Manual of Critical Care Nursing 7th Edition
Manual of Critical Care Nursing 7th Edition
Critical Care
Nursing
Nursing Interventions and
Collaborative Management
SEVENTH EDITION
2
3
Table of Contents
Cover image
Title page
Copyright
Contributors
Preface
Hemodynamic monitoring
Mechanical ventilation
Nutrition support
Pain
Prolonged immobility
4
Sedation and neuromuscular blockade
Selected references
Emerging infections
Patient safety
Selected references
3. Trauma
Major trauma
Abdominal trauma
Burns
Drowning
Pelvic fractures
Thoracic trauma
Selected references
5
4. Respiratory disorders
Respiratory assessment: General
Acute pneumonia
Pneumothorax
Pulmonary embolism
Pulmonary hypertension
Selected references
Heart failure
Acute pericarditis
Aortic aneurysm/dissection
Cardiogenic shock
Cardiomyopathy
Hypertensive emergencies
6
Selected references
6. Kidney injury
Genitourinary assessment: General
Selected references
7. Neurologic disorders
General neurologic assessment
Brain death
Meningitis
Status epilepticus
Selected references
8. Endocrinologic disorders
Endocrine assessment
Diabetes insipidus
Hyperglycemia
Myxedema coma
7
Syndrome of inappropriate antidiuretic hormone
Selected references
9. Gastrointestinal disorders
Gastrointestinal assessment: General
Acute pancreatitis
Enterocutaneous fistula
Hepatic failure
Peritonitis
Selected references
Anaphylactic shock
Selected references
Drug overdose
Stimulants
8
Oncologic emergencies
Organ transplantation
Selected references
Index
Ibc
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Copyright
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Notices
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11
NANDA International, Inc. Nursing Diagnoses: Definitions &
Classifications 2015-2017, Tenth Edition. Edited by T. Heather
Herdman and Shigemi Kamitsuru. 2014 NANDA International, Inc.
Published 2014 by John Wiley & Sons, Ltd. Companion website:
www.wiley.com/go/nursingdiagnoses.
12
Contributors
Patrice C. Al-Saden, BS, RN, CCRC, Senior Clinical Research
Associate, Comprehensive Transplant Center, Feinberg School of
Medicine, Chicago, Illinois
13
Madalina Boitor, BScN, RN, PhD Student, Ingram School of
Nursing, McGill University, Montreal, Canada
14
Beverly George Gay, MSN, RN, Assistant Professor, Department
of Nurse Anesthesia, School of Allied Health Professions, Virginia
Commonwealth University, Richmond, Virginia
15
Kiersten Henry, MSN, ACNP-BC, CCNS, CCRN-CMC, Acute
Care Nurse Practitioner, Chief Advanced Practice Provider,
MedStar Montgomery Medical Center, Olney, Maryland
16
Alice S. Kerber, MN, APRN, ACNS-BC, AOCN, APNG, Clinical
Nurse Specialist, Oncology, Advanced Practice Nurse in Genetics,
Georgia Center for Oncology Research and, Education (Georgia
CORE), Atlanta, Georgia
17
Clinical Practice Consultant, Clinical Effectiveness Team, Kaiser
Permanente Northern California, Regional Quality and Regulatory
Services, Oakland, California
Critical Care Transport RN, Bayshore Ambulance, Foster City,
California
18
Clinical Assistant Professor, Stony Brook University, Stony Brook,
New York
Reviewers
Bimbola Fola Akintade, PhD, ACNP-BC, MBA, MHA, Co-
Specialty Director and Assistant Professor, Adult Gerontological
Acute Care Nurse, Practitioner/Clinical Nurse Specialist, Program,
University of Maryland Baltimore, School of Nursing, Baltimore,
Maryland
19
Diane Dressler, MSN, RN, CCRN, Clinical Assistant Professor,
Marquette University College of Nursing, Milwaukee, WI
20
Julene B. Kruithof, MSN, RN, CCRN, Nurse Educator, Spectrum
Health, Grand Rapids, Michigan
Fadi B. Nahab, MD
Associate Professor, Department of Necrology and Pediatrics,
Emory University
Medical Director, Stroke Program, Emory University Hospitals,
Atlanta, Georgia
21
Tara L. Sacco, MS, RN, CCRN, ACNS-BC, ACCNS-AG, Visiting
Assistant Professor, St. John Fisher College Wegmans School of,
Nursing, Rochester, New York
22
Preface
Manual of Critical Care Nursing is a clinical reference for both
practicing nurses and students in critical care, progressive care, and
complex medical-surgical units. It is the most comprehensive of the
critical care handbooks available, yet is a concise and easy reference
with an abbreviated outline format and a portable, trim size. This
handbook provides quick information for more than 75 clinical
phenomena seen in critical care and other high acuity care
environments, which promotes evidence-based practice in planning
goal-driven care.
23
collaboration. Both a collaborative plan of care, and specific nursing
care plans are presented. Given the increasing acuity of
hospitalized patients, problems previously managed in critical care
such as using arterial blood gas interpretation to correct acid-base
imbalances, medically managing dysrhythmias with medication
infusions, or controlling blood pressure with vasoactive drugs can
be part of daily care of patients in progressive care units, telemetry,
stepdown units, and high-acuity medical-surgical units.
Accordingly, the care plans presented are applicable across the
spectrum of high-acuity care, from complex medical-surgical to
critical care. The book addresses the highly technical life-support
equipment as part of the care options for each condition, and in
detail for those who are actively using the technology in separate,
detailed sections.
24
Each body system–specific chapter includes a general physical
assessment, and several chapters include generic plans of care
applicable to patients with all disease processes affecting that body
system. Each disorder includes a brief review of pathophysiology,
physical assessment, diagnostic testing, collaborative management,
NANDA-approved nursing diagnoses and nursing interventions,
patient/significant other teaching, desired outcomes, and disease-
specific discharge planning considerations. Gerontologic icons
highlight material relevant to the care of older adults, bariatric icons
have been added for care specific to people of size, and safety alerts
highlight key information needed to prevent complications. Desired
nursing care outcomes and interventions are based on the
University of Iowa’s Nursing Intervention Classification (NIC) and
Nursing Outcomes Classification (NOC) systems and are
highlighted throughout the text. Nursing interventions are linked to
nursing diagnoses, and suggested outcomes include specific
measurement criteria for physical parameters and time frames for
attainment of expected outcomes. The suggested time frames for
outcomes achievement are guidelines. Each patient’s response to
the illness and interventions is unique.
For clarity and consistency throughout the book, normal values
are given for hemodynamic monitoring and other measurements.
All values should be individualized to each patient’s baseline
health status.
25
• Information to help assess and plan care for bariatric patients.
Acknowledgments
I want to thank many individuals who supported the development
of this manuscript. In particular, I am grateful for the time and
efforts of the Elsevier Science staff, including Melissa Rawe,
Content Development Specialist, and Marquita Parker, Senior
Project Manager, Book Production. I appreciate the guidance of Lee
Henderson, Executive Content Strategist. I thank all the
contributors for their work, as well as all the reviewers whose
comments helped guide our revisions. All are recognized as shining
stars in their own right. Both perseverance and patience are the
fundamental characteristics inherent in all participants.
Marianne Saunorus Baird
I acknowledge the support of my daughter Rachel, my best
cheerleader, and my husband Thom for his patience. I also cannot
thank the authors enough for your attention to detail; particularly
all the new authors who “filled the gaps” from Emory Healthcare,
Atlanta, Georgia. I would also like to acknowledge Savannah Davis,
who helped the team begin our process with Elsevier Science.
MSB
26
CHAPTER 1
General concepts in
caring for the
critically ill
Acid-base imbalances
Cells must transport ions, metabolites, and gases to function
appropriately in their respective roles in the body. For this to occur,
the chemical environment of the bloodstream must be electrically
stable. The stability of the environment is measured by the arterial
pH and must be chemically neutral (pH 7.40) for all systems to
function properly. The arterial blood gas (ABG) is the most
commonly used analysis to measure acid-base balance and to assess
the efficacy of oxygenation. Respiratory (CO2) and metabolic acids
(H+) are generated as cells work and must be buffered or eliminated
to maintain a neutral chemical environment. When the chemical
environment is no longer neutral, the patient has an acid-base
imbalance. Ineffective metabolism (tissue level), renal dysfunction,
and/or problems with ventilation (breathing gasses effectively) are
often the cause of acid-base imbalance.
There are two main types of acid-base imbalance: acidosis and
alkalosis. The kidneys and lungs work in tandem to maintain
chemical neutrality, but it is actually cellular function that produces
acid. When either the kidneys or lungs are overfunctioning or
underfunctioning, the other system is designed to have the opposite
response to compensate and bring the pH back to a normal range.
27
When the kidneys fail to regulate metabolic acids (H+), the lungs
must compensate. When the lungs fail to regulate respiratory acid
(CO2), the kidneys must compensate. Additional buffering
mechanisms are also available to help regulate the accumulation of
acids. Control of alkaline states, resulting from accumulation of
bases or loss of acids, is maintained in a similar manner between
the lungs and kidneys.
28
processing proteins to yield glucose, there is an
increase in lactic acid or ketoacid.
29
3. Acid excretion (kidneys): A functional kidney
will use increased carbonic acid by breaking
H2CO3 into bicarbonate and H+, excreting H+ and
retaining bicarbonate. This should compensate
for the increased respiratory acidosis but is very
slow, taking 4 to 48 hours for compensation to
occur.
• Alkalosis: Extra base is present or there is loss of acid, with a pH
greater than 7.45.
30
alkalosis from any cause. This response occurs
within minutes.
31
patient will remain in acid-base imbalance. If the pH is outside the
normal range, then there is a primary problem and compensation is
inadequate or has failed. Patients may have a pure acidosis or
alkalosis and the overall problem may be masked by compensation
or two problems presenting at the same time.
Unless the patient has ingested acid (aspirin, ethanol, etc.), all
acid in the bloodstream has been produced at the cellular level
(Table 1-1). When evaluating patients, care providers must have a
basic understanding of the acid-base balancing system. The main
formula for maintenance of acid-base balance is:
Table 1-1
PRODUCERS AND REGULATORS OF ACID
Acid
Cause Measure
Pathways
Cells Hypermetabolic states, such as pain, hyperthermia, or HCO3−
produce inflammation. The respiratory and heart rates
acid (acid increase, and bicarbonate is initially consumed by
production buffering.
increases). Tissues are hypoxic; anaerobic metabolism ensues Lactate level ↑
resulting in lactic acidosis.
Absolute insulin deficiency results in failure of Blood glucose level ↑
glucose to be transported into cells. Ketoacids ↑
Cells When acid production (H+) increases, pH decreases, pH ↓
regulate bicarbonate is initially consumed by buffering, and HCO3↓
acids. CO2 is exhaled in larger amounts, and H+ exchanges K+↑
for K+ as cells buffer acid. Total serum CO2↓
Lungs When acid increases as a result of hypermetabolic Paco2↓
regulate states such as pain, hyperthermia, or inflammation,
acid. carbonic acid (H2CO3) increases and rapidly converts
to CO2 and H2O. The respiratory rate increases to
blow off CO2.
Kidneys When acid increases, tubules are affected by low HCO3↑
regulate blood pH, and work to neutralize increased carbonic Kidney function is
acid. acid (H2CO3) by separating it into H+ and bicarbonate assessed by serum blood
HCO3. Kidneys excrete what is necessary to sustain urea nitrogen and
normal pH if renal function is normal. If abnormal, creatinine; elevated
kidneys may not perform this task. blood urea nitrogen and
creatinine indicate
abnormal kidney
function.
32
The most important component identified is H2CO3 or carbonic
acid. As carbonic acid increases (“goes up”), the pH decreases
(“goes down”), reflecting the presence of acid. If carbonic acid
decreases (“goes down”), the pH increases (“goes up”), reflecting
the absence of acid. The equation is constantly shifting from left to
right and right to left to maintain a normal H2CO3 and therefore a
normal pH. Whatever causes the change of carbonic acid
concentration (may be related to a regulation failure by either the
lungs or kidneys or a metabolic acid production state) is the
“primary culprit.” Identifying the origin or cause of the change in
pH direction identifies the problem. Therefore, if the problem is too
much acid (either increased CO2 or H+), carbonic acid increases and
pH decreases. The primary problem is acidosis. Further evaluation
is needed to determine whether failure to regulate the acid was
ineffective regulation by the lungs, the kidneys, or an increase in
cellular acid production (ketoacidosis or lactic acidosis).
pH (perfect 7.40, normal range 7.35 to 7.45): This reflects the level
of respiratory and metabolic acids found in the blood during the
continuous “balancing act” that regulates the acid environment. If
this balance is altered, derangements in pH occur. Any alteration in
pH should be evaluated. If the pH has changed from perfect, it can
only be one of two reasons: normal variation or abnormality with
compensation. When pH is less than 7.35 or greater than 7.45, it is
considered an acute change that is uncompensated. When full
compensation is attained for an acid-base imbalance, the pH
normalizes. Failure to bring the pH into normal range means there
is failure to compensate, despite the body attempting to mount a
response. Traditionally, if the body made an attempt to
compensate, this was known as partial compensation. This term is
no longer advocated.
PaCO2 (perfect 40, normal range 35 to 45 mm Hg): This is a
measure of pressure (partial pressure designated by the P) that the
dissolved CO2 exerts in the arterial blood. The dissolved gas exerts
34
the pressure of CO2, enabling it to diffuse across the capillary and
alveolar cell wall.
CO2 is released during aerobic metabolism and is the main
contributor to serum acid. CO2 is controlled through ventilation. In
the normal lung, CO2 is regulated by changes in the rate and depth
of alveolar ventilation. CO2 is carried both bound to hemoglobin
and dissolved in the blood. The measured CO2 is termed PaCO2.
PaCO2 is directly measured (not calculated) and is a reliable
indicator of respiratory acid-base regulation. The correlation
between PaCO2 and respiratory-based pH changes is direct,
consistent, and linear. In other words, if PaCO2 is up and pH is
down, the cause is respiratory deregulation. If the issue is
metabolic, and respiratory compensation has occurred, the PaCO2
will decrease to bring pH back to normal levels. Respiratory
compensation typically occurs rapidly in metabolic acid-base
disturbances as long as respiratory function is not impaired. When
a patient hyperventilates, PaCO2 decreases as it is “blown off” by
rapid exhalations. During hypoventilation (slow and/or shallow
breathing), PaCO2 increases. Although the only way to evaluate true
lung function is by the gas exchange, the capacity of the lungs (CO2
regulation response) is measured via the minute ventilation (VE or
MV). This measures the amount of volume exhaled per minute (VE)
calculated as respiratory rate (RR) multiplied by tidal volume (VT).
Normal MV is approximately 8 to 10 L/min.
PaO2 (perfect 95 to 100 mm Hg, normal range 80 to 100 mm Hg):
The partial pressure of oxygen (O2), or PaO2, is a measure of the
dissolved (usable) gas in the arteries. The dissolved gas exerts the
pressure of O2, enabling it to diffuse across the capillary and cell
wall to oxygenate cells. PaO2 normally declines in the older adult.
35
• FIO2: Fraction of inspired O2 or the percentage of the atmospheric
pressure that is oxygenated. Room air is 21% or 0.21 O2. O2
delivery devices can increase the FIO2 to 100% or 1.00.
36
oximetry is initiated, to assess accuracy of SpO2 readings. Pulse
oximetry is a close correlate to SaO2 under normal physiologic
conditions, but if perfusion decreases, the pulse needed for
accurate measurement by the SpO2 probe is decreased, prompting
inaccurate readings. Patients with anemia should have
consistently high readings, thus what is usually considered a
normal SpO2 reading may be too low in a patient with anemia.
The measure of true oxyhemoglobin (Hgb saturated with O2)
requires an ABG analysis. Many centers do not perform a
correlation analysis when oximetry is initiated.
37
significant contribution to buffering acids. Hgb not
only transports O2 but also provides a very strong
buffer for hydrogen ions (H+). Albumin is also a
significant buffer, and hypoalbuminemia must be
considered when performing anion gap
calculations.
38
CO2” rather than as bicarbonate (HCO3−). The
serum HCO3− concentration is usually calculated
and reported separately with ABG analysis. Either
value may be used as part of the assessment of acid-
base balance (Table 1-2).
39
the blood.
Table 1-2
DIAGNOSTIC TESTS FOR ACID-BASE BALANCE
40
Role of ABG Measures Normals
Evaluation of arterial oxygen Arterial oxygen saturation Sao2: 0.95 to 1.0 or 95%
(dissolved oxygen and oxygen (oxygen bound to hemoglobin) to 100%
bound to hemoglobin)
Partial pressure of arterial Pao2: 80 to 100 mm Hg
oxygen (dissolved oxygen) (decreased over the age
of 70 years)
Calculation of alveolar-arterial (A- Alveolar-arterial gradient A-a Do2: <20 mm Hg
a) oxygen gradient Pao2/Fio2 ratio PF ratio: 300
Evaluation of cellular environment pH (reflects H2CO3) i.e., ↑ H2CO3 pH
then pH ↓ Perfect: 7.40
Normal range: 7.35 to
7.45
Evaluation of ventilation Paco2 Paco2 Normal range: 35
to 45 mm Hg
Evaluation of tissue metabolism H+ inversely (indirectly) pH
reflected by buffers: Perfect: 7.40
bicarbonate (HCO3−) Total Normal range: 7.35 to
CO2 7.45
−
+
i.e., ↑ H then buffers ↑ HCO 3 : 22 to 26 mEq/L
Total CO2: 20 to 26
Base
Normal range: −2 to +2
Anion gap: 12 ±2
Additional measures of tissue Both contribute H+ to blood Lactic acid: 1 to 2
metabolism Lactic acid mmol/L
Ketoacids Lactic acid: 1 to 2
mmol/L
Ketoacids
Blood: 0.27 to 0.5
mmol/L
Urine levels
Small: ≤20 mg/dL
Moderate: 30 to 40
mg/dL
Large: >50 mg/dL
Evaluation of renal clearance Appropriate clearance of pH
excessive components: Perfect: 7.40
H+ or (HCO3−) Range: 7.35 to 7.45
Appropriate clearance of BUN: 0 to 20 mg/dL
excessive components: BUN Creatinine: <2.0 mEq/L
and creatinine
ABG, Arterial blood gas; BUN, blood urea nitrogen.
41
When there is a perfect balance of acid and buffer (base), the pH is
termed neutral or perfect. If it is not perfect, determine if the
direction of the difference is above or below 7.40. Next, determine if
it is in the normal range (7.35 to 7.45). If it is abnormal, identify
whether it is on the acidotic (less than 7.35) or alkalotic (greater
than 7.45) side of normal. “Perfect pH” occurs when the system
preserves neutrality (pH 6.8) inside the cells, where most chemistry
occurs, and maintains the serum pH at 7.40. For the purposes of
learning, the perfect pH is where all measurement begins. When the
system contains too many acid ions (in the form of ↑CO2 or ↑H+),
this causes acidemia. When the system contains too few acid ions
(in the form of ↓CO2 or ↓H+), this causes alkalemia, and the pH will
reflect the change. Any variation in the pH in relationship to perfect
(7.40) must be noted by the provider. If the pH is in the range of
7.35 to 7.45, there are only two possibilities. First, the deviation is a
normal variation, wherein no abnormalities exist on either the
respiratory side (PaCO2) or the metabolic side (HCO3−) of the pH
equation. Second, there is a problem with ventilation (respiratory),
cellular acid production (metabolic), or the ability of the kidneys
(metabolic) to balance the pH. Diagnosis of a problem with
metabolic acid-base balance is more complex, because many
conditions generate metabolic acids and renal failure creates an acid
clearance deficit.
pH less than 7.35, Acidosis: Extra acids are present or base is lost.
If pH is 7.35 to 7.39, the pH is normal but not perfect (7.40); the pH
is considered “on the acidotic side.”
42
effectively ventilate results in the inability to
exhale CO2, and that failure causes carbonic acid
to increase (more acid) and pH to decrease.
43
removes acidic secretions and influences the acid-
base balance.
44
PaCO2) or metabolic (reflected by HCO3−), or both.
Respiratory acidosis
Pathophysiology
45
changes are a symptom of a problem. Thus, the first issue is to
identify the problem.
pH: The primary problem with pH regulation is identified by the
direction of the pH change with regard to perfect: Is it on the acid
side (less than 7.40) or the alkaline side (greater than 7.40)?
Investigation begins
46
side).
Investigation begins
47
2. Problem: No apparent kidney or metabolic problems.
48
respond to the first device change or values further deteriorate, a
100% nonrebreather mask may be applied to provide close to 100%
O2. Note: All ABG readings must be recorded with consideration of
the mode of O2 delivery recorded, as well as the FIO2 or
concentration of O2. Otherwise, evaluation of the PaO2 and SaO2
values is meaningless. If the values are NOT recorded, the
assumption is made that the readings are done on room air, without
O2 in place.
49
expansion, particularly if the patient was recently admitted for
trauma, has recently had central line placement, or has recently
been intubated or extubated. A pneumothorax may be present,
which may cause ineffective ventilation.
2. Normalize the pH
50
slow (4 to 48 hours), they are able to facilitate a nearly normal pH
level by excreting or retaining large quantities of HCO3− or H+
from the body. Note that the level of available HCO3− is always
opposite the level of H+ present in the plasma. HCO3 is partnered
as it buffers H+ which yields carbonic acid.
51
Over time, if ventilation is not effectively managed, the HCO3− will
increase to 32, which will correct the pH to 7.35 if kidneys are
functioning normally. The CO2 remains 55. O2 provided at 4 L/min
by nasal cannula increases the PaO2 to 100% and the SaO2 to 100%.
With the same PaCO2, the pH is corrected, primarily by the
kidneys, to 7.35: on the acid side of the normal range. Whenever the
pH is less than 7.40, it reflects either a normal variation OR
abnormality with compensation.
52
hemothorax, Pickwickian syndrome), neuromuscular abnormalities
(e.g., myasthenia gravis, Guillain-Barré syndrome, amyotrophic
lateral sclerosis), respiratory center depression (e.g., brain tumor,
stroke, bleed, head injury), and poor ventilation management. In
patients with a chronic lung disease, a near-normal pH is the result
of kidney compensatory mechanisms, as discussed earlier.
Patients with chronic lung disease can experience acute increases
in PaCO2 or lose their metabolic compensation (increased
production of metabolic acid or loss of renal function) secondary to
superimposed disease states, such as pneumonia, hypermetabolic
cellular hypoxia, or renal dysfunction. If the chronic compensatory
mechanisms in place (e.g., elevated) are inadequate to meet the
sudden increase in PaCO2 or if the circulation of metabolic acids
increases, pH may change rapidly. In fact, these patients frequently
have normal HCO3− measures upward of 30. As an acute (on top of
chronic) process begins, the pH decreases, but the bicarbonate may
be slower to reflect the real problem. Care must be taken when
evaluating patients with chronic respiratory acidosis who have
secondary issues.
Clinical presentation
Patients may have possible increased work of breathing, anxiety,
pallor, sweating, reflective of respiratory distress. In advanced
respiratory acidosis, somnolence and inability to awaken the
patient are common. CO2-based acidosis has a sedative-like effect
on patients. Sleep may ensue following distress, giving the false
impression that the problem has resolved, when in reality, the
problem has resulted in sufficient CO2 accumulation for the patient
to lose consciousness from the sedative effect of severe
hypercapnia. Patients with obstructive sleep apnea are at risk for
developing respiratory acidosis.
Physical assessment
Patients have decreased depth of respirations with an initially
increased rate or decreased rate and depth of respirations in severe
respiratory acidosis. With obstructive lung disease or acute asthma
exacerbation, audible wheezing may be present. With severe
53
asthma, the chest can become silent, indicative gas exchange is
extremely impaired, and the patient is close to respiratory arrest.
Monitoring parameters
Use pulse oximetry to assess if hypoxemia ensues because of
ineffective ventilation. The patient needs close observation for
deterioration, so appropriate steps can be taken to provide
noninvasive positive-pressure ventilation (NPPV), such as bilevel
positive airway pressure (BiPAP) or endotracheal (ET) intubation
with mechanical ventilation.
Respiratory monitoring
54
breath sounds. Compare findings before and after (e.g., O2 therapy,
physiotherapy, medications) for improvement.
Oxygen therapy
Ventilation assistance
55
fluid occupation of lung or pleural space (e.g., hemothorax, pleural
effusion, and hyperplasia).
Respiratory alkalosis
Pathophysiology
The problem is alveolar hyperventilation, which results in an
increased pH.
Example: pH 7.48, PaCO2 30, HCO3 23.
56
This signals alveolar hyperventilation (decreased respiratory acid
causing an alkaline pH). When minute ventilation is increased, CO2
decreases, which causes H2CO3 to also decrease (production of
carbonic acid decreases) and the pH becomes alkalotic. Question: Is
there a problem? The CO2 has decreased and the pH has increased.
The problem is respiratory alkalosis.
Step 3: The HCO3− is 23, which is less than perfect but still
in the normal range
It must be determined if there is a metabolic contribution to the
alkalosis or if there is compensation provided by the kidney
retaining acid and excreting bicarbonate. The BE is –1, within the
normal range.
57
and asystole.
In the alkalotic environment, cells release H+ and K+. The result is
frequently serum hypokalemia (low serum K+ with intracellular
hyperkalemia). Kidney compensation for the respiratory alkalosis is
not clinically apparent for 4 to 48 hours. Acute respiratory alkalosis
progresses to chronic respiratory alkalosis if it persists for longer
than 6 hours and/or renal compensation occurs.
58
retention by the opposing system.
In alkalotic environments
Clinical presentation
Presentation includes lightheadedness, anxiety, paresthesias
(especially of the fingers), and circumoral numbness. In extreme
alkalosis, confusion, tetany, syncope, and seizures may occur.
59
Physical assessment
Increased rate and depth of respirations (hyperventilation) are
present.
Monitoring parameters
Cardiac dysrhythmias are present.
Ventilation assistance
60
3. Manage fatigue: Provide uninterrupted rest after the breathing
pattern has stabilized. Hyperventilation can result in fatigue.
Metabolic acidosis
Pathophysiology
Accumulation of metabolic acids, reflected by decreased HCO3−
(less than 22 mEq/L) with a pH decreased below 7.40. Metabolic
acids are circulating acids that cannot be exhaled. These acids
should be neutralized by buffers, excreted by the kidneys, or
metabolized.
Example: pH 7.28, PaCO2 39, HCO3− 16, PaO2 98 mm Hg, SaO2 99%.
61
because the role of bicarbonate is to buffer H+. The conjugation of
H+ and HCO3− yields an increase in carbonic acid. As carbonic
acid (H2CO3) increases, the pH decreases.
62
ketosis).
Step 5: The PaO2 and SaO2 are normal because the patient
is breathing normally
The patient has normal oxygenation.
63
compensatory response for respiratory alkalosis.
64
therapy. When cells are in a shock state, O2 delivery shock is
present. Shock effects the mechanics of delivery, whereas systemic
inflammatory response or severe sepsis, with the secondary effects
of endothelial dysfunction, vasodilation, inflammatory mediation,
and unopposed procoagulation, interfere with the use of O2 at a
microcirculatory and cellular level. Large areas of the capillary beds
may be hypoperfused, resulting in cells resorting to anaerobic
metabolism to survive.
Anaerobic metabolism results in the production of lactic acid, a
metabolic acid that can create acidosis if compensation fails. The
ABG reflects a decreased pH but does NOT always reflect a
markedly decreased PaO2 and SaO2. Persistent tissue-level hypoxia
further exacerbates the systemic inflammatory response and may
lead to multi-organ dysfunction syndrome (MODS) and eventually
death.
Arterial lactate concentration is dependent on the balance
between its production and consumption. In the critically ill septic
population, increased glucose metabolism, increased energy
expenditures, and profound catabolism are the norm. The
corresponding lactic acidosis signals physiologic stress but may not
necessarily be evidence of tissue hypoxia. The concomitant energy
expenditures, along with metabolic dysfunction, will increase
lactate production, but high levels of clearance may mask this
disturbing trend.
These conditions, coupled with an out-of-control inflammatory
response and increasing oxygenation dysfunction at the tissue level,
combine to produce a profound tissue acidosis. The lactate
production is further increased via other abnormal pathways that
are specifically related to metabolic dysfunction, even in the
absence of tissue hypoxia (type B lactic acidosis).
The main cause of the significantly increased lactate is still a
puzzle. One factor is the failure of adenosine triphosphate (ATP)
production, which clearly occurs in the presence of a profound O2
supply/demand imbalance (type A lactic acidosis). This in turn
affects the mitochondrial ability to use pyruvate, and the increased
pyruvate is indicative of a profound metabolic hyperlactatemia, an
elevated lactate/pyruvate ratio, increased glucose, and low energy
production. Ultimately, as severe sepsis progresses, it evolves into a
65
mediator-induced cardiac failure state, with profound intraarterial
hypovolemia.
1. Lactate level: All patients who run the risk of cellular hypoxia
must have a sample drawn for a lactate level to evaluate for lactic
acidosis. An arterial lactate sample should be placed on ice and
taken as soon as possible to the laboratory. Any lactate greater than
4 mmol/L needs to be investigated for severe tissue hypoxia and
hypoperfusion. Lactates greater than 2 mmol/L should be observed
along with the clinical conditions of the patient. Serial lactates
should be performed to evaluate therapy effectiveness and follow
the clearance level. A lactate clearance greater than 10% in 24 hours
is considered a successful measure of therapeutic intervention for
severe sepsis.
66
themselves will not give as much beneficial
information as those in the presence of wide
anion gap and low or normal ScVO2.
67
tip of a catheter placed in the central vein (CV catheter) or PA
(PA catheter). Measurement may provide an early indication of
perfusion failure or increased tissue demands for O2, reflected by
a decreased mixed venous saturation of Hgb. If this saturation is
normal or high, but the patient has an increased lactate level, the
cells may be unable to extract or use O2, which frequently occurs
in the later stages of severe sepsis.
68
line is to release O2 from Hgb to provide more dissolved O2 at the
cell level, resulting in a shift to the right in the dissociation curve
(Figure 1-1).
69
elevated. If H+ is elevated, resulting in increased carbonic acid, and
the pH is decreased even slightly, the problem is acid accumulation.
In this case, it is acute metabolic acidosis, without compensation.
70
2. Compensated metabolic acidosis: pH 7.36, PaCO2 30, HCO3− 16,
SaO2 99%, PaO2 100%.
Step 2: PaCO2 30 mm Hg
Level is decreased, which should reflect toward the alkaline side,
which does not coincide with the direction of the pH change.
Step 5: The PaO2 and SaO2 are normal because the patient
is breathing normally
The patient has normal oxygenation.
71
Collaborative management: Acute metabolic
acidosis
Care priorities
72
thorough discussion was provided earlier in this chapter. The gap is
not affected when a patient has metabolic acidosis purely from
kidney failure. The formula for calculation of anion gap (AG) is:
3. Treat the pH
Treat the pH only if the patient’s life is threatened. Sodium
bicarbonate (NaHCO3) may be indicated when arterial pH is ≤7.15.
The usual mode of delivery is IV drip: 2 or 3 ampules (44.5
mEq/ampule) in 1000 mL D5W, although NaHCO3 may be given by
IV push in emergencies. Deficit should be calculated and replaced
accordingly. Concentration depends on severity of the acidosis and
presence of any serum sodium disorders. NaHCO3 must be given
very cautiously to avoid metabolic alkalosis and pulmonary edema
as a result of the sodium load. Dose (mmol) = BE × weight/10 to
replace half of the loss. Usual dose for full replacement is 1
mmol/kg IV (repeated as required).
4. Manage hyperkalemia
Usually serum hyperkalemia is present, but an intracellular
potassium deficit may be present. If a potassium deficit exists (K+
less than 3.5), it must be corrected before NaHCO3 is administered,
because when the acidosis is corrected, the potassium shifts back to
intracellular spaces. This shift in K+ could result in a profound
serum hypokalemia with serious consequences, such as cardiac
irritability with fatal dysrhythmias and generalized muscle
weakness. See Hypokalemia for more information.
5. Support ventilation
If mechanical ventilation is required on the basis of ABG results and
clinical signs, it is important that the patient’s compensatory
hyperventilation be allowed to continue to prevent acidosis from
becoming more severe. Therefore, the respiratory rate on the
ventilator should not be set lower than the rate at which the patient
has been breathing spontaneously, and the tidal volume should be
73
large enough to maintain compensatory hyperventilation until the
underlying disorder can be resolved.
Clinical presentation
Usually the process leading to chronic metabolic acidosis is gradual
and the patient is symptom-free until serum HCO3− is ≤15 mEq/L.
Fatigue, malaise, and anorexia may be present in relation to the
underlying disease. Findings vary, depending on underlying
disease states and the severity of the acid-base disturbance and the
speed with which it developed. There may be changes in LOC that
range from fatigue and confusion to stupor and coma.
Physical assessment
Tachycardia (until pH is less than 7.0, then bradycardia), decreased
BP, tachypnea leading to alveolar hyperventilation (may be
Kussmaul respirations), dysrhythmias, and shock state. Depending
on the type of shock and the vascular response, skin temperature
and color will be affected. Mild metabolic acidosis (HCO3− 15 to 18
mEq/L) may result in no symptoms, whereas symptoms will
74
develop with a pH less than 7.2.
Monitoring parameters
A waveform suggestive of hyperkalemia (prolonged PR interval,
widened QRS, and peaked T waves) may occur. Persistent
tachycardia may indicate tissue hypoperfusion.
Electrocardiography (ECG): Detects dysrhythmias, which may
be caused by metabolic acidosis or hyperkalemia. Changes seen
with hyperkalemia include peaked T waves, depressed ST segment,
decreased size of R waves, decreased or absent P waves, and
widened QRS complex. Ventricular fibrillation may occur.
• For serum HCO3− levels less than 15 mEq/L, oral alkalis may be
administered (NaHCO3 tablets or sodium citrate and citric acid
oral solution [Shohl solution]). They are used cautiously to
prevent fluid overload and tetany caused by hypocalcemia.
75
(CRRT), or peritoneal dialysis may be indicated for chronic renal
failure or other disease processes (see Acute Renal Failure,
Chapter 6).
Metabolic alkalosis
Pathophysiology
Elevated HCO3− levels (greater than 26 mEq/L) reflect decreasing
circulating metabolic acids (H+). Caution must be applied to
differentiate compensatory alterations in response to respiratory
acidosis versus primary disorder. The diagnosis is made by the
presence of elevated serum HCO3− (up to 45 to 50 mEq/L). Acute
metabolic alkalosis most commonly reflects:
Even when the causative factors have been removed, the alkalosis
will be sustained until volume and electrolyte disturbances that are
contributing to the alkalosis have been corrected. Severe alkalosis
(pH greater than 7.6) is associated with high morbidity and
mortality. Acidosis is better tolerated than alkalosis. SpO2 will be
used for Step 5, because a discussion of PaO2 and SaO2 does not add
to knowledge of metabolic alkalosis.
76
Example: pH 7.58, PaCO2 40 mm Hg, HCO3− 35, SaO2 99%, PaO2 99
mm Hg.
Step 5: The PaO2 and SaO2 are normal because the patient
is breathing normally
The patient has a normal oxygenation, but has an abnormal
response to alkalosis. The respiratory rate and depth should
decrease to promote CO2 retention to compensate.
77
When H+ (acid) decreases, pH increases. The central respiratory
center in the brain responds by decreasing the rate and depth of
ventilation (in the normal lung) to 50% to 75% of the normal level.
This method of compensation is very poorly tolerated, because
patients will almost stop breathing.
Uncompensated metabolic alkalosis: pH 7.58, PaCO2 40 mm Hg,
HCO3− 35.
Step 2: PaCO2 59 mm Hg
Increased level, which reflects toward the acid side; change is
opposite the pH, which is toward the alkaline side. The PaCO2 is not
the problem but rather a compensation. The increased PaCO2 would
not increase the pH to alkaline. This measure is in the wrong
direction to be the cause.
78
decreased.
Care priorities
2. Correct hypokalemia
Potassium chloride (KCl) is indicated for patients with low
potassium levels. KCl is preferred over other potassium salts
because chloride losses can be replaced simultaneously.
79
renal excretion of excess HCO3− is impaired and metabolic alkalosis
continues.
80
ventilation.
Clinical presentation
Muscular weakness, neuromuscular instability, and hyporeflexia
because of accompanying hypokalemia are present. Decrease in GI
tract motility may result in an ileus. Severe alkalosis can result in
apathy, confusion, and stupor. Seizures may occur.
Physical assessment
Decreased respiratory rate and depth, periods of apnea, and
tachycardia (atrial or ventricular) are present.
Monitoring parameters
Atrial and ventricular dysrhythmias as a result of cardiac irritability
secondary to hypokalemia; prolonged QT intervals are present (see
Hypokalemia).
• Urinalysis: Urine chloride levels can help identify the cause of the
metabolic alkalosis. Urine chloride level will be less than 15
mEq/L if hypovolemia and hypochloremia are present, and
greater than 20 mEq/L with excess retained HCO3−. This test is
not reliable if diuretics have been used within the previous 12
81
hours.
Care priorities
1. Fluid management
If volume depletion exists, normal saline infusions are given.
2. Potassium replacement
If a chloride deficit is also present, KCl is the drug of choice. If a
chloride deficit does not exist, other potassium salts are acceptable.
3. Dietary
The normal diet contains 3 g or 75 mEq potassium but not in the
form of KCl. Dietary supplementation of potassium is not effective
if a concurrent chloride deficit is also present.
4. Potassium-sparing diuretics
82
These may be added to treatment if thiazide diuretics are the cause
of hypokalemia and metabolic alkalosis.
Clinical presentation
The patient may be symptom-free. With severe potassium depletion
and profound alkalosis, the patient may experience weakness,
neuromuscular instability, and a decrease in GI tract motility,
which can result in ileus.
Physical assessment
Decreased respiratory rate and depth, and tachycardia (atrial or
ventricular) are present.
Monitoring parameters
Frequent premature ventricular contractions (PVCs) or U waves with
hypokalemia and alkalosis are present.
83
tissue resulting from perfusion defects (ischemia), brain injury, and
tumors. Mental status change also occurs as a result of systemic
problems, including infection, metabolic, or endocrine problems. A
change in mental status is also associated with dementia, delirium,
coma, encephalopathy, and psychiatric disorders. Mental status
change may be as subtle as a variation in behavior or as profound
as loss of consciousness. Whatever the cause, confusion, memory
loss, change in alertness, disorientation, lack of judgment or insight,
emotional dysregulation, anxiety, agitation, restlessness, and
change in psychomotor skills or behavior are critical clues to a
changing condition.
Factors precipitating various alterations in consciousness or
mental status are listed in Table 1-3. These precipitating factors
arise from intrinsic causes (medical condition and associated
problems) and extrinsic causes (environmentally produced).
Impaired consciousness or change in mental status, regardless of
etiology, results in higher complication rates, puts the patient’s
safety at risk, causes longer hospital stays, and is linked to higher
morbidity and mortality. Three states of mental status change or
impaired consciousness, coma, delirium, and cognitive dysfunction,
can be recognized in emergency department and hospitalized
patients. Although each of these conditions may arise from distinct
medical problems, the clinical features are often similar and may be
superimposed on each other, making diagnosis and treatment more
complex. Change in mental status or change in behavior are often
the early warning signs of a medical emergency. The differential
diagnosis is crucial to the proper treatment of these mental status
changes. The following are descriptions of common mental status
variants that require further evaluation.
Table 1-3
FACTORS PRECIPITATING ALTERATIONS IN CONSCIOUSNESS
OR CHANGE IN MENTAL STATUS
84
CNS, Central nervous system; DKA, diabetic ketoacidosis; ICU, intensive care unit.
Abnormal behavior
Often a precursor to alterations in consciousness, acute change in
behavior is a frequent predictor of an underlying medical or
psychiatric problem. Abnormal behavior described as an objective
change in a person’s normal activity pattern is often associated with
confusion. Although there are no specific medical definitions of
abnormal behavior or confusion, subtle changes in normal routine
are identified by family members and caregivers. Reported
behavioral changes may be simply a variation in daily pattern,
inability to articulate a common word or do a familiar task, failure
to recognize danger, fear, euphoria, somnolence, or change in
interaction with a known person (friend, family member, caregiver,
or authority figure). Individuals do not have insight into their
change in behavior, thus the reports of others must be recognized
as valid. Although the causes of abnormal behavior and associated
confusion are varied, the first step in the evaluation of abnormal
behavior is to identify life-threatening causes. Screening for vital
sign changes (BP, HR, RR, and temperature), hypoxia, and
hypoglycemia provide initial data to differentiate acute medical
conditions such as sepsis, DKA, and respiratory compromise that
85
require immediate attention or hypovolemia caused by
dehydration. For elderly persons and persons with existing chronic
conditions, behavior change may be the single indicator of
declining medical status. The second step in evaluation of a patient
with change in behavior is determining if the problem is
disorientation and memory (linked to medical or neurologic
problems) or changes in thought content (linked to psychiatric
problems). In addition to the history of the present illness, taking a
thorough medical and substance abuse history is imperative. Quick
bedside tests such as the Six-Item Screen, Quick Confusion Scale, or
Vigilance A Test provide reliable information for cognitive
function, attention, and confusion.
Delirium
This is a state of disordered attention that reflects an underlying
acute or subacute process. It is usually a transient condition (may be
prolonged) that develops along a continuum including a clouding
of consciousness, confusion, attention deficit, global cognitive
impairment, and psychosis. Symptoms include disorientation to
time, place, and person; disorganized thinking; fear; irritability;
misinterpretation of sensory stimuli (e.g., pulling at tubes and
dressings); appearance of being distracted; altered psychomotor
activity; altered sleep-wake cycles; memory impairment;
hallucinations; inappropriate communication (e.g., yelling,
swearing, nonsensical speech); and dreamlike delusions. Lucid
intervals alternate with episodes of delirium. Patients may have
difficulty following commands. Daytime drowsiness is contrasted
with nighttime agitation. Clinical variants of delirium include the
hyperactive-hyperalert form, the quiet form, and a combination
form that combines the hyperactive-hyperalert and quiet forms to
produce both lethargy and agitation (Figure 1-2).
86
FIGURE 1-2 Linking sedation and delirium monitoring;
a two-step approach to assess
consciousness. Source: (Copyright © E. Wesley Ely, MD, MPH, and
Vanderbilt University, 2002.)
Coma
Coma is an alteration in arousal and diminished awareness of self
and environment. No understandable response to external stimuli
or inner need is elicited. No language is spoken. There are no covert
or overt attempts at communication or eye opening. Spontaneous
purposeful movement and/or localizing movements are absent.
Motor responses to noxious stimuli are reflexive and do not result
in recognizable defensive movements. Sleep-wake cycles are absent
on the electroencephalogram (EEG). The extent of coma is difficult
to quantify because limits of consciousness are difficult to define.
Self-awareness can only be inferred from appearance and actions.
Coma occurs when normal central nervous system (CNS) function
is disrupted by alteration in the cerebral structure (brain injury),
cerebrovascular impairment (hemorrhage, ischemia, or edema), or
metabolic conditions (hepatic encephalopathy). If coma persists for
longer than 4 weeks, it is defined as transitioning to a vegetative
87
state.
88
(eyes are open and sleep patterns may be observed) with return
of spontaneous control of autonomic function but without
observable signs of cognitive function. The patient cannot follow
commands, offers no comprehensible sounds, and displays no
localization to stimuli. There is complete loss of meaningful
interaction with the environment. When the VS continues for
weeks or months, it is considered persistent vegetative state
(PVS). PVS may exist for many years because the autonomic and
vegetative functions necessary for life have been preserved. PVS
generally resolves more quickly in patients with a traumatic brain
injury than in patients with no trauma.
Cognitive dysfunction
This is an alteration in thought process involving many of the
following brain functions: memory, learning, language, attention,
judgment, reasoning, reading, and writing. Aphasia, or difficulty
understanding language or with responding with the proper
words, may also be present. Dysphagia, or difficulty swallowing,
occurs because of attention deficits or muscle weakness. These
cognitive impairments, whether permanent or transitory, if
overlooked, underdiagnosed or incorrectly diagnosed may result in
failure to correct a new acute illness or an exacerbation of a chronic
89
illness. See Table 1-3 for factors contributing to cognitive
dysfunction in acute, critical, or chronic illnesses. Acute changes in
behavior or mental status superimposed on chronic cognitive
dysfunction (dementia) is a harbinger of an underlying condition
that needs immediate attention.
90
History and risk factors
• Age : Older adults (age 60 years and older) are more prone to
alterations in consciousness, especially with changes in the
environment, subclinical response to infection or other medical
conditions including myocardial infarction (MI), and prescription
drug toxicity.
• Medication review
91
consciousness: Sympathomimetics, anticholinergics,
hallucinogens, opioid, sedative-hypnotic,
cholinergic, and serotonin uptake inhibitors.
• Surgical factors: Nature (hip, cardiac, neurosurgery patients at
increased risk) and extent of surgery and anesthesia time.
Vital signs
All of the following vital sign changes may be associated with an
alteration in consciousness:
92
CO will cause a change in HR initially.
93
• In patients who are unconscious or demonstrate low-level
function, assessment techniques are used that do not require
patient participation, such as coma and cognitive functioning
scales. The purpose of assessment is to determine the extent of
wakefulness and cognition through observed responses, such as
eye opening, movement of the head and body, verbalization, and
ability to follow commands. These observations alone will not
fully discriminate the subtle differences in altered states of
arousal.
Screening labwork
• ABGs evaluate ventilation, perfusion, estimated Hgb, and acid-
base status.
Neurologic evaluation
• Mental status testing: Subjective assessment requiring patient
cooperation for best results (Box 1-1).
94
• Quick Confusion Scale: Consists of six items and is used for
screening impaired mental status in the emergency department.
Total points are 15 with a total score of 11 suggesting the need for
further evaluation and a score of ≤7 confirming impairment (Box
1-2).
95
Unit): Four-part scale used to evaluate confusion. Onset and
course, inattention, disorganized thinking, and LOC are assessed
(Box 1-6).
Table 1-4
INTENSIVE CARE DELIRIUM SCREENING CHECKLIST
Table 1-5
RICHMOND AGITATION-SEDATION SCALE (RASS)
96
+3 Very agitated Pulls on or removes tubes or catheters, aggressive behavior toward staff
+2 Agitated Frequent nonpurposeful movement or patient-ventilator dyssynchrony
+1 Restless Anxious or apprehensive but movements not aggressive or vigorous
2. If the patient is not alert, in a loud-speaking voice state the patient’s name and direct the
patient to open his or her eyes and look at the speaker. Repeat once if necessary. Can prompt
the patient to continue looking at the speaker.
The patient has eye opening and eye contact, which is sustained for more than 10 seconds
(score −1).
The patient has eye opening and eye contact, but this is not sustained for 10 seconds (score −2).
The patient has any movement in response to voice, excluding eye contact (score −3).
3. If the patient does not respond to voice, physically stimulate the patient by shaking shoulder
and then rubbing sternum if there is no response.
The patient has any movement to physical stimulation (score −4).
The patient has no response to voice or physical stimulation (score −5).
2. If not alert, state the patient’s name and say to open eyes and look at the speaker.
• The patient awakens with sustained eye opening and eye contact (score −1).
• The patient awakens with eye opening and eye contact, but not sustained (score −2).
• The patient has any movement in response to voice but no eye contact (score −3).
3. When no response to verbal stimulation, physically stimulate the patient by shaking shoulder
and/or rubbing sternum.
• The patient has any movement to physical stimulation (score −4).
• The patient has no response to any stimulation (score −5).
97
Reproduced, with permission, from Sessler CN, Gosnell M, Grap MJ, et al: The
Richmond Agitation-Sedation scale: validity and reliability in adult intensive care unit
patients. Am J Respir Crit Care Med 166(10):1338-1344, 2002. Copyright © 2002
American Thoracic Society. From Ely EW, Truman B, Shintani A, et al: Monitoring
sedation status over time in ICU patients: the reliability and validity of the Richmond
Agitation-Sedation Scale (RASS). JAMA 289(22):2983-2991, 2003.
Table 1-6
COGNITIVE REHABILITATION GOALS
98
care, ed 4, St Louis, 1999, Mosby.
Box 1-1
MENTAL STATUS COMPONENT OF THE
NEUROLOGIC EXAMINATION
1. General appearance
5. Judgment
6. Abstract thinking
Box 1-2
QUICK CONFUSION SCALE
99
Adapted from Huff J, Farace E, Brady W, et al: The Quick Confusion Scale in the
emergency department: comparison with the Mini-Mental State Examination. Am J
Emerg Med 19:461-464, 2001.
Box 1-3
MINI-MENTAL STATUS EXAMINATION
1. What is the year, season, date, day, month? (5 points)
4. Count backward by sevens (e.g., 100, 93, 86, 79, 72). (5 points)
100
9. Follow the command “close your eyes.” (1 point)
Box 1-4
SIX-ITEM SCREEN
Six-item screen (used to detect problems with cognition,
attention, short-term memory, and orientation; subset of
the mmse, the blessed dementia rating scale (bdrs), and
the word list recall)
1. Examiner names three items and asks patient to repeat each item.
(3)
2. Examiner asks what year, what month, what day of the week? (3)
Box 1-5
VIGILANCE A TEST
Vigilance A Test Scoring
Random list of 60 letters with the letter A appearing greater Count number of omissions or
than random frequency. The patient is asked to tap or commission of the target letter (A).
indicate when the target letter (A) is spoken by the Greater than two missed is
examiner. abnormal
Box 1-6
CONFUSION ASSESSMENT METHOD-
101
INTENSIVE CARE UNIT (CAM-ICU)
WORKSHEET
Feature 1: Acute onset or fluctuating course
Positive if you answer “yes” to either 1A or 1B.
Positive or Negative
1A: Is the patient different than his/her baseline mental status?
Or
1B: Has the patient had any fluctuation in mental status in the
past 24 hours as evidenced by fluctuation on a sedation scale (e.g.,
RASS), GCS, or previous delirium assessment?
Yes or No
Feature 2: Inattention
Positive if either score for 2A or 2B is less than 8.
Attempt the ASE Letters first. If the patient is able to perform
this test and the score is clear, record this score and move to
Feature 3. If the patient is unable to perform this test or the score is
unclear, then perform the ASE Pictures. If you perform both tests,
use the results of the ASE Pictures to score the feature.
Positive or Negative
2A: ASE Letters: Record score (enter NT for not tested)
Directions: Say to the patient, “I am going to read you a series of 10
letters. Whenever you hear the letter ‘A,’ indicate by squeezing my hand.”
Read letters from the following letter list in a normal tone.
SAVEAHAART
Scoring: Errors are counted when patient fails to squeeze on the
letter “A” and when the patient squeezes on any letter other than
“A.”
Score (out of 10): ______
2B: ASE Pictures: record score (enter NT for not tested)
Directions are included on the picture packets.
Score (out of 10): ______
Feature 3: Disorganized thinking
Positive if the combined score is less than 4
Positive or Negative
3A: Yes/No Questions
102
(Use either Set A or Set B, alternate on consecutive days if
necessary):
Set A Set B
1. Will a stone float on water? 1. Will a leaf float on water?
2. Are there fish in the sea? 2. Are there elephants in the sea?
3. Does one pound weigh more than two 3. Do two pounds weigh more than one
pounds? pound?
4. Can you use a hammer to pound a nail? 4. Can you use a hammer to cut wood?
Score ___ (Patient earns 1 point for each correct answer out of 4)
3B: Command
Say to patient: “Hold up this many fingers” (Examiner holds two
fingers in front of patient). “Now do the same thing with the other
hand” (Not repeating the number of fingers). (If patient is unable
to move both arms, for the second part of the command ask patient
“Add one more finger”). Score___ (Patient earns 1 point if able to
successfully complete the entire command)
Combined Score (3A + 3B):_____ (out of 5)
Feature 4: Altered level of consciousness
Positive if the Actual RASS score is anything other than “0”
(zero)
Positive Negative
Overall CAM-ICU (Features 1 and 2 and either Feature 3 or 4):
Positive Negative
Copyright © 2002, E. Wesley Ely, MD, MPH and Vanderbilt University, all rights reserved.
Diagnostic tests
Neurodiagnostic testing
See the section on Traumatic Brain Injury in Chapter 3.
Neuropsychological testing
Although not a routine part of critical care, neuropsychological
testing should be planned and implemented for patients with brain
injury or altered consciousness when they enter the recovery phase.
This testing provides a comprehensive baseline for rehabilitation by
evaluating higher cortical functions, such as memory, learning, and
103
language.
Laboratory studies
If there is an acute or unexpected mental status change, laboratory
studies include complete blood count (CBC), electrolytes, cardiac
profile, blood and sputum cultures, urinalysis and culture, ABG,
chest radiograph, ECG, and other tests as determined by signs and
symptoms.
Collaborative management
Care priorities
When evaluating alteration in consciousness or a change in mental
status, there are two primary targets: (1) recognize that the disorder
is present and (2) uncover the underlying cause. Acute and/or life-
threatening problems must be ruled out before proceeding.
Therefore, signs and symptoms such as lethargy, somnolence,
fatigue, anxiety, or sleeplessness should not be normalized as part
of illness behavior but as signs and symptoms prompting further
investigation. Although severe agitation is difficult to manage, it is
imperative that physiologic causes of agitation are ruled out before
sedating the patient. Once acute causes of the problem are ruled
out, the following measures may be implemented for other causes
of behavioral changes:
1. Delirium
104
• Manage pain and assess effectiveness.
• Treat agitation.
2. Coma
105
(e.g., spasticity, swallowing disorders) and complications of
immobility (e.g., disuse syndrome, contractures, and pressure
ulcers).
3. Locked-in syndrome
4. Vegetative state
106
FIGURE 1-3 Sensory stimulation (SS) programs as an
intervention technique in the critically ill. Source: (From Kater
K: Response of head-injured patients to sensory stimulation. West J Nurs
Res 11[1]:20-33, 1989; Lewinn E, Dimancescu M: Environmental
deprivation and enrichment in coma. Lancet 2[8081]:156-157, 1978; Mackay
L, Bernstein BA, Chapman PE, et al: Early intervention in severe head
injury: long-term benefits of a formalized program. Arch Phys Med Rehabil
73[7]:635-641, 1992; Mitchell S, Bradley VA, Welch JL, et al: Coma arousal
procedure: a therapeutic intervention in the treatment of head injury. Brain
Inj 4[3]: 273-279, 1990; Schinner K, Chisholm AH, Grap MJ, et al: Effects of
auditory stimuli on intracranial pressure and cerebral perfusion pressure in
traumatic brain injury. J Neurosci Nurs 27[6]:336-341, 1994; and Wilson S,
Powell GE, Brock D, et al: Vegetative state and response to sensory
stimulation: an analysis of 24 cases. Brain Inj 10[11]:807-818, 1996.)
107
interventions designed to reduce delirium in the intensive care unit
—one was to reduce delirium in postoperative patients by
controlling disturbances in the sleep-wake cycle. The second
involved the daily visit of a geriatric consult service, which
provided targeted recommendations using a 10-item protocol. The
protocol included (1) maintenance of central nervous system O2
delivery, (2) fluid and electrolyte corrections, (3) pain management,
(4) removal of unnecessary medications, (5) bowel/bladder
regulation, (6) establishing adequate nutrition, (7) mobilization
and rehabilitation, (8) detection/prevention and treatment of
surgical complications, (9) sensory stimulation, and (10) treatment
of agitational variant of delirium.
108
cause of the problem and correct it. This may include limiting
sedation or pain medication, monitoring for withdrawal
syndromes, drug interactions, or impending sepsis (SIRS, see
Chapter 11).
109
• Assess underlying cause of confusion or delirium
before using sedation, anxiolytic, analgesic, or
antipsychotic drug therapy (see Sedation and
Neuromuscular Blockade).
Communication enhancement
4. Assure the patient that you are attempting to find methods that
promote communication if the patient’s needs cannot always be
understood.
110
5. For the patient who does not respond to or acknowledge verbal
stimulation, continue communication attempts.
111
• Maintain body alignment and positioning.
5. Maintain the patient’s skin integrity. See Wound and Skin Care.
112
sputum is present.
113
magnesium (Mg+), phosphates (PO4−), proteins, and sulfates. The
extracellular fluid compartment (ECF) is composed of interstitial
fluid, which surrounds the cells (14% of body weight), intravascular
fluid, contained within blood vessels (5% of body weight), and
transcellular fluid, which includes cerebral spinal fluid and fluid
contained in other body spaces such as joint spaces, pleural,
peritoneal, and pericardial spaces (1% to 2% of total body weight.)
ECF contains the remaining one third of body fluid and has a high
concentration of the plasma ions sodium (Na+), chloride (Cl−), and
bicarbonate (HCO3−).
The composition and concentration of ECF are primarily
regulated by the concentration of Na+, which defines the relative
relationship of sodium and water. Although ECF is altered and
then modified as the body reacts with its surrounding environment,
ICF remains relatively stable. Intracellular stability is important for
maintaining normal cellular function.
In addition to water, body fluids contain two types of dissolved
substances: electrolytes and nonelectrolytes. Electrolytes are
substances that carry an electrical current and can dissociate into
ions, which have either a positive or a negative charge. They are
measured by their capacity to combine (milliequivalents/liter
[mEq/L]) or by the molecular weight in milligrams (millimoles/liter
[mmol/L]). Nonelectrolytes are substances such as glucose and urea
that do not dissociate in solution and are measured by weight
(milligrams per 100 milliliters, or mg/dL) and mmol/L. The
intravascular and extravascular components of the ECF are
separated by a semipermeable or porous capillary membrane,
which allows movement of dissolved substance/particles between
compartments, and slow passage of albumin (5% per hour), which
is returned to the circulation via the lymphatic system at the same
rate. The unique composition of each compartment is maintained
(Table 1-7) in a state of equilibrium. Whereas the hydrostatic
pressure within the circulation tends to drive fluid out, the oncotic
pressure of the plasma proteins (e.g., albumin) draws fluid in and
maintains the relative constancy of the plasma volume.
Table 1-7
PRIMARY CONSTITUENTS OF BODY WATER COMPARTMENTS*
114
*
This is a partial list. Other constituents include calcium (Ca2+), magnesium (Mg2+),
and proteins.
Cl−, Chloride; HCO3−, bicarbonate; HPO4−, phosphate; K+, potassium; Na+, sodium.
Osmolality
Osmolality is the number of particles in solution. This concentration
of particles determines the relationship of fluid between the ICF
and ECF. Normal osmolality is regulated by a wide variety of
mechanisms, which include arterial BP, sympathetic stimulation,
renal regulation, and hormonal outflow.
Osmolality = 2(Na+) + Glucose/18 + BUN/2.8 (normal value: 265 to
285 mOsm/L)
Hormonal influence
Three hormones are responsible for fluid volume regulation:
115
sodium (along with water), and increases potassium and
hydrogen excretion.
Fluid disturbances
Fluid changes affect the volume status, regulation, and the
composition of body fluids. Fluid loss or gain changes the
concentration of particles in fluid compartments.
Hypovolemia
Pathophysiology
ECF volume depletion or hypovolemia may be caused by abnormal
skin losses, GI losses, polyuria/diuresis, bleeding, decreased intake,
and movement of fluid into a third space (e.g., pleura, peritoneum,
interstitium). Depending on the type of fluid lost or “third-spaced,”
hypovolemia may be accompanied by acid-base, osmolar, or
electrolyte imbalances. Severe ECF volume depletion can lead to
hypovolemic shock and cellular dehydration, which causes
alterations in electric potentials (the ability to conduct impulse)
throughout the body.
Compensatory mechanisms in hypovolemia include increased
sympathetic nervous system stimulation: increased HR, increased
force of cardiac contraction (positive inotropic effect),
vasoconstriction to maintain perfusion to O2-dependent organs (i.e.,
heart, lungs, brain), increased thirst, and increased release of
aldosterone and ADH (vasopressin). Reduced perfusion to high-
flow, low O2–consuming organs (i.e., kidney, mesenteric bed,
skeletal muscles) may lead to acute renal failure, ischemic bowel,
and skeletal muscle cell rupture.
Hypovolemic shock develops when the intravascular volume
116
decreases to the point where compensatory mechanisms can no
longer maintain the perfusion needed for normal, aerobic cellular
function. Without normal levels of O2, cellular metabolism becomes
anaerobic, resulting in acidosis, cardiac depression, intravascular
coagulation, increased capillary permeability, and release of toxins.
If shock is not adequately treated, it may become irreversible,
leading to death.
Hypovolemia assessment
Goal of assessment
Identify the signs and symptoms of hypovolemia.
117
Vital signs
Evaluate BP, HR, temperature, weight, central venous pressure
(CVP), pulmonary artery wedge pressure (PAWP), and urine
output to determine the extent of volume depletion.
• Increased temperature.
Table 1-8
WEIGHT LOSS AS AN INDICATOR OF EXTRACELLULAR FLUID
DEFICIT IN THE ADULT
Observation
Evaluate the skin, mucous membranes, and clinical presentation for
signs of dehydration including furrowed tongue, dry mucous
membranes, sunken eyeballs, flat neck veins, clinical pallor,
dizziness, weakness, fatigue, syncope, anorexia, nausea, vomiting,
thirst, confusion, and constipation.
Palpation
118
Chest and abdominal palpation are performed to elicit pain in the
abdomen or chest.
Screening labwork
Blood studies can reveal the extent of hypovolemia, because the
blood becomes more concentrated as fluid is lost. If bleeding is
present, studies will reveal blood loss.
• Serum and urine osmolality depend on the type of fluid lost and a
comparison assists in the diagnosis of renal insufficiency.
119
As shock progresses, pulse pressure may widen as the
compensatory response fails. Heart rate decreases, ventricular
compliance is reduced, and with impaired ventricular relaxation
during diastole, ventricular filling time is reduced, resulting in
decreased central venous pressure and pulmonary artery pressure.
Volume status may be underestimated. If the difference in systolic
and diastolic blood pressure is less than 25% of the systolic blood
pressure, the pulse pressure is considered to be narrow. A wide
pulse pressure is considered to be greater than 50% of the systolic
blood pressure.
Collaborative management
Care priorities
Identification of patients at risk for volume loss and prevention of
continued losses and fluid replacement guide the care plan for these
patients.
120
5. Protect skin with lotions and egg crate or alternating pressure
mattress.
Management of Hypovolemia
1. Restore Normal Fluid Volume and Correct Acid-Base and Electrolyte Disturbances
The type of fluid replacement depends on the type of fluid lost and the severity of the deficit and on serum
electrolytes, serum osmolality, and acid-base status. Intravenous (IV) fluids are provided to expand
intravascular volume or to correct an underlying imbalance in fluids or electrolytes. Fluids should be
infused at a rate resulting in a positive fluid balance (e.g., 50 to 100 mL in excess of all hourly losses).
Replacement fluids
• Isotonic solutions (normal saline 0.9%): Expand the extracellular fluid compartment (ECF)
only; do not enter the intracellular fluid compartment (ICF). Appropriate for rapid volume
replacement.
• Hypotonic saline solutions (0.45% saline): Expand the ECF and provide some free water to
the cells. Used in the management of the patient who is both volume-depleted and
hyperosmolar (e.g., in cases of hypernatremia or hyperglycemia).
• Dextrose and water (5% dextrose in water): Provide free water only that will be distributed
evenly through both the ICF and ECF; used to treat water deficit.
• Mixed isotonic saline/electrolyte solutions: Provide additional electrolytes (e.g., potassium
and calcium) and a buffer (e.g., lactate or acetate). Example: Lactated Ringer solution (Ringer
lactate): Isotonic solution containing a small amount of K+ and lactate, which metabolizes to
bicarbonate in the liver to assist blood buffering.
• Blood and albumin: Expand only the intravascular portion of the ECF. Both packed red
blood cells and fresh-frozen plasma expand the intravascular volume.
• Dextran or hetastarch, hypertonic saline, hextend: Synthetic colloidal solutions used to
expand the intravascular volume.
2. Restore Tissue Perfusion (Hypovolemic Shock)
• Rapid volume replacement with crystalloids: Fluids may be given rapidly as long as cardiac
filling pressures and blood pressure remain low. Overaggressive fluid resuscitation in
uncontrolled hemorrhage can increase the risk of secondary hemorrhage as the intravascular
hydrostatic pressure increases.
• Volume replacement with colloids: Use of volume replacement with colloids to prevent the
development of pulmonary edema secondary to rapid volume replacement remains
controversial. Solutions include albumin and synthetics such as hetastarch.
• Blood: Administered only if necessary to maintain oxygen-carrying capacity. Hematocrit
should not be raised greater than 35%.
• Vasopressors: Used to reduce the size of blood vessels while volume infusions continue to
increase blood pressure. Effective for false hypovolemia induced by vasogenic (septic,
anaphylactic, neurogenic) shock to control severe vasodilation.
121
to 6 mm Hg, pulmonary artery pressure (PAP) 20 to 30/8 to 15 mm
Hg, CO 4 to 7 L/min, mean airway pressure (MAP) 70 to 105 mm
Hg, HR 60 to 100 beats per minute (bpm), and systemic vascular
resistance (SVR) 900 to 1200 dynes/s/cm5.
Fluid Balance, Hydration, Kidney Function.
Fluid monitoring
122
increase in ventilator pressures and a decrease in SpO2.
Fluid management
123
Membranes.
Positioning
1. Protect patients who are at high risk for falling: those who are
confused, dizzy, or weak. Keep side rails up and bed in lowest
position with wheels locked. Assist with ambulation. Raise the
patient to sitting or standing positions slowly.
124
Neurologic Monitoring
Hypervolemia
Pathophysiology
Hypervolemia is a state of higher-than-normal intravascular
volume that occurs in four situations: (1) excessive retention of
sodium and water caused by a chronic renal stimulus to conserve
sodium and water; (2) abnormal renal functioning causing reduced
excretion of sodium and water; (3) excessive administration of IV
fluids; and (4) interstitial-to-plasma fluid shifting. Hypervolemia
may lead to heart failure and pulmonary edema, especially in the
patient with cardiovascular dysfunction.
Hypervolemia assessment
Goal of assessment
• Evaluate the potential causes and sequelae of hypervolemia.
125
colloid oncotic solutions (i.e., albumin).
Observation
• Evaluate for the clinical signs of volume overload: SOB,
orthopnea, peripheral edema, distended neck veins, and moist
skin.
Vital signs
• HR, BP, and hemodynamic measurements to evaluate volume
status.
• Increased BP.
• HR: tachycardia.
• Respirations: tachypnea.
• O2 saturation decreased.
Palpation
• Pulse assessment to evaluate tissue perfusion: Bounding pulses,
ascites, and peripheral and sacral edema.
Auscultation
• Heart and lung assessment to evaluate signs of volume overload:
Tachycardia, gallop rhythm, crackles, rhonchi, and wheezes.
126
Screening labwork
• Blood studies are variable and nonspecific: Hematocrit, BUN and
creatinine, ABGs, serum sodium and osmolality, urinary sodium,
and urine specific gravity.
Radiology
• Chest radiograph may reveal signs of pulmonary vascular
congestion.
Collaborative management
127
Care priorities
The priorities include prevention of further volume overload and
returning the patient to a euvolemic state.
Box 1-7
FOODS HIGH IN SODIUM
Bouillon
Celery
Cheeses
Dried fruits
128
Mustard
Olives
Pickles
Preserved meat
Sauerkraut
Soy sauce
Fluid/electrolyte management
129
1. Monitor intake and output hourly. Urine output should be ≥0.5
mL/kg/h unless the patient is in oliguric renal failure.
130
turgor, flat neck veins, and acute weight loss.
Respiratory monitoring
131
Increased O2 requirements may signal increased pulmonary
vascular congestion.
132
Goals/Outcomes: The patient’s skin and tissue remain intact.
Tissue Integrity: Skin and Mucous Membranes.
Pressure management
3. Check tissue areas at risk with each position change (e.g., heels,
sacrum, areas over bony prominences).
133
gain Na2+). The most common cause of hyponatremia is water gain
from renal dysfunction. The kidneys should increase output if
intake increases. As serum osmolality decreases, fluid shifts into
cells, causing swelling and sometimes compartment syndromes.
There are three types of hyponatremia: hypovolemic,
hypervolemic, and euvolemic. Dilutional states are the most
frequent cause of hyponatremia in the critically ill. Clinical
indicators and treatments depend on the cause of hyponatremia
and whether it is associated with normal, decreased, or increased
ECF volume. For more information, see Burns (Chapter 3), Heart
Failure (Chapter 5), Acute Renal Failure/Acute Kidney Injury
(Chapter 6), and Syndrome of Inappropriate Antidiuretic Hormone
(Chapter 8).
Hyponatremia assessment
Goal of assessment
• Evaluate for the signs and symptoms of hyponatremia.
134
History and risk factors
• Decreased ECF volume. GI losses: diarrhea, vomiting, fistulas,
and nasogastric suction; renal losses: diuretics, salt-wasting
kidney disease, and adrenal insufficiency; skin losses: burns,
wound drainage, and excessive diaphoresis.
Observation
• Hyponatremia with decreased ECF volume: Irritability,
135
apprehension, dizziness, personality changes, poor skin turgor,
dry mucous membranes, tremors, seizures, and coma.
Palpation
• Cold clammy skin with decreased ECF volume.
Screening labwork
• Serum sodium.
• Serum osmolality.
• Urine sodium.
Collaborative management
136
Care priorities
• Administer diuretics.
137
6. Assess for resolution of the signs and symptoms of
neurologic changes.
HIGH ALERT!
Osmotic Demyelination Syndrome
Overly aggressive or inappropriate treatment of hyponatremia can also
cause permanent neurologic damage secondary to osmotic demyelination
syndrome. Osmotic demyelination is poorly understood but should
always be suspected after hypertonic resuscitation when patients
display bilateral neurologic deficits, flaccidity, and quadriparesis.
Initially, sodium levels should not increase at a level greater than
0.5 to 1.0 mEq/L/h in patients being treated for symptomatic
hyponatremia with hypertonic NaCl. For those symptomatic with
severe hyponatremia (less than 120 mEq/L), the rate of correction
should be 1 to 2 mEq/h for 3 to 4 hours. After an initial 6 to 8
mEq/L increase in the serum sodium level, the rate of increase
should not be greater than 0.5 mEq/L/h. Levels should not increase
at an average rate of greater than 0.5 mEq/L/h in patients without
symptoms. The total increase in the first 24 hours of treatment
should not exceed 12 mEq/L.
138
RR 12 to 20 breaths/min), BP within the patient’s normal range,
CVP 2 to 6 mm Hg, and PAP 20 to 30 mm HG systolic, 8 to 15 mm
Hg diastolic or within the patient’s normal range.
Fluid Balance, Kidney Function, Hydration.
Fluid monitoring
If the patient is receiving hypertonic saline, assess carefully for
signs of intravascular fluid overload: tachypnea, tachycardia, acute
SOB, crackles (rales), rhonchi, increased CVP and PAP, gallop
rhythm, and increased BP. For other interventions, see
Hypovolemia or Hypervolemia.
Electrolyte Management: Hyponatremia; Fluid/Electrolyte
Management; Intravenous (IV) Therapy; Invasive Hemodynamic
Monitoring.
Acute confusion
related to hyponatremia
Goals/Outcomes: Within 48 hours of treatment, the patient more
consistently verbalizes orientation to time, place, and person and
has not sustained physical injury related to altered sensorium.
Serum sodium level should ideally increase to greater than 125
mEq/L in the first 48 hours after treatment.
Cognitive Orientation; Distorted Thought Self-Control;
Information Processing; Neurologic Status: Consciousness.
Neurologic monitoring
4. Keep side rails up and bed in lowest position with wheels locked.
139
5. Use reality therapy such as clocks, calendars, and familiar objects;
keep these items at the bedside within the patient’s visual field.
HIGH ALERT!
Overly rapid correction of chronic hyponatremia may result in
permanent neurologic damage.
Hypernatremia assessment
Goal of assessment
Evaluate the risk factors and clinical symptoms of hypernatremia.
140
hyperglycemia), and osmotic diarrhea.
Observation
• Symptoms related to hypertonicity, intracellular dehydration, and
electrolyte imbalance: Intense thirst, fatigue, restlessness,
agitation, coma, flushed skin, and peripheral edema.
Vital signs
• Low-grade fever.
• Postural hypotension.
141
osmolality helps to rehydrate the cells. Individuals with chronic
hypernatremia exhibit few symptoms. This adaptive mechanism
plays a key role in the treatment of hypernatremia.
HIGH ALERT!
Overly aggressive water administration may cause rapid movement of
water into the cells, which can result in dangerous cerebral edema caused
by a too-rapid reduction of sodium.
Collaborative management
Care priorities
1. Assess the patient for fluid losses or gains.
142
gain.
Fluid/electrolyte management
143
4. Inform the patient and significant others that altered sensorium is
temporary and will improve with treatment.
5. Keep side rails up and bed in lowest position with wheels locked.
144
The body gains potassium through foods (primarily meats, fruits,
and vegetables) and medications. The ECF also gains potassium
from breakdown or death of cells, when a large amount of
intracellular K+ is released from the cell contents. Potassium is
eliminated from the body through the kidneys, the GI tract, and the
skin. The potassium level may decrease in the serum (ECF) when K+
shifts inside the cells. The serum potassium level increases when
renal function decreases, when circulation is reduced to a large
amount of cells causing cell death, with cellular lysis, and with
rhabdomyolysis. Changes in insulin production, insulin and other
receptor activity, and catecholamine level affect the movement of K+
across the cell wall. The kidneys are the primary regulators of
potassium balance.
145
Changes in serum potassium levels reflect changes in
extracellular fluid potassium—not necessarily changes in total
body levels.
Hypokalemia assessment
Goal of assessment
Evaluate for the risk factors and signs and symptoms of
hypokalemia and use the information to manage the symptoms.
The patient is at risk for torsades de pointes and ventricular
tachycardia.
Vital signs
• Postural hypotension.
146
Auscultation
• Decreased bowel sounds.
Palpation
• Weak and irregular pulse.
• Decreased reflexes.
• Paresthesias.
Screening
12-Lead ECG: Evaluate changes typically seen with hypokalemia,
including ST segment depression, flattened T waves, presence of U
waves; with severe hypokalemia, P wave amplitude is increased,
PR interval is prolonged, QRS and QT complexes widen, and
patient is at risk for torsades de pointes.
147
Hypokalemia potentiates the effect of digitalis.
Electrocardiography may reveal signs of digitalis toxicity despite
a normal serum digitalis level.
Collaborative management
Care priorities
Box 1-8
FOODS HIGH IN POTASSIUM
Apricots
Artichokes
Avocados
Bananas
Cantaloupes
148
Carrots
Cauliflower
Chocolate
Dried fruit
Mushrooms
Nuts
Peanuts
Potatoes
Prune juice
Pumpkins
Spinach
Swiss chard
Sweet potatoes
149
4. Monitor for signs of hyperkalemia
When replacing K+ monitor for signs of hyperkalemia.
HIGH ALERT!
Patients receiving 10 to 20 mEq/h should be on a continuous
cardiac monitor.
If potassium is administered via a peripheral line, the rate of
administration may need to be decreased to prevent irritation of
vessels. The development of tall, peaked T waves suggests the
presence of hyperkalemia and should be reported to the advanced
practice provider. Intravenous potassium may be administered as
potassium chloride or potassium phosphate.
Electrolyte management
150
Potassium chloride should not be added to intravenous (IV)
bags while they are hanging on a pole, to avoid accumulation of K+
at the bottom of the IV bag. The solution container should be
inverted before adding the medication and mixed well.
4. Monitor I&O hourly. Report urine output less than 0.5 mL/kg/h.
Unless severe symptoms of hypokalemia are present, potassium
supplements should not be given to patients with low urine output;
hyperkalemia may develop in patients with oliguria (output less
than 15 to 20 mL/h). High urine output (diuresis or polyuria)
increases the risk of hypokalemia.
151
gastric suction.
Respiratory monitoring
Ventilation Assistance.
152
greater than 5 mEq/L)
Pathophysiology
Hyperkalemia results from increased intake of potassium,
decreased urinary excretion of K+, or sudden movement of K+ out of
cells. The rate of change in serum K+ is as important as the level.
Rapid increases do not allow time to compensate. Hyperkalemia is
often associated with acidosis.
Hyperkalemia assessment
Goal of assessment
Evaluate for the risk factors and signs and symptoms of
hyperkalemia. Information should be used immediately to manage
potentially life-threatening dysrhythmias. Hyperkalemia is often
associated with acidosis.
153
catabolism (e.g., fever, sepsis, trauma, surgery).
Observation
• Irritability.
• Abdominal distention.
• Diarrhea.
• Ascending weakness.
• Parethesias.
Vital signs
• Irregular pulse.
• Hypotension.
Screening
• 12-Lead ECG: Tall, thin T waves, prolonged PR interval, ST
depression, widened QRS complex with progression to cardiac
arrest, loss of P wave; eventually, QRS widens further and
cardiac arrest occurs.
154
specimen. If red blood cells hemolyze (are injured), potassium is
released from damaged cells while or after specimen has been
drawn.
Collaborative management
Care priorities
155
6. Provide hemodialysis to lower K+ level if rapid removal
for K+ is needed
Fluid/electrolyte management
156
and irregular pulse. Assess for hidden sources of potassium:
medications (e.g., potassium penicillin G), banked blood, salt
substitute, GI bleeding, or catabolic conditions (i.e., infection or
trauma).
157
Electrolyte Management: Hyperkalemia; Dysrhythmia
Management; Hemodialysis Therapy.
158
produced by the thyroid gland when serum Ca2+ increases to inhibit
bone resorption.
Calcium regulates skeletal and cardiac muscle contractions, is
part of the clotting cascade, and has other essential functions. It is
imperative to maintain the Ca2+ balance.
Hypocalcemia assessment
Goal of assessment
Evaluate the signs and symptoms of hypocalcemia.
• Alkalosis.
159
replacement with normal saline after massive
hemorrhage).
• Increased calcium loss in body fluids.
Observation
• Numbness with tingling of fingers and circumoral region.
• Tetany.
• Convulsions.
Vital signs
• Hypotension secondary to vasodilation.
Percussion
• Positive Trousseau sign: Ischemia-induced carpopedal spasms.
Elicited by applying a BP cuff to the upper arm and inflating it
past systolic BP for 2 minutes.
160
muscles. Elicited by stimulating the facial nerve during
percussion of the face just in front of the ear.
Screening
• 12-Lead ECG: Prolonged QT interval caused by elongation and
elevation of ST segment.
Collaborative management
Care priorities
161
maintain calcium levels over time.
HIGH ALERT!
Administer intravenous (IV) calcium slowly. Undiluted IV 10%
calcium should not be given faster than 0.5 to 1 mL/min. Diluted
162
calcium given in an infusion is preferred. Rapid administration can
cause hypotension. Observe IV insertion site for infiltration; calcium
will slough tissue. Concentrated calcium solutions (calcium chloride)
should be administered through a central line. Do not add calcium to
solutions containing sodium bicarbonate or sodium phosphate to
avoid dangerous precipitates. Digitalis toxicity may develop,
because calcium potentiates digitalis. Monitor for hypercalcemia:
lethargy, confusion, irritability, nausea, and vomiting.
6. Monitor for calcium loss (e.g., with loop diuretics, renal tubular
163
dysfunction) or conditions that place the patient at risk for it (e.g.,
acute pancreatitis).
164
more comfortable work of breathing with RR 12 to 20 breaths/min
and absence of the indicators of laryngeal spasm: laryngeal stridor,
dyspnea, or crowing.
Respiratory Status: Ventilation; Respiratory Status: Airway
Patency.
Respiratory monitoring
Hypercalcemia assessment
Goal of assessment
Evaluate the signs, symptoms, and risk factors for hypercalcemia.
165
• Hyperparathyroidism: May be stress-related in critical illness.
Observation
• Symptoms absent unless serum calcium is greater than 11 mg/dL.
Vital signs
• Hypertension.
• Heart block.
• Cardiac arrest.
166
12-Lead ECG
• Shortening ST segment and QT interval.
• Ventricular dysrhythmias.
Collaborative management
Care priorities
167
parathyroidectomy for hyperparathyroidism, discontinuation of
calcium supplements, vitamins A and D, and thiazide diuretics.
168
by neurosensory changes.
Cognitive Orientation; Distorted Thought Self-Control;
Neurologic Status.
Neurologic monitoring
169
Fluid Monitoring; Dysrhythmia Management; Fluid
Management.
Fluid management
170
Phosphorus imbalance (normal serum level
2.5 to 4.5 mg/dL or 1.7 to 2.6 mEq/L)
Phosphorus, the primary anion (− or negative ion) of the ICF, has a
wide variety of vital functions: formation of energy-storing
substances (e.g., ATP); formation of red blood cell 2,3-
diphosphoglycerate (2,3-DPG) (facilitates the release of O2 from the
Hgb to be used by the cells); metabolism of carbohydrates, protein,
and fat; and maintenance of acid-base balance. In addition,
phosphorus is critical to normal nerve and muscle function and
provides structural support to bones and teeth.
Plasma phosphorus levels vary with diet and acid-base balance.
Glucose, insulin, or sugar-containing foods cause a temporary drop
in phosphorus because of a shift of serum phosphorus into the cells.
Phosphorous and calcium have an interdependent effect on each
other and share many of the common causes of abnormalities.
Alkalosis, particularly respiratory alkalosis, may cause
hypophosphatemia as a result of an intracellular shift of
phosphorus. Although the exact mechanism for this shift is not
fully understood, it may be related to an alkalosis-induced cellular
glycolysis, with increased formation of phosphorus-containing
metabolic intermediates. Respiratory acidosis may cause a shift of
phosphorus out of the cells and contribute to hyperphosphatemia.
Although the level of ECF phosphate is affected by a combination
of factors, including dietary intake, intestinal absorption, and
hormonally regulated bone resorption and deposition, phosphorus
balance depends largely on renal excretion.
171
conditions such as chronic alcohol abuse and DKA.
Hypophosphatemia assessment
Goal of assessment
Evaluate the signs, symptoms, and risk factors for
hypophosphatemia. Acute, severe hypophosphatemia can be a life-
threatening condition. Symptoms can be so profound that care
providers focus on extensive workups while sometimes
overlooking the hypophosphatemia.
Observation
172
Symptoms may be caused by sudden decreases in serum
phosphorus, or they may develop gradually because of chronic
deficiency. The majority of symptoms are secondary to decreases in
ATP and 2,3-DPG; therefore, the patient will become acutely
hypoxic at the cellular level, producing a high lactate and metabolic
acid load, resulting in poor coordination, confusion, seizures, and
coma. Other acute symptoms include:
• Rhabdomyolysis, hemolysis.
Vital signs
• Decreased respiratory rate.
• Increased PAWP.
• Decreased CO.
173
Respiratory alkalosis causes phosphorus to move
intracellularly, aggravating the existing hypophosphatemia.
Collaborative management
Care priorities
Box 1-9
FOODS HIGH IN PHOSPHORUS
174
Dried beans and peas
Fish
Milk and milk products (e.g., cheese, ice cream, cottage cheese)
Poultry
175
Goals/Outcomes: Within 24 hours of initiation of treatment the
patient exhibits improvement of acute confusion and normalization
of associated electrolyte imbalances.
Cognitive Orientation; Distorted Thought Self-Control;
Neurologic Status.
Neurologic monitoring
5. Keep the side rails up and the bed in its lowest position with
wheels locked.
7. If the patient is at risk for seizures, pad the side rails and keep an
appropriate-size airway at the bedside.
176
and metabolic acidosis.
HIGH ALERT!
Do not administer intravenous (IV) phosphate at a rate greater than that
recommended by the manufacturer. Potential complications of IV
phosphorus administration include tetany as a result of
hypocalcemia (serum calcium levels may drop suddenly if serum
phosphorus levels increase suddenly; see Hypocalcemia, for
additional information); soft tissue calcification (if
hyperphosphatemia develops, the calcium and phosphorus in the
extracellular fluid compartment may combine and form deposits in
tissue); and hypotension, caused by a too-rapid delivery.
Medication Administration.
177
With decreased 2,3-diphosphoglycerate levels, the
oxyhemoglobin dissociation curve will shift to the left. At a given
PaO2 level, more O2 will be bound to hemoglobin and less will be
available to the tissues.
Respiratory monitoring
178
1. Monitor all patients with suspected hypophosphatemia for
decreasing muscle strength. Perform serial assessments of hand
grasp strength and clarity of speech. Consult the advanced practice
provider for changes.
Cardiac care
179
Ineffective protection
related to compromised immunity resulting from hypophosphatemia
Goals/Outcomes: The patient is free of infection, as evidenced by
normothermia and absence of erythema, swelling, warmth, and
purulent drainage at invasive sites.
Immune Status.
Infection protection
Risk Identification.
180
after IV administration of phosphates) or in patients prone to
hypocalcemia (e.g., those with chronic renal failure).
The primary complication of hyperphosphatemia is metastatic
calcification (i.e., the precipitation of calcium phosphate in the soft
tissue, joints, and arteries). Chronic hyperphosphatemia in the
patient with chronic renal failure may contribute to the
development of renal osteodystrophy.
Precipitation of calcium phosphate occurs when the product of
the serum calcium and serum phosphorus (i.e., calcium ×
phosphorus) exceeds 70 mg/dL.
Hyperphosphatemia assessment
Goal of assessment
Evaluate the signs, symptoms, history, and risk factors for
hyperphosphatemia.
• Increased intake
• Massive transfusion.
181
• Cellular destruction
• Rhabdomyolysis.
• Decreased urinary losses: Hypoparathyroidism, volume
depletion.
Observation
• GI symptoms: Anorexia, nausea, and vomiting.
Vital signs
• Hypotension secondary to vasodilation.
• Tachycardia.
Percussion
• Positive Trousseau sign: Ischemia-induced carpopedal spasms.
Elicited by applying a BP cuff to the upper arm and inflating it
past systolic BP for 2 minutes.
182
Usually patients experience few symptoms with
hyperphosphatemia. The majority of symptoms relate to
development of hypocalcemia or soft tissue (metastatic)
calcifications. Indicators of metastatic calcification include
oliguria, corneal haziness, conjunctivitis, irregular heart rate, and
popular eruptions.
Screening
• 12-Lead ECG: Deposition of calcium phosphate in the heart may
lead to dysrhythmias and conduction disturbance; prolonged QT
interval caused by elongation and elevation of ST segment.
Collaborative management
Care priorities
183
Positive Chvostek and/or positive Trousseau sign.
184
binders. Encourage use of bulk-building supplements or stool
softener if constipation occurs. Phosphate-containing laxatives and
enemas must be avoided (i.e., Fleet’s Phospho-Soda products).
Ineffective protection
related to the inability to avoid internal complications associated with
hyperphosphatemia
Goals/Outcomes: The patient does not develop symptoms of
physical injury caused by precipitation of calcium phosphate in the
soft tissue or joints, or by hypocalcemic tetany.
Activity Tolerance; Mobility; Energy Conservation.
185
for abnormal values. Phosphorus values may be kept slightly
higher (4 to 6 mg/dL) to ensure adequate levels of 2,3-DPG in
patients with chronic renal failure, to minimize effects of chronic
anemia on O2 delivery to the tissues.
186
of neuromuscular activity, neural transmission within the CNS, and
myocardial functioning.
Hypomagnesemia assessment
Goal of assessment
Evaluate for the signs, symptoms, and risk factors for
hypomagnesemia and investigate further whether the patient may
also have hypokalemia and/or hypocalcemia.
187
• Decreased GI absorption: Cancer, colitis, pancreatic insufficiency,
surgical resection in the GI tract, use of laxatives, and diarrhea.
• Protein-calorie malnutrition.
• Cardiopulmonary bypass.
Observation
• Behavioral changes: Mood changes, lethargy, hallucinations, and
confusion.
Vital signs
• Hypotension.
• Tachycardia.
188
• Laryngeal stridor.
Percussion
• Increased reflexes.
Screening
• 12-Lead ECG: PVCs, possible torsades de pointes, prolonged PR
interval, widened QRS complex, prolonged QT interval,
depressed ST segment, flattened T wave, prominent U wave,
atrial fibrillation, paroxysmal atrial tachycardia with variable
block, or other heart blocks related to digitalis effect (in those
taking digitalis derivatives).
Collaborative management
Care priorities
189
1. Increase magnesium level
Box 1-10
FOODS HIGH IN MAGNESIUM
Bananas
Chocolate
Coconuts
Grapefruits
Kelp
Legumes
Molasses
Oranges
Refined sugar
Seafood
Soy flour
190
Wheat bran
191
2. Administer IV MgSO4 slowly. Refer to the manufacturer’s
guidelines. Too-rapid administration may lead to dangerous
hypermagnesemia, with cardiac or respiratory arrest. Patients
receiving IV magnesium should be monitored for decreasing BP,
labored respirations, and diminished patellar reflex (knee jerk). An
absent patellar reflex signals hyporeflexia (seen with dangerous
hypermagnesemia). Should any of these changes occur, stop the
infusion and consult the physician or midlevel practitioner
immediately (see Hypermagnesemia). Keep calcium gluconate at
the bedside in the event of hypocalcemic tetany or sudden
hypermagnesemia.
192
the physician or midlevel practitioner for significant changes.
Inform the patient and significant others that altered mood and
sensorium are temporary and will improve with treatment.
Cardiac care
193
3. Because hypomagnesemia (and hypokalemia) potentiate the
cardiac effects of digitalis, monitor for digitalis-induced
dysrhythmias. ECG changes may include multifocal or bigeminal
PVCs, paroxysmal atrial tachycardia with varying AV block, and
other heart blocks.
Dysrhythmia Management.
194
Hypermagnesemia (serum magnesium level
greater than 2.5 mEq/L)
Pathophysiology
Hypermagnesemia occurs almost exclusively in individuals with
renal failure who have an increased intake of magnesium (e.g.,
those who use magnesium-containing medications). It may also
occur in acute cases of adrenocortical insufficiency (Addison
disease) or in obstetric patients treated with parenteral magnesium
for pregnancy-induced hypertension. In rare cases
hypermagnesemia occurs because of excessive use of magnesium-
containing medications (e.g., antacids, laxatives, enemas). The
primary symptoms of hypermagnesemia are the result of depressed
peripheral and central neuromuscular transmission. Symptoms
usually do not occur until the magnesium level exceeds 4 mEq/L.
Hypermagnesemia assessment
Goal of assessment
Evaluate the signs, symptoms, and risk factors for the development
of hypermagnesemia.
Observation
• Neurologic/neuromuscular symptoms: Altered mental status,
drowsiness, coma, muscular weakness or paralysis, sensation of
195
warmth, diaphoresis, flushing, and thirst.
Vital signs
• Hypotension.
• Bradycardia.
Palpation
• Soft tissue calcification (metastatic).
Screening
• 12-Lead ECG: Prolonged PR interval, prolonged QRS and QT
intervals with levels greater than 5 mEq/L, complete heart block,
cardiac arrest in severe hypermagnesemia.
Collaborative management
196
Care priorities
197
Ineffective protection
related to inability to control internal changes caused by hypermagnesemia
Goals/Outcomes: Within 12 hours of initiation of treatment, the
patient verbalizes orientation to time, place, and person. The patient
does not exhibit evidence of injury as a result of complications of
hypermagnesemia, including no symptoms of soft tissue
(metastatic) calcifications: oliguria, corneal haziness, conjunctivitis,
irregular HR, and papular eruptions.
Neurologic Status.
Neurologic monitoring
4. Keep side rails up and the bed in its lowest position with the
wheels locked.
198
Deficient knowledge
related to magnesium-containing medications
Goals/Outcomes: Within the 24-hour period before discharge
from ICU, the patient verbalizes the importance of avoiding
unusual magnesium intake and identifies potential sources of
unwanted magnesium.
Knowledge: Medication.
Teaching: Individual
Table 1-9
MAGNESIUM-CONTAINING MEDICATIONS
Hemodynamic monitoring
Hemodynamic monitoring is continuous monitoring of the
pressures being exerted on or within the veins, arteries, and heart.
Hemodynamic monitoring is a diagnostic tool, not a treatment or
199
therapy. The information gained from hemodynamic monitoring is
used to evaluate cardiovascular performance, which includes
information about the cardiac output (CO), tissue perfusion, blood
volume, tissue oxygenation, and vascular tone. Hemodynamic
monitoring readings encompass a broad array of measurements,
depending on the technology used. Understanding hemodynamic
values and the trends of the information provided is important in
determining actions used to improve cardiac function, oxygenation,
oxygen use, overall circulation, and tissue perfusion. Accurately
determined hemodynamic values are used to guide fluid and
occasionally blood administration and cardiovascular drug–based
and device-based therapies provided to patients who are critically
ill.
The three overarching assessment parameters provided by
hemodynamic monitoring are calculation of preload (end-diastolic
volume and pressure in both ventricles before contraction),
afterload (pressure created by blood volume and arterial tone,
which the heart must overcome to open the aortic and pulmonic
heart valves), and contractility (ability of the heart muscle to
pump/contract effectively). Preload, afterload, contractility, and HR
ultimately determine stroke volume (SV), CO, and BP. Changes in
any of the four determinants of CO (preload, afterload, contractility,
or HR) may produce significant adverse effects on BP with resulting
adverse changes in cellular function and energy production as a
result of altered tissue perfusion. Hemodynamic monitoring helps
to assess these parameters in the patient who is critically ill so that
appropriate treatment with medications or devices can be provided.
Usage guidelines were developed to outline when use of
hemodynamic monitoring provides the most benefit (Box 1-11).
Box 1-11
OPTIMAL USE OF PULMONARY ARTERY
CATHETERS
Rajaram et al., in 2013, published a review of studies of pulmonary
artery catheter (PA catheter) use in adult patients in intensive care
units (ICUs). The total number of patients included in the review
was 5686. The authors concluded that there was no difference in
200
ICU or hospital length of stay, mortality, or cost between patients
who had a PA catheter and those that did not. The evidence does
not support the argument that the PA catheter is costly and
unnecessary. However, the authors remind their readers that
hemodynamic monitoring is a diagnostic tool not a treatment.
A 2013 guideline for the management of heart failure from the
American College of Cardiology Foundation and the American
Heart Association (ACCF/AHA) gave a Class I recommendation
for use of a PA catheter. The report indicated that the PA catheter
should be used to guide therapy in patients who have respiratory
distress or clinical evidence of impaired perfusion such that cardiac
filling pressures could not be determined via clinical assessment.
The ACCF/AHA 2011 guideline for coronary bypass surgery
included placement of a PA catheter as a Class I recommendation
for patients in cardiogenic shock undergoing coronary bypass
surgery.
In 2007, the ACCF/AHA produced guidelines on perioperative
cardiovascular evaluation and care for patients undergoing
noncardiac surgery. The following excerpts concern their
recommendations on the use of hemodynamic monitoring.
The use of a PA catheter may be helpful in the surgical patient at
risk for hemodynamic disturbances detectable using a PA catheter.
The guideline suggests that three parameters should be assessed
before use: patient disease (incidence of fluid shifts), surgical
procedure (anticipate fluid shifts), and practice setting (presence of
skilled personnel to maintain the PA catheter and interpret data).
Routine use of a PA catheter perioperatively, especially in patients
at low risk of developing hemodynamic disturbances, is not
recommended.
In 2003, Practice Guidelines for Pulmonary Artery Catheterization:
An Updated Report by the American Society of Anesthesiologists Task
Force on Pulmonary Artery Catheterization was published.
The task force recommended looking at the patient, surgery, and
setting before making a clinical decision to use hemodynamic
monitoring. “Patients at increased risk for hemodynamic
disturbances are those with clinical evidence of significant
cardiovascular disease, pulmonary dysfunction, hypoxia, renal
insufficiency, or other conditions associated with hemodynamic
201
instability (e.g., advanced age, endocrine disorders, sepsis, trauma,
burns).
Low-risk patients: Include those with an American Society of
Anesthesiologists (ASA) physical status score of 1 or 2, with
hemodynamic disturbances unlikely to cause organ dysfunction.
Moderate-risk patients: Category ASA 3 who have hemodynamic
disturbances that occasionally cause organ dysfunction. High-risk
patients: Category ASA 4 or 5 who have hemodynamic
disturbances with a great chance of causing organ dysfunction or
death. “The assessment of risk should be based on a thorough
analysis of the medical history and physical examination findings,
rather than on exclusive consideration of specific laboratory results
or other quantitative criteria. Surgical procedures associated with
an increased risk of complications from hemodynamic changes,
including damage to the heart, vascular tree, kidneys, liver, lungs,
or brain, may increase the chance of benefiting from PA
catheterization.”
Pathophysiology
Determinants of cardiac output and blood pressure
The most powerful determinant of CO is tissue oxygen (O2)
demand. The primary function of circulation is to provide a
medium for exchange of oxygen, nutrients, and waste products
between the blood and tissues. The flow of blood throughout the
microcirculation, where the exchange occurs, is dependent on
arterioles (regulate blood flow through changing level of
resistance), capillaries (primary exchange vessels), and venules
(collect and exchange vessels). As metabolism and O2 consumption
increase or decrease, the heart responds, and CO increases or
decreases in direct response to increased or decreased need. The
heart works as a two-sided pump, with the right side pumping
deoxygenated blood into the lower pressure pulmonary circulation
(reflected by PA pressure) and the left side pumping oxygenated
blood into the higher pressure systemic circulation (reflected by
202
BP). Evaluation of CO requires an assessment of the components
that determine SV (preload, afterload, and contractility) for both
sides of the heart and factors affecting the HR.
In the absence of underlying pathology, such as intracardiac
right-to-left or left-to-right shunting, the output of the ventricles
should be the same. If the output of one of the ventricles changes,
the other ventricle should adjust its output to compensate for the
difference. The right and left sides of the heart are connected by the
pulmonary arteries and veins. Many specialized types of central
vessel and arterial catheters are available to measure the pressures
within the cardiopulmonary circulation and provide a means to
calculate CO. The original PA catheter was known as the Swan-
Ganz catheter named after the physicians who developed it. All PA
catheters provide information about the right side and left side of
the heart, as well as systemic circulation. Options for measurements
vary with each uniquely configured catheter. Once the
hemodynamic data are evaluated, strategies may be implemented
to manipulate preload, afterload, contractility, and HR.
Preload
Understanding Frank Starling’s law is fundamental to
understanding preload. Starling’s law of the heart states, “The
greater the ability of the myocardial muscle to stretch at the end of
diastole, the greater is the force of myocardial contraction.”
However, if the stretch becomes consistently excessive, the force of
contraction will diminish. Preload is determined by the compliance
(ability to stretch) of the ventricles during diastole as the blood
volume fills the ventricles. As the blood volume increases, the heart
must “stretch” with each heartbeat to accommodate it. As the blood
volume decreases, the heart stretches much less but must still
generate the force needed to propel the blood volume forward
during systole. This mechanism enables the heart to adjust
ventricular size to varying blood volumes. Preload coupled with
the electrical conduction system of the heart coordinates the output
of the right and left ventricles.
Factors that affect ventricular blood volume include venous
return, circulating blood volume, condition of the heart valves, and
atrial contractility. Ventricular compliance is affected by stiffness
203
and thickness of the cardiac muscle. Any stressor that influences
one of these factors will result in a change in preload, with a
concomitant change in CO. Heart disease affects preload. Patients
with biventricular heart failure and/or “stiff ventricles” are not able
to handle increased intravascular volume. Their preload is always
high because the heart cannot stretch normally to accommodate
more volume. The diseased heart has little ability to compensate for
volume changes. Patients with a right ventricular (RV) infarction
are in a difficult position, as they require a higher preload to
maintain a normal CO because the infarct zone cannot stretch. Extra
ventricular blood volume, or higher preload, creates more stretch in
the normal RV tissues to promote better RV output but can result in
excessive work for the left ventricle. All patients with heart disease
may develop heart failure, thus expert monitoring by the clinician is
required to optimize CO (see Heart Failure, Chapter 5).
Clinically, preload is measured as ventricular end-diastolic
pressure (VEDP), because pressure in the ventricles correlates
closely with volume. For the right side of the heart, RV end-
diastolic (filling) pressure (RVEDP) is reflected by right atrial (RA)
pressure (RAP) or CVP. Left ventricular (LV) end-diastolic (filling)
pressure (LVEDP) is reflected by left atrial (LA), PA diastolic
(PAD), or PA occlusive (PAOP) or wedge (PAWP) pressure
measurements. If preload begins to increase in a patient with heart
disease, appropriate medications, including diuretics, may be given
to help decrease CVP and PAOP. Vasodilating drugs with strong
venodilating properties may also be used to decrease venous return
so that a heart with limited ability to stretch can accommodate and
pump the lesser blood volume. An increase in preload signals that
the ventricles may be unable to eject enough of the end-diastolic
volume, causing more blood to be retained in the ventricles. As a
result, venous congestion and fluid overload occurs, leading to the
clinical signs of congestive heart failure. Conversely, decreased
preload is seen with hypovolemia and certain types of shock where
vasomotor tone is affected causing vasodilation. Decreased preload
can lead to a decrease in CO related to the decrease in SV.
Hypovolemia may be difficult to assess, because the patient may
have pitting edema but is deficient of fluid volume within the blood
vessels. The CVP may not always provide a complete picture of
204
volume status. Stroke volume variability (SVV) can assist the
clinician in assessment of the need for fluid replacement and the
adequacy of the volume delivered. SVV is determined using the
arterial waveform to calculate the change in SV from beat to beat of
the heart (see Septic Shock).
Afterload
Afterload refers to the pressure or force that must be generated
within the right and left ventricles/ventricular myocardium during
systole to overcome the vascular resistance to ejection. The
pressures created by the blood volume and vascular tone within the
pulmonary, aortic, and systemic circulation create resistance against
the aortic and pulmonic valves, which can impede ventricular
ejection. Other resistant forces include increased blood viscosity,
reduced distensibility of the vascular system (created by
atherosclerosis or “hardening of the arteries”), and diseased heart
valves. The clinician should be aware that diseased ventricles are
extremely sensitive to abrupt changes in afterload because the
diseased tissue cannot readily generate additional force to
overcome additional resistance to ejection. Paying close attention to
PA pressures, as well as systemic arterial pressure, is of paramount
importance. If blood volume starts to be retained in the ventricles,
rather than being normally ejected, VEDP increases, followed by
increases in PA pressure. When these changes are observed,
measures such as administration of diuretics or vasodilating drugs
with strong arterial dilating properties may be initiated to decrease
afterload and help improve ventricular ejection. Medications used
for management of hypertension are administered to reduce
afterload.
Because vascular resistance plays a major role in determining
pressures throughout the heart and lungs, RV afterload is evaluated
by calculating pulmonary vascular resistance (PVR), whereas LV
afterload is reflected by SVR. The higher the afterload, the greater
the myocardial wall tension/pressure must be to open the aortic
and/or pulmonic valves, and the greater is the work of the heart to
overcome resistance to flow. This explains why hypertension is
called “the silent killer,” because the constantly increased afterload
strains the heart. Increased cardiac work requires increased
205
myocardial blood flow to deliver additional O2. When blood
flowing through the coronary arteries is diminished by
atherosclerosis, the demand for the increased blood flow required
to manage energy needs created by increased afterload may not be
met, resulting in myocardial ischemia, injury, and possibly
infarction.
Contractility
This is the inherent capacity of the myocardium to contract during
systole. This mechanism functions independently of variations in
preload and afterload. Changes in ventricular contractility have a
significant effect on tissue perfusion and the shape/slope of the
ventricular function curves generated during CO measurement.
Although contractility is not measured directly, a change in
contractility can be inferred when CO is decreased and other
variables that affect CO (i.e., preload, SV, afterload, HR) remain the
same. Changes in ventricular function curves infer changes in
contractility. Several factors positively influence contractility:
sympathetic stimulation, calcium, and positive inotropic agents,
such as digitalis, dobutamine, milrinone, and beta-adrenergic
drugs. Factors such as acidemia, hypoxia, myocardial ischemia,
myocardial infarct, cardiomyopathies, beta-blocker drugs, and
antidysrhythmic drugs can decrease contractility.
Heart rate
Changes in HR affect myocardial functioning significantly. Slight
increases in HR with a constant SV result in increased CO. Very
rapid HRs are associated with a reduction in CO as the duration of
diastole is shortened, resulting in decreased coronary perfusion and
reduced ventricular filling time. Patients who are critically ill often
manifest sinus tachycardia to maintain a CO that meets the demand
for O2 and nutrients at the cellular level. The heart requires more O2
when the HR increases, and as long as coronary artery perfusion is
adequate, HR increases provide compensation needed for increased
metabolic demands. Tachycardia can, however, reach a critical
point where the heart is receiving less O2 if filling time becomes too
brief to provide appropriate coronary artery perfusion. Bradycardia
206
often results in decreased CO unless there are increases in SV
during the longer ventricular filling times. Athletes are able to
maintain excellent CO with slower HRs, but the patient who is
critically ill may not be as fortunate when HR decreases.
Algorithms have been created for advanced cardiac life support,
which include both pharmacologic and electrical therapies to
manage HR.
Hemodynamic assessment
The goal of hemodynamic monitoring is to obtain accurate
measurements and to observe trends in values that are used in
combination with physical assessment findings to provide
appropriate, effective therapies to maintain adequate BP, CO, and
tissue perfusion. The hemodynamic measurements listed in Table 1-
10 are considered the values needed in a complete hemodynamic
profile.
Table 1-10
HEMODYNAMIC NORMAL VALUES AND DERIVED VALUES
207
− PAOP
Stroke volume (SV) CO/HR × 55 to 100 mL/beat
1000
Stroke volume index (SVI) SV/BSA 30 to 60 mL/beat/m2
Right ventricular stroke work index (RVSWI) SVI (PAM − 4 to 8 g/m2/beat
RAP) ×
0.0136
208
using a stethoscope and manometer. Manual or auscultatory BP
readings are wrought with pitfalls that cause false-high and false-
low readings. Proper cuff size, proper cuff position, arm position
being level with the heart, and skill in determining the onset of
the first Korotkoff sound are imperative components for accurate
readings.
209
20 mm Hg and/or the diastolic BP falls by 10 mm
Hg, or greater change when in the standing
position. Clinically the patient may be dizzy or
light-headed. Prepare to safely assist the patient
back to a sitting or lying position to prevent a fall.
210
• Specialized CV catheters allow continuous venous oximetry
(ScVO2) monitoring that provides information on oxygen use.
Cardiac output
CO can be calculated using several methods.
211
catheter to determine the flow rate of a room temperature IV
solution (injectate) passing through the heart. The temperature of
the injectate is lower than the temperature of the blood in the
central circulation. IV solution is injected into a more proximally
located port in the PA catheter and travels through the heart to a
more distally located port. A temperature sensor is used to track
the flow rate of the injectate. The speed of the flow from the
proximal to the distal port is used to calculate CO. It is
considered accurate and reliable. The TD method of CO
determination is now used as the standard for comparing other
methods of CO determination.
Tissue oxygenation
212
Adequate tissue oxygenation is the goal of therapy for patients in
critical care. The regulation of oxygenation is dependent on
regulation of blood flow. The cardiovascular system controls blood
flow by maintaining the appropriate perfusion pressure throughout
the arterial system supplying blood to each organ, and by allowing
each organ to regulate vascular resistance based on the needs of the
organ. CO can be redistributed at the organ or tissue level based on
need. Vasoregulation occurs at the local level by the arterioles or
resistance vessels. Vasoactive medications used to support
perfusion pressure require careful titration based on an analysis of
meaningful data. To assist the clinician in meeting this goal, oxygen
use is measured via specialized catheters.
• The SVO2 PA catheter not only gives a CCO but also measures the
venous O2 saturation (SVO2) via a fiber optic tip in the PA, and is
used for determination of the balance between O2 delivery and O2
use. O2 delivery is the result of CO multiplied by the arterial O2
content (CaO2). The arterial O2 content is determined by Hgb and
arterial O2 saturation (SaO2). The balance between oxygen
delivery (DO2) and oxygen use (VO2) is reflected by the SVO2.
213
up equipment
Ensuring proper setup and maintenance of the pressure monitoring
system will prevent most inaccuracies. Normal waveform
configurations must be understood for all readings so that
abnormal waveforms can be readily identified. Abnormal
waveforms can sometimes reflect a problem with the system setup
or maintenance.
2. During the initial setup, flush or prime the monitoring system (all
tubing and the transducer[s]) without pressure applied to the flush
bag to help prevent formation of air bubbles from turbulent flow
within the empty tubing. Slower priming allows for more even
fluid dispersion throughout the system.
3. Remove excess air from the flush bag before flushing to help
prevent an air embolus from entering the patient’s vasculature. The
excess air can be accidentally introduced into the patient.
4. Flush all stopcocks and apply sterile dead-end caps to seal the
system. Vented caps are not recommended, because the venting
offers an entry point for organisms and could create a leak in the
system.
214
7. Maintain electrical safety guidelines to avoid microshocks
entering the heart via the fluid column created by the monitoring
system.
3. Leveling and zeroing should be done at least once a shift, for any
change in patient position, when the system has been opened to air,
and/or if there is a question of accuracy in values or waveforms
obtained.
215
Hg and a continuous fluid column contained within rigid tubing
between the transducer and the patient. The number of transducers,
and type and length of tubing may vary. Flaws within the system
directly affect the accuracy of pressure readings. The test indicates
if the system is normal, overdamped, or underdamped.
4. Testing should be done when the system is set up, once every
shift, when the system is opened to air for any reason (including
blood sampling), and when waves appear distorted from the usual
appearance.
216
to 2 oscillations (Figure 1-4, A). If the resulting
waveform is abnormally shaped, lacks shape, lacks
amplitude, or does not return to baseline, the
response is abnormal.
217
FIGURE 1-4 Dynamic response testing (square wave,
frequency response testing) using the fast-flush
system. A, Optimally damped system. B, Overdamped
system. C, Underdamped system.
218
Arterial pressure monitoring
219
from Daily E, Schroeder J: Techniques in bedside hemodynamic monitoring,
ed 4, St Louis, 1989, Mosby.)
Table 1-12
ABNORMAL PULMONARY ARTERY PRESSURES
Hemodynamic Normal
Clinical Conditions
Pressure Range
Pulmonary artery 20 to 30 Increased: Right ventricular failure, chronic left ventricular failure,
systolic (PAS) mm Hg constrictive pericarditis, cardiac tamponade, pulmonary
pressure hypertension (primary or related to lung disease).
Decreased: Hypovolemia, preload reduction.
Pulmonary artery 8 to 15 Increased: Left ventricular failure, mitral stenosis, left-to-right
diastolic (PAD) mm Hg shunts, pulmonary hypertension (primary or related to lung
pressure* disease).
Decreased: Hypovolemia, preload reduction.
Pulmonary artery 6 to 12 Increased: Left ventricular failure, cardiac tamponade, mitral valve
occlusive mm Hg regurgitation, mitral valve stenosis, acute ventricular septal
pressure (PAOP)† defect, fluid volume overload.
Decreased: Hypovolemia, afterload reduction.
*
PAD may exceed PAOP by ≥5 mm Hg in patients with pulmonary hypertension,
hypoxemia, acidosis, pulmonary emboli, and other lung disease.
†
PAOP > PAD signals a mechanical problem (i.e., overwedging or improper
identification of PAD).
• The most common sites used for PA catheter insertion are the
internal jugular or subclavian veins. Femoral and brachial veins
may also be used. The most common PA catheter placement
technique is percutaneous insertion of the catheter
introducer/introducing needle using the Seldinger technique for
insertion, in combination with waveform analysis provided by
the hemodynamic monitoring system as the catheter passes
through the heart. Waveform analysis and pressure readings
provide the practitioner with the information needed to know the
position of the catheter. Insertion may also be done using a
cutdown to expose the vessel but is rarely needed. Catheter
placement is occasionally done under fluoroscopy for patients
with abnormal cardiac or vasculature structures.
220
of the PA catheter if the catheter is inserted too far or migrates
out of position. This can cause pulmonary tissue ischemia or
infarction, if it is severe. Slower blood flow can lead to thrombus
formation. If air inadvertently enters the system during line
insertion, through a crack or other flaw in the closed system, an
air embolus may result. If the closed system is cracked or
becomes disconnected, exsanguination may occur. The cardiac
chambers can be perforated during insertion, resulting in
hemorrhage into the mediastinum and cardiac tamponade. The
vasculature can be perforated during insertion, resulting in the
extravascular catheter tip causing fluid or blood accumulation in
the pleural space or the mediastinum and/or a pneumothorax.
Dysrhythmias may occur, particularly when the catheter passes
through the right ventricle.
Diagnostic tests
221
Factors affecting hemodynamic measurements
222
BP.
223
FIGURE 1-6 Right atrial pressure waveform with
electrocardiography (ECG). Source: (Redrawn from Daily E,
Schroeder J: Techniques in bedside hemodynamic monitoring, ed 4, St
Louis, 1989, Mosby.)
224
Right ventricular pressure (RVP)
The normal RVP is 15 to 25 mm Hg systolic, 0 to 8 mm Hg diastolic.
RVP is measured only during catheter insertion and provides
information about the function of the right ventricle and the
tricuspid and pulmonic valves. Elevation of RV systolic pressure
may be seen in pulmonic stenosis, pulmonary hypertension, or
ventricular septal defect (VSD) with left-to-right shunt. Elevation of
RV diastolic pressure may occur with RV failure, cardiac
tamponade, or constrictive pericarditis.
225
FIGURE 1-7 Location of catheter tip and waveforms
obtained during insertion of pulmonary artery catheter.
PAOP, Pulmonary artery occlusion
pressure. Source: (From Urden LD, Stacy KM, Lough ME: Priorities in
critical care nursing, ed 5, St Louis, 2008, Mosby.)
226
(see Table 1-10). All values are helpful in determining how to
manage the patient’s fluid balance, heart function, and vascular
tone and can be individualized to the patient’s body size (index
values). There is ongoing research on the usefulness of indexing
hemodynamic values to body weight in the morbidly obese
population; no consensus has been formed. Abnormal PA pressures
are discussed in Table 1-12. Complications of PA catheters include
ventricular or atrial dysrhythmias, pulmonary ischemia or
infarction, valvular damage (tricuspid, pulmonic), PA rupture,
infection, emboli (thrombotic, air, balloon), and pneumothorax. The
incidence of PA catheter complications ranges from less than 1% to
3% and most are related to insertion.
227
FIGURE 1-8 Pulmonary artery pressure
waveform. Source: (Redrawn from Daily E, Schroeder J: Techniques in
bedside hemodynamic monitoring, ed 4, St Louis, 1989, Mosby.)
228
FIGURE 1-9 Pulmonary artery occlusive pressure
waveform. Source: (From American Association of Critical-Care Nurses
(AACN): AACN procedure manual for critical care, ed 5, Philadelphia, 2005,
Saunders.)
229
management of preload, afterload, contractility, and HR. The
presence of intracardiac shunts renders CO measurements invalid,
because pulmonary and systemic blood flows are erratic and
unequal.
230
Any factor that increases SVR will increase the workload of the
heart and may reduce CO. Vasodilator therapy is used to reduce
SVR to normal limits. A low SVR can indicate systemic
vasodilation, commonly seen with septic, anaphylactic, and
neurogenic shocks, and seen immediately postoperatively when
recovering vascular tone. Vasopressors and IV fluids are
administered to manage vasodilatation along with medications
directed at the cause. Patients with low SVR often have high CO as
a result of low resistance to ventricular ejection. Medications may
affect SVR: norepinephrine, vasopressin, and phenylephrine (Neo-
Synephrine) increase it, whereas isoproterenol, nifedipine,
prostaglandins, sodium nitroprusside, and acetylcholine decrease
it.
231
considerations discussed with SVO2 also apply to ScVO2. Traditional
belief was that hemodynamic stability and normal ABG levels
meant O2 delivery (DO2) to tissues was adequate to meet and
address cellular O2 needs. As technology developed, it became clear
that conventional methods were unable to measure cellular O2
needs (O2 demand) or use (O2 consumption) by assessing O2
delivery alone. With the development of monitors displaying SVO2
continuously, the onset of O2 supply/demand/consumption
imbalance can be more readily identified. SVO2 can be measured
intermittently using mixed venous blood samples from the distal
port of the PA catheter or continuously using a specialized fiber
optic SVO2 PA catheter. CO, Hgb level, and arterial O2 saturation
impact O2 delivery. SVO2 is reflective of O2 delivery and
consumption. If O2 delivery is inadequate, or O2 demand is high,
more O2 will be extracted from Hgb. If the patient is anemic, there
are fewer red blood cells carrying oxyhemoglobin, thus more O2 is
extracted. If the patient has pulmonary disease, such as ARDS, O2
saturation is less, thus less O2 is delivered. Normal O2 delivery is
600 mL O2/min/m2 if CO, Hgb level, and O2 saturation (SaO2 or
SpO2) are normal. Normal O2 consumption ( O2), which should
mirror demand, is 150 mL/min/m2, which means 450 mL/min/m2 of
O2 should be left in the red blood cells returning to the heart. In
other words, approximately 25% of O2 is used, leaving behind
approximately 75%. The textbook normal value for SVO2 is 0.75, or
75%. Very low levels (less than 30%) indicate poor perfusion and
are often associated with lactic acidosis (see Acid-Base Balance). If
the SVO2 value changes by more than 10% for longer than 10
minutes, the nurse should evaluate SaO2, CO, Hgb, and O2. SVO2
monitoring can be used to evaluate the effects of medical and
nursing interventions on tissue O2 use. By examining the variables
involved in tissue oxygenation, the nurse can help determine which
parameters may need to be better managed to meet the current
metabolic demands (Table 1-13).
232
Table 1-13
FACTORS AFFECTING MIXED VENOUS OXYGEN SATURATION
Svo2 is a sensitive indicator of oxygen supply/demand balance. Scvo2 will respond in the same
manner as Svo2. If Svo2 decreases to less than 50%, the patient should be rapidly assessed for
the cause of an increased oxygen demand, or decrease in supply. Anemia, hypoxemia, and
decreased CO may result in markedly reduced oxygen delivery. In the presence of the high
metabolic demands imposed by critical illness, a reduction in O2 delivery or further increase in
O2 demand can produce profound instability in the patient. Changes in Svo2 often precede
overt changes reflective of physiologic instability.
Factor Effect Clinical Examples
on
Svo2
Arterial Oxygen Saturation
↑ Sao2 ↑ Supplemental oxygen
Svo2
↓ Sao2
↓Svo2 Reduced oxygen supply (e.g., ARDS, ET suctioning, removal of
supplemental oxygen, pulmonary disease, asthma, respiratory failure,
obstructive sleep apnea)
Cardiac Output
↑ CO ↑ Administration of inotropes to increase contractility
Svo2
↓ CO ↓ Dysrhythmias, increased SVR, MI, hypovolemia, ↑HR, or ↓HR
Svo2
Hemoglobin
↓ Hgb ↓ Hemorrhage, hemolysis, severe anemia in patients with cardiovascular
Svo2 disease
Oxygen Consumption
↑ Vo2 ↓ States in which metabolic demand exceeds oxygen supply (e.g., shivering,
Svo2 seizures, hyperthermia, hyperdynamic states)
↓ Vo2 ↑ States in which there is failure of peripheral tissue to extract or use oxygen.
Svo2 Significant peripheral arteriovenous shunting: cirrhosis, renal failure.
Redistribution of blood away from beds where oxygen extraction occurs:
sepsis, acute pancreatitis, major burns.
Blockage of oxygen uptake or use: cyanide poisoning (including
nitroprusside toxicity), carbon monoxide poisoning.
Mechanical ↑ Wedged PA catheter creates falsely elevated Svo2
problems Svo2
ARDS, Acute respiratory distress syndrome; CO, cardiac output; ET, endotracheal;
Hgb, hemoglobin; HR, heart rate; MI, myocardial infarction; PA, pulmonary artery;
SVR, systemic vascular resistance.
233
adequacy of the volume delivered. The normal range for SVV is
10% to 15% with the goal of therapy 13% or less.
Collaborative management
The need for accuracy of hemodynamic values cannot be stressed
enough. Making clinical decisions based on these values and the
calculations derived from them is the reason for using
hemodynamic monitoring in patients who are critically ill.
Continuous monitoring of hemodynamic and oxygen use values
allow the clinical team to see trends so that they can intervene
earlier and accurately monitor response to treatment.
Care priorities
234
suspected, square wave testing is done to assess proper
compliance within the system, which is essential for accurate
readings.
235
• Suspected air embolus: Complications are seen more frequently
from venous air emboli, which may happen during any central
catheter insertion, including PA catheters. Symptoms include
acute respiratory distress, apnea, possible wheezing, sudden
hypotension, syncope, hypoxia, cyanosis, possible murmur,
elevated CVP, neurologic deficits, cardiac arrest with asystole,
pulseless electrical activity (PEA), or ventricular fibrillation.
Arterial monitoring systems connected to intraaortic balloon
catheters can cause life-threatening air embolism in the central
circulation, including the aorta, but this is rarely seen in clinical
practice.
HIGH ALERT!
Suspected Air Embolus
The patient should immediately be placed in left lateral
Trendelenburg (head down) position and 100% O2 administered.
Have the patient try to perform a Valsalva maneuver. Aspirate air
from the system: intravenous tubing, arterial line tubing, or the
catheter itself. If severe complications ensue, hyperbaric O2
treatment using the Diving Accident Protocol may be used if
available. Perform cardiopulmonary resuscitation if necessary. Air
can cause stroke or death in the patient.
236
• PA waveform: Has the same waveform components as arterial
pressure, except that the dicrotic notch represents pulmonic valve
closure, followed by runoff flow in the pulmonary vasculature
during diastole. The PA pressure measurements are taken at the
peak systolic and end-diastolic pressures (see Figure 1-8).
• Timing waveforms with the ECG: The a-wave and v-wave are
distinguished by their timing with the ECG. The electrical
conduction of the heart occurs before mechanical contraction.
This is why the RAP/CVP a-wave is found just before the QRS
and the v-wave is found at the T wave. The PAOP wave has
farther to travel to be transmitted; therefore, the a-wave follows
the QRS and the v-wave is found after the T wave and before the
next P wave (see Figure 1-6).
237
important diagnostic adjuncts, because a-waves are absent in an
atrioventricular junctional or idioventricular rhythm. Large,
abnormal a-waves called cannon waves are caused by the atria
trying to contract against a closed AV valve, which may occur
during atrial fibrillation and complete heart block. PAOP with a
large v-wave is an indication of mitral insufficiency.
HIGH ALERT!
Pulmonary Artery Rupture and Occlusion
Overwedging or rapid balloon inflation can cause pulmonary
artery (PA) rupture. Prolonged balloon inflation or PA catheter
migration can lead to balloon rupture, as well as clot formation and
pulmonary infarction. Pulmonary artery occlusive pressure
(PAOP) may be assessed less frequently if a strong correlation is
established between the PAOP and the PA diastolic to avoid
repeated trauma to the pulmonary vessels and to prolong the life
of the balloon. The PA waveform must be continually monitored to
observe for distal migration of the catheter, or proximal
displacement resulting from pulling on the catheter or movement
of the external monitoring system during patient care procedures
(see Table 1-11).
Table 1-11
MECHANICAL PROBLEMS AFFECTING HEMODYNAMIC
MEASUREMENTS
238
*
Whenever the amplitude of an arterial or PA waveform decreases, the patient should
first be assessed for hypovolemia or shock.
†
If line has become disconnected or a portion open to air, the patient must be
assessed for any potential air embolus; then, the line should be changed to prevent
sepsis. PA catheters must always be transduced, as it is necessary to assess
catheter migration through waveform analysis. Catheter migration may result in
pulmonary infarction if not identified and managed.
CPR, Cardiopulmonary resuscitation; PA, pulmonary artery; PAOP, pulmonary artery
occlusive pressure; PEA, pulseless electrical activity; RV, right ventricular.
239
Teaching: Procedure/treatment
240
Hemodynamic regulation
241
7. Consult the advanced practice provider if the PA waveform
remains in wedged position after balloon deflation. This may
indicate that the catheter has lodged in the vessel, which can lead to
pulmonary infarction resulting from lack of perfusion distal to the
lodged catheter.
Ineffective protection
related to inability to control internal responses and external threats posed
by the presence of invasive hemodynamic catheters
Goals/Outcomes: The patient is free of infection, as evidenced by
normothermia, white blood cell (WBC) count <11,000/mm3,
negative culture results, and absence of erythema, heat, swelling, or
purulent drainage at the insertion site.
Immune Status Uncompromised.
Infection protection
242
solution, because dextrose solutions better support bacterial
growth.
10. Record the date of catheter insertion: Ensure that the catheter is
changed according to agency protocol.
243
Ineffective peripheral tissue perfusion (involved extremity)
related to interrupted blood flow secondary to presence of arterial catheter
or thrombosis caused by the catheter.
244
Goals/Outcomes: Within 15 minutes of this diagnosis, the patient
has adequate perfusion to affected extremity, as evidenced by brisk
capillary refill (less than 2 seconds), natural color, warm skin,
normal sensation, and the ability to move the fingers.
Circulation Status.
Circulatory precautions
Ineffective protection
related to potential for insertion complications secondary to ventricular
irritability, patient movement during insertion procedure, or difficult
anatomy.
Goals/Outcomes: The patient has no complications from PA or
CVP catheter insertion, as evidenced by normal sinus rhythm on
ECG, BP within the patient’s normal range, HR <100 bpm, RR <20
breaths/min with normal pattern and depth, normal breath sounds,
and absence of adventitious breath sounds or muffled heart sounds.
Circulation Status.
Risk identification
245
to conduct a preprocedure verification process; mark the correct site
and use of “Time Out” to assure patient safety.
Mechanical ventilation
Mechanical ventilation provides assistance with movement of gases
in and out of the lungs to facilitate blood-alveolar clearance of CO2
and uptake of O2 into the blood. For ventilation to be effective, the
nervous system must be intact, the diaphragm and respiratory
muscle groups must contract, the rib cage must be intact, the
external fibrous level of the pleural sac must be attached to the rib
cage, and intrapleural or intraalveolar pressures should be normal.
This combination of conditions decreases the alveolar resting
pressures, promoting a pressure gradient that facilitates gas
movement into the conducting tubes that ultimately distends
(recruits) the alveoli.
Spontaneous ventilation (whether or not supported) depends on
246
the ability to generate alveolar distention, or negative pressure, and
therefore increases compliance. This is referred to as increasing
alveolar compliance (static compliance), a decreasing alveolar
pressure (pPlat), or negative pressure breathing. There are other
conditions required for patients to generate negative pressure and
breathe spontaneously (Box 1-12). When patients are too weak to
generate adequate force (negative pressure), too weak to maintain
their airway, too sick or sedated to stimulate and contract the
diaphragm, or when the conducting airways or the alveolar units
are constricted, collapsed, or congested (Box 1-13), ventilator
support may be unavoidable. To ensure optimal care of the patient
who requires mechanical ventilation, the practitioner must have
adequate knowledge of the equipment and processes involved in
mechanical ventilation. An exhaustive review of mechanical
ventilation is not possible in this chapter; however, basic concepts
must be addressed.
Box 1-12
FACTORS AFFECTING NORMAL
SPONTANEOUS VENTILATION
1. Having intact phrenic nerve innervation of the diaphragm
Box 1-13
CONDITIONS THAT MAY REQUIRE
VENTILATOR SUPPORT
247
Acute obstructive disease: acute severe asthma; airway mucosal
edema
248
• Charted as breaths per minute.
249
exchange, while helping to reduce the incidence of
ventilator induced lung injury.
• Charted as: VT or tidal volume (i.e., 375 mL/breath).
• Normal is 8 to 10 L/min.
250
• Average proximal airway pressure during the entire respiratory
cycle; a major determinate for oxygenation and a focus for the
settings of alternative ventilation.
Flow rate ( )
• The delivery method and rate of speed for the tidal volume
breath (also affects time spent in inspiration versus exhalation, as
well as pressure reached).
• Normally 40 to 60 L/min.
251
circuit).
Sensitivity
• A setting on the ventilator that adjusts how much negative
inspiratory pressure the patient must generate (see Patient effort)
before the ventilator delivers a breath. Is activated only in assist-
control ventilation (ACMV) or synchronized intermittent
mandatory ventilation (SIMV).
3. Time cycle: Delivers air/gas over a set time after which the
inspiration ends (affects the I:E)—inspiratory time/exhalation time
(I:E).
252
shorter and “exhalation (E) time” will be longer.
This strategy is used in compliant lungs when CO2
retention or ventilator dyssynchrony is evaluated.
253
subatmospheric pressure to the thorax and trunk (similar to
applying an external vacuum) to initiate respiration and do not
require intubation for use. The iron lung, chest cuirass shell, and
poncho chest shell are examples. Because these devices are
noninvasive and do not require intensive monitoring, there has
been a resurgence of interest in their use for long-term home
therapy. They are not discussed here.
Positive-pressure ventilation
All methods of mechanical ventilation require a means of
administering positive pressure for delivery of a predetermined
volume of gas. Positive-pressure ventilation creates a super
atmospheric pressure (greater than 760 mm Hg), which is generated
at the upper airway. The resultant pressure gradient between the
upper airway and the alveoli then allows for the “pushing” gas
volume. This delivery system may be administered via a mask
system (noninvasive) or invasively via an ET tube or tracheostomy.
The concept, put very simply, is to decrease the need for the
development of a significant negative pressure or force,
supplanting that requirement with the super atmospheric pressure.
254
be unable to remove the system to eat or drink without
deterioration. Consideration for additional support is needed when
patients cannot remove the system for short periods of time.
2. Mark and chart the centimeter mark on the tube using the teeth
as a reference point.
4. Cut/shorten the tube to reduce dead space, taking care not to cut
255
the pilot balloon, so only 4 cm protrudes from the teeth.
Box 1-14
REASONS TO CONSIDER INTUBATION
Severe acidosis or hypoxemia
Severe dyspnea
Respiratory arrest
Cardiovascular instability
Aspiration risk
Copious/viscous secretions
Extreme obesity
256
breath, the machine senses the negative-pressure event (sensitivity
set on the ventilator), which triggers the ventilator to deliver a
breath of identical duration and magnitude as the mandatory
breath. The patient receives a breath each time a spontaneous
breath is initiated, regardless of actual minute ventilation
requirement. The “interactive” feature of this mode is that the
patient receives a breath when he or she generates enough negative
pressure to turn the ventilator on. The advantage of this mode is
that patients breathe spontaneously with small amounts of work.
Conventional assist-control (A/C) delivers a preset breath based on
time intervals (defined by frequency). The inspiratory flow rate is
measured in liters per minute, and it determines how quickly the
breath is delivered. The time required to complete inspiration is
determined by the tidal volume delivered and the flow rate: Ti =
VT/Flow rate. The breath is limited by reaching either the preset
volume (volume control [VC]) or pressure (when volume is
delivered reaching a predetermined pressure [pressure control,
PC]). Every breath is controlled (either pressure or volume), but the
patient may take more breaths than the mandatory rate determines
(Table 1-14).
Table 1-14
VOLUME-CONTROLLED VERSUS PRESSURE-CONTROLLED
MECHANICAL VENTILATION
257
pressure or volume control.
258
Only set breath is a ventilator breath and predetermined for
either pressure or volume control. All patient breaths are
volume/pressure variable.
259
These two methods are flow-triggered/limited and (pressure) and
volume-controlled. In ACMV when the patient takes a breath, the
controlled method (volume) turns on. In SIMV when the patient
takes a breath, the breath may either be a synchronized ventilator
breath or a spontaneous volume breath.
Mode and method of ventilation should be determined by
patient need and provider expertise rather than by individual
bias.
Breath limit
• Time limited or cycled: Relates to time that inspiratory flow is
administered and is determined by a preset time or percent of
cycle that relates to inspiration. Inspiratory time is increased to
deliver a volume-controlled or pressure-controlled breath over a
longer time of the breath cycle. Depending on the manufacturer,
inspiratory (I) and expiratory (E) times or flow rate may be the
direct setting to adjust. In either case, the provider may maintain
the tidal volume, minute ventilation, and frequency when
adjusting the E time. I time is increased to deliver a volume-
controlled or pressure-controlled breath over a longer time of the
breath cycle. This will affect the frequency and therefore the tidal
volume delivered. This may be used for noncompliant lungs and
alveolar recruitment to promote better oxygenation and is
referred to as inverse I to E.
260
Table 1-15
MODES OF MECHANICAL VENTILATION
261
application of or increase in PEEP may prompt a decrease in BP.
Generally, PEEP pressures range from 2.5 to 20 cm H2O. Higher
pressures (greater than 24 cm H2O) may be used if the patient can
tolerate the increase and if the condition is warranted. Tolerance is
primarily determined by monitoring BP and regularly assessing for
a pneumothorax.
The role of PEEP in lung ventilation is to stabilize alveoli,
decreasing alveolar collapse, and promoting better gas exchange.
PEEP is applied when the exhalation valve in the circuit closes,
promoting lung trapping of gas (refreshed), which is then measured
as pressure sustained at the end of expiration. When PEEP is
increased, the valve closes earlier. In lung-protective ventilation,
PEEP allows for better distribution of gas over a larger open lung
surface, while preventing alveolar over distention. Gattinoni et al.
showed that injured lungs have less lung surface, which
participates in ventilation, and the application of PEEP in this
diagnosis can open collapsed alveoli and prevent the shear stresses
caused by alveolar recruitment/derecruitment. In the open lung
approach, alveoli and small airways are stented open with a
constant airway pressure. This allows the breath to reach more
functional surface area early in inspiration, as alveolar opening is
maintained by the application. PEEP promotes better gas exchange,
increases the P/F ratio, and allows for reduction of Fio2, and is
frequently used in conjunction with mechanical ventilation to
improve oxygenation. Clinical improvements are reflected by
increased partial pressure of O2 in arterial blood (PaO2) and the
ability to decrease Fio2.
Application of PEEP increases intrathoracic pressure and can
compromise the patient’s hemodynamic status by compressing the
heart and great vessels. Increased intrathoracic pressure decreases
venous return, RV-filling pressures, and CO, which may cause or
potentiate hypotension and shock. Patients with intravascular
volume depletion are at higher risk for associated hemodynamic
instability. High levels of PEEP can cause pneumothorax,
particularly if lung compliance is diminished. The understanding
gained through the study of alveolar mechanics would suggest that
an open lung approach might minimize shear stress and improve
262
oxygenation. Multiple modes of ventilation will allow for open lung
ventilation: high-frequency oscillatory ventilation (HFOV), airway
pressure-release ventilation (APRV), and alveolar recruitment
maneuvers (high levels of PEEP applied for short times to open
collapsed alveoli), followed by the application of PEEP. The
decision-making strategies for patient management are discussed in
Table 1-16.
Table 1-16
FACTORS CONSIDERED WHEN CHOOSING MODES OF
VENTILATION
263
lung to “rest” until the resolution of the underlying lung injury.
Formulas:
1-1
RESEARCH BRIEF BOX
Higher positive end-expiratory pressure (PEEP) should be used for
moderate and severe acute respiratory distress syndrome (ARDS),
whereas lower PEEP may be more appropriate in patients with
mild ARDS. PEEP should be set to maximize alveolar recruitment
while avoiding overdistention. Volume and pressure limitation
during mechanical ventilation can be described in terms of stress
and strain. Fraction of inspired oxygen and PEEP are typically
titrated to maintain arterial oxygen saturation (SpO2) of 88% to 95%
(PaO2 55 to 80 mm Hg).
From Biehl M, Kashiouris MG, Gajic O: Ventilator-induced lung injury: minimizing its
impact in patients with or at risk for ARDS. Respir Care 58(6):927-937, 2013.
264
When Fio2 is at a toxic level (levels of oxygen that promote radical
byproducts, which may actually cause alveolar lining destruction),
it may be of vital importance to consider alternative strategies
designed to increase the functional lung surface available for gas
exchange. The following list is a small sample of current and
experimental ventilator modes designed to optimize MAP and
alveolar recruitment.
265
will be synchronized whenever possible (SIMV). Spontaneous
breathing is not required, but facilitated. No breathing occurs
during low time until weaning begins.
Bilevel ventilation
BiLevel is a method of switching between low-pressure and high-
pressure limits based on the patient’s inspiration and exhalation. In
BiPAP, the circuit switches between a high-airway and low-airway
pressure in an adjustable time sequence. If the patient is not
breathing spontaneously, the I:E ratio and the ventilatory frequency
can be adjusted to optimize ventilation and oxygenation. If the I:E
ratio is reversed, then APRV has to be set up, and mandatory
breaths can be applied. Breathing is allowed during both high-
pressure and low-pressure times. Airway pressure is not as well
controlled. BiLevel can be used initially as pressure-controlled
ventilation, can be weaned to BiPAP, and then weaned to CPAP
before extubation.
266
Mandatory minute ventilation or minimum minute ventilation
(MMV) provides a predetermined minute ventilation to augment
the patient’s spontaneous minute ventilation (breathing efforts).
It is used to prevent hypoventilation and respiratory acidosis
during ventilator weaning when SIMV is supporting the patient.
267
ALI, Acute lung injury; ARDS, acute respiratory distress syndrome; IBW, ideal body
weight; PEEP, positive end-expiratory pressure; PAWP, pulmonary artery wedge
pressure; PIP, peak inspiratory pressure.
Tension pneumothorax
This develops when pressurized air escapes from the lungs and
enters and collects in the thoracic cavity, causing one or both lungs
to collapse. High pressure from mechanical positive-pressure
ventilation may tear diseased or fragile lung tissue, leading to this
life-threatening complication. Symptoms include respiratory
distress, fluctuations in BP, shifting of the trachea toward the
unaffected side, and sudden and sustained increases in PIP.
HIGH ALERT!
If tension pneumothorax is suspected, the patient should be
disconnected from the ventilator immediately and ventilated using
a bag/valve/tube device (Ambu bag). While the primary
nurse/therapist is using tube/mask ventilation, others will facilitate
an emergency physician call and set up the patient for immediate
chest tube insertion/placement.
Gastrointestinal complications
268
Peptic ulcers with profound hemorrhage may develop as a result of
physiologic pressures and stress. Histamine H2-receptor antagonists
(e.g., ranitidine) or proton-pump inhibitors (e.g., omeprazole
[Prilosec], lansoprazole [Prevacid], rabeprazole [Aciphex],
pantoprazole [Protonix], esomeprazole [Nexium], and Zegerid), or
sucralfate (Carafate) may be administered to prevent these ulcers
from developing. A great deal of controversy surrounds the best
strategy for peptic ulcer prevention and the evidence is evolving. In
addition, gastric dilation can occur as a result of the large amounts
of air swallowed in the presence of an artificial airway. If gastric
dilation is left untreated, paralytic ileus, vomiting, and aspiration
may develop. Extreme dilation can compromise respiratory effort
because of the restriction of diaphragmatic movement. Treatment
includes insertion of a gastric tube orally or nasally (oral placement
may be preferred) connected to low intermittent suction to remove
air from the GI tract.
269
Increased ICP occurs as a result of decreased cerebral venous return
to the heart resulting from compression of intrathoracic blood
vessels when using PEEP greater than 5 cm H2O or mean airway
pressure management strategies. This may limit cerebral venous
outflow, therefore increasing the ICP. See the section on Traumatic
Brain Injury in Chapter 3 for additional information.
Fluid imbalance
Increased production of ADH occurs as a result of increased
pressure on baroreceptors in the thoracic aorta, which causes the
system to react as if the body were volume-depleted. ADH
stimulates the renal system to retain water. Patients may need
diuretics if signs of hypervolemia are present. Be alert to new
symptoms of dependent edema or adventitious breath sounds.
270
effective for the prevention of VAP and may be associated with
reduced duration of mechanical ventilation.
Anxiety
Many individuals experience anxiety related to the discomfort
associated with loss of control over their ventilatory process and the
perception that their health status is threatened. Hypoxemia and air
hunger, if present, contribute to anxiety and prompt rapid, shallow,
and often irregular respiratory efforts. The first approach is always
to evaluate mode and method of ventilation to insure appropriate
ventilatory support. The flow rate of the volume must be
considered, and can best be evaluated with a volume-pressure loop.
Coordinated and effective ventilation may not be possible with
severe anxiety and agitation. Diligent administration of anxiolytic
drugs and analgesics, along with close monitoring of the patient’s
response to potent medications, may be necessary to reduce the
work of breathing and facilitate effective mechanical ventilation.
The use of an approved sedation scale is also recommended (see
Sedation and Neuromuscular Blockade). In extreme cases, if the
patient is unable to tolerate the ventilator mode most appropriate
for his or her condition and cannot be managed using high-dose
anxiolytic agents, sedatives, and analgesics, the advanced practice
provider may consider use of neuromuscular blockade (induced
paralysis) to facilitate more effective ventilation. Neuromuscular
blockade should be reserved for only the most extreme situations,
wherein the patient’s life is threatened by the overall energy
271
expenditure related to fear, anxiety, or inability to attain control
over his or her breathing pattern despite other efforts (see Sedation
and Neuromuscular Blockade).
Table 1-17
PARAMETERS FOR WEANING FROM MECHANICAL VENTILATION
Optimal
Pulmonary Function Definition
Parameters
Minute ventilation >10 L/min Tidal volume × respiratory rate; if adequate, it indicates that
the patient is breathing at a stable rate with adequate tidal
volume
Negative inspiratory >−20 cm Measures respiratory muscle strength; maximum negative
force H2O pressure indicates that the patient is able to generate and
272
initiate spontaneous respirations; indicative of the patient’s
ability to initiate inspiration independently
Maximum voluntary 2 × resting Measures respiratory muscle endurance; indicates the
ventilation minute patient’s ability to sustain maximal respiratory effort
ventilation
Tidal volume 5 to 10 Indicates the patient’s ability to ventilate lungs adequately
mL/kg
Arterial blood gases Pao2 >60
Fractional mm Hg
concentration of Pao2 <45
inspired oxygen mm Hg
(Fio2) 0.40 pH 7.35 to
7.45
or
patient’s
baseline
Table 1-18
COMMON ADJUSTMENTS DURING WEANING TO IMPROVE GAS
EXCHANGE
273
Patients with nonchronic pulmonary disease decrease
rate every 30-minute interval. After 2 hours at a
mandatory rate of zero with CPAP, if the patient is
clinically stable, he or she may be extubated.
274
this manner, the patient builds strength and endurance for
independent respiratory effort.
HIGH ALERT!
Apnea
Frequent patient assessments with vigilant monitoring must be
done, because there may not be ventilator backup or an apnea
program to support the patient if the patient fails to breathe.
Failure to wean
Patients who need prolonged mechanical ventilation are increasing
in numbers. These complex patients require high resource use and
achieve suboptimal outcomes, especially if elderly. Patients who fail
the transition from ventilator support to sustained spontaneous
breathing do so primarily because of weakness of the respiratory
muscles, including the diaphragm. Considerations regarding the
following parameters should be evaluated before attempting
weaning. The following parameters should be evaluated when
patients are unable to be weaned from the ventilator.
275
• Left ventricular dysfunction, cardiomyopathy, and
myocardial ischemia.
• Chronic renal failure, which alters capacity for compensation.
Table 1-19
CAUSES OF HIGH-PRESSURE ALARMS DURING MECHANICAL
VENTILATION
276
Patient biting ET tube ARDS
Bronchospasm
Box 1-15
CAUSES OF LOW-PRESSURE ALARMS
Patient disconnected from machine
277
Care plans for mechanical ventilation
Impaired gas exchange
related to altered oxygen supply resulting from an abnormal tidal volume
distribution associated with mechanical ventilation.
Goals/Outcomes: The patient has adequate gas exchange, as
evidenced by PaO2 greater than 60 mm Hg, Paco2 35 to 45 mm Hg,
SpO2 greater than 92%, SvO2 greater than 60%, and RR 12 to 20
breaths/min.
Respiratory Status: Gas Exchange.
Mechanical ventilation
278
right lung has more surface area. If ABG results
show that the patient tolerates left lateral decubitus
position, alternate between the two positions.
Rotational therapy (rotating the patient and/or use
of a chest percussion bed) may be effective.
4. Auscultate the upper chest over the artificial airway to assess for
leaks.
279
8. Notify the advanced practice provider of dysrhythmias, which
can occur even with modest alkalosis if the patient has heart disease
or is receiving inotropic medications (see Appendix 6).
9. If changes in patient status are noted, note the SpO2 reading and
end-tidal CO2, if used, or follow institutional protocol for
addressing deterioration in the status of a patient receiving
mechanical ventilation. An ABG analysis may be warranted.
Airway management
2. Monitor the patient for restlessness and anxiety, which can signal
early airway obstruction and hypoxia.
280
in a secure and proper alignment.
Ventilation assistance
2. Monitor the respiratory rate and quality, and for early signs of
respiratory distress (e.g., tachypnea, hyperventilation, anxiety,
restlessness, lethargy). Cyanosis is a late sign of respiratory
insufficiency.
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HIGH ALERT!
Restlessness Management
Administer prescribed medication for restlessness only after any
physiologic causes, including hypoxia and hypoglycemia, have
been ruled out. Restlessness, if attributable to a nonphysiologic
cause such as anxiety or unrelieved pain, should be managed with
either sedation or analgesia, because it increases O2 demand and
consumption and can interfere with adequate ventilation.
Ineffective protection
related to increased environmental exposure (contaminated respiratory
equipment); tissue destruction (during intubation or suctioning); invasive
procedures (intubation, suctioning, presence of ET tube);
immunocompromised state; and/or the physiologic stress resulting from a
critical illness.
Goals/Outcomes: The patient is free of infection, as evidenced by
normothermia, WBC count ≤11,000/mm3, clear sputum, and
negative sputum culture results.
Immune Status.
Infection protection
282
bundle:
283
suction device is dedicated to use exclusively in the
oropharynx.
284
data suggest that disposable bags be changed with
any frequency, reusable bags should not be used
between patients without sterilization.
10. Be aware of special risk factors for patients with tracheostomy
tubes, and intervene accordingly:
285
Anxiety
related to actual or perceived threat to health status as a result of the need
for or the presence of mechanical ventilation.
Goals/Outcomes: During the interval of mechanical ventilation,
the patient relates the presence of emotional comfort and exhibits a
decrease in irritability, with an HR within the patient’s normal
range.
Anxiety Level.
Anxiety reduction
3. Explain all procedures before they are initiated to the patient and
significant others. Inform the patient of his or her progress.
4. Describe and point out the alarm system, explaining that it will
alert staff in the event of any problem with the ventilator, including
an accidental disconnection.
286
the daily sedation vacation. Analgesics should be administered to
control pain.
3. Assess and record vital signs every 15 minutes for the first hour
of weaning, then hourly if the patient is stable. Report significant
findings to the advanced practice provider such as increased
respiratory effort, hyperventilation, anxiety, lethargy, and cyanosis.
Anxiety
related to perceived threat to health status secondary to the weaning
287
process
Goals/Outcomes: During the weaning process, the patient
expresses the attainment of emotional comfort and is free of the
signs of harmful anxiety, as evidenced by HR less than 100 bpm, RR
less than 20 breaths/min, and BP within the patient’s normal range.
Anxiety Self-Control.
Anxiety reduction
2. Stay with the patient during the initial phase of weaning, keeping
the patient informed of progress being made. Provide positive
feedback for positive efforts.
6. Leave call light within the patient’s reach before leaving bedside.
Reassure the patient that help is nearby.
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Additional nursing diagnoses
Also see nursing diagnoses and interventions under Prolonged
Immobility and Emotional and Spiritual Support of the Patient and
Significant Others, Chapter 2.
Nutrition support
Malnutrition in patients who are hospitalized is common, with an
incidence ranging from 24% to over 50% in different studies. The
impact of malnutrition on patient outcomes is significant, including
decreased wound healing, immune dysfunction, increased
infection, and increased mortality. Length of stay and costs can be
as much as three times higher in patients with a diagnosis of
malnutrition than in patients who are well nourished. The patient
who is critically ill is at high risk for malnutrition and its negative
sequelae. The metabolic response to critical illness includes
increased energy expenditure, protein catabolism, oxidation of
stored lipids, and altered carbohydrate metabolism. Because the
body has no protein stores, protein is transported from the
periphery (muscle mass) to the liver during critical illness for
production of acute phase proteins and gluconeogenesis and to the
gut for preservation of the GI lining and gut-associated lymphoid
tissue. The resting energy expenditure in patients who are critically
ill can be elevated by up to 120% to 160% and remains elevated for
up to 21 days in patients with sepsis or trauma, even when these
conditions are being adequately managed. In patients with sepsis
and trauma, 13% of total body protein stores are lost in the first 21
days of illness despite the provision of adequate nutrition support.
In the patient who is unfed, stressed, and critically ill, up to 250 g
(∼0.5 lb) of lean body mass can be broken down daily. Patients
who are critically ill are often admitted to ICU with some degree of
malnutrition. Those who were not previously suffering from
malnutrition have poor volitional intake in ICU. The role of
nutrition support in the management of patients who are critically
ill cannot be overestimated.
Nutrition support is defined as the administration of parenteral
or enteral nutrition. The goals of nutrition support therapy in the
289
patient who is critically ill are to preserve lean body mass, maintain
immune function, prevent metabolic complications, and in certain
instances to attenuate the disease process. Since the publication of
the last edition of this handbook, the American Society of
Parenteral and Enteral Nutrition (ASPEN) and the Society of
Critical Care Medicine (SCCM) have published joint guidelines for
the provision of nutrition support in the adult patient who is
critically ill. The Canadian Critical Care Nutrition (CCCN)
guidelines were updated in 2013 to include additional
recommendations for the administration of nutrition support in
patients who are critically ill. The revised guidelines underscore the
importance of nutrition support in improving patient outcomes.
The recommendations will be discussed throughout this chapter.
Nutrition assessment
Multiple sources of information are used for the assessment of
nutritional status in the hospitalized patient who is critically ill
including medical and nutrition history, anthropometric data (body
measurements), biochemical analysis of blood and urine, and type
and duration of the disease process. With an individual who is
critically ill, the medical and nutrition history may be obtained from
significant others. Although clinical dietitians in ICU are
responsible for a complete nutrition assessment during the patient’s
stay, according to The Joint Commission, screening for nutrition
risk should be done within 48 hours of admission and is usually
performed by the nurse.
Medical/diet history
A diet history identifies individuals who are or may be at risk for
malnutrition resulting from inadequate intake or an imbalance in
food intake. It should describe the adequacy of both usual and
recent food intake, as well as focus on factors that may have
impaired adequate selection, preparation, ingestion, digestion,
absorption, and excretion of nutrients. The medical history is
included to assess diseases or conditions affecting nutritional status.
The following should be included in the medical and diet history
assessment:
290
• Comprehensive review of usual dietary intake, including food
allergies, food aversions, use of nutritional supplements
including vitamins, supplements, and alternative/complementary
therapies.
291
at older than 75 years).
• NPO (nil per os [nothing by mouth]) status for more than 3 days.
292
including length of stay, infectious morbidity, mortality, and
attainment of nutritional goals.
Physical assessment
Most physical findings are not conclusive for particular nutritional
deficiencies. It is important to compare current assessment findings
with past assessments, especially related to the following:
Anthropometric data
Anthropometrics is the measurement of the body or its parts.
Pounds and inches are converted to metric measurements using the
following formulas:
293
women:
294
stores.
Table 1-20
HEIGHT AND WEIGHT GUIDELINES FOR MEN AND WOMEN
Diagnostic tests
No laboratory test specifically measures nutritional status. Status
can be estimated, however, using the following parameters.
295
Visceral protein status
Normal values may vary with different laboratory procedures and
standards. If the hydration status is normal and anemia is absent,
albumin and transferrin levels may be the initial parameters used
for a general assessment of nutritional status. The following are all
visceral proteins:
296
muscle loss, edema, and reduced grip strength, as well as the
presence or absence of acute illness or injury, chronic illness, or
social or environmental circumstances that would predispose
patients to malnutrition. Regarding interpretation of weight loss,
percent of weight change over time is used to differentiate between
moderate and severe malnutrition. Of note, both the AND-ASPEN
guidelines and the ASPEN-SCCM guidelines do not recommend
using visceral protein markers to identify malnutrition.
Nitrogen balance
Nitrogen balance is used in the clinical setting to measure protein
metabolism and protein status. Nitrogen balance is calculated as
follows: Nitrogen balance = Nitrogen in (calculated from total
protein intake) − Nitrogen out (the sum of nitrogen lost in urine,
stool, and body fluids). Most nitrogen loss occurs through the urine,
with a small, constant amount lost via the skin and feces. Nitrogen
balance studies should be performed by nutrition support
specialists, because accurate calculation is important to determine
the patient’s protein status and protein requirements. Nitrogen
balance studies require a 24-hour urine collection and accurate
measurement of protein intake. Heavy losses of protein in the
presence of ascites, large wounds, malabsorption, and excessive
chest tube drainage are difficult to measure but are considered by
the nutrition support specialist when calculating the nitrogen
balance. A positive or neutral nitrogen balance is optimal, but is
sometimes difficult to attain during critical illness because of the
catabolic nature of the disease.
297
following options.
Indirect calorimetry
Indirect calorimetry is the “gold standard” for calculating energy
needs in the patient who is critically ill and mechanically ventilated.
This test measures O2 consumption and CO2 production as a
byproduct of metabolism and gives the resting metabolic rate
(RMR) and the respiratory quotient (RQ). The RMR is slightly
higher than the basal metabolic rate (BMR). The RQ is the ratio of
carbon dioxide produced relative to oxygen consumption, and can
determine if the patient is being adequately fed (RQ 0.85), underfed
(RQ < 0.82), or overfed (RQ > 1). Indirect calorimetry accuracy can
be affected by many factors including Fio2 ≥ 60, leaking chest tubes,
bronchopleural fistulas, and renal replacement therapy. Specialized
personnel and access to a metabolic cart are required to provide
accurate results.
Predictive equations
Many predictive equations have been validated over the years. The
Harris Benedict Equation was formerly the most common and
accepted formula used to determine RMR. Published originally in
1919, it was widely accepted until 2003 when the American Dietetic
Association recommended other more reliable equations.
Currently, there are many available equations for estimating
energy needs. We will focus on the two equations that are
commonly endorsed and are validated for use for patients who are
critically ill, including the patient with obesity who is critically ill.
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Mifflin St Jeor (MSJ)
The MSJ formula is based on patient age, height, weight, and
gender. The MSJ formula has been shown to be one of the most
accurate formulas for predicting RMR in both obese and nonobese
patients. It has been endorsed by the American Dietetic Association
and by the American Society of Parenteral and Enteral Nutrition.
The MSJ formula is appropriate for most healthy patients. For
critically ill hospital patients who are not mechanically ventilated,
adding a stress factor of 1.2 to 1.3 × MSJ is recommended.
299
carbohydrate daily is required to prevent ketosis.
300
vitamins A and C for burns; thiamine, folate, and vitamin B12 for
chronic alcohol ingestion). Patients who are malnourished and who
are at increased risk of refeeding syndrome should receive
additional thiamine (B1). Enteral formulas contain the RDA for most
vitamins and minerals. However, it is not uncommon for patients
who are tube fed to receive additional multivitamin preparations.
Parenteral multivitamin infusion (MVI) is added to TPN. Trace
elements include zinc, copper, manganese, chromium, and
selenium. Trace elements are usually included in enteral or oral
multivitamin preparations. They are available as a separate
multitrace element preparation for IV administration in TPN. For a
list of common signs and symptoms of vitamin and mineral
deficiency and toxicity, see Table 1-21. For a list of common signs
and symptoms of trace element deficiencies, see Table 1-22.
Table 1-21
SIGNS AND SYMPTOMS OF VITAMIN DEFICIENCY AND TOXICITY
From Clark SF. Vitamins and Trace Elements. The A.S.P.E.N. Adult Nutrition
Support Core Curriculum, 2nd Edition. Charles M. Mueller, Editor. 2012.
301
Fluid requirements
Many factors affect fluid balance. All sources of intake (oral, enteral,
intravenous, and medications), as well as output (urine, stool,
drainage, emesis, fluid shifts, and respiratory and evaporative
losses), must be considered. Fluid intake is closely associated with
energy provided. Approximately 1 mL fluid per calorie is one
method to calculate fluid requirements; however, this often
underestimates fluid needs. Another method to determine fluid
requirements is according to patient weight. Most patients require
between 30 and 40 mL/kg of fluid daily. For patients with fluid
restriction, use less than 25 mL/kg or 1.4 to 1.9 L daily. It is
important to remember to calculate fluid received from enteral
nutrition and PN to avoid fluid overload. Fever increases fluid
needs, and fluid intake should be closely monitored in renal and
cardiac dysfunction.
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benefits of enteral nutrition, patients in the ICU setting frequently
receive only up to 50% of their goal calories. This is as a result of
unnecessary holding of enteral feeds around procedures, ordering
inadequate calories, or tube feeding intolerance. It is also
attributable to a common misconception that enteral feeding cannot
be started until bowel sounds are present. According to the ASPEN-
SCCM 2009 guidelines, as well as the CCCN guidelines, neither the
presence of bowel sounds nor the presence of flatus or stool is
necessary to initiate tube feeding in the patient who is critically ill.
The rationale for this is that bowel sounds are indicators of gut
contractility and do not necessarily correlate with gut function or
absorptive capacity. The reasons for patient intolerance of enteral
feeds in the critical care setting are multifactorial and can be
attributed to inappropriate enteral formula selection, enteral access,
mode of enteral feeding (e.g., bolus versus continuous tube
feeding), medications, or the patient’s underlying disease process.
A dedicated interdisciplinary nutrition support team can address
these issues and prevent tube feeding intolerance in many if not
most circumstances.
1-2
RESEARCH BRIEF BOX
Early enteral nutrition in patients who are critically ill
Another recent trial, by Elke et al., was a secondary analysis of
pooled data that were collected prospectively from nutrition
studies. This trial looked at clinical outcomes of critically ill
mechanically ventilated patients with sepsis and/or pneumonia (N
= 2207) who were enterally fed at either close to goal calories or
hypocaloric or trophic feeding. The study results showed that an
increase of 1000 kcal daily was associated with a statistically
significant reduction in 60-day mortality (odds ratio 0.61, 95%
confidence interval 0.53 to 5.08, P = 0.02) and a statistically
significant increase in ventilator-free days (2.81 days, 95%
confidence interval 0.48 to 0.77, P <0.001). Similar results were
found regarding an increase of 30 g daily of protein
From Elke G, Wang M, Weiler N, et al: Close to recommended caloric and protein intake
303
by enteral nutrition is associated with better clinical outcome of critically ill septic patients:
secondary analysis of a large international nutrition database. Crit Care 18(1):R29, 2014.
Enteral formulas
Enteral formulas are composed of a wide variety of standard and
modular formulas. See Table 1-23 for a more detailed discussion of
currently available enteral formulas.
Table 1-23
TYPES OF ENTERAL FORMULATIONS
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Nutrihep Nutritionally complete; has a greater ratio of branched chain
to aromatic amino acids while restricting total amino acid
concentrations and adding nonprotein calories. Calorie-
dense to prevent fluid overload.
Renal failure
Suplena Low-protein, calorie-dense, low-electrolyte (no electrolytes
Renalcal in Renalcal) formulas designed for patients with reduced
kidney function but not yet on dialysis; restricted total
protein content may reduce or postpone need for dialysis.
High in vitamin B6 and folic acid.
Respiratory Insufficiency
Pulmocare Nutritionally complete; contains a higher proportion of fat to
Novasource Pulmonary carbohydrates; may help prevent an increase in CO2
production. Helpful in patients with COPD, cystic fibrosis,
or respiratory failure.
Oxepa Specialized formula with unique blend of patented oils (EPA
and GLA) to help modulate the inflammatory response in
patients who are critically ill and ventilated, especially those
with ALI, ARDS, and sepsis.
Hypermetabolic and Trauma States
Impact Peptide 1.5, Pivot 1.5 Very-high protein, calorie-dense, immune-enhancing
formulas with added arginine for the patient who is
metabolically stressed and immunosuppressed.
Impact, Impact with fiber, Impact Specialized nutrition for surgical and trauma patients.
glutamine, Pivot 1.5
Peptamen bariatric Very-high protein, low-calorie to meet the needs of patients
who are critically ill and obese.
Oxepa Specialized formula with unique blend of patented oils (EPA
and GLA) to help modulate the inflammatory response in
patients who are critically ill and ventilated, especially those
with ALI, ARDS, and sepsis.
Diabetes or Hyperglycemia
Diabetisource AC, Glucerna Reduced carbohydrate, fiber-containing formulas to help
products, Glytrol minimize glycemic response. Lactose-free.
Fiber-Enhanced
Compleat, FiberSource Replete Fiber blends help to support digestive health and normal
fiber, Promote with Fiber Jevity, bowel function. Products contain soluble or insoluble fiber
Nutren Fiber, Impact with Fiber, or a blend of both. Insoluble fiber is NOT recommended in
Peptamen 1.5 with Prebio, critically ill patients in the ICU setting.
Glucerna products, Diabetisource
AC, Glytrol
Calorie-Dense Products
TwoCal HN, Nutren 2.0 Calorie content is 2 calories/mL to provide adequate
nutrients in lower volume for volume-restricted patients;
some standard products also come in 1.5 calories/mL
concentration.
High-Protein Formulas
Promote, Replete Increased protein to help support wound healing. Meets or
exceeds 100% of recommended daily intake for vitamins and
minerals.
Soy-Based Products
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FiberSource HN, Isosource HN Soy protein isolate and soy fiber for patients who cannot
tolerate milk protein. Not suitable for patients with
galactosemia.
Elemental or Semielemental
Vivonex, Optimental, Peptamen Designed for easy absorption for the patient who has
products, Perative, Impact malabsorption or intestinal atrophy; protein source is free
Peptide 1.5, Vital products amino acids or protein hydrolysates (peptides) or both; fat
sources are oils easily absorbed: MCT, soybean, canola,
safflower; some formulas contain fiber; some have flavor
packets for oral use.
ALI, Acute lung injury; ARDS, acute respiratory distress syndrome; COPD, chronic
obstructive pulmonary disease; EPA, eicosapentaenoic acid; GLA, gamma linolenic
acid; MCT, medium chain triglycerides.
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recommend avoiding insoluble fiber in patients who are critically ill
and at high risk for gut dysmotility and ischemia. Adverse side
effects of fiber and prebiotics include bloating, abdominal pain, and
flatulence.
307
essential fatty acids and calories. MCTs are more easily absorbed
and digested because they do not require pancreatic enzymes for
digestion and are absorbed immediately into the GI tract without
having to be absorbed via the lymph system. However, MCTs do
not contain essential fatty acids and are therefore not a sole fat
source in enteral formulas. Some enteral formulas contain
“structured” lipids. Structured lipids have been chemically
modified to contain both LCTs and MCTs on the same lipid
backbone.
308
are higher in fat. The high-fat content can lead to intolerance in
some patients. Although these formulas are still available, they
are not widely used, and nutrition support clinicians prefer to use
standard formulas and to avoid overfeeding. There are specific
formulas for ARDS and acute lung injury (ALI) that have an
antiinflammatory lipid profile (borage oil and omega-3 fatty
acids) and high amounts of antioxidants. The ASPEN-SCCM
guidelines for nutrition support in the patient who is critically ill
recommend these formulas for ICU patients with ALI/ARDS,
with a high level of recommendation. However, recent
randomized, controlled trials failed to show any benefit of these
products in patients with ALI, thus these recommendations may
be downgraded in updated guidelines. The recently updated
CCCN guidelines did downgrade the recommendation for use of
these formulas in patients with ALI/ARDS from “recommended”
to “should be considered.”
Enteral access
There are many different options for enteral access based on length
of therapy desired (short term versus long term), site of entry (nasal
versus enterostomy), and terminal site (stomach, duodenum,
jejunum).
309
Site of delivery
Stomach: The stomach is the easiest site for enteral tube placement;
gastric feeding simulates normal GI function, and may be used
for bolus, intermittent, cyclic, or continuous feedings. Entry site
into the stomach is nasal (NG), oral (OG), percutaneous (PEG),
laparoscopic, or surgical (open gastrostomy).
Site of Entry
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Procedure-related: The most common procedure-related
complications are epistaxis, aspiration, and circulatory or
respiratory arrest. The most serious complication is misplacement
into the bronchi. For this reason, verification of feeding tube
placement is imperative when placing a nasoenteric feeding tube.
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Methods of administration of enteral nutrition
Enteral nutrition can be delivered either as continuous infusion,
cyclic infusion, intermittent feeding, or bolus or gravity drip
feeding. For patients with feeding tubes terminating in the jejunum,
only continuous or cyclic infusion is appropriate because the
jejunum cannot tolerate large boluses of fluid.
Continuous, pump-assisted, tube feeding is the most common
and preferred method of enteral nutrition delivery in ICU patients.
Other indications for continuous infusion are patients at risk for
refeeding syndrome, patients receiving feeding via a jejunostomy
tube, patients with poor glycemic control, or those who have not
tolerated bolus or intermittent feeding. Continuous tube feeding is
usually started at a low rate (10 to 25 mL/h) and is advanced slowly
every 4 to 6 hours to the goal rate. The goal rate can be calculated
by determining the total daily volume to be infused and dividing
by 24 hours.
Cyclic tube feeding is almost the same as continuous tube
feeding, but the total volume is infused over a shorter amount of
time, usually 12 to 16 hours, but sometimes as little as 8 hours. This
method is also used to infuse tube feeds at night (nocturnal tube
feeding) as a method to help the patient transition to an oral diet.
Intermittent tube feeding can be delivered via a pump or by the
gravity drip method. Larger volumes of formula (240 to 720 mL or 1
to 3 cans) are infused over a shorter period of time (usually from 20
to 60 minutes) several times a day, depending on the volume
needed to meet the patient’s caloric needs.
Bolus or gravity drip feedings are similar to intermittent tube
feeding, but the volume of enteral formula is given over a shorter
period of time (5 to 10 minutes) several times a day instead of being
allowed to infuse over a longer period of time. Bolus feeding is
most similar to normal feeding, and is the least expensive and
cumbersome method of tube feeding. It is generally not used in
patients who are critically ill and who cannot tolerate such rapid
infusion of large amounts of volume (Table 1-24).
Table 1-24
METHODS OF ADMINISTRATION FOR ENTERAL PRODUCTS
312
Type Typical Rate of Administration Comments
Bolus 250 to 400 mL four to six times daily. Recommended for stable,
Administer using an open-ended, 60-mL ambulating patients. May cause
catheter-tipped syringe allowing infusion by cramping, bloating, nausea,
gravity. Do not push until feeding tolerance diarrhea, aspiration; not
is well established. recommended for unstable
critically ill patients. Higher risk for
aspiration.
Intermittent Bolus feeding infused by pump: Begin with Starting regimen
120 mL formula (half a can) over 1 hour, Should not exceed 30 mL/hr; may
with 30 to 50 mL water flush before and cause cramping, nausea,
after feeding. bloating, diarrhea, aspiration;
Advancement: Increase formula by 60 mL may need to reduce infusion rate
every 8 to 12 hours if residual is less than to decrease discomfort and
half the volume of the previous feeding to increase tolerance.
a maximum of 450 mL of feeding.
Cyclic Continuous tube feeding generally infused Recommended for patients who
over 12 to 20 hours daily. Rate to be cannot tolerate bolus or
determined by formula and caloric needs. intermittent feeding and patients
Full-strength formula should be used to with J-tubes. Allows more time for
afford the patient the best opportunity to absorption of nutrients while also
receive maximal support from the feeding. allowing time for gut rest and
allowing time for patient to
ambulate freely.
Continuous Rate to be determined by formula and Allows more time for absorption of
caloric needs. Full-strength formula should nutrients. Less risk of aspiration.
be used. If not well tolerated, reducing the Recommended for patients who are
infusion rate may be warranted. Be mindful critically ill and patients with J-
of the number of interruptions in feedings, tubes.
as each interruption reduces the amount of
nutrition support the patient receives.
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For patients receiving bolus or intermittent bolus enteral feeding,
gastric residuals should be checked before initiation of the bolus
feeding.
To minimize aspiration, the following factors should be
considered:
Table 1-25
MANAGEMENT OF COMPLICATIONS IN THE TUBE-FED PATIENT
Complication/Possible
Suggested Management Strategy
Causes
Nausea and Vomiting
Fast rate Decrease rate
Fat intolerance Change to a low-fat formula
Fiber content Change to a low-fiber formula
Delayed gastric Change from bolus to continuous or cyclic tube feeding
emptying Decrease rate or hold tube feeding, consult the physician to rule out
Gastrointestinal ileus, gut ischemia
intolerance (high
residuals, abdominal
pain and distension)
Clogged Tube
Inadequate flushing Flush tube with at least 30 mL water after each feeding and before and
after medication administration. Flush every 4 hours with a
minimum of 30 mL water as ordered. For clogged feeding tubes,
flush with warm water (60 to 100 mL), repeat as necessary. If feeding
tube is still clogged, consider an enzyme solution to unclog feeding
tube, such as Viokace or Clog-Zapper.
Do not use Coca-Cola or pineapple juice to unclog feeding tube
because this can further denature the protein and exacerbate the
clog.
Instillation of crushed Do not instill crushed medications in small-bore tubes. Substitute
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medications liquid preparations after consulting the pharmacist and prescriber.
Some medications may be crushed into a fine powder and dissolved.
Check with the pharmacist, because crushing can alter medication
characteristics. Never crush time-released medications.
Incompatibilities between drugs and feeding formulas are possible.
Some medications that require that tube feeding be held around
administration include phenytoin, warfarin, fluoroquinolone, and
tetracyclines.
Viscous medications Dilute viscous medications with water before administering.
Dislodged feeding If a standard tube for replacement is not immediately available, insert
tube (enterostomy a Foley catheter of suitable size to keep the entry site open until a
tube) feeding tube is available.
1. Use oral route when possible (if the patient is taking some PO,
PO administration is preferred).
315
3. Check osmolality and sorbitol content if the patient experiences
diarrhea. If medication has high osmolality, dilute before
administration.
1. Phenytoin: Hold tube feeding for 2 hours before and after drug
administration.
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feeding 1 hour before and 2 hours after drug administration.
Table 1-26
SELECTED “DO NOT CRUSH” MEDICATIONS AND MEDICATIONS
THAT REQUIRE CAUTION WITH CRUSHING
Table 1-27
SELECTED MEDICATIONS THAT CAN CAUSE OR EXACERBATE
DIARRHEA
317
Common Medications with High Osmolality Common Medications with High
Sorbitol Content
Acetaminophen liquid Hydroxyzine HCl Acetaminophen liquid
syrup
Acetaminophen with codeine Lithium citrate Guaifenesin/dextromethorphan
elixir syrup syrup
Dexamethasone solution Metoclopramide Lithium citrate syrup
HCl syrup
Parenteral nutrition
Parenteral (IV) nutrition provides some or all of the patient’s
required nutrients using either a peripheral venous catheter (PIV)
or central venous catheter (CVC). TPN or hyperalimentation (HAL)
are interchangeable terms referring to the administration of IV
nutrition. TPN that is administered via a peripheral vein is called
peripheral parenteral nutrition (PPN). TPN administered via a
central line is called central parenteral nutrition (CPN). CPN can
meet total nutritional needs in patients who cannot be given enteral
support safely or whose GI tract cannot be accessed. Parenteral
nutrition is also used when the GI tract is unable to function, such
as in the case of motility disorders, for example, postoperative ileus
or small bowel obstruction. PPN, by contrast, usually does not meet
the nutritional needs of the patient and is generally reserved for
short-term IV nutrition.
Parenteral nutrition solutions are compounded from a
combination of dextrose, amino acids, electrolytes, vitamins, trace
elements, sterile water for injection (SWFI), and IV fat emulsion (IV
lipids). Total nutrient admixtures (TNAs) are formulated by
combining dextrose, fat, and amino acids together in one container.
2-in-1 TPN admixtures combine dextrose and amino acids, and are
combined with electrolytes, vitamins, and minerals, and IV fat
emulsion is given separately. A 0.22-micron in-line filter must be
used with 2-in-1 TPN formulas (amino acids and dextrose
solutions). The 0.22-micron filter cannot be used for TNA solutions
because it can disrupt the lipid emulsion. Instead, a 1.2-micron filter
318
should be used with TNA. A 1.2 micron filter should be used for IV
fat emulsions hung separately. TPN can be infused as a continuous
infusion or as a cyclic TPN. Cyclic TPN is usually infused over 8 to
16 hours and is beneficial in long-term TPN patients to increase
patient mobility and to allow for organ rest.
Components of TPN
• Fat: IV fat emulsion (lipids) are available as 10%, 20%, and 30%
emulsions. The 10% and 20% emulsions can be administered as
part of TPN or separately; 30% fat emulsion can only be used to
compound TNA and cannot be administered separately. IV fat
emulsions (IVFEs) are isotonic solutions that provide essential
fatty acids and a source of concentrated calories. IVFEs in the
United States have traditionally consisted of polyunsaturated
319
LCTs only. Recently, a new IVFE has been approved by the U.S.
Food and Drug Administration (FDA) that also contains olive oil
(a monounsaturated LCT). Outside of the United States, IVFEs
containing MCTs and fish oil are also available. As stated earlier,
an IVFE that is administered separately can be infused without
an in-line filter. As stated earlier, an IVFE that is administered
separately should be infused a 1.2 micron in-line filter.
Additionally, for TNA a 1.2 micron filter (not a 0.22-micron filter)
should be used.
320
hours. Patients receiving propofol (Diprivan),
which is lipid-based, should receive fat emulsion
with caution, not to exceed 60% of total calories
from fat. Current recommendations for patients
who are critically ill recommend no more than 1
g/kg of IVFE daily.
• Multivitamins: Multivitamins for TPN are available as MVI-12
and MVI-13. The IV MVI contain fat-soluble vitamins (A, E, D,
and K) and water-soluble vitamins (B complex and C). The only
difference between the two formulations is that MVI-12 does not
contain vitamin K. Usually 10 mL of MVI is added to the TPN
daily.
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4. Use imported products if use is approved by the
specific institution.
Table 1-28
CATHETERS USED IN PARENTERAL NUTRITION
Catheter Description
Temporary/Short-Term Use
Peripherally May be inserted into a peripheral vein and threaded into a central vein at
inserted bedside by a physician or specially trained infusion therapy nurse. May be a
central single or double lumen.
catheter May be used for total parenteral nutrition (TPN) administration at home.
(PICC) Catheter may remain in place for several months. Multiple uses of a single
lumen for blood sampling, nutrition support, and medication administration
increase the risk of infection, especially in patients who are
immunocompromised. Note: A midline PICC is NOT a central catheter and
only peripheral parenteral nutrition should be infused via this type of line.
Multilumen Inserted at bedside. May have up to four lumens. Subclavian or jugular vein
central accessed. Dedicate one lumen, preferably the most distal, for administration of
venous TPN. Other lumen(s) are used for medication administration and drawing of
catheter blood samples.
(CVC)
Permanent/Long-Term Use
Right atrial Generally placed surgically by a physician into the subclavian or jugular vein
catheter (e.g., with the catheter tunneled and exiting from the skin. The catheter usually
Hickman, includes a Dacron cuff from which the catheter exits the vessel. This type of
Broviac) catheter is associated with the lowest infection rates of all central lines.
Implantable May be placed by a radiologist or surgeon. Designed for repeated access,
venous making the need for repeated venipuncture unnecessary.
access device
(IVAD, such
as Infuse-a-
Port, or Port-
a-Cath)
Modified from Eisenberg P. In Swearingen PL, editor: Manual of medical-surgical
nursing care, ed 6, St Louis, 2007, Mosby Elsevier.
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Central venous IV catheter (CVC): Used for infusion of large
amounts of nutrients or electrolytes with smaller fluid volumes
(hypertonic solutions) than those in PPN. The solution is usually
delivered through a large-diameter vein (e.g., superior vena cava
via the subclavian vein). The volume of blood flow rapidly dilutes
the hypertonic solutions and decreases irritation of vein walls.
Nontunneled catheters are usually placed in the ICU for short-term
infusion of medications and TPN. Tunneled catheters are more
difficult to insert, but are better suited for long-term TPN. For a list
of complications associated with central lines, refer to Table 1-29.
Table 1-29
LINE COMPLICATIONS IN PATIENTS RECEIVING PARENTERAL
NUTRITION
Potential
Management Strategy
Complications
Upon Central Line Insertion
Pneumothorax Position a rolled towel under the patient’s back, parallel to the spine before the
temporary catheter is inserted. Ensure that x-ray is done immediately after
insertion to determine placement of catheter before initiating total parenteral
nutrition (TPN). Monitor for diminished or unequal breath sounds, tachypnea,
dyspnea, and labored breathing. The greater the number of catheter attempts,
the greater the chance for pneumothorax.
Accidental If pulsatile, bright red blood returns into the syringe during central catheter
subclavian insertion into the subclavian vein, assist with immediate removal of the needle
artery and apply pressure for 10 minutes anteriorly and posteriorly at the point of
penetration penetration. If internal bleeding is unable to be controlled, the patient will
leading to develop a hemothorax and hemorrhagic shock.
hemothorax
During Catheter Maintenance
Catheter If solution is infusing sluggishly, flush line using positive pressure with saline.
occlusion Check to see if line or tubing is kinked. If line is occluded, try to aspirate clot
and contact the physician or midlevel practitioner who may prescribe a
thrombolytic agent, such as Cathflo TPA, TPA (tissue plasminogen activator),
or urokinase, according to agency protocol.
Leakage or Do not insert needles into central line port lumen caps to avoid damaging the
catheter catheter. If the lumen is accidentally punctured and begins leaking, notify the
puncture physician or midlevel practitioner immediately for further action.
Air embolism If signs of air embolism occur, examine the catheter to determine whether an
(a medical open port enabled air to enter the infusion system. Clamp the catheter distal to
emergency) any opening discovered. Turn the patient onto their left side and place in the
Trendelenburg position (head down, feet up) and notify the physician or
midlevel practitioner immediately while administering oxygen.
Central line– Assess for swelling of the upper extremities and perform a neurovascular
related assessment. If limb is swollen, is cool, and has reduced or absent pulses, the
thrombosis physician or midlevel practitioner should be notified and consideration given
leading to to removing the central venous catheter. The extremity should be elevated and
upper the thrombosis managed as ordered to address anticoagulation.
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extremity deep
vein
thrombosis
324
postpyloric placement and elemental feedings, and other GI
dysfunction that precludes oral or enteral intake.
Although the initiation of enteral nutrition support in the patient
who is critically ill is highly recommended within the first 24 hours
of admission to ICU, early initiation of TPN in the patient who is
critically ill and who cannot maintain volitional oral intake or who
is not a candidate for enteral nutrition is no longer routinely
recommended. In general, it is recommended to wait at least 5 days
before initiating TPN in patients who are critically ill. These
recommendations were based on studies that found a decreased
risk of infectious morbidity and complications in patients who were
NPO compared with those who received TPN.
Early initiation of TPN in patients who are critically ill is
recommended for patients who are already malnourished on
admission (10% to 15% recent weight loss or a patient weighing less
than 90% of his or her IBW), especially those who are going to
undergo major GI surgery. Some clinicians will recommend
holding IVFE for the first week of PN therapy in patients who are
critically ill because fat metabolism is impaired in critical illness and
soy-based IVFE may have immunosuppressive properties. It is
important to note that TPN therapy that is provided for a very short
time period (less than 5 to 7 days) is not recommended because it
will not improve the patient’s nutritional status and only puts the
patient at risk for complications. It is also important that patients
who are receiving TPN be reassessed frequently for the possibility
of transitioning to either enteral or oral nutrition.
TPN complications
Complications with TPN can be divided into two categories: early
complications and late complications. Early complications from
TPN include hyperglycemia, hyperlipidemia, line infections,
phlebitis, azotemia, refeeding syndrome, and electrolyte
abnormalities. Late complications include trace element
deficiencies, hepatobiliary disorders (hepatic steatosis, PNALD
(PN-associated liver disease), metabolic bone disease, and central
line infections.
For information regarding managing macronutrient-related and
micronutrient-related complications, see Table 1-30.
325
Table 1-30
MACRONUTRIENT AND MICRONUTRIENT COMPLICATIONS IN
PATIENTS ON TOTAL PARENTERAL NUTRITION
Hypertriglyceridemia Can result from either excessive intravenous (IV) fat emulsion or by
infusing IV fat emulsion too quickly.
Hypertriglyceridemia can also result from excessive dextrose
administration.
Monitor triglycerides weekly. Hold IV fats for triglycerides >400 mg/dL.
Essential fatty acid Usually seen in patients who are not receiving IV fat emulsion with
deficiency (EFAD) TPN.
Can occur within 1 to 3 weeks of IV fat emulsion-free TPN.
Minimum IV fat emulsion necessary to prevent EFAD is 100 g weekly
(500 mL of 20% IV fat emulsion)
Azotemia Usually occurs because the patient is either receiving excessive protein,
inadequate fluid, or both.
Monitor input and output for signs of dehydration. Ensure adequate
fluid intake.
Micronutrient and Fluid and Electrolyte Disturbances: See Tables 1-21, 1-22
Refeeding syndrome Usually attributable to carbohydrate administration in patients who are
malnourished or prolonged NPO (nil per os) status. Initiate TPN slowly
(lower % dextrose). Monitor electrolytes (especially phosphorus,
potassium, and magnesium). Consider the addition of thiamine in TPN
to prevent thiamine deficiency and subsequent lactic acidosis, beriberi,
and Wernicke encephalopathy.
From Kumpf VJ, Gervasio J. Complications of Parenteral Nutrition. The A.S.P.E.N.
Adult Nutrition Support Core Curriculum, 2nd Edition. Charles M. Mueller, Editor.
2012.
Table 1-22
SIGNS AND SYMPTOMS OF TRACE ELEMENT DEFICIENCY AND
TOXICITY
326
Trace
Signs of Deficiency Toxicity
Element
Chromium Glucose intolerance, hyperlipidemia, Renal failure, anemia,
peripheral neuropathy, encephalopathy thrombocytopenia, liver failure
Copper Common: hypochromic, microcytic anemia Gastrointestinal symptoms, hepatic
and neutropenia (similar to signs and failure
symptoms of vitamin B12 deficiency) Biliary excretion – caution in liver
Central nervous system dysfunction, failure
hypotonia
Selenium Cardiomyopathy, myalgia, myositis, Chronic: nail and hair changes, N/V,
hemolysis, and impaired cellular immunity weight loss, paresthesias, fatigue,
garlic odor on breath, ↑ incidence
of diabetes
Acute (rare): cardiac abnormalities,
hypotension
Electrolyte imbalances
Electrolyte imbalances can occur during the administration of both
enteral nutrition and PN (Table 1-31).
Table 1-31
POSSIBLE ELECTROLYTE IMBALANCES OCCURRING IN
ENTERAL AND PARENTERAL NUTRITION
327
Parenteral: Increase free water, decrease sodium in TPN, increase volume
of TPN.
Enteral: All enteral formulas are low sodium. Change tube feeding
formula to less concentrated formula and increase water flushes.
Hyponatremia Most common cause in patients receiving TPN is administration of
hypotonic fluids or volume overload. In patients who are tube-fed,
hyponatremia may be caused by excessive fluid administration or
excessive water flushes. Other causes of hyponatremia include adrenal
insufficiency, renal insufficiency, SIADH (syndrome of inappropriate
antidiuretic hormone), cirrhosis, and chronic heart failure.
Management
Parenteral: Decrease fluid and/or increase sodium in TPN.
Enteral: Switch to calorie-dense, fluid-restricted tube-feeding formula,
decrease water flushes via feeding tube or flush with normal saline as
directed.
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exogenous administration of phosphorus. Medications that can cause
hyperphosphatemia include phosphorus-rich solutions, antacids,
diuretic agents, and steroids. Associated with metabolic acidosis.
Management
Parenteral: Decrease phosphate in TPN or other exogenous phosphate
administration.
Enteral: May require treatment with phosphate binders such as
sevelamer (Renvela) and calcium acetate (PhosLo). Change to a renal
tube-feeding formula.
Hypophosphatemia A complication with a high mortality, often found in malnourished
patients with refeeding syndrome. As the patient receives fluids
containing dextrose, phosphorus shifts rapidly into the intracellular
space, causing hypophosphatemia. Refeeding syndrome also affects
other intracellular electrolytes, particularly potassium and magnesium.
Associated with metabolic alkalosis.
Management
Parenteral and Enteral: Initiate tube feeding or TPN slowly to avoid
refeeding syndrome.
Parenteral: Increase phosphorus in TPN or provide other sources of
phosphorus (sodium phosphate, potassium phosphate) in patients
with low phosphorus levels.
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hypercalcemia. Bisphosphonates can be used to treat chronic
hypercalcemia.
Parenteral: Decrease calcium in TPN.
Hypocalcemia Occurs with reduced vitamin D intake, hypoparathyroidism, and
hypomagnesemia. Medications that can cause hypocalcemia include
loop diuretics, bisphosphonates, calcitonin, phenobarbital, and
phenytoin.
Management
Parenteral and Enteral: Calcium supplementation (parenteral or oral).
Ionized calcium level should be used as a guide to replacement,
because serum calcium is bound to albumin. If albumin level is low,
calcium level will appear falsely low.
Transitional feeding
A period of adjustment is needed before discontinuing nutrition
support. It is good practice to taper enteral nutrition and PN as oral
intake increases instead of discontinuing nutrition support as soon
as the patient is able to take a PO diet. Often, parenteral or enteral
nutrition can be cycled over a period of hours as a means of
tapering. For example, the nutrition support clinician may cycle the
enteral or parenteral feeding at night to allow the patient to increase
PO intake during the day. If nutrition support is not tapered when
the patient begins an oral diet, this can interfere with the patient’s
appetite and minimize his or her PO intake, keeping him or her on
nutrition support for longer than necessary.
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infection (see Risk for Infection).
Nutritional Status: Nutrient Intake.
Nutrition monitoring
331
11. Be aware that residual volumes of gastric feedings include not
only feeding but also gastric secretions. The amount of residual
feeding is NOT purely feeding. More recent studies indicate that
caregivers may not need to be concerned about residual volumes of
less than 250 to 500 mL. Patient positioning also effects the amount
of residual volume that may be found by the caregiver.
5. Elevate the HOB at least 30 degrees during and for 1 hour after
feeding. If the patient is receiving continuous enteral nutrition, the
HOB should always be elevated at least 30 degrees.
332
6. Notify the advanced practice provider if gastric residual is
greater than 250 to 500 mL (per institution protocol) or if the patient
is having any signs of abdominal pain or distention. The patient
should be positioned on their right side for 20 minutes before
aspirating the enteral tube for residual volume to ensure that
feeding is being directed toward the small bowel. False high
volumes may be reported if feeding has pooled in the body of the
stomach in a supine patient. If the caregiver is certain that the
residual volume was properly obtained, hold feeding for 1 hour,
and then recheck residuals.
Diarrhea
related to adjustment to formula, method of administration, and volume of
enteral feeding.
Goals/Outcomes: The patient has begun to form normal stools
within 24 to 48 hours of intervention.
Bowel Elimination, Electrolyte and Acid-Base Balance;
Nutritional Status: Food and Fluid Intake
Diarrhea management
333
dehydration.
6. Bacterial contamination:
334
• Hang time for closed-system enteral formulas is 24
to 48 hours per manufacturer’s guidelines.
8. Medications:
335
a recommendation for administration of probiotics
in patients in ICU. The 2013 CCCN guidelines
currently recommend that probiotics be considered
in patients who are critically ill. There have been
reports of gut ischemia with probiotic use in
patients with acute pancreatitis (PROPATRIA trial)
and there have been several cases of fungemia
associated with the use of Saccharomyces boulardii
(Florastor). Therefore, it would be prudent to avoid
use of probiotics in patients with acute pancreatitis
and to avoid the use of Florastor in patients in ICU
or those with CV catheters.
Skin surveillance
336
Nasoenteric tube/postpyloric feeding tube
7. Give ice chips, chewing gum, or hard candies PRN (pro re nata
[when necessary]) if permitted.
Gastrostomy tube/PEG
10. Assess site for erythema, drainage, tenderness, and odor every 4
hours.
12. Secure tube so that there is no tension on the patient’s tissue and
skin.
13. After insertion, clean skin with mild soap and water. Rinse and
dry the area thoroughly. Routine use of antibiotic ointment and
hydrogen peroxide is no longer recommended.
Jejunostomy tube/PEJ
14. Assess site for erythema, drainage, tenderness, and odor every 4
hours.
337
necessary.
16. Provide frequent oral care to maintain integrity of teeth and oral
mucosa.
17. Skin care for a PEG tube is the same as for gastrostomy tube.
18. Avoid large-volume water flushes (greater than 120 mL) as this
may cause small bowel necrosis.
19. Avoid bolus feeding via a jejunal feeding tube as this can cause
abdominal pain and can lead to small bowel necrosis.
Infection protection
1. When the central line is inserted, ensure that the CDC central line
insertion guidelines are followed, including use of full barrier
precautions.
2. Twice weekly and PRN, monitor CBC and differential for values
outside the normal range.
338
6. Avoid using the nutrition support port on the central IV or PIV
catheter for blood drawing, pressure monitoring, or administration
of medications or other fluids.
IV insertion
339
4. Check chest radiograph film to determine catheter position
following insertion.
IV therapy
4. Use occlusive dressing over insertion site for 24 hours after the
catheter is removed to prevent air entry via catheter-sinus tract.
Fluid monitoring
2. Consult advanced practice provider for urine output less than 0.5
mL/kg/h.
340
3. Check urine specific gravity; consult the physician or midlevel
practitioner for elevated specific gravity according to institutional
guidelines.
Pain
341
Advances in pharmacologic and complementary therapies, ongoing
research in pain management and numerous guidelines, position
statements, and practice recommendations have flourished over the
past decades. Despite these innovations and national and
international efforts, pain remains a common phenomenon in ICU.
Patients who are critically ill experience moderate to severe pain at
rest and during procedures such as turning, drain removal,
coughing, and endotracheal suctioning. Removal of endotracheal
tubes, a common procedure in ICU, is a substantial trigger of severe
pain in patients in ICU, and the majority of patients who are
mechanically ventilated experience moderate to severe pain despite
an unrestricted use of fentanyl and morphine. In addition to
procedure-induced pain, pathologic conditions, tissue damage, and
immobility are common sources of pain. The acuity and care
requirements of patients admitted in ICU expose them to multiple
sources of pain. These are presently addressed with pharmacologic
and nonpharmacologic treatments, yet pain remains undertreated
in most of these patients.
Advances in medical technology and an aging population have
resulted in an increased demand for intensive care services
including the use of invasive procedures such as endotracheal
intubation. Ultimately, the need for better pain relief of patients in
ICU will only continue to grow.
Unrelieved pain is not benign but affects every aspect of the
patient’s experience with critical care. It is a significant stressor for
patients who are critically ill and contributes to and potentiates
other problems such as confusion, inadequate ventilation,
immobility, sleep deprivation, depression, and
immunosuppression, which can lead to extended healing times. The
cardiovascular effects of unrelieved pain are increased HR, BP,
SVR; increased myocardial O2 consumption; altered regional blood
flow; and deep vein thrombosis (DVT). The pulmonary effects
noted of uncontrolled pain are decreased lung volumes, atelectasis,
decreased cough effort, increased sputum retention, and
hypoxemia. GI and genitourinary effects are decreased gastric and
bowel motility and urinary retention. The neuroendocrine response
to uncontrolled pain is to release more of the stress hormones such
as catecholamines, cortisol, and glucagon. Psychological effects are
342
anxiety, fear, and sleeplessness.
Unrelieved pain can also lead to multisystem complications,
anatomic changes, and physiologic changes in the nervous system
contributing to the development of chronic disabling pain and
posttraumatic stress disorder, which in turn may seriously impact
the patient’s functioning, quality of life, and well-being. The
negative impacts of pain are not only experienced by the patient
admitted in ICU but they also extend to family members and
significant others. Admission of a relative who is critically ill to ICU
causes both stress and anxiety to family members. They are
exposed to a number of potential stressors including deterioration
in the patient’s condition, uncertain prognosis, an unfamiliar
environment loaded with mechanical equipment, and pain and
suffering experienced by the patient. Posttraumatic stress disorder,
anxiety, guilt, frustration, and depression are some of the emotional
reactions of families to such stressors.
Pathophysiology
Pain is a warning signal to which the body responds to prevent
further injury. Nociception represents the neural processes of
encoding and processing noxious stimuli that can be perceived as
painful. Four processes are involved in nociception: (1)
transduction, (2), transmission, (3) perception, and (4) modulation.
In summary, transduction refers to the mechanical (e.g., surgical
incision), thermal (e.g., burn), or chemical (e.g., toxic substance)
noxious stimuli that damage tissues. These noxious stimuli lead to
the release of excitatory neurotransmitters that stimulate
nociceptors and thus serve to initiate transmission. Afferent nerve
fibers such as A delta (Aδ) and C fibers respond to pain stimuli
peripherally and relay this information to the spinal cord entering
through the dorsal horn. Aδ fibers are small, myelinated, fast-
conducting fibers that transmit pain sensation that is well localized.
C fibers are small, unmyelinated, slow-conducting fibers that
transmit poorly localized, dull, aching pain sensations. In the dorsal
horn, neurotransmitters such as substance P are released in
response to the nociceptive input that activates the second-order
dorsal horn neurons. The activation of the second-order neurons
343
results in (1) spinal reflex responses such as muscle spasm, and
increased sensitization; and (2) activation of the ascending tracts,
which transmits the nociceptive input to several regions within the
brain. This is where several responses to pain occur, including the
perception of pain and the emotional and behavioral responses.
Modulation refers to the release of endogenous opioids, which
inhibit, through the descending pathways, the transmission of the
nociceptive signal in the spinal cord and produce analgesia.
Assessment
Definition and types of pain
Pain is described as an unpleasant sensory and emotional
experience associated with actual or potential tissue damage. Such a
definition highlights the subjectivity of a complex multidimensional
pain experience. Indeed, the “gold standard” measure for pain is
the patient’s self-report. However, in the critical care setting, many
patients are unable to self-report their pain. In such a situation,
behavioral changes caused by pain are valuable forms of self-report
and should be considered as alternative measures of pain. The
inability to self-report does not negate the possibility that an
individual is experiencing pain and is in need of appropriate pain-
relieving treatment, and pain assessment methods must be adapted
to the patient’s cognitive capacity and condition.
Pain can be classified as acute or chronic, and nociceptive or
neuropathic. Acute pain implies tissue damage that is usually from
an identifiable cause that lasts for the healing process, which is
approximately 30 days. Chronic pain persists for more than 3 to 6
months following the healing process. Pain can be nociceptive or
neuropathic. Nociceptive pain arises from the activation of
nociceptors and can be of somatic or visceral origin. Somatic pain
involves peripheral tissues such as the skin, muscles, joints, and
bones. Visceral pain involves organs such as the heart, stomach,
and liver. Neuropathic pain arises as a direct consequence of an
injury or disease affecting the somatosensory system. It can
originate from the peripheral (e.g., neuropathy) or central (e.g.,
phantom pain, stroke) somatosensory system.
344
Goal of assessment
Pain assessment is an integral part of nursing care and is a
prerequisite for adequate pain management. Pain is a subjective
and multidimensional concept that requires complex assessment.
Many factors may alter verbal communication in patients who are
critically ill, making pain assessment more difficult. The American
Society for Pain Management Nursing has described a stepwise
approach for pain assessment in vulnerable patients including the
critically ill:
345
1. Attempt to obtain the patient’s self-report of pain: A
comprehensive initial assessment of pain, whenever possible, is
important in accurately evaluating and managing pain. Regular
follow-up pain assessments are necessary postoperatively and
during ICU stay until the pain is well controlled. A simple yes or no
for presence or absence of pain communicated verbally or using
signs (e.g., head nodding, hand grasping) should be considered as a
valid self-report.
346
1-3
RESEARCH BRIEF BOX
Puntillo et al. compared patient, family member, nurse reports, and
physician reports of the perceived intensity and distressing aspects
of pain in patients in the intensive care unit. Family members’
reports of both the intensity and distress of the patient’s pain was
positively moderately correlated with the patient’s self-report.
Interestingly, these family members were more accurate at
determining the intensity and distress of their loved one’s pain
than that of the physicians and nurses currently in charge of the
patient’s care. Proxy pain assessments should be combined with
other evidence such as direct observation using validated
behavioral pain scales, and the patient’s diagnosis, health history
and physical examination, and evaluation of treatment response.
Derived from Puntillo KA, White C, Morris AB, et al: Patients’ perceptions and responses
to procedural pain: results from Thunder Project II. Am J Crit Care 10(4):238-251, 2001.
347
professional attitudes and beliefs (e.g., certain patients do not have
pain [e.g., neonates], pain management is low priority); (6)
inappropriate patients’ attitudes and beliefs (e.g., pain builds
character, pain is a part of procedures); (7) cultural norms that
frame the expected response to pain (e.g., succumbing to pain is a
sign of weakness); (8) views of the spiritual significance of enduring
suffering (e.g., suffering on earth will entitle the person to more
rewards in the afterlife); and (9) fear of tolerance, addiction, and
analgesic side effects by both professionals and patients.
Assessment
348
into account the patient’s preference. A vertical pain intensity scale
seems to be easier to use for patients who are elderly because it
reminds them of a thermometer. Also, in a recent study, an
enlarged, readable horizontal 0 to 10 NRS-Visual was the most
feasible scale in patients in ICU. Once the nurse determines which
scale the patient can use, the same scale should be used for the
duration of clinical care so that accurate comparisons can be made
regarding the patient’s pain intensity, effectiveness of pain
management strategies, and to guide further alterations in pain
relief efforts.
349
improved over time? Intensive Crit Care Nurs 23(5):298-303, 2007).
Collaborative management
350
treatment as well as tapering of the analgesics and implementation
of adjuvant therapies. In the recent clinical guidelines of the SCCM,
the use of nonpharmacologic interventions is recommended for the
management of pain in adults who are critically ill, and nurses
should attempt to employ these interventions in their efforts to
promote optimal pain relief.
• There are many sources of pain in ICU and unrelieved pain can
have multiple negative impacts on the patient’s recovery.
2. Pharmacologic therapies
The pharmacologic management of pain is widely used in the
critical care setting. Pain pharmacology can be divided into three
main categories of action: opioids, nonopioids, and adjuvants. The
mechanism of action of these different agents in association with
nociception, their administration routes, therapeutic uses, and side
effects are described in Table 1-32. Pain can be managed using a
combination of the available agents, and must consider the type of
pain and the patient response to treatment.
Table 1-32
EQUIANALGESIC DOSES OF NARCOTIC ANALGESICS
351
*
Recommended starting dose; actual dose must be titrated to patient response.
†
Starting doses lower (codeine 30 mg, oxycodone 5 mg, meperidine 50 mg,
propoxyphene 65 to 130 mg, pentazocine 50 mg).
‡
Respiratory depressant effects persist longer than analgesic effects.
Modified from Hazard V, Hopfer DJ: Davis’ drug guide for nurses, ed 5, Philadelphia,
1997, Davis; Macintyre PE, Ready LBN: Acute pain management: a practical guide,
London, 1996, Saunders; and Salerno E: Pharmacologic approaches. In Salerno E,
Willens JS, editors: Pain management handbook: an interdisciplinary approach, St
Louis, 1996, Mosby.
IM, Intramuscular; IV, intravenous; PO, oral; SC, subcutaneous.
352
analgesia with minimal side effects. “As needed” dosing provides
poor pain management because of delays in administration and
fluctuations in the patient’s analgesic blood levels. Patient-
controlled analgesia (PCA) pumps, continuous peripheral or
epidural infusions, and small, frequent IV bolus dosing are effective
methods used for patients in critical care settings. Opioid tolerance,
physiologic or psychological dependence, and addiction are
unusual when opioids are used to manage acute pain in patients
without a history of chemical dependency. Parenteral opioids may
cause hypotension in patients with hypovolemia. Restore fluid
volume before or concurrently with administration. Some patients
are at a greater risk for respiratory depression such as the opioid
naïve, those with compromised pulmonary status or
neuromuscular disease, the extremely young (neonates), and older
adults. Opioid-induced respiratory depression can be prevented
with careful titration and monitoring.
353
the critical care unit, it may be indicated for brief courses (i.e., <
48 hours, < 600 mg/24 h) in patients with allergy or intolerance to
morphine, hydromorphone, or other opioids, and for the
treatment of postoperative shivering. Morphine is approximately
7 to 10 times stronger than meperidine, thus meperidine doses
are much higher (see Table 1-32). The drug is not well tolerated
by older adults . Its toxic metabolite, normeperidine, is a
cerebral irritant and may cause seizures, which has decreased
its usage in both older adults and the critically ill. Some patients
report little pain relief from meperidine, despite stating a strong
feeling of intoxication.
HIGH ALERT!
A fentanyl patch may be used for continuous analgesia, usually
with supplemental doses of morphine or another opiate titrated to
produce analgesia for breakthrough pain but should be used only
for patients with opiate tolerance. A fentanyl patch is not
recommended for mild pain, acute postoperative pain, or
354
intermittent pain because of its slow onset (12 to 16 hours) and
long duration, and because it is difficult to reverse its side effects
and adverse effects. Respiratory depression with hypoventilation
occurs, as with morphine. Transdermal fentanyl absorption can be
increased in patients with elevated temperatures.
355
drug has been effective when given on an alternate schedule with
morphine or another opioid analgesic during ventilator weaning
of postoperative patients. Renal toxicity is possible, which limits
use to patients with normal renal function. Bleeding
complications are more likely with high-dose therapy and in
older adults.
356
Older adults
Older adults are more sensitive to the therapeutic and toxic
effects of analgesics. The distribution of medications is altered by
age. With aging, lean body mass decreases and body fat increases.
Also, muscle and soft tissue mass decrease, and body water
declines. This results in water-soluble opioid analgesics such as
morphine having a lower volume of distribution. This causes an
increased rate of the onset of action and raises the peak
concentration, which is associated with increased toxicity. Lipid-
soluble opioid analgesics (e.g., fentanyl) may be more widely
distributed, resulting in a delayed onset of action and accumulation
with repeated doses. Because of age-related changes in metabolism
and elimination, older adults are also at risk for drug-accumulation
toxicity.
In treating older adults, it is best to start at lower doses (50%
to 75% of recommended younger adult doses). The interval
between doses can be increased, using opioids with shorter half-
lives (morphine, hydromorphone, oxycodone). All older adults
should be monitored for signs of opioid toxicity, including
increased sedative effects, inability to awaken the patient easily,
and respiratory depression. With careful assessment, proper dosing
and titration, knowledge of analgesic onset and peak times, and
careful monitoring, the risk for respiratory depression is low.
However, naloxone (Narcan), an opioid antagonist, should be
immediately available to reverse respiratory depression.
357
Nonpharmacologic interventions
In light of the recognition of the high prevalence of pain in the
critically ill despite the administration of standard pharmacologic
treatments, a multimodal approach to pain management in patients
in ICU is recommended. A multimodal approach supports the
combination of nonopioid with opioid analgesics for optimal pain
relief versus an increase in the dosage of opioids administered to
prevent the adverse effects of high opioid doses on patients.
Moreover, the recent clinical practice guidelines of the SCCM for
the management of pain in ICUs suggest the use of complementary,
nonpharmacologic interventions for pain management (massage,
music therapy, relaxation techniques) in addition to a multimodal
approach.
The general belief of ICU nurses is that pain is primarily
managed with pharmacologic treatments such as indicated in most
ICU pain management protocols, but when this type of treatment is
not sufficient, they try different nonpharmacologic approaches.
Several nonpharmacologic interventions such as deep breathing
exercises, massage, and positioning were reported to be already
used by nurses for the management of pain in ICU.
These nonpharmacologic interventions are intended to
supplement pharmacologic treatments to maximize pain relief.
Even though they are commonly used in clinical practice, there is
still limited evidence to support their effectiveness in critical care
settings. These interventions include sensory, emotional, and
cognitive interventions, such as massage, relaxation, distraction,
guided imagery, repositioning, and transcutaneous electrical nerve
stimulation, and are used for mild pain and anxiety and as adjuncts
to pharmacologic management of moderate to severe pain.
Physical techniques
358
documented for the administration of massage in various clinical
settings. It has been shown to reduce fatigue and improve sleep
quality, to promote relaxation and decrease muscle tension, and
to impact vital signs by decreasing systolic and diastolic BP,
cardiac, and respiratory rates.
Cognitive-behavioral techniques
359
impact pain levels both physiologically and psychologically. At
the physiologic level, it can reduce the sympathetic response to
pain with subsequent decreases in oxygen consumption, BP, HR,
and respiration. Psychologically, through distraction, this
technique decreases the cognitive awareness of pain by
encouraging the patient to focus on something unrelated to the
pain. Examples include conversing, reading, watching television
or videos, and listening to music.
1-4
RESEARCH BRIEF BOX
Owens and Flom indicate that family members of patients in the
intensive care unit are able to predict when their loved one is in
pain approximately 75% of the time, but the severity is usually
underestimated
From Owens D, Flom J: Integrating palliative and neurological critical care. AACN Clin
Issues 16(4):542-550, 2005.
360
a decrease in pain, and the use of valid and reliable scales for pain
assessment in patients who are noncommunicative will indicate
lower pain scores.
Pain Control.
Pain management
Analgesic administration
361
sedation, respiratory depression, nausea, vomiting, and
constipation.
4. Check the patient’s analgesia record for the last dose and amount
of medication given during surgery and in the postanesthesia care
unit. Be careful to coordinate timing and dose of postoperative
analgesics with previously administered medication.
Medication management
362
analgesics for moderate-to-severe pain.
363
tranquilizers for analgesics.
Self-responsibility facilitation
364
interventions, using the pain scale or other formalized method.
Respiratory monitoring
365
the last dose of epidural morphine. Monitor for respiratory
depression during and for 24 hours after the patient has received
epidural or intrathecal opioids.
Urinary retention
related to inhibition of reflex arc secondary to opioid action
Goals/Outcomes: Within 4 hours of this diagnosis, complete
bladder emptying is achieved. Overflow incontinence is absent.
Urinary Elimination.
Urinary Catheterization.
Medication management
366
Monitor sedation when antihistamine is added.
Prolonged immobility
Prolonged immobility is a common consequence of prolonged
hospitalization for severe and critical illness. Morbidity related to
prolonged immobility is often profoundly impacted by nursing
care. Nurses attend to patients continuously, providing ongoing,
expert assessments and interventions. Significant adverse outcomes
of prolonged immobility have been demonstrated to be preventable
(Box 1-16).
Box 1-16
PHYSIOLOGIC EFFECTS AND
COMPLICATIONS OF BED REST
(DECONDITIONING)
Cardiovascular
• Increased heart rate and blood pressure for submaximal
workload
367
• Orthostatic hypotension
• Reflex tachycardia
Pulmonary
• Modest decrease in pulmonary function
• Atelectasis
• Pneumonia
• Pulmonary embolus
Gastrointestinal
• Ileus
Musculoskeletal
• Loss of muscle mass
• Bone demineralization
• Joint contractures
Skin
• Decubitus ulcers
368
include:
• Others:
• Severe sepsis.
• Failure to thrive.
369
Standard 1. Establish a culture of safety
The employer and healthcare workers partner to establish a culture
of safety that encompasses the core values and behaviors resulting
from a collective and sustained commitment by organizational
leadership, managers, healthcare workers, and ancillary/support
staff to emphasize safety over competing goals.
1.1 Employer
370
patient handling and mobility, including allocated time for training
and education.
1. Assess the patient’s height and weight. Weight alone may be the
determining factor in deciding how much assistance is needed or if
an assistive device is needed.
371
assistive devices (e.g., cane or walker), without staff
assistance?
Assistive devices
Assistive devices are very helpful in preventing injury and
decreasing the number of staff needed to assist. There are many
assistive devises on the market, usually in the form of slings. Some
types of slings may be independent, roll on wheels, and be able to
be moved from one patient to another. Another type of sling, which
is not portable, may be attached to the ceiling and slide.
It is important to know how to use the sling properly and to have
enough staff to assist with the use safely. Read the instructions
before using any new device that is not familiar.
The following set of nursing care plans frames the care of those
who require prolonged periods of bed rest and/or those who are
immobile.
372
later), as evidenced by:
• SVO2 ≥60%.
• RR ≤20 breaths/min.
HIGH ALERT!
373
Avoid isometric exercises in patients with cardiac disease. Stop any
exercise that causes muscular or skeletal pain. Consult with a
physical therapist for necessary modifications to allow for exercise
without causing muscular or skeletal pain.
• Dysrhythmias.
374
• A new S3 or a systolic murmur indicating mitral
regurgitation that may occur.
375
• Plan to increase duration:
376
every 2 hours.
Table 1-33
RATING PERCEIVED EXERTION
377
5 Strong effort
6
7 Very strong effort
8
9 Very, very strong effort
10 Maximal effort
From Borg G: Psychophysical bases of perceived exertion. Med Sci Sports Exerc
14(5):377-381, 1982.
Exercise promotion
378
extension and alter the gait.
• Prevent contractures.
• Hips extended.
379
• Fingertips to extend over the edge of the pillows to
maintain normal arching of hands.
HIGH ALERT!
Because elevating the head of the bed promotes hip flexion, ensure
that the patient spends equal time with the hips in extension. When
the patient is in the side-lying position, extend the lower leg from
the hip to help prevent hip flexion contracture.
380
• Foam boots or “high top” tennis shoes may be used
to support the feet.
6. Ensure that the patient does not exceed his or her tolerance by
performing constant assessment of activity tolerance. Provide
passive exercises for patients unable to perform active or active-
assistive exercises. Incorporate exercising all joints with ADLs, such
as changing position, giving bed baths, using bedpan, and changing
the patient’s gown.
• Perform ROM.
9. Reinforce progress.
381
• Post the exercise regimen at the patient’s bedside to
ensure consistency by all healthcare personnel.
382
continuously during oral hygiene to remove fluid
and debris.
Self-care deficit
related to cognitive, neuromuscular, or musculoskeletal impairment;
activity intolerance secondary to prolonged bed rest.
Goals/Outcomes: The patient’s physical needs are met by the
patient, nursing staff, and/or significant others while the patient is
being encouraged to participate as much as possible.
Self-Care: Activities of Daily Living.
383
• Use assessment criteria for activity tolerance: If the
patient experiences a decrease in BP of more than
20 mm Hg, an increase in HR of more than 20 bpm
above resting HR, or a HR above 120 bpm in a
patient receiving beta-adrenergic drugs, the patient
is not fully tolerating the activity.
2. If the patient is comatose, meet all the patient’s physical needs:
bathing, oral hygiene, feeding, and elimination.
384
5. If the patient is alert, keep toiletries and other necessary items
within reach.
385
2. Identify patients at risk for DVT: chronic infection, malignancy,
peripheral vascular disease, history of smoking, obesity, anemia,
prolonged bed rest, and advanced age.
Note: All patients who are in bed greater than 50% of the
time, including at night, should have deep vein thrombosis
prophylaxis, either medical (heparin, enoxaparin) or mechanical.
Embolus precautions
The following measures are generally a part of a DVT prevention
program.
1. Assess for a positive Homan sign. The Homan sign is not very
sensitive or specific for DVT but can be elicited by flexing the knee
30 degrees and dorsiflexing the foot. Pain elicited with the
dorsiflexion may indicate DVT and may warrant further evaluation
by the physician.
• Fever.
• Tachycardia.
386
• Patients who are “hypercoagulable” are at higher
risk for DVT.
• Pain.
387
4. Advise the patient and family to perform only the exercises
prescribed by the healthcare team. Discourage practices such as
massaging the legs when swelling and discomfort are noted.
388
breakdown.
• Heparin
• Low-molecular-weight heparin
• Aspirin
• Platelet inhibitors
• Sodium warfarin
• Prothrombin time
389
• Heparin level
• Epistaxis
• Bleeding gums
• Hematemesis
• Hemoptysis
• Melena
• Hematuria
• Ecchymoses
Circulatory Precautions.
390
Neurologic Status; Neurologic Status: Consciousness.
1. Assess the patient for factors that increase the risk of orthostatic
hypotension.
• Recent diuresis
• Diaphoresis
• Advanced age
• Severe LV dysfunction
391
4. Prepare the patient for getting out of bed. Encourage position
changes within necessary confines. Consider using a tilt table to
reacclimate the patient to upright positions.
• Diaphoresis
• Pallor
• Tachycardia
• Hypotension
• Syncope
• Drop in systolic BP of 20 mm Hg
• Feeling of vertigo
392
• Impending syncope
Constipation
related to less-than-adequate fluid or dietary intake and bulk; immobility;
lack of privacy; positional restrictions; use of opioid analgesics.
Goals/Outcomes: Within 24 hours of this diagnosis, the patient
verbalizes knowledge of measures that promote bowel elimination.
The patient relates the return of his or her normal pattern and
character of bowel elimination within 3 to 5 days of this diagnosis.
Older adults often experience constipation.
Bowel Elimination.
Bowel management
• Straining at stool.
393
• Fecal impaction, which may be manifested by
oozing of liquid stool and confirmed via digital
examination.
3. Auscultate each abdominal quadrant for at least 1 minute to
determine the presence of bowel sounds. Normal sounds are clicks
or gurgles occurring at a rate of 5 to 34 per minute.
• Ensure privacy.
394
bowel movement.
• Medicated suppositories
• Enemas
9. Discuss, with the patient, the role narcotics and other medications
have in constipation. Consider alternative methods of pain control
(see Box 1-15) in an attempt to reduce narcotic dosage.
Constipation/Impaction Management.
395
Deficient diversional activity
related to prolonged illness and hospitalization
Goals/Outcomes: Within 24 hours of intervention, the patient
engages in diversional activities and relates the absence of
boredom.
Motivation.
Self-responsibility facilitation
396
patient. Arrange for hospital volunteers to visit, play cards, read
books, or play board games as appropriate. Consider relocation to a
room in an area of high traffic if the patient desires more social
interaction.
Risk of injury
related to falls
Goals/Outcomes: The patient will remain free from falls
throughout stay in ICU.
Cognitive Orientation, Distorted Thought Self-Control,
Information Processing.
• History of falls.
• Sensory impairment.
• Confused or disoriented.
397
• Needs assistance with elimination (bowel or
bladder).
398
• Have the patient demonstrate use of the call light.
399
For patients who are immobile, turn patients every
2 hours.
Footwear.
400
Box 1-17
PATHOLOGIC CONDITIONS
CONTRIBUTING TO AGITATION
Addisonian crisis
Alzheimer disease
Anxiety disorder
Delirium
Delirium tremens
Developmental disability
Diabetes
Drugs
Subtherapeutic
Supratherapeutic (toxic)
Withdrawal syndromes
Idiosyncratic reactions
Drug interactions
Steroids
Encephalopathy
Hepatic
401
Metabolic
Uremic
Fear
Fluid/electrolyte abnormalities
Hypercarbia
Hyperthyroidism
Hypoglycemia
Hyponatremia
Hypophosphatemia
Hypoxemia
Cerebral thrombosis
Subarachnoid hemorrhage
Intracranial bleeding
Cerebral vasospasm
Cerebral edema
Increased intracranial pressure
Tumor
Cerebrovascular accident
402
Hydrocephalus
Infection
Meningitis
Encephalitis
Brain abscess
Sepsis syndrome
Pain, inadequately controlled
Sleep deprivation
Stress
Thyroid disease
403
control, life-threatening illness, inability to communicate (e.g.,
mechanical ventilation), and feelings of helplessness.
Environmental factors such as noise, temperature extremes, and
sleep deprivation add to anxiety and agitation. The influence of
environmental factors is sometimes more pronounced in those with
altered LOC (see Alterations in Consciousness). Common
pathophysiologic factors that contribute to agitation include
hypoxemia, impaired cerebral perfusion, infection, alcohol
withdrawal, and encephalopathy (Box 1-17). These causes must be
ruled out before initiating sedation because the use of sedative
medications may mask a treatable problem. Litigation resulting
from patient harm induced by use of sedation to manage hypoxia-
induced agitation is not rare in the United States.
Delirium
Consideration of the possibility of delirium is imperative when
beginning the management of agitation. Many of the clinical factors
associated with agitation (see Box 1-17) are also causative for
delirium, occurring in up to 50% of patients in ICU and up to 80%
of patients who are mechanically ventilated. Causes are
multifactorial and include the presence of invasive devices, use of
benzodiazepines, sleep deprivation, and prolonged immobility.
Following ruling out of other causes for agitation, the
recommendation of the SCCM is to deliver light sedation to the
patient using a validated agitation assessment scale, either the
RASS or the Sedation-Agitation Scale (SAS) (see Appendices 1 and
2). A fluctuation in the patient’s RASS or SAS score can be the first
indication that delirium may be present. It is recommended that
assessments be done on all patients in ICU every 12 hours, given
that fluctuation in mental status is common. The diagnosis is made
using one of two validated scales: the Confusion Assessment
Method for the ICU (CAM-ICU) or the Intensive Care Delirium
Screening Checklist (ICDSC). Delirium can be hyperactive
(previously known as ICU-psychosis), but is much more commonly
hypoactive or a mixture between the two. Hypoactive delirium may
be manifested as a flat affect, withdrawal, lethargy, apathy, or an
otherwise relatively unremarkable change in mental status. The
unfortunate term “pleasantly confused” is sometimes used for these
404
patients, but the outcome is often worse than for the hyperactive
patient because it is so easy to ignore or undertreat. Delirium is
associated with increased ICU and hospital length of stay, increased
ventilator time, increased mortality, and some degree of permanent
cognitive impairment in up to one third of patients. Studies have
calculated that delirium may increase hospital costs by an average
of almost $15,000. Treatment involves discontinuing medications
that can be deliriogenic, identifying and modifying preexisting or
precipitating risk factors if possible, nondrug treatment strategies
(Box 1-18), and finally haloperidol or atypical antipsychotic
medications. There is insufficient evidence to support the use of
antipsychotics for prophylaxis in patients who are at high risk for
delirium.
Box 1-18
NONDRUG TREATMENT STRATEGIES
FOR DELIRIUM AND CONFUSION
Repeated reorientation of the patient
Adequate hydration
405
Administering sedation
Assuming that pain and delirium are addressed, the goal of further
pharmacologic sedation is to reduce anxiety and produce a calm
but communicative state, if possible. This is best accomplished by
administering frequent, incremental doses of sedatives only until
the desired effects are achieved. For a majority of patients, the goal
of therapy is light sedation, or 0 to −1 on the RASS, 3 to 4 on the
SAS. Light sedation, as opposed to deeper levels, has been
associated with decreased time on the ventilator, decreased hospital
and ICU length of stay, and decreased incidence of delirium.
Deeper levels of sedation may be appropriate for certain clinical
conditions including elevated intracranial pressures, alcohol or
other drug withdrawal, seizures, ARDS, hemodynamic instability,
ventilator dyssynchrony, concomitant therapy with neuromuscular
blocking agents (NMBAs), or comfort care.
If intermittent boluses of sedatives fail, it may be necessary to use
a continuous infusion. SCCM guidelines recommend fentanyl as the
initial infusion, followed by propofol or dexmedetomidine. If large
amounts of medication are necessary, careful consideration should
be given for consultation with a physician or midlevel practitioner
who specializes in the management of patients who are critically ill
using sedation, analgesia, and, if necessary, neuromuscular
blockade. Major organ dysfunction, multiple medications, tissue
catabolism, and other factors render patients who are critically ill
especially vulnerable to the toxic effects of many sedatives.
Oversedation and toxicity should be carefully avoided through
close monitoring, individualized dosing, and titration to desired
effect. Excessive sedation has been associated with delayed
recognition of neurologic events, muscle wasting, and nosocomial
complications such as DVT, compression injury, and pneumonia.
The literature supports performing daily wake up assessments on
patients with continuous drips to assure that there has been no
underlying neurologic changes and that the drips are at the lowest
effective dose, if indeed they are still required at all.
When providing sedation, if anxiolytic or other adjunctive agents
fail to help stabilize ventilation and perfusion in patients who are
406
mechanically ventilated, NMBAs may need to be added.
Neuromuscular blockade results in total paralysis of the striated
muscle at the neuromuscular junction. Neither the nondepolarizing
paralytic agents (see Table 1-36) nor succinylcholine possess
anxiolytic nor analgesic properties. The patient may be terrified,
given that they are fully aware that they have no ability to move,
communicate, or breathe. Paralysis is always done in conjunction
with sedation and analgesia to ensure that the patient is not
overwhelmed with fear. If not done, the patient undergoes extreme
stress, which can be further exacerbated if they also have
unrelieved pain. The pain should be addressed with either
scheduled (not PRN) opiates or a continuous opiate drip, usually
fentanyl, and potential anxiety with a sedative drip such as
propofol.
Patients may not tolerate or may inadvertently “fight” necessary
treatments. Those with severe respiratory dysfunction may require
use of specialized ventilator settings (ventilator dyssynchrony) such
as reversing the inspiration to expiration time (reverse I:E ratios), or
the use of oscillatory ventilation. Successful ventilation may not be
possible without use of NMBAs to stop the patient from tensing in
response to the treatment. Tensing reduces tidal volume and
requires increased energy expenditure. Care providers must create
an anticipatory plan for pain management and anxiolysis when the
patient is no longer able to voice his or her needs.
1-5
RESEARCH BRIEF BOX
Delirium evaluation in patients in the intensive care unit (ICU)
requires the use of an arousal/sedation assessment tool before
assessing consciousness. The Richmond Agitation-Sedation Scale
(RASS) and the Riker Sedation-Agitation Scale (SAS) are well-
validated arousal/sedation tools. The concordance of RASS and
SAS assessments in determining eligibility of patients in ICU for
delirium screening using the confusion assessment method for ICU
(CAM-ICU) was assessed. A prospective cohort study was
performed in the adult medical, surgical, and progressive (step-
down) ICUs of a tertiary care, university-affiliated, urban hospital
407
in Indianapolis, Indiana. The cohort included 975 admissions to
ICU between January and October 2009. In total, 2469 RASS and
SAS paired screens were performed and the conclusion was that
both SAS and RASS led to similar rates of delirium assessment
using CAM-ICU.
From Khan BA: Comparison and agreement between the Richmond Agitation-Sedation
Scale and the Riker Sedation-Agitation Scale in evaluating patients’ eligibility for delirium
assessment in the ICU. Chest 142(1):48-54, 2012.
Neuromuscular blockade
Monitoring paralytic agents: When a patient is paralyzed using
NMBA therapy, it is of paramount importance to be able to
evaluate whether the levels of sedation, analgesia, and paralysis are
appropriate. The previously mentioned means of monitoring pain
and agitation do not apply in the patient who is paralyzed, hence
the need for continuous infusions or around-the-clock boluses of
each for the duration of paralysis, without decreasing the doses.
The “gold standard” for monitoring paralytics is the use of a
peripheral nerve stimulator to deliver four (train of four or TO4)
tiny, sequential stimulating shocks to nerves on the wrist, foot, or
face. The muscle response is measured to evaluate how many of the
four signals are blocked by the NMBA compared with the number
perceived. In the absence of neuromuscular blockade, the muscle
should move four times equally in response to four signals. As
receptors are saturated with NMBAs, fewer muscle contractions are
seen (Table 1-34). Nerve stimulators are the best monitoring option,
with bispectral index (BIS) monitoring and drug holidays largely
falling from favor, but can be uncomfortable for the patient being
evaluated on an hourly basis. To avoid this, a baseline setting
should be established before the paralytic is started. Termed the
“supramaximal stimulation point,” it is the electrical setting on the
nerve stimulator after which no increased muscle movement is
noted. Once the drip is started, under no circumstances should this
electrical setting be increased. Also, it is very important to
recognize that the purpose of the nerve stimulator is to avoid
overexposure to these exceptionally dangerous drugs, in other
words the nurse should attempt to decrease the drip rate if one or
fewer twitches are present. Increasing the drip should only be done
408
based on clinical necessity, never TO4 results, even if all four
twitches are present.
Table 1-34
NERVE STIMULATION IN RELATIONSHIP TO PERCENT
BLOCKAGE
Collaborative management
Care priorities
409
Other opiates commonly used include hydromorphone (Dilaudid)
and fentanyl citrate (Sublimaze). Fentanyl and hydromorphone are
rapidly absorbed by the CNS and therefore are more potent than
morphine. Fentanyl is the shortest acting opiate and is best used as
a continuous infusion. The SCCM recommends that fentanyl be
used for rapid onset of analgesia and in patients who are
hemodynamically unstable. Meperidine (Demerol) is not
recommended as a primary analgesic, particularly in older adults
and those with renal failure. Patients often report inadequate pain
control, while experiencing euphoria. Meperidine accumulates with
repeated doses and causes an increased risk of neurotoxicity (see
Table 1-32).
410
slow increases in the infusion rate. Propofol is particularly useful
for patients with neurologic impairment, because the short action
facilitates daily awakening during the sedation vacation to
evaluate underlying mental status. The drug is not an analgesic,
thus pain medication should be prescribed. Effectiveness of pain
management should be assessed during daily awakening.
Scheduled doses or a continuous infusion of opiate analgesics
provide effective pain control when used in combination with
propofol. Doses in ventilated ICU patients should rarely exceed
50 µg/kg/min (or 3 mg/kg/h) because the agent is considered an
anesthetic at higher doses. It is metabolized and eliminated
largely independent of renal and hepatic function. The lipophilic
drug accumulates more readily in patients who are obese, and
dosing should be based on either IBW or adjusted body weight
(ABW), (ABW − IBW) × 0.4 + IBW, in patients who are obese.
These patients may also be at increased risk for a more prolonged
recovery time after the infusion is discontinued. Prolonged
recovery time may occur with any patient when the infusion is
continued for more than 3 days at high doses.
411
doses. Early recognition is the key to successful
management. If symptoms of PRIS are noted,
propofol should be discontinued and an alternative
sedative agent initiated. Measures to support
cardiac and renal function should be promptly
initiated.
Dexmedetomidine (Precedex): A novel agent with a mechanism of
action similar to clonidine. The drug blocks sympathetic outflow
through a central alpha stimulation to produce sedation when
used as a continuous infusion. Although not an analgesic,
dexmedetomidine has been shown to have opiate-sparing
properties. Level of awareness may be assessed without
downward titration of the drip. The drug is effective in managing
alcohol withdrawal syndrome, delirium, and failed extubation.
Dexmedetomidine is not associated with respiratory depression
but can cause hypotension and bradycardia. The drug should be
initiated in well-hydrated patients to avoid hypotension. The
recommended initial bolus dose may be omitted in borderline
hypovolemic patients. The SCCM has positioned the drug, as
well as propofol, ahead of benzodiazepines in the treatment of
agitation after analgosedation has been adequately attempted.
Although the labeling gives a maximum duration of 24 hours,
there are sufficient data that support extended use of the drug,
up to 72 hours or more. The maximum dose is 1 µg/kg/h,
although safety has been established at up to 1.5 µg/kg/h. It can
also be used in nonintubated patients, unlike propofol.
412
(Versed) is considered superior to other benzodiazepines in
preventing recall. Ease of use, a general lack of paradoxic
agitation, and lack of recall are advantages of benzodiazepines,
but these are offset by a higher incidence of delirium and some
pharmacokinetic disadvantages (see later). They are the primary
drugs used to alleviate symptoms of acute alcohol withdrawal,
which commonly contribute to agitation in the critically ill.
However, benzodiazepines do not have analgesic properties
present in opiates, thus pain should always be ruled out as a
cause of agitation before using benzodiazepines solely. If present,
pain should be treated with analgesics before these drugs are
initiated. Table 1-35 describes specific characteristics of the
widely used benzodiazepines.
413
complications, it is the benzodiazepine of choice for
prolonged sedation. Patients who are lightly
sedated should awaken within 30 minutes during
the daily wake up assessment (sedation vacation).
When patients have difficulty awakening during
these assessments, the dosage should be decreased.
414
to avoid hypotension if given parenterally. Antipsychotics may
be used as part of management of alcohol withdrawal syndrome.
415
cleanest side effect profile of the injectable atypical
antipsychotics, it is also less sedating, which can be
a disadvantage.
416
started at 25 mg every 8 to 12 hours and increased
to 300 mg or more daily if needed. QT prolongation
and orthostatic hypotension can occur with
quetiapine.
417
paralysis, most often during emergent intubation.
Long-term blockade is not practical because of
rapid tachyphylaxis and desensitization of
receptors to blocking effects.
Table 1-35
418
BENZODIAZEPINE CHARACTERISTICS
Table 1-36
NEUROMUSCULAR BLOCKING AGENT CHARACTERISTICS
BP, Blood pressure; CO, cardiac output; HR, heart rate; MAP, mean airway
pressure; PRN, pro re nata (when necessary).
Box 1-19
DRUGS AND PHYSIOLOGIC CONDITIONS
THAT AFFECT NEUROMUSCULAR
BLOCKADE
Drugs that augment neuromuscular blockade
Aminoglycoside antibiotics
Bacitracin
419
Calcium channel blockers
Clindamycin
Colistimethate
Cyclosporine
Inhaled anesthetics
Lidocaine
Piperacillin
Procainamide
Propranolol
Quinidine
Vancomycin
Azathioprine
Carbamazepine
Corticosteroids
Phenytoin
Ranitidine
Theophylline
420
Acidosis
Dehydration
Hypercalcemia
Hypermagnesemia
Hypocalcemia
Hypokalemia
Hyponatremia
Hypothermia
Myasthenia gravis
Hyperkalemia
Hypernatremia
421
Care plans for sedation and neuromuscular
blockade
Anxiety
related to actual or perceived threat of death; change in health status;
threat to self-concept or role; unfamiliar people or environment; the
unknown.
Goals/Outcomes: Within 4 to 6 hours of initiating therapy, the
patient’s anxiety is diminished, as evidenced by verbalization of
same, HR less than 100 bpm, RR less than 20 breaths/min, and
decrease in restlessness and extraneous motor movement.
Anxiety Self-Control.
Anxiety reduction
422
available for reversal of drug effects.
Ventilation assistance
423
Mechanical Ventilation).
6. Continuously monitor SpO2 via pulse oximetry and end tidal CO2.
9. Position the patient to promote full lung expansion, and turn the
patient to mobilize sputum.
Deficient knowledge
related to lack of recall, related to interrupted memory consolidation
secondary to benzodiazepine use.
Goals/Outcomes: Within 12 hours of cessation of benzodiazepine
therapy, the patient recalls information essential to self-protection
and self-care.
Knowledge: Treatment Procedures.
Teaching: Procedure/treatment
424
comprehension is demonstrated.
425
studied and found to be valid for the prediction of pressure ulcer
risk. As a result of the emphasis on prevention of avoidable
pressure ulcers and the accompanying economic impact of fiscal
restraints, more effort is being placed on prevention. Norton scores
of 14 are indicative of mild risk; a score of 12 indicates “high risk.”
Braden scores of 18 to 15 indicate mild risk, and 12 is high risk. A
risk assessment tool should be used in acute care on admission and
reassessment should be done at least every 24 to 48 hours or when
the patient’s condition changes or deteriorates.
Assessment
Optimal wound healing
Immediately after a surgical injury, the incision is warm, red,
indurated, and tender. Inflammation normally subsides in 3 to 5
days. A healing ridge can be palpated just under the intact suture
line by days 5 to 9. It is produced by the newly formed connective
426
tissue (see Table 1-37).
Impaired healing
Impaired healing is recognized by the lack of an adequate
inflammatory response surrounding a wound, continued drainage
from an incision line 2 days after injury (when no drain is present),
absence of a healing ridge by day 9 after injury, and/or presence of
purulent drainage (see Table 1-37). A chronic wound is one that
fails to proceed to healing within a reasonable time, to progress
through a normal repair process, and is usually associated with
pathology (i.e., diabetes or pressure damage). Wound assessment
should be done on an ongoing basis to determine the progress or
deterioration of the wound. Assessment includes anatomic location,
dimensions (length, width depth), percent of tissue type
(granulation, slough, necrotic), exudate (amount, color, odor), and
condition of the periwound skin. The wound should be cleansed
before assessment to allow for visualization of the wound base.
Table 1-37
ASSESSMENT OF HEALING OF WOUNDS CLOSED BY PRIMARY
427
INTENTION
Collaborative management
Care priorities for surgical wounds healing by primary
intention
1. Application of a sterile dressing in surgery or at the time of
injury: Protects wound from external contamination, trauma, or
pressure injury. Usually, the surgeon or advanced practice nurse
changes the initial dressing.
428
from many sources, including the SCCM and the American
Association of Critical-Care Nurses. Choice of protocol is based on
the ability of each nurse to comply with the recommended insulin
dosage regime and associated monitoring. Protocols vary with
number of steps, frequency of monitoring blood glucose, and need
for available technology, such as access to computers, the Internet,
point-of-care blood glucose meters, and other variables. Control of
blood glucose has been consistently associated with more timely
and effective would healing. Glucose stabilization must be done
with a protocol that given the available resources, nurses are able to
appropriately monitor blood glucose and manage hypoglycemia to
maintain patient safety.
429
wound healing: well-approximated wound edges, good initial
postinjury inflammatory response (erythema, warmth, induration,
pain), no inflammatory response after the fifth day postinjury, no
drainage (without drain present) 48 hours after closure, and healing
ridge present by postoperative days 5 to 9. Tissue integrity is
restored.
Tissue Integrity: Skin and Mucous Membranes.
Wound care
430
smoking increases vasoconstriction, which
compromises perfusion impacting negatively on
wound healing.
Assessment
Optimal healing
Initially, the wound edges are inflamed, indurated, and tender. Pale
granulation tissue on the wound floor and wound wall proliferates
and progresses to a deeper pink and then red; the tissue should be
431
moist. As the wound fills with granulation tissue, epithelial cells
from the surrounding tissue migrate across the granulation tissue,
fill the defect, and contraction occurs simultaneously to close the
wound. As healing continues, the wound edges approximate and
the newly resurfaced epithelium is pink and dry. If present, a
wound tract or sinus gradually decreases in size. The time frame for
healing depends on the size and location of the wound, as well as
the patient’s physical and psychological status (Table 1-38).
Table 1-38
ASSESSMENT OF HEALING OF WOUNDS CLOSING BY
SECONDARY INTENTION
Impaired healing
Exudate, slough, and necrotic material appear on the base and walls
of the wound, indicating that healing has not progressed. The
percentage of nonviable tissue in the wound must be assessed for
distribution, color, presence of odor, and presence of wound
exudate (color, amount, and consistency). Assess the periwound
skin for signs of tissue damage, including disruption, moisture-
related skin damage, discoloration, and increasing pain. Volume,
color, and odor of drainage are assessed and measured if possible
(see Table 1-38).
Diagnostic tests
See discussion on Wounds Closed by Primary Intention.
432
Test Purpose Abnormal Findings
Culture Test for the presence Culture will identify the specific aerobic and anaerobic
of infection organisms and their susceptibility to antibiotics. Preliminary
culture results in 24 hours, final in 48 hours.
Biopsy To rule out the Consult appropriate treating specialty as needed (e.g.,
presence of cancer or oncology or dermatology). Incorrect diagnosis of wound
dermatologic etiology can have untoward delay in treatment.
diagnosis
Collaborative management
Care priorities
1. Débride slough and necrotic tissue: To remove nonviable tissue,
use surgical or sharp débridement (done by provider certified to
perform débridement) for rapid removal and enzymatic (e.g.,
Santyl) or autolytic (e.g., hydrocolloid dressing) for slower removal.
433
8. Negative pressure wound therapy: Reduces edema and wound
exudate, promotes wound contraction, reduces bacterial bioburden,
and stimulates granulation tissue formation.
10. Tissue flap: Fills tissue defect and provides wound closure with
its own blood supply. Requires pressure redistribution bed surface
to minimize pressure on operative flap.
Wound care
434
1. Impaired wound healing: Assess and document wound condition
daily. Report and manage decreased inflammatory response or
inflammatory response lasting more than 5 days; epithelialization
slowed or mechanically disrupted; granulation tissue remains pale
or becomes dry; presence of odor, exudate, necrotic tissue, pain,
wound breakdown, or if the wound edges close prematurely
(epibole).
435
Table 1-39
DRESSINGS USED FOR WOUND CARE
Calcium Dressing is seaweed and is highly absorptive, Cannot be used for dry
Alginate used for heavily exudative wounds, wounds; requires secondary
(e.g., appearance is gel-like upon removal. dressing; may have foul odor
SeaSorb, when removed.
Algisite)
Gauze (e.g., 2 Inexpensive; easy to use; ideal for packing May result in tissue maceration
× 2, 4 × 4, wound. if inserted too moist; may result
rolled gauze) in tissue disruption if allowed
to dry.
Composites Use for partial- to full-thickness wounds. Adhesive borders may disrupt
(e.g., surrounding skin. Composite
Alldress, dressings come in a variety of
Covaderm sizes, may be difficult to carry a
Plus) large supply.
Silver Antiseptic capability while in the wound. Silver sensitivity or allergy.
dressings: Different manufacturers will identify the length Rare cases of issues of tattooing
foam, of time their dressing has in continuing to shed have been noted. Silver ions
alginates, silver. will be deactivated by some
gels solutions.
Pressure ulcers
The National Pressure Ulcer Advisory Panel (NPUAP) defines a
pressure ulcer as localized injury to the skin and/or underlying
tissue usually over a bony prominence, as a result of pressure, or
pressure in combination with shear. High-risk patients include
436
patients with impaired sensory perception, advanced age, skin
moisture (incontinence, excessive sweating), decreased activity and
mobility levels, poor nutritional intake, and exposure to friction and
shear.
437
related skin tears, tape burns, incontinence-associated dermatitis,
maceration, or excoriation.
*Note: Bruising indicates deep tissue injury.
438
pressure and/or shear. The area may be preceded by tissue that is
painful, firm, mushy, boggy, warmer, or cooler compared with
adjacent tissue. Deep tissue injury may be difficult to detect in
individuals with dark skin tones. Evolution may include a thin
blister over a dark wound bed. The wound may further evolve and
become covered by thin eschar. Evolution may be rapid exposing
additional layers of tissue even with optimal treatment.
Diagnostic tests
See Diagnostic Tests.
Collaborative management
See Collaborative Management in Surgical Wounds Healing by
Primary Intention and Collaborative Management in Surgical or
Traumatic Wounds Healing by Secondary Intention.
439
1. Risk assessment: Identify individuals at risk daily with a
reliable/valid risk assessment tool; systematically document skin
condition from head to toe according to institutional policy.
3. Heels: Float the heels using pillows placed under the length of
440
the calf.
441
cleansers are available. If soap must be used, then thoroughly rinse
from the skin.
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CHAPTER 2
2. Most can be aerosolized, but not all are transmitted in the air.
462
6. They have high morbidity and/or mortality rates.
Key signs
Bioterrorism should be suspected when the following situations are
seen:
• Those indoors are not as affected as or “as are those” who have
been outdoors.
463
• Those presenting within 48 to 72 hours of exposure have likely
been exposed to a biological agent, as opposed to those exposed
to a toxin, who present within a few hours.
Monitor
• Observe for an unusual or unexplained increase in an illness,
especially with the characteristics listed in Key Signs.
464
steps are taken to increase worldwide security against infectious
diseases.
The proposed strategy for international security against
bioterrorism is as follows:
Report
• All occurrences of the six Category A diseases must be reported
to the CDC.
465
Shigella], glanders [Burkholderia mallei], melioidosis [Burkholderia
pseudomallei], psittacosis [Chlamydia psittaci], Q fever [Coxiella
burnetii], ricin toxin from Ricinus communis [castor beans],
staphylococcal enterotoxin B, typhus fever [Rickettsia prowazekii],
viral encephalitis [alphaviruses, e.g., Venezuelan equine
encephalitis, Eastern equine encephalitis, Western equine
encephalitis], and water safety threats [e.g., Vibrio cholerae,
Cryptosporidium parvum]). These organisms are the second highest
priority.
Labwork
• Appropriate laboratory studies should be done to confirm the
presence of the suspected biological agent. Many of these
diseases require testing at specialty laboratories because these are
uncommon bacteria and most hospital laboratories are not set up
to test for these agents.
Anthrax
466
Pathophysiology
Anthrax is a serious disease caused by Bacillus anthracis, a spore-
forming bacterium. A spore is a dormant (inactive) cell that
activates under the right conditions. Anthrax spores, once inside
the human body, are able to germinate. Once germinated, the
replicating bacteria release endotoxins leading to hemorrhage,
edema, and necrosis.
There are three types of anthrax: skin (cutaneous), lung
(inhalation), and digestive (gastrointestinal). Hemorrhagic
mediastinitis is present with the inhalation form, and bloody
diarrhea is seen with the intestinal form. When enough endotoxin is
released into the bloodstream, the disease can be fatal even if
antibiotics eradicate the bacteria. Anthrax infections are usually
very rare because it takes thousands of spores to cause an infection.
Inhalation anthrax is usually fatal even with treatment.
Gastrointestinal anthrax has a mortality rate of 25% to 60%,
whereas 20% of those with untreated cutaneous anthrax die.
Cutaneous anthrax is rarely fatal unless untreated.
Transmission
Anthrax has not been known to spread from one person to another.
Humans may acquire anthrax by handling products from infected
animals or inhaling anthrax spores from infected animal products
(e.g., wool). People acquire gastrointestinal anthrax by eating
undercooked meat from infected animals. Anthrax in soil may enter
the body through open skin. The organism is easy to obtain,
produce, and store.
Assessment
The symptoms (warning signs) of anthrax differ depending on the
type of disease:
• Inhalation: The most serious form with the highest mortality rate,
this begins 1 to 6 days after exposure with cold or influenza (flu)-
like symptoms, with sore throat, mild fever, and muscle aches.
Later symptoms include cough, chest discomfort, shortness of
467
breath, fatigue, and muscle aches. Inhalation anthrax quickly
progresses to respiratory failure and shock. Chest radiograph
reveals a widened mediastinum and pleural effusions.
Diagnostic tests
Diagnostic tests to isolate anthrax antigen are not widely available.
Confirmation of the diagnosis is made by sending a specimen to a
national reference laboratory after the treatment begins. Clinicians
should begin treatment based on clinical signs and symptoms,
because early treatment is imperative to enhance chances of
survival from inhalation anthrax. Standard blood culture may be
useful if the laboratory is told to look for bacillus species. A Gram
stain, enzyme-linked immunosorbent assay (ELISA), and nasal
swab check for spores may also be useful.
Collaborative management
Care priorities
1. Antibiotics
Used to treat all three types of anthrax. Ideally, the antibiotic should
be based on culture and sensitivity results. If those are not
available, the antibiotics of choice are doxycycline and
ciprofloxacin. Additionally, levofloxacin is recommended for
adults. Occasionally, rifampin may also be used. Early
identification and treatment are crucial to minimize the amount of
468
endotoxin released.
6. Vaccination
A vaccine to prevent anthrax exists, but it is not yet available to the
general public. Anyone at risk for anthrax exposure, including
certain members of the U.S. Armed Forces, laboratory workers, and
workers who may enter or reenter contaminated areas, may be
vaccinated. If anthrax is used as a weapon, a vaccination program
will be initiated to vaccinate as many exposed people as possible.
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Goals/Outcomes: Within 12 to 24 hours of treatment, the patient
has adequate gas exchange, as evidenced by PaO2 at least 80 mm
Hg, Paco2 35 to 45 mm Hg, pH 7.35 to 7.45, presence of normal
breath sounds, and absence of adventitious breath sounds. The
respiratory rate (RR) is 12 to 20 breaths/min with normal pattern
and depth.
Respiratory Status: Gas Exchange.
Respiratory monitoring
Oxygen therapy
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ordered. Add humidity as appropriate.
Mechanical ventilation
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6. Provide the patient with means of communication.
Botulism
Pathophysiology
Botulism is a muscle-paralyzing disease associated with respiratory
dysfunction caused by a toxin produced from Clostridium botulinum
bacteria. The toxin is the most potent lethal substance known to
humans. Man-made inhalational botulism is brought into being
when aerosolized botulinum toxin is inhaled. The bacterium
naturally lives for weeks in nonmoving water and food. There are
three naturally acquired types of botulism:
Transmission
Botulism is not spread from person to person. Botulinum toxin is
absorbed through lung or intestinal mucosa and nonintact skin.
Foodborne botulism occurs in all age groups.
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Assessment
• Foodborne: Double vision, drooping eyelids, slurred speech,
dysphagia, dry mouth, and descending muscle weakness are
symptoms. Weakness starts in the shoulders and upper arms,
descends to the lower arms and upper thighs, and eventually
spreads down to the lower legs and feet. Paralysis of the
respiratory muscles leads to respiratory failure unless ventilation
is supported with mechanical ventilation. Patients are generally
afebrile and alert.
Diagnostic tests
Currently, the CDC and fewer than 25 public health laboratories
perform the diagnostic test for botulism. Diagnosis is made
clinically, after ruling out other causes of paralysis. Classic botulism
paralysis is descending in nature and involves the cranial nerves.
Collaborative management
Care priorities
1. Antitoxin
Botulinum antitoxin is available in two forms from the CDC.
Because both are equine derivatives, it is important to perform a
skin test as directed in the package insert to check for
hypersensitivity before administering. Antitoxin helps prevent
further nerve damage from the botulinum toxin but cannot reverse
the existing paralysis. It is most effective if given within the first 24
hours. The antitoxin is not effective in infant botulism. For infant
botulism, botulism immune globulin-intravenous (BIG-IV) is
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administered.
2. Antibiotic
Antibiotics are given to treat wounds infected with C. botulinum
and secondary infections. Antibiotics have no effect on botulinum
toxin.
3. Supportive care
Includes mechanical ventilation, nutrition support, care for
immobility, and treatment for secondary infections.
Respiratory monitoring
Ventilation assistance
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1. Position the patient to alleviate dyspnea and insure maximal
ventilation, generally in a sitting upright position unless severe
hypotension is present.
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Transmission
HFVs reside in many animal hosts and arthropod vectors. Humans
become infected when bitten by an infected arthropod, by inhaling
aerosolized virus from infected rodent excreta, from direct contact
with infected animal carcasses, and from other human beings.
Humans infected with Ebola, Marburg, Lassa fever, and
arenaviruses can spread the disease through contact with body
fluids.
Isolation
Strict droplet and contact precautions are required if a patient is
suspected of infection. The recommendations for management of
Ebola patients has evolved worldwide. It was recognized that a
large number of secondary infections from Ebola virus disease
during the 2014 outbreak occurred in health care workers exposed
during care of infected patients. Leading U.S. special contagious
disease centers have used full-body Tyvek suits and powered air
purifying respirator (PAPR) hoods as part of the contact and
droplet precautions protocol.
Assessment
Clinical scenarios vary depending on the virus. The most common
symptom is a fever.
Diagnostic tests
Only the CDC and U.S. Army Research Institute of Infectious
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Diseases laboratories have testing available.
Collaborative management
Care priorities
1. Supportive care
Maintain fluid and electrolyte balances, and treat hypotension with
early use of vasopressors if fluid therapy is not effective,
mechanical ventilation, renal dialysis, and anticonvulsive therapy.
Administration of clotting factor concentrates, platelets, fresh-
frozen plasma, and heparin in patients with DIC.
2. Antivirals
These agents are not effective against these diseases.
3. Ribavirin
Institute a 10-day course if Lassa fever or New World arenavirus is
confirmed.
5. Vaccine
A vaccine is available for yellow fever, which is only recommended
for travelers going to South America or Africa where yellow fever is
endemic and for laboratory personnel who are exposed to yellow
fever samples. The vaccine is not helpful postexposure because the
short incubation period does not allow immunity to develop if the
vaccine is administered following exposure.
Plague
Pathophysiology
Plague is an infectious disease caused by the bacterium Yersinia
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pestis that is found in rodents and their fleas. Several forms of
plague can occur individually or in combination: bubonic,
pneumonic, and septicemic plague. Bubonic plague is the most
common, occurring when an infected flea bites a human or when
infectious materials enter through a break in the skin. Pneumonic
plague occurs when Y. pestis infects the lungs through direct or
close contact with a person who has pneumonic plague or in
untreated patients with bubonic or septicemic plague, allowing
bacterial spread to the lungs. Septicemic plague can occur as a
complication of either of the previous types of plague or alone. The
bacteria enter the bloodstream and multiply, prompting the
systemic effects of sepsis.
The Y. pestis bacteria travel to lymph nodes, where they resist
defense mechanisms and rapidly multiply, causing destruction of
lymph nodes. Bacteria enter the bloodstream and prompt sepsis,
septic shock, DIC, and coma. Without treatment, mortality
approaches 100%; with treatment, the mortality can be as low as
5%.
Transmission
Pneumonic plague is spread through direct contact with an infected
person. Neither bubonic nor septicemic plagues are transmitted by
person-to-person contact.
Assessment
• Pneumonic plague: Fever, headache, weakness, and rapidly
developing pneumonia with shortness of breath, chest pain,
cough, and sometimes bloody or watery sputum. The pneumonia
progresses and in 2 to 4 days can cause respiratory failure and
shock. Without treatment, patients with pneumonic plague will
die.
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• Bubonic plague: Swollen, tender lymph glands (called buboes),
fever, headache, chills, and weakness.
Diagnostic tests
• Gram stain of sputum or blood: Reveals gram-negative bacilli. A
laboratory may misidentify the bacteria unless notified that Y.
pestis is suspected.
Collaborative management
Care priorities
1. Antibiotics
Given within the first 24 hours of symptoms. Streptomycin,
gentamicin, tetracyclines, and chloramphenicol are all effective in
treating pneumonic plague. The preferred choice in adults is
streptomycin 1 g intramuscularly (IM) twice a day for 10 days or
gentamicin 5 mg/kg either IM or IV once a day or 2 mg/kg loading
dose followed by 1.7 mg/kg administered IM or IV three times a
day for 10 days. In children, the drug of choice is streptomycin 15
mg/kg IM twice a day with maximum dose of 2 g or gentamicin 2.5
mg/kg IM or IV three times a day for 10 days.
2. Vaccine
There currently is no vaccine available in the United States. Work is
currently under way to develop a vaccine.
3. Supportive care
Ventilatory support, pain management, and treatment for shock,
DIC, and multiorgan dysfunction syndrome, as appropriate.
Smallpox (variola)
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Pathophysiology
Smallpox is a serious, contagious, and sometimes fatal infectious
disease. It is a member of the orthopoxvirus family, along with
monkeypox, vaccinia, and cowpox. Although all of these can cause
skin lesions, only smallpox is readily transmitted from person to
person. There are two main clinical forms of smallpox: Variola
major and Variola minor, with several additional strains. Variola
major is the severe and most common form of smallpox, with a
more extensive rash and higher fever. Historically, Variola major
had a 30% mortality rate. Variola minor was less common and
much less severe. Smallpox was eradicated after a successful
worldwide vaccination program. The last case of smallpox in the
United States was in 1949. The last naturally occurring case in the
world was in Somalia in 1977. There is currently questionable
access to the virus since the separation of the Soviet Union, because
Moscow and the United States housed the only two storage
laboratories at that time.
Smallpox virus enters the body through the mucosa in the
oropharyngeal and respiratory tracts. The virus multiplies in the
lymph nodes, the spleen, and the bone marrow. Eventually the
virus, contained in lymphocytes, localizes in small blood vessels of
the dermis and infects adjacent cells, causing the pustules to form.
Smallpox is an excellent agent for bioterrorism because it is easy
to both transport and store, and because it is very stable and
markedly virulent when aerosolized.
Transmission
Smallpox is transmitted via droplet nuclei or aerosols expelled from
the oropharynx of an infected person. Usually direct and fairly
prolonged face-to-face contact was required to spread smallpox
from person to person. Smallpox can be spread through direct
contact with infected bodily fluids or contaminated objects (e.g.,
bedding or clothing). Rarely, the virus spreads through the air in
enclosed settings (e.g., buildings, buses, trains). Humans are the
only natural hosts of variola (there is no recorded transmissions
from animals or insects).
A person with smallpox is sometimes contagious with onset of
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fever (prodrome phase). Most infected persons become contagious
with the onset of rash. At this stage, the person is usually very sick,
unable to move around in the community. The person remains
contagious until the last smallpox scab falls off.
Assessment
• Clinical case definition: An illness with acute onset of fever ≥101°
F (38.3° C), followed by a rash characterized by firm, deep-seated
vesicles or pustules in the same stage of development without
any other apparent cause. These characteristics help differentiate
the smallpox from chickenpox. Smallpox may be easily missed in
the early stage by health care providers.
Diagnostic tests
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Laboratory diagnostic testing for variola should be done by a CDC
Laboratory Response Network (LRN) laboratory using LRN-
approved polymerase chain reaction (PCR) tests and protocols for
variola virus. Laboratory testing should be reserved for cases that
meet the clinical case definition, thus classified as being a potential
high risk for smallpox.
Collaborative management
There are no approved treatments for smallpox. Currently,
treatment consists of supportive care. However, cidofovir, an
antiviral, is currently being studied to see if it is effective against the
smallpox virus.
Care priorities
1. Vaccine
A key is to identify smallpox exposure and administer vaccine
within 3 days, to prevent or significantly lessen the severity of the
disease process. Vaccine administered within 4 to 7 days after
exposure may provide some protection and lessen the disease
severity.
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2. Isolation
Patients presenting with symptoms should be isolated immediately
in a negative-pressure room. The door should be kept closed at all
times. All health care workers entering the room should wear an N-
95 respirator mask. Because smallpox is also transmitted via body
fluids (contaminating the bedding), health care workers should use
contact precautions (i.e., gown, gloves, and shoe covers) when
entering the room. Other infection control practices, such as
limiting patient transport, designating patient care equipment, and
so forth, should follow the institution’s policies. Linen should be
autoclaved and corpses cremated.
3. Supportive management
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1. Use anticipatory guidance to prepare the patient for predictable
changes in body image.
4. Identify the effects of the patient’s culture, religion, race, sex, and
age in terms of body image.
Emotional support
Tularemia
Pathophysiology
Tularemia is caused by a bacterial zoonosis called Francisella
tularensis. One of the most infectious pathogenic bacteria known, it
is found in infected water, soil, vegetation, small mammals, ticks,
fleas, and mosquitoes. F. tularensis is a small, nonmotile, aerobic,
gram-negative coccobacillus that targets the lymph nodes, lungs,
pleura, spleen, liver, and kidneys. Bacteria enter through skin,
mucous membranes, gastrointestinal tract, and lungs to invade
cells, causing inflammation and permanent damage if untreated.
Transmission
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Tularemia is transmitted by bites from infected arthropods;
handling infectious animal tissues or fluids; direct contact with or
ingestion of contaminated water, food, or soil; and inhaling infected
aerosols. There is no evidence of person-to-person transmission.
Patients should be placed on standard precautions.
Assessment
• Disease presentation: May vary depending on the infecting
organism, dose, and site of inoculation. It usually starts abruptly
with a fever of 100.1° F to 104° F (38° C to 40° C), headache, chills,
generalized body aches, rhinitis, and a sore throat. Some patients
have a dry cough, substernal pain, skin or mouth ulcers, swollen
painful lymph glands, and swollen and painful eyes.
Diagnostic tests
Rapid diagnostic testing for F. tularensis is not widely available. If
tularemia is suspected, specimens of respiratory secretions and
blood should be collected and sent to a designated laboratory for
microscopic identification using fluorescent-labeled antibodies.
Collaborative management
Care priorities
1. Antibiotics
Several types of antibiotics have been effective. Oral tetracyclines
(i.e., doxycycline) or fluoroquinolones (i.e., ciprofloxacin) can be
used. IV streptomycin and gentamicin are effective. Bacterial
cultures and sensitivity data are used to determine the most
appropriate treatment. The patient may be placed on a 10-day
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course.
Emerging infections
Infectious diseases pose a serious health care threat. Although
medicine has been able to develop strategies to successfully prevent
and treat infections, both familiar and lesser known organisms
continue to present treatment challenges. Emerging infections are
complex, and their evolution has been challenging for health care
personnel to recognize, understand, and treat. Many infections,
such as H1N1, H5N1, hantavirus, and “mad cow” disease, originate
from different species of animals and spread to humans. Other
infectious diseases are acquired from exposure to specific
environments such as health care settings, or are transmitted from
person to person. Regardless of how infections and infectious
diseases are transmitted, prevention and control are challenging.
486
precautions. Universal precautions and other infection prevention
methods are the long-standing strategies used in hospitals
commonly referred to as isolation precautions. The most recent
revision (2007) by the CDC and the Healthcare Infection Control
Practices Advisory Committee reflects evidence-based practices and
the knowledge base of 2007. These techniques and procedures are
transmission-based, interrupting the transmission of infectious
agents and adhere to five basic principles:
487
or suspected to be infected with microorganisms
transmitted person to person by airborne droplet
nuclei that remain suspended in the air and that
can be dispersed widely by air currents.
488
infectious disease can strike at any time and may lead to significant
morbidity and mortality.
Multidrug-resistant organisms
MDROs pose a serious health risk to the patient who is
hospitalized. These organisms are resistant to one or more classes of
antimicrobial agents and thus are difficult to successfully manage.
Prolonged treatment leads to increased length of stay, increased
health care costs, and increased morbidity and mortality.
Methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-
resistant Enterococci (VRE) are the most common MDROs. Several
gram-negative bacilli, including Carbapenem-resistant
Enterobacteriaceae (CRE), are developing increased resistance to
treatment. MDROs are spread by person-to-person contact and by
contact with contaminated environmental surfaces. Treatment is
prescribed based on the sensitivity of the causative organism to the
available antimicrobial agents.
Many individuals are colonized with MDROs rather than having
active infections. The organism is present within the body without
signs or symptoms of infection. These patients are carriers. Patients
are placed on contact precautions to prevent the spread of the
MDRO to others. Hand hygiene remains the most important
infection control measure for the prevention of MDROs.
489
Vancomycin-resistant Enterococcus (VRE)
VRE developed from the enterococci normally present in the
intestines, female genitalia, and the environment, which most often
cause urinary tract, bloodstream, and surgical wound infections.
Enterococcal infections have often been treated with vancomycin.
After many years of managing these infections with vancomycin,
various strains of enterococci developed resistance to eradication by
vancomycin. Patients most likely to develop VRE infections include
those previously treated with a prolonged regimen of vancomycin
or other antibiotics; patients who are hospitalized and receiving
antibiotics for an extended period of time; patients who are
immunosuppressed, including critically ill, oncology, and patients
who have had a transplant procedure; patients who have
undergone abdominal and chest surgical procedures; those with the
need for prolonged management using a urinary catheter or central
IV catheter; and those already colonized with VRE.
490
Filoviridae, genus Ebolavirus. There are five Ebolavirus species but
only four are known to cause disease in humans, Zaire ebolavirus,
Sudan ebolavirus, Tai Forest ebolavirus, and Bundibugyo ebolavirus.
EVD was first identified in 1976 near the Ebola River in the
Democratic Republic of the Congo. Since first identified, there have
been sporadic outbreaks in Africa.
The 2014 Ebola outbreak is the largest in world history. The first
cases reported occurred in Guinea in March of 2014 and is the first
outbreak in West Africa. The 2014 West Africa outbreak has
affected several countries with the majority of the cases occurring in
Sierra Leone, Liberia, Guinea, and more recently, Mali. As of March
2015, there have been over 25,000 cases reported with over 10,000
confirmed deaths.
The natural reservoir remains unknown; however, researchers
believe the virus is animal-borne with bats being the most likely
reservoir. Ebola is also considered an agent of bioterrorism. Of the
five subtypes listed earlier, four occur in an animal host that is
native to Africa.
Transmission
Ebola is spread through direct contact to mucous membranes or
broken skin with blood and body fluids, including but not limited
to blood, sweat, vomit, feces, saliva, breast milk, and semen. It is
not spread through the air or by water.
Screening tools should be used in all health care settings to
establish risk factors for EVD. These include recent travel to areas
that have active EVD and a fever of greater than 38.6° C or 101.5° F.
Additional symptoms are severe headache, muscle pain, vomiting,
diarrhea, unexplained hemorrhage, or abdominal pain. Health care
providers should also include malaria as a working diagnosis
because it is also the most common febrile illness in people who
have recently travelled to the affected countries.
Case definitions
Early recognition and detection is crucial, and health care providers
need to be alert and evaluate any patients suspected with EVD. The
following categories have been defined by the CDC.
491
Person Under Investigation (PUI): A person who has both risk
factors and symptoms as follows:
AND
• Close contact with a person who has EVD, such as being within 3
feet of a patient with EVD, in the room or in the care area of the
person who is ill for a prolonged period of time.
492
No Known Exposure: A person who has been in a country where
there is an EVD outbreak in the past 21 days but does not report a
high-risk or low-risk exposure.
493
environment or airborne isolation room. Powered air purifying
respirator (PAPR) hoods have been used to provide additional
protection with enhanced comfort.
Diligent environmental cleaning and disinfection measures
should be used along with safe handling of potentially
contaminated materials. Use of Environmental Protection Agency-
registered hospital disinfectants with a label claim for
nonenveloped viruses should be used to disinfect environmental
surfaces in the patient’s room with suspected or confirmed EVD.
Patients with EVD should not be placed in rooms with carpet,
upholstered furniture, or curtains. Mattresses or pillows should
have a nonporous covering that fluids cannot penetrate. Any cloth
products or textiles should not be laundered. These items should be
disposed of into the waste stream. Any disposable single-use items
should be placed in leak-proof containment. Any plastic waste bags
should be placed in a rigid waste receptacle. U.S. centers have used
more extensive environmental protection measures including
autoclaving trash prior to placing it in rigid waste receptacles,
treating toilet water with disinfectants when waste is deposited,
and extensive terminal cleaning measures, based on lessons learned
from care providers managing the EVD outbreak in West Africa.
Diagnosis
Diagnosis is made by recent travel to areas where EVD is endemic
and by symptoms. This can be difficult in the early stages but
health care providers can follow the case definitions previously
listed.
Laboratory tests include:
Timeline of Infection Diagnostic Tests Available
Within a few days after Antigen-capture enzyme-linked immunosorbent assay
symptoms begin (ELISA) testing
• Immunoglobulin M (IgM) ELISA
• Polymerase chain reaction (PCR)
• Virus isolation
Later in disease course or after • IgM and IgG antibodies
recovery
Retrospectively in deceased • Immunohistochemistry testing
patients • PCR
• Virus isolation
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Treatment
Treatment is dependent on symptoms and patients are provided
supportive care. Early treatment and interventions increase the
chance of survival. Managing fluid and electrolytes by providing IV
fluids, maintaining oxygen levels and blood pressure are all
essential to survival. Patients may produce 10 liters of diarrhea
daily.
There are currently no U.S. Food and Drug Administration
(FDA)-approved vaccines or medications available for EVD. There
have been some experimental vaccines and treatments but they
have not been fully tested for effectiveness and safety.
Recovery depends on good supportive care and the patient’s
immune response. Patients who recover develop antibodies that
last for at least 10 years. At present, it is not known if they are
immune for life or can become infected with different species of
EVD. Long-term complications have occurred in patients who have
recovered from EVD, such as joint and vision problems.
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civet cat and raccoon dog). Both are considered delicacies in China
and are consumed by humans. One theory states that this CoV had
mutated and was transmitted to humans through handling of these
animals or contact with their saliva and feces.
Pathophysiology
SARS begins much like the common flu, progressing to pneumonia,
and potentially to acute respiratory distress syndrome (ARDS) and
death. Lymphopenia, thrombocytopenia, and leucopenia are noted.
SARS-CoV may infect blood cells and/or induce autoantibodies to
damage these cells, leading to immunologic dysregulation in
response to SARS-CoV.
Transmission
The most common mode of transmission for SARS is close person-
to-person contact: kissing, sharing eating or drinking utensils, close
conversation (less than 3 feet), physical examination, and any other
direct physical contact. Respiratory droplets are expelled by the
infected person by a cough or sneeze into the air. Droplets then
reach the mucosal membrane of the nose, mouth, or eyes of a
nearby person, infecting him or her.
Surfaces contaminated with SARS droplets may serve as a
reservoir for the virus. SARS droplets can remain viable up to
several days depending on the type of surface.
Assessment
Goal of assessment
Evaluate for early clinical and epidemiologic features of SARS.
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SARS-CoV disease among persons presenting with community-
acquired illness. The suspicion of SARS-CoV disease is raised if,
within 10 days of symptom onset, the patient:
OR
OR
OR
OR
497
contains live SARS-CoV) or close contact with an ill
person with such an exposure history.
Early illness
498
• ARDS (see Acute Lung Injury and Acute
Respiratory Distress Syndrome, Chapter 4), or
Screening labwork
Laboratory studies such as bacterial cultures and respiratory viral
panels can be used to rule out other potential causes of respiratory
tract infection. SARS-CoV reverse transcription (RT)-PCR and
enzyme immunoassay (EIA) tests are not typically ordered until
after a high index of suspicion by the physician and notification of
public health officials.
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Collaborative management
500
Care priorities for SARS-CoV
(see Care Priorities for MERS-CoV)
Pathophysiology
The clinical signs and symptoms of MERS-CoV include fever,
cough, dyspnea, chills, rigor, headache, myalgia, and malaise.
Other reported symptoms included nausea, vomiting, diarrhea,
abdominal pain, and sore throat. Patients present with acute
respiratory illness and can rapidly progress to pneumonitis,
respiratory failure, septic shock, and multiorgan failure, which may
result in death.
The incubation period ranges from 2 to 13 days with a median
incubation period of 5 days. Most patients present to the hospital on
day 4. The median time of onset of illness to death in the patient
who is critically ill is 12 days.
Transmission
MERS-CoV can spread from a person who is ill to others through
close contact. Close contact means individuals who care for the
individual who is ill or those living with the person who is infected.
501
There has been transmission to health care providers by patients
who are infected. There have been no reported community
outbreaks at this time, although this is being closely monitored. All
cases that have been reported have been linked to countries in or
near the Arabian Peninsula, and most people who have become ill
have lived or recently traveled to the area.
Assessment
Goal of assessment
Evaluate for early clinical and epidemiologic features of MERS-
CoV.
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Care priorities for MERS-CoV and SARS-CoV
2. Infection control
Patients are to be placed in a negative-pressure room under
airborne, contact, and standard precautions. Anyone who enters the
patient’s room must wear gowns, gloves, an N-95 respirator, and
eye protection. Hand hygiene should be performed after contact
with a patient on precaution. If there is a lack of negative-pressure
rooms and/or there is a need to concentrate infection control efforts
and resources, patients may be cohorted on a floor or nursing unit
designated for the care of patients with MERS only if air-handling
systems can be modified to allow these areas to operate under
negative pressure relative to surrounding areas.
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Maintain a stock of clean patient care and PPE supplies outside
the patient’s room. Decide where contaminated linen and waste
will be placed. Locate receptacles close to the point of use and
separate from clean supplies.
Creutzfeldt-Jakob disease
504
Pathophysiology
Creutzfeldt-Jakob disease (CJD) is a rare, fatal, neurodegenerative
disorder, believed to be caused by an abnormal isoform of a
glycoprotein known as a prion, a proteinaceous infectious particle.
The most common disorder is bovine spongiform encephalopathy,
or “mad cow” disease. A new form of CJD has emerged, called new
variant CJD (vCJD or nvCJD). This form of CJD is linked to
consumption of cattle with “mad cow” disease. Clinical and
epidemiologic evidence supporting this link between “mad cow”
disease and vCJD has become stronger. vCJD generally affects
younger people with a mean age of 29 years, whereas CJD occurs in
those aged 65 to 69 years.
CJD is classified as a transmissible spongiform encephalopathy.
Prion disease occurs in animals, particularly cattle, sheep, and goats.
CJD is endemic around the world and its estimated incidence report
is 1 case per 1 million population. Three forms of “classic” CJD
have been identified. Sporadic CJD affects older adults with rapid-
onset dementia and neurologic symptoms of unknown cause.
Familial CJD is an inherited disease and generally strikes younger
individuals. It has a longer course in comparison to sporadic CJD.
Iatrogenic CJD occurs through contact with infected tissue via
medical procedures or treatments.
Prion proteins are normal proteins in the body and brain. In CJD,
these proteins become abnormally shaped, as a result either of
genetics or of contamination from an outside source. This leads to
surrounding normal prion proteins taking on the abnormal shape.
Central nervous system (CNS) function is disrupted, leading to
cognitive impairment and cerebellar dysfunction. As the process
continues, the abnormal prions accumulate in the brain, causing
neuronal dysfunction, neuron death, gliosis (proliferation of
neuroglial tissue in the CNS), and ultimately death.
Transmission
CJD can spread via infectious or hereditary means. Prion infections
are transmitted via the peripheral route, either orally or
transcutaneously. They may be introduced to lymphatic organs,
particularly the spleen and lymph nodes, where initial replication
505
of the infected prions occurs. Infections can either enter the
circulatory system and be hematogenously spread to the brain, or
infected prions may travel via the vagus nerve to the brain. Genetic
mutation of the human prion gene PrP on chromosome 20 leads to
the dysfunction of the prion protein. More than 20 reported
mutations of this chromosome have been reported. All mutations
influence the onset and duration of CJD. vCJD is theorized to be
caused by the consumption of meat from cattle that is infected.
Once ingested, the infected prions follow the same neuroinvasion
route of CJD.
Sporadic CJD
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• At end stage, patients are unable to move or speak and need 24-
hour care.
Familial CJD
vCJD
• Persistent pain and odd sensations in the face and extremities are
common. As disease progresses, the patient develops ataxia,
sudden erratic movements, and progressive dementia with
marked memory loss.
• Ultimately, the patient will lose the ability to move or speak and
will require 24-hour care. Death soon follows.
Diagnostic tests
CJD is diagnosed based on typical signs, symptoms, and
progression of disease.
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Diagnostic Tests for Creutzfeldt-Jakob Disease (CJD)
Collaborative management
There is no known treatment or cure for CJD. Management of these
patients is supportive and palliative in nature. There is no vaccine
for CJD.
Care priorities
1. Supportive care
Ventilatory support, pain management, patient safety, intensive
skin care, assessment, nutrition support, care for immobility, and
treatment for secondary infections.
2. Infection control
Standard precautions are used to care for patients with CJD. If a
brain biopsy or other procedure is performed on a patient with CJD
or suspected CJD, inform the central sterile department so that
stringent chemical and autoclave sterilization methods can be used
to reprocess instruments.
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Mechanical Ventilation, Alterations in Consciousness, Wound and
Skin Care, Prolonged Immobility (Chapter 1), Emotional and
Spiritual Support for the Patient and Significant Others, and Ethical
Considerations in Critical Care (Chapter 2).
Transmission
WNV is a disease that has spread worldwide. Initially, WNV was a
disease that only occurred in bird species. Approximately 146
different species of birds have been reported to acquire this disease.
This disease is spread among the bird population by 29 different
species of mosquitoes (vectors). The natural cycle is from bird 1 to
mosquito 1 to bird 2 to mosquito 2, and so forth. Because of a
complex intensification of this natural cycle, bridge vectors
(mosquitoes that bite both birds and humans) became infected with
the WNV and spread the disease to humans. Only birds and
humans in the United States and Israel have been known to die
from WNV.
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Exposure to mosquitoes where WNV exists increases risk. WNV is
common in areas such as Africa, West Asia, and the Middle East. It
first appeared in the United States in the summer of 1999 and since
then has been found in all 48 contiguous states. Older age is
associated with a higher risk for developing more serious CNS
disease.
Incubation period
• Generally 2 to 14 days, although longer incubation periods have
been documented in persons who are immunosuppressed.
510
including limb paralysis and cranial nerve palsies, may be
observed. Tremor and movement disorders have also been
identified.
Clinical features
• Fever
• Seizures
• Myelitis
• Polyradiculitis
• Optic neuritis
• Severe weakness
• Ataxia/extrapyramidal signs
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Labwork
Certain findings are seen in patients with severe disease.
Collaborative management
Treatment of WNV infection is supportive. High-dose ribavirin and
interferon alfa-2b have some activity against WNV in vitro. There is
no specific antibiotic or antidote for the viral infection. Also, there is
no vaccine.
Care priorities
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Supportive care
Includes IV fluids to prevent dehydration, antipyretics for fever
management, oxygen therapy and ventilatory support, patient
safety, nutrition support, and treatment for secondary infections.
Standard precautions should be taken at all times; follow
organization’s policy for appropriate personal protection category.
Pandemic flu
An epidemic occurs when there are an unusually high number of
people affected by a disease. A pandemic is an international
epidemic. An influenza pandemic may occur when a new influenza
virus is detected and the human population has no immunity. With
the increase in global travel and transportation, and urban
development with areas of overcrowding, epidemics that result
from a new influenza virus are likely to be disseminated around the
world and rapidly become a pandemic. The WHO has defined the
phases of a pandemic to create a global framework to aid countries
in pandemic preparedness and response planning. Pandemics can
be either mild or severe in the illness and death they cause. The
severity of a pandemic can change during the time the illness
continues to spread.
The WHO has developed a global influenza preparedness plan
that outlines the responsibilities of WHO and national authorities in
the event of an influenza pandemic. The WHO also offers guidance
tools and training to assist in the development of national pandemic
preparedness plans (www.who.int/csr/disease/influenza/A58_13-
en.pdf).
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Avian influenza (“bird flu”)
Pathophysiology
Avian influenza is an infection caused by avian (bird) flu viruses,
type A strains. These viruses occur naturally among birds. Wild
birds carry the viruses in their intestines but usually do not get sick
from them. However, domesticated birds such as poultry can
become very ill and die from avian influenza viruses.
It is theorized that certain subgroups of avian influenza mutated,
crossed species, and infected humans. The subgroups of avian
influenza linked to human infections include but are not limited to
H5N1, H7N7, H9N2, H7N3, and H7N9. The H5N1 subgroup is of
particular concern to humans because of its ability to mutate and its
tendency to acquire genes from viruses from other animal species.
It has demonstrated high pathogenicity and causes severe disease
in humans. The H7N9 is a new subgroup first reported in March
2013, characterized by rapid development of serious pneumonia,
which leads to sepsis, ARDS, and multisystem organ failure.
Transmission
Avian influenza is most commonly spread from infected birds to
humans. The virus is harbored in birds (in the intestine), which
shed the virus through their saliva, nasal secretions, and feces. The
most common means of transmission among birds is fecal to oral.
Humans who come in direct contact with infected poultry are
susceptible to infection. Avian influenza survives on inanimate
objects. Items contaminated with secretions/excretions of infected
birds can be a vector for transmission to humans. The spread of
avian influenza from one person who is ill to another has been
reported very rarely, and transmission has not been observed to
continue beyond one person.
Assessment
History and risk factors
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• Direct or close contact with infected poultry or contaminated
surfaces. In outbreaks, most cases have occurred in previously
healthy children and young adults.
• A Health Safety Alert will be sent out by the CDC to all hospitals
if there are avian influenza outbreaks that lead this federal
organization to recommend heightened surveillance and
diagnostic testing of targeted patients. In this situation, the CDC
will outline triage guidelines, which will likely include travel to
the outbreak location within the past 10 days and hospitalization
with a severe respiratory illness.
Diagnostic tests
Diagnostic Tests for Avian Influenza
Abnormal
Test Purpose
Findings
Laboratory Studies
Complete blood count Assess for changes Elevated white
suggestive of other blood cell count
bacterial infections.
Influenza A/H5 (Asian lineage) virus real-time To identify causative Positive
reverse transcription–polymerase chain reaction agent.
(RT-PCR) assay:
Must consult with and have authorization from
local or state health departments. Test is
conducted only in designated laboratories.
Rapid bedside tests: Conduct for rapid Positive.
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Available but results are not confirmatory. screening for virus. Confirmatory
tests should
be
performed.
Viral culture: Identify causative agent. Positive for
Must be conducted in biosafety Level 3 laboratory. pathogen
Radiology
Chest radiograph Identify progression of Infiltrates,
lung disease and atelectasis
anatomic involvement.
Respiratory Tests
Arterial blood gas (if patient is in respiratory Determination of Acidosis,
distress) oxygen saturation and alkalosis
blood gases.
Pulse oximetry Measure oxygen <90%
saturation.
Collaborative management
At present, the primary medication therapy option is oseltamivir
(Tamiflu) and zanamivir (Relenza); however, there is concern that
viruses may become resistant to both of these drugs. Treatment is
supportive in accordance to the clinical status of the patient.
Care priorities
1. Supportive management
Includes IV fluids to prevent dehydration, antipyretics for fever
management, oxygen therapy and ventilatory support, patient
safety, nutrition support, and treatment for secondary infections.
2. Infection control
Place patients in a negative-pressure room under airborne, contact,
and standard precautions. An N-95 respirator should be worn by
everyone who enters the room. Gowns and gloves are to be worn
for all patient contact, and eye protection should be worn when
within 3 feet of the patient. Good hand hygiene should be practiced.
Precautions should be continued for 14 days after onset of
symptoms or until either an alternative diagnosis is established or
diagnostic test results indicate that the patient is not infected.
Restricted visitation should be implemented and an ongoing log
kept of all people entering the patient’s room. Minimize the number
516
of health care personnel caring for the patient. All equipment and
other items should remain in the patient’s room and should not be
used with other patients or outside the isolation room.
517
possible inconsistency of nurse assignment, and the amount of
coverage available by other disciplines, time constraints may lead to
dysfunctional situations that are not handled in the best manner to
produce a sustainable solution or, in worst-case scenarios, to not
being noticed at all.
It is of paramount importance that nurses are familiar with how
to provide both emotional and spiritual support to patients and
significant others, and to help guide them through the challenges
posed by critical illness and hospitalization. Complex support
system issues may include identification of high-risk dependent
relationships among older adults, family members, domestic
partners, children, or religious leaders. Actions required may
include steps to prevent infliction of physical, emotional, or sexual
harm, exploitation, or neglect of basic life necessities.
Effective exchange of information is foundational for
collaboration among the health care team, patients, and their
significant others. Accurate and timely information should be
shared throughout the hospitalization to ensure the delivery of
holistic patient care. In our current fast-paced, dynamic health care
environment, relationships among health care professionals and
their clients vary, and can evolve over time.
With less opportunity to establish relationships, trusting the
clinical knowledge, decisions, and judgment of unknown providers
may be difficult. In large teaching hospitals, the problem is
compounded as the monthly rotation of multiple levels of physician
house staff ensues. Nursing care is often delivered on a dynamic
schedule and includes increasing numbers of contract and per diem
clinical staff. Therefore, stabilizing the team and taking the time
needed to provide effective communication can be challenging. The
larger the number of health care team members or
family/significant others involved, the greater the challenge of
adequate communication. In addition, emotionally charged events
are common in the critical care environment. To help provide care
of the whole patient and family system, emotional support can be
of assistance to promote healthy coping.
Occasionally, however, providers are also in need of emotional
support to cope with difficult situations. Emotional support is
defined as support for emotions that will help provide the best
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outcomes. Key elements of holistic care include providing
encouragement, reassurance, and acceptance during times of stress.
Mental, emotional, and spiritual interventions are often needed to
help with coping and decision-making during critical illness.
Emotional responses may be closely associated with mental
processes; in other words, thoughts or perceptions drive feelings
about life events. Knowledge affects perception, so keeping patients
and families informed and up to date is of paramount importance
to their emotional well-being. Knowledge will promote them
having more perceived control of the situation. Frequent, repetitive,
simple explanations are often needed. During emotional upset, the
ability to recall and retain information is often impaired.
Nurses can facilitate adaptation to perceived stressors, changes,
or threats that interfere with meeting the demands present in the
lives of patients and their significant others. Coping techniques that
are used vary with individuals, including health care providers,
and are often affected by culture. Counseling or family-centered
care team conferences may be provided, using an interactive,
helpful approach, and may focus on the needs, problems, or
feelings of the patient, significant others, and health care team
members. Actions are designed to enhance or support coping, crisis
management, problem-solving, and interpersonal relationships.
Emotionally charged ethical issues frequently arise in the critical
care environment. Care providers are prompted to address end-of-
life decision-making, including “Do Not Resuscitate” issues,
withdrawal of care, and whether or not the family desires to be
present if resuscitation is needed. Involvement of the
interdisciplinary team (which may include members such as
pastoral care, mental health professionals, social work, palliative
care, and an ethics professional) may be warranted on admission to
the critical care unit and throughout the stay if complex end-of-life
issues arise.
2-1
RESEARCH BRIEF
A large percentage of the U.S. general public has stated they would
like to have loved ones present during resuscitation. Despite the
519
countless benefits reported, family presence during resuscitation is
still a controversial, highly debated issue among health
professionals in adult critical care units. Baumhover and Hughes
(2009) designed an exploratory, descriptive, and correlational
study to determine the relationship between the spirituality of
health care professionals and support for family presence during
invasive procedures and resuscitation. The holistic Spirituality
Assessment Scale (SAS) developed by Howden (1992) was used to
obtain information regarding a more comprehensive meaning of
spirituality; not focused exclusively on religious beliefs and
feelings of patients but also including the feelings of health care
providers. Data were collected from 73 nurses, 31 physicians, and 4
physician assistants. Results suggested a link between a holistic
perspective and support for family presence. The higher the scores
of spirituality for health care providers, the greater the likelihood
that they supported family presence as a patient’s right and
essential part of holistic care. This study helps to fill the gap in the
current literature regarding certain demographic characteristics
affecting whether or not health care providers are willing to allow
families to be present during invasive procedures and
resuscitation. Further analysis of extraneous variables is needed
before the results of this study can be generalized.
From Baumhover N, Hughes L: Spirituality and support for family presence during
invasive procedures and resuscitations in adults. Am J Crit Care 18:357-367, 2009.
520
appropriate avenues are not initiated to repair damages. The
American College of Critical Care Medicine has developed patient
and family guidelines that help widen perspectives, open new
options, and suggest different ideas for health care providers to
help abate situations before they escalate to the point of physical
violence.
Spiritual support is regarded as a part of providing holistic care.
Spirituality is not to be confused with religion. Although the vast
majority of nurses believe spiritual care is a part of providing
patient-centered, holistic care, over half feel inadequate to perform
spiritual care interventions. Spirituality has been described as the
values, beliefs, and behaviors of an individual related to purpose
and meaning in life; connectedness to self, others, and life and
universal dimensions; innerness or inner resources and capacity for
transcendence. Using these characteristics, Howden developed the
Spirituality Assessment Scale or SAS (Box 2-1). The 28 items on the
SAS provide a strong operational framework for evaluating the
ability of all involved with patient care and decision-making to
connect or to be sensitive to the spiritual dimensions of others, and
possibly frame the approach on addressing the emotional needs of
others. If a health care provider has not developed the capacity to
connect with others, providing care that requires embracing a
viewpoint outside of his or her personal sphere of perception is
extremely difficult. Behavior modification of the patient, significant
others, or health care team members may be necessary as part of
facilitating adaptation to life changes for the patient and significant
others resulting from hospitalization. Values may collide, based on
past experiences of all involved; therefore, staying focused on the
present can assist all involved in remaining objective when
approaching the situation.
Box 2-1
ELEMENTS OF THE HOWDEN SPIRITUAL
ASSESSMENT SCALE (SAS)*
Has a sense of belongingness Feels part of the community lived in
Has capacity to forgive Feels reconciling relationships is important
Can rise above or go beyond mental and Can rise above or go beyond body changes or
521
physical problems body losses
Is concerned about environmental Feels responsible for preserving the planet
destruction
Can find peace during a devastating event Has inner resources for dealing with uncertainty
Has a sense of kinship to others Has found inner strength during past struggles
Has a connection to all of life Possesses life goals and aims
Relies on inner strength when struggling Possesses inner strength
Enjoys serving others Feels a sense of fulfillment in life
Has a sense of inner spiritual guidance Trusts life is good despite discouraging events
Perceives ability for self-healing Feels good about themselves
Perceives meaning of life provides peace Has the sense life has meaning and purpose
Feels a sense of balance within life Feels inner harmony and peace
Boundaries of personal universe extend Inner strength is related to belief in a higher
beyond space and time power or supreme being
*
Items are rated 1 (Strongly disagree) through 6 (Strongly agree) on a Likert scale after
reading statements about the elements listed here.
From Howden JW: Development and psychometric characteristics of the Spirituality
Assessment Scale. Dissert Abstr Int 54:166B, 1992. Abstract reproduced with permission
from ProQuest LLC. © 2007 ProQuest LLC; all rights reserved. Further reproduction is
prohibited without permission.
522
abilities. The factors listed in Box 2-1 have been demonstrated by
various studies to affect how decisions are made and how they may
adversely affect coping because of a difference in beliefs related to
spirituality. The following characteristics in any member of a
decision-making team may be associated with ineffective coping:
poor self-image, a lack of fulfillment, significant financial problems,
existing unhealthy and/or unrepaired relationships, resistance to
change, a lack of meaning or purpose in life, difficulty in learning, a
poor sense of belonging or connectedness, a lack of inner peace or
strength, the inability to forgive others, difficulty relating to others,
and/or unclear life goals.
Anxiety reduction
a. Mild: Restless.
523
b. Moderate: Inattentive, expresses concern,
narrowed perceptions, disturbed sleep pattern,
altered vital signs.
524
9. Reduce sensory overload by providing an organized, quiet
environment. (See Alterations in Consciousness, Chapter 1).
10. Introduce one self and other health care team members; explain
each individual’s role as it relates to the plan of care or care map.
Box 2-2
TYPES OF TOUCH
Instrumental touch
• Task- or procedure-related
Affective touch
• Expressive, personal
• Caring
• Comforting
Therapeutic touch
• Deliberate intervention to accomplish a purpose
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• Acupressure
Social isolation
related to altered health status; inability to engage in satisfying personal
relationships; altered mental status; altered physical appearance.
Goals/Outcomes: Within 24 hours after diagnosis, the patient
demonstrates interaction and communication with others.
Loneliness Severity, Mood Equilibrium, Personal Well-Being.
Socialization enhancement
• Denial or withdrawal.
526
loneliness and isolation. (“You seem very sad when your family
leaves the room. Can you tell me more about your feelings?”)
Coping enhancement
527
aware of? Knowing about it may help us better care for your
mother.”)
Fear
related to patient’s life-threatening condition; lack of information
Goals/Outcomes: After the intervention, the patient and
family/significant others relate that fear has been lessened or is
manageable.
Fear Level, Fear Self-Control.
528
Security enhancement
Box 2-3
SAFETY PRECAUTIONS IN THE EVENT OF
VIOLENT BEHAVIOR
529
Patient safety
• Remove harmful objects from the environment, such as heavy
objects, scissors, tubing.
• If available, use bed alarms. Ensure all unit staff members are
aware of potential for violence.
Caregiver safety
• Place the patient in bed closest to nursing station. Maintain
visibility at all times by keeping door open.
530
• Remain alert.
From Bureau of Labor Statistics (BLS), U.S. Department of Labor, for the National Institute
for Occupational Safety and Health (NIOSH), Centers for Disease Control and Prevention:
Survey of workplace violence prevention, Washington, 2005, U.S. Department of Labor.
Retrieved from www.bls.gov/iif/osh_wpvs.htm.
Grieving
related to perceived potential loss of physiologic well-being (e.g., expected
loss of body function or body part, changes in self-concept or body image,
terminal illness).
Goals/Outcomes: After interventions, patient and significant
others/family express grief, participate in decisions about the
future, and communicate concerns to health care team members
and to one another.
Adaptation to Physical Disability, Body Image Enhancement.
Table 2-1
STAGES OF GRIEVING
531
Disbelief: “But I just saw her this morning”
Anger
Hostility
Resentment
Bargaining to postpone loss
Appeal for help to recover loss
Loud complaints
Altered sleep and appetite
Disorganization Depression
Withdrawal
Social isolation
Psychomotor retardation
Silence
Reorganization Acceptance of loss
Development of new interests and attachments
Restructuring of lifestyle
Return to preloss level of functioning
Emotional support
Spiritual distress
related to separation from spiritual/religious/cultural supports; challenged
532
belief and value system.
Goals/Outcomes: After diagnosis, the patient and family
verbalize spiritual or religious beliefs and express hope for the
future, the attainment of spiritual or religious support, and the
availability of what is required to resolve conflicts.
Spiritual Health, Dignified Life Closure.
Spiritual support
533
blood transfusions been discussed with you?”)
Coping enhancement
534
Support system enhancement
Caregiver support
535
manage the situation?” “I hear that your loved one is very ill. How
can I help you?”)
536
11. Encourage healthy functioning. For example, facilitate open
communication and encourage behaviors that support
cohesiveness. (“Your mother seemed to enjoy your last visit. Would
you like to see her now?”)
13. Assist with developing realistic goals, plans, and actions. Refer
to clergy, case manager, psychiatric nurse, social services, financial
counseling, and family therapy as appropriate.
Powerlessness
related to health care environment; treatment regimen
Goals/Outcomes: After diagnosis, assess the patient’s and
family’s preferences, needs, values, and attitudes. The patient
makes decisions about self-care and therapies and relates an
attitude of realistic hope and a sense of self-control and the family
accepts decisions.
Depression Self-Control, Family Participation in Professional
Care, Health Beliefs: Perceived Control.
Self-responsibility facilitation
537
responsibilities of the hospital with regard to patient care.
2. Ensure the patient and family know who is taking care of the
patient. Tell the patient and family if a staff member does not have
an identification badge visible, it is alright to ask for their name and
their role in patient care.
9. Encourage the patient and family to ask to speak with the charge
nurse, nurse manager, nurse supervisor, or patient advocate/patient
representative if there is a problem with any member of the health
care team.
538
acquaintances request information about the patient’s status, refer
them to the patient or a family member who can provide acceptable
amounts of information.
Sleep enhancement
539
medications, underlying illness, sleep apnea, respiratory disorder,
caffeine, fear, and medical and nursing interventions.
Table 2-2
NONPHARMACOLOGIC MEASURES TO PROMOTE SLEEP
Activity Example(s)
Mask or eliminate Use eye shields, ear plugs
environmental stimuli Play soothing music
Dim lights at bedtime
Mask odors from dressings/drainage; change dressing or
drainage container as indicated
Promote muscle relaxation Encourage ambulation as tolerated throughout the day
Teach and encourage in-bed exercises and position change
Perform back massage at bedtime
If not contraindicated, use a heating pad
Reduce anxiety Ensure adequate pain control
Keep the patient informed of his or her progress and treatment
measures
Avoid overstimulation by visitors or other activities
immediately before bedtime
Avoid stimulant drugs (e.g., caffeine)
Promote comfort Encourage the patient to use own pillows, bedclothes if not
contraindicated
Adjust bed; rearrange linens
Regulate room temperature
Promote usual presleep Offer oral hygiene at bedtime
routine Provide warm beverage at bedtime
Encourage reading or other quiet activity
540
Minimize sleep disruption Maintain quiet environment throughout the night
Plan nursing activities to allow long periods (at least 90
minutes) of undisturbed sleep
Use dim lights when checking on the patient during the night
4. Discuss the loss or change with the patient. Recognize that what
may seem to be a small change may be of great significance to the
patient (e.g., arm immobilizer, catheter, hair loss, ecchymoses, facial
abrasions).
541
patient’s feelings related to the changed body part or function. (“It
seems as though your son looks very different to you now, but it
would help if you speak to him and touch him as you would
normally.”)
Box 2-4
INDICATORS SUGGESTING BODY IMAGE
DISTURBANCE
Nonverbal indicators
• Missing body part: internal or external (e.g., splenectomy,
amputated extremity)
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• Avoiding looking at or touching body part
Verbal indicators
• Expression of negative feelings about body
Complicated grieving
related to loss of physiologic well-being; fatal illness.
Goals/Outcomes: After diagnosis, the patient and family express
grief, explain the meaning of the loss, and talk with each other. The
patient assumes necessary self-care activities.
Mood Equilibrium, Grief Resolution, Depression Self-
Control.
1. Assess grief stage (see Table 2-1) and previous coping abilities.
Discuss feelings of the patient and family, the meaning of loss, and
goals. (“How do you feel about your condition/illness or your loved
one’s condition? What do you hope to accomplish in these next few
days/weeks? Are you afraid your family will not be taken care of if
you pass away?”)
543
must feel very angry, but for the safety of others, you may not
throw equipment.”)
Hope instillation
544
7. Set realistic, attainable goals, and reward achievement.
545
5. For acute confusion that becomes aggressive, do not attempt to
reorient patient and avoid arguing. Instead, provide support by
stating, “I believe that you (see, hear) that; however, I do not (see,
hear) that.” Use nonthreatening mannerisms, facial expressions,
and tone of voice.
546
and substance abuse as maladaptive coping behaviors (see Box 2-3).
Normalization promotion
547
like some private time together?”)
Deficient knowledge
related to disease process, diet, medication, prescribed activity, fall
prevention, infection control, health resources, treatment procedures,
treatment regimen, substance use control, personal safety.
Goals/Outcomes: The patient and family/significant others
verbalize understanding of current diet, disease process, health
resources, medication, prescribed activity, treatment procedures,
and treatment regimen before discharge from the critical care unit.
Knowledge: Disease Process, Diet, Fall Prevention, Health
Behavior, Illness Care, Infection Control, Medication, Personal
Safety, Substance Use Control.
548
4. Assess learning needs and establish short- and long-term goals.
549
understand your husband’s status and what we are doing to care
for him?”)
14. Ask if needs for information are being met. (“Do you have any
questions about the care your mother is receiving or about her
condition?”)
550
2. With the patient and significant others, assess the patient’s ability
to hear, see, speak, read, write, and comprehend English. If the
patient speaks a language other than English, collaborate with an
English-speaking family member or interpreter to establish effective
communication.
551
stress; altered sensory reception, transmission, or integration; chemical
alteration.
Goals/Outcomes: At the time of intervention, the patient
verbalizes orientation to time, place, and person; relates the ability
to concentrate; and expresses satisfaction with the degree and type
of sensory stimulation being received.
Distorted Thought Self-Control, Neurologic Status:
Cranial/Sensory Motor Function, Vision Compensation Behavior.
Environmental management
552
• Depending on the patient’s preferences, provide a
radio, music, reading materials, and tape recordings
of family and significant others. Earphones help
block out external stimuli.
553
6. Encourage participation in health care planning and decision-
making whenever possible by asking the patient first.
Informed consent
Without adequate knowledge, patients and their significant others
cannot make good decisions. Part of a nurse’s obligation is to
inform patients and families, in a caring manner, what is to be
554
expected from different treatment options. Informed consent serves
not only to protect the health care provider from liability but its
primary purpose is to support the ethical principle of respect for
autonomy. Informed consent is instrumental to a patient’s right to
accept, continue, or reject all or part of health care interventions.
The elements of informed consent should be used as a guide but are
not absolutely necessary for all nursing or medical interventions
(Box 2-5).
Box 2-5
ELEMENTS OF INFORMED CONSENT
Threshold elements (preconditions)
1. Competence (to understand and decide)
Information elements
3. Disclosure (of material information)
Consent elements
6. Decision (in favor of a plan)
From Beauchamp TL, Childress JF: Principles of biomedical ethics, ed 6, New York, 2009,
Oxford University Press.
555
Decision-making capacity
A patient’s ability to make a decision is fundamental to informed
consent. The four components of decision-making capacity are the
ability to: (1) express a choice, either verbally or via another means,
(2) understand the relevant information, (3) appreciate the
importance of the information to one’s own situation, including
risks and benefits of options, and (4) reason about options
consistently with one’s beliefs, values, etc.
Patients are presumed to have decision-making capacity. Lack of
orientation to person and place, medications, psychological
disorders, and cognitive decline may be reasons to question a
patient’s capacity, but they are not sufficient reasons to declare that
a patient cannot make a decision. Health care professionals should
try to maximize the patients’ capacity, such as removing or adding
medications, having discussions during a certain part of the day, or
discussing in the presence of family members.
Decision-making capacity is decision-specific. The more critical
and complex the decision, the higher level of decision-making
capacity required. Capacity should be assessed on an ongoing basis
as decisions need to be made. All health care providers must be
familiar with individual state laws regarding who can legally assess
a patient’s capacity and how it should be documented.
Advance directives
Advance directives refer to a patient’s directions on how to provide
care in the event that the patient becomes unable to make decisions
or verbalize them on his or her own behalf. An advance directive
can be written or verbal and can be in the form of a living will or a
durable power of attorney for health care (DPAHC).
A living will specifies what treatment a patient wants or does not
want in the event that the condition is terminal and the patient
cannot make health care decisions. A DPAHC appoints a person to
make decisions for a patient when the patient cannot make
decisions.
A surrogate decision-maker is someone named in the DPAHC.
When no DPAHC exists, the legal next of kin becomes the surrogate
decision-maker for the patient. If the patient does not have family
556
or a DPAHC, a court-appointed guardian becomes the surrogate
decision-maker. This person is obligated to make choices that the
patient would make if able. If those choices are unknown, the
surrogate decision-maker must try to determine, based on the
patient’s values, what the patient would want.
Interpretation of advance directives can be problematic.
Although many patients express a desire for no “extraordinary
measures,” the meaning of this term can vary. For example, a
ventilator can be considered “extraordinary,” but it is also part of
very common temporary treatments regularly used in critical care.
Despite problems with interpretation, caregivers must responsibly
deal with these ambiguities and seek to honor the patient’s wishes.
Many states are adopting Physician Orders for Life Sustaining
Treatment (POLST, also known as MOST and POST) to clarify
patient choices. POLST forms differ from a living will insofar as the
form becomes a physician order as soon as it is signed. Therefore,
there should be careful deliberation regarding when it is
appropriate for a patient to complete a POLST form.
Confidentiality
Confidentiality in a relationship between a health care provider and
a patient means that one does not identify or expose information
that is not relevant to care. Also, one does not communicate
information gained from a patient except with providers and
decision-maker identified by the patient. Health care provider
codes of ethics generally include provisions for keeping all
information about a patient confidential. Any disclosure of patient
information should be considered very carefully.
The Health Insurance Portability and Accountability Act of 1996
(HIPAA) was mandated by the U.S. Congress to establish a federal
standard regarding confidentiality of specific electronic medical
information. Individual states may have stricter privacy laws.
HIPAA sets the lowest acceptable standard for privacy. State laws
apply over HIPAA.
There are situations in which one is legally obligated to breach
patient confidentiality. These situations include public welfare
risks, sexually transmitted diseases, gunshot wounds, and
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suspected abuse and/or neglect of children, older adults, or
developmentally disabled individuals. HIPAA supports the
disclosure of protected health information when required by law.
Quality of life
A person’s quality of life is based on physical, intellectual,
emotional, and social components. Although improving quality of
life is a primary focus of health care, assessing quality of life is
difficult at best. Numerous studies have demonstrated that health
care providers consistently rate patients’ quality of life lower than
the patients do themselves. Studies also reveal that such judgments
by health care providers do affect care. A life of dependence on
medications, treatments, and care rendered by others is generally
viewed as “not desirable” by many people, including health care
providers, until they are actually faced with the choice between a
dependent life versus death involving a family member or
themselves. Nurses and care team members in critical care should
be aware of all the dynamics underlying choices of patients and
families, because hospitalization reflects a minuscule part of a
patient’s entire life.
A patient’s assessment of quality of life may be compromised
when that patient becomes depressed or newly disabled (e.g.,
stroke, paraplegia, quadriplegia). Although critical care nurses care
for many patients in such situations, it is usually the first time that
this patient or family has faced such life-altering circumstances. The
stress of the situation makes evaluation of quality of life difficult for
them. It is important to provide the patient and family with support
and time before making critical decisions.
Studies indicate that health care providers not only base quality
of life on the patient’s medical condition but also have social
prejudices that affect care. These include biases against older adults,
people with alternative lifestyles, those with alcohol and/or other
substance abuse, and patients with a history of criminal activity.
Comments about perceived flawed decision-making by patients
and families may be passed on to others during nursing reports and
hand-off communications between other team members. Rather
than viewing care with objectivity, the team is at risk of developing
558
the plan of care with biases shared in conversation. The team must
regularly evaluate the plan of care and patterns of communication
with the patient and family. Poor communication may undermine
the relationship between the health care team with
patients/significant others and overall success of the
interdisciplinary plan of care.
Truth telling
Respect for patient autonomy and the principles of informed
consent require that patients are told the truth about their medical
condition. There are times when family members or treating
professionals believe that telling patients the truth about their
condition may negatively affect their outcomes. Sometimes called
the therapeutic exception to truth telling, it should be used very
rarely, and only with confirming evidence that telling the truth
would truly harm the patient. Sometimes requests from family
members to withhold medical information from a patient entail
religious and/or cultural considerations. These requests should be
addressed on a case-by-case basis.
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decision has been made to withhold resuscitation, it is important to
clearly define treatments to be withheld or provided.
Comfort care
Patients who are chronically ill, debilitated, or dying are generally
isolated from and by society, as well as by health care providers.
Health care providers now recognize that pain and depression may
be undertreated in the routine care of patients and while caring for
those who are chronically ill or dying. Health care professionals
express fears of causing dependence, unresponsiveness, and even
death resulting from use of sedatives and narcotic analgesics. When
faced with a patient who is dying, it is unreasonable to worry about
potential dependence on medication. The benefits of analgesics far
outweigh the risks of dependence. Health care providers should try
to provide the maximal pain relief possible while preserving
responsiveness. When that is not possible, many patients and
families choose to accept a decreased responsiveness to ensure that
adequate pain relief is provided for the patient who is dying.
560
Many health care providers voice concerns that giving potent
opioids or opiates to a patient who is dying may actually kill the
patient. This concern is magnified when decisions to withdraw and
withhold treatments have been made simultaneously. Opioid and
opiate analgesics afford a broad therapeutic index and have a long
history of safe use in patients who are medically frail. Many
patients can tolerate increasing doses of these drugs without
adverse respiratory or cardiovascular effects. Doses must be
individualized or titrated based on pain relief using a pain scale. It
is nearly impossible to predict a “perfect dose” of medication, given
that not everyone responds to opioid analgesics the same way.
Even though it is very difficult to determine what amount of
opioid or opiate will cause a person’s death, such medicines can
still be given by applying the principle of double effect. Simplified,
this principle explains that giving narcotics to relieve pain is
morally acceptable, even while knowing that it may also cause the
patient to die sooner. However, growing evidence suggests that
opiates, even at high doses, when given according to the latest
palliative care guidelines, do not hasten death while meeting the
patient’s needs for comfort. The principle of double effect rarely
needs to be used to justify the administration of opioids.
Ethical reasoning
When nurses find themselves in a situation in which they think
something is “wrong,” they should first consider the situation
logically and systematically. By doing this, nurses can defend their
positions rationally and provide ethically as well as medically
sound care.
1. Determine the relevant facts of the case: These facts include the
patient’s medical, mental, and emotional condition, as well as the
current plan of care.
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3. Identify the problem: Do the facts support your view of the
problem? Would others view the problem differently? If so, how?
Preventive ethics
Just as it is easier to prevent heart disease than it is to cure it, it is
easier to prevent an ethical conflict than it is to resolve one. When
evaluating actions taken to resolve a dilemma, nurses should
consider how those actions can provide guidance in future
situations. When the bedside nurse first detects a problem,
strategies used in previous, similar situations can be employed to
prevent this situation from developing into a conflict. Many
problems may be resolved after the first few steps of an ethical
inquiry; gathering information and coordinating a patient care
conference involving all relevant people. The interdisciplinary team
should refrain from speculation or gossip and instead openly
communicate with the patient, family, and other members of the
care team about the plan of care. The nurse should promote
discussions regarding the possible patient outcomes, ensuring that
significant others have considered that they could be facing the
patient’s lifelong debility, the possibility of death, and are aware of
the extent of time that may be needed to achieve a reasonable
recovery. Lastly and most importantly, nurses should respect each
562
patient as a person and treat that patient accordingly. The local
ethics committee or team may be consulted for assistance with any
ethical questions or concerns.
Teaching: Procedure/treatment
3. Determine that the patient has not been coerced into making
decisions that are not in harmony with their wishes.
Deficient knowledge
related to end-of-life decisions related to available documents.
Goals/Outcomes: The patient will verbalize understanding of the
options available regarding advance directives (living wills and
DPAHC).
Knowledge: Disease Process
Decision-making support
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1. Provide the patient with information regarding living wills and
DPAHC.
Grieving
related to withholding/withdrawal of treatment; anticipation of loss.
Goals/Outcomes: After intervention, the patient and significant
others communicate feelings and participate in decisions regarding
death and dying.
Grief Resolution.
Anticipatory guidance
Patient safety
In 1999, the Institute of Medicine (IOM) released the report, To Err
564
Is Human: Building a Safer Health Care System, which focused
national attention on patient safety. The IOM estimated that
between 44,000 and 98,000 persons die annually as a result of health
care errors and that more than 1 million patients sustain injury as a
result of health care errors. Since its release over 10 years ago,
regulatory agencies, health care facilities, and consumers have
joined together to enhance patient safety with minimal
improvement. The report emphasized that individual clinicians’
competency, hard work, and good intentions were not the cause of
these errors but that the complex health care system with
complicated processes were leading to these errors.
Shifting the goal from eliminating individual errors to reducing
or eliminating the potential for patients to be harmed is significant.
A proactive approach generally yields more globally successful
outcomes. Nurses can contribute significantly to keeping patients
safe by focusing on system-wide improvements, rather than
reacting to adverse events. Nurses spend extensive periods of time
with patients and are placed in roles that require interdisciplinary
care coordination. The coordinative role prompts familiarity with a
variety of hospital processes that may place the patient at risk for
harm. Although it is not an easy journey, health care facilities now
focus attention on designing systems where errors are prevented,
and when they occur, practitioners can easily recognize and recover
from actual and potential errors.
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AHRQ
The mission of the AHRQ (www.AHRQ.gov) is to improve the
quality, safety, efficiency, and effectiveness of health care for all
Americans. The agency’s research assists both consumers and
professionals in making more informed decisions about health care
and facilitate quality improvement in health care services. The
AHRQ was formerly known as the Agency for Health Care Policy
and Research.
CMS
The Medicare and Medicaid programs were signed into law on July
30, 1965. The CMS (www.cms.gov) administers the Medicare
program and jointly with state governments administers the
Medicaid program. The CMS activities are focused to ensure access
to safe and quality health care for beneficiaries.
IHI
The IHI (www.ihi.org) is an independent, nonprofit organization
that strives to lead the improvement of worldwide health care. The
IHI facilitates improvement by augmenting the desire or will for
change, developing concepts for improving patient care, and
helping health care systems put those ideas into action.
566
• Nurse job satisfaction, retention, and quality of care
were all expected to improve.
NQF
The NQF (www.qualityforum.org) is a not-for-profit organization
focused on improving the quality of health care for all Americans.
Their three-part mission includes setting priorities for performance
improvement, supporting national consensus standards for
performance measurement and public reporting of this information,
and facilitating attainment of national goals by offering education
and outreach programs.
NPSF
The NPSF (www.npsf.org) is an independent, not-for-profit
organization founded in 1997, with a mission to improve safety of
patients and families within the health care system. The NPSF is
committed to a collaborative, interprofessional approach including
key stakeholders. The goal of the group is to unite professional
disciplines with organizational leaders across the continuum of
care.
TJC
The mission of TJC (www.jointcommission.org) is to continuously
improve the safety and quality of care provided to patients through
the provision of health care accreditation. The organization has set
standards that include National Patient Safety Goals and Sentinel
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Event Alerts. The 2007 Joint Commission Annual Report on Quality
and Safety revealed inadequate communication between health
care providers, or between providers and the patient and family
members, as the main or root cause of at least half the serious
adverse events in hospitals. Other causes included inadequate
assessment of the patient’s condition and poor leadership or
training. TJC has launched several patient safety initiatives
including the “Do Not Use Abbreviation” list, Infection Control,
“Speak Up,” and Universal Protocol (“Time Out”). Many of these
initiatives have risen as a result of sentinel events that have
occurred across the United States. TJC was formerly known as the
Joint Commission on Accreditation of Health care Organizations
(JCAHO).
Websites for additional resources are listed in Table 2-3.
Table 2-3
RESOURCES ON PATIENT SAFETY
568
practices outlined by sentinel event alerts and close any
inconsistencies that may exist in practice.
Box 2-6
SENTINEL EVENT POLICY
A sentinel event is an unexpected occurrence involving death or
serious physical or psychological injury, or the risk thereof. The
terms “Sentinel Event” and “Health Care Error” are not
synonymous. Not all sentinel events are caused by a health care
error, nor do all health care errors result in a sentinel event. All
accredited organizations are required to define “sentinel event” for
its own purpose and establish how all sentinel events will be
identified and managed. Accredited organizations’ response to a
“sentinel event” includes conducting a timely, thorough, and
credible root cause analysis, and development of an action plan.
From The Joint Commission. Retrieved from www.jointcommission.org.
Box 2-7
OCCURRENCES THAT ARE SUBJECT TO
REVIEW BY THE JOINT COMMISSION
UNDER THE SENTINEL EVENT POLICY
• Event has resulted in an unanticipated death or major permanent
loss of function, not related to the natural course of the patient’s
illness or underlying condition
OR
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• Discharge of an infant to the wrong family
570
chapter to the main body of standards in the TJC standards manual
over time. Patient safety goals evolve into the standard of care.
Box 2-8
THE 2014 JOINT COMMISSION NATIONAL
PATIENT SAFETY GOALS
For acute care hospitals
• Identify patients correctly
• Prevent infections
571
Box 2-9
“SERIOUS REPORTABLE EVENTS”
(previously known as “Never Events”)
Seven categories
1. Surgical or invasive procedure events
5. Environmental events
6. Radiologic events
Culture of safety
Health care organizations have identified that 95% of health care
errors are directly related to system flaws, whereas only 5% of
health care errors are caused by incompetent or poorly intended
care (Sexton and Thomas, 2004). System flaws are largely related to
flawed communication, which may lead to disjointed or
572
uncoordinated care. Not all members of the team are consistently
aware of key information that, if omitted, may cause harm to the
patient. Therefore, to improve patient safety and address health
care errors, health care organizational culture must value
communication and team collaboration. Focus on these two factors
will result in improved clinical effectiveness and job satisfaction
among health care professionals (Box 2-10).
Box 2-10
COMPONENTS OF SUCCESSFUL
TEAMWORK
• Trust
• Respect
• Collaboration
• Open communication
• Nonpunitive environment
• Clear direction
• Atmosphere of respect
573
Communication
Despite years of training, coaching, and experience, communication
among health care professionals remains a challenge and a leading
root cause of sentinel events in many facilities. In a metaanalysis of
research studies, Seago (2008) found that the evidence remains
mixed on a preferred format for communication strategies. In the
AACN Standards for Establishing and Sustaining a Healthy Work
Environment, Skilled Communication is the first standard
addressed and is the one standard that weaves its way into the five
other standards. The emphasis by the AACN on healthy work
environment standards is a testimony to the importance of excellent
communication skills in acute and critical care (Table 2-4).
Table 2-4
AMERICAN ASSOCIATION OF CRITICAL-CARE NURSES
STANDARDS FOR ESTABLISHING AND SUSTAINING HEALTHY
WORK ENVIRONMENTS
574
communicates with a physician or midlevel practitioner and does
not provide a focused report, key patient care data may not be
communicated effectively.
The power of structured communication methods has been
successfully used in many industries including the airline industry,
nuclear power, and the U.S. Department of Defense. One such
method of structured communications is the Situation-Background-
Assessment-Recommendation (SBAR) documentation format.
Using SBAR is helpful to those who have difficulty with focused,
concise communications. The AHRQ and others across the United
States have advocated for SBAR as a form of standardized
communication among complex health care teams (Table 2-5).
575
Table 2-5
STRUCTURED COMMUNICATION: SITUATION-BACKGROUND-
ASSESSMENT-RECOMMENDATION (SBAR)
Before initiating an SBAR conversation, nurses should assess the patient; review the health care
record for appropriate physician or other care provider to call; know the patient’s diagnoses,
procedures, and medical history; read all recent physician progress notes (especially from the
past 12 hours); have available the following clinical data (chart, allergies, medications recently
given, recent diagnostic tests, and patient code status); and, last, take a moment to organize all
data, thoughts, and requests.
S Situation Give your name and unit “Dr. James, I’m Susie, a critical care RN. Mr.
you are calling from, Smith is a 42-year-old currently in radiology for
the patient’s full name, a computed tomography (CT) of the head after a
room number, and motor vehicle crash (MVC). I am the rapid
attending physician response nurse and was called to see him for
name if calling the on- anxiety and shortness of breath.”
call physician.
If the problem is urgent,
please notify the
provider at the
beginning of the call.
The patient’s code status
if appropriate.
B Background The patient’s admission “Mr. Smith was the driver and sustained blunt
diagnosis, admission chest trauma during the MVC approximately 3
date, and pertinent hours ago. There is no significant medical
medical history. history.”
Provide a brief synopsis
of the treatments and
plan of care thus far.
A Assessment Provide a brief “I think Mr. Smith has a pneumothorax on the
description of the right. Breath sounds are absent in the right
problem or primary middle and lower lobes. He is short of breath,
concern. anxious, and tachypneic with an oxygen
If uncertain of the saturation of 88% on 4 liters of oxygen.”
problem, acknowledge
the uncertainty.
Provide clinical data such
as most recent vital
signs, physical
assessment findings,
and clinical changes
specific to the problem
you are calling about.
Provide update of all
pertinent therapies (IVs,
O2, etc.).
R Express what you think “I think Mr. Smith needs more oxygen and a
Recommendation the patient needs to chest tube right away. I have asked the
address the problem. radiology technician to obtain the supplies for
If unclear on what chest tube placement. Can you come to
interventions are radiology to assess the patient for chest tube
needed, acknowledge placement, or is there someone else we should
576
uncertainty. call?”
If requesting the
practitioner to come
and assess the patient,
clarify with the
practitioner the exact
time frame to expect
their arrival.
Box 2-11
HAND-OFF COMMUNICATION
Elements of hand-off communication
• Standardized to the situation to which it applies
577
• Limit interruptions and distractions.
TeamSTEPPS
The AHRQ and the U.S. Department of Defense have partnered
together to develop an evidence-based curriculum and training
program with the goal of promoting patient safety through
improving communication and teamwork skills among health care
professionals (Table 2-6).
Table 2-6
THREE PHASES OF THE TeamSTEPPS IMPLEMENTATION
578
Phase 3 Sustain and spread improvements in teamwork performance, clinical
Sustainment processes, and outcomes.
Continual learning and reinforcement of skills on the unit or within the
facility:
• Provide opportunities for clinicians to practice skills.
• Ensure leaders emphasize new skills.
• Provide regular feedback and coaching.
• Celebrate and measure successes.
• Update the plan.
“Just culture”
The creation of a “Just Culture” has been advocated as a means to
enhance the patient safety culture of an organization. A culture of
learning must exist that encourages the reporting of adverse events
and near misses without the fear of retribution. The practitioner
must be offered protection from disciplinary action when they
report injuries, errors, and near misses when personally involved.
This implies that errors are most often not intentional, nor are they
caused by human failures alone. Most are often a series of system
failures that come together at an intersection involving the patient.
The creation of a “Just Culture” does acknowledge that there are
exceptions where health care workers do not have protection.
Protection should not be granted for risky and/or criminal behavior,
for active malfeasance, or in cases in which an injury is not reported
in a timely manner (Box 2-12).
Box 2-12
“JUST CULTURE”
Creation of a culture where clinicians are willing to report errors so
that the process can be analyzed and solutions found, but clinician
responsibility for events is maintained. The culture is not “blame-
free” but blame-appropriate.
From Marx D: Patient safety and the “just culture”: a primer for health care executives, New
579
York, 2001, Columbia University. Retrieved from www.psnet.ah rq.gov/resource.aspx?
resourceID-1582.
Patient/family involvement
Patient and family involvement in the plan of care can be a crucial
element of patient safety, because both are familiar with key
information that, if known, may prevent harm. Understanding of
medications, the health history, and proposed plan of care is vital to
a safe patient care experience. Patients and families may feel
reluctant to challenge, remind, or question their health care
providers. There has been a recent shift within all patient safety
organizations as well as professional organizations to include the
patient in daily rounds, to provide time for daily goal setting, and
to ensure all parts of the treatment plan have been communicated
and are understood. Several national programs have been
developed and promoted to facilitate the involvement of patients
and families in the plan of care (Box 2-13).
Box 2-13
STEPS TO INVOLVING PATIENTS IN
PATIENT SAFETY
Obtain patient feedback through a variety of sources such as
patient satisfaction, focus groups, community groups, hotlines, etc.
Review patient plan of care and daily goals with patients and
their families.
Never separate a patient from their family unless that is desired;
allow patient access 24 hours per day.
Never deny a patient information; a variety of tools can be used
to enhance communication and sharing of information such as
reviewing the health care record; orientation to the unit,
equipment, and team members; wipe boards; sharing clinical
pathways; patient conferences with interdisciplinary team; and
customized discharge instructions.
Encourage patient’s and family’s involvement in care by inviting
them to participate through creative campaigns; staff wearing
buttons asking “Ask me if I’ve washed my hands”; tent cards in
580
patient rooms; brochures and pamphlets educating patients on
how to be involved in their care.
From Roizen M, Oz M, The Joint Commission: You: the smart patient, New York, 2006,
Simon & Schuster Inc. Retrieved from
www.jointcommission.org/GeneralPublic/smart_patient.htm.
Speak up
TJC supports a national campaign urging patients to partner with
their health care provider to prevent health care errors by becoming
involved in their care. The campaign offers a variety of tools
(videos, brochures, artwork, etc.) to educate patients on steps they
can take to partner with health care workers to enhance safe care
delivery. Topics include but are not limited to “Help Avoid
Mistakes with Your Medication,” “Five Things You Can Do to
Prevent Infection,” and “What You Should Know about Pain
Management” (Box 2-14).
Box 2-14
SPEAK UP
Speak up if you have questions or concerns. If you still do not
understand, ask again. It is your body and you have a right to
know.
Pay attention to the care you get. Always make sure you are
getting the right treatments and medicines by the right health care
professionals. Do not assume anything.
Educate yourself about your illness. Learn about the medical
tests you get and your treatment plan.
Ask a trusted family member or friend to be your advocate
(advisor or supporter).
Know what medicines you take and why you take them. Health
care errors are the most common health care mistakes.
Use a hospital, clinic, surgery center, or other type of health care
organization that has been carefully checked out. For example, The
Joint Commission visits hospitals to see if they are meeting The
Joint Commission’s quality standards.
Participate in all decisions about your treatment. You are the
center of the health care team.
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From The Joint Commission: Speak Up: help prevent errors in your
care, and speak up: know your rights. Retrieved from
www.jointcommission.org/assets/1/18/speakup_hc.pdf.
Table 2-7
NATIONAL AGENDA FOR ACTION: PATIENTS AND FAMILIES IN
PATIENT SAFETY: ROAD MAP FOR ACTION
Education and Awareness • Raise public awareness on the definition and frequency
of health care error and patient safety.
• Educate the public on how to aid in safeguarding their
own care.
• Educate health care professionals and leadership about
the importance of the patient/family perspective.
• Raise health care providers’ awareness of the experiences
of patients and their families.
• Raise awareness in the behavioral health community on
health care errors.
• Educate the media.
• Build patient safety and health care error prevention into
all health care professional education curricula.
• Build interactive, interdisciplinary education programs.
• Develop a central clearinghouse and interactive resource
center.
Build a Culture of Patient- and • Teach and encourage effective communication skills.
Family-Centered Patient Safety • Engage leadership in promoting and training providers
in open communication about health care error.
• Empower hospital patient representatives to effectively
advocate.
• Establish patient and family advisory councils.
• Represent patients’ interests on boards and trustees.
582
• Establish patient safety task forces.
• Create a national forum for state coalitions.
Research • “Bridging the gap.”
• Disclosure.
• Short- and long-term effects of incorporating patients
and families into the system.
• Current patient safety information and resource
landscape for patients and families.
• Posttraumatic stress specific to health care error.
• Team relationships.
High-reliability organizations
High-reliability organizations (HROs) are those that are known to
be complex and risky yet maintain safety and effectiveness. Key
characteristics of HROs include preoccupation with failure and
safety, deference to expertise, sensitivity to operations, commitment
to resilience, and reluctance to simplify. HROs are continually
analyzing and asking questions to prevent failures within the
systems and analyzing how to minimize effects from failures when
and if they occur. The use of the prospective tool of a failure mode
and effects analysis (FMEA) and the use of a retrospective tool such
as a root cause analysis (RCA) have proven valuable to health care
organizations (Table 2-8).
Table 2-8
FAILURE MODE AND EFFECTS ANALYSIS VERSUS ROOT CAUSE
ANALYSIS
Failure Mode and Effects Analysis (FMEA) Root Cause Analysis (RCA)
Proactive analysis of a process or equipment to Retrospective analysis of an event that has
anticipate any potential process or product already occurred; actual failure
failure
Looks forward through a process to identify any Looks back chronologically after a process
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potential failure points has failed
Multidisciplinary team involvement is key to Multidisciplinary team involvement by all
success who were involved in the failure is key to
success
Three key questions are addressed: Three key questions are addressed:
• How likely is the equipment or process to • What happened?
fail? • Why did it happen?
• What is the significance of the failure? • What can be done to prevent it from
• How likely it is that someone will be able to happening again?
detect this failure?
Analytical tools used: Analytical tools used:
• Flow diagrams of all main and subprocesses • Timeline
• Brainstorm • Cause-and-effect diagrams
• Cause-and-effect diagrams • Frequency plots
• Scatterplots
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CHAPTER 3
Trauma
Major trauma
Pathophysiology
Traumatic injuries account for over 5 million deaths worldwide. In
the United States, traumatic injuries are the leading cause of death
for patients between the ages of 1 and 44 years. Traumatic injuries
also account for over 2.6 million hospitalizations each year. Major
trauma occurs when energy is applied to body tissues in excess of
what the tissues are able to absorb. The energy can be in the form of
kinetic, thermal, chemical, electrical, and radiant energy. Trauma
can also occur when the body is deprived of an essential element
such as oxygen or heat. Kinetic energy is the most common cause of
trauma and includes mechanisms such as motor vehicle collisions
(MVCs), falls, and gunshot wounds. Thermal, chemical, electrical,
and radiation energy cause burns. Lack of oxygen occurs in
drowning and hanging injuries. The amount of damage to the tissue
will depend on the amount of force applied, the length of time the
force is applied, and the resiliency of the tissue. Hollow organs tend
to absorb more energy and are injured less frequently than are solid
organs because the organ tissue has more flexibility to withstand
the forces.
The primary pathophysiologic process that occurs with major
trauma is shock. Patients with major trauma are at risk for all types
of shock, but the most common type is hypovolemic shock resulting
from hemorrhage. Hypovolemic shock is usually broken into four
stages that are used to describe the physiologic response to
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hemorrhage and are useful in estimating the amount of blood loss.
All body systems require both oxygen and glucose for cellular
energy production. The classic signs of hypovolemic shock occur
from activation of the central nervous system (CNS). Following
major injury, the CNS triggers a series of reactions to increase
delivery of oxygen and glucose to the cells. Catecholamines
(epinephrine and norepinephrine) and glucocorticoids are released
from the adrenal glands to preserve perfusion to vital organs,
mobilize glycogen stores, increase available glucose and oxygen,
suppress pancreatic insulin secretion, and enhance glucose uptake.
Hyperglycemia is common following major trauma. Glycogen
stores are rapidly depleted (within 24 hours). Without nutrition,
energy is generated from the breakdown of the body or catabolism.
Breakdown of muscle tissue, fat, and viscera creates a negative
nitrogen balance. Subclinical adrenal insufficiency may become
clinically apparent after severe injury.
The posterior pituitary release of antidiuretic hormone promotes
water absorption in the distal renal tubules. Intravascular volume
increases as urinary output decreases. Blood pressure (BP) is
increased by the renin-angiotensin-aldosterone system. Aldosterone
promotes sodium and water reabsorption to increase intravascular
volume, and angiotensin II causes vasoconstriction.
Several factors can alter the patient’s response to blood loss and
must be considered in the resuscitation of these patients. These
factors include the patient’s age, location of injury, type and
severity of the injury, the amount of time that has elapsed since the
injury, prehospital interventions to address blood loss, and
medications taken for chronic conditions, especially anticoagulants
and beta-blockers. Because the patient has many other injuries, the
classic signs of shock may be altered.
The source of the bleeding must be identified and stopped as
soon as possible. The patient must be adequately resuscitated or the
patient is at risk of developing acidosis, coagulopathy, and
hypothermia, which are considered the deadly triad of trauma.
Once these conditions occur, they tend to stimulate each other and
become a vicious cycle that is difficult to break.
Acidosis occurs when the number of red blood cells is reduced
from blood loss and cellular oxygen supply is reduced, resulting in
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end-organ hypoxia caused by inadequate tissue perfusion.
Anaerobic metabolism may ensue if blood and volume replacement
is inadequate to maintain perfusion. While anaerobic metabolism
continues, lactic acid builds up, leading to an increase in the base
deficit and decrease in the pH.
After initial restoration of circulating fluid volume, the body may
develop a hyperdynamic circulatory state to help compensate for
the cellular oxygen debt incurred. This phase should peak at 48 to
72 hours and diminish within 7 to 10 days. The hyperdynamic state
is evidenced by an increased cardiac index (CI), oxygen delivery
(DO2), and oxygen consumption ( O2). Inability to achieve and
maintain a hyperdynamic state is associated with higher mortality
and shock-related organ failure.
Coagulopathy develops from both the consumption of clotting
factors as the body forms clots in an attempt to stop the bleeding of
injured tissues and the dilution of the blood from infusion of
crystalloids and massive transfusion of packed red blood cells
when clotting factors are not replaced. If coagulopathy is not
reversed, disseminated intravascular coagulopathy (DIC) can occur.
Factors contributing to development of DIC include hypotension,
impaired tissue perfusion, and capillary dysfunction leading to
stasis, hypoxemia, and hypothermia.
Multiple factors increase the likelihood of hypothermia in major
trauma. Exposed body surface area or viscera may occur at the
scene of injury or during the initial resuscitation. If blood and
resuscitation fluids are infused without warming, the core body
temperature can drop. Prolonged exposure to cool temperatures in
resuscitation or operative areas can also lower the body
temperature. When present, central thermoregulatory failure
caused by CNS injury, intoxication, or hypoperfusion contributes to
hypothermia. Mild hypothermia can help preserve the function and
viability of major organs, particularly when tissue perfusion is
diminished as a result of injury, shock, or surgical clamping of
arteries. Severe hypothermia creates significant physiologic
alterations, including CNS depression, dysrhythmias, acidosis, and
substantial electrolyte imbalances. Catecholamine infusions are
often ineffective until body temperature approaches 33.9 °C (93
°F).
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In patients who sustain major trauma, a widespread
inflammatory response known as systemic inflammatory response
syndrome (SIRS) may be triggered by massive tissue injury and the
presence of foreign bodies such as road dirt, shrapnel, and invasive
medical devices. Inflammatory mediators activate the coagulation
cascade, increased catecholamines stimulate the production and
release of white blood cells, and endothelial dysfunction ensues.
The hemodynamic response and clinical findings are similar to
those with sepsis. (See Chapter 11 for information on SIRS.)
The overwhelming inflammation associated with SIRS may lead
to multiple organ dysfunction syndrome (MODS). MODS is a
leading cause of late mortality in patients with multitrauma,
accounting for approximately 10% of trauma deaths. Inadequate
initial resuscitation or inability to achieve and maintain a
compensatory hyperdynamic state contributes to the development
of organ failure in patients with trauma. Presence of endotoxin,
tumor necrosis factor, interleukin-1, and other inflammatory
mediators cause vasodilation, leading to hypotension. Capillary
dysfunction results in poor cellular circulation and subsequent
tissue destruction. Acidosis, pulmonary compromise, and
circulatory collapse may result. Clinical trials are under way for
therapies to help control inflammatory mediators.
Psychological response
Victims of major trauma sustain life-threatening injuries. The
patient often is aware of the situation and fears death. Even after
the physical condition stabilizes, the patient may have a prolonged
and severe psychological reaction triggered by the trauma called
posttraumatic stress disorder.
Airway assessment
Determine airway patency.
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• Is the airway open?
Breathing assessment
• Is there adequate air exchange?
• Inspect the chest for signs of trauma that could interfere with
chest excursion.
• Inspect the neck for tracheal deviation and jugular vein distention
(JVD).
• Palpate the chest for crepitus, tenderness over the ribs or sternum.
Circulatory assessment
• Observe skin color.
Disability assessment
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• Observe the patient’s responsiveness.
Exposure
• Expose the patient to observe for signs of trauma.
Vital signs
• Pulse rate may be elevated if the patient has experienced
blood loss or stimulation of the sympathetic nervous system
(SNS) or be decreased in response to elevated intracranial
pressure (ICP) from a severe head injury.
History
• AMPLE (Allergies, Medications, Past surgeries and pertinent
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medical conditions, Last meal, Events leading up to incident).
• Tetanus status.
Head-to-toe assessment
• Observe each area for signs of trauma including bruising,
abrasions, lacerations, and contusions.
• Auscultate for lung sounds, heart sounds, bowel signs, and bruits.
Chest
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• Listen to breath sounds, noting equality and for any abnormal
breath sounds.
Extremities
Posterior surface
• Inspect the posterior surface; if the patient’s spine has not been
cleared, the patient must be logrolled, maintaining spinal
precautions.
Laboratory work
Blood studies can reveal indications of hypoxia and/or continued
bleeding and developing shock, as well as identify special
circumstances such as pregnancy and intoxication.
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ratio (INR).
• Electrolytes.
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Collaborative management
The primary goals of initial assessment in major trauma are to
identify life-threatening injuries, stop bleeding, and restore
adequate oxygenation to the tissues. Once life-threatening injuries
have been addressed, a secondary assessment is performed to
identify all injuries the patient may have sustained; perform a
thorough organized head-to-toe assessment to minimize the chance
of missing injuries. The following treatments may be required.
601
Care priorities
2. Support ventilation
If the patient is not adequately ventilating to maintain oxygen
saturations greater than 93%, the patient should be placed on
supplemental oxygen. Most patients with major trauma will require
supplemental oxygen. Blood loss creates reduced oxygen-carrying
capacity, and tissue demand for oxygen is greatly increased during
the hypermetabolic phase. High-flow oxygen by mask is indicated
initially. Oxygen therapy can be titrated according to ABG and
pulse oximetry values. Mechanical ventilation may be required if
the patient is not ventilating well enough to remove CO2. If the
patient does not have equal breath sounds, a pneumothorax or
hemothorax may have occurred and a tube thoracotomy may be
indicated. Capnography should be considered for patients who are
mechanically ventilated, because it is an early marker of
hypoventilation and apnea.
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internal diameter (trauma tubing), absence of stopcocks, and use of
external pressure are techniques used to promote rapid fluid
volume therapy when indicated. In some cases, the patient may
require large central venous access, such as an 8.5 Fr introducer.
When rapid infusion of large amounts of fluid is required, all fluid
should be warmed to body temperature to prevent hypothermia.
Rapid warmer/infuser devices are available to facilitate rapid
administration of blood products. Fluid resuscitation should be
used more judiciously in pediatric and older patients, as well as
patients with significant craniocerebral trauma, who have precise
fluid requirements (see Traumatic Brain Injury).
603
transfusion is hypocalcemia caused by calcium binding with
citrate in stored PRBCs, resulting in depressed myocardial
contractility, particularly in patients with hypothermia or in those
with impaired liver function. One ampule of 10% calcium
chloride should be considered for administration after every 4
units of PRBCs.
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4. Identify, prevent, and/or manage hypothermia
Warmed blankets, forced warm air blankets, and warmers for
IV fluids and blood should be used to prevent hypothermia. If the
patient is already hypothermic, more aggressive measures to
rewarm the patient may be necessary. Warming lights are useful for
pediatric patients. Core rewarming measures can include irrigation
of the peritoneal and/or thoracic cavities with warmed saline, use of
heated humidified oxygen, and extracorporeal blood rewarming.
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Tetanus immunoglobulin (TIG) and tetanus-toxoid (Tt) are
considered on the basis of the Centers for Disease Control and
Prevention recommendations (Table 3-1).
Table 3-1
GUIDE TO TETANUS PROPHYLAXIS IN ROUTINE WOUND
MANAGEMENT
*
Such as (but not limited to) wounds contaminated with dirt, feces, soil, and saliva;
puncture wounds; avulsions; and wounds resulting from missiles, crushing, burns,
and frostbite.
†
For children younger than 7 years, DTaP (Diphtheria, Tetanus, and Pertussis) is
recommended; if pertussis vaccine is contraindicated, DT is given. For individuals 7
to 9 years of age or 65 years or older, Td is recommended. For individuals 10 to 64
years, Tdap is preferred to Td if the patient has never received Tdap and has no
contraindication to pertussis vaccine. For individuals 7 years of age or older, if Tdap
is not available or not indicated because of age, Td is preferred to TT.
‡
TIG is human tetanus immunoglobulin. Equine tetanus antitoxin should be used
when TIG is not available.
§
If only three doses of fluid toxoid have been received, a fourth dose of toxoid,
preferably an adsorbed toxoid, should be given. Although licensed, fluid tetanus
toxoid is rarely used.
||
Yes, if it has been 10 years or longer since the last dose.
¶
Yes, if it has been 5 years or longer since the last dose. More frequent boosters are
not needed and can accentuate side effects.
From Centers for Disease Control and Prevention: Manual for the surveillance of
vaccine-preventable diseases, Atlanta, 2008, Centers for Disease Control and
Prevention.
606
Parenteral nutrition or postpyloric (jejunal) feedings may be used if
postoperative ileus or injury to the gastrointestinal (GI) tract is
present. For more information, see Nutrition Support.
607
increased thirst, increased HR, increased systemic vascular
resistance [SVR], decreased urinary output [urine output],
decreased bowel sounds, decreased peripheral perfusion, altered
mental status, or altered respirations).
608
3. Auscultate BPs in both arms and compare, as appropriate.
Acid-base monitoring
Airway management
609
1. Assess for patent airway; if snoring, crowing, or strained
respirations are present, indicative of partial or full airway
obstruction, open airway using chin-lift or jaw-thrust technique and
maintain cervical spine alignment.
Oxygen therapy
610
4. Document pulse oximetry with oxygen liter flow in place at time
of reading as ordered. Oxygen is a drug; the dose of the drug must
be associated with the oxygen saturation reading or the reading is
meaningless.
Respiratory monitoring
611
end-tidal CO2 (etco2), and ABGs as appropriate.
Acute pain
related to physical injury
Goals/Outcomes: Within 30 minutes of intervention, the patient’s
subjective evaluation of discomfort improves, as documented by a
pain scale. Nonverbal indicators, such as grimacing, are absent.
Vital signs return to baseline. ECG changes present during event
resolve.
Comfort Status: Physical, Pain Level.
Pain management
612
Hypothermia
related to altered temperature regulation
Goals/Outcomes: The patient will maintain a normal body
temperature greater than 36° C (96.8° F).
Thermoregulation.
Temperature regulation
Posttrauma syndrome
related to inadequate coping ability resulting from major physical and
emotional stress.
Goals/Outcomes: The patient exhibits appropriate coping
mechanism and reduced anxiety, as evidenced by decreased
613
restlessness, pulse rate 60 to 100 bpm, RR 12 to 20 breaths per
minute, and decrease in the amount of pain medication requested.
Anxiety Level; Coping.
Anxiety reduction
Coping enhancement
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7. Encourage family involvement, as appropriate.
Emotional support
Abdominal trauma
Pathophysiology
The patient with abdominal injury can be the most challenging and
difficult to manage. Forces may be blunt or penetrating and the
organs are either solid (pancreas, kidneys, adrenal glands, liver,
and spleen) or hollow (stomach, small bowel, and colon).This
patient may have subtle signs of internal hemorrhage, which can be
a major contributor to the increase in mortality and morbidity noted
after the initial injury has been managed. The severity of abdominal
injury is related to the type of force applied to the organs
suspended inside the peritoneum. Motor vehicle collision (MVC),
either auto-auto or auto-pedestrian, is the most common cause of
blunt abdominal trauma worldwide.
Blunt trauma
There are three mechanisms of action with blunt trauma.
615
inside the abdominal cavity move at different speeds depending on
their density. This creates what is known as shear force, that is, two
different directions applied to the organ, usually at the point of
attachment, causing injury to other organs such as the aorta.
Intrathoracic abdomen
The upper abdomen resides beneath the rib cage and includes the
diaphragm, liver, spleen, and stomach.
616
blunt trauma, the tear is best visualized by chest radiograph,
which reveals an elevation of the left hemidiaphragm and air
under the diaphragm.
Pelvic abdomen
As defined by bony pelvis, this includes the urinary bladder,
urethra, rectum, small intestine, and, in females, the ovaries,
fallopian tubes, and uterus. Diagnosis is difficult because many of
these injuries are extraperitoneal (outside the peritoneal cavity).
Retroperitoneal abdomen
This includes the kidneys, ureters, pancreas, aorta, and vena cava.
Evaluation may require a computed tomography (CT) scan,
angiography, and an IV pyelogram (IVP).
617
associated with pelvic fractures or damage to retroperitoneal
organs (pancreas, duodenum, and kidney) can cause bleeding
into the retroperitoneum.
True abdomen
This includes the small and large intestines, uterus (when
enlarged), and bladder (when distended). Perforation usually
presents with peritonitis such as pain and tenderness.
• Pelvis: See Renal and Lower Urinary Tract Trauma (Chapter 3).
618
difficult to detect and may be associated with massive injury to
nearby organs, prompting spillage of irritating fluids, activated
enzymes, and bile, which augments the inflammatory response.
Pancreatic injury is rare; however, the pancreas can be contused or
lacerated. Clinical indicators of injury to these retroperitoneal
organs may not be obvious for several hours.
Injuries to major vessels such as the abdominal aorta and inferior
vena cava most often are caused by penetrating trauma but also
occur with deceleration injury. Hepatic vein injuries are frequently
associated with juxtahepatic vena cava injury and result in rapid
hemorrhage. Blood loss after major vascular injury is massive.
Survival depends on rapid transport to a trauma center and
immediate surgical intervention.
619
First and foremost, it is essential to establish how the injury
occurred (Box 3-1). Details regarding circumstances of the accident
and mechanism of injury are invaluable in detecting the presence of
specific injuries. Second, allergies, medications, and last meal eaten
will play an important role in the maintenance of good
resuscitation. Other information, previous abdominal surgeries,
and use of safety restraints (if appropriate) should be noted. Hollow
viscous injury is often missed but is more likely to be present when
a contusion is seen on the abdomen. Medical information including
current medications and last Tt immunization should be obtained.
The history is sometimes difficult to obtain because of alcohol or
drug intoxication, head injury, breathing difficulties, or impaired
cerebral perfusion. Family members and emergency personnel may
be valuable sources of information.
Vital signs
Assess for impending hemorrhagic shock: Pulse greater than
100 bpm, decreased pulse pressure, oliguria: blood loss 750 to 1500
mL; pulse greater than 120 bpm, hypotension, oliguria, confusion:
blood loss 1500 to 2000 mL; pulse greater than 140 bpm, severe
oliguria, lethargy: blood loss greater than 2000 mL.
HIGH ALERT!
Persistent Tachycardia
Persistent tachycardia: Should always be considered a clue to
tissue hypoxia. While the neuroendocrine response ensues,
persistent tachycardia indicates a response to tissue
hypermetabolism and inadequate resuscitation.
620
(promoting preservation of fluid), resulting in significant
tachycardia, profound vasoconstriction, and progressive oliguria.
These responses may mask the severity of hemorrhage. Patients
on alpha- or beta-antagonists or those with acute spinal cord
injuries (above C5) will not manifest these responses and
therefore will have few compensatory mechanisms.
Box 3-2
MEASURING PARADOXICAL PULSE
• After placing blood pressure (BP) cuff on the patient, inflate it
above the known systolic BP. Instruct the patient to breathe
normally.
• Listen for the first Korotkoff sound, which will occur during
expiration with cardiac tamponade.
• Note the manometer reading when the first sound occurs, and
continue to deflate the cuff slowly until Korotkoff sounds are
audible throughout inspiration and expiration.
621
Observation and subjective/objective symptoms
• Inspection of all surfaces of trunk, head, neck, and extremities,
including anterior lateral and posterior exposure, with notation
of all penetrating wounds, contusions, tenderness, ecchymosis, or
other marks and indicators. Multiple wounds may represent
entrance or exit wounds but do not eliminate the possibility of
objects that may remain internally.
• Nausea and vomiting may occur, and the conscious patient who
has sustained blood loss often complains of thirst; an early sign of
hemorrhagic shock.
622
Inspection
• Abrasions and ecchymoses may indicate underlying injury. The
absence of ecchymosis does not exclude major abdominal trauma
and massive internal bleeding. In the event of gunshot wounds,
entrance and exit (if present) wounds should be identified.
Auscultation
It is important to auscultate before palpation and percussion,
because these maneuvers can stimulate the bowel and confound
assessment findings.
Palpation
623
• Tenderness to light palpation suggests pain from superficial or
abdominal wall lesions, such as that occurring with seat belt
contusions.
HIGH ALERT!
Flank (Grey-Turner sign) or umbilical (Cullen sign) ecchymosis
may be delayed several hours to days in patients with
retroperitoneal hemorrhage. Based on the index of suspicion,
persistent hypotension is always investigated with ultrasound or
radiography.
Box 3-3
SIGNS AND SYMPTOMS THAT SUGGEST
PERITONEAL IRRITATION
• Generalized abdominal pain and tenderness.
624
• Involuntary guarding of the abdomen.
• Rebound tenderness.
Percussion
• Unusually large areas of dullness may be percussed over
ruptured blood-filled organs. For example, a fixed area of
dullness in the left upper quadrant suggests a ruptured spleen.
An absence (or decrease in the size) of liver dullness may be
caused by free air below the diaphragm, a consequence of hollow
viscous perforation, or, in unusual cases, displacement of the
liver through a ruptured diaphragm.
HIGH ALERT!
Massive intestinal edema is common following laparotomy
and prolonged shock. Inflammatory response, neuroendocrine
stimulation, aggressive crystalloid resuscitation, bowel handling,
intraabdominal packing, and retroperitoneal hematomas may
625
cause a delay in abdominal closure. If the abdomen is closed, the
intraabdominal volume may compress arteries, capillaries, the
bladder, and the ureters. This compartment hypertension
(abdominal compartment syndrome) may cause significant
hypotension, oliguria, and base deficit that will be difficult to
combat. (See Abdominal Hypertension and Abdominal
Compartment Syndrome, Chapter 10).
Collaborative management
The initial focus should be stabilization and supporting
hemodynamics, but the highest priority is to diagnose and repair
626
causes of hemorrhage. Timely provision of needed surgery,
preferably in a trauma center, is the crucial factor impacting
survival. Prolonged hypovolemia and shock result in organ
ischemia and ultimately failure. See Major Trauma (Chapter 3)
Acute Respiratory Distress Syndrome (Chapter 4) Cardiogenic
Shock (Chapter 5), Acute Renal Failure (Chapter 6), and Hepatic
Failure (Chapter 9).
Care priorities
• Remove all wet clothing and make sure the patient is dry. The
patient should be actively warmed with blankets, air-warming
devices, or possibly continuous arteriovenous warming
techniques. A simple method is to cover all extremities and the
abdomen with plastic (e.g., blue side of underpads or trash bags)
to trap all heat produced.
627
cross-matched fresh blood is the optimal fluid for replacement of
large blood losses. However, because fresh whole blood is rarely
available, a combination of packed cells and fresh-frozen plasma is
often used. Overaggressive use of colloids and PRBCs may increase
third spacing and SIRS. (See Major Trauma for more information.)
• Signs of peritonitis.
628
or DPL (diagnostic peritoneal lavage) examinations.
629
• Blunt, nonpenetrating abdominal injuries: Physical examination is
important in determining the necessity for surgery in patients
who are alert, cooperative, and nonintoxicated. Additional
diagnostic tests such as abdominal ultrasound, DPL, or CT are
necessary to evaluate the need for surgery in the patient who is
intoxicated or unconscious or who has sustained head or spinal
cord trauma.
630
trauma is indicated under the following
circumstances: (1) clear signs of peritoneal irritation
(see Box 3-3); (2) free air in the peritoneum; (3)
hypotension caused by suspected abdominal injury,
or persistent and unexplained hypotension; (4)
positive DPL findings; (5) GI aspirate or rectal
smear-positive result for blood; and (6) other
positive findings in diagnostic tests such as CT or
arteriogram.
• Need for immediate surgery versus triad of failure: Once in the
operating room, it may become apparent that the patient cannot
survive a long procedure, or that the triad of failure (acidosis,
hypothermia, and coagulopathy) may cause death. At this point
the surgeon may do limited repair and packing, choosing to
delay major surgical repair.
631
room. There are multiple methods discussed in the literature to
supplement closure.
1. Silo bag closure: A 3-L sterile plastic irrigation bag is emptied and
cut to lie flat. The edges are trimmed and sutured to the skin.
HIGH ALERT!
Sudden release of abdominal pressure may lead to further
injuries such as ischemia-reperfusion, acute vasodilatation, and
cardiac dysfunction and arrest. The nurse should hydrate the
patient with at least 2 L of intravenous fluids and vasopressors
should be immediately available in case severe hypotension occurs.
632
8. Prevent infection with antibiotics
Abdominal trauma is associated with a high incidence of
intraabdominal abscess, sepsis, and wound infection, particularly
with injury to the terminal ileum and colon. Patients with
penetrating or blunt trauma and suspected intestinal injury are
started on parenteral antibiotic therapy immediately. Broad-
spectrum antibiotics are continued postoperatively and stopped
after approximately 72 hours unless there is evidence of infection.
Fluid management
633
Even a small but sudden decrease in blood pressure signals
the need to consult the advanced practice provider and/or surgeon,
especially for the patient with trauma in whom the extent of injury
is unknown.
HIGH ALERT!
Evaluate patency of intravenous catheters continuously during
rapid volume resuscitation.
634
HIGH ALERT!
An elevated heart rate (HR), along with decreased pulmonary
artery wedge pressure, decreased cardiac output/cardiac index
(CO/CI), and increased systemic vascular resistance suggest
hypovolemia (see Table 5-10 for hemodynamic profile of
hypovolemic shock). Anticipate slightly elevated HR and CO
caused by hyperdynamic cardiovascular state in some patients
who have undergone volume resuscitation, particularly during the
preoperative phase. Also anticipate mild to moderate pulmonary
hypertension, especially in patients with concurrent thoracic
injury, such as pulmonary contusion, smoke inhalation, or early
acute respiratory distress syndrome. Acute respiratory distress
syndrome is a concern in patients who have sustained major
abdominal injury, considering that there are many potential
sources of infection and sepsis that make the development of acute
respiratory distress syndrome more likely (see Acute Respiratory
Distress Syndrome).
Table 3-2
CHARACTERISTICS OF GASTROINTESTINAL DRAINAGE*
635
Source Composition and Usual Characteristics
Acute pain
related to physical injury secondary to trauma or surgical intervention.
Goals/Outcomes: The patient’s subjective evaluation of
discomfort improves, as assessed by use of a pain scale and/or
assessed by nonverbal indicators of discomfort, such as grimacing,
restlessness, and/or physiologic indicators.
Pain Control; Comfort Level.
Pain management
636
regarding pain relief measures.
Infection protection
1. Note color, character, and odor of all drainage from any surgical
site, orifice, drain, or site of invasive catheters.
637
related to interruption of arterial or venous blood flow or episodes of
hypovolemia resulting in decreased perfusion to GI organs.
Goals/Outcomes: The patient has adequate GI tract tissue
perfusion, as evidenced by normoactive bowel sounds; soft,
nondistended abdomen; and return of bowel elimination.
Tissue Perfusion: Abdominal Organs.
Circulatory precautions
2. Evaluate the patient for peritoneal signs (see Box 3-3), which may
occur initially as a result of injury or may not develop until days or
weeks later, if complications caused by slow bleeding or other
mechanisms occur.
638
HIGH ALERT!
Note changes that suggest bleeding (presence of frank or occult
blood), infection (e.g., increased or purulent drainage), or
obstruction (e.g., failure to eliminate flatus or stool within 3 to 4
days after surgery).
Skin surveillance
639
Goals/Outcomes: The patient has adequate nutrition, as
evidenced by maintenance of baseline body weight and state of
nitrogen balance on nitrogen studies.
Nutritional Status: Food and Fluid Intake; Nutritional Status.
Nutrition management
640
Feeding.
641
important to verify the type of colostomy with the surgeon before
explaining this to the patient.
Box 3-4
HOROWITZ CLASSIFICATION OF
PERICARDIAL EFFUSIONS
Grade 1: Small: Echo-free space in diastole less than 10 mm.
Ostomy Care.
642
caused by decreased filling of the chambers of the heart from
pressure exerted by fluid, blood, purulent liquid, or gas in the
pericardial space surrounding the heart. Cardiac tamponade is
classified as acute, subacute, occult, or regional. Acute cardiac
tamponade occurs when there is a rapid accumulation of fluid in
the pericardial space that compresses the heart, resulting in sudden
hemodynamic instability that can be life threatening.
Potential causes of cardiac tamponade include the following:
643
compressed within the pericardial sac to the point where the
chambers of the heart cannot fill. The pressure within the sac must
be relieved. The rapid detection and treatment of acute tamponade
are key to patient survival. The pericardial sac contains 20 to 50 mL
of fluid to protect and provide a friction-free surface for the beating
heart. The pericardial sac has a fibroelastic quality, which allows
limited stretching ability. A sudden addition of 50 to 100 mL of
fluid can markedly increase intrapericardial pressure. Conversely, a
slowly accumulating tamponade can result in 2000 mL of fluid
collection without life-threatening cardiac compromise because the
pericardial sac has an opportunity to stretch slowly, expanding to
accommodate the slow accumulation of fluid volume within the
pericardial sac.
When there is a rapid increase in intrapericardial pressure, the
heart is compressed causing a decrease in intraventricular filling.
The compliance of the right side of the heart is limited, because it is
competing for the fixed volume within the pericardium. The right
atrium (RA), as a low pressure heart chamber is the most
susceptible to collapse, which decreases filling of the right ventricle.
This decreased filling results in JVD. While the pressure continues
to increase, the right ventricle has partial collapse during early
diastole. The decreased right ventricle free wall compliance causes a
right-to-left shift of the septum, which is pronounced during
inspiration, causing the pulsus paradoxus seen with cardiac
tamponade. An unresolved tamponade puts pressure on all
chambers of the heart, pulmonary vessels, and coronary arteries,
causing hemodynamic instability. Hemodynamically, while
pulmonary artery pressures (PAPs) increase, an equalization of
pressures of the right and left atria are seen, and decreased
ventricular filling occurs. This hemodynamic compromise results in
decreased CO and hypotension with decreased tissue perfusion.
644
HIGH ALERT!
Pulseless electrical activity may be the presenting sign of cardiac
tamponade. Have a high suspicion of tamponade if presenting
rhythm is narrow-complex tachycardia without a pulse.
Cardiopulmonary resuscitation must be initiated immediately.
• Emergent pericardiocentesis.
Observation
• Early signs and symptoms: Beck triad consisting of muffled or
distant heart tones, distended neck veins, and hypotension; an
unwillingness to lay flat/supine, high anxiety, dyspnea, a change
in mental status and pulsus paradoxus. Pulsus paradoxus is a
decrease of greater than 10 mm Hg in systolic BP that occurs
during inspiration in the setting of increased intrathoracic
pressure. Stroke volume is reduced by the increased intrathoracic
pressure compressing the heart and blood vessels. The decrease
in systolic BP during inspiration is heard when slowly
auscultating the BP.
645
cuff, the subtle drop in the systolic BP heard during inspiration
when auscultating the BP is almost impossible to recognize.
Vital signs
• Sinus tachycardia, commonly seen as compensatory response to
decreased stroke volume.
• Low urine output is a result of low CO, and taken with other
signs should be viewed as a signal for intervention in the absence
of hemodynamic monitoring.
Auscultation
• Beck triad, although described as classic, is seen in 10% to
33% of patients. Muffled heart tones may not be apparent with
the patient sitting upright, depending on the volume of
tamponade, and may be difficult to hear in a busy, noisy
environment. JVD is not always present in acute tamponade, but
is commonly seen in constrictive pericarditis. Differentiating
646
constrictive pericarditis from cardiac tamponade is important. In
the presence of hypovolemia, blood flowing toward the RA
during inspiration makes the finding of JVD less likely with
tamponade. Pericardial friction rub may be heard with
pericarditis.
Percussion
• Dullness to percussion under the left scapula posteriorly,
related to compression of the left lower lobe. The Bamberger-
Pins-Ewart sign is a localized pulmonary auscultation and
percussion finding noted in the setting of large pericardial
effusions. There is dullness to percussion, increased fremitus, and
bronchial breathing between the vertebral column and the
scapula. A blowing sound can be heard, generally on the left side,
resulting from atelectasis caused by the enlarged pericardial sac.
Hemodynamic monitoring
If hemodynamic monitoring is not already in progress, do not delay
other treatments, but prepare for appropriate monitoring, according
to the hemodynamic system used. This may include insertion and
monitoring of an arterial line and pulmonary artery catheter or
another system capable of CO measurement.
647
pericarditis, but rarely with cardiac tamponade. The right
ventricle can accommodate increased volume with inspiration in
the setting of tamponade, and thus a decline in JV pressure can
be seen on the CVP waveform. With cardiac tamponade, jugular
veins are distended with a prominent x descent and an absent y
descent on the CVP waveform. The right atrial y descent is lost
because no blood can enter the atrium. Patients with constrictive
pericarditis have a prominent x and y descent. This is important
in differentiating tamponade from constrictive pericarditis.
• PAP: Increased.
648
with fluid administration alone.
Collaborative management
From www.acc.org/qualityandscience/clinical/statements.htm.
649
Pericardiocentesis should be avoided when cardiac
tamponade is associated with aortic dissection; immediate
surgical intervention is indicated.
The American College of Cardiology Foundation
(ACCF)/American Heart Association (AHA)/American Association
for Thoracic Surgery (AATS)/American College of
Radiology(ACR)/Society of Cardiovascular Anesthesiologists
(SCA)/Society for Cardiovascular Angiography and Interventions
(SCAI)/Society of Interventional Radiology (SIR)/Society of
Thoracic Surgeons (STS)/Society for Vascular Medicine (SVM)
issued Guidelines for the Diagnosis and Management of Patients
With Thoracic Aortic Disease in 2010. This safety alert information
was derived from that report.
Care priorities
650
2. Facilitate providing pericardiocentesis
Needle aspiration of the pericardium can be performed using a
subxiphoid or left parasternal approach to drain excess fluid from
the pericardial space. The blood removed often will not clot,
because the heart action can cause clotting factors within the
pericardial sac to break down (defibrination). Pericardiocentesis
alone may not suffice to manage acute pericardial tamponade.
Surgical exploration with pericardial window is recommended
because of the high incidence of recurrent bleeding if surgery is not
performed. A drain may stay in place until fluid output decreases
or ceases.
5. Administer vasoconstrictors
Medications used to increase BP by stimulating vasoconstriction in
the peripheral vasculature include neosynephrine or
norepinephrine. These medications are less effective in a setting of
hypovolemia.
651
include dopamine, dobutamine, and milrinone (see Appendix 6).
652
BP SVV greater than 13% and pulsus paradoxus. Later signs include
equalization of CVP and left atrial pressure (pulmonary artery
occlusive pressure) and elevated PAP in the presence of
hypotension, SVV greater than 13% and not fluid responsive, low
CO and CI (see Box 3-4).
653
Fluid Monitoring; Fluid Management; Blood Product
Administration; Medication Administration; Oxygen Therapy;
Resuscitation; Shock Management: Cardiac; Vital Signs Monitoring;
Dysrhythmia Management.
654
lines for evidence of infiltration. If vasopressor agents infiltrate
subcutaneous tissues, necrosis occurs. Follow appropriate
management protocol for your institution.
655
Pathophysiology
Injury to the spinal cord can be a devastating event initiating a
cascade of physical and psychological changes that may last a
lifetime. Spinal cord injury (SCI) affects approximately 12,000
people each year; this number depicts a continuing trend in injuries
associated with motor vehicle crashes (39.2%), falls (28.3%), and
violent acts, primarily gunshot wounds (14.6%) but a decreasing
trend in sports injuries (8.2%) with 9.7% classified as other. The
average age at injury is increasing and is now 41.6 years; the rising
trend may reflect referral patterns survival of older adults at the
scene, or an increase in the number of injuries in those who are 60
years and older. Young white males continue to be injured most
frequently but a mixed racial/ethnicity pattern has emerged since
2005 that may reflect the U.S. population trend; a decrease in white
populations with an increase in African-American and Hispanic
populations being injured. Cervical injuries occur most frequently
at a rate of 56% over lumbar and thoracic injuries. There are
estimated to be between 250,000 and 400,000 people living with an
SCI, and approximately 85% of patients with SCI who survive the
initial 24 hours live at least 10 years. Less than 1% of patients
experience complete recovery at the time of discharge from the
hospital.
The spinal cord is approximately 18 inches in length running
from the base of the brain to the lumbar (L) spine area between L1
and L2 where the cord tapers to form the conus medullaris, a
bulbous end that terminates into a collection of nerve roots known
as the cauda equina (horse’s tail). The spinal nerve roots exit the
spinal cord at corresponding levels below the vertebral body of the
spinal column and are the anatomic connection between the central
and peripheral nervous system. Because the spinal cord ends at L1
and L2, the nerves descending from the conus medullaris making
up the cauda equina are considered peripheral nerves. The brain
and spinal cord communicate sensory and motor information along
a complex system of tracts, some descending from the brain (motor)
and others ascending from the periphery (sensory). Damage to
pathways along this communication system results in unique but
very distinguishable syndromes that include upper motor neurons
(UMNs), which carry messages between the brain and the
656
periphery along the spinal cord, and lower motor neurons (LMNs),
those nerves that branch out from the vertebrae (peripheral nerves).
Damage to UMNs results in muscle spasticity and hyperreflexia,
whereas damage to LMNs results in muscle flaccidity and areflexia.
Mechanisms of injury to the spinal cord can be traumatic or
nontraumatic. Traumatic injuries include MVCs, falls, sports
injuries, or acts of violence (e.g., gunshot wounds or stabbings).
These mechanical force injuries result in sudden flexion,
hyperextension, vertebral fracture, compression of the cord,
rotation of the cord, or direct injury to the cord such as in a stabbing
or gunshot wound. Nontraumatic injuries may be a result of
vascular injury (aortic disruption or spinal artery occlusion),
degenerative diseases (spondylosis), inflammatory events,
neoplasms, or autoimmune diseases (multiple sclerosis). Injuries to
the spinal cord regardless of mechanism of injury include
concussion, contusion, laceration, transsection, hemorrhage,
ischemia, and avascularization. See SCI classifications and
terminology in Table 3-3.
Table 3-3
SPINAL CORD INJURY CLASSIFICATIONS AND TERMINOLOGY
657
cord), paralysis almost always occurs. Penetration of the spinal cord
with bony fragments may cause hemorrhage, infection, and leakage
of cerebrospinal fluid (CSF).
Spinal shock
Spinal shock occurs following both complete and partial
transsection of the cord. It is a temporary loss of reflex and
sensorimotor function in all segments below the level of injury.
Spinal shock does not involve the classic shock symptoms,
including hypotension, tachycardia, and cardiovascular
compensation to help support the BP. The “shock” manifests as
temporarily “stunning” the function of the spinal cord. Spinal shock
occurs immediately after SCI, lasting several hours to weeks and is
a separate phenomenon from neurogenic shock. Sensorimotor
function of the disrupted portion of the spinal cord can return once
spinal shock resolves.
Neurogenic shock
Neurogenic shock occurs in patients who injure the cervical or
upper thoracic cord, disrupting sympathetic innervation to the
vasculature and the heart. Cardiovascular compensatory
mechanisms controlled by sympathetic nerves in the upper thoracic
cord are lost. The loss of sympathetic innervation causes
widespread vasodilation and venous pooling in the extremities and
splanchnic vasculature. Loss of sympathetic innervation to the heart
leads to bradycardia. The ensuing hypotension and bradycardia
reduce CO as a result of decreased preload (decreased venous
return) and inability to increase heart rate, putting patients at risk
for secondary injury related to ischemia.
658
(neurogenic shock) occurs most dramatically in high cervical spine
injuries, with interruption of the sympathetic nervous system.
Profound bradycardia and hypotension are possible. With SCIs
lower than the midthoracic area, the patient will experience a
phase of neurogenic shock, with loss of sympathetic innervation to
vasculature below the level of the lesion; however, the effects of
that loss are not as dramatic.
Septic shock
Septic shock (see Septic Shock) may occur in patients with SCI as a
result of infections related to pneumonia, urinary tract infections
(UTIs), pressure sores, overuse of corticosteroids, and other causes.
HIGH ALERT!
Autonomic Dysreflexia
A life-threatening condition affecting victims with lesions at or
above T6, stemming from stimulation of the SNS by relatively
minor events. The resultant uncompensated cardiovascular
response may cause seizures, subarachnoid hemorrhage, fatal
cerebrovascular accident, and myocardial infarction if not
immediately recognized and treated.
Once spinal shock resolves, autonomic dysreflexia may occur at
any time from the acute phase to several years following the injury.
Causes
Most commonly, stimuli to the bladder, including distention,
infection, calculi, cystoscopy; or from the bowel with fecal
impaction, rectal examination, suppository insertion; or from the
skin, such as tight clothing or sheets, temperature extremes, sores,
or areas of broken skin. Initiating a regular toileting program is of
paramount importance as the patient recovers.
659
Acute phase assessment
Goal of assessment
There are two goals for spinal cord assessment: (1) identify and
initiate management of fractures, spinal shock, and cord
syndromes; and (2) prevent further injury.
Clinical assessment
The clinical assessment of the patient with SCI begins with the
trauma primary survey at the time of arrival to the emergency
department (see sections on Major and Abdominal Trauma
discussed earlier). Once stabilized the secondary trauma survey can
be completed and an extensive neurologic and functional
assessment can be performed.
Neurologic examination: Use of the American Spinal Injury
Association Scale (ASIA) documents the motor and sensory
impairment related to the injury (Table 3-4).
Table 3-4
AMERICAN SPINAL INJURY ASSOCIATION SCALE
660
signs, respiratory status, including oxygen saturation (pulse
oximetry), vital capacity, and monitoring for ascending edema.
Consideration for cardiac monitoring, placement of nasogastric
(NG) tubes, or Foley catheters occurs as a result of cardiac, GI, and
genitourinary assessment. Interpretation of laboratory values and
diagnostic studies assist in the development of the plan of care.
Types of injury
Complete SCI is total loss of motor and sensory function below the
level of the lesion. Symptoms are a result of physiologic
transsection of the cord either from bruising or compression of cord
and blood vessels. Both sides of the body are affected equally.
Approximately 50% of injuries are complete.
Incomplete SCI has preservation of some motor or sensory
function below the level of the lesion. The pattern of injury may not
be symmetrical. Several cord syndromes (anterior cord syndrome,
central cord syndrome, lateral cord/Brown-Séquard syndrome,
posterior cord syndrome, conus medullaris syndrome, and cauda
equina syndrome) have been identified and will be discussed under
Acute Phase Assessment.
Levels of injury
Tetraplegia (quadriplegia): Injury to the cervical cord resulting in
motor loss in all four extremities.
Paraplegia: Injury to the thoracic and lumbar cord resulting in
motor loss in the lower trunk and extremities.
The patient should be evaluated for the following SCI specific
conditions:
Spinal shock initial symptoms:
661
• Loss of vasomotor tone.
• Vasodilation.
• Hypotension.
• Bradycardia.
• Vasodilation.
• Hypotension.
662
• Pounding headache.
• Flushing of the skin with sweating above the level of the lesion.
• Nasal congestion.
• Blurred vision.
• Nausea.
• Chest pain.
Table 3-5
LEVELS OF CORD INJURY
Level
of Manifestation
Injury
C4 Loss of muscle function, including respiratory function; fatal outcome unless
and ventilation is provided immediately.
above
C4-C5 Same as above; phrenic nerve may be spared; assisted ventilation;
quadriplegia/tetraplegia.
C6-C8 Diaphragm and accessory muscles or respiration retained; movement of neck,
shoulders, chest, and upper arms; quadriplegia.
T1-T3 Neck, chest, shoulder, arm, hand, and respiratory function retained; difficulty
maintaining a sitting position; paraplegia.
T4- More stability of trunk muscles; paraplegia.
T10
T11- Use of upper extremities, neck, and shoulders; some function of upper thigh; reflex
L2 emptying of bowel; males may have difficulty achieving and maintaining an erection;
decreased seminal emission.
L3-S1 Reflex emptying of bowel/bladder; decreased/lack of ability to have an erection;
decreased seminal emission; all muscle groups in upper body function; most muscles of
lower extremities function.
S2-S4 Flaccid bowel and bladder; lower extremity weakness; all muscle groups function; no
ability to have a reflex erection.
Cord syndromes
663
Anterior cord syndrome: Injury to the anterior two thirds of the
spinal cord supplied by the anterior spinal artery caused by an
acute burst fracture, herniation of an intervertebral disk, a vascular
injury or occlusion resulting from trauma, clot, or surgical
procedure, such as aortic aneurysm repair.
The prognosis varies with each patient and depends on the
degree of structural damage and edema.
Symptoms include:
• Sacral and some lumbar fibers are spared, therefore motor and
sensory function in the perineum, genitalia, and lower
extremities is present.
664
• Bladder dysfunction varies with each patient.
• Ipsilateral weakness.
• Usually there are bilateral motor and sensory deficits, but motor
activity will be better on the contralateral side and sensory
activity will be better on the ipsilateral side.
• Loss of proprioception.
665
presenting a mixed clinical picture of UMN and LMN lesions.
Symptoms include:
666
• Sensation is diminished or lost to pinprick and light touch
along the dermatome pattern of the nerve; often there is saddle
anesthesia with diminished or absent sensation to the glans penis
or clitoris.
HIGH ALERT!
Requires immediate attention (decompression) to prevent
permanent injury.
HIGH ALERT!
Vertebral artery injury (VAI): Recognizing the potential for
VAI in patients with cervical spine injuries is important. These are
667
occult injuries but may account for changes in mental status in a
patient without a history of brain injury. Patients may be
asymptomatic or complain of headache. Some go on to have
posterior fossa infarcts. Magnetic resonance imaging should be
part of the diagnostic workup for early detection of VAI. Patients
with VAI may be placed on anticoagulants.
Diagnostic tests
Following trauma, the commonly used radiologic investigations do
not rule out injury to the spinal cord, especially for children,
particularly resulting from the elasticity of the cervical spine. There
is a possibility of SCI without radiologic abnormality (SCIWORA).
The changes may be identified using magnetic resonance imaging
(MRI). SCIWORA may be present in patients who have experienced
blunt trauma who report immediate or transient symptoms of
neurologic deficit or who exhibit symptoms upon initial
assessment. Treatment within 6 hours with high-dose
methylprednisolone improves the outcome. It is possible to reduce
the incidence of neurologic complications by increasing awareness
and initiating early treatment with steroids and immobilization of
the affected area, most often, the cervical spine.
Spinal radiograph
Plain radiographs provide information on the bony anatomy of the
spine, thereby delineating fractures, dislocations, and subluxations
of the vertebral bodies, as well as demonstrating narrowing of the
spinal canal and level of hematomas, neoplasms, or abscesses.
Additional views such as open mouth, bilateral oblique, or flexion-
extension films also aid in diagnosis.
Cervical spine x-rays taken to rule out fracture on patients with
traumatic brain injury or SCI include three views: anterior posterior
(AP), lateral, and odontoid. Visualization from C1 to T1 is
imperative but may be difficult in patients with large necks and
shoulder muscles. If visualization is clear, CT or MRI must be done
before removing cervical spine collars.
668
HIGH ALERT!
Films must be obtained with extreme caution in the evaluation
of the patient with a possible spinal cord injury because any
sudden or incorrect movement of the injured area could cause
further trauma to the spinal cord or cause injury in a patient who is
neurologically intact. Flexion-extension films should only be
obtained when a patient is alert and able to describe pain on
manipulation or under the supervision of a radiologist using
fluoroscopy techniques.
CT scans
The CT scan provides detailed information on the bony structures
of the vertebral bodies, especially related to encroachment on the
spinal canal by bone fragments or vertebral body displacement. CT
images are especially useful for evaluation of the cervical thoracic
junction. Helical or spiral CT scans are used to reconstruct the
sagittal and coronal planes. The entire spine should be imaged
if there is an SCI to identify injuries at other levels.
Collaborative management
Care priorities
669
SCI. Immobilization continues until the spine is stable either by
traction or surgical decompression and fixation. Remove the patient
from the spine board as soon as possible to prevent skin
breakdown. This is usually done after the primary survey is
completed. There is new evidence to suggest that use of spine
boards should be reserved only for those with obvious SCI during
prehospital care.
670
compression is imminent, in the presence of an expanding
hematoma or neoplasm; (2) in the presence of compound
fractures; (3) if there is a penetrating wound of the spine; (4) if
bone fragments are localized in the spinal canal; or (5) if there is
acute anterior spinal cord trauma. Surgeries may include
decompression laminectomy, closed or open reduction of the
fracture, or spinal fusion for stabilization. Anterior cervical
decompression is advocated for significant disk herniation. Once
stabilization of the spine occurs, the patient can be mobilized
unless contraindicated for other reasons.
671
derivative), use of calcium channel blockers to aid in axonal
conduction, use of Cethrin (a Rho antagonist) for neuroregeneration
and neuroprotection, and the use of anti-Nogo monoclonal
antibodies to augment plasticity and regeneration. Cell-mediated
repair is being investigated using stem cells and bone marrow
stromal cells. The use of GM1 gangliosides to improve spinal cord
outcomes has not been supported.
Methylprednisolone protocol is as follows: Within 8 hours of
injury, a loading dose (30 mg/kg) is administered by IV bolus over a
15-minute period. After a 45-minute wait, 5.4 mg/kg/h is then
administered in a continuous IV infusion over a 23-hour period and
then stopped. If the infusion is interrupted for any reason, it must
be recalibrated so that the entire dose can be completed within the
original 23-hour time frame.
HIGH ALERT!
Use of this protocol and the 48-hour protocol is no longer the
standard of care and is used only if benefit outweighs the risk.
672
hypotension during the immediate postinjury stage caused by
loss of vasomotor control below the level of injury, with resultant
vasodilation and a relative hypovolemia (see Appendix 6).
HIGH ALERT!
Vasopressor support should be initiated only after fluid
resuscitation has been done or in cases of refractory hypotension or
low systemic vascular resistance.
5. Support ventilation
Respiratory insufficiency is a hallmark in SCI, and the higher the
level of injury, the more likely the injury will affect ventilation. The
need for assisted ventilation is based on the level of injury, ABG
values, pulse oximetry, capnography, and the results of pulmonary
function tests, pulmonary fluoroscopy, and physical assessment
data. The need for mechanical ventilation is likely with injuries at
C4 and above, patients older than 40 years, smokers, and patients
with associated chest trauma and immersion injuries. Initially, the
673
patient may require intubation and, later, tracheotomy. Patients
with low cervical or high thoracic injuries whose respiratory status
is stable initially may need temporary intubation later if ascending
edema develops. Patients with high cervical injury who survive the
initial injury but have paralysis of the muscles of respiration may
require permanent tracheotomy and mechanical ventilation.
674
are recommended over histamine blockers for stress ulcer (a
Cushing ulcer) prophylaxis. Cushing ulcers are related to CNS
trauma and occur more often in the stomach than the duodenum,
and occasionally affect the esophagus. PPIs reduce the production
of acid in the stomach by blocking gastric parietal cell hydrogen-
potassium ATPase. Recommended therapy for PPIs is 4 weeks.
675
Early detection of vascular complications: Use of Doppler
ultrasonography or plethysmography for detection of deep
venous thrombosis (DVT) is recommended. CT angiography has
a greater specificity to diagnose PE than D dimer and ventilation-
perfusion scan.
HIGH ALERT!
Patients who are not candidates for anticoagulation therapy
may have an inferior vena cava filter inserted to trap emboli
traveling from the lower extremities to the lungs.
676
13. Bladder program
Once the stability of the patient is ensured, a bladder program
using an intermittent straight catheterization procedure is
recommended.
HIGH ALERT!
Early bladder decompression and drainage using a Foley
catheter is necessary during the acute phase (3 to 4 days after
injury). To prevent bladder infections, begin bladder training and
remove the Foley catheter once the patient is stable. Bladder
distention can be a trigger for onset of autonomic dysreflexia.
677
function and prevents constipation and impaction. Liquid or oral
stool softeners (e.g., docusate sodium), suppositories, and small-
volume enemas are used.
678
inspiration) is ≥1 L. Motor and sensory losses remain at the same
spinal cord level as the initial findings.
HIGH ALERT!
Patients with cervical injuries usually arrive in the intensive
care unit (ICU) already intubated. However, with some high
thoracic or low cervical lesions, patients who ventilate
independently in the emergency department may arrive in the ICU
without assisted ventilation. This patient is at risk for an
increasingly higher level of cord damage because of hemorrhage
and edema, which can result in a higher level of dysfunction and a
change in respiratory status that requires assisted ventilation.
Before attempting oral intubation with neck flexion, ensure that
cervical x-ray studies have confirmed the absence of cervical
involvement. Use either nasal intubation or orotracheal intubation
with manual cervical spine immobilization if cervical spine injury
is not ruled out. Fiber optic intubation may also be considered.
Respiratory monitoring
679
respiratory fatigue.
HIGH ALERT!
680
Be alert for bradycardia associated with tracheal suctioning. If
the patient’s cough is ineffective, implement the following method,
known as quad coughing: place palm of hand under the patient’s
diaphragm, and push up on the abdominal muscles as the patient
exhales. Be aware that using the quad cough maneuver in patients
with intracaval filters to prevent pulmonary emboli has been
reported to have significant complications, including bowel
perforation and filter migration and deformation.
HIGH ALERT!
Have a plan to remove the vest if cardiopulmonary
resuscitation is needed.
681
Autonomic dysreflexia (or risk for same)
related to abnormal response of the autonomic nervous system to a
stimulus.
Goals/Outcomes: The patient has no symptoms of autonomic
dysreflexia, as evidenced by dry skin above the level of injury, BP
within the patient’s normal range, HR ≥60 bpm, and absence of
headache and other clinical indicators of autonomic dysreflexia.
ECG demonstrates normal sinus rhythm.
Risk Detection.
Dysreflexia management
682
• Monitor BP and HR every 3 to 5 minutes until the
patient stabilizes.
683
has sustained injury above T6, because these patients are at risk for
autonomic dysreflexia for life.
Dysreflexia Management.
Decreased CO
related to relative hypovolemia secondary to enlarged vascular space
occurring with neurogenic shock.
Goals/Outcomes: The patient has adequate CO, as evidenced by
orientation to time, place, and person; systolic BP ≥90 mm Hg (or
within the patient’s normal range); HR 60 to 100 bpm; RAP 4 to 6
mm Hg; PAP 20 to 30/8 to 15 mm Hg; PAWP 6 to 12 mm Hg; SVR
900 to 1200 dynes/s/cm−5; normal amplitude of peripheral pulses
(greater than 2+ on a 0-to-4+ scale); urinary output ≥0.5 mL/kg/h;
and normal sinus rhythm on ECG.
Circulation Status.
Hemodynamic regulation
684
• Perform range-of-motion (ROM) exercises every 2
hours to prevent venous pooling.
HIGH ALERT!
Patients sustaining major trauma are at high risk for
685
development of gastritis/gastric ulcers caused by increased
production of gastric acid. Although ulceration can occur at any
time in the patient with spinal cord injury, it is most likely to occur
within 3 weeks of the injury. Cushing ulcers develop in the
stomach, duodenum, and rarely the esophagus in the setting of
central nervous system trauma, whereas Curling ulcers are stress
ulcers related to burns and other trauma that occur almost
exclusively in the duodenum.
Risk Control.
Bleeding precautions
2. Test gastric aspirate and stools for blood q8h. Promptly consult
the physician if blood is present.
686
5. For the patient with GI ulceration and hemorrhage, bowel
perforation is an added risk. Be alert to the following indicators:
pallor, shock state, abdominal distention, may or may not have
voluntary or involuntary guarding, vomiting of material that
resembles coffee grounds, absent bowel sounds, elevated WBC
count (greater than 11,000/mm3), and presence of air on abdominal
x-ray view. In some cases the only indicators are tachycardia and
shoulder pain. Lack of pain is not a reliable indicator of bowel
perforation in the patient with SCI. Bowel perforation is an
emergency situation, requiring immediate surgical intervention.
687
definitive diagnosis of DVT.
688
concomitant increase in blood viscosity, which can
promote thrombus formation.
HIGH ALERT!
Patients with spinal cord injury who are not candidates for
anticoagulation because comorbidities may require surgical
intervention (insertion of intracaval filter) to prevent pulmonary
emboli as a result of thrombophlebitis or deep venous thrombosis.
Pressure management
689
warmth, open or macerated tissue, and foul odors (indicative of
infection with tissue necrosis).
HIGH ALERT!
Do not turn the patient until the injury has been stabilized or a
turning protocol has been ordered. If turning is allowed before
immobilization with tongs, halo, or surgery, use the logrolling
technique only, using at least three people to turn the patient: one
to support the head and neck and keep them in alignment during
the procedure, and two to turn the patient.
690
evidenced by balanced nitrogen state per nitrogen balance studies,
serum albumin 3.5 to 5.5 g/dL, thyroxine-binding prealbumin 20 to
30 mg/dL, and retinol-binding protein 4 to 5 mg/dL.
Nutritional Status.
Nutrition management
691
may compromise respiratory movement; and less
fatiguing.
HIGH ALERT!
Urinary retention with stretching of the bladder muscle may
trigger autonomic dysreflexia. Therefore, it is crucial to assess for
retention and to treat it promptly.
Urinary Elimination.
692
2. Assess for effects of medications that can cause urinary retention
such as tricyclic antidepressants and anticholinergics.
HIGH ALERT!
Urinary tract infection (UTI) is one of the leading causes of
morbidity and mortality in the patient with spinal cord injury. This
693
patient may not be aware of the presence of UTI until he or she is
severely ill as a result of pyelonephritis (calculi, infection,
septicemia).
Ineffective thermoregulation
related to inability of the body to adapt to environmental temperature
changes secondary to poikilothermic reaction occurring with SCI.
Goals/Outcome: Within 2 to 4 hours of this diagnosis, the patient
becomes normothermic.
HIGH ALERT!
With spinal cord injury the patient is poikilothermic, that is, the
patient has a decreased ability to regulate temperature below the
level of the lesion through vasodilation or vasoconstriction
(sweating and shivering). Because there is no autonomic control of
core body temperature, the patient is susceptible to temperature
variations in the environment. Attention to room temperature and
use of external cooling or warming devices may be necessary.
Thermoregulation.
Temperature regulation
694
1. Monitor the patient’s temperature at least every 4 hours and
assess the patient for signs of ineffective thermoregulation:
complaints of being too warm, excessive diaphoresis, warmth of
skin above the level of injury, complaints of being too cold,
pilomotor erection (goose bumps), or cool skin above the level of
injury.
Constipation
related to atonic bowel, paralytic ileus with concomitant autonomic
dysreflexia or loss of anal sphincter control.
Goals/Outcomes: The patient remains free of symptoms of
constipation and/or paralytic ileus, as evidenced by auscultation of
normal bowel sounds, and free of symptoms of autonomic
dysreflexia, and the patient has bowel elimination of soft and
formed stools.
HIGH ALERT!
Paralytic ileus occurs most often in patients with spinal cord
injury at T6 and above and usually within the first 72 hours after
injury.
Bowel Elimination.
Constipation/impaction management
695
2. Assess for indicators of paralytic ileus: decreased or absent bowel
sounds, abdominal distention, anorexia, vomiting, and altered
respirations as a result of pressure on the diaphragm. Report
significant findings promptly.
3. Keep the patient NPO (nil per os) until evidence of return of
bowel function (flatus or bowel movements are the most reliable
signs).
696
HIGH ALERT!
Be aware that overdistention of the bowel or stimulation of the
anal sphincter caused by impaction, rectal tube, rectal examination,
or enema may precipitate autonomic dysreflexia. Use generous
amounts of anesthetic lubricant when performing a rectal
examination or administering an enema.
697
of invasive immobilization devices.
Goals/Outcomes: The patient is free of infection at insertion site
for tongs or halo device, as evidenced by normothermia; negative
culture results; and absence of erythema, swelling, warmth,
purulent drainage, or tenderness at insertion site.
Risk Control.
Infection protection
2. Perform pin care as prescribed. Cleanse the site with soap and
water or NS; the area may be left open to air. Monitor for drainage
or infection.
Environmental management
698
• Position mirrors to increase the amount of area that
can be visualized from the patient’s position.
Positioning.
Sexual counseling
699
resolution of the spinal shock, particularly for individuals with
lesions in the cervical and thoracic areas. Reassure the patient that
this is normal and minimize embarrassment by providing coping
skills.
Burns
Pathophysiology
Burn injuries involve damage to the skin and underlying tissues,
700
but other organ systems may be affected, especially with extensive
(greater than 20% total body surface area [TBSA]) burn injuries. The
cause of injury may be thermal (flame/flash; contact with hot
liquids, semiliquids, hot objects), electrical, chemical, or radiation.
Relative risk of injury differs by age, gender, occupation, and
recreational activities. Estimates for the number of burn injuries in
the United States range from 1.4 to 2 million injuries annually, and
of those, approximately 450,000 seek medical treatment. Of these, it
is estimated that 40,000, including 30,000 at hospital burn centers,
require hospitalization. For those who survive their injury, the
average hospital length of stay is slightly greater than 1 day per 1%
TBSA burn. The number of deaths as a result of fire, burns, and/or
smoke inhalation each year is approximately 3400. In the United
States, the two most common reported etiologies are fire/flame
(43%) and scalds (34%); electrical burn injuries account for 4% of all
admissions to burn centers each year. The burning agent, intensity,
and duration of exposure, location, and depth of burn, and the
extent or size of injury, determine overall injury severity.
Burn injuries are categorized based on depth of injury. The longer
and more intense the exposure to the burning agent, the greater is
the depth of injury. A burn injury is described as either a partial-
thickness or full-thickness injury, relative to the layer(s) of skin and
tissues injured. A superficial injury, commonly referred to as “first-
degree” burn (e.g., sunburn), damages only the epidermis. These
burns typically heal within 3 to 5 days and without permanent
scarring. Partial-thickness injury, called a “second-degree” burn,
involves varying levels of the dermis, which contain structures
essential to skin function (e.g., sweat and sebaceous glands, hair
follicles, sensory nerves, capillary network). These burns typically
heal within 14 to 21 days, depending on the depth. Full-thickness
injury, a “third-degree” burn, destroys the epidermis and dermis
and exposes the less vascularized fat layer, which contains adipose
tissue, roots of sweat glands, and hair follicles. These wounds
require surgical excision of the dead tissue and skin grafting to
provide the best functional and cosmetic outcomes. In very small
full-thickness wounds (e.g., size of a quarter or smaller), healing
may occur by granulation and migration of healthy epithelium
from the wound margins. When full-thickness injuries include
701
destruction of tendon and bone, clinicians often describe these
injuries as “fourth-degree” burns. These injuries are the deepest
and require excision, possibly amputation of extremities, and skin
grafting to heal. Refer to Table 3-6 for detailed burn wound
classification and descriptions.
In patients admitted to burn centers, approximately 10% to 20%
have an associated inhalation injury. Inhalation injury commonly
occurs with flame injuries, particularly if the victim is trapped in an
enclosed, smoke-filled space, and is an important determinant of
survival (60% to 70% of patients who die in burn centers have
inhalation injuries). The associated pathophysiology can be divided
into three types of injury as follows.
702
• Injury above the glottis: Injury above the glottis (nasopharynx,
oropharynx, and larynx) can be thermal or chemical in nature.
The heat exchange capability of the respiratory tract is very
efficient such that tissue damage from breathing in heated air
occurs most often above the vocal cords. Heat damage to the
pharynx can be severe enough to cause upper airway edema
resulting in obstruction.
• Injury below the glottis: Injury below the glottis is almost always
chemical in nature, causing direct damage to airway epithelium
from inhalation of the noxious chemicals (e.g., aldehyde, sulfur
oxide, phosgene) of smoke.
703
not necessarily in a burn center, and minor burns are often treated
on an outpatient basis. Box 3-5 outlines the ABA criteria for patients
who should be referred to a recognized burn center.
Box 3-5
AMERICAN BURN ASSOCIATION BURN
CENTER REFERRAL GUIDELINES
• Partial-thickness burns greater than 10% total body surface area
(TBSA) burn in patients younger than 10 years or older than 50
years.
• Chemical burns.
704
Excerpted from American Burn Association/American College of
Surgeons Committee on Trauma: Guidelines for the operation of burn
centers. Resources for optimal care of the injured patient 2006, Chicago,
2006, American Burn Association, pp. 79-86.
Initial assessment
In the prehospital setting or emergency department, patients with a
burn injury should be evaluated using a primary survey followed
by a more thorough, secondary survey; the principles of which are
taught in the Advanced Burn Life Support (ABLS) course. The
primary patient survey includes the basic ABCs, with the addition
of D and E: A: airway and cervical spine immobilization (based on
mechanism of injury); B: breathing; C: circulation; D: disability or
neurologic deficit; and E: exposure and evaluation. Once the
primary survey is complete, a secondary survey should be
705
performed and includes a detailed head-to-toe assessment,
exploration of the circumstances of the injury, and the patient’s
medical history. Injury severity is assessed according to patient’s
age, potential for inhalation injury, TBSA burn, depth and location,
past medical history, and concomitant trauma.
Airway/breathing
• Observe for foreign objects in mouth, including a large tongue
that may obstruct the airway.
706
• Take BP on uninjured extremity if possible. Arterial line may be
necessary for BP monitoring if burn injury to bilateral extremities
is extensive and/or patient exhibits hemodynamic instability.
Compare cuff BP to arterial line BP if arterial line is in place;
decide which pressure is deemed the most accurate.
• Pallor.
• Pulselessness.
• Paresthesias.
• Paralysis.
707
be used for both children and adults and is frequently used in
critical and acute care settings. More recent studies have called into
question the use of these measures in the morbidly obese
population and suggest that as the body mass index increases, the
size of the palmer surface in relation to the percent TBSA burn
decreases.
708
FIGURE 3-2 Estimation of burn injury: Lund and
Browder chart. Areas represent percentages of body
surface area that vary according to age. The
accompanying table indicates the relative percentages
of these areas in various stages of life. Source: (From
Sabeston DC Jr, editor: Textbook of surgery: the biographical basis of
modern surgical practice, ed. 11, Philadelphia, 1977, Saunders.)
709
• Estimate wound size (percent TBSA burn) and assess depth
(partial- or full-thickness burn injury).
Palpation
• Pulse assessment to evaluate for decreased tissue perfusion of all
extremities:
Auscultation
• Respiratory sounds to assess for adventitious breath sounds;
confirm for bilateral breath sounds.
Respiratory system
710
Respiratory compromise may occur as a result of upper airway
swelling, inhalation injury, carbon monoxide poisoning, or
respiratory tract infection. The upper airway is injured when hot air
causes heat injury to the respiratory mucosa. The lower respiratory
tract can be damaged by contact with products of combustion and
inhalation of vaporized caustic substances, such as sulfur, hydrogen
cyanide, ammonia, acrolein, aldehydes, and hydrochloric acid.
These noxious gases are produced from the combustion of common
household items, such as carpeting, furniture, and decorations.
Airway injury, obstruction, or respiratory distress may not occur
immediately following injury.
• Secure and protect airway; check for any cervical injuries and
need to stabilize neck area for appropriate airway protection
positioning.
711
Table 3-7
CARBON MONOXIDE POISONING
712
decreased compliance, and abnormal ABG values.
Cardiovascular system
Circulatory compromise results from the fluid shifts that occur
following a significant (typically greater than 20% TBSA) burn
injury. Increased capillary permeability caused by the inflammatory
response results in a shift of intravascular fluid into the interstitial
spaces in the first 72 hours postburn. This causes a decrease in
circulating volume and increased blood viscosity. Other systemic
responses include increases in catecholamines, cortisol, renin-
angiotensin, antidiuretic hormone, and aldosterone production as
the body attempts to retain sodium and water to replenish
intravascular fluid. Rapid fluid shifts can result in massive edema
in unburned and burned areas, hemoconcentration, and thrombus
formation.
713
Gastrointestinal system
Initially, blood flow is shunted away from the GI tract and
peristalsis is slowed or stopped completely, causing a gastric ileus
(usually resolves within 72 hours after burn injury).
Renal system
Hemoconcentration and reduced circulatory volumes result in
decreased renal blood flow and low urinary output. Dark
concentrated urine in the presence of muscle injury implies
myoglobinuria or hemoglobinuria. Continued poor renal perfusion
results in acute tubular necrosis and renal failure. Urine output
guides fluid resuscitation measures and recognition of renal
compromise or poor CO is essential.
714
Bladder pressures exceeding 20 mm Hg may constitute an
emergency as it may indicate abdominal compartment syndrome.
Thus it is important for the nurse to monitor any increases in
trending of bladder pressures.
Integumentary system
Loss of skin integrity results in increased fluid loss through
evaporation, hypothermia, pain, and increased risk of infection.
Evaporative fluid losses can be substantial, especially in patients
with large surface area burns and in pediatric patients with burn
injuries who have larger surface area per kilogram of body weight.
Significant hypothermia can result in patients with large surface
area burns, long transports to the hospital, and long surgeries and
in those who require prolonged wound care.
Patients with burn injuries can experience three types of pain:
715
Circumferential full-thickness burns can cause constriction of
underlying tissue, blood vessels, and muscles with circulatory
compromise to underlying muscles and distal extremities. Healed
skin may result in some scar formation, which can lead to
contractures that limit joint ROM.
See Table 3-6 for a complete description of partial-thickness and
full-thickness burn wound injuries.
Wound infection
Loss of skin integrity means that the body’s first line of defense
against infection is compromised. Ongoing evaluation for burn
wound infection is imperative because a significant infection may
lead to delayed healing, tissue loss, and sepsis. Typically, the larger
the wound or delay in complete healing, the greater is the risk for
wound infection. Early signs of wound infection include fever,
increase or decrease in WBC count, erythema surrounding the burn
wound, increased wound pain, change in exudate or wound
appearance, and loss of previously healed skin grafts. Invasive
wound infection is indicated by rapid eschar separation (invasive
fungal infections); focal, dark red, brown, or black discolorations in
the eschar; rapid conversion of an area of partial- to full-thickness
injury; and hemorrhagic fat necrosis.
716
• Decreased BP with low SVR.
717
Diagnostic tests
Bronchoscopy
The ABA Consensus Conference on Burn Sepsis and Infection
Group has determined that bronchoscopy is the best and most
reliable test for diagnosis of smoke inhalation injury below the
glottis. Signs of injury below the glottis that can be observed with
bronchoscopy include carbonaceous material, edema, and
ulceration. Therapeutic bronchoscopy facilitates removal of
carbonaceous material and nonviable tissue.
718
Fluorescein examination
This procedure uses orange dye (fluorescein) and an ultraviolet
light (Wood lamp) to detect foreign bodies in the eye and/or
damage to the cornea. This examination should occur in all patients
with possible eye injury and should be performed early (first 24
hours after burn injury), before swelling prevents a thorough
examination.
Urine collections
Perform urinalysis and culture and sensitivity early to detect UTI. A
24-hour urine collection to measure total nitrogen, urea nitrogen,
creatinine, and amino acid nitrogen values may indicate return of
capillary integrity (3 to 5 days after burn occurrence) and
mobilization of third-spaced fluids, the degree of catabolism
present, and the onset or resolution of acute renal failure.
Myoglobinuria can result from muscle injury sustained from an
electrical injury or deep full-thickness burn.
Hematology
719
Elevated Hct resulting from hemoconcentration during initial
resuscitation. Hgb will be decreased secondary to dilution, surgical
burn wound excision, hemolysis, or multiple laboratory draws.
During the first 24 hours postburn, neither the Hgb level nor the
Hct is a reliable guide to fluid resuscitation. WBCs may be
elevated resulting from systemic inflammatory response or sepsis.
Patients with burn injuries will typically be leukopenic initially
because WBCs migrate to areas of burned tissue.
Electrolyte panel
Hyperglycemia is common in patients related to the normal stress
response of injury. Hyperglycemia may also be seen in patients
with sepsis and multiple organ failure. Sodium shifts occur during
resuscitation; carefully monitor and adjust type of resuscitation
fluid 24 hours postinjury. Vigilant monitoring of the ECG for T
wave elevation indicative of hyperkalemia is of paramount
importance. Early identification of hyperkalemia facilitates prompt
treatment. Potassium may be elevated as a result of cell lysis, fluid
shifts, or renal insufficiency. Blood urea nitrogen (BUN) is elevated
because of hypovolemic state, increased protein catabolism, or
possible acute renal failure. Persistent elevation of BUN and
creatinine signals inadequate fluid intake or acute renal failure.
Total protein and albumin are decreased secondary to leakage of
plasma proteins into interstitial spaces. Creatine kinase (CK) is
sometimes used as an index of muscle damage, but a burn injury
that damages even a small quantity of muscle tissue will result in
markedly elevated CK levels in the first 24 hours. Troponin levels
are more indicative of cardiac damage. Increase in lactate may
indicate inadequate fluid resuscitation (first 12 to 24 hours
postburn), infection, or shock state from decreased tissue perfusion
or sepsis.
ECG
Evaluate for tachycardia secondary to hypovolemia or pain.
Tachycardia of 100 to 120 bpm is common in the adult patient who
appears adequately resuscitated. Myocardial damage secondary to
high-voltage electrical burn injury may be evident (e.g.,
dysrhythmias, prolonged QT interval). Dysrhythmias related to
720
electrolyte imbalance may occur. Hyperkalemia is relatively
common and, if extreme, requires immediate care to avoid a lethal
dysrhythmia.
Collaborative management
Care priorities
721
failure is present, airway obstruction from laryngeal edema
associated with the superheated gases is imminent (e.g.,
progressive hoarseness and/or stridor), or the patient cannot protect
their airway (impaired LOC). Large burn injury (more than 40%
TBSA) may result in generalized tissue edema even in the absence
of inhalation injury, requiring prophylactic intubation for airway
protection. Because laryngeal edema typically resolves in 3 to 5
days after the burn injury, tracheostomy is avoided for upper
airway distress unless there is acute obstruction or prolonged need
for ventilatory support.
For patients requiring intubation and mechanical ventilation,
implementation of measures (e.g., Ventilator Bundle) to prevent
ventilator-associated pneumonia are instituted. Ventilator-
associated events are identified by using a combination of objective
criteria: deterioration in respiratory status after a period of stability
or improvement on the ventilator, evidence of infection or
inflammation, and laboratory evidence of respiratory tract infection
(www.cdc.gov/nhsn/pdfs/pscManual/10-VAE_FINAL.pdf).
Ventilator-associated pneumonia is the leading cause of death
among patients with hospital-acquired infections; it prolongs time
spent on the ventilator, in the ICU, and the total hospital length of
stay.
The key components of the Institute for Healthcare Improvement
(IHI) Ventilator Bundle are noted as follows (*); other key
preventative interventions are also suggested:
• Hand hygiene.
722
• Lung protective ventilator strategies.
• Early mobilization.
723
necessary. If peripheral IV access is not possible, obtain central
venous line access (preferably through nonburned skin) for IV
administration. Intraosseous infusion may be necessary if
peripheral or central venous access is not possible.
Patients with less than 20% total body surface area burns
may be candidates for oral fluid resuscitation. Oral resuscitation
should be considered when the patient is able to tolerate oral
intake (intact gastrointestinal tract) or when resources are limited
(e.g., mass casualty situation).
6. Fluid resuscitation
The goal of fluid resuscitation is to maintain tissue perfusion
and organ function while avoiding the complications of inadequate
or excessive fluid therapy (Advanced Burn Life Support). Fluid
replacement protocols are based on body weight and percent of
TBSA burned and provide an estimate for resuscitation. The ABA
Consensus formula recommends administration of 2 to 4 mL fluid
per kilogram body weight per percent TBSA burned (adult) and 3
to 4 mL fluid per kilogram body weight per percent TBSA burned
(infants and young children weighing less than 30 kg) to provide
the total estimate of fluids to be administered in the first 24 hours
following the time the burn occurred. Give half in the first 8 hours
and then the second half over the next 16 hours. The initial infusion
rate is calculated using the Consensus formula and subsequent
hourly titration is guided by urinary output (30 to 50 mL/h for
adults and 1 mL/kg/h in children weighing less than 30 kg). LR
solution is used in the first 24 hours, with small amounts of colloid
fluids added during the second 24 hours after injury. Colloids are
generally avoided during the first 12 to 24 hours after injury
because increased capillary permeability allows leakage of protein
into the interstitial tissues. The greater surface area–to–body mass
ratio of children necessitates the administration of relatively greater
amounts of resuscitation fluid. In addition, infants and young
724
children should receive fluid with 5% dextrose (e.g., D51⁄4 NS or D51⁄2
NS) at a maintenance rate in addition to the LR resuscitation fluid.
Maintenance fluids are provided at a constant rate and are based on
the child’s dry weight. A child weighing up to 10 kg should receive
4 mL/kg/h; those 11 to 20 kg should receive 2 mL/kg/h, and those 21
to 30 kg should receive 1 mL/kg/h during the first 24 hours
following injury. Patients who are particularly sensitive to excessive
fluid resuscitation include children, older adults, and those with
preexisting cardiac disease.
Calculate fluid infusion from the time of injury, not the time
of hospital admission. Fluid resuscitation and maintenance
formulas should be modified based on individual patient responses
and needs. Hourly urine output serves to guide infusion rates.
Patients with electrical injuries, very deep burns, inhalation
injury, prior dehydration, ethanol intoxication, and concomitant
trauma (e.g., crushing injuries) may have greater fluid needs than
suggested by their cutaneous burn injury alone.
725
resuscitative phase because of the potential for gastric ileus in
patients with greater than 20% TBSA burn and in patients with
intubated airway.
726
intake alone. Enteral feedings are preferred in these patients and
have the added benefit of decreasing GI acidity and ulcer
formation. Either gastric or postpyloric jejunal feedings may be
used. Elemental jejunal feedings may be tolerated when
conventional feedings are not. Total parenteral nutrition may be
initiated for the patient with gastric ileus or inability to tolerate an
adequate amount of enteral feedings.
For patients who are difficult to wean from the ventilator, it has
been suggested that the use of higher-fat, lower-carbohydrate diets
may be beneficial because excess carbohydrate increases CO2
production.
727
(pigskin); provides temporary wound coverage until the wound
bed beneath is healed or is ready for permanent autografting.
Pharmacotherapy
728
2. Manage pain with IV analgesics and anxiolytics
Morphine sulfate and fentanyl are common agents used for pain
management. They are administered in small, frequent IV doses, as
needed for comfort and before painful procedures. Consider
adjunctive treatment using benzodiazepines (e.g., lorazepam,
diazepam, midazolam) to decrease anxiety. Anxiety increases the
perception of pain.
729
logical to assume that this patient population is at high risk because
of hypercoagulability, altered vascular integrity from the burn
injury, imposed immobilization, and multiple operative
procedures.
Airway management
730
coughing.
Respiratory monitoring
731
work of breathing and predisposes patients to apneic episodes
and/or oxygen desaturations.
732
Outcomes for urine output should be adjusted for those patients
with preexisting renal failure/compromise. In the presence of
myoglobinuria (red-pigmented urine indicative of myoglobin or
red blood cells in the urine), a urinary output of 1 to 1.5 mL/kg/h
(approximately 75 to 100 mL/h in the adult) is the desired outcome
until the heme pigments clear from the urine (urine color returns to
normal).
Fluid Balance.
Fluid management
733
during rapid volume resuscitation.
5. Monitor serial Hct and Hgb values. During the first 24 hours
postburn, neither the Hct nor Hgb levels are reliable guides to fluid
resuscitation. While the circulating volume is restored,
hemoconcentration is no longer present and Hct returns to within
normal limits. Consult the physician for significant anemia.
6. Monitor the patient for signs and symptoms of large volume fluid
administration (shortness of breath, tachypnea, excessive urine
output). Central hemodynamic monitoring is recommended for
patients who have preexisting heart or lung disease.
734
Ineffective tissue perfusion: Peripheral
related to thermal injury, circumferential burns, edema, hypovolemia.
Goals/Outcomes: The patient maintains adequate tissue
perfusion.
Note: Tissue perfusion in burned extremities is adequate when
peripheral pulses are greater than 2+ on a 0-to-4+ scale, capillary
refill is brisk (less than 2 seconds), and uninjured and healing skin
is warm to the touch.
Tissue Perfusion: Peripheral; Circulation Status.
Circulatory precautions
Hypothermia
related to exposure at the scene of injury; large body surface area burns,
administration of large volumes of unwarmed fluid.
Goals/Outcomes: The patient’s temperature returns to normal
(smaller burn injuries) or is slightly elevated (38.5° C; extensive
burn injuries) within 24 hours of this diagnosis. Complications of
hypothermia have been avoided.
Thermoregulation.
Temperature management
735
2. Avoid unnecessary exposure of the body. Keep the patient
covered with warmed or warming blanket.
Infection prevention
736
4. Assess burn wound daily for signs of infection.
6. Wash burn wound with a mild soap and rinse thoroughly with
water.
10. Assess all invasive lines and devices (e.g., urinary catheters)
daily. Review necessity with prompt removal of unnecessary lines
and devices.
737
11. For patients with a central line, implement the IHI central line
bundle:
• Hand hygiene.
Acute pain
related to burn injury and treatment
Goals/Outcomes: Within 30 minutes of treatment/intervention,
the patient’s subjective evaluation of discomfort improves and/or
nonverbal indicators of discomfort are absent or diminished.
Pain Control.
738
painful procedures, and sleep deprivation.
739
Healing
1. Assess and document extent and depth of burn wound (see Table
3-6).
Table 3-6
BURN WOUND DESCRIPTION AND CHARACTERISTICS
Modified from Carrougher GJ, editor: Burn care and therapy, St Louis, 1998, Mosby.
740
report the presence of bright red bleeding, which would inhibit
graft take, or purulent exudate, which indicates infection.
741
Gastrointestinal intubation
742
Nutrition management
7. Recognize that patients with an ileus that persists for longer than
4 days or those unable to meet caloric needs enterally may require
total parenteral nutrition.
743
Fear
related to potentially threatening situation (e.g., serious injury,
hospitalization) and supported by presence of pain, unfamiliarity, and
noxious environmental stimuli present in critical care area;
communication barrier (e.g., intubation); sensory impairment from direct
injuries.
Goals/Outcomes: The patient exhibits decreased symptoms of
fear: apprehension, tension, nervousness, tachycardia,
aggressiveness, and withdrawal.
Fear Control.
Anxiety reduction
744
understanding) for necessary treatments.
Vision Compensation Behavior: Cognitive Orientation.
3. For the patient with cutaneous burn injury, explain why tactile
sensation is decreased or absent. If the patient’s eyelids are swollen
shut because of facial edema, reassure the patient that he or she is
not blind and that swelling will resolve within 3 to 5 days. Apply
eye lubricant, as prescribed, for those patients with excessive
swelling and/or inhibited blink.
Positioning
745
possible, combine when medicated with analgesics for other
procedures and during activities of daily living.
746
National Headquarters Office, website: www.ameriburn.org,
phone: (312) 642-9260; the Phoenix Society for Burn Survivors, Inc.,
National Headquarters Office, website: www.phoenix-society.org,
phone: (800) 888-2876.
Deficient knowledge
related to lack of knowledge regarding ability for self-care management
and/or use of resources for supportive care.
Goals/Outcomes: Within 24 hours of initiation of acute care, the
patient and significant others verbalize knowledge about prescribed
medications and techniques that facilitate continued wound healing
and limb mobility.
Knowledge: Medication; Knowledge: Treatment Regimen.
747
Additional nursing diagnoses
For other nursing diagnoses and interventions, see the following, as
appropriate: Nutrition Support, (Chapter 1); Mechanical
Ventilation, (Chapter 1); Prolonged Immobility, (Chapter 1);
Compartment Syndrome/Ischemic Myositis, (Chapter 3); Emotional
and Spiritual Support of the Patient and Significant Others,
(Chapter 2).
Compartment syndrome/ischemic
myositis
Pathophysiology
Compartment syndrome is caused by pathologic elevation of
intercompartmental pressures within nonexpansible tissue
envelopes. The pressure increase may come from either an increase
in volume within a tissue compartment or externally applied
pressure compressing a tissue compartment. While pressure within
the anatomic space increases, local perfusion is compromised,
leading, if untreated, to irreversible damage of the tissues within
the compartment. Compartment syndrome is a surgical emergency
that requires rapid intervention to prevent permanent cosmetic or
functional deformity or loss of limb. Compartment syndrome may
be acute or chronic (exercise-related forms); this section focuses on
the acute peripheral type.
Most compartment syndromes are associated with trauma, but
the condition may also occur from multiple other etiologies
including reperfusion injuries, ischemia, burns, prolonged limb
compression, drug abuse, or poor positioning during prolonged
surgical procedures (Table 3-8). The incidence of compartment
syndrome in those younger than 35 years is increased probably
secondary to the larger muscle mass contained within the
osteofascial space.
Any muscle may be affected as long as the pressure within a
muscle is sustained for a prolonged period of time. Most often the
muscles affected are those that are contained within an osteofascial
748
space in the upper or lower extremity. The most common site in the
upper arm is the forearm. The forearm contains two compartments:
the volar and dorsal. The volar compartment contains the flexors of
the wrist and fingers and the dorsal compartment contains the
extensors. The lower extremity contains a total of seven
compartments: three in the thigh and four in the calf. The three
compartments of the thigh are the anterior, posterior, and medial.
The calf compartments are the anterior, lateral/peroneal, deep
posterior, and superficial posterior. The tibial nerve lies within the
posterior compartment and provides sensation to the plantar
surface of the foot and flexion of the toes. The anterior
compartment contains the peroneal nerve providing sensation to
the first web space and motor function of the extensors of the calf
and foot. The anterior compartment of the calf is the most common
site of compartment syndrome.
Increased and sustained pressure within a muscle compartment
can develop because of increased volume in the compartment from
a hematoma or edema. A second etiology is prolonged ischemia,
which may be as a result of external compression or arterial
compromise. Finally, compartment syndrome may be caused by
decreased overall size of the muscle compartment from scar
formation, especially following circumferential burns (see Table 3-
8).
Regardless of the etiology or location, ischemia begins when the
metabolic demands of the tissues cannot be met. The normal
pressure in muscle compartments is less than 10 to 12 mm Hg.
Whitesides’ theory states that the development of compartment
syndrome depends on both the intracompartmental pressure and
the systemic BP. The diastolic BP minus the compartmental
pressure should be greater than 30 mm Hg to avoid ischemia in the
tissues. Thus, increasing the compartmental pressure or decreasing
the perfusion pressure can each lead to a compartment syndrome.
When injury occurs, the depletion of intracellular energy stores
causes cellular swelling and increasing venous pressures, allowing
edema to develop and local blood flow to decrease. Lymphatic
drainage initially increases and then decreases as a result of
congestion from the growing tissue edema. Compartmental tissue
pressure increases, compromising capillary blood flow. Histamine
749
is released, producing vasodilation and increased capillary
permeability. Rising compartmental pressure further increases
venous congestion and results in reduction in the arteriovenous
pressure gradient, reducing local tissue perfusion and further
increasing capillary pressure. Fluids and proteins escape from the
capillaries and contribute to even higher tissue pressures. The
higher tissue pressures eventually exceed both capillary and venous
pressures, stopping nutrient blood flow and promoting further
ischemia. Local blood flow to muscles is severely compromised
when the interstitial tissue pressure equals or exceeds the diastolic
pressure. As a result of impaired venous return, anaerobic
metabolism creates more lactic acid, which stimulates vasodilation
further, decreasing BP and elevating tissue pressure. The pressure
within the compartment continues to increase, equaling or
exceeding the capillary pressure and leading to arteriolar
compression, causing further ischemia of the muscle and nerves.
Sustained hypotension and shock are associated with greater
incidence of compartment syndrome resulting from the lowered
pressure gradient. Less compartmental pressure is needed to result
in arteriolar spasm and ischemic changes in the muscles.
The earliest signs of compartment syndrome are often subtle but
are primarily neurologic as a result of the susceptibility to hypoxia
of the nonmyelinated sensory fibers. Sensory changes in the
extremity begin with paresthesias or hyperesthesias within 30
minutes of the onset of ischemia and may become functionally
irreversible after 12 to 24 hours. The average interval between the
initial injury to the compartment and the beginning symptoms of
compartment syndrome is 2 hours. Compartmental tissue ischemia
that lasts longer than 6 hours results in muscle necrosis and
irreversible tissue changes.
Late-onset compartment syndrome is seen in patients who are
comatose or confused and who are unable to communicate
symptoms. Late-onset compartment syndrome is often more
difficult to recognize and manage, sometimes worsening following
treatment with fasciotomy. The late syndrome may occur in
compartments already treated with fasciotomy. Healthy
granulation tissue may cover necrotic muscle within partially
opened compartments. With sufficient muscle tissue injury (e.g.,
750
after crush injuries) or undiagnosed compartment syndrome,
rhabdomyolysis may develop with the release of metabolic toxin
and intracellular components, especially myoglobin. The release of
toxins can result in secondary myoglobinemia, leading to acute
tubular necrosis, which may progress to acute kidney injury and
multisystem failure.
• Patients admitted for acute renal failure after treatment for crush
injuries or compartment syndrome should be suspected of having
late-onset or continuing compartment syndrome.
Table 3-8
CAUSES OF COMPARTMENT SYNDROME
751
Vital signs
• Hypotension potentiates compartment syndrome.
Early indicators
Late findings
• Paralysis.
Palpation
752
• Feel for temperature of affected area; polar (coolness) of affected
area is a late sign.
753
pressure.
Near-infrared Based on the different light absorption More studies are needed,
spectroscopy properties, NIRS can measure the local but NIRS may provide
(NIRS) changes in concentration of oxygenated and the benefit of a rapid,
deoxygenated hemoglobin and perfusion in continuous, noninvasive,
different tissues including muscle. sensitive, and specific
tool for early detection of
acute compartment
syndrome.
754
Compartmental pressure monitoring continues to be the preferred
method of definitive diagnosis of acute compartment syndrome.
Several methods of direct compartment measurement exist
including the needle manometer, the wick catheter, and the slit
catheter. Continuous readings are not possible with the needle
manometer method and may result in falsely high levels caused by
the injection of saline into the muscle. Pressures within
compartments may be continuously monitored with either the wick
method or the slit catheter method by attaching a pressure
transducer to an implanted catheter within a muscle compartment.
Indications for continuous or intermittent pressure monitoring are
in the patient who is unconscious, children or other patients
difficult to assess, patients with nerve injury, and those with
multiple orthopedic traumas. Regardless of technique,
compartmental pressures greater than 30 mm Hg above the
systemic diastolic pressure indicate the need for a compartment
fasciotomy.
Early indicators
Collaborative management
Care priorities
755
circumferential casts and padding or dressings; escharotomy for
circumferential burns or frostbite.
2. Manage pain
Analgesia: Parenteral opiates often with sedative adjuncts.
756
Multiple methods of wound closure have been used, including
mechanical closure devices, dynamic skin sutures, vacuum-
assisted closure, and healing by secondary intention.
6. Renal protection
757
• Administer 500 mL/h IV crystalloid solution and
22.4 mEq bicarbonate (total 12 L/day, prompting
diuresis of approximately 8 L/day).
Circulatory precautions
758
1. Monitor neurovascular status of injured extremity at least every 2
hours.
• Pallor.
• Polar (coolness).
• Pulselessness.
• Paresthesia.
• Paralysis.
759
9. Monitor tissue pressures continuously, with an
intracompartmental pressure device if needed.
HIGH ALERT!
Pressures greater than 10 mm Hg may reflect significant
elevation. Myoglobinuria may indicate that rhabdomyolysis has
ensued, which if not immediately managed may lead to acute renal
failure.
Acute pain
related to physical factors (tissue ischemia) secondary to compartment
syndrome.
Goals/Outcomes: Throughout the hospitalization, the patient’s
pain is controlled, as reflected by a pain scale. Nonverbal indicators
of discomfort (e.g., grimacing) are reduced or absent. Within 2
hours of admission, the patient verbalizes understanding of the
need to report uncontrolled or increasing pain.
Pain Control; Comfort Level.
Pain management
760
noncommunicative or of low-level intellect may require a simpler
or different pain scale.
Infection protection
761
1. Monitor the patient for fever, increasing pain, and laboratory
data indicative of infection (e.g., increased WBC count or
erythrocyte sedimentation rate).
762
Body image enhancement
2. Provide time for the patient to share feelings about his or her
changed appearance and function. Encourage questions and
discussion of these feelings with the patient’s significant others.
Drowning
Incidence
Drowning accounts for over 4000 deaths annually in the United
States according to the Centers for Disease Control and Prevention
and 388,000 deaths worldwide according to the World Health
Organization, making drowning the third leading cause of
unintentional deaths worldwide. The highest mortality rates are in
children younger than 5 years of age; drowning occurs more
763
frequently among males than females.
Pathophysiology
Drowning is defined as a process of experiencing respiratory
impairment from submersion/immersion in a liquid by the World
Health Organization. The terms drowning and near-drowning are
often used to distinguish between individuals who die within 24
hours of the drowning incident and those who live 24 hours or
longer following the incident (termed “near-drowning”).
Individuals classified as “near-drowning” may eventually die from
the submersion/immersion. Healthcare providers cannot always
determine who will die within the first 24 hours. Both populations
receive the same treatment. The 2010 American Heart Association
guidelines support these definitions to maintain consistency in the
reporting of data related to drowning. A current term used to
describe patients who survive a submersion is nonfatal drowning.
The main effects of drowning are decreased lung compliance,
ventilator-perfusion mismatch, and intrapulmonary shunting
leading to hypoxemia and decreased oxygen delivery to the tissues,
which can lead to failure of multiple organs, most importantly, the
CNS. Hypotension, pulmonary edema, hypothermia, and
respiratory and metabolic acidosis occur after nonfatal drowning,
compounding the detrimental effects of the hypoxemia. In addition
to the neurologic deficits from cerebral anoxia, acute lung injury or
acute respiratory distress syndrome, pneumonia, acute renal failure
secondary to acute tubular necrosis, and DIC can occur. Cervical
SCI is not common in nonfatal drowning. Any aspirated
contaminants (e.g., algae, chemicals, sand) may cause or contribute
to obstruction and lead to asphyxiation. Bacterial pneumonia can
develop, depending on the type of contaminant in the aspirant, and
chemical pneumonitis can occur if gastric contents were aspirated.
Drowning was formerly categorized by the type of water
(freshwater versus saltwater) and whether the person aspirated
fluid into the lungs (wet versus dry drowning). These distinctions
are thought to be irrelevant in providing care to patients following
nonfatal drowning.
764
Wet versus dry drowning
An individual experiencing the drowning process will initially
attempt to hold their breath. During breath holding there is some
degree of laryngospasm that is followed by falling oxygen levels
and increasing carbon dioxide levels in the blood. Eventually, the
drive to breathe takes over and the individual begins to aspirate
fluid into the lung (wet drowning). In individuals with prolonged
laryngospasms, oxygen tension drops and the laryngospasm
eventually subsides, prompting aspiration of water before cardiac
arrest. Other causes of cardiac arrest are possible in individuals
found in water without water in their lungs (dry drowning).
765
resuscitation. Resuscitation should be continued until the victim is
rewarmed to at least 32° C (89.6° F), because the heart may start
beating at that temperature. The adage, “a patient is not dead until
warm and dead,” describes the need to ensure that proper
rewarming has occurred in all patients who are hypothermic before
pronouncing them dead. Many medications used during
resuscitation are ineffective until the patient is warmed.
Resuscitation remains possible after 30 minutes of submersion.
Resuscitation efforts frequently should be continued for at least 1
hour.
Assessment: Drowning
Goal of system assessment
Evaluate for respiratory and neurologic functioning, as well as
determining if concurrent injuries were sustained such as head
and/or spinal trauma.
Vital signs
• Temperature may be low if drowning occurred in cold water.
• Hypotension.
766
• RR may be increased with dyspnea or may be absent if arrest has
occurred. Absent respiratory effort may indicate a high cervical
spinal cord injury (SCI).
Observation
Evaluate for signs of trauma to head and neck, skin coloring as an
indication of hypoxia, signs of neurologic functioning including
pupil size and equality and response to stimuli.
Palpation
• Evaluate skin for temperature, neck for deformities, and head for
signs of trauma including swelling.
Auscultation
Evaluate lung fields to identify abnormal breath sounds.
767
Collaborative management
Care priorities
The primary goal of treatment is to restore ventilation and correct
hypoxemia and acidosis. Once ventilation is normal, hypoxemia
and acidosis may resolve without further treatment; however,
many patients, especially those submerged for more than a few
minutes may require additional measures. The following
treatments may be required:
768
goal is to rewarm as safely and quickly as possible to achieve a
normal core temperature. Care must be taken not to rewarm too
quickly because blood can pool in the extremities, especially with
external rewarming strategies, prompting hypotension. IV fluids
should also be warmed to prevent further exacerbation of the
hypothermia. Rewarming cannot be safely accomplished as quickly
as cooling.
6. Consider bronchoscopy
To remove aspirated contaminants, if necessary.
769
oxygenation
Extracorporeal membrane oxygenation (ECMO), if available,
may be useful when the patient is unable to maintain good
oxygenation despite intubation and mechanical ventilation.
770
Impaired gas exchange
related to asphyxiation and aspiration
Goals/Outcomes: Within 12 hours of initiation of treatment, the
patient has adequate gas exchange, as evidenced by the following
ABG values: PaO2 greater than 80 mm Hg and Paco2 less than 45 mm
Hg. Within 3 days of treatment, RR is less than 20 breaths/min with
normal depth and pattern; breath sounds are clear and bilaterally
equal; and the patient is oriented to time, place, and person
(depending on degree of permanent neurologic impairment).
Respiratory Status: Gas Exchange.
Respiratory monitoring
Oxygen therapy
771
1. Administer supplemental oxygen using liter flow and device as
ordered.
Mechanical ventilation
772
4. Administer muscle paralyzing agents, sedatives, and narcotics
analgesics as appropriate.
Hypothermia
related to immersion in cold water
Goals/Outcomes: Within 24 hours of initiating therapy, the
patient’s core temperature increases to 35° C to 37° C (95° F to 98.6°
F). BP, RR, and HR are normalizing for the patient.
Thermoregulation.
Hypothermia treatment
773
lights, warmed baths, warmed blankets, forced air warming
blankets), as appropriate. Do not attempt surface or external
warming until core temperature is within acceptable limits (i.e., 35°
C to 37° C [95° F to 98.6° F]). Premature surface rewarming can lead
to the return of cold blood to the heart and precipitate an “after
drop” in core temperature.
Infection protection
774
Pelvic fractures
Pathophysiology
The pelvis is composed of three bones: two innominate bones and
the sacrum. The innominate bones are each composed of three
bones (ilium, pubis, and ischium) that fuse after childhood. The two
innominate bones are joined by the symphysis pubis, a fibrous
cartilage joint that connects the two pubic bones anteriorly; they are
attached posteriorly to a third bone, the sacrum, by a system of
ligaments termed the posterior osseous ligamentous structures. Many
blood vessels run through the pelvis and join to form the large
venous plexus.
MVCs and auto-pedestrian trauma cause approximately two
thirds of all pelvic fractures, which have a mortality rate of up to
50% in some studies. A large force is needed for a pelvic fracture to
occur, because these bones are stabilized by a strong network of
ligaments. Pelvic fractures have been classified by several systems,
but perhaps the most helpful are the systems that classify fractures
by their stability and the mechanism of injury (Table 3-9). Pelvic
fractures are considered stable fractures when the posterior osseous
ligamentous structures are intact. An unstable pelvic fracture occurs
when the osseous ligamentous structures are disrupted posteriorly
and portions of the pelvis can move in any direction.
Table 3-9
CLASSIFICATION OF PELVIC FRACTURES
Pelvic fractures are most commonly classified using one of two systems: the Tile Classification
System and the Young Classification System.
1. Tile Classification System: Focuses on whether the posterior sacroiliac complex is intact:
• Type A Injuries: The sacroiliac complex is intact with a pelvic ring stable fracture that can be
managed without surgery.
• Type B Injuries: The posterior sacroiliac complex is partially disrupted, are often unstable,
and result from internal rotational forces.
• Type C Injuries: The posterior sacroiliac complex is completely disrupted, have both
rotational and vertical instability, and result from motor vehicle collisions, a fall from great
heights, or severe compression.
775
contralateral to a posterior injury.
• Grade I: Associated sacral compression on side of impact.
• Grade II: Associated posterior iliac (“crescent”) fracture on side of impact.
• Grade III: Associated contralateral sacroiliac joint injury.
776
a pelvic fracture have a 20% mortality rate. Older adults have more
problems related to preexisting conditions. Cardiovascular disease
often causes insufficient compensatory function to manage the
stress of injury. Despite a less severe mechanism of injury, rates of
sepsis and death are higher in older adults than in patients with
trauma who are younger than 65 years with similar injuries.
• Age.
• Smoking.
• Previous hysterectomy.
• Use of anticoagulants.
777
deformation.
• Fracture of the pelvic ring in more than one place that results in
displacement.
Vital signs
• Temperature may be low if the patient is developing shock.
Observation
Evaluate for signs of trauma to the abdominal and pelvic regions.
Palpation
The pelvis is palpated by placing inward and posterior compression
on the iliac crests.
778
• Assess for pain with palpation.
779
besides the pelvic fracture. If contrast
extravasation or a false aneurysm is
identified, then embolization can be done.
Angiography is currently the gold standard
for diagnosis of arterial bleeding secondary
to pelvic fracture.
Collaborative management
Care priorities
• A sheet wrapped around the pelvis and secured with towel clips.
780
If abnormal shortening or rotation has occurred with the injury,
the lower extremities should be supported and stabilized in the
position in which they were found. A backboard supported by
pillows, towels, or blankets taped in place with cloth tape are used
until a traction splint can be applied.
781
by eliminating the deadly triad of acidosis, hypothermia, and
coagulopathy. See Major Trauma for further discussion of massive
transfusion protocols. Some studies have supported withholding
aggressive fluid resuscitation until after operative or embolic repair
because an increase in MAP will increase intravascular hydrostatic
pressure and may increase bleeding from torn vessels.
782
place, and person without restlessness or confusion.
Tissue Perfusion: Peripheral; Blood Loss Severity.
Hemorrhage control
Hypovolemia management
5. Monitor serial Hct and Hgb values. While the circulating volume
is restored, hemoconcentration is no longer present and Hct returns
to within normal limits (WNL).
783
fluid administration (shortness of breath, tachypnea, excessive
urine output).
Infection prevention
5. Encourage rest.
784
Impaired physical mobility
related to limitation in movement of pelvis needed to stabilize fracture
with fixation device and other loss of joint movement or ability to ambulate
independently.
Goals/Outcomes: The patient will not develop complications of
impaired mobility such as skin breakdown on any dependent areas
or areas involved with fracture stabilization; venous
thromboembolism; or constipation.
Immobility Consequences: Physiologic.
Positioning
785
4. Monitor fixation/traction devices for proper setup, and maintain
position and integrity of traction when repositioning the patient.
786
sexual assault and rough consensual sexual intercourse. Injury to
the vulva or penis is uncommon and should alert one for prompt
screening for interpersonal violence. Pathophysiology for renal and
LUT trauma is shown in Table 3-10.
Table 3-10
PATHOPHYSIOLOGY FOR RENAL AND LOWER URINARY TRACT
TRAUMA
787
Goal of system assessment
Identify specific location of physical injuries and presence of signs
and symptoms indicating injury to organs affected by the renal
system or surrounding organs.
HIGH ALERT!
Gross hematuria is present in only slightly more than half of
patients with renal trauma and is considered an unreliable
diagnostic sign.
788
• Ureter trauma: Gross hematuria may be present; if the ureter is
transected, normal urine from the unaffected kidney may still be
voided. Late signs may include fever and flank or abdominal
discomfort. Urine may be found at the entrance or exit sites of
penetrating abdominal wounds or wounds of the middle to lower
back areas.
HIGH ALERT!
Physical signs may be masked because the kidneys are located
beneath abdominal organs, back muscles, and bony structures.
Vital signs
• Hypotension.
• Tachycardia.
Palpation
789
• Bladder trauma: Suprapubic tenderness.
Inspection
• Digital rectal examination to check for rectal tone, gross blood,
and the position of the prostate. Posterior urethral disruption
may result in a “high riding” prostate in males, which moves
away from the examiner during the procedure. The finding
indicates rupture of the urethra, which requires surgical repair or
“railroading” as soon as the patient’s general condition permits.
Diminished rectal tone may indicate SCI or imply that the patient
engages in anal intercourse.
Collaborative management
Care priorities
2. Manage pain
790
• Phenazopyridine (Pyridium) is a urinary antispasmodic agent
that helps to relieve burning and frequency.
791
Catheterization
792
Table 3-11 for examples of procedures for the various types of
renal and LUT injuries.
Table 3-11
SURGICAL PROCEDURES FOR RENAL AND LOWER URINARY
TRACT TRAUMA
Type of
Surgical Indications/Surgical Management
Injury
Minor renal Conservative management. Rest and observation with careful follow-up to
trauma prevent progressive deformity and to evaluate blood pressure.
Major renal Surgical intervention if hypotension and hemodynamic instability occur.
trauma
Critical renal Immediate surgical exploration; low rates of renal salvage.
trauma
Proximal Primary ureterostomy with end-to-end anastomosis.
ureteral
injury
Distal Ureteral stenting or percutaneous nephrostomy, depending on location and
ureteral extent of injury.
injury
Bladder Use of urinary or suprapubic drainage. Surgical repair may be indicated.
injury
Urethral Urinary or suprapubic catheterization is used for long-term management.
injury
Table 3-12
AMERICAN ASSOCIATION FOR THE SURGERY OF TRAUMA
ORGAN INJURY SEVERITY SCORE FOR THE KIDNEY
793
2 Parenchyma Laceration less than 2 cm in depth and into the cortex, small hematoma
contained within Gerota fascia
Collecting No injury
system
3 Parenchyma Laceration greater than 1 cm in depth and into the medulla, hematoma
contained within Gerota fascia
Collecting No injury
system
4 Parenchyma Laceration through the parenchyma into the urinary collecting system
Collecting Vascular segmental vein or artery injury
system Laceration, one or more in the collecting system with urinary
extravasation
Renal pelvis laceration and/or complete ureteral pelvic disruption
5 Vascular Main renal artery or vein laceration or avulsion main renal artery or vein
thrombosis
From Buckley JC, McAninch JW: Revision of the current American Association for
the Surgery of Trauma Renal Injury Grading System. J Trauma 70:35-37, 2011.
794
• Difficult or unsuccessful urinary catheterization.
• Hematuria.
795
Urinary Catheterization; Fluid Management; Fluid
Monitoring; Tube Care: Urinary.
Infection protection
2. Record the color and odor of urine each shift. Culture urine
specimen when signs or symptoms of infection are present.
5. Assess catheter exit site each shift for the presence of erythema,
swelling, or drainage.
796
the physician of purulent or foul-smelling drainage. Consider
obtaining a culture.
Pain management
797
5. Implement nonpharmacologic measures for coping with pain:
diversion, touch, and conversation.
Thoracic trauma
Pathophysiology
Thoracic trauma may be caused by blunt or penetrating injuries to
the chest, back, flanks, and upper abdomen region. Thoracic trauma
accounts for up to 60% of all trauma-related deaths in the United
States. Careful assessment is needed to quickly identify life-
threatening injuries to the heart, lungs, and great vessels. Close
monitoring is required to prevent complications secondary to
injuries that develop over the first 24 hours, such as pulmonary
contusions.
Thoracic injuries can result from both direct and indirect forces.
Direct force such as direct impact involving an object can result in
bony fractures, tissue bruising, and ruptured organs. Indirect forces
can cause tissues to stretch beyond their limits and can result in
tears leading to rupture of blood vessels and disruption of organs,
such as the bronchus and esophagus. Thoracic injuries often lead to
problems with ventilation, oxygenation, and perfusion, causing a
decrease in the delivery of oxygen and nutrients to the tissues.
The lungs are often affected by space-occupying injuries, such as
hemothoraces, pneumothoraces, and hemopneumothoraces, which
compress lung tissue, interfering with lung expansion, thereby
limiting the amount of ventilation and decreasing oxygen exchange
at the alveoli level. The most serious of these injuries is a tension
pneumothorax where the pressure in the chest is so high that not
only is oxygenation impaired but also venous return to the heart is
diminished, leading to decreased CO and shock.
One of the most common thoracic injuries is contusions to the
lungs. When the lung tissue is bruised, alveolar hemorrhage and
parenchymal destruction occur, leading to both local and systemic
consequences. The reduced compliance impairs ventilation and
causes an increase in shunting with decreased pulmonary blood
798
flow. Hypoxemia and hypercarbia develop and usually worsen
over the following 72 hours.
Blunt thoracic trauma can cause injury to the heart muscle by one
or more of the following four mechanisms: compression of the heart
between the sternum and vertebrae, bruising of heart tissue by
bony structures, rupture or compression of coronary arteries by the
blow, or cardiac rupture caused by intrathoracic or intraabdominal
pressure. Causes of blunt cardiac injury are MVCs, direct blows to
the chest, falls from great heights, sporting and industrial injuries,
and kicks from animals. There are no reliable diagnostic tests to
identify blunt cardiac injury. Cardiac injury is considered
significant when the patient has new findings, such as new
dysrhythmias, abnormal cardiac wall motion, or injury to the heart.
Penetrating thoracic trauma is caused by gunshot wounds, stab
wounds, or foreign bodies entering the chest or upper abdomen.
Open chest injuries can result in an open pneumothorax or
lacerations to the lung tissue or the airways, heart, great vessels,
and/or the esophagus. Penetrating injuries to the heart are the most
common cause of intrapericardial hemorrhage.
Vital signs
• RR may be increased if hypoxia is present.
• BP may be decreased.
799
Observation
Check chest for signs of trauma and chest excursion.
Percussion
• Percuss over the lung fields to identify areas of hyperresonance,
indicating a collection of air in the pleural space. Dullness may
indicate atelectasis or a collection of blood in the pleural space.
Palpation
• Over the ribs, sternum, and scapula to identify areas of
tenderness and step-offs.
Auscultation
• Lung fields to identify abnormal breath sounds.
800
• Muffled heart sounds may indicate a pericardial tamponade.
Assessment
The nurse and interdisciplinary team assess for the following
common injuries.
Pneumothorax/tension pneumothorax
• Chest pain.
• Respiratory distress.
• Hypoxia.
• Tachycardia.
Hemothorax
• Chest pain.
• Respiratory distress.
Flail chest
• Hypoxia.
801
• Decreased chest excursion resulting from pain.
Pulmonary contusion
• Hypoxia.
• Respiratory distress.
• Arrhythmias.
• Chest pain.
Aortic trauma
• Hypotension/hypertension.
• Tachycardia.
802
803
Collaborative management
Collaborative management should start with addressing the ABCs
as outlined in the section on Major Trauma, including oxygen, IV
fluids, and blood as indicated. During the initial assessment, several
conditions involving injuries to the thoracic organs may warrant
immediate intervention. These include the following:
• Open pneumothorax.
• Tension pneumothorax.
• Massive hemothorax.
• Flail chest.
• Cardiac tamponade.
Care priorities
With pulmonary injuries, interventions are directed toward
managing acute respiratory compromise while correcting the
underlying injuries that may cause deterioration in the patient’s
condition. Intervention should be aimed at correcting and
preventing hypoxia. With cardiac and great vessel injuries, the care
priorities are focused on stopping hemorrhage, restoring perfusion,
and supporting cardiac function.
804
2. Restore intrathoracic negative pressure
805
breathing. Opioid analgesics are used cautiously to avoid
respiratory depression. An epidural patient-controlled analgesia
pump or an intercostal nerve block may help to relieve local rib
pain.
806
hospital. Repair using endovascular stenting has been shown to
decrease patient morbidity.
807
Ineffective breathing pattern
related to pulmonary and/or cardiac injury
Goals/Outcomes: Within 24 hours of this diagnosis, RR stabilizes
to 12 to 20 breaths/min with normal work of breathing; lung injuries
are managed to provide expanded lungs with minimal fluid and/or
blood accumulation in the thoracic cavity; sources of bleeding are
identified and managed to provide adequate Hgb level for
adequate oxygenation; lost intravascular volume is replaced to
reflect a CVP of 6 to 12 mm Hg; oxygen saturation is at least 95%,
with PaO2 at least 80 mm Hg with oxygen and Paco2 less than 45 mm
Hg with (or without) mechanical ventilation; and HR is 60 to 100
bpm with BP stable (at least 100 mm Hg systolic and 60 mm Hg
diastolic).
Respiratory Status: Ventilation.
Airway management
Ventilation assistance
Respiratory monitoring
808
3. Initiate and maintain a continuous temperature-monitoring
device.
Decreased CO
related to cardiac injury or ineffective cardiac compensatory response to
oxygenation or perfusion deficits.
Goals/Outcomes: Within 24 hours of this diagnosis, the patient
exhibits adequate CO, as evidenced by BP within normal limits for
the patient; HR 60 to 100 bpm; normal sinus rhythm on ECG;
peripheral pulses at least 2+ on a 0-to-4+ scale; warm and dry skin;
hourly urine output at least 0.5 mL/kg; measured CO 4 to 7 L/min;
CVP 2 to 6 mm Hg; PAP 20 to 30/8 to 15 mm Hg; PAWP 6 to 12 mm
Hg; and patient awake, alert, oriented, and free from angina pain.
Blood Loss Severity, Cardiac Pump Effectiveness.
Hemorrhage control
Shock management
809
Hgb levels, CO), if available.
810
neuronal damage, vascular insufficiency, and inflammation. The
cerebral vasculature and skull are often damaged. Tissue stresses
result in contusions, diffuse axonal injuries, and compression
injuries. Biomolecular processes cause neuroexcitation and
deafferentation of the neurons. The neuroexcitatory injury activates
excitatory neurotransmitters (glutamate and aspartate), which
depolarize neurons. This neurotransmitter surge causes aberrant
cell signaling, leading to long-lasting or permanent neuronal
dysfunction. Deafferentation destroys the neurofilament of the
axon, and the axon swells and retracts. Reduced blood flow,
through cerebral edema or vasoconstrictive mechanisms, causes
ischemia and augments cell death.
Outcome after TBI can be predicted to some extent based on the
type of lesion, severity of injury, and length of coma. Age, preinjury
medical status, mechanism of injury, ICP, and brainstem integrity
are important factors influencing outcome.
Box 3-1
811
INITIAL HISTORY TAKING OF PATIENTS
IN MOTOR VEHICLE COLLISIONS
(BYSTANDERS, PASSENGERS, AND
RESCUE PERSONNEL)
• Extent of damage to the vehicle
• Approximate speed
• Alcohol or drugs?
812
of injuries in the cerebral cortex, brainstem, or cerebellum may
change CPP. Severity of brain injuries is classified using the GCS:
mild (GCS score = 13 to 15), moderate (GCS score = 9 to 12), and
severe (GCS score ≤8). The FOUR score (Full Outline of
UnResponsiveness) has been used with increasing frequency as a
predictor of outcomes in patients with TBI. Verbal assessment is not
possible with intubated patients using the GCS, which also lacks
testing of brainstem reflexes. The FOUR score features four
elements: eye, motor, brainstem, and respiration with a maximum
score of 4 points for each element. The FOUR score provides
additional details lacking in the GCS, can recognize locked-in
syndrome, assesses brainstem reflexes, breathing patterns, and can
recognize the different stages of herniation. Specific injuries arising
from the mechanical forces are as follows:
813
disorientation); moderate (brief loss of consciousness, transient
focal neurologic deficits); or severe (prolonged loss of
consciousness with sustained neurologic deficits lasting less than
24 hours). No changes are seen on CT scan, but patients with
neurologic deficits require observation.
• Extra axial: Injuries are located outside the brain and are
attributable to forces that disrupt the superficial layers of the
brain resulting in bleeding (see Hematomas discussed later).
814
• Linear skull fractures: Nondisplaced, associated with low-velocity
impact.
Vascular injuries
Vascular injuries are intrinsic brain injuries resulting from impact
force that causes bleeding of cerebral arteries or veins. These
injuries usually accompany moderate and severe primary injuries.
Neurologic complications
Herniation syndromes
815
Displacement of a portion of the brain through openings within the
intracranial cavity that result from increased ICP. Herniation occurs
when there is a pressure difference between the supratentorial
and infratentorial compartments within the skull. When herniation
occurs, significant portions of the cerebral vasculature are
compressed, destroyed, or lacerated, resulting in ischemia, necrosis,
and ultimately death.
816
bilaterally. Symptoms of increased ICP often occur too rapidly to
be observed. Changes in respiratory patterns may not be seen in
patients who are critically ill and mechanically ventilated,
depending on mode of ventilation (e.g., controlled or intermittent
mandatory ventilation).
• Mental status
• Cranial nerves
• Motor status
• Sensory status
• Reflexes
817
part of the neurologic assessment.
The following are assessment findings related to specific types of
brain injuries.
• Headache
818
• Comminuted fractures are open wounds with or without dural
tears, CSF leak, and transcalvarial herniation.
Concussion
• Headache, although there are no overt signs of injury
• Dizziness
• Vomiting
• Memory loss
HIGH ALERT!
Moderate and severe injuries require close observation because
cerebral edema and increased intracranial pressure can develop.
Changes in behavior, level of consciousness, or refractory
intracranial pressure require an immediate computed tomography
scan.
Contusion
• Loss of consciousness is common. May have surface bruising of
face or scalp along with hematoma.
819
prolonged and recovery of function is minimal to moderate.
Subdural hematoma
• With acute subdural hematoma, neurologic deterioration is seen
within 24 to 72 hours (or earlier), changing LOC, ipsilateral
dilated pupil, and contralateral extremity weakness.
HIGH ALERT!
Neurologic signs associated with a chronic subdural hematoma
may occur weeks or months after injury.
Subarachnoid hemorrhage
• Severe headache often reported as “the worst headache of my
life.”
• Changes in LOC.
820
leg when thigh is flexed on abdomen).
Intracranial hematoma
• Neurologic deficits are based on the site and severity of injury.
821
external stimulus (i.e., auditory, of the cortex or ascending
visual, somatosensory). Evoked pathways of the spinal cord,
potentials are used to determine brainstem, or thalamus
the extent of injury in patients who
are uncooperative, confused, or
comatose.
CSF analysis Evaluate for infection and bleeding Abnormal color,
turbidity/cloudiness, red blood
cell (RBC) and white blood cell
(WBC) counts, protein, glucose,
electrolytes, gram stain, culture,
and sensitivity.
Laboratory work Evaluate for metabolic imbalances, Can indicate infection, anemia,
WBCs infection, coagulation status, nutritional deficiencies,
Hemoglobin bleeding, and drug use. electrolyte imbalances, and drug
Hematocrit use. All need to be monitored
Partial thromboplastin closely during emergency and
time, prothrombin acute phases.
time/international
normalized ratio
Electrolyte panel
Glucose
Osmolality
Alcohol and urine drug
screen (admission)
Collaborative management
Care priorities
1. Surgical intervention
822
• Subdural hematomas or intracerebral hemorrhage are more
common in patients on clopidogrel (Plavix), aspirin, warfarin, or
other anticoagulants.
• For patients on warfarin with INR greater than 1.2, infuse fresh-
frozen plasma, or factor VII, and administer vitamin K until INR
is in nontherapeutic range (less than 1.2). Monitor PT/INR daily
and continue infusion of fresh-frozen plasma and administration
of vitamin K based on results.
HIGH ALERT!
There are no evidence-based studies for reversing
coagulopathies because patients’ response to medication is very
individual. These strategies are aimed at monitoring the
coagulopathy while they wax and wane over the postoperative
course.
823
3. Management of ICP dynamics
Table 3-14
TYPES OF INTRACRANIAL MONITORING
3-1
RESEARCH BRIEF
Intracranial pressure (ICP) monitoring is indicated for patients
with a Glasgow Coma Scale (GCS) score ≤8 after resuscitation and
an abnormal admission computed tomography (CT) scan.
Placement of an ICP monitor is also suggested in patients who
have a GCS ≤8 with a normal CT scan and if two or more of the
824
following are noted on admission: (1) the patient is older than 40
years, (2) the patient has unilateral or bilateral abnormal posturing,
or (3) the patient’s systolic blood pressure is less than 90 mm Hg.
Physician discretion may also determine the use of ICP monitoring.
Adapted from Brain Trauma Foundation: Guidelines for the management of severe head
injury. J Neurotrauma 24(Suppl 1):S1-S106, 2007.
825
• Used to measure cerebral oxygenation by determining oxygen
content of cerebral venous blood as a global measurement of
oxygen supply and demand. Three types of blood flow can be
discriminated:
HIGH ALERT!
Optimal management of a severe traumatic brain injury should
include monitoring of cerebral perfusion pressure (CPP),
intracranial pressure (ICP), and PbTO2, as well as ventilation
management. ICP threshold should be less than 20 mm Hg,
optimal CPP is 50 to 70 mm Hg, and optimal PbTO2 is greater than
20 mm Hg. While ICP rises and PbTO2 falls, it may be necessary to
adjust the Fio2 to keep PbTO2 greater than 20. It is not uncommon
for Fio2 to be 0.1 or 100% to maintain adequate cerebral
826
oxygenation. PaO2 less than 60 mm Hg should be avoided.
8. Hyperosmolar therapy
827
MAP and thus CPP. Glucose solutions are not used for fluid
resuscitation in TBI.
828
contusions, lacerations, and penetrating injuries.
Table 3-15
ANALGESICS AND SEDATIVES RECOMMENDATIONS FOR USE IN
TRAUMATIC BRAIN INJURY
829
• Barbiturate coma: A less-often used method of reducing
metabolic demand, barbiturate administration, is recommended
to control ICP refractory to standard medical and surgical
treatment.
830
HIGH ALERT!
Normal temperatures range from 35.8° C to 37.5° C (96.4° F to
99.5° F) with a diurnal variation of 1° C. Rectal temperatures are
0.2° C to 0.6° C higher than oral and can be 0.8° C higher than right
atrial, esophageal, and oral temperatures. Evaluation of the
etiology of fever is important with brain injury, because it
influences treatment choice.
HIGH ALERT!
Shivering increases metabolic demand and may increase
intracranial pressure. Shivering may be controlled by wrapping
distal extremities in bath towels before initiating hypothermia or
using chlorpromazine (Thorazine), which, must be used with
caution because it may cause hypotension. Research on use of
831
hypothermia in treatment of acute brain injury is evolving. If used,
follow a strict hypothermia protocol. Currently, there is no support
for prophylactic hypothermia.
HIGH ALERT!
All nursing care activities that increase intracranial pressure
(ICP) should be spaced to enable a return of ICP to baseline and
maximizing of cerebral perfusion pressure. Clustering nursing care
such as bathing, turning, and suctioning creates a stair-step rise in
ICP. Sustained increases (longer than 5 minutes) should be
avoided.
832
• Turning: Turning is necessary to prevent pressure ulcer formation
and is not contraindicated. Individual patient responses to
turning should be evaluated. Initially, turning from side to side
will elevate pressure, but ICP should return to resting baseline
after a few minutes. If ICP does not return to resting baseline
within 5 minutes, CPP may be compromised and the patient
should be returned to a position that reduces ICP and maximizes
CPP. Hip flexion also increases ICP. If independent nursing
activities do not decrease ICP, then medical protocols must be
used.
Table 3-16
MANAGEMENT OF SEVERE BRAIN INJURY
Level of
Treatment Recommendation
Evidence*
Blood pressure Level II† Avoid early postinjury episodes of hypotension <90 mm Hg.
Oxygenation Level III Avoid Pao2<60 mm Hg and O2 saturation <90%.
ICP treatment Level II Treatment to lower ICP should be initiated at 20 mm Hg.
threshold
CPP treatment Level III CPP should be maintained at ≥50 mm Hg. Maintain MAP >90
mm Hg.
Cerebral Level III Keep PbTO2>20.
oxygenation
Hyperventilation Level II Avoid prophylactic hyperventilation; hyperventilate for short
duration for refractory increased ICP >25 mm Hg.
Level III Avoid hyperventilation in the first 24 hours postinjury.
833
Hyperosmolar Level II Mannitol: use intermittent boluses of 0.25 to 1 mg/kg.
therapy
Option Hypertonic saline (3%). No recommended dose.
Barbiturates Level II May be considered in patients with hemodynamic stability
refractory to other methods to reduce ICP.
Propofol Level II Use for control of ICP.
Glucocorticoids Standard Use is not recommended.
Nutrition Level II Full caloric replacement by postinjury day 7
Seizure Level II Anticonvulsants can be considered an option for high-risk
prophylaxis patients early after injury.
Box 3-6
GUIDELINES FOR SUCTIONING
SECRETIONS FROM PATIENTS AT RISK
FOR INCREASED INTRACRANIAL
PRESSURE
• Suction only if the clinical status of the patient warrants.
834
• Use a suction catheter with an outer-to-inner diameter ratio of 2:1.
835
result of prolonged bed rest. There is concern for the use of
anticoagulation therapies because there is risk for expansion of
intracranial hemorrhage. There is level III support for the
prophylactic use of low–molecular-weight heparin or
unfractionated heparin along with mechanical measures to
prevent DVT (sequential compression devices); however, there is
no evidence to support optimum doses or time when to begin
therapy. Clinical practice guidelines for TBI also support the use
of graduated compression stockings, unless the lower extremity
injuries prevent their use. However, there are no
recommendations for the therapeutic treatment of DVT or PE.
DVT management is determined by the attending physician
based on risk-benefit ratios.
17. Glucocorticoid
836
18. Rehabilitation
Respiratory monitoring
837
1. Assess the patient’s RR, depth, and rhythm. Auscultate lung
fields for breath sounds every 1 to 2 hours and as needed. Monitor
for respiratory patterns described in Table 3-13. Be alert to IICP (see
Box 7-1).
Table 3-13
ASSESSMENT OF CENTRAL AND UNCAL HERNIATIONS
838
Modified from Plum F, Posner J: Diagnostic of stupor and coma, ed 3, Philadelphia,
1980, Davis.
Infection protection
839
infection. Be alert to elevated temperature and increased HR and
BP.
5. Other infection sites: Monitor for signs of UTI if the patient has
an indwelling Foley catheter. Monitor other injury and surgical
sites.
9. Apply basic principles for care of any invasive device used with
ICP monitoring:
840
causing straining and agitation.
Neurologic monitoring
1. Assess neurologic status at least hourly (GCS and FOUR score are
commonly used). Monitor pupils, LOC, and motor activity; also
perform cranial nerve assessments (see Appendix 3). A decrease in
LOC is an early indicator of IICP. Changes in the size and reaction
of the pupils, a decrease in motor function (e.g., hemiplegia,
abnormal flexion posturing), and cranial nerve palsies.
841
is greater than 50 mm Hg. Be alert to decreases in mean systolic
arterial BP (less than 80 mm Hg) or increases in MAP. Perform
ongoing assessment of ICP, CPP, and PbTO2 recording levels
hourly until stable. Consult the physician if pressure changes
significantly (e.g., ICP greater than 20 mm Hg; PbTO2 less than 20
or other preestablished ranges for PbTO2). Perform ongoing
calibration and zeroing of transducer to ensure accuracy of
readings.
Box 3-7
NURSING INTERVENTIONS FOR
PATIENTS WITH INCREASED
INTRACRANIAL PRESSURE
• Maintain head of bed elevation at level that keeps intracranial
pressure (ICP) less than 20 mm Hg and cerebral perfusion
pressure (CPP) greater than 50 mm Hg.
842
• Maintain head in neutral position.
Ineffective thermoregulation
related to trauma associated with injury to or pressure on the
hypothalamus.
Goals/Outcomes: The patient becomes normothermic within 24
hours of the diagnosis.
Thermoregulation.
Temperature regulation
843
6. As prescribed, administer antipyretics such as acetaminophen.
9. Assess for possible drug fever reaction, which can occur with
antimicrobial therapy.
Fever Treatment.
Positioning
5. For the patient with spasticity, use foot cradles to keep linens off
the feet. To maintain dorsiflexion, provide the patient with shoes
that are cut off at the toes, with the shoes ending just proximal to
the head of the patient’s metatarsal joints. Because there is no
844
contact of the balls of the feet with a hard surface, the risk of
spasticity will be minimized. Consult the occupational therapist for
use of splints or other supportive device.
Risk identification
3. Lubricate the patient’s eyes every 2 hours with isotonic eye drops
or ointment.
845
Aneurysm and Subarachnoid Hemorrhage (Chapter 7). As
appropriate, see nursing diagnoses and interventions under
Alterations in Consciousness (Chapter 1), Care of the Patient after
Intracranial Surgery (Chapter 7), and Meningitis (Chapter 7). See
Risk for Trauma in Status Epilepticus (Chapter 7). Also see nursing
diagnoses and interventions under Nutrition Support (Chapter 1),
Mechanical Ventilation (Chapter 1), Hemodynamic Monitoring
(Chapter 1), Prolonged Immobility (Chapter 1), Emotional and
Spiritual Support of the Patient and Significant Others (Chapter 2).
The patient with craniocerebral trauma is at risk for diabetes
insipidus and syndrome of inappropriate antidiuretic hormone. See
Diabetes Insipidus (Chapter 8) and Syndrome of Inappropriate
Antidiuretic Hormone (Chapter 8).
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CHAPTER 4
Respiratory disorders
Respiratory assessment: General
Goal of system assessment
Evaluate for ineffective breathing patterns, impaired gas exchange,
and airway obstruction.
858
Continuous pulse oximetry (SpO2
monitoring)
• Evaluate for changes over time and/or since the last recorded
reading. Results should be correlated with the arterial oxygen
saturation (SaO2) readings derived from arterial blood gases
(ABGs).
Observation
• Evaluate for use of accessory muscles, shortness of breath, and air
hunger.
859
therapy so that appropriate liter flow is determined to prevent
respiratory impairment.
Auscultation
• Listen to breath sounds to evaluate for presence of adventitious
sounds that reflect factors contributing to respiratory distress,
including those related to both airway obstruction and impaired
gas exchange.
860
Screening labwork
• ABG analysis can reveal increases or decreases in pH; levels of O2,
O2 saturation, CO2, and bicarbonate; base excess or base deficit
indicative of impending respiratory failure;
hyperpnea/tachypnea; and metabolic derangements affecting
breathing patterns. Blood gas analysis may be done using either
arterial blood or mixed venous blood samples. Mixed venous
blood samples are available only using a pulmonary artery
catheter and can be used to calculate efficacy of both O2 delivery
and O2 consumption. ABGs cannot be used to calculate O2
consumption.
861
Respiratory Status: Gas Exchange, Symptom Control Behavior,
Comfort Level, Endurance.
Ventilation assistance
862
10. Provide chest physical therapy as appropriate, if other methods
of secretion removal are ineffective.
Oxygen therapy
863
higher concentrations of O2 (greater than 45% Fio2) for longer than
24 hours. Changes will be apparent in chest radiograph and breath
sounds. Absorption atelectasis may be present. The higher the O2
concentration, the greater is the chance of toxicity.
Respiratory monitoring
864
7. Evaluate changes in SaO2, SpO2, ETco2, ScVO2, and ABGs as
appropriate.
865
and eventually mucus plugging, which further decreases airflow.
Eventually, irreversible changes in airway structure occur,
including fibrosis, smooth muscle hypertrophy, mucus
hypersecretion, injury to epithelial cells, and angiogenesis. Persons
with asthma eventually develop air trapping, increased functional
residual capacity, and decreased forced vital capacity. Several types
of cells and cellular elements are affected including mast cells,
epithelial cells, T lymphocytes, macrophages, eosinophils, and
neutrophils, which when triggered can sometimes prompt sudden,
fatal exacerbations of coughing, wheezing, chest tightness, and
breathlessness.
Life-threatening asthma exacerbation results from bronchial
smooth muscle contraction (bronchospasm), bronchial
inflammation leading to airway edema, and mucus plugging. When
an episode of bronchospasm (critical airway narrowing) is not
reversed after 24 hours of maximal doses of traditional inhaled
short-acting beta2-adrenergic agonists (SABAs) such as albuterol or
levalbuterol, injected systemic beta2-agonists such as epinephrine,
inhaled anticholinergics such as ipratropium, and systemic steroid
therapy with prednisone, prednisolone, or methylprednisolone, the
refractory patient may be diagnosed with status asthmaticus.
Common triggers for asthma exacerbations include respiratory tract
infections, allergens (airborne or ingested), air pollutants, smoke,
and physical irritants (e.g., cold air, exercise). Anxiety or “panic”
attacks and use of beta-adrenergic blocking agents and nonsteroidal
antiinflammatory drugs (NSAIDs) may predispose patients to
development or exacerbation of severe asthma. Activities that
prompt deeper inhalation, such as vigorous laugher or physical
exertion, can trigger an episode. Exercise-induced asthma or
exercise-induced bronchospasms are well recognized in the
literature.
Several clinical patterns for development of an asthma
exacerbation are recognized. An “attack” can happen suddenly
(over several hours) or it may take several days to reach critical
airway obstruction. The more common gradual presentation
manifests with increasing symptoms of sputum production,
coughing, wheezing, and dyspnea. As air trapping increases, lung
hyperinflation prompts increased work of breathing. Rapid
866
exhalations increase insensible water loss through exhaled water
vapor and diaphoresis. Oral intake may be decreased, contributing
to hypovolemia. Without adequate oral intake to promote
hydration, mucus becomes thick and begins to plug the airways.
Terminal bronchioles can become occluded completely from
mucosal edema and tenacious secretions. Ventilation-perfusion
mismatch or shunting occurs as poorly ventilated alveoli continue
to be perfused, which leads to hypoxemia. Tachycardia is an early
compensatory mechanism to increase O2 delivery to the body cells,
but it increases myocardial O2 demand. Oxygen requirements and
work of breathing increase, leading to respiratory failure,
hypercapnia, and respiratory arrest if not managed promptly and
appropriately.
Assessment
Goal of system assessment
• Evaluate for ineffective breathing patterns, impaired gas
exchange, and airway obstruction.
For asthma
867
disease are at higher risk of asthma.
868
following endotracheal intubation, general anesthesia, and
ventilation provided during surgical or other invasive
procedures. Impaired cough, hypoxemia, and hypercapnia may
trigger exacerbation.
869
• Hypotension may be present; hypotension is exacerbated by
underlying dehydration often present in patients with severe
asthma.
Observation
• Severe attacks render patients unable to speak resulting from
breathlessness.
Auscultation
• Wheezing bronchial breath sounds; wheezing on inspiration is
more indicative of acute airway narrowing, versus wheezing on
expiration, which is more common.
870
Palpation
• Palpate to assess for chest expansion; chest may be hyperinflated
or may be asymmetrical; chest expansion during inspiration may
be decreased.
Percussion
• May reveal hyperresonance (pneumothorax), a complication of
asthma.
Screening labwork
• Complete blood count (CBC) with white blood cell (WBC)
differential: Evaluates for elevated WBCs indicative of chronic
inflammation as a result of allergic response and infection
including presence of eosinophils, neutrophils, and mononuclear
cells.
4-1
RESEARCH BRIEF
Important changes in prescribing practices resulting from recent
studies are occurring in primary care. The Asthma Clinical
Research Network is reporting evidence that improvement in FEV1
(forced expiratory volume in 1 second) in response to albuterol is a
reliable predictor of improved asthma control using tiotropium, a
long-acting muscarinic antagonist. This holds particular promise
for long-term control in patients with severe asthma. There is
evidence supporting improvement in lung function with
tiotropium as an add-on therapy to inhaled corticosteroids and
long-acting beta-agonists. These practical studies are examples of
what is commonly referred to as real-world research, an effort to
investigate the patient’s disease course at the interface of their daily
871
life and activities. Patient-reported outcome measures (PROMs) are
guiding investigators toward a better appreciation of the relevance
of investigational end points. Improvements in PROMs include
morning peak expiratory flow and asthma control days among
other outcomes.
From Peter SP, Bleecker ER, Kunselman SJ, et al: Predictors of response to tiotropium
versus salmeterol in asthmatic adults. J Allergy Clin Immunol 132:1068-1074, 2013.
872
tests/spirometry FEV1 (forced expiratory volume in 1 acute episodes; if less than
second)/FVC (forced vital capacity). If peak 0.7, narrowed airways
expiratory flow (PEF) rate does not improve prevent forceful exhalation
with initial aggressive inhaled of inspired volume (Table 4-
bronchodilator treatments, morbidity 1).
increases. PEF rate: Less than 100 to
125 L/min in a normal-sized
adult indicates severe
obstruction to air flow.
Pulse oximetry Noninvasive technology that measures the Normal Spo2: Greater than
(SpO2) oxygen saturation of arterial blood 95%. Correlation of Spo2
intermittently or continuously using a probe with Sao (arterial
2
placed on the patient’s finger or ear. When
using pulse oximetry, it is helpful to obtain saturation) is within 2%
when Sao2 is greater than
ABG values to compare the oxygen
saturation and evaluate the Pao2, Paco2, and 50%. Temperature, pH,
Paco2, anemia, and
pH.
hemodynamic status may
reduce the accuracy of pulse
oximetry measurements.
Presence of other forms of
hemoglobin in the blood
(carboxyhemoglobin or
methemoglobin) can
produce falsely high
readings.
Serologic studies Acute and convalescent titers are drawn to Increased antibody titers: A
diagnose a viral infection. positive sign for viral
infection.
Chest radiograph Evaluates the severity of air trapping; also Lung hyperinflation: Caused
useful in ruling out other causes of by air trapping
respiratory failure (e.g., foreign body Flat diaphragm: Related to
aspiration, pulmonary edema, pulmonary increased intrathoracic
embolism, pneumonia). volume.
12-Lead ECG Evaluates for dysrhythmias associated with Sinus tachycardia: Important
(electrocardiogram) stress response and asthma medications. baseline indicator; use of
some bronchodilators (e.g.,
metaproterenol) may
produce cardiac stimulant
effects and dysrhythmias.
Sputum Gram Culture and sensitivity may show Gross examination may
stain, culture, and microorganisms if infection is the show increased viscosity
sensitivity precipitating event. or actual mucous plugs.
The most reliable specimens are obtained Gram stain positive: Indicates
via bronchoalveolar lavage (BAL) during organism is present.
bronchoscopy, or using a protected Culture: Identifies organism.
telescoping catheter (mini-BAL or using Sensitivity: Reflects
BAL) to decrease the risk of effectiveness of drugs on
contamination from oral flora. identified organism.
Diagnostic fiber Obtains specimens during simple Gram stain positive: Indicates
optic bronchoscopy bronchoscopy without contaminating the organism is present.
using a PSB aspirate; modified technique (mini-BAL) is Culture: Identifies organism.
(protected also effective without the need of full Sensitivity: Reflects
specimen brush) bronchoscopy. effectiveness of drugs on
and BAL identified organism.
Serum theophylline Important baseline indicator for patients Acceptable therapeutic
level who take theophylline regularly; range is 10 to 20 µg/mL.
873
therapeutic level is close to toxic level. If There is little evidence to
additional theophylline is given, serial support clinical benefit for
levels should be measured within the first adding theophylline to
12 to 24 hours of treatment and daily inhaled beta-adrenergic
thereafter. Patients are monitored for side blocking agents and steroids
effects (e.g., nausea, nervousness, for patients with acute,
dysrhythmias). severe asthma who were not
already using theophylline
regularly.
Collaborative management
Care priorities
The goal of asthma management is to control the disease using a
stepwise approach to therapies. Ideal control is attained when
patients are free of daytime symptoms, do not awaken breathless or
coughing at night, have few or no limitations on activities, do not
regularly use rescue medications, have no exacerbations, and
maintain a forced expiratory volume in 1 second (FEV1) and/or
peak expiratory flow rate (PEFR) greater than 80% of the predicted
value. When prevention fails, the potential for life-threatening
respiratory failure is high during exacerbations unresponsive to
treatment within the first hour. Management is directed toward
decreasing bronchospasm and increasing ventilation. Other
interventions are directed toward treatment of complications (Table
4-1).
Table 4-1
PULMONARY FUNCTION TESTS IN ASTHMA EXACERBATION
874
1. Determine severity of asthma exacerbation
2. Oxygen therapy
Patients have profound hypoxia and can tolerate high doses of O2
(Fio2) unless they retain CO2 and breathe by hypoxic drive. Most
patients with asthma are able to tolerate high flow O2, versus those
with other obstructive lung disease who cannot. Oxygen dosage
must be limited in nonintubated, mechanically ventilated patients
who breathe via hypoxic drive to avoid hypoventilation and
respiratory arrest. Humidified O2 therapy is begun immediately to
correct hypoxemia and thin secretions. PaO2 is maintained slightly
above normal unless the patient retains CO2 to compensate for the
increased O2 demands imposed by the increased work of breathing.
The degree of hypoxemia and patient response determines the
method of O2 delivery. A high-flow device (e.g., 100%
nonrebreather mask) delivers more precise and higher Fio2.
Management of anxiety must be considered, especially if the patient
will not wear a mask because of feelings of suffocation.
3. Heliox therapy
875
A blended mixture of helium and O2, available in mixtures of 60:40,
70:30, and 80:20, which is delivered either through a tight-fitting
face mask or through a mechanical ventilator circuit. Heliox
reduces the turbulent flow of air in narrowed airways. Helium is
not as dense as nitrogen, which accounts for the decreased
turbulence, therefore reducing the work of breathing and
improving gas exchange. Findings of upper airway sounds in the
bronchopulmonary system are inconsistent with the diagnosis of
asthma. The advanced practice provider should be consulted for
further actions should auscultation reveal this finding.
876
functional airways. SABAs are the mainstay of asthma
exacerbation management, whereas long-acting beta-adrenergic
agonists (LABAs) are used for long-term control of asthma.
Theophylline and aminophylline are no longer recommended for
management of acute bronchospasms.
877
with therapy. These agents depress the central nervous system
(CNS) response to hypoxia and hypercapnia. Once mechanical
ventilation is in place, the dosage is titrated until the patient is
comfortable and/or hypoxemia or hypercapnia begins to resolve.
Table 4-2
MEDICATIONS USED FOR ASTHMA EXACERBATION*
*
Recommendations originate from the National Institutes of Health (NIH) Expert
Panel on the Diagnosis and Management of Asthma (2007). Intravenous
theophylline and magnesium are not recommended for general use in a hospitalized
patient with acute asthma by the NIH guidelines. A 20-minute intravenous
magnesium sulfate infusion for poorly responding patients is recommended by the
British Thoracic Society guidelines. All patients receiving theophylline before
hospitalization should have a theophylline level determined before a loading dose is
given.
878
6. Fluid replacement
To liquefy secretions and replace insensible losses. Generally,
crystalloid fluids (e.g., 5% dextrose in water [D5W], 5% dextrose in
normal saline [D5NS]) are used.
7. Chest physiotherapy
Generally contraindicated in acute phases of exacerbation because
of acute respiratory decompensation and hyperreactive airways.
Once the crisis is over, the patient may benefit from percussion and
postural drainage every 2 to 4 hours to help mobilize secretions.
Ventilation assistance
879
respiratory failure and near-fatal asthma exacerbation.
Mechanical ventilation
880
(DHI) causing pressure increases inside the thorax, which impede
venous return to the heart.
Cough enhancement
881
respiratory failure. If the patient can manage to take deep breaths,
respiratory failure is manageable.
9. Explain that the patient may need to repeat this technique several
times before the cough becomes productive.
Asthma management
882
6. Note onset, frequency, and duration of coughing and advise the
patient to avoid triggers of coughing if identified.
Table 4-3
STEPPED MEDICATION MANAGEMENT FOR ASTHMA CONTROL
883
*
Information based on National Institutes of Health Asthma Management Guidelines
(2007). Retrieved from www.nhlbi.nih.gov/health-pro/guidelines/current/asthma-
guidelines. Accessed February 6, 2014.
CNS, Central nervous system; DPI, dry powder inhaler; HFA, hydrofluoroalkanes
(ozone-benign propellant for inhalation); ICS, inhaled corticosteroid; IgE,
immunoglobulin E; LABA, long-acting beta2-agonist; LTRA, leukotriene receptor
antagonist; MDI, metered dose inhaler; PUD, peptic ulcer disease; SABA, short-
acting beta2-agonist; SVT, supraventricular tachycardia.
Anxiety reduction
884
anxiety, which can increase O2 demands.
885
ventilation failure or hypercapnia. A wide variety of disease states
create a single or mixed respiratory failure. One of the simplest
methods of evaluating patients relates to the understanding of basic
gas exchange. Oxygenation occurs primarily during inspiration and
the removal of CO2 occurs during exhalation. The basic concepts
applied here include compliance and recoil. Lung compliance is the
measure of expansion of the alveoli (the gas-exchanging surface),
which occurs on inspiration, whereas elasticity refers to the ability
of the alveoli to recoil, as they do on exhalation. Restrictive airway
diseases generally present with significant hypoxemia, whereas
obstructive disorders are more likely to develop a persistent and
chronic hypercapnia. See Box 4-1 for a description of some of the
disease processes that can lead to acute respiratory failure.
Box 4-1
DISEASE PROCESSES LEADING TO THE
DEVELOPMENT OF RESPIRATORY
FAILURE
Obstructive disease states, impaired exhalation, impaired
minute ventilation, CO2 retention
886
effusion, pneumothorax, kyphoscoliosis, obesity, diaphragmatic
paralysis)
• Pulmonary emboli
• Atelectasis
• Pneumonia
• Bronchiolitis
Diffusion disturbances
• Pulmonary/interstitial fibrosis
• Pulmonary edema
The terms acute lung injury (ALI) and ARDS were historically
used to differentiate and describe a continuum of lung dysfunction.
ARDS was defined in 1994 by the American-European Consensus
Conference. Many concerns regarding the evaluation methods and
categorization of lung dysfunction and interventions have evolved
since that time. In 2011, the Berlin definition equalized the
diagnosis and divided the disorder by levels of hypoxemia, as well
as Fio2 and PEEP requirements (Table 4-4).
Table 4-4
STAGING ACUTE RESPIRATORY DISTRESS SYNDROME BASED
ON BERLIN DEFINITIONS
887
Mild Pao2/Fio2 < 200 mm Hg Pao2/Fio2 < 300 mm Hg with PEEP or
CPAP ≥5 cm H2O
Moderate Pao2/Fio2 < 100 mm Hg Pao2/Fio2 < 200 mm Hg with PEEP or
CPAP ≥5 cm H2O
Severe Pao2/Fio2 < 100 mm Hg with PEEP or
CPAP ≥5 cm H2O
888
noncompliant, derecruited, and gas dysfunctional state.
The evaluation of respiratory failure includes the understanding
of the following:
Match
This general term refers to the relationship of gas distribution ( )
to the amount of blood ( ), which passes the total alveolar
surface in 1 minute of time. Normal alveolar ventilation occurs at a
rate of 4 L/min, and normal pulmonary vascular blood flow occurs
at a rate of 5 L/min. The normal ratio is therefore 4 L/min
divided by 5 L/min, or a ratio of 0.8, almost in a 1:1 ratio. Any
disease process that interferes with either side of the equation
upsets the physiologic balance, causing a mismatch.
889
must be interpreted in conjunction with the volume exhaled,
especially in patients who are mechanically ventilated. Many
vagaries of CO2 flux can be eliminated by controlling ventilation
and muscular activity. Current evidence supports that the
overdistension and shear force of opening-closing also profoundly
affect the healthy lung.
Intrapulmonary right-to-left shunt: Large amounts of blood pass
from the right side of the heart to the left side of the heart and out
into the general circulation without adequate oxygenation. This
process occurs when alveoli are not recruited on inspiration
resulting from atelectasis or the alveoli are flooded. Primary causes
of intrapulmonary shunt are atelectasis and ARDS.
ARDS is primarily defined once the injury creates a hypoxemia
requiring intubation and mechanical ventilation. The presence of
refractory hypoxemia in conjunction with diffuse pulmonary
infiltrates in the absence of left atrial hypertension is considered to
be the primary indicator of the continuum of acute respiratory
failure. Despite advances in the treatment of the primary
inflammatory process and progress in the method of ventilatory
support, the continuum of ALI/ARDS continues to be associated
with high morbidity and mortality, reaching greater than 60%.
Since 1964, when the continuum was first described, the
understanding of the etiology, pathophysiology, and epidemiology,
as well as the relationship of genetic prodrome and ventilator-
induced lung injury process, has significantly increased (Table 4-5).
Table 4-5
RISK FACTORS FOR ACUTE RESPIRATORY DISTRESS
SYNDROME
Assessment
890
Goal of system assessment
Evaluate for decreasing PaO2/Fio2 and increasing requirements for
pressure control and PEEP. (See Acid-Base Imbalances, Chapter 1).
Vital signs
• If breathing spontaneously (with or without ventilation support),
RR may be rapid and compensatory for metabolic acidosis.
• May present with ashen, pale, or gray/blue facial color, lip color,
or nail beds.
891
• Chest expansion may be decreased, restricted, or asymmetrical
with severe changes in one lung manifesting severe atelectasis or
pleuritic pain.
• The patient with a loss of lung function will have a decreased P/F
ratio (defined later). Initially, there may be a shift from volume
control ventilation to pressure control as well as an increase in
PEEP (see Table 4-1).
892
tachycardia, diaphoresis, and mental obtundation.
Auscultation
• Decreased or bronchial breath sounds.
Palpation
• Palpate chest wall for tenderness indicative of inflammation.
Percussion
• May reveal presence of consolidation or fluid (dullness) or
hyperresonance (pneumothorax).
Screening labwork
• CBC: Evaluates for elevated WBCs indicative of infection.
Bandemia (immature neutrophils) of greater than 10% is
especially concerning.
893
systemic infection.
A-a gradient/A-aDO2/P(A-a)o2
• P/F ratio: The PaO2 divided by the Fio2 (PaO2/Fio2 ratio known as
the P/F ratio) can be used to more simply assess the severity of
the gas exchange defect. The normal value for the ratio of the
partial pressure of arterial blood O2 to Fio2 {PaO2/Fio2} (Fio2 is
expressed as a decimal ranging from 0.21 to 1.00) is 300 to 500. A
value of less than 300 indicates gas exchange derangement, and a
value below 200 or greater than 40% Fio2 is indicative of severe
impairment and is a major component of the diagnostic criteria
for ARDS. The inverse relationship of the P/F and the A to a
894
difference is important to consider when discussing the level of
gas exchange failure.
Diagnostic tests
Diagnostic Tests for Acute Respiratory Distress Syndrome
895
Collaborative management
Maintaining adequate arterial oxygenation while protecting the
functional lung is the highest priority in both traditional and more
recent approaches to ventilator management for ARDS. Careful
consideration should be given to evaluate neurologic conditions
and OSA because these are commonly overlooked causes of
respiratory failure. In addition, the primary goal is to determine
896
and treat the underlying pathophysiologic condition.
Care priorities
897
volutrauma and pressure trauma, both of which cause
overdistension and stimulation of inflammation. Lung-
protective ventilator strategies are considered standard practice
in the care of patients with ARDS. To minimize ventilator-
induced lung injury, attention is directed at avoidance of alveolar
overdistension and cyclical opening and closing. The lowest
possible plateau pressure and tidal volume should be selected. A
reasonable target tidal volume in patients who are mechanically
ventilated is 6 mL/kg. A topic of much controversy is the optimal
setting of PEEP.
4-2
RESEARCH BRIEF
Evidence suggests that higher positive end-expiratory pressure
(PEEP) should be used for moderate and severe acute respiratory
distress syndrome (ARDS), whereas lower PEEP may be more
appropriate in patients with mild ARDS. PEEP should be set to
maximize alveolar recruitment while avoiding overdistension.
Volume and pressure limitation during mechanical ventilation can
be described in terms of stress and strain. Fraction of inspired
oxygen and PEEP are typically titrated to maintain arterial oxygen
saturation (SpO2) of 88% to 95% (PaO2 55 to 80’ mm Hg).
From Biehl M, Kashiouris MG, Gajic O: Ventilator-induced lung
injury: minimizing its impact in patients with or at risk for ARDS.
Respir Care 58:927-937, 2013.
898
in the dependent areas of the lung. Repositioning the patient at
least every 2 hours is indicated in patients with hypoxemia;
however, if staffing allows and the patient can tolerate it, more
frequent (every 30 minutes) turning could be beneficial.
Continuous lateral motion therapy beds may also be used to
continuously turn the patient. Motion therapy assists in the
redistribution of interstitial edema and may improve
oxygenation.
4-3
RESEARCH BRIEF
Successful early mobilization of patients who are critically ill can
reduce several complications including atelectasis and ventilator-
associated pneumonia and shorten ventilator time. In addition,
evidence shows that cognitive and functional limitations may last 1
to 5 years after discharge from the intensive care unit (ICU).
A schedule of repositioning every 2 hours was not superior to
every 4 hours to prevent pressure ulcers in ICU patients under
mechanical ventilation and on modern support surfaces. These
position changes require a higher nursing workload and increases
the likelihood of an adverse effect.
From Manzano F, Colmenero M, Perez-Perez AM, et al:
Comparison of two repositioning schedules for the prevention of
pressure ulcers in patients on mechanical ventilation with
alternating pressure air mattresses. Intensive Care Med 40:1679-1687,
2014.
899
Usually, the patient’s cardiac output is supported with fluid
therapy. The balance between dehydration and euvolemia is a
difficult one to achieve. New measures of total blood volume and
arterial stroke volume may assist the provider in achieving
adequate fluid without causing volume overload. The use of
crystalloid versus colloid fluids has been and remains controversial,
but the SAFE Study Investigators (2004) validated that the use of
colloids in the general population of patients did not improve
outcomes but significantly increased cost. More recently, concerns
have been studied regarding the presence of extravascular lung
water.
4-4
RESEARCH BRIEF
Managing thirst in the patient who is mechanically ventilated can
be challenging. Thirst is a prevalent, intense, and distressing
symptom in patients in the intensive care unit. Simple bundled
therapies including ice water spray, mouth hygiene, and lip
wetting reduced the perception and memory of severe thirst.
Integrating this practice with routine thirst assessment can relieve
one of the most distressing symptoms experienced by patients who
are critically ill.
From Rose L, Nokoyama N, Rezai S, et al: Psychological
wellbeing, health related quality of life and memories of intensive
care and a specialised weaning centre reported by survivors of
prolonged mechanical ventilation. Intensive Crit Care Nurs 30:145-
151, 2013; Puntillo K, Arai SR, Cooper BA, et al: A randomized
clinical trial of an intervention to relieve thirst and dry mouth in
intensive care unit patients. Intensive Care Med 40:1295-1302, 2014.
4. Reduce anxiety
Before any medication is administered, the provider must ascertain
that the ventilation is tailored to the patient. This can best be
evaluated by analyzing the volume-pressure loop and the flow/time
graph. The respiratory therapist is an invaluable resource for this
900
method of evaluation. After ensuring adequate ventilation, many
patients will require anxiety reduction with medication such as
fentanyl and anxiolytics. Those patients who cannot be adequately
oxygenated and ventilated with mechanical ventilation may be
given anxiety-reducing agents such as propofol and
dexmedetomidine. A sedation scale and protocol should be used to
standardize this practice. The use of sedating agents has been
linked to ICU delirium and post-ICU syndrome. In addition, the
bedside nurse must ascertain if the patient is in pain and administer
analgesics appropriately. A wide variety of pain scales can be used
effectively.
Patients who are unable to achieve appropriate ventilation as a
result of agitation and dyssynchrony or are hemodynamically
unstable may require heavy sedation with agents such as propofol
(Diprivan) or, in extreme cases, the diaphragm may need to be
paralyzed with a neuromuscular blocking agent such as
vecuronium bromide (Norcuron) or cisatracurium (Nimbex).
Although very user-dependent, train of four should be performed
when evaluating level of pharmacologic paralysis. The caregiver
must recognize that, although the patient who is pharmacologically
paralyzed may appear to be resting quietly or may even be
comatose, he or she may be alert and extremely anxious because of
the total lack of muscle control. These patients must receive
appropriate sedation (e.g., lorazepam [Ativan]) and analgesia (e.g.,
morphine), and they will require expert psychosocial nursing
interventions. (See Sedating and Neuromuscular Blockade, Chapter
1.) When patients appear agitated, ventilation should be evaluated
first (as long as the patient is not in danger of extubation or self-
harm) followed by pain evaluation and analgesia, followed by
anxiety-relieving medications. Neuromuscular paralysis should be
performed as a last resort and only when necessary to control
ventilation.
901
patient’s caloric and metabolic needs to make certain that the
patient is being adequately nourished but not overfed. All efforts
should be made to feed enterally so that the gut is used. Newer
elemental feedings require no digestion and can be used in the
stomach, duodenum, or jejunum. (See Nutrition Support, Chapter
1.)
4-5
RESEARCH BRIEF
Risk Factors for Physical Impairment After Acute Lung Injury in a
National Multicenter Study
The investigators of this study set out to determine what risk
factors could be found that predicted physical impairment after
acute lung injury/acute respiratory distress syndrome (ALI/ARDS).
They evaluated patients enrolled from the ARDS Network studies
around the United States using the physical measures from the
Short Form-36 (SF-36). At 6 and 12 months, strength was 92% and
93% of maximal strength, 6-minute walk distance was 64% and
67% of predicted values, and SF-36 Physical Function Score was
61% and 67% of predicted values.
When adjusted for risk and acuity, corticosteroid dosage and
intensive care unit length of stay were highly associated with poor
or reduced physical outcomes.
From Needham DM, Wozniak AW, Hough CL, et al: National Institutes of Health NHLBI
ARDS Network. Am J Respir Crit Care Med 189:1214-1224, 2014.
902
decreases.
Respiratory Status: Ventilation, Vital Signs Status;
Respiratory Status: Gas Exchange, Symptom Control Behavior,
Comfort Level, Endurance.
Respiratory monitoring
903
equipment at the bedside.
904
Acute pneumonia
Pathophysiology
Pneumonia is the ninth leading cause of death in the United States
and the leading cause of death as a result of infectious disease
(www.cdc.gov/Features/Pneumonia/). The hallmark
pathophysiology of pneumonia is inflammation of the lung
parenchyma, which include the alveolar spaces, respiratory
bronchioles, and interstitial tissue. Pneumonia can be classified as
community-acquired pneumonia (CAP) or hospital-acquired
pneumonia (HAP).
Predisposing factors in the development of pneumonia are
immunosuppression and neutropenia. The microorganisms
involved include bacteria, protozoa, fungi (Candida, Aspergillus),
and viruses (cytomegalovirus). Patients who have a severely
compromised immune system, that is, acquired immune deficiency
syndrome, are most often infected by Pneumocystis jirovecii, a
fungus.
Sepsis, septic shock, respiratory failure, ARDS, emphysema,
or lung abscesses are complications of pneumonia that may require
intensive critical care. Those with the highest risk are older adults,
the very young, and those with chronic medical conditions.
Common disorders include COPD, cardiac disease, diabetes
mellitus, liver disease, renal disease, or cerebrovascular disease,
malignancy, or an immunocompromised state.
Community-acquired pneumonia
Pneumonia that occurs outside of the inpatient or “in facility”
healthcare environment is associated with high mortality and
morbidity rates. The most common pathogen is Streptococcus
pneumoniae. Approximately 4 million patients develop CAP
annually, resulting in 600,000 hospitalizations at a cost of
approximately $23 billion. Mortality rates range from 5.1% for
patients who are hospitalized and ambulatory to 36.5% for patients
requiring critical care. The disease occurs in all age groups but is
most common in those from the mid-50s to the late 60s.
905
Nosocomial pneumonia
Nosocomial pneumonia is the second most common cause of
hospital infections and has proven to be a fatal complication for
many patients, especially the critically ill. The three types of
nosocomial pneumonia are hospital acquired pneumonia (HAP),
which transpires 48 hours or more after hospital admission noting
that the infection was not incubating at the time of admission.
Healthcare-associated pneumonia includes patients with recent
hospitalization within 90 days of infection, exposure to healthcare
environments such as nursing homes, long-term care facilities, and
chronic hemodialysis; and receiving IV antimicrobial therapy,
chemotherapy, or wound care with 30 days of pneumonia. The final
type is ventilator-associated pneumonia (VAP), which develops 48 or
more hours after ET intubation. VAP has been very difficult to
define, resulting in inconsistent tracking and reporting of the
hospital-acquired condition. VAP is now part of a broader
classification of conditions associated with mechanical ventilation
termed ventilator-associated events (VAEs). For practical purposes,
HAP is the term used in this chapter to cover all the
aforementioned types.
A diagnosis of HAP requires new or advanced infectious
infiltrate on chest imaging and the presence of two of the following:
fever, leukopenia and leukocytosis (which is WBC count less than
5000 cells/mm3 or 10,000 cells/mm3), or purulent-appearing sputum
or ET aspirate. Other clinical manifestations used by the Centers for
Disease Control and Prevention (CDC) include change in mental
status, increase in respiratory secretions, new onset of dyspnea or
cough, rales, and adventitious bronchial lungs sounds. Another
criterion by the CDC is at least one positive result from a blood
culture or pleural fluid, or bronchoalveolar culture. The risk factors
for HAP are multifactorial from severe illness related to
comorbidities, hemodynamic compromise, and depressed immune
system. The use of conventional treatment modalities such as
antibiotics, corticosteroids, sedatives, and acid-relieving
medications (proton pump inhibitors and histamine blockers),
which increase gram-negative colonization of the aerodigestive
tract, artificial airway in the trachea, and respiratory therapy
equipment (e.g., mechanical ventilation where bacteria can be
906
inhaled from aerosols) also increase the risk of HAP.
Aspiration pneumonia
Aspiration pneumonia occurs when oropharyngeal flora or gastric
material are aspirated into the lower respiratory tract resulting
from dysphagia or impaired coughing mechanisms. Aspiration
pneumonia can lead to ALI, ARDS, empyema, or lung abscess. The
patient population at highest risk is the older adult population.
Other predictors of aspiration pneumonia in older adults include
COPD, congestive heart failure, tube feeding, delirium, immobility,
cerebrovascular accident, GERD, and obesity. Pathogens
associated with aspiration pneumonia are gram-negative bacilli,
given gastric pH-altering medications, anaerobes, and
Staphylococcus aureus.
Ventilator-associated pneumonia
A patient who acquires pneumonia more than 48 hours following
ET intubation and initiation of mechanical ventilation may be
classified as having VAP. VAP is associated with increased
duration of ET intubation, mechanical ventilation, intensive care
stay, and hospital cost (approximately $99,600 per case). Hospital
mortality of mechanically ventilated patients who develop VAP is
46% compared with 32% for those without VAP, with 4.4% of
deaths occurring at day 30 and 5.9% on day 60 in 2011. In 2010, the
National Healthcare Safety Network (NHSN) facilities reported
more than 3525 VAP cases. VAP incidence for hospital units ranged
from 0.0 to 5.8 per 1000 ventilator days; a very broad range,
indicative of a problem with consistency of reporting. Currently,
there is no valid, reliable definition for VAP. The most widely used
VAP definitions and criteria were evaluated and were found to be
neither sensitive nor specific.
Ventilator-associated events
Surveillance for VAEs by the NHSN was limited to VAP until 2013.
In 2011, the Centers for Disease Control and Prevention composed a
Working Group of key stakeholder organizations to evaluate the
limitations of the NHSN pneumonia definitions and to develop a
907
more reliable approach to VAE surveillance by the NHSN. A VAE
surveillance algorithm was developed by the Working Group and
implemented by the NHSN in January 2013. The approach is based
on measurable, simplified, and “automation-friendly” criteria
designed to identify a comprehensive list of conditions and
complications associated with adult patients who are mechanically
ventilated. The three tiers of the VAE algorithm include: ventilator-
associated condition, infection-related ventilator-associated
complication, and possible and probable VAP. The Centers for
Medicare and Medicaid Services has recognized VAP as a
preventable illness when appropriate patient care is provided. The
key components for improvement in outcomes of patients who are
mechanically ventilated are defined within the “ventilator bundle”
developed by the Institute for Healthcare Improvement. The
evidence-based practices include elevation of the head of the bed,
daily sedation vacation and assessment of readiness to extubate,
peptic ulcer disease prophylaxis, daily oral care with chlorhexidine,
and deep venous thrombosis (DVT) prophylaxis.
Assessment
Goal of system assessment
Identify ineffective breathing patterns, impaired gas exchange, and
airway obstruction. Findings are influenced by the patient’s age,
extent of the disease process, underlying medical condition, and
pathogen involved. Severity of pneumonia should be determined
following initial assessment and diagnostic testing.
908
Cough
• Can be unrelenting and severe; may induce vomiting in some
patients.
Chest radiograph
• Determines presence of pneumonia, but initial radiograph finding
is often negative if the patient is dehydrated.
Vital signs
• Fever occurs in response to infection; some patients are not
febrile, especially if being cooled or on continuous renal
replacement therapy.
909
• Hypovolemia alone may prompt tachycardia.
Observation
• Nasal flaring and expiratory grunt may be present.
Auscultation
• Decreased or bronchial breath sounds.
Palpation
• Palpate chest wall for tenderness indicative of inflammation.
Percussion
910
• May reveal presence of consolidation or fluid (dullness) or
hyperresonance (pneumothorax).
Screening labwork
• CBC: Evaluates for elevated WBCs indicative of infection.
Abnormal
Test Purpose
Findings
Arterial Oxygenation status and acid-base balance are evaluated pH changes:
blood gas with ABGs. Acidosis may
(ABG) reflect
analysis respiratory
failure; alkalosis
may reflect
tachypnea.
Carbon
dioxide:Elevated
CO2 reflects
respiratory
failure;
decreased CO2
reflects
tachypnea.
Hypoxemia: Pao2
less than 80 mm
Hg.
Oxygen saturation:
Sao2 less than
92%.
Bicarbonate: HCO3
less than 22
mEq/L.
Base deficit: less
than −2.
Complete Evaluates for presence of infection. Increased white
911
blood count blood cell (WBC)
(CBC) count: less than
11,000/mm3 is
seen with
bacterial
pneumonias.
Normal or low
WBC count: Seen
with viral or
mycoplasma
pneumonias.
Sputum Identifies infecting organism. Gram stain
Gram stain, A sputum culture should be obtained from the lower positive:
culture, and respiratory tract before initiation of antimicrobial Indicates
sensitivity therapy. The most reliable specimens are obtained via organism is
bronchoalveolar lavage (BAL) during bronchoscopy, present.
suctioning with a protected telescoping catheter (mini- Culture: Identifies
BAL), or open-lung biopsy (used occasionally to reduce organism.
contamination of specimen with oral flora). Sensitivity:
Reflects
effectiveness of
drugs on
identified
organism.
Blood culture Identifies whether pneumonia organism has become Secondary
and systemic; blood cultures help to identify the causative bacteremia: A
sensitivity organism. frequent finding;
patients with
bacteremia are at
higher risk for
developing
respiratory failure.
Serologic Acute and convalescent titers are drawn to diagnose viral Increased antibody
studies pneumonia. Both serologic and urine tests are available for titers: A positive
Legionnaires’ pneumonia. sign for viral
infection.
Acid-fast To rule out mycobacterial infection (e.g., tuberculosis). Positive:
stain Mycobacterial
infection is
present.
Chest Identifies anatomic involvement, extent of disease, presence Lobar: Entire lobe
radiograph of consolidation, pleural effusions, or cavitation. involved.
Segmental
(lobular): Only
parts of a lobe
involved.
Bronchopneumonia:
Affects alveoli
contiguous to
the involved
bronchi.
Diagnostic Obtains specimens during simple bronchoscopy without Gram stain
fiber optic contaminating the aspirate; modified technique (mini-BAL) positive:
bronchoscopy is also effective without the need of full bronchoscopy. Indicates
using a PSB organism is
(protected present.
specimen Culture: Identifies
912
brush) and organism.
BAL Sensitivity:
Reflects
effectiveness of
drugs on
identified
organism.
Thoracentesis Removal of pleural effusion fluid from the pleural space Gram stain
using a needle to drain the chest cavity. Pleural effusion positive:
fluid may be cultured following thoracentesis to identify Indicates
the causative organism. organism is
present.
Culture: Identifies
organism.
Sensitivity:
Reflects
effectiveness of
drugs on
identified
organism.
PNEUMONIA MEASURES*
Indicators Measure
Appropriate PN-6: Initial antibiotic is appropriate for community-acquired pneumonia in
antibiotic immunocompetent patients
selection
Appropriate PN-6A: Initial antibiotic selection for community-acquired pneumonia in an
antibiotic immunocompetent patient-intensive care unit patient
selection
Appropriate PN-6B: Initial antibiotic selection for community-acquired pneumonia in an
antibiotic immunocompetent patient-non–intensive care unit patient
selection
Blood PN-3A: Blood cultures performed within 24 hours before or 24 hours after
cultures hospital arrival for patients who were transferred or admitted to the intensive
drawn care unit within 24 hours of hospital arrival
*
Criteria to include vaccinations PN-2 (pneumococcal vaccination) and PN-7
(influenza vaccination) were retired effective 1 January 2012. These measures have
been replaced with the two immunization measures from The Joint Commission that
are applicable to all patients regardless of diagnosis, rather than restricting the need
for the vaccinations to patients with community-acquired pneumonia.
Retrieved from www.jointcommission.org/pneumonia/
913
Collaborative management
Care priorities
1. Relieve hypoxemia
914
Failure.)
• Confusion/disorientation.
• Thrombocytopenia.
• Septic shock.
• Leukopenia.
3. Control infection
915
radiograph results until sputum or blood culture results are
available. Pneumococcus is the most common pathogen associated
with CAP, whereas enteric gram-negative bacteria are the most
common pathogens identified with HAP. Pseudomonas aeruginosa
and methicillin-resistant Staphylococcus aureus are the most
common organisms seen in patients on long-term mechanical
ventilation. Antimicrobial therapy in patients who are critically ill
is usually parenteral and guided by sensitivity of the causative
organism. Many of the organisms responsible for nosocomial
pneumonias are resistant to multiple antibiotics or antimicrobials.
Proper identification of the organism, determination of sensitivity
to the medication, and attainment of therapeutic drug levels are
crucial for effective therapy.
4. Control cough
Antitussives are used to relieve coughing. Occasionally, narcotics
such as codeine are required if coughing is unrelieved by other
agents. Patients receiving narcotics for pleuritic or other pain
control may experience a reduction in coughing as a beneficial side
effect of the narcotics. If cough is productive, adding an expectorant
to help manage thicker secretions may assist the patient. Additional
IV or enteral fluids may also help thin secretions by augmenting
overall hydration. Coughing should be controlled to a reasonable
level, but not at the expense of expectorating sputum.
5. Provide hydration
IV fluids may be necessary to replace insensible fluid loss and help
thin secretions (e.g., tachypnea, diaphoresis with fever), in addition
to providing enteral fluids. Volume resuscitation for dehydration
must be done carefully to avoid volume overload in patients with
multiple comorbidities. Dehydration causes secretions to become
thick, tenacious, and difficult to expectorate.
6. Reduce fever
Analgesic antipyretics such as acetaminophen are used to reduce
916
body temperature. Aspirin is generally not used for temperature
control.
9. Relieve congestion
Percussion and postural drainage are indicated if deep breathing,
coughing, hydration (either enteral or parenteral fluids), and
moving about in bed or ambulation are found to be ineffective in
raising and expectorating sputum. Consult with the respiratory care
provider as indicated.
917
Retrieved from www.jsicm.org/pdf/VAPbundle2010kaitei_ENGLISH.pdf.
Infection control
918
with these activities.
Infection risk
919
• Cross-contamination is more likely with
manipulation of these tubes.
920
12. Elevate the head of the bed to at least 30 degrees during
feedings and for 1 hour after any feeding or medication to reduce
the risk of aspiration.
Fluid management
921
Document the patient’s response to fluid replacement therapy.
922
lungs is the first step to oxygen delivery to the tissues. Carbon
dioxide must also diffuse from the bloodstream into the alveoli to
be exhaled. Type I respiratory failure (hypoxemic) is oxygenation
failure, whereas type II (hypercapnic) is ventilation failure. Many
patients manifest respiratory failure of types I and II
simultaneously. Clinically, type I failure exists when PaO2 is less
than 50 mm Hg with the patient at rest and breathing room air (Fio2
0.21 or 21% of the atmospheric pressure, which is 760 mm Hg at sea
level). Paco2 greater than 50 mm Hg is significant for acute
ventilation failure or hypercapnia. The PaO2 provides the “driving
pressure” for the saturation of hemoglobin. Without adequate
pressure (PaO2), the hemoglobin is inadequately saturated.
Approximately 98% of the oxygen delivered to tissues is provided
by oxyhemoglobin. The amount of oxygen combined with
hemoglobin depends on the PaO2. The relationship is articulated
within the oxyhemoglobin dissociation curve.
Carbon dioxide is transported in three main forms: (1) in simple
solution, (2) as bicarbonate, and (3) combined with protein of
hemoglobin as a carbamino compound. Under healthy conditions,
the amount of carbon dioxide produced by the tissues is constant
and equals the amount of carbon dioxide eliminated by the lung. A
wide variety of disease states creates a single or mixed respiratory
failure; some affecting ventilation, others, perfusion. One of the
simplest methods of evaluating patients relates to the
understanding of basic gas exchange. Oxygenation occurs primarily
during inspiration and the removal of CO2 occurs during
exhalation. The basic concepts applied here include compliance and
recoil. Lung compliance is the measure of expansion of the alveoli
(the gas-exchanging surface), which occurs on inspiration, whereas
elasticity refers to the ability of the alveoli to recoil, as they do on
exhalation. Restrictive airway diseases [generally] present with
significant hypoxemia, whereas obstructive disorders are more
likely to develop a persistent and chronic hypercapnia. See Box 4-1
for a description of some of the disease processes that can lead to
acute respiratory failure.
The evaluation of respiratory failure includes the understanding
of the following:
923
Ventilation and perfusion matching ( match)
This general term refers to the relationship of gas distribution ( )
to the amount of blood ( ), which passes the total alveolar
surface in 1 minute of time. Normal alveolar ventilation occurs at a
rate of 4 L/min, and normal pulmonary vascular blood flow occurs
at a rate of 5 L/min. The normal ratio is therefore 4 L/min
divided by 5 L/min, or a ratio of 0.8, almost in a 1:1 ratio. Any
disease process that interferes with either side of the equation
upsets the physiologic balance, causing a mismatch.
924
Volume of CO2: The volume of CO2 produced by the body tissues
varies with metabolic rate (fever, pain, agitation, sepsis, and so
forth). The Paco2 must be interpreted in conjunction with the
volume exhaled, especially in patients who are mechanically
ventilated. Many of the variables impacting CO2 flux can be
eliminated by controlling ventilation and muscular activity.
Current evidence supports that the overdistension and shear
force of opening-closing also profoundly affect the healthy lung.
Assessment
Goal of system assessment
To evaluate for poor gas exchange and increased ventilatory
support requirements (see sections on Acid-Base Balance and
Mechanical Ventilation, Chapter 1).
925
agitated and combative as a result of hypoxia. Patients with COPD
have reduced airway diameter as well as chronic inflammation and
airway remodeling, and when the underlying chronic condition is
exacerbated, mucus hypersecretion and airway edema compound
the initial condition. Increased effort is needed to mobilize gas in
and out of the lungs, particularly during exhalation. The failure to
exhale leads to air trapping and hyperinflation, which further
compromise inspiratory effort and contribute to increasing hypoxia
and hypercapnia. Patients with impending shock are at high risk
for respiratory failure. Inhalation of toxic substances, pneumonia,
severe pneumonitis, aspiration of gastric contents, drowning, and
air or fat embolus may prompt respiratory failure. Other causes
include acute pancreatitis, drug overdose, neurologic injury,
hemorrhage, sepsis, extreme obesity, or any condition that has
enlarged the abdomen to the point of exerting upward pressure on
the diaphragm.
Vital signs
• Early indicators: Dyspnea, restlessness, anxiety, headache,
fatigue, cool and dry skin, increased BP, tachycardia, and
persistent rapid RR, which indicate hypoxia. Hypercapnia results
in slurred speech and headache.
926
Vital signs
• RR is rapid. If the patient is experiencing impending shock, RR is
compensatory for metabolic acidosis.
A-a gradient/A-aDO2/P(A-a)o2
• When the Fio2 is greater than 0.21, the A-a gradient becomes less
accurate as in the measurement of proportional gas exchange,
although the difference should always be less than 150 mm Hg.
927
Fio2 should be considered abnormal and indicative of pulmonary
dysfunction.
Observation
• Nasal flaring and expiratory grunt may be present.
• May present with ashen, pale, or gray/blue facial color, lip color,
or nail beds.
Auscultation
Evaluate the presence of normal breath sounds and synchronous
lung expansion. Auscultate for the presence of:
928
4. Inspiratory wheezes: Anterior, lateral, and posterior: early airway
narrowing.
Palpation
• Palpate chest wall for tenderness indicative of inflammation.
Percussion
• May reveal presence of consolidation or fluid (dullness) or
hyperresonance (pneumothorax).
Screening labwork
• Blood gas evaluation can determine primary and secondary
problems, or primary problems with compensation (see Acid-
Base Balance, Chapter 1).
929
Collaborative management
Careful consideration should be given to evaluate neurologic
conditions and OSA because these are commonly overlooked
causes of respiratory failure. In addition, the primary goal is to
determine and treat the underlying pathophysiologic condition.
Care priorities
930
NPPV or NiPPV, CPAP or BiPAP, or invasive mechanical
ventilation.
931
vasopressors, IV sodium bicarbonate may be used conservatively to
return the pH to a level higher than 7.25. The use of sodium
bicarbonate is a short-term solution for most acid-base disturbances
and its use may actually make the overall situation worse.
4-6
RESEARCH BRIEF
Clinical research to evaluate the effectiveness of life support
systems in acute fatal illness has unique problems of logistics,
932
ethics, and consent. There have been 10 prospective comparative
trials of extracorporeal membrane oxygenation in acute fatal
respiratory failure, using different study designs. The trial designs
were prospective controlled randomized, prospective adaptive
randomized, sequential, and matched pairs. The trials were
reviewed with regard to logistics, ethics, consent, statistical
methods, economics, and impact. The matched pairs method is the
best study design for evaluation of life support systems in acute
fatal illness.
From Bartlett RH: Clinical research in acute fatal illness: lessons from extracorporeal
membrane oxygenation. J Intensive Care Med Sep 15;pii: 0885066614550278 [Epub ahead of
print], 2014.
Respiratory monitoring
933
near-fatal asthma exacerbation.
Anxiety reduction
Oxygen therapy
934
the skin, such as nares, and around edges of mask devices.
Ventilation assistance
935
Vital Signs Monitoring.
Pneumothorax
Pathophysiology
Pneumothorax is an accumulation of air between the parietal and
visceral pleura with secondary lung collapse. There are three types
of pneumothorax: spontaneous, traumatic, and tension.
Spontaneous
A portion of the lung may spontaneously collapse, while the chest
wall remains intact with no leak to the atmosphere. Both primary
and secondary spontaneous pneumothoraces may result from the
rupture of a bleb or bullae on the visceral pleural surface, usually
near the apex, resulting in air entering the thorax. A primary
spontaneous pneumothorax is rarely life threatening and generally
occurs in healthy, 20- to 40-year-old lean, thin men who smoke. The
cause of the bleb/bullae rupture is unknown, although it may result
from a weakness related to a respiratory infection. Symptoms most
often occur at rest rather than with vigorous exercise or coughing.
There is a high probability for recurrence within 2 to 3 years.
A secondary spontaneous pneumothorax may occur in all age
groups resulting from an underlying lung disease (COPD, cystic
fibrosis, tuberculosis, malignant neoplasm). Symptoms are
more likely to be life threatening than with a primary spontaneous
pneumothorax, and recurrence rates are high in this population.
The rate of reabsorption of spontaneous pneumothoraces is 1.25%
to 1.8% of the volume of the hemithorax every 24 hours. A 15%
pneumothorax requires 8 to 12 days to fully resolve without
treatment.
936
Traumatic
The integrity of the chest wall may or may not be disrupted before
lung collapse in a pneumothorax resulting from trauma. An open
pneumothorax occurs when air enters the pleural space from the
atmosphere through an opening in the chest wall, such as with a
penetrating injury (includes stabbing, gunshot wound to the chest)
or an invasive medical procedure (e.g., lung biopsy, thoracentesis,
placement of a central line into a subclavian vein). A closed
pneumothorax occurs when the visceral pleura is penetrated but
the chest wall remains intact, with no atmospheric leak. Closed
chest wall lung collapse occurs with blunt trauma, including
cardiopulmonary resuscitation, when an external impact on the
chest fractures and dislocates the ribs (i.e., motor vehicle crash with
the chest hitting the steering wheel). It may also occur from the use
of high-level PEEP therapy. For more information about blunt chest
injuries, see Chest Trauma, Chapter 3.
Tension
Tension pneumothorax is a life-threatening medical emergency
most often associated with trauma or infection. Tension can ensue
with a spontaneous pneumothorax or during positive-pressure
mechanical ventilation. The integrity of the chest wall may or may
not be disrupted before lung collapse. Air enters the pleural space
during inspiration through a pleural tear and continues to
accumulate inside the pleural cavity. The air cannot escape during
expiration because the intrapleural pressure is greater than alveolar
pressure, which creates a one-way or flap-valve effect. The
increasing intrathoracic pressure is transmitted to the mediastinum,
resulting in a mediastinal shift toward the unaffected side. The
encroachment of the enlarging affected side makes it impossible for
the unaffected side to fully expand. The increased pressure also
compresses the vena cava, which impedes venous return, and
reduces preload/end-diastolic volume. Cardiac output is
progressively reduced while intrathoracic pressure and
compression of the vena cava increases, leading to circulatory
collapse if not promptly diagnosed and managed. Bilateral tension
pneumothoraces may occur and generally result in cardiac arrest
shortly after the lungs collapse.
937
Assessment
Goal of system assessment
Identify ineffective breathing patterns and impaired gas exchange.
The clinical presentation will vary in degree, depending on the type
and size of the pneumothorax. With tension pneumothorax,
evaluate for decreased cardiac output and decreased tissue
perfusion. See the section on Respiratory Assessment General:
(earlier in Chapter 4), and Cardiac Assessment: General (Chapter 5).
Chest radiograph
• Determines presence of pneumothorax, usually estimated in
percentages depending on the size of the lung collapsed.
Vital signs
• Tachycardia, tachypnea.
• Possible fever.
938
• Small pneumothoraces may not affect vital signs at all.
Observation/inspection
Tension pneumothorax
• Severe dyspnea.
939
• Decreased chest wall movement on affected side.
Palpation
Tension pneumothorax
Percussion
Tension pneumothorax
Auscultation
940
• Increased RR.
Tension pneumothorax
941
placement may be
present, and when the
chest radiograph is
obscured by surgical
emphysema.
Arterial blood gas (ABG) Assesses for Hypoxemia (Pao2 <80 mm Hg on room
analysis hypoxemia and air) is generally present with a 20% or
acidosis. greater lung collapse. Mild hypoxemia is
present with smaller pneumothoraces.
Tension pneumothoraces may cause
both respiratory and lactic acidosis (pH
<7.35) from impending respiratory
failure and circulatory collapse. Elevated
carbon dioxide and lactate lower the
blood pH.
12-Lead ECG Rules out acute Vena cava compression from tension
(electrocardiogram) coronary syndrome as pneumothorax affects perfusion of the
a cause for chest pain coronary arteries if pneumothorax is not
with vital sign changes diagnosed and managed promptly. ST
indicative of segment depression, indicative of
deterioration. myocardial ischemia, may be present,
along with decreased QRS
amplitude/decreased R waves,
rightward axis deviation.
Pulmonary function tests Pulmonary function Not recommended.
tests provide
minimally sensitive
data to validate
presence or size of
pneumothorax.
Collaborative management
Care priorities
Patients with shortness of breath should not be left without
intervention regardless of the size of the pneumothorax seen on the
chest radiograph.
1. Relieve hypoxemia
942
suspected cause of the pneumothorax, positive pressure is
reduced if possible.
943
simple pneumothorax is done by passing a small (approximately
8 Fr) catheter over a guide wire into the pleural space. A three-
way stopcock is attached and air may be aspirated via a 50-mL
syringe. Addition of a Heimlich valve and suction may improve
success rates to over 60%. If simple aspiration or catheter
aspiration drainage is unsuccessful, a chest/intercostal tube
should be inserted.
944
tube insertion, but rather added after 48 hours if persistent air
leak is present or the pneumothorax fails to reexpand. High-
volume, low-pressure (greater than 10 to less than 20 cm H2O)
suction systems are recommended. Patients requiring suction
should be managed by physicians and nurses who have
experience managing complex pneumothoraces. There is no
evidence to support routine use of immediate suction with chest
drain systems in the treatment of spontaneous pneumothorax.
3. Relieve pain
945
• Chest radiograph before tube removal: Chest radiographs are
obtained following the last evidence of air leak but before chest
tube removal at intervals ranging from less than 4 to 24 hours
after the last air leak assessment. Nearly two thirds of
practitioners wait 5 to 12 hours after last evidence of air leak
before obtaining the preremoval radiograph. Practices range from
less than 4 to 24 hours.
946
solution or talc, both of which result in pleural adhesions to
prevent recurrence. A partial pleurectomy may be performed
instead of mechanical or chemical abrasion.
Ventilation assistance
947
1. Assist the advanced practice provider with chest tube insertion
according to institutional guidelines.
948
• Ensure that the system is appropriately vented at all
times to help prevent the possibility of tension
pneumothorax should the system be disrupted. Air
should be released if the system is vented.
949
• Bubbling in the underwater-seal chamber occurs
only during expiration and reflects air is leaving the
pleural space through the drainage system.
Oxygen therapy
950
2. Administer supplemental O2 using liter flow device as ordered.
Respiratory monitoring
Acid-Base Management.
Acute pain
related to chest tube placement and pleural irritation
Goals/Outcomes: Within 1 to 2 hours of initiating analgesic
therapy, the patient’s subjective evaluation of discomfort improves
as documented by a pain scale. Nonverbal indicators of discomfort,
such as grimacing and splinting on inspiration, are absent.
Comfort Level; Pain Control Behavior; Pain Level.
Pain management
951
with the patient, rating discomfort on a scale of 0 (no pain) to 10
(worst pain). Medicate with analgesics as prescribed, evaluating
and documenting the effectiveness of the medication on the basis of
the pain scale.
Self-responsibility facilitation
952
in Chapter 2 on Emotional and Spiritual Support of the Patient and
Significant Others.
4-7
RESEARCH BRIEF
A faster and more efficient method for assessing pneumothorax
progression in patients receiving positive-pressure mechanical
ventilation would certainly lead to earlier intervention and
improved patient safety. Ultrasonography is a common bedside
tool that can offer clinicians a less expensive and more accessible
alternative to computed tomography scanning in the assessment of
pneumothorax. Research using animal models has provided
reliable evidence that could possibly contribute to the development
of best practice. Pneumothorax progression is known as the best
indicator for the need for chest tube placement.
From Oveland NP, Lossius HM, Wemmelund K, et al: Using thoracic ultrasonography to
accurately assess pneumothorax progression during positive pressure ventilation: a
comparison with CT scanning. Chest 143:415-422, 2013.
Pulmonary embolism
Pathophysiology
Pulmonary embolism (PE) is a blockage in the pulmonary
circulation created by a lodged blood clot, vasculitis from fatty
acids, or presence of air or other endogenous substances.
Pulmonary emboli resulting from DVT affect from 300,000 to
600,000 patients (1 to 2 per 1000 patients; and in those older than 80
years, 1 per 100 patients) annually in the United States. It is
estimated that from 60,000 to 10,000 people die of DVT/PE, with
10% to 30% dying in the first 30 days. Sudden death is the first
symptom of a problem in approximately 25% of patients. PE occurs
in nearly 70% of patients with venous thrombosis in veins proximal
to the knee and is less common with more distal thrombosis. PE is
associated with recurrent embolic events (within 10 years) in over
33% of affected patients. Venous thromboembolism (VTE)
953
prevention augments both public health and patient safety. Despite
efforts to prevent hospital-acquired VTE, the number of secondary
diagnoses has increased. During 2007 to 2009, the data from each
year revealed that approximately 550,000 adult hospital stays had a
discharge diagnosis of VTE. Prevention of VTE has recently been
the focus of attention from both researchers and quality
improvement organizations as a leading strategy to help reduce
morbidity and mortality in patients who are hospitalized. Acute
right ventricular failure with resultant low cardiac output is the
leading cause of death related to PE. Despite strong evidence,
recommended evidence-based practices are inconsistently
implemented. VTE rates are increasing as the U.S. population ages,
is progressively obese, and is living longer with chronic
diseases, which may promote thrombus formation. Venous
thrombosis is the most common cause of PE, followed by fat
emboli. Emboli related to venous air, foreign bodies, and other
sources (amniotic fluid, sepsis/infection, and tumors) occur more
rarely.
Venous thromboembolism
A formed blood clot from a large vein dislodges and travels to the
pulmonary circulation, where it may obstruct one (massive PE) or
both branches (saddle emboli) of the pulmonary artery or a smaller,
distal vessel. Blood clots typically originate in the deep veins of the
legs, the iliofemoral system, or pelvis. Many patients with VTEs
have no symptoms of DVT. Thrombus formation can result from
blood stasis, alterations in clotting factors, and injury to vessel
walls. Emboli are classified by size and location and include
submassive, massive, and saddle emboli. Total obstruction of blood
flow leading to pulmonary infarction is rare. Prevention, early
diagnosis, and appropriate treatment may reduce development of
DVT and PE by 68% and mortality to less than 10%. Although most
thrombotic emboli resolve completely, leaving no residual deficits,
some patients may be left with chronic pulmonary hypertension
(Table 4-6).
Table 4-6
954
INCIDENCE OF VENOUS THROMBOEMBOLISM IN HOSPITALIZED
PATIENTS
955
resorbed. Surgical procedures, insertion of pulmonary artery
catheters, central venous catheters, hemodialysis, endoscopy, and
use of automatic injectors such as those used for contrast media can
prompt symptomatic air emboli. A larger bolus of air into the right
ventricle may completely obstruct pulmonary blood flow, leading
to cardiac arrest. In severe cases, venous air embolus has a
mortality rate greater than 50%. Rapid diagnosis and treatment are
essential. Case reports describe the adult lethal volume of air as
approximately 200 to 300 mL delivered rapidly. Air occludes the
right ventricular pulmonary outflow tract, or the smaller
pulmonary arteriole with a mixture of air and fibrin clots, which
results in right ventricular failure and cardiogenic shock.
956
Assessment
Goal of system assessment
Evaluate for ineffective breathing patterns and impaired gas
exchange. The clinical presentation will vary in degree, depending
on the type and size of the embolus. With a submassive or massive
embolism, evaluate for decreased cardiac output and decreased
tissue perfusion. Massive embolism may prompt cardiogenic shock.
For saddle emboli, identifying pulmonary embolus as the cause for
acute cardiopulmonary decompensation is of paramount
importance so that life-saving treatments can be provided. (See the
section on Respiratory Assessment: General, and Cardiac
Assessment: General in Chapter 5.)
Table 4-8
RISK FACTORS FOR VENOUS THROMBOEMBOLISM
957
Determine probability based on risk factors
• Helps determine presence of pulmonary embolus: More than six
factors is considered high, two to six is moderate, and less than
two is considered low probability.
Vital signs
• Severity of all findings varies with size of the embolus; patients
with small emboli may be asymptomatic.
Observation/inspection
• Dyspnea, nonproductive cough, and nausea.
958
above.
959
• Massive embolus: Severe chest pain, cyanosis, and acute
respiratory distress.
Palpation
• Possible reduced chest excursion on affected side attributable to
splinting for pain.
Percussion
• Unchanged.
Auscultation
• Crackles.
HIGH ALERT!
Saddle pulmonary embolus is life threatening. Immediate medical
or surgical intervention is crucial. Thrombolysis directed at the
pulmonary embolus will also prompt lysis of other clots and may
lead to other bleeding complications. If thrombolysis is
contraindicated, surgical or percutaneous catheter-mediated
embolectomy is performed immediately.
Fat embolism
960
• Multiple long bone fractures, particularly the femur and pelvis.
• Osteomyelitis.
Observation/inspection
Patients are often asymptomatic for 12 to 24 hours after the
embolization occurs. This period ends with a sudden deterioration
in cardiopulmonary and neurologic status.
• Petechial rash may appear especially over the upper torso and
axillae, secondary to thrombocytopenia. The platelets aggregate
in the presence of circulating fats.
Vital signs
Auscultation
961
• Pulmonary artery/central venous catheter insertion.
• Cardiopulmonary bypass.
• Hemodialysis.
• Endoscopy.
Clinical presentation
Depends on severity of the bolus.
Observation/inspection
Agitation, confusion, cough, dyspnea, and chest pain.
Vital signs
RR greater than 20 breaths/min, HR greater than 100 bpm, and
hypotension.
Auscultation
Wheezing, “mill wheel heart murmur,” which can be defined as a
temporary loud, machinery-like sound resulting from right
ventricular blood mixing with air.
Foreign bodies
• Vena cava filter has not been retrieved within recommended time
frame.
962
Diagnostic Tests for Venous Thrombotic Pulmonary Embolism
963
12-Lead ECG Rules out acute coronary If VTE is extensive, signs of acute
(electrocardiogram) syndrome as a cause for chest pulmonary hypertension may be
Vitally important because pain with vital sign changes present: right-shift QRS axes, tall
chest pain can mimic indicative of deterioration. and peaked P waves, ST segment
severe angina or acute changes, and T wave inversion in
myocardial infarction leads V1 to V4.
Fat embolism
• ABG values: Hypoxemia (PaO2 less than 80 mm Hg) and
hypercapnia (Paco2 greater than 45 mm Hg) will be present with
respiratory acidosis (pH less than 7.35).
964
• ABG values: Hypoxemia (PaO2 less than 80 mm Hg), hypercapnia
(Paco2 greater than 45 mm Hg), and respiratory acidosis (pH less
than 7.35) are generally present in severe cases.
Foreign bodies
• Chest radiograph: All devices are radiopaque for easy
identification using radiographs. The “lost” device should be
easily visible using a chest radiograph.
Collaborative management
Care priorities: Venous thromboembolism
Patients with shortness of breath should not be left without
intervention regardless of the probability that VTE is present.
1. Relieve hypoxemia
Patent foramen ovale (or atrial septal defect) may augment
hypoxemia if right atrial pressure exceeds left atrial pressure,
causing deoxygenated blood to shunt from the right to the left
atrium.
965
hypotension or shock
Hemodynamic stabilization is achieved using a combination of
fluid therapy to increase the end-diastolic volume in the right
ventricle and positive inotropic agents to increase the force of right
ventricular contraction. Management of right ventricular failure is
complex. Efforts should be directed at restoring patency of
pulmonary circulation in patients with VTE. When the obstruction
is relieved, the patient generally improves rapidly. See the sections
on Heart Failure and Cardiogenic Shock in Chapter 5.
966
year
Severe head or spinal cord trauma within Craniotomy within Epidural analgesia; catheter
4 weeks 2 weeks present, or will be present in the
spine
967
sequential compression devices
devices
968
• Heparin requirements are the largest in the initial
72 hours of therapy. Maintenance continues for 7 to
14 days, during which time the patient is placed on
bed rest to ensure that the thrombus is firmly
attached to the vessel wall before ambulation.
Platelets should be monitored, because patients
sometimes experience heparin-induced
thrombocytopenia (HIT) or low platelets. Protamine
sulfate is a heparin antidote, which should be
readily available during heparin therapy. Fatal
hemorrhage occurs in 1% to 2% of patients
undergoing heparin therapy. Risk of bleeding is
greatest in women older than 60 years.
• Subcutaneous low–molecular-weight heparin (dalteparin,
enoxaparin): An alternative to unfractionated heparin with
longer half-life, greater bioavailability, and more predictable
anticoagulant activity. Enoxaparin is given 1 mg/kg
subcutaneously (SC) every 12 hours or 1.5 mg/kg SC daily.
Dalteparin is given 200 units (international units)/kg SC daily to a
maximum daily dose of 18,000 international units, while the
patient is being bridged to warfarin.
969
• 10 mg SC daily: Weight greater than 100 kg.
Table 4-9
UNFRACTIONATED HEPARIN INTRAVENOUS INFUSION DOSAGE
TITRATION
970
process of clot lysis. These medications are not often used but can
be used immediately when severe cardiopulmonary compromise or
arrest has occurred. Heparin therapy is used following
thrombolytic infusion. As many as 33% of patients who receive
thrombolytic therapy have hemorrhagic complications. The drug
should be discontinued and fresh-frozen plasma infusion may be
initiated for severe bleeding complications.
971
• Endovascular ultrasound delivered thrombolysis: Intended for
controlled and selective infusion of thrombolytics in the
peripheral vasculature for treatment of DVTs and PE including
“saddle emboli.” This therapy may be used in veins, arteries,
behind valves, and through IVC filters. Ultrasonic energy
prepares the clot by thinning fibrin, which increases permeability
of the clot and creates a pressure gradient to transport clot-
dissolving drugs inside the thrombus. This form is used in
difficult-to-reach areas such as behind valves, reduces the risk of
thrombus breakages and emboli, and uses less drug as the
thrombus is directly exposed to the lytic, preventing hemolysis.
972
condition has stabilized and the heparin is
discontinued, weekly monitoring of INR is
acceptable. After hospital discharge the PT should
be monitored every 2 weeks for as long as the
patient continues to take warfarin.
973
Warfarin or another VKA is not recommended during the first and
third trimesters and is used with caution during the second
trimester. Anticoagulant therapy should be continued for 3 months
postpartum.
1. Manage hypoxemia
Concentration of O2 is based on clinical presentation, ABG results,
and the patient’s previous respiratory status. Intubation and
mechanical ventilation may be required.
974
1. Prevent further air entry
If central line is being inserted, catheter hub should be occluded
using a clamp, or the inserter’s gloved finger.
2. Manage hypoxemia
Oxygen using 100% Fio2 is initiated immediately.
975
at risk of DVT and/or VTE and other pulmonary emboli.
Goals/Outcomes: The patient is free of hemodynamic instability
and shortness of breath reflected by normal (return to the patient’s
stable baseline) vital signs and normal work of breathing. Within 12
hours of initiation of therapy, the patient has adequate gas
exchange reflected by the following ABG values: PaO2 greater than
60 mm Hg, Paco2 35 to 45 mm Hg, and pH 7.35 to 7.45. Within 2 to 4
days of initiating anticoagulant therapy, the patient’s RR is 12 to 20
breaths/min with normal depth and pattern. Unobstructed,
unidirectional blood flow at an appropriate pressure is restored
through large vessels of the pulmonary and systemic circuits.
Circulation Status; Cardiac Pump Effectiveness; Respiratory
Status: Gas Exchange.
Embolus precautions
1. Assess the patient for risk factors associated with VTE (see Table
4-7).
3. Instruct the patient not to cross legs, either when in bed or sitting
in a chair.
Table 4-7
RISK FACTORS FOR VENOUS THROMBOEMBOLISM IN
HOSPITALIZED PATIENTS*
976
Age >50 years Previous history of venous Myocardial infarction
thromboembolism (VTE)
Myeloproliferative Impaired mobility, paresis, or Acute or chronic lung disease
disease paralysis
Dehydration Recently bedridden >3 days Obesity
Congestive heart Inflammatory bowel disease Known thrombophilic stroke
failure
Active Active rheumatic disease Varicose veins or chronic
malignancy/cancer venous stasis
Moderate to major Nephrotic syndrome Pregnancy
surgery
Hormone replacement Sickle cell disease Recently postpartum with
therapy immobility
Central venous Estrogen therapy or estrogen
catheter in place contraceptives
*
Patients who have more than a single condition are at increased risk of developing
venous thromboembolism. The more conditions present, the higher the risk.
977
tests needed as part of differential diagnosis.
8. Screen the patient for risk of bleeding (see the VTE prophylaxis
chart) in preparation for anticoagulant and possibly thrombolytic
drug administration.
11. Consult with the dietician to ensure that the patient maintains a
diet with consistent intake of vitamin K if VKAs, such as warfarin
(Coumadin) are initiated. Varying vitamin K intake may have a
marked effect on the ability to regulate the appropriate dose of
medication to avoid bleeding and clotting complications.
978
medication profile.
Hemodynamic regulation
979
and may worsen heart failure. Inodilator drugs
such as milrinone, amrinone, and, to a lesser extent,
dobutamine may not work well, because all
decrease venous return, which may also worsen
right ventricular failure.
980
Bleeding precautions
Bleeding reduction
981
5. Administer blood products if needed and monitor for transfusion
reaction.
982
2. Discuss the drug name, purpose, dosage, schedule, potential side
effects, and complications of therapy.
983
Pulmonary hypertension
Pathophysiology
Pulmonary hypertension and pulmonary arterial hypertension
(PAH) are complex, progressive, often fatal diseases caused by
elevated pulmonary pressures. PAH is defined as a mean
pulmonary artery pressure (MPAP) greater than 25 mm Hg,
pulmonary capillary wedge pressure (PCWP) or left atrial pressure
or left ventricular end-diastolic pressure less than 15 mm Hg, and
PVR greater than 3 Wood units. Wood units are a calculated PVR
that is obtained by subtracting the PCWP from the PAP systolic and
dividing by the cardiac output. The pulmonary vasculature is
normally a highly distensible, low-resistance system. All types of
pulmonary hypertension or PAH may result in right ventricular
failure, because the right ventricle is under constant strain to pump
into the highly resistant pulmonary vasculature. (See Table 4-10 for
World Health Organization classifications.) Each classification of
pulmonary hypertension has a different cause and different
approach to therapy.
Idiopathic pulmonary arterial hypertension (IPAH) is rare, has a
poor prognosis, and affects primarily middle-aged and young
women. Causes of IPAH are unclear. Heritable PAH is thought to
be familial with a link to germline mutations, such as bone
morphogenetic receptor 2 (BMPR2) or other causes. Associated
pulmonary arterial hypertension (APAH) is attributable to
secondary causes such as scleroderma or portopulmonary
hypertension. Other causes of pulmonary hypertension are more
common, with management directed at treating the underlying
cause and lowering PAPs using vasodilator drugs. IPAH and
APAH are often unresponsive to conventional treatments and may
require specialty therapies.
In PAH, there is dysfunction and imbalance between vasodilation
and vasoconstriction of the pulmonary vasculature from the right
side of the heart to the lungs resulting in chronic vasoconstriction.
The vessel walls thicken and hypertrophy causing vascular
remodeling from a non–muscular low-pressure system to a high-
pressure, low-flow system. The endogenous vasodilators, nitric
984
oxide and prostacyclin production, are impaired. In addition,
endothelin-1, a potent endogenous vasoconstrictor, is increased.
This increase in PVR and impedance to flow causes right
ventricular strain, impaired filling, and increased right ventricular
dilatation. This then leads to right ventricular ischemia. Eventually,
the right side of the heart weakens and is unable to accommodate
venous blood returning to the heart. PAH is generally a primary
disease of the right side of the heart.
The pathophysiology of pulmonary hypertension differs from
PAH in that it is generally attributable to primary disease of the left
side of the heart such as left ventricular diastolic dysfunction or
valvular heart disease. See the section on Heart Failure (Chapter 5)
for further discussion of left-sided to right-sided heart failure.
Pulmonary hypertension may also be caused by chronic
pulmonary diseases such as COPD or PE leading to cor pulmonale.
The pulmonary vasculature responds to alveolar hypoxia by
vasoconstriction, a beneficial mechanism that shunts blood away
from underventilated areas to better ventilated areas in the lungs,
thereby improving oxygenation. The resulting rise in PAP and
increase in PVR from acute hypoxia are completely reversible once
the hypoxia has been resolved. However, in the presence of chronic
hypoxia, the pulmonary vasculature undergoes permanent changes
similar to the changes in PAH, causing vascular remodeling. The
right ventricle dilates and hypertrophies under the constant strain
and workload. Eventually, the right side of the heart weakens and
is unable to accommodate venous blood returning to the heart. As a
result, pressure in the systemic venous circulation increases,
causing cor pulmonale, or right-sided heart failure.
Assessment
Goal of assessment
Because the low-resistance pulmonary vascular bed is clinically
silent until late in the disease process, onset is insidious.
Assessment before late stages of the disease should focus on
discerning the cause of early indicators and classifying functional
status (Box 4-2) so that an appropriate plan of care is created.
985
Box 4-2
WORLD HEALTH ORGANIZATION
CLASSIFICATION: FUNCTIONAL STATUS
OF PATIENTS WITH PULMONARY
HYPERTENSION
Class I: Patients with pulmonary hypertension (PH) but without
resulting limitation of physical activity. Ordinary physical
activity does not cause undue dyspnea or fatigue, chest pain, or
near syncope.
Class IV: Patients with PH with inability to carry out any physical
activity without symptoms. These patients manifest signs of
right-sided heart failure. Dyspnea and/or fatigue may even be
present at rest. Discomfort is increased by any physical activity.
986
pulmonary edema, and an array of other causes. See Table 4-10 for
etiologic factors.
Table 4-10
WORLD HEALTH ORGANIZATION CLINICAL CLASSIFICATION OF
PULMONARY HYPERTENSION
World Health
Organization Subsets/Examples of Causes
Class/Group
1. Pulmonary 1.1 Idiopathic PAH (IPAH): Occurs at random. Also known as primary
arterial pulmonary hypertension.
hypertension 1.2 Heritable: Formerly familial PAH; includes two types of PAH.
(PAH) 1.3 Drug- and toxin-induced: Includes antiobesity drugs such as [fen-phen]
(fenfluramine + phentermine), methamphetamine, and cocaine.
1.4 Associated with other disorders: Diseases include connective tissue
diseases, human immunodeficiency virus (HIV), portal hypertension,
congenital heart disease, schistosomiasis, chronic hemolytic anemia, and
persistent pulmonary hypertension of the newborn.
2. Pulmonary 2.1 Systolic dysfunction
hypertension 2.2 Diastolic dysfunction
(PH) with left- 2.3 Valvular disease
sided heart
disease
3. PH associated 3.1 Chronic obstructive pulmonary disease
with lung 3.2 Interstitial lung disease
diseases and/or3.3 Other pulmonary diseases with mixed restrictive and obstructive
hypoxemia pattern
3.4 Sleep-disordered breathing
3.5 Alveolar hypoventilation disorders
3.6 Chronic exposure to high altitude
3.7 Developmental abnormalities
4. Chronic Pulmonary thromboembolism or embolism attributable to fat, tumor,
thromboembolic parasites, and foreign material.
pulmonary
hypertension
5. Unclear 5.1 Hematologic disorders
multifactorial 5.2 Systemic disorders: sarcoidosis, pulmonary Langerhans’ cell
mechanisms histiocytosis, lymphangioleiomyomatosis, neurofibromatosis, and
vasculitis.
5.3 Metabolic disorders: glycogen storage disease, Gaucher disease, and
thyroid disorders.
5.4 Others: tumoral obstruction, fibrosing mediastinitis, and chronic renal
failure on dialysis.
From Simonneau G, Robbins IM, Beghetti M, et al: Updated clinical classification of
pulmonary hypertension. J Am Coll Cardiol 54 S43-S54, 2009.
Clinical presentation
Early indicators
987
Exertional dyspnea, fatigue, and weakness.
Late indicators
Chest pain, dizziness, syncope, palpitations, and lower extremity
edema.
Vital signs
• Tachycardia and tachypnea.
Observation/inspection
• Cyanosis of the lips and nail beds.
• Peripheral edema.
Palpation
• Right ventricular heave (visible left parasternal systolic lift).
Auscultation
• Accentuated pulmonary component of the second heart sound.
• S3 or S4.
988
• Distant breath sounds.
989
diagnosis. positive results are common with
echocardiography.
Pulmonary Important for differential Will vary according to cause.
function tests diagnosis of the underlying
pathologic condition.
Pulmonary To rule out an embolic event as the Will not be positive if the cause is
angiography and underlying cause. pulmonary hypertension.
perfusion scans
Type B natriuretic Monitors the progress of any Will be progressively elevated as heart
peptide level associated heart failure. failure worsens.
Other blood tests Used to rule out other possible Various values will be positive for
diagnoses, such as liver disease, specific pathologies.
human immunodeficiency virus
(HIV), and autoimmune disease.
Collaborative management
The goal of interdisciplinary management is to diagnose and treat
the underlying disorder or process causing the pulmonary
hypertension and improve the patient’s symptoms, functional
status, quality of life, and survival. Treatment is directed primarily
toward preventing progression of the disease, preventing thrombi
in situ, and reducing pulmonary artery vasoconstriction.
Care priorities
990
therapy is not available. It is currently under research as a
portable device.
• Vasodilators:
991
NSAIDs, so the patient must be educated to avoid
them.
• Phosphodiesterase-5 (PDE-5) inhibitors: Vasodilates the
pulmonary vessels. Sildenafil (Revatio) and tadalafil (Adcirca)
while used for pulmonary hypertension are also marketed under
the trade names of Viagra and Cialis at much lower doses for
erectile dysfunction.
992
pulmonary emboli (blood clots in the lungs).
HIGH ALERT!
Complex Parenteral Therapy
Epoprostenol and treprostinil are the only intravenous
medications delivered in nanogram per kilogram per minute
(1,000,000 [1 million] nanograms = 1 milligram). Because of the
high risk of dose errors, verification of correct dose and dose
weight should occur with the patient and family, specialty
pharmacy, inpatient pharmacy, pulmonary arterial hypertension
team if the institution has one, and provider team. Parenteral
therapy should not be stopped, flushed, or diluted for any reason,
and must be infused in a dedicated line without any flush bag.
Owing to the short half-life of the medication epoprostenol, there
must be an immediate backup bag available at all times. Any
interruption or error in calculation can lead to rebound pulmonary
hypertension and risk of death.
993
Circulation Status.
Hemodynamic regulation
994
Respiratory Status: Gas Exchange.
Oxygen therapy
Ventilation assistance
2. Provide emotional and spiritual support for the patient and his or
her support system. (See Emotional and Spiritual Support of the
Patient and Significant Others, Chapter 2.)
995
nitric oxide, the advanced practice provider may need to approach
the patient (if aware and oriented) and support system about
extracorporeal membrane oxygenation if they are a candidate for
heart-lung transplantation. If there are no further options available,
discontinuation of life support may need to be addressed (see
Ethical Considerations in Critical Care, Chapter 2).
Deficient knowledge
related to disease process and treatment of pulmonary hypertension and
associated underlying diseases if present.
Goals/Outcomes: Throughout the hospitalization, the patient and
support system voice understanding of the plan of care; within 24
hours of hospital discharge, the patient and support system
verbalize sufficient knowledge of management of the disease
process(es) and treatments to sustain the patient outside the
hospital.
Knowledge: Disease Process; Knowledge: Treatment and
Procedure(s).
996
4. If the patient requires mechanical ventilation, ensure that the
patient understands how to communicate with care providers (see
Mechanical Ventilation care plans for further details).
6. Ensure that the patient is familiar with the home health providers
who will provide O2 therapy and other ventilation strategies, such
as a nebulizer or aerosol, if needed.
1. Assess the patient’s level and key support system members’ level
of understanding of the disease process.
997
6. If activity has been progressively impaired, consult with a
physical therapist and respiratory therapist regarding an
appropriate exercise program.
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1008
CHAPTER 5
1009
12-lead electrocardiogram
Evaluate for changes from last electrocardiogram (ECG) to assess
for worsened heart disease (myocardial damage) or for electrolyte
imbalances, which may decrease CO; this should be done on every
patient to use for comparison.
Observation
• Evaluate for facial and lip color, appearance of skin and nails, and
patterns of edema (especially dependent areas) to evaluate for
decreased tissue perfusion.
1010
prescribed.
Palpation
Pulse assessment to evaluate for decreased tissue perfusion:
• Capillary refill
Auscultation
• Heart sounds to evaluate for contributors to decreased CO (note
changes with body positioning and respirations):
1011
• Extra sounds: Murmurs, clicks (may indicate valve disease)
Labwork
Blood studies can reveal causes of dysrhythmias or changes in
pacing/conduction or HR changes:
• Coagulation studies
• Lipid profile
• Cardiac enzymes/isoenzymes/troponin
1012
Energy management
1013
Decreased cardiac output
related to altered cardiac pump function.
Goals/Outcome: Within 24 hours of this diagnosis, the patient
exhibits adequate CO, as evidenced by BP within normal limits for
the patient, HR 60 to 100 bpm, NSR on ECG, peripheral pulses
greater than 2+ on a 0 to 4+ scale, warm and dry skin, hourly urine
output greater than 0.5 mL/kg, measured CO 4 to 7 L/min, CVP 4 to
6 mm Hg, PAP 20 to 30/8 to 15 mm Hg, pulmonary artery wedge
pressure (PAWP) 6 to 12 mm Hg, and patient awake, alert, oriented,
and free from anginal pain.
Considerations for the bariatric patient: Preload and after
load may be increased because of increased blood volume.
Circulation Status
1014
7. Monitor effects of negative inotropic medications (e.g., beta
blockers) carefully, as the decreased myocardial workload may
prompt hypotension.
15. Record intake and output (I&O), urine output, and daily weight
and evaluate for fluid retention, which may indicate compromised
renal perfusion.
1015
17. Monitor for increasing activity intolerance, dyspnea, excessive
fatigue, and orthopnea, which may all indicate CO is lessening.
18. Keep head of the bed (HOB) elevated if the patient is unable to
breathe comfortably when flat in bed.
Hemodynamic regulation
1016
Respiratory Status: Ventilation
Airway management
1017
Oxygen therapy
1018
receiving higher concentrations of oxygen (greater than Fio2 45%)
for longer than 24 hours. The higher the oxygen concentration, the
greater the chance of toxicity.
Respiratory monitoring
1019
oxygen therapy (if present) to either NiPPV or endotracheal
intubation with mechanical ventilation to help support the work of
breathing.
Heart failure
Pathophysiology
Heart failure (HF) is the inability of the heart to adequately fill with
blood or pump blood through the body. Effective pumping of the
heart is determined by the components of CO: preload (end-
diastolic volume in the ventricles, which stretches the myocardial
fibers); afterload (resistance to ejection); and contractility of the
myocardium. Myocardial contractility depends heavily on the
delivery of oxygen and nutrients to the heart.
Functional and structural factors that affect any component of CO
can lead to impaired cardiac function and eventual HF. Preload
may be impacted by valvular disorders, cardiac tamponade,
pericarditis, or cardiac arrhythmias such as atrial fibrillation.
Conditions that may increase afterload include aortic stenosis and
hypertension. Contractility may be reduced by direct damage to the
cardiac muscle during myocardial infarction, myocarditis,
cardiomyopathy, or during times of increased metabolic demand
such as thyroid storm. Damaged areas of myocardium can become
hypokinetic (weakly contractile), akinetic (noncontractile), or
dyskinetic (moving opposite from the normal cardiac muscle).
1020
cardiomyopathy, and valvular heart disease. Less common causes
include alcohol- and substance-induced cardiomyopathy, viral
cardiomyopathy, and peripartum cardiomyopathy.
In diastolic failure, cardiac relaxation and ventricular filling are
impaired but EF is preserved. Common causes of diastolic
dysfunction include CAD, ischemic cardiomyopathy, hypertension,
arrhythmias, and aging. Some patients manifest the symptoms of
HF without evidence of systolic or diastolic dysfunction .
Obesity, chronic lung disease, pulmonary embolism, or acute
coronary ischemia can be alternate causes of these symptoms.
1021
components of effective HF management. The progression of HF
symptoms varies with each patient.
Death results from HF-related complications (such as lethal
dysrhythmias) before some patients develop symptoms, while
others are managed for years with an effective medical regimen.
Patients with EF less than 35% are at significantly increased risk of
sudden cardiac death. Advanced HF is classified by severity of
symptoms, cardiac dysfunction, frequency of hospitalization, and
reduction in functional status. Patients with advanced or end-stage
HF may require advanced intervention such as implanted
defibrillator, cardiac resynchronization therapy, inotropic therapy,
ventricular assist device, or cardiac transplantation.
Table 5-2
AMERICAN COLLEGE OF CARDIOLOGY/AMERICAN HEART
ASSOCIATION HEART FAILURE CLASSES
1022
History and risk factors
• History of HF, CAD, myocardial infarction (MI), hypertension,
hypercholesterolemia, obstructive sleep apnea, diabetes,
arrhythmias, and recent viral illness.
• Obesity
1023
1024
Collaborative management
Care priorities
1025
2. Provide oxygen therapy and support ventilation
Supplemental oxygen is required to optimize the patient’s oxygen
saturation.
1026
have been shown to improve survival (carvedilol,
metoprolol succinate, and bisoprolol). All stable
patients with current or prior symptoms of HF and
reduced EF should receive a beta blocker unless
contraindicated. These drugs block the pathologic
effects of circulating catecholamines (epinephrine
and norepinephrine) in patients with HF. Beta
blockers reduce contractility and HR, resulting in
decreased myocardial oxygen consumption and
demand. While a reduction in HR and CO seems
counterintuitive for a patient with HF, allowing the
heart more time to fill and pump with each beat
leads to more effective function. COPD is not a
contraindication to beta-blocker therapy in patients
without significant active wheezing. A
cardioselective beta blocker such as metoprolol
succinate or bisoprolol would be preferable in
patients with a history of COPD. The combination
of ACEI, diuretics, and beta blockers administered
together may cause hypotension. Spacing
medication administration and indicating clear
“hold” parameters for BP in hospitalized patients
can help to reduce this effect.
1027
and systemic tissue perfusion. Treatment with an
ACEI has been shown to reduce mortality and HF
symptoms while improving exercise tolerance and
LVEF. All patients with an EF ≤ 40% should be
treated with an ACEI unless they have a
contraindication or intolerance. ACEIs are
considered reasonable therapy and likely beneficial
in all other patients with HF, regardless of EF. They
help prevent HF in patients at high risk with
atherosclerosis, diabetes mellitus, or hypertension
with other cardiovascular risk factors. ACEI dose
should be titrated to the maximum tolerated;
however, 10% to 20% of patients are ACEI
intolerant. The most troubling side effect from
ACEIs is cough, which may prompt a change to an
ARB or a combination of hydralazine and a nitrate.
Most patients who cough on ACEIs are doing so
because of HF rather than intolerance to the ACEI.
Cough may disappear with increased diuresis.
Development of either angioedema or acute renal
failure requires that the drug be stopped
immediately.
1028
failure and hyperkalemia.
1029
alternative therapy.
1030
• Inodilators (milrinone and inamrinone):
Phosphodiesterase-inhibiting drugs increase
myocardial contractility and lower SVR through
vasodilation. This allows the failing heart to pump
against less pressure (reduced afterload), resulting
in increased CO. Milrinone is used for hypotensive
patients with low-CO HF and pulmonary
hypertension. It is a more potent pulmonary
vasodilator than dobutamine. Milrinone is superior
to dobutamine for patients on chronic oral beta-
blocker therapy who develop acute hypotensive
HF.
1031
• Nitroprusside can induce significant hypotension
and must be titrated carefully. Nitroprusside is
ideally used only for a short time in patients with
advanced renal disease to avoid thiocyanate
toxicity, resulting from an accumulation of this
byproduct of the hepatic metabolism of
nitroprusside. Nitroprusside should also be
avoided in patients with ACS because it may cause
coronary steal syndrome, which shunts blood away
from the ischemic myocardium to better-perfused
muscle.
Table 5-1
HEART FAILURE ASSESSMENT
Left-Sided Heart Failure Pulmonary Edema and Right-Sided Heart Failure Cor Pulmonale
Congestion and Systemic Congestion
Symptoms
• Decreased exercise tolerance • Decreased exercise tolerance
• Fatigue • Fatigue
• Weakness • Peripheral edema (legs, hands,
• Anxiety abdomen, sacrum)
• Dyspnea • Weight gain
At rest • Decreased urination
On exertion • Abdominal tenderness
Orthopnea (inability to lie flat) • Nausea, vomiting, constipation, and
Paroxysmal anorexia
nocturnal dyspnea (awakening from sleep with
significant dyspnea)
• Cough (possibly moist with frothy sputum)
• Diaphoresis
• Palpitations
Physical Assessment
1032
• Tachypnea • Dependent pitting edema
• Rales (most often dependent, in lung bases) • Jugular venous distention
• Unilateral or bilateral diminished lung sounds at • Hepatomegaly
the base (pleural effusion) • Splenomegaly
• Hypertension or hypotension • Ascites
• Orthostasis (drop in BP ≥20 mm Hg with sitting • Positive hepatojugular reflex
or standing) • Cardiogenic shock in acutely ill patients
• Tachycardia (significant hypotension, tachycardia,
• Atrial or ventricular arrhythmia altered mental status)
• S3
• Cyanosis or pallor
• Cardiogenic shock in acutely ill patients
(significant hypotension, tachycardia, altered
mental status, significant dyspnea)
• The combination of skin and pulmonary
assessment can provide information about
perfusion and volume status:
• Warm and dry
• Well-perfused and euvolemic
• Warm and wet
• Well-perfused with volume overload
• Cold and dry
• Hypoperfused without volume overload
• Cold and wet
• Hypoperfused with volume overload
Monitoring
Daily weight Daily weight
Arrhythmias Arrhythmias
SpO2 less than 90% In patients with advanced hemodynamic
Signs of decreased cardiac output: monitoring:
Hypotension Elevated right atrial pressure and central
Tachycardia venous pressure
Decreased urine output Decrease in Svo2 with minimal activity
Weak peripheral pulses Possible decrease in CO/CI caused by
In patients with advanced hemodynamic right ventricular failure causing reduced
monitoring: left ventricular preload
• Decreased CO/CI
• Decreased Svo2
• Elevated pulmonary artery pressures and
pulmonary artery wedge pressure
• Elevated systemic vascular resistance
Table 5-3
DIURETIC DOSING IN HEART FAILURE
Generic (Trade
Type of
Name) and Initial Usage Information
Diuretic
Dose
Loop Furosemide (Lasix) 20 Given per os (PO) or intravenously (IV); PO dosage is
mg doubled for the equivalent effect of IV dosing.
1033
Bumetanide (Bumex) PO and IV administrations result in the same effects from the
0.5 mg same dosage.
Torsemide Given PO or IV. Has the strongest PO effects of all loop
(Demadex) 10 to 20 diuretics.
mg
Ethacrynic acid Given IV to patients who are allergic to furosemide or other
(Edecrin) 50 mg loop diuretics.
Thiazide Hydrochlorothiazide Given PO mainly to manage hypertension; can easily lead to
12.5 mg hypokalemia, hyponatremia, and dehydration.
Metolazone Given PO; should be given 30 minutes before furosemide if
(Zaroxolyn) 2.5 mg used together; has high incidence of hypokalemia.
1034
5. Initiate a low-cholesterol and low-sodium diet
• Extra salt and water are held in the circulatory system, causing
increased strain on the heart. Limiting sodium (Table 5-4) will
reduce the amount of fluid retained by the body. In addition,
fluids may be limited to 1500 to 2000 mL/day in patients who are
hyponatremic.
Table 5-4
REDUCING DIETARY SODIUM
1035
instances, LVEF will improve with medical therapy and/or
treatment of CAD.) ICD therapy has been shown to significantly
reduce mortality in patients with reduced LVEF. Patients should
have a life expectancy of at least 1 year before implantation. In
patients with end-stage HF symptoms who have an ICD in place,
the decision can be made to deactivate the defibrillator to avoid
unnecessary discomfort at end of life.
1036
• LV assist devices (LVADs): Some patients with CS unresponsive
to intraaortic balloon counterpulsation and IV inotrope therapy
may be referred for mechanical circulatory support. LVADs may
be used as a bridge to cardiac transplantation or as a destination
therapy for those ineligible for transplant. The inflow cannula of
an LVAD is connected to the apex of the left ventricle. Blood is
pumped by the device via the outflow cannula to the aorta.
Complications include stroke, infection, coagulopathy with
bleeding, multiple organ dysfunction syndrome (MODS), and
prosthetic valve insufficiency. Most modern LVADs have
continuous flow, leaving the patient without a palpable pulse
despite adequate perfusion.
1037
continued to prevent abrupt worsening of clinical condition.
Fluid/electrolyte management
1038
6. Administer medications as prescribed.
Decreased CO
related to disease process that has resulted in decreased ability of the heart
to provide adequate pumping to maintain effective oxygenation and
nutrition of body systems.
Goals/Outcomes: Within 24 hours of initiating treatment, the
patient has attained a cardiac index (CI) of at least 2.0, PAP is
reduced to within 10% of patient’s normal baseline, BP has
stabilized to within 10% of baseline, and HR is controlled to within
10% of normal baseline.
Cardiac Pump Effectiveness; Circulation Status
1039
6. Hepatic congestion: Monitor liver function (SGOT/AST,
SGPT/ALT, and/or bilirubin), as appropriate.
Respiratory monitoring
1040
90% or greater.
Activity intolerance
related to imbalance between oxygen supply and demand secondary to
decreased functioning of the myocardium.
Goals/Outcomes: Within the 12- to 24-hour period before
discharge from the critical care unit, the patient exhibits cardiac
tolerance to increasing levels of activity as evidenced by RR less
than 24 breaths/min, NSR on ECG, and HR 120 bpm or less (or
within 20 bpm of resting HR).
Activity Tolerance; Energy Conservation
Energy management
1041
active/passive range-of-motion exercises, as appropriate. Encourage
the patient to do as much as possible within prescribed activity
allowances.
Deficient knowledge
related to disease process with HF; need to stop smoking, if applicable;
activity requirements and limitations; need for daily weight log; symptoms
to report; prescribed diet and fluid restriction and medications.
Goals/Outcomes: Within the 24-hour period before discharge
from the critical care unit, the patient and significant others
verbalize understanding of the disease, as well as the prescribed
diet and medication regimens.
Knowledge: Cardiac Disease Management
1042
2. Smoking cessation: Teach the patient about the adverse effects of
smoking and how smoking cessation may benefit him or her.
Provide information about smoking cessation classes and nicotine
patches and medications prescribed to help people stop smoking,
such as varenicline and bupropion.
4. Fluid volume excess: Teach the patient the signs and symptoms
of fluid volume excess that necessitate medical attention: irregular
or slow pulse, increased SOB, orthopnea, decreased exercise
tolerance, and steady weight gain (≥1 kg/day for 2 successive days).
The importance of daily weights should be stressed.
5. Daily weight: Advise the patient about the need to keep a journal
of daily weight. Explain that an increase of ≥1 kg/day on 2
successive days of normal eating necessitates notification of
advanced practice provider.
1043
rest and relaxation.
1044
arteries that results in insufficient perfusion of the myocardium.
ACS includes unstable angina (UA), non-ST-elevation myocardial
infarction (NSTEMI), and ST-segment elevation myocardial
infarction (STEMI). Angina pectoris, or angina as it is commonly
called, is chest discomfort or pain associated with myocardial
ischemia. Angina may be caused by reduced coronary blood flow
as a result of vessel lumen narrowing by plaque or vasospasm. It
can also occur when perfusion pressure is low, as in sudden
hypotension, or when there is increased myocardial workload, as in
aortic stenosis caused by the tremendous resistance to ejection
created by the narrowed aortic valve. Dysrhythmias may also cause
chest discomfort caused by either increased workload (e.g., with
tachycardias) or coronary perfusion deficit (e.g., with bradycardias).
If the chest pain has a predictable pattern, such as being triggered
by increased demand as in exertion (e.g., exercise), it is considered
stable. Those with chest pain or chest discomfort that occurs at rest
or with normal activity, as well as with exertion, have UA. There is
also a variant form of angina, called Prinzmetal angina, which is
caused by vasospasm of the coronary arteries.
Acute myocardial infarction (AMI), either ST elevation or non-ST
elevation, results from necrosis of myocardial tissue caused by
relative or absolute lack of blood supply to the myocardium. Most
AMIs are caused by atherosclerosis, which results in plaque
formation within the coronary arteries. Plaque deposition results in
endothelial changes, which over time cause narrowing of the lumen
of the coronary artery. If an unstable plaque ruptures, the immune
system responds with localized inflammation: platelets aggregate at
the site of the injured plaque, and a thrombus forms. If the lesion is
large enough to fill the vessel lumen, this process results in total
occlusion of blood flow. Occlusion can also be caused by coronary
artery vasospasm. The site of the MI is determined by the location
of the arterial occlusion. In addition to known biomarkers that are
used to diagnose MI, novel biomarkers to help predict plaque
instability that can lead to ACS are being researched.
American Heart Association (AHA)/American College of
Cardiology (ACC) standards recommend treatment protocols for
three types of ACSs: UA, MI with ST-segment elevation (STEMI),
and MI without ST-segment elevation (NSTEMI or non-STEMI).
1045
Patients with STEMI evolve to an ECG with Q waves. Infarcts with
Q waves are larger, although Q waves resolve in 15% of STEMIs.
ECGs in patients with NSTEMIs do not show Q waves. The type of
clot present in the coronary artery may determine the type of event
that evolves. Platelet-rich clots often result in UA or NSTEMI, but
as the rupture of the plaque leads to thrombus formation, it may
result in a STEMI.
The cause of acute chest pain may not be related to myocardial
ischemia. Differential diagnosis of cardiac pain versus other origins
is critical and can challenge the most experienced clinician.
Extracardiac causes of chest pain include pulmonary embolus,
pneumonia, bronchitis, pneumothorax, pleurisy, aortic arch or high
thoracic aortic aneurysm, esophagitis, esophageal motility
disorders, hiatal hernia, cholecystitis, cholelithiasis,
gastroesophageal reflux disease, costochondritis, musculoskeletal
strain, anemia, hypoglycemia, fractured ribs or sternum, thyroid
disease, anxiety disorder, obstipation, and bowel obstruction.
Cardiac causes of chest pain not directly related to ischemia include
valvular disease, aortic dissection, cardiac trauma, cardiac
tamponade, pericarditis, and endocarditis.
The diagnostic process should initially focus on ruling out MI. It
is the most common cause of severe, unrelieved chest pain and
requires immediate intervention to minimize loss of myocardium.
Left unchecked, patients with large areas of necrosis can progress to
cardiogenic shock (CS) quickly. The patient’s history and physical
examination provide the initial framework for treatment decisions,
coupled with the initial diagnostic ECG and assessment of serum
biomarkers. If MI does not appear likely from these findings,
differential diagnosis of chest pain should then focus on
identification of other life-threatening events such as dissecting
thoracic or aortic arch aneurysms, large pulmonary embolism, or
cardiac tamponade.
1046
• Evaluate for decreased CO and decreased tissue perfusion
initially with General Assessment, (Chapter 4).
1047
sided chest discomfort, pain in the teeth, nausea, epigastric pain,
syncope, extreme sudden fatigue, or SOB
• No pain: Does not rule out infarction; 25% of MIs are “silent”
or without pain; common in older adults, women, and diabetic
persons who may feel extreme, sudden-onset fatigue rather than
pain
1048
• AMI: Review for ST-segment elevation in at least two contiguous
leads, which indicates active myocardial damage (acute
infarction); Q waves may or may not form
Vital signs
• Possible fever in patients with AMI
Observation
Evaluate for facial and lip pallor, ashen or diaphoretic appearance
of skin, ashen or cyanotic nail beds, and edema (especially in
dependent areas) to determine decreased tissue perfusion
Palpation
Pulse amplitude may be increased or decreased, depending on SNS
response; evaluate for:
1049
• Slow capillary refill (longer than 2 seconds)
Auscultation
Heart sounds to evaluate for contributors to decreased CO (note
changes with body positioning and respirations):
• S3 indicative of HF (systolic)
• S4 indicative of HF (diastolic)
Labwork
Blood studies can indicate MI and reveal causes of dysrhythmias or
changes in pacing/conduction or HR changes:
1050
1051
Electrocardiographic monitoring and interpretation
First ECG
The first ECG is done immediately upon complaint of chest pain
and is used as part of the process to differentiate STEMI from
NSTEMI/UA or other causes of chest pain and to help determine
diagnosis. It is also helpful in determining the possible need for
thrombolytic therapy or percutaneous coronary intervention (PCI)
for STEMI or antiplatelet medications for patients with
NSTEMI/UA. Reperfusion strategies should be implemented
1052
immediately for STEMI patients.
Serial ECGS
ECGs are then done in a series (initially and then every 30 minutes
for the first 2 hours). Characteristic changes in certain lead groups
identify the area and evolution of infarct. After the initial evaluation
phase, ECGs may be done every 8 to 24 hours and as needed for
complaints of chest pain.
1053
minutes of arrival.
Not all patients experience STEMI. The 2012 ACCF/AHA practice
guidelines outline treatment options for UA/NSTEMI patients. They
include treatment with P2Y12 receptor inhibitors such as
clopidogrel, prasugrel, or ticagrelor.
Q waves
Q waves are a later ECG change and may or may not be present in
patients presenting with an MI. Q waves are indicative of MI and
are “pathologic” if they meet the following criteria: wider than 0.03
seconds, ≥ 1 mm in depth, and present in 2 contiguous leads. Q
waves may develop later, or the tissue necrosis may extend itself if
a reperfusion strategy is withheld.
1054
T-wave changes
Within the initial hour of infarction, tall, peaked, “hyperacute”
upright T waves may be seen in leads over the infarct. Within
several hours to days, the T wave becomes inverted. Gradually over
time, the ST segment becomes isoelectric and the T wave may
remain inverted. T-wave changes may last for weeks and return to
normal or remain inverted for the rest of the patient’s life. T-wave
changes reflective of posterior and RV MI are not clearly seen on
the 12-lead ECG. Use of 15- or 18-lead ECGs should provide better
information about these areas (Table 5-5).
Table 5-5
12- TO 18-LEAD ECG LOCATION OF MYOCARDIAL INFARCTION
(MI)
*
Leads must be added to normal 12-lead ECG.
LAD, Left anterior descending artery; LV, left ventricle.
Collaborative management
ACUTE MYOCARDIAL INFARCTION HOSPITAL QUALITY
ALLIANCE INDICATORS
1055
Care priorities for all acute coronary syndromes
Prevention of initial or further coronary thrombus formation may
include administration of anticoagulant/antithrombin medications
(i.e., unfractionated or low-molecular-weight heparin [LMWH])
and antiplatelet drugs (e.g., aspirin, clopidogrel, or glycoprotein
[GP] IIb/IIIa inhibitors such as abciximab, eptifibatide, or tirofiban).
In patients evolving toward AMI, these agents are thought to abate
complete closure of the coronary arteries or to prevent more
extensive clot formation. Cardiac catheterization is often performed
to assess the size and location of coronary lesions. If significant
lesions are found, PCI can immediately follow catheterization in
facilities that offer PCI.
1056
heart is enhanced, pain can be relieved. If the patient deteriorates,
other methods of oxygen delivery may be implemented (e.g.,
nonrebreather mask with reservoir and mechanical ventilation
for those who deteriorate markedly).
1057
the only anticoagulant during PCI because of the increased risk of
catheter thrombosis.
• Administer medications:
1058
prevention and treatment of HF. Should be used for
patients with diabetes, chronic kidney disease,
and/or reduced EF unless contraindicated.
HIGH ALERT!
Caution should be exercised in the use of antiarrhythmic agents in
patients with acute myocardial infarction (AMI), especially to
manage reperfusion dysrhythmias, because instability of the
conduction system with AMI is sometimes aggravated by use of
antiarrhythmic agents. Electrical therapies such as synchronized
cardioversion, defibrillation, external/transthoracic pacing, or
transvenous pacing may provide a safer management strategy for
these patients.
1059
5. Prevention of contrast-induced nephropathy related
to use of contrast during coronary angiography/PCI
Additional treatments
1060
determine whether the stenosis has been reduced to less than
50% of the vessel diameter, which is the goal of the procedure.
The femoral artery site may be closed using a device, or the
introducer sheath is left in the femoral artery until the effect of
anticoagulant medications has diminished. In the case of radial
access, a radial artery band is applied.
1061
3. Surgical revascularization
1062
Box 5-1
THROMBOLYTICS
First-generation (nonselective) thrombolytics
Streptokinase: An enzyme derived from group C beta-hemolytic
streptococci. Because it is an antigen, patients who have had
previous exposure to streptococcal organisms may have
antibodies against streptokinase. Therefore steroids or
antihistamines are administered before streptokinase therapy to
prevent a hypersensitivity reaction.
1063
conversion of plasminogen to plasmin is increased relative to its
conversion in the absence of fibrin. Following administration of
tenecteplase, there are decreases in circulating fibrinogen and
plasminogen. It has a half-life of up to 130 minutes for final
clearance and is mostly metabolized through the liver. There are
less bleeding complications than with alteplase. Tenecteplase is
given as a single 5-second bolus and is dosed by weight.
Box 5-2
CONTRAINDICATIONS AND WARNINGS
FOR THROMBOLYTIC THERAPY
Absolute contraindications
• Known hypersensitivity to thrombolytic agents
• Cerebrovascular disease
1064
• Recent internal bleeding (within 2 to 4 weeks)
• Recent trauma
• Dementia
• Pregnancy
• Advanced age
1065
discharge from the CCU, the patient exhibits cardiac tolerance to
increasing levels of activity as evidenced by RR less than 24
breaths/min, NSR on ECG, BP within 20 mm Hg of patient’s normal
range, HR less than 120 bpm (or within 20 bpm of resting HR for
patients on beta-blocker therapy), and absence of chest pain.
Energy Conservation, Instrumental Activities of Daily Living
(IADL)
Energy management
Bleeding precautions
1066
including aspirin and other antiplatelet drugs, GP IIb/IIIa
inhibitors, direct thrombin inhibitors, and thrombolytics.
2. Monitor Hgb and Hct closely. Report Hgb drop greater than 2 g
to physician immediately.
4. After PCI via femoral sheath, keep HOB less than 30 degrees and
affected leg straight as ordered.
5. After PCI, monitor vital signs, sheath site, and distal pulses every
15 minutes until sheath is removed, then every 15 minutes x2, then
every 30 minutes x2, then every 4 hours.
1067
to 4+ scale, warm and dry skin, and hourly urine output >0.5
mL/kg/h. Patient is awake, alert, and oriented without palpitations,
chest pain, or dizziness. Within 48 hours, the patient maintains
stability as just described.
Circulation Status
Cardiac care
1068
9. Monitor for signs of bleeding and bleeding complications:
bleeding at sheath site or at IV sites, back pain (may indicate
retroperitoneal bleed), signs and symptoms of cerebrovascular
accident (CVA)/stroke (see Stroke: Acute Ischemic and
Hemorrhagic, Chapter 7).
Risk identification
1069
antihistamine as prescribed.
Hemodynamic regulation
1070
1. Monitor for unstable BP and use hemodynamic readings to help
assess need for titration of vasoactive, inotropic, and antiarrhythmic
medications.
1071
Goals/Outcomes: Within the 24-hour period before discharge
from the step-down unit, the patient verbalizes understanding of
his or her disease, as well as the necessary lifestyle changes that
may modify risk factors.
Knowledge: Disease Process; Knowledge: Medication;
Knowledge: Diet; Knowledge: Energy Conservation; Sexual
Identity: Acceptance; Knowledge: Sexual Functioning
1. Teach the patient about ischemia and its resultant chest pain,
referred to as angina pectoris.
3. Assist the patient in identifying his or her own risk factors (e.g.,
cigarette smoking, high-stress lifestyle, hyperglycemia, high-fat
diet).
1072
Teaching: Individual; Teaching: Disease Process,
Thrombolysis
Altered protection
related to risk of bleeding/hemorrhage secondary to nonspecific
thrombolytic effects of therapy.
Goals/Outcomes: Symptoms of bleeding complications are absent
as evidenced by BP within patient’s normal range, HR less than 100
bpm, blood-free secretions and excretions, natural skin color,
baseline or normal level of consciousness (LOC), and absence of
back and abdominal pain, hematoma, headache, dizziness, and
vomiting.
Risk Control
Risk identification
1073
drip to maintain PTT at 1.5 to 2 times control levels or according to
protocol. Never discontinue heparin without consulting with the
provider.
8. Use care with oral hygiene and when shaving patient. For more
information about safety precautions, see Pulmonary Embolus,
(Chapter 4).
1074
• Teach the patient about the prescribed medications,
including name, purpose, dosage, action, schedule,
precautions, and potential side effects.
Teaching: Activity/exercise
If chest pain occurs:
1075
warm up and cool down with stretches for 5 to 7
minutes and to walk 3 to 5 times each week.
Table 5-6
THROMBOLYTIC DOSAGE REGIMENS
1076
Teaching: Sexuality
Sexual activity guidelines: Because sexual activity is a physical
activity, certain guidelines can help the patient and his or her
partner enjoy a satisfying sexual relationship while minimizing the
workload of the heart:
1077
6. Do not take phosphodiesterase type-5 (PDE-5) inhibitors
(sildenafil, vardenafil) if taking nitrates.
Pain management
1078
than 80 mm Hg systolic BP) occurs, stop the infusion and contact
the provider for further directions.
10. Instruct the patient to report any further episodes of chest pain.
Dysrhythmia management
1079
1. Obtain a 12/15/18-lead ECG during patient’s episode of chest
pain. During angina, ischemia usually is demonstrated on the ECG
by ST-segment depression and T-wave inversion.
1080
Medications; Knowledge: Disease Process
Teaching: Procedure/treatment
1081
with another patient who has had a successful intervention.
1082
hemolytic, Intermedius, Lugdunensis, Enterococcal gram-negative
bacilli, Legionella, Haemophilus, Aphrophilus, Actinobacilus,
Actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens,
Kingella kingae, Bartonella, Candida, Aspergillus, and Pseudomonas
aeruginosa. Forty percent of patients with IE have no underlying
heart disease. Despite diagnosis and treatment strategies, the
fatality rate has not decreased since the 1970s. The age of a patient,
proliferation of implanted biomechanical devices, rise in resistant
organisms, and the incidence of hospital-associated infection may
have influenced that. Antibiotic prophylaxis has had little effect on
decreasing the incidence.
Portals of entry for the infecting organism include the mouth and
GI tract, upper airway, skin, and external genitourinary (GU) tract.
All heart valves are at risk for infection, but the aortic and mitral
valves are more commonly affected than the right-sided pulmonic
and tricuspid valves. IV drug abuse, along with right-side insertion
of invasive lines increases the possibility of tricuspid IE. Once the
infection process begins, valvular dysfunction, manifested by
insufficiency with regurgitant blood flow, can occur, ultimately
resulting in a decrease in CO. The vegetation may enlarge and
obstruct the valve orifice, further reducing CO. The vegetation may
break apart and embolize to vital organs. In severe cases, the
affected valve may necrose, develop an aneurysm, and rupture; or
the infection may extend through the myocardium and epicardium
to cause a pericarditis (see Acute Pericarditis, Chapter 5). If the
conduction system is affected by the spreading infection, bundle
branch block may occur. The chordae tendineae can become
infected and rupture, resulting in severe acute mitral or tricuspid
regurgitation. Complications of IE occur suddenly, with a dramatic
change in the clinical picture. Mortality rates between 20% and 50%
have been reported. The infection recurrence rate is 10% to 20%.
The incidence of IE is higher in patients older than 50 years of age,
is more common in men than in women, and is uncommon in
children.
Types of IE include:
1083
• Prosthetic valve endocarditis, early and late: 10% to 20%
• IV drug abuse
• Pacemaker
• Nosocomial
Assessment
Goal of assessment
The goal is to identify the severity of symptoms. The severity of
symptoms varies depending on the infective organism. (For
example, Staphylococcus aureus infection is more severe than that
with Streptococcus viridans.) Acute presentation is defined as onset
within 1 week of infection, while subacute infections may take up to
4 weeks to present.
Vital signs
• Fever, tachycardia, possible dysrhythmias, possible hypotension,
fatigue, and valvular dysfunction
Hemodynamic measurements
Invasive monitoring devices are used cautiously with these
patients, as they may cause further valvular dysfunction,
embolization, and infection.
1084
necessary.
Observation
• The skin is often pale.
1085
If emboli of the vegetations occur in other areas, signs and
symptoms of stroke or peripheral, myocardial, renal, or mesenteric
arterial insufficiency, occlusion, or infarct will be seen.
Auscultation
• A new or changed murmur may be heard as a result of the
valvular dysfunction.
Screening labwork
Blood studies can reveal presence of infection or further and
progressive worsening heart status, such as HF, conduction
problems, or ischemia.
12-lead electrocardiogram
Evaluates for changes from last ECG to assess for worsening of
heart disease (myocardial damage). ECG changes resulting from
electrolyte imbalances may also decrease CO. An initial 12-lead
ECG should be done on every patient and used for comparison
over the course of hospitalization.
1086
contractions, atrial flutter, or atrial fibrillation may occur.
1087
Collaborative management
Care priorities
• A history of endocarditis
1088
• Certain congenital heart defects including:
Table 5-9
ECG CHANGES FREQUENTLY FOUND WITH VENTRICULAR AND
ATRIAL HYPERTROPHY
Table 5-8
ASSESSMENT FINDINGS WITH VALVULAR HEART DISEASE
1089
BP, Blood pressure; CO, cardiac output; CVP, central venous pressure; ICS,
intercostal space; LSB, left sternal border; LV, left ventricle/ventricular; LVEDP, left
ventricular end-diastolic pressure; MCL, midclavicular line; PA, pulmonary artery;
PAEDP, pulmonary artery end-diastolic pressure; PAP, pulmonary artery pressure;
RA, right atrium; RAP, right atrial pressure; RSB, right sternal border; RV, right
ventricle/ventricular.
• Fluid and sodium restriction: Used for optimal fluid balance with
1090
reduced heart function or HF. Specific restrictions must be
individualized and based on severity of symptoms.
• Bed rest: May be used initially, with activity as tolerated for the
remainder of treatment
3. Pharmacotherapy
1091
antibiotics (see Valvular Heart Disease, Chapter 5). An abscess or
infected tissue may be surgically removed if there is no response to
long-term antibiotics. If the patient is hemodynamically stable,
surgery may not be needed. A surgeon is usually consulted in case
of an HF emergency. Early surgical intervention with severe
valvular damage may decrease hospital mortality.
1092
Ring abscess may lead to valve dehiscence,
perivalvular leakage, and formation of myocardial
abscesses. Extension to the conduction system may
prompt a new atrioventricular block. Valve stenosis
and purulent pericarditis are seen less often. Valve
stenosis is more common with bioprosthetic valves
than mechanical valves. Bioprosthetic valve PVE
results in leaflet tears or perforations. Ring
abscesses, purulent pericarditis, and myocardial
abscesses are seen less often in bioprosthetic valve
PVE.
• Early PVE: Occurs within 60 days of valve insertion and is usually
the result of perioperative contamination
• Late PVE: Occurs 60 days or later after insertion and is usually the
result of transient bacteremia from dental or GU sources, GI
manipulation, or IV drug abuse
1093
Cardiac care
1094
patient’s MAP is high, decrease afterload with
prescribed arterial dilators (e.g., nitroprusside).
1095
related to alveolar-capillary membrane changes with decreased diffusion of
oxygen secondary to pulmonary congestion.
Goals/Outcomes: Within 24 hours of initiation of oxygen therapy
and during the weaning process, the patient has adequate gas
exchange as evidenced by RR less than 20 breaths/min with normal
pattern and depth, SVO2 60% to 80%, PaO2 greater than 80 mm Hg,
SaO2 greater than 95%, and natural skin color.
Respiratory Status: Gas Exchange; Tissue Perfusion:
Pulmonary
Ventilation assistance
1096
• Assess arterial oxygen saturation with pulse
oximetry. Normal oxygen saturation is 95% to 99%.
Levels of 90% to 95% necessitate frequent
assessment. Oxygen levels that trend down to less
than 90% require aggressive interventions to
increase oxygen saturation. Consider increasing
FIO2, decreasing preload, and taking measures to
improve ventilation.
Infection protection
1097
1. Prevent central line-associated bloodstream infection: Use strict
aseptic technique to care for all invasive monitoring device
insertion sites and IV lines. Rotate central lines per hospital
protocol. Discuss feasibility of a tunneled catheter or peripherally
inserted central catheter (PICC) line with advanced practice
provider.
1098
procedures such as dental examinations or surgery. The AHA
publishes general guidelines for prophylactic antibiotic treatment to
prevent IE.
Hemodynamic regulation
1099
4. Monitor patient for confusion and changes in sensorimotor
capabilities or cognition, which may signal cerebral emboli.
Acute pericarditis
Pathophysiology
Pericarditis is the general term for an inflammatory process
involving the pericardium and the epicardial surface of the heart.
Inflammation can occur as the result of an AMI, an infection,
chronic renal failure, or an immunologic, chemical, or mechanical
event (Box 5-3). Often, early pericarditis manifests as a dry
irritation, whereas late pericarditis (after 6 weeks) involves
pericardial effusions that can lead to cardiac tamponade if severe.
Pericarditis is often seen in the CCU as a secondary finding
following coronary revascularization surgery or valve replacement
or associated with chronic renal failure. A thorough assessment and
recognition are essential for appropriate treatment, as symptoms
1100
can be masked by the primary condition. For example, patients are
sometimes transferred into a CCU with acute cardiac
decompensation resembling ACS, when in reality, the condition is
caused by pericardial effusions.
Box 5-3
CAUSES OF PERICARDITIS
• Autoimmune cardiac injury
• Hypothyroidism
• Idiopathic
• Myocardial infarction
• Metabolic disorders
• Neoplasms
• Postpericardiotomy syndrome
• Radiation injury
• Rheumatologic disease
• Rheumatic fever
• Rheumatoid arthritis
• Sarcoidosis
1101
• Trauma
• Uremia
Assessment
Goal of assessment
The goal is to assess severity of the symptoms and to rule out ACS
as the cause of ECG changes (ST-segment elevation and/or
depression) and chest pain. Acute pericarditis is characterized by
chest pain, pericardial friction rub, and serial electrocardiographic
changes. Severe pericardial effusions can cause cardiac tamponade.
Observation
The patient presents with chest pain, but the location and quality
can vary. Pain can be knifelike and stabbing and may radiate to the
neck or shoulder. Usually the pain is aggravated by a supine
position, coughing, deep inspiration, and swallowing. Pain may be
1102
lessened when leaning forward. Dyspnea develops because of
shallow breathing to prevent pain.
1103
Hemodynamic measurements
If used, the PA catheter reveals elevated CVP, PAP, and PAWP.
Auscultation
Heart sounds may reveal an intermittent pericardial friction rub.
The pericardial friction rub has three components; one systolic and
two diastolic: one early in diastole when the heart begins to stretch
during ventricular filling and the other during late diastole when
the ventricles are fully stretched. The first and second heart sounds
are obscured by the rubbing sounds, which are sometimes
described as the sound of squeaky leather shoes. S1 and S2 are no
longer crisp and clear. If all three components of the rub are
audible, S2 may sound split.
Pericardial friction rub: The rub is heard best with the diaphragm
of the stethoscope positioned at the left lower sternal border. The
rub is often positional, so auscultation should be done with the
patient in several positions (i.e., supine, sitting and leaning forward,
lying on the left lateral side). A friction rub may not be heard, even
in the presence of pericarditis.
Screening labwork
• CBC: May reveal elevated WBCs and anemia
12-lead electrocardiogram
Evaluates for changes from last ECG; assesses for worsened heart
disease (myocardial damage) or electrolyte imbalances that may
decrease CO; should be done on every patient to use for
1104
comparison.
1105
1106
Table 5-10
ECG CHANGES WITH PERICARDITIS
Time of
Stage Pattern
Change
1 Onset of pain ST segments have a concave elevation in all leads except AVL and V1; T
waves are upright
2 1 to 7 days Return of ST segments to baseline with T wave flattening and invert
3 1 to 2 weeks Inversion of T waves without R or Q changes
4 Weeks to ECG returns to prepericarditis state
months
Collaborative management
Care priorities
1107
• Colchicine: Reduces inflammation in the body; may be prescribed
as a first-line treatment for pericarditis or for recurrent
symptoms. Colchicine can reduce the length of pericarditis
symptoms and decrease the risk that the condition will recur.
However, the drug is not safe for people with certain preexisting
health problems, such as liver or kidney disease. Carefully check
the patient’s health history before prescribing colchicine.
1108
Ineffective breathing pattern
related to guarding as a result of chest pain
Goals/Outcomes: Within 48 hours of this diagnosis, the patient
demonstrates RR 12 to 20 breaths/min with normal depth and
pattern and reports that chest pain is controlled.
Respiratory Status: Ventilation
Respiratory monitoring
Activity intolerance
related to bed rest, weakness, and fatigue secondary to impaired cardiac
function, ineffective breathing pattern, or deconditioning.
Goals/Outcomes: Within 72 hours of this diagnosis, the patient
exhibits cardiac tolerance to increasing levels of exercise as
evidenced by peak HR less than 20 bpm over patient’s resting HR,
peak systolic BP less than 20 mm Hg over patient’s resting systolic
BP, SVO2 at least 60%, RR less than 24 breaths/min, NSR on ECG,
warm and dry skin, and absence of crackles, murmurs, and chest
pain during or immediately after activity.
1109
Energy Conservation; Endurance; Activity Tolerance
Energy management
2. Modify the activity plan for the patient with post-MI pericarditis
who is receiving steroids. A lower activity level may help prevent
thinning of the ventricular wall and reduce the risk of an aneurysm
or rupture of the ventricle.
1110
Aortic aneurysm/dissection
Pathophysiology
The aorta is exposed to high pulsatile pressure, making it
susceptible to injury and disease from mechanical trauma.
Conditions that weaken the medial layer or increase stress on the
vessel wall can lead to dilation, aneurysmal formation, and
eventually rupture or dissection of the aorta. Pathologies related to
the aorta can be life-threatening because of the potential for
disruption of blood flow to a large portion of the body, including
vital organs such as the brain, heart, kidneys, and GI tract.
Symptoms may mimic other conditions, and survival depends
largely on timely diagnosis and rapid intervention to preserve end-
organ function.
An aortic aneurysm is an abnormal dilation of the vessel, with an
increase of at least 50% its normal diameter. Aneurysms are usually
described based on their location along the aorta (thoracic,
abdominal) and their morphology. A true aneurysm involves all
three layers of the arterial wall (intima, media, adventitia). The two
forms of a true aneurysm are fusiform (symmetrical dilation of the
entire circumference of the aorta) and saccular (eccentric ballooning
of only a portion of the aortic wall). A false aneurysm or
“pseudoaneurysm” is a hematoma caused by injury to the aortic
wall, resulting in blood contained by the adventitia or surrounding
tissue.
Most often aneurysms develop at the site of an atherosclerotic
lesion, which precipitates degeneration of the tissue and allows the
arterial wall to dilate. With advancing age, the elastin in the aorta is
decreased, which further weakens the vessel wall. Hypertension
increases mechanical stress on the vessel, promoting further
expansion of the aneurysm. Smoking has been linked to accelerated
expansion of both thoracic and abdominal aneurysms. The rate at
which the aneurysm increases is not predictable; however, the
likelihood of rupture or dissection increases dramatically when the
size exceeds 6 cm. Aortic aneurysms result in approximately 17,000
deaths per year, the majority because of rupture.
An aortic dissection is a longitudinal tear in the intimal layer of
1111
the aortic wall. Dissection can occur without the presence of an
aneurysm. As blood enters the tear, pulsatile pressure creates a
false channel between the intimal and medial layers. The force of
pressure generated by ventricular contraction and systemic BP can
cause the dissection to extend either distally or proximally—
compromising flow to structures perfused by that segment of the
aorta. Precipitating factors for aortic dissection include medial
degeneration from inherited (e.g., connective tissue diseases,
congenital defects) or acquired (e.g., hypertension, inflammation)
disorders, trauma, pregnancy, and cocaine abuse (see Hypertensive
Emergencies, Chapter 5).
Aortic dissection is classified by location, using two different
systems. The DeBakey classification defines a dissection as type I if
it involves the entire aorta, type II if it is confined to the ascending
aorta only, and type III if the dissection originates in the descending
aorta, distal to the left subclavian artery. The Stanford system
classifies dissections into two groups: type A, which involves both
the ascending and descending aorta (DeBakey types I and II), and
type B, which affects only the descending aorta (DeBakey type III).
Ascending dissections occur much more frequently (65%) than
descending dissections and are considered more lethal.
The morbidity and mortality associated with aortic dissection are
greatest near the time of the initial injury. Patients who present for
medical evaluation within 2 weeks or less of symptom onset are
characterized as “acute,” while a dissection diagnosed after this
time is considered “chronic.” Approximately 2000 episodes of acute
aortic dissection occur annually, with mortality approaching 75% if
left untreated.
Assessment
Goal of the assessment
Gather information that can assist in making the differential
diagnosis so appropriate management can be initiated immediately.
1112
(e.g., smoking, CAD, hyperlipidemia), connective tissue disorders
(e.g., Marfan syndrome, Ehlers-Danlos syndrome), congenital
defects (e.g., coarctation of the aorta, bicuspid aortic valve), family
history of aneurysm or dissection, blunt chest trauma, pregnancy,
cocaine use, advanced age (older than 60 years), and male sex.
Vital signs
• Hypertension may be preexisting or an SNS response to pain;
more common in descending dissections.
Observation
Pain
1113
• Symptoms vary based on location of the dissection and resultant
compromise in tissue perfusion.
Palpation
• Pulse deficits (difference in pulse volume or absent pulses) are
considered a classic finding; they occur in only 30% of patients.
Auscultation
• Diastolic murmur: With aortic regurgitation
Diagnostic tests
1114
HIGH ALERT!
Rapid diagnostic imaging is essential, because mortality from
aortic dissection increases by the hour. Transesophageal
echocardiography, CT angiography, and magnetic resonance
imaging are all highly accurate in identifying the presence and
extent of dissection. The choice of study is usually determined by
the patient’s clinical stability and the facility’s resources. Although
the definitive diagnosis is made by imaging studies, additional
diagnostic tests may be helpful in ruling out other potential causes
of chest pain (pulmonary embolism, MI, pericarditis) or evaluating
the extent of end-organ involvement (see Diagnostic Tests Table).
Collaborative management
1115
Because of the emergent nature of this disorder, limited
randomized controlled trials are available to guide the treatment of
patients with aortic dissection or rupture. The establishment of the
International Registry of Acute Aortic Dissection has provided
valuable information regarding presentation, management, and
outcomes for this patient population. This information was
combined with an appraisal of available cohort studies and
retrospective reviews to develop the practice guidelines described
in the following table.
In 2010 the American College of Cardiology, American Heart Association, and a number of other
professional groups issued guidelines for diagnosis and management of patients with thoracic aortic
disease. Some of the class I recommendations for managing acute and chronic dissection are listed below:
Initial Management of Acute Dissection
1. Initial management of thoracic aortic dissection should be directed at decreasing aortic wall
stress by controlling heart rate and blood pressure as follows:
• In the absence of contraindications, intravenous beta blockade should be initiated and
titrated to a target heart rate of 60 beats per minute (bpm) or less.
• In patients with clear contraindications to beta blockade, nondihydropyridine calcium
channel-blocking agents should be used as an alternative for rate control.
• If systolic blood pressure remains greater than 120 mm Hg after adequate heart rate control
has been obtained, then ACEIs and/or other vasodilators should be administered
intravenously to further reduce blood pressure to a level that maintains adequate end-organ
perfusion.
• Beta blockers should be used cautiously in the setting of acute aortic regurgitation because
they will block compensatory tachycardia.
1116
atherosclerosis.
From: Hiratzka LF, Bakris GL, Beckman JA, et al: 2010 ACCF/AHA/AATS/ACR/ASA/
SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients
with thoracic aortic disease: executive summary. J Am Coll Cardiol 55:1509-1544,
2010.
Care priorities
The immediate goal of therapy for aortic dissection or rupture is to
limit propagation of the dissection by reducing the shearing forces
created by myocardial contractility and BP.
2. Control pain
Usually achieved with IV morphine sulfate, 2 to 10 mg, since
morphine helps diminish sympathetic outflow. If additional
sedation is required, midazolam may be used.
1117
3. Evaluate for and facilitate surgical or endovascular
treatment
Urgent intervention is recommended for type A (ascending)
dissection and type B (descending) dissection when impending
rupture, significant organ ischemia, or refractory hypertension
occurs. Surgery involves removal of the affected section of the aorta
and replacement with a prosthetic graft. Repair or replacement of
the aortic valve may also be needed. For patients who meet clinical
and anatomic criteria, endovascular repair is increasingly an option.
This involves placement of a stent graft to occlude the false lumen,
thus restoring flow in the true lumen. Fenestration, a technique in
which holes are created either in the dissection flap or in the graft to
reestablish flow from the aorta into branching arteries, may also be
used.
1118
sensations in the extremities, bilaterally equal systolic BP less than
120 mm Hg, HR less than or equal to 60 bpm, NSR on ECG, urine
output greater than 0.5 mL/kg/h, equal and normoreactive pupils,
and orientation to time, place, and person.
Circulation Status
Shock prevention
1119
8. Decreased renal perfusion: Monitor urine output hourly. Consult
advanced practice provider if urine output is less than 0.5 mL/kg/h
for 2 consecutive hours.
Acute pain
related to biophysical injury secondary to necrosis at the aortic media and
distal tissue hypoperfusion.
Goals/Outcomes: Within 24 to 48 hours of this diagnosis,
patient’s subjective evaluation of pain improves, as documented by
a pain scale. Nonverbal indicators, such as grimacing, are decreased
or absent.
Pain Control
Pain management
1120
Additional nursing diagnoses
For other nursing diagnoses and interventions, also see the
following as appropriate: Hemodynamic Monitoring (Chapter 1),
Prolonged Immobility (Chapter 1), Emotional and Spiritual Support
of the Patient and Significant Others (Chapter 2), and Chest Trauma
(Chapter 3).
Cardiogenic shock
Pathophysiology
Cardiogenic shock (CS) represents the final pathway of a large
number of pathologic conditions, which lead to severe impairment
of CO (cardiac function) and result in significant impaired end-
organ perfusion. Initial perfusion changes resulting from CS are
associated with a cycle of inflammation, ischemia, and progressive
myocardial dysfunction. Morbidity and mortality are the end result
of severe LV failure. CS may be caused by several conditions:
primary LV failure, RV failure, severe valvular regurgitation, or
ventricular septal rupture, which may occur alone or in
combination. Because of the wide spectrum of causes of CS, the true
incidence is unknown; however, the most common cause of CS is
AMI. CS occurs in 5% to 8% of patients experiencing an AMI, most
commonly in patients with STEMI. Although uncommon, NSTEMI
can result in CS. There are few studies characterizing the
differences in shock in patients presenting with STEMI versus
NSTEMI. Despite high mortality rates in all patients with shock, no
definitive guideline recommendations exist for the management of
shock in patients with NSTEMI.
CS is initiated by a severe impairment in CO leading to decreased
perfusion of the coronary arteries. The result is ischemia, which
further reduces myocardial performance, commonly known as
“pump failure.” Myocardial necrosis or stunning of the
myocardium can occur from reperfusion injury during invasive
intervention such as primary PCI or reocclusion of the infarcted
artery. Next in the cascade of events is the compensatory
neurohumoral response to reduced blood flow. Activation of the
1121
SNS and renin-angiotensin-aldosterone system result in
vasoconstriction and salt and water retention. As resistance to
ventricular ejection increases, the result is worsening myocardial
ischemia and end-organ hypoperfusion, with an increased
incidence of ventricular dysrhythmias. Catecholamine release from
the SNS also induces tachycardia, which further increases
myocardial oxygen demand and worsens pump failure. As
perfusion continues to decrease, compensation fails and vascular
beds begin dilating, resulting in anaerobic metabolism and lactic
acidosis, which further decreases myocardial contractility.
Inflammatory mediators including interleukin-6 and tumor necrosis
factor-alpha are elevated, which adds to the negative inotropic
effects. Nitric oxide level increases are the result of high levels of
cytokines. Vasodilatation progressively increases, which results in
hypotension and worsening of lactic acidosis.
Despite decades of studies, the mortality rate from CS remains
high. In the future, improved outcomes for patients with CS will
result from an improved understanding of the pathophysiology
and advances in pharmacologic and mechanical therapies.
Assessment
Goals of assessment
The goals are to identify the severity of symptoms and the stage of
shock and provide the patient’s clinical and laboratory data to assist
with the differential diagnosis of the cause.
The diagnosis of CS is dependent on several findings.
1122
from renal hypoperfusion, disorientation, lethargy, elevated lactic
acid indicating visceral hypoperfusion
Observation
As shock progresses from the low CO state, there is evidence of
vital organ hypoperfusion: disorientation (altered mental status),
oliguria, and acidosis. Skin is cool to cold (mottling may be present)
and diaphoretic caused by decreased peripheral perfusion.
3) HR ≥ 60 bpm
Auscultation
• S3 or S4 heart sounds may be present resulting from an
overdistended, noncompliant ventricle.
1123
regurgitation. Electrocardiographic changes in mitral
regurgitation are nonspecific and are primary changes of LV
hypertrophy and strain.
Hemodynamic measurements
Hemodynamic monitoring
An arterial line is used to guide initial therapy. The role of invasive
hemodynamic monitoring with a pulmonary artery catheter in
patients with CS is uncertain. Although no clinical trial has
established a clinical benefit from its use, it is still being
recommended for use in this patient population. Currently less
invasive methods are also being used including:
• Transpulmonary thermodilution
• Diagnostic accuracy
1124
• Measuring mixed venous oxygen, SVO2, which is an indicator of
how well oxygen supply meets tissue demand for energy
production
Diagnostic tests
See Diagnostic Tests for Heart Failure page and Acute Coronary
Syndromes (Chapter 5).
Collaborative management
Care priorities
Patients in CS have high mortality rates. Early and rapid relief of
ischemia when the cause of CS is AMI is essential to avoid
refractory multiorgan dysfunction and death. Treatment of CS is
aimed at improving symptoms and stabilizing the hemodynamics.
The goals are to:
1125
oxygen demand.
Initial therapy
Limited fluid resuscitation is reasonable unless there is pulmonary
edema upon presentation. The maintenance of adequate
oxygenation and airway protection is required, along with
mechanical intubation if needed. Excessive levels of positive end-
expiratory pressure should be avoided to prevent oxygen toxicity.
Hypokalemia and hypomagnesemia contribute to ventricular
arrhythmias and should be treated immediately. Amiodarone can
be used to prevent arrhythmia recurrence. Bradycardia caused by
heart block or drug effects should be corrected. Anxiety and pain
can be treated with narcotic analgesics as they will also reduce
preload, afterload, and sympathetic activity.
1126
Dopamine: Dopamine is used to increase CO and BP when the HR
is below 110 bpm Dopamine is used in both low and high doses:
• Vasodilation
1127
• Cardioprotection
Table 5-11
HEMODYNAMIC EFFECTS OF DRUGS USED IN CARDIOGENIC
SHOCK
1128
BP, Blood pressure; CO, cardiac output; D, decrease; HR, heart rate; I, increase; O,
no effect; SVR, systemic vascular resistance.
Loop diuretics
Furosemide is a loop diuretic that blocks the sodium potassium
chloride transporter and increases urinary excretion of sodium and
chloride. LV filling pressures are reduced because of the ability of
furosemide to increase the systemic venous capacitance.
Other loop diuretics that can be used are bumetanide and
torsemide.
1129
IABP is the most widely used form of mechanical hemodynamic
support in patients with CS. The IABP is a balloon inserted into the
descending aorta between the arch vessels and renal arteries. The
balloon inflates after cardiac ejection and deflates before the onset
of the following systole. The balloon displaces blood proximally,
increasing coronary perfusion pressure and raising diastolic aortic
pressure. Deflation of the balloon during systole reduces end-
diastolic pressure and LV afterload. The main aims of the use of
IABP are to improve hemodynamics, increase perfusion of vital
organs, and reduce myocardial oxygen consumption. Results of
recent studies have resulted in the ACCF/AHA downgrading the
use of the IABP to class IIa (can be useful) in the guidelines for the
management of STEMI.
TandemHeart
1130
The Impella device is minimally invasive and the least
invasive of the LVADs. It consists of a catheter-
based 12-French pump motor inserted via a femoral
artery and positioned across the aortic valve. The
pump pulls blood from the LV through an inlet area
and expels blood into the proximal ascending aorta.
The Impella can generate up to 2.5 L/min of
forward flow into the systemic circulation. After the
pump is inserted and positioned, an activated
clotting time (ACT) between 160 and 180 seconds is
required to prevent clot formation in the motor. The
current ACCF/AHA guidelines provide a IIb
recommendation (may be considered) for the use of
alternative LVADs for patients with refractory CS.
1131
Provide other treatments for cardiogenic shock after the
cause of pump failure has been identified
3. Heart transplantation
1132
the BP.
1133
reflexes, and pupillary response to light should be reported to the
physician.
Ventilation assistance
1134
90%, notify physician.
1135
serum creatinine (greater than 1.5 mg/dL) indicative of acute renal
failure.
10. Monitor Hgb and Hct values daily as loss of blood reduces
oxygen delivery to the cells, resulting in tachycardia and tachypnea.
1136
and every 2 hours thereafter if assessment is within normal limits.
Assess pulses, temperature, color and sensation, and mobility of the
toes in the involved leg. Consult physician or midlevel provider
immediately if any changes occur.
1137
2. Reposition patient every 2 hours keeping involved leg extended
and log-roll patient onto side.
3. Provide care to keep skin dry and clean, inspect pressure areas at
the beginning of each shift.
Respiratory monitoring
1138
temperature, SOB, increased sputum production or coughing, and
altered color of sputum).
8. Monitor I&O.
Ineffective protection
related to risk of bleeding secondary to coagulopathy or IV
anticoagulants needed to maintain therapeutic equipment (left
ventricular assist devices).
Goals/Outcomes: Throughout hospitalization, patient’s bleeding
is controlled as evidenced by secretions and excretions negative for
blood, chest tube drainage within acceptable amounts, and absence
of abdominal pain or ecchymosis.
Blood Coagulation
Bleeding precautions
1. Monitor PTT, ACT (or other blood clotting labwork), and platelet
levels daily.
1139
Bleeding Reduction
Energy Management
1140
Circulatory care: Mechanical assist device
Infection protection
1141
Imbalanced nutrition less than body requirements
related to decreased intake secondary to oral intubation; increased
nutrition needs secondary to debilitated state and impaired tissue
perfusion with concomitant nitrogen malabsorption.
Goals/Outcomes: Within the 24- to 48-hour period before
discharge from the ICU, the patient will have adequate nutrition as
evidenced by a balanced nitrogen state and stable weight.
(Optimal nutrition in the ICU patient is still being debated in the
literature.)
Nutritional Status: Nutrient Intake
Nutritional management
Cardiomyopathy
Pathophysiology
Cardiomyopathy (CM) refers to a heterogeneous group of
myocardial diseases that are often genetic and associated with
mechanical and electrical dysfunction. Most types of CM result in
1142
inappropriate ventricular hypertrophy or dilation. The AHA 2006
Expert Panel on Contemporary Definitions and Classification of
Cardiomyopathy categorized CM into two major groups: primary
and secondary CM. Primary CMs are caused by pathology confined
to the heart muscle alone; whereas secondary CMs are caused by
pathology from a variety of generalized systemic (multiorgan)
disorders (Table 5-12). Some common disease entities involving the
heart muscle have been excluded from the present contemporary
CM classification. These include pathologic myocardial processes
and cardiac dysfunction caused by another cardiovascular
abnormality, such as valvular heart disease, systemic hypertension,
congenital heart disease, and atherosclerotic CAD. Other conditions
not included in this CM classification are cardiac tumors, diseases
affecting the endocardium with little or no myocardial
involvement, and hypertensive hypertrophic CM. Primary and
secondary CMs included in the 2006 AHA definition of CM are
further classified into the following: hypertrophic CM (HCM),
dilated CM (DCM), arrhythmogenic RV CM/dysplasia (ARVC/D),
and LV noncompaction (LVNC). Be aware that one disease, be it
primary or secondary CM, may fall into more than one CM
classification, causing confusion if there is an overlap between
categories. For example, some genetic primary CMs are known to
cause both DCM and HCM. Furthermore, a CM may evolve as a
consequence of remodeling from one category to another as the
disease progresses. CMs, whether confined to the heart (primary
CM) or part of a generalized systemic disorder (secondary CM),
often lead to cardiovascular death or progressive HF-related
disability.
Table 5-12
TYPES AND CAUSES OF CARDIOMYOPATHY
Primary Types of
Secondary Causes of Cardiomyopathy
Cardiomyopathy
Genetic Autoimmune/Collagen
Hypertrophic Systemic lupus erythematosus, dermatomyositis, rheumatoid
cardiomyopathy arthritis, scleroderma, polyarteritis, nodosa
Arrhythmogenic right
ventricular Storage
cardiomyopathy/dysplasia Hemochromatosis, Fabry disease, glycogen storage disease (type
Left ventricular II, Pompe), Niemann-Pick disease
1143
noncompaction Friedreich ataxia, Duchenne-Becker muscular dystrophy,
Mixed Type (Genetic and Emery-Dreifuss muscular dystrophy, myotonic dystrophy,
Nongenetic) neurofibromatosis, tuberous sclerosis
Dilated cardiomyopathy
Infiltrative
Restrictive cardiomyopathy
(nonhypertrophied and Amyloidosis, Gaucher disease, Hurler disease, Hunter disease
nondilated) Inflammatory (Granulomatous)
Acquired Type Sarcoidosis
Inflammatory (myocarditis) Endocrine
Stress-induced (“tako- Diabetes mellitus, hyperthyroidism, hypothyroidism,
tsubo” or “broken heart hyperparathyroidism, pheochromocytoma, acromegaly
syndrome”) Cardiofacial
Peripartum Noonan syndrome, lentiginosis
Tachycardia induced Endomyocardial
Endomyocardial fibrosis, hypereosinophilic syndrome (Löeffler
endocarditis)
Nutritional Deficiencies
Beriberi (thiamine), pellagra, scurvy, selenium, carnitine,
kwashiorkor
Toxicity
Drugs, heavy metals, chemical agents
Electrolyte Imbalance
Consequence of Cancer Therapy
Anthracyclines: doxorubicin (Adriamycin), daunorubicin,
cyclophosphamide, radiation
Infectious
HIV, Lyme disease, Chagas, coxsackie, influenza
Note: This table lists common diseases associated with primary and secondary CM
and is not intended to represent an exhaustive and complete list of conditions
associated with CM. Some disagreement exists in the scientific community regarding
the classification, definition, and nomenclature of CM; therefore, discrepancies and
contradictions may occur among various scientific resources.
Dilated cardiomyopathy
Dilated cardiomyopathy (DCM) is characterized by marked,
progressive dilation of the ventricles, resulting in decreased
myocardial contractility and a reduced systolic ejection fraction
(less than 40%). DCM is the most common cause of
cardiomyopathy. Infectious agents (particularly viruses producing
myocarditis), cocaine, chronic excessive alcohol consumption, and
chemotherapeutic agents are common causes of DCM, along with
other autoimmune, neurologic, metabolic, endocrine, nutritional,
and other systemic disorders. About 20% to 35% of DCM cases have
been reported as familial, and they are frequently associated with
skeletal muscle or neuromuscular disorders. In patients with severe
1144
dilation, the increase in total cardiac mass may lead to ventricular
hypertrophy. Alternatively, DCM may occur as a late manifestation
of hypertrophic heart disease. DCM may ultimately lead to a
decline in LV contractile function, ventricular and supraventricular
arrhythmias, conduction system abnormalities, thromboembolism,
progressive HF, and sudden or HF-related death.
Hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy (HCM) is characterized by
inappropriate hypertrophy of the ventricular muscle, leading to LV
stiffness and diastolic dysfunction. HCM is most often a genetically
acquired illness and is the most common inherited heart defect.
Approximately 60% to 70% of patients with HCM have familial
HCM, an inherited autosomal dominant condition. Other
cardiovascular diseases, including hypertension and aortic stenosis,
are capable of producing the same magnitude of wall thickening
seen with HCM. HCM is the most common cause of sudden cardiac
death in the young, especially in athletes, but may lead to HF and
disability at any age. Obstructive HCM (also called hypertrophic
obstructive cardiomyopathy or HOCM) occurs when the enlarged
heart muscle, usually the ventricular septum, obstructs the
ventricular outflow channel. HOCM may result in angina, HF, and
sudden death.
Restrictive cardiomyopathy
Restrictive cardiomyopathy (RCM) is less common than HCM or
DCM and is characterized by nondilated ventricles with impaired
ventricular filling from rigid or fibrotic ventricular walls. LV
diastolic dysfunction occurs, often associated with very high end-
diastolic pressures and moderate to marked biatrial enlargement
secondary to elevated atrial pressures. Hypertrophy is typically
absent, although the infiltrative and storage diseases (such as
amyloid and hemochromatosis) may cause an increase in LV wall
thickness. Systolic function usually remains normal, at least early in
the disease. Treatment is difficult and prognosis is poor.
Differentiating RCM from constrictive pericarditis is important
since the two clinical pictures are similar, while management is
markedly different.
1145
Arrhythmogenic right ventricular cardiomyopathy/dysplasia
Arrhythmogenic right ventricular cardiomyopathy/dysplasia
(ARVC/D) is an uncommon genetic disease characterized by
progressive replacement of normal myocardial cells with fatty or
fibrofatty tissue. Initially thought to be a disease isolated to the
right ventricle, more recent evidence shows that the left ventricle is
also involved in as many as 75% of cases. Clinical manifestations
include ventricular arrhythmias and HF. In young adults, ARVC/D
often presents with sudden death.
Assessment
Goal of assessment
The physical assessment of patients with CM attempts to
characterize the etiology and severity of cardiac dysfunction, the
level of functional impairment, and the optimal therapeutic
approach. Furthermore, the physical assessment should identify
factors that precipitated clinical decompensation, for example,
exercise or exacerbation of autoimmune disease. A good physical
assessment will help differentiate heart and circulatory failure from
entities that cause similar complaints and findings. During the
course of treatment, the physical assessment will also provide
feedback about the patient’s response to therapies (Table 5-13).
Table 5-13
SIGNS AND SYMPTOMS OF CARDIOMYOPATHY
1146
AV, atrioventricular; CHF, congestive heart failure; CM, cardiomyopathy; CO, cardiac
output; HCM, hypertrophic cardiomyopathy; HF, heart failure; JVD, jugular venous
distention; LV, left ventricular; LVH, left ventricular hypertrophy; PMI, point of
maximal impulse; PND, paroxysmal nocturnal dyspnea; RCM, restrictive
cardiomyopathy; RV, right ventricular.
Observation
A patient’s clinical presentation will vary according to the type and
extent of the CM and whether the patient has progressed to overt
HF. The clinical presentation will reflect both the hemodynamic
abnormalities caused by cardiac dysfunction and the degree of
secondary compensatory mechanisms. Patients’ presenting
symptoms may range from asymptomatic to, unfortunately,
symptoms continuous with cardiogenic shock (CS) or sudden
death. Most commonly, patients will present with symptoms of HF
or arrhythmias. Diagnostic tests used in patients with suspected
cardiomyopathy are outlined in the following table.
1147
1148
Collaborative management
Care priorities
1149
2. Initiate pharmacotherapy to maintain or reestablish
hemodynamic stability, control symptoms, and prevent
cardiac remodeling, all of which aid in halting further
disease progression
Medications commonly used in the treatment of CM and their
nursing implications (also see Heart Failure, Chapter 5, and
Cardiogenic Shock, Chapter 5):
1150
obstructive HCM. Monitor the patient for weakness, postural
hypotension, hypokalemia (see Hypokalemia, Chapter 1),
hypomagnesemia, dehydration, and worsening renal function.
1151
diagnosis of amyloidosis.
1152
life expectancy of at least 1 year before implantation. In patients
with end-stage HF symptoms who have an ICD in place, the
decision can be made to deactivate the defibrillator to avoid
unnecessary discomfort at end of life.
1153
Intraaortic balloon pump (IABP): In the presence of a failing
myocardium, an IABP helps to decrease afterload and increase
coronary artery perfusion
1154
therapy. Each institution has criteria that must be met before
transplantation is considered a treatment option (see Organ
Transplantation, Chapter 11).
SBP, Systolic blood pressure; MAP, Mean arterial pressure; CI, Cardiac Index; CO,
Cardiac Output; PAWP, Pulmonary artery wedge pressure; CVP, Central venous
pressure; RR, Respiratory Rate; HR, Heart rate.
1155
Cardiac Pump Effectiveness; Circulation Status
1156
medication.
Table 5-7
ACTIVITY LEVEL PROGRESSION FOR HOSPITALIZED PATIENTS*
Level Activity
I Bed rest Flexion and extension of extremities 4 times daily, 15 times each extremity;
deep breathing 4 times daily, 15 breaths; position change from side to side
every 2 hours
II Out of As tolerated, 3 times daily for 20 to 30 minutes
bed to
chair
III Ambulate As tolerated, 3 times daily for 20 to 30 minutes
in room
IV Ambulate Initially, 50 to 200 ft twice daily; progressing to 50 to 200 ft 4 times daily
in hall
*
Signs of activity intolerance: Decrease in blood pressure less than 20 mm Hg;
increase in heart rate to greater than 120 bpm (or more than 20 bpm above resting
heart rate in patients receiving beta-blocker therapy).
Activity intolerance
related to imbalance between oxygen supply and demand secondary to
decreased functioning of the myocardium.
Goals/Outcomes: Within the 12- to 24-hour period before
discharge from the CCU, patients should exhibit cardiac tolerance
to increasing levels of activity as evidenced by respiratory rate less
than 24 breaths/min, BP within 20 mm Hg of patient’s normal
range, HR within 20 bpm of patient’s normal resting HR, return to a
stable baseline ECG rhythm, and activity tolerance to a level
without presence of angina/chest pain or worsening dyspnea.
Activity Tolerance; Energy Conservation
Energy management
1157
in systolic BP greater than 20 mm Hg.
1158
the vagus nerve, which slows the rate of pacing by the SA node and
AV junction, and decreases force of contraction. Sympathetic nerve
fibers originate from T1 to T5 and, when stimulated, produce the
neurotransmitter norepinephrine, which increases HR during the
stress response. Sympathetic stimulation also promotes production
of catecholamines by the adrenal glands, and the hormones are
received by catecholamine receptors (alpha receptors, beta
receptors, dopaminergic receptors), which increase HR, force of
contraction, BP, and CO. Electrical dysfunction can markedly
change the CO and cause prompt deterioration in the patient’s
hemodynamic status (Figure 5-1).
1159
intracellular ion. The resting cells have a threshold for activation,
based on the difference in the ion concentrations (action potential).
Stimulation of a cardiac muscle cell, or depolarization, is created by
a rapid influx of Na+ followed by a slower influx of Ca2+ into the
cell. Normally, the influx is followed by muscle contraction. The cell
responds to the influx by K+ diffusing out of the cell to help
rebalance the positive ions (early repolarization and plateau phase)
on both sides of the cell membrane. A slower efflux is followed by a
rapid efflux of K+ (rapid repolarization). Finally, the sodium-
potassium pump must activate to fully rebalance the electrical
potential of the cell, restore the ions to their original position, and
achieve resting membrane potential or polarization.
Normal electrical activity of the heart produces waves or
deflections on the ECG (Figure 5-2). The waves and intervals that
comprise the components of the ECG make up one electrical cardiac
cycle (Figure 5-3).
1160
deflection from the baseline). Some normal positive complexes
are “missing” a distinct Q or S wave. The complex is
predominantly negative in leads aVR, V1, and V2 and biphasic in
leads V3, V4, and, occasionally, lead III (which represents stronger
Q- and S-wave activity, which are the negative deflections that
precede and follow the R wave).
1161
of the T wave and beginning of the P wave. It reflects the time the
cardiac cells are electrically silent or neutral.
1162
FIGURE 5-2 Electrical basis of the ECG. Source: (From
Huszar RJ: Basic dysrhythmias: interpretation and management, ed 3, St.
Louis, 2002, Mosby.)
1163
FIGURE 5-3 Components of the ECG. Source: (From Huszar
RJ: Basic dysrhythmias: interpretation and management, ed 3, St. Louis,
2002, Mosby.)
1164
of catecholamines. Imbalance of these regulators can cause a
disturbance in automaticity, conduction/conductivity, or
myocardial contractility.
Disturbances in automaticity
May involve an acceleration or deceleration in pacing or
automaticity of the SA node, such as sinus tachycardia (HR greater
than 100 bpm) or sinus bradycardia (HR less than 60 bpm).
Premature beats or possibly an escape or compensatory heart
rhythm may arise from the atria, junction, or ventricles if the SA
node is dysfunctional or arrests. Without additional catecholamines
prompted by the stress response, escape rhythms generated from
the AV junction or the ventricles are usually bradycardic (HR less
than 60 bpm). Abnormal rhythms, such as atrial or ventricular
tachycardia, may also result from excessive sympathetic stimulation
or electrolyte imbalance.
1165
Disturbances in conduction
Conduction may be too rapid, as in conditions that induce the stress
response (e.g., severe/critical illness, certain endocrine diseases,
profound emotional stress) or in the presence of an accessory
pathway (e.g., Wolff-Parkinson-White [WPW] syndrome).
Accessory pathways are extraconduction fibers that provide a
direct connection between the atria and the ventricles,
circumventing the AV node. Rhythms generated from these
anatomically incorrect conduction systems are called AV
reciprocating tachycardias and may have rates greater than 250
bpm. Reentry is a situation in which a misdirected electrical
impulse reexcites a conduction pathway through which it has
already passed. Once started, this impulse may circulate through
the same area repeatedly, prompting an AV reentrant tachycardia.
The trapped impulse becomes the pacemaker in this circumstance.
Impulse conduction may be delayed or too slow (e.g., first- and
second-degree AV block), or become totally blocked from
continuing down the pathway by abnormal electrical tissues (e.g.,
third-degree or complete heart block) (Figure 5-4).
1166
FIGURE 5-4 Anomalous AV conduction. Source: (From
Huszar RJ: Basic dysrhythmias: interpretation and management, ed 3, St.
Louis, 2002, Mosby.)
1167
Combinations of disturbed automaticity and conduction
Several dysrhythmias may occur simultaneously (e.g., first-degree
AV block [disturbance in conductivity], premature atrial complexes
[PACs] [disturbance in automaticity]).
Assessment
Goal of assessment
To diagnose the type of dysrhythmia, the cause of the rhythm
(electrolyte or acid-base imbalance, structural abnormality, heart
and/or renal disease, nervous system or neuroendocrine
dysfunction), the impact of the dysrhythmia on the CO
(BP)/coronary artery perfusion (may prompt chest discomfort), and
to determine the urgency and type of treatment. Lethal
dysrhythmias result in cardiac arrest.
Observation
The patient’s appearance varies from absence of symptoms to
complete cardiopulmonary arrest. Common symptoms include
1168
activity intolerance, weakness, pallor, hypotension, dizziness, SOB,
dyspnea, palpitations, chest discomfort or pressure, and sensation
of “racing heart” or “skipped beats.” More serious symptoms
include altered mental status, anxiety, respiratory insufficiency,
syncope, and seizures, which may lead to HF and cardiopulmonary
arrest. Pulseless ventricular tachycardia, ventricular fibrillation,
asystole, and pulseless electrical activity (PEA) result in immediate
cardiac arrest.
Vital signs
Vary with type of dysrhythmia. Vital signs may be unaffected or
affected slightly. Accelerated or decelerated HR may cause
hypotension, result in HF, or deteriorate into pulselessness.
Symptomatic dysrhythmias most often result in a very rapid, slow,
or irregular pulse, changed pulse quality, hypotension, pallor,
possibly a variable HR (fast, then slow), and tachypnea. If the CO is
markedly decreased, shocklike symptoms ensue including cold,
clammy skin, dusky or cyanotic appearance, decreased urine
output, and feeling of impending doom or imminent death.
1169
and their treatment. Occasionally, patients have an electrical
rhythm without corresponding mechanical pumping. This
condition is known as PEA. Initially, the rhythm may appear nearly
normal but rapidly deteriorates as the conduction pathway
becomes hypoxic.
1170
FIGURE 5-6 Sinus tachycardia. Source: (From Huszar RJ: Basic
dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)
1171
FIGURE 5-7 Sinus bradycardia. Source: (From Huszar RJ: Basic
dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)
1172
FIGURE 5-8 Sinus dysrhythmia. Source: (From Huszar RJ:
Basic dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)
1173
FIGURE 5-10 Sinus tachycardia with premature atrial
complexes (PACs). Source: (Top, from Emergency Nurses
Association: Sheehy’s manual of emergency care, ed 6, St. Louis, 2005,
Mosby. Bottom, from Aehlert B: ECGs made easy: pocket reference, ed 2,
St. Louis, 2002, Mosby.)
1174
FIGURE 5-11 Atrial tachycardia. Source: (From Huszar RJ:
Basic dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)
1175
FIGURE 5-12 Atrial flutter (type I). Source: (From Huszar RJ:
Basic dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)
1176
FIGURE 5-13 Atrial fibrillation (AF). Source: (From Huszar RJ:
Basic dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)
1177
FIGURE 5-14 AV junctional rhythm or junctional escape
rhythm. Source: (From Huszar RJ: Basic dysrhythmias: interpretation and
management, ed 3, St. Louis, 2002, Mosby.)
1178
FIGURE 5-16 Premature junctional
complexes. Source: (Top, from Emergency Nurses Association:
Sheehy’s manual of emergency care, ed 6, St. Louis, 2005, Mosby. Bottom,
from Huszar RJ: Basic dysrhythmias: interpretation and management, ed 3,
St. Louis, 2002, Mosby.)
1179
Aehlert B: ECGs made easy: pocket reference, ed 2, St. Louis, 2002,
Mosby.)
1180
St. Louis, 2005, Mosby. Bottom, from Huszar RJ: Basic dysrhythmias:
interpretation and management, ed 3, St. Louis, 2002, Mosby.)
1181
FIGURE 5-20 Ventricular fibrillation. Source: (From Huszar RJ:
Basic dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)
1182
FIGURE 5-21 Idioventricular rhythm. Source: (From Aehlert B:
ACLS Study Guide, ed 3, St. Louis, 2007, Mosby.)
1183
FIGURE 5-23 First-degree AV block. Source: (From Huszar RJ:
Basic dysrhythmias: interpretation and management, ed 3, St Louis, 2002,
Mosby.)
1184
FIGURE 5-24 Second-degree AV block (type I)
(Wenckebach). Source: (From Huszar RJ: Basic dysrhythmias:
interpretation and management, ed 3, St. Louis, 2002, Mosby.)
1185
FIGURE 5-25 Second-degree AV block (type
II). Source: (From Huszar RJ: Basic dysrhythmias: interpretation and
management, ed 3, St. Louis, 2002, Mosby.)
1186
FIGURE 5-26 Complete (third-degree) AV
block. Source: (Top, from Emergency Nurses Association: Sheehy’s
manual of emergency care, ed 6, St. Louis, 2005, Mosby. Bottom, from
Huszar RJ: Basic dysrhythmias: interpretation and management, ed 3, St.
Louis, 2002, Mosby.)
1187
FIGURE 5-28 Dual-chambered pacemaker. Source: (From
Aehlert B: ECGs made easy: pocket reference, ed 2, St. Louis, 2002,
Mosby.)
Auscultation
If HF is present, heart sounds may include S3 and S4; basilar crackles
or rales are audible with lung auscultation; and a wet cough with
frothy sputum may be present. If atrial fibrillation or other
1188
dysrhythmias that prompt an irregular ventricular response are
present, the irregularity is audible with auscultation.
Palpation
With HF, jugular veins are distended and peripheral edema is
present. ECG rhythms reflecting an irregular ventricular response
will prompt an irregular pulse upon palpation. Electrical complexes
that resulted in decreased stroke volume will be reflected as a lesser
or absent pulse beat.
1189
Collaborative management
Care priorities
1190
HR and rhythm: Too fast or too slow? Regular or irregular? When
the HR exceeds 150 or is less than 50 bpm, patients are more
likely to experience adverse effects. Fast rhythms include sinus
tachycardia, atrial tachycardia, atrial flutter, atrial fibrillation,
junctional tachycardia, and VT with a pulse. Slow rhythms
include sinus bradycardia, junctional rhythms, ventricular or
idioventricular rhythms, and second- and third-degree heart
blocks.
1191
FIGURE 5-31 Placement of the left and right chest
leads. Source: (From Aehlert B: ACLS study guide, ed 3, St. Louis, 2007,
Mosby.)
1192
FIGURE 5-32 Posterior chest lead
placement. Source: (From Aehlert B: ACLS study guide, ed 3, St. Louis,
2007, Mosby.)
1193
thorough evaluation of his or her history and under the guidance of
the AHA guidelines for ACLS. A handbook of emergency cardiac
care for health providers is updated regularly to reflect current
research. The resource includes information reviewed by AHA
Committee on Emergency Cardiovascular Care, and Subcommittees
on Basic Life Support, Pediatric Resuscitation, and Advanced
Cardiac Life Support.
Box 5-4
ANTIDYSRHYTHMIC DRUGS
Class I (sodium channel blockers)
Block the rapid, inward sodium current. Local anesthetics and
other drugs that decrease automaticity of ventricular conduction,
delay ventricular repolarization, decrease conduction velocity,
increase conduction via AV node, and suppress ventricular
automaticity. Class IA decreases depolarization moderately and
prolongs repolarization. May prolong the QT interval. Class IB
decreases depolarization and shortens repolarization. Class IC
significantly decreases depolarization with minimal effect on
repolarization.
Class IA Class IB Class IC
Disopyramide (PO) Lidocaine (IV, IM) Encainide (PO)
Procainamide (PO, IV, IM) Mexiletine (PO) Flecainide (PO)
1194
Quinidine (PO, IV) Phenytoin (PO) Propafenone (PO)
Tocainide (PO)
Moricizine (PO)
Unclassified
Depress activity of the AV node.
Adenosine (IV)
1195
* Available in Great Britain.
AV, Atrioventricular; IV, intravenous; IM, intramuscular; PO, by mouth; SA, sinoatrial.
1196
synchronizing the patient’s R waves with the cardioverter; lower
energy is also required to convert the rhythm to NSR.
1197
increased with subsequent shocks (AHA Advanced
Cardiac Life Support Guidelines, 2011.
Synchronized cardioversion
The defibrillator will not discharge the energy until R wave
synchronization is achieved, which sometimes takes several
seconds. Providers need to exercise extreme caution to remain
“clear” and not touch the patient, bed, or anything connected to the
patient until the energy is delivered.
1198
after ensuring a patent airway, providing manual ventilation if
breathing is absent, and providing cardiac compressions if the
pulse is absent. The operator must be able to assess for
pulselessness and apnea, along with applying hands-free
defibrillator pads in the proper position at the right sternal
border and anterior axillary line, fifth intercostal space. If
healthcare providers are using the AED, the anterior-posterior
pad position may also be used.
AEDs
Not all automated external defibrillators are programmed per
current ACLS guidelines. Some still deliver three stacked shocks
(per older ACLS guidelines) when it is time to defibrillate, rather
than the currently recommended one shock. If a healthcare
provider comes across this type of defibrillator, the provider is
generally advised to follow the instructions and not interrupt the
cycle. Interruption may cause the device to malfunction, resulting
in the patient not receiving any further electrical therapy, or the
device ceasing to give associated instructions regarding the proper
steps of resuscitation.
1199
• ICD: A battery-powered pulse generator (electrical device)
implanted into the pectoral area, with a lead system and shocking
coil positioned inside the heart and superior vena cava, which
can recognize and terminate potentially lethal dysrhythmias.
Risks and complications of thoracotomy versus nonthoracotomy
implantation are outlined in Table 5-14. Newer, third-generation
devices do not require thoracotomy for insertion. The devices are
smaller and lighter, allowing prepectoral implantation. These
devices may also provide antitachycardia pacing (ATP), low-
energy cardioversion, high-energy cardioversion,
antibradycardia pacing, and high-energy defibrillation along
with the ability to score performance data. Algorithms for
treatment of recognized dysrhythmias are programmed into the
device. Maximal energy output is 30 to 40 joules, which can
defibrillate malignant or lethal rhythms such as pulseless
ventricular tachycardia and ventricular fibrillation. Magnets may
be used for emergency deactivation/activation or suppression of
all or part of programmed therapies in newer devices. If the
patient has a combination ICD/pacemaker, the magnet will
deactivate the ICD and change from demand (discharges
electrical impulses or “fires” as needed to maintain the selected
HR) pacing to fixed mode (discharges the selected number of
impulses per minute, regardless of the patient’s underlying heart
rhythm). When the device discharges or fires, the patient’s status
should be documented in the medical record.
Table 5-14
IMPLICATIONS FOR PATIENT CARE AND COSTS: IMPLANTABLE
CARDIOVERTER-DEFIBRILLATORS (ICDs)
1200
Immediate intervention is required for a device that is not
delivering appropriate therapy. If the device does not deliver
therapy, external cardioversion can be used. A patient with an
implantable cardioverter defibrillator (ICD) who has a sustained
hemodynamically unstable ventricular rhythm should be treated
exactly as one who does not have an ICD. The placement of the
external pads should not be over the ICD generator. When
inappropriate firing occurs in the absence of a treatable
dysrhythmia, there is a high probability that an ICD lead has
become dislodged, a connection has become loose, or the device
sensitivity setting is too “low,” which causes the device to respond
“too soon” to certain rhythm changes.
1201
abnormal rapid conduction in these areas, which produces
supraventricular tachycardia. Ablation can be done as adjunctive
therapy for management of monomorphic VT, following
placement of an ICD to enhance rhythm control. Postablation
assessment of the patient involves careful monitoring of the
cardiac rhythm, vital signs, catheter insertion sites, LOC, and
peripheral pulses. Complications include cardiac perforation,
cardiac tamponade, coronary artery spasm, cerebral or
pulmonary embolus, bleeding, thrombosis, and dysrhythmias
including AV blocks.
• Specific tachycardias:
1202
biphasic defibrillator (or 360 joules using a
monophasic device), along with CPR and advanced
life support measures. See ACLS guidelines for
tachycardia with pulses or pulseless arrest for
specific management algorithms.
1203
the patient is stable; if the patient is unstable,
attempt defibrillation as for VF. These patients may
be resistant to defibrillation. If the patient continues
to experience TdP, an agent such as isoproterenol
may be infused to increase the HR, thereby
shortening the QT interval. This may be especially
necessary if TdP is caused by medications with a
long half-life. Antidysrhythmic drugs including
class 3 amiodarone and sotalol prolong the QT
interval and, like class 1 agents (e.g., quinidine,
disopyramide), are proarrhythmic. Initiate a
magnesium infusion if not done initially. Other
drugs, including certain antibiotics and
antihistamines, may promote polymorphic VT,
particularly when used in combination. Congenital
causes include long-QT syndrome, Brugada
syndrome (possibly congenital), and
catecholaminergic polymorphic VT.
1204
unstable (signs of decreased CO, congestive HF, or
ACS) or become hemodynamically unstable are
generally managed with synchronized
cardioversion. Atrial fibrillation may occur post-
CABG, producing CO compromise and danger of
stroke. Rate control to slow the rapid ventricular
response can be achieved by diltiazem. Loading
dose is 0.75 mg/kg IV followed by a continuous
infusion at 5 mg/h. If atrial fibrillation reoccurs or
persists over a 24-hour period, warfarin
anticoagulation for 4 weeks will be needed. For
patients with normal QTc interval, immediate
chemical conversion might be attained using
ibutilide, 1 mg diluted in 10-mL IV solution given
over 10 minutes, and repeated once if atrial
fibrillation has been present for less than 48 hours.
Ibutilide is reserved for patients with a normal QTc
interval to avoid lethal ventricular dysrhythmias
following administration. An alternative is
amiodarone in a loading dose of 150 mg IV over 10
minutes followed by 1 mg/min drip for 6 hours and
then 0.5 mg/min drip for 18 hours. For chronic atrial
fibrillation patients, conversion to NSR without
anticoagulation is not a goal because of the risk of
atrial thrombus formation and possible
embolization. If synchronized cardioversion is
needed during the immediate postoperative period
and anticoagulation is not an option, Doppler or
transesophageal echocardiography may be used to
check for atrial thrombus formation. In addition to
1205
cardioversion, other nonpharmaceutical treatments
for atrial fibrillation include AV node and focal
ablation, surgical correction such as the Maze
procedure, and implanted permanent pacing with
atrial fibrillation suppression algorithms.
1206
patients with New York Heart Association (NYHA) functional
class III or ambulatory class IV HF symptoms.
Table 5-15
NBG PACEMAKER CODES
1207
’• Temporary epicardial pacing: Placement of temporary pacing
wires on the epicardial surface of the heart while the chest is open
during cardiac surgery so that cardiac pacing can be used in the
postoperative period. Usually two atrial and two ventricular
wires (pacing and ground wires) are attached to the outside
surface of the heart and exit through the skin incision allowing
attachment to a temporary pacing generator. The exposed pacing
wires may be capped and later connected to a generator if pacing
is needed. The end of the leads, connection points, and pacing
generator terminals should be protected and insulated from
electrical microshock. The temporary pacing wires are removed
when no longer needed by slowly and gently pulling them out
through the skin. The patient is monitored carefully after the
pacing wires are removed for dysrhythmias, cardiac tamponade,
hemorrhage, hematoma, and hemodynamic changes. If left in for
a prolonged period of time, tissue may adhere to the wires and
the provider may elect to cut the external wires at the level of the
skin. The skin will then grow over the entry points and heal.
1208
result in ventricular tachycardia or ventricular fibrillation.
The pads cannot both sense and pace; therefore, the device
includes an electrocardiogram (ECG) monitor so that efficacy
(capture) of pacing can be assessed. Leads should be applied to the
chest in addition to the pads to assess capture. Capture should
reflect that the level of electrical stimulation (mA) provided was
able to prompt ventricular contraction. The ECG tracing generally
becomes larger and wider when capture is achieved. When pacing
is effective, the patient’s vital signs should improve. If the level of
energy needed to achieve capture is high, sedation may be
necessary for the patient to tolerate transcutaneous cardiac
pacing.
1209
• LV aneurysmectomy and infarctectomy: Excision of possible focal
spots of ventricular dysrhythmias.
1210
Decreased cardiac output
related to altered rate, rhythm, or conduction or negative inotropic
changes secondary to cardiac disease.
Goals/Outcomes: Within 15 minutes of development of serious
dysrhythmias, the patient has adequate CO as evidenced by BP at
least 90/60 mm Hg or baseline, HR 60 to 100 bpm, and NSR on
ECG. CVP is less than 7 mm Hg, and CO is 4 to 7 L/min.
Circulation Status
Cardiac care
1211
treatment.
Energy management
1212
Deficient knowledge of disease process or other
mechanisms by which dysrhythmias occur
related to lifestyle implications.
Goals/Outcomes: Within the 24-hour period before discharge
from critical care, the patient and significant others verbalize
knowledge about causes of dysrhythmias and the implications for
modification of patient’s lifestyle.
Knowledge: Disease Process; Knowledge: Health Promotion;
Knowledge: Medication
Teaching: Individual
3. Teach the patient and significant others how to check pulse rate
for 1 full minute.
1213
6. Stress the importance of leading a normal and productive life,
even though the patient may fear breakthrough of life-threatening
dysrhythmias. If the patient is going on vacation, advise him or her
to take along sufficient medication and to be aware of healthcare
facilities in the vacation area.
Anxiety reduction
1214
dysrhythmias may benefit from practicing a relaxation response.
Many different techniques can be used, including use of breathing
alone or in conjunction with muscle group contraction and
relaxation. Other techniques incorporate use of imagery.
Deficient knowledge:
ICD or related to pacemaker insertion procedure and follow-up
care.
Goals/Outcomes: Within the 24-hour period before the
procedure, the patient and significant others describe rationale for
the procedure and method of insertion. Within the 24-hour period
before discharge from ICU, the patient and significant others
describe postinsertion care and need for continued advanced
practice provider follow-up.
Knowledge: Illness Care
Teaching: Procedure/treatment
1215
• Possible need for temporary transvenous pacemaker
insertion before ICD or permanent pacemaker
procedure.
1216
• No lifting of arm above level of shoulder for at least
4 weeks; may resume showering at 72 hours.
1217
incision site and in the respiratory tract.
Infection Severity
Infection protection
6. Teach the patient and significant others the signs and symptoms
of infection of both the incision site and the respiratory tract: cough,
sputum production, fever, dyspnea, chills, headache, myalgia.
Explain that the older adult with an infection may be confused and
disoriented and may run low-grade fevers even though few other
indicators are present.
1218
Decreased cardiac output
related to malfunction of cardiac pacemaker
Goals/Outcomes: Within the 24-hour period preceding hospital
discharge or throughout the duration of temporary cardiac pacing,
the patient has adequate CO as evidenced by systolic BP at least 90
mm Hg, RR 12 to 20 breaths/min, HR less than 100 bpm, urinary
output at least 0.5 mL/kg/h, warm and dry skin, and ECG indicative
of effective capture, sensing, response to sensing, and function of
antitachycardia pacing (if operational).
Circulation Status
1219
of the heart that could lead to cardiac tamponade, pericarditis,
infection, and bleeding.
Table 5-18
ELECTROMAGNETIC INTERFERENCE AND THE THIRD-
GENERATION ICDs AND SOME PROGRAMMABLE PACEMAKERS
1220
Sexual Identity; Role Performance
Sexual counseling
4. Explain that the device may shock at any time. If the patient’s
partner is in contact with the patient’s body at that time, the shock
may be experienced as a tingling sensation by the partner.
1221
see Pneumothorax, Chapter 4, for information related to this
disorder. Also see nursing diagnoses and interventions in
Hemodynamic Monitoring (Chapter 1) and Emotional and Spiritual
Support of the Patient and Significant Others (Chapter 2).
Hypertensive emergencies
Pathophysiology
A hypertensive emergency is present when severely elevated BP
results in end-organ damage. Severe hypertension adversely affects
the CNS, cardiovascular, and renal systems. Both malignant
hypertension and accelerated hypertension are considered
emergencies, and they have similar outcomes and management
strategies. Malignant hypertension is BP elevation with
encephalopathy or nephropathy with papilledema. Progressive
kidney failure and permanent blindness can occur if treatment is
not provided. Accelerated hypertension is defined as a recent
marked increase of BP over normal baseline pressure, associated
with end-organ damage. Vascular damage is seen on funduscopic
examination, including hemorrhages or exudates, but without
papilledema.
Hypertensive urgency is managed differently from hypertensive
emergency. Urgency is present when severely elevated BP is noted
(e.g., systolic BP greater than 220 mm Hg or diastolic BP greater
than 120 mm Hg) without end-organ damage. Signs and symptoms
include severe headache, severe anxiety, and SOB. BP can be
reduced within the subsequent 24 to 48 hours following diagnosis.
IV treatment of BP is not necessary. Oral treatment is satisfactory.
Hypertensive emergencies require immediate management to
reduce the BP. The patient may experience life-threatening signs
and symptoms, such as severe pulmonary edema, cerebral edema,
ischemia or hemorrhage of the brain, aortic dissection, AMI, and
eclampsia (during pregnancy). Immediate vascular necrosis is
possible if the diastolic pressure exceeds 120 mm Hg. Necrosis has
also manifested with MAPs greater than 150 mm Hg. Conversely,
no evidence suggests patients benefit from rapidly reducing BP in
1222
minutes to a few hours during hypertensive urgency. Aggressive
therapy may result in cardiac, renal, or cerebral perfusion deficits
resulting from low BP.
The morbidity and mortality of hypertensive emergencies
depend on the extent of end-organ damage when the patient
presents and subsequent BP control. Following a crisis, those with
BP control and medication compliance have a 10-year survival rate
of nearly 70%.
Hypertension causes more deaths and disease than any other
cardiovascular risk factor worldwide. Hypertension prompts
ventricular remodeling and increases the risk of heart attack, HF,
stroke, and kidney failure. The Eighth Joint National Committee (8)
did not define “hypertension,” but rather prescribed thresholds for
treatment applicable to all hypertensive populations except when
the evidence supported variance in a particular subgroup. The
guideline was submitted for external peer review in January 2013
by the National Heart, Lung, and Blood Institute (NHLBI) to 20
expert reviewers and 16 federal agencies. The guideline review
focused on 3 key questions surrounding management of adults
with hypertension: (1) Does initiating antihypertensive medications
at specific BP thresholds improve outcomes? (2) Do medications
targeted at a specific BP goal improve outcomes? (3) Do various
classes of medications differ in benefits vs harms reflected in the
outcomes? Lifestyle modifications were not revised, but rather,
were supported by endorsing the evidence-based recommendations
of the 2013 Lifestyle Work Group.
Following an exhaustive review of the literature, the following
nine recommendations emerged from JNC-8:
• For those older than 60 years of age, initiate drug therapy for
a systolic BP greater than 150 mm Hg and diastolic BP greater
than 90 mm Hg. Goal: Systolic BP less than 90 mm Hg, diastolic
BP less than 90 mm Hg.
1223
• For those younger than 60 years of age, initiate drug therapy for a
diastolic BP above 90 mm Hg. Goal: Diastolic BP less than 90 mm
Hg.
• For those younger than 60 years of age, initiate drug therapy for a
systolic BP above 140 mm Hg. Goal: Systolic BP less than 140 mm
Hg.
• For those older than 18 years of age with chronic kidney disease
(CKD), initiate drug therapy to keep systolic BP below 140 mm
Hg and diastolic BP below 90 mm Hg.
• In those older than 18 years of age with CKD, initial (or added)
medications should include an ACEI or ARB to improve kidney
outcomes. This applies to people of all races, with or without
diabetes mellitus.
1224
may be used. Referral to a hypertension specialist may be needed
when the patient’s BP is not controlled with three medications.
Pathophysiology
The pathophysiology of hypertensive emergencies is not well
understood. Initially, there is a failure of the normal autoregulation
and an abrupt rise in SVR. It is thought that the wall of a stressed
vessel causes the release of humoral vasoconstrictors, which
increases the SVR. The increased pressure within the vessel then
starts a cycle of endothelial damage, local intravascular activation
of the clotting cascade, fibrinoid necrosis of small blood vessels, and
release of more vasoconstrictors. The cycle of vascular injury leads
to tissue ischemia and autoregulatory dysfunction. Single-organ
involvement is found in approximately 83% of patients presenting
with hypertensive emergencies. Two-organ involvement is found in
14% of patients, and multiorgan involvement (more than three
organ systems) is found in approximately 3% of patients presenting
with a hypertensive emergency.
Hypertensive crisis can lead to hypertensive encephalopathy as
cerebral blood vessels dilate resulting from inability to affect
autoregulation. Cerebral autoregulation is the ability of the cerebral
vasculature to maintain a constant pressure or cerebral blood flow
(CBF). When autoregulation is disrupted, increased intercranial
1225
pressure and cerebral edema may result. Hallmark signs of
hypertensive encephalopathy include cerebral edema and
microhemorrhages, altered mental status, and papilledema. Blood
flow is increased, and the excessive pressure drives fluid into the
perivascular tissue, resulting in cerebral edema. The extreme
pressure can cause arteriolar damage, as demonstrated by fibrinoid
necrosis of the intima and media of the vessel wall. Although any
organ is vulnerable, the eyes and the kidneys are most likely to
suffer damage, leading to retinopathy, blindness, and renal failure.
Patients with hypertension who are admitted to the ICU may have
a rebound elevation of the BP if their usual antihypertensive
regimen is interrupted. In addition, a loss of BP control can occur
because of the nature of the primary disorder, trauma, or the stress
of being in the ICU.
Patients also have increased cerebrovascular resistance and are
more prone to ischemia when the BP decreases. Normotension
achieved with BP control may result in decreased CBF. Rapid rises
in BP can cause hyperperfusion with an increased CBF. The
rapidity of the rise in pressure may be more destructive than the
level of BP elevation. The 1-year mortality rate is 79% for patients
with untreated hypertensive emergencies. The 5-year survival rate
among all patients with treated hypertensive crisis is approximately
74%. Progressive stiffness occurs in the arteries, which increases
systolic BP, resulting in a widened pulse pressure, which decreases
coronary perfusion pressures, increases myocardial oxygen
consumption, and causes the left ventricle to enlarge. The
remodeled left ventricle is unable to compensate for an acute rise in
SVR, leading to LV failure, pulmonary edema, and myocardial
ischemia. Small renal arteries exhibit endothelial dysfunction and
impaired vasodilation, which affects renal autoregulation. Once the
renal autoregulatory system is disrupted, the intraglomerular
pressure varies directly with the systemic arterial pressure. The
kidney is no longer protected from fluctuations in perfusion caused
by BP changes, resulting in acute renal ischemia during a
hypertensive crisis.
Assessment
1226
Goal of assessment
The history and physical examination determine the nature,
severity, and management of the hypertensive event. Patients
should be questioned regarding compliance with antihypertensive
drug therapy, intake of over-the-counter preparations and
sympathomimetic agents, and illicit drug use. Identifying the
presence of end-organ dysfunction, particularly renal and
cerebrovascular disease, is of paramount importance. Duration and
severity of preexisting hypertension and the degree of BP control
should be clearly defined by the history.
• Postoperative hypertension
1227
pyelonephritis, primary glomerulonephritis, tubulointerstitial
nephritis (comprises 80% of all secondary causes),
atherosclerosis, fibromuscular dysplasia, polyarteritis nodosa
Box 5-5
CAUSES OF SECONDARY HYPERTENSION
Renal disease
• Acute glomerulonephritis
• Chronic pyelonephritis
• Hydronephrosis
• Renal tumors
• Renovascular hypertension
Endocrine disorders
• Cushing syndrome
• Pheochromocytoma
• Primary aldosteronism
• Thyroid/parathyroid disease
Congenital disorders
• Adrenal hyperplasia
1228
• Coarctation of the aorta
Pregnancy-induced disorders
• Pregnancy-induced hypertension
• Preeclampsia
• Eclampsia
Drug-induced disorders
• Cyclosporine
• Oral contraceptives
• Steroids
Other
• Sleep apnea
Observation
Early indicators
Although most patients are free of symptoms, vague discomfort,
fatigue, dizziness, and headache can occur. The heart’s initial
response to systemic hypertension is to develop LV hypertrophy,
which progresses to dilated cardiomyopathy.
1229
symptoms include hematuria, nocturia, and azotemia. Nausea and
vomiting also may occur.
Eye assessment
A funduscopic examination is performed to determine whether
hemorrhage, fluffy cotton exudates, or arteriovenous nicking of the
vessels has occurred. When these changes occur, visual perception
is decreased. Nurses should assess the patient’s gross visual acuity
by the ability to read and recognize objects and people. Retinal
hemorrhages and exudates as well as papilledema may occur.
Neurologic assessment
Assess level of consciousness, visual fields, and focal neurologic
signs. May reveal evidence of a residual neurologic deficit from a
cerebral infarct or ischemic event, as manifested by a positive
Babinski reflex (upgoing toe), hemiparesis, hemiplegia, ataxia,
confusion, or cognitive alterations. Assessment should include any
onset of headache, nausea, vomiting, lethargy, restlessness, or
agitation. Neurologic presentations during crisis include occipital
headache, stroke (infarction or hemorrhage), and visual
disturbances. Hypertensive encephalopathy (severe hypertension,
headache, vomiting, visual disturbances, altered mental status,
seizures, and retinopathy with papilledema) may be present. A
complete neurologic examination should be done to screen for
localizing signs. Focal neurologic signs might not be attributable to
encephalopathy; focal signs may reflect cerebral hemorrhage,
infarct, or presence of a mass.
Vital signs
1230
fitting cuff or an automatic BP recorder should be selected for use.
The bladder of the cuff must encircle 80% of the arm and cover two
thirds of the length of the upper portion of the arm. BP
measurement in both the supine and standing positions (if able)
may help in assessment for volume depletion. A significant
difference between the arms may be suggestive of an aortic
dissection. Note when the patient last smoked or used any nicotine
product, how much caffeine was consumed during the previous 4
hours, and whether adrenergic stimulants (e.g., over-the-counter
decongestants or bronchodilators) have been used within the past
24 hours, as they elevate BP.
Pheochromocytoma assessment
Paroxysmal elevations of BP associated with palpitations,
tachycardia, headache, diaphoresis, pallor, warmth or flushing,
tremor, excitation, fright, nervousness, feelings of impending doom,
tachypnea, abdominal pain, nausea, and vomiting. Episodes also
are associated with hyperglycemia and hypermetabolism. Postural
hypotension and paradoxic response to antihypertensive
medications may occur.
Palpation
Peripheral pulses
Pulsus alternans, an alteration in pulse pressure with a regular
rhythm, may be palpated at any of the major pulse points. All
1231
peripheral pulses should be palpated bilaterally. With coarctation
of the aorta, the femoral pulses will be bilaterally weak with a slow
upstroke; whereas the radial and brachial pulses will be normal or
bounding
Auscultation
Heart sounds
When dilated cardiomyopathy is developing, an S3 or S4 heart
sound may be auscultated in the mitral area with the bell of the
stethoscope. Murmurs may be audible. In addition, crackles may be
auscultated in the presence of cardiac failure along with jugular
venous distention and peripheral edema.
Vascular sounds
Screen for carotid or renal bruits.
Diagnostic tests
The definitive test for hypertension is BP measurement. Once
hypertension has been documented, many tests may be performed
to determine the amount of end-organ damage or to diagnose the
condition responsible for the development of secondary
hypertension.
1232
See diagnostic tests for patients with Acute Coronary Syndrome
(Chapter 5), Aortic Aneurysm/Dissection (Chapter 5), Heart Failure
(Chapter 5), Stroke: Acute Ischemic and Hemorrhagic (Chapter 7),
and Acute Kidney Injury/Acute Renal Failure (Chapter 6).
Additional studies such as a toxicology screen, pregnancy test, and
endocrine testing may be necessary.
Collaborative management
1233
Care priorities
In the treatment of hypertensive emergencies complicated by (or
precipitated by) CNS injury, IV labetalol or nicardipine may be
recommended, since they both are nonsedating and do not cause
significant cerebral vasodilation, which can increase intracranial
pressure (a potential problem with sodium nitroprusside). In
hypertensive emergencies arising from catecholaminergic
mechanisms, such as pheochromocytoma or cocaine use, beta
blockers can worsen the hypertension because of unopposed
peripheral vasoconstriction; phentolamine may be effective.
Labetalol is useful in these patients if the HR must be controlled.
1234
prevent further bleeding while maintaining cerebral perfusion in
the face of cerebral vasospasm.
1235
recommended dose is 1.7 µg/kg/min. The half-life is
9.8 minutes. The patient must still be kept in the
ICU and undergo arterial monitoring with this
drug.
1236
effects persist for up to 50 hours. It may cause
tachycardia, headache, flushing, and aggravation of
angina. Do not exceed 150 mL/h (15 mg/h).
1237
3 to 5 minutes. Headache is common and controlled
with analgesics.
HIGH ALERT!
Nifedipine is no longer recommended for the management of
hypertensive emergencies.
Liquid nifedipine had been used for rapid treatment of
hypertension; the capsule was pierced and the contents were
squeezed out under the tongue, with rapid sublingual absorption
the goal. However, the drug was not absorbed sublingually but
rather was swallowed and absorbed in the stomach, producing a
quick onset of action. Effects were varying and dangerous.
Variations in dosage occurred, since the amount removed from the
capsule by squeezing liquid from the small pierced hole was
variable, as was the amount actually swallowed, versus that left
pooled in the mouth. Serious side effects, including stroke, have
been reported.
1238
combinations. If ineffective in a combination of three of the four
categories, medications in other categories, including beta blockers
and alpha-adrenergic blockers, may be used. A hypertension
specialist may be needed for optimal medication management for
patients with resistant hypertension. For persons with severe
hypertension, three to five medications are often needed to achieve
normal BP. Resistant hypertension is defined as BP that remains
above goal despite the concurrent use of three antihypertensive
agents of different classes.
1239
prompt hypertension
Although there is no surgical intervention for primary
hypertension, several forms of secondary hypertension respond
well to the surgical correction of the primary problem. A
coarctation of the aorta can be repaired by removing the narrowed
area of the vessel and inserting an aortic graft. Renal artery stenosis
may be corrected by grafting or by renal artery angioplasty. For
patients with pheochromocytoma, surgical removal of the tumor(s)
will return the patient to a normotensive state.
Hemodynamic regulation
1240
• Correlate cuff pressure with pressure from arterial
cannulation.
Table 5-19
MEDICATIONS USED IN THE TREATMENT OF HYPERTENSION
1241
1242
1243
*
Cardioselective.
BP, Blood pressure; ISA, intrinsic sympathomimetic activity; IV, intravenous; PO, by
mouth.
Some drug combinations available in multiple fixed doses. Each drug dose is
reported in milligrams.
Acute pain
related to headache secondary to cerebral edema occurring with high
perfusion pressures.
Goals/Outcomes: Patient’s subjective evaluation of pain
improves within 12 to 24 hours, as documented by a pain scale.
Nonverbal indicators, such as grimacing, are absent or diminished.
Pain Control
Pain management
1244
pain scale with patient, rating discomfort from 0 (no pain) to 10
(severe pain).
1245
patient’s ability to read and recognize objects or people. Evaluate
patient’s movement coordination to determine depth perception.
Perform a funduscopic examination per institutional guidelines, if
appropriate and allowable.
2. If the patient has decreased visual acuity, assist with feeding and
other ADLs and keep patient’s personal effects within his or her
visual field.
Surveillance: Safety
1246
collagen and elastin fibers. The media is the thick middle layer of
the vessel composed of varying amounts of smooth muscle,
collagen, and elastic fibers. The adventitia is the outermost layer
composed of collagen and elastin, making it a key element in
providing the strength of the arterial wall.
Atherosclerotic plaque formation occurs in three stages. The early
stage is development of fatty streaks during childhood or young
adult life. The fatty streaks are formed from lipid-laden
macrophages called foam cells. Low-density lipoprotein cholesterol
is the main lipid component of the fatty streaks. The second stage is
the appearance of fibrous plaque later in life from progression of
the fatty streaks from foam cells to a more permanent fibrous
plaque. These plaques are most often found at areas of bifurcation
of the arterial vessels. The last stage occurs as the fibrous plaque
develops into a complicated lesion with necrosis and ulceration of
the plaque surface with exposure, leading to thrombogenesis
through platelet aggregation and thrombus formation. Elasticity of
the arterial wall is lost and there is progressive narrowing of the
vessel lumen. The vessel wall may also degenerate and dilate,
leading to aneurysmal development.
The primary risk factors known to accelerate this process are
smoking, hypertension, hyperlipidemia, and diabetes mellitus. The
presence of CAD and renal artery stenosis has been correlated with
carotid artery disease of 50% stenosis or greater. Exercise and
modification of risk factors can slow the progression and even
promote regression of the fatty streaks.
Symptoms of atherosclerosis emerge over time with the
progressive narrowing and occlusion of the arterial bed until the
vessel that provides the main perfusion of a limb or tissue is
critically narrowed to 50% or more of lumen diameter (noted as a
hemodynamically significant stenosis). Symptoms of chronic
progressive atherosclerosis include subtle changes in skin
appearance, color, and temperature. Other factors, such as length of
stenosis, blood viscosity, peripheral resistance, and acute versus
chronic development, affect blood flow and tissue perfusion. As
plaque progresses along the arterial walls in an uneven pattern, the
laminar flow of blood becomes turbulent and can be heard with a
stethoscope as a bruit. Generally, the progressive and chronic
1247
development of disease allows for the development of collateral
blood flow and perfusion to be maintained at a minimal level for
the person at rest without symptoms present at this time. Pain
occurs when the tissue needs more oxygen, such as with walking or
other exercises.
Autonomic neuropathy, which occurs when blood is shunted
away from peripheral cutaneous capillary beds, may occur with
PAD alone, or in conjunction with diabetes or other comorbidities.
Motor neuropathy causes changes in gait and pressure distribution,
which may lead to ulceration. Skin is less elastic with diminished
capillary perfusion and reparative mechanisms. Loss of protective
sensation and proprioception resulting in increased force with each
step can lead to callus formation at pressure areas, which decreases
elasticity and increases skin ischemia. Bone and joint changes
occurring with comorbidities, such as diabetes, can add additional
abnormal weight-bearing mechanisms to the feet, leading to callus
and ulcer formation. This can become critical in the presence of
PAD and diminished perfusion.
Sudden blockage of an artery presents with an acute onset of
symptoms that are more pronounced. An acute blockage of a lower
extremity artery (acute limb ischemia [ALI]) may present with pain,
pallor, and neurosensory impairment in the lower limb, while an
acute occlusion of a cerebrovascular artery may present as a stroke.
1248
goal of treating significant carotid stenosis is to prevent stroke.
Box 5-6
CAUSES OF ACUTE ARTERIAL
OCCLUSION
General pathologic processes
Arterial versus atheroembolization
Thrombosis of a diseased artery (acute-on-chronic disease)
Acute occlusion of a vascular bypass graft
Arterial traumas
Specific sources or processes
Cardiac Causes Noncardiac Causes
Atherosclerotic heart disease (most Aneurysms (most common noncardiac source)
common cardiac source)
Arrhythmias—atrial fibrillation
Myocardial infarction (left ventricular mural Atherosclerotic plaque ulcers (in aorta or
thrombus formation) (second most common common iliac artery; also source of stroke in
source) carotid artery disease)
Cardiomyopathy Prosthetic grafts
Left ventricular aneurysms Iatrogenic sources or arterial trauma (such as
catheter-induced thrombus formation)
Endocarditis (valvular vegetation) Paradoxical sources (secondary to an intracardiac
defect and a patent foramen ovale)
Prosthetic cardiac valves
Rheumatic heart disease
1249
detailed listing of manifestations of TIA or stroke relating to
stenosis of the right or left internal carotid artery. TIA or strokes
may also occur from ischemia or infarction of the vertebrobasilar
system secondary to stenosis of the vertebral arteries. Symptoms
related to vertebral artery stenosis include cranial nerve deficits,
visual field loss, ataxia, dizziness, imbalance, incoordination, and
ataxic gait.
1250
with irreversible anoxic injury to skeletal muscle or peripheral
nerves within 4 to 6 hours. Skin and subcutaneous tissue remain
viable for longer periods because of increased tolerance to ischemia.
In less than 8 hours’ duration of acute ischemia, the limb may
appear pale, waxy white with a cadaveric appearance. At 8 to 12
hours, areas of local stasis develop with bluish skin mottling
followed by blebs, superficial skin necrosis, and dry gangrene
mummification of toes.
Evaluation and diagnosis of the cause of ALI are crucial to
prevent tissue injury and necrosis. In general, an onset of symptoms
indicative of ALI presenting within the past 14 days is considered
acute. Early diagnosis would include duplex ultrasound or vascular
noninvasive Doppler studies, angiography, echocardiogram, and
possible magnetic resonance angiography (MRA) or computer
tomography angiography (CTA). Treatment will include a number
of options including anticoagulation, thrombolytic therapy, surgical
thromboembolectomy, endovascular procedures of stent,
angioplasty, or atherectomy, and surgical bypass or amputation of
the limb. Complications include those secondary to the treatment,
as well as complications related to the acute ischemic event and
reperfusion injury. These include catheter-induced vessel injury,
bleeding, reocclusion, compartment syndrome, and reperfusion
injury.
Compartment syndrome and reperfusion injury occur when
ischemia to a limb is absent for an extended period of time.
Compartment syndrome is defined by the swelling of tissues within
closed fascial compartments leading to increased pressure,
compression, and further necrosis and nerve injury. In anticipation
of this, a fasciotomy of the involved limb may be performed at the
time of surgical thromboembolectomy or at a later time.
Reperfusion injury also involves the development of severe
acidosis, hyperkalemia, renal failure secondary to myoglobinuria,
and pulmonary insufficiency (see Compartment Syndrome
Ischemic Myositis, Chapter 3).
1251
Goal of system assessment
• Evaluate for decreased blood flow and tissue perfusion so as to
evaluate for focal diminished perfusion of the cerebrovascular or
lower extremity peripheral arterial systems.
• Patients with a bruit and/or two or more risk factors for PAD
1252
should be evaluated for carotid stenosis.
Box 5-7
SYMPTOMS OF TIA AND ISCHEMIC
STROKE RELATED TO STENOSIS OF THE
CAROTID ARTERY
Right Internal Carotid Artery (RICA) Left Internal Carotid Artery (LICA)
Right eye monocular blindness (amaurosis Left eye monocular blindness (amaurosis
fugax) fugax)
Right homonymous hemianopsia (visual loss Left homonymous hemianopsia (visual loss
involving right visual field) involving left visual field)
Aphasia in ambidextrous or left-handed Aphasia
persons
Left-sided weakness (hemiparesis) Right-sided weakness (hemiparesis)
Left-sided sensory loss (paresthesia) Right-sided sensory loss (paresthesia)
1253
• Intermittent claudication is the most common manifestation of
PAD.
• Rest pain, which is present all the time without relief, indicates a
critically ischemic limb and is generally present in the distal foot,
forefoot, and toes.
1254
• Acute occlusions are commonly associated with a
thromboembolic source, which needs to be identified.
Observation
Symptoms of PAD may vary depending on the vessels involved
and may include intermittent claudication if it involves the limbs or
TIAs if it involves the carotid arteries, which provide perfusion to
the brain. Most patients with intermittent claudication require no
intervention, approximately 20% require surgical reconstruction,
and approximately 5% to 10% progress to require an amputation.
The presence of pain at rest or a nonhealing necrotic ulcer defines
CLI and indicates disease in greater than one artery and impending
loss of the limb without treatment. Evaluate blood flow quality and
tissue perfusion of cerebrovascular and peripheral vascular vessels:
• Cerebrovascular perfusion
1255
• Neurologic assessment of cranial nerve function
1256
movement; injury may affect tongue movement,
dysphagia, or dystonia.
Vital signs
Check temperature, HR, BP, and peripheral pulses to evaluate
blood flow quality and tissue perfusion.
1257
• HR: Symptomatic bradycardia may develop post carotid
procedure caused by vagal stimulation.
Box 5-8
ANKLE-BRACHIAL INDEX
To obtain an ankle-branchial index (ABI):
• With the patient lying flat, measure blood pressure (BP) of both
arms. If the BP differs between arms, use the higher reading.
1258
• Calculate the ABI by dividing the systolic reading at the DP/PT
level by the systolic reading at the arm (brachial artery).
Palpation
• Check skin temperature and pulse assessment to evaluate for
decreased tissue perfusion.
1259
• Presence of edema (scale 0 to 4+) of extremities is indicative of
other secondary problems (such as HF, liver or renal disease,
venous insufficiency, or venous thrombosis)
Auscultation
Listen for presence of bruits, which indicate disturbances in flow
(plaque formation).
• Bruits in the carotid arteries, the aorta, or the renal arteries may
be indicative of stenosis or dilation of arteries.
1260
and correlate with the presence of turbulent flow.
Screening labwork
Blood studies can help to determine risk of vascular disease or its
complications.
1261
• Coagulation studies: PT/INR or PTT evaluating for increased
clotting/bleeding propensity.
1262
1263
ALI, acute limb ischemia; ASCVD, atherosclerotic cardiovascular disease; AST,
aspartate aminotransferase; CLI, critical limb ischemia; CPK, creatine
phosphokinase; CT, computed tomography; EDV, end-diastolic velocity; HDL-C,
high-density lipoprotein cholesterol; LDH, lactate dehydrogenase; LDL-C, low-density
lipoprotein cholesterol; LE, lower extremity; PAD, peripheral artery disease; PSV,
peak systolic velocity; TBI, toe brachial index; VLDL, very low-density lipoprotein.
1264
disease. Stenosis greater than 70% may indicate the need for CTA or
angiogram, especially if symptoms are present. A CTA may also be
used if unilateral symptoms are present and there are conflicting
findings on the DUS.
Ankle-brachial index
BP is taken in both arms, with the highest pressure used for
calculating indices (unequal arm pressures may indicate the
presence of carotid or subclavian artery disease and the need for a
carotid/subclavian DUS). Segmental pressures are also taken with a
thigh cuff placed above the knee for a low thigh pressure and above
the ankle to obtain ankle pressures of the dorsalis pedis and
posterior tibial artery. A hand-held Doppler is used to acquire the
dorsalis pedis and posterior tibial pulses. Normally, the pressure in
the leg is equal to or slightly higher than brachial pressure. A
difference of greater than 30 mm Hg between segments indicates
disease of the artery proximal to where the pressure was taken. The
ankle pressure is divided by the brachial pressure to obtain the ABI.
Calcification of the arterial wall provides a falsely high
measurement preventing compression of the vessel to obtain the
pressure; this is referred to as a “noncompressible” vessel. In these
patients, diagnosis must be based on Doppler waveform analysis.
Collaborative management
Care priorities: Peripheral artery occlusive disease
Priorities for the care of a patient with chronic peripheral artery
occlusive disease should focus on early identification of disease and
prevention of disease progression, disability secondary to ischemic
injury, and thrombotic ischemic events. Prevention of disease
progression would include the control of risk factors, prevention of
thrombus formation (i.e., antiplatelet therapy or other
anticoagulants), and management of medications to control risk
factors.
To assist and guide the identification and management of
patients with PAD, many national organizations have collaborated
to produce evidence-based guidelines. Selective recommendations
1265
from the guidelines that are related to acute care settings are
outlined in the following tables.
1266
*
2014, JNC-8 Guidelines for Management of Hypertension in Adults
†
2013, ACC/AHA Task Force Cholesterol Management Guidelines
ABI, Ankle-brachial index; ACEI, angiotensin-converting enzyme inhibitor; ASCVD,
atherosclerotic cardiovascular disease; CHF, congestive heart failure; CV,
cardiovascular; DM, diabetes mellitus; HLD, hyperlipidemia; HTN, hypertension;
LDL-C, low-density lipoprotein cholesterol; LE, lower extremity; MI, myocardial
infarction; PAD, peripheral artery disease; PTFE, polytetrafluoroethylene; PVR, pulse
volume recording; TBI, toe-brachial index.
1267
with ischemic ulcers, specific care priorities would include wound
care, preventing or treating infection, and protecting the limb to
prevent further tissue damage. Additional measures would include
the following.
1268
patient who has undergone lower extremity bypass or stent
placement are important to prevent graft occlusion. Hypotension
decreases perfusion to the graft and dehydration increases blood
viscosity, leading to thrombosis and graft or stent occlusion.
1269
• Ticagrelor is a newer antiplatelet medication that is currently
recommended only for coronary patients as there is no data on its
use in PAD patients.
1270
• Thromboendarterectomy or endarterectomy: This procedure is
similar to that described above with a carotid endarterectomy
(CEA). An incision is made along the length of the artery where
the stenosis is located. The plaque is removed and the artery is
sewn closed. A vein patch may be placed in the vessel during
closure to provide an adequate size for blood flow. This is
generally performed on the proximal vessels of the distal aorta,
iliac, or femoral arteries. A shunt, as may be used in the CEA to
ensure cerebral perfusion, is not required in the distal limbs.
1271
ischemic time and restore blood flow to the ischemic limb. In the
limb with an acute arterial occlusion, thrombolysis is the
recommended emergent procedure used to dissolve the arterial clot
and restore limb perfusion. Time is of great concern in an acute
arterial occlusion. Anticoagulation may be initiated with a heparin
bolus and continuous infusion. If the patient is unable to undergo
thrombolytic therapy, a thromboembolectomy may be performed to
treat an acute arterial occlusion to quickly restore perfusion of the
limb.
1. Thrombolysis
See Acute Coronary Syndromes Chapter 5, for a complete
discussion of this procedure and care priorities related to its use.
Care priorities for a patient undergoing thrombolysis for an acute
peripheral artery occlusion are essentially the same as in the patient
with an acute coronary thrombus.
2. Thromboembolectomy
A surgical arteriotomy is performed and an embolectomy balloon
catheter is passed past the thrombus, the balloon is inflated, and the
clot is extracted. Neighboring arteries are checked for clot. Distal
embolization is of great concern with this procedure because of the
manipulation of the catheter around the thrombus.
Care priorities for ALI also include monitoring and early
recognition of compartment syndrome, thromboembolic injury, and
neuromuscular injury. For a full discussion and care priorities of
compartment syndrome, see Compartment Syndrome/Ischemic
Myositis, Chapter 3.
In ALI, care priorities would also include facilitating the
identification of the source of emboli. Given that the heart is a
common source, an echocardiogram will be performed as soon as
perfusion to the limb has been restored. Additional studies that
would be considered include an abdominal/pelvic CTA scan or
angiogram to look for any aneurysmal source. A lower extremity
ultrasound may be performed to look for peripheral aneurysms of
the femoral or popliteal arteries.
1272
High potential for distal emboli to the foot, referred to as
“trashed foot” or “blue toe syndrome.” The risk for distal
embolism from dislodgment of thrombus or thrombotic plaque is
significant in any procedure in which catheters are manipulated
around or through the clot, causing clot fragmentation, such as
with thrombolysis, thromboendarterectomy, angioplasty, or
stenting. Incorporate monitoring for distal emboli into care
priorities.
Collaborative management
Care priorities: Carotid artery occlusive disease
The focus of care is similar to PAD but includes the early
recognition and intervention of carotid artery stenosis to reduce
progression of disease and to prevent stroke. Multiple large
randomized trials have demonstrated an association between
carotid stenosis and other significant risk factors (ischemic heart
disease, TIA/stroke, PAD, hypertension, dyslipidemia, and
smoking). Many of these same trials have demonstrated a
decreased risk of stroke and MI with medical management. Several
trials have evaluated the risk of stroke in asymptomatic persons
with carotid artery stenosis, finding that persons with 60% to 80%
stenosis had higher stroke rates. Many trials have demonstrated
decrease in stroke and cardiovascular events with management of
the risk factors. Treatment of carotid disease includes medical
management and possibly a surgical approach of CEA or
endovascular placement of a carotid artery stent.
1273
1274
*
2014, JNC-8 Guidelines for Management of Hypertension in Adults
†
2013, ACC/AHA Task Force Cholesterol Management Guidelines
ASCVD, Atherosclerotic cardiovascular disease; BP, blood pressure; CAD, coronary
artery disease; CAS, carotid artery stent; CEA, carotid endarterectomy; CTA,
computed tomography angiography; CV, cardiovascular; DUS, duplex
ultrasonography; HTN, hypertension; IMT, intramural thickness; LDL-C, low-density
lipoprotein cholesterol; LVEF, left ventricular ejection fraction; MI, myocardial
infarction; MRA, magnetic resonance angiography; TIA, transient ischemic attack.
1275
1. Facilitate recovery from cea
• Observe for and prevent limb ischemia related to the access site
for the endovascular procedure.
1276
4. Initiate medical management, including antiplatelet
medications
Energy management
1277
3. Monitor for muscle pain during activity.
Fluid/electrolyte management
1278
2. Assess urine output, condition of skin, wound drainage, and
I&O.
Hemorrhage control
1279
4. Promote smoking cessation and decreased caffeine intake.
1280
viscosity, thus decreasing blood flow to the brain,
muscles, and tissues.
1281
Table 5-16
LOW-CHOLESTEROL DIETARY GUIDELINES
Egg yolks (no more than 3/week) Egg whites; cholesterol-free egg substitutes
Foods made with many egg yolks (e.g., Lean, well-trimmed meats; minimize servings of
sponge cakes) beef, lamb, and pork
Fatty cuts of meat, fat on meats Fish (except shellfish), chicken, and turkey
Skin on chicken and turkey (without the skin)
Luncheon meats and cold cuts Dried peas and beans as meat substitutes
Sausage, frankfurters Nonfat (skim) or low-fat (2%) milk
Shellfish (e.g., lobster, shrimp, crab) Low-fat cheese
Whole milk, cream, whole milk cheese Ice milk, sherbet, low-fat yogurt
Ice cream Monosaturated oils for cooking and food
Commercially prepared foods with preparation: canola, safflower, olive
hydrogenated shortening, which is Margarines that list one of the above oils as their
saturated fat first ingredients
Coconut and palm oils and products Foods prepared “from scratch” with the above
made with them (e.g., cream suggested oils
substitutes) Meats (in acceptable quantity) and vegetables
Butter, lard, hydrogenated shortening prepared by broiling, steaming, or baking (never
Meats and vegetables prepared by frying frying)
Seasonings containing large amounts of Spices, herbs, lemon juice, wine, flavored wine
sugar and saturated fats vinegars
Sauces and gravies
Salad dressings containing cream, cheese,
or mayonnaise
Table 5-17
GUIDELINES FOR A DIET LOW IN SATURATED FAT
Teaching: Activity/exercise
Discharge Instruction:
1282
1. Increase activity slowly; do not push, pull, or lift anything over
10 lb for 2 to 6 weeks. Do not drive until you talk with your
practitioner.
3. Plan for regular rest periods; let your body guide you in
decreasing or increasing activities.
1283
3. Assess for decreased BP, increased HR, and increased
respirations (may indicate cerebral ischemia).
Neurologic monitoring
Hemorrhage control
1284
deviation related to cervical hematoma.
Neurologic monitoring
1285
2. Ask the patient to wiggle his or her toes and flex and extend foot
and knee to assess motor function.
Skin surveillance
3. Promote proper foot care for operative leg and opposite foot as
opposite foot will be bearing more weight during convalescence.
Pressure management
Wound care
1286
2. Avoid further skin injury by not using tape directly on the skin.
4. Use aseptic technique for all dressing changes and incisional care.
Deficient knowledge
related to endovascular procedure and postprocedure care.
Goals/Outcomes: Within the 24-hour period before the
procedure, the patient describes the rationale for the procedure,
how it is performed, and postprocedure care. Patient relates
discharge instructions within the 24-hour period before discharge
from the ICU.
Knowledge: Treatment Procedures; Knowledge: Disease
Process; Knowledge: Medication; Knowledge: Prescribed Activity
1287
and degree of information desired.
Teaching: Procedure/treatment
As appropriate for coping style, discuss the following with patient
and significant others:
8. Need for increased fluid intake after procedure to flush dye from
system
1288
2. Avoidance of strenuous activity during the first few weeks at
home
1289
Pathophysiology
Valves facilitate the unidirectional flow of blood from atrium to
ventricles (AV valves) or ventricles to pulmonary and systemic
circulation (semilunar valves). Disease that alters the valve’s
structure can affect any or all of the cardiac valves, resulting in
either stenosis or insufficiency. Stenosis results from the narrowing
of the valve orifice because of the inability of the valve to open
properly, causing partial obstruction. Insufficiency is the leaking of
blood around the orifice when the valve does not close properly,
resulting in regurgitation or backward flow of blood through the
valve. Both conditions result in higher pressure behind the valve
that reduces forward blood flow and CO. Stenosis and insufficiency
can occur independently or together and affect a single or multiple
valves.
Atrioventricular valves
AV valves are connected by chordae tendineae to papillary
muscles, enabling the valve cusp to point in the direction of blood
flow. Papillary muscle contraction holds the AV valves in place,
preventing them from being forced into the atria by the increased
ventricular pressure during contraction.
Semilunar valves
Semilunar describes the half-moon shape of the valves. When
intraventricular pressures increase and exceed atrial and
pulmonary pressures, valves open, allowing blood to flow forward
into the pulmonary and systemic vasculature. Closure of the valves,
after ventricular contraction and ejection, prevents blood from
reversing or flowing backwards.
1290
located between the right ventricle and the pulmonary artery.
1291
after the acute phase of rheumatic endocarditis. Diastolic doming
of the anterior leaflet (hockey-stick deformity) and an immobile
posterior leaflet give the valve a fish-mouth appearance and
restrict the valve orifice. Pressure in the left atrium increases
caused by the extra force needed to drive blood through the
narrowed opening. Eventually, left atrial hypertrophy and
stiffening of the left atrial wall change the surrounding structures
and increase pulmonary artery pressure. Additionally, the
structural abnormalities of the atria contribute to changes in atrial
conduction patterns leading to atrial fibrillation in half of
individuals with mitral stenosis.
1292
abnormality of the leaflets because of a variety of disease
processes. Medications used to treat migraine (e.g.,
methysergide), Parkinson disease (e.g., pergolide), and obesity
(e.g., fenfluramine) have been associated with TR.
1293
• Chronic AR occurs in response to gradual dilatation of the left
ventricle and symptoms are masked by compensatory
mechanisms. Once symptoms become severe, rapid decline
follows.
1294
History and risk factors
Causes of valvular heart disease
• Congenital malformations
• Rheumatoid arthritis
• Advanced age
• Infective endocarditis
• Annular calcification
• Cancer
• Syphilis
• Pulmonary hypertension
• Cardiomyopathy
Physical assessment
Murmurs: Auscultation of heart sounds is the most effective
1295
screening tool for valvular disease. Evaluate changes in quality,
pitch, and intensity to obtain insight into the patient’s clinical
condition, functional capacity, and quality of life. Changes in the
quality and sound of murmurs can provide essential information
regarding the clinical condition of patients with valvular heart
disease.
1296
ascites, and pedal edema. LV end- dysfunction decreases both TSV and
diastolic pressure (LVEDP) and CO are FSV, but EF may be normal. ESV
often normal when only the mitral and EDV increase, then LAP and
valve is stenosed. With progressive LVEDP increase, pulmonary edema
stenosis, the CO becomes subnormal at may occur, and if unmanaged,
rest and fails to increase during cardiogenic shock ensues.
exercise.
Assessment
Aortic Stenosis Aortic Insufficiency
Findings
Observation Faint slow radial pulse, low blood Dyspnea, pulmonary congestion, edema,
pressure and pulse pressure, symptoms related to left-sided heart
dizziness, fainting, syncope, failure. Aortic regurgitation (AR) is
pallor, dyspnea, fatigue; chest indicated by three findings: Corrigan
pain caused by coronary pulse is a palpated pulse with rapid and
insufficiency, irregular heart forceful distention of the artery followed
1297
sounds, and left-sided heart by quick collapse. DeMusset sign is
failure forward and backward bobbing of the
head. Quincke sign is visible pulsation
seen with slight compression of nail beds.
Hill sign is popliteal cuff systolic blood
pressure 40 mm Hg higher than brachial
cuff systolic blood pressure.
Auscultation Increased amplitude of S1; Diastolic blowing murmur heard loudest
opening snap and mid-diastolic at the second right intercostal space
murmur at the mitral area beginning with S2. Duroziez sign is a
systolic murmur over the femoral artery
with proximal compression of the artery,
and a diastolic murmur with distal
compression of the artery.
Chest Left ventricular (LV) enlargement LV enlargement
radiograph and dilation of the ascending
aorta
12-lead ECG LV hypertrophy; large S in V2, LV hypertrophy; large S in V2, large R in
large R in V5; strain results in V5; strain results in inverted T and
inverted T and depressed ST depressed ST segments in I and II and Vl,
segments in I and II and Vl, V5, V5, and V6.
and V6, bradydysrhythmias
Hemodynamics Increased LV pressure, increased Increased LV pressure, increased
pulmonary artery end-diastolic peripheral artery disease (PAD) and
pressure and wedge pressure; pulmonary artery occlusive pressure
increased gradient across the (PAOP), decreased cardiac output;
aortic valve on pullback from LV increased systolic blood pressure and
end-diastolic pressure to aortic widened pulse pressure. Peripheral pulses
pressure; narrow pulse pressure, are prominent or bounding. Symptoms
decreased cardiac output. LV may result from the elevated stroke
systolic function is preserved and volume during systole and the
cardiac output is maintained for incompetent aortic valve allowing
many years despite an elevated significantly decreased aortic diastolic
LV systolic pressure. Despite the pressure (often <60 mm Hg), with pulse
cardiac output at rest being pressures often >100 mm Hg. During early
normal, it fails to increase chronic AR, the LV ejection fraction (EF) is
appropriately during exercise, normal or increased. As AR progresses,
causing exercise-induced syncope LV enlargement exceeds preload reserve
or near syncope. With severe and the EF decreases to normal and then
aortic stenosis, atrial contraction subnormal levels. The LV end-systolic
is vital to diastolic filling of the volume increases and reflects progressive
LV so atrial fibrillation can be myocardial dysfunction. The LV gradually
catastrophic to maintaining stroke transforms from an elliptical to a spherical
volume. configuration.
1298
Collaborative management
Care priorities
1299
High-Risk Recommended Not Recommended
•Patients with prosthetic valves • Aggregated lifetime risk of endocarditis
• Prior infective endocarditis • GU and GI procedures (TEE,
• Cardiac transplant patients with esophagogastroduodenoscopy, colonoscopy,
regurgitation caused by abnormal valve cystoscopy) (See Acute Infective Endocarditis,
structure Chapter 5).
• Unrepaired and palliated cyanotic
congenital heart defects (surgically
constructed palliative shunts and conduits)
• Repaired congenital heart defects
(prosthetic material or devices) first 6
months postprocedure
• Congenital heart defects with residual
defects at or adjacent to the prosthetic
patch or device that inhibits
endothelialization
1300
• Decision about surgery: Need is based largely on the patient’s
symptoms, rather than exclusively on the transvalvular pressure
gradient. Angina, syncope, and HF can develop suddenly,
sometimes following a lengthy asymptomatic period. Following
onset of symptoms, survival averages 2 to 3 years.
1301
greatly outweigh risks in inoperable patients with severe
symptomatic AS. Results show significantly improved quality of
life during the first year following TAVR/TAVI.
1302
with management of afterload (BP/SVR) using vasodilators.
1303
• Transcatheter interventions: Increasingly studied for carefully
selected patients with severe MR. Data are limited and there is
FDA approval for only one device to date. ACC, AATS, SCAIF,
and STS recommendations and guidelines are in development.
1304
• Pulmonic regurgitation: Generally not seen unless other valve
disease is present. It is also likely to be a congenital defect and
typically managed with pulmonic valve replacement if HF is
present.
1305
appropriate. In the case of uncontrolled bleeding, fresh-frozen
plasma or prothrombin complex concentrate is recommended
over higher-dose parenteral (IV) vitamin K1, which often results
in a hypercoagulable state. Low-dose IV vitamin K (1 mg) has
been found to be safer, if needed. Aspirin should also be
discontinued.
Surgical interventions
• Valve replacement: Procedure with a mortality rate of about 6%,
performed in patients with moderate to severe calcification,
stenosis with insufficiency, and pure insufficiency. Three types of
replacement valves are available: homografts and heterografts,
which are tissue grafts, and mechanical valves. Homografts are
specially treated human cadaver valves and are seldom used
because of a lack of availability. The more commonly used
heterograft is a specially prepared valve from an animal, usually
a pig or a cow. These valves are readily available and more
advantageous because there is less of a tendency for clot
formation and adherence to the valve structures. Thus, patients
do not require anticoagulation therapy after valve replacement.
The disadvantage is that they function for only 5 to 8 years.
Mechanical valves are made from stainless steel, carbon, plastic,
and other durable materials. Mechanical valves have a 10- to 15-
year life span and require lifelong anticoagulation because of
their susceptibility to clot formation. Postoperative care is similar
to that of the patient who has undergone myocardial
revascularization for CAD (see Acute Coronary Syndromes,
1306
Chapter 5). Patients undergoing valve surgery are at increased
risk for thrombosis, embolism, and valvular endocarditis
(particularly with mechanical mitral valves and patients with
atrial fibrillation).
1307
perforation of the left ventricle, and dysrhythmias.
Ineffective protection
related to risk of bleeding/hemorrhage secondary to
anticoagulation.
Circulatory precautions
1308
3. Monitor hemodynamics for hypovolemia: RAP less than 4 mm
Hg, PAWP less than 6 mm Hg, decreased BP, decreased measured
CO/CI, urine output less than 0.5 mL/kg/h, increased urine specific
gravity, and excessive chest tube drainage (more than 100 mL/h). Be
alert to a decreased Hct. Optimal values are Hct greater than 37%
(female) and greater than 40% (male).
Box 5-9
NURSING IMPLICATIONS FOR
ADMINISTRATION OF EPSILON-
AMINOCAPROIC ACID
• Be aware that rapid administration may induce hypotension,
bradycardia, or cardiac dysrhythmias.
• Monitor for and report the following side effects: nausea, cramps,
diarrhea, dizziness, tinnitus, headache, skin rash, malaise, nasal
stuffiness, postural hypotension.
1309
stockings as prescribed.
1310
Shock prevention
1311
An air embolus, particulate emboli from calcified valves, and
thrombotic emboli from prosthetic valves may lodge in the brain,
leading to varying degrees of stroke.
Neurologic monitoring
3. Assess patient’s PT, PTT, and INR as heparin is tapered off and
warfarin therapy is instituted. Heparin and warfarin may be
initiated simultaneously to reduce the time needed to stabilize the
lab values.
1312
assist with moving.
Deficient knowledge
related to risk of infective endocarditis after valve surgery and preventive
strategies.
1313
affect the repaired valve.
Deficient knowledge
related to risk of bleeding or clotting caused by excessive or insufficient
anticoagulation therapy.
1314
2. To call advanced practice provider if bleeding or bruising is
noted.
Deficient knowledge
related to procedure for percutaneous balloon valvuloplasty (PBV) and
postprocedural assessment.
Goals/Outcomes: Within the 24-hour period before PBV, the
patient verbalizes rationale for the procedure, the technique, and
postprocedural care.
Knowledge: Treatment Regimen
Teaching: Preoperative
1315
• Use of fluoroscopy during procedure. Evaluate
patient for a history of sensitivity to contrast
material.
Teaching: Procedure/Treatment
Shock prevention
1316
3. Monitor Hct and electrolyte values. Observe for a decrease in Hct
or any change in electrolyte levels (particularly potassium) that
could precipitate dysrhythmias. Optimal values are Hct greater
than 37% (female) or greater than 40% (male) and serum potassium
3.5 to 5 mEq/L.
Ineffective protection
related to risk of hemorrhage or hematoma formation secondary to
heparinization with PBV.
Goals/Outcomes: Throughout the postoperative course, the
patient has minimal or absent bleeding or hematoma formation at
the catheter insertion site. PTT is within therapeutic anticoagulation
range (as prescribed or according to institutional procedure).
Circulation Status
Bleeding precautions
1317
that of normal.
1318
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1340
CHAPTER 6
Kidney injury
Genitourinary assessment: General
Goal of system assessment
Evaluate for decreased renal function and assess the severity of
renal dysfunction.
• Exposure to chemicals.
1341
urinary catheterization
Observation
Evidence of chronic versus acute process:
• Temperature.
Palpation
Abdominal assessment to identify renal pathology:
1342
• Kidneys are difficult to palpate because of location. If they are
enlarged and palpable, this could represent polycystic kidney
disease or hydronephrosis.
Auscultation
• Cardiac auscultation for the presence of murmurs, pericardial
friction rub, S3 and/or S4 and congestive heart failure.
Labwork
Renal dysfunction causes marked changes in fluid and electrolyte
balance, acid-base balance, and red cell production, and increased
concentrations of blood urea nitrogen (BUN) and creatinine.
• Urinalysis.
• Urine electrolytes.
1343
levels.
Table 6-1
KIDNEY DISEASE/IMPROVING GLOBAL OUTCOMES (KDIGO)
CRITERIA FOR THE DIAGNOSIS OF ACUTE KIDNEY INJURY
1344
prerenal, intrarenal, and postrenal (Table 6-2).
Table 6-2
CAUSES OF ACUTE KIDNEY INJURY
1345
perfusion, stretch receptors in the glomerular afferent arterioles
cause vasodilation. Vasodilation is also enhanced by the production
of prostaglandins, kallikrein, kinins, and nitric oxide. NSAIDs
inhibit prostaglandin production, thereby diminishing afferent
arteriole vasodilation prompting low filtration pressure. Efferent
arterioles normally increase vasoconstriction in response to
angiotensin II. Angiotensin II inhibitors and blockers interfere with
the efferent arteriole response to hypoperfusion. Patients receiving
ACEIs with a glomerular filtration critically dependent on the
angiotensin II–regulated efferent arteriole vascular tone (patients
with heart failure or severe volume depletion) can experience low
efferent arteriolar pressure, which contributes to reduced filtration.
Prerenal AKI is reversible if treated promptly. Treatment is directed
at the underlying cause of decreased renal blood flow. Intravascular
volume depletion, reduced cardiac output, systemic vasodilation,
renal vasoconstriction, and increased intraabdominal pressure are
causes of hypoperfusion. A consequence of prolonged
hypoperfusion includes renal tissue ischemia and the subsequent
development of intrarenal AKI.
Intrarenal AKI is caused by direct insults to the glomerular or
tubular structures. The most common form of intrarenal AKI is
acute tubular necrosis (ATN). In addition to renal ischemia, ATN
may be the result of nephrotoxic injury produced by medications,
radiocontrast media, infection, and exposure to toxic substances
such as heavy metals, pesticides, and organic solvents. Conditions
that produce myoglobinuria and hemoglobinuria can also lead to
tubular injury. Contrast material–induced nephropathy (CIN) is a
form of ATN that develops within 12 to 48 hours of contrast
administration. Risk factors for CIN include diabetes mellitus,
chronic kidney disease, hypotension, volume depletion, cirrhosis,
heart failure, and administration of nephrotoxic agents. Although
the development of low-osmolality contrast agents and prevention
protocols have reduced the incidence of CIN, most patients in the
intensive care unit would have one or more risk factors for the
development of CIN. Clinicians weigh the diagnostic benefit of
using contrast material during imaging procedures and the risk of
CIN.
1346
6-1
RESEARCH BRIEF
Purpose: The authors conducted a systematic review and
metaanalysis of controlled studies comparing the incidence of
acute kidney injury (AKI) in patients who received intravenous
(IV) contrast media with patients who underwent an imaging
procedure without contrast media.
Methods: MEDLINE, EMBASE, Scopus, and the Cochrane
Library were searched for studies that compared the incidence of
AKI in patients exposed to IV contrast medium with the incidence
of AKI in unexposed patients. Changes in serum creatinine level or
estimated glomerular filtration rate 48 to 72 hours following
imaging procedures or admission were used for the detection of
AKI. Relative risk was calculated and tested in subgroups of
different patient comorbidities, contrast medium types, and AKI
diagnostic criteria.
Results: Thirteen nonrandomized studies (25,950 patients) met
inclusion criteria. The average rate of AKI was 6.4% in the contrast
medium group and 6.5% in the noncontrast group. The risks of
AKI, dialysis, and death were similar for both groups regardless of
IV contrast medium type, diagnostic criteria for AKI, or whether
patients had diabetes mellitus or renal insufficiency.
Conclusion: Controlled contrast medium–induced nephropathy
studies demonstrate a similar incidence of AKI, dialysis, and death
between the contrast medium group and control group.
ATN is characterized by tubular cell necrosis, cast formation,
and tubular obstruction caused by casts and cellular debris.
Therapy is focused on maintenance of renal perfusion pressure,
administering renal vasodilators to restore blood flow, and
promoting diuresis to “wash out” the intratubular debris. ATN is
sometimes nonoliguric. Oliguria may occur with both toxic ATN
and ischemic ATN. Common nephrotoxic agents are found in
Table 6-3.
From McDonald J, McDonald R, Comin J, et al: Frequency of acute kidney injury following
intravenous contrast medium administration: a systematic review and meta-analysis.
Radiology 267:119-128, 2013.
1347
Table 6-3
COMMON NEPHROTOXINS
Exogenous Endogenous
Antineoplastics Rhabdomyolysis
• Methotrexate Hemolysis
• Cisplatin Tumor Lysis Syndrome
Antimicrobials
• Amphotericin
• Aminoglycosides
• Acyclovir
• Penicillins
Chemicals
• Ethylene glycol
• Pesticides
• Organic solvents
• Radiocontrast Medium
1348
4 mg/dL) and is rarely symptomatic unless the patient receives
magnesium-containing antacids (e.g., Maalox, Milk of Magnesia).
Table 6-4
ALTERED ELECTROLYTE BALANCE IN ACUTE KIDNEY INJURY
1349
• Neuromuscular symptoms are seen at serum
levels of approximately 2.5 mEq/L.
• Teach the patient and significant others the
indicators of hypokalemia and the importance of
notifying the nurse promptly if they occur.
• Provide a list of foods high in potassium and
assist with planning menus that incorporate them.
• Administer potassium-sparing diuretics (e.g.,
spironolactone, triamterene) as prescribed.
• Administer oral or IV potassium supplements as
prescribed; for oral route, administer with at least
4 oz water or juice to minimize gastric irritation.
Hypernatremia
The inability of the kidneys to excrete • Monitor serum sodium levels for serum Na+
excess sodium; decreased water intake; greater than 147 mEq/L.
increased water losses via osmotic • Monitor VS and I&O hourly; weigh the patient
diuresis; excessive parenteral daily.
administration of sodium-containing • Be alert to dry mucous membranes, flushed skin,
solutions (e.g., sodium bicarbonate, 3% firm and rubbery tissue turgor, hyperthermia,
sodium chloride) oliguria, or anuria.
• Assess sensorium for restlessness and agitation;
institute seizure precautions as indicated.
• Administer prescribed IV replacement fluids.
• Administer diuretics as prescribed.
Hyponatremia
Loss through vomiting, diarrhea, profuse • Monitor for serum Na+ less than 137 mEq/L.
diaphoresis; use of potent diuretics; salt- • Monitor input and output hourly; record weight
losing nephropathies; administration of daily for trend.
large amount of sodium-free IV fluids • Assess the patient for abdominal cramps,
(may be associated with fluid volume diarrhea, nausea, dizziness when changing
excess or postobstructive diuresis) position, postural hypotension, cold and clammy
skin, and apprehension.
• Provide parenteral replacement therapy as
prescribed.
• Institute a safe environment for individuals with
altered LOC.
Hypocalcemia
Poor absorption of dietary calcium; • Monitor for serum Ca2+ less than 8.5 mg/dL.
precipitation of calcium out of tissues in • Monitor for numbness and tingling around the
the presence of elevated phosphorus mouth, muscle twitching, facial twitching, and
level; inadequate absorption and use of tonic muscle spasms.
calcium occurring with lack of • Assess for Trousseau sign (carpopedal spasm)
conversion of vitamin D to its usable and Chvostek sign (spasm of lip and cheek).
form • Administer calcium and vitamin D supplements
as prescribed.
• Reinforce the necessity of taking these
medications as prescribed.
• Teach the patient and significant others the
indicators of hypocalcemia.
• Teach the importance of continued medical
follow-up to check serum Ca2+ levels.
Hyperphosphatemia
Abnormal retention of phosphates • Monitor for serum phosphate greater than 4.5
caused by the inability of the kidneys to g/dL.
excrete excess phosphorus • Although most foods contain generous amounts
of phosphate, those especially high in phosphate
include beef, pork, dried beans, dried mature
1350
peas, and dairy products. Monitor the patient’s
diet accordingly.
• Administer phosphate binders as prescribed.
Assess for constipation, which may result from
use of phosphate binders.
• Teach the patient and significant others the
relationship between calcium and phosphate
levels in the body.
• Emphasize that maintaining good phosphate
control and calcium balance may help control
itching and prevent future problems with bone
disease.
• Reinforce the need for follow-up visits to check
serum phosphate levels.
Hypermagnesemia
Administration of magnesium- • Monitor serum Mg2+ levels greater than 2.5
containing medications to patients with mEq/L.
impaired renal function • Assess for diaphoresis, flushing, hypotension,
drowsiness, weak-to-absent DTRs, bradycardia,
lethargy, and respiratory impairment.
• Teach the indicators listed above to the patient
and significant others.
• Avoid giving medications that contain
magnesium (see Box 1-7). Emphasize to the
patient that such medications should not be taken
without the physician’s approval.
Metabolic Acidosis
The inability of the kidneys to excrete • Monitor for HCO3− less than 22 mEq/L and pH
excess acid produced by normal less than 7.35.
metabolic processes; marked tissue • Monitor input and output, LOC, and VS.
trauma, infection, and diarrhea may • Be alert to Kussmaul’s respirations, SOB,
contribute to a more rapid development anorexia, headache, nausea, vomiting, weakness,
of acidosis (often associated with K+ apathy, fatigue, and coma.
greater than 5 mEq/L) • Institute seizure precautions in the presence of
altered LOC.
• Administer IV fluids and bicarbonate as
prescribed.
• Teach the patient the importance of dietary
restrictions, particularly of protein, and of
maintaining adequate carbohydrate intake to
prevent worsening acidosis.
• Emphasize that the patient should report to the
advanced practice provider increased temperature
and other signs of infection.
• Teach the patient the importance of taking
sodium bicarbonate as prescribed and of
maintaining the dialysis schedule (both
hemodialysis and peritoneal dialysis help correct
acidosis)
Uremia
Failure of the kidneys to excrete urea, • Monitor the patient for chronic fatigue, insomnia,
creatinine, uric acid, and other metabolic anorexia, vomiting, metallic taste in the mouth,
waste products pruritus, increased bleeding tendency, muscular
twitching, involuntary leg movements, decreasing
attention span, anemia, muscle wasting, and
weakness.
• Teach the patient and significant others that the
1351
indicators of uremia develop gradually and are
very subtle. Explain the importance of notifying
the nurse of sudden worsening of the symptoms
that may be present.
• Monitor and record dietary intake of protein,
potassium, and sodium.
• Use lotions and oils to lubricate the patient’s skin
and relieve drying and cracking.
• Provide oral hygiene at frequent intervals, using a
soft-bristle toothbrush and mouthwash, to help
combat the patient’s thirst and the metallic taste
caused by uremia. Chewing gum and hard candy
may also help alleviate thirst and the unpleasant
taste.
• Encourage isometric exercises and short walks, if
the patient is able, to help maintain the patient’s
muscle strength and tone, especially in the legs.
• Teach significant others that because of the
patient’s decreasing concentration level, they
should communicate with the patient by using
simple and direct statements.
• Teach the patient to maintain good nutrition by
ingesting the allotted amounts of carbohydrates
and high–biological value protein to support cell
rebuilding and decrease waste products from
protein breakdown.
• Explain that profuse bleeding can occur with
uremia and that knives, scissors, and other sharp
instruments should be used with caution.
• Stress that OTC medications such as aspirin and
ibuprofen may enhance bleeding tendency.
• Emphasize the importance of follow-up visits to
evaluate the progression of uremia.
• Stress that the dialysis schedule should be
maintained to decrease the symptoms of uremia
and correct many of the metabolic abnormalities
that occur.
AKI, Acute kidney injury; Ca2+, calcium; DTR, deep tendon reflex; ECG,
electrocardiogram; HCO3−, bicarbonate; HR, heart rate; I&O, intake and output; IV,
intravenous; K+, potassium; LOC, level of consciousness; Mg2+, magnesium; Na+,
sodium; OTC, over-the-counter; SOB, shortness of breath; VS, vital signs.
1352
3. Recovery phase: A return to a normal 24-hour volume (1500 to
1800 mL). Usually, kidney function continues to improve and may
take 6 months to 1 year from the initial insult to return to baseline
functional status.
Assessment
Goal of assessment
AKI impacts most of the major organs and the focus of assessment
is to determine how AKI is affecting these organs. Assessment
findings contribute to the development of a treatment plan that
manages fluid, electrolyte, and acid-base imbalances, as well as
prevents or minimizes metabolic encephalopathy, anemia, and
infection.
1353
secretion capacity of the intestine, oxalate enters the circulatory
system with subsequent renal tubular exposure. Recreational drug
use (e.g., cocaine, methamphetamines, and bath salts) has also been
implicated in the development of AKI.
1354
thirst sensation, and the structural /functional changes of aging
increase the risk of AKI in older adult patients. There is a natural
decline in kidney size, GFR, and renal blood flow with advancing
age. An impaired ability to concentrate urine increases the risk of
volume depletion and may predispose the older adult patient to
prerenal azotemia. Diagnosis of AKI in older adults can be
challenging. KDIGO guidelines use serum creatinine and urine
production for staging AKI. Serum creatinine levels are influenced
by age, muscle mass, hydration status, and race. AKI may be
obscured by a low or normal serum creatinine level in the older
adult population. Serial changes in creatinine values, urine output,
and weight may be more helpful in the detection of AKI in the older
adult.
Prerenal presentation
• Oliguric or nonoliguric.
Intrarenal presentation
• Oliguric or nonoliguric.
1355
• Urine specific gravity 1.010.
• Abnormal sediment with red blood cell (RBC) casts and cellular
debris in the urine.
Postrenal presentation
• Likely oliguric but may be nonoliguric.
Vital signs
• BP may be elevated in states of fluid volume excess or decreased
in states of fluid volume deficit.
1356
• Temperature: may be hyperthermic or hypothermic with sepsis.
Observation
• Peripheral edema and periorbital edema.
• Shortness of breath.
• Pallor.
• Purpura.
• Weakness.
• Neuromuscular dysfunction.
• Dysrhythmias.
Palpation
• Edema (scale 0 to 4+): extremities and sacrum.
• Muscle tenderness.
• Flank tenderness.
Auscultation
• S3 and S4 gallops indicative of heart failure.
1357
• Pericardial friction rub.
• Tachycardia or dysrhythmias.
• Crackles.
Uremic manifestations
• Drowsiness, confusion, irritability, and coma.
• Hypertension.
• Heart failure.
• Pulmonary edema.
1358
• GFR: Most reliable estimation of GFR is the measurement of 24-
hour creatinine clearance.
1359
Blood Studies
Complete blood Assesses for anemia, inflammation, Decreased RBCs, Hgb, or Hct reflects
count (CBC) and infection; assists with anemia or recent blood loss.
Hemoglobin differential diagnosis of septic
(Hgb) cause of acute renal failure/acute
Hematocrit (Hct) kidney injury (ARF/AKI)
Red blood cell
(RBC) count
White blood cell
(WBC) count
Coagulation Assesses for the presence of Decreased PT with low INR promotes
profile: bleeding or clotting and clotting; elevation promotes bleeding.
Prothrombin disseminated intravascular
time (PT) with coagulation (DIC)
international
normalized
ratio (INR)
Partial
thromboplastin
time (PTT)
Blood urea Assesses for the severity of renal Elevation indicates renal dysfunction.
nitrogen (BUN) dysfunction Creatinine may be markedly elevated
Creatinine in the presence of massive skeletal
Estimated muscle injury (e.g., multiple trauma,
glomerular crush injuries).
filtration rate BUN is influenced by hydration,
(eGFR) catabolism, gastrointestinal
bleeding, infection fever, and
corticosteroid therapy.
The eGFR in ARF/AKI is usually less
than 50 mL/min. BUN may elevate
before creatinine in the setting of
dehydration or hypovolemia,
particularly in older adults.
Electrolytes: Assesses for abnormalities Increase or decrease in K+ may cause
Potassium (K+) associated with AKI arrhythmias. Elevated Na+ may
Sodium (Na+) indicate dehydration.
Calcium (Ca2+) Decreased Na+ may indicate fluid
Magnesium retention.
(Mg2+) Low Mg2+ or Ca2+ may cause
dysrhythmias.
Arterial blood Assesses for the presence of Low Paco2 and plasma pH values
gases metabolic acidosis reflect metabolic acidosis.
Urinalysis Assesses for the presence of Presence of sediment containing
sediment tubular epithelial cells, cellular
debris, and tubular casts supports
diagnosis of ARF/AKI.
Increased protein and many RBC
casts are common in intrarenal
disease.
Sediment is normal in prerenal
causes.
Large amounts of myoglobin may be
present in severe skeletal muscle
injury or rhabdomyolysis.
Urinary sodium Differentiates prerenal from Urinary Na+ is less than 20 mEq/L
1360
intrarenal cause; often overlooked (prerenal).
as a significant finding Urinary Na+ is more than 20 mEq/L in
intrarenal causes.
Box 6-1
INVESTIGATIONAL BIOMARKERS FOR
ACUTE KIDNEY INJURY
• Interleukin-18
• Cystatin C
• N-Acetyl-beta-d-glucosaminidase
Collaborative management
1361
Care priorities for AKI
The management of AKI focuses on interventions to limit nephron
damage and restore fluid, electrolyte, and acid-base balances.
Supportive therapies are implemented to manage uremia and
associated complications (Table 6-5).
Table 6-5
MANAGEMENT CONSIDERATIONS: ACUTE KIDNEY INJURY
Issue Treatment
Intravascular volume Restriction of salt (1 to 1.5 g/day) and water (1 L/day).
overload Consider diuretic therapy to decrease filtrate reabsorption and
enhance water excretion. Use only after adequate hydration to
increase urine output or in an attempt to prevent onset of oliguria.
If volume overload is present, they are used to prevent pulmonary
edema. Osmotic diuretics such as mannitol may be used to increase
intravascular volume, promote renal blood flow, increase
glomerular filtration rate, and stimulate urinary output.
Ultrafiltration may be considered for extracorporeal fluid removal.
Hemodynamic monitoring of central venous pressure.
Oxygen/high flow, continuous positive airway pressure
Rhabdomyolysis/Tumor Forced alkaline diuresis with isotonic sodium bicarbonate solution at
lysis syndrome 100 mL/h to manage pigmenturia (myoglobinuria, hemoglobinuria)
resulting from rhabdomyolysis or severe crush or skeletal muscle
injury. In addition, aggressive volume replacement to maintain renal
perfusion pressure and reduce cast formation leading to renal tubular
obstruction.
Hyponatremia Restriction of oral and intravenous free water.
Hyperkalemia Restriction of dietary potassium.
Discontinuation of potassium supplements or potassium-sparing
diuretics.
Loop diuretics in diuretic-responsive patients.
Potassium-binding resin.
Glucose (50 mL of 50% with regular insulin 10 units intravenously).
Calcium gluconate (10 mL of 10% solution over 5 minutes).
Sodium bicarbonate (50 mEq intravenously): Sodium bicarbonate is
given in acidosis to promote the shift of potassium back into the
cells.
Albuterol 20 mg nebulized.
Renal replacement therapy.
Metabolic acidosis Careful management of dietary protein.
Renal replacement therapy.
Sodium bicarbonate: Sodium bicarbonate is given to control
metabolic acidosis and promote the shift of potassium back into the
cells.
Management of Restriction of dietary phosphate intake.
hyperphosphatemia Phosphate-binding agents: Phosphate binders (calcium carbonate
antacids, calcium acetate) that bind phosphorus and control
hyperphosphatemia and hypermagnesemia are given with meals.
Hypermagnesemia Discontinuation of magnesium-containing drugs such as antacids.
Prevention of contrast- Aggressive hydration with normal saline or bicarbonate solution 12
induced nephropathy hours before contrast administration. N-Acetylcysteine may be added
1362
with hydration for patients with glomerular filtration rate of less than
30 undergoing major procedures.
Uremic Renal replacement therapy.
encephalopathy/ Monitor for high risk of bleeding and injury.
Uremic pericarditis
1363
b. Aminoglycosides should be avoided unless a therapeutic
alternative is not available.
Table 6-6
DIURETIC USE IN ACUTE KIDNEY INJURY
Potential Fluid
Types Mechanisms of Action and Electrolyte
Abnormalities
Osmotic Diuretics
Mannitol Increase osmotic pressure of the filtrate, which Hyponatremia
Urea attracts water and electrolytes and prevents their Hypokalemia
reabsorption Rebound volume
expansion
Loop Diuretics
Furosemide Inhibit reabsorption of Na+ and Cl− at the ascending Hypokalemia
Ethacrynic acid loop of Henle in the medulla; they produce a Hyperuricemia
Bumetanide vasodilatory effect on the renal vasculature Hypocalcemia
Torsemide Hyperglycemia
and impairment
of glucose
tolerance
Dilutional
hyponatremia
Hypochloremic
alkalosis
Thiazides
Bendroflumethiazide Inhibit Na+ in the ascending loop of Henle at the Hypokalemia
Benzthiazide beginning of the distal loop Dilutional
Chlorothiazide hyponatremia
sodium Hypercalcemia
Hydrochlorothiazide Metabolic
Hydroflumethiazide alkalosis
Polythiazide Hypochloremia
Trichlormethiazide Hyperuricemia
Hyperglycemia
and impaired
glucose
tolerance
Thiazide-like Diuretics
Chlorthalidone Action same as thiazides Same as thiazides
Indapamide
Metolazone
Quinethazone
Potassium-sparing Diuretics*
1364
Amiloride HCl Inhibit aldosterone effect on the distal tubule, Hyperkalemia
Spironolactone causing Na+ excretion and K+ reabsorption Hyponatremia
Triamterene Dehydration
Acidosis
Transient increase
in BUN
Carbonic Anhydrase Inhibitors
1365
3. Provide nutrition support
4. Avoid hyperglycemia
Provide insulin therapy targeting plasma glucose 110 to 149
mg/day.
b. Hyperkalemia.
c. Metabolic acidosis.
d. Uncontrolled azotemia.
e. Drug overdose.
1366
related to inability of kidney to normally excrete urine
Goals/Outcomes: Within 24 to 48 hours of onset, intravascular
volume is stabilized, as evidenced by balanced intake and output
(I&O), urinary output greater than 0.5 mL/kg/h, body weight within
the patient’s normal range, MAP greater than 60 mm Hg and within
the patient’s normal range, CVP 10 to 12 mm Hg, HR 60 to 100
beats/min (bpm), and improvement of edema, crackles, gallop, and
other clinical indicators of fluid overload.
Fluid Overload Severity; Fluid Balance.
Fluid management
1367
6. Provide ice chips, chewing gum, or hard candy to help quench
thirst and moisten mouth.
1368
Hypovolemia management
6. Monitor for occult bleeding: Test all stools, emesis, and peritoneal
dialysate drainage for occult blood. Check urine and dialysate
1369
drainage at least every 8 hours.
Nutrition therapy
3. Control catabolism:
1370
antipyretic agents to control fever. Fever increases
tissue catabolism, which in turn increases metabolic
needs. Patients who are critically ill are often
catabolic and require careful nutrition management,
especially when hemodialysis, peritoneal dialysis,
or CRRT is implemented. Protein target is 0.8 to 1.0
g/kg/day to provide essential amino acids for a
noncatabolic patient with AKI. The end products of
protein metabolism that accumulate are reflected by
an increase in BUN level. Ensure intake of protein
with high biological value (e.g., eggs, meat, fowl,
milk, fish), which contains essential amino acids
necessary for cell building.
4. Manage electrolytes:
1371
greatly. If oliguria is present, sodium intake may be
restricted in the diet. If diuresis is present, sodium
intake may be increased because of excess sodium
loss in the urine. Intervene accordingly.
1372
related to immunocompromised state associated with renal failure
Goals/Outcomes: At the time of discharge from the intensive care
unit, infection is controlled, as evidenced by normothermia,
negative culture results of dialysate and body secretions, and white
blood cell (WBC) count less than 11,000/mm3.
Immune Status.
Infection protection
1373
anuria. The presence of a catheter further increases the risk of
infection.
Knowledge deficit
related to disease process of AKI
Goals/Outcomes: Within 72 hours of admission, the patient and
significant others verbalize accurate information regarding AKI and
the plan of care.
Knowledge: Disease Process.
1374
without approval of the advanced practice provider.
11. Teach the patient to use lotions and oils to lubricate the skin and
relieve drying and cracking.
1375
Teaching: Individual; Teaching: Prescribed Medication.
Additional, optional interventions include Discharge Planning;
Medication Management; and Weight Management.
Acute confusion
related to altered level of consciousness that results from fluid and
electrolyte imbalance and/or uremia.
Goals/Outcomes: Within 48 to 72 hours of onset, the patient
verbalizes orientation to time, place, and person and maintains his
or her normal mobility.
Neurologic Status.
Neurologic monitoring
1376
• Hypermagnesemia: drowsiness, lethargy, sensation
of heat.
9. Use splints and braces to aid in mobility for patients with severe
neuropathic effects.
1377
Counseling; Pressure Management; Pressure Ulcer Prevention; and
Teaching: Individual.
Constipation
related to fluid and electrolyte imbalance and reduced activity level.
Goals/Outcomes: Within 48 hours of onset, the patient has bowel
movements of soft consistency.
Bowel Elimination.
Constipation/impaction management
1378
Pruritus management
3. Ensure that the patient’s fingernails are cut short and that the nail
tips are smooth.
1379
Additional nursing diagnoses
For patients undergoing dialytic therapy (conventional
hemodialysis), see nursing diagnoses and interventions in
Continuous Renal Replacement Therapies, as follows.
2. Acid-base balance.
1380
4. Uremic intoxication.
• Neurologic (encephalopathy).
• Cardiovascular (pericarditis).
5. Need for removal of dialyzable substances (metabolites, drugs,
toxins).
1381
4. ARF/AKI in the presence of sepsis or systemic inflammatory
response syndrome.
Pathophysiology
Historically, CRRT has evolved from an arteriovenous to a
venovenous extracorporeal process to achieve solute and fluid
removal in the patient who is critically ill. For this reason,
arteriovenous therapy will not be included in this chapter. Venous
access has proven to be safer, and the evolving technology has
improved the efficacy of treatment. CRRT has been traditionally
limited to the intensive care unit setting based on the requirement
for close hourly monitoring and fluid adjustments. The multiple
acronyms and description of therapies are available in Table 6-7.
Table 6-7
COMPARISON OF MODES OF CONTINUOUS RENAL
REPLACEMENT THERAPY
SCUF Slow continuous ultrafiltration: Indicated primarily to remove fluids. A filter with a
large surface area, high sieving coefficient, and low resistance facilitates continuous
fluid removal and minimal solute removal.
CVVH Continuous venovenous hemofiltration: Ultrafiltration is used to remove fluid.
Convective clearance is used to remove solutes. Replacement solution is infused via
prefilter, postfilter, or both prefilter and postfilter to create a solute drag effect (a
large volume of fluid is infused into the patient’s bloodstream, which facilitates
solutes to be returned or “dragged” to the filter. CVVH does not use dialysate
solution.
CVVHD Continuous venovenous hemodialysis: Ultrafiltration is used to remove fluid.
Diffusive clearance is used to remove solutes. Dialysate solution is infused into the
filter countercurrent to the blood flow. Solutes diffuse from the blood (high solute
concentration) to the dialysate solution (low solute concentration). Replacement
solution is not used.
CVVHDF Continuous venovenous hemodiafiltration: Ultrafiltration is used to remove fluid.
Both convective and diffusive clearance is used to remove solute so that both
replacement and dialysis fluids are used.
SLED Sustained low-efficiency dialysis: Hybrid form of continuous renal replacement
therapy using a reduced blood flow and rate of dialysate infusion to remove both
solute through diffusive clearance and fluid by ultrafiltration. Therapy is usually
sustained 4 to 12 hours per day.
1382
and may not be tolerated in unstable patients.
1383
consistent therapy as a result of machine problems, such as clotting
of the filter. Frequent machine alarms indicate that therapy has
ceased or will cease shortly, which undermines the efficacy of
CRRT. Continuous replacement requires a fully operational system
that provides uninterrupted therapy. If the system is frequently
alarming, diffusion, ultrafiltration, and convection are interrupted
with the sounding of each alarm.
Assessment: Pre-CRRT
Goal of assessment
Evaluate fluid, electrolyte, and acid-base balances to prevent the
development of metabolic complications attributable to AKI.
Vital signs
• BP may be elevated in states of fluid volume excess or decreased
in states of fluid volume deficit.
1384
• Weight may be increased or decreased based on fluid volume
status.
• Pulse oximetry.
Observation
• Peripheral edema and periorbital edema.
• Dyspnea.
• Kussmaul respirations.
• Pallor.
• Purpura.
• Weakness.
• Neuromuscular dysfunction.
• Asterixis.
Palpation
1385
• Edema (scale 0 to 4+): extremities and sacrum.
• Muscle tenderness.
• Flank tenderness.
Auscultation
• S3 and S4 gallops indicative of heart failure.
• Tachycardia or dysrhythmias.
• Crackles.
Uremic manifestations
• Accumulation of urea, creatinine, and uric acid.
• Increased BP.
• Pulmonary edema.
• Behavioral changes.
1386
• Decreased wound-healing ability.
Screening labwork
Blood and urine tests will determine the level of renal dysfunction
and can provide clues to the cause of ARF/AKI.
1387
Coagulation Assesses for the presence of bleeding or Decreased PT, aPTT with low
profile: clotting and disseminated intravascular INR promotes clotting.
Prothrombin coagulation (DIC). Elevation promotes bleeding.
time (PT) with
international
normalized
ratio (INR)
Activated partial
thromboplastin
time (aPTT)
Blood urea Assesses for the severity of renal Elevation indicates renal
nitrogen dysfunction. dysfunction.
(BUN) Creatinine may be markedly
Creatinine elevated in the presence of
Estimated massive skeletal muscle injury
glomerular (e.g., multiple trauma, crush
filtration rate injuries).
(eGFR) BUN is influenced by hydration,
catabolism, gastrointestinal
bleeding, infection, fever, and
corticosteroid therapy.
The eGFR in ARF/AKI is usually
less than 50 mL/min.
Electrolytes: Assesses for abnormalities associated Increase or decrease in K+ may
Potassium (K+) with ARF/AKI. cause dysrhythmias. Elevated
Sodium (Na+) Na+ may indicate dehydration.
Calcium (Ca2+) Decreased Na+ may indicate
Magnesium fluid retention.
(Mg2+) Low Mg2+ or Ca2+ may cause
dysrhythmias.
Arterial blood Assesses for the presence of metabolic Low Paco2 and plasma pH values
gases acidosis. reflect metabolic acidosis.
Urinalysis Assesses for the presence of sediment. Presence of sediment containing
tubular epithelial cells, cellular
debris, and tubular casts
supports diagnosis of
ARF/AKI.
Increased protein and many RBC
casts are common in intrarenal
disease.
Sediment is normal in prerenal
causes.
Large amounts of myoglobin
may be present in severe
skeletal muscle injury or
rhabdomyolysis.
Urinary sodium Differentiates prerenal from intrarenal Urinary Na+ <20 mEq/L indicates
etiology. prerenal etiology.
Urinary Na+ >20 mEq/L indicates
intrarenal etiology.
1388
options available on existing equipment are part of the
considerations used to determine the modality of CRRT used.
Treatment goals for removal of water and potentially toxic solutes
are considered. Therapeutic options may target removal of water
plus solutes, water only, or solutes only to be removed. All
modalities use a highly permeable, hollow-fiber filter. The type of
filter used is a crucial element contributing to efficacy of treatment
when removing solutes, coupled with the functionality of the
venous access device. Dysfunctional vascular access can undermine
the best of technology and filters, given that the blood flow through
the extracorporeal system must be adequate to achieve treatment
goals. Solutes removed are generally unbound substances,
including urea, calcium, sodium, potassium, chloride, vitamins, and
unbound drugs with a molecular weight between 500 and 10,000
Da. Types/modalities of CRRT include:
Table 6-8
INDICATIONS, ADVANTAGES, AND
DISADVANTAGES/COMPLICATIONS OF MODES OF CONTINUOUS
RENAL REPLACEMENT THERAPY
1389
CVVH, Continuous venovenous hemofiltration; CVVHD, continuous venovenous
hemodialysis; CVVHDF, continuous venovenous hemodiafiltration; SCUF, slow
continuous ultrafiltration.
Table 6-9
TROUBLESHOOTING MAJOR PROBLEMS IN CONTINUOUS
RENAL REPLACEMENT THERAPY
1390
Principles applied to specific therapies
Ultrafiltration: For ultrafiltration to occur, there must be a pressure
gradient across the filter compartments; the pressure in the blood
compartment must exceed the pressure in the filtrate compartment.
This pressure gradient is called transmembrane pressure (TMP). Its
major determinants are hydrostatic pressure and oncotic pressure.
The rate of ultrafiltration depends on the type of filter, the
hydrostatic pressure of the blood, and blood flow. The hydrostatic
pressure forces small and middle size molecules such as creatinine,
urea, glucose, and cytokines from the blood across the filter. The
longer it takes for blood to exit the filter, the longer the blood is in
contact with the porous filter surface, the dialysate (if used), and the
filtration pressure. Longer exposure increases the likelihood that
the molecules of solute will be filtered from the patient’s blood.
Hydrostatic pressure from the dialysis system is opposed by
oncotic pressure, which is maintained by plasma proteins that do
not pass through the filter because of their larger size. When
hydrostatic pressure exceeds oncotic pressure, filtration of water
and solutes occurs.
Ultrafiltration Prescription: To achieve optimal fluid
management, the right amount of ultrafiltration must be prescribed
and delivered. The net ultrafiltrate (fluid loss) is the difference
between the amount of urine output and plasma water removed
and the amount of fluid administered to the patient. Fluid balance
is normally calculated hourly and is adjusted in response to
hemodynamic changes.
Calculation of the ultrafiltration prescription can be found in Box
6-2.
1391
membrane. The SC is equal to the ultrafiltrate concentration of
the drug divided by the plasma concentration. Drugs that are
more protein-bound have a lower clearance during CRRT.
However, as a result of the long duration of CRRT, more of these
drugs may be removed.
Box 6-2
ULTRAFILTRATION PRESCRIPTION
Example 1: Calculate ultrafiltrate based on anticipated
fluid balance
• Anticipated fluid intake is 4 L/24 h
Procedure
The filter and lines are primed with normal saline to remove all air
bubbles before the treatment is initiated. A large, double-lumen
1392
catheter is placed in the internal jugular, subclavian, or femoral
vein. The catheter must have radiographic confirmation of
placement before beginning therapy. Although the system is driven
by venous access, dialysis terminology states that blood flows from
the patient into the “arterial” or proximal port of the vascular access
through the filter and returns to the patient through the “venous”
or distal port of the access. If the “arterial” or proximal lumen of the
catheter becomes occluded by being pulled up against the vessel
wall, the proximal and distal lumens may be interchanged so that
the blood is being removed from the patient via the “venous” or
distal lumen of the catheter and returned via the “arterial” or
proximal lumen. This phenomenon is sometimes signaled by the
presence of increased air in the system, or low-flow alarms, which
indicate that lower blood volume is being filtered.
For most patients, a continuous method of anticoagulation is
necessary to prevent clotting in the lines and filter, heparin or
citrate is most commonly used. A pump is used to drive the blood
flow. While the blood flows through the filter, water, electrolytes,
and most drugs not bound to plasma protein diffuse across the
filter and thus become part of the filtrate, referred to as effluent.
If the objective is the removal of large amounts of fluid and solute
(e.g., urea, potassium, creatinine) through convective clearance, it is
necessary to infuse large volumes of replacement fluid to maintain
fluid and electrolyte balance. Nursing responsibilities include
initiating treatment, monitoring the patient and the system, and
discontinuing treatment. Tables 6-9 and 6-10 list the advantages,
disadvantages, and complications of the various therapeutic CRRT
modes. Table 6-9 evaluates troubleshooting major problems with
CRRT.
Table 6-10
APPROACHES TO CONTINUOUS RENAL REPLACEMENT
THERAPY FILTRATION FLUID REPLACEMENT
1393
Used to enhance urea clearance to ≥18%; decreases oncotic Used to maintain fluid and
pressure, increasing net TMP; moves urea from erythrocytes electrolyte balance
into plasma
Increases net fluid removal Less replacement fluid
required
Potentially increases filter life Simplified clearance
determination
*Urea clearance 12.5 mL/min Urea clearance 10.6 mL/min
*
If increased urea clearance is desired, predilution mode of fluid replacement is used.
BUN, Blood urea nitrogen; Hct, hematocrit; TMP, transmembrane pressure.
Anticoagulation
Patients who are critically ill may have an increased tendency for
coagulation and/or bleeding. All CRRT modalities require the
patient’s blood to be in contact with artificial tubing and
membranes, which stimulates the coagulation cascade. The
complement cascade may also be stimulated if a biocompatible
filter is not used. The goal of anticoagulation is to prevent clotting
in the CRRT circuit, preserve filter performance, and optimize
survival of the circuit. Care providers strive to achieve a balance
between preventing blood loss within the circuit as a result of
clotting and preventing excessive anticoagulation leading to
bleeding. Clotted blood remaining in the circuit is “lost” from the
patient. The patient who is critically ill is at increased risk for
bleeding as a result of coagulopathy and endothelial disruption.
AKI/ARF may be associated with a procoagulant state because of
downregulation of natural anticoagulants and inhibition of
fibrinolysis. If AKI has evolved slowly resulting from an underlying
disease, platelets may also be dysfunctional.
Patient factors
1394
• Decrease in natural anticoagulants.
• Transfusions.
• Fibrinolysis inhibition.
• Kinking or malposition.
Treatment variations
Heparin
Heparin is the most common and least expensive of the choices. It
can be administered either systemically or regionally.
1395
CRRT device. In addition to the complication of bleeding,
heparin-induced thrombocytopenia can occur. Potential for
thrombocytopenia has limited the use of systemic heparin in
recent years.
Citrate
Citrate is a common alternative to heparin for regional
1396
anticoagulation. Citrate is infused into the arterial line to chelate or
bind with calcium and magnesium, thus inhibiting the coagulation
cascade in the extracorporeal circulation. The deficit in ionized
calcium is present only outside the body in the extracorporeal
circuit, because before reinfusion of the filtered blood, calcium is
substituted into the venous line to target normal ionized calcium.
The goal is to maintain ionized calcium less than 0.35 mmol/L in the
extracorporeal circuit to prevent clotting within the filter. It is
important to infuse calcium systemically to maintain normal levels
of ionized calcium in the patient’s circulation. If dialysate and
predilution replacement fluids are used, they should be calcium-
free to prevent reversal of the citrate effect in the circuit. The
amount of citrate infused into the preblood pump is determined by
systemic ionized calcium levels, which are sampled every 6 hours.
During regional citrate anticoagulation, a minimum amount of
citrate enters the systemic circulation; however, a systemic calcium
infusion is used to assure that normal levels of ionized calcium are
maintained in the patient’s circulation.
Monitoring all laboratory values, including ionized calcium,
sodium, and acid-base balance, is essential.
Replacement fluid
1397
Electrolyte imbalances that may occur with CRRT include
hypokalemia, hypocalcemia, hypophosphatemia, and
hypoglycemia. Free water can be depleted. Use of large amounts of
normal saline replacement fluid can prompt hyperchloremic
acidosis. The replacement fluid may be infused prefilter or
postfilter and is tailored to the specific needs of individual patients.
Three types of solutions are available: citrate-based, lactate-based,
and bicarbonate-based. Lactate solutions can prompt the
development of acidosis, and are not used in patients with liver
abnormalities or in patients with lactic acidosis. Citrate is generally
not used in patients with liver dysfunction.
• Nutritional state.
• Neurologic status.
Vital signs
• BP may increase or decrease based on fluid volume status.
1398
• A change in baseline temperature in the presence of sepsis.
• Urine output and other fluid losses (blood loss drainage fluid).
Observation
• Filter pressures.
• Balance pressures.
• Effluent pressures.
• Transmembrane pressure.
1399
• Ultrafiltration rate.
• Filter patency.
• Anticoagulation.
• Catheter patency.
• Access pressure.
• Return pressure.
Palpation
• Pulse quality and regularity bilaterally (scale 0 to 4+).
Auscultation
• Heart sounds to evaluate for contributors to decreased cardiac
output.
Screening labwork
1400
• Electrolytes, BUN, and creatinine to determine renal function and
effectiveness of CRRT.
Collaborative management
Goals for patients undergoing CRRT: The goal is the removal of
excess fluid and solutes, while maintaining electrolyte balance and
adequate fluid intake for homeostasis. In the adult patient who is
critically ill, catabolic rate is two to three times that of normal.
Key Considerations Goals
Enteral nutrition Maintain nutritional requirements
Predilution fluid Used if increased solute removal is required
replacement
Replacement fluid Used for convective clearance and to maintain fluid and electrolyte
balance
Anticoagulation Used to prevent clotting in the circuit
Vasopressors Used to maintain adequate blood pressure
Vascular access Double-lumen catheter, preferably in the subclavian or internal
jugular vein
Care priorities
Prevention of hemodynamic instability and maintenance of
homeostasis are the goals of CRRT. This includes fluid removal and
electrolyte replacement. Continuous monitoring and frequent
prescription changes based on patient condition and needs are
required to meet the goal of therapy. Fluid removal, electrolyte
balance, and maintaining nutrition in these catabolic patients who
are critically ill present a major care challenge for the treatment
team.
1401
hypervolemia or hypovolemia. Determine electrolyte balance with
particular attention to sodium, potassium, and calcium. Determine
the state of catabolism based on BUN and creatinine levels, along
with the presence of metabolic acidosis.
3. Replacement fluids
Use physiologic solutions (more chemically similar to normal body
chemistry) to replace the majority of the filtrate removed hourly,
maintain volume stability, and replace electrolyte losses. The use of
plain normal saline may not be appropriate for patients with high-
volume replacement fluid, because electrolyte imbalances or
hyperchloremic acidosis may ensue. Determine hourly fluid
balance to maintain hemodynamic stability. Frequent changes in
the CRRT prescription (orders) may be necessary based on intake
changes. If the patient is receiving citrate-based anticoagulation,
systemic calcium must be measured by ionized calcium levels, and
replaced by a calcium infusion to prevent hypocalcemia.
1402
there is evidence of clotting. If using regional anticoagulation of the
circuit, adjust the rate of the anticoagulant infusion as necessary to
maintain blood flow within the circuit without causing systemic
anticoagulation of the patient.
Hemodynamic regulation
1403
T waves and ST segments, associated with intravascular fluid
volume or electrolyte changes.
Fluid monitoring
2. Weigh the patient daily. Be alert to a daily loss of greater than 2.5
kg.
1404
diarrhea, fever, and wound drainage.
Fluid/electrolyte management
1405
BP elevated greater than 20 mm Hg over baseline, tachycardia,
jugular venous distention, basilar crackles, increasing edema
(peripheral, sacral, periorbital), and tachypnea.
Deficient knowledge
related to CRRT procedure/treatment
Goals/Outcomes: The patient or significant other verbalizes
accurate information about the CRRT procedure within 24 to 48
hours of instruction.
Knowledge: Treatment/Procedure.
Teaching: Procedure/treatment
4. Discuss that vital signs will be assessed and blood tests will be
performed at frequent intervals to monitor for stability throughout
therapy. Reinforce that staff members are close at all times to
provide support and additional information as needed.
1406
5. Explain that the use of CRRT may require 24 hours or longer to
attain fluid balance.
Positioning
2. Explain to patient the need for care and assistance when moving.
1407
extremities. Encourage isometric, isotonic, and quadriceps setting
exercises on uninvolved extremities.
Fluid monitoring
4. If the test result is positive for blood, clamp the ultrafiltrate port
and consult the advanced practice provider for further
interventions.
1408
Additional nursing diagnoses
For more information about fluid and electrolytes, see sections on
Fluid and Electrolyte Disturbances, and Prolonged Immobility,
Chapter 1.
Selected references
1. ACT Investigators. Acetylcysteine for prevention of renal
outcomes in patients undergoing coronary and peripheral
vascular angiography: main results from the randomized
Acetylcysteine for Contrast-induced nephropathy Trial
(ACT). Circulation. 2011;124:1250-1259.
2. Adedotun A, Perazella M. Recurrent acute kidney injury
following bath salts intoxication. Am J Kidney Dis.
2012;59:273-275.
3. American Nephrology Nurses Association: Core curriculum for
nephrology nursing. Pitman: Anthony J. Jannetti. 2008.
4. Bagshaw SM, Berthiaume LR, Delaney A, Bellomo R.
Continuous versus intermittent renal replacement therapy
for acute kidney injury: a meta-analysis. Crit Care Med.
2008;35:610-617.
5. Balemans C, Reichert L, vanSchelven B. Epidemiology of
contrast material-induced nephropathy in the era of
hydration. Radiology. 2012;263:706-713.
6. Banks DS. Prescribing continuous renal replacement
therapy using a JavaScript calculator improves delivered
dose. JICS. 2011;12:289-292.
7. Bellomo R, Lipesey M, Calzavacca P. Early acid-base and
blood pressure effects of continuous renal replacement
therapy intensity in patients with metabolic acidosis.
Intensive Care Med. 2013;39:429-436.
8. Boling B. Renal issues in older adults in critical care. Crit
Care Nurs Clin North Am. 2014;26:99-104.
9. Bouchard J, Mehta RL. Acid-base disturbances in the
intensive care unit: current issues and the use of renal
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1409
10. Bouchard J, Mehta RL. Volume management in continuous
renal replacement therapy. Semin Dial. 2009;22:146-150.
11. Bucaloiu I, Perkins R, DiFilippo W. Acute kidney injury in
the critically ill, morbidly obese patient: diagnostic and
therapeutic challenges in a unique population. Crit Care
Clin. 2010;26:607-624.
12. Cerda J, Lameire N, Eggers P. Epidemiology of acute
kidney injury. Clin J Am Soc Nephrol. 2008;3:881-886.
13. Chrysochoou G, Marcus RJ, Sureshkumar KK. Renal
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14. Cruz DN, Goh CY, Marenzi G. Renal replacement therapies
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15. Davenport M, Khlaltbari S, Dillman J. Contrast material-
induced nephrotoxicity and intravenous low-osmolality
iodinated contrast material. Radiology. 2013;267:94-105.
16. Dennen P, Douglas I, Anderson R. Acute kidney injury in
the intensive care unit: an update and primer for the
intensivist. Crit Care Med. 2010;38:261-275.
17. Erdbruegger U, Okusa M. Palevsky PM UptoDate
http://www.uptodate.com/contents/investigational-
biomarkers-and-the-evaluation-of-acute-tubular-
necrosis/abstact/54 (Updated January 31, 2014)
Investigational biomarkers and the evaluation of acute tubular
necrosis. Waltham: Wolters Kluwer. 2014.
18. Fiaccadori E, Regolisti G, Maggiore U. Specialized
nutritional support interventions in critically ill patients on
renal replacement therapy. Curr Opin Clin Nutr Metab Care.
2013;16:217-224.
19. Filiponi TC, de Souza Durao M. How to choose the ideal
renal replacement therapy in sepsis. Shock. 2013;39:50-53.
20. Getting J, Gregoire J, Phul A, Kasten M. Oxalate
nephropathy due to “juicing”; case report and review. Am J
Med. 2013;126:768-772.
21. Ghossein C, Grouper S, Soong W. Renal replacement
therapy in the intensive care unit. Int Anesthesiol Clin.
2009;47:15-34.
1410
22. Himmelfarb J, Joannidis M, Molitoris B. Evaluation and
initial management of acute kidney injury. Clin J Am Soc
Nephrol. 2008;3:962-967.
23. Honiden S. http://69.36.35.38/accp/pccsu/caring-critically-
ill-obese-patient?page=0,3 Caring for the critically ill, obese
patient. Northbrook: American College of Chest Physicians.
2011.
24. Honore PM, Jacobs R, Joannes-Boyau O. Newly designed
CRRT membranes for sepsis and SIRS – a pragmatic
approach for bedside intensivists summarizing the more
recent advances: a systematic structured review. ASAIO J.
2013;59:99-106.
25. Hoste E, Schurgers M. Epidemiology of acute kidney
injury: how big is the problem. Crit Care Med. 2008;36(Suppl
4):S146-S151.
26. Kidney Disease/Improving Global Outcomes (KDIGO)
Acute Kidney Injury Work Group: KDIGO clinical practice
guidelines for acute kidney injury. Kidney Int Suppl.
2012;2:1-138.
27. Kinsey G, Okusa M. Pathogenesis of acute kidney injury:
foundation for clinical practice. Am J Kidney Dis.
2011;58:291-301.
28. Lameire N, Bagga A, Cruz D. Acute kidney injury: an
increasing global concern. Lancet. 2013;382:170-179.
29. Legrand M, Darmon M, Joannidis M, Payen D.
Management of renal replacement therapy in ICU patients:
an international survey. Intensive Care Med. 2013;39:101-108.
30. Luber S, Fischer D, Venkat A.
http://www.medscape.com/viewarticle/572923 Accessed on
Feb. 20, 2014 Care of the bariatric surgery patient in the
emergency department, Medscape. New York: WebMD. 2008.
31. Lyndon WD, Wille KM, Tolwani AJ. Solute clearance in
CRRT: prescribed dose versus actual delivered dose.
Nephrol Dial Transplant. 2012;27:952-956.
32. Mayrtenson J, Martling C, Bell M. Novel biomarkers of
acute kidney injury and failure: clinical applicability. Br J
Anaesth. 2012;109:843-850.
33. McDonald J, McDonald R, Comin J. Frequency of acute
1411
kidney injury following contrast medium administration: a
systematic review and meta-analysis. Radiology.
2013;267:119-128.
34. Oh JH, Shin DH, Lee MJ. Urine output is associated with
prognosis in patients with acute kidney injury requiring
continuous renal replacement therapy. J Crit Care.
2013;28:379-388.
35. Palevsky P. Curhan GC UptoDate
http://www.uptodate.com/contents/definition-of-acute-
kidney-injury-acute-renal-failure Definition of acute kidney
injury (acute renal failure). Waltham: Wolters Kluwer. 2008.
36. Pannu N, Klarenbach S, Wiebe N. Renal replacement
therapy in patients with acute renal failure: a systematic
review. JAMA. 2008;299:793-805.
37. Pieracci F, Barie P, Pomp A.
http://www.medscape.com/viewarticle/533570 Critical care
of the bariatric patient. In Medscape. New York: WebMD.
2006.
38. Ricci Z, Ronco C. Timing, dose and mode of dialysis in
acute kidney injury. Curr Opin Crit Care. 2011;17:556-561.
39. Rosner M. Acute kidney injury in the elderly. Clin Geriatr
Med. 2013;29:565-578.
40. Schefold JC, Haehling SV, Pschowski R. The effect of
continuous versus intermittent renal replacement therapy
on outcome of critically ill patients with acute renal failure
(CONVINT): a prospective randomized controlled trial. Crit
Care. 2014;18:R11.
41. Scoville BA, Mueller BA. Medication dosing in critically ill
patients with acute kidney injury treated with renal
replacement therapy. Am J Kidney Dis. 2013;61:490-500.
42. Sharfuddin A, Weisbord S, Palevsky P, Molitoris B. Taal M
Chertow G Marsden P Brenner & Rector’s the kidney ed 9
Acute kidney injury. Philadelphia: Saunders. 2011;1044-1099.
43. Shashaty M, Meyer N, Localio A. African race, obesity and
blood product transfusion are risk factors for acute kidney
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1412
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acute respiratory distress syndrome. Crit Care Med.
2012;40:2601-2608.
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injury. N Engl J Med. 2008;359:7-20.
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Care Med. 2008;36(Suppl 4):S166-S171.
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1413
CHAPTER 7
Neurologic disorders
General neurologic assessment
Level of consciousness
• Assess for orientation, drowsiness, inappropriate use of words,
slurred speech, arousability, confusion, and amnesia.
1414
benzodiazepines, when the drugs are weaned. Underlying mood
changes and memory loss may be present, because these
conditions are associated with obesity.
Vital signs
Refer to specific sections for key vital sign changes specific for the
type of neurologic disorder.
• All functions are evaluated bilaterally (e.g., both eyes, both sides
of face, etc.).
• Ask the patient to walk heel to toe to check for balance and
1415
coordination.
• Perform Romberg test: Ask the patient to close eyes and stand
with feet close together while you stand nearby in case the
patient sways/falls (abnormal response indicative of cerebellar
dysfunction).
• Ask the patient to squeeze your hands and push feet against your
hands, to assess if strength is equal on both sides.
• Flaccidity.
1416
Motor deficits (weakness or paralysis) are caused by injury or
edema to the primary motor cortex and corticospinal (pyramidal)
tracts.
1417
reasons for limited mobility, in addition to reduced level of
endurance. Posture analysis is done to help classify the body
type, which helps to anticipate risk factors. Functional ability,
mobility, and disabilities should be noted, including simple
findings such as the ability to transfer from bed to chair.
Sensory assessment
Sensory deficits occur when the primary sensory cortex, the sensory
association areas of the parietal lobe, or the spinothalamic tracts are
injured or edematous. Sensory deficits include inability to
distinguish objects according to characteristics (e.g., size, shape,
weight) and inability to distinguish overall changes in temperature,
touch, pressure, and position.
• Test vibratory sense (with vibrating tuning fork) distally (on the
tip of big toe or finger) and ask when the patient feels the
vibration stop.
• For position sense, move distal joints about using very light touch
and ask about the position the patient perceives of the joint.
1418
Improvement in both motor and sensory perception may be seen
while cerebral edema subsides.
Fundoscopic assessment
Generally done by the advanced practice provider and may
reveal retinal hemorrhage(s) at the side of the optic disc.
Hemorrhage is caused by blood from the subarachnoid space (SAS)
being forced along the optic nerve sheath under high pressure. The
patient may complain of blurred vision or blind spots (scotomata).
Terson hemorrhage associated with vitreous and/or subhyaloid
hemorrhage has been seen as a subarachnoid complication and its
presence has been noted with increased mortality and morbidity
rates.
Dysphagia screening
Should be performed early, particularly when stroke has
occurred, to prevent complications of aspiration and to initiate
appropriate nutrition therapy. People with neurologic dysfunction
are poor judges of their own ability to swallow, thus a thorough
evaluation and intervention by a speech pathologist may be
required, following routine screening procedures recommended by
institutional protocol.
1419
progress. Can visualize facial skeleton and
Assesses details of structures soft tissue structures for
of bone, tissue, and fluid- abnormalities (e.g., tumors, brain
filled space. injury).
Detects exudate, abscesses, Within the first few hours after an
and intracranial pathology acute ischemic stroke, the scan
(e.g., tumors, brain injury). may appear normal. Intracranial
Assesses for hydrocephalus. hemorrhage is easily diagnosed
on CT—blood appears as a bright
white signal.
Continuous Evaluates cardiovascular Phenytoin and other antiepileptic
electrocardiographic status, especially during drugs can cause dysrhythmias and
monitoring medication administration. hypotension.
CT angiography Less invasive than cerebral Visualizes intraarterial clot, small
angiography; involves use of intracranial aneurysm, and AVM.
contrast media injection into
peripheral vein and use of CT
scanner.
CT perfusion or CT- Provides information related Compromised blood flow; a limited
xenon scan to cerebral blood flow (CBF) test; cannot detect infarcted tissue.
and volume.
Used to guide clinical
decision-making regarding
the use of thrombolysis or
interventional procedures.
Electroencephalography Evaluates electrical activity of Diagnosis of seizures and
the brain for ongoing seizures, localization of structural
even if there are no clinical abnormalities.
signs of seizures. Also used as element of criteria for
brain death.
Electromyography Assesses NCV deficit as a result EMG and NCV demonstrate
(EMG) or nerve of the demyelination of profound slowing of motor
conduction velocity peripheral nerves. conduction velocities and
(NCV) conduction blocks several weeks
into the illness.
Lumbar puncture (LP) Measures CSF pressures and Elevated protein, low glucose,
with cerebrospinal fluid obtains CSF specimen when elevated white blood cell count.
(CSF) specimen for infection, such as meningitis
analysis or neurosyphilis, is
suspected.
May be performed when
subarachnoid hemorrhage is
suspected and CT is normal.
Magnetic resonance Minute oscillations of Infarcts, areas at risk or ischemic
imaging (MRI) and hydrogen atoms in the brain areas, vascular defects, stenosis,
arteriography (MRA) of create graphic image of bone, occlusion.
brain fluid, and soft tissue.
Provides a more detailed
image.
MRI is most useful for patients
with ischemia in identifying
the cause and area involved.
Provides detailed information
regarding the area of injury
or its vascular supply
(magnetic resonance
arteriogram or MRA).
1420
Diffusion-weighted imaging is
a measurement of edema,
whereas perfusion-weighted
imaging is a measurement of
global CBF.
Positron emission To evaluate brain metabolism Demonstrates abnormal function of
tomography (PET) and and blood flow using three- the brain by revealing abnormal
single-photon emission dimensional imaging produced structures, metabolism, and
computed tomography using a radioactive tracer. perfusion.
Locates areas of brain causing
seizures, head injury, and some
disorders (e.g., Alzheimer
disease).
Radioisotope brain scan Examines areas of blood flow Increased or decreased blood flow
through concentration of intraoperatively or assesses for
isotope uptake in the brain. postoperative cerebral infarction.
Lack of uptake may indicate
cerebral brain death.
Transcranial Doppler Noninvasive and can be done Arterial narrowing, vasospasm,
serially at the bedside. cerebral circulatory arrest, emboli
Evaluates the intracranial as a result of vasospasm.
vessels and assesses the Can also be used to confirm absent
velocity of blood flow in the blood flow in brain death.
anterior and posterior
cerebral circulation.
Also used to evaluate
vasospasm, to determine
brain death via detection of
cerebral circulatory arrest,
for intraoperative
monitoring, and to locate
emboli.
Brain death
Pathophysiology
Brain death is defined as irreversible loss of function of the brain,
including the brainstem and respiratory centers. Cardiac death is
the cessation of mechanical action/pumping of the heart, resulting
in absence of pulse, heart sounds, blood pressure (BP), and
respirations. Brain death is most frequently the result of increased
intracranial pressure (ICP) caused by severe traumatic head injury
or hemorrhagic stroke caused by ruptured cerebral aneurysm with
subarachnoid hemorrhage (SAH) or intracranial hemorrhage (ICH).
A significant number of patients with large acute ischemic strokes
(AIS) experience cerebral edema and herniation. Hypoxic-ischemic
1421
encephalopathy with massive brain swelling after prolonged
cardiopulmonary resuscitation or asphyxia and encephalopathy
with cerebral edema resulting from fulminant hepatic failure may
also result in increased ICP, herniation, and brain death.
If brain death occurs quickly, cardiac death may occur
immediately. If brain death occurs more slowly, with time to
initiate mechanical ventilation before cardiac death, the heart can
continue to beat/pump because the cardiac pacing cells operate
independently from brain regulation. Mechanical ventilation
provides the oxygen necessary to maintain viable cardiac pacing
cells and conduction pathways if the patient is circulating adequate
amounts of blood cells carrying oxyhemoglobin, acidosis is
controlled, and electrolytes are managed. Over time, without a
functional hypothalamus and pituitary gland, patients experience
further instability of BP caused by loss of regulation of the thyroid
and adrenal glands. Massive diuresis is common when the
posterior pituitary gland ceases to function.
If the patient is an organ donor, the organs must be sustained
before removal, requiring management of all sequelae of brain
death. Guidelines for managing brain dead organ donors have
common elements internationally, with most controversy stemming
from the need to provide additional hormones to help control
endocrine-related crises associated with loss of function of the
pituitary and hypothalamus and use of prophylactic antibiotics to
prevent infection.
The President’s Commission report regarding “guidelines for the
determination of death” drafted a proposal for a legal definition of
death resulting in the Uniform Determination of Death Act
(UDDA). The document states: “An individual who has sustained
either (1) irreversible cessation of circulatory and respiratory
functions, or (2) irreversible cessation of all functions of the entire
brain, including the brainstem, is dead. A determination of death
must be made with accepted medical standards.” In the United
States, the majority of state laws reflect the UDDA. Amendments
including physician qualifications, confirmation by a second
physician, or religious exemption have also been included by
legislators in several states.
The UDDA does not define “accepted medical standards.” The
1422
American Academy of Neurology (AAN) brain death practice
guidelines were initially written in 1995 to define medical standards
for determination of brain death. The guidelines highlighted that
three key clinical findings must be present to confirm irreversible
cessation of brain functions, including the brainstem: coma (with a
known cause), absence of brainstem reflexes, and apnea. Despite
the AAN guidelines, patients are inconsistently managed in U.S.
hospitals and worldwide. Differences in prerequisites, the number
of required physician assessments, the lowest “living person” core
temperature, and other measurements varied. Medical record
documentation of those diagnosed with brain death consistently
reveals deficiencies in documentation.
In 2010, the AAN incorporated the majority of available evidence
into updated guidelines. Five questions emerged, and were
answered following a thorough review of the literature, to address
variations in brain death determination and to facilitate more
consistency in diagnosis:
1423
determine apnea is safe, but there is insufficient evidence to
determine the comparative safety of techniques used for apnea
testing.
1424
skull. If additional blood or cerebrospinal fluid (CSF), edematous
tissue, or tumor occupies space inside the skull, there is little ability
to expand to “make room” for anything not normally present.
These “mass lesions” or “space-occupying lesions” cause
“crowding” within their cavity, which increases the pressure.
When pressure in one of the two compartments (supratentorial or
infratentorial) is markedly elevated, the brain structures and blood
vessels within the cavity are compressed, resulting in ischemia,
hypoxia, and, if uncontrolled, cerebral anoxia. When blood flow is
minimal to absent, the hypoxic/anoxic brain tissues become more
edematous. Eventually, no space remains for further expansion.
The skull cannot expand and the tentorium expands minimally,
thus the brain is forced through the available openings. The
movement or displacement through an opening causes further
compression of blood vessels, with possible laceration and
destruction, which leads to necrosis of brain tissues and brain death
(see Traumatic Brain Injury, Neurologic Herniation Syndromes,
Chapter 3).
1425
• Prolonged cardiopulmonary resuscitation.
Vital signs
• Mild hypothermia: Core temperature greater than 32° C (90° F),
but less than 36.5° C (97° F).
Observation/inspection/palpation
• Coma: The patient does not respond to verbal stimuli, touch, or
deep pain induced by pressure exerted on nail beds, the
supraorbital area of the skull, or the temporomandibular joint or
rubbing the sternum. The cause of coma is most often determined
by history and physical examination, coupled with
neuroradiologic imaging and laboratory testing. If the patient has
received central nervous system (CNS) depressing medications,
neuromuscular blocking agents, has consumed alcohol, has
1426
severe electrolyte, acid-base, or endocrine disease, diagnosis of
brain death cannot be made until residual effects of the drugs or
other conditions are fully resolved. Core temperature must be
raised and maintained at ≥36° C. Two neurologic examinations
should be done. Any physician is legally allowed to perform the
examination in most U.S. states, but neurologists, neurosurgeons,
and intensivists may have a great level of comfort and expertise
in determining a brain death diagnosis.
1427
Prerequisites for testing include normotension, normothermia,
euvolemia, normal Paco2 level, absence of hypoxia and no
previous history of CO2 retention (chronic obstructive pulmonary
disease, severe obesity). All prerequisite conditions must be
normalized before testing.
Screening labwork
• Toxicology screen: Evaluates for presence of toxic doses of
recreational drugs, medications, or poisons (see Drug Overdose,
Chapter 11).
1428
Collaborative management
ORGAN DONOR MANAGEMENT FOLLOWING BRAIN DEATH
1429
Care priorities
1430
responses.
1431
• Phrases to avoid: artificial life support, will live on in others,
deeply comatose.
1432
Decreased intracranial adaptive capacity
related to increased ICP resulting from imminent brain death. When brain
death is imminent, mechanisms that normally compensate for increases in
ICP are failing. When failed, brain herniation occurs.
Goals/Outcomes: The patient is maximally supported for
reduction of ICP until efforts are proved futile, when brain
herniation ensues, resulting in brain death. Following brain death,
hemodynamic status is supported until decisions are made
regarding organ donation and/or discontinuation of life support.
Tissue Perfusion: Cerebral; Neurologic Status: Consciousness.
1433
response to patient care activities. Minimize activities that result in
further increases in ICP.
Neurologic monitoring
Decisional conflict
related to the uncertainty regarding the proper course of action related to
the discontinuation of life support and possible organ donation following
brain death.
Goals/Outcomes: Family/support system is maximally supported
in making judgments, and choosing between immediate
discontinuation of life support, organ donation, or possibly
continuing life support until information about brain death can be
processed and accepted.
Decision-Making; Information Processing; Dignified Life
Closure; Acceptance: Health Status.
Dying care
1434
capabilities.
Coping enhancement
7. Ensure that the family understands that brain dead patients are
dead. Patients are no longer able to breathe without mechanical
ventilation, will experience cardiac death when removed from
mechanical ventilation, will never regain consciousness, will never
interact with others, and have no ability to experience joy related to
human life.
1435
breathing spontaneously. Families may not be able to comprehend
why when the brain is dead, the heart still functions unless
mechanical ventilation is removed. Guilt may be associated with
removal of mechanical ventilation because the patient appears
“alive” with mechanical ventilation in place.
1436
unruptured aneurysm or those postrupture with a diagnosis of
SAH. Unruptured aneurysms may be asymptomatic, but nearly half
of the affected population experiences some warning sign or
symptom before rupture as a result of expansion of the lesion and
compression of cerebral tissue. When an aneurysm ruptures, a
hemorrhage occurs in the SAS and basal cisterns. If the patient
survives the initial compromise of cerebral circulation from the
force of the arterial hemorrhage resulting in sharply increased ICP,
the next challenges are surviving possible rebleeding and cerebral
arterial vasospasms. The greatest incidence of rebleeding following
SAH is between 3 and 11 days following the rupture, with the peak
at day 7. Mortality is approximately 70% from SAH. Theories
regarding the cause(s) of rebleeding propose a problem with the
normal process of clot dissolution coupled with “spikes” in arterial
pressure.
The major complication postrupture is the occurrence of
delayed cerebral ischemia from cerebral arterial vasospasm. This
occurs as a result of the constriction of the arterial smooth muscle
layer of the major cerebral arteries and causes a dramatic decrease
in cerebral blood flow that leads to cerebral ischemia and
progressive neurologic deficit. Vasospasm occurs in as many as
60% of patients from 4 to 21 days following SAH, with incidence
peaking between 7 and 10 days. The pathogenesis of the
vasospasms is poorly understood, but ongoing research indicates a
direct relationship to the amount of blood in the SAS and basal
cisterns. The greater the volume of blood, the greater is the risk of
vasospasm. While clots in the basal cisterns begin to hemolyze,
substances may be released that prompt vasospasms. A current
prophylactic treatment includes careful fluid balance and “triple H”
(hypervolemia-hemodilution-hypertension) therapy. Recent
evidence has suggested that intravascular volume management
should target euvolemia and avoid prophylactic hypervolemic
therapy. Aggressive administration of fluid aimed at achieving
hypervolemia has been shown to be harmful by several studies.
Other treatments include the use of calcium antagonists to relieve
vasospasms, balloon or chemical angioplasty to normalize the
vessel lumen, and possibly cisternal fibrinolytic drugs to alter the
natural process of clot breakdown for those with a larger cisternal
1437
blood accumulation. The patient with a ruptured cerebral aneurysm
and SAH is also at risk for communicating or obstructive
hydrocephalus, hypothalamic dysfunction, and hyponatremia.
Some patients present with an obstructive hydrocephalus from
intraventricular blood. However, communicating hydrocephalus
develops in approximately 20% of patients with SAH as a result of
the presence of blood in the SAS and ventricular system.
Hydrocephalus may be acute (occurs within less than 24 hours),
subacute (occurs within less than 4 hours to 1 week), or delayed
(beginning 10 or more days after SAH). Blood in the SAS and
ventricles obstructs the flow of CSF, interferes with circulation and
resorption of CSF, and causes increased ICP, with concomitant
worsening of neurologic status. Hydrocephalus sometimes
produces minimal symptoms and resolves without medical
intervention, whereas some patients may require temporary or
permanent diversion of CSF circulation to achieve symptom relief.
Hypothalamic dysfunction, seen in approximately one third of
patients with hydrocephalus after SAH, may result from
mechanical pressure on the hypothalamus from a dilated third
ventricle. The increased pressure causes an increase in the releasing
hormones from the hypothalamus, which activates the
hypothalamic-pituitary axis of the anterior pituitary, as well as
stimulating the production of antidiuretic hormone (ADH) by the
posterior pituitary gland. The response to the increased
adrenocorticotropic hormone from the anterior pituitary gland
mimics an exaggerated stress response, which includes a marked
increase in serum catecholamines leading to overstimulation of the
sympathetic nervous system. The vasoconstrictive response is
severe enough in a subset of patients to cause “stunned
myocardium,” similar to what is seen with an acute myocardial
infarction (MI).
The surge of ADH from the posterior pituitary results in
syndrome of inappropriate antidiuretic hormone (SIADH), which
may include hyponatremia caused by cerebral salt-wasting (CSW)
syndrome, or a combination of factors influencing sodium and
water metabolism (Table 7-1). Recent studies emphasize that the
diagnosis of CSW requires the presence of hypovolemia versus
SIADH, which usually results in euvolemia or moderate
1438
hypovolemia. Patients with an SAH may have CSW and SIADH
occurring simultaneously, manifested by excessive urine output
coupled with excessive free water retention. Fluid management
strategies in this patient population may be difficult (see Syndrome
of Inappropriate Antidiuretic Hormone, p. 734). Hyponatremia
occurs in 30% to 50% of patients with SAH. Untreated
hyponatremia may lead to intracranial hypertension, cerebral
ischemia, seizures, coma, and death.
Table 7-1
CLINICAL PRESENTATION WITH CEREBRAL SALT-WASTING
SYNDROME VERSUS SYNDROME OF INAPPROPRIATE
ANTIDIURETIC HORMONE
1439
decreased intracranial adaptive capacity, risk for seizure activity
with potential impairment of cerebral tissue perfusion, impaired
gas exchange or ineffective airway clearance attributable to altered
LOC, potential need for management of hyperglycemia, and fluid
volume imbalance and potential for aspiration.
1440
symptoms and is used to predict clinical outcomes and for choosing
treatments. Critical care nurses can benefit from using this grading
system. Grading is first determined by the initial symptoms and
LOC upon presentation, and is used as a basis of comparison over
time.
The critical care nurse must carefully review the patient’s history
and diagnostic findings to understand the potential risk for
complications. Patients with unruptured aneurysms are at risk for
rupture, depending on the location and size of the aneurysm.
Unruptured aneurysms may be found during diagnostic testing for
headaches or other neurologic symptoms and may produce
symptoms of cerebral ischemia. A patient with new onset of
oculomotor nerve palsy, visual field loss, or lower cranial nerve
deficits should be evaluated for a potential aneurysm. Patients with
unruptured aneurysms are typically encountered in the critical care
setting after elective aneurysm securement (treatment). The two
main options for aneurysm treatment are craniotomy with
aneurysm neck clipping, wrapping or ligation; and the more
recently developed option of a neurovascular interventionalist
performing endovascular coiling or embolization (“chemical
gluing”). Patients admitted for management of a ruptured cerebral
aneurysm may have additional unruptured aneurysms, which will
be secured at a later date.
The distinguishing characteristic of a ruptured aneurysm is often
a patient who complains of the “worst headache of my life.” This is
1441
usually accompanied by severe nausea and vomiting, nuchal
rigidity, visual disturbances, and photophobia. There is a 2% to 4%
risk for rebleeding within the first 24 hours. “Sentinel” or warning
headaches are associated with an aneurysm that begins leaking
days to weeks before rupturing. Very few patients report having a
sentinel headache before aneurysm rupture.
Rupture results in hemorrhage producing seizures, neurologic
deficits, deterioration in LOC, and a mortality rate of 20% to 50% if
the aneurysm rebleeds. Vasospasms may ensue, which increases the
probability for a negative outcome.
Vital signs
BP, HR, and respiratory rate (RR)/pattern may change
secondary to altered cerebral tissue perfusion. BP control is an
essential strategy to prevent rebleeding of an aneurysm.
Continuous intraarterial monitoring is essential for prompt
detection of subtle changes/trends. Many patients are hypertensive
following hemorrhage. BP and headache may fluctuate in tandem;
higher BP increases the severity of the headache. Treatment
involving intravascular volume expansion can increase BP, and is
generally withheld until after the aneurysm has been surgically
clipped or managed with endovascular coils or chemical
embolization. Conversely, hypotension can decrease cerebral blood
flow and perfusion. Hypertension must be managed with great care
to avoid creating hypotension. Temperature should be monitored
closely to avoid worsening outcomes post-SAH. Fever increases
cerebral metabolic rate, which can worsen cerebral ischemia, with
resultant negative outcomes.
Intracranial pressure
Blood in the SAS can produce acute hydrocephalus within the
first 24 hours, which may result in increased ICP. Subacute, or
chronic, hydrocephalus occurs in approximately 10% to 15% of
patients, usually 10 or more days following the SAH. It is caused by
a clot within the ventricular system that blocks the pathways for the
resorption of CSF leading to ventricular enlargement and nonfocal
neurologic deterioration. Intraventricular extension (distension of
the ventricles) at the time of aneurysm rupture can result in acute
1442
hydrocephalus and requires temporary external ventricular
drainage for management of ICP. Nuchal rigidity may be present.
Indicators of increased ICP are listed in Box 7-1.
Box 7-1
INDICATORS OF INCREASED
INTRACRANIAL PRESSURE*
• Alterations in consciousness: increasing restlessness, confusion,
irritability, disorientation, increasing drowsiness, and lethargy.
• Bradycardia.
• Worsening headache.
• Papillary changes.
• Seizures.
1443
rapidly to permanent brain damage or death. For additional
information about herniation syndromes, see Traumatic Brain
Injury (Chapter 3).
Indicators of hydrocephalus
• Acute: Persistent or sudden onset of coma with loss of
pupillary reflexes within 24 hours of SAH.
Pupillary changes
Depending on location of the aneurysm, visual changes may vary;
assess for visual field loss, oculomotor palsy, diplopia, immobile
eye, retroorbital pain, or hemianopsia.
1444
Motor/sensory assessment
Fluctuating hemiparesis or aphasia with increasing confusion can
be clinical symptoms of vasospasm. Hydrocephalus is generally not
associated with focal neurologic deficits. Anxiety, confusion,
agitation, disorientation, lethargy, stupor, and coma may indicate
hydrocephalus, vasospasm, or early hyponatremia. Anorexia,
nausea, vomiting, abdominal pain, cold and clammy skin,
generalized weakness, and lower extremity muscle cramps are late
signs of untreated hyponatremia. Flushing, diaphoresis, pupillary
dilation, decreased gastric motility, increased serum glucose, fever,
hypertension, tachycardia, cardiac dysrhythmias, ischemia, and
infarction can be attributable to increased circulating
catecholamines.
Fundoscopic assessment
See Chapter 7 “General Neurologic Assessment.”
Screening labwork
• CSF analysis may be performed to confirm the presence of blood
in the CSF in patients with symptoms suggestive of SAH but with
no clear abnormalities detected on the CT scan. The presence of
xanthochromia (yellow-tinged) CSF is caused by the breakdown
of hemoglobin and signals possible hemorrhage. CSF pressure,
normally 0 to 15 mm Hg (75 to 180 mm H2O), may be elevated.
The pressure is proportionate to the amount of bleeding. Protein
may increase to 80 to 130 mg/dL (normal is 15 to 50 mg/dL).
Note: Performance of lumbar puncture in the patient with SAH
and increased ICP carries substantial risk of herniation and
rebleeding; thus, it is not a routine study in this patient
population. In patients with SAH and an external ventricular
drain for the management of hydrocephalus, CSF may be
sampled as part of a workup of infectious causes of sustained
fever.
1445
hypokalemia, hypomagnesemia, and hypophosphatemia, thus
these electrolytes should also be monitored on at least a daily
basis.
Diagnostic testing
Refer to Neurologic Diagnostic Testing, Chapter 7.
Collaborative management
Care priorities
1. Pharmacotherapy
1446
in desired measurements. Maintaining BP at less than 200 mm
Hg has been recommended.
HIGH ALERT!
With the rapid movement of extracellular fluid from brain
tissue to plasma with associated decrease in brain volume,
potential for rebleeding may be increased after giving mannitol.
Mannitol may cause a rebound increase in intracranial pressure 8
to 12 hours after administration, while fluid shifts from cells into
the vascular compartment. Furosemide (Lasix) is often used to
decrease the rebound effect of mannitol.
1447
bleeding. In patients requiring multiple interventions to manage
increased ICP, sustained fever can compromise outcome and
aggressive measures may be required to control the fever.
Clinical trials have been conducted to evaluate conventional
treatment (use of acetaminophen and cooling blankets) compared
with addition of an intravascular catheter–based heat exchange
system for patients with temperatures higher than 38° C and
have shown the effect to decrease fever.
1448
deficits, and affects mortality. Liver function tests and creatine
kinase should be assessed before initiation of statin therapy and
then monitored on a weekly basis during acute management of
aneurysmal SAH. Patients who do not otherwise require statin
therapy will require it only during hospitalization.
1449
• Hemodilution (albumin and crystalloid fluids): Decreases blood
viscosity. CVP greater than 8 mm Hg is usually sufficient to
maintain hypervolemia and dilute the hematocrit to less than
35%.
2. Surgical/endovascular intervention
Initial management involves stabilizing the patient and minimizing
the risk of rerupture of the aneurysm. The National Institute of
Neurological Disorders and Stroke (NINDS), a division of the
National Institutes of Health (NIH), is recognized as the leader in
research on the brain and nervous system in the United States. The
NINDS sponsored the International Study of Unruptured
Intracranial Aneurysms, including more than 4000 patients at 61
sites in the United States, Canada, and Europe. Results revealed
that the risk of rupture for aneurysms less than 7 mm in size is low.
The findings provide a comprehensive evaluation of these vascular
defects, offering guidance to both patients and healthcare
professionals facing the difficult decision about the best treatment
for a cerebral aneurysm.
Advances in imaging, use of microscopes intraoperatively,
dedicated neurologic intensive care units, endovascular treatment
methods, and aggressive cerebral vasospasm prevention and
management have reduced morbidity and mortality. Treatment
options depend on assessment of preoperative risk factors,
predictive indicators, and location and size of the aneurysm.
Successful treatments include endovascular embolization
(“gluing”), surgical clipping, and endovascular detachable coiling.
Recent studies confirm improved patient outcomes when the
1450
ruptured aneurysm is secured within the first 24 to 72 hours for
patients with grade I or II symptoms (Hunt and Hess Scale). Early
intervention may prevent rebleeding, an often fatal complication,
and allows for the management of vasospasm without risk of
rebleeding. Securing of the aneurysm during the time period
associated with the highest risk of development of cerebral arterial
vasospasm has been shown to be associated with increased
morbidity and mortality. If the aneurysm is not secured within 24
to 72 hours of rupture, repair should be delayed until the peak time
for vasospasm (7 to 10 days after SAH) has passed. Patients with
grades III to V symptoms are generally considered poor
interventional risks, especially in the period immediately after
SAH. If these patients are clinically unstable, they may be treated
medically until they improve or stabilize enough for endovascular
or surgical intervention. Surgery is considered for a patient with a
large intracranial clot causing life-threatening, intracranial brain
shifting. Intervention is delayed for a patient with cerebral
vasospasm until the vasospasm subsides.
Although surgical clipping of aneurysms had previously been the
only method of intervention available, neurovascular
interventionalists can now use an alternative to surgery using
Guglielmi detachable coils (GDC coils). The overall size and
location of the aneurysm and the aneurysmal neck size are
evaluated to decide if this option is feasible. GDC coils are
microcoils composed of a soft platinum alloy that are placed with
use of a microcatheter through the femoral artery. The catheter is
advanced into the cerebral circulation using radiographic imaging.
Low-voltage current is applied to the guide wire to detach the
coil(s) placed into the sac of the aneurysm. Placement of one or
more coils fills the sac, reduces the pressure inside, and isolates the
aneurysm from normal circulation. When this is performed for the
management of unruptured aneurysm, the patient’s hospital stay is
very brief (24 to 48 hours) unless the aneurysm ruptures or another
complication of angiography occurs. Endovascular treatment
complications differ from those associated with surgical clipping
and can include arterial dissection, arterial perforation, distal
embolization, and groin hematomas. Aneurysmal recurrence has
been seen in a small number of cases. However, endovascular
1451
methods have become an acceptable alternative to microsurgical
clipping in appropriate cases.
Neurovascular interventionalists can also perform cerebral
angioplasty for arterial vasospasm to decrease vascular narrowing
and reverse ischemia in patients with new-onset vasospasm within
6 to 12 hours of onset. Patient selection for this is limited to those
whose vasospasm involves accessible major cerebral vessels; distal
cerebral arterial vasospasm is not amenable to angioplasty.
3. Management of hydrocephalus
Box 7-2
1452
NURSING INTERVENTIONS AFTER
SHUNT PLACEMENT
• After the shunting, assess the patient for indicators of increased
ICP (see Box 7-1) caused by either the disease itself or shunt
malfunction.
• Position the patient on side opposite the insertion site, either flat
or with head elevated slightly (as prescribed) to prevent pressure
on shunt mechanism.
1453
Care plans for cerebral aneurysm and
subarachnoid hemorrhage
Risk for ineffective cerebral tissue perfusion
related to vasospasm of cerebral vessels and/or decreased intracranial
adaptive capacity related to increased ICP.
Goals/Outcomes: Maintain normal ICP and/or minimize clinical
effects on cerebral adaptability through preventive measures,
aggressive volume management, regulation of cerebral blood flow,
and close hemodynamic monitoring.
Circulation Status.
1454
(e.g., coma or death). Elevated ICP that does not respond to
treatment has been associated with poor patient outcomes.
Ventilation assistance
1455
possible when hyperventilation has been used. Improper use of
hypocapnia may result in more harm than benefit.
Oxygen therapy
Risk identification
1456
control of fluid volumes affecting systemic and cerebral blood flow
and electrolyte levels.
Fluid Balance.
Fluid/electrolyte management
1457
Additional nursing diagnoses
As appropriate, see nursing diagnoses and interventions in
Nutrition Support (Chapter 1), Mechanical Ventilation (Chapter 1),
Alterations in Consciousness (Chapter 1), Prolonged Immobility
(Chapter 1), Emotional and Spiritual Support of the Patient and
Significant Others (Chapter 2), Diabetes Insipidus (Chapter 8), and
Syndrome of Inappropriate Antidiuretic Hormone (Chapter 8).
1458
Goal of system assessment
Evaluate for several key nursing diagnoses requiring emergent
intervention:
• Impaired mobility.
• Pain.
1459
Vital signs
• BP, HR, and RR changes: May further alter cerebral tissue
perfusion. Uncontrolled high BP can lead to intracranial
hemorrhage (ICH); therefore, close monitoring is important to
keep the SBP less than 160 to 200 mm Hg to prevent bleeding.
Hypotension reduces cerebral perfusion and may cause cerebral
ischemia. Monitor rate, rhythm, and depth of respirations for
changes or abnormal breathing patterns.
Observation
• Level of consciousness: The improvement in the degree of LOC
depends on preoperative damage to cerebral tissue.
Consciousness often improves while anesthesia wears off, or
while cerebral edema subsides, and while ICP approaches
normal.
1460
• Communicative and cognitive deficits: The ability to
communicate and understand spoken or written words after
surgery depends on the level of preoperative dysfunction, the site
of the lesion, extent of the procedure, and the degree of
postoperative cerebral edema.
1461
(pyramidal) tracts.
Screening labwork
• Sodium levels and osmolality: Important for management of
SIADH and diabetes insipidus (DI). Close monitoring during
hyperosmolar therapy is important. Hypernatremia may indicate
dehydration if associated with DI. Hyponatremia may be
associated with SIADH. If sodium level is not managed
appropriately, cerebral edema may result.
1462
• Cerebrospinal fluid (CSF) analysis: Evaluates the color, white
blood cell (WBC) count, differential, glucose content, and protein
level, which are important whenever a CSF leak develops.
Diagnostic testing
Refer to Neurologic Diagnostic Testing, Chapter 5.
1. Respiratory support
Supplemental oxygen, intubation, and mechanical ventilation as
needed. In patients requiring mechanical ventilation who have
potential or actual increased ICP, use of hyperventilation needs
careful monitoring to avoid cerebral vasoconstriction. The Brain
Trauma Foundation standard emphasizes that in the absence of
increased ICP, prophylactic hyperventilation (Paco2 less than 25 mm
Hg) is not recommended. Paco2 is maintained within normal limits
unless acute elevation in ICP is present with the possibility of
imminent cerebral herniation. A brief period of hyperventilation
may be instituted in the setting of imminent herniation. Use of
prophylactic hyperventilation (Paco2 less than 35 mm Hg) should be
avoided during the first 24 hours or used only if increased ICP does
not respond to other measures such as CSF drainage, sedation, or
use of neuromuscular blocking agents.
1463
2. Positioning
The HOB is most often elevated 30 degrees to promote venous
drainage, which reduces ICP. The head should be kept in straight
alignment with the trunk to prevent increased ICP and to facilitate
venous return.
3. Manage pain
1464
• Corticosteroids (e.g., dexamethasone): To decrease cerebral
edema.
Note: Not indicated for patients with traumatic brain injury (TBI).
Research is ongoing to determine whether steroids are effective in
the treatment of cerebral edema. They are prescribed for the
treatment of vasogenic cerebral edema and edema caused by
cerebral tumor.
1465
A systematic review of literature done for the Agency for
Healthcare Research and Quality (AHRQ) showed that the risk of
neurosurgical patients for deep venous thrombosis (DVT) is 28%.
The 5 Million Lives Campaign, National Hospital Quality
Measure of The Joint Commission, National Hospital Quality
Measure by the Centers for Medicare and Medicaid Services, and
the National Quality Forum all endorse aspects of DVT
prophylaxis. Craniotomy patients without contraindications for
anticoagulation should receive DVT prophylaxis using either a
low–molecular-weight heparin or low-dose unfractionated heparin
given as an alternative. Pharmacologic agents can be used as an
adjunct to mechanical prophylaxis using intermittent pneumatic
compression, elastic stockings, or both. Venous imaging techniques
such as ultrasonography can be used before discharge to detect
thrombosis.
6. Control seizures
Antiepileptic agents: Phenytoin, fosphenytoin, and levetiracetam
should be considered for prophylaxis of provoked or early seizures
occurring within 7 days of surgery. Use of other agents such as
carbamazepine, phenobarbital, and valproate remains controversial
and in some studies has not shown to reduce postoperative
seizures.
7. Prevent infection
Antibiotics: Prevent postoperative surgical site infection or
respiratory or urinary tract infection. Randomized controlled trials
have shown that in patients undergoing craniotomy, the use of
prophylactic antibiotics reduces the frequency of postoperative
meningitis.
The American Society of Health System Pharmacists and the
Centers for Disease Control and Prevention have recommended
that antibiotic administration be via the intravenous route at
induction of anesthesia and/or that the bactericidal concentration of
the drug be established in the tissues and serum when the incision
1466
is made.
8. Nutrition support
The method and type of nutrition support are determined by the
patient’s condition and may include any of the following: oral
feedings, enteral feedings, supplements, or parenteral nutrition (i.e.,
total parenteral nutrition, fat emulsion therapy). See Nutrition
Support (p. 117).
9. Reduce fever
Antipyretics: Treat elevated temperature, which can increase use of
oxygen and glucose supplies.
1467
surgery
Decreased intracranial adaptive capacity
related to possible changes in intracranial fluid or brain tissue volume
following surgery.
Goals/Outcomes: Maintain normal ICP (0 to 10 mm Hg with
upper limit of 15 mm Hg) through regulation of cerebral flow and
cerebral spinal circulation.
Neurologic Status: Consciousness.
1468
caused by a slowing or complete stoppage of the flow of CSF
through the ventricular system secondary to edema, bleeding,
scarring, or obstruction. For further discussion, see Cerebral
Aneurysm and Subarachnoid Hemorrhage (p. 629).
Ventilation assistance
1469
pneumonia.
Infection control
Fluid management
1470
posterior lobe of the pituitary gland. ADH is produced in the
hypothalamus and stored in the posterior pituitary.
1471
occur, such as constipation, after neurologic surgery. Decreased or
absent peristalsis results from prolonged anesthesia, immobility,
trauma, electrolyte deficiencies, and mechanical bowel obstruction
(e.g., obstipation).
Exercise promotion
Cardiac precautions
Pain
1472
related to headache or discomfort secondary to surgical intervention
Goals/Outcomes: Pain and discomfort are controlled based on
the patient’s self-reported pain score (if verbal) or appropriate
nonverbal pain scale, stable vital signs, and lack of skeletal muscle
tension and behavioral signs. Pain and autonomic system
stimulation and physical agitation can increase ICP, produce sleep
deprivation, and mask neurologic changes and thereby lead to
further complications.
Pain Control.
Pain management
Meningitis
Pathophysiology
Meningitis is an inflammation of the brain and spinal cord, the
1473
CNS, affecting the meninges (i.e., dura, arachnoid, pia), brain
surface, and cranial nerves. Meningeal infection comes about
through environmental exposure or as a result of direct
contamination through invasive procedures or surgeries.
Meningitis is a reportable disease in all states. There are several
types of meningitis, broadly classified as bacterial (pyogenic), viral,
aseptic, tuberculous, fungal, and eosinophilic (parasitic). The
causative agent travels in the bloodstream from various sources
before entering the cerebral spinal fluid (CSF. The CSF is unable to
mount an antimicrobial response because it lacks immunoglobulins
and complement. Therefore, when contamination of the CSF takes
place, phagocytosis and opsonization of the microbes do not occur.
Bacterial meningitis, a consequence of bacterial invasion, progresses
through four interconnected phases: (1) invasion of host leading to
central nervous system (CNS) infection, (2) inflammation of the
subarachnoid and ventricular space while bacteria multiply, (3)
pathophysiologic changes consistent with progression of
inflammation, and (4) neuronal damage.
Bacterial meningitis
The most common type of meningitis is bacteria, which can be
community-acquired or hospital-acquired. Transmission of
bacterial meningitis can occur through environmental exposure or
because of an invasive procedure (placement of external ventricular
device or craniotomy), injury (e.g., open/penetrating wounds),
facial or basilar skull fractures, shunt occlusion/malfunction, otitis
media, sinusitis, or bacteremia (e.g., endocarditis, pneumonia).
Bacterial types usually appear within 3 to 7 days after exposure.
The most common agents associated with bacterial meningitis are
discussed as follows.
Streptococcus pneumoniae, a gram-positive cocci, has been the
leading cause of adult meningitis in the United States.
Pneumococcal meningitis occurs in crowded conditions and is
spread seasonally (fall and winter). S. pneumoniae is not as prevalent
a cause of meningitis since the development of Pneumovax and
Prevnar vaccines. Pneumococcal meningitis may occur following an
upper respiratory tract infection or nasopharyngeal colonization
with a pneumococcal strain, is a complication of conditions
1474
associated with CSF leaks, is associated with asplenia, and is more
prevalent in immunocompromised persons and in older adults.
Neisseria meningitidis, a gram-negative cocci, is the second
leading cause of meningitis in the United States. N. meningitidis is
endemic in the United States, can cause community epidemics, and
has resulted in death in previously healthy young adults. Infection
is more likely to occur in young children, persons with immune
deficiencies (human immunodeficiency virus [HIV]), or
complement component deficiencies (e.g., congenital, associated
with nephrotic syndrome, hepatic failure, systemic lupus
erythematosus, or multiple myeloma). Other risk factors include
nasopharyngeal carrier states and high-risk sexual behaviors.
Vaccinations have reduced the number of cases since 2005.
Haemophilus influenzae, a gram-negative bacilli, had been the most
common cause of meningitis in children before 1990. Since 1990, the
H. influenzae vaccine type B (Hib vaccine) has reduced the incidence
of bacterial meningitis substantially in infants and children, making
it a disease predominantly of adults. Before 1990, H. influenzae type
B serotype was the leading cause of bacterial meningitis in all age
groups. Other serotypes continue to affect children and adults.
Predisposing factors include upper respiratory tract infections,
diabetes mellitus, hypogammaglobulinemia, alcoholism, and head
trauma.
Listeria monocytogenes, a gram-positive bacilli, is being seen more
frequently as a cause of meningitis, especially in patients who are
immunocompromised and those of extreme ages (very young
and very old). Outbreaks have been linked to consumption of
contaminated dairy products, undercooked chicken, fish, and
meats.
Gram-negative species (Escherichia coli, Klebsiella pneumoniae,
Proteus mirabilis, and Pseudomonas aeruginosa) are increasing in
prevalence as a hospital-acquired cause secondary to trauma or
neurosurgical procedures. Spontaneous gram-negative
meningitis is found in older adults, the immunocompromised, or
persons with underlying conditions such as cirrhosis, diabetes
mellitus, malignancy, or splenectomy. The urinary tract is the usual
portal of entry of bacteria. Other surgical procedures complicated
by gram-negative infections are ventriculoperitoneal shunts,
1475
craniofacial repair, ventriculostomy, hypophysectomy, reservoir
insertion, and myelography.
Other microbes
Also associated with meningitis are Mycobacterium pneumoniae,
Borrelia burgdorferi, and Treponema pallidum.
Tuberculous meningitis
Mycobacterium tuberculosis as a CNS disease and manifested as
meningitis is documented in children and adults where
tuberculosis has a regional prevalence. In more developed regions,
M. tuberculosis meningitis is related more to reactivation of the
disease. Other risk factors for development of M. tuberculosis are
older age, alcoholism, malnutrition, and immunocompromised
states including HIV and patients with malignancies. Older adults
and children living among people with tuberculosis have increased
risk.
Fungal meningitis
Cryptococcus neoformans, an opportunistic organism seen with
acquired immune deficiency syndrome (AIDS), is the leading cause
of CNS fungal infection. Other fungi-associated meningitis include
Candida albicans, and histoplasmosis meningitis is also seen in
immunocompromised patients and evolving from progressive
disseminated histoplasmosis.
Viral meningitis
Enteroviruses are the most common cause of viral meningitis that
occurs in the spring and fall seasons. The condition generally lasts 7
to 10 days and, although serious, is rarely fatal in people with
normal immune systems. Herpes viruses, including herpes simplex
viruses (the cause of chickenpox, Epstein-Barr virus, and shingles),
measles, and influenza may lead to viral meningitis. Mosquitoes
and other insects spread arboviruses, which cause infections that
lead to viral meningitis.
Eosinophilic meningitis
1476
Infestation by Angiostrongylus cantonensis, a parasitic nematode,
results in severe gastrointestinal (GI) or CNS disease in humans,
depending on the species. A. cantonensis, also known as the rat
lungworm, causes eosinophilic meningitis. Prevalent in Southeast
Asia and Tropical Pacific Islands, the nematode resides in rodents
and transmission is through larvae found in rat feces. Slugs or
mollusks ingest the larvae. Humans are incidental hosts as a result
of eating infected slugs, raw vegetables, or vegetable juices
contaminated with the slugs or their slime.
Noninfectious causes
Sarcoidosis, leptomeningeal carcinomatosis, systemic lupus
erythematosus, Wegener granulomatosis, and Behçet disease.
1477
Neurologic assessment: Meningitis
Goal of system assessment
A complete neurologic examination should be performed to
establish the patient’s baseline neurologic function. Examination of
associated systems (head, eye, ear, nose, and throat [HEENT] and
respiratory) provides additional data. When diagnosed one or more
signs of meningitis are positive (Table 7-2).
Table 7-2
POSITIVE MENINGEAL SIGNS
• Community setting
1478
• Recent surgery or medical problems
• Antibiotic use
• Tuberculosis risk
• Lifestyle
• Recent travel
• IV drug use
• Immunocompromised
• Splenectomy
• HIV
• Hepatitis
• Chemotherapy
1479
• Recent trauma to the head
• Exposure to meningitis
• Use of antibiotics
• Drug allergies
• Immunocompromising condition
• IV drug use
• Critical History
• Exposure
• Drug allergies
1480
Vital signs
• BP, HR, and RR changes: May further alter cerebral tissue
perfusion. Monitor rate, rhythm, and depth of respirations for
changes or abnormal breathing patterns. Use of pulse oximetry
and electrocardiographic (ECG) monitoring is recommended.
Observation
A constellation of early symptoms is associated with most types of
meningitis and includes headache, fever, neck stiffness, and altered
mental status. At least one of these symptoms is found in most
types of meningitis. Other symptoms such as papilledema, seizures,
focal deficits (cranial nerve palsies), and coma may be seen early or
late in the development of meningitis. Meningitis is associated with
cerebral infarction and arthritis in some cases. The clinical features
of specific types of meningitis are described as follows. Common
meningeal signs demonstrated in meningitis are found in Table 7-2.
Level of consciousness
When assessing LOC it is important not to use subjective terms
such as “stupor or lethargy” but rather to assess and communicate
clearly the description of the patient’s spontaneous activity,
response to verbal stimuli and reaction to painful stimuli, and how
this differs from previous assessment. Assess for an acute change in
mental status or fluctuation in mental status; various scales can be
used that include LOC and other key indicators. Examples are the
Richmond Agitation and Sedation Score (RASS) and Glascow Coma
Scale (GCS).
Pupillary changes
Examine pupils for size (in mm), shape, symmetry, reactivity to
1481
light, constriction, consensual response, and accommodation.
Pupillary abnormalities can indicate unilateral or bilateral brain
dysfunction, interruption of sympathetic or parasympathetic
pathways, damage in the brainstem, cranial nerve damage, and
herniation.
Clinical presentation
1482
pneumonia are commonly reported. Nuchal rigidity in older
adults must be differentiated from degenerative changes of the
cervical spine.
1483
• C. neoformans: Because the infection is subacute, fever and
headache may have a subtle pattern lasting for weeks while other
symptoms of meningitis occur, including positive meningeal
signs (Table 7-2), alterations in mental status (e.g., hyperactivity,
bizarre behavior, emotional labiality, poor judgment),
photophobia, focal cranial nerve deficits, nausea, vomiting, and
(rarely) seizures.
Functional assessment
1484
Chapter 7 General Neurologic Assessment.
• Sensory: Assess perception of touch, proprioception, pain,
temperature, and vibration (if possible). Superficial and deep
reflexes are tested on symmetrical sides of the body and
compared noting the strength of contraction. Sensory deficits
occur when the primary sensory cortex, the sensory association
areas of the parietal lobe, or the spinothalamic tracts are injured
or edematous. Sensory deficits include the inability to distinguish
objects according to characteristics (e.g., size, shape, weight) and
inability to distinguish overall changes in temperature, touch,
pressure, and position. Improvement in both motor and sensory
perception may be seen while cerebral edema subsides.
Screening labwork
• CSF analysis: Evaluates the color, WBC count, differential,
glucose content, and protein level.
Diagnostic tests
1485
Bacterial meningitis presents with classic symptoms of fever,
altered mental status, headache, and nuchal rigidity. Immediate
diagnosis and isolation of the organisms are paramount in this life-
threatening disease. Delay in obtaining the necessary information
needed to diagnosis and treat the underlying organism will increase
morbidity and mortality.
Table 7-3
MENINGITIS: TYPICAL CEREBROSPINAL FLUID FINDINGS
Collaborative management
Care priorities
1. Control infection
1486
(Table 7-4): Prophylaxis, using appropriate antimicrobials for
people exposed to N. meningitidis (rifampin or spiramycin) or H.
influenzae meningitis, is recommended.
Table 7-4
COMMON DRUG THERAPY FOR THE MANAGEMENT OF
MENINGITIS*
1487
*
These therapies are subject to change based on the Centers for Disease Control
and Prevention recommendations and new studies.
Adapted from Tunkel A: Initial therapy and prognosis of bacterial meningitis in adults.
In Calderwood S, editor: UpToDate, Waltham, 2014, Wolters Kluwer. Retrieved from
www.uptodate.com/contents/initial-therapy-and-prognosis-of-bacterial-meningitis-in-
adults; Friedman N, Sexton D: Gram-negative bacillary meningitis: epidemiology,
clinical features, and diagnosis. In Sexton D, editor: UpToDate, Waltham, 2014,
Wolters Kluwer. Retrieved from www.uptodate.com/contents/gram-negative-
bacillary-meningitis-epidemiology-clinical-features-and-diagnosis?source=see_link;
Tunkel A, Hartman B, Kaplan S, et al: Practice guidelines for the management of
bacterial meningitis. Clin Infect Dis 39:1267-1284, 2004.
3. Monitor
It is important to monitor neurologic status, vital signs, and
respiratory status. The patient may need to be intubated and placed
on a ventilator. Watch for signs of increased ICP or hydrocephalus.
1488
restriction during the first 48 hours of treatment of bacterial
meningitis. Electrolyte imbalances should be corrected. Monitor
urine output and serum osmolality and watch for signs and
symptoms of SIADH.
8. Prevent infection
Vaccines are currently available for meningitis prophylaxis. These
include the following: (1) influenza type B (Hib), given as a
childhood immunization; (2) bacillus Calmette-Guérin (BCG), used
for tuberculosis, also prevents tuberculosis meningitis; (3)
pneumococcal vaccine recommended for those who are chronically
ill and adults older than 65 years of age; and (4) N. meningitides
vaccines for specific or combined prophylaxis for five
investigational subgroups. The Centers for Disease Control and
Prevention (CDC) guidelines recommend that “Transmission-Based
Precautions” be implemented until effectiveness of antimicrobial
treatment is established.
9. Facilitate mobility
1489
Physical therapy, occupational therapy, and speech therapy should
be initiated as soon as the patient is stable, to minimize physical
(contractures and muscle atrophy) and cognitive complications.
Prevent pressure ulcers, pneumonia, or DVTs related to immobility.
Initiate DVT prophylaxis including sequential stockings and
prophylactic anticoagulants as indicated.
Neurologic monitoring
1490
cranial nerve palsies.
Acute pain
related to headache, photophobia, and fever secondary to meningeal
irritation
Goals/Outcomes: Within 2 hours of initiating interventions to
relieve pain, the patient reports pain relief, as documented by a
pain scale.
Comfort Level.
1491
Pain management
1. Monitor the patient for pain and discomfort. Devise a pain rating
scale with the patient. Administer analgesics as prescribed. (See
Pain, Chapter 1.)
Infection control
1492
antimicrobial therapy.
Neurodegenerative and
neuromuscular disorders
Pathophysiology
Neurodegenerative diseases are conditions wherein the neurons, or
the myelin sheath of the neurons of the brain and spinal cord, are
destroyed. Cells of the brain and spinal cord do not effectively
regenerate in large numbers, thus profound destruction is
sometimes devastating. Over time, the progressive destruction
leads to dysfunction and disabilities. The disorders are divided into
two groups: conditions affecting movements (e.g., ataxia) and
conditions affecting memory (e.g., dementia), which are not
1493
mutually exclusive. Alzheimer, Pick, Parkinson, Huntington, and
Lou Gehrig (amyotrophic lateral sclerosis[ALS]) diseases, prion
diseases (Creutzfeldt-Jakob[CJD]), and multiple sclerosis are a few
of the more commonly recognized conditions. Some of the diseases
are genetic, whereas alcoholism, cancer, and vascular disease are
associated with other conditions. Environmental toxins, chemicals,
or viruses may cause other disorders. Neurodegeneration often
begins long before the patient manifests symptoms. Treatments
vary with each disorder.
Neuromuscular disorders include the neurodegenerative
diseases, which affect voluntary movements. Communication
between the nervous system and muscles is not possible when
nerves are destroyed. Muscles weaken and atrophy as a result of
disuse. Weakness may also be associated with muscle twitching,
cramps, and pain, along with joint and movement deficits. These
disorders may affect the heart and respiratory muscles. Many
neuromuscular disorders are genetic, whereas others are immune-
mediated (associated with an immunologic disorder). Myasthenia
gravis (MG), Guillain-Barré syndrome (GBS), and muscular
dystrophy are several of the more commonly recognized
conditions. Most of the diseases are incurable. The goal of treatment
is to improve symptoms, increase mobility, and lengthen life.
Patients with MG may experience difficulties with medication
management resulting in a crisis, which is rather easily corrected
with the proper medication adjustment. Patients with other
neuromuscular disorders may require more elaborate treatments
including high-dose corticosteroids, plasmapheresis, and more
prolonged hospitalization.
Diagnosis of neuromuscular diseases depends on the
identification of a specific defect of neuromuscular function. The
functional defect can sometimes be inferred by a physical
examination done by a physician or advanced practice provider
coupled with laboratory testing of blood and possibly CSF. A more
extensive diagnostic process evaluates the function of nerves,
muscles, and the connections between them by using two
complementary techniques—nerve conduction velocity (NCV)
testing and electromyography (EMG).
Care of patients who are critically ill may involve managing
1494
patients with respiratory failure and cardiovascular instability
related to exacerbations of neuromuscular disorders. Patients at this
stage of instability may be terminally ill. Patients with either MG or
GBS may be treated and fully recover. This chapter will focus on
MG and GBS; however, the nursing diagnoses, interventions, and
outcomes are common to most neurodegenerative and
neuromuscular disorders.
Myasthenia gravis
Pathophysiology
Myasthenia gravis (MG) is a chronic, progressive autoimmune
disorder causing weakness and abnormal fatigability of the
voluntary striated skeletal muscles. MG usually affects women
between 20 and 40 years of age and men after age 40 years; the peak
incidence for women is during the second and third decades and
for men during the sixth decade. The overall ratio of affected
women to men is 3:2. Of patients with MG, 85% to 90% have an
anti–acetylcholine receptor (anti-AChR) antibody
(immunoglobulin). MG is associated with other autoimmune
disorders. The thymus gland undergoes pathologic changes in 80%
of patients with MG and may produce anti-AChR antibodies when
exposed to inflammation. The course of the disease depends on the
muscle groups involved and the degree of their involvement.
MG causes changes in the structural integrity of the postsynaptic
membrane at the neuromuscular junction by markedly reducing the
number of AChRs. Acetylcholine (ACh), a neurotransmitter, is
synthesized and stored in the terminal expansion of motor nerve
axons. ACh is released into the synaptic cleft. The attachment of
ACh to AChR on the postsynaptic membrane activates muscle
action potential, resulting in muscle contraction. Contraction
terminates when ACh is deactivated by acetylcholinesterase in the
neuromuscular junction.
Patients may experience remissions and exacerbations. Many
medications can increase the weakness associated with MG,
including several commonly administered antibiotics
(erythromycin, aminoglycosides, and azithromycin) and cardiac
1495
medications such as magnesium or antidysrhythmic agents
including procainamide, beta-adrenergic–blocking agents, and
quinidine. Paradoxical weakness may occur when a patient receives
an excessive dose of anticholinesterase medications (cholinesterase
inhibitors such as physostigmine or neostigmine), which are used to
treat MG. Distinguishing worsening MG from side effects from
prescribed medication effects can be difficult. Exacerbations can be
profound, and thus are called crises.
A myasthenic or cholinergic crisis may occur rapidly or
incipiently. Myasthenic crisis can occur as part of the natural course
of MG or may result from other factors, including infection,
tapering of immunosuppressive medications, administration of
various other medications, pregnancy, childbirth, or following a
surgical procedure, ultimately resulting in respiratory failure from
weakness of the respiratory muscles. Severe weakness of the
oropharyngeal muscles (bulbar signs) is often associated with
respiratory muscle weakness, resulting in dysphagia and
aspiration. Endotracheal (ET) intubation with mechanical
ventilation may be needed. A cholinergic crisis results from excessive
doses of anticholinesterase medications and rarely occurs if the
dose of medications remains within the normally prescribed range.
The patient is acutely aware of all sensations. Crisis is dramatic and
frightening.
Assessment
Goal of assessment
The assessment differentiates between acute and chronic neurologic
assessment findings. Signs of myasthenic and cholinergic crises
may be subtle. Increasing anxiety, apprehension, or insomnia may
indicate the onset of crisis.
1496
imbalance, or intake of medications with neuromuscular-blocking
properties, such as sedatives, tranquilizers, opiates, or antibiotics
(e.g., neomycin, kanamycin, gentamicin, streptomycin, tetracycline),
may prompt crisis.
Vital signs
• Findings vary significantly, depending on whether the patient is
experiencing a crisis.
Observation
• Patients may be asymptomatic or have mild symptoms if crisis
develops slowly.
Symptom progression
1497
Weakness is greater in proximal muscles than distal. Strength is
decreased in all extremities, with inability to maintain position
without support. Diaphragmatic and intercostal weakness,
dyspnea, ineffective cough, and accumulation of secretions are
present, which increases the risk for respiratory arrest.
Auscultation
• Breath sounds may reflect reduced movement of air or shallow
breaths.
1498
Collaborative management
Care priorities for patients with myasthenia gravis
1499
4. Manage pharmacotherapy during noncrisis periods
Medications must be given on time to maintain therapeutic effects.
Drug combinations are patient-specific.
1500
other treatments have been unsuccessful or are contraindicated.
5. Consider plasmapheresis
A complete exchange of plasma with removal of abnormal
circulating antibodies that interfere with AChRs. Box 7-3 describes
potential complications, nursing assessments, and interventions.
(For additional information, see Fluid and Electrolyte Disturbances,
Chapter 1.)
Respiratory monitoring
1501
rate, rhythm, or depth of respirations; pallor; nasal flaring; use of
accessory muscles; and restlessness, irritability, confusion, or
somnolence.
3. Monitor ABG and pulse oximetry results. Falling PaO2 (less than
60 mm Hg), rising Paco2 (greater than 50 mm Hg), and falling
oxygen saturation, coupled with changes in vital capacity, tidal
volume, and increasing RR, indicate the need for additional
respiratory support.
1502
intervention/treatment, the patient’s airway is clear, as evidenced
by absence of adventitious breath sounds.
Aspiration Prevention; Respiratory Status: Airway Patency.
Airway management
1503
Artificial Airway Management; Cough Enhancement:
Oxygen Therapy; Ventilation Assistance.
Health screening
Impaired swallowing
related to decreased or absent gag reflex; decreased strength or excursion of
muscles involved in mastication; facial paralysis; mechanical obstruction
(tracheostomy tube).
Goals/Outcomes: Before oral foods and fluids are given or
reintroduced, the patient demonstrates capability for safe and
1504
effective swallowing, as evidenced by the presence of gag reflex
and adequate strength and excursion of muscles involved in
mastication.
Aspiration Prevention; Swallowing Status.
Aspiration precautions
1. Assess the patient for the presence of the gag reflex, ability to
swallow, and strength and excursion of muscles involved in
mastication. As indicated, consult with a speech therapist to
determine the patient’s ability to swallow.
3. After the patient’s gag reflex and ability to swallow return, begin
oral feedings cautiously.
1505
• Keep suction equipment at the bedside; suction
excess secretions as necessary after each feeding.
Inspect the mouth for residual food after meals.
Provide for oral hygiene after every meal.
2. Provide an eye patch or frosted lens for the patient with diplopia;
alternate the patch or lens to the opposite eye every 2 to 3 hours
during the patient’s waking hours.
3. Provide eyelid crutches for the patient with ptosis, or loosely tape
eyelids open but only when providing direct care.
1506
4. Administer artificial tears in each eye at least every 4 to 6 hours to
lubricate and protect corneal tissue.
Deficient knowledge
related to thymectomy procedure, including preoperative and postoperative
care.
Goals/Outcomes: Before surgery, the patient verbalizes
understanding of the surgical procedure, including preoperative
and postoperative care.
Knowledge: Treatment Procedure(s).
Teaching: Procedure/treatment
1507
performed preoperatively and postoperatively to assist in
determining the patient’s respiratory status.
Deficient knowledge
related to purpose and procedure for plasmapheresis
Goals/Outcomes: Before the first plasma exchange, the patient
verbalizes knowledge of the purpose and procedure for
plasmapheresis.
Knowledge: Treatment Procedure(s).
Teaching: Procedure/treatment
4. Explain that the nurse will make assessments before, during, and
after plasmapheresis (see Box 7-3).
1508
5. Advise the patient that the procedure takes several hours and
may be performed daily.
Deficient knowledge
related to signs and symptoms of myasthenic and cholinergic crises.
Goals/Outcomes: Within 24 hours of stabilization of respiratory
status, the patient and significant others verbalize the signs and
symptoms of impending myasthenic and cholinergic crises.
Knowledge: Disease Process.
1509
suction apparatus) and facilitate it being available in the home if the
patient has a history of crisis events.
Guillain-barré syndrome
Pathophysiology
Guillain-Barré syndrome (GBS) is a disorder wherein the immune
system mistakenly attacks the peripheral nervous system, causing
weakness and paresthesias of the lower extremities. Symptoms can
intensify and ascend toward the head, resulting in loss of ability to
use all muscles. When severe, the patient is totally paralyzed and
the disorder is life threatening, with impending respiratory muscle
paralysis and cardiovascular instability. GBS is not considered a
classic neuromuscular or neurodegenerative disorder, because the
onset is sudden, with rapid progression, and once peaked, patients
have the potential for a complete recovery.
This disorder is an acute inflammatory, immune-mediated,
demyelinating polyneuropathy of the peripheral nervous system,
affecting 1.5 to 2 individuals per 100,000 population.
GBS affects mainly the Schwann cell, which synthesizes and
maintains the peripheral nerve myelin sheath. Studies suggest that
macrophages penetrate the basement membrane and strip
apparently normal myelin from intact peripheral nerve axons,
1510
causing the characteristic signs and symptoms of GBS. The ventral
(motor) root axons of the anterior horn cells, which innervate
voluntary skeletal muscles, are primarily involved. Dorsal (sensory)
root axons of the posterior horn are not as affected. Recovery of
neurologic function depends on proliferation of Schwann cells and
remyelination of axons. Recovery can be expected in 80% to 90% of
cases, with minor residual deficits in less than half of the patients,
and 2% to 5% experiencing recurrence after complete recovery.
Vital signs
• Autonomic nervous system involvement (a type of autonomic
dysreflexia): Occurs in most patients with GBS: sinus tachycardia,
bradycardia, orthostatic hypotension, hypertension, excessive
diaphoresis, bowel and bladder dysfunction, loss of sphincter
1511
control, increased pulmonary secretions, SIADH, and cardiac
dysrhythmias (a common cause of death).
Observation
• Ascending flaccid motor paralysis is the most common presenting
sign and is associated with the early loss of deep tendon reflexes.
1512
Collaborative management
Care priorities
2. Perform plasmapheresis
Involves a complete exchange of plasma with the removal of
abnormal circulating antibodies that affect the peripheral nerve
myelin sheath. Removal of these autoantibodies may lessen the
duration and severity of GBS. For nursing interventions for
complications of plasmapheresis, see Box 7-3.
1513
administered to maintain BP within normal levels.
7. Rehabilitation
Active and passive ROM exercises are performed at frequent
intervals during all phases of GBS. Activity must be balanced with
caloric intake to prevent muscle wasting. When the patient’s
condition stabilizes, a physiatrist consultation to plan rehabilitation
with physical and occupational therapy should be done while the
patient is in critical care. The primary goal is to pace recovery to
obtain maximum mobility, promote self-care, and adapt to changes
in body image. Rehabilitation does not improve nerve regeneration.
1514
secondary to weakness or paralysis of intercostal and diaphragmatic
muscles.
Goals/Outcomes: Within 12 to 24 hours of this diagnosis, the
patient has adequate gas exchange, as evidenced by orientation to
time, place, and person; RR 12 to 20 breaths/min with normal
pattern and depth; HR less than 100 bpm; BP within the patient’s
normal range; PaO2 greater than 80 mm Hg; Paco2 less than 45 mm
Hg; and oxygen saturation greater than 94%.
Respiratory Status: Gas Exchange; Respiratory Status:
Ventilation; Mechanical Ventilation Response: Adult.
Respiratory monitoring
1515
Goals/Outcomes: Within 12 to 24 hours of this diagnosis, the
patient’s airway is clear, as evidenced by absence of adventitious
breath sounds; HR 60 to 100 bpm; BP within the patient’s baseline
range; RR 12 to 20 breaths/min with normal depth and pattern; tidal
volume within baseline measurements; PaO2 greater than 80 mm
Hg; Paco2 less than 45 mm Hg.
Aspiration Prevention; Respiratory Status: Airway Patency.
Airway management
1516
Goals/Outcomes: The patient maintains baseline/optimal ROM of
all joints and baseline muscle size and strength; no evidence of
DVT.
Endurance.
Energy management
1517
• Assess position sense by moving the patient’s big
toe or thumb up and down while patient’s eyes are
closed. Note vibratory sense by placing a vibrating
tuning fork over bony prominences.
Activity therapy
1518
2. Obtain a physical therapy referral, and begin rehabilitation
planning process during the early stages of the disorder.
Dysreflexia management
1519
1. Assess for signs of AD: cardiac dysrhythmias; HR less than 60
bpm or greater than 100 bpm; elevated and sustained BP (greater
than 250 to 300/150 mm Hg); facial flushing; increased sweating,
possibly caused by loss of thermal regulation; extreme generalized
warmth; profound weakness; and complaints of severe headache or
tightening in the chest and abdomen.
1520
• Sensory stimuli: pressure caused by tight clothing,
dressings, bed covers, thigh straps on urinary
drainage bags; prolonged pressure on skin surface
or over bony prominences; temperature changes,
such as exposure to a cool breeze or draft.
1521
6. Consult the advanced practice provider if symptoms do not abate
within 15 to 30 minutes, especially elevated BP. This may lead to
seizures, subarachnoid (SAH) or intracerebral hemorrhage (ICH),
or other stroke.
Hemodynamic regulation
1522
3. Implement measures to prevent decreased cardiac output caused
by orthostatic hypotension:
1523
• If the patient experiences a deficit, place objects
where the patient can see them and assist with
ADLs.
Constipation
related to hypoperistalsis or paralytic ileus associated with neuromuscular
impairment.
Goals/Outcomes: Within 3 to 5 days of this diagnosis, the patient
has a bowel movement.
Bowel Elimination; Hydration.
Bowel management
1524
1. Assess the patient’s GI status: bowel sounds, abdominal
distension, nausea, vomiting, and abdominal discomfort. In the
presence of hypoperistalsis or paralytic ileus, the patient will
exhibit (1) high-pitched, tinkling sounds that will be heard early in
obstruction or ileus or (2) a decrease or absence of sounds occurring
with complete obstruction or paralytic ileus.
1525
suppositories.
Box 7-3
NURSING INTERVENTIONS FOR
COMPLICATIONS OF PLASMAPHERESIS
Hypovolemia
Can result from rapid removal of up to 3 L of body fluid during
plasmapheresis with volume replacement that is too slow during
the procedure.
1526
• Monitor and record I&O throughout the procedure. Be alert to
oliguria (urinary output less than 30 mL/h for 2 consecutive
hours).
Clotting abnormalities
Can result from removal of clotting factors during plasmapheresis.
• Assess PT, PTT, and platelet count before and after procedure. Be
alert to PT and PTT greater than those of control values and to
increased platelet count. Normal ranges are as follows: PT 11 to
15 seconds, PTT 30 to 40 seconds, and platelet count 150,000 to
400,000/mm3.
Hypokalemia*
Can result from removal of potassium during the plasma exchange.
1527
• Observe cardiac monitor for signs of cardiac dysrhythmias: ST
segment depression, flattened T wave, presence of U wave, and
ventricular dysrhythmias. Report abnormal cardiac rhythms to
the physician.
Hypocalcemia
Can result from binding of calcium to ACD, the anticoagulant used
during plasmapheresis.
• Encourage the patient to drink milk before and during the plasma
exchange.
Myasthenic crisis
Can result from removal of circulating anticholinesterase drugs
during plasmapheresis.
Cholinergic crisis
Can result from removal of antibodies and decreased need for
anticholinesterase drugs after plasmapheresis.
1528
• In the event of either crisis, have the following available: IV
infusion apparatus, medications (edrophonium chloride
[Tensilon], neostigmine bromide, atropine, and pralidoxime
chloride [Protopam Chloride]), manual resuscitator bag,
automatic external defibrillator (antiepileptic drug), oxygen,
suction equipment, and intubation tray if intubation is not
already in place.
E-mail: info@gbs-cidp.com
Website: www.gbs-cidp.org
Fax: 610-667-7036
1529
For more information on neurologic disorders or research
programs funded by the National Institute of Neurological
Disorders and Stroke, contact the Institute’s Brain Resources and
Information Network (BRAIN) at:
Bethesda, MD 20824
Tel: 800-352-9424
Fax: 301-402-2186
Email: braininfo@ninds.nih.gov
http://www.ninds.nih.gov
Status epilepticus
Pathophysiology
Status epilepticus (SE) is a state of recurring or continuous seizures
of at least 30 minutes’ duration, in which the patient does not return
to full consciousness from the postictal state before another seizure
occurs. A practical definition of SE may be revised to include
seizures of only 5 minutes’ duration, because of a high likelihood
that they will continue. If possible, treatment should be initiated
1530
immediately to prevent neuronal injury, which may begin within 20
to 30 minutes of the onset of SE. The mortality rate for SE is
estimated to be from 12% to 25%.
There are two major types of SE: convulsive and nonconvulsive.
Another classification is based on Gastaut and used by Engel in
which generalized SE includes convulsive SE (generalized tonic-
clonic seizures) and partial SE. Convulsive SE is more common and
is considered a life-threatening medical emergency, because the
hypoxia and metabolic exhaustion of neuronal tissue may cause
neuronal death. Partial SE includes simple partial SE (focal motor or
epilepsia partialis continua) and complex partial SE (temporal or
nontemporal seizures). The term “nonconvulsive status” may also
be used to describe absence, complex partial SE, and simple partial
SE. Clinical diagnosis of the type of nonconvulsive seizure activity
is difficult, and thus requires continuous video-
electroencephalographic (video-EEG) monitoring to validate that
the condition is present.
Refractory SE is present when the seizures, either convulsive or
nonconvulsive, continue despite treatment with a therapeutic dose
of a benzodiazepine and an initial loading dose of an
anticonvulsant.
SE in persons with epilepsy is often as a result of nonadherence
with medications or a drop in anticonvulsant serum levels caused
by alcohol abuse or infection. Other causes for individuals with and
without preexisting epilepsy include acute metabolic disturbances
(e.g., hypoglycemia, hyponatremia, hypocalcemia), stroke, CNS
infection (e.g., meningitis, encephalitis), CNS trauma or tumors,
sepsis, hypoxia, and alcohol or drug abuse. Prompt treatment may
prevent complications including cardiac dysrhythmias,
hyperthermia, aspiration, hypertension or hypotension, anoxia,
hyperglycemia or hypoglycemia, dehydration, rhabdomyolysis,
myoglobinuria, and oral and/or musculoskeletal injuries. The
prognosis of SE is thought to be related to the etiology and how fast
treatment is initiated.
Assessment
Goal of system assessment
1531
Evaluate for cessation of seizures, return to baseline neurologic
function, injury, and to determine cause of seizures.
Vital signs
Changes resulting from the massive sympathetic nervous system
response to continuous, generalized seizures include hypertension,
tachycardia, dysrhythmias, tachypnea, and hyperthermia.
• Automatisms.
• Speech difficulty.
Screening labwork
1532
Blood tests can reveal causes of seizures.
Electroencephalography
Continuous EEG monitoring is used to determine whether the
patient is still in SE even though there are no clinical signs or very
subtle clinical signs and for those patients who are placed in a
medication-induced coma for refractory SE.
1533
brain scan abnormalities responsible for See meningitis section
Lumbar puncture SE
Assesses for abnormalities in the
central nervous system that
may indicate infection as a
reason for refractory status
Collaborative management
Care priorities
2. Establish IV access
For medication administration, fluid resuscitation, and to draw
blood for needed labwork.
3. Pharmacotherapy
Prevention of Wernicke-Korsakoff syndrome: 100 mg IV thiamine
and 50 mL of 50% glucose are administered if chronic alcohol
ingestion or hypoglycemia is suspected.
First-line or emergent therapies
Administration of fast-acting anticonvulsant: Given to quickly
achieve high serum and brain concentrations. Not used as long-
acting anticonvulsant. First-line agents are benzodiazepines.
Treatment is most effective when started promptly.
1534
• Lorazepam (Ativan)
• Diazepam (Valium)
OR
• Midazolam (Versed)
1535
• Monitor respiratory and cardiovascular status.
• Fosphenytoin (Cerebyx)
• Phenytoin (Dilantin)
1536
dysrhythmias, including asystole.
• Infuse at 3 to 6 mg/kg/min.
1537
Administration of IV phenobarbital: Used if the patient is allergic
to phenytoin.
Pentobarbital coma
1538
mg/kg/h to stop seizures.
Propofol
Midazolam
1539
dosage of 0.05 to 2 µg/kg/h to stop seizure activity.
Use of Sedation
1540
intravenous hypnotic agent that is also cautiously used for sedation.
Pentobarbital coma is occasionally used for patients who experience
high ICP that does not respond to other forms of therapy. (See
Sedation and Neuromuscular Blockade, Chapter 1.)
5. Nutrition support
Enteral or parenteral nutrition may be necessary, depending on the
duration of the SE and the patient’s underlying nutritional state.
Respiratory monitoring
1. Monitor for respiratory distress. Note RR, depth, and rhythm and
skin color. Report use of accessory muscles, rapid or labored
respirations, and cyanosis.
1541
6. Administer oxygen as prescribed.
1542
the presence of focal findings that suggest an expanding lesion.
1. Keep side rails padded and up at all times, with bed in the lowest
position.
1543
• Avoid use of tongue blade, which could splinter
and cut the mouth.
1544
5. Once the cause of noncompliance is identified, work to find a
solution. If the patient has side effects from the medication, such as
gastric upset, suggest that the patient try taking the medication
after meals. If the gastric upset is a result of increasing the
medication, advise the patient to increase the dose more slowly.
Deficient knowledge
related to disease process, treatment, and lifestyle changes that epilepsy
necessitates.
Goals/Outcomes: Within the 24-hour period before discharge
from the critical care unit, the patient verbalizes understanding of
epilepsy, including its etiology and pathophysiology and seizure
classification, as well as its treatment and the lifestyle changes it
necessitates.
Knowledge: Disease Process.
1545
level of medication by taking it as prescribed. Reinforce importance
of keeping appointments for labwork. Explain if the medication is
missed or taken erratically, he or she cannot attain the blood level
needed to prevent seizure breakthrough. If a dosage of medication
is missed, instruct the patient to notify the physician and/or
advanced practice provider.
Ineffective coping
related to frustration related to unpredictable nature of the disease.
Goals/Outcomes: Within 24 to 48 hours of this diagnosis, the
patient verbalizes feelings, identifies strengths and ineffective
coping behaviors, and understands responsibility for self-care.
Coping.
Coping enhancement
1546
3. Involve the patient in decisions regarding care so that he or she
has more sense of control over life (e.g., encourage the patient to
participate in the decision for scheduling the medications). Problem
solve for major concerns.
4. Help the patient set realistic goals for employment and living
arrangements. Refer the patient to regional or local EFA as
appropriate.
1547
cause of death in 129,476 cases in 2010. Stroke is the leading cause
of long-term disability in the United States. Cost to treat stroke may
increase from $71.55 billion in 2010 to $183.13 billion in 2030 per
year, according to the American Heart Association/American Stroke
Association (AHA/ASA). One third of patients with stroke do not
survive, one third suffer with long-term disability, and one third
with no or minimal disability. Although men have a higher
incidence of stroke at younger ages, the incidence is reversed
and higher for women by age 75 years and older. Women
experience 55,000 more strokes each year than do men. In addition,
the risk of stroke varies with ethnicity and age. Blacks and
Hispanics are at increased risk compared with whites. The risk of
stroke increases with age; however, in 2009 34% of hospitalized
patients with stroke were younger than 65 years of age.
The classification of stroke depends on the preceding
pathophysiologic event. Eighty-seven percent are ischemic strokes,
10% are ICHs, and the remaining 3% are SAHs. Subcategories are
shown in Figure 7-1. Acute ischemic stroke (AIS) and ICH are
discussed here. Subarachnoid hemorrhage (SAH) from cerebral
aneurysmal rupture was discussed in an earlier section of this
chapter (see Cerebral Aneurysm and Subarachnoid Hemorrhage,
Chapter 7). A transient ischemic attack (TIA) is a temporary episode
of neurologic dysfunction, caused by focal brain, spinal cord, or
retinal ischemia, without acute infarction. Although not considered
a stroke, TIAs presage 15% of all strokes, and 12% of patients with a
TIA will die within 1 year. A TIA may precede an AIS by hours to
years. Studies of patients in Northern California showed that 5%
had strokes within 2 days, 11% within 3 months, and 33% within 1
year of having a TIA. Atherosclerosis of the arteries supplying the
brain is the most common cause of TIA. TIAs generally last less
than 24 hours, with most episodes persisting less than 1 hour.
1548
FIGURE 7-1 Types of Stroke.
1549
any anticoagulant use before admission (even if international
normalized ratio [INR] is less than 1.7), NIH Stroke Scale greater
than 25, and CT findings involving more than one third of the
middle cerebral artery (MCA) territory (as evidenced by
hypodensity, sulcal effacement, or mass effect estimated by visual
inspection or use of the ABC/2 formula (ellipsoid) revealing a mass
of greater than 100 mL). Ideally, thrombolytics should be
administered within the first hour of arrival in a hospital/stroke
center. In many states, emergency medical services (EMS) have
been instructed to bypass noncertified primary stroke centers, and
take patients with stroke to advanced primary stroke centers or
comprehensive stroke centers for evidence-based care and best
possible outcomes. Patieents with hemorrhagic strokes may require
immediate treatment intervention to reduce intracranial pressure
(ICP), such as inserting a ventriculostomy to drain cerebral spinal
fluid (CSF). Regardless of the type of stroke, early assessment and
intervention is crucial in minimizing complications.
AIS most commonly results from atherosclerosis of blood vessels
perfusing the brain. Approximately 20% of AIS results from large
artery atherosclerotic disease (extracranial or intracranial), most
often associated with thrombus formation related to an unstable
plaque. A thrombus is a clot formed in the artery, usually in
branches with low flow resulting from plaque. Thrombotic strokes
are usually caused by local atherosclerosis of cerebral arteries.
Characteristic deficits are produced depending on the artery
involved (Table 7-5). Another 25% of AIS results from thrombosis of
small perforating intracranial arteries that result in lacunar or
subcortical strokes. An additional 20% of AIS results from low to
absent cerebral perfusion caused by cardiogenic emboli, most often
resulting from atrial fibrillation. Cerebral emboli may be formed in
the heart, in the carotid, or other cerebral arteries, and migrate to
occlude an artery in the brain. The remaining 30% are cryptogenic
and can include critically ill patients in shock experiencing systemic
hypoperfusion.
Table 7-5
CEREBRAL PERFUSION NEUROANATOMY RELATED TO
NEUROLOGIC DEFICIT
1550
Vessel Area Supplied Deficit
Internal Right or left hemisphere Contralateral motor or sensory deficit, aphasia with
carotid dominant hemisphere, neglect with nondominant
artery hemisphere, contralateral visual field deficit
(hemianopia), contralateral eye deviation
Middle Right or left convex surface of Contralateral hemiplegia (arm and face and leg),
cerebral the brain, most of the basal sensory involvement, aphasia of dominant
artery ganglia, internal capsule, hemisphere, neglect of nondominant hemisphere
putamen, and globus pallidus (denial of weakness), homonymous hemianopsia
Anterior Right or left frontal lobe, Weakness or sensory loss of contralateral leg and
cerebral corpus callosum, caudate proximal arm; behavior disturbance: abulia,
artery nucleus, internal capsule confusion, memory loss, urinary incontinence
Posterior Midbrain thalamus, choroid Contralateral visual field deficit, color blindness,
cerebral plexus, occipital lobe, and impaired depth perception, occasional sparing of
artery medial temporal lobe central vision, memory loss, sensory loss,
nystagmus, pupillary abnormalities, ataxia
Vertebral Medulla and/or cerebellum Face, nose, or eye ipsilateral numbness with
artery contralateral body numbness, facial weakness,
vertigo, ataxia, nystagmus, dysphagia, dysarthria
Basilar Pons, midbrain, and/or Quadriplegia or hemiplegia/paresis, dysarthria,
artery locked-in syndrome (pons) dysphagia, ataxia, nystagmus, vertigo, coma
cerebellum
1551
Disrupted tissue and the ruptured vessel reduce normal blood flow
to the area that surrounds the already injured brain tissue, resulting
in some ischemic injury. Intracerebral blood may rupture into the
ventricles, creating risk for communicating hydrocephalus. Lobar
hemorrhages are less common and most often occur in older adults
with cerebral amyloid angiopathy. Other common causes of
hemorrhage include vascular anomalies such as arterial venous
malformations (AVMs), arterial venous fistulas (AVFs), vasculitis,
neoplasms, hematologic disorders, and stimulant abuse (e.g.,
cocaine, amphetamines). Tighter BP control in the setting of acute
ICH to less than 160/90 mm Hg can limit the increase in ICH size
during the acute period.
Table 7-6
HEMORRHAGIC LOCATIONS AND SYNDROMES
Area Syndrome
Putamen Contralateral hemiplegia, hemisensory loss, hemianopsia, slurred speech
Thalamic Contralateral hemiplegia; hemisensory loss; small, poorly reactive pupils; decreased
level of consciousness
Pontine Locked-in syndrome (awake, aware, unable to verbally communicate,
quadriplegia), coma
Cerebellar Occipital headache, ataxia, dizziness, headache, nausea, vomiting
Lobar Mimics cerebral infarct (e.g., contralateral motor and sensory signs)
1552
stroke with residual disability, and history of recent surgeries,
bleeding, or any previous history of ICH.
1553
rapidly decreasing GCS scores, or compromised
ventilation require emergent airway control via
rapid sequence intubation.
1554
• Blood glucose should be maintained with a goal of
normoglycemia (less than 180 mg/dL).
Normoglycemic patients should not be given IV
fluids with excessive glucose, to avoid exacerbation
of ischemic injury resulting from hyperglycemia.
1555
• Obtain information regarding baseline neurologic function (e.g.,
dementia, previous stroke, and neuropathy) and identify risk
factors associated with stroke.
• Women more often report stroke symptoms such as face and limb
pain, hiccups, nausea, general weakness, chest pain, palpitations,
fainting, shortness of breath, and seizures. Further research is
being conducted to better understand the gender differences
related to stroke.
1556
• Symptoms of ICH depend on the size and location of the
hematoma. A relatively small hemorrhage into the brainstem
may produce quadriplegia and coma, whereas a hematoma of
similar size in the basal ganglia may produce hemiparesis
without altered LOC. A larger hematoma (as measured by CT
brain scan) may indicate a poorer prognosis.
Screening labwork
• Biochemical profile: Evaluates for abnormal glucose and
electrolyte imbalances.
1557
neurologic changes.
1558
Collaborative management
AMERICAN HEART ASSOCIATION/AMERICAN STROKE
ASSOCIATION GUIDELINES FOR ACUTE ISCHEMIC STROKE AND
HEMORRHAGIC STROKE MANAGEMENT ARE THE MOST
REFERENCED PUBLICATIONS FOR SETTING THE STANDARDS
OF PRACTICE
*
Indicators for both acute ischemic stroke and intracranial hemorrhage.
Care priorities
1559
Goals of management are to prevent secondary neurologic damage,
secondary complications, and to promote optimal functional
outcome. Early detection via accurate neurologic examination and
immediate medical or surgical intervention help prevent stroke
extension, increased brain edema, and hydrocephalus. Physical
examination findings guide medical and nursing interventions. The
Joint Commission requires the following list of interventions for
certified stroke centers: initiation of DVT prophylaxis, discharge on
antithrombotic medications, anticoagulation therapy for patients
with atrial fibrillation/flutter, administration of thrombolytic
therapy, initiation of antithrombotic therapy by the end of the
second hospital day, stroke education, and assessment for
rehabilitation.
1560
neurologic examinations every 30 minutes for 6 hours and then
every hour for 16 hours. Heparin, aspirin, clopidogrel,
dipyridamole, or warfarin should NOT be given for the initial 24
hours, after which these antithrombotic agents should be started
as prescribed. During and following infusion, monitor for major
and minor bleeding complications. Continuous cardiac
monitoring should remain in place for at least 72 hours.
HIGH ALERT!
If the patient experiences profound deterioration in neurologic
status during recombinant tissue plasminogen activator (rtPA)
infusion, a hemorrhagic complication may have ensued. If
suspected, the rtPA infusion should be discontinued immediately.
Subsequent measurements include vital signs and neurologic
assessments every 15 minutes, and consideration of
hyperventilation, mannitol infusion, administration of blood
products (cryoprecipitate, fresh-frozen plasma, platelets, factor
VIIa, and packed red blood cells), possible initiation of
hemodynamic monitoring, and further neurodiagnostic testing and
laboratory tests to evaluate the potential for further bleeding.
Antithrombotic Therapy: Antithrombotics should be ordered
within the first 24 hours of admission for those who are ineligible
for thrombolysis. Continuous cardiac monitoring should be
provided for up to 48 hours for patients ineligible for thrombolysis.
1561
patient is converted to oral warfarin (Coumadin) therapy or
newer anticoagulants, including direct thrombin inhibitors.
1562
on the individual’s medical history. Long-term therapy may be
prescribed based on the Eighth Joint National Committee (JNC 8)
guidelines (Table 7-7). SBP is often elevated in the acute phase and
requires vasoactive IV medications such as nicardipine (Cardene
IV) or labetalol (Normodyne). Hypotension is a concern, especially
in the patient with ICH, because MAP is decreased. If MAP is
decreased in the presence of normal or elevated ICP, a decrease in
CPP results, further compromising neurologic status. Vasopressors
and/or inotropes may be titrated to keep MAP high enough to
maintain CPP greater than 60 mm Hg.
Acute Ischemic Stroke:
1563
Intracranial Hemorrhage:
The AHA/ASA guidelines recommend the following for
management of BP in patients with ICH/acute cerebral hemorrhage:
1564
• ICP monitoring: Ensure an adequate wave form, zero balance
equipment, and patency of tubing (if applicable), and maintain
sterility of system. Increased ICP is attributable to extension of
the infarct or hematoma and its associated edema. May cause
midline shift and herniation; increased ICP is associated with
hydrocephalus after ICH; seizures generally occur within the first
24 hours but may present at any time.
Table 7-7
CLASSIFICATION AND MANAGEMENT OF BLOOD PRESSURE
FOR ADULTS
*
ACEIs and ARBs should not be used in combination. Beta-blockers, aldosterone
1565
antagonists, or other antihypertensives may be added if initial therapy combination is
ineffective.
†
Initial combined therapy should be used cautiously in those at risk for orthostatic
hypotension.
From Dennison-Himmelfarb C, Handler J, Lackland DT, et al: 2014 evidence-based
guideline for the management of high blood pressure in adults report from the panel
members appointed to the Eighth Joint National Committee (JNC 8). JAMA 311:507-
520, 2014.
ACEI, Angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker;
BP, blood pressure; CCB, calcium channel blocker.
6. Manage agitation
1566
Antibiotics are given immediately after lumbar puncture or
CT and after blood cultures.
Table 7-9
MAINTENANCE OF NORMAL REGULATORY FUNCTIONS IN
STROKE
1567
maintain normal circulating
blood volume.
Digestion and Prevent aspiration pneumonia: NPO until ability to swallow has been
bowel Swallowing dysfunction may be evaluated within the 24 hours of
elimination present. Reduce incidence of stress hospitalization. Bedside swallow may
ulcers and constipation: Straining precede modified barium swallow.
with bowel movements increases Initiate proton pump inhibitors or H2-
ICP. blockers and a bowel program. H2-
blockers may cause delirium.
Cellular glucose Maintain a normal blood glucose Aggressively manage blood glucose to
supply level: Optimizes brain cell function control hyperglycemia and prevent/treat
by ensuring adequate intracellular hypoglycemia; avoid glucose-containing
supply of glucose. IV solutions in the emergency
department.
Nourishment Maintain an anabolic state; prevent Initiate nutrition as soon as possible;
catabolism: Promote optimal enteral feeding, then long-term diet to
healing opportunity and prevent meet caloric needs; low-Na+, low-fat,
recurrent stroke by controlling weight reduction if needed.
CVD/ASHD risk factors.
Urinary Prevent urinary tract infection and Prevent unnecessary use of urinary
continence skin breakdown: Removal of Foley Foley catheter; remove within 48 hours
catheter may prompt skin if possible; bladder training as soon as
breakdown if the patient is possible.
incontinent.
Mobility and Promote proper body alignment Perform ROM exercises, regular
endurance and muscle strengthening: repositioning; increase activity as
Prevents contractures, DVT, and tolerated; use mobility beds if needed.
complications of immobility. Initiate DVT prophylaxis.
Skin integrity Prevent skin breakdown and Keep skin clean and dry; use pressure
dependent edema relief surfaces.
Communication Develop appropriate Provide pictorial board so that the
communication techniques; patient can point at needs, ask yes and
promotes sense of well-being and no questions that do not require long
facilitates more timely response to answers, provide pencil and paper for
patient needs when requests are those who can write; ensure glasses and
understood. hearing aides are in place for those who
use them.
CO, Cardiac output; CVD/ASHD, cardiovascular disease/atherosclerotic heart
disease; DVT, deep venous thrombosis; HOB, head of the bed; ICP, intracranial
pressure; IV, intravenous; Na1, sodium; NPO, nothing by mouth; O2, oxygen; ROM,
range of motion.
8. Provide rehabilitation
Should begin immediately once stabilized. Consults to a physiatrist,
physical therapist, occupational therapist, and speech therapist
should be made within the first 24 hours. Death within the first
month after stroke is commonly caused by acute MI, pneumonia,
and sepsis, which can result from inactivity. Pulmonary embolism,
DVT, skin breakdown, and depression are also common.
1568
9. Manage seizures
Anticonvulsant therapy is used for seizures in the acute phase.
Generally, the patient is given a loading dose of phenytoin
(Dilantin) or fosphenytoin (Cerebyx), followed by a maintenance
dosage. Benzodiazepines (e.g., Ativan) may be used initially.
Patients with ICH are given seizure prophylaxis, whereas patients
with AIS are managed only when active seizures are present.
Temperature greater than 38° C (100.4° F) should be treated with
acetaminophen.
1569
new or further deterioration of language, cognition, or visual field
per NIHSS (see Table 7-8).
Table 7-8
NATIONAL INSTITUTES OF HEALTH STROKE SCALE (NIHSS)
1570
command, the task should be demonstrated to him or
her (pantomime), and the result scored (i.e., follows
none, one, or two commands). Patients with trauma,
amputation, or other physical impediments should be
given suitable one-step commands. Only the first
attempt is scored.
2. Best Gaze: Only horizontal eye movements will be 0 Normal. ______
tested. Voluntary or reflexive (oculocephalic) eye 1 Partial gaze palsy; gaze
movements will be scored, but caloric testing is not is abnormal in one or
done. If the patient has a conjugate deviation of the eyes both eyes, but forced
that can be overcome by voluntary or reflexive activity, deviation or total gaze
the score will be 1. If a patient has an isolated peripheral paresis is not present.
nerve paresis (cranial nerves III, IV, or VI), score a 1. 2 Forced deviation, or
Gaze is testable in all aphasic patients. Patients with total gaze paresis not
ocular trauma, bandages, preexisting blindness, or other overcome by the
disorder of visual acuity or fields should be tested with oculocephalic maneuver.
reflexive movements, and a choice made by the
investigator. Establishing eye contact and then moving
about the patient from side to side will occasionally
clarify the presence of a partial gaze palsy.
3. Visual: Visual fields (upper and lower quadrants) are 0 No visual loss.
tested by confrontation, using finger counting or visual 1 Partial hemianopia.
threat, as appropriate. Patients may be encouraged, but 2 Complete hemianopia.
if they look at the side of the moving fingers 3 Bilateral hemianopia (blind
appropriately, this can be scored as normal. If there is including cortical blindness).
unilateral blindness or enucleation, visual fields in the
remaining eye are scored. Score 1 only if a clear-cut
asymmetry, including quadrantanopia, is found. If the
patient is blind from any cause, score 3. Double
simultaneous stimulation is performed at this point. If
there is extinction, the patient receives a 1, and the
results are used to respond to item 11.
4. Facial Palsy: Ask or use pantomime to encourage the 0 Normal symmetrical
patient to show teeth or raise eyebrows and close eyes. movements.
Score symmetry of grimace in response to noxious 1 Minor paralysis (flattened
stimuli in the poorly responsive or noncomprehending nasolabial fold, asymmetry on
patient. If facial trauma/bandages, orotracheal tube, smiling).
tape, or other physical barriers obscure the face, these 2 Partial paralysis (total or near-
should be removed to the extent possible. total paralysis of lower face).
3 Complete paralysis of one or
both sides (absence of facial
movement in the upper and
lower face).
5. Motor Arm: The limb is placed in the appropriate 0 No drift; limb holds 90 (or 45)
position: extend the arms (palms down) 90 degrees (if degrees for full 10 seconds.
sitting) or 45 degrees (if supine). Drift is scored if the 1 Drift; limb holds 90 (or 45)
arm falls before 10 seconds. The aphasic patient is degrees, but drifts down before
encouraged using urgency in the voice and pantomime, full 10 seconds; does not hit bed
but not noxious stimulation. Each limb is tested in turn, or other support.
beginning with the nonparetic arm. Only in the case of 2 Some effort against gravity; limb
amputation or joint fusion at the shoulder, the examiner cannot get to or maintain (if
should record the score as untestable (UN), and clearly cued) 90 (or 45) degrees, drifts
write the explanation for this choice. down to bed, but has some effort
against gravity.
3 No effort against gravity; limb
falls.
4 No movement.
1571
UN Amputation or joint fusion,
explain: _______
5a. Left Arm
5b. Right Arm
6. Motor Leg: The limb is placed in the appropriate 0 No drift; leg holds 30-degree
position: hold the leg at 30 degrees (always tested position for full 5 seconds.
supine). Drift is scored if the leg falls before 5 seconds. 1 Drift; leg falls by the end of the
The aphasic patient is encouraged using urgency in the 5-second period but does not hit
voice and pantomime, but not noxious stimulation. Each bed.
limb is tested in turn, beginning with the nonparetic leg. 2 Some effort against gravity; leg
Only in the case of amputation or joint fusion at the hip, falls to bed by 5 seconds, but has
the examiner should record the score as untestable (UN), some effort against gravity.
and clearly write the explanation for this choice. 3 No effort against gravity; leg
falls to bed immediately.
4 No movement.
UN Amputation or joint fusion,
explain: _______
6a. Left Leg
6b. Right Leg
7. Limb Ataxia: This item is aimed at finding evidence of a 0 Absent.
unilateral cerebellar lesion. Test with eyes open. In case 1 Present in one limb.
of visual defect, ensure testing is done in intact visual 2 Present in two limbs.
field. The finger-nose-finger and heel-shin tests are UN Amputation or joint fusion,
performed on both sides, and ataxia is scored only if explain: _______
present out of proportion to weakness. Ataxia is absent
in the patient who cannot understand or is paralyzed.
Only in the case of amputation or joint fusion, the
examiner should record the score as untestable (UN),
and clearly write the explanation for this choice. In case
of blindness, test by having the patient touch nose from
extended arm position.
8. Sensory: Sensation or grimace to pinprick when tested, 0 Normal; no sensory loss.
or withdrawal from noxious stimulus in the obtunded or 1 Mild-to-moderate sensory loss;
aphasic patient. Only sensory loss attributed to stroke is the patient feels pinprick is less
scored as abnormal, and the examiner should test as sharp or is dull on the affected
many body areas (arms [not hands], legs, trunk, face) as side; or there is a loss of
needed to accurately check for hemisensory loss. A score superficial pain with pinprick,
of 2, “severe or total sensory loss,” should only be given but the patient is aware of being
when a severe or total loss of sensation can be clearly touched.
demonstrated. Stuporous and aphasic patients will, 2 Severe-to-total sensory loss; the
therefore, probably score 1 or 0. The patient with patient is not aware of being
brainstem stroke who has bilateral loss of sensation is touched in the face, arm, and
scored 2. If the patient does not respond and is leg.
quadriplegic, score 2. Patients in a coma (item 1a = 3) are
automatically given a 2 on this item.
9. Best Language: A great deal of information about 0 No aphasia; normal.
comprehension will be obtained during the preceding 1 Mild-to-moderate aphasia; some
sections of the examination. For this scale item, the obvious loss of fluency or facility
patient is asked to describe what is happening in the of comprehension, without
attached picture, to name the items on the attached significant limitation on ideas
naming sheet, and to read from the attached list of expressed or form of expression.
sentences. Comprehension is judged from responses Reduction of speech and/or
here, as well as to all of the commands in the preceding comprehension, however, makes
general neurologic exam. If visual loss interferes with conversation about provided
the tests, ask the patient to identify objects placed in the materials difficult or impossible.
hand, repeat, and produce speech. The intubated patient For example, in conversation
should be asked to write. The patient in a coma (item 1a about provided materials, the
1572
= 3) will automatically score 3 on this item. The examiner can identify picture or
examiner must choose a score for the patient with stupor naming card content from the
or limited cooperation, but a score of 3 should be used patient’s response.
only if the patient is mute and follows no one-step 2 Severe aphasia; all
commands. communication is through
fragmentary expression; great
need for inference, questioning,
and guessing by the listener.
Range of information that can be
exchanged is limited; listener
carries burden of
communication. The examiner
cannot identify materials
provided from the patient
response.
3 Mute, global aphasia; no usable
speech or auditory
comprehension.
10. Dysarthria: If the patient is thought to be normal, an 0 Normal.
adequate sample of speech must be obtained by asking 1 Mild-to-moderate dysarthria;
the patient to read or repeat words from the attached the patient slurs at least some
list. If the patient has severe aphasia, the clarity of words and, at worst, can be
articulation of spontaneous speech can be rated. Only if understood with some difficulty.
the patient is intubated or has other physical barriers to 2 Severe dysarthria; the patient’s
producing speech, the examiner should record the score speech is so slurred as to be
as untestable (UN), and clearly write an explanation for unintelligible in the absence of
this choice. Do not tell the patient why he or she is being or out of proportion to any
tested. dysphasia, or is mute/anarthric.
Intubated or other physical
barrier, explain:
11. Extinction and Inattention (formerly Neglect): 0 No abnormality.
Sufficient information to identify neglect may be 1 Visual, tactile, auditory, spatial,
obtained during the previous test. If the patient has a or personal inattention or
severe visual loss preventing visual double extinction to bilateral
simultaneous stimulation, and the cutaneous stimuli are simultaneous stimulation in one
normal, the score is normal. If the patient has aphasia of the sensory modalities.
but does appear to attend to both sides, the score is 2 Profound hemiinattention or
normal. The presence of visual spatial neglect or extinction to more than one
anosognosia may also be taken as evidence of modality; does not recognize
abnormality. Because the abnormality is scored only if own hand or orients to only one
present, the item is never untestable. side of space.
______
Neurologic Status.
Neurologic monitoring
1573
3. Position the patient to maintain adequate cerebral perfusion.
Keep the HOB at 25 to 30 degrees or less as tolerated for patients
with ischemic stroke. Keep the HOB raised at 30 degrees as
tolerated for patients with hemorrhagic stroke. Avoid extreme hip
flexion. When positioning, monitor tolerance to position change.
1574
1. Turn and position frequently as tolerated. Transfer toward
unaffected side.
1575
Inability to comprehend spoken words. The patient
may respond to nonverbal cues.
1576
their speech may not speak sensible language but may think they
are making sense.
8. Ensure that call light is available and the patient knows how to
use it. If the patient is unable to use call light, check frequently and
anticipate needs to ensure safety and trust.
Selected references
1. Adams HP Jr, del Zoppo G, Alberts MJ. (published
corrections appear in Stroke 38:e38, 2007, and 38:e96, 2007)
Guidelines for the early management of adults with
ischemic stroke: a guideline from the American Heart
Association/American Stroke Association Stroke Council,
Clinical Cardiology Council, Cardiovascular Radiology and
Intervention Council, and the Atherosclerotic Peripheral
Vascular Disease and Quality of Care Outcomes in Research
Interdisciplinary Working Groupsthe American Academy
of Neurology affirms the value of this guideline as an
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CHAPTER 8
Endocrinologic
disorders
Endocrine assessment
Assessment of the endocrine system is complex when assessing the
system as a whole because it regulates all body functions in
conjunction with the nervous system. Focusing on assessment
appropriate to critically ill patients, the following principles should
be considered:
1587
FIGURE 8-1 Endocrine system: hypothalamic-pituitary
axis feedback loop.
1588
hyperglycemia, adrenal crisis, and myxedema coma. Patients with
adequate function of the pancreas, thyroid, and adrenal glands
under normal conditions may not be able to maintain balance when
exposed to the stress of critical illness. Those with underlying
hypofunction are more likely to experience crises.
1589
are found to have underlying endocrine dysfunction.
1590
The most common disease process associated with adrenal
insufficiency is severe sepsis with pituitary suppression.
Inappropriately rapid withdrawal of pharmacologic steroids can
also result in a crisis during critical illness or may cause critical
illness. Adrenal crisis is also associated with acute exacerbation of
chronic adrenocortical insufficiency in patients who become
stressed by sepsis, surgery, adrenal hemorrhage (septicemia-
induced Waterhouse-Friderichsen syndrome from
meningococcemia), and anticoagulation complications. There are
approximately 50 total hormones produced by the adrenal glands,
with cortisol and aldosterone being by far the most abundant.
If primary adrenal insufficiency is the cause of the crisis, the
adrenal glands are the root cause of the problem. Addison disease
manifests when the entire adrenal cortex is destroyed, which stops
the production of glucocorticoids (cortisol) and mineralocorticoids
(aldosterone). Glucocorticoids are essential hormones produced by
the adrenal cortex that help maintain vascular tone and cardiac
contractility, facilitate wound healing, and support immunity.
Cortisol deficiency intensifies the clinical effects of hypovolemia by
promoting a decrease in vascular tone, which is partially related to
unopposed endothelial production of nitric oxide, and a decreased
vascular response to the catecholamine hormones epinephrine and
norepinephrine. Relative hypoglycemia may be present, as the
breakdown of stored glycogen is not possible without cortisol.
Mineralocorticoid hormones are primary regulators of fluid and
electrolyte balance, and, when unavailable, patients experience
hyponatremia, hypovolemia, hyperkalemia, and metabolic acidosis.
Large amounts of sodium and water are excreted in the urine.
Severe hypotension, shock, and eventually death may occur
without intravenous (IV) adrenocortical hormone and fluid
replacement. In patients with chronic primary adrenocortical
insufficiency or Addison disease, physical stress or trauma may
exacerbate a crisis. Acute crises may be prevented by tripling
hormone replacement doses during periods of stress.
Primary adrenal insufficiency is relatively rare, can be acute or
chronic, and is most often caused by autoimmune-mediated,
idiopathic atrophy. Other causes include tuberculosis, fungal
infection, hemorrhage, congenital adrenal hyperplasia, enzyme
1591
inhibitors (e.g., metyrapone), cytotoxic agents (e.g., mitotane), and
other diseases infiltrating the adrenal glands.
Secondary adrenal insufficiency results from any process that
involves the hypothalamus and/or pituitary gland which reduces
corticotropin secretion. Inflammatory mediators or trauma may
suppress or damage the hypothalamus or pituitary. Pituitary or
other tumors may impair pituitary function or, in rarer cases,
produce glucocorticoids, which suppress the hypothalamic-
pituitary axis.
Exogenous or pharmacologic glucocorticoids (e.g.,
hydrocortisone) elevate the circulating level of the hormones, which
results in hypothalamic-pituitary-adrenal axis dysfunction. With
higher levels of circulating glucocorticoids, the adrenal glands do
not receive signals to produce endogenous cortisol. When
glucocorticoid therapy is abruptly discontinued or weaned too
quickly, the adrenal gland cannot immediately respond, given the
axis has been “turned off” during pharmacologic therapy and the
patient experiences adrenal crisis.
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and result in osmotic changes that temporarily recruit volume from
the intracellular fluid. Catecholamines not only augment vascular
tone but also liberate free fatty acids to fuel the heart and skeletal
muscles and hepatic gluconeogenesis and to serve as substrates for
hepatic ketone body production. If sustained, however, these
profound responses come with substantial costs. Substrate
mobilization via proteolysis results in unsustainable losses of
structural and muscle proteins that manifest as atrophy and
wasting. Unbalanced stress metabolism leads to hyperglycemia
with far-reaching effects on immune competence and neurologic
morbidities. Often the presenting signs are hemodynamic
instability and persistent hypotension, as well as a
petechial/purpuric rash. This syndrome is complicated by
hypoglycemia, hyponatremia, and hyperkalemia. It is a medical
emergency and needs to be treated urgently with antibiotics and
hydrocortisone. Critical illness-induced adrenal insufficiency is not
readily identified by all practitioners. Patients with pituitary
dysfunction generally do not require mineralocorticoid
replacement, because the release of aldosterone is dependent on
release of angiotensin II rather than ACTH from the pituitary.
8-1
RESEARCH BRIEF
Sprung and colleagues published a multicenter, double-blind,
randomized clinical trial in 2008. Fifty-two ICUs enrolled 500
patients who were older than 18 years of age with onset of septic
shock within the previous 72 hours (SBP less than 90 mm Hg
systolic despite fluids or need for vasopressors for longer than 1
hour). An ACTH 250 µg stimulation test was performed on all
patients meeting criteria. Nonresponders were those patients
whose serum cortisol level rose less than 9 µg/dL after stimulation.
All of these patients then received hydrocortisone dosing or
placebo. Hydrocortisone was administered in the following pattern
of deceleration:
1593
2. 50 mg IV every 12 hours on Days 6 to 8
1594
Observation and vital signs: Primary (first-degree)
insufficiency only
• Prominent nausea and vomiting, weight loss
1595
At this time, free cortisol is the most reliable test.
1596
The 2012 Surviving Sepsis Campaign Guidelines recommend
an evidence-based protocol approach to possible adrenal
insufficiency in severe sepsis:
1597
Collaborative management
DIAGNOSIS AND MANAGEMENT OF CORTICOSTEROID
INSUFFICIENCY IN CRITICALLY ILL PATIENTS
From Marik PE, Pastores SM, Annane D, et al: Crit Care Med 36:1937–1949, 2008.
1598
Care priorities
1. Correct hypovolemia
Initiate replacement of intravascular fluid volume. Rapid volume
replacement is essential, using normal saline crystalloid IV solution.
Administer 1 L over the first hour, followed by an additional 1 to 2
L over the next 6 to 8 hours. If hypovolemia persists,
colloid/volume-expanding IV solutions may be necessary.
2. Manage hypotension
Use vasopressors if intravascular volume replacement fails to
effectively increase BP (see Appendix 6). Response to catecholamine
infusions (epinephrine, norepinephrine, dopamine) is reduced in
adrenal insufficiency; higher-than-normal doses may be needed to
manage refractory hypotension.
3. Replace cortisol
During stressful situations, the normal adrenal gland output of
cortisol is approximately 250 to 300 mg over 24 hours. IV
hydrocortisone should be given only to adult patients with septic
shock after it has been confirmed their BP is poorly responsive to
fluid resuscitation and vasopressor therapy.
1599
to 75 mg over 24 h) and eventually to daily oral replacement
doses when oral intake is possible.
1600
Deficient fluid volume
related to failure of regulatory mechanisms secondary to impaired
secretion of aldosterone, causing increased sodium excretion with resultant
diuresis.
Goals/Outcomes: Within 12 hours of initiating treatment, the
patient is moving toward normovolemia as evidenced by BP
approaching normal range; heart rate (HR) 60 to 100 beats/min
(bpm); respiratory rate (RR) 12 to 20 breaths/min with normal
pattern and depth, or, if on the ventilator, weaning from the
ventilator; central venous pressure (CVP) 2 to 6 mm Hg; if
hemodynamic monitoring is in place, pulmonary artery wedge
pressure (PAWP) approaching 6 to 12 mm Hg; normal sinus
rhythm on electrocardiogram (ECG); and improvement in level of
consciousness (LOC).
Fluid Balance
1601
extremities, muscle weakness. Be aware that
hyperkalemia will worsen in the presence of
metabolic acidosis.
5. Monitor ECG continuously; observe for potassium-related
changes. Increased ventricular irritability may signal hypokalemia.
(See Fluid and Electrolyte Disturbances, Hypokalemia, Chapter 1.)
Box 8-1
PATIENT AND FAMILY EDUCATION
CONCERNING GLUCOCORTICOID AND
MINERALOCORTICOID REPLACEMENT
Glucocorticoids (e.g., cortisone acetate, prednisone)
Glucocorticoids (e.g., Cortisone Acetate, Prednisone) and
mineralocorticoids: two-thirds of dose in the morning and one-
1602
third of dose in the afternoon).
1603
stable weight, urine output less than 80 to 125 mL/h, HR 60 to 100
bpm, BP within the patient’s normal range, and normothermia.
Immune Status; Infection Status; Energy Conservation
Energy management
1604
1. Teach the patient about prescribed medications, including
purpose, dosage, route of administration, and potential side effects
(Box 8-1). Medication administration should mimic normal diurnal
pattern of plasma cortisol levels (e.g., two-thirds in the morning
and one-third in late afternoon).
Diabetes insipidus
Pathophysiology
Diabetes insipidus (DI) is a metabolic disorder that affects total
body free water regulation, resulting in an abnormally high output
of extremely dilute urine, increased fluid intake, and constant thirst.
The volume of hypotonic urine excreted is 3 to 20 L per day.
1605
Vasopressin (antidiuretic hormone [ADH]) is a key component in
the regulation of fluid and electrolyte balance through direct effects
on renal water regulation. Vasopressin is produced in the
hypothalamus, is stored in the posterior pituitary gland, and exerts
action in the kidneys for water regulation. Three subtypes of
receptors respond to the effects of vasopressin (Table 8-1).
Table 8-1
LOCATIONS AND ACTIONS OF VASOPRESSIN RECEPTORS
When any aspect of water regulation fails, if free water is lost, the
extracellular fluid volume rapidly decreases, causing plasma
osmolality and serum sodium to rise. Plasma osmolality is the main
determinant of vasopressin secretion from the posterior pituitary.
The osmoregulatory systems for thirst and vasopressin secretion,
and the actions of ADH on renal water excretion, maintain plasma
osmolality between 284 and 295 mOsmol/kg. Thirst and drinking
are key processes in the maintenance of fluid and electrolyte
balance. Thirst perception and the regulation of water ingestion
involve complex neural and neurohormonal pathways. Thirst
occurs when plasma osmolality rises above 281 mOsmol/kg, similar
to the threshold for ADH release. The osmoreceptors regulating
thirst are located in the hypothalamus.
Situations that alter the balance between plasma osmolality and
vasopressin concentration include:
1606
• Drinking fluids: Oral fluid consumption rapidly suppresses the
release of ADH, through afferent pathways originating in the
oropharynx.
1607
• Gestational or gestogenic DI results from a lack of vasopressin
that develops during the third trimester of pregnancy if the
pregnant woman’s thirst center is abnormal, causing a blunted
thirst response, and/or the placenta destroys vasopressin too
rapidly. The placenta may increase the action of vasopressinase,
the enzyme that breaks down vasopressin. The condition is
controlled using synthetic vasopressin until the DI resolves.
Vasopressin can generally be discontinued 4 to 6 weeks after
delivery. Signs and symptoms of DI will recur with subsequent
pregnancies.
Table 8-2
FOUR MAJOR SUBTYPES OF DIABETES INSIPIDUS
Subtypes of
Pathophysiology Common Etiology
DI
Central Lack of ADH production by the Head injury, pituitary tumor and
posterior pituitary gland postpituitary tumor resection, cerebral
ischemia, intracerebral hemorrhage, CNS
infection, brain death, idiopathic
Nephrogenic Inability of the kidneys to respond Medications, ethanol abuse, chronic
to normal amounts of ADH hypercalcemia, hypokalemia osmotic
diuresis, congenital disorder, polycystic
kidney disease, pyelonephritis, Sjögren
syndrome, sickle cell anemia
Gestational Blunted thirst response related to Last trimester of pregnancy in women who
pregnancy, and placenta increases have oligohydramnios, preeclampsia, and/or
the action of vasopressinase, hepatic dysfunction
which results in decreased
circulating ADH
Dipsogenic ADH suppression Unquenchable thirst, massive water intake;
Caused by increased fluid intake psychogenic causes may be associated with
mental illness
1608
The most common presentation of DI is following head trauma or
intracranial surgery. When a person cannot adequately respond to
stimulation of the thirst center by drinking fluids, extracellular and
intracellular dehydration may result. Electrolyte imbalance,
primarily hypernatremia, may produce neurologic symptoms
ranging from confusion, restlessness, and irritability to seizures and
coma. DI sometimes occurs in brain-dead organ donors and must
be managed to effectively preserve organs.
In normal individuals, a more concentrated circulating volume
stimulates ADH release through activation of osmoreceptors that
monitor serum osmolality. ADH is also released as part of the
renin-angiotensin-aldosterone mechanism as a result of
hypotension sensed by the juxtomedullary apparatus located
outside the glomerulus of the kidney. A 5% to 10% decrease in
arterial BP is necessary to increase circulating vasopressin
concentrations. Progressive hypotension in individuals who are
healthy results in an exponential increase in plasma ADH via
baroreceptor stimulation, whereas osmoregulated ADH release in
response to dehydration is more linear. If the hypothalamus is
damaged, production of ADH may not be possible and both the
ability to regulate circulating volume and vascular tone may be
affected. Baroregulated (pressure response) release of vasopressin is
a key physiologic mediator in an integrated hemodynamic response
to volume depletion.
1609
electrolyte imbalance must be prevented or managed immediately
to avoid possible organ damage.
1610
(hyponatremia).
Vital signs
• Tachycardia and tachypnea are present with dehydration.
Observation
• Polyuria with dilute urine; 3 to 20 Ld of urine may be excreted,
with specific gravity of 1.000 to 1.005.
• Extreme thirst
1611
DI, but if DI develops in a critically ill patient,
readings typically reflect hypovolemia.
• Altered mental status: Serum hyperosmolality and hypernatremia
affect consciousness and behavior. Changes may also be related
to the underlying disease.
Auscultation
• In rare cases, bowel sounds may be lessened if hypovolemic
shock has reduced abdominal vessel perfusion.
1612
c. Urinary and serum osmolality: Values may
become similar. When kidneys properly
concentrate urine, urine osmolality is generally
four times the value of serum osmolality.
Collaborative management
Care priorities
1613
• Place at least two large-bore IV lines, or have a central line
inserted.
1614
patient’s response to DI management. Vasopressin’s potential
vasoconstrictive effects occur rarely with appropriate dosing for
management of DI. Excessive dosing of ADH may cause
hypertension and cardiac symptoms; other side effects include
abdominal cramping and increased peristalsis.
Table 8-3
VASOPRESSIN PREPARATIONS
1615
deprivation test and ADH test. A thorough history and physical
examination may help identify possible causes. Consider NDI in
the elderly patients using polypharmacy. Consider NDI in
patients with a history of mental illness. NDI can occur in
patients with a remote history of lithium use.
1616
Fluid Balance, Electrolyte and Acid-Base Balance, Hydration
Hypovolemia management
1. Monitor vital signs every 15 minutes until the patient is stable for
1 hour. Monitor CVP, MAP, and, if hemodynamic monitoring was
in place, pulmonary artery pressure (PAP), and pulmonary
capillary wedge pressure (PCWP), if ordered. Consult advanced
practice provider for the following: HR greater than 140 bpm or BP
less than 90/60 mm Hg or decreased more than 20 mm Hg from
baseline, or MAP decreased more than 10 mm Hg from baseline,
CVP less than 2 mm Hg, and PAWP less than 6 mm Hg. Manage
judiciously in all patients, including organ donors who are brain-
dead.
5. Weigh the patient daily, at the same time and using the same
scale and while the patient is wearing the same garments to prevent
error. Consult an advanced practice provider for weight loss greater
than 1 kg/d.
1617
membranes, hypotension).
Fluid/electrolyte management
1618
Goals/Outcomes: The patient verbalizes orientation to time,
place, and person; the patient is protected from unnecessary
complications and bodily injury.
Cognitive Orientation
Surveillance
2. Keep bed in lowest position with side rails raised if the patient is
confused.
Neurologic Monitoring
Infection protection
1619
indicates a flaw in cranial bone integrity. (See Care of the Patient
After Intracranial Surgery, Chapter 7.)
Teaching: Procedure/treatment
1620
gland was damaged or removed during surgery. If the patient is
also experiencing anterior pituitary dysfunction
(panhypopituitarism), teach the indicators of hormone replacement
excess or deficiency.
1621
card outlining diagnosis and appropriate treatment in the event of
an emergency.
Hyperglycemia
Pathophysiology
Over the last several decades, the incidence of diabetes mellitus has
risen. According to the 2014 National Diabetes Statistics Report,
29.1 million Americans, or 9.3% of the U.S. population, have
diabetes. Of these, 8.1 million people are undiagnosed. The disease
is associated with serious complications, including heart disease,
stroke, kidney disease, various eye diseases, and nerve damage,
which contribute to increased medical costs. Direct costs of care are
about $176 billion dollars; 2.3 times higher than for people without
diabetes.
Type 1 and type 2 diabetes result from separate causes. People
with type 1 diabetes are genetically predisposed to a trigger, often a
viral illness, which results in destruction of the insulin-producing
beta cells in the pancreas, leading to an abrupt, permanent loss of
insulin production. Insulin is the hormone that attaches cells,
allowing passage of glucose from the bloodstream into the cell.
People with type 1 diabetes require daily insulin injections to
support their basal metabolic needs and to manage hyperglycemia
resulting from food ingestion.
People with type 2 diabetes are initially insulin-resistant and
1622
subsequently have a gradual decline in insulin production and
secretion over years of time. T-defective cellular insulin receptors
do not allow transport of glucose into the cell by insulin. The lack of
receptor insulin sensitivity is associated with increased hepatic
glucose production, given cells “signal” that the intracellular
environment lacks glucose needed to produce sufficient energy for
effective cellular function of all organs and body systems.
Additional hepatic glucose production further increases blood
glucose levels. Type 2 diabetes is initially treated with oral agents
and is likely to require insulin as the disease progresses.
The importance of managing hyperglycemia in hospitalized
patients came to the forefront in 2001 with a landmark study by
Van den Berghe and colleagues. The study revealed dramatic
improvement in outcomes of postoperative cardiovascular surgical
intensive care patients when glucose was maintained at 80 to 110
mg/dL using IV insulin as opposed to a conventional treatment goal
of 180 to 200 mg/dL. With this goal for “tight control,” patients with
no previous history of diabetes often required treatment as well
because, postoperatively, the stress response elevated blood
glucose. After 12 months of study, intensive insulin therapy
reduced ICU mortality to 4.6% from 8.0% with conventional
therapy (P < 0.04 with adjustment for sequential analyses). For
patients who remained in the unit longer than 5 days, mortality
using intensive insulin therapy was reduced to 10.6% from 20.2%
using conventional therapy. Total in-hospital mortality was
reduced 34%, BSIs by 46%, acute renal failure requiring dialysis or
hemofiltration by 41%, the median number of red blood cell
transfusions by 50%, and critical illness polyneuropathy by 44%.
The greatest reduction in mortality involved deaths caused by
multiple organ failure with a proven sepsis focus. Many hospitals
found this target unachievable, given that the risk of hypoglycemia
was too high, unless there was a knowledgeable champion to
oversee safe, effective, and efficient methods of insulin
administration.
The Van den Berghe study raised awareness of the importance of
glycemic control. In early 2009, the NICE SUGAR study improved
practice by providing a more realistic, safer, and achievable target
glucose range. The trial highlighted the unacceptably high
1623
incidence of hypoglycemia seen with tight control and
recommended hypoglycemia could be avoided while maintaining
glucose control using a less stringent target. On the basis of this
study, the American Diabetes Association (ADA) and American
Association of Clinical Endocrinologists (AACE) now recommend
patients who are critically ill be controlled to glucose values of 140
to 180 mg/dL. For more stable hospitalized patients who are eating
meals, the recommendation is for premeal blood glucose values be
less than 140 mg/dL. There are patients who may benefit from a
lower target, but, given the nature of critical illness, the target
glucose range should not be lower than 110 mg/dL for patients who
are critically ill. The Society of Thoracic Surgeons recognizes use of
IV insulin for cardiac surgery patients to maintain a target of 110 to
140 mg/dL as a class I treatment recommendation.
No “best” method for dosing and delivery of IV insulin has
been established. Evidence revealed insulin binds to IV tubing, and
therefore 20 to 50 ml must be flushed through the tubing into an
external receptacle before initiating the insulin infusion. Binding
sites within the wall of the tubing are “saturated” with insulin by
this procedure, allowing for all insulin within the infusion to be
delivered to the patient. There are no guidelines for standardization
of a “loading dose” or initial IV bolus, at what rate to begin the
infusion, or titration to the patient’s response. Thus, glucose
management targets have been set without a “road map” for how
to safely achieve them. Institutions are best served to have an
interprofessional committee decide the type of dosing and
monitoring regimen that is both safe and feasible. The patient
population, available infusion pumps, nurse and physician
expertise with evidence-based hyperglycemia management
practices, nurse staffing, and physician support must be considered
to both control blood glucose and protect patients from
hypoglycemia. Many published protocols require hourly glucose
monitoring and dosage adjustment. Given the workload associated
with hourly monitoring, several computerized insulin-dosing
systems are available to assist nurses with ongoing infusion
management.
Despite quality organizations and insurers’ familiarity with the
challenges of glycemic control, in October 2009, occurrences of
1624
hypoglycemia, diabetic ketoacidosis (DKA), and hyperglycemic
hyperosmolar syndrome (HHS) were deemed “never events” for
hospitalized patients. If patients can be harmed by the occurrence of
a problem acquired in the hospital, insurers are not required to pay
for care associated with a selection of those events considered
preventable. If patients are admitted with a history of the selected
condition, hospitals are paid if the problem reoccurs during
hospitalization. Careful admission screening of all patients related
to past experience with both hyperglycemia and hypoglycemia is of
paramount importance to realize payment for treatment of the
patients.
Diabetic ketoacidosis
Pathophysiology
DKA is a life-threatening complication of diabetes mellitus
characterized by hyperglycemic crisis, ketosis, acidosis,
hypovolemic shock caused by dehydration, and electrolyte
imbalance involving potassium. Progressive hyperglycemia occurs
because of inadequate circulating insulin, preventing cellular
uptake of glucose and resulting in a state of starvation at the
cellular level. Without glucose available inside the cells, the cells are
unable to perform their work effectively. Starvation prompts
glucagon secretion from the pancreas and release of other stress
hormones, including catecholamines, cortisol, and GH, which
facilitate glycogenolysis and gluconeogenesis, further raising
plasma glucose. Intracellular hypoglycemia continues to prompt a
series of responses in an effort to produce glucose to “feed” the
“starving cell.” Proteolysis and lipolysis ensue, forming free fatty
acids, which are converted to ketoacids (acetoacetate, β-
hydroxybutyrate, and acetone), caused by lack of intracellular
glucose required for normal metabolic conversion of the acids.
Accumulation of ketones creates a metabolic acidosis. The
excessive glucose and ketones in the blood cause severe osmotic
diuresis as intracellular fluids move into the vascular compartment
to dilute the blood; however, the excess fluid is eliminated by the
kidneys, which also lose the ability to effectively eliminate excess
1625
glucose. A vicious cycle of progressive metabolic disruption begins
and will continue until hydration, insulin, and additional
management of acidosis/fluid and electrolyte imbalance are
provided. Osmotic diuresis causes loss of sodium, potassium,
phosphorus, magnesium, and body water, which leads to
dehydration and, possibly, hypovolemic shock. Increased blood
viscosity and platelet aggregation can result in thromboembolism.
Despite significant loss of potassium in the urine, the patient may
initially manifest normal or elevated plasma potassium because of
the dramatic shift of potassium out of the cells secondary to insulin
deficiency, acidosis, and tissue catabolism. Dehydration lowers BP
and decreases tissue perfusion. Because of a lack of oxygen
delivery, cells begin anaerobic metabolism. The resulting lactic acid
waste products worsen acidosis. Low pH stimulates the respiratory
center, producing deep, rapid Kussmaul respirations. Abundant
plasma ketones cause fruity or acetone breath. If not managed,
elevated serum osmolality, acidosis, and dehydration depress
consciousness to a coma state. Death can result.
The cause of death in patients with DKA and the other
hyperglycemic emergency, HHS, is rarely caused by the metabolic
complications of hyperglycemia or metabolic acidosis. Death is
related to the underlying medical illness that caused the metabolic
decompensation. Successful treatment depends on a prompt and
careful evaluation for the precipitating cause(s). The clinical
symptoms of DKA generally appear within 24 hours of failure to
manage hyperglycemia.
1626
hyperglycemia hyperosmolar nonketotic syndrome (HHNS), and,
traditionally, hyperosmolar hyperglycemic nonketotic coma
(HHNK). HHNK, HHNS, HNS, and HONK are somewhat incorrect
titles for the syndrome, as recent evidence reveals a mild degree of
ketosis is often present with HHS, and true coma is uncommon. The
mortality rate of HHS ranges from 10% to 50%, higher than that for
DKA (1.2% to 9%). Mortality data are difficult to interpret because
of the high incidence of coexisting diseases or comorbidities.
Historically, HHS and DKA were described as distinct
syndromes, but one-third of patients exhibit findings of both
conditions. HHS and DKA may be at opposite ends of a range of
decompensated diabetes, differing in time of onset, degree of
dehydration, and severity of ketosis. HHS occurs most commonly
in older people with type 2 diabetes, but with the recent obesity
epidemic, occasionally obese children and teenagers with both
diagnosed and undiagnosed type 2 diabetes manifest HHS. The
cascade of events in HHS begins with osmotic diuresis. Glycosuria
impairs the ability of the kidney to concentrate urine, which
exacerbates the water loss. Normally, the kidneys eliminate glucose
above a certain threshold and prevent a subsequent rise in blood
glucose level. In HHS, the decreased intravascular volume or
possible underlying renal disease decreases the glomerular
filtration rate, causing the glucose level to increase. More water is
lost than sodium, resulting in hyperosmolarity. Insulin is present,
but not in adequate amounts to decrease blood glucose levels, and
with type 2 diabetes, significant insulin resistance is present. DKA
and HHS are compared in Table 8-4.
Table 8-4
COMPARISON OF DIABETIC KETOACIDOSIS (DKA) AND
HYPERGLYCEMIC HYPEROSMOLAR SYNDROME (HHS)
1627
Physical Dry and flushed skin, poor skin Same as DKA, but no Kussmaul
assessment turgor, dry mucous membranes, respirations or fruity odor to the breath;
decreased BP, tachycardia, altered instead, occurrence of tachypnea with
LOC (irritability, lethargy, coma), shallow respirations
Kussmaul respirations, fruity odor to
the breath
History Recent stressors such as surgery, Undiagnosed type 2 diabetes mellitus;
and risk trauma, infection, MI; insufficient recent stressors such as surgery, trauma,
factors exogenous insulin; undiagnosed type 1 pancreatitis, MI, infection; high-calorie
diabetes mellitus enteral or parenteral feedings in a
compromised patient; use of diabetogenic
drugs (e.g., phenytoin, thiazide diuretics,
thyroid preparations, mannitol,
corticosteroids, sympathomimetics)
Monitoring ECG: Dysrhythmias associated with ECG evidence of hypokalemia as listed
parameters hyperkalemia: peaked T waves, with DKA Hemodynamic measurements:
widened QRS complex, prolonged PR CVP <3 mm Hg below patient’s baseline;
interval, flattened or absent P wave. PADP and PAWP <4 mm Hg below
Hypokalemia (K+ <3 mEq/L), which patient’s baseline
may produce depressed ST segments,
flat or inverted T waves, or increased
ventricular dysrhythmias
Diagnostic Serum glucose: >250 mg/dL >600 mg/dL
tests
Serum ketones: Large presence Usually absent to mild presence because
of dehydration
Urine glucose: Positive Positive
Urine acetone: “Large” Usually negative
Serum osmolality: >290 mOsmol/L >320 mOsmol/L
Bicarbonate: <15 mEq/L >15 mEq/L
Serum pH: <7.2 Normal or mildly acidotic (pH ≤7.4)
Anion Gap: Elevated >13 Normal
Serum potassium: normal or elevated Normal or >3.5 mEq/L
>5.0 mEq/L initially and then
decreased
Serum sodium: elevated, normal, or Elevated, normal, or low
low
Serum Hct: elevated because of Elevated because of hemoconcentration
osmotic diuresis with
hemoconcentration
BUN: elevated >20 mg/dL Elevated
Serum creatinine: >1.5 mg/dL Elevated
Serum phosphorus, magnesium, Elevated
chloride: decreased
WBC: elevated, even in the absence of Normal unless infection present
infection
Onset A few days Days to weeks
Mortality 1 to 10% 14 to 58% because of age group and
complications such as stroke, thrombosis,
renal failure
BP, Blood pressure; BUN, blood urea nitrogen; CVP, central venous pressure; DKA,
diabetic ketoacidosis; ECG, electrocardiogram; Hct, hematocrit; HHS, hyperglycemic
hyperosmolar syndrome; LOC, level of consciousness; MI, myocardial infarction;
PADP, pulmonary artery diastolic pressure; PAWP, pulmonary artery wedge
pressure; WBC, white blood cell count.
1628
Primary causes of HHS include infections, noncompliance with a
diabetes management regimen, undiagnosed diabetes, medications,
substance abuse, and coexisting diseases. Infections are the leading
cause (57% of patients); pneumonia (often Gram-negative) is the
most common, followed by urinary tract infection (UTI) and sepsis.
Lack of compliance with diabetic medications or other aspects of
diabetes management may be a frequent cause (21%). Undiagnosed
diabetes prompts a failure to recognize early symptoms of the
complications of unmanaged hyperglycemia. Acute coronary
syndrome (myocardial infarction [MI]), stroke, pulmonary embolus,
and mesenteric thrombosis have caused HHS. At least one study
revealed that, in urban populations, the three leading causes are
lack of compliance with medications, drinking alcohol, and using
cocaine. Chronic use of steroids and gastroenteritis are commonly
associated with HHS in children.
The blood glucose level is higher with HHS than with DKA. A
global electrolyte loss is present. Sodium and potassium levels vary
at diagnosis, but deficiencies of both are present. Magnesium,
calcium, phosphate, and chloride deficiencies evolve. Patients may
lose from 15% to 25% of total body water, or approximately 100 to
200 mL/kg. Fluids are drawn from cells to dilute the concentrated
bloodstream, resulting in significant intracellular dehydration.
Neurologic deficits occur in response to severe dehydration and
hyperosmolality. The blood is highly viscous and flow slows,
increasing risk for the formation of thromboemboli. Increased
cardiac workload and decreased renal and cerebral blood flow may
result in MI, renal failure, and stroke.
Unlike DKA, wherein acidosis produces severe symptoms,
HHS develops slowly, and frequently symptoms are nonspecific.
Polyuria and polydipsia occur but may be ignored. Neurologic
deficits may be mistaken for dementia. Similarity of symptoms to
other disease processes in older adults may delay diagnosis and
treatment, allowing the process to progress.
1629
Evaluate for degree of hyperglycemia and its effects on overall
hemodynamics, respiratory rate/pattern, and mental status.
Hyperglycemia may be asymptomatic or, with DKA, result in
hypotension causing decreased perfusion, increased work of
breathing with Kussmaul respirations, ineffective breathing
patterns, abdominal pain, and neurologic deficits, including coma
and/or stroke-like symptoms. HHS findings are similar but are
more likely to result in neurologic changes, cause abdominal pain
less often, and almost never cause compensatory Kussmaul
respirations, because acidosis is mild, if present at all. Dehydration,
hyperglycemia, and acidosis must be managed immediately.
Associated electrolyte imbalances may be managed as the patient’s
glucose level normalizes and hydration is provided.
1630
islet cells in the pancreas, they have no ability to produce insulin.
1631
2. Cardiovascular disease: MI or other acute coronary syndromes
6. Pancreatitis
7. Pulmonary embolism
8. Acute abdomen
10. Burns
11. Hyperthyroidism
12. GI bleeding
Medication-related
1632
7. Glucocorticoids/steroids: Cortisone, hydrocortisone, prednisone,
methylprednisolone
9. Anticonvulsants: Phenytoin
Vital signs
• Findings vary significantly, depending on patient’s situation.
Mild to moderate hyperglycemia generally has no effect on vital
signs.
Observation
• Mild to moderate hyperglycemia alone may not cause overt
physical assessment changes.
1633
• DKA and HHS:
Auscultation
• Hyperglycemia does not change baseline physical assessment,
unless it has progressed to crisis level (DKA, HHS).
1634
present.
• Heart sounds may reflect heart failure with DKA and HHS.
Palpation
• DKA: Abdomen may be palpated if abdominal pain is present.
Percussion
• DKA and HHS: Lung percussion may reveal presence of
consolidation or fluid (dullness) indicative of a pulmonary
infection.
1635
Diagnostic Tests for Hyperglycemia and Hyperglycemic
Emergencies
1636
least 8 hours glucose (FBG) is used at the FBG 111 to 125 mg/dL with 2-hour
of fasting, oral beginning of the test. Additional reading >140 mg/dL: Patient has
glucose is readings are done 2 hours later. impaired glucose tolerance (IGT)
consumed by Fasting readings are compared to 2 FBG 111< to 125 mg/dL with 2-hour
the patient to hours after glucose ingestion to reading >140 mg/dL: Patient has
determine determine extent of glucose impaired fasting glucose (IFT)
how quickly it intolerance.
is cleared from
the blood.
Arterial blood Assess for abnormal gas exchange pH changes: With DKA, may be 6.8 to
gas analysis or compensation for metabolic 7.2; acidosis results from ketosis or
(ABG): derangements in patients in lactic acidosis
Done promptly, hyperglycemic crisis; profound Carbon dioxide: With DKA, decreased
following acidosis can indicate DKA is CO2 reflects tachypnea and
confirmation present, since HHS typically Kussmaul respirations
of presents with minimal to mild Hypoxemia: With DKA or HHS, Pao2
hyperglycemia acidosis unless prolonged, severe <80 mm Hg may indicate
to assess for hypovolemic shock is present. pneumonia precipitated the crisis
DKA and Oxygen saturation: If pneumonia or
HHS. heart failure is present, Sao2 may be
<92%
Bicarbonate:
HHS: HCO32 15 to 22 mEq/L;
DKA: HCO32 may be <15 mEq/L
Base deficit: HHS at or above −2;
DKA, above −10
Complete blood Evaluates for presence of infection Increased WBC count: >11,000/mm3 is
count (CBC) seen with bacterial pneumonias,
urinary tract infections and other
infections.
Sputum Gram Screens for pneumonia, a common Gram stain-positive: Indicates
stain, culture, underlying cause of hyperglycemic organism is present
and sensitivity crisis; identifies infecting organism Culture: Identifies organism
Sensitivity: Reflects effectiveness of
drugs on identified organism
Blood culture Screens for sepsis, a common Secondary bacteremia: A frequent
and sensitivity underlying cause of finding; patients with bacteremia are at
hyperglycemic crisis higher risk for developing respiratory
Identifies whether an organism has failure.
become systemic
Blood chemistry Screens for electrolyte imbalances; DKA and HHS: Hypernatremia is
potassium imbalances may create present: BUN, creatinine, and K1
potentially dangerous dysrhythmias may be elevated, normal, or low.
Anion gap DKA: >13
Anion gap HHS: 10 to 12
Plasma Screens for elevated osmolality Osmolality is increased more with
osmolality associated with severe HHS than with DKA.
hyperglycemia DKA: 290 to 320 mmol/L
HHS: >320 mmol/L
Urine ketones Screens for the presence of ketones DKA: Ketones strongly positive
to confirm diagnosis of DKA; HHS: Ketones negative, or mildly
HHS does not cause ketonuria. positive
12-Lead ECG Used to rule out myocardial Hyperkalemia: Tall, peaked T waves if
infarction as the cause of HHS or increased K+ is present before
DKA management of hyperglycemia,
hypovolemia and acidosis;
1637
PVCs/ventricular irritability is seen
with decreased K+ seen as insulin
normalizes glucose.
Chest Screens for pneumonia and acute “Fluffy whiteness” may not initially be
radiograph respiratory distress syndrome, present caused by dehydration, but
which may prompt DKA and HHS may appear as patient is rehydrated if
patient has underlying pneumonia or
ARDS
Computed Screens for ischemic and Generally not done until patient has
tomography hemorrhagic stroke, which may had at least 1 hour of rehydration and
(CT) brain scan prompt DKA and HHS insulin therapy to see if symptoms
to altered mental resolve spontaneously.
status or “stroke-
like” symptoms
Collaborative management
When managing hyperglycemia in hospitalized patients, the
following key elements should be considered in evaluating current
management blood glucose control strategies:
1638
than 1 mL accurately, and staffing with competent nurses must be
considered before implementation of a glycemic control program.
1639
both glucose control and incidence of hypoglycemia?
Care priorities
HHS:
1640
administered during the first hour of therapy. The remaining 8 L
should ideally be infused within the next 24 hours.
• Once the blood sugar falls below 300 mg/dL, change the IV fluid
to 5% dextrose with 45% NaCl at 150 to 250 ml/h.
DKA:
• Once the blood sugar falls below 300 mg/dL, change the IV fluid
to 5% dextrose with 45% NaCl at 150–250 ml/h.
3. Support hemodynamics/perfusion
Hemodynamic monitoring may be useful in guiding fluid
replacement tolerance and efficacy and may help recognize the
patient’s response to the effects of other comorbidities. Although
hypovolemic shock is the primary problem associated with
hyperglycemia, cardiogenic shock may ensue if the patient has had
1641
an MI, or septic shock is possible if severe infection is present. Use
of catecholamine infusions and steroids should be avoided, if
possible, until hyperglycemia is resolved.
4. Control hyperglycemia
Continuous IV insulin infusion via infusion pump is the preferred
method for delivering insulin. An initial IV insulin bolus may be
administered at 0.1 U/kg. Many institutions use a concentration of 1
U of insulin in 1 mL of IV fluid to simplify rate and dosage
calculations. The IV insulin infusion dose may be initiated at up to
0.1 U/kg/h during crisis states. It is imperative to perform hourly
glucose monitoring for drip titration to ensure effectiveness of the
dosage regimen. If the blood glucose does not decreased by 10%, or
50 mg/dL in the first hour, the infusion dose may need to be
increased by 0.05–0.1 U/kg/h. Titrate the infusion to achieve a
gradual blood glucose decrease of 50–70 mg/dL/h. Once the blood
glucose is below 200 mg/dL for DKA and 300 mg/dL for HHS,
decrease the insulin infusion rate by 50% to very gradually decrease
blood glucose to achieve a target range of 140 to 180 mg/dL. For
blood sugar less than 80 mg/dL, the insulin infusion can be held
(paused) for 1 hour, then restarted at a lower rate. Achievement of
target range or overshooting target range does not mean the insulin
infusion can be permanently discontinued. The rationale is similar
to the use of BP control medications. Achievement of the target is
only the first step to sustained control. The transition from the
insulin drip to a subcutaneous basal/bolus insulin regimen can
occur when the patient can tolerate eating, the blood glucose falls is
200 mg/dL, HCO32 is above 18 mEq/L, pH is higher than 7.3, and
anion gap is normal.
1642
probability of creating hypokalemia. Electrolytes should be
measured every 2 hours. Begin adding 20 to 30 mEq/L potassium to
the IV solution when the level falls below 5.2 mEq/L, with the aim
of keeping the potassium level between 4–5 mEq/L. Should the
potassium level fall below 3.3 mEq/L during the process of
controlling the hyperglycemic crisis, immediately hold (pause) the
IV insulin to slow movement of potassium out of the blood stream
and into the cell, to avoid life-threatening dysrhythmias.
Replacement of calcium, magnesium, and phosphates may be done
as needed. Chlorides are replaced by the normal saline IV solutions.
Use of bicarbonate for management of acidosis is not
recommended, unless the acidosis does not respond to hydration
and insulin or when essential medications needed for support of
hemodynamics fail to work in the acidotic environment (e.g., if
catecholamines are needed to support BP).
Hyperglycemia management
1643
1. Monitor blood glucose levels as ordered or according to protocol.
1644
provide the best opportunity for glycemic control. Explain the
difference in simple (bad) and complex (good) carbohydrates and
how they are metabolized.
13. Ensure the patient understands the need for adherence to the
prescribed diet and exercise regimen.
14. Assess whether or not the patient has the financial means to
procure the proper food and medications to control hyperglycemia
following discharge from the hospital.
Hypoglycemia management
6. Keep the patient off oral food and fluids or on a no-calorie liquid
diet while receiving an insulin infusion. If patients receive meals
while insulin is infusing, additional mealtime subcutaneous insulin
should be given, rather than adjusting IV insulin to cover glucose
increases resulting from meals. If the IV insulin infusion is titrated
upward throughout the day for meals, the probability of
hypoglycemia is high when the patient stops eating meals at night.
1645
7. Instruct the patient and significant others regarding the signs,
symptoms, and management of hypoglycemia.
Hypovolemia management
1. Monitor vital signs every 15 minutes until the patient is stable for
1 hour. Monitor CVP, MAP, and possibly PAP and PCWP, if
ordered. Consult advanced practice provider for the following: HR
greater than 140 bpm or BP less than 90/60 or decreased 20 mm Hg
or greater, or MAP decreased 10 mm Hg or greater from baseline,
CVP less than 4 mm Hg, and PAWP less than 6 mm Hg.
Fluid/electrolyte management
1646
1. Monitor for abnormal electrolyte levels as ordered.
1647
Infection Severity, Immune Status
Infection protection
Skin Surveillance
Confusion, acute
related to hyperosmolality, dehydration, or hypoglycemia
Goals/Outcomes: The patient verbalizes orientation to time,
place, and person; the patient is protected from unnecessary
complications and bodily injury.
Cognitive orientation
Neurologic monitoring
2. Keep bed in lowest position with side rails raised, if the patient is
confused.
1648
glucose drops faster than 100 mg/dL/h or if it drops to less than 250
mg/dL. Obtain prescription for glucose-containing IV solution to
prevent hypoglycemia and allow the continued administration of
insulin necessary to correct acidosis.
Deficient knowledge
related to new-onset diabetes or misunderstanding of the causes and
prevention of DKA or HHS.
Goals/Outcomes: By discharge from the hospital, the patient will
be able to explain causes, symptoms, and prevention of DKA or
hyperglycemic crisis.
Hyperglycemia management, hypoglycemia management
1649
it every 2 to 4 hours or more.
1650
Additional nursing diagnoses
See also nursing diagnoses and interventions in Hyperkalemia,
Hypokalemia, and Hypovolemia in Fluid and Electrolyte
Disturbances, Chapter 1; Alterations in Consciousness, Chapter 1;
Prolonged Immobility, Chapter 1; and Emotional and Spiritual
Support of the Patient and Significant Others, Chapter 2.
Myxedema coma
Pathophysiology
Myxedema coma is a life-threatening condition that occurs
when hypothyroidism is untreated or when a stressor such as
infection affects an individual with known or unknown
hypothyroidism. The clinical picture of myxedema coma includes
exaggerated hypothyroidism, with decreased mental status or
coma, hypoventilation, hypothermia, hypotension, seizures, and
shock. Myxedema coma usually develops slowly, has a greater than
50% mortality rate, and requires prompt, aggressive treatment.
Even with early diagnosis and treatment, mortality is nearly 45%.
Hypothyroidism is a common endocrine disorder reflecting
inadequacy of production or uptake of the thyroid hormone.
Localized disease of the thyroid gland that results in decreased
thyroid hormone production is the most common cause of
hypothyroidism. Normally, the thyroid gland releases 100 to 125
nmol of thyroxine (T4) daily and only small amounts of
triiodothyronine (T3). T4 is a prohormone that functions as a
reservoir for the more metabolically active form of the thyroid
hormone, T3. Primary conversion occurs in the peripheral tissues
via 5’-deiodination. Decreased production of T4 and failure of
deiodinization to T3 causes an increase in the secretion of thyroid-
stimulating hormone (TSH) by the functional pituitary gland. TSH
stimulates hypertrophy and hyperplasia of the thyroid gland and
an increase in thyroid T4–5’-deiodinase activity. Early in the disease
process, compensatory mechanisms maintain T3 levels; however,
this compensatory mechanism may be short-lived.
1651
Individuals who are acutely or critically ill may have an extreme
disruption of the normal hypothalamic–anterior pituitary–thyroid
axis, particularly related to the nocturnal surge that is normally
seen with thyrotropin. These patients will have a low T3 level even
after the TSH is restored to normal, and they are commonly
referred to as presenting with low T3 syndrome. Patients with poor
heart function or more intense inflammatory reaction show more
pronounced downregulation of the thyroid system. During sepsis,
the pituitary gland is activated via blood-borne proinflammatory
cytokines and through a complex interaction between the
autonomic nervous system and the immune cells. Sepsis elicits a
pattern of pituitary hormone dysfunction that may cause a
significant decrease in the secretion of TSH.
Hypothyroidism results in inadequate amount of circulating
thyroid hormone, causing a decrease in metabolic rate that affects
all body systems.
Primary hypothyroidism, the most common presenting form of
thyroidal disorders, is caused by thyroid suppression for any direct
reason (i.e., cancer, radiation, autoimmune dysfunction).
1652
viral syndromes may be associated with transient hyperthyroidism
followed by transient hypothyroidism. This presentation is linked
to fever, malaise, and a painful and tender gland.
Box 8-2
COMMON CAUSES OF ACUTE
HYPOTHYROIDISM
Primary hypothyroidism
• Hashimoto thyroiditis (autoimmune)
• External irradiation
• Thyroid tumor
• Drug related
• Lithium
• Interferon
• Amiodarone
1653
Secondary hypothyroidism
• Pituitary or hypothalamic disease
1654
myxedema (polysaccharide accumulation).
Vital signs
Cardinal signs and symptoms of myxedema coma include
hypothermia (may be less than 26.6° C, 80° F), hypoventilation,
hypotension, and bradycardia, as well as hyponatremia and
hypoglycemia. The presentation of any three of these signs and
symptoms together should be considered in differential diagnosis
as signs of acute hypothyroidism until proven otherwise.
Observation
Cardiac: Nonspecific ECG changes, prolonged conduction times,
prolonged QT syndrome. Cardiac enlargement, possible effusion,
or low cardiac output. If hypotensive, may be refractory to
1655
volume and vasopressors until thyroid hormone given.
Hypothyroidism
• Possible presence of obesity and/or weight gain from fluid
retention
• The skin may be dry, cool, and coarse, and the hair may be
thin, coarse, and brittle. The tongue may be enlarged
(macroglossia), and the reflexes may be slowed. Periorbital
edema may be noted.
1656
Screening lab work
Blood studies may reveal the presence of thyroid dysfunction.
Expected abnormalities include (see also Figure 8-2):
• T4 decreased
• Hypercholesterolemia
• Hypoglycemia
• Hyponatremia
• Hypoxemia
• Hypercapnia
1657
FIGURE 8-2 Diagnosing hypothyroidism.
1658
Collaborative management
Care priorities
1659
ultimately by the institution of thyroid hormone, it may take
several days. Extreme caution must be taken when rewarming
(only passive techniques should be used) to avoid
uncompensated vasodilation and profound hypotension.
1660
Use of IV triiodothyronine (LT3): Controversial therapy because it
has a higher frequency of adverse cardiac events and is generally
reserved for patients who are not improving clinically on LT4. Oral
thyroid hormone (i.e., levothyroxine): This is not the avenue of
choice in myxedema coma. It is given early in treatment for primary
hypothyroidism. To prevent hyperthyroidism caused by too much
exogenous hormone, patients are started on low doses that are
increased gradually based on serial laboratory tests (TSH and T4)
and adjusted until the TSH is in a normal range. This therapy is
continued for the patient’s lifetime. For patients with secondary
hypothyroidism, thyroid supplements can promote acute
symptoms and therefore are contraindicated.
3. Manage hyponatremia
If serum Na1 is greater than 120 mEq/L, fluids are restricted. If
serum Na1 is less than 120 mEq/L, consider administration
hypertonic (3%) saline followed by water diuresis.
4. Manage hypoglycemia
IV solutions containing glucose or 50% dextrose (D50).
7. Avoid barbiturates
1661
Because of alterations in metabolism, patients with hypothyroidism
do not tolerate barbiturates and sedatives, and therefore central
nervous system (CNS) depressants are contraindicated.
Risk identification
1662
range (usually to no greater than 120 mEq/L) rather
than to a normal value.
4. Administer IV thyroid replacement hormones with IV
hydrocortisone and IV glucose to treat hypoglycemia.
Respiratory monitoring
1663
3. Teach the patient coughing, deep breathing, and use of incentive
spirometer. For respiratory distress, assist provider with intubation
or tracheostomy and maintenance of mechanical ventilatory
assistance. Suction upper airway as needed.
Airway Management
Hypervolemia management
2. Weigh the patient at the same time every day, using the same
scale. Monitor for the following indicators of heart failure: jugular
vein distention, crackles (rales), SOB, dependent edema of
extremities, and decreased pulse amplitude. Report significant
findings to provider.
Activity intolerance
related to weakness and fatigue secondary to slowed metabolism and
decreased cardiac output caused by pericardial effusions, atherosclerosis,
and decreased adrenergic stimulation.
Goals/Outcomes: During activity patient rates perceived exertion
at 3 or less on a 0 to 10 scale and exhibits cardiac tolerance to
activity as evidenced by HR 20 bpm or less over resting HR, systolic
BP 20 mm Hg or less over or under resting systolic BP, warm and
1664
dry skin, and absence of crackles (rales), murmurs, chest pain, and
new dysrhythmias.
Activity Tolerance; Endurance; Energy Conservation
Energy management
Infection protection
1665
communicable disease not to enter patient’s room without
appropriate infection control precautions.
Nutritional management
2. Encourage foods that are high in fiber content (e.g., fruits with
skins, vegetables, whole-grain breads and cereals, nuts) to improve
gastric motility and elimination.
Constipation
related to inadequate dietary intake of roughage and fluids, bed rest, and/or
decreased peristalsis secondary to slowed metabolism.
Goals/Outcomes: Within 48 to 72 hours of admission, the patient
resumes normal pattern of bowel elimination.
Elimination
Bowel management
1666
2. Encourage the patient to maintain a diet with adequate roughage
and fluids. Ensure that fluid intake in persons without underlying
cardiac or renal disease is at least 2 to 3 L/d.
1667
4. Stress the importance of continued, frequent medical follow-up.
Syndrome of inappropriate
antidiuretic hormone
Syndrome of inappropriate antidiuretic hormone (SIADH), also
known as syndrome of inappropriate antidiuresis (SIAD), is a
potentially lethal condition that involves an alteration in sodium
and water balance. It is associated with water retention caused by a
failure to suppress ADH secretion. SIADH is one of the most
common etiologies of hyponatremia in hospitalized patients,
including those in the ICU. The syndrome occurs in the absence of
renal dysfunction or recognized stimuli that would typically induce
release of ADH. Patients with SIADH have hypoosmolality and
hyponatremia, but are euvolemic. The sodium level is normal, but
there is an increase in total body water in the intravascular space.
SIADH is considered a paraneoplastic syndrome as it can be
caused by an alteration in the immune system caused by the
presence of tumor cells. Several other etiologies, including those
that are pulmonary, neurologic, or hormonal in nature, as well as
several medications, have been implicated in its development.
Prompt and accurate diagnosis and initiation of therapies to correct
1668
serum sodium levels are essential. Management depends on the
degree of hyponatremia, associated manifestations, and how
rapidly it occurred. Meticulous critical care nursing care is pivotal
to avoid life-threatening sequelae in the acute phase of this
condition.
Pathophysiology
ADH (the type in humans is termed arginine vasopressin [AVP]) is
a hormone composed of nine amino acids. It is therefore considered
a peptide hormone (as opposed to a steroid hormone). Its two main
functions are to control levels of body water and BP. For the
purposes of this chapter, the focus is on ADH’s role in control of
body water.
ADH is synthesized by the supraoptic nucleus (a collection of
nerve cell bodies) in the hypothalamus and is secreted from the
posterior pituitary gland (neurohypophysis). When triggered, the
nerve cells release ADH. Production of ADH triggers absorption of
free water in the distal convoluted tubules and collecting duct of
the kidneys. This occurs because of binding of ADH to the V2
receptor.
The primary trigger of the supraoptic nucleus to release ADH is
an elevated serum osmolality. Other significant triggers include a
decrease in circulating blood volume, hypotension, and angiotensin
II (part of the renin-angiotensin-aldosterone system). Pain, other
sources of stress, nausea, pregnancy, hypoglycemia, nicotine, and
some drugs (e.g., morphine sulfate) are also implicated as stimuli
affecting ADH release. Cancer cells may also secrete ADH; this is
especially true of small cell lung cancer. Conversely, the two main
inhibitors of ADH secretion are hypoosmolality and hypervolemia.
Normally, ADH is secreted by the posterior pituitary when
triggered by an increase in serum osmolality; changes in serum
osmolality are detected by osmoreceptors in the hypothalamus.
ADH secretion is also stimulated by decreased circulating blood
volume or BP. These pressure changes are sensed by baroreceptors
located in the aortic arch, carotid sinus, and right atrium. ADH then
stimulates V2 receptors in the collecting duct cells of the kidney,
causing reabsorption of water, which lowers serum osmolality.
1669
Secretion of ADH results in urine concentration and decreased
urine output. There is a direct relationship between serum ADH
levels and concentration of urine, meaning that as serum ADH
levels increase, the concentration of urine increases.
In SIADH, the amount of ADH release is higher than expected,
given the patient’s serum osmolality. AVP secretion remains
increased despite a serum osmolality that normalizes. Further, in
patients with SIADH, increasing water intake does not decrease
ADH secretion and concentrated urine persists. When the body
produces excess ADH, the kidneys are unable to eliminate the
excess water. This results in an increase in total body water, despite
the absence of renal dysfunction. As fluid accumulates, sodium
levels are diluted; this results in hypotonic hyponatremia.
Four types of SIADH have been identified based on the
impairment in patterns of AVP secretion. These are delineated in
Table 8-5.
Table 8-5
TYPES OF SIADH
8-2
RESEARCH BRIEF
The incidence of SIADH-induced hyponatremia is up to 15% in
patients with small cell lung cancer (SCLC). This condition has
high morbidity and mortality rates and frequently delays initiation
of antineoplastic therapies. This prospective case series describes
management of hyponatremia with tolvaptan in 10 patients with
1670
SCLC. Treatment with tolvaptan led to an improved performance
status on all patients, allowing them to begin chemotherapy in
time. Rapid and effective correction of symptoms and serum
sodium levels were achieved. There were no prolonged
hospitalizations associated with the patient’s condition or
therapies.
From: Petereit C, Zaba O, Teber I, et al: A rapid and efficient way to manage hyponatremia
in patients with SIADH and small cell lung cancer: treatment with tolvaptan. BMC Pulm
Med 13:55, 2013.
Assessment
History and risk factors
A number of etiologic factors for the development of SIADH have
been identified. These factors can cause release of ADH but are not
directly related to serum osmolality or fluid volume status. These
factors are listed in Table 8-6.
Table 8-6
ETIOLOGIC FACTORS OF SYNDROME OF INAPPROPRIATE
ANTIDIURETIC HORMONE AND HYPONATREMIA
Pulmonary-related Medication-related
Abscess Amantadine
Acute respiratory failure Amiodarone
Asthma Amitriptyline
Atelectasis Angiotensin-converting enzyme inhibitors
Pneumonia (e.g., Legionella, Bromocriptine
Mycoplasma) Carbamazepine
Pneumothorax Carboplatin
Tuberculosis Chlorpropamide
Vasculitis Ciprofloxacin
Cisplatin
Cyclophosphamide (high-dose)
Haloperidol
Ifosfamide
Imatinib (high-dose)
Interferon-α
Interferon-γ
Lamotrigine
Levetiracetam
Lorcainide
1671
Melphalan
Methotrexate
Monoamine oxidase inhibitors
Moxifloxacin
Nonsteroidal anti-inflammatory drugs
Opiates
Oxcarbazepine
Phenothiazines
Prostaglandins
Quinolones
Serotonin and norepinephrine reuptake inhibitors (e.g.,
venlafaxine)
Selective serotonin reuptake inhibitors
Sodium valproate
Tacrolimus
Thioridazine
Thiothixene
Tolbutamide
Tolterodine
Tricyclic antidepressants
Vinblastine
Vincristine
Vinorelbine
Neurology-related Hormone-related
Brain trauma Hypopituitarism
CNS infection (e.g., meningitis, Hypothyroidism
meningoencephalitis) Exogenous hormone administration (e.g., vasopressin,
Guillain-Barré syndrome desmopressin, oxytocin)
Intracranial
bleeding/hemorrhage (e.g.,
subdural or subarachnoid
hemorrhage)
Lambert-Eaton myasthenic
syndrome
Multiple sclerosis
Psychosis
Stroke
Cancer-related Other
Adrenal tumors Chemotherapy-induced nausea
Brain tumors “Ecstasy” (3,4-methylenedioxymethamphetamine)
Breast cancer Exercise (prolonged, strenuous)
Endometrial cancer Genetic abnormalities (i.e., gene for renal vasopressin-2 (V2)
Extrapulmonary small cell receptor, gene affecting hypothalamic osmolality sensing)
carcinomas Graft-versus-host disease (acute)
Gastric cancer HIV infection (symptomatic) or AIDS
Genitourinary tract malignancy Idiopathic
(e.g., bladder, ureteral) Interventional procedures (e.g., cardiac catheterization)
Head and neck cancer (e.g., Porphyria (acute intermittent)
oropharyngeal, Positive pressure ventilation
nasopharyngeal) Stem cell transplant
Lymphoma Surgical procedures (e.g., transphenoidal pituitary, surgery
Mesothelioma on bones and joints, carotid endarterectomy, cardiac, open
Multiple myeloma and laparoscopic abdominal)
Olfactory neuroblastoma Vasculitis
Pancreatic cancer
Prostate (poorly differentiated
acinar adenocarcinoma)
1672
Sarcoma (Ewing)
Small cell lung cancer
Thymoma
Vital signs
In the absence of comorbidities (e.g., heart failure, hypokalemia), as
patients with SIADH are euvolemic, they will not have orthostatic
BP changes. HR and CVP values will be within the expected range
for the patient.
Observation
The manifestations of SIADH depend on the degree of
hyponatremia and how rapidly it developed. Patients are more
likely to be symptomatic if sodium levels decline rapidly and may
be asymptomatic if serum sodium levels are 130 mEq/L or above.
Manifestations based on degree of hyponatremia appear in Table 8-
7.
Table 8-7
MANIFESTATIONS OF SIADH BASED ON DEGREE OF
HYPONATREMIA
1673
Abdominal pain
Severe: sodium <125 mEq/L Altered mental status (e.g., lethargy, delirium)
Seizures
Decreased deep tendon reflexes
Agitation
Hallucinations
Incontinence
Pseudobulbar palsy
Coma
Respiratory collapse
Death
Lab work
Blood and urine test results are evaluated concomitantly with
assessment of extracellular fluid volume status. Evaluation of
volume status is essential for accurate interpretation of laboratory
results. Results of blood and urine tests in SIADH are as follows:
• Serum uric acid level low or within range: Less than 4 mg/dL
1674
• Serum glucose level: Within appropriate range for the patient (to
validate that hyperglycemia is not causing a false hyponatremia)
Differential diagnosis
When attempting to diagnose a patient with SIADH, the following
conditions associated with hyponatremia and euvolemic
hyponatremia should be ruled out:
• Hypothyroidism
• Hypocortisolism
• Adrenal insufficiency
• Primary polydipsia
Collaborative management
The management of patients with SIADH varies, depending on the
patient symptomatology and associated degree of hyponatremia. It
is essential for patients with severe hyponatremia that developed
within the past 48 hours to be treated to avoid life-threatening
neurologic complications. Mainstays of treatment for all patients
include eliminating the underlying cause of SIADH and correction
of serum sodium levels. The latter may be accomplished in a
number of different ways, including fluid restriction,
1675
administration of sodium, vasopressin receptor antagonist
administration, or combinations of these therapies. Each of these
treatment modalities has associated drawbacks. Hyponatremia is
the primary complication associated with SIADH. The suggested
treatment goal for patients with SIADH is serum sodium of at least
130 mEq/L. This will help mitigate neurologic symptoms associated
with lower sodium levels.
Care priorities
• Hypertonic saline
1676
correct less than 10 mEq/L in 24 hours and no more
than 18 mEq/L in 48 hours.
• Fluid restriction
1677
results in an increase in free water excretion. Loop
diuretics are typically indicated for patients with a
urine osmolality two times greater than serum
osmolality. Administration results in decreased
concentration of urine and increased water
excretion. Loop diuretics are reported not to be
useful in long-term therapy. Monitoring for
hypokalemia and hypovolemia is essential with
loop diuretic therapy as the diuretic effect is more
significant in patients with SIADH and normal
renal function.
1678
AVP from binding to receptors in the collecting ducts, thereby
inhibiting the actions of vasopressin. Administration of a
vasopressin receptor antagonist results in an increase of free water
excretion by the kidneys (aquaresis); sodium and potassium
excretion are not affected. This results in an increased sodium level
and decreased urine osmolality. Mental status improvement has
also been reported in patients with SIADH who have a serum
sodium level less than 130 mEq/L. Vasopressin receptor antagonists
are not indicated in patients who are hyponatremic but
asymptomatic.
Vasopressin receptor antagonists are available in oral and IV
formulations. As it may be challenging to predict the rate of sodium
correction with vasopressin receptor antagonists, their use is
generally reserved for when fluid restriction has not been
successful.
Tolvaptan is the oral agent and conivaptan is an IV formulation
of this class of drugs that are approved by the Food and Drug
Administration (FDA). Dosing of tolvaptan starts at 15 mg/d; up to
60 mg/d may be given. It is FDA-approved for patients with
hypervolemic or euvolemic hyponatremia (serum sodium 125
mEq/L or less.). Patients with less severe hyponatremia who have
not been successfully treated with fluid restriction may also be
given tolvaptan. Side effects of tolvaptan include liver toxicity, dry
mouth, constipation, and excess thirst. Because of the risk of
hepatotoxicity, administration of tolvaptan is typically limited to no
more than 30 days and is contraindicated in patients with liver
dysfunction, as an increase in liver enzymes was reported in clinical
trials. Tolvaptan is also contraindicated in patients with
hypovolemic hyponatremia or anuria and in those with inability to
recognize and respond to thirst.
Conivaptan, because it is an IV formulation, requires hospital
admission. However, its administration will increase sodium levels
more quickly than fluid restriction and salt tablets (for patients with
mild to moderate levels of hyponatremia and who have few or no
related symptoms). Patients with more severe levels of
hyponatremia or with mild or moderate symptoms may receive
conivaptan with or without hypertonic saline. The initial dose of
conivaptan is 20 mg over 30 minutes; this is followed by another
1679
infusion of 20 mg over 24 hours. Side effects include nausea,
vomiting, diarrhea, and infusion site reactions.
1680
useful in patients in the ICU with hyponatremia associated with
SIADH. Its use seems limited to patients who have a moderate
increase in urine osmolality. Urea administration is rarely used in
the United States because of its lack of availability in pharmacies.
Correction of chronic hyponatremia should not exceed 10 mEq/L
over 24 hours and 18 mEq/L over 48 hours. Monitoring of serum
sodium should be conducted initially every 2 to 3 hours and then
every 3 to 4 hours until the patient’s condition stabilizes.
1681
recommended to protect the patient from harm.
Patients with severe SIADH and chronic hyponatremia are at risk
for the development of alterations in bone metabolism that can lead
to osteoporosis. Bone protection therapy and monitoring of bone
density is recommended in these patients.
1682
prescribed. Note and document efficacy.
1683
Graves disease, also known as diffuse toxic goiter. Causes of acute
hyperthyroid states are listed in Box 8-3. Not all conditions listed
are associated with thyroid storm.
Box 8-3
COMMON CAUSES OF ACUTE
HYPERTHYROID STATES
• Graves disease
• Thyrotropin-secreting tumors
• Iodine-induced hyperthyroidism
1684
(ESS). When serum thyrotropin is decreased or suppressed by
severe or critical illness or by medications, particularly high doses
of glucocorticoids and dopamine, this abnormality may be the
diagnosis.
1685
metabolically active hormone. The increased circulating levels of
active thyroid hormone increase the response of β-adrenergic
receptors (sympathetic stimulation increase) and also increase the
system responsiveness to catecholamines.
Vital signs
• May have hyperpyrexia (fever)
1686
Observation
• Confused, possibly psychotic, disoriented person with CNS
irritability
• Males often have gynecomastia. Many patients have fine hair and
thin skin.
Palpation
• The thyroid gland in Graves disease will usually be enlarged, soft,
and symmetrical, although occasionally it may be firm and
irregular.
• Older patients may not have enlarged thyroid glands, which may
lead to dismissal of the diagnosis.
1687
testing has made the diagnosis of thyroid dysfunction much
simpler.
Collaborative management
Care priorities
1688
• Reduce the stress response with β-adrenergic–blocking agents
(e.g., esmolol, metoprolol, propranolol): Control tachycardia,
manage atrial fibrillation if present, anxiety, heat intolerance, and
tremor. Does not decrease the metabolic rate and has a mild effect
on global oxygen consumption. Do not assume improvement in
the thyroid disorder itself, only its symptoms. Calcium channel
blockers may be used if β-blockers are contraindicated.
1689
• Propylthiouracil (PTU) has been the first line of treatment and is
more effective in thyroid storm than methimazole. Can be used in
pregnant patients. If the patient is unable to swallow, the
medication is given using a nasogastric tube. Iodides (potassium
iodide or Lugol solution) are given several hours after PTU to
avoid a buildup of hormones stored in the thyroid gland.
• Noncompliant patients
1690
Most invasive and expensive therapy; hypothyroidism is inevitable.
Surgical removal of part of the gland often is the best treatment for
patients with extremely enlarged glands or multinodular goiter.
Surgery is avoided in the pregnant patient because of risk of
miscarriage or preterm delivery. The patient is prepared with
antithyroid agents until normal thyroid function is achieved
(usually 6 to 8 weeks). The most frequent postoperative
complication is hemorrhage at the operative site. The following
complications are rare but can be extremely serious:
hypoparathyroidism, laryngeal nerve injury, and tetany from
damage to the parathyroid glands.
Risk identification
1691
they are noted. Maternal and fetal monitoring is initiated on
pregnant patients.
1692
11. Administer iodides as prescribed, 1 hour after administering
PTU.
Aspiration precautions
1693
hoarseness indicates laryngeal nerve damage. If bilateral nerve
damage is present, upper airway obstruction can occur. Report
findings to advanced practice provider promptly.
Anxiety
related to SNS stimulation
Goals/Outcomes: Within 24 hours of hospital admission, the
patient is free of harmful anxiety as evidenced by a HR 100 bpm or
less, RR 12–20 breaths/min with normal depth and pattern, and
absence of or decreases in irritability and restlessness. The patient
and significant others verbalize knowledge about the causes of the
patient’s behavior.
Anxiety Level, Anxiety Self-control
Anxiety reduction
3. Limit number of visitors and the amount of time they spend with
patient. Advise significant others to avoid discussing stressful
topics and to refrain from arguing with the patient.
1694
4. Administer β-blockers as prescribed to reduce anxiety,
tachycardia, and heat intolerance.
5. Reassure the patient that anxiety is related to the disease and that
treatment decreases severity.
Nutrition therapy
1695
Sleep enhancement
Eye care
1. Teach the patient to wear dark glasses in the sun or for highly lit
areas to protect the cornea.
1696
discharge, the patient verbalizes knowledge about potential side
effects of prescribed medications, signs and symptoms of
hypothyroidism and hyperthyroidism, and the importance of
following the prescribed medical regimen. The patient understands
that he or she must be seen within 4 months for endocrine follow-
up.
Knowledge: Medications; Knowledge: Illness Care
Teaching: Individual
1697
8. Stress the importance of avoiding physical and emotional stress
early in the recuperative stage and maximizing coping mechanisms
for dealing with stress.
Selected references
1. Abraham A, Shafi F, Iqbal M. Syndrome of inappropriate
antidiuretic hormone due to multiple myeloma. Mo Med.
2011;108:377-379.
2. Afshinnia F, Sheth N, Perlman R. Syndrome of
inappropriate antidiuretic hormone in association with
amiodarone therapy: a case report and review of literature.
Ren Fail. 2011;33:456-468.
3. Agha A, Thornton E, O’Kelly P. Posterior pituitary
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1706
CHAPTER 9
Gastrointestinal
disorders
Gastrointestinal assessment: General
Goal of system assessment
Evaluate for dysfunctional ingestion and digestion of food and
elimination of waste products. When assessing the surgical
bariatric patient (person of size), assess the type of gastric bypass
performed, the number of days that have elapsed since surgery,
and the amount of weight lost as a result of the surgical procedure.
1707
Observation
Observe the abdomen for distension and skin color changes, which
may be signs of other system disorders.
Auscultation
Evaluate bowel sounds in each of the quadrants in a systemic
manner.
1708
Evaluate for systolic bruits (humming, swishing, or blowing
sounds) over:
Palpation
The normal abdomen should be soft and nontender to palpation.
Palpate for liver enlargement and tenderness. The spleen is not
normally palpable. If found palpable, the spleen is enlarged.
Further palpation must be discontinued, because it may cause
splenic rupture.
Nutrition assessment
Evaluate for risk factors and indications of malnutrition for which
patients who are critically ill are at risk. Malnutrition may occur
resulting from negative caloric intake with concomitant GI
obstruction, malabsorption syndromes, infectious diseases, certain
medications, and surgical treatment. Additionally, caloric needs are
greatly increased in the critically ill as a result of hypermetabolic
states produced by trauma, fever, sepsis, and wound healing.
1709
gastric bypass surgery has altered the anatomy of the stomach.
Table 9-1
GENERAL SIGNS OF MALNUTRITION
1710
Brittle nails; spooned-shaped nails Iron deficiency
Considerations for the surgical bariatric patient:
Will have vitamin deficiencies if not on
multivitamins
Screening labwork
• Serum electrolyte levels.
• Serum amylase.
• Serum lipase.
1711
14%. Mortality may reach 40% in the presence of hemodynamic
instability. The occurrence of acute GI bleeding is decreasing in the
United States resulting from a reduced incidence of Helicobacter
pylori infection and advances in ulcer-prevention strategies
including consistent use of prophylactic medications in
nonsteroidal antiinflammatory drug (NSAID) users. The following
overview presents common GI bleeding sites and occurrences.
Esophagus
Esophageal varices (EVs) are the most common cause of massive
and persistent esophageal hemorrhage. EVs are caused by
significant portal hypertension causing bleeding to occur under
high pressure. Acute variceal bleeding is severe, difficult to control,
and rarely resolves spontaneously. Less frequent causes of EV
bleeding include esophagitis, esophageal ulcers, and tumors.
Maneuvers that increase intraabdominal pressure (IAP) (e.g.,
retching, vomiting, straining, coughing, blunt abdominal trauma)
can lead to a Mallory-Weiss (MW) tear (a laceration at the
esophagogastric junction), which can result in massive bleeding.
MW tears are commonly found in patients with hiatal hernia.
1712
phenomenon that occurs in patients who are critically ill, with
higher incidence in those who are mechanically ventilated. Stress
ulcers comprise multiple lesions, generally confined to the gastric
fundus. Ulcers primarily result from stress-related hyperacidity of
critical illness and gastric mucosal ischemia secondary to diversion
of blood away from the GI tract during the stress response. Curling
ulcers occur in the proximal duodenum and are seen in patients
with major burn injuries or major trauma. Ischemia and necrosis of
the mucosa results from decreased plasma volume. Cushing ulcers
are a related condition associated with high gastric acid output and
prone to perforation that occurs in patients with increased
intracranial pressure. These patients have sustained a serious head
injury or are experiencing a critical central nervous system (CNS)
disorder. PUD resulting from a hypersecretory state is observed in
Zöllinger-Ellison syndrome (ZES). In ZES, ulcerations occur in the
stomach, duodenum, and jejunum resulting from excessive gastrin
secretion by a tumor, resulting in hyperacidity with mucosal
erosion. Benign or malignant GI neoplasms may initiate severe
bleeding episodes, especially tumors located in the vascular system
that supplies the GI tract.
Ulcer bleeding from the upper GI (UGI) tract is usually self-
limiting, most often ceasing spontaneously with the exception of
EVs. Recurrent bleeding arises in a substantial proportion of
patients and is associated with a poor prognosis. The need for
accurate diagnosis and effective therapy is crucial.
Small intestine
The structures distal to the ligament of Treitz (a thin muscular band
that wraps around the small intestine where the duodenum and
jejunum meet) are affected by conditions including arteriovenous
malformation, intussusception of the small bowel, acute superior
mesenteric artery occlusion, and Crohn disease.
Large intestine
The most common cause of significant lower GI bleeding (LGIB) is
colonic diverticulosis, accounting for up to 50% of all cases.
1713
Arteriovenous malformation of the ascending colon and the cecum
is also a usual cause of massive colonic bleeding. Inflammatory
bowel diseases such as ulcerative colitis and Crohn disease result in
friable intestinal mucosa, which can lead to massive hemorrhage
and other serious complications, including bowel obstruction and
perforation. Other causes include colonic polyps, benign or
malignant neoplasms and congenital malformation such as
hemangioma or telangiectasia.
Rectum
Hemorrhoids and neoplasms frequently cause LGIB but are usually
hemodynamically insignificant.
Neighboring organs
Medications
Long-standing use of aspirin, corticosteroids, or anticoagulants is
associated with serious GI bleeding. Ethanol may cause or
1714
potentiate ulcer bleeding because it induces gastric mucosal injury.
NSAIDs cause increased risk of serious GI bleeding, ulceration, and
perforation of the stomach and intestines. Traditional NSAIDs are
nonselective inhibitors of both cyclooxygenase-1 (COX-1) and
cyclooxygenase-2 (COX-2) enzymes. COX-1 enzymes regulate
gastroduodenal mucosal protective mechanisms. COX-2 enzymes
are involved in inflammatory and pain responses. The newer COX-
2 selective inhibitors were believed to block pain and inflammation
while leaving protective mucosal mechanisms intact, thereby
significantly lowering the incidence of GI ulceration and bleeding
compared with traditional NSAIDs. However, the COX-2 inhibitors
were shown to increase the risk of cardiovascular disease,
especially in older adults, resulting in the removal of two of three
COX-2 agents from the market. Currently, celecoxib (celebrex)
is the only COX-2 selective inhibitor available in the United States.
This COX-2 inhibitor is still associated with an increased risk for GI
bleeding, while to a lesser degree than traditional NSAIDS;
additionally, it does not appear to pose any greater risk for
cardiovascular disease than traditional NSAIDs.
Other
Obscure GI bleeding is bleeding from an unknown site despite
endoscopic and colonoscopy evaluation. These patients are believed
to have a source in the small intestine that cannot be pinpointed.
These patients may present with visible or occult bleeding (iron
deficiency anemia and/or positive for fecal occult blood). Bleeding
as a result of minor trauma: In addition to major abdominal trauma
(Chapter 3), foreign bodies such as razors, screws, or nails may
lacerate gastric or intestinal mucosa, causing bleeding.
1715
History and risk factors
History and risk factors include critical illness, especially that
caused by major injury, surgery, CNS disorder, or burns; prolonged
shock or hypoperfusion; organ failure; EVs, excessive alcohol,
NSAIDs, or corticosteroid ingestion; inflammatory bowel disease;
foreign body ingestion; hiatal hernia; hepatic, pancreatic, or biliary
tract disease; blood dyscrasias; penetrating or blunt trauma; familial
cancer; recent abdominal surgery; and the presence of H. pylori.
Identification of those at risk for recurrent bleeding is essential to
guide therapy and prevent recurrence. Risk factors associated with
rebleeding are listed in Box 9-1.
Box 9-1
RISK FACTORS TO PREDICT RECURRENT
BLEEDING
• Large-volume blood loss on admission with transfusion of greater
than 6 units
• Shock
1716
• Orthostatic hypotension signs will be positive revealing a
decrease in systolic BP greater than 10 mm Hg with an increase in
HR of 10 bpm. Orthostatic hypotension is indicative of recent
blood loss of 500 to 1000 mL in the adult.
Blood loss
• The amount of blood lost and rate of bleeding will have varying
effects on cardiovascular and other body systems.
Abdominal pain
• Mild to severe epigastric pain is often associated with
gastroduodenal ulcerative or erosive disease. The pain is
described as dull or gnawing.
• Pain may diminish when blood covers and protects the eroded
tissue.
1717
• Blood can irritate the bowels, thereby increasing transit time in
the lower GI tract, causing diarrhea.
Observation
• Extremities are cool and diaphoretic.
• Abnormal stool:
1718
• Massive LGIB is associated with dark red “currant
jelly” stools or passing fresh blood with clots.
• Jaundice, vascular spiders, ascites, and hepatosplenomegaly are
suggestive of liver disease.
Auscultation
• Abdominal auscultation may reveal hyperactive bowel sounds
caused by mucosal irritation by blood.
Palpation
• Palpation may reveal epigastric tenderness, which is expected in
peptic ulceration.
Nutrition assessment
• Evidence of malnutrition will be noted in the presence of chronic
liver disease or active, excessive alcohol use.
Screening labwork
• CBC: May identify decreased hemoglobin (Hgb) and decreased
hematocrit (Hct).
1719
Hemodynamic measurements
• Decreased central venous pressure (CVP).
1720
Elevated BUN:creatinine ratio up to 36:1 mg/dL reflects a
disproportionate increase in BUN compared with a mild increase in
serum creatinine with UGIB resulting from red blood cells (RBCs)
that have bled and pooled in the UGI tract being consumed and
digested by duodenal/proximal small intestinal bacteria. The
resulting urea is absorbed. BUN increases without a corresponding
increase in creatinine. BUN increases are NOT seen with bleeding
from the colon or the lower portion of the small intestine.
Dehydration contributes to the increased BUN and total protein
levels. Mild reduction in glomerular filtration rate from volume
depletion causes a mild creatinine elevation.
Esophagogastroduodenoscopy
Esophagogastroduodenoscopy is the most accurate means of
determining the source of UGI ulcer bleeding. Visualization of the
esophagus, stomach, and duodenum using a fiber optic endoscope
passed through the mouth is usually performed within the first 12
hours after admission of the patient to identify the exact source of
bleeding and characteristics of ulcers, if present. Endoscopic ulcer
findings are referred to as endoscopic stigmata. Stigmata indicative
of bleeding ulcers, bleeding EVs, or ulcers at risk for rebleeding are
identified in Box 9-2, Stigmata of Active or Recent Hemorrhage
(SARH). SARH findings are helpful in determining the course of
direct therapy as well as providing prognostic information.
Antacids and sucralfate should be withheld until after the
procedure, because they can alter the appearance of lesions. Gastric
biopsy is usually obtained with endoscopy for H. pylori diagnosis as
well as to exclude gastric malignancy.
Box 9-2
STIGMATA OF ACTIVE OR RECENT
HEMORRHAGE
Endoscopic Ulcer Findings From Active or Recent Upper
Gastrointestinal Hemorrhage:
Diagnostic Endoscopic Findings Rebleeding Rate Without Rebleeding Rate With
(Prevalence) Treatment (%) Treatment (%)
• Active arterial spurting (12%) 90 15-30
1721
• Nonbleeding visible vessel (22%) 50 15-30
• Active oozing of blood (14%) 10
• Adherent or overlying clot without 33 5
oozing (10%)
• Flat, pigmented slough or spot on 7
the ulcer base (10%)
• Clean ulcer base (32%) 3
Colonoscopy
Colonoscopy is diagnostic for patients with LGIB for identification
of bleeding through visualization. Colonoscopy is usually
performed within 12 to 24 hours of presentation. If a visible vessel
or adherent clot is noted, direct therapy can be provided. Direct
therapy includes laser therapy, heater probes, electrocoagulation,
injection, and argon plasma coagulation. Bleeding from colonic
diverticula is usually from multiple sites and intermittent,
therefore, direct intervention is frequently limited.
Collaborative management
Acute GI bleeding can occur from various lesions or sites in the GI
tract. The amount of blood loss can vary from minor to massive
(Table 9-2) depending on the cause, resulting in hypovolemic shock
with significant associated mortality. The patients requiring
intensive care management are those with severe bleeding,
advanced age, and significant comorbidities such as end-stage renal
disease, hepatic disease, or cardiovascular disease. Severe
gastrointestinal bleeding is defined as GI bleeding:
1722
• Identified by documented hematemesis, melena, hematochezia,
or positive NG lavage;
Table 9-2
SEVERITY OF BLOOD LOSS
Severity of Percent of Intravascular Blood Pressure (BP, bpm) and Heart Rate (HR,
Bleed Blood Loss mm Hg) Findings
Massive 20% to 25% Systolic BP < 90 mm Hg HR >100 bpm
Moderate 10% to 20% Orthostatic hypotension HR ≥100 bpm
Minor <10% Normal BP HR ≤100 bpm
Adapted from Rockey DC: Gastrointestinal bleeding. In Sleisenger MH, Feldman M,
Fordtran JS, et al, editors: Sleisenger & Fordtran’s gastrointestinal and liver disease:
pathophysiology, diagnosis, management, ed 8, Philadelphia, 2006, Saunders.
Care priorities
Assessing the bleeding severity and restoration of
hemodynamic stability of the patient are immediate priorities in the
acute phase of GI bleeding. Intensive care unit monitoring is
necessary to reduce morbidity and mortality. Once stabilized, care
priorities will shift to the identification and management of the
bleeding source.
1723
resuscitation initiated. Volume replacement should include a
combination of crystalloid and blood products. Unstable patients
with poor tissue perfusion may require blood products. Packed
cells and fresh-frozen plasma should be balanced to provide for
both the replacement of cells and clotting components. Large
transfusions will cause Ca2+ to bind with the citrate (the
preservative in stored blood) and deplete free Ca2+ levels. In
addition, large-volume blood transfusions can lead to coagulation
disorders. Vasopressors and inotropic agents should be used only if
tissue perfusion remains compromised despite adequate
intravascular volume replacement. Hemodynamic monitoring is
essential for continuous evaluation of the patient’s volume status,
especially in patients older than 50 years or those with chronic
illnesses such as cardiovascular, pulmonary, renal, or hepatic
disease. Overaggressive volume resuscitation may result in fluid
volume excess with complications of cardiac failure and pulmonary
edema. Electrolyte levels should be closely monitored, especially in
patients with renal or hepatic disease.
2. Respiratory support
Provide oxygen therapy by nasal cannula or face mask.
Supplemental oxygen is necessary as a result of blood loss, which
reduces the number of RBCs available for oxygen-carrying capacity.
Continuous or frequent pulse oximetry monitoring is
recommended in patients who are actively bleeding to monitor
oxygen saturation, but arterial blood gas (ABG) analysis may be
needed to check SaO2 if the patient is markedly anemic. More
aggressive ventilatory support may be required for patients with
persistent hypoxemia, evidence of early respiratory failure, or
impending acute respiratory distress syndrome (ARDS), as well as
for patients who were aggressively volume resuscitated.
3. Nutrition support
As soon as the hemodynamic status of the patient stabilizes,
nutrition support must be considered. Patients with active bleeding,
visible vessels, or clots may receive clear liquids following
successful endoscopic hemostasis. Patients with clean-based ulcers
may receive a regular diet following endoscopy.
1724
4. Gastric intubation
Gastric intubation may be performed but is not required for
patients with UGIB for diagnosis, prognosis, visualization, or
therapeutic effect. Gastric lavage is performed using room
temperature normal saline or water to clear blood and clots from
the stomach and to allow for estimation of ongoing blood loss. A
lavage free of blood suggests a lower GI source of bleeding. There is
no evidence that lavage stops the bleeding. Gastric intubation is
avoided if EVs are the suspected bleeding source. Balloon
tamponade may be necessary for the patient with variceal bleeding
refractory to medical and endoscopic therapy.
5. Endoscopic therapies
Coagulopathy and thrombocytopenia should be corrected before
endoscopy. In cases of respiratory insufficiency, altered mental
status, with ongoing bleeding, endotracheal intubation is indicated
before endoscopy to stabilize the patient and protect the airway.
Early endoscopy, within the first 24 hours of admission increases
diagnostic accuracy, reduces the risk of rebleeding, and decreases
the length of hospitalization. Endoscopy should be performed
within 12 hours of admission for the patient with suspected varices.
Endoscopic modalities for the achievement of hemostasis include:
thermal therapy (electrocoagulation or heater probe and injection of
sclerosant), epinephrine injection therapy (should be used in
conjunction with second modality), and the application of
hemoclips (clips that serve to apply mechanical pressure to the
bleeding site) are generally effective in stopping bleeding for both
UGIB and LGIB. Complications of endoscopy include perforation
and MW tears.
6. Pharmacotherapy
Pharmacotherapy including vasopressin and nitroglycerin is only
available for the management of UGIB. No pharmacologic therapies
for LGIB are currently available. In the upper GI tract, increased
gastric acidity is believed to impede blood clotting, although gastric
alkalinization may facilitate platelet aggregation, thus promoting
acid-lowering pharmacotherapies. Pharmacologic agents involved
in ulcer treatment include antacids, H2-receptor antagonists,
1725
proton-pump inhibitors (PPIs), prostaglandin analogues,
somatostatin, and octreotide.
Antacids (aluminum hydroxide, calcium carbonate,
citrocarbonate, magaldrate, magnesium hydroxide, simethicone):
Oral antacids raise gastric pH levels and decrease the corrosiveness
of gastric acid. They may relieve dyspepsia but have no effect on
bleeding ulcers.
Histamine H2-receptor antagonists (e.g., famotidine, ranitidine,
cimetidine, nizatidine): Inhibit gastric acid and pepsin secretion,
and are useful in the treatment of ulcerative disease and for stress
ulcer prophylaxis. The usefulness in an active bleeding ulcer is
unsupported. They provide inferior acid inhibition to PPIs.
Cimetidine is avoided in patients who are critically ill because it
inhibits certain liver enzymes, resulting in potential drug
interactions.
Proton-pump inhibitors (e.g., esomeprazole, lansoprazole,
omeprazole, pantoprazole, rabeprazole): PPIs deactivate the
enzyme system that pumps hydrogen ions from parietal cells,
thereby inhibiting gastric acid secretion. PPIs have become the
preferred agent for erosive ulcer disease with bleeding. Acid-
inhibitory effects of PPIs are significantly stronger than H2-receptor
antagonists. IV PPIs or high-dose oral PPIs following a bleeding
episode are effective in reducing the incidence of rebleeding, the
number of transfusions, and the need for further endoscopic
therapy. Preendoscopic IV PPIs may reduce high-risk stigmata in
patients with UGIB and is recommended. IV PPIs are additionally
recommended in patients for whom endoscopy must be delayed or
cannot be tolerated.
Prostaglandin analogues (e.g., misoprostol [Cytotec]): Synthetic
prostaglandin E1 enhances the body’s normal mucosal protective
mechanisms by stimulating mucosal blood flow and bicarbonate
secretion, and reducing mucosal cell turnover. They are useful in
reducing the incidence of ulcer development in patients taking
NSAIDs.
Vasoconstrictors: Vasopressin may help slow variceal bleeding.
Octreotide, a somatostatin analogue: Causes splanchnic
vasoconstriction and reduced portal pressure. In combination with
endoscopic therapies, it has been shown to control variceal bleeding
1726
and reduce the risk of recurrence. No improvement in mortality has
been shown with its use in this population.
Sucralfate (Carafate): Oral sucralfate may be prescribed for
patients with gastric erosions. Sucralfate combines with gastric acid
and forms an adhesive-protective coating over damaged mucosa
and does not alter gastric pH. Sucralfate frequently causes
constipation and should be avoided in patients with chronic renal
insufficiency.
Pharmacotherapy for H. pylori: Eradication of H. pylori is
effective with combination therapies, monotherapy is useless.
“Triple therapy” includes two antibiotics (clarithromycin and
amoxicillin or metronidazole) and a PPI. “Quadruple therapy”
includes bismuth salicylate, metronidazole, tetracycline, and a PPI
or H2-blocker. There are several triple therapy combination
preparations available to allow the patient to receive the
combination in one pill.
7. Surgical management
Many surgical techniques are used for both acute UGIB and LGIB,
depending on the location and severity of the lesion. EVs are best
managed with endoscopic ligation (banding) or sclerotherapy. Band
ligation involves wrapping elastic bands over the varices in the
distal esophagus; sclerotherapy involves the injection of a
sclerosing agent. Ulcerative disease requires surgery if the lesion
continues to bleed despite aggressive medical and endoscopic
therapy or if complications such as perforation or obstruction
develop. Oversewing of the bleeding vessel is usually followed by
an acid-reducing procedure such as antrectomy, which removes
acid-secreting cells, or vagotomy, which denervates the acid-
producing fundic mucosa. Pyloroplasty is performed if there is
impairment of gastric emptying. In the patient whose condition is
unstable, both vagotomy and pyloroplasty are performed.
Antrectomy and vagotomy may be performed in patients whose
condition is more stable with anastomosis of the stomach to the
duodenum (Billroth I procedure). Also common is the Billroth II
procedure for duodenal ulcers involving antrectomy with
gastrojejunostomy. Massive LGIB is difficult to control and may
require aggressive surgical procedures such as a colectomy with the
1727
creation of a permanent ileostomy or internal ileal pouch.
Fluid management
2. Monitor postural vital signs for the patient with mild to moderate
GI bleeding on admission, every 4 to 8 hours, and more frequently
if recurrence of active bleeding is suspected: measure BP and HR
with the patient in a supine position, followed immediately by
measurement of BP and HR with the patient in a sitting position (as
tolerated). A decrease in systolic BP greater than 10 mm Hg or an
increase in HR of 10 bpm with the patient in a sitting position
suggests a significant intravascular volume deficit, with
approximately 15% to 20% loss of volume.
1728
available. Assist-control mode is recommended for patients
undergoing SVV monitoring. Be alert to low or decreasing CVP.
CVP less than 2 mm Hg, SI less than 33, and SVV greater than 13%
to 15% are suggestive of hypovolemia and the need for volume
restoration.
Fluid resuscitation
Shock management
1729
1. Initiate fluid replacement (see Fluid and Electrolyte Disturbances,
Chapter 1).
1730
lightheadedness, and passage of frank blood in stools. Reinforce the
importance of seeking medical attention promptly if signs of
bleeding occur.
Hemodynamic regulation
4. Monitor vital signs and CO, and replace volume as indicated (see
Fluid and Electrolyte Disturbances, Chapter 1).
1731
5. Monitor for oliguria hourly; report urine output less than 0.5
mL/kg/h for 2 consecutive hours.
Respiratory monitoring
Acute pain
related to chemical or physical injury of GI mucosal surfaces caused by
digestive juices and enzymes or tissue trauma.
Goals/Outcomes: Within 2 hours of diagnosis, the patient’s
subjective evaluation of discomfort improves, as demonstrated by a
decreased reported pain level. Nonverbal indicators of discomfort,
such as grimacing, are absent.
Comfort Level; Pain Control.
Pain management
1732
hypovolemic to avoid hypotension and respiratory depression.
Diarrhea
related to irritation and increased motility secondary to the presence of
blood in the GI tract.
Goals/Outcomes: By hospital discharge, the patient’s stools are
normal in consistency and frequency, and results are negative for
occult blood.
Fluid Balance; Bowel Elimination; Electrolyte and Acid-Base
Balance.
Diarrhea management
1733
hyperdynamic bowel sounds. Absence of bowel sounds (especially
in association with severe pain or abdominal distension) may signal
serious complications such as ileus or perforation.
Nutrition management
4. Weigh the patient daily at the same time of day, using the same
scale. Weight can be a practical indicator of nutrition status if the
patient’s weight changes are interpreted on the basis of the
following factors: fluid shifts (edema, diuresis, third spacing),
surgical resection, and weight of dressings and equipment.
1734
Additional nursing diagnoses
See other nursing diagnoses and interventions as appropriate:
Hemodynamic Monitoring (Chapter 1), Prolonged Immobility
(Chapter 1), and Emotional and Spiritual Support of the Patient and
Significant Others (Chapter 2).
Acute pancreatitis
Pathophysiology
Acute pancreatitis (AP) is an autodigestive process of the pancreas
and surrounding tissue by pancreatic enzymes, resulting in the
most common cause of GI disease–related hospitalizations in the
United States. Normally, pancreatic acinar cells produce and secrete
inactive proteolytic enzymes. These proenzymes travel through the
pancreatic duct safely until reaching the duodenum, where they are
activated by other enzymes found in the intestinal brush border. In
AP, the proenzyme trypsinogen is prematurely activated to the
proteolytic enzyme trypsin within the acinar cells of the pancreas.
Once secreted into the pancreatic duct, trypsin activates other
proenzymes, resulting in enzymatic autodigestion of the pancreas.
The exact mechanisms prompting trypsin to be prematurely
activated remains unanswered. AP is created by a series of events.
Initially, the activated digestive enzymes within the pancreas digest
pancreatic tissue, leading to inflammation and capillary leakage.
Eventually, these enzymes may also digest elastin in blood vessel
walls, causing vascular injury that sometimes leads to hemorrhage.
The spread of inflammatory mediators (kinins, complement,
coagulation factors) released at the site of tissue and vessel injury
cause further edema, inflammation, thrombosis, and result in
systemic inflammatory response syndrome (SIRS). Significant
pancreatic edema leads to rupture of the pancreatic ducts and
spillage of pancreatic enzymes into the peripancreatic tissue,
resulting in injury. Pancreatic necrosis develops when the
pancreatic blood supply is significantly disrupted. Pancreatic
necrosis along with organ failure are defining features of severe
disease. Shock, distant organ dysfunction, and/or multiple organ
1735
dysfunction syndrome (MODS) can ensue.
AP is clinically classified as mild or severe. In cases of mild AP,
there is local inflammation, interstitial edema identified by imaging,
and the absence of pancreatic necrosis and/or organ failure. The
pancreatic blood supply is preserved. Patients usually improve in
48 to 72 hours with supportive management. Mild AP accounts for
the majority of cases with a mortality rate of less than 1%. The
incidence of progression from mild to severe AP may be increasing.
Approximately, 15% to 20% of patients with mild AP will develop
severe disease. Severe acute pancreatitis (SAP) is a life-threatening
condition currently described in two distinct phases: early (within
the first week) and late (after the first week). Early disease is
characterized by persistent organ failure and/or SIRS lasting longer
than 48 hours. Organ failure may be identified by two or more of
the following: shock (systolic BP less than 90 mm Hg), pulmonary
insufficiency (PaO2 ≤60 mm Hg), kidney failure (serum creatinine
greater than 2 mg/dL), or GI bleeding (greater than 500 mL/24 h).
Late SAP involves the development of one or more local
complications that include sterile or infected
pancreatic/peripancreatic necrosis, acute pseudocyst, acute
peripancreatic fluid collection, and walled-off pancreatic necrosis
(WOPN) (see Complications).
Alcoholism and gallstones account for 80% of all AP cases.
Alcohol sometimes has a direct toxic effect on the pancreatic acinar
cells or may cause inflammation of the sphincter of Oddi, resulting
in the retention of enzymes in the pancreatic duct. In patients with
gallstones, AP may be caused by obstruction of the pancreatic duct
by gallstones lodged at the shared outlet of the pancreatic duct and
common bile duct into the duodenum. When the outlet is blocked,
bile can reflux into the pancreatic duct. Once AP ensues,
hypercalcemia, hyperlipidemia, and hypertriglyceridemia are often
found to be present and may cause AP. AP is often associated with
a recent endoscopic retrograde cholangiopancreatography (ERCP)
procedure: the most common iatrogenic cause. Other causative
factors include blunt or penetrating trauma, metabolic factors,
infectious agents, and certain drugs (Box 9-3). Despite the capacity
for thorough investigation, the cause of AP is idiopathic in
approximately 15% to 20% of cases.
1736
Box 9-3
PRECIPITATING FACTORS FOR ACUTE
PANCREATITIS
Mechanical blockage of pancreatic ducts
• Biliary tract disease (e.g., gallstones)
• Post-ERCP
• Tumors
Toxic/metabolic factors
• Ethyl alcohol
• Hyperlipidemia
• Hypercalcemia
• Pregnancy
Infection
• Viral (e.g., mumps, Coxsackie virus B, hepatitis B, HIV, CMV)
Trauma
• External
• Surgical
1737
Ischemia
• Prolonged/severe shock
• Vasculitis
Drugs
• Corticosteroids
• Estrogens
• NSAIDs
• Sulfonamides
• Thiazides
• Tetracycline
Risk stratification
Timely identification of patients at risk for developing SAP is
crucial to planning appropriate care to achieve the best outcomes.
Predicting severity early is crucial in preventing complications and
mortality. It is difficult to distinguish mild from severe disease in
the early stages. Several classification systems have been developed
to determine severity. Ranson’s criteria for non–gallstone AP
provide a scale of severity for AP based on age, blood gas,
hematologic, and biochemical changes. Pancreatitis is classified as
severe when three or more of Ranson’s 11 criteria are met during
the first 48 hours following presentation (Box 9-4). The Acute
Physiology and Chronic Health Evaluation (APACHE) II scoring
system (Table 9-3) is another tool to determine severity. An
APACHE II score of less than 8 points within the first 48 hours is
directly related to better survival. Higher scores during this time
1738
interval are associated with increased morbidity and mortality
rates. Scoring systems are often cumbersome and should be used in
conjunction with ongoing clinical findings and other laboratory
data. The less cumbersome Bedside Index of Severity in Acute
Pancreatitis (BISAP) was recently developed for risk stratification
during the first 12 hours of admission. The index includes five
commonly available clinical variables that are each assigned 1
point. A simple score of 3 points or greater is associated with
increased risk of complications and mortality (Box 9-5).
Table 9-3
THE ACUTE PHYSIOLOGY AND CHRONIC HEALTH EVALUATION
(APACHE) II SCORING SYSTEM
*
Use if Fio2 <50%.
†
Use if percentage of inspired oxygen (Fio2) >50%.
‡
Use only if no arterial blood gas measurements are available.
§
APACHE II score ≥ 8 identifies severe acute pancreatitis and the need for intensive
care.
From Knaus WA, Draper EA, Wagner DP, Zimmerman JE: APACHE II: a severity of
disease classification system. Crit Care Med 13:818-829, 1985.
1739
A-aPo2, alveolar-arterial oxygen pressure; Pao2, partial pressure of oxygen in arterial
blood.
Box 9-4
RANSON CRITERIA FOR CLASSIFYING
THE SEVERITY OF PANCREATITIS
At presentation
• Age ≥55 years
• WBCs ≥16,000/mm3
• Fluid sequestration ≥6 L
1740
ABG, Arterial blood gas; AST, aspartate aminotransferase; BUN,
blood urea nitrogen; Ca2+, calcium; LDH, lactate dehydrogenase;
PO2, partial pressure of oxygen; WBCs, white blood cells.
Box 9-5
BEDSIDE INDEX OF SEVERITY IN ACUTE
PANCREATITIS (BISAP) SCORE
Clinical Variables Point Allocation
BUN (blood urea nitrogen) >25 mg/dL 1
Impaired mental status 1
SIRS (systemic inflammatory response syndrome) 1
2 or more of the following:
• Temperature <36° C or >38° C
• Pulse >90bpm
• Respiratory rate >20 breaths/min or Pao2 <32 mm Hg
• White blood cell count <4000 or >12,000 or 10% bands
Age >60 years 1
Pleural effusion 1
Complications
The inflammation associated with AP is nonbacterial. Pancreatic
necrosis is usually sterile but can become infected. In SAP, the
inflammatory process results in extensive pancreatic and
peripancreatic necrosis of mesenteric and retroperitoneal fat tissue
that prompts late-phase local complications, which increase
mortality and significantly lengthen the clinical course of disease.
Infected pancreatic necrosis should be suspected when worsening
of pain, fever, and leukocytosis manifest between 7 and 10 days
after admission. Infective necrosis often leads to sepsis and MODS
as a result of translocation of bacteria from the poorly functioning
gut. Pancreatic pseudocysts can form, comprising encapsulated
fluid collections with high enzyme concentration and variable
amounts of tissue debris. Although the majority of pseudocysts are
sterile, some become infected resulting in hemorrhage or rupture,
which prompts pancreatic ascites. Pseudocysts usually form within
or adjacent to the pancreas but can migrate into the chest or other
1741
locations. Other unencapsulated acute peripancreatic fluid
collections form in the peripancreatic area in approximately 30% of
AP cases. WOPN defines a collection of pancreatic and
peripancreatic debris and liquefied dead tissue encased in a fibrous
tissue wall. WOPN develops over a 4-week period in patients with
necrotizing pancreatitis.
A major initial complication of SAP is hypovolemia resulting
from plasma volume fluid sequestration into the interstitium,
retroperitoneum, and the gut. Massive, life-threatening hemorrhage
from rupture of necrotic tissue results in severe anemia and
hypotension. SIRS ensues, wherein inflammatory mediators trigger
vasodilation and increased capillary permeability, which further
contributes to severe hypovolemia and hypotension.
Hypoalbuminemia is frequently present, which prompts
intravascular fluids to move through the permeable capillaries
more rapidly, because oncotic pressure is reduced. Severe
hypotension may persist despite volume repletion given there is too
little protein to hold the volume within the blood vessels. If
hypovolemia is not adequately corrected promptly, acute kidney
injury and MODS may develop (see Systemic Inflammatory
Response Syndrome, Sepsis, Septic Shock, and Multiple Organ
Dysfunction Syndrome, Chapter 11).
Mild to severe respiratory failure with hypoxemia is common in
AP patients with SIRS. Respiratory complications are related to
right-to-left vascular shunting within the lung and alveolar-
capillary leakage caused by the circulating inflammatory mediators
resulting in ARDS (see Acute Lung Injury and Acute Respiratory
Distress Syndrome, Chapter 4). In addition, elevation of the
diaphragm, atelectasis, and pleural effusion caused by
subdiaphragmatic inflammation of the pancreas and surrounding
tissues, and/or pancreatic ascites, can compromise ventilation
further. Inflammatory mediators and vascular injury may lead to
intravascular coagulopathy or DIC, resulting in life-threatening
complications such as major thrombus formation and pulmonary
emboli. The circulatory and respiratory failures that ensue are often
the cause of death in these patients.
Assessment
1742
Goal of system assessment: Acute pancreatitis
Evaluate for organ and systemic involvement of dysfunctional
pancreatic secretions.
Abdominal pain
• Sudden onset of epigastric pain (often after excessive food or
alcohol ingestion) lasting 12 to 48 hours, described as mild
discomfort to severe distress, and located from the
midepigastrium to the right upper quadrant (RUQ). Occasionally
pain is reported in the left upper quadrant.
Observation
• Mild to moderate ascites may be present.
1743
• Dyspnea and cyanosis may be observed if ARDS is present (see
Acute Lung Injury and Acute Respiratory Distress Syndrome,
Chapter 4).
Auscultation
• Diminished, sluggish, or absent bowel sounds reflective of GI
dysfunction and paralytic ileus.
Palpation
• Abdominal tenderness is common.
1744
• In the presence of hemorrhage or severe hypovolemia, the hands
are cool and sweaty to touch.
Nutrition assessment
• Malnutrition may be present, especially if there is a history of
alcoholism (see Table 9-1).
Screening labwork
• Serum electrolyte levels: Hypercalcemia.
• CBC: Leukocytosis.
1745
The diagnosis of acute pancreatitis (AP) is based on the presence
of two of the following three criteria:
The following tests are used to support the diagnosis and trend
the progression of the disease.
1746
Serum lipase and amylase
Serum lipase has become a primary diagnostic marker for AP.
Serum amylase is not sensitive diagnostically in cases of delayed
clinical presentation; pancreatitis caused by hypertriglyceridemia;
and in patients with chronic pancreatitis experiencing an acute
attack. Prolonged clamp time with coronary artery bypass grafting
or valve replacement can lead to AP in which only amylase is
elevated.
Collaborative management
Management includes risk stratification, monitored supportive care,
efforts to prevent, limit and treat complications, and recurrences.
The American College of Gastroenterology (ACG) guidelines
“Management of Acute Pancreatitis” frame the management
priorities. Because AP is a disease of significant variability, there is
a paucity of large randomized controlled trials. The ACG practice
guidelines (Box 9-6) present recommendations based on: scientific
studies and best evidence of new understandings and
developments in the diagnosis, etiology, and management of AP.
Box 9-6
AMERICAN GASTROENTEROLOGY
ASSOCIATION RECOMMENDATIONS FOR
ACUTE PANCREATITIS
Diagnosis
• Established by the presence of two out of three of the following
criteria: abdominal pain consistent with the disease, serum
amylase and/or lipase greater than three times the upper normal
limit, and/or characteristic findings from abdominal imaging.
1747
Determination of etiology
• Transabdominal ultrasound should be performed on all patients.
Assessment of severity
• Assess hemodynamic status on presentation and begin
resuscitative measures.
Management
• Aggressive fluid resuscitation is most beneficial in the first 12 to
24 hours.
1748
• The use of antibiotics in patients with sterile necrosis to prevent
the development of infected necrosis is not recommended.
1749
In SAP-related pulmonary congestion, pleural effusion and
atelectasis result in respiratory insufficiency or failure. Abdominal
distension and retroperitoneal fluid sequestration cause
diaphragmatic elevation and ventilatory restriction. Oxygen
administration is initiated if hypoxemia is present. Early respiratory
failure is detected by a decrease in PaO2 with increase in Paco2. If
severe pulmonary insufficiency develops, intubation and positive-
pressure ventilation is required. Mechanical ventilation is
frequently necessary for the patient with SAP. ARDS is a
complication found in 20% of patients with SAP. IV fluids are given
cautiously to prevent fluid overload resulting in cardiopulmonary
compromise.
1750
depending on the severity of the pain. Patient-controlled analgesia
(PCA) is a helpful mode of delivery. Morphine has been implicated
in the past as causing spasm of the sphincter of Oddi, thus
worsening the pancreatitis. However, no evidence has been found
to demonstrate this in humans. Its use in AP has not been shown to
adversely affect outcomes. Meperidine was the analgesic of choice
but has an active neurotoxic metabolite that accumulates with long-
term use, causing agitation, seizures, and muscle fibrosis. Because
of these side effects, many hospitals have limited the availability of
IV meperidine. Hydromorphone or sublimaze are alternatives.
1751
feeding tolerance and consulting with dieticians and nutrition
support pharmacists regarding elemental or polymeric feedings
(see Nutrition Support, Chapter 1). If enteral feedings are not
tolerated, total parenteral nutrition (TPN) can be administered as
second-line therapy, necessitating insertion of a central IV catheter.
TPN continues to be associated with significant complications from
the catheter, ranging from catheter-related sepsis, local abscess,
localized hematomas, pneumothorax, venous thrombosis, venous
air embolism, and metabolic complications such as hyperglycemia
and electrolyte imbalance. Low-fat oral feedings are begun after the
initial episode subsides and bowel function returns.
1752
patients with asymptomatic pseudocysts and sterile necrosis
regardless of size or location. Minimally invasive necrosectomy by
laparoscopic, radiologic, or endoscopic approach is indicated for
stable patients with infected necrosis or pseudocysts, but should be
delayed for more than 4 weeks after initial presentation to allow
liquefaction of the contents and for the development of a fibrous
wall. Any type of invasive intervention before the 4-week period is
associated with increased mortality.
1753
IAP greater than 25 mm Hg refractory to medical therapy (see
Abdominal Hypertension and Abdominal Compartment
Syndrome, Chapter 11).
Fluid resuscitation
1754
3. Aggressive IV hydration with volumes of 250 to 500 mL/h may be
necessary in patients with no cardiac or renal comorbidities and is
of most benefit the first 12 to 24 hours.
Fluid management
1755
5. Monitor for indicators of hypovolemia, including cool
extremities, delayed capillary refill (greater than 2 seconds), and
decreased amplitude of or absent distal pulses.
11. Consider fluid bolus for urine output less than 0.5 mL/kg/h for 2
consecutive hours. If SAP is present, initiate fluid resuscitation and
shock management.
12. Weigh the patient daily, using the same scales and method.
Weight may increase as a result of significant capillary leak and
anasarca with intravascular volume depletion.
13. Evaluate characteristics of all fluids lost. Note color and odor. Be
alert to the presence of particulate matter, fibrin, and clots. Test GI
aspirate, drainage, and excretions (including stool) for the presence
of occult blood.
Shock management
1756
1. Monitor fluid status (see Fluid Management, Fluid Resuscitation).
Electrolyte management
1757
Fluid/Electrolyte Management; Fluid Monitoring;
Hemodynamic Regulation; Hypovolemia Management; Invasive
Hemodynamic Monitoring; Shock Prevention; Bleeding
Precautions; Bleeding Reduction; Hypervolemia Management.
Hemodynamic regulation
Acute pain
related to chemical injury to the pancreas and peripancreatic tissue
secondary to release of pancreatic enzymes.
Goals/Outcomes: Within 2 to 4 hours of diagnosis, the patient’s
1758
subjective evaluation of discomfort improves, as documented by a
pain scale. Ventilation and hemodynamic status are
uncompromised, as evidenced by MAP greater than 70 mm Hg, HR
60 to 100 bpm, and RR 12 to 20 breaths/min with normal depth and
pattern (eupnea).
Pain Control; Pain Level; Comfort Level.
Analgesia administration
1759
Opioid analgesics decrease intestinal motility and delay
return to normal bowel function.
Pain management
1760
related to atelectasis and ARDS; elevation of the diaphragm and pleural
effusion caused by subdiaphragmatic inflammation of the pancreas, and
with SAP, alveolar-capillary membrane changes secondary to
microatelectasis, inflammatory mediators, and pulmonary fluid
accumulation.
Goals/Outcomes: Within 4 hours of diagnosis, the patient has
adequate gas exchange, as evidenced by SaO2 greater than 92%;
PaO2 greater than 80 mm Hg; Paco2 35 to 45 mm Hg; RR 12 to 20
breaths/min with normal depth and pattern; orientation to time,
place, and person; and clear and audible breath sounds.
Respiratory Status: Gas Exchange; Respiratory Status:
Ventilation.
Airway management
1761
6. Maintain a body position that optimizes ventilation and
oxygenation. Elevate HOB 30 degrees or higher, depending on the
patient’s comfort. If pleural effusion or other defect is present on
one side, position the patient with the unaffected lung dependent to
maximize the ventilation-perfusion relationship.
Hypervolemia management
1762
2. Consider administering furosemide (Lasix) or other diuretic as
prescribed to promote diuresis, after volume status has been
evaluated. Patients may be intravascularly hypovolemic despite
significant weight gain resulting from third spacing of fluids.
Diuresis may not prove to be beneficial. Document response to
diuretic therapy.
Infection protection
1763
inflammatory response or sepsis. Be alert to increases in HR and RR
associated with temperature elevations.
Nutrition management
1764
pharmacist to estimate the patient’s individual metabolic needs,
based on activity level, presence of infection or other stressor, and
nutrition status before hospitalization. Overuse of calcium
supplements can cause AP; this mechanism should be added as
noted earlier. Develop a plan of care accordingly.
8. Begin low-fat oral feedings when acute episode has subsided and
bowel function has returned. This may take several weeks in some
patients.
1765
Parenteral Nutrition (TPN) Administration; Venous Access Device
(VAD) Maintenance; Hyperglycemia Management; Hypoglycemia
Management.
For additional details, see Nutrition Support, Chapter 1.
Deficient knowledge
related to lack of exposure to healthcare information
Goals/Outcomes: Before hospital discharge, the patient
verbalizes knowledge regarding availability of alcohol
rehabilitation programs, prescribed medications, importance of a
low-fat diet, indicators of actual or impending GI hemorrhage,
indicators of infection, and the importance of seeking medical
attention promptly if signs of recurring pancreatitis appear.
Knowledge: Disease Process; Knowledge Treatment:
Regimen.
1766
passing blood in the stools, or vomiting blood) or infection (see Risk
for Infection) appear.
Enterocutaneous fistula
Pathophysiology
Enterocutaneous fistulas (ECFs) are formed when trauma, surgery,
infection, neoplastic disease, or other pathologic condition results in
a GI-cutaneous communication. Classifications include
spontaneous (15% to 25%) or postoperative (75% to 85%) (.
Spontaneous fistulas occur in patients with inflammatory bowel
disease (IBD) (Crohn disease > indeterminate colitis > ulcerative
colitis), cancer, diverticular disease, appendicitis, perforated bowel
disease, radiation enteritis, or ischemic bowel. Postoperative fistulas
account for the majority of ECFs and are observed following
abdominal surgery for IBD, intestinal malignancy, recurrent
explorations, or after extensive lysis of adhesions for conditions
such as small bowel obstruction. For patients with severe
abdominal trauma, severe intraabdominal sepsis, or complex
surgical pathologies, open abdominal (OA) management has
become a recurrent treatment option. In OA management, the
peritoneal cavity is left open and abdominal contents are protected
with a temporary dressing until bowel edema reduces or washouts
1767
are no longer required and the peritoneum can be closed. A new
type of ECF has emerged as a complication of OA management
called enteroatmospheric fistula (EAF). EAFs develop from
edematous loops of bowel within the wound bed of an open
abdomen that became injured.
Fistulas can be classified as high output (greater than 500 mL/d),
moderate output (200 to 500 mL/d), and low output (less than 200
mL/d). High-output proximal small bowel fistulas are the most
difficult to manage with losses as high as 2 L in 24 hours. Drainage
from proximal fistulas is hypertonic; rich in enzymes, electrolytes,
and proteins; thin in consistency and tends to be copious. Extensive
skin and tissue breakdown often occur because of the presence of
activated pancreatic enzymes in fistula drainage. Electrolyte and
protein loss is great with high-output proximal fistulas. Drainage
from distal sites, such as the ileum and colon, is thick and of less
volume than is proximal fistula drainage.
Three factors are associated with mortality in patients with ECFs:
(1) fluid and electrolyte imbalance, (2) malnutrition, and (3) sepsis.
Fluid, potassium, sodium, proteins, and bicarbonate may be lost in
great quantities. Replacement by enteral nutrition or parenteral
nutrition (TPN) is complex, and proper balance is often difficult to
achieve. Sepsis is frequently associated with bowel fistulization
caused by anastomotic breakdown, local wound contamination, or
inadequate drainage. Hypercatabolism and malnutrition are
associated with both sepsis and fistulization, creating a great
demand for calories and protein. Aggressive nutrition support and
meticulous local wound management are crucial to patient survival.
Mortality rates for ECF have declined overall because of advances
in nutrition, wound care, and surgical technique to 5% to 15%.
Gastrointestinal assessment:
Enterocutaneous fistula
Goal of assessment: Enterocutaneous fistula
Evaluate the functional integrity of the intestinal tract.
1768
• Direct trauma to the GI system, especially the bowel.
Abdominal pain
• Tenderness, erythema, and possibly pain at the incision/fistula
site caused by irritation from fistula output or infection.
Abdominal drainage
• Discharge of bile, enteric contents, or gas through a surgical
incision.
1769
• Sudden increase in the amount of drainage from a surgical
incision or drainage catheter.
Observation
• Mental confusion is often present as a result of electrolyte
imbalance, dehydration, or early sepsis.
• Sunken eyes, poor skin turgor, and dry oral mucosa are
associated with dehydration.
Auscultation
• Diminished or absent bowel sounds if peritonitis or ileus is
present.
Palpation
• Discomfort and guarding on abdominal palpation over an
abdominal mass (abscess) or near a drain site or surgical incision.
Nutrition assessment
• Weight loss and loss of muscle mass resulting from protein losses
and hypercatabolism.
1770
Screening labwork
• Serum electrolyte levels: Depleted as a result of external losses
through the fistula.
Hemodynamic measurements
• Decreased BP, MAP, and CVP if severe dehydration is present.
1771
drainage.
Nutrition profile: Evaluates nutrition These laboratory tests will vary in individual patients.
Serum albumin, status and initiates Serum transferrin levels >140 mg/dL have been
transferrin, aggressive shown to correlate with the spontaneous closure of
prealbumin nutrition support enterocutaneous fistulas, thereby reducing mortality
early. among these patients. Levels <140 is a poor
prognostic finding. Serum albumin 3 g/dL or less at
the time of fistula presentation is a poor prognostic
indicator.
Prealbumin levels will rise with effective nutrition
therapy.
Noninvasive
Cardiology
Electrocardiogram Assesses and Hypokalemia may result in flattening of T wave or U
monitors for wave development. Hypocalcemia, hypokalemia, and
cardiac rhythm hypomagnesemia can result in widening of the QT
disturbances interval.
related to
hypokalemia,
hypocalcemia, and
hypomagnesemia.
Radiology
Fistulogram: To identify the Radiographs will confirm anatomic site of origin and
Water-soluble anatomy and fistula tract.
contrast characteristics of
medium the fistula tract.
injected into the
suspected
fistula
Computed CT may be used to Confirmation of intraperitoneal abscess is made.
tomography (CT) identify abscesses Percutaneous drainage may be performed.
scan associated with
fistulization.
Upper An upper GI series Upper GI series may reveal esophageal, gastric, or
gastrointestinal may be indicated if duodenal fistulas.
(GI) series the suspected
fistula is proximal
to the intestines.
Nonradiographic evaluation
Bedside maneuver: An external fistula can be simply confirmed
without radiology by the oral administration of charcoal. The
visible presence of dye in the drainage confirms the presence of a
fistula.
Biopsy: In patients with neoplastic disease, a biopsy specimen of
the fistula tract may be obtained to determine the presence of
malignancy within the tract.
Culture: Fistula effluent from the stomach, duodenum, biliary
tree, and pancreas may be cultured for evidence of infection. Small
1772
and large bowel fistulas are generally not cultured because of the
expected presence of bacteria.
Collaborative management
Early management of ECF presents a considerable challenge
requiring advanced support of a multidisciplinary team in a
surgical intensive care unit setting. The patient with ECF is
typically malnourished with a recent history of malignancy,
inflammatory or infectious disease, postoperative or traumatic
bowel injury, dehiscence, or inadvertent enterotomy. Their
physiologic and nutrition reserves are significantly compromised.
Treatment is usually complicated by sepsis and the metabolic and
fluid derangements caused by the fistula. Early fistula identification
is imperative to implement appropriate management strategies,
including patient stabilization, investigation of the fistula,
evaluation of surgical need, and the promotion of healing.
Care priorities
Once the fistula is diagnosed, immediate management should focus
on fluid restoration and the correction of electrolyte abnormalities.
The control of sepsis and septic complications, nutrition support,
and fistula management are key components to positive outcomes
and should be addressed concurrently.
2. Control of sepsis
Sepsis is often seen in the patient with postoperative ECF following
a bowel procedure where bowel contents escape into the
peritoneum. All team members should participate in the evaluation
of a septic foci. Blood, wound, fistula drainage, sputum, and venous
1773
catheter tips should be cultured. Empirical antibiotic therapy is
indicated with diagnosis of sepsis followed by specific therapy.
Intraperitoneal abscesses should be drained cautiously, because
manipulation of the septic foci may lead to its spread. If no
evidence of sepsis is observed, antibiotic therapy should be
withheld in the postoperative period. In patients with ECF,
indiscriminate antibiotic use will lead to the emergence of highly
resistant bacteria. (See Sepsis, Chapter 11.)
3. Nutrition support
Patients with a fistula are typically malnourished because of their
postoperative NPO status, the hypercatabolism of sepsis, and the
protein- and mineral-rich intestinal fluid loss from the fistula. Both
TPN and enteral nutrition can be used to manage patients with ECF
based on a thorough nutrition assessment.
Enteral nutrition is currently advocated over TPN, because
enteral nutrition enhances mucosal proliferation, promotes villus
growth, improves hepatic protein synthesis, and stimulates the
enterocyte, whereas TPN has been shown to cause intestinal
mucosal atrophy. However, TPN remains a valuable therapeutic
modality for patients who cannot tolerate enteral nutrition and in
combination with enteral nutrition for patients who are unable to
absorb sufficient calories from enteral feedings alone. Enteral
feedings can be initiated by a weighted nasoduodenal intestinal
feeding tube if there is sufficient (approximately 4 feet) functioning
small bowel length between the ligament of Treitz (a thin muscle
that wraps around the small intestine where the duodenum and
jejunum meet) and the fistula. Enteral feedings can be optimized in
patients with a feeding jejunostomy (placed at the time of their
surgery) distal to the fistula, as is the case of many postoperative
ECFs. In some cases, enteral feedings may be infused into the fistula
itself. The volume and concentration of enteral feedings are started
low and increased incrementally; supplementation with TPN is
necessary to meet caloric and protein requirements during this
time. For some patients, TPN supplementation is needed
throughout the duration of care. Enteral feedings are slowed or
discontinued if fistula output increases after initiation of feedings.
Patients with proximal small bowel fistulas, prolonged ileus, or
1774
extensive intraabdominal sepsis usually require TPN. Optimizing
nutrition status will enhance the immune system, preserve lean cell
mass, and promote wound healing. Improved nutrition status
correlates with spontaneous fistula closure.
4. Fistula management
Ideally, drainage from each fistula is collected separately to assess
individual fistula activity and healing. Individualized systems of
gravity or gentle suction drainage and barrier skin protection are
devised for each patient. Good local management reduces the
incidence of wound-related bacteremias and increases the rate of
wound healing. EAFs are managed with negative pressure wound
management therapy (NPWT) devices previously referred to as
vacuum-assisted closure (VAC) systems. The system consists of a
porous foam pad that connects to subatmospheric suction under an
occlusive dressing. NPWT devices divert fistula drainage away
from the wound by providing continuous negative pressure suction
to the wound surface. NPWTs protect the skin and reduce patient
discomfort from multiple dressing changes, because they require
changes only once every 2 to 3 days. This system effectively
promotes wound healing by increasing the rate of tissue
granulation and augmenting wound contracture.
Somatostatin analogues: Somatostatin analogues such as
octreotide have been shown to inhibit gastric secretions and should
decrease fistula output. However, studies showed no significant
improvement in fistula closure rate or improvement in mortality
rates. Somatostatin is associated with a frequent incidence of
hyperglycemia and can cause increased nausea. Therefore,
somatostatin analogs are not indicated for routine use in patients
with ECF. Octreotide has been shown to provide improved healing
time in patients with high-output fistulas, perhaps by decreasing a
high-output fistula to a low-output fistula. The role of octreotide is
currently limited for use with high-output fistulas.
Surgery: Spontaneous fistula closure occurs in approximately
30% of patients with ECF with adequate nutrition support and
successful treatment of sepsis. If spontaneous closure does not
occur after 4 to 6 weeks of management, surgical resection is
considered. Surgery is indicated in the following instances: (1) to
1775
close fistulas that continue to drain significant amounts despite
absence of infection and appropriate nutrition support; (2) to
explore and drain fistula tracts that could not be identified or
drained by less invasive techniques; and (3) if overwhelming sepsis
fails to respond to antibiotics and supportive therapy. Persistently
draining fistulas are surgically closed with a procedure involving
resection with end-to-end anastomosis. Postoperatively, parenteral
nutrition and antibiotic coverage are continued. A gastrostomy is
usually created to allow for prolonged intestinal decompression
and drainage. The patient may remain NPO for greater than 1 to 2
weeks after surgery, depending on the rate of healing and the
return of bowel function. An alternate feeding strategy is initiated
during this time.
Fluid/electrolyte management
1776
2. Administer IV crystalloids to replace fistula output. Generally,
fistula output is isosmotic with high potassium content. Thus,
normal saline with a potassium supplement should be
administered.
1777
11. Monitor ECG for prolongation of the QT interval, a result of
hypokalemia, hypocalcemia, and hypomagnesemia.
Infection control
1778
5. Administer IV antibiotics in a timely manner. Reschedule
antibiotics if a dose is delayed for greater than 1 hour. Recognize
that failure to administer antibiotics on schedule can result in
inadequate blood levels and treatment failure.
Nutrition management
1779
5. If fistula output increases in response to enteral feedings, slow
the rate of infusion or reduce the strength of the feeding. If the
patient tolerates oral feedings but they increase fistula output,
increase the frequency of the feedings and decrease the amount
consumed at each feeding.
Wound care
1. Assess the extent of the local problem (Box 9-7). Consult the
physician for signs of extensive damage to the tissue adjacent to the
fistula (i.e., severe local erythema, excoriation, edema, maceration).
1780
3. Note characteristic, color, odor, and volume of output from each
fistula. Consult the advanced practice provider for significant
changes in these indicators.
Box 9-7
NURSING ASSESSMENT OF
ENTEROCUTANEOUS FISTULA
• Evaluate size, shape, and location of the fistula. Reposition or lift
skin folds as necessary.
1781
Box 9-8
RECOMMENDATIONS FOR CONTAINING
FISTULA DRAINAGE
• Clean the intact skin surrounding the fistula with a nonirritating
antibacterial cleanser.
1782
related to biophysical change secondary to presence of external fistula.
Goals/Outcomes: By hospital discharge, the patient
acknowledges body changes, as evidenced by viewing fistula and
not exhibiting preoccupation with or depersonalization of fistula.
Body Image.
1783
Coping Enhancement; Self-Care Assistance; Support System
Enhancement.
3. For patients with altered LOC, massage gums and teeth with
saline-moistened, sponge-tipped applicator and brush teeth gently
if there is no evidence of bleeding. Carefully suction the solution
from the oral cavity throughout the procedure with a tonsil suction
device.
4. Keep the lips moist with emollients such as lanolin. Take care to
apply emollient to external tissue only. Oil-containing emollients
are harmful if aspirated or otherwise introduced into the
respiratory tract.
1784
Inflammatory Response Syndrome, Sepsis, Septic Shock, and
Multiple Organ Dysfunction Syndrome (Chapter 11).
Hepatic failure
Pathophysiology
There are various manifestations of acute and chronic liver failure.
Fluid retention, edema, and ascites are common to acute and
chronic hepatic failure and are attributed to: (1) intrahepatic
vascular obstruction with transudation of fluid into the peritoneum;
(2) defective albumin synthesis, resulting in decreased colloid
osmotic pressure with failure to retain intravascular fluid; and (3)
disturbances of various hormones, including renin, aldosterone,
and renal prostaglandins, resulting in sodium and water retention.
Massive ascites is usually the result of cirrhosis.
Hepatic encephalopathy occurs in both acute and chronic liver
failure. A state of decreased mentation, neuromuscular function,
and consciousness are the hallmarks of hepatic encephalopathy.
Patients with stage one (mild) hepatic encephalopathy have
problems concentrating, difficulty writing, memory loss, subtle
personality changes, mood swings, and sleep alteration that may
result in loss of awareness of time of day or night; often switching
daytime activities into night activities. Patients with stage two
(moderate) hepatic encephalopathy have less energy, have slurred
speech, behave strangely, forget more frequently, and have
problems with basic math. Patients with stage three (severe) hepatic
encephalopathy are somnolent, may have syncopal episodes, and
exhibit extreme changes in behavior. Monitoring patients for
seizures and dementia is crucial. These patients are often poorly
functional at home and are reported to be jumpy, fearful, and have
absolutely no basic math skills. Patients in stage four (hepatic coma)
are admitted directly to the ICU, usually arriving unconscious or
semiconscious. Patients with stage one and two are usually
ambulatory and receive outpatient treatment for hepatic
encephalopathy with oral medications. Patients with stage three are
often bordering on critical illness, whereas patients with stage four
1785
generally require mechanical ventilation and sedation in the ICU.
Complications of hepatic encephalopathy include brain swelling
with herniation, coma, and death.
Both acute and chronic hepatic failure affect the physiologic
status of all organs. Key differences between the two include
progression rate of liver failure, previous history of liver disease,
type of treatments required, and prognosis.
1786
Heart failure may occur in worsening ALF. While the condition
progresses, dysrhythmias result from reduced beta-adrenergic
receptor signal transduction, defective cardiac excitation-
contraction coupling, and conduction abnormalities. Right
ventricular failure ensues and causes venous engorgement resulting
in hepatic congestion. The decreased forward flow of blood from
the failing right-to-left heart circulation results in reduced CO.
Decreased hepatic blood flow, with congestion of the vena cava
from blood “backing up” from the failing right side of the heart,
impedes the emptying of the portal vein into the vena cava.
Heart failure progressively damages the hepatocytes attributable
to hypoxia resulting from circulatory impairment. The portal vein
supplies up to 83% of the blood flow to the liver, with the hepatic
artery supplying up to 34% (varies from person to person by
approximately ±17%). In the final stages of ALF, profound
peripheral vasodilation results in severe vascular congestion and
third spacing of intravascular fluids including ascites, which causes
hemodynamic collapse. Hypotension, tachycardia, heart murmur,
warm extremities, an exaggerated precordial impulse, palmar
erythema, and/or spider angiomas are present.
1787
United States are attributable to ESLD secondary to hepatitis C. The
U.S. Food and Drug Administration (FDA) has recently approved
direct-acting antivirals for hepatitis C that will profoundly change
the face of ESLD and liver transplantation in the future.
Nonalcoholic fatty liver disease attributable to risk factors such as
lipidemia (hypertriglyceridemia), obesity, and diabetes is quickly
becoming a more prevalent liver disease and in the near future will
be responsible for more cases of ESLD. In the great majority of
cases, CLF takes decades to manifest itself with symptoms
requiring treatment and eventual referral to a liver transplant
center.
In patients with cirrhosis, portal hypertension creates
hyperdynamic circulation, reflected by decreased SVR,
hypotension, increased CO, tachycardia, and bounding pulses.
Progression to advanced liver disease correlates with worsening
hyperdynamic circulation.
Patients with chronic liver disease may have hepatopulmonary
syndrome (HPS) that results from intrapulmonary microvascular
dilation that may or may not be coupled with portal hypertension.
There may be diffuse or localized dilated pulmonary capillaries.
Less common are the presence of pleural and pulmonary
arteriovenous communications. Arterial hypoxemia, commonly
present in chronic liver disease, is attributable to multiple
coexisting causes such as ascites, hepatic hydrothorax, and/or
chronic obstructive pulmonary disease. Dyspnea (shortness of
breath) may be present at rest or during exertion and is the main
symptom, particularly after long-standing liver disease. Upon
examination, spider angioma, digital clubbing, cyanosis, and
platypnea (shortness of breath relieved when lying down) are
common findings. Liver transplantation can reverse HPS if the
patient survives longer than 6 months posttransplant and can
improve to the point that supplemental oxygen may no longer be
needed.
As defined by the National Institutes of Health Patient Registry
for the Characterization of Primary Pulmonary Hypertension, a
patient has portopulmonary hypertension (POPH) in the presence
of portal hypertension with a mean pulmonary artery pressure ≥25
mm Hg and pulmonary capillary wedge pressure less than 15 mm
1788
Hg. Symptoms include fatigue, dyspnea, peripheral edema,
syncope, chest pain, and a systolic murmur. ECG in 90% of patients
reflects right bundle branch block, right-axis deviation, or a right
ventricular hypertrophy. According to the American Association
for the Study of Liver Diseases (AASLD) practice guidelines, POPH
can potentially improve with liver transplantation and has
acceptable short-term outcomes. In some patients, vasodilator
therapy can even be discontinued posttransplant. Transjugular
intrahepatic portosystemic shunting (TIPS) is useful for treating
portal hypertension associated with refractory ascites and
esophageal varices in the patient with cirrhosis who has ESLD. In
over 90% of patients, TIPS procedures decompress the portal vein.
Studies have shown that the rate of new or worsening hepatic
encephalopathy after TIPS is 20% to 31%.
Spontaneous bacterial peritonitis is a spontaneous infection that
affects up to one third of patients with ESLD. The most common
organism found in the peritoneal fluid of patients with spontaneous
bacterial peritonitis is Escherichia coli, believed to be attributable to
translocation of the bacteria from the intestinal lumen. Prevention
of spontaneous bacterial peritonitis is key with the use of oral
antibiotics.
Hepatorenal syndrome (HRS) is defined by the International
Club of Ascites as renal impairment or failure that occurs in
patients with advanced chronic liver disease, liver failure, and
portal hypertension. Patients have marked abnormalities in the
arterial circulation and activity of the endogenous vasoactive
systems. There are two types of HRS defined by the International
Club of Ascites: type 1 is rapidly progressive, with baseline
creatinine level doubling in less than 2 weeks to a value greater
than 2.5 mg/dL. Type 2 is a slower disease that consists of moderate
renal failure and is commonly associated with refractory ascites.
The vast majority of patients have no intrinsic renal disease.
Significant renal vasoconstriction results in low glomerular
filtration rate, whereas arterial vasodilation in the extrarenal
circulation results in reduction of SVR and hypotension. Factors
that reduce renal perfusion in patients with chronic liver disease are
dehydration, lactulose therapy, use of NSAIDs, hemorrhage, and
paracentesis. For patients with cirrhosis who develop renal
1789
dysfunction, the risk of death increases sevenfold and 50% of
patients die within a month of onset.
Hepatic assessment
Goal of system assessment
A thorough physical assessment along with an accurate history
should produce a correct liver disease diagnosis in the majority of
cases. Evaluate for cause of and subsequent hepatic and
multisystem effects of ALF, because severe liver damage has
already occurred upon presentation for care.
1790
Vital sign assessment
• Neurologic assessment, including Glasgow Coma Scale score, in
some cases an intracranial pressure (ICP) monitor, and an arterial
line may be needed for patients who are severely ill.
• Take BP while the patient is lying down, sitting up, and standing
(if able)—this also helps to observe for platypnea.
Observation
• Evaluate for pallor, jaundice, and scleral icterus and signs of
coagulopathies.
1791
• Note if asterixis (brief periods of “flapping” or irregular flexion of
the hands at the wrist) is present.
Palpation
Liver palpation can aid in the diagnosis of liver disease etiology
and confirm cirrhosis.
• Palpate the liver and other abdominal organs (i.e., spleen). Note
liver firmness, size, edges, and possible pain with palpation.
Hepatomegaly may be evident. Many times in liver disease,
splenomegaly is also appreciated. Gallbladder (if not previously
removed) may be palpated (and if palpable and/or painful may
be attributable to stones or infection); also assess for the presence
of any abdominal masses.
1792
• Ascites can be diagnosed if not obvious with palpation and
observation of an abdominal fluid wave upon palpation.
Auscultation
• Listen to the heart, carotid artery, lungs, and abdomen.
Screening labwork
Blood testing may differentiate between ALF and chronic liver
disease, as well as aid in diagnosing the severity of liver injury and
degree of liver function/dysfunction.
1793
decreased albumin to check for hepatocyte injury, or a cholestatic
cause for liver disease (see chart).
Liver biopsy
Once thought of as a diagnostic tool, liver biopsy now serves three
important roles according to the AASLD liver biopsy position
paper: (1) for diagnosis, (2) for assessment of prognosis (disease
staging), and/or (3) to assist in making therapeutic management
decisions. Liver biopsy is invaluable in patients that present with
atypical clinical features, coexisting disorders, and “overlap”
syndrome of two liver diseases (such as primary biliary cirrhosis
and autoimmune hepatitis).
Other studies
1794
Chest radiography, Doppler echocardiography, and ABGs are
useful in the diagnoses of HPS and POPH.
1795
occur in viral hepatitis and
cirrhosis. Consistently elevated
levels are a poor prognostic sign.
Gamma-glutamyl To assist with diagnosing Present in numerous tissues, but
transpeptidase (GGT) that liver disease is present. highest in liver disorders. This
test can be used to confirm that
Alk Phos is elevated resulting
from a hepatic-related condition.
Usually elevated in cholestatic
liver disease, cirrhosis, alcoholic
liver disease, and metastasis to
the liver.
1796
Hematologic Tests
Hemoglobin (Hgb) To assess if anemia is GI bleeding may be present with
Hematocrit (Hct) present. decreased Hgb/Hct. Anemia seen
in hepatic failure is termed
macrocytic (attributable to
increase in mean corpuscular
volume) and normochromic
(normal Hgb).
1797
results in 2 to 3 minutes bacterial peritonitis if PMN
count is ≥250 cells/mm3
while awaiting culture and
sensitivity results.
Radiology
Chest x-ray Assesses for any pathology Tumors, lymph nodes, atelectasis,
in the lungs and chest cardiomegaly, infiltrates,
cavity, confirms diagnosis of tortuous cardiac vessels, and
portopulmonary diaphragm elevation (bilateral or
hypertension and unilateral).
hepatopulmonary
syndrome.
Magnetic resonance imagingAssesses liver size, Enlarged liver, cirrhosis, tumors,
(MRI): morphology, function, cysts, hemangiomas, steatosis,
Hepatic MRI presence of cirrhosis, macronodular lesions,
steatosis, and lesions. Used hemochromatosis (if large iron
to characterize known stores are present), sarcoid
lesions and status of hepatic nodules, biliary cystadenomas,
circulation. Can produce a adenomas, focal nodular
sharp contrast between hyperplastic nodules,
tissues and water and/or fat. cholangiocarcinoma, abscesses,
Can image in transverse, thromboses, and hepatic
longitudinal, coronal, or congestion.
oblique planes.
Computed tomography (CT): Assesses liver size, Enlarged liver, cirrhosis, tumors,
Hepatic CT scan presence of cirrhosis, cysts, hemangiomas, steatosis,
looks for the presence of macronodular lesions,
lesions to characterize hemochromatosis (if large iron
known lesions and status stores are present), sarcoid
of hepatic circulation. nodules, biliary cystadenomas,
Oral or intravenous adenomas, focal nodular
contrast can be hyperplastic nodules,
administered to help cholangiocarcinoma, abscesses,
distinguish the bowel thromboses, and hepatic
lumen and blood vessels congestion.
and tissue, respectively.
Ultrasound: Assesses for fluid-filled Main anatomic features of the
Hepatic ultrasound lesions and vascular liver can be identified, as well as
abnormalities. Also used cysts, infections, abscesses,
to “mark the spot” before steatosis, hemangiomas,
liver biopsy. malignant neoplasms, adenomas,
Note: Ultrasound is best hyperplastic lesions, lymphomas,
suited to thinner patients. increased echogenicity, hydatid
cysts, amebiasis (caused by
Entamoeba histolytica that can
spread to the liver causing liver
abscesses), and fungal disease.
Cerebral CT Used for diagnosis when a Cortical and subcortical atrophy;
subdural hematoma or benign, neoplastic, and metastatic
doubt about etiology of lesions; hemorrhaging;
altered consciousness in the aneurysms; and hematomas.
patient with end-stage liver
disease is in question.
Brain flow studies: To confirm brain death Brain death, as evidenced by lack
Technetium scan of the brain when the patient is in a of blood flow into the brain.
hepatic coma when EEG is
not confirmatory.
1798
Radioisotope liver scan To determine the presence Hepatocellular carcinoma,
Injection with radioactive of three-dimensional lesions melanoma, Hodgkin and non–
compound and scanned in the liver. Hodgkin lymphoma.
with a scintillation camera
or radiography
Invasive Testing
Liver biopsy (can be Used as a diagnostic and Inflammation, fibrosis, cirrhosis,
percutaneous at the bedside prognostic tool. Can grade hepatocellular carcinoma,
or transvenous in and stage liver disease. Can regenerative changes, apoptosis,
interventional radiology) differentiate between necrosis, iron, complex
Note: Even when platelets are various liver diseases. Can carbohydrates, steatosis, copper,
low, this test can still be be used to follow the granulomas, hepatitis B surface
performed in interventional progression of liver antigen, Mallory bodies, talc
radiology transjugularly after diseases. crystals, inflammatory cells,
platelet infusions, microabscesses, Cowdry type A
desmopressin (DDAVP), or inclusions, etc.
recombinant factor VIIa,
according to local practice.
Box 9-9
KING’S COLLEGE HOSPITAL CRITERIA
ALF from acetaminophen
• pH <7.30 (24 hours after ingestion and after adequate fluid
resuscitation)—irrespective of coma grade
1799
• PT >100 seconds (INR >6.5)—regardless of coma grade or any
three of the following regardless of encephalopathy grade:
1800
jaundice in a patient. Usually, bilirubin levels are higher in a
neoplastic process in the liver than in other causes of liver disease.
Alkaline phosphatase
Similar to the other “liver function” tests, alkaline phosphatase is
found in many parts of the body. The liver and bone appear to be
the main sources of this enzyme. Elevation of this enzyme is usually
seen in hepatobiliary diseases.
Serum albumin
Albumin levels tend to be normal regardless of the cause of liver
disease. Hypoalbuminemia is usually found in patients with ESLD
and/or cirrhosis where decreased albumin synthesis, ascites, and
severe liver damage are present.
Liver biopsy
Liver biopsy is the “gold standard” of testing used to diagnose the
type of liver disease, screen for familial disease, monitor and stage
the disease, evaluate the degree of hepatocellular injury, evaluate
effectiveness of treatment, and confirm rejection episodes in the
transplanted liver.
HIGH ALERT!
Risk of death from a liver biopsy complication is estimated to be 1
in 10,000. The patient MUST be adequately prepared for the liver
biopsy procedure and the aftercare to minimize potential
complications and prevent mortality. The patient and their vital
signs must be monitored very closely for signs and symptoms of
complications from a biopsy if they are in a hepatic coma or
induced coma. If platelets are less than 60,000, the biopsy can still
1801
be performed transjugularly in interventional radiology after
administration of a platelet transfusion, desmopressin (DDAVP),
or administration of recombinant factor VIIa.
Before biopsy
• Ensure that the patient has not had salicylates (e.g., aspirin or
bismuth) or NSAIDs (e.g., ibuprofen, naproxen) for 7 days before
the biopsy.
• The patient should not have eaten for 4 to 8 hours before the
procedure.
During biopsy
• Coach the alert patient to exhale and hold their breath during the
procedure (or manually ventilate the intubated patient to prevent
lung inflation during puncture) to avoid movement of the lung
and possible resulting pneumothorax.
1802
After biopsy
• Remind the patient that mild shoulder pain may persist for 24 to
48 hours after the biopsy.
Collaborative management
1803
HEPATIC FAILURE MANAGEMENT GUIDELINES
*
All guidelines and position papers are available on the AASLD website:
www.aasld.org. AASLD, American Association for the Study of Liver Diseases.
Care priorities
Hepatic failure may develop suddenly in a patient with
compensated liver disease. Sustained hypoxia or hypotension from
any cause can aggravate hepatocellular failure and must be
corrected promptly. EtOH, hepatotoxic drugs, and hepatotoxic
alternative therapies are eliminated. Minimize use of sedatives and
tranquilizers because they may contribute to hepatic
encephalopathy.
1804
When the patient first presents for care, a central line should be
inserted. This will assist with restoration of intravascular volume
thereby ensuring systemic perfusion, which can help to keep other
organs from failing. Maintaining hemodynamics is particularly
important if intracranial hemorrhage (ICH) is present or renal
function is compromised. The AASLD guidelines recommend that
hypotensive patients with ALF be resuscitated with normal saline
first. After initial resuscitation, if the patient is acidotic, half-normal
saline containing 75 mEq/L sodium bicarbonate should be given.
Inotropic or pressors may be needed to maintain an MAP of at least
75 mm Hg or a cerebral perfusion pressure of 60 to 80 mm Hg.
Norepinephrine may be used to assist peripheral organ perfusion
and preserve splanchnic (hepatic) blood flow. CVP monitoring may
be initiated to ensure adequate tissue perfusion without fluid
overload. Hypoglycemia is common and a continuous glucose
infusion should be used. In addition, potassium, magnesium, and
phosphorus move from the intravascular space to the intracellular
space, thereby necessitating the need to monitor these electrolytes
closely and supplement as needed.
HIGH ALERT
Accurate measurements and careful interpretation of
hemodynamic measurements are essential because fluid balance is
delicate in critically ill patients with hepatic failure. Hemodynamic
measurements can be difficult to interpret because circulation is
hyperdynamic. SVO2 or ScVO2 monitoring is helpful in evaluating
the adequacy of tissue oxygenation.
1805
parenteral feedings be initiated early. Restriction of protein should
be avoided. It is recommended that 60 g/d be given initially.
Sodium is moderately restricted (up to 2000 mg/d) unless
significant ascites and peripheral edema are present, wherein a less
than 500-mg sodium diet is prescribed. Total caloric intake should
be 2500 to 3000 per day.
1806
admission and then every 2 to 4 hours once stabilized.
Hypoglycemia should be corrected expeditiously with a bolus of
50% dextrose (D50) or continual infusion of a 10% dextrose
solution (D10).
1807
of flora can be given. PPIs have been associated with the rate of
spontaneous bacterial peritonitis in patients with cirrhosis. The
majority of patients may have no documented indication for their
use.
1808
stent to decompress the portal vein and create a new circulatory
pathway for blood to flow around the liver back to the heart to
help relieve portal hypertension. AASLD guidelines recommend
that a polytetrafluoroethylene-covered stent is preferable for TIPS
procedures versus bare stents, with studies showing less stent
dysfunction, and perhaps improved patient outcomes. In
addition, a TIPS can prevent rebleeding from varices and reduce
or stop ascites. See Box 9-11 and Fluid Volume Excess, Chapter 9,
for nursing implications.
1809
must be processed by the liver.
1810
guide pharmacologic management (e.g., mannitol, furosemide)
and other therapeutic measures. See discussion in Traumatic
Brain Injury, Chapter 3.
7. Infection control
Whether in acute or chronic liver failure, patients are susceptible to
infections. These patients have decreased phagocyte function,
decreased complement, and their need for invasive procedures
makes them more exposed to various bacteria, viruses, and fungi.
1811
• Monitor ascitic fluid: Bedside dipsticks are available that will
provide a result within 2 to 3 minutes to inform healthcare
providers if an infection is present in ascites. This can easily be
done at the bedside during a paracentesis. These results can
correlate with an upward trend of WBCs.
1812
of the skin to retain it causing it to weep. The limb
may feel cold and wet, blistering may be evident.
This can lead to erysipelas and cellulitis. More
frequent sheet changes to keep the rest of the skin
dry, dressing changes of the area with foam, or a
hydrofiber composite dressing material and a
compression dressing may help. Severe weeping
may call for hourly dressing changes.
9. Pain management
Patients with ascites and edema are uncomfortable as a result of
excess fluid compressing internal organs and the skin stretching. In
severe cases, skin splitting prompts more significant pain, similar to
a burn or ruptured blister. Pain assessments should be done at least
every 2 hours and medication for pain administered as needed.
Any changes in vital signs must be thoroughly evaluated to discern
if fluctuations are attributable to worsening pain or worsening of
condition. Nonpharmacologic pain-relief strategies including a
change of position, imagery, relaxation exercises, biofeedback, hot
or cold compresses, or distraction techniques may be helpful.
Spiritual support during a time of suffering may be meaningful,
such as having a chaplain or other appropriate religious figure visit
the patient. All measures that are effective in relieving pain should
be reported to team members and documented in the healthcare
record.
1813
• Monitor for change in location of pain: A change in location of
pain can herald disease progression.
1814
pressure (PAWP) 6 to 12 mm Hg, CI greater than 5 L/min/m2, SVR
900 to 1200 dynes/s/cm-5, urinary output greater than 0.5 mL/kg/h,
and orientation to person, place, time, and situation. The goals of
improvement for patients who are extremely ill are adjusted
according to the predicted best values the patient can achieve with
their level of organ impairment.
Risk Control: Fluid Volume Deficit, Fluid Balance, Fluid
Status, Electrolyte, and Acid-Base Balance.
Fluid management
1815
provider if serum albumin and total protein are trending
downward.
Hemodynamic regulation
Fluid management
1816
1. Fluid overload: Consult the advanced practice provider for fluid
overload: weight gain, presence of dyspnea, tachypnea, rhonchi,
orthopnea, basilar crackles that do not clear with coughing, labored
and/or shallow breathing, elevated BP, or S3 heart sound.
Box 9-11
NURSING CARE AFTER TRANSJUGULAR
INTRAHEPATIC PORTOSYSTEMIC SHUNT
OR PERITONEAL VENOUS SHUNT
PROCEDURE
Measure urinary output hourly and CVP every 1 to 2 hours.
1817
• Anticipate rapid fluid mobilization, as evidenced by increased
CVP and increased urinary output.
1818
• Expanded blood volume may increase variceal pressure, resulting
in bleeding. Bleeding is evidenced by a sudden decrease in
hematocrit (a mild dilutional decrease is anticipated in the
immediate postprocedural period), unexplained nausea,
lightheadedness, dark stools, or hematemesis.
1819
Goals/Outcomes: The patient has adequate nutrition, as
evidenced by a state of nitrogen balance as shown by daily fecal
excretion of 2 to 3 g of nitrogen and 4 to 20 g of urinary nitrogen,
thyroxine-binding prealbumin 200 to 300 µg/mL, and retinol-
binding protein 40 to 50 µg/mL. During protein catabolism
(proteolysis), nitrogen is excreted in the feces, urine, and blood. If
nitrogen balance is negative, the patient is using muscle for protein.
At least 5 g of feces needs to be collected with for the test. Urine
should be collected for 24 hours. Thyroxine-binding prealbumin
(measures protein-calorie malnutrition) and retinol-binding protein
(measures visceral protein mass) are serum tests. Blood glucose
levels remain within an acceptable range of 100 to 160 mg/dL.
Nutrition Status; Biochemical Measures.
Nutrition monitoring
1820
desired by the patient and ensure it meets prescribed dietary
restrictions.
Energy management
Hypoglycemia management
1821
Level of consciousness is difficult to evaluate in the presence
of moderate to severe hepatic encephalopathy, and obtaining a
baseline level of consciousness is imperative.
Oxygen therapy
Aspiration precautions
1822
Disturbed sensory perception
related to endogenous chemical alteration (accumulation of ammonia or
other CNS toxins occurring with hepatic dysfunction), therapeutically
restricted environment, sleep deprivation, hypoxia, sensory overload
(noise, personnel) in ICU, and medication (side effects, toxic levels from
the inability of the liver to detoxify appropriately).
Goals/Outcomes: By the time of hospital discharge, the patient
exhibits stable personality patterns, age-appropriate behavior,
intact intellect appropriate for level of education, distinct speech,
and coordinated gross and fine motor movements. Handwriting is
legible, and psychometric test scores are improved from baseline
range.
Distorted Thought Self-Control; Information Processing;
Neurologic Status: Consciousness.
1823
significant elevations from baseline. Ammonia
values and their measurement vary greatly and
do not always correlate directly with
encephalopathy.
1824
production of cerebral intoxicants. Monitor the
patient for evidence of ototoxic effects (i.e.,
decreased hearing) and nephrotoxic effects (e.g.,
urinary output less than 0.5 mL/kg/h, increased
creatinine levels) of neomycin use. Avoid
neomycin administration for patients with renal
insufficiency.
1825
prescribed. Sedation or coma induction may be indicated if cerebral
edema does not respond to the measures just mentioned.
Box 9-12
FACTORS THAT CONTRIBUTE TO
HEPATIC ENCEPHALOPATHY
Chronic factors
• Portal-systemic shunting (entry of portal blood into systemic
veins without being metabolized by the liver): May occur via
damaged liver, collateral vessels, or surgically created portacaval
anastomosis
• Intestinal bacteria
• Acid-base imbalance
Precipitating factors
• Dehydration/electrolyte imbalance: May occur with overdiuresis,
diarrhea, vomiting, or other factors
• Excessive paracentesis
• Sedatives/hypnotics
• Infection
1826
• Constipation
• Viral hepatitis
• Alcoholic hepatitis
Box 9-10
DRUGS AND SUBSTANCES WITH
HEPATOTOXIC POTENTIAL
• Acetaminophen
• Allopurinol
• Amiodarone
• Amoxicillin-clavulanate
• Amphetamines
• Ampicillin
• Antidepressants
• Carbamazepine
• Carbenicillin
• Carbon tetrachloride
• Chloramphenicol
1827
• Chlorpromazine
• Clindamycin
• Cocaine
• Dantrolene
• Dapsone
• Didanosine
• Diclofenac
• Disulfiram
• Efavirenz
• Ethanol
• Etoposide
• Flutamide
• Gemtuzumab
• Halothane
• Hydrochlorothiazide
• Imipramine
• Isoflurane
• Isoniazid
• Ketoconazole
• Labetalol
1828
• Lisinopril
• Metformin
• Methotrexate
• Methyldopa
• Nefazodone
• Nicotinic acid
• Ofloxacin
• Oral contraceptives
• Penicillin
• Phenytoin
• Propylthiouracil
• Pyrazinamide
• Quetiapine
• Rifampin
• Rifampin-isoniazid
• Salicylates
• Statins
• Sulfonamides
1829
• Tolcapone
• Trimethoprim-sulfamethoxazole
• Troglitazone
• Valproic acid
• Yellow phosphorus
Infection protection
1830
for positive culture results.
Ineffective protection
related to clotting anomaly, thrombocytopenia, itching, and disorientation.
Goals/Outcomes: The patient’s bleeding, if it occurs, is not
prolonged. The patient’s skin is not damaged from scratching. The
patient’s confusion (if present) and LOC will not lead to injury (see
Alterations in Consciousness, Chapter 1).
Blood Coagulation.
1831
Bleeding precautions
6. Avoid trauma: Use electric rather than safety razor for patient
shaving. Provide soft-bristle toothbrush or sponge-tipped
applicator and mouthwash for oral hygiene. Avoid indwelling,
large-bore gastric drainage tubes if possible, because they may
irritate gastric mucosa or varices, causing bleeding to occur.
1832
products are present in the blood and thrombocytopenia is
significant, the patient may have DIC (see Bleeding and Thrombotic
Disorders: Disseminated Intravascular Coagulation, Chapter 10).
Fluid/electrolyte management
1833
Impaired tissue integrity
related to chemical irritants (bile salts), impaired mobility, and fluid excess
(tissue edema).
Goals/Outcomes: The patient’s tissue remains intact; pruritus is
relieved or reduced within 12 hours of this diagnosis.
Comfort.
Skin surveillance
1834
5. Prevent skin damage:
Deficient knowledge
related to lack of exposure to healthcare information; cognitive limitation
secondary to hepatic encephalopathy.
Goals/Outcomes: The patient/family/significant other states signs
and symptoms of early hepatic encephalopathy, importance of
medical follow-up, understanding of disease state, and how to keep
it stabilized (i.e., alcohol/drug treatment programs, proper diet,
proper infection control methods, taking prescribed medications).
Knowledge: Disease Process; Knowledge: Diet; Knowledge:
Medication; Knowledge: Substance Use Control, Risk Control Drug
Use, Risk Control Alcohol Use.
1835
unknowingly shared a toothbrush or razor).
1836
infectious disease consult may be indicated, along with possible
treatment. It is important to note, however, that those with sexual
exposure have less than a 5% chance of seroconversion. Those with
exposure to blood, particularly through hollow-bore needles, have
the greatest chance of seroconversion.
1837
HCV NS5B RNA-dependent RNA polymerase. The
combination of SOF plus RBV has been shown to be
effective against multiple genotypes without PEG
use and thereby decreases numerous side effects,
including severe effects. Response rates are nearly
100% in patients with genotypes 2 and 3 HCV using
an oral regimen, and greater than 90% in patients
with genotype 1 HCV. Simeprevir, a second-
generation protease inhibitor developed to treat
patients with genotype 1, binds to its target
differently than boceprevir or telaprevir. Response
rates are in the 75% to 80% range in combination
with PEG plus RBV. Other treatments are in various
stages of development including NS3 protease
inhibitors, NS4B inhibitors, NS5A inhibitors, NS5B
nucleoside inhibitors, and NS5B nonnucleoside
inhibitors. Drugs being developed to attack other
host targets include cyclophilin A inhibitors,
MiR122 inhibitors, and entry inhibitors.
1838
paracentesis or other invasive procedure sites; warmth and
erythema surrounding the invasive sites; or abdominal pain. Have
the patient demonstrate the technique for measuring oral
temperature with type of thermometer used at home.
10. Alcohol use: Caution about the necessity of alcohol cessation for
at least several months after complete recovery from the acute
episode. After full recovery, one or two glasses of beer or wine a
week are usually allowed if hepatic failure was not related to
alcoholism or alcohol ingestion.
Teaching individual
1839
1. Liver biopsy: Fully prepare the patient emotionally and
physically for the procedure.
Peritonitis
Pathophysiology
Peritonitis is an inflammation of the peritoneum and can be
classified as primary, secondary, or tertiary. Secondary peritonitis,
the most common form of peritonitis, is an inflammation of all or
part of the peritoneal cavity caused by diffuse microbial
proliferation or chemical irritation from leakage of corrosive gastric
or intestinal contents into the peritoneum. Ruptured appendix,
leaky anastomoses from weight loss surgery (e.g., Roux-en-Y,
1840
gastric bypass), perforated peptic ulcer, bowel rupture related to
ulcerative colitis or Crohn disease, pancreatitis, abdominal trauma,
and ruptured abdominal abscesses are among the many etiologic
factors associated with secondary peritonitis. Indwelling tubes and
catheters, such as those used for postoperative drainage and
peritoneal dialysis, are foreign bodies that compromise peritoneal
integrity and permit the entry of infective organisms that can
trigger peritonitis. Peritonitis is a leading cause of morbidity in
patients with kidney failure who are treated with continuous
ambulatory peritoneal dialysis (CAPD). CAPD-associated
peritonitis is caused by bacteria (Staphylococcus epidermidis and other
skin flora) most often, entering the abdominal cavity by the dialysis
catheter site.
Primary peritonitis is a bacterial infection of the serous
membrane lining the abdominal cavity that occurs spontaneously
without any apparent source of contamination, such as bowel
perforation. The most common etiology of primary peritonitis is
spontaneous bacterial peritonitis, which occurs most commonly in
patients with cirrhosis of the liver with ascites. Bacterial seeding of
ascitic fluid is believed to result from the translocation of enteric
bacteria across the gut wall or mesenteric lymphatic vessels and is
associated with a high mortality rate. Tertiary peritonitis represents
persistent or recurrent infection following an apparently
successfully treated episode of primary spontaneous bacterial
peritonitis or secondary peritonitis. Tuberculosis-related peritonitis
is rare in the United States with the exception of patients with
acquired immunodeficiency syndrome (AIDS), who are frequently
infected with multidrug-resistant strains of the bacillus.
Regardless of the initiating factor, the inflammatory process is
similar. Initial manifestations are triggered by histamine release and
include hyperemia, edema, and vascular congestion. Fluid shifts
from intravascular to interstitial spaces creating hypovolemia as a
result of increased vascular permeability caused by inflammatory
mediators. The circulating blood volume is depleted and
hypovolemic shock may ensue. The transudated fluid within the
interstitium contains high levels of fibrinogen and thromboplastin.
The fibrinogen is converted to fibrin by the thromboplastin. Under
normal conditions, the healthy peritoneum is naturally fibrinolytic,
1841
and can block fibrin formation. When the peritoneum is weakened
or injured, fibrinolysis is hampered and fibrin adheres to the
damaged area and forms a barrier that harbors and protects
bacteria from the normal immune responses, resulting in pockets of
infection and abscess formation. In most cases, the fibrin deposits
dissolve. The continued presence of fibrin can lead to adhesions
and potentially bowel obstruction. With severe inflammation,
intraabdominal sepsis may develop.
1842
sepsis.
Abdominal pain
• Abdominal pain is the hallmark of peritonitis and may be severe,
causing the patient to maintain a fetal position and resist any
movement that aggravates the pain. The onset can be sudden or
insidious, with the location varying according to the underlying
pathology.
Observation
• Occasionally, mild to moderate ascites is observed, depending on
the cause of the peritonitis.
Auscultation
• Auscultation of all four quadrants usually reveals diminished or
absent bowel sounds. The complete absence of bowel sounds
suggests an ileus—a frequent complication of peritonitis.
1843
Palpation
• Palpation of the abdomen elicits tympany and tenderness that can
be generalized or localized, depending on the nature and extent
of infection.
Nutrition assessment
• Evidence of malnutrition will be noted in the presence of chronic
liver or renal disease.
Screening labwork
• Abdominal paracentesis: Ascitic fluid for cell count, Gram stain,
and culture.
• LFTs: Elevated.
Hemodynamic measurements
• Hypovolemia with marked tachycardia, hypotension, decreased
MAP, and decreased urine output may occur as a result of
1844
massive fluid shifts from the intravascular space into the
abdominal interstitium and peritoneum and from vasodilation
caused by inflammatory mediators.
1845
Peritoneal total Useful in confirming the Total protein >1 g/dL; ascetic low-density
protein and diagnosis of bacterial lipoprotein greater than serum low-density
lactate peritonitis. lipoprotein.
dehydrogenase
levels
Peritoneal Useful in confirming the Decreased peritoneal fluid glucose level (<50
glucose level diagnosis of bacterial mg/dL).
peritonitis.
Hematologic tests
Leukocytosis will be present. A low total WBC count may indicate
an exhausted bone marrow, with a poor prognosis. Initially, the
Hgb and Hct values may be increased because of
hemoconcentration, but they will decrease to baseline levels when
normal intravascular volume is restored.
1846
Radiologic procedures
The abdominal radiograph test usually reveals dilation of the large
and small bowel, with edema of the small bowel wall. Free air in
the abdomen suggests visceral perforation. With abdominal CT,
abscesses can be visualized and sometimes drained during the
procedure, thus avoiding surgery. Free fluid in the abdomen on
ultrasound suggests hemorrhage or ascites.
Diagnostic paracentesis
Abdominal paracentesis involves the insertion of a catheter or
trocar into the abdomen to obtain a specimen. Sterile saline is
infused through the catheter, and the return fluid is analyzed for
RBC, WBC, and bacteria content. If ascites is present, it may not be
necessary to infuse saline because fluid can be removed directly for
analysis. Paracentesis may be repeated 48 hours after the initiation
of treatment to assess patient response. Multiple organisms on
peritoneal or ascitic fluid Gram stain or culture are diagnostic of
secondary peritonitis, whereas spontaneous bacterial peritonitis is
caused by monomicrobial infection.
Collaborative management
Management should be geared toward controlling the infectious
source, eliminating bacteria and toxins, modulating the
inflammatory process, and preventing organ system failure.
Patients should be cared for in an intensive care setting, even if they
do not appear critically ill initially.
Care priorities
Care priorities begin with volume resuscitation, electrolyte
replacement, and empirical antibiotic coverage. Medical, nursing,
interventional, and surgical therapies should be complementary
involving hemodynamic management, pulmonary support, and
1847
renal replacement therapy, and nutrition and metabolic support.
1848
according to the infectious source, infection severity, underlying
disease, and the patient’s response to therapy. Therapy for 5 to 10
days is sufficient for most patients.
1849
• Interventional therapies include percutaneous drainage of
abscesses and percutaneous and endoscopic stent placements.
Ultrasound- and CT-guided percutaneous drainage has been
shown to be efficacious and safe and preferred in some cases,
allowing for a delay in surgery until the acute process and sepsis
can be resolved.
1850
the return of GI motility, enteral nutrition with nonelemental
(conventional) tube feedings can begin.
Fluid/electrolyte management
1851
hypovolemia. Usually, the ECG will show sinus tachycardia. In the
presence of hypokalemia caused by prolonged vomiting or gastric
suction, ECG may show ventricular ectopy, prominent U wave, and
depression of the ST segment.
1852
using the same scales and method. Compare 24-hour body fluid
output with 24-hour fluid intake, and record the difference.
Medication management
1853
blood flow. Vasopressin or epinephrine may be added as ordered.
Dopamine is not recommended except in highly selective patients
such as those with low risk for tachydysrhythmias or with absolute
or relative bradycardia according to the 2012 Surviving Sepsis
Campaign guidelines.
Wound care
1854
and other body fluids from wounds.
Hyperthermia
related to infectious process, increased metabolic rate, and dehydration
secondary to peritonitis.
Goals/Outcomes: The patient’s temperature remains within
acceptable limits (36° C to 38.9° C [97° F to 102° F]) or returns to
acceptable limits within 4 to 6 hours of diagnosis. An open airway
is secured in the event of hyperthermic seizures.
Thermoregulation.
Temperature regulation
1855
minimize tissue damage.
Infection control
Wound care
1856
purulent drainage).
Acute pain
related to biological or chemical agents causing injury to the peritoneum
and intraperitoneal organs.
Goals/Outcomes: Within 2 hours of diagnosis, the patient’s
subjective evaluation of discomfort improves, as documented by a
pain scale. Nonverbal indicators of discomfort, such as grimacing,
are absent.
Pain Control.
1857
Analgesic administration
1858
Goals/Outcomes: The patient maintains baseline body weight,
and nitrogen tests show a state of nitrogen balance within 5 to 7
days of this diagnosis.
Nutrition Status: Food and Fluid Intake.
Nutrition management
1859
Goals/Outcomes: The patient displays no signs of increased IAPs
through discharge.
(See Abdominal Hypertension and Abdominal Compartment
Syndrome, Chapter 11.)
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1860
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1861
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CHAPTER 10
Hematologic/immunologi
disorders
General hematology assessment
Goal of assessment
The goal of a basic hematology assessment is to identify assessment
and historical factors that correlate with findings on the complete
blood count (CBC) to assist in diagnosing a hematologic disorder.
Correlation of findings helps with diagnosis and treatment of
anemias, allergies, bleeding and clotting disorders, infections, and
cancer (especially in patients requiring chemotherapy). The use of
many medications and chemotherapy may have a negative effect on
the bone marrow, resulting in reduced production of cells reflected
on the CBC.
Observation
Changes in various blood components place patients at higher risk
for infection, fatigue, weakness, lethargy, bleeding, and clotting.
Patients may report:
1866
• Respiratory: Shortness of breath (SOB), exertional or chronic
dyspnea, cough, hemoptysis, orthopnea.
History
Patients at risk of hematologic or immunologic problems may
report having the following disorders:
1867
diabetes mellitus, rheumatoid arthritis, systemic lupus
erythematosus, Sjögren syndrome, Hashimoto thyroiditis.
1868
Absolute The number of neutrophils (mature white cells) in the blood. 2000/mm3 and
neutrophil Neutrophils are a type of WBC that help fight infection. greater
count (ANC) When ANC decreases, the patient is neutropenic and more
prone to infection. Risk of infection increases when the ANC
falls below 2000 and the greatest risk is below 500; a “right
shift” on the WBC differential.
WBC Measures the percentage of each type of WBC in the total Neutrophils:
differential WBC count; a “left shift.” Indicates that a large percentage 50% to 62%
of WBCs are neutrophils; indicates that the bone marrow Bands: 3% to
has been stimulated by a severe infection to produce 6%
neutrophils to fight the infection. Bands are immature Monocytes: 3%
neutrophils. to 7%
“Right shift”: Indicates that a small percentage of WBCs are Basophils: 0%
neutrophils, putting the patient at higher risk for an to 1%
infection; neutropenia. Eosinophils:
Eosinophilia: Increased eosinophils indicate that an allergic 0% to 3%
reaction is present. Lymphocytes:
Monocytes and lymphocytes: Act as “backup” to the 25% to 40%
neutrophils. Percentages increase during infection when
oncology patients begin bone marrow recovery. If levels
do not rise and then fall in a normal pattern, this can be an
indication that the patient has a poor prognosis for
recovery.
Platelets Cells that form the matrix on which blood clots are formed. 150,000 to
(thrombocytes) 400,000/mm3
*
Information specific to hematologic and/or immunologic findings for each section is
presented in disease-specific sections. The basic assessment can be a part of every
patient’s assessment to determine the risk of development or presence of a
hematologic or immunologic disorder.
Anaphylactic shock
Pathophysiology
Anaphylaxis (anaphylactic shock) is a potentially life-
threatening condition resulting from an exaggerated or
hypersensitive response to an antigen or allergen. The typical
presentation occurs in a sensitized person (i.e., someone who has
been exposed previously to the same antigen) and is within 1 to 30
minutes of exposure to the antigenic substance, although symptoms
may not develop for several hours. The most common triggers
include drugs, foods, insect stings or bites, antisera, and blood
products. Recent studies have found that exercise may induce
anaphylaxis. This syndrome may or may not occur independently
of food-allergen ingestion. The hypersensitive response results in
1869
airway inflammation that causes obstruction and respiratory
distress, which can lead to respiratory arrest. In addition, there is a
relative hypovolemia caused by massive vasodilation. Fluids shift
from the vasculature into interstitial spaces, creating a false
hypovolemia or vasogenic (vasodilated) shock, which progresses to
end-organ dysfunction secondary to tissue hypoxia from poor
perfusion.
The hypersensitivity response occurs primarily on the surface of
the mast cells of the lungs, small blood vessels, and connective
tissue. The antigen combines with sensitized antibodies from
previous exposure (usually immunoglobulin E [IgE] type) and
attaches to basophils circulating in the blood. Inflammatory
mediators, including histamine, serotonin, kinins, and eosinophil
and neutrophil chemotactic factors, are then released from the
granules within the cells. Histamine is the primary mediator of an
anaphylactic response. Activation of histamine receptors causes
increased capillary permeability, increased pulmonary secretions,
bronchoconstriction, and systemic vasodilation.
The antigen-antibody complexes activate production of
prostaglandins and leukotrienes, which are termed slow-reacting
substances of anaphylaxis. These chemical mediators produce
systemic effects with potentially deadly results, including profound
shock. The leukotrienes produce severe bronchoconstriction and
cause venule dilation and increased vascular permeability. The
prostaglandins exaggerate bronchoconstriction and potentiate the
effects of histamine on vascular permeability and pulmonary
secretions. Kinins contribute to bronchoconstriction, vasodilation,
and increased vascular permeability. Eosinophilic chemotactic
factor of anaphylaxis is then released to attract eosinophils, which
work to neutralize mediators such as histamine. However, the
amount of neutralization is ineffective in reversing the anaphylaxis.
(See Figure 10-1 for a depiction of the pathophysiologic process of
anaphylaxis.)
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FIGURE 10-1 Pathophysiologic process of
anaphylaxis. Source: (Major chemical mediators are in boldface.) SRS-
A, Slow-reacting substance of anaphylaxis.
1871
symptoms, treatment, and mortality risk are identical, but “true”
anaphylaxis results directly from degranulation of mast cells or
basophils mediated by IgE. Pseudoanaphylaxis results from other
causes not directly mediated by antibodies. Differential diagnosis is
based on studying the allergic reaction.
10-1
RESEARCH BRIEF
Exercise-induced anaphylaxis (EIA) is a rare and unpredictable
form of anaphylaxis that is poorly understood. Between 5% and
10% of anaphylactic episodes are associated with or caused by
exercise. EIA may be food-dependent or occur independent of
food.
Although the pathophysiology behind EIA is not fully
understood, researchers believe that possible causes may include
alterations in plasma osmolality and/or pH during exercise, tissue
transglutaminase activity, redistribution of blood flow, and
changes in gut permeability. Additional research is needed to
better understand EIA. Based on current knowledge, if food is
contributing to EIA, dietary management is required, and the
specific food should be avoided 3 hours before exercise and 1 hour
after exercise.
From Robson-Ansley P, Du Toit G: Pathophysiology, diagnosis and management of
exercise-induced anaphylaxis. Curr Opin Allergy Clin Immunol 10:312-317, 2010.
1872
breathing patterns, and impaired gas exchange, along with
altered tissue perfusion related to vasodilation and third-spaced
intravascular fluids. Symptoms vary with means of antigen entry.
• Latex.
Vital signs
• Severity of all findings varies with the level of sensitivity to the
antigen. Patients who are highly sensitive are at risk for
1873
impending death if the condition is inappropriately managed.
1874
• General late indicators (occurring within minutes to hours)
include rapid progression of urticaria involving large areas of
skin; angioedema (tissue swelling; more commonly the eyes, lips,
tongue, hands, feet, and genitalia); cough, hoarseness, dyspnea,
and respiratory distress; lightheadedness or syncope; and
abdominal cramps, diarrhea, and vomiting.
Table 10-1
SYSTEMIC EFFECTS OF ANAPHYLAXIS
1875
capillary permeability;
decreased oxygen
saturation
BP, Blood pressure; HR, heart rate; GI, gastrointestinal; LOC, level of
consciousness.
Auscultation
• Wheezing bronchial breath sounds.
Palpation
• Palpate to assess for chest expansion; chest may be hyperinflated
if the patient is asthmatic.
Percussion
• May reveal hyperresonance (pneumothorax), a complication of
asthma (if present).
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Collaborative management (see figure 10-2)
Care priorities
Prevention
The goal of management of patients with severe allergies is to
quickly identify the offending stimulant and control the allergic
response using a stepwise approach to therapies and to prevent
exposure to the antigen. Ideally, patients should be educated
regarding avoidance of the allergen, but for those with severe
allergies, avoidance may not be possible for all substances, such as
various substances in the air. For patients with asthma, ideal control
is attained when patients are free of daytime symptoms, do not
awaken breathless or coughing at night, and have few or no
limitations on activities. For those with allergies to insects,
immunotherapy with hymenoptera venoms is used worldwide as
an effective treatment for most patients hypersensitive to stings
from bees, wasps, hornets, yellow jackets, or white-faced hornets or
bites from fire ants. Food allergy research, including sublingual
preparations and vaccines to prevent anaphylaxis from peanuts and
other common foods, is underway in leading research centers,
including the Johns Hopkins Children’s Center. A recent report
from the Centers for Disease Control and Prevention revealed that
incidence of all food allergies is increasing. Up to 6 million children
1877
in the United States, including almost 8% of young children, have at
least one food allergy.
1878
2):S465-S528, 1998.)
1879
epinephrine and may require higher or additional doses. Glucagon
may help to counteract the effects of beta-blocking drugs.
1880
Appendix 6). Usual doses are as follows:
1881
To detect dysrhythmias.
Airway management
1882
and elbows propped on the over-the-bed table to promote maximal
chest excursion, may reduce use of accessory muscles and
diaphoresis resulting from work of breathing. May not be possible
with severe hypotension, as further decrease in BP may result.
Ventilation assistance
Anaphylaxis management
1883
support. If the patient retains CO2 and is unrelieved by positioning,
lower-dose oxygen, bronchodilators and steroids, intubation, and
mechanical ventilation may be necessary sooner than in patients
who are able to receive higher doses of oxygen by mask.
6. Stay with the patient to promote safety and reduce fear. Use
calm, reassuring approach.
Hemodynamic regulation
1884
• Palpate peripheral pulses for decreasing amplitude,
assess the patient for mottling, decreased urine
output, or altered mental status.
1885
Continued swelling, despite treatment, may indicate
ineffective treatment, overaggressive fluid therapy, or heart or
kidney failure.
1886
patient has adequate perfusion, as evidenced by strong proximal
peripheral pulses, brisk capillary refill, warm extremities
temperature, urinary output 0.5 mL/kg/h or greater,
uncompromised neurologic status, and no restlessness, listlessness,
and unexplained anxiety.
Tissue Perfusion: Abdominal Organs; Tissue Perfusion:
Peripheral; Tissue Perfusion: Cerebral.
Hypovolemia management
HIGH ALERT!
Changes in level of consciousness may signal either decreased
cerebral perfusion (tissue hypoxia) or increasing intracranial
pressure caused by interstitial swelling from capillary
permeability. This may be a late sign.
1887
8. Administer fluid and pharmacologic agents as prescribed (see
previous nursing diagnosis).
Pruritus management
1. Assess the patient for urticaria (hives) and itching of hands, feet,
neck, and genitalia.
1888
in contact with allergen, and the necessity of informing the primary
healthcare provider immediately of any allergic symptoms.
Knowledge: Treatment Regimen; Knowledge: Illness Care;
Knowledge: Health Behavior; Knowledge: Disease Process.
1889
Anemia
Anemia reflects a reduction in total body hemoglobin (Hgb)
concentration and is common in patients who are critically ill. By
the third day in an intensive care unit, 95% of patients have reduced
Hgb concentrations. While Hgb decreases, the oxygen-carrying
capacity of the blood is reduced, resulting in tissue hypoxia unless
compensatory mechanisms are adequate to assist the body with
oxygen delivery. Anemia may be classified under one of three
functional classes after initial evaluation of the CBC and
reticulocyte index. (See Table 10-2 for functional classification.)
Table 10-2
FUNCTIONAL CLASSES OF ANEMIA WITH EXAMPLES
Hemolytic crisis
Hemolytic crisis is an acute disorder that frequently accompanies
hemolytic anemias. It is characterized by premature pathologic
destruction (hemolysis) of red blood cells (RBCs). While RBC
destruction accelerates, the oxygen-carrying capacity of the blood
decreases, which results in a reduction in the amount of oxygen
1890
delivered to the tissues. This hypoxic state produces tissue ischemia
and can progress to tissue infarction. Hemolytic episodes can be
triggered by both emotional and physiologic states, including
stress, trauma, surgery, acute infectious processes, and abnormal
immune responses.
Assessment
Goal of system assessment
Evaluate for decreased oxygen-carrying capacity with subsequent
organ dysfunction as a result of decreased production or increased
destruction or loss of RBCs.
Anemia
Risk factors
Advanced age; environmental exposure to certain chemicals,
liver dysfunction, autoimmune or other immunologic disorders,
malignancy (and its treatment), drug use (such as aspirin, NSAIDs,
warfarin); diets low in protein and iron, iron or folic acid deficiency,
B12 deficiency, chronic alcoholism, autoimmune disorders.
Vital signs
1891
• Tachypnea, orthopnea, tachycardia, fever.
Observation
• ECG changes.
Palpation
• Bone tenderness (especially rib and sternal areas), joint
tenderness.
Auscultation
• Crackles associated with heart failure.
Hemolytic crisis
Risk factors
Individuals with mild or chronic hemolytic anemia may be
asymptomatic until they are exposed to a severe stressor, such as an
acute infectious process, profound emotional upset, critical illness,
surgery, or trauma. With added stress, hemolysis can accelerate to a
crisis state in which patients experience organ congestion from
massive amounts of hemolyzed blood cells, precipitating multiple
organ dysfunction syndrome (MODS), and shock.
1892
splenomegaly; and signs of peripheral nerve damage including
paresthesias, paralysis, chills, and vomiting.
Vital signs
Observation
• Hemiplegia, paresthesias.
Palpation
Auscultation
1893
Test Purpose Abnormal Findings
Red blood cell Enumeration of red cells found in Reduced; in hemolytic crisis, an
(RBC) count each cubic millimeter of blood increased number of premature RBCs
(nucleated RBCs) will be present
1894
Total iron- Measures the capacity of the blood Normal or reduced, depending on the
binding capacity to bind iron with transferrin; also type of anemia
(TIBC) indirect test of liver function
(although rarely used).
TIBC is typically measured along
with serum iron to evaluate
people suspected of having either
iron deficiency or iron overload
Ferritin Iron stores: With damage to organs Reduced with iron deficiency anemia;
that contain ferritin (especially the normal or elevated with anemia of
liver, spleen, and bone marrow), critical illness; elevated with
ferritin levels can become elevated hemochromatosis
even though the total amount of
iron in the body is normal
Transferrin Used to determine the cause of Reduced with anemia of chronic
anemia, to examine iron metabolism inflammation, anemia of critical illness
(e.g., in iron deficiency anemia), and
to determine the iron-carrying
capacity of the blood
Transferrin The iron concentration divided by Reduced with anemia of chronic
saturation TIBC; a more useful indicator of inflammation, anemia of critical illness
iron status than iron or TIBC alone
Folate; folic acid Measures folic acid in the blood Reduced with nutrition deficiency
leading to megaloblastic anemia
Erythropoietin Measures the amount of a hormone Reduced with renal disease and
(EPO) called erythropoietin (EPO) in the normal in those who are critically ill
blood; acts on stem cells in the bone who should have an elevated level if
marrow to increase the production anemia of any cause is present.
of RBCs; made by cells in the Reticulocyte response to EPO has been
kidney, which release the hormone shown to be reduced in many critically
when oxygen levels are low ill patients with elevated EPO levels.
Vitamin B12 Measures the amount of vitamin B12 Reduced with pernicious or
in the blood; used with folic acid megaloblastic anemia
test, because a lack of either can
cause megaloblastic anemia
Unconjugated Measures bilirubin that has not been Elevated in hemolytic anemia as a
bilirubin: Free conjugated in the liver. It gives an result of the inability of the liver to
bilirubin, indirect reaction to the Van Den process increasing bilirubin released
indirect bilirubin Bergh test during hemolysis
Serum lactic General indicator of the existence Elevated in hemolytic anemia because
dehydrogenase and severity of acute or chronic of their release when an RBC is
isoenzymes tissue damage and, sometimes, as a destroyed
(LDH1 and monitor of progressive conditions;
LDH2) monitor damage caused by muscle
trauma or injury and to help
identify hemolytic anemia
Haptoglobin Used to detect and evaluate Decreased in hemolytic anemia as a
level hemolytic anemia; not to diagnose result of increased binding of
cause of the hemolysis. Haptoglobin haptoglobin, which facilitates removal
levels should be drawn before of increased Hgb from blood
transfusion
Peripheral blood Microscopic examination of cells May reveal abnormally shaped RBCs,
smear from a drop of blood; investigates such as spherocytes. RBC hyperplasia
hematologic problems or parasites (abnormal number) is present in nearly
such as malaria and filarial all cases of chronic hemolysis with
intact bone marrow
1895
Bone marrow Evaluates bone marrow status; May reveal abnormal size, shape, or
aspiration diagnoses blood disorders and amounts of RBCs, WBCs, or platelets
determines if cancer or infection has
spread to the bone marrow
Coombs test: Detects antibodies that may bind to Positive in antibody-mediated
Direct RBCs and cause premature RBC immunologic hemolysis
antiglobulin test; destruction
indirect
antiglobulin test
Immunoglobulin Measures the level of Elevated: Autoimmune disorders,
levels immunoglobulins, also known as sickle cell; lower in
antibodies, in the blood. immunocompromised states
Glucose-6- Measures G6PD—enzyme levels are Decreased in G6PD deficiency,
phosphate normal in newly produced cells but hemolysis Elevated: myocardial
dehydrogenase fall as RBCs age and only deficient infarction, liver failure, chronic blood
(G6PD) levels cells are destroyed loss, hyperthyroidism
Radiologic x-rays and bone scans Liver/spleen Decreased density, aseptic necrosis of
examinations scans bones Hepatomegaly, splenomegaly,
lesions
1896
10-2
RESEARCH BRIEF
Marik and colleagues conducted a systematic review of 45 cohort
studies to determine the correlation between red blood cell
transfusion and negative outcome. Outcome measures included
mortality, infection, multiorgan dysfunction, and acute respiratory
distress syndrome. Forty-two of the 45 studies revealed that risks
of transfusion outweighed benefit in treating anemia. Transfusion-
related acute lung injury and transfusion-related circulatory
overload are some of the most common adverse events. Risks of
transfusion must be weighed individually against the risks of
anemia, and other treatments such as iron or erythropoiesis-
stimulating agents.
From Marik PE, Corwin HL: Efficacy of red blood cell transfusion in the critically ill: a
systematic review of the literature. Crit Care Med 36:2667-2674, 2008.
3. Volume replacement
If the patient is hypovolemic, aggressive fluid and/or blood
replacement is mandatory to prevent profound hypotension and
shock. Fluid challenges/boluses also assist in prevention of
deposition of hemolyzed RBCs in the microvasculature.
1897
6. Iron supplements
Administered for iron-deficiency states to help increase production
of normal-size RBCs. May be given IV or enterally. Iron levels must
be normal to facilitate the action of erythropoietin injections.
8. Vitamin B12
Administered by injections or IV infusion for management of
pernicious anemia, a type of megaloblastic anemia caused by failure
of the gastric mucosa to absorb vitamin B12.
1898
Pulmonary.
Respiratory monitoring
5. Note changes in SaO2, SVO2, ScVO2, Sto2 (if available) and changes
in ABG values, as appropriate.
Table 10-3
BLOOD AND BLOOD PRODUCTS*
1899
*
Use correct filter with each blood product; most filters can be used to administer 2 to
4 units; either piggyback or flush products with normal saline solution only.
Activity intolerance
related to anemia/lack of oxygen-carrying capacity of the blood
Goals/Outcomes: Within 24 hours of onset of treatment, the
patient’s activity tolerance improves, as evidenced by HR and RR
returning to within 10% of baseline (or HR 60 to 100 bpm and RR 12
to 20 breaths/min) and BP returning to within 10% of the patient’s
baseline (or systolic BP greater than 90% mm Hg). Within 24 hours
of initiation of treatment, the patient is able to assist minimally with
self-care activities.
Endurance; Activity Tolerance.
Energy management
1900
1. Alternate periods of rest and activity to avoid stress that increases
oxygen demand.
10. Teach the patient and significant others about the specific
anemia affecting the patient.
Pressure management
1901
1. Keep extremities warm to promote circulation and help prevent
tissue hypoxia.
13. For additional interventions, see Wound and Skin Care, Chapter
1.
1902
Collaborative management: Hemolytic crisis
Care priorities
1. Oxygen therapy
Administered to relieve SOB or dyspnea. Methods of oxygen
delivery range from nasal cannulas, to various face masks, to
mechanical ventilation in severe cases.
2. Pain management
Aspirin, acetaminophen, NSAIDs, narcotics, and sedatives may be
necessary for relief of pain and anxiety associated with hemolytic
anemia, particularly during hemolytic crisis.
3. Volume replacement
If the patient is hypovolemic, aggressive fluid and/or blood
replacement is mandatory to prevent profound hypotension and
shock. Fluid challenges/boluses also assist in the prevention of
deposition of hemolyzed RBCs in the microvasculature.
1903
RBCs for patients who are unresponsive to other treatments for
sickle cell disease.
6. Thrombocytapheresis
Cytapheresis procedure for patients experiencing symptoms of
excessive thrombosis, to attempt rapid platelet reduction to
decrease clotting before onset of MODS (see Multiple Organ
Dysfunction Syndrome in Systemic Inflammatory Response
Syndrome, Sepsis, and Multiple Organ Dysfunction Syndrome,
Chapter 11).
7. Therapeutic phlebotomy
Removal of 200 to 500 mL of whole blood from the patient when
iron overload exists.
8. Corticosteroids
Therapy used with limited success in the management of hemolytic
anemia.
9. Splenectomy
Removal of the spleen is sometimes recommended for patients
suspected of having splenic sequestration crisis related to hemolytic
anemia.
1904
pattern), oxygen saturation greater than 95%, urinary output 0.5
mL/kg/h or greater, and orientation to time, place, and person.
Circulation Status.
1905
10. Teach the patient and significant others about hemolytic anemia,
including the signs of impending hemolytic crisis, rendering
information on the following:
1906
Cardiac Care: Acute; Circulatory Care: Venous Insufficiency;
Respiratory Monitoring; Shock Management: Cardiac; Cerebral
Perfusion Promotion; Neurologic Monitoring; Peripheral Sensation
Management; Fluid/Electrolyte Management; Fluid Management;
Vital Signs Monitoring.
Acute pain
Related to tissue ischemia secondary to vessel occlusion;
inflammation/injury secondary to blood within the joints.
Goals/Outcomes: Within 1 to 2 hours of initiating treatment, the
patient’s subjective evaluation of discomfort improves, as
documented by a pain scale; nonverbal indicators of discomfort are
reduced or absent.
Pain Control; Pain Level.
Pain management
1907
6. Administer adjuvant analgesics and/or medications when needed
to potentiate analgesia.
14. Help allay fears by reassuring the patient that pain will decrease
when the crisis subsides.
1908
attempt to prevent severe pain.
Fluid/electrolyte management
1909
6. Monitor electrolytes and serum osmolality. A universal increase
in electrolytes and osmolality is indicative of dehydration. A
universal decrease signals fluid overload.
1910
2. Increased platelet destruction or consumption: Includes heparin-
induced thrombocytopenia (HIT); antiphospholipid antibody
syndrome or lupus anticoagulant syndrome; idiopathic
thrombocytopenic purpura (ITP); thrombotic thrombocytopenic
purpura (TTP); hemolytic-uremic syndrome; febrile reactions;
severe sepsis; and hemolysis, elevated liver enzymes, and low
platelet count (HELLP) syndrome. Disseminated intravascular
coagulation (DIC) presents with a combined coagulopathy and
platelet consumption.
1911
hemophilia, Von Willebrand disease, and DIC.
Patients prone to thromboembolic conditions include those with
platelet abnormalities, including thrombocytosis, diabetes mellitus,
hyperlipidemia, heparin-induced thrombocytopenia, systemic
lupus erythematosus; blood vessel defects, including venous
disease/stasis, roughened surface of vascular endothelium (seen
with arteriosclerosis, trauma, severe sepsis, SIRS, or infection), atrial
fibrillation, grafts or other devices in place, hyperviscosity, TTP,
hemolytic uremic syndrome, vasculitis; and those with systemic
illness and conditions, including long bone fractures, orthopedic
surgery, abdominal surgery, malignancy, pregnancy or postpartum
(risk of venous thromboembolism is five times higher than for
nonpregnant women), oral contraceptives, nephrotic syndrome,
inflammatory bowel disease, slow/stagnant blood flow through the
vessels (e.g., shock states, severe peripheral vascular disease),
infusion of prothrombin complex, and sickle cell disease.
When patients are evaluated for a bleeding disorder, the process
should include evaluation of platelets, deficiency of a single
coagulation factor (factors VII, VIII, IX, X, or XI) or multiple
coagulation factors, for endogenous or exogenous antibiotics in the
circulation, and consumptive coagulopathy (e.g., ITP, TTP,
vasculitis, hemolytic uremic syndrome, paroxysmal nocturnal
hematuria, obstetric complication, trauma, liver disease). Adequate
levels of calcium and vitamin K are also needed for adequate
function of the clotting cascade.
Those suspected of having thromboembolic disease may require
evaluation of coagulation factors, circulating antibodies, abnormal
proteins (deficient protein C or S), and other endogenous chemicals.
Normal blood coagulation is activated most often as a result of
injury to blood vessels, causing the following series of events:
1912
3. Activation of plasma clotting factors: Stimulation of factors that
leads to the formation of a fibrin clot. The pathways that initiate
clotting factors (Figure 10-3) include the following:
1913
Tissue thromboplastin from the vessel initiates the extrinsic
pathway, whereas contact of factor XII and platelets with the
injured vessel wall traumatizes the blood and initiates the intrinsic
pathway. The extrinsic pathway is able to form clots in as little as 15
seconds with severe trauma, whereas the intrinsic pathway requires
2 to 6 minutes for clot formation. Both are necessary to maintain
clot.
Heparin-induced thrombocytopenia
Pathophysiology
Heparin is the most widely used IV anticoagulant and one of the
most frequently prescribed drugs in the United States. Heparin
prevents the conversion of fibrinogen to fibrin. HIT, also called
heparin-induced thrombocytopenic thrombosis (HITT), white clot
syndrome, or heparin-associated thrombocytopenia (HAT), types I
and II, occurs when heparin therapy causes either a mild to
1914
moderate (i.e., HAT type I) or severe (i.e., HAT type II) decrease in
the number of freely circulating platelets. Platelets in affected
patients exhibit unusual aggregation and can result in heparin
resistance, arterial and venous thrombosis, and subsequent emboli
in extreme cases (Figure 10-4). Depending on the source of the
heparin received, HIT is reported in approximately 5% of all
patients receiving heparin. Bovine (beef-based) heparin has been
associated with HIT more frequently than other heparins. It is
estimated that as many as 50% of patients on heparin may be
asymptomatic but generate antibodies to heparin-platelet factor 4
(H-PF4), which increases the risk of HIT on their next exposure to
heparin. HIT is not related to the heparin dose and has been seen in
patients receiving low-dose subcutaneous heparin, as well as in
patients receiving simple heparin “flushes” to maintain patency of
IV lines.
1915
FIGURE 10-4 Heparin-induced thrombocytopenia. IgG,
Immunoglobulin G.
1916
• High morbidity (immune-mediated): Generally begins 5 to 7 days
after initiation of heparin. Symptoms persist until heparin is
discontinued. Platelets decrease to less than 100,000/mm3.
Thrombosis with subsequent embolization and bleeding is
apparent. Complications may include pulmonary emboli,
myocardial infarction, cerebral infarction, and circulatory
impairment resulting in limb amputations. Mortality rate is 29%.
Overall, 0.6% of all patients receiving heparin therapy develop
thromboembolization.
Assessment
Goal of system assessment
Evaluate for increased risk of inappropriate bleeding or clotting as a
result of qualitative or quantitative dysfunction of platelets and
clotting factors.
Risk factors
Previous drug-induced or immunologic thrombocytopenia.
Vital signs
Tachypnea, tachycardia, hypertension.
Observation
Patients may present with high or low acuity states. Those without
clinical symptoms with a slight decrease in platelets are much
easier to manage than patients with severe, high morbidity.
Extreme cases manifest arterial thrombosis of the distal aorta and
proximal lower limb arteries. High morbidity patients present with:
• Paresthesias; paralysis.
1917
• Severe chest pain and SOB, indicative of myocardial ischemia.
Palpation
• Bone tenderness (especially rib and sternal areas).
• Joint tenderness.
• Abdominal tenderness.
1918
because of release of platelet
membrane antibody leading to
“clumping”
Heparin-induced Adds patient platelet-poor plasma Reflects abnormal aggregation
platelet aggregation (as a source of immunoglobulin) curve with a decrease in the optical
to normal platelet-rich plasma in density in the aggregometer
the presence of heparin to induce
platelet aggregation
Serotonin release Detects the presence of antibodies Helps in the differential diagnosis
testing and ELISA to PF4/heparin/TSP-1 complexes of heparin-induced
heparin PF4 thrombocytopenia
Bone marrow Evaluates bone marrow status; Normal or increased number of
aspiration diagnoses blood disorders and megakaryocytes (platelet
determines if cancer or infection precursors), indicative of normal
has spread to the bone marrow production of platelets or
increased response to need for
platelets
Collaborative management
Care priorities
1919
2. Administer defibrinogenating agents if high morbidity
symptoms are present
Ancrod (Arvin) may be given to reduce the possibility of
thrombosis.
1920
idraparinux inhibit clot propagation. Direct thrombin inhibitors
(antithrombins) block fibrin formation for clot completion.
Bleeding precautions
1921
2. Assess for signs of internal bleeding including tachycardia and
dysrhythmias, tachypnea and hypotension. Sustained increase in
HR and RR or ECG changes, such as ST segment depression or
elevation, may precede hypotension.
3. Protect the patient from trauma that may cause bleeding. Do not
use rectal temperatures to monitor for fever. Avoid IM injections
and venous and arterial punctures as possible until bleeding time
normalizes.
1922
9. Assess the patient’s neurologic status hourly if platelet count
decreases to less than 30,000.
11. Teach the patient and significant others about the basic
pathophysiology of HIT, and instruct them to report this problem
to all subsequent healthcare providers. Teach the patient to wear a
medical-alert bracelet to alert healthcare providers if the patient
becomes unable to speak.
Hypovolemia management
1923
5. Check excretions for occult blood, and observe for blood in
emesis, sputum, feces, urine, nasogastric drainage, and wound
drainage as appropriate.
1924
Usually it occurs within 21 days following a viral infection. At the
onset, platelets decrease to less than 20,000/mm3. The chronic form
is typically a disease of adults aged 20 to 50 years, but it has
occurred in a small percentage of children and older adults. The
chronic disease rarely resolves spontaneously, sometimes responds
to treatment of the underlying disorder, and usually is not
associated with infection but can be related to autoimmune
disorders (e.g., systemic lupus erythematosus, rheumatoid arthritis)
and neoplastic disorders (e.g., chronic lymphocytic leukemia,
lymphoma). Women are affected three times more often than men.
Petechiae and purpura are commonly seen on the distal upper and
lower extremities. Patients may feel symptom-free until actual
bleeding begins. Intracranial hemorrhage is a potential
complication. Platelet counts decrease to as low as 5000/mm3 in
some patients, but may be as high as 75,000/mm3 in others.
Assessment
Goal of system assessment
Evaluate for increased risk of inappropriate bleeding or clotting as a
result of qualitative or quantitative dysfunction of platelets and
clotting factors.
Risk factors
• Acute ITP: History of antecedent viral infection occurring
approximately 3 weeks before the hemorrhagic episode.
Vital signs
• Tachypnea, tachycardia, hypotension, fever.
1925
Observation
• Petechiae, purpura, bruising on skin and mucous membranes,
prolonged bleeding; intracranial hemorrhage occurs in less than
1% of patients if the thrombocytopenia is severe.
• Retinal disturbances.
Palpation
• Enlargement of the liver and/or spleen.
• Joint tenderness.
1926
count with (WBCs), platelets, and the WBC differential hematocrit resulting from
differential insidious blood loss or
simultaneous hemolytic
anemia (Evans syndrome)
Normal WBC count: Unless
idiopathic thrombocytopenic
purpura is associated with
another disease impacting
differential leukocyte count
Capillary- Method to determine a patient’s Will show >1+, which signals
fragility test: hemorrhagic tendency: Assesses fragility of that more than 11 petechiae
Rumpel-Leede capillary walls: Used to identify were present in a 2.5-cm radial
capillary- thrombocytopenia. Seldom used in current area on the skin after prolonged
fragility test practice, but may be used to discern from application of a blood pressure
damage as a result of prolonged cuff cuff Normal is 1+ or <10
inflation in patients with blood dyscrasias petechiae
Bone marrow Evaluates bone marrow status; diagnoses Biopsy will reveal
aspiration blood disorders and determines if cancer or megakaryocytes (platelet
infection has spread to the bone marrow precursors) in normal or
increased numbers with a
“nonbudding” appearance,
possibly indicating defective
maturation or failure of platelet
production
1927
• IV immunoglobulin (IVIG): Given at 400 mg/kg/day for 2 to 5
consecutive days, resulting in increased platelet count in 60% to
70% of patients. Serum sickness (fever, chills, rash) is not
uncommon between 9 and 14 days. It is less effective in patients
with long-standing chronic ITP. The platelet level at initiation of
treatment and incidence of serum sickness is not necessarily
correlated to individual response. Duration of response may be
longest in individuals who achieve the highest initial platelet
increases.
1928
• Colchicine: A small percentage of patients refractory to other
treatments may improve with 1.2 mg colchicine daily for 2 weeks
or longer. The drug has been used successfully in limited studies.
1929
Goals/Outcomes: Within 72 hours of onset of treatment, the
patient exhibits no clinical signs of new bleeding or bruising
episodes. Secretions and excretions are negative for blood, and vital
signs are within 10% of the patient’s normal range. Within the 24-
hour period before discharge from intensive care, the patient and
significant others verbalize understanding of the indicators of
potential or actual bleeding.
Blood Coagulation.
Bleeding precautions
2. Protect the patient from trauma that may cause bleeding. Avoid
taking rectal temperatures.
1930
pads or tampons.
10. Teach the patient that it is always safer to use an electric razor
for shaving.
12. Teach the patient and significant others to recognize the signs of
impending hemorrhage: more rapid pulse and breathing, easy
bruising, painful joints, and blood in sputum, urine, or stool.
Skin Surveillance.
Neurologic monitoring
1931
2. Monitor trend of Glasgow Coma Scale (Appendix 2), intracranial
pressure, and cerebral perfusion pressure.
1932
related to active loss secondary to intraabdominal bleeding or
postsplenectomy intraabdominal bleeding.
Goals/Outcomes: The patient remains normovolemic, as
evidenced by HR, RR, and BP within 10% of the patient’s normal
range (or HR 60 to 100 bpm, RR 12 to 20 breaths/min with normal
depth and pattern, systolic BP ≥90 mm Hg); urinary output at least
0.5 mL/kg/h; and absence of abdominal pain or tenderness, back
pain, and frank bleeding from the splenectomy incision.
Fluid Balance.
Fluid management
Acute pain
Related to joint inflammation and injury secondary to bleeding into the
synovial cavity of the joint(s); postsplenectomy pain.
Goals/Outcomes: Within 4 hours of initiating treatment, the
1933
patient’s subjective evaluation of discomfort improves, as
documented by a pain scale, nonverbal indicators of discomfort are
absent or decreased, and HR, RR, and BP are within 10% of the
patient’s baseline.
Pain Control.
Pain management
1. Devise a pain scale with the patient, rating discomfort from 0 (no
pain) to 10. Perform a comprehensive assessment of pain to include
location, characteristics, onset/duration, frequency, quality,
intensity or severity, and precipitating factors.
3. Teach the patient causes of the pain, how long it may last, and
about discomforts from procedures.
1934
Enhancement; Anxiety Reduction.
1935
• FDPs (or FSPs) result from fibrinolysis, which changes platelet
aggregation and inhibits fibrin polymerization. See Figure 10-3
for the normal coagulation pathway.
Table 10-4
CLOTTING FACTORS: PRIMARY ACTIONS
Table 10-5
DISSEMINATED INTRAVASCULAR COAGULATION:
PREDISPOSING CONDITIONS
1936
A predisposing event that damages the vascular endothelium
initiates the clotting cascade. Studies reflect that both the intrinsic
and extrinsic pathways are activated initially, resulting in an
abnormal acceleration of the clotting process. Thrombocytopenia
occurs because of thrombin production and microvascular
thrombus formation.
Assessment
Goal of system assessment
Evaluate for increased risk of inappropriate bleeding or clotting as a
result of qualitative or quantitative dysfunction of platelets and
clotting factors.
Risk factors
Any clinical state or pharmacologic therapy (e.g., chemotherapy)
that inhibits the removal of activated clotting factors, FDPs, and
thromboplastin by the reticuloendothelial system. Any patient is at
high risk following severe trauma or with SIRS, a severe infection,
sepsis, severe sepsis, septic shock, or invasive procedures.
Obstetrics patients with abruptio placentae, amniotic fluid
embolism, or eclampsia release procoagulation factors, placing
them at risk. DIC can occur as a paraneoplastic syndrome or
oncologic emergency related to certain malignancies such as acute
promyelocytic leukemia (APL), multiple myeloma, and some solid
tumors. DIC may manifest as a profound bleeding/clotting disorder
in the acute phase or as a less symptomatic chronic disorder.
1937
In chronic (compensated) DIC, activation of coagulation and
fibrinolysis does not occur rapidly enough to exceed the rate of
production of clotting factors or inhibitors. The course of DIC
depends on the intensity of the stimulus, coupled with the status of
the liver, bone marrow, and vascular endothelium. Whether DIC
leads to bleeding or to thrombosis is profoundly affected by the
underlying disease process.
Vital signs
• Tachypnea, tachycardia, hypotension.
Observation
• Bleeding with abrupt onset: From invasive procedure sites and
mucosal surfaces (e.g., oral, nasal, tracheal, gastric, urethral,
vaginal, rectal); may include hematuria, petechiae, stools or
gastric aspirate positive for occult blood, pallor, tachycardia,
tachypnea, vertigo, hypotension, ecchymoses (e.g., on palate,
gums, skin, conjunctivae), lethargy, irritability, or feeling of
impending doom, and possible back pain and abdominal
tenderness.
• Anxiety, restlessness.
• Acrocyanosis.
1938
headaches.
Palpation
• Hepatosplenomegaly.
• Abdominal tenderness.
Auscultation
• Diminished or absent bowel sounds.
1939
activated common pathways of the coagulation of activation of the intrinsic
partial cascade. The aPTT is the time, in seconds, pathway, causing consumption
thromboplastin for patient plasma to clot after the additionof coagulation factors. Critical
time (aPTT) of an intrinsic pathway activator, value: >70 seconds. In chronic
phospholipid, and calcium disseminated intravascular
coagulation (DIC), the value may
be normal (25 to 35 seconds) or
less than normal
PT, Measure of the integrity of the extrinsic Prolonged (>15 seconds) because
international pathway of the coagulation cascade of activation of the extrinsic
normalized pathway, causing consumption
ratio (INR) of the extrinsic clotting factors.
Critical value: >40 seconds
Thrombin Test of the time it takes for a clot to form, Prolonged (>1.5 times the control
time, thrombin measuring the conversion of fibrinogen to value or >2 seconds in excess of a
clotting time fibrin 9- to 13-second control value)
because of rapid conversion of
fibrinogen into fibrin
Antithrombin Evaluates whether the total amount of Decreased (<50% of control value
III (AT-III), functional antithrombin is normal. Activity using a plasma sample, or <80%
functional will be decreased with both type 1 and type using functional values) because
antithrombin 2 antithrombin deficiencies, thus this test of rapid consumption of this
III, can be used as an initial screen for both. If thrombin inhibitor. The action of
antithrombin, the antithrombin activity is low, then the AT-III is catalyzed by heparin
activity, and antithrombin antigen test is performed to
antigen determine the quantity of antithrombin
present
Euglobulin clot Measures overall fibrinolysis; measures Decreased time is seen with DIC.
lysis time fibrinogen activity via measurement of Normal: Lysis in 2 to 4 hours.
plasminogen and plasminogen activator, Critical value: 100% lysis in 1
which assist in prevention of fibrin clot hour
formations
Platelet count Used to diagnose bleeding disorders or Decreased (<140,000/mm3)
bone marrow disease because of rapid rate of platelet
aggregation to form clots during
DIC. Aggregation decreases the
freely circulating platelets
Alpha2- Measures alpha2-antiplasmin, which is an Decreased because of rapid
antiplasmin inhibitor that regulates the fibrinolytic consumption resulting from large
system primarily by blocking the enzymatic amounts of plasmin generated.
activity of plasmin When all alpha2-antiplasmin is
depleted, excessive
hyperfibrinolysis (massive, rapid
clot lysis) occurs
Protamine Associated with the formation of excessive Results are positive (normal:
sulfate test amounts of thrombin and secondary negative), indicative of presence
fibrinolysis of fibrin strands
Peripheral Microscopic examination of cells from a For visualization during
blood smear drop of blood; investigates hematologic microscopic examination of
problems or parasites such as malaria and schistocytes and burr cells, which
filarial indicate the deposition of fibrin
in the small blood vessels
1940
intravascular coagulation
Care priorities
• Underlying malignancy/carcinoma.
1941
Patients who have acute promyelocytic leukemia with
disseminated intravascular coagulation often experience
accelerated symptoms of fibrinolysis (declotting) when receiving
chemotherapy. If these individuals receive heparin, an
antifibrinolytic agent such as epsilon- (ε-)aminocaproic acid
(Amicar) may be added to decrease bleeding.
1942
transfusions are used if the patient has impaired platelet production
and profuse bleeding. Antithrombin III (AT-III) concentrate has
been used on a limited basis (see Table 10-3). More recently, DIC is
being managed with antithrombin concentrate, activated protein C
(drotrecogin alfa), tissue factor pathway inhibitor, and synthetic
serine protease inhibitors (e.g., aprotinin).
1943
mucosal surfaces; secretions and excretions that are negative for
blood; absence of large or increasing ecchymoses; decreasing
purpura; and HR, RR, and BP within 10% of the patient’s baseline
(or HR 60 to 100 bpm, RR 12 to 20 breaths/min, systolic BP greater
than 90 mm Hg).
Blood Coagulation.
Bleeding precautions
1944
bleeding.
7. Use electric rather than safety razor for shaving the patient.
Table 10-6
MEDICATIONS THAT MAY PROMOTE BLEEDING
1945
Penicillin Phenothiazines
Pentamidine Chlorpromazine
Streptomycin Promethazine
Sulfonamides (antibiotics) Trifluoperazine
Chloramphenicol Phosphodiesterase
Isoniazid inhibitors
Nitrofurantoin Caffeine
Rifampin Dipyridamole
Trimethoprim Theophyllines
Anticoagulants Antiplatelet drugs
Heparin Aspirin (acetylsalicylic
Enoxaparin acid)
Dalteparin Ticlopidine
Thrombolytics Clopidogrel
Alteplase Prostaglandin I2
Reteplase Prostaglandin D2
Streptokinase Prostaglandin E
Urokinase Sedative-hypnotics
Anisoylated plasminogen Benzodiazepines
streptokinase Clonazepam
Tenecteplase Diazepam
Vasodilators
Nitroglycerin
Nitroprusside
Table 10-7
DISSEMINATED INTRAVASCULAR COAGULATION:
LABORATORY VALUES
1946
DIC, Disseminated intravascular coagulation
Fluid monitoring
1947
6. Ensure that the patient has typed and cross-matched blood
available for transfusion.
Table 10-8
COMPLETE BLOOD COUNT VALUES
1948
Peripheral, cardiopulmonary, cerebral, gastrointestinal, and
renal
related to blood loss or presence of microthrombi.
Goals/Outcomes: The patient has adequate perfusion, as
evidenced by peripheral pulses greater than 2+ on a scale of 0-to-4+,
brisk capillary refill (less than 2 seconds), BP within the patient’s
normal range, CVP 2 to 6 mm Hg, and HR regular and less than 100
bpm. The patient is oriented to time, place, person, and self and has
urinary output at least 30 mL/h (0.5 mL/kg/h) and oxygen
saturation greater than 96%.
Circulation Status.
Shock prevention
1949
bowel habits (e.g., constipation, diarrhea), characteristic of stool
(e.g., tarry, bloody), and presence or absence of bowel sounds.
Respiratory monitoring
1950
5. Monitor the patient’s respiratory secretions. Institute respiratory
therapy treatments as needed.
Surveillance: Safety
3. When blood products are being infused, check vital signs every
15 minutes for the first hour. Check the patient frequently
1951
throughout the first 15 minutes of the transfusion to observe for
signs of an acute hemolytic transfusion reaction, including fever,
chills, dyspnea, hypotension, flushing, tachycardia, back pain,
hematuria, mentation changes, and shock.
1952
fibrinogen levels (see Table 10-7).
Table 10-9
ACUTE TRANSFUSION REACTIONS
1953
of the Patient and Significant Others, Chapter 2. For patients who
manifest activity intolerance, see nursing diagnosis in Prolonged
Immobility, Chapter 1. For patients with sepsis or septic shock, see
Systemic Inflammatory Response Syndrome, Sepsis, and Multiple
Organ Dysfunction Syndrome, Chapter 11.
Selected references
1. Abraham J. Romiplostim for treating thrombocytopenia in
chronic idiopathic thrombocytopenic purpura. Commun
Oncol. 2008;5:651-656.
2. American Association of Blood Banks.
http://www.aabb.org/tm/coi/Documents/coi1113.pdf
Circular of information for the use of human blood and blood
components. Bethesda: American Association of Blood
Banks. 2013.
3. American Society of Anesthesiologists. Practice guidelines
for perioperative blood transfusion and adjuvant therapies.
Anesthesiology. 2006;105:198-208.
4. American Society of Anesthesiologists Committee on
Standards and Practice Parameters. Practice guidelines for
perioperative blood management. An updated report by the
American Society of Anesthesiologists Task Force on
Perioperative Blood Management. Anesthesiology.
2015;122:1A.
5. American Society of Hematology. Red blood cell
transfusions: a clinical practice guideline from AABB. Ann
Intern Med. 2012;157:49-58.
6. Bickley L. Bates guide to physical examination and history
taking ed 11. Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins. 2013.
7. Gentry CA, Gross KB, Sud B, Drevets DA. Adverse
outcomes associated with the use of drotrecogin alfa
(activated) in patients with severe sepsis and baseline
bleeding precautions. Crit Care Med. 2009;37:19-25.
8. Ghanima W, Godeau B, Cines DB, Bussel JB. How I treat
immune thrombocytopenia: the choice between
splenectomy or a medical therapy as a second-line
1954
treatment. Blood. 2012;120:960-969.
9. Gould S, Cimino M, Gerber D. Packed red cell transfusion
in the intensive care unit: limitations and consequences. Am
J Crit Care. 2007;16:39-49.
10. Harmon S. http://www.scientificamerican.com/article/food-
allergy-therapies/ Bring on the peanuts: food allergy
therapies move closer to approval. Scientific American. June
30, 2011.
11. Hebert P, Tinmouth A, Corwin H. Controversies in RBC
transfusion in the critically ill. Chest. 2007;131:1583-1590.
12. Horvath KA, Acker MA, Chang H. Blood transfusion and
infection after cardiac surgery. Ann Thorac Surg.
2013;95:2194-2201.
13. Keating GM. Romiplostin: a review of its use in immune
thrombocytopenia. Drugs. 2012;72:415-435.
14. Kelton J, Warkentin T. Heparin induced thrombocytopenia:
a historical perspective. Blood. 2008;112:2607-2616.
15. Klein H, Spahn D, Carson J. Red blood cell transfusion in
clinical practice. Lancet. 2007;370:415-426.
16. Lee A, Peterson E. Treatment of cancer-associated
thrombosis. Blood. 2013;122:2310-2317.
17. Lelubre C, Vincent J. Red blood cell transfusion in the
critically ill patient. Ann Intensive Care. 2011;1:43.
18. Marik P, Corwin H. Efficacy of red blood cell transfusion in
the critically ill: a systematic review of the literature. Crit
Care Med. 2008;36:2667-2674.
19. McEvoy M, Shandra A. Anemia, bleeding, and blood
transfusion in the intensive care unit: causes, risks, costs,
and new strategies. Am J Crit Care. 2013;22:eS1-eS13.
20. McMahon B. Malignancy-associated thrombosis. Oncol
Issues. 2009;24:20-23.
21. Pieracci FM, Barle PS, Pomp A. Critical care of the bariatric
patient. Crit Care Med. 2006;34:1796-1804.
22. Robson-Ansley P, Du Toit G. Pathophysiology, diagnosis
and management of exercise-induced anaphylaxis. Curr
Opin Allergy Clin Immunol. 2010;10:312-317.
23. Rome S, Doss D, Miller K, Westphal J. IMF Nurse
Leadership Board: Thromboembolic events associated with
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novel therapies in patients with multiple
myelomaconsensus statement of the IMF nurse leadership
board. Clin J Oncol Nurs. 2008;12(Suppl 3):21-28.
24. Sampson HA, Muñoz-Furlong A, Campbell RL. Second
symposium on the definition and management of
anaphylaxis: summary report—Second National Institute of
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Anaphylaxis Network symposium. J Allergy Clin Immunol.
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25. Simons FE. Anaphylaxis. J Allergy Clin Immunol.
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26. Simons FE. Anaphylaxis: recent advances in assessment
and treatment. J Allergy Clin Immunol. 2009;124:625-636.
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organization guidelines for the assessment and
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2011;4:13-37.
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immunotherapy in peanut allergic subjects in a single
center trial. J Allergy Clin Immunol. 2011;127:AB25.
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1956
C H A P T E R 11
Complex special
situations
Abdominal hypertension and
abdominal compartment syndrome
“ . . . the end result of a progressive, unchecked increase in intra-abdominal
pressure from a myriad of disorders that eventually leads to multiple organ
dysfunction.”
John Hunt, MD
Pathophysiology
Intraabdominal hypertension (IAH) occurs when the amount of
intraabdominal contents (through edematous bowel or fluid
accumulating in the cavity) exceeds the distendable capability of
the fascia. The result is an intraabdominal hypertensive state, which
can lead to abdominal compartment syndrome (ACS). As the fluid
accumulates (because of bleeding, ascites, volume overload, and
other causes), the resulting increase in pressure (change in
compliance/change in volume) initially affects regional blood flow
and results in impaired tissue perfusion, which is then associated
with a systemic inflammatory response. The resulting ischemia and
inflammatory response further cause capillary leakage and
1957
compression of the intraabdominal viscera. If untreated, the
continually elevated free fluid and measured pressure begin to
compress blood vessels, causing organ dysfunction both inside and
outside the abdomen, and lead to ACS. The inflammatory response
promotes the release of cytokines, causing vasodilation and cell
membrane dysfunction. The cell membrane loses integrity, which
causes further inflammation, profound edema, and ultimately cell
death. The elevated pressure in the abdominal cavity generated by
the severe increase in extravascular fluid load increases the
intraabdominal contents (free water) and further impairs intestinal
tissue perfusion as compression of the arteries and veins continues.
This process underlies the multiorgan effects of rising
intraabdominal pressure (IAP). When the IAP rises above critical
level, blood flow to the abdominal viscera and organs decreases
and ACS is imminent. Although initially described in surgical
patients, IAH and ACS also occur in medical patients without
abdominal conditions. IAP can be measured easily and reliably in
patients through the bladder using simple tools.
Risk factors
Diminished abdominal wall compliance
• Ascites/liver dysfunction;
hemoperitoneum/pneumoperitoneum.
Capillary leak/fluid resuscitation
1958
• Acidosis (pH less than 7.2); hypotension;
hypothermia (below 33°C [91.4° F]); massive fluid
resuscitation; poly transfusion; coagulopathy;
sepsis, major trauma and burns.
Definitions
Bladder pressure reflects the IAP and is measured using the
indwelling urinary catheter. The pressure is expressed in mm Hg.
1959
Abdominal compartment syndrome is defined as an IAP greater
than 15 mm Hg and the onset of new organ failure. ACS is
defined as “intraabdominal hypertension with a gradual and
consistent increase in the IAP value of [equal to or greater than]
20 mm Hg,” recorded by at least 3 standardized measurements
taken 1 to 6 hours apart and in conjunction with at least one new-
onset organ dysfunction. ACS can be fatal and often complicates
or results in a clinical condition refractory to treatment. The
astute clinician suspects IAH and ACS when MODS is evolving
and/or the patient presents with persistent lactic acidosis.
Table 11-1
PRESSURE AND SYMPTOM GRADE FOR INTRAABDOMINAL
HYPERTENSION
Pressure
Graded
Measurement and Physiologic Events and Clinical Signs
Measurement
Relevance
Pressure 12 to 15 mm Hg Cytokine release and capillary leak
grade I Significant in the Third spacing of resuscitative fluid
presence of organ Decreasing venous return and preload
dysfunction Early effects on ICP and CPP
Abdominal wall perfusion decreases 42%
Marked reduction in intestinal and intraabdominal
organ blood flow leading to regional acidosis and free
radical formation
Pressure 16 to 20 mm Hg Markedly decreased venous return, CO, and splanchnic
grade II Significant in most perfusion
patients Increased SVR, CVP, PAWP
Decreased blood pressure, particularly systolic blood
pressure, and pulse pressure
Decreased TLC, FRC, RV
Increased vent pressures, hypercapnia, hypoxia
Reduction to 61% of baseline mucosal blood flow and
increasing gut acidosis
Oliguria, anuria
Increasing ICP and decreasing CPP
Pressure 21 to 25 mm Hg Hemodynamic collapse, worsening acidosis, hypoxia,
grade III Significant in all hypercapnia, anuria
patients Inability to oxygenate, ventilate, or resuscitate
Pressure >25 mm Hg Hemodynamic collapse, worsening acidosis, hypoxia,
grade IV Significant in all hypercapnia, anuria
patients Inability to oxygenate, ventilate, or resuscitate
1960
If both pressure and clinical symptoms are met for grade III and/or grade IV, patient
has abdominal compartment syndrome. CPP: Cerebral Perfusion Pressure. CVP:
Central Venous Pressure; FRC: Functional Residual Capacity; ICP: Intracranial
Pressure; PAWP: Pulmonary Artery Wedge Pressure; RV: Residual Volume; SVR:
Systemic Vascular Resistance; TLC: Total Lung Capacity.
1961
abdominal injury that creates IAH, including sepsis or any
condition prompting capillary leak (e.g., major burns, conditions
requiring massive fluid resuscitation). A large multicenter study by
Malbrain and colleagues in 2005 found the prevalence of IAH was
54% among medical intensive care unit (ICU) patients and 65% in
surgical ICU patients. This was remarkable, as most medical
patients are not evaluated for or even considered to have IAH and
ACS.
ACS treatments are the same regardless of the cause; however,
the caregiver must be very careful in managing secondary ACS. The
opportunity for early intervention may be lost because of the subtle
development of signs and symptoms of IAH and ACS. The lack of
definitive signs often leads to delayed diagnosis and delayed
recognition, and an urgent medical condition becomes an
emergency surgical situation. Increased organ failure, increased
mortality, increased resource use, and longer ICU lengths of stay
may result. Similar to sepsis and severe sepsis, the greatest
challenge is early recognition and diagnosis. Monitoring all high-
risk patients would enable clinicians to trend the IAP, facilitating
early, appropriate interventions when the syndrome is more likely
to be responsive to medical therapy. The best management strategy
is to prevent ACS via early monitoring, early medical interventions,
and early surgical decompression if needed.
Assessment
Goal of system assessment
To rapidly evaluate for significant primary and secondary IAH and
correlating reduction of blood flow to other organs
1962
pneumoperitoneum, hypovolemic or vasogenic shock or any
patient with aggressive fluid resuscitation, acute ascites, and/or
pancreatitis.
Observation
Observe for upward trends in respiratory and heart rates (RR and
HR, respectively) and decrease in urine output. Signs and
symptoms are nonspecific and subtle and may be attributed to
other clinical conditions (Table 11-1). Elevated IAP affects the
cardiovascular, pulmonary, renal, and neurologic systems.
1963
Increased IAP compresses the aorta, resulting in elevated SVR
(increased afterload), which reduces CO. The compensatory
vasoconstriction affects blood flow to the hepatic and renal veins,
leading to renal compromise, oliguria, and hepatic
hypoperfusion; if untreated, kidney and liver failure can result.
11-1
RESEARCH BRIEF
The findings of this study revealed the mean IAP within 24 hours
of ICU admission is an independent predictor of mortality. IAP
measurements assist with the identification of patients at increased
1964
risk of death in the first 24 hours of admission. This is a time when
therapy could save the patient’s life. Although no definitive risk
factor profile is identified, serial IAP measurements are an
excellent indicator when patients have significant evidence of lactic
acidosis.
Reintam Blaser A, Sarapuu S, Tamme K, et al: Expanded measurements of intra-
abdominal pressure do not increase the detection rate of intra-abdominal hypertension: a
single-center observational study. Crit Care Med 42:378-386, 2014.
Diagnostic tests
Methods of intraabdominal pressure measurement
The best method for measurement of IAP is controversial. The most
common method is measuring the response of intrabladder
compliance to an instillation of 25 mL of sterile fluid by measuring
the resulting pressure.
Indirect methods
Bladder pressure is commonly used, while other methods are
infrequently used. Indirect methods include gastric pressure
measurement through gastrostomy or a nasogastric tube, intrarectal
pressure measurement using an esophageal stethoscope catheter, or
bladder pressure measurement through a urinary catheter.
Bladder pressure measurement: As physical examination is
notoriously inaccurate in detecting the presence of IAH, bedside
IAP monitoring is essential to both recognizing IAH and avoiding
IAP-induced organ failure. An indwelling urinary catheter is
connected to either a pressure transducer or a fluid manometer to
measure the pressure. Readings are reliable and easier to perform
than direct intraperitoneal measurement. More information
regarding the different methods to measure IAP, including the pros
1965
and cons of each technique, can be found on the WSACS website
(www.wsacs.org).
The urinary bladder normally has a compliant wall. Many studies
reveal compliance decreases when there is a high presence of
intraabdominal fluids, which increases the pressure in the
abdominal cavity and compresses the bladder, increasing
resistance. When fluid is injected into the bladder pressure system,
any decrease in bladder compliance is reflected by increased
intrabladder pressure. The procedure is generally easier and safer if
a prepackaged closed bladder pressure system is used. If
assembling the system without a prepackaged tool, use the
urinary/Foley catheter with an aspiration or infusion port:
2. The cable connecting the system to the monitor should allow for
visualization of a small pressure (scale either at auto or 30 mm Hg).
5. Using the stopcock, the system will be turned off to the monitor
and 25 mL of sterile fluid (an intravenous [IV] fluid is fine) will be
injected rapidly into the infusion port on the urinary catheter. The
stopcock will be then turned off to the injecting port, leaving a
connected pressure system from patient to monitor.
1966
7. A normal value is generally considered between 0 and 5 mm Hg,
although levels as high as 15 mm Hg are not unusual in the first 24
hours after abdominal surgery (see Table 11-1). If the pressures are
elevated, document and repeat in the next hour using the same
techniques. Inform the physician or midlevel practitioner if both
measures are elevated.
11-2
RESEARCH BRIEF
In this retrospective, nonexperimental, observational analysis
performed in a large urban trauma center, many risk factors
appeared for IAH and ACS. As expected, there was a very strong
relationship between polytransfusion and death in patients with
ACS. However, what was most significant was that, in the setting
where ACS is highly probable, developing and adhering to a
protocol for assessing ACS and monitoring IAP were considered
essential. Serial measures were not performed, much to the
authors’ dismay, and the suggestion is that, were they performed
according to a protocol, mortality may be decreased.
Harrell BR, Melander S: Identifying the association among risk
1967
factors and mortality in trauma patients with intra-abdominal
hypertension and abdominal compartment syndrome. J Trauma
Nurs 19:182–189, 2012.
Collaborative management
Care priorities
Box 11-1
MANAGEMENT OF ABDOMINAL
COMPARTMENT SYNDROME
1. Improvement of abdominal wall compliance
Sedation
Neuromuscular blockade
Body positioning
1968
Percutaneous abdominal wall component separation
Nasogastric suction
Rectal tube/enemas
Paracentesis
Diuretics/colloids/hypertonic fluids
Hemodialysis/ultrafiltration
1969
Ascorbic acid in burn patients
Modified from Ivatury R, Cheatham M, Malbrain M et al: In Vincent JL, editor: Yearbook of
intensive care and emergency medicine. Berlin, 2008, Springer, Chapter 5.
Therapies include:
1970
vasculature, hypotension ensues. Patients should be hydrated with
at least 2 L of IV fluid, which may include a “cellular protection
cocktail,” such as 25 g of mannitol 12.5% given along with 2
ampules of bicarbonate/L. IV fluids and vasopressors should be
immediately available in case severe hypotension occurs as the
abdomen is decompressed.
After opening the abdomen, temporary closure will be applied.
The goal is to permanently close the abdomen as soon as possible.
For most patients who require emergent opening of the abdomen
for ACS, a vacuum-assisted closure device (abdominal wound
VAC) attached to a negative pressure device is commonly applied.
An open abdomen may precipitate loss of liters of volume. The
modified negative pressure wound VAC facilitates open wound
fluid management and supports tissue granulation, as well as local
perfusion, which facilitate eventual closure of the open wound.
1971
Fluid/electrolyte management
1972
than 0.5 mL/kg/h usually reflects inadequate intravascular volume
in the patient with abdominal trauma. Decreasing urine output may
also signify compression of the renal arteries in ACS.
1973
2. Monitor BP at least hourly or more frequently in the presence of
unstable vital signs.
5. Evaluate the patient for peritoneal signs (see Box 3-3, Chapter 3),
which may occur initially as a result of injury or may not develop
until days or weeks later, if complications caused by slow bleeding
or other mechanisms occur.
1974
related to inadequate primary defenses secondary to physical trauma,
surgery, underlying infection, temporary closure of abdomen, or insertion
of urinary catheter for measurement of IAP; inadequate secondary defenses
caused by debilitated condition, decreased hemoglobin, or inadequate
immune response; tissue destruction and environmental exposure
(especially to intestinal contents); multiple invasive procedures.
Goals/Outcomes: The patient is free of infection as evidenced by
core or rectal temperature less than 37.7°C (100°F); normal white
blood cell count and no bandemia; HR less than 100 bpm;
orientation to time, place, and person; and absence of unusual
redness, warmth, or drainage at surgical incisions and drain sites.
Immune Status; Infection Severity
Infection protection
Table 11-2
COMMON BARBITURATES
1975
taken. Withdrawal from drugs with shorter half-lives produces more intense
symptoms that last for shorter periods; whereas, withdrawal from drugs with longer
half-lives produces less intense symptoms that can be prolonged. Moreover, the
severity of the withdrawal is directly related to the drug’s dosage.
Infection Control
Drug overdose
Overview/epidemiology
Over 2.3 million human toxic exposure cases are reported annually
to American poison control centers. Most cases are unintentional,
involve a single agent, and can be handled on site with help from a
poison control center. Although the overall mortality of these cases
is low, over a quarter of them require an emergency department
visit and 7.1% result in inpatient admissions.
The type, amount, and route of the agent determine the
signs/symptoms, physical presentation, prognosis, management,
and outcome of a toxic exposure. Every drug has a threshold for
occurrence of serious toxic effects. Drugs of abuse are more
dangerous than prescription drugs, as they are uncontrolled and
unregulated, with a haphazard nature of administration. The
patient’s history is often unavailable or of poor quality. Time is
critical to successful treatment. A thoughtful and stepwise approach
to laboratory testing, medical and nursing interventions,
pharmacologic support, and general supportive measures is
essential. No organ or body system is protected from the
detrimental effects of drug overdose.
1976
Ingestion of unknown substances
Many patients with drug overdose present with altered mental
status and without a useful or reliable history. Identification of the
ingested substance is difficult. Labwork is done for common drugs
of abuse, including amphetamines, barbiturates, benzodiazepines,
cocaine, opioids, phencyclidine, and cannabinoids. Specific drug
levels are available for salicylates, acetaminophen, digoxin,
theophylline, iron, and lithium. When one of these drugs is not the
offending agent, a number of signs and symptoms should be noted
and tests done to determine the list of potential offending agents.
Assessment
It is beyond the scope of this chapter to include all the drugs and
toxins leading to common presenting symptoms, but important
clues to the poison may be gleaned from answering the following
questions:
1977
• Arterial blood gas (ABG): Is the pH acidotic or alkalotic?
Activated charcoal
Activated charcoal (AC) is a fine, insoluble, nonabsorbable powder
that binds with many toxic drugs to enhance their elimination. A
review of the literature yields mixed results on the efficacy of AC.
The dose is 25 to 100 g initially. Repeat dosing of half that amount
every 4 hours is recommended by the American Academy of
Clinical Toxicology if the poisoning involves life-threatening
overdoses of carbamazepine, dapsone, phenobarbital, quinine, or
theophylline. A combination product of AC and sorbitol is
available; the latter component increases the tolerability of charcoal
and may help reduce constipation. Contraindications to AC are
bowel obstruction or perforation, depressed mental status (unless
the airway is protected), delayed presentation, and need for
endoscopy. AC does not bind with inorganic ions such as lithium,
potassium, and magnesium; with alcohols such as ethanol,
methanol, propylene glycol, and isopropyl alcohol; with heavy
1978
metals such as iron, lead, mercury, and arsenic; with acidic or
alkaline corrosives; or with hydrocarbons.
Gastric lavage
Commonly known as “pumping the stomach,” gastric lavage is the
insertion of an orogastric tube followed by repeatedly instilling and
aspirating small quantities of fluid. It is no longer recommended as
routine management by American and European toxicology
associations. In the rare case that it is used, it must be done as soon
as possible, within 60 minutes of the ingestion. When using lavage,
the airway must be protected and lavage should continue until the
fluid is clear of fragments (it usually requires about 5 L of fluid).
Gastric lavage should not be attempted if it delays or interferes with
AC administration in appropriate patients.
Large, life-threatening amounts of recently ingested toxin (which
may be poorly bound to AC used before lavage) may justify use.
Contraindications include the risk or presence of esophageal
hemorrhage or perforation, unprotected airways, and caustic or
hydrocarbon ingestions.
1979
theophylline, salicylates, sotalol, and phenobarbital. Extracorporeal
therapies may be used in extreme cases when other management
strategies are ineffective for drugs that are not highly protein
bound, have a reasonable molecular size, are water soluble (rather
than lipid soluble), have a limited volume of distribution, and are
not highly charged or ionized. Hemofilters used for continuous
renal replacement therapy are often able to accommodate larger-
sized molecules than conventional hemodialysis therapy.
Routes of administration
Oral (most common); rectal per suppository.
1980
and tachypnea have been reported as a hypersensitivity reaction
or as a side effect of N-acetylcysteine. See the Collaborative
Management section that follows.
Hepatic: Acute ingestion will cause hepatic necrosis, which can lead
to liver failure. Hypoglycemia, right-sided abdominal pain, and
nausea with vomiting may be noted, usually 1 to 2 days after
ingestion.
Collaborative management
Care priorities
1981
closely
Alcohols
Ethanol
Route of administration
Oral.
1982
hypoglycemia, hypothermia, lactic acidosis, hypokalemia.
Collaborative management
Care priorities
1983
benzodiazepines may be given on a schedule. If withdrawal is
severe and benzodiazepine doses become excessive, barbiturates
may be added. Agents that have glutamate-blocking properties,
such as lamotrigine, memantine, and topiramate, are showing
promise in alcohol detoxification.
1984
Ingestion of carbohydrates, either orally or parenterally, increases
the body’s demand for thiamine. Traditionally thiamine has been
recommended to be administered before glucose, but evidence
supporting a benefit of this practice is lacking. One reason for this
may be that thiamine is taken up into the cells more slowly than
dextrose, so the order of administration is consequently relatively
minor. Thiamine repletion is very important, however, and 100
mg should be administered promptly, via a parenteral route for the
first dose in severe cases.
Route of administration
Oral; found in household cleaning and automotive products,
especially antifreeze. Methanol poisoning can be associated with
illicit distillation of alcohol (“moonshine”) or intentional
substitution for ethanol.
Collaborative management
Similar to ethanol for hypoglycemia/seizures. Administer
bicarbonate if the pH is less than 7.3 and provide thiamine, folate,
and multivitamins in all patients. Fomepizole is a specific antidote,
followed by hemodialysis if the patient does not respond. In severe
cases (pH less than 7.25, high plasma levels of alcohol, kidney
1985
injury, or severe electrolyte disturbances), hemodialysis should be
done immediately. Ethanol has also traditionally been used as an
antidote for methanol and ethylene glycol but, while cheaper, has a
worse side effect profile. The preferred IV dosage form has also
been removed from the market.
Routes of administration
Oral, rectal (suppository), topical.
1986
symptoms of pneumonia, caused by the presence of tachypnea and
fever.
Later signs and symptoms include the following:
1987
disease characterized by nausea, vomiting, hypoglycemia,
elevated levels of liver enzymes and ammonia, fatty infiltration of
the liver, increased intracranial pressure, and coma.
Collaborative management
Care priorities
1988
6. Glucose administration/treatment of hypoglycemia: Blood
glucoses should be maintained in the upper normal range (110 to
140 mg/dL). There is a risk of cerebral hypoglycemia even with
normal blood glucoses so glucose should be administered to
patients with altered mental status even if normoglycemic.
Barbiturates
Street names
Barbs, downers, ludes, rainbows, red dolls, reds, sleepers,
stumblers, tootsies, yellow jackets.
Routes of administration
Oral, IV, IM.
1989
Neurologic: Symptoms may include headache, vertigo, dizziness,
lethargy, ataxia, stupor, flaccidity, seizures, absent dolls-eye
reflex, coma, loss of deep tendon reflexes, and nystagmus.
Collaborative management
Care priorities
1990
5. Prevention of aspiration: A gastric tube is inserted, which is then
connected to low suction.
Benzodiazepines
Common agents
See Table 11-3.
Table 11-3
COMMON BENZODIAZEPINES
Street names
Benzos, BZDs, downers, heavenly blues, qual, robital, stupes, tranx,
Valley girl.
Routes of administration
Oral, IM, IV.
1991
Effects on body systems
Collaborative management
Care priorities
1992
cause protein to precipitate in the kidneys, leading to renal failure.
Creatine kinase levels of five times the upper limit of normal, with
possible increases in BUN, creatinine, and urine protein, are noted
when rhabdomyolysis is present. Prevention of seizures and
aggressive fluid administration are the best means of preventing
rhabdomyolysis; fluids are also the main treatment modality.
Patients should be monitored closely for hyperkalemia if
rhabdomyolysis develops.
Beta blockers
Common agents
Metoprolol, propranolol, nadolol, atenolol, bisoprolol, carvedilol,
sotalol, acebutolol, and nebivolol.
Routes of administration
Oral (for chronic use).
Respiratory: Depression.
1993
Other: Hypoglycemia, hyperkalemia, rhabdomyolysis, renal failure,
mesenteric ischemia.
Collaborative management
Decontamination strategies can be used if 1 to 2 hours since
ingestion. ACLS measures, including fluids for hypotension and
atropine for severe bradycardia or heart block, may be necessary. IV
calcium and glucagon are given to address negative inotropy and
chronotropy. Glucose and insulin may be needed for blood sugar
and electrolyte imbalances. Beta agonists (vasopressors) such as
norepinephrine or epinephrine and sometimes inotropes such as
dobutamine or milrinone are often needed to maintain
hemodynamics in severe overdose.
Common agents
Verapamil, diltiazem, nifedipine, amlodipine, felodipine,
isradipine, nisoldipine, and nicardipine.
Routes of administration
Oral (for chronic use).
Collaborative management
Decontamination strategies can be used if 1 to 2 hours since
ingestion. ACLS measures should be initiated, including fluids for
hypotension, atropine for severe bradycardia or heart block, and
airway and hemodynamic stabilization as necessary. IV calcium is
1994
given at high doses in an attempt to displace the overdosed drug
and reopen calcium channels, though it is often ineffective. In
animal models high-dose insulin has been effective in severe
overdose, with or without dextrose depending on blood glucose
levels. Other modalities that may be used include glucagon and
vasopressors. Electrolytes should be closely monitored and treated
accordingly.
Cannabinoids
Marijuana
Street names
Ashes, ashitshi, Aunt Mary, baby bhang, blanket, blunt, bobo,
bomber, boom, broccoli, cheeba, chronic, cripple, dinky dow, Dona
Juana, dope, flower tops, gange, giggle smoke, grass, hash, herb, jay
joints, jolly green, joy smoke, Maryjane, pot, reefer, roach, skunk,
weed.
Sometimes marijuana is combined with other drugs (narcotics,
heroin, PCP, LSD, crack, cocaine, alcohol) to achieve a certain high.
Routes of administration
Smoked or ingested most commonly. Less common but presenting
as more severely symptomatic is IV use of hashish oil.
Cannabinoids contain tetrahydrocannabinol (THC).
1995
Collaborative management
Supportive care, benzodiazepines, gastric decontamination
measures if ingested recently, IV fluids.
Synthetic cannabinoids
Street names
Aroma, barely legal, bliss, K2, krypto buds, spice, spicestar fire.
Routes of administration
Like bath salts these are relatively recent drugs of abuse (use
beginning around 2008), which are composed of a plant/herbal
component, such as bay beans, dwarf skullcap, lousewart, red
clover, rose, or vanilla, mixed with synthetic cannabinoid
derivatives to mimic the effects of marijuana. They are marketed as
incense or potpourri (as with bath salts labeled “not for human
consumption”), sold via the internet, convenience stores, liquor
stores, and head shops, and usually smoked. These synthetic agents
bind as full agonists to the CB1 cannabinoid receptor, which is the
target receptor, as opposed to THC, which is only a partial agonist,
so the effects are more potent and the potential for
overdose/toxicity is greater.
Collaborative management
Supportive care. No antidote is available similar to THC. Some of
the synthetic cannabinoids have a longer duration (CP-47, 497) and
some shorter (JWH018 and JWH-073). Benzodiazepines for
agitation and seizures, antipsychotics for severe or prolonged
psychotic symptoms or a comorbid history of psychotic disorder,
and IV fluids as needed are given.
Cocaine
1996
Street names
Badrock, base, ball, bazooka, beam, beat, berni, big C, big flake,
biscuits, blast, blizzard, blow, bones, boost, bouncing powder,
boulders, boy, brick, bump, bunk, C, Cabello, cakes, caine, candy,
casper, caviar, chalk, Charlie, chicken scratch, coca, cocaine blues,
cocktail, coconut, coke, cola, Colombian, cooking up, cookies, crack,
crumbs, cubes, do a line, Damablanca, devil drug, dust, esnortiar,
everclear, fatbags, flake, flame cooking, flame throwers, flash, flex,
Florida snow, foo, freebase, freeze, G rock, girl, goofball, gravel,
happy dust, happy powder, happy trails, hardball, heaven, hell,
kibbles ‘n bits, king, kryptonite, lady, lady caine, late night, line,
love, mama coca, marching dust, marching powder, mojo, monster,
moonrocks, mujer and nieve (Spanish words), nose, nose candy,
nuggets, onion, P dogs, pebbles, Peruvian, piedras (Spanish word),
peace, pimp, powder, press, prime time, ready rock, Roca, rock,
rock star, Roxanne, rush, Scott, Scottie, Scrabble, shootin’ caine,
sleigh ride, smoke houses, smoking gun, sniff, snow, snort, soda,
speedball, sporting, stardust, stone, sugar, sweet stuff, teeth, toke,
toot, tornado, trails, white horse, white lady, white powder,
working bags, Yeyo (Spanish), zip.
Routes of administration
Nasal or IV (cocaine, snow); smoked (crack, rock); cooked;
freebased (flame cooking, flame throwers).
1997
bronchospasm, pulmonary edema, and respiratory failure. Both
lactic acidosis and metabolic acidosis have been seen.
Renal: Renal failure can occur and has been related to profound
hypotension and rhabdomyolysis. Renal infarction has been
reported.
Peak action
1998
• Intranasal: 20 to 60 minutes.
• Oral: 60 to 90 minutes.
• IV: 5 minutes.
Cutting agents
Cutting agents are substances mixed with pure cocaine to increase
bulk. Cutting agents are often unknown but may include procaine,
caffeine, ephedrine, APAP, theophylline, phencyclidine,
amphetamine, quinine, talc, and strychnine, and the clinical effects
of a mixed intoxication may vary accordingly. Agents used in the
preparation of crack include powdered cocaine, water, baking soda,
and lidocaine. Cutting agents can become emboli that shower into
cerebral and pulmonary circulation, with subsequent effects.
Collaborative management
Care priorities
1999
4. Treatment of hypotension or hypertension: Antihypertensives or
vasopressors are administered as indicated.
Cyclic antidepressants
Examples include amitriptyline hydrochloride (Elavil), doxepin
hydrochloride (Sinequan), imipramine hydrochloride (Presamine,
Tofranil), trimipramine maleate (Surmontil), nortriptyline (Pamelor,
Aventyl), and desipramine (Norpramin).
Route of administration
Oral. Overdose has become less common with the much more
widespread use of the safer antidepressant class of serotonin
reuptake inhibitors (SSRIs) such as fluoxetine, paroxetine,
citalopram, escitalopram, and sertraline. Rarely, an SSRI can cause
dangerously high levels of serotonin resulting in serotonin
syndrome. The condition is often accidental, resulting from when
two medications that raise serotonin levels are combined.
Offending agents include other antidepressants, pain or headache
medications, and St. John’s Wort (herbal supplement). Signs and
symptoms include restlessness, agitation, confusion, diaphoresis,
anxiety, tremors, lack of coordination, and tachycardia.
2000
Cardiovascular: Hypotension, sinus tachycardia, supraventricular
tachycardia, ventricular dysrhythmias, conduction defects,
myocardial infarction, cardiopulmonary arrest. Hypertension has
been noted. Monitor ECG for widening QRS complex.
Progressive QRS widening signals worsening toxicity.
Pancreatic: Pancreatitis.
Collaborative management
Care priorities
2001
5. Prevention/treatment of seizures: Phenytoin and diazepam are
administered.
Digoxin
Routes of administration
Oral/IV.
Digitalis glycosides like digoxin are very serious and potentially
life threatening in the event of an overdose; these drugs can
accumulate quickly if renal dysfunction develops or worsens. Like
tricyclic antidepressants, reports of toxicities are decreasing in
frequency as evidence-based use of the drug in heart failure and
arrhythmias is decreasing.
2002
serum digoxin levels are readily available to evaluate.
Collaborative management
AC if recent ingestion. Digoxin immune fab is a specific binding
antidote that will quickly reverse toxicity. Since it is expensive and
whole digoxin levels are unusable after administration, it should be
reserved for cases where arrhythmias or other serious signs and
symptoms are present and not used to treat moderately elevated,
asymptomatic digoxin levels.
Hallucinogens
Street names
Acid, battery acid, blotter, boomers, California sunshine, cids,
doses, dots, golden dragon, heavenly blue, hippie, looney tunes,
LSD, Lucy in the sky with diamonds, mesc, microdot, pane, purple
heart, superman, tab, window pane, yellow sunshine, Zen.
Common agents
Lysergic acid diethylamide (LSD), mescaline (peyote cactus),
ketamine (special K, K, ket, kitkat, super K), morning glory seeds,
nutmeg, psilocybin (mushrooms, magic mushrooms, shrooms,
magics, blue meanies, liberty caps, golden tops, mushies),
phencylclidine (PCP, angel dust, peace pill).
Routes of administration
Oral, IV, nasal, smoked.
2003
Mescaline: Sense of being followed by moving geometric shapes.
Collaborative management
Care priorities
Opioids
Common agents
Codeine, fentanyl, heroin, hydrocodone, hydromorphone
(Dilaudid), levorphanol (Levo-Dromoran), pethidine or meperidine
(Demerol), methadone (Dolophine), morphine, opium, oxycodone
hydrochloride (Percocet-5, Tylox, Oxycontin), buprenorphine
(Subutex), and oxymorphone (Numorphan). Heroin is the most
abused opioid. There has been a steady increase in abuse of
prescription opioids such as morphine.
Street names
2004
China white, Chinese H, dope, dragon, Harry cone, junk, OC, oxy,
painkillers, white, white dynamite.
Routes of administration
Oral, IV, IM, smoked.
Collaborative management
Care priorities
2005
hydrochloride (Narcan) to manage respiratory depression. After the
initial dose of naloxone, the patient’s respiratory status must be
monitored closely, since additional doses may be required.
Respiratory depression and coma may occur when the effects of
naloxone wear off and the opiate effects predominate. The half-life
of naloxone is 60 to 90 minutes, and effects last 2 to 3 hours. If the
narcotic effects last longer than the effects of the naloxone, the
patient may slip into coma once the naloxone wears off. If persistent
respiratory depression is present, a continuous naloxone infusion
may be considered.
Phencyclidine
Street names
Angel dust, mist, PCP, peep, hog, crystal.
Routes of administration
Oral, nasal, smoked.
2006
Respiratory: Respiratory depression, respiratory arrest, laryngeal
stridor, bronchospasm.
Collaborative management
Care priorities
2007
4. Respiratory support: Pulmonary edema is treated with diuretics
and restriction of IV fluid intake. Persons with hypoxia and
respiratory distress require monitoring of pulse oximetry and may
require mechanical ventilation.
Stimulants
Amphetamines
Street names
Crank, crystal meth, ecstasy, ice, methamphetamine, speed, white
crosses.
Routes of administration
Oral, IV, IM, intranasal, smoked.
2008
Renal: Renal failure related to dehydration and rhabdomyolysis.
Collaborative management
1. Support of cardiovascular and respiratory systems to prevent
collapse: Antidysrhythmic agents are given per ACLS guidelines to
manage tachycardias. Ischemia is treated with nitrates; myocardial
infarction is treated per ACLS guidelines for acute coronary
syndromes.
2009
Bloom, blue silk, cloud nine, ivory snow, ivory wave, lunar wave,
white rush, scarface, sextacy, stardust, vanilla sky, white lightning,
and zoom. The energizing and agitating effects mimic other drugs
such as amphetamines and cocaine, which raise the level of
dopamine, a neurotransmitter, in the brain areas that regulate
reward and movement. The surge in dopamine prompts feelings of
euphoria and increased energy.
Routes of administration
Oral or nasally insufflated. Less commonly used rectally IV, IM,
gingivally, or via inhalation. A recently emerging drug of abuse,
bath salts are popular because they are generally cheap, easy to
acquire through the internet or at gas stations, convenience stores,
liquor stores, or head shops, and have only recently (September
2011) been placed under Schedule 1 as a drug with no medical
value and high abuse potential. An easily manipulated chemical
structure has been exploited to weaken such control; this chemical
family in part led to the Drug Abuse Prevention Act of 2012, which
broadened the spectrum and gave a general definition to Schedule 1
substances.
Collaborative management
Primarily supportive; similar to amphetamines.
2010
Table 11-4 gives specific drug treatments for a few of the more
common and critical drug overdoses not discussed in the preceding
section.
Table 11-4
MANAGEMENT OF DRUG OVERDOSE/TOXICITIES
2011
Respiratory monitoring
Hyperthermia
related to overdose of cocaine, hallucinogens, phencyclidine, salicylates, or
cyclic antidepressants.
Goals/Outcomes: Optimally, within 24 to 72 hours of
intervention, the patient becomes normothermic.
Thermoregulation
2012
be achieved.
Temperature regulation
Fluid management
2013
1. Monitor hydration status. Note signs of continuing dehydration:
poor skin turgor, dry mucous membranes, thirst, weight loss
greater than 0.5 kg/day, urine specific gravity greater than 1.020,
weak pulse with tachycardia, and postural hypotension.
• Monitor CO as appropriate.
2014
7. Maintain fluid intake as prescribed; administer prescribed
electrolyte supplements.
Reality orientation
2015
the patient may have more trust in them.
Behavior management
2. Speak with the patient in a quiet and calm voice, using short
sentences.
2016
6. Limit the number of interventions as much as possible to avoid
frequently disturbing the patient.
2017
Most pregnant women are healthy and rarely in need of critical
care. The high-risk obstetric patient presents the unique challenge
of caring for the mother and the fetus simultaneously. In most
cases, the survival of the mother will take precedence over fetal
survival, but the optimal outcome is survival of both. Two basic
principles should underlie the care of the pregnant patient. First,
maternal anatomic and physiologic changes occur during
pregnancy to facilitate adequate blood flow to the fetus and protect
the mother after delivery (Box 11-2). The pregnant patient may
require hemodynamic monitoring, and the critical care nurse
should be familiar with the different hemodynamic changes and
pressure values in pregnancy and labor as outlined in Table 11-5.
Second, the fetus is totally dependent on the mother for all of his or
her oxygenation and growth needs, so any intervention performed
on the mother will most likely affect the fetus. Despite the unique
challenges presented by the critically ill obstetric patient, transfer of
the patient to a critical care unit should not be delayed.
Table 11-5
EXPECTED HEMODYNAMIC CHANGES DURING PREGNANCY,
LABOR, DELIVERY, AND POSTPARTUM
2018
Box 11-2
PHYSIOLOGIC ANATOMICAL CHANGES
IN PREGNANCY
Body position
Supine hypotension: After 20 weeks, supine positioning
significantly reduces CO and uterine blood flow by compressing
the inferior vena cava.
Cardiovascular
Heart rate: 10 to 15 bpm increase from prepregnancy rate by 32
weeks
Fetal circulation
More than 10% of maternal CO is diverted into the uterine
circulation. Maternal CO increases by at least 25% during
pregnancy. Fetal oxygenation is dependent on maintenance of
sufficient maternal CO.
Gastrointestinal
Gastric motility: decreased
2019
Gastric emptying time: decreased
IAP: increased
Neck/throat
Larynx: displaced anteriorly, prompting increased incidence of
airway edema and bleeding, leading to failed intubation.
Renal
Glomerular filtration rate: increased by 50% at term
2020
conditions. The most prevalent indication for obstetric ICU
admissions is hypertension in pregnancy. This chapter will focus on
the hypertensive complications of pregnancy that may result in
admission to a critical care unit.
Hypertension in pregnancy
Classification
Hypertensive disease occurs in up to 22% of pregnancies. The study
of hypertension in pregnancy has been hindered by a lack of
agreement on a set of definitions to define subsets of the disease.
This chapter uses terms recommended by the American Congress
of Obstetricians and Gynecologists and endorsed by the National
Institutes of Health Working Group on High Blood Pressure to
define hypertensive disease in pregnancy (refer to Box 11-3). Of
these hypertensive disorders, preeclampsia, eclampsia, and HELLP
(hemolysis, elevated liver enzymes and low platelet count)
syndrome were responsible for 30% of obstetric ICU admissions.
These conditions, their management, and care will be discussed.
Box 11-3
CLASSIFICATION OF HYPERTENSIVE
STATES OF PREGNANCY
• Chronic hypertension: Hypertension that is present before
pregnancy or develops before 20 weeks’ gestation.
2021
of pregnancy without proteinuria.
Pathophysiology
Preeclampsia has been called the “disease of theories” because true
mechanisms behind the pathogenesis remain unclear. Many women
with preeclampsia have smaller than normal blood vessels feeding
the placenta. However, why this happens to some women and not
others is not completely understood. Preeclampsia is characterized
by widespread arteriolar vasospasm resulting in increased
peripheral vascular resistance. Areas of vasospasm cause breaks or
roughened areas in the endothelial layer. These roughened areas
2022
trigger fibrin deposition and leakage of intravascular fluid into the
extravascular space. Decreased colloid oncotic pressure, a normal
physiologic change during pregnancy, also contributes to fluid
leakage and proteinuria. These widespread arteriolar vasospasms
result in decreased perfusion to virtually all organs, including the
placenta, a decrease in plasma volume, activation of coagulation
cascade, and alteration in glomerular capillary endothelium. The
physiologic process of vasospasm manifests in the development of
classic symptoms associated with preeclampsia resulting in
decreased blood flow to the major maternal organs such as the
kidney, brain, and liver, as well as the placenta. These generalized
cyclic vasospasms lead to tissue ischemia and eventually end-organ
dysfunction. One of the more common problems related to
preeclampsia is pulmonary edema caused by increased capillary
permeability. Thrombocytopenia complicates severe preeclampsia
in about 7% to 11% percent of women. Abruptio placentae and the
release of procoagulants, such as thromboplastin, can result in acute
disseminated intravascular coagulation (DIC).
2023
• Low platelet count (may be rapidly falling).
Table 11-6
HEMODYNAMIC PROFILES IN OLIGURIC PATIENTS WITH
PREECLAMPSIA
2024
diabetes, vascular disease, connective tissue disease, and
maternal infections.
HELLP syndrome
HELLP syndrome is an acronym for a unique pregnancy condition
representing increased severity of a variant of severe preeclampsia
or eclampsia. HELLP syndrome affects 2% to 20% of patients with
severe preeclampsia or eclampsia. Maternal mortality ranges from
3.5% to 24%, with perinatal mortality ranging from 10% to 60%. The
etiology of HELLP is uncertain. Approximately 10% to 15% of
pregnant patients with HELLP syndrome do not have elevated
proteinuria of hypertensive disease. The clinical manifestations of
HELLP syndrome, which include nausea, vomiting, malaise, flulike
symptoms, and epigastric pain, may suggest a multitude of other
clinical diagnoses. Misdiagnosis is common and may result in a
delay of correct treatment. Any pregnant woman demonstrating
clinical manifestations and hemolysis, elevated liver enzymes, and
low platelets must be diagnosed with HELLP syndrome.
Worsening of systemic arteriolar vasospasm produces such
complications as liver damage, subcapsular hematoma, pulmonary
edema, liver rupture, abruption placentae, DIC, and acute renal
failure. The HELLP patient should be closely monitored for right
upper quadrant pain or shoulder pain because these complaints
may be indicative of liver hematoma or liver rupture. The only
known treatment for HELLP syndrome is to empty the uterus of the
fetus and the placenta.
Test Findings
Complete blood Hemoglobin and hematocrit (Hct) may be elevated (>35 Hct) and steadily
2025
count rising with severe preeclampsia-eclampsia.
Peripheral blood Schistocytes or burr cells are present with HELLP syndrome.
smear
Urinalysis Positive for protein spillage
24-hour urine Mild/moderate: 0.3 to 5 g protein with normal urine output. Severe
collection preeclampsia-eclampsia: >5 g protein with low urine output.
Serum albumin Decreases as urine protein spillage increases; severe: <2.5 mg/dL.
Liver enzymes Aspartate transaminase, alanine amino transferase, and lactate
dehydrogenase are elevated with severe preeclampsia-eclampsia and
HELLP syndrome. Bilirubin may be elevated with HELLP.
Renal serum Mild-moderate: BUN, creatinine, and uric acid levels may be elevated.
chemistry Severe preeclampsia-eclampsia: BUN, creatinine, and uric acid will be
elevated.
Platelet count Mild-moderate: <100,000/mm3. Severe preeclampsia-eclampsia and
HELLP syndrome: <100,000/mm3
Bleeding time Prolonged when platelet count is <100,000/mm3.
Fibrinogen Decreased (<300 mg/dL)
Screening Normal unless the patient develops HELLP syndrome that progresses to
coagulation tests DIC, wherein all values are elevated.
(PT, PTT, thrombin
time)
2026
aid the critical care nurse, but optimally, there would be an
obstetric nurse as part of the care team for any obstetric patient
admitted to the ICU for severe hypertensive conditions.
2027
4. Biophysical profile: The biophysical profile uses a combination of
NST and fetal parameters observed via ultrasound to measure fetal
well-being. The fetus is scored as 0, 1, or 2 for each of 5 parameters:
fetal breathing movement, gross fetal movement, fetal tone,
amniotic fluid volume, and NST test results.
2028
symptoms of preterm labor:
• Dull backache.
2029
obstetrician or midlevel practitioner, because
cervical examination is the most accurate method
for diagnosing preterm labor.
3. Monitor uterine contractions (preterm labor) and fetal status:
2030
indicated because of the maternal condition or fetal compromise.
The goal of the healthcare team is to accurately monitor ongoing
organ system dysfunction and prevent further damage leading to
end-organ failure and maternal-fetal mortality.
Mode of administration:
Magnesium is given iv as a loading (bolus) dose followed by a
continuous drip.
2031
• Administer using an infusion pump. Two nurses should verify
the infusion pump settings when magnesium is initiated or
dosage changed.
2032
present at the bedside with the critical care nurse to monitor fetal
and uterine response during magnesium infusion.
Table 11-7
CLINICAL EFFECTS OF MAGNESIUM
2033
Fluid management
Severely preeclamptic patients are easily overloaded with IV fluid,
predisposing them to pulmonary edema. Strict observation of I&O
is warranted. Total fluid intake is typically maintained at 125 to 150
mL/h. Hemodynamic monitoring may be indicated if pulmonary
edema develops. Urine output of less than 0.5 mL/kg/h should be
reported to the physician or midlevel practitioner.
A nonglucose solution should always be available as part of a
fetal resuscitation protocol, and a bolus of 500 to 1000 mL of
lactated Ringer or normal saline is usually given to improve
maternal circulating volume and subsequently improve uterine
perfusion and fetal oxygenation.
Pain management
Medications used in pregnancy are generally limited to classes A
and B, to decrease potential negative effects on the fetus. The
benefits of medications in classes C, D, and E should be carefully
weighed against the risk to the fetus. Butorphanol (Stadol),
nalbuphine (Nubain), and fentanyl (Sublimaze) may all be given IM
or as an IV bolus/IV push and are commonly given for pain relief
during labor.
2034
molecular-weight heparin within 12 hours, coagulation disorders,
maternal shock, or infection at the insertion site. Common side
effects of neuraxial analgesia include maternal hypotension and
itching. Hypotension is generally treated with IV fluid boluses
and/or IV ephedrine. Ephedrine is the preferred vasopressor
because it causes peripheral vasoconstriction without affecting the
umbilical vessels. Loratadine (Claritin) or cetirizine (Zyrtec) may be
given to alleviate itching.
2035
clinical placement for the patient based on availability of
equipment, skills, and trained personnel:
2036
selected, since regional anesthesia (entering the spine) is generally
contraindicated with thrombocytopenia. Because of the potential
for difficult intubation caused by airway edema and hyperemia,
fiberoptic intubation may be used. The patient will require close
observation postoperatively for the first 24 to 48 hours.
Intrapartum
2037
2. Monitor BP of mother at least every 5 minutes if severe
hypertension or seizures have occurred. Monitor FHR for slowing,
indicative of fetal distress.
10. Note hemoglobin and Hct levels before and after blood loss, as
indicated.
Ineffective protection
related to potential for seizures and neurologic complications secondary to
eclampsia or HELLP syndrome.
Goals/Outcomes: Throughout the hospitalization, the patient
remains free of seizures and neurologic complications as evidenced
2038
by orientation to time, place, and person; normoreactive pupils and
reflexes; her normal visual acuity, motor strength, and
coordination; and absence of headache and other clinical indicators
of increased intracranial pressure.
Risk control
Seizure precautions
2039
stimuli, decorticate or decerebrate posturing, Cushing triad (i.e.,
bradycardia, increased systolic BP, widening pulse pressure),
nonreactive/fixed pupils, unequal pupils, or fixed and dilated
pupils. See Traumatic Brain Injury, Chapter 3, for more information
about herniation. For additional interventions for increased
intracranial pressure, see Box 3-7.
Fluid monitoring
2040
petechiae. Maintain patent IV access.
Infection protection
2041
3. Monitor CBC, and consult advanced practice provider for
significant increases in WBCs. Be aware that a normal or mildly
elevated leukocyte count may signify infection in patients with liver
dysfunction.
7. Provide daily breast care by cleansing the breasts with mild soap
and water. Breast engorgement should be managed per physician’s
orders to help prevent infection and control pain. If left unrelieved,
breast engorgement can result in stoppage of lactation. If breast-
feeding is planned, breasts can be massaged and milk manually
expressed or pumped.
Medication management;
2042
Compromised family coping
related to abnormal circumstances surrounding labor, delivery, and
postpartum; creating need for mother to be separated from infant and other
family members.
Goals/Outcomes: The patient and family demonstrate adequate
coping behaviors and are facilitated in being together as soon as
possible in the postpartal hospitalization.
Surveillance: Safety; Anxiety: Self-Control, Concentration,
Coping.
Coping enhancement
Oncologic emergencies
An oncologic emergency is defined as a life-threatening situation
occurring as a manifestation of a malignancy or the result of
2043
antineoplastic treatment or tumor progression. Such emergencies
most commonly arise from the ability of cancer to (1) spread by
direct infringement on adjacent structures or metastasize to distant
sites leading to thrombosis or hemorrhage; (2) produce abnormal
amounts of hormones or cellular products leading to fluid and
electrolyte imbalances and organ failure; (3) infiltrate serous
membranes with effusion; (4) obstruct vessels, ducts, or hollow
viscera; or (5) replace normal organ parenchyma. As more
aggressive therapies are used in the treatment of these cancers, side
effects are more intense and the use of critical care to manage such
side effects will only increase.
Early recognition and intervention are essential to enhance
positive outcomes. Once an oncologic emergency is recognized, the
aggressiveness of management is influenced by the reversibility of
the immediate situation, the probability of long-term survival, and
the ability to provide effective supportive care.
Oncologic emergencies can be classified as hematologic,
structural, metabolic, or side effects from treatment such as
chemotherapy, radiation therapy, biologic therapy, surgery, or bone
marrow transplantation. Neutropenic sepsis, tumor lysis syndrome
(TLS), and superior vena cava syndrome (SVCS) will be discussed
in this chapter as examples of oncologic emergencies seen in the
critical care arena. When recognized early and managed
appropriately, these acutely ill individuals have a high likelihood of
recovery. An overview of additional oncologic emergencies,
associated causes, and signs and symptoms is given in Table 11-8.
Table 11-8
ONCOLOGIC EMERGENCIES DEFINED
2044
2045
Sources: Recommendations for end-of-life care in the intensive care unit: a
consensus statement by the American College of Critical Care Medicine. Crit Care
Med 36:1394-1396, 2008; Guidelines for evaluation of new fever in critically ill adult
patients: 2008 update from the American College of Critical Care Medicine and the
Infectious Diseases Society of America. Crit Care Med 2008 36:1330-1349, 2008;
Clinical practice guideline: red blood cell transfusion in adult trauma and critical care.
Crit Care Med 37:3124-3157, 2009; Dellinger RP, Levy MM, Carlet JM, et al:
Surviving Sepsis Campaign: international guidelines for management of severe
sepsis and septic shock: 2008 [correction appears in Crit Care Med 41(2):580-637,
2013; Crit Care Med 2008;36:296-327; National Comprehensive Cancer Network
Clinical Practice Guidelines in Oncology, retrieved from www.nccn.org; American
Society of Clinical Oncology Practice Guidelines, retrieved from http://www.asco.org;
Oncology Nursing Society Practice Guidelines and Resources, retrieved from
www.ons.org/ClinicalResources/
Cancer patients may require intensive care for several reasons: (1)
overwhelming infection and sepsis; (2) structural complications of
cancer or cancer treatment; or (3) metabolic complications of cancer
or cancer treatment. Intensivists sometimes refuse admission to
cancer patients needing critical care, which may result in denial of
effective care for some deserving patients. A cancer patient may
need admission to an intensive care unit for a variety of reasons.
The outcomes of patients with hematologic malignancies,
previously dismal, have improved over the last 10 years. The
previously known indicators of poor outcome are no longer valid in
view of recent advances in intensive care. A select group of patients
with hematologic malignancies may be offered aggressive therapy
for a limited duration and then prognosis can be reassessed. Cancer
chemotherapy can produce toxicities affecting all major organ
systems. Such patients may be admitted with acute organ
dysfunction or years afterward for incidental illnesses. Knowledge
of these toxicities is essential for early diagnosis, management, and
prognostication in such patients. The postsurgical cancer patient
has unique problems; care can range from monitoring alone after
major surgery to fully aggressive intensive care for postsurgical
anastomotic dehiscence, mediastinitis, septic shock, and multiorgan
dysfunction. The metabolic and mechanical complications
commonly seen in nonsurgical cancer patients are also reasons for
admission. Intensive care should be offered to all patients who have
a reasonable chance of cure or supportive care of their disease. The
intensivist must be able to recognize the potentially reversible
critical illnesses among the various groups of cancer patients and
2046
discourage admission to terminally ill cancer patients. He or she
must also be aware that alleviation of suffering in the last hours of
life for a terminal cancer patient is one of the functions of an ICU,
once a decision to discontinue aggressive therapy has been made, if
there isn’t time for transfer to a hospice.
Neutropenic sepsis
Pathophysiology
Neutropenia is defined as an abnormally low level of neutrophils in
the blood. The normal level of neutrophils in human blood varies
slightly by age and race. Infants have lower counts than older
children and adults, and African Americans have lower counts than
whites or Asians. The average adult level is 1500 cells/mm3 of
blood. Neutrophil counts (in cells/mm3) are interpreted as follows:
2047
Asssessment: Neutropenic sepsis
History and risk factors
Granulocytopenia, immunosuppression, recent cancer treatment,
diabetes, organ-related disease, age older than 65 years, indwelling
catheters, long hospital stays, loss of skin or mucosal integrity,
malnutrition, hypothermia, intubation/mechanical ventilation,
aspiration, alcoholism, renal failure, hepatic failure, chronic illness.
The risk of death is twice as great for sepsis patients with cancer as
for those without and is comparable to the risk observed in sepsis
patients who are HIV positive.
Stage 1
Systemic inflammatory response syndrome (SIRS) describes a
systemic inflammation without a defined source of infection
resulting from any major insult to the body, such as trauma, burns,
or myocardial infarction, in which two or more of the following are
present:
• HR at least 90 bpm.
2048
Stage 2
Sepsis is identified by the presence of two of the SIRS criteria in
response to pathogenic microorganisms and associated endotoxins
in the blood. However, in many cases of sepsis, the actual cause of
infection is never identified. The delay in waiting for confirmation
of infection can slow the treatment of sepsis; the most effective
course of action once SIRS is identified and infection is suspected is
to treat the infection and monitor the patient for signs and
symptoms of organ failure, which will indicate that the condition
has progressed to severe sepsis.
Stage 3
Severe sepsis occurs when a patient who meets the sepsis criteria
shows one of the signs and symptoms of organ failure. Once severe
sepsis is suspected, the patient requires aggressive treatment in a
critical care area.
Stage 4
Septic shock is defined as severe sepsis plus hypotension (a systolic
BP less than 90 mm Hg) that does not respond to fluid resuscitation.
Septic shock is associated with a high mortality rate. The patient’s
chances of recovery are significantly reduced if, by this stage of
sepsis, she or he has not already been transferred to the ICU.
2049
• Digestive: Nausea, vomiting, anorexia, decreased GI motility, GI
bleed.
Collaborative management
Fever (even low grade) is often the only reliable sign of infection in
2050
the neutropenic patient. No specific patterns of fever or clinical
features can positively distinguish between fever because of
infection and one of noninfectious cause. Therefore, all febrile
neutropenic patients should be considered for the administration of
empirical broad-spectrum antibiotics within 1 hour of presentation.
Many patients are outpatients during their cancer treatments, and it
is vital to their survival that they and their significant others be
educated about early recognition (and timing during treatment) of
neutropenia to minimize the risk of sepsis. All healthcare providers
should be educated about this potential life-threatening situation
and be aware of strategies to minimize risk to patients by
systematically and regularly evaluating response to treatment and
progress toward desired outcomes.
Because sepsis-related mortality is unacceptably high, the Society
of Critical Care Medicine (SCCM) set a quality improvement goal to
reduce mortality caused by severe sepsis and septic shock by 25%.
Clearer definitions of sepsis, severe sepsis, and septic shock will
help in achieving this goal, as will recently updated evidence-based
management guidelines for severe sepsis and septic shock. To be
effective, these definitions and guidelines need to be applied to the
early identification and aggressive treatment of patients who have
severe sepsis or septic shock. Early goal-directed therapy to achieve
hemodynamic stabilization has been demonstrated to decrease
mortality in patients who have septic shock. See SIRS, Sepsis, and
MODS, Chapter 11.
Care priorities
1. Manage hypovolemia
Once severe sepsis or septic shock has been identified, the highest
management priorities are to establish vascular access and initiate
fluid resuscitation to improve tissue perfusion. Failure to manage
global hypoxia can lead to MODS. Fluid resuscitation guidelines are
defined by the SCCM and are a part of early goal-directed therapy
(see Sepsis, SIRS, and MODS, Chapter 11).
2051
values indicate several possible causes of poor oxygenation,
including inadequate oxygen delivery, high oxygen demand, or
inability of tissues to extract oxygen from hemoglobin (see Sepsis,
SIRS, and MODS, Chapter 11).
Infection control
2052
• Monitor WBC and differential for evidence of
infection and response to interventions.
• Strict handwashing.
• Universal precautions.
2053
• Assist with daily bathing, oral, and perineal
hygiene; change linens daily.
Hypovolemia management
2054
2. Monitor and document HR, rhythm, pulses, and BP.
Acute pain
related to fever, chills, headaches, myalgias, and arthralgias associated
with neutropenia and infection.
Goals/Outcomes: The patient will not experience chills and will
be able to perform activities of daily living without discomfort;
temperature will stay below 38° C (100.4° F).
Comfort Level
Pain management
2055
3. Apply warmth to muscles or joints or cool compress to head as
needed.
2056
Complications include laryngeal edema, cerebral edema,
decreased CO with hypotension, and pulmonary embolism (when
an associated thrombus is present). Potential issues include:
Assessment
Goal of assessment
Minimize life-threatening complications of cancer and its treatment
through early recognition and effective management.
Malignancy
Primary intrathoracic malignancies are the cause of SVCS in
approximately 87% to 97% of cases. The most frequent malignancy
associated with the syndrome is lung cancer, followed by
lymphomas and solid tumors that metastasize to the mediastinum.
SVCS develops in approximately 3% to 15% of patients with
bronchogenic carcinoma, and it is 4 times more likely to occur in
patients with right- rather than left-sided lesions. Breast and
testicular cancers are the most common metastatic malignancies
causing SVCS, accounting for more than 7% of cases. Metastatic
disease to the thorax is responsible for SVCS in about 3% to 20% of
patients.
Nonmalignant causes
2057
The most common nonmalignant cause of SVCS in cancer patients
is thrombosis secondary to venous access devices. Other
nonmalignant causes include cystic hygroma, substernal thyroid
goiter, benign teratoma, dermoid cyst, thymoma, tuberculosis,
histoplasmosis, actinomycosis, syphilis, pyogenic infections,
radiation therapy, silicosis, and sarcoidosis. Some cases are
idiopathic.
Observation
Classic symptoms
Patients with SVCS most often present with complaints of facial
edema or erythema, dyspnea, cough, orthopnea, or arm and neck
edema. These classic symptoms are seen most commonly in
patients with complete obstruction, as opposed to those with mildly
obstructive disease.
2058
radiograph baseline and every 24 hours lobe congestion, masses, or nodes between clavicle
(CXR) if signs and symptoms of and scapula.
sepsis persist.
Spiral chest Further evaluates lung status Precisely identify location and size of masses
CT scan to help clarify findings from around SVC, clarify growth versus compression.
with CXR.
contrast
Magnetic Provides further data Precisely identifies location and size of masses
resonance regarding the area of the around SVC.
imaging of superior vena cava.
the chest
Doppler Noninvasively assesses the Presence of thrombus or ineffective thrombolysis
ultrasound entire vascular tree to when therapies are rendered.
of the identify thrombosis or
vasculature effects of thrombolysis.
Contrast Invasively assesses the entire Presence of thrombus or ineffective thrombolysis
and vascular tree to identify when therapies are rendered.
radionuclide thrombolysis; may be used
venography to validate Doppler
ultrasound findings.
Complete Evaluates the composition Declining platelet count may signal the presence of
blood count: and concentration of the heparin-induced thrombocytopenia or “white clot
platelet cellular components of syndrome.” If unmanaged, may lead to extremity
count blood, particularly platelets. gangrene and life-threatening venous
thromboembolism.
Collaborative management
Care priorities
2059
possibility of platelet-induced thrombocytopenia syndrome (white
clot syndrome). This rare syndrome may lead to extremity
gangrene and life-threatening venous thromboembolism.
Management requires urgent discontinuation of heparin and urgent
evaluation by a hematologist for appropriate pharmacotherapy.
Vascular surgical evaluation may also be indicated.
2060
maintaining patency of the superior vena cava
Balloon angioplasty is rare but may be considered in patients with
SVCS, significant clinical symptoms, and critical SVC obstruction
demonstrated by angiography.
7. Assess skin and mucous membranes for cyanosis and pallor and
2061
skin temperature for signs of change in perfusion.
Respiratory monitoring
2062
pain, dyspnea, pallor, cyanosis, pupillary dilation, rapid or
irregular pulse, profuse diaphoresis, and anxiety. Assess need for
supplemental oxygen, and consult advanced practice provider
immediately. Patients with severe pulmonary emboli may require
mechanical ventilation. See Pulmonary Embolus, Chapter 4.
2063
treatment are at greatest risk of developing TLS.
TLS is also seen in small-cell lung cancer and metastatic breast
cancer. Because of clinicians’ increased awareness of TLS during the
past decade and the use of adequate prophylaxis before initiation of
chemotherapy, the number of cases has decreased. Occasionally,
TLS occurs following treatment with radiation, glucocorticoids,
tamoxifen, or interferon.
Assessment
History and risk factors
The typical patient at risk for TLS tends to be young (under 25 years
of age) and male with an advanced, highly proliferative, high-grade
disease (lymphoma, leukemia, etc.), and a markedly elevated lactate
dehydrogenase level. Abdominal disease is often present.
Comorbid conditions include renal insufficiency and diabetes.
Volume depletion, concentrated acidic urine pH, and excessive
urinary uric acid excretion rates may also increase the risk.
TLS most commonly develops during the rapid growth phase of
high-grade lymphomas and leukemia in patients with high
leukocyte counts; it is less common in patients with solid tumors.
The syndrome is often iatrogenic, caused by cytotoxic
chemotherapy.
Observation
Signs and symptoms reflect electrolyte imbalance, coupled with
those of acute renal failure. The syndrome is characterized by
hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia,
and oliguric renal failure (see Fluid and Electrolyte Disturbances,
Chapter 1, and Acute Renal Failure, Chapter 6). The diagnosis of
TLS is based on the development of increased levels of serum uric
acid, phosphorus, and potassium; decreased levels of serum
calcium; and renal dysfunction following chemotherapy.
Collaborative care
Care priorities
2064
1. Identify patients at risk and initiate prophylactic
measures
Patients at risk for TLS should be identified before the initiation of
chemotherapy and should be adequately hydrated and given
agents to alkalinize the urine. Treatment with allopurinol (IV or
PO) may be instituted to minimize hyperuricemia. The
recommended dosage of IV allopurinol ranges from 200 to 400
mg/m2/day. This regimen should be started 24 to 48 hours before
initiation of cytotoxic treatment. The dose may be equally divided
into 6-, 8-, or 12-hour increments, but the final concentration should
not exceed 6 mg/mL.
2. Monitor electrolytes
Serum electrolytes, uric acid, phosphorus, calcium, and creatinine
levels should be checked repeatedly for 3 to 4 days after
chemotherapy is initiated, with the frequency of monitoring
dependent on the patient’s clinical condition and risk profile.
2065
and creatinine levels will be within normal limits.
Electrolyte and Acid-Base Balance
Fluid/electrolyte management
2066
Shock Management: Volume
Organ transplantation
Solid organ transplantation remains a viable option for end-stage
organ failure. As of May 2014, there were nearly 122,900 people on
the United Network for Organ Sharing (UNOS) organ transplant
waiting list. The major constraint to meeting the demand for
transplants is the availability of donated (cadaver) organs. Dialysis
remains the main lifeline for kidney disease and mechanical devices
for heart failure are becoming increasingly available throughout the
United States. A small number of patients are living at home on
mechanical ventilation. In general, those with end stage liver end-
stage, pancreatic, and lung disease remain dependent on organ
transplantation to sustain life.
Several steps have been taken to alleviate the organ shortage.
National laws mandate that families of every appropriate potential
donor be offered the option to donate organs and tissues. In
addition, the ongoing efforts of the National Organ Donation
Collaborative and laws requiring all deaths to be reported to organ
procurement agencies have prompted an increase in organ
donations. Ongoing efforts of organ recovery coordinators and
others to improve public awareness of organ donation will help
reduce the shortage, as will use of extended donors.
Nationally, major improvements are being made to optimize
organ distribution, improve procurement, and ensure good
matches. Inclusion criteria for the waiting list are being
standardized using listing criteria for all degrees of sickness (see
Box 11-4 for allocation of cardiac organs). UNOS maintains a
computerized registry of all patients awaiting organs for
transplantations. Organs procured within a region are shared first
2067
within that region. If a recipient cannot be found there, UNOS
directs the organ to the recipient in another region with the greatest
need. Organ recovery coordinators are available 24 hours a day, 7
days a week to arrange serologic testing and organ removal from
donors, preserve organs pretransplant, and distribute organs to
appropriate recipients.
Labwork
• General laboratory assessment profiles including biochemical,
hematologic, lipid, hepatic, renal, and thyroid studies, and
urinalysis. If findings indicate several organs are impaired, the
patient may be inappropriate for transplant, since
immunosuppressive drugs can cause renal failure, those with
heart disease may have a myocardial infarction in the
postoperative period, those with lung disease may be unable to
wean from mechanical ventilation, and those with liver disease
may be immunocompromised and at higher risk for sepsis and
metabolic complications.
2068
• Cancer screening: May include pap smears, prostate examination,
prostate-specific antigen, mammogram, colonoscopy, and chest
radiography
Diagnostic testing
• Pulmonary evaluation: Oxygenation assessment using pulmonary
function testing and chest radiograph.
2069
• Osteoporosis screening: Osteoporosis may place a patient at
higher risk for complications following transplantation, as
maintenance medication may increase the severity, which
increases the probability of bone fractures.
Organ-specific evaluation
• Cardiac: Cardiac catheterization (right and left heart),
cardiopulmonary exercise testing, cardiac magnetic resonance
imaging or positron emission tomography scan, and MVo2
testing.
2070
hepatic vasculature. A GI evaluation is done to assess for bowel
diseases.
Table 11-9
SELECTION CRITERIA FOR CARDIAC TRANSPLANTATION
2071
• 1-year survival expectancy <50% and poor • History of cancer in remission
short-term prognosis or poor functional • Absolute
capacity • Complicated IDDM with end-organ damage
• Age <60 to 65 years • Poor compliance
• Left ventricular ejection fraction 20% to • Severe obesity
35% • Pulmonary hypertension: PVR >6 Wood units
• Chronic, unstable angina • Comorbid diseases
• Peak O2 consumption 14 mL/kg/min • Active infection (until resolved) and infection
• Onset of atrial fibrillation with highly resistant organisms that are nearly
• Decreasing cardiac output impossible to eradicate
• Refractory ventricular dysrhythmias • Irreversible liver and kidney dysfunction
• Otherwise good health • Active peptic ulcer disease
• Coexisting cancer
• Symptomatic peripheral and cerebral vascular
disease
• Severe osteoporosis
• Amyloidosis
ACE: Angiotensin Converting Enzyme; BMI: Body Mass Index; IDDM: Insulin
Dependent Diabetes Mellitus; PVR: Pulmonary Vascular Resistance;
Box 11-4
ALLOCATION OF CARDIAC ORGANS
Status 1A
A patient is admitted to the transplant center and has at least one
of the following:
2072
arrhythmias
C. Mechanical ventilation
E. Patient does not meet the above criteria but has a life expectancy
without a heart transplant of less than 7 days.
Status 1B
A patient listed as status 1B has at least one of the following
devices or therapies in place:
A. Left and/or right ventricular assist device implanted for >30 days
Status 2
A patient who does not meet the criteria for status 1A or 1B is
listed as a status 2.
Status 7
A patient listed as status 7 is considered temporarily unsuitable to
receive a thoracic organ transplant.
From the United Network for Organ Sharing (UNOS) for allocation of thoracic organs. For
complete, detailed criteria, see actual policy at www.UNOS.org.
Lung
Lung transplant candidates generally have a life expectancy of less
than 18 months, are dependent on supplemental oxygen, have
severe exercise intolerance, are under 65 years of age, and report
poor quality of life.
Indications
In adults, irreversible, progressively disabling, end-stage
pulmonary disease encompassing a wide variety of etiologies. The
majority of lung transplants are performed for chronic obstructive
2073
pulmonary disease, followed by idiopathic pulmonary fibrosis,
pulmonary hypertension, and cystic fibrosis (CF). Four groupings
of lung diseases that may result in transplantation are:
2074
Contraindications
Relative
• Body weight: Patients with BMI less than 16 likely have a poor
nutritional status, which impairs healing. Those with BMI greater
than 30 are at higher risk of developing postoperative atelectasis
and pneumonia.
Absolute
2075
• Malignancy within the past 2 years (except cutaneous squamous
and basal cell tumors).
Liver
Indications
Patients with chronic or acute liver disease who cannot sustain a
normal quality of life or have life-threatening complications are
probable candidates for liver transplant. Complications that
warrant liver transplantation generally include recurrent variceal
hemorrhage, intractable ascites, spontaneous bacterial peritonitis,
refractory encephalopathy, severe jaundice, and sudden
deterioration in status. Reduced-size, split, and living-related liver
transplantation continue to expand the number of donors, and yet
these efforts still fail to meet the demand for organs.
2076
are exposed to or ingest toxins or toxic doses of illicit drugs or
medications (e.g., acetaminophen toxicity) are included in this
group. Hepatotoxic drugs include acetaminophen (paracetamol),
salicylates (aspirin, Pepto-Bismol), methanol (wood alcohol),
isoniazid, IV tetracycline, chlorinated hydrocarbons, and sodium
valproate. The most commonly involved drug is acetaminophen,
and, in some locations, it is the most common cause of FHF.
Other diseases that may cause FHF include heart failure,
cardiomyopathy, sepsis, shock, cyanotic heart disease,
obstructive lesions of the aorta, vascular occlusions, myocarditis,
Hodgkin disease, and severe asphyxia.
Contraindications
Relative
• Advanced cachexia.
• Active infections.
• MODS.
Absolute
2077
• Active alcohol or other substance abuse.
Kidney
Indications
Relative
Absolute
• Active infection.
2078
• Obesity.
• Noncompliance.
Pancreas
Preexisting advanced renal disease is observed in significant
numbers of pancreas transplantation candidates. Many pancreas
transplantation candidates may benefit from a combined
pancreas/kidney transplant.
Indications
2079
• C-reactive peptide less than 0.8 ng/mL.
Contraindications
Relative
Absolute
• Active/chronic hepatitis B.
Organ donors
The mainstay of organ supply is the deceased donor or cadaveric
donation. Nationwide, approximately 30% to 40% of all deceased
2080
organ donors are trauma patients. Evaluation of the trauma patient
as a potential organ donor is critical to maximizing the availability
of deceased donor organs for transplantation. Regional transplant
centers vary in absolute and relative criteria for excluding potential
organ donors. Early criteria limited evaluation to ideal donors aged
10 to 50 years without comorbid conditions. In response to the
increasing demand for organs, restrictions have loosened
considerably and the donor pool has expanded. Organs are
now often procured from patients younger than 10 years and older
than 50 years of age. Factors such as hepatitis C or active bacterial
infection are no longer absolute contraindications. “Nonideal”
donors are often used for specific recipients.
There are relatively few absolute contraindications, and most
potential donors are reviewed on an individual or a case-by-case
basis. Additional absolute and relative contraindications are
assessed for donation of specific organs. Some organs must be
transplanted within a very short time following brain death, while
other organs can be preserved for much longer periods of time. The
following are types of organ donors:
2081
patient is pronounced dead. The donation should not hasten the
death, and the transplant procurement team enters the operating
room after the patient is pronounced dead and is not part of the
end-of-life care. All normal care, including palliative measures,
occurs until the patient is pronounced. Donation may also be
considered if there is an unplanned cardiac arrest.
Living donors
Living donors are considered for kidney and liver transplants. The
evaluation process is critical for living donors. Postoperative care
for the donor and donor family must also be clearly defined.
Considerations to be assessed include:
2082
3. Understanding the Costs: Does the donor understand the
potential financial costs he or she will incur and the amount of time
that will be lost from work?
2083
• HLA typing.
• Blood cultures.
Heart donor
• ECG.
• Chest radiograph.
• Echocardiogram.
Lung donor
• ABG on 100% Fio2; then, serial ABGs.
• Chest radiograph.
• Bronchoscopy.
Pancreas donor
2084
• Serial blood glucose determinations.
Liver donor
• Liver function tests.
• Liver biopsy for patients with BMI greater than 32, age older
than 70 years (older than 60 years if diabetic), past medical
history suggestive of liver disease, significant history of alcohol
abuse, radiographic studies suggestive of fatty liver infiltration,
or positive hepatitis serology.
• PT/INR.
• aPTT.
Kidney donor
• Electrolytes.
• BUN.
• Creatinine.
2085
status 1A and status 1B candidates was 2.4 months and 6.9 months,
respectively, in 2012. The median waiting time for status 1A
candidates has not changed appreciably during the last decade,
although it has increased for status 1B and status 2 candidates. The
median time to transplant among candidates with ventricular assist
devices (when listed) was 3 months in 2006-2007 and has since
increased to 8.7 months in 2012, the same as for candidates without
them.
Lungs
The Lung Allocation Score (LAS) is a numerical scale (0 to 100)
computed from a list of criteria and updated every 6 months.
People who are most likely to die before transplantation and have a
chance of greater survival after transplantation are the candidates
given the highest scores on the list. Along with the LAS, blood type,
age, and distance from the donor are used to determine priority for
the organ. Also under consideration is the bilirubin level and
changes in this level while on the waiting list. A current bilirubin of
at least 1.0 mg/dL or an increase by at least 50% during a 6-month
time period increases the candidate’s risk of dying while on the list.
Pediatric and adolescent patients have priority over adults. LAS
testing is updated every 6 months.
Since implementation of the LAS, transplant rates have increased
for all candidates and are most profound in candidates aged 65
years or older and those in diagnosis group D. Overall median
waiting time for candidates listed for lung transplant in 2012 was 4
months and 3.1 months for group D patients. Median months to
transplant for group B patients listed in 2011 was 9.7 months.
Although 65.3% of lung transplant candidates underwent
transplant within 1 year of listing, the percentage of candidates
undergoing lung transplant was highly variable based on donation
service area (DSA). The variation was from 37.5% to 93.5% for those
with at least 10 listings.
Kidneys
Living donor allocation/timing is dependent on availability and
matching. The waiting time may be less than for a deceased donor.
2086
Waiting times can vary from 2 to 5 years for a deceased donor.
Recipients must have a glomerular filtration rate of no more than 20
mL/min to be considered. Recipient status is either active or
inactive. There is no urgent status. Extended criteria donors are on
the rise. Considerations include ABO type, HLA antibodies, cross-
match, and PRAs. PRAs can be tested as frequently as monthly. A
new algorithm—Life Years from Transplantation—will attempt to
determine the donor and recipient combination that will achieve
the greatest survival benefit relative to dialysis.
Liver
Transplant-appropriate patients are generally determined using the
model for end-stage liver disease (MELD) score. Those patients in
the ICU with life expectancy of less than 7 days with acute liver
failure, hepatic artery thrombosis, primary graft nonfunction, or
acute decompensated Wilson disease are considered status 1 and
are excluded from other requirements of the MELD score. The
overall transplant rate has been gradually declining since 2006. The
greatest decline is in candidates with hepatocellular cancer and
those aged 18 to 34 years. The decrease in transplant rates reflects
the gradually worsening donor shortage. Despite a decline in wait-
list registration, the median pretransplant waiting time among
active wait-listed adult patients increased from 12.9 months in 2009
to 17.6 months in 2010 and to 18.5 months in 2011. Pretransplant
mortality rates decreased in 2012, for the first time in several years.
MELD Score: This score ranges from 6 (less ill) to 40 (gravely ill)
and is used to prioritize liver transplant candidates at least 12 years
of age. It is predictive of risk of 3-month mortality from liver
disease. The number is calculated using a formula that considers
three blood studies: bilirubin, which measures liver excretion of
bile; INR (international normalized ratio), which measures the
ability of the liver to manufacture clotting factors; and creatinine,
which measures kidney function. Bile excretion and the ability to
synthesize clotting factors are impaired by chronic liver disease.
Renal impairment is often associated with liver disease. A
numerical scale is used for liver allocation for chronic liver disease
only. Status 7 patients are considered inactive.
2087
Pancreas
Waiting lists and allocation of organs vary by institution and are
generally based on time waiting and PRA level. Frequent
evaluation is necessary, that is, every 6 months or per program
standard. There are four main types of pancreas transplantation:
Pharmacotherapy
2088
Posttransplant immunosuppression
Goals of therapy include:
1. Prevent rejection.
Induction
Immunosuppression, usually in high doses, in the initial period of
organ transplantation wipes out T cells completely. Commonly
used drugs typically consist of corticosteroids and monoclonal and
polyclonal antibodies: Orthoclone OKT3, antithymocyte globulin
(ATG), basiliximab, daclizumab, alemtuzumab.
Maintenance
A maintenance dose of immunosuppression for transplant patients
in stable condition serves to maintain a gradual process of healing
and to prevent rejection. The potential for weaning patients off
some of their medication therapies is a high priority. Commonly
used drugs are corticosteroids, calcineurin inhibitors (CNIs),
antiproliferative agents, and mammalian target of rapamycin
(mTOR) inhibitors.
Rejection
Immunosuppression, usually in high doses for a patient whose
2089
organs are acutely rejecting. Commonly used drugs are
corticosteroids and polyclonal and monoclonal antibodies:
Orthoclone OKT3, ATG, basiliximab, daclizumab, and
alemtuzumab.
Desensitization
Therapies to reduce newly formed or preexisting alloantibodies.
Commonly used drugs are IVIG, rituximab, and
cyclophosphamide. Plasmapheresis mechanically removes
antibodies but does not treat the underlying problem.
Categories of drugs
Interleukin 1 inhibitors
Corticosteroids are used to treat and prevent organ rejection and to
suppress production of cytotoxic T-lymphocytes from noncytotoxic
precursor cells. They can be used for maintenance to prevent
rejection or as part of an acute rejection protocol. Evidence indicates
that steroids may prevent release of interleukin (IL)-1 and IL-2. IL-1
is released by the macrophages and promotes differentiation of
helper T cells. The release of IL-2 promotes differentiation of
cytotoxic cells and helps to reduce or prevent edema, to promote
normal capillary permeability, and to prevent vasodilation. Side
effects are numerous, including mood changes, sodium retention,
blurred vision, fragile skin, bleeding, glucose intolerance, increase
in appetite and subsequent weight gain, osteoporosis, and “moon
face” appearance from an accumulation of fatty tissue on cheeks
and upper back.
2090
cytokine release syndrome. The drug is tapered to as low a dose
as tolerated.
Calcineurin inhibitors
Calcineurin is a protein phosphatase (also known as protein
phosphatase 3, and calcium-dependent serine-threonine
phosphatase), which activates the T cells of the immune system.
CNIs are used to block T-cell activation.
2091
Another dose is given at 96 hours and then at weeks 2, 4, 8, and 12.
Starting at week 16, a maintenance dose of 5 mg/kg is given every 4
weeks.
Antiproliferative agents
Antiproliferative agents are used in maintenance
immunosuppression and treatment of rejection to block the
proliferative phase of activated T- and B-lymphocyte generation.
They are an integral part of most immunosuppression regimens.
2092
by a maintenance dose of 2 mg/day regulated by blood level
assessment, divided into 2 doses given every 12 hours.
Therapeutic trough blood levels are seen between 8 and 15
ng/mL. The drug is associated with impaired wound healing, so
it is not used during induction in the posttransplantation period.
Monoclonal antibodies
Monoclonal antibodies are monospecific antibodies made by fusing
the spleen cells from a mouse immunized with a target antigen with
myeloma cells. These highly specialized antibodies can detect and
bind to the target antigen to purify the substance. Rabbit B cells
have been used more recently in the production of monoclonal
antibodies.
2093
• Basiliximab (Simulect): A chimeric (murine/human) monoclonal
antibody produced by recombinant DNA technology that is used
as an immunosuppressive agent during induction to inhibit IL-2
activation of T lymphocytes. It is not used to treat rejection, but
rather to prevent it. The dosage is 20 mg within 2 hours of
transplantation surgery and repeated 4 days after transplant. Side
effects are rare.
Polyclonal antibodies
Polyclonal antibodies are antibodies secreted by various lineages of
B cells within the body. In contrast, monoclonal antibodies originate
from a single cell type. This collection of immunoglobulin
molecules has the capacity to identify and purify many different
2094
antigens. Each type of molecule targets a specific antigen.
Antivirals:
2095
transplant.
Pain management
Opiates: Fentanyl is commonly used because it is short acting and,
unlike morphine, does not cause histamine-mediated hypotension.
2096
lymphoproliferative disorder, and an increased incidence of
rejection, have been associated with pretransplant sensitization.
Collaborative management
Care priorities
1. Prevent infection
Infection control is paramount because of immunosuppression
therapy. Immunosuppressed patients are vulnerable to bacterial
(Staphylococcus, Streptococcus, Klebsiella, Pseudomonas), viral (CMV,
EBV, herpes simplex, varicella zoster,) and fungal (Aspergillus,
Candida, Cryptococcus, histoplasmosis, Coccidioides, pneumocystis,
and Toxoplasma gondii) infections. Prophylactic antibiotics,
antivirals, and antifungals are used.
Steps to reduce infection postoperatively and beyond:
Table 11-10
CHARACTERISTICS OF ORGAN REJECTION BY CATEGORY
2097
Type of
Characteristics Outcome
Rejection
Hyperacute Occurs immediately Usually irreversible and untreatable
Antibody-mediated Preventable with crossmatching
Result of preformed circulatory
antibodies
Accelerated Occurs 3–5 days after transplant Irreversible and untreatable
acute Antibody-mediated Preventable with crossmatching
Rapid loss of function
Fever and oliguria
Acute Primarily T cell-mediated Treatable and reversible Multiple
Possible presence of humoral episodes affect long-term graft survival
component
Occurs weeks, months, or years after
transplant
Chronic Develops slowly over months to years Untreatable, eventually leads to graft loss
Probably a combination of cellular-
and humoral-mediated processes
Table 11-11
CLINICAL PRESENTATION WITH ACUTE ORGAN REJECTION
2098
lymphocyte enlarges, divides, and differentiates into a plasma cell
that produces and secretes antigen-specific immunoglobulins, or
antibodies. The formation of this antigen-antibody complex triggers
events that augment the nonspecific responses of inflammation and
phagocytosis. Cell-mediated immune response involves T-
lymphocytes that recognize a foreign antigen on the surface of the
macrophage, bind to the antigen, enlarge, and produce a sensitized
clone, which migrates through the body to the site of the antigen.
When the sensitized T cell combines with the antigen, chemicals are
released that kill foreign cells directly and facilitate phagocytosis
and the inflammatory response.
Heart
Biopsy is performed in a cardiac catheterization lab/biopsy lab or
surgery. The cannulation site is generally the right internal jugular
or sometimes the femoral vein. Biopsy samples are graded
according to one of several grading systems. Biopsies are generally
performed at 7 and 14 days after surgery and at specified intervals
thereafter, and the Biopsy Rejection Scale is used:
2099
Biopsy Rejection Scale
Grade Description
0R No evidence of acute cellular rejection
1R Interstitial and/or perivascular infiltrate with up to 1 focus of myocyte damage
2R Two or more foci of infiltrate with associated myocyte damage
3R Diffuse infiltrate with multifocal myocyte damage +/− edema, +/− hemorrhage, +/−
vasculitis
Lung
2100
• Transbronchial biopsy: Not particularly helpful in detecting
rejection; the morbidity risk increases with open biopsy.
• Biopsy grading:
Kidney
• Renal biopsy: Determines presence, type, and severity of
rejection.
2101
• Kidney biopsy grading: (Table 11-12).
Table 11-12
BANFF DIAGNOSTIC CATEGORIES FOR RENAL ALLOGRAFT
BIOPSIES
2102
tender on palpation.
Liver
Several methods are used to obtain liver samples, including
laparoscopic liver biopsy, percutaneous image-guided liver biopsy,
and open surgical liver biopsy.
2103
• Serum bilirubin level: Total bilirubin will rise in relation to
baseline postoperative level.
Table 11-13
LIVER TRANSPLANT DATABASE (LTD GRADING SCHEME)
Grade Criteria
AO No rejection
A Rejection without bile duct loss
1 Rejection infiltrate in some, but not all, of the triads confined within the portal spaces.
2 Rejection infiltrate involving all of the triads, with or without spillover into the lobule.
No evidence of centrilobular hepatocyte necrosis, ballooning, or dropout
3 Infiltrate in some or all of the triads, with or without spillover into the lobule, with or
without inflammatory cell linkage of the triads, associated with centrilobular
hepatocyte ballooning or necrosis and dropout
Pancreas
Open biopsy is the only means by which a definitive diagnosis can
be made.
The following signs also assist in the diagnosis of rejection of the
transplanted pancreas:
2104
• Serum creatinine: Elevated.
2. Provide the patient with verbal and written information for the
type of immunosuppressive agent that has been prescribed. Discuss
the generic name, trade name, purpose, usual dosage, route, side
effects, and precautions.
2105
transplant coordinator. Encourage the patient to bring a significant
other to the visit.
Infection protection
2106
practice provider for any of these findings.
2107
and Therapy Medication Management; Respiratory Monitoring;
Teaching: Disease Process; Tube Care: Urinary; Vital Signs
Monitoring.
1. Inspect the mouth daily for signs of exudate and lesions and
report abnormal findings to the physician. Teach the patient to
perform self-inspection of mouth.
Skin surveillance
2108
2. Assess for and document the presence of rashes or lesions in the
perineal area. Herpetic lesions are common in the
immunosuppressed patient.
3. Inspect the trunk area daily for the presence of flat, itchy rashes.
Skin fungal rashes are common in the immunosuppressed patient.
4. Teach the patient the importance of daily skin care with water,
nondrying soap, and lubricating lotion.
2109
response to a stimulus that represents a danger to the host, it has
also been directly related to current treatments rendered to
critically ill patients who previously would have died. It accounts
for 1,000,000 cases and 200,000 deaths annually in the US alone, but
unlike other major epidemic illnesses, treatment for sepsis is
nonspecific, limited primarily to support of organ function and
administration of IV fluids, antibiotics, and oxygen. There are no
approved drugs that specifically target and treat sepsis. Current
evidence supports that acute infections worsen preexisting chronic
diseases or result in new chronic diseases, which lead to poorer
outcomes and increased morbidity in survivors.
Sepsis represents a syndrome, not a disease, and it is difficult to
identify because the signs and symptoms are often subtle and
evolving and generally mirror the signs and symptoms of other
conditions. This clinical diagnostic term used to describe patients
who have a continuum of abnormalities in organ function evolved
from a 1991 Consensus Conference that defined “sepsis” as
documented or suspected infection combined with two or more
abnormalities in body temperature, HR, RR, or WBC count. Those
individuals with sepsis and evidence of organ dysfunction
(cardiovascular, renal, hepatic, or neurologic) were further
classified as having “severe sepsis,” and those with cardiovascular
dysfunction not responsive to fluid were said to have “septic
shock.” Ten years later the diagnosis of septic shock was expanded
to include evidence of inadequate tissue perfusion (low SVO2, lactic
acidosis, wide anion gap). Recently, evidence shows that patients
with sepsis or septic shock go on to develop “persistent critical
illness” with overt organ dysfunction that may last for weeks or
months. These survivors may be disabled by cognitive dysfunction,
neuropathies, and other complications.
2110
elevated HR and RR, and an altered WBC count as well as a
suspected or proven source of infection. Sepsis is a syndrome
consisting of the combination of a systemic inflammatory response
and the presence of infection. Risk factors for poor outcome in
sepsis include hypothermia, leukopenia, low arterial pH, shock,
multiorgan dysfunction, age greater than 40 years, and medical
comorbidities. The issues associated with identification are related
to this generalized presentation. Almost all acutely ill patients meet
SIRS criteria and often have infection, which is not necessarily
sepsis. Sepsis with one or more organ dysfunctions is considered
severe sepsis.
11-3
RESEARCH BRIEF
The latest definition is that sepsis is a life-threatening condition
when the body’s response to an infection injures its own tissues
and organs. Using this criteria, sepsis cannot be identified until
there is organ dysfunction in the primary easily evaluable
sixsystems: renal, neurological, hepatic, cardiovascular,
respiratory, and coagulation. Other systems may be more difficult
to assess; however, any acute dysfunction in this situation must be
considered a sign of sepsis.
Czura CJ: Merinoff symposium 2010: sepsis—speaking with one
voice. Mol Med 17:2-3, 2011.
Severe sepsis
Severe sepsis is the compounding of sepsis by comorbid conditions,
wherein the inflammatory response to a nidus of infection or
inflammation is fulminating and out of control. Severe sepsis has
2111
more recently been viewed as endothelial dysfunction resulting
from overwhelming inflammatory mediation, in conjunction with
profound, unopposed coagulation. The capillary vasculature
sustains a significant injury by a cascade of events that ends in
capillary occlusion. The more massive the occlusion, the greater the
potential for organ failure, as cellular level circulation requires a
functional capillary network for delivery of oxygen and nutrients
and removal of cellular metabolic waste products. When infection
or other injury prompts an initially widespread inflammatory
response, or SIRS, the normally smooth surface of microvascular
(capillary) endothelium is roughened or damaged by the response.
Release of inflammatory mediators prompts vasodilation with
increased capillary permeability. Microscopically, the endothelium
resembles a road riddled with tiny “potholes.” Systemic mediators
are released to facilitate healing of the endothelium, which is aimed
at “filling the tiny potholes.”
The four main factors associated with severe sepsis that may
evolve to septic shock are hyperinflammation, hypercoagulation,
microvascular obstruction, and increased endothelial permeability.
Because endothelial damage is generalized, the extensive or
hyperinflammatory response leads to accelerated formation of
microclots on the non–smooth capillary endothelium, consuming
platelets and inhibiting clot lysis (fibrinolysis). This progresses to
uncontrolled alterations in the vascular tone with vasodilation in
the large vessels (where BP is measured). Both vasodilation and
constriction occur in capillaries, where oxygen delivery takes place.
Stimulated by products of antigen ingestion, activated
neutrophils and other humoral mediators combine, activate, and
potentiate an ongoing vascular endothelial injury with a
concomitant proinflammatory, procoagulating, antifibrinolytic
response. Among other mediators, an increased presence of tissue
factor persistently stimulates thrombin, which ultimately increases
fibrinogen conversion to fibrin and promotes platelet aggregation.
Coupled with microvascular clotting, the process limits oxygen
delivery and may lead to organ ischemia. Unopposed, this process
may lead to a profound consumptive coagulopathy (DIC),
diminished distal blood flow, and cell death by activated cellular
suicide (apoptosis). The blood flow necessary to maintain tissue
2112
oxygenation and aerobic metabolism, nutrient transfer, and
metabolic waste removal is profoundly threatened.
Excessive thrombin production and a secondary decrease in
endothelial production of plasminogen activator, thrombomodulin,
protein C, and other prothrombin and antithrombin mediators,
ultimately, activated protein C, illustrate the overwhelming
response that separates simple infection from severe sepsis. The
endothelial regulation of appropriate blood flow requires a balance
of vasodilators (i.e., nitric oxide) and vasoconstrictors (e.g.,
endothelin). In severe sepsis, when the balance cannot be
maintained, the corresponding maldistribution of blood flow and
loss of vascular tone at the macro- and microvascular levels result
in both ischemia and hyperemia in the cells supplied by the same
capillary beds. In addition, myocardial depressant factor is released
and may contribute to the loss of the compensatory CO, which is
required to keep blood moving through the vascular beds.
2113
continuum that often begins with the same event (Table 11-14).
SIRS initiates a process of relative hypovolemia. To the
unsuspecting practitioner, the early signs of arterial hypoperfusion
may be masked by the patient’s near normal appearance resulting
from compensatory vasoconstriction and increased CO, which
maintains a normal BP. If SIRS and/or sepsis is managed
aggressively in the early stages, the incidence of MODS is
decreased. The American College of Chest Physicians
(ACCP)/SCCM Consensus Conference first initiated a suggested
approach to the identification of profound and uncontrolled
inflammatory response in 1992. These guidelines have been
modified and updated several times, with the most recent revisions
reflected in the 2012 Surviving Sepsis Campaign International
Guidelines (Table 11-15). Some of the more specific recognized
signs and laboratory profiles are listed in Table 11-16.
Table 11-14
SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)
If two or more of the following are present, the patient meets criteria for SIRS:
1 Temperature >38° C or 100.4°F or <36° C or 96.8°F.
2 Heart rate >90 bpm
3 Respiratory rate >20 breaths/min or Paco2 <32 mm Hg
4 White blood cell count >12,000 cells/mm3 or <4000 cells/mm3 or >10% immature (band) forms
Adapted from Levy MM, Fink MP, Marshall JC, et al: 2001
SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care
Med 31:1250-1256, 2003.
Table 11-15
ASSESSMENT FINDINGS FOR THE PATIENT WITH SEPSIS IN THE
EARLY HYPERDYNAMIC STAGE
2114
Svo2 >80% Decreased use of oxygen by cells
PAWP usually <6 mm Venous dilation, decreased preload
Hg
SVR <900 Vasodilation
dynes/sec/cm-5
2115
to resolve without hospitalization.
In addition to infection, sepsis is associated with multiple injuries
in trauma patients and other patients with significant inflammation
such as pancreatitis. Critically ill patients with sepsis resulting from
infection are often not easily managed, with microorganisms that
require considerable skill to control. Microorganisms commonly
seen in the critically ill include gram-negative enteric pathogens
(e.g., Escherichia coli, Klebsiella spp., Enterobacter spp., Pseudomonas
aeruginosa), Staphylococcus aureus, coagulase-negative staphylococci,
Enterococcus spp., and Candida spp. Antibiotic-resistant bacteria
(e.g., methicillin-resistant S. aureus [MRSA]) are commonly seen.
The American College of Chest Physicians (ACCP)/SCCM
Consensus Conference first initiated one suggested approach to the
identification of profound and uncontrolled inflammatory response
in 1992. The Surviving Sepsis Guidelines for Management of Severe
Sepsis and Septic Shock were first published in 2004, revised in
2008, and recently revised again and published in 2013. The
evidence-based update supports components of the overall
campaign, but there are other directives that have come under
increasing scrutiny. Early identification, antibiotics, and source
control as well as initial volume resuscitation remain as the
foundation of sepsis management, although the endpoints may not
be as clear as they first appeared to be.
Key points
• Shock is a clinical diagnosis defined by inadequate end-organ
perfusion in the setting of hemodynamic instability.
2116
Assessment: Systemic inflammatory
response syndrome, sepsis, severe sepsis,
septic shock and multiorgan dysfunction
syndrome
Goal of system assessment
Evaluate for hypermetabolism, progressive tissue hypoxia, and
prevention of organ dysfunction.
Vital signs
• Patients may present with tachycardia, tachypnea, hyper- or
hypothermia, and hyper- or hypoglycemia. Hypoglycemia is
being increasingly recognized and is thought to be related to
depletion of glycogen stores, increased cellular glucose use,
and/or impaired gluconeogenesis. Criteria for diagnosis of sepsis
are evolving.
2117
associated with sepsis, which is now defined as infection
accompanied by two or more of the following signs of systemic
inflammation: hypo- or hyperthermia, tachycardia, tachypnea, or
elevated or depressed leukocyte count. Decreased Paco2, positive
culture, tissue stain, polymerase chain reaction testing, clinical
examination, radiologic imaging, or other laboratory findings
may support the diagnosis of infection. Older adults may
manifest normal or slightly decreased temperature.
2118
indicator of the SV response to therapy is to note whether it
increases by 10% to 15% after a specific therapy. Dynamic methods
used to evaluate volume levels and volume responsiveness
measure heart-lung interactions during inspiration. Spontaneous
breathers (negative pressure breathing) may be evaluated using
pulse pressure variation or systolic pressure variation. Pulse
pressure variation, estimated from the arterial waveform, and
stroke volume variations, from pulse contour analysis, pulse
oximeter plethysmographic waveform, or thoracic bioreactance,
have been found to be reliable predictors of fluid responsiveness
when patients receive a challenge test, such as passive leg raise. If
patients are mechanically ventilated, using the pulse contour
analysis, pulse oximeter plethysmographic waveform, or thoracic
bioreactance has been found to be reliable in predicting fluid
responsiveness when patients receive a challenge test, such as
passive leg raise.
2119
• Threats to tissue oxygenation occur, such as a
decrease in blood flow from hypovolemia or low
CO (relative to tissue demand). The compensatory
mechanism is to release more oxygen from
hemoglobin (shift to right), which reflects a lower
than normal measured ScVO2.
2120
that is normal to high, in the presence of significant
lactic acidosis.
4. Lactate level: Should be reviewed to assess progress, as increases
in ScVO2 are not always indicative of improvement. Although
lactate provides a valuable reflection of tissue hypoxia, it cannot be
continuously monitored and it changes over time. Lactate is
produced excessively when poor circulation and oxygenation
prompt cells to initiate anaerobic metabolism. Blood lactate
concentrations reflect the balance between lactate production and
clearance. The normal blood lactate concentration in physiologically
unstressed patients is 0.5 to 1 mmol/L. In critical illness, lactate
concentrations of less than 2 mmol/L are considered acceptable.
Hyperlactatemia is defined as a mild to moderate persistent
increase in blood lactate concentration (2 to 4 mmol/L) without
metabolic acidosis. Depending on the hospital or clinical laboratory
protocol, lactic acidosis is diagnosed when increased blood lactate
levels rise above 3 mmol/L. When patients are at risk of cellular
hypoxia, a blood sample to measure the lactate level should be
drawn. This may apply to a patient with suspected sepsis, but also
to those with sustained tachycardia, tachypnea, hyperventilation,
and persistent hypotension.
Table 11-16
ASSESSMENT FINDINGS FOR THE PATIENT WITH SEPSIS IN THE
LATE STAGE
2121
hemoglobin because of acidosis
Respiratory
Increased >30 breaths/min (even at late stage) or Metabolic acidosis and acute lung
decreased respiratory rate <12 breaths/min injury lead to tachypnea; whereas,
central respiratory center depression
can cause hypopnea
Decreased respiratory rate (< 12 breaths/min) and Central respiratory center depression
depth
Crackles, rhonchi, wheezes Accumulation of lung secretions
Increased Fio2 required to maintain Pao2 (possible Ventilation/perfusion mismatch and
ARDS) decreased lung compliance
Renal
Decreased urine output progressing to anuria Decreased renal perfusion and tubular
ischemia
Low urinary excretion of sodium, with possibly Activation of the aldosterone
decreased fractional excretion of sodium; if patient mechanism and release of ADH, which
develops acute tubular necrosis, sodium excretion stimulate sodium and water retention
typically increases.
Cutaneous
Cool, pale skin or cyanosis Sustained vasoconstriction
Neurologic
Decreased LOC, coma Severe hypoxia and metabolic
derangements leading to reversible
encephalopathy
Hematologic
Oozing from previous venipuncture sites Development of DIC caused by
stimulation of coagulation process, and
fibrinolysis
Acid-Base Status
pH <7.35; Mixed acid-base disorder: respiratory
Paco2 >45 mm Hg, HCO3 <22 mEq/L (or less than acidosis and metabolic acidosis
expected)
ARDS, Acute respiratory distress syndrome; ADH, antidiuretic hormone; BP, blood
pressure; CI, cardiac index; CO, cardiac output; CVP, central venous pressure; DIC,
disseminated intravascular coagulation; LOC, level of consciousness; PAWP,
pulmonary artery wedge pressure; SVR, systemic vascular resistance.
2122
consciousness with possible obtundation or unresponsiveness as
cerebral perfusion is failing; rales caused by heart failure;
respiratory failure requiring endotracheal intubation and
mechanical ventilation; oliguria; diminished bowel sounds; and
diminished peripheral pulses. Vasodilation may maintain warm-
to-hot skin until the patient totally decompensates with cool-to-
cold, clammy skin.
2123
Collaborative management
Care priorities
Early recognition and therapy are still the cornerstones of acute care
of the septic patient. The advent of new technologies and
biomolecular testing should improve survival rates and give rise to
more accurate incidence statistics. The treatment of severe sepsis
and septic shock is an evolving process, and the guidelines continue
to be updated. Reduction of septic inflammation may involve
several pharmacologic therapies and adjunct therapies.
Management of sepsis and septic shock includes respiratory
support, aggressive fluid resuscitation, inotropic support,
vasopressor therapy, and early antibiotic therapy. In the future less
invasive methods of optimizing a patient’s fluid status and
hemodynamics, along with monitoring the microcirculatory
dysfunction common in sepsis, may become more routine.
There are several models available to simplify the identification
process. The use of standardized order sets for the management of
sepsis should be recommended strongly for better performance in
treatment. Standard order sets use serum lactate values because of
their relationship to organ dysfunction in sepsis. To reduce
mortality rates, sepsis must be identified and treated as early as
possible.
Summary of immediate steps: Identify the patient and engage in
collaborative practices to begin treatment. Delays in patient
identification are often directly related to the nurse’s ability to have
the appropriate conversation with colleagues on the factors present
that are indicative of sepsis. Nurses are crucial to successful patient
identification. Broad-spectrum antibiotics are initiated immediately;
ideally, after blood cultures are drawn to provide therapy within 1
hour in the setting of severe sepsis, with or without septic shock.
Imaging should be done as soon as possible; ideally during the first
hour to try to identify and/or confirm the source of infection so
necessary steps can be initiated as soon as possible to manage the
source. It is crucial to provide aggressive resuscitation within the
first 6 hours of diagnosis. As noted, blood cultures should be
obtained within 1 hour of recognition, before initiating antibiotics if
possible, but delaying antibiotics in lieu of cultures is unacceptable.
2124
Large-bore IV access should be secured in preparation for large
volume fluid resuscitation, which should be initiated as soon as
possible within the first hour of patient identification. Vasopressor
therapy with norepinephrine is used to stabilize the patient.
2125
3. Use early goal-directed therapy to prevent or slow patient
progression to multiorgan dysfunction syndrome and
multiple organ failure
According to current ACCP/SCCM guidelines, the following are
points of early goal-directed therapy:
• All blood for labwork for the sepsis profile (serum lactate, blood
culture, biomedical profile, CBC with differential, coagulation
profile, and biomarkers such as presence of TNF, IL-6, or
procalcitonin if available) should be drawn and then repeated
every 2 to 4 hours initially to assess for progress.
2126
veins and arteries, to assist in the management of terminal heart
failure. Given that both vasodilation and vasoconstriction are
present throughout the circulation, it is difficult to predict the
most effective strategy for support of circulation. Some
institutions may use noncatecholamine inodilator medications
such as milrinone to provide inotropic support as well as to
decrease resistance to ventricular ejection.
11-4
RESEARCH BRIEF
An increased circulating NT-pro-B-type natriuretic peptide plasma
level is an independent marker of greater systolic cardiac
dysfunction and a better predictor of fluid nonresponsiveness in
septic versus nonseptic critically ill patients.
Turner KL, Moore LJ, Todd SR, et al: Identification of cardiac dysfunction in sepsis with B-
type natriuretic peptide. J Am Coll Surg 213:139-146, 2011.
2127
adequate tissue perfusion (i.e., the initial MAP is very low or
MAP is persistently less than 60 mm Hg). If norepinephrine is
ineffective, phenylephrine, vasopressin, and high-dose
epinephrine may be used. The goal of therapy is to optimize
cardiac index by providing a balance among promoting venous
return, augmenting cardiac contractility, and creating the ideal
level of resistance to ventricular ejection.
2128
hours.
2129
• Control the source of the infection: Other methods for controlling
the source of infection should be weighed carefully for risks and
benefits. Identifying the source of infection is critical. Localizing
and draining an abscess, removing new pleural fluid collections,
and discontinuing infected indwelling catheters are keys to better
outcomes.
2130
Care plans for systemic inflammatory
response syndrome, sepsis, and multiorgan
dysfunction syndrome
Deficient fluid volume
related to active loss from vascular compartment secondary to increased
capillary permeability and shift of intravascular volume into interstitial
spaces and relative hypovolemia resulting from vasodilation.
Goals/Outcomes: Within 4 hours of initiation of therapy, the
patient is normovolemic as evidenced by peripheral pulses greater
than 2+ on a 0 to 4+ scale, stable body weight, urine output 0.5
mL/kg/h or greater, mean BP 60 mm Hg or greater (or within
patient’s normal range), sustained systolic BP 90 mm Hg or greater
(or within patient’s normal range), and absence of edema and
adventitious lung sounds. SVI is 30 to 40 mL/min /m3, SVV is less
than 15%, and ScVO2 or SVO2 is 60% to 80%.
Fluid Balance; Electrolyte and Acid-Base Balance
Hemodynamic regulation
2131
and/or PAWP. Current literature does not support the routine
use of pulmonary artery pressures in lieu of SVO2 and ScVO2 when
managing septic patients, given challenges associated with cellular
oxygenation, which are not reflected unless technology reflective of
oxygen delivery, demand, and consumption is used.
2132
mL/min/m3, SVV is less than 15%, and ScVO2 or SVO2 is 60% to 80%.
Cardiac Pump Effectiveness; Circulation Status
2133
900 to 1200 dynes/sec/cm–5. SVI is 30 to 40 mL/min/m3, SVV is less
than 15%, and ScVO2 or SVO2 is 60% to 80%.
Circulation Status
Circulatory precautions
2134
using a centrally placed central line or peripherally inserted line is a
good alternative. The goal range is CVP of 2 to 6 mm Hg (add 3 mm
Hg when positive pressure ventilation is used). Pulmonary artery
catheters are associated with high risk and are not used as often for
management of septic patients. When in place, SVR and CO can be
assessed to determine drug effects. Optimally, SVR will increase to
at least 900 dynes/sec/cm-5, CO will be 4 to 7 L/min, and CI will be
2.5 to 4 L/min/m2. Fluid boluses are administered rapidly to obtain
the goal.
Ventilation assistance
2135
patient’s condition. The presence of crackles may indicate fluid
accumulation.
2136
Respiratory monitoring
Ineffective thermoregulation
related to illness with concomitant endotoxin effect on hypothalamic
temperature-regulating center.
Goals/Outcomes: Within 24 hours of initiation of treatment, the
patient becomes normothermic.
Thermoregulation
Temperature regulation
2137
may be allowed in the septic patient, as increased temperature may
help control bacteremia. The following are weighed for each patient
to determine the extent of treatment that should be used to decrease
fever (e.g., acetaminophen administration):
2138
related to increased need secondary to increased metabolic rate.
Goals/Outcomes: Within 48 hours of initiation of treatment, the
patient has adequate nutrition as evidenced by stable weight, serum
albumin 3.5 g/dL, prealbumin 20 to 30 mg/dL, retinol-binding
protein 4 to 5 mg/dL, urine urea nitrogen 10 to 20 mg/dL, and a
state of nitrogen balance as determined by nitrogen studies.
Nutritional Status
Nutrition management
2139
parenteral nutrition solutions are not metabolized
well in the septic state. Branched-chain amino acid
solutions and short-to medium-chain fatty acid
solutions may be used (e.g., MCT Oil or FreAmine
HBC).
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2152
APPENDIX 1. Heart and breath sounds
ASSESSING HEART SOUNDS
A, Aortic; ICS, intercostal space; LSB, left sternal border; M, mitral; MI, myocardial
infarction; P, pulmonic; RSB, right sternal border; T, tricuspid.
2153
ICS, Intercostal space; LSB, left sternal border; MCL, midclavicular line; RSB, right
sternal border.
I, Inspiration; E, expiration.
2154
CNS, Central nervous system; DKA, diabetic ketoacidosis; IICP, increased
intracranial pressure; MODS, multiple organ dysfunction syndrome; SIRS, systemic
inflammatory response syndrome.
2155
APPENDIX 2. Glasgow coma scale
2156
APPENDIX 3. Cranial nerves: Assessment
and dysfunctions
2157
APPENDIX 4. Major deep tendon (muscle-
stretch) reflexes
Scale (0 to
Interpretation
4+)
4+ Very brisk, hyperactive, repetitive, rhythmic flexion and extension (clonus);
indicative of disease
3+ Brisker than average; may be normal for certain individuals or may indicate
disease.
2+ Average/normal
1+ Diminished response or low normal
0 No response
2158
APPENDIX 5. Major superficial
(cutaneous) reflexes
2159
APPENDIX 6. Inotropic and vasoactive
medication infusions
—, No effect; ↑or ↓ minimal effect; ↑↑or ↓↓, moderate effect; ↑↑↑ or ↓↓↓, major effect;
CO, cardiac output; HR, heart rate; IV, intravenous; PAOP, pulmonary artery
occlusive pressure; SVR, systemic vascular resistance.
2160
APPENDIX 7. Sample relaxation technique
3. Breathe through your nose. As you breathe out, say the word
“one” silently to yourself. Become aware of your breathing.
Continue this process for about 20 minutes.
2161
APPENDIX 8. Abbreviations used in this
manual
A—aortic valve
ACE—angiotensin-converting enzyme
ACh—acetylcholine
AChR—acetylcholine receptor
AD—autonomic dysreflexia
ADH—antidiuretic hormone
2162
AEG—atrial electrogram
AF—atrial fibrillation
ALP—alkaline phosphatase
ALT—alanine aminotransferase
AM—akinetic mutism
ASO—antistreptolysin O
2163
AST—aspartate aminotransferase
AT—antithrombin
AT1—receptor antagonist
atm—atmosphere (standard)
ATP—adenosine triphosphate
AV—atrioventricular; arteriovenous
AVM—arteriovenous malformation
BAL—bronchoalveolar lavage
BG—blood glucose
BIS—bispectral index
BP—blood pressure
BS—bowel sounds
2164
C—centigrade; Celsius
Ca2+—calcium
CD—Cotrel-Dubousset
CI—cardiac index
CIE—counterimmunoelectrophoresis
CJD—Creutzfeldt-Jakob disease
CK—creatine kinase
Cl—chloride
CM—cardiomyopathy
2165
CNS—central nervous system
CO2—carbon dioxide
CPK—creatine phosphokinase
CSF—cerebrospinal fluid
CT—computed tomography
cTnI—cardiac troponin I
CXR—chest radiograph
CyA—cyclosporine
2166
DAI—diffuse axonal injury
DCM—dilated cardiomyopathy
DI—diabetes insipidus
DKA—diabetic ketoacidosis
DM—diabetes mellitus
Do2—oxygen delivery
DOE—dyspnea on exertion
EACA—epsilon-(e)aminocaproic acid
EBV—Epstein-Barr virus
ECG—electrocardiogram
ECHO—electrocardiography
EEG—electroencephalogram
2167
EMI—electromagnetic interference
EPS—electrophysiologic studies
ET—endotracheal
ETOH—alcohol
ETT—endotracheal tube
F—Fahrenheit
Fr—French
GBS—Guillain-Barré syndrome
2168
GERD—gastroesophageal reflux disease
GI—gastrointestinal
GKI—glucose-potassium-insulin
G6PD—glucose-6-phosphate dehydrogenase
GU—genitourinary
H2O—water
HAT—heparin-associated thrombocytopenia
HCM—hypertrophic cardiomyopathy
HCO32—bicarbonate
Hct—hematocrit
HDL—high-density lipoprotein
Hgb—hemoglobin
HOB—head of bed
HPO4—phosphate
HR—heart rate
HRS—hepatorenal syndrome
2169
HUS—hemolytic-uremic syndrome
IAP—intraabdominal pressure
ICD—implantable cardioverter-defibrillator
ICH—intracerebral hematoma
ICP—intracranial pressure
ICS—intercostal space
IE—infective endocarditis
I/E—inspiration/expiration
IgG—immunoglobulin G
IM—intramuscular
2170
IPD—intermittent peritoneal dialysis; intracranial pressure
dynamics
IV—intravenous
IVP—intravenous pyelogram
JT—junctional tachycardia
K+—potassium
kcal—kilocalorie
kg—kilogram
L—liter; lumbar
LDL—low-density lipoprotein
LIS—locked-in-syndrome
2171
LMW—low molecular weight
LOC—level of consciousness
LOS—length of stay
LP—lumbar puncture
LR—lactated Ringer
LV—left ventricular
m—meter
M—mitral valve
MCT—medium-chain triglycerides
Mg2+—magnesium
MG—myasthenia gravis
mg—milligram
2172
MI—myocardial infarction
mOsm—milliosmole
MS—multiple sclerosis
MSO4—morphine sulfate
Na/Na+—sodium
NaCl—sodium chloride/saline
NG—nasogastric
nl—normal
NPO—nothing by mouth
2173
NSTEMI—non–ST-segment elevation myocardial infarction
NTG—nitroglycerin
OT—occupational therapist
OTC—over-the-counter
P—pulmonic valve
PA—pulmonary artery
PCA—patient-controlled analgesia
PE—pulmonary embolus
2174
PEG—percutaneous endoscopic gastrostomy
PIH—pregnancy-induced hypertension
PK—pyruvate kinase
PN—parenteral nutrition
PO—by mouth
PO4—phosphates
Pplat—plateau pressure
PRA—panel-reactive antibody
2175
PTCA—percutaneous transluminal coronary angioplasty
PTH—parathyroid hormone
PWI—perfusion-weighted imaging
RCM—restrictive cardiomyopathy
ROM—range of motion
RR—respiratory rate
SA—status asthmaticus
SAH—subarachnoid hemorrhage
2176
SAS—subarachnoid space
SOB—shortness of breath
SS—sensory stimulation
SV—stroke volume
2177
T—tricuspid valve
TCD—transcranial Doppler
TE—thrombotic emboli
TEA—tranexamic acid
TMP—transmembrane pressure
TOF—train-of-four
UF—ultrafiltration
2178
UTI—urinary tract infection
VC—vital capacity
VF—ventricular fibrillation
VLDL—very-low-density lipoprotein
VMA—vanillylmandelic acid
Vo2—oxygen consumption
VT—ventricular tachycardia
Vt—tidal volume
WPW—Wolff-Parkinson-White syndrome
2179
Index
Page numbers followed by “b” indicate boxes; “f, ” figures; “t, ”
tables.
A
A/C., See Assist-control ventilation (A/C, ACV).
Abdomen,
intrathoracic, 271–272
pelvic, 272
retroperitoneal, 272
trauma to, 271-284. See also Abdominal trauma.
true, 272
Abdominal compartment syndrome (ACS), 937–945
2180
diagnostic tests for, 941–942
with fluid volume deficit, care plan for, 943–944
history and risk factors for, 939
with ineffective tissue perfusion, care plan for, 944
with infection risk, care plan for, 945
observation in, 940
pathophysiology of, 937–939
prevention of, 942–943
risk factors for, 937
vital signs in, 940
Abdominal hypertension, 937–945
2181
risk factors for, 937
vital signs in, 940
Abdominal trauma, 271–284
2182
mechanisms of action of, 271–272
surgery for, 278–279
percussion in, 275–277
with risk for infection, care plan for, 281–282
subjective/objective symptoms in, 274
vital signs in, 273–274
ABG., See Arterial blood gas (ABG).
ABI., See Ankle-brachial index (ABI).
Abilify., See Aripiprazole (Abilify).
Accelerated junctional rhythm, 552f
Acetaminophen,
arterial blood gas and, 4-8. See also Arterial blood gas
(ABG).
pathophysiology of, 1–3
pH regulation and, 2–3
Acid-base regulation, principles of, 1–3
Acid producers and regulators, 184t
Acidosis, 1, 7
cellular, 1
compensation for, 2
2183
metabolic, 15-16. See also Metabolic acidosis.
renal, 2
respiratory, 1, 8-10. See also Respiratory acidosis.
ACS., See Abdominal compartment syndrome (ACS); See Coronary
syndrome, acute (ACS).
Acute limb ischemia (ALI), 590–592
2184
history and risk factors for, 759
with injury risk, care plan for, 763–764
observation and vital signs in, 759
pathophysiology of, 757–759
primary adrenal insufficiency and, 758
screening labwork in, 760–761
secondary adrenal insufficiency and, 758
Adrenal glands, endocrine assessment of, 759–761
Adrenal insufficiency, acute, 757-765. See also Adrenal crisis.
Adrenocortical insufficiency, noncritical, screening labwork for,
760–761
Advance directives, 243
Afterload, 82
Agitation, pathologic conditions contributing to, 173b
AI., See Aortic insufficiency (AI)/regurgitation (AR).
Airway,
2185
Alcohol overdose, 948–954
Alcoholism, acute pancreatitis and, 828–829
Aldosterone, 42
Aldosterone antagonists, for cardiomyopathy, 534
Alemtuzumab (Campath, MabCampth, Campath-1H), 1000
ALI., See Acute limb ischemia (ALI).
Alkalosis, 2, 7–8
2186
with deficient knowledge, care plan for, 902
diagnostic tests for, 896t
history and risk factors for, 895
with impaired gas exchange, care plan for, 899–900
with impaired skin integrity, care plan for, 901
with ineffective airway clearance, care plan for, 899
observation in, 895–896, 895t
palpation in, 896
pathophysiology of, 892–893, 894f
percussion in, 896
systemic effects of, 895t
vital signs in, 895
Anaphylaxis., See also Anaphylactic shock.
exercise-induced, 893
Anectine., See Succinylcholine (Anectine).
Anemia,
2187
collaborative management of, 906–907
diagnostic tests for, 904–906t
with impaired gas exchange, care plan for, 908
with impaired skin integrity risk, care plan for, 908–
910
pathophysiology of, 902
in trauma patient, management of, 277–278
Aneurysm,
2188
cutaneous, 201
diagnostic tests for, 201
gastrointestinal, 201
with impaired gas exchange, care plan for, 202–203
inhalation, 201
pathophysiology of, 201
transmission of, 201
Anthropometric data, in nutrition assessment, 125
Antiarrhythmic agents, for cardiomyopathy, 534
Antibiotics,
2189
for prosthetic heart valves, 621
for superior vena cava syndrome, 985
Anticonvulsants,
2190
Antiplatelet therapy, in stroke, 713
Antiproliferative agents, in posttransplant immunosuppression, 999
Antipsychotics,
2191
guidelines for, 515–516t
history and risk factors for, 513
with ineffective tissue profusion, care plan for, 517
observation in, 513
palpation in, 513–514
vital signs in, 513
Aortic insufficiency (AI)/regurgitation (AR), 613
2192
values for, 4–7
Arterial occlusive disease., See also Peripheral vascular disease
(PVD).
mean, 93
right, 94, 94f
Arteriogram, carotid, 598
Aseptic meningitis syndrome, 702
Aspiration, prevention of, in spinal cord injured patient, 300
Aspirin overdose, 949–950
Assist-control ventilation (A/C, ACV), 108–109
Assisted suicide, 244–245
Asthma exacerbation, acute, 393–404
2193
collaborative management of, 397–400
diagnostic tests for, 396–397t
history and risk factors for, 393–394
with impaired gas exchange, care plan for, 400–401
with ineffective airway clearance, care plan for, 401–
404
observation in, 394–395
palpation in, 395
pathophysiology of, 393
peak expiratory flow in, 394
percussion in, 395
pulmonary function test for, 398t
screening labwork in, 395–397
spirometry in, 394
stepped medication management for, 402–403t
vital signs in, 394
Asystole, 556f
Atherosclerosis, 589. See also Peripheral vascular disease (PVD).
2194
catheter ablation for, 568
Atrial flutter, 550f
Atrial hypertrophy, ECG changes found with, 503t
Atrial natriuretic peptide (ANP), 42
Atrial pacemaker, wandering, 549f
Atrial tachycardia, 550f
Atrioventricular (AV) block,
first-degree, 556f
second-degree,
type I (Wenckebach), 557f
type II, 557f
third-degree (complete), 558f
Atrioventricular junctional rhythm, 552f
Autoflow, 113
Automaticity, 539
2195
pathophysiology of, 224–225
signs and symptoms of, 225
transmission of, 225
Axonal injury, diffuse, in traumatic brain injury, 372
Azathioprine (Imuran), 999
Azotemia, 637–638
B
Bacterial meningitis, 701–702
Balloon counterpulsation therapy/IABP, for failing heart, 521–522
Barbiturate coma, in traumatic brain injury management, 378
Barbiturate overdose, 951, 951t
Bariatric patient,
abnormal, 27
violent, safety precautions in event of, 232b
Behavioral pain scales, 153
2196
Belatacept, 999
Benzodiazepines,
2197
assessment of, 199–201
botulism in, 203
containment of, 200
hemorrhagic fever viruses in, 204–205
key signs of, 199–200
labwork on, 201
monitoring for, 200
plague in, 206
reporting on, 200
smallpox in, 207
surveillance for, 199–201
tularemia in, 209
BioWatch, 199
“Bird flu”, 224-225. See also Avian influenza (“bird flu”).
BiVent (airway pressure-release ventilation), 112–113
Bladder program, in spinal cord injury, 301–302
Bleeding,
2198
blood products and, 909t
coagulation of., See Coagulation.
Blood count, complete,
afterload and, 82
in burn assessment, 314
classification and management of, for adults, 743t
contractility and, 82–83
control and management of, in pregnancy, 971
determinants of, 80–83
diastolic, hemodynamic measurements and, 93
heart rate and, 11–12
measurements of, in hypertensive emergencies, 580
preload and, 80–82
systolic, hemodynamic measurements and, 93
Blood transfusions,
2199
Blood urea nitrogen-to-creatinine ratio, in acute gastrointestinal
bleeding, 821
Blood vessel injuries, in traumatic brain injury, 370
Body fluid disturbances, 42–45, 46–47, 48. See also Fluid and
electrolyte disturbances.
Body image disturbance, indicators of, 237b
Bone marrow transplantation, for anemia, 907
Botulism, 203
Bowel irrigation, for drug overdose, 946
Bowel management, in spinal cord injury, 302
BP., See Blood pressure (BP).
Bradycardia, sinus, 547f
Brain,
2200
diagnostic tests for, 680–681t
history and risk factors for, 678–679
inspection in, 679
neurologic assessment for, 678–681
observation in, 679
organ donation after, 995
organ donation management after, 681–682t
palpation in, 679
pathophysiology of, 677–678
screening labwork in, 679–681
vital signs and, 679
Brain tissue oxygenation monitoring, in traumatic brain injury, 377
Breathing,
2201
with acute pain, care plan for, 330
airway/breathing in, 313
assessment of, 312–321
auscultation in, 316
cardiac output and perfusion in, 314
cardiovascular system in, 317
care plans for, 326–333
care priorities for, 322–326
classification of, 311
collaborative management of, 322–326
with deficient knowledge, care plan for, 333
description and characteristics of, 310–311, 312t
diagnostic tests for, 319–321t, 321–322
with disturbed body image, care plan for, 333
with disturbed sensory perception, care plan for, 332
with disuse syndrome risk, care plan for, 332–333
with fear, care plan for, 332
with fluid volume deficit, care plan for, 327–328
gastrointestinal system in, 317
heart rate and rhythm in, 314
history and risk factors for, 312–313
with hypothermia, care plan for, 329
2202
with impaired gas exchange, care plan for, 327
with impaired tissue integrity, care plan for, 330–331
with ineffective airway clearance, care plan for, 326–
327
with ineffective tissue perfusion, care plan for, 328–
329, 331
with infection risk, care plan for, 329–330
integumentary system in, 318
Lund-Browder chart for extent of, 314, 315f
with nutritional imbalance, care plan for, 331–332
palpation in, 315
pathophysiology of, 310–311
renal system in, 317–318
respiratory system in, 316–317, 316t
rule of nines for, 314, 314f
septic shock in, 318–321
systemic inflammatory response syndrome in, 318–
321
wound extent in, 314–315
wound infection in, 318
C
Calcineurin inhibitors, in posttransplant immunosuppression, 999
2203
Calcium,
2204
Carbonic acid, 2, 3
Cardiac cycle, 538–539
Cardiac death, organ donation after, 995
Cardiac dysrhythmias, 537–576
2205
hemodynamic measurements in, 544–546
history and risk factors for, 544
idioventricular rhythm, 556f
with ineffective health maintenance, care plan for, 573
junctional escape rhythm, 552f
junctional tachycardia, 553f
normal sinus rhythm, 546f
with sinus arrest, 548f
observation in, 544
palpation in, 546–561
pathophysiology of, 537–544
pharmacologic management of, 563, 564b
premature junctional complexes, 553f
with risk for activity intolerance, care plan for, 572
second-degree AV block,
type I (Wenckebach), 557f
type II, 557f
sinus bradycardia, 547f
sinus dysrhythmia, 548f
sinus tachycardia, 547f
with premature atrial complexes, 549f
third-degree (complete) AV block, 558f
2206
torsade de pointes, 554f
in traumatic brain injury, management of, 381
ventricular demand (VVI) pacemaker, 558f
with failure to capture, 559f
with failure to sense, 559f
ventricular fibrillation, 555f
ventricular tachycardia, 554f
vital signs in, 544
Cardiac index (CI), hemodynamic measurements and, 96
Cardiac injury, blunt, in thoracic trauma, 363
Cardiac output (CO),
afterload and, 82
in burn assessment, 314
contractility and, 82–83
decreased,
acute cardiac tamponade with, care plan for, 290–291
acute coronary syndrome with, care plan for, 492–494
acute GI bleeding with, care plan for, 826–827
acute infective endocarditis with, care plan for, 504–
505
acute pancreatitis with, care plan for, 842
acute spinal cord injury with, care plan for, 304
after intracranial surgery, care plan for, 700
2207
anaphylactic shock with, care plan for, 900–901
cardiogenic shock with, care plan for, 522–524, 525–
526
cardiomyopathy with, care plan for, 536–537
cardiovascular disorders with, care plan for, 463–464
continuous renal replacement therapies with, care
plan for, 667–668
Guillain-Barré syndrome with, care plan for, 725
heart failure with, care plan for, 477
from hyperkalemia, care plan for, 60
from hypocalcemia, care plan for, 63
from hypokalemia, care plan for, 57–58
from hypomagnesemia, care plan for, 76
hypotension with, from mechanical ventilation, 115
neutropenic sepsis with, care plan for, 983
patients undergoing percutaneous balloon
valvuloplasty with, care plan for, 626
pelvic fracture with, care plan for, 351
septic patients with, care plan for, 1020
superior vena cava syndrome with, care plan for, 986
thoracic trauma with, care plan for, 367–368
valve replacement with, care plan for, 623–624
determinants of, 80–83
2208
heart rate and, 11–12
hemodynamic measurements and, 96
preload and, 80–82
Cardiac pacing., See Pacemakers.
Cardiac Resynchronization Therapy (CRT), for cardiomyopathy,
535
Cardiac tamponade, acute, 284–291
2209
auscultation in, 519
care plans for, 522–526
care priorities for, 520
collaborative management of, 520–522
with decreased cardiac output, care plan for, 522–524,
525–526
diagnostic criteria for, 519
hemodynamic measurements in, 519
with imbalanced nutrition, care plan for, 526
with impaired gas exchange, care plan for, 523
with impaired tissue integrity, care plan for, 524–525
with ineffective breathing pattern, care plan for, 525
with ineffective protection, care plan for, 525
with ineffective tissue perfusion, care plan for, 523,
524
with infection risk, care plan for, 526
observation in, 519
pathophysiology of, 518
with risk for complications from immobility, care plan
for, 525
vital signs in, 519
Cardiography, impedance, in cardiac output measurement, 85–86
Cardiomyopathy, 526–537
2210
with activity intolerance, care plan for, 537
arrhythmogenic right ventricular, 528
assessment of, 529–532
care plans for, 536–537
care priorities for, 533–536
collaborative management of, 533–536
with decreased cardiac output, care plan for, 536–537
diagnostic tests for, 529–532t
dilated, 528
functional classifications of, 528–529
hypertrophic, 528
observation of, 529–532
pathophysiology of, 526–529
restrictive, 528
types and causes of, 527t
Cardiovascular disorders,
2211
aneurysm/dissection.
assessment of, 462–465
auscultation in, 463
cardiogenic shock as, 518-526. See also Cardiogenic
shock (CS).
dysrhythmias and conduction disturbances as, 537-
576. See also Cardiac dysrhythmias; See
also Conduction, disturbances of.
electrocardiogram in., See Electrocardiogram (ECG).
generalized,
with activity intolerance, care plan for, 463
care plans for, 463–465
with decreased cardiac output, care plan for, 463–464
with impaired gas exchange, care plan for, 464–465
heart failure as, 466-479. See also Heart failure.
hypertensive emergencies as, 576–589
labwork in, 463
observation in, 462
palpation in, 462
peripheral vascular disease as, 589-612. See
also Peripheral vascular disease (PVD).
valvular heart disease as, 612-627. See also Valvular
heart disease.
2212
Cardiovascular system, in burn assessment, 317
Cardioversion., See Defibrillation/cardioversion.
Carotid artery occlusive disease, 590, 591b
2213
Cerebellar function, in neurologic assessment, 673–674
Cerebral aneurysm, 684–694
2214
Cerebral perfusion pressure (CPP) maintenance, in traumatic brain
injury, 377
Cerebral salt-wasting syndrome, clinical presentation of syndrome
of inappropriate antidiuretic hormone versus, 686t
Cerebrospinal fluid findings, in meningitis, 707t
Cerebyx., See Fosphenytoin (Cerebyx).
Certican (everolimus), 1000
Cervical spine injury, care priorities for, 298–299
Chain donations, 995
Charcoal, activated, for drug overdose, 946
Chemotherapy, for superior vena cava syndrome, 986
Chest pain., See Angina.
Chest physiotherapy, for acute asthma exacerbation, 400
Cholesterol, diet low in, guidelines for, 571t
Cholinergic crisis, 713
2215
Coagulation,
2216
abdominal, 937-945. See also Abdominal compartment
syndrome (ACS).
with acute pain, care plan for, 340
assessment of, 335–338
with body image disturbance, care plan for, 341
care plans for, 339–341
care priorities for, 338–339
causes of, 334t
collaborative management of, 338–339
compartmental pressure monitoring in, 338
diagnostic tests for, 336t
history and risk factors for, 335–336
for ineffective tissue perfusion, care plan for, 339–340
with infection risk, care plan for, 340–341
observation and subjective symptoms of, 336
palpation in, 336–338
pathophysiology of, 334–335
vital signs in, 336
Compensation,
for acidosis, 2
for alkalosis, 2
Complete blood count, components of, commonly reviewed, 892t
Concussion, 372
2217
Conduction,
acute,
acute renal failure with, care plan for, 654–655
hypernatremia-related, care plan for, 54
hyponatremia-related, care plan for, 52–53
nondrug treatment strategies for, 174b
Confusion Assessment Method for ICU (CAM-ICU), 175b
Confusion Assessment Method for ICU (CAM-ICU) Worksheet, 31,
34b
Consciousness, 25
alterations in, 84
assessment of, 29–31
care plans for, 39–40
care priorities for, 33–38
in cerebral aneurysm/subarachnoid hemorrhage, 688
collaborative management of, 33–38
2218
coma as., See Coma.
delirium as., See Delirium.
diagnostic tests for, 31–33
history and risk factors for, 29–30
with impaired physical mobility, care plan for, 40
with impaired verbal communication, care plan for,
39
laboratory studies in, 33
neurologic evaluation in, 31
neuropsychological testing in, 33
observation in, 30–31
pathophysiology of, 25–29
screening labwork in, 31
vegetative state as., See also Vegetative state (VS).
vital signs in, 30
level of,
in meningitis, 704
in neurologic assessment, 673
Consent, informed, 241–242
2219
Contusion,
2220
observation in, 481
palpation in, 481
pathophysiology of, 479
with risk for deficient fluid volume, care plan for, 492
vital signs in, 480–481
Corticol replacement, in adrenal crisis, 762–763
Corticosteroids,
2221
CRE (carbapenem-resistant Enterobacteriaceae), 211
Creutzfeldt-Jakob disease (CJD), 220
2222
Daclizumab (Zenapax), 1000
Death, brain, 677-684. See also Brain death.
Decision-making capacity, 243
Decompressive laparotomy, for abdominal compartment
syndrome, 943
Deconditioning, 162-172. See also Immobility, prolonged.
Deep venous thrombosis (DVT) prevention,
2223
Dexmedetomidine (Precedex),
2224
pathophysiology of, 765–767, 765t
screening labwork for, 768–769
subtypes of, 766t
vital signs in, 767
Diabetes mellitus,
low-cholesterol, 571t
low saturated fat, 464
Dietary support., See Nutrition support.
Diffuse axonal injury, in traumatic brain injury, 372
Digoxin,
2225
Dilantin., See Phenytoin (Dilantin).
Dilated cardiomyopathy (DCM), 528
Dilaudid., See Hydromorphone (Dilaudid).
Diprivan., See Propofol (Diprivan).
Direct renin inhibitors, for hypertension, 586–588t
Direct thrombin inhibitors,
2226
laboratory values in, 932t
observation in, 927
palpation in, 927
pathophysiology of, 924–925
risk factors for, 927
vital signs in, 927
Diuretics,
2227
collaborative management of, 344–345
diagnostic tests for, 343–344t
freshwater versus saltwater, 342
history and risk factors for, 342
with hypothermia, care plan for, 346
with impaired gas exchange, care plan for, 345–346
incidence of, 341
with infection risk, care plan for, 346
observation in, 343
palpation in, 343
pathophysiology of, 341–342
vital signs in, 342–343
wet versus dry, 342
Drug-nutrient interactions, in enteral nutrition, 138
acetaminophen, 947
alcohols, 948–954
amphetamine, 959–960
aspirin, 949–950
assessment in, 946
barbiturate, 951, 951t
benzodiazepine, 952, 952t
beta-blocker, 953
2228
calcium channel blocker, 953–954
cannabinoids, 954–959
care plans for, 961–963
cathinone, 960
cocaine, 955–956
cyclic antidepressant, 956
digoxin, 957
with disturbed sensory/perceptual perception, care
plan for, 963
epidemiology of, 945
ethanol, 948
ethylene glycol, 949
with fluid volume deficit, care plan for, 962–963
gastric decontamination for, 946
hallucinogen, 957–958
with hyperthermia, care plan for, 962
with ineffective airway clearance, care plan for, 961–
962
management of, 961t
methanol, 949
opioid, 958
phencyclidine, 959
2229
salicylates, 949–950
stimulant, 959–964
treatment options for, 946, 947
unknown substance ingestion and, 945
with violence risk, care plan for, 963
Dual-Chamber Pacemaker, for cardiomyopathy, 535
Duodenal bleeding, 816
Durable power of attorney for health care (DPAHC), 243
DVT., See Deep venous thrombosis (DVT).
Dynamic response test, 87–88, 88f
Dysphagia screening, in neurologic assessment, 675–676
Dysreflexia, autonomic,
E
Ebola virus disease (EVD), 211–212
2230
signs and symptoms of, 212
transmission of, 212
treatment of, 213
ECF., See Enterocutaneous fistula (ECF).
Echocardiogram,
2231
atrial tachycardia, 550f
atrioventricular junctional rhythm, 552f
in cardiac dysrhythmias, 544–546
in cardiovascular assessment, 462
chest lead placement for,
left and right leads, 562f
posterior leads, 562f
components of, 543f
dual-chambered pacemaker, 559f
electrical basis of, 541f
first-degree AV block, 556f
idioventricular rhythm, 556f
junctional escape rhythm, 552f
junctional tachycardia, 553f
for myocardial infarction, 485t
normal sinus rhythm, 546f
with sinus arrest, 548f
P wave on, 538
PR interval on, 538
premature junctional complexes, 553f
Q waves in, 485
QRS complex on, 538–539
2232
QT interval on, 539
second-degree AV block,
type I (Wenckebach), 557f
type II, 557f
sinus bradycardia, 547f
sinus dysrhythmia, 548f
sinus tachycardia, 547f
with premature atrial complexes, 549f
ST segment on, 539
changes in, 484–485
T wave on, 539
changes in, 485
third-degree (complete) AV block, 558f
torsade de pointes, 554f
TP segment on, 539
U wave on, 539
ventricular demand (VVI) pacemaker, 558f
with failure to capture, 559f
with failure to sense, 559f
ventricular fibrillation, 555f
ventricular tachycardia, 554f
Electroencephalography (EEG), in status epilepticus, 728
2233
Electrolyte imbalances, in enteral and parenteral nutrition, 143
Electrolytes, 41
2234
history and risk factors, 229
Howden Spiritual Assessment Scale and, 229b
ineffective denial and, care plan for, 234
ineffective individual coping, care plan for, 234
need for, assessment of, 229
powerlessness and, care plan for, 235–236
sensory perception disturbance and, care plan for,
241–242
sleep pattern disturbance and, care plan for, 236
social isolation and, care plan for, 231
spiritual distress and, care plan for, 233–234
verbal communication impairment and, care plan for,
241
violence prevention and, care plan for, 239
Enalaprilat, for hypertensive emergency, 583
Encephalitis, WNV, 223
Encephalopathy, hepatic, 854
2235
care plans for, 504–507
care priorities for, 502–504
collaborative management of, 502–504
with decreased cardiac output, care plan for, 504–505
diagnostic tests for, 500–501t
electrocardiogram in, 499–501
hemodynamic measurements in, 499
history and risk factors for, 499
with impaired gas exchange, care plan for, 505
with ineffective tissue perfusion, care plan for, 506–
507
with infection risk, care plan for, 506
observation in, 499
pathophysiology of, 498
prophylaxis for, 618–619, 619t
screening labwork in, 499
vital signs in, 499
Endocrine assessment, 756–757
Endocrinologic disorders, 756–813
2236
myxedema coma as, 787-795. See also Myxedema
coma.
thyrotoxicosis crisis as, 803-810. See
also Thyrotoxicosis crisis.
Endoscopic therapies, in acute gastrointestinal bleeding, 824
Endovascular interventions,
2237
auscultation in, 847
with body image disturbance, care plan for, 853
care plans for, 850–853
care priorities for, 849–850
collaborative management of, 848–850
diagnostic tests for, 847–848t
drainage from, containing, recommendations for, 852b
with fluid volume deficit, care plan for, 850–851
gastrointestinal assessment of, 846–848
hemodynamic measurements in, 847–848
history and risk factors for, 846
with impaired oral mucous membrane, care plan for,
853
with impaired tissue integrity, care plan for, 852–853
with infection risk, care plan for, 851
nonradiographic evaluation of, 848
nursing assessment of, 852b
nutrition assessment in, 847
with nutritional imbalance, care plan for, 851–852
observation in, 847
palpation in, 847
pathophysiology of, 845–846
2238
screening labwork in, 847
vital sign assessment in, 846
Enterostomy tube placement, complications of, 135–136
Eosinophilic meningitis, 702
Epidural hematoma, 372
Epinephrine,
2239
decision-making capacity as, 243
with deficient knowledge, care plans for, 246
ethical reasoning as, 245
euthanasia as, 244–245
on grieving, care plan for, 246–247
informed consent as, 242
preventive ethics as, 245–246
quality of life as, 244
truth telling as, 244
withholding and withdrawing treatment as, 244
Ethical reasoning, 245
Ethics, preventive, 245–246
Ethylene glycol overdose, 949
Euthanasia, 244–245
Euthyroid sick syndrome, 803b
EVD., See Ebola virus disease (EVD).
Everolimus (Certican), 1000
Exercise-induced anaphylaxis, 893
Extracellular fluid (ECF) compartment, 41
Extracorporeal membrane oxygenation, for cardiogenic shock, 522
Extracorporeal membrane oxygenation (ECMO), for nonfatal
drowning patient, 345
Extracorporeal removal of toxins, for drug overdose, 947
Extracranial herniation, 370
2240
F
Faces Scales for pain, 153, 154f
Family, in patient safety, 254–255, 254b, 255–256t
Family coping,
2241
in anxiety management, 176
in pain management, 155, 156b
Fetus,
atrial, 551f
catheter ablation for, 568
ventricular, 555f
Fick oxygen consumption method, of cardiac output calculation, 85
Fio2., See Fraction of inspired oxygen (Fio2).
Fistula, enterocutaneous, 845-854. See also Enterocutaneous fistula
(ECF).
Flail chest, in thoracic trauma, 363
Flow rate (V), 106
Flu,
2242
hormonal influence on, 42
hypercalcemia as, 64–65
hyperkalemia as, 58–60
hypernatremia as, 53–54
hyperphosphatemia as, 71–72
hypervolemia as, 46–47, 48
hypocalcemia as, 61–62
hypokalemia as, 55–57
hypomagnesemia as, 73–75
hyponatremia as, 50–52
hypophosphatemia as, 67–68
hypovolemia as, 42–45
osmolality and, 41
Fluid and electrolyte management,
2243
Fluid resuscitation,
2244
G
Gallstones, acute pancreatitis and, 828–829
Gas exchange, impaired, in mechanical ventilation, care plans for,
118–120, 122
Gastric bleeding, 816
Gastric decompression, in major trauma management, 267
Gastric decontamination, for drug overdose, 946
Gastric intubation, in acute gastrointestinal bleeding, 824
Gastric lavage, for drug overdose, 946
Gastric ulcer prevention,
2245
blood loss in, 818, 823t
blood urea nitrogen-to-creatinine ratio in, 821
care plans for, 825–828
care priorities for, 823–825
collaborative management of, 822–825
colonoscopy in, 822
with decreased cardiac output, care plan for, 826–827
diagnostic tests for, 820–821t
with diarrhea, care plan for, 827
esophagogastroduodenoscopy in, 821–822
with fluid volume deficit, care plan for, 825–826
gastrointestinal assessment in, 818–822
hemodynamic measurements in, 819–821
history and risk factors for, 818
lower, 817
nutrition assessment in, 819
with nutritional imbalance, care plan for, 827–828
observation in, 819
palpation in, 819
pathophysiology of, 816–818
recurrent, risk factors to predict, 818b
screening labwork in, 819
2246
stigmata of, 822b
upper, 816
vital sign assessment in, 818
Gastrointestinal disorders, 814–890
2247
detailed health history in, 636
labwork in, 637
observation in, 636
palpation in, 636
vital sign assessment in, 636
Genitourinary tract trauma, 352–361
2248
Geodon., See Ziprasidon (Geodon).
Glasgow Coma Scale, 31
Global Health Security Agenda (2014), 200
Glucagon IV bolus, for anaphylactic shock, 899
Glucocorticoids,
2249
history and risk factors for, 720
with impaired gas exchange, care plan for, 722–723
with ineffective airway clearance, care plan for, 723
observation in, 721
pathophysiology of, 720
with sensory/perceptual alterations, care plan for,
725–726
vital signs in, 721
H
Hallucinogens, overdose of, 957–958
Haloperidol lactate (Haldol), in agitation/anxiety management, 179
H2CO3, 2, 3
Healing., See Wound closure/healing.
Health Insurance Portability and Accountability Act of 1996
(HIPAA), 243
Heart,
2250
disease of, 612-627. See also Valvular heart disease.
prosthetic,
anticoagulation for, 621
thrombosis of, management of, 621
replacement of., See Valve replacement, patients
undergoing.
semilunar, 612
Heart disease, valvular, 612-627. See also Valvular heart disease.
Heart failure (HF), 466–479
2251
left- versus right-sided, 466
pathophysiology of, 466
progression of, 466
systolic and diastolic dysfunction in, 466
Heart rate, 11–12
2252
bleeding disorders as, 913–935. See also specific disorder.
hemolytic crisis as, 902-913. See also Hemolytic crisis.
profound anemia as, 902-913. See also Anemia,
profound.
thrombotic disorders as, 913–935. See also specific
disorder.
Hematology assessment, 891–892
general, 891–892
history in, 891–892
observation in, 891
Hematoma,
epidural, 372
intracranial, 373–374
subdural, 373
Hemodilution, for cerebral aneurysm/subarachnoid hemorrhage,
691
Hemodynamic monitoring, 79–104
2253
in cardiac dysrhythmias, 544–546
cardiac index and, 96
cardiac output in, 85–86, 96
in cardiogenic shock, 519
for cardiomyopathy, 535
care plans for, 101–104
care priorities for, 100–101
central venous pressure in, 85, 93–94
in collaborative management, 99–101
for complications of acute pancreatitis, 834–837
considerations during setup, line insertion and
placement, 90–93
with deficient knowledge, care plan for, 101–104
diagnostic tests in, 92–93t, 93–98
in enterocutaneous fistula, 847–848
equipment setup for, 86–88
for ineffective peripheral tissue perfusion, care plan
for, 103
with ineffective protection, care plan for, 102–104
left atrial pressure and, 97
pathophysiology and, 80–83
in peritonitis, 881–882
2254
pulmonary artery occlusive pressure and, 96
pulmonary artery pressure monitoring, 91–93
pulmonary artery pressures in, 85, 95–96
right atrial pressure, 85, 94, 94f
right ventricular pressure and, 94–95
with risk for ineffective cardiac tissue perfusion, care
plan for, 102
systemic arterial pressure in, 83–85
tissue oxygenation in, 86
Hemodynamic stability maintenance, in spinal cord injured patient,
299–300
Hemodynamic values,
2255
with ineffective tissue perfusion, care plan for, 911–
912
pathophysiology of, 902
Hemorrhage,
2256
care priorities for, 917–918
collaborative management of, 917t
with fluid volume deficit, care plan for, 919
with ineffective protection, care plan for, 918–919
observation in, 915–916
palpation in, 916–917
pathophysiology of, 915, 916f
risk factors for, 915
in superior vena cava syndrome, monitoring for, 985–
986
vital signs in, 915
Heparin therapy,
acute, 854–855
ascites in, management of, 868
assessment of, 856–864
auscultation in, 857
2257
care for, in transplant center, benefits of, 856
care plans for, 871–879
care priorities for, 866–871
chronic, 855–856
collaborative management of, 864–871
with deficient knowledge, care plan for, 877–878
diagnostic tests for, 858–862t
with disturbed sensory perception, care plan for, 874–
875
enteral formulas for, 134
with fluid volume deficit, care plan for, 871–872
with fluid volume excess, care plan for, 872
history and risk factors for, 856
with imbalanced nutrition, care plan for, 873
with impaired gas exchange, care plan for, 873–874
with impaired tissue integrity, care plan for, 877
with ineffective protection, care plan for, 876
with ineffective tissue perfusion, care plan for, 876–
877
with infection risk, care plan for, 875–876
with injury risk, care plan for, 879
King’s College Hospital criteria for, 863b
2258
liver biopsy in, 858, 863–864, 863b
liver function tests in, 862–863
management guidelines for, 864–865t
observation in, 857
palpation in, 857
screening labwork in, 857–858
spontaneous bacterial peritonitis in, prevention of,
867–868
vital sign assessment in, 856–857
Hepatic transplantation., See Liver transplantation.
Hepatopulmonary syndrome (HPS), 855
Hepatorenal syndrome (HRS), 856
Herniation syndromes, in traumatic brain injury, 370, 371t
HF., See Heart failure (HF).
HFOV (high-frequency oscillatory ventilation), 113
HFVs (hemorrhagic fever viruses), 204–205
HHS., See Hyperglycemic hyperosmolar syndrome (HHS).
High-frequency oscillatory ventilation (HFOV), 113
High-reliability organizations (HROs), 255–257, 256t
Histamine H2-receptor antagonists,
2259
Howde Spiritual Assessment Scale (SAS), 229b
HROs (high-reliability organizations), 255–257, 256t
Hunt and Hess classification system, 687
Hydralazine,
2260
pathophysiology of, 64
12-lead ECG in, 64–65
vital signs in, 64
Hypercapnia, permissive, in mechanical ventilation, 111–113
Hyperglycemia, 773–787
2261
784–785
screening labwork for, 780–782
vital signs in, 779
Hyperglycemic hyperosmolar syndrome (HHS), 775–777
2262
collaborative management of, 78
with deficient knowledge, care plan for, 79
diagnostic tests for, 78t
history and risk factors for, 77
with ineffective protection, care plan for, 78–79
observation in, 77
palpation in, 77
pathophysiology of, 77
screening for, 78
vital signs in, 77
Hypernatremia, 53
2263
Hyperosmolar therapy,
2264
medications for, 586–588t
in pregnancy, 964-975. See also Pregnancy,
hypertension in.
pulmonary, 450-457. See also Pulmonary
hypertension.
secondary, causes of, 579b
in stroke, management of, 742–744
Hypertensive emergencies, 578
2265
vital signs in, 580
Hyperthyroidism, uncontrolled, 803-810. See also Thyrotoxicosis
crisis.
Hypertrophic cardiomyopathy (HCM), 528
Hyperventilation,
2266
palpation in, 47
pathophysiology of, 46
radiology in, 47
screening labwork in, 47
vital signs in, 47
Hypocalcemia, 61
2267
in acute kidney injury, 640–643t
assessment of, 55–56
auscultation in, 56
care plans for, 57–58
care priorities for, 56–57
collaborative management of, 56–57
complicating plasmapheresis, 716
with decreased cardiac output, care plan for, 57–58
diagnostic tests for, 56t
history and risk factors for, 55–56
with ineffective breathing pattern, care plan for, 58
palpation in, 56
pathophysiology of, 55
screening for, 56
vital signs in, 56
Hypomagnesemia, 73–74
2268
history and risk factors for, 74
with ineffective protection, care plan for, 75–76
with nutritional imbalance, care plan for, 76–77
observation in, 74
pathophysiology of, 73–74
percussion in, 74
screening for, 74–75
vital signs in, 74
Hyponatremia, 50
2269
for, 52
screening labwork for, 51
SIADH-induced, 796b
vital sign assessment in, 50
Hypophosphatemia, 67
2270
therapeutic, after intracranial surgery, 698
in trauma patient, management of, 267, 270, 277
Hypothyroidism,
2271
pathophysiology of, 42
screening labwork for, 43–44
in trauma patient, management of, 266, 277–278
vasodilation-induced, management of, in spinal cord
injured patient, 300
vital signs in, 43
Hypovolemic shock, 42, 43–44b
Hypoxemic hypoxia, in acute respiratory distress syndrome, 407
I
ICG., See Impedance cardiography (ICG).
ICH., See Intracranial hemorrhage (ICH).
ICP., See Intracranial pressure (ICP).
Idioventricular rhythm, 556f
Imagery, guided, in pain management, 159
Immobility, prolonged, 162–172
2272
for, 168–169
with injury risk, care plan for, 172
physiologic effects and complications of, 162b
with risk for disuse syndrome, care plan for, 166–167
with self-care deficit, care plan for, 167–168
Immune globulin, intravenous, in posttransplant
immunosuppression, 1001
Immune thrombocytopenic purpura (ITP), 920
2273
Immunologic disorders, 891-936. See
also Hematologic/immunologic disorders.
Immunosuppression therapy,
patients with,
care plans for, 573–574
with sexual dysfunction, care plan for, 576
third-generation,
electromagnetic interference and, 575t
patients with, care plans for, 575
Imuran (azathioprine), 999
Indirect calorimetry, in nutrition requirements estimation,
2274
127
Infection(s),
emerging, 209–226
avian influenza as, 224-225. See also Avian influenza
(“bird flu”).
Creutzfeldt-Jakob disease as, 220. See also Creutzfeldt-
Jakob disease (CJD).
Ebola virus disease as, 211-212. See also Ebola virus
disease (EVD).
Middle Eastern respiratory syndrome as, 217. See
also Middle Eastern respiratory syndrome (MERS-
CoV).
multidrug-resistant organisms as, 210–211
pandemic flu as, 224
prevention and control of, 209–210
severe acute respiratory syndrome as, 214. See
also Severe acute respiratory syndrome (SARS).
West Nile virus as, 222. See also West Nile virus.
opportunistic, in organ transplantation, prevention of,
1001
prevention/control of,
after intracranial surgery, 698
in genitourinary tract trauma, 358
in hepatic failure, 870
2275
in meningitis, 708–709
in nonfatal drowning patient, 345
in septic patients, 1017, 1019
in spinal cord injury, 302
in transplant patients, 1001–1002
wound, in burn assessment, 318
Infective endocarditis, acute, 498-507. See also Endocarditis, acute
infective.
Influenza, avian, 224-225. See also Avian influenza (“bird flu”).
Informed consent, 241–242
2276
in pancreatitis patient, 840
in peritonitis, 884
Intraaortic balloon pump (IABP), for cardiomyopathy, 535
Intracellular fluid compartment (ICF), 41
Intracranial hematoma, 373–374
Intracranial hemorrhage (ICH), 734, 735–736
2277
with decreased intracranial adaptive capacity, care
plan for, 698–699
with fluid volume deficit or excess, care plan for, 699–
700
functional assessment in, 696
history and risk factors for, 695
with impaired physical mobility, care plan for, 700
with ineffective breathing pattern, care plan for, 699
with infection risk, care plan for, 699
neurologic assessment for, 694–696
observation in, 695
with pain, care plan for, 700–701
screening labwork for, 696
vital signs in, 695
Intravascular foreign bodies,
2278
Ipratropium bromide, for acute asthma exacerbation, 399t
Iron, supplemental, for anemia, 907
IRV (inverse ratio ventilation), 112
Ischemic myositis, 334-341. See also Compartment syndrome.
Ischemic stroke, acute, 734-752. See also Stroke.
Isoproterenol, for failing heart, 520
Isotonic sodium chloride solution, in continuous renal replacement
therapies, 665
ITP., See Immune thrombocytopenic purpura (ITP).
J
Joint Commission National Patient Safety Goals (2014), 249–250,
250b
Jugular venous oxygen saturation monitoring, in traumatic brain
injury, 376
Junctional complexes, premature, 553f
Junctional escape rhythm, 552f
Junctional rhythm,
accelerated, 552f
atrioventricular, 463–465
Junctional tachycardia, 553f
“Just Culture”, 252–254, 254b
K
Ketamine, in pain management, 157
Ketorolac (Toradol), in pain management, 157
Kidney(s),
2279
AAST Organ Injury Severity Score for, 360t
failure of, 636-672. See also Renal failure, acute.
injury to, acute., See Renal failure, acute.
protection of, in compartment syndrome, 339
transplantation of, selection criteria for, 993–994
trauma to, 352-361. See also Genitourinary tract
trauma.
Kidney transplantation,
L
Labetalol, for hypertensive emergency, 583
Labor and delivery,
2280
Laparotomy, decompressive, for abdominal compartment
syndrome, 943
Large intestine, bleeding in, 817
Lateral cord syndrome, 296
Left atrial pressure (LAP), hemodynamic measurements and, 97
Left ventricular noncompaction (LVNC), 528–529
Levalbuterol, for acute asthma exacerbation, 399t
Levosimendan, for failing heart, 520, 521, 521t
Lifestyle alterations, for hypertensive patients, education on, 584
Liver,
2281
in agitation/anxiety management, 178
for status epilepticus, 729
Lower extremity peripheral artery occlusive disease, 590–592
M
MabCampth (alemtuzumab), 1000
Macronutrient requirements, 128
“Mad cow” disease, 220
Magnesium,
2282
excess of, 77. See also Hypermagnesemia.
foods high in, 75b
imbalances of, 73
Magnesium sulfate,
2283
for acute respiratory distress syndrome, 419
adjuncts to, 110–114
airway pressure-release, 112–113
alveolar mechanics in, 110–111
for anthrax, 202
with anxiety, care plans for, 122–123
anxiety from, 116
appropriate, diagnostic evaluation of, 113–114t
assist-control, 108–109
autoflow in, 113
barotrauma in, 114
bilevel, 113
breath limit, 110
for burns patient, 323
care plans for, 118–123
complications related to, 114–116
fluid imbalance from, 115
gastrointestinal complications of, 115
high-frequency oscillatory, 113
hypotension with decreased cardiac output from, 115
with impaired gas exchange, care plans for, 118–120,
122
2284
with ineffective airway clearance, care plan for, 120
with ineffective breathing pattern, 120–122
with ineffective protection, care plan for, 121–122
intracranial pressure increase from, 115
invasive, 107–108
inverse ratio, 112
low-tidal volume, 111–113
in meningitis, 708b
basic, 108–110
to promote alveolar recruitment, 112–113
negative pressure, 107
for nonfatal drowning patient, 344
noninvasive positive-pressure, 107
permissive hypercapnia, 111–113
for pneumothorax, 432
pneumothorax in, 114
positive end-expiratory pressure in, 110–111
positive-pressure, 107
pressure support, 109
protective lung ventilation, 111–113
restlessness in, management of, 120–122b
for septic patients, 1018
2285
for spinal cord injured patient, 300
spontaneous breathing trials during, 118
synchronized intermittent mandatory, 109
tension pneumothorax in, 114–115
in thoracic trauma, 366
for traumatic brain injury patient, 375–376
troubleshooting ventilator problems in, 118, 119b
ventilator-associated events from, 115–116, 415
volutrauma in, 114
weaning from, 116–118
failure of, 118
traditional methods of, 116–118
Medications., See also Pharmacotherapy.
2286
collaborative management of, 708–710
with decreased intracranial adaptive capacity, care
plan for, 710
diagnostic tests for, 706–707t, 706–707
eosinophilic, 702
functional assessment of, 705–706
fungal, 702
history and risk factors for, 703–704
with infection risk, care plan for, 711
neurologic assessment in, 703–706
noninfectious causes of, 702–703
observation in, 704–705
pathophysiology of, 701–703
positive signs of, 703t
screening labwork in, 706
tuberculous, 702
viral, 702
vital signs in, 704
WNV, 223
Mental status,
2287
Mental status testing, 31, 32b
Meperidine (Demerol),
acute, 18–21
in acute kidney injury, 640–643t
chronic, 21–22
lactic acidosis, 17–18
pathophysiology of, 15–16
Metabolic alkalosis, 22–23
acute, 23–24
chronic, 24–25
pathophysiology of, 22–23
Metabolic demand, reduction of, in traumatic brain injury
management, 377–379, 378t
Methanol overdose, 949
Methicillin-resistant Staphylococcus aureus (MRSA), 211
Methimazole, for thyrotoxicosis crisis, 806
Methylprednisolone, for acute asthma exacerbation, 399t
Methylprednisolone (Solu-Medrol), 999
MG., See Myasthenia gravis (MG).
MI., See Mitral insufficiency (MI)/regurgitation (MR).
2288
Midazolam (Versed),
2289
Mitral stenosis, 612–613
2290
with fluid volume deficit, care plan for, 1019–1020
history and risk factors for, 1013
with imbalanced nutrition, care plan for, 1023
with impaired gas exchange, care plan for, 1021–1022
with ineffective breathing pattern, care plan for, 1022
with ineffective tissue perfusion, care plan for, 1021
infection control in, 1017, 1019
observation and assessment findings in, 1015–1016
pathophysiology of, 1009–1010
with thermoregulation ineffectiveness, care plan for,
1022–1023
ventilation assistance in, 1018
Multivitamins, in TPN, 141
Murmurs, in valvular heart disease, 614
Muscle strength rating, 674t
Mutism, akinetic, 28
Myasthenia gravis (MG), 712
2291
with impaired gas exchange, care plan for, 715
with impaired swallowing, care plan for, 718
with ineffective airway clearance, care plan for, 717
with infection risk, care plan for, 717–718
observation in, 713
pathophysiology of, 712
symptom progression in, 713
with visual perception disturbance, care plan for, 718–
719
vital signs in, 713
Myasthenic crisis, 713
2292
Myositis, ischemic, 334-341. See also Compartment syndrome.
Myxedema coma, 787–795
2293
N
N-Acetylcysteine, in hepatic failure, 867
Naloxone, in pain management, 158b
Nasoenteric feeding tube placement, complications of, 135
Nasogastric intubation, for burn patient, 324
Negative pressure ventilation, 107
Neoral (cyclosporine), 999
Nephrotoxins, common, 640t
Neurodegenerative disorders, 711-727. See
also Neurodegenerative/neuromuscular disorders.
Neurodegenerative/neuromuscular disorders, 711–727
2294
in meningitis, 703–706
motor and cerebellar function in, 673–674
sensory assessment in, 674–675
vital signs in, 673
Neurologic complications, of traumatic brain injury, 370
Neurologic deficit, cerebral perfusion neuroanatomy related to, 736t
Neurologic disorders, 673–755
2295
Neurologic evaluation,
2296
collaborative management of, 982
with decreased cardiac output, care plan for, 983
diagnostic tests for, 981t
history and risk factors for, 980
with ineffective protection, care plan for, 982–983
observation of, 981
pathophysiology of, 980
stages of, 980
Nicardipine, for hypertensive emergency, 583
Nimbex., See Cisatracurium (Nimbex).
Nimodipine (Nimotop), for cerebral aneurysm/subarachnoid
hemorrhage, 689
Nimotop., See Nimodipine (Nimotop).
NiPPV (noninvasive positive-pressure ventilation), 107
Nipride., See Nitroprusside (Nipride).
Nitrates, for cardiomyopathy, 534
Nitrogen balance, in nutrition assessment, 127
Nitroglycerin, for hypertensive emergency, 583
Nitroprusside (Nipride), for hypertensive emergency, 583
NMBAs., See Neuromuscular blocking agents (NMBAs).
Noninvasive positive-pressure ventilation (NiPPV, NPPV), 107
2297
GI bleeding from, 817
in pain management, 157
Norepinephrine,
2298
Nutrition requirements,
2299
in enterocutaneous fistula, 849
with fluid volume imbalance risk, care plan for, 150
in hepatic failure, 866
with impaired tissue integrity, care plan for, 148
with ineffective protection from aspiration, care plan
for, 147
with infection risk, care plan for, 149
with injury risk, care plan for, 149
in meningitis, 708
modalities for, 131–143
with nutritional imbalance, care plan for, 144–150
for pancreatitis patient, 839
parenteral nutrition in, 138-143. See also Parenteral
(IV) nutrition.
for peritonitis, 884
for septic patients, 1019
in spinal cord injury, 301
transitional feeding in, 143
in trauma management, 268, 279
for traumatic brain injury patient, 380
Nystan, 1001
2300
Obese patient., See Bariatric patient.
Obstetrics., See also Pregnancy.
2301
after brain death, 995
management of, 681–682t
after cardiac death, 995
living, 995
paired an chain, 995
Organ transplant rejection,
2302
with impaired skin integrity, care plan for, 1007
infection control/prevention in, 1001–1002
with infection risk, care plan for, 1006–1007
with injury risk, care plan for, 1006
laboratory and diagnostic tests for, 996
labwork for, 989–990
pharmacotherapy for, 998–1001
priority/waiting lists/medical urgency determination for, 996–998
rejection in., See Organ transplant rejection.
selection criteria for, organ-specific, 991–994
2303
for acute respiratory distress syndrome, 410
for anemia, 906
for burn patient, 322–323
for heart failure, 472
for hemolytic crisis, 910
for nonfatal drowning patient, 344
for pneumothorax, 432
for trauma patient, 277
Oxyhemoglobin dissociation curve, 19f
P
P wave, 538
PA pressures., See Pulmonary artery (PA) pressures.
Pacemaker(s),
2304
transcutaneous, transthoracic cardiac, 570
ventricular demand (VVI), 558f
with failure to capture, 559f
with failure to sense, 559f
wandering atrial, 549f
PACs., See Premature atrial complexes (PACs).
Pain, 150–162
abdominal,
in acute gastrointestinal bleeding assessment, 819
in acute pancreatitis, 833
in enterocutaneous fistula, 846
in peritonitis, 880
assessment of, 151–159
definition of, 151
history and risk factors for, 152–153
management of, 153-158. See also Pain management.
pathophysiology of, 151
types of, 151
undertreated, in ICU, origins for, 152–153
Pain management, 153–158
2305
after intracranial surgery, 697
for burn patient, 326
care plans for, 159–162
cognitive-behavioral techniques in, 159
ethical obligation for, 153–154
in genitourinary tract trauma, 358
for hemolytic crisis, 910
in hepatic failure, 871
in hypertensive obstetric disorders, 971–972
with impaired skin integrity, care plan for, 162
with ineffective breathing pattern, care plan for, 161
nonpharmacologic interventions in, 158–159
in older adults, 157–158
for organ transplantation, 1001
in pancreatitis patient, 839
pharmacologic therapies in, 155–157
physical techniques in, 158–159
in pneumothorax, 433–434
in spinal cord injured patient, 301
in trauma patient, 267, 269–270, 279–280
with urinary retention, care plan for, 161
Paired organ donation, 995
2306
Pancreas, bleeding in, 817
Pancreas transplantation,
2307
with fluid volume excess, care plan for, 843–844
hemodynamic measurements for complications of,
834–837
history and risk factors for, 830
with imbalanced nutrition, care plan for, 844–845
with impaired gas exchange, care plan for, 843
with infection risk, care plan for, 844
nutrition assessment in, 834
observation in, 833
palpation in, 834
risk stratification for, 829, 830b, 831t, 833b
screening labwork in, 834
serum lipase and amylase in, 837
severity of,
Acute Physiology and Chronic Health Evaluation
(APACHE) II scoring system for, 831t
Bedside Index of, 833b
Ransons criteria for classifying, 830b
vital sign assessment in, 833
Pancuronium (Pavulon), in agitation/anxiety management, 180
Pandemic flu, 224
PAOP., See Pulmonary artery occlusive pressure (PAOP).
PAPs., See Pulmonary artery pressures (PAPs).
2308
Paracentesis, for ascites in hepatic failure, 868
Paradoxical pulse, measuring, 274b
Parenteral (IV) nutrition, 138-143. See also Nutrition support.
2309
resources on, 248t
sentinel events policy and, 248–249, 249b
standards for, 247–250
TeamSTEPPS and, 252, 253t
PAV., Proportional-assist ventilation (PAV).
Pavulon., See Pancuronium (Pavulon).
PCIs., See Percutaneous coronary interventions (PCIs).
PE., See Pulmonary embolism (PE).
Peak expiratory flow (PEF), in acute asthma exacerbation, 394
Peak inspiratory pressure (PIP), 105–106
PEEP., See Positive end-expiratory pressure (PEEP).
PEF., See Peak expiratory flow (PEF).
Pelvic fractures, 347–352
2310
observation in, 349
palpation in, 349–350
pathophysiology of, 347
vital signs in, 348
Pelvis, structures of, 347
Penicillin/silibinin, in hepatic failure, 867
Pentobarbital coma, for status epilepticus, 730
Peptic ulcer disease (PUD), bleeding in, 816
Peptic ulcers, in mechanical ventilation, 115
Percutaneous balloon valvuloplasty, 622
patients undergoing,
care plans for, 625–626
with decreased cardiac output, care plan for, 626
with deficient knowledge, care plan for, 625–626
with ineffective protection, care plan for, 626
Percutaneous coronary interventions (PCIs),
2311
assessment of, 507–510
auscultation in, 508
care plans for, 511–512
care priorities for, 510–511
causes of, 507b
collaborative management of, 510–511
diagnostic tests for, 509t
ECG changes in, 509–510, 509t
hemodynamic measurements in, 508
history and risk factors for, 508
with ineffective breathing pattern, care plan for, 511
observation of, 508
pathophysiology of, 507
screening labwork in, 508
vital sign assessment in, 508
Peripheral artery occlusive disease,
2312
Peripheral vascular disease (PVD), 589–612
2313
abdominal pain in, 880
with acute pain, care plan for, 887
auscultation in, 880
blood chemistry tests for, 882
care plans for, 884–888
care priorities for, 883–884
collaborative management of, 883–884
diagnostic procedures for, 882
with fluid volume deficits, care plan for, 884–885
gastrointestinal assessment in, 880–882
hematologic tests for, 882
hemodynamic measurements in, 881–882
history and risk factors for, 880
with hyperthermia, care plan for, 886
with impaired tissue integrity, care plan for, 886–887
with infection risk, care plan for, 885–886
nuclear medicine scans for, 882
nutrition assessment in, 880
with nutritional imbalance, care plan for, 887
observation in, 880
palpation in, 880
pathophysiology of, 879–880
2314
radiologic procedures for, 882
with risk for intraabdominal hypertension, care plan
for, 888
screening labwork for, 881
vital sign assessment in, 880
pH regulation, 2–3
Pharmacotherapy,
2315
Phencyclidine overdose, 959
Phentolamine, for hypertensive emergency, 583
Phenylephrine, in cardiogenic shock, 521t
Phenytoin (Dilantin), for status epilepticus, 729–730
Pheochromocytoma, assessment of, in hypertensive emergencies,
580
Phlebotomy, therapeutic, for hemolytic crisis, 911
Phosphorus,
aspiration, 415
assessment of, 416–421
auscultation in, 416
care plans for, 421–422
2316
care priorities for, 418–421
chest radiograph in, 416
collaborative management of, 418–421
community-acquired, 414
congestion relief in, 420–421
cough control in, 419–420
cough in, 416
diagnostic tests for, 417–418t
fever reduction in, 420
with fluid volume deficit, care plan for, 422
history and risk factors for, 416
hydration in, 420
infection control in, 419
with injury risk, care plan for, 421–422
nosocomial, 414–415
nutritional support in, 420
observation in, 416
pain relief in, 420
palpation in, 417
pathophysiology of, 414–415
percussion in, 418–421
screening labwork in, 417–418
2317
severity of, determining, 418–421
ventilator-associated, 415
Institute for Healthcare Improvement bundle for, 420–
421t
pressure ulcers and, 190b
ventilator-associated events and, 415
vital signs in, 416
Pneumothorax, 429–436
2318
palpation in, 431
pathophysiology of, 429–430
percussion in, 431
spontaneous, 429, 430, 431
tension, 429–430
in mechanical ventilation, 114–115
in thoracic trauma, 363
traumatic, 429, 430, 431
vital signs in, 430
Poisoning, carbon monoxide, signs and symptoms of, 316, 316t
Poliomyelitis, WNV, 223
Polyclonal antibodies, in posttransplant immunosuppression, 1000–
1001
Positioning, patient, in acute respiratory distress syndrome, 419
Positive end-expiratory pressure (PEEP), 110–111
2319
imbalances of, 55
supplemental, for cardiomyopathy, 534
PR interval, 538
Prealbumin, 126
Prebiotics, in enteral formulas, 133
Precedex., See Dexmedetomidine.
Prednisolone, for acute asthma exacerbation, 399t
Prednisone, for acute asthma exacerbation, 399t
Preeclampsia, 966
2320
monitoring for preterm labor in, 969–970
pathophysiology of, 966–967
patient positioning for, 969
risk factors for, 967
signs and symptoms of, 966–967
hyperthyroidism in, 803b
physiologic anatomical changes in, 964b
venous thromboembolism prophylaxis during, 447
Preload, 80–82
Premature atrial complexes (PACs), sinus tachycardia with, 549f
Premature junctional complexes, 553f
Pressure controlled ventilation, 110
Pressure measured during inspiratory hold (PPlateau, PPlat), 106
Pressure support ventilation (PSV), 109
Pressure ulcers, 183
2321
Propofol (Diprivan),
2322
auscultation in, 440
care plans for, 448–450
care priorities for, 443–447
collaborative management of, 443–448
fat embolism and, 438. See also Fat embolism.
history and risk factors for, 438–439
with ineffective cardiopulmonary tissue perfusion,
care plan for, 448–450
intravascular foreign bodies and, 438. See
also Intravascular foreign bodies.
observation/inspection in, 440
palpation in, 440
percussion in, 440
saddle, 440b
saddle, thrombolytic drugs for, 446
venous air embolism and, 438. See also Venous air
embolism.
venous thrombotic, diagnostic tests for, 441–442t
vital signs in, 439–440
Pulmonary hypertension, 450–457
2323
care priorities for, 454–455
classifications of, WHO, 451t, 452b
clinical presentation of, 452
collaborative management of, 454–455
with deficient knowledge, care plan for, 456–457
history and risk factors for, 452
with impaired gas exchange, care plan for, 456
observation/inspection in, 453
palpation in, 453
pathophysiology of, 450–452
with risk for ineffective cardiopulmonary tissue
perfusion, care plan for, 455–456
screening diagnostic tests for, 453–454t, 453–454
vital signs in, 452
Pulmonary transplantation., See Lung transplantation.
Pulmonary vascular resistance (PVR), in hemodynamic values
adjustment, 98
Pulmonic insufficiency/regurgitation, 614
Pulmonic stenosis, 614
Pulmonic valve, 612
Pulmonic valve disease, 614, 615–616t
2324
continuous, in respiratory assessment, 390
in heart failure management, 472, 472b
Pupillary changes,
Q
QRS complex, 538–539
QT interval, 539
Quality of life, as ethical consideration, 244
Quetiapine (Seroquel), in agitation/anxiety management, 179
Quick Confusion Scale, 31, 32b
R
Radioactive iodine, for thyrotoxicosis crisis, 806–807
Radiotherapy, for superior vena cava syndrome, 986
Rancho Los Amigos (RLA) Cognitive Functioning Scale, 31
RAP., See Right atrial pressure (RAP).
Rapamune (sirolimus), 1000
Rectal bleeding, 817
Red cell exchange therapy, for sickle cell crisis, 910
Reginol-binding protein, 126
Rehabilitation,
2325
for stroke, 748
for traumatic brain injury, 381–382
Rejection, organ., See Organ transplant rejection.
Relaxation, in pain management, 159
Renal acidosis, 2
Renal alkalosis, 2
Renal disease, enteral formulas for, 134
Renal failure, acute, 636–672
2326
with fluid volume excess, care plan for, 651–652
history and risk factors for, 644
with imbalanced nutrition, care plan for, 652–653
with impaired skin integrity, care plan for, 655–656
with infection risk, care plan for, 653–654
intrarenal presentation of, 638–639, 638t, 645
with knowledge deficit, care plan for, 654
observation in, 645
palpation in, 645
pathophysiology of, 637–643
postrenal presentation of, 638t, 639, 645
prerenal presentation of, 637–638, 638t, 644–645
renal replacement therapies for, 656-670. See
also Renal replacement therapies.
screening laboratory tests in, 646–647
special populations at risk for, 644
uremic manifestations in, 646
vital signs in, 645
Renal replacement therapies,
continuous, 656–670
continuous (CRRT), 656–670
anticoagulation in, 663–665
2327
approaches to, 663t
assessment for,
before, 658–660
during, 665–666
auscultation before, 659
care plans for, 667–670
care priorities for, 667
collaborative management of, 666–667
with decreased cardiac output, care plan for, 667–668
with deficient knowledge, care plan for, 669
determining types and modality of, 660–663
diagnostic tests used in association with, 659–660t
with fluid volume deficit risk, care plan for, 668
with fluid volume excess, care plan for, 668
heparin therapy in, 664
with impaired physical mobility, care plan for, 669
with injury risk, care plan for, 669–670
modes of,
comparison of, 657t
indications, advantages, and
disadvantages/complications of, 661t
pathophysiology of, 657–658
2328
principles applied to, 662
procedure for, 662–663
replacement fluid in, 665
troubleshooting major problems in, 661t
uremic manifestations before, 659
initiation of, 651
Renal system, in burn assessment, 317–318
Renal transplantation., See Kidney transplantation.
Renal trauma, 352-361. See also Genitourinary tract trauma.
Renin inhibitors, direct, for hypertension, 586–588t
Reperfusion injury, 592
Respiratory acidosis, 1, 8–10
acute, 14
care plan for, 15
chronic, 14–15
pathophysiology of, 13
2329
Respiratory disorders, 390–461
2330
assessment of, 406–408
auscultation in, 408
care plans for, 413–414
care priorities for, 410–413
collaborative management of, 410–413
diagnostic tests for, 409–410t, 409–410
history and risk factors for, 406–407, 407t
with impaired gas exchange, care plan for, 413
mild, hypoxemic hypoxia in, 407
moderate to severe, hypoxemic hypoxia in, 407
observation in, 407
palpation in, 408
pathophysiology of, 404–406
percussion in, 408
with risk for injury, care plan for, 413–414
screening labwork in, 408
staging of, based on Berlin definitions, 405t
vital signs in, 407
Respiratory failure, acute, 423–429
2331
care plans for, 428–429
care priorities for, 426–428
collaborative management of, 426–428
diagnostic tests for, 426t
disease processes leading to, 405b
history and risk factors for, 424
with impaired gas exchange, care plan for, 428–429
observation in, 425
palpation in, 425
pathophysiology of, 423–424
percussion in, 425
screening labwork in, 425–426
ventilation-perfusion matching in, 423–424
vital signs in, 424
Respiratory rate (RR), 104
Respiratory support, after intracranial surgery, 696
Respiratory system,
2332
Rheumatic fever, prophylaxis for, 618–619
Richmond Agitation-Sedation Scale (RASS), 31, 37
Right atrial pressure (RAP), 85
S
Saddle pulmonary embolism, 440b
Safe patient handling, 163–164
Safety,
2333
administering, 174–175
for anxiety reduction, care plan for, 181
care plans for, 181–182
care priorities for, 176–180
collaborative management of, 176–180
with deficient knowledge, care plan for, 182
delirium monitoring and, 28f
in hepatic failure, 866
with risk for injury, care plan for, 182
in traumatic brain injury management, 377, 378t
Seizures,
control of,
after intracranial surgery, 698
in meningitis, 708
in traumatic brain injury management, 377–378
prevention of, in eclampsia, 970–971
Selective T-cell costimulation blocker, in posttransplant
immunosuppression, 999
Sensory function, in neurologic assessment, 674–675
Sensory stimulation programs, for critically ill, 38f
Sepsis, 1008–1023
2334
in late stage, 1012t
with cardiac output decrease, care plan for, 1020
care plans for, 1019–1023
care priorities for, 1016–1019
collaborative management of, 1016–1019
definition of, 1008–1009b
diagnostic tests for, 1015–1016t
in enterocutaneous fistula, control of, 849
with fluid volume deficit, care plan for, 1019–1020
history and risk factors for, 1013
with imbalanced nutrition, care plan for, 1023
with impaired gas exchange, care plan for, 1021–1022
with ineffective breathing pattern, care plan for, 1022
with ineffective tissue perfusion, care plan for, 1021
infection control in, 1017, 1019
neutropenic, 980. See also Neutropenic sepsis.
observation and assessment findings in, 1014
pathophysiology of, 1008
severe,
assessment of, 1013–1016
diagnostic tests for, 1015–1016t
observation and assessment findings in, 1015–1016
2335
pathophysiology of, 1009
with thermoregulation ineffectiveness, care plan for,
1022–1023
ventilation assistance in, 1018
vital signs in, 1013
Septic shock, 1008–1023
2336
in spinal cord injury, 293
with thermoregulation ineffectiveness, care plan for,
1022–1023
ventilation assistance in, 1018
Seroquel., See Quetiapine (Seroquel).
Serum albumin, 126
Severe acute respiratory syndrome (SARS), 214
2337
spinal, 292, 293
Shunts,
2338
basilar, 372
compound depressed, 372
linear, 372
Sleep promotion, nonpharmacologic measures in, 237t
Small intestine, bleeding in, 817
Smallpox (variola), 207
Sodium,
acute, 291–310
assessment of, acute phase, 294–297
with autonomic dysreflexia, care plan for, 303–304
care plans for, 302–310
care priorities for, 298–302
collaborative management of, 298–302
with constipation, care plan for, 308–309
2339
cord syndromes in, 295–297
with decreased cardiac output, care plan for, 304
diagnostic tests for, 297–298
with disturbed visual perception, care plan for, 310
with gastric injury risk, care plan for, 305
with impaired gas exchange, care plan for, 302–303
with impaired skin integrity, care plan for, 306
with ineffective thermoregulation, care plan for, 308
with ineffective tissue perfusion, care plan for, 305–
306
with infection risk, care plan for, 309
levels of, 296t
neurogenic shock in, 292–293
with nutritional imbalance, care plan for, 306–307
pathophysiology of, 291–294
with reflex urinary incontinence, care plan for, 307–
308
with sexual dysfunction, care plan for, 310
spinal shock in, 292
with urinary retention, care plan for, 307–308
vertebral fractures in, 292
classifications and terminology of, 293t
2340
Spinal cord syndromes,
2341
electroencephalography in, 728
history and risk factors for, 727
with impaired gas exchange, care plan for, 731
with ineffective coping, care plan for, 733
with noncompliance with prescribed medication
regimen, care plan for, 732
observation in, 728
pathophysiology of, 727
refractory, treatment of, 730–731
screening labwork in, 728
seizure assessment in, 728
with trauma risk, care plan for, 732
vital signs in, 727
Stimulant overdose, 959–964
Stomach, bleeding in, 816
Stool softeners, for cerebral aneurysm/subarachnoid hemorrhage,
690
Streptokinase, 489, 490t
Stress ulceration, bleeding in, 816
Stroke,
2342
collaborative management of, 741–750
with decreased intracranial adaptive capacity, care
plan for, 750–751
diagnosis of, 739–740t
extension of, preventing, 744
hemorrhagic locations and syndromes in, 736t
history and risk factors for, 737
with impaired physical mobility, care plan for, 751
with impaired verbal communication, care plan for,
751–752
ischemic,
with carotid artery stenosis, symptoms of, 591b
hypertensive emergency and, management of, 582
neurologic evaluation in, 737–738
NIH scale for, 745–748t
pathophysiology of, 734–736
recurrent, preventing, 744
regulatory functions in, maintaining, 748, 749–750t
screening labwork in, 738–740
screening neurologic imaging in, 738
types of, 734f
vital sign assessment in, 737
2343
Stroke volume variability (SVV), in hemodynamic values
adjustment, 98
Stupor, 27
Subarachnoid hemorrhage, 373
2344
685
vital signs in, 687
Subdural hematoma, 373
Sublimaze., See Fentanyl (Sublimaze).
Succinylcholine (Anectine), in agitation/anxiety management, 179–
180
Sucralfate (Carafate),
2345
for acute infective endocarditis, 504
for acute ischemic stroke, 742
for acute myocardial infarction, 489
for aortic aneurysm/dissection, 516
for cardiac tamponade, 290
for cardiomyopathy, 535–536
for cerebral aneurysm/subarachnoid hemorrhage, 691
for compartment syndrome, 338–339
for critical limb ischemia, 603
for dysrhythmias, 570
for genitourinary tract trauma, 359, 359t
for intracranial hemorrhage, 742
for major trauma, 268
for pelvic fractures, 350–351
for peritonitis, 883–884
for recurrent pneumothorax, 434
for superior vena cava syndrome, 986
for traumatic brain injury, 374
for valvular heart disease, 621–622
SVCS., See Superior vena cava syndrome (SVCS).
SVR., See Systemic vascular resistance (SVR).
SVV., See Stroke volume variability (SVV).
2346
Synchronized intermittent mandatory ventilation (SIMV), 109
Syndrome of inappropriate antidiuretic hormone (SIADH), 795–803
2347
care plans for, 1019–1023
care priorities for, 1016–1019
collaborative management of, 1016–1019
diagnostic tests for, 1015–1016t
with fluid volume deficit, care plan for, 1019–1020
history and risk factors for, 1013
with imbalanced nutrition, care plan for, 1023
with impaired gas exchange, care plan for, 1021–1022
with ineffective breathing pattern, care plan for, 1022
with ineffective tissue perfusion, care plan for, 1021
infection control in, 1017, 1019
observation and assessment findings in, 1014
pathophysiology of, 1008–1009, 1010t
with thermoregulation ineffectiveness, care plan for,
1022–1023
ventilation assistance in, 1018
vital signs in, 1013
Systemic vascular resistance (SVR), in hemodynamic values
adjustment, 97–98
Systolic blood pressure, hemodynamic measurements and, 93
T
T wave, 539
Tachycardia,
2348
atrial, 550f
junctional, 553f
persistent, in abdominal trauma, 273b
sinus, 547f
ventricular, 554f
catheter ablation for, 567–568
Tacrolimus (Prograf), 999
Talc embolism, 438
TandemHeart, for cardiogenic shock, 522
TBI., See Traumatic brain injury (TBI).
TeamSTEPPS, 252, 253t
Teamwork, successful, components of, 251b
TEE., See Transesophageal echocardiogram (TEE).
Temperature regulation,
2349
in thoracic trauma, 363
Terbutaline, for acute asthma exacerbation, 399t
Tetanus prophylaxis,
2350
therapies, 664
Thrombocytopenia,
2351
Thyrotoxicosis crisis, 803–810
2352
low, in mechanical ventilation, 111–113
Time limited ventilation, 110
Tiotropium, in asthma control, 395b
TIPS., See Transjugular intrahepatic portosystemic shunt (TIPS).
TLS (tumor lysis syndrome), 987
Toradol., See Ketorolac (Toradol).
Torsade de pointes, 554f
Total body surface area (TBSA) burn calculation, 314–315, 314f, 315f
Total parenteral nutrition (TPN), components of, 140–141
Touch, types of, 230b
Toxins, extracorporeal removal of, for drug overdose, 947
TP segment, 539
TPN (total parenteral nutrition), components of, 140–141
Trace minerals,
2353
symptoms of, 591b
Transjugular intrahepatic portosystemic shunt (TIPS), for ascites in
hepatic failure, 868, 869b
Transplantation, organ, 989-1007. See also Organ transplantation.
Transtentorial herniation, 370
Transthoracic echocardiogram (TTE), in cardiac output calculation,
86
Trauma, 260–391
2354
exposure in, 262
head-to-toe assessment in, 263
history in, 262
with hypothermia, care plan for, 270
with impaired gas exchange, care plan for, 269
with ineffective tissue perfusion, care plan for, 268
laboratory work in, 263–265
pathophysiology of, 260–261
with posttrauma syndrome, care plan for, 270–271
psychological response to, 261
vital signs in, 262
thoracic, 361-368. See also Thoracic trauma.
Traumatic brain injury (TBI), 368–385
2355
with impaired gas exchange, care plan for, 382
with impaired tissue integrity, care plan for, 385
with ineffective thermoregulation, care plan for, 383–
384
with infection risk, care plan for, 382–383
management of, 381t
neurological complications of, 370
pathophysiology of, 368–370
primary, 368–369
secondary, 369
skull fractures associated with, 369
vascular injuries in, 370
Tricuspid regurgitation/insufficiency, 613
Tricuspid stenosis, 613
Tricuspid valve, 612
Tricuspid valve disease, 613, 616t
2356
U
U wave, 539
Ulcers,
V
Vaccination,
2357
Valcyte (valganciclovir), 1001
Valganciclovir (Valcyte), 1001
Valium., See Diazepam (Valium).
Valve replacement, patients undergoing,
2358
surgical interventions for, 621–622
tricuspid valve disease as, 613, 616t
valve replacement for, care plans for, 622-625. See
also Valve replacement, patients undergoing.
Valvuloplasty, 622
Vancomycin-resistant Enterococcus (VRE), 211
Variola (smallpox), 207
Vascular grafts, intraabdominal, bleeding from, 817
Vascular injuries, in traumatic brain injury, 370
Vasculopathy, in organ rejection, 1002
Vasoconstrictors, for acute GI bleeding, 824
Vasodilators, for cardiomyopathy, 534
Vasopressin, 42
2359
Vena cava filter, in heparin-induced thrombocytopenia, 918
Venous air embolism,
2360
fraction of inspired oxygen in, 105
inspiratory flow begins in, 106
inspiratory flow end in, 106–107
mean airway pressure in, 106
mechanical, 104-123. See also Mechanical ventilation.
minute ventilation in, 105
peak inspiratory pressure in, 105–106
respiratory rate in, 104
spontaneous, factors affecting, 104b
support of, in major trauma, 265–266
terminology for, 104–107
tidal volume in, 105
Ventilation assistance., See also Mechanical ventilation.
Ventilator-acquired pneumonia, pressure ulcers and, 190b
Ventilator-associated events (VAEs), 115–116, 415
Ventricular demand (VVI) pacemaker, 558f
2361
Vertebral artery injury (VAI), 297b
Vertebral fractures, 292
Vigilance A Test, 31, 33b
Violence, risk for, care plan for, 239
Violent behavior, safety precautions in event of, 232b
Viral meningitis, 702
Virus(es),
2362
in acute renal failure, 645
in acute respiratory failure, 425
in adrenal crisis, 759
in anaphylactic shock, 895
in aortic aneurysm/dissection, 513
in brain death, 679
in cardiac dysrhythmias, 544
in cardiogenic shock, 519
in cerebral aneurysm, 687
in continuous renal replacement therapies,
before, 658
during, 665
in diabetes insipidus, 767
in disseminated intravascular coagulation, 927
in drowning, 342–343
in enterocutaneous fistula, 846
in fat embolism, 440
in gastrointestinal assessment, 814
in Guillain-Barré syndrome, 721
in heparin-induced thrombocytopenia, 915
in hepatic failure, 856–857
in hypercalcemia, 64
2363
in hyperglycemia, 779
in hypermagnesemia, 77
in hypernatremia, 53–54
in hyperphosphatemia, 71
in hypertensive emergencies, 580
in hypervolemia, 47
in hypocalcemia, 61
in hypomagnesemia, 74
in hyponatremia, 50
in hypophosphatemia, 68
in hypovolemia, 43
in immune thrombocytopenic purpura, 920
in intracranial surgery, 695
in major trauma, 262
in meningitis, 673
in mental status/consciousness assessment, 30
in myasthenia gravis, 713
in myxedema coma, 789, 789b
in neurologic assessment, 673
in pain assessment, 153
in pelvic fractures, 348
in peripheral vascular disease, 594
2364
in peritonitis, 880
in pneumothorax, 430
in pulmonary embolism, 439–440
in pulmonary hypertension, 452
in respiratory disorders, assessment of, 390
in status epilepticus, 727
in stroke, assessment of, 737
in subarachnoid hemorrhage, 687
in syndrome of inappropriate antidiuretic hormone,
798
in thyrotoxicosis crisis, 804
Vitamin B12, for anemia, 907
Vitamins,
2365
W
Wandering atrial pacemaker, 549f
Water, body, compartments of, primary constituents of, 41
Weaning, from mechanical ventilation, 116–118
Weight, nutrition requirement calculations based on, 127
West Nile virus (WNV), 222
2366
assessment of, 183–184
care plans for, 185
care priorities for, 184–185
collaborative management of, 184–185
diagnostic tests during, 184t
with impaired tissue integrity, care plan for, 185
by secondary intention, 185
assessment of, 185–186
2367
care plans for, 187
care priorities for, 186–187
collaborative management of, 186–187
diagnostic tests for, 186t
with impaired tissue integrity, care plan for, 187
Wounds, burn,
Z
Zemuron (rocuronium), in agitation/anxiety management, 180
Zenapax (daclizumab), 1000
Zinc, in hepatic failure, 867
Ziprasidone (Geodon), in agitation/anxiety management, 179
Zyprexa., See Olanzapine (Zyprexa).
2368
Ibc
2369
Table of Contents
Title page 2
Table of Contents 4
Copyright 10
Contributors 13
Preface 23
1. General concepts in caring for the critically ill 27
Acid-base imbalances 27
Altered mental status 83
Fluid and electrolyte disturbances 113
Hemodynamic monitoring 199
Mechanical ventilation 246
Nutrition support 289
Pain 341
Prolonged immobility 367
Sedation and neuromuscular blockade 400
Wound and skin care 425
Selected references 442
2. Managing the critical care environment 462
Bioterrorism 462
Emerging infections 486
Emotional and spiritual support of the patient and significant
517
others
Ethical considerations in critical care 554
Patient safety 564
Selected references 584
3. Trauma 592
Major trauma 592
Abdominal trauma 615
Acute cardiac tamponade 642
Acute spinal cord injury 655
Burns 700
2370
Compartment syndrome/ischemic myositis 748
Drowning 763
Pelvic fractures 775
Renal and lower urinary tract trauma 786
Thoracic trauma 798
Traumatic brain injury 810
Selected references 846
4. Respiratory disorders 858
Respiratory assessment: General 858
Acute asthma exacerbation 865
Acute respiratory distress syndrome 885
Acute pneumonia 905
Acute respiratory failure 922
Pneumothorax 936
Pulmonary embolism 953
Pulmonary hypertension 983
Selected references 998
5. Cardiac and vascular disorders 1009
Cardiovascular assessment: General 1009
Heart failure 1020
Acute coronary syndrome 1044
Acute infective endocarditis 1082
Acute pericarditis 1100
Aortic aneurysm/dissection 1111
Cardiogenic shock 1121
Cardiomyopathy 1142
Dysrhythmias and conduction disturbances 1158
Hypertensive emergencies 1222
Peripheral vascular disease 1246
Valvular heart disease 1289
Selected references 1319
6. Kidney injury 1341
Genitourinary assessment: General 1341
2371
Acute kidney injury 1344
Continuous renal replacement therapies 1380
Selected references 1408
7. Neurologic disorders 1414
General neurologic assessment 1414
Brain death 1421
Cerebral aneurysm and subarachnoid hemorrhage 1436
Care of the patient after intracranial surgery 1458
Meningitis 1473
Neurodegenerative and neuromuscular disorders 1493
Status epilepticus 1530
Stroke: Acute ischemic and hemorrhagic 1547
Selected references 1577
8. Endocrinologic disorders 1587
Endocrine assessment 1587
Acute adrenal insufficiency (adrenal crisis) 1590
Diabetes insipidus 1605
Hyperglycemia 1622
Myxedema coma 1651
Syndrome of inappropriate antidiuretic hormone 1668
Thyrotoxicosis crisis (thyroid storm) 1683
Selected references 1698
9. Gastrointestinal disorders 1707
Gastrointestinal assessment: General 1707
Acute gastrointestinal bleeding 1711
Acute pancreatitis 1735
Enterocutaneous fistula 1767
Hepatic failure 1785
Peritonitis 1840
Selected references 1860
10. Hematologic/immunologic disorders 1866
General hematology assessment 1866
Anaphylactic shock 1869
2372
Profound anemia and hemolytic crisis 1889
Bleeding and thrombotic disorders 1910
Selected references 1954
11. Complex special situations 1957
Abdominal hypertension and abdominal compartment syndrome 1957
Drug overdose 1976
Stimulants 2008
High-risk obstetrics: Hypertension in pregnancy 2017
Oncologic emergencies 2043
Organ transplantation 2067
Sepsis, septic shock, systemic inflammatory response syndrome,
2109
and multiple organ dysfunction syndrome
Selected references 2140
Heart and breath sounds 2153
Glasgow coma scale 2156
Cranial nerves Assessment and dysfunctions 2157
Major deep tendon muscle stretch reflexes 2158
Major superficial cutaneous reflexes 2159
Inotropic and vasoactive medication infusions 2160
Sample relaxation technique 2161
Abbreviations used in this manual 2162
Index 2180
Ibc 2369
2373