CCRN REVIEW PART 2

Education is a progressive discovery of our own ignorance

- Will Durant -

Sherry L. Knowles, RN, CCRN, CRNI

CCRN REVIEW PART 2

TOPICS
Renal Alterations Acute Renal Failure Electrolytes IV Fluid Therapy AVMs & Cerebral Aneurysms Intracranial Hemorrhage Stroke

Metabolic Alterations DKA & HNNK

DI & SIADH
DIC Shock States Sepsis

Neurological Alterations

CCRN REVIEW PART 2

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.

OBJECTIVES
List the main functions of the kidney. List the common diagnostic tests associated with renal function. List the complications associated with acute renal failure. Describe the common treatments of acute renal failure. List the major signs & symptoms associated with electrolyte disturbances of sodium, potassium magnesium and calcium and phosphorus. Define serum osmolality. List the intracellular & extracellular fluid compartments of the body. Describe the effects of hypotonic, isotonic and hypertonic IV fluids. Describe the different treatments for intravascular depletion verses cellular dehydration. Identify the risk factors and signs & symptoms of brain aneurysms and AVMs. Explain the current treatments available for brain aneurysms and AVMs. Describe the different types of intracranial hemorrhage and their associated signs & symptoms.

CCRN REVIEW PART 2

13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26.

OBJECTIVES
List the potential complications of associated with intracranial hemorrhages, brain aneurysms and AVM repairs. List the types of CVAs, their risk factors and related pathophysiology. Identify the recommended treatments for CVAs. Differentiate between the signs and symptoms of DKA and HHNK. Describe the treatment of DKA and HHNK. Differentiate between the signs and symptoms of DI and SIADH. Describe the treatment of DI and SIADH. List the signs & symptoms of Disseminated Intravascular Coagulation. Explain the treatments for disseminated intravascular coagulation. Understand the different stages of shock. Differentiate between different types of shock. Identify the different treatments used for the different types of shock. Describe the stages of the sepsis syndrome. Explain the treatment of septic shock.

Renal Alterations

Acute Renal Failure Electrolytes IV Fluid Therapy

Acute Renal Failure

WHAT DO THE KIDNEYS DO?

Filter blood

Regulates electrolytes

Regulate blood pressure

Renin-angiotensin system (RAS)

Maintain acid/base balance

Removes wastes, detoxifies blood

Acute Renal Failure

WHAT ELSE DO THE KIDNEYS DO?

Stimulate RBC production

Make erythopoietin

Make corticosteroids

Regulate kidney function

Increase calcium absorption

Convert Vitamin D to its active form Calcitriol

The Kidney

The Nephron

The Nephron

Glomerulus
Network of capillaries

Bowmans capsule
Membrane that surrounds the glomerulus

Renal Tubules
Travel from cortex to medulla and back to cortex

Collecting duct
Within the medulla

The Kidney

The Renal Cortex Contains

Bowman's Capsules Glomerulus Proximal Tubules Distal Convoluted Tubules

The Renal Medulla Contains

The Pyramids

Loop of Henle Collecting Duct Blood Vessels

The Juxtaglomerular Apparatus

Lies within Cortex Controls the activity of the nephron Plays major role in the renin-angiontensionaldosterone system

Urine Formation

Acute Renal Failure

DEFINITIONS
Sudden interruption of kidney function resulting from obstruction, reduced circulation, or disease of the renal tissue Rapid deterioration of renal function

increase of creatinine of >0.5 mg/dl in <72hrs azotemia (accumulation of nitrogenous wastes) elevated BUN and Creatinine levels decreased urine output (usually but not always)

Acute Renal Failure

TERMINOLOGY
Anuria: No UOP (or <100mL/24hrs) Oliguria: UOP<400-500 mL/24hrs

Azotemia: (Increased BUN, Cr, Urea)

May be prerenal, renal, postrenal Does not require any clinical findings

Chronic Renal Insufficiency

Deterioration over months-years

GFR 10-20 mL/min, or 20-50% of normal

ESRD: GFR <5% of mL/min

Acute Renal Failure

PERSONS AT RISK
Major surgery Major trauma Receiving nephrotoxic medications Hypovolemia > 40 minutes

Elderly

Acute Renal Failure

SIGNS & SYMPTOMS

Azotemia Hyperkalemia Electrolyte Disturbances K+ Na+ phosphate calcium Oliguria - anuria HTN Hypovolemia Pulmonary edema Ascites Metabolic acidosis Asterixis Encephalopathy

Cr BUN Metabolic acidosis Nausea/Vomiting

Acute Renal Failure

COMPLICATIONS
Results in retention of toxins, fluids, and end products of metabolism May be reversible with medical treatment

Acute Renal Failure

DIAGNOSTIC TESTS
H&P BUN, creatinine, sodium, potassium, pH, bicarb, Hgb and Hct Urine studies US of kidneys 24 hour urine for protein and creatinine Urine eosinophils

Acute Renal Failure

OTHER DIAGNOSTIC TESTS

Albumin, glucose, prealbumin KUB

Abd and Renal CT/MRI

Retrograde pyloegram Renal biopsy

Post-void residual or catheterization

Acute Renal Failure

PHASES
Onset

1-3 days with BUN and creatinine and possible decreased UOP UOP < 400/day, BUN, Cr, P04, K, may last up to 14 days UOP to as much as 4000 mL/day but without waste products, may begin to see improvement at end of this stage Things go back to normal or may remain insufficient and become chronic

Oliguric

Diuretic

Recovery

Acute Renal Failure

CAUSES
Pre-renal (hypoperfusion)

Renal (intrinsic)
Post-renal (obstructive)

Acute Renal Failure

SPECIFIC CAUSES
Prerenal

Hypovolemia, shock, blood loss, embolism, pooling of fluid due to ascites or burns, cardiovascular disorders, sepsis ATN, nephrotoxic agents, infections, ischemia acute tubular necrosis, acute nephritis, polycystic kidney disease Stones, blood clots, BPH, urethral edema from invasive procedures, renal calculi

Intrarenal

Postrenal

Pre-Renal or Intra-Renal?
Pre-renal
BUN/Cr Urine Na (mEq/L) Urine Specific Gravity BUN/CR Ratio

Intra-renal < 20 > 40 Low < 10-15:1

> 20 < 20 High > 20:1

Acute Renal Failure

TREATMENT
Make/consider the diagnosis Treat life threatening conditions Identify the cause if possible

Hypovolemia Toxic agents (drugs, myoglobin) Obstruction Hydrate Remove drug Relieve obstruction

Treat reversible elements

Acute Renal Failure

NURSING CARE
Fluid and dietary restrictions

Protein, potassium & phosphate restriction

Maintain electrolytes
D/C or reduce causative agent Adjust medication doses May need dialysis to jump start renal function May need to stimulate production of urine with IV fluids, Dopamine, diuretics, etc.

Acute Renal Failure

DIALYSIS
Hemodialysis Peritoneal Dialysis Continuous Renal Replacement Therapy (CRRT)

Chronic Renal Failure

TREATMENT
Strict I&O Daily weights Watch for hyper/hypoglycemia Maintain nutrition Mouth care Monitor skin

Watch for heart failure

Monitor lab results Watch for hyperkalemia
S&S

S & S of Hyperkalemia: Malaise, anorexia, parenthesia, muscle weakness, EKG changes

CCRN REVIEW PART 2

BREAK

K+

HCO3Ca++ Mg+

PO4

Cu

Na+

Electrolyte Disturbances
ClNH3

NaCl

Potassium (K+)

Dominant intracellular electrolyte Primary buffer in the cell

K+
Normal serum K+ level: 3.5-5.5 mEq/L

Potassium (K+)

INVOLVED IN
Muscle contraction Nerve impulses Cell membrane function Attracting water into the ICF Imbalances interfere with neuromuscular function and may cause cardiac rhythm disturbances

Hyperkalemia

SIGNS & SYMPTOMS

Weakness, malaise, lethargy Anorexia Muscle cramps Paresthesias Dysrhythmias

Hyperkalemia

K > 5.5 -6
Tall, peaked Ts Wide QRS

Prolong PR
Diminished P Prolonged QT

QRS-T wave merge = sine wave

Sine (Off) Wave

Hyperkalemia

CAUSES
Chronic or acute renal failure Burns Crush injuries Excessive use of Potassium salts

Hyperkalemia

TREATMENT
Calcium Gluconate (carbonate) Calcium Chloride Sodium Bicarbonate Insulin/glucose Kayexalate Lasix Albuterol Hemodialysis

Hypokalemia

SIGNS & SYMPTOMS

Malaise Skeletal muscle weakness Decreased reflexes Hypotension Vomiting Excessive thirst Cardiac arrhythmias and cardiac arrest Flattened T wave U wave

Hypokalemia

CAUSES
Reduced dietary intake Poor absorption by the body Vomiting and/or diarrhea Renal disease Medications (typically diuretics)

Hypo Verses Hyper Potassium

Hypoglycemia

SIGNS & SYMPTOMS

Cold, clammy, pale skin Nervousness Shakiness, lack of coordination, staggering gait Irritability, hostility, and strange behavior Difficulty concentrating Fatigue Excessive hunger Headache Blurred vision and dizziness Abdominal pain or nausea Fainting and unconsciousness

Acute Hypoglycemia
SIGNS & SYMPTOMS
Cardiovascular Signs
Palpitations

Neurological Signs
Agitation Confusion Slurred Speech Staggering Gait Paraplegia Seizures Coma

Tachycardia
Anxiety Irritability Diaphoresis Pale, cool skin Tachypnea

Hyperglycemia

SIGNS & SYMPTOMS

Thirst Polyuria Dehydration Nausea, vomiting DKA HNNK

Normal serum Glu level: 70 - 110 mg/dL

Sodium (Na+)

Dominant extracellur electrolyte Chief determinant of osmolality

NaCl

Normal serum Na+ level: 135-145 mEq/L

Hyponatremia

SIGNS & SYMPTOMS

Deficiency of sodium in the blood Hypotension Tachycardia Muscle weakness

Mental Confusion

Hypernatremia

SIGNS & SYMPTOMS

Excess sodium in the blood Hypertension Muscle twitching Mental confusion Coma

Magnesium (Mg+)

Activates many enzymes

50% is insoluble in bone
Mg+

45% is intracellular 5% is extracellular

Normal serum Mg+ level: 1.5 - 2.5 mg/dL

Hypomagnesemia

SIGNS & SYMPTOMS

Tremors Positive Chvostek & Trousseau Nystagmus Dysrhythmias Confusion/Hallucinations ECG Changes Diarrhea Flat T wave

Hyperactive deep reflexes

ST interval depression

Seizures

Prolonged QT interval
May lead to Torsade de Pointes

Hypomagnesemia

CAUSES
Alcoholism Malabsorption Starvation Diarrhea

Diuresis

Hypermagnesemia

SIGNS & SYMPTOMS

Peaked T wave Bradycardia CNS Depression Areflexia Sedation Respiratory paralysis

Hypermagnesemia

CAUSES
Not common Occurs with chronic renal insufficiency Treatment is hemodialysis

Calcium (Ca++)
ESSENTIAL FOR
Neuromuscular transmission Growth and ossification of bones

Muscle contraction

Ca++

Normal serum Ca++ level: 8 - 11 mg/dL

Calcium (Ca++)
INVOLVED IN
Blood clotting Nerve impulse

Muscle contraction
Excreted through urine, feces, and perspiration

Ca++

Hypocalcemia

SIGNS & SYMPTOMS

Tetany (cramps/convulsions in wrists and ankles) Weak heart muscle Increased clotting time Prolonged QT interval

May lead to Torsade de Pointes

Abnormal behavior Chvostek's sign (facial twitching) Trousseaus Sign (carpopedal spasm) Paresthesia

Hypocalcemia

CAUSES
Renal insufficiency Decreased intake or malabsorption of Calcium Deficiency in or inability to activate Vitamin D

Hypercalcemia

SIGNS & SYMPTOMS

Kidney stones Bone pain Hypotonicity of muscles (decreased tone) Altered mental status Cardiac arrhythmias Shortened QT interval

Hypercalcemia

CAUSES
Neoplasms (tumors) Excessive administration of Vitamin D

TREATMENT
Usually aimed at underlying disease and hydration Severe hypercalcemia may be treated with forced diuresis

Phosphorus (P, PO4)

INVOLVED IN
Energy metabolism Genetic coding

PO4

Cell function
Bone formation

Normal serum PO4 level: 2.5-4.5 mg/dL

Hypophosphatemia

SIGNS & SYMPTOMS

Respiratory difficulty Confusion Irritability Coma

Hypophosphatemia

CAUSES
Severe infections Kidney failure Thyroid failure Parathyroid Failure Often associated with hypercalcemia or hypomagnesemia or too much Vitamin D Cell destruction - from chemotherapy, when the tumor cells die at a fast rate

Can cause tumor lysis syndrome

Hyperphosphatemia

SIGNS & SYMPTOMS

Elevated blood phosphate level

There are no symptoms of hyperphosphatemia

Hyperphosphatemia

TREATMENT
Calcium Carbonate tablets

Aluminum hydroxide

Can cause aluminum toxicity

IV Fluid Therapy

OSMOLALITY
Concentration of a solution Concentration of solutes per kilogram The higher the osmolality the greater its pulling power for water
Normal serum osmolality is 275 to 295 mOsm/L

Serum Osmolality

Sodium = major solute in plasma

Estimated serum osmolality = 2 X serum Na

Urea (BUN) and Glucose are large molecules that serum osmolality
When either or both are elevated, the serum osmolality will be higher than 2 times the sodium level, so the following formula is more accurate:

Serum osmolality = 2 X serum Na + BUN + glucose 3 18

Major Mediators of Sodium and Water Balance

Angiotensin II Aldosterone

Antidiuretic hormone (ADH)

Renin-Angiotensin-Aldosterone

Angiotensin II 1. Stimulates production of aldosterone 2. Acts directly on arterioles to cause vasoconstriction 3. Stimulates Na+/H+ exchange in the proximal tubule Aldosterone 1. Stimulates reabsorption of Na+ and excretion of K+ in the late distal tubule 2. Stimulates activity of H+ ATPase pumps in the late distal tubule

Antidiuretic Hormone (ADH)

Synthesized in the hypothalamus and stored in the posterior pituitary Released in response to plasma hyperosmolality and decreased circulating volume Actions of ADH
Increases the water permeability of the collecting tubule (makes kidneys reabsorb more water) Mildly increases vascular resistance

IV Fluid Therapy
Isotonic same osmolality as serum Hypotonic lower osmolality than serum Hypertonic higher osmolality than serum

Effect on Cells

IV Solutions
D5W Hypotonic Solutions Isotonic Solutions Hypertonic Solutions Hypotonic in the body Used for cellular dehydration Not used with head injuries

Hydrates extracellular compartment

Pulls fluid into vascular space

IV Solutions
D5W
D10W D50W NS NS Isotonic

3% NaCl
LR D5LR Albumin Dextran

Hypertonic
Isotonic Hypertonic Hypertonic Hypertonic

Hypertonic
Hypertonic Hypotonic Isotonic Hypertonic Hypertonic

D51/2 NS
D5NS

Hetastarch
PRBCs

Hypertonic
Hypertonic

D5W

Hypotonic in the body

Daily Fluid Balance

Intake: 1-1.5 L

Insensible Loss - Lungs 0.3 L - Sweat 0.1 L

Urine: 1.0 to 1.5 L

Solids 40% of Wt Intracellular (2/3) Extracellular (1/3)

H 2O

H 2O

Na

E.C.F. COMPARTMENTS

Interstitial (3/4)

Intravascular (1/4)
H2O Na
Colloids & RBCs

H2O Na

Third Space

Third space refers to collection of fluids (usually isotonic) that is sequestered in potential spaces.
This situation is not normal and the fluid is derived from extracellular fluid.

Principles of Treatment

How much volume?

Need to estimate fluid deficit

Which fluid?
Which fluid compartment is predominantly affected? Must evaluate other acid/base, electrolyte & nutrition needs

Fluid Replacement Products

Crystalloids

able to pass through semi permeable membranes

Isotonic solutions Hypotonic solutions Hypertonic solutions

Colloids do not cross the semi permeable membrane and remain

in the intravascular space for several days (pulling fluid out of the intracellular and interstitial space)

Albumin Dextran Hetastarch

1 liter 5% Albumin
Total body water

ECF ICF

Intravascular =1 liter

1 Liter 0.9% saline

Total body water

ECF=1 liter

ICF=0

Interstitial=3/4 of ECF=750ml Intravascular =1/4 ECF=250 ml

1 liter 5% Dextrose
Total body water

ECF=1/3 = 300ml

ICF=2/3 = 700ml

Intravascular =1/4 of ECF~75ml

Ringers Lactate

Infusion of Ringer Lactate solution may lead to metabolic alkalosis because of the presence of lactate ions Lactated Ringers should be used with great care with patients with hyperkalemia, severe renal failure, and hepatic insufficiency Solutions containing lactate are not for use in the treatment of lactic acidosis

CCRN REVIEW PART 2

BREAK

Neurological Alterations

Brain Aneurysms & AVMs Intracranial Hemorrhage Stroke

The Human Brain

Cerebral Spinal Fluid

The serum-like fluid that circulates through the ventricles of the brain, the cavity of the spinal cord, and the subarachnoid space

Spinal Cord Nerve Tracts

Descending Motor Tract
(Corticospinal Tract)

(Spinothalmic Tract)

Ascending Sensory Tract

Brown-Squard syndrome
Incomplete Spinal Cord Injury

(Hemi-section)

Central Cord Syndrome

Walking Quads

Homonymous Hemianopia

Brain Aneurysms & AVMs

Brain Aneurysm
An intracranial aneurysm is a weak or thin spot on a blood vessel in the brain that balloons out and fills with blood

AV Malformation (AVM)
Arteriovenous malformation (AVM) of the brain is a "short circuit between the arteries and veins

Intracranial Aneurysms

Usually occur at bifurcations and branches of the large arteries located in the Circle of Willis The most common sites include the:
Anterior Communicating artery (30 - 35%) Bifurcation of the Internal Carotid and Posterior Communicating artery (30 - 35%) Bifurcation of Middle cerebral (20%) Basilar artery bifurcation (5%) Remaining posterior circulation arteries (5%)

Types of Aneurysms

Saccular aneurysm
Occurs at bifurcations

Fusiform aneurysm
Often in basilar artery

Dissecting aneurysm

Ruptured aneurysm

Brain Circulation

Arterial Circulation in the Brain

Intracranial Aneurysms

RISK FACTORS
Smoking Hypertension Coarctation of the aorta Dissections/trauma Intracranial neoplasm Polycystic kidney disease Abnormal vessels or High-flow states (eg, vascular malformations, fistulae) Hypercholesterolemia Connective tissue disorders (eg, Marfan, Ehlers-Danlos)

Intracranial Aneurysms

SIGNS & SYMPTOMS

Usually asymptomatic until rupture

Cranial Nerve Palsy Dilated Pupils Double Vision Pain Above and Behind Eye Localized Headache

Warning signs prior rupture

Localized Headache Nausea & Vomiting Stiff Neck Blurred or Double Vision Sensitivity to Light (photophobia) Loss of Sensation

Treatment of Brain Aneurysms

Surgery
Craniotomy and clipping

Endovascular coiling

Aneurysm Post-Op Risks

Rebleeding
Most frequently within the first 24 hours Up to 20% of patients rebleed within 14 days Main preventative measure is control of blood pressure (preferably beta blockers)

Vasospasm
Usually occurs before 3 days or after 10 days (post bleed) May require hypervolemic therapy

Hydrocephalus Hyponatremia Fluids / Electrolytes

Arterio-Venous Malformation

Arterio-Venous Malformation

The arteries and veins have a direct connection, bypassing the capillary network

Presents with ongoing headaches, seizures, hemorrhage, or progressive neurological dysfunction

Arterio-Venous Malformation

SIGNS & SYMPTOMS

Seizures Headaches Whooshing" Sound (Bruit) Other Signs

Subtle behavioral changes Communication or thinking disturbances Loss of coordination and balance Paralysis or weakness in one part of the body Visual disturbances Abnormal sensations

Arterio-Venous Malformation

COMPLICATIONS
Hemorrhage (into surrounding tissue)

Ischemia
Seizures Brain Cell Death

Arterio-Venous Malformation

DIAGNOSIS
MRI (including MR Angiography) as well as CT Angiography help identify AVMs

Cerebral Angiography is a prerequisite to treatment

To identify the precise anatomy and configuration of both the lesion and the feeding and draining vessels

Arterio-Venous Malformation

TREATMENT
Surgery

Usually delayed

Open ligation and/or resection of the AVM

Radiosurgery Embolization

Usually as adjunct to surgery

Observation

Arterio-Venous Malformation

RADIOSURGERY
Believed to "work" by initiating an "inflammatory" response in the pathological blood vessels ultimately resulting in their progressive narrowing and ultimate closure The risk for hemorrhage is not reduced during this lag time

There is the added risk of radiation necrosis of adjacent healthy brain tissue or brain cyst formation

Brain Radiosurgery

ADVANTAGES
Noninvasive Can access all anatomic locations of the brain

DISADVANTAGES
Can only treat smaller lesions (<3 cm in diameter) Requires 2 or more years to complete

AVM Post-Op Risks

Perfusion-breakthrough bleeding Endovascular occlusion

Intracranial Hemorrhage

Sudden onset of the worst headache of my life

Intracranial Hemorrhage

Epidural Subdural Subarachnoid Intraparencymal Intraventricular Cerebellar

Intracranial Hemorrhage

ICH is a dynamic, not a static process Hemorrhage volume can increase over time CT scan is the most important diagnostic tool Managing blood pressure is extremely important Must aggressively manage fever and seizures

Consider hyperventilation and paralytics in setting of increased ICP and deterioration

Treatment of ICH

KEY CONCEPTS
1) Intracranial Pressure
Elevated when ICP >20 mm Hg

2) Cerebral Perfusion Pressure

CPP = MAP - ICP Must maintain CPP > 70 mm Hg Example: MAP = 100, ICP = 20 CPP = 80 mmHg

Subarachnoid Hemorrhage (SAH)

DEFINITION
When a blood vessel just outside the brain ruptures, the area of the skull surrounding the brain (the subarachnoid space) rapidly fills with blood

Subarachnoid Hemorrhage (SAH)

SIGNS & SYMPTOMS

Sudden, intense headache Neck pain Nausea or vomiting Neck stiffness Photophobia

Sudden onset of the worst headache of my life

Subarachnoid Hemorrhage (SAH)

SAH may be spontaneous or traumatic Spontaneous SAH causes

Cerebral aneurysms AV malformations Trauma

Uncommon causes
Neoplasms, venous angiomas, infections

Subarachnoid Hemorrhage

Warning bleeds are relatively common Sentinel headache 30-50%

Early diagnosis prior to rupture will improve outcomes

50% of patients die within 48 hours irrespective of therapy

Subarachnoid Hemorrhage

Often accompanied by a period of unconsciousness (50% never wake up) Common signs include neck stiffness, photophobia, headache 20% have ECG evidence of myocardial ischemia

Complications of SAH

Hydrocephalus

may develop within the first 24 hours because of obstruction of CSF outflow in the ventricular system by clotted blood

Rebleeding of SAH occurs in 20% of patients in the

first 2 weeks. Peak incidence of rebleeding occurs the day after SAH and may be from lysis of the aneurysmal clot

Vasospasm from arterial smooth muscle contraction

(symptomatic in 36% of patients)

Re-bleeding After SAH

Re-bleeding occurs most frequently within the first 24 hrs Up to 20% of patients rebleed within 14 days The main preventative measure is to control the blood pressure preferably beta blockers Early clipping of the aneurysm allows hypertensive and hypervolemic therapy to prevent vasospasm

Vasospasm After SAH

Worst time is day 7 to day 10 (most frequent time for vasospasms) Diagnosed by neurologic exam, transcranial doppler and angiography May use calcium channel blockers
Reduces vasospasm, neurological deficit, cerebral infarction and mortality

May use some antispasmodics

Vasospasm & HHH Therapy

Hemodilution
Hct 30-35%

Hypertension
Phenylephrine / Norepinephrine BP titration to CPP/exam

Hypervolemia
Colloids/crystalloids

Other Vasospasm Therapy

Angioplasty
BP management during procedure Reperfusion issues Timing

Papaverine Infusion
Side effects Repeated trips

Other Complications of SAH

Neurologic deficits from cerebral ischemia, peaks at days 4-12 Hypothalamic dysfunction causes excessive sympathetic stimulation, which may lead to myocardial ischemia or labile BP Hyponatremia may result from cerebral salt wasting / SIADH Nosocomial pneumonia and other such complications Pulmonary edema neurogenic & non-neurogenic

Treatment of SAH
1)

Identify and treat the causative lesion

Thus preventing re-bleeding

2)

Treat hydrocephalus
Treating and prevent vasospasm

3)

Treatment of SAH

Maintain systolic BP >130mmHg

Use vasopressors if necessary to maintain CPP and reduce ischemic complications from vasospasm Generally avoid vasodilators (except calcium channel blockers)

CCRN REVIEW PART 2

BREAK

Stroke

Stroke

Stroke

RISK FACTORS
TIA CAD High Blood Pressure High Cholesterol Smoking Heart Disease Diabetes

Excessive alcohol Family History Age Sex Race Obesity

Annual risk of stroke: Increases with age

Stroke Tests

Computed Tomography (CT) Magnetic Resonance Imaging (MRI) Cerebral Angiography: identify responsible vessel Carotid Ultrasound: carotid artery stenosis Echocardiogram: identify blood clot from heart Electrocardiogram (ECG): underlying heart conditions Heart monitors, blood work and more tests!!

http://www.strokecenter.org/education/ais_ct_tool/index.htm

CT

MRI

p : / / w w w . s t r o k e c e n t e r . o r g / e d u c a t i o n / a i s _ c t _ t o o l / c t 0 4 / c t 0 4 f r a e s . h t

Treatment of Ischemic CVA

Tissue plasminogen activator (tPA) can be given within three hours from the onset of symptoms
Heparin Intra-arterial thrombolysis Hemicraniectomy In addition to being used to treat strokes, the following can also be used as preventative measures
Anticoagulants/Antiplatelets
Carotid Endarterectomy Angioplasty/Stents

Treatment of Hemorrhagic CVA

Surgery is often required to remove pooled blood from the brain and to repair damaged blood vessels Prevention:
An obstruction is introduced to prevent rupture and bleeding of aneurysms and AVMs Surgical Intervention Endovascular Procedures

Prevention of CVA

Control high Blood Pressure Lower cholesterol Quit smoking

Control diabetes
Maintain healthy weight Exercise

Manage stress
Eat a healthy diet

CCRN REVIEW PART 2

BREAK

Metabolic Alterations

DKA & HHNK DI & SIADH

DIC
Shock States

Sepsis

Diabetic Ketoacidosis

What is DKA?

Diabetic Ketoacidosis

A life-threatening complication seen with Diabetes Mellitus Type 1

Diabetic Ketoacidosis

SIGNS & SYMPTOMS

Serum Glucose 300-800 Ketoacidosis Present Large Serum And Urine Ketones Fruity Breath Kussmaul Respirations

Serum pH < 7.3

Dehydration

HHNK

What is HHNK?

Hyperglycemic Hyperosmolar Nonketonic Coma

A life threatening complication seen with Diabetes Mellitus Type 2

HHNK

SIGNS & SYMPTOMS

Serum Glucose 600-2000 Ketoacidosis Not Present Absent Or Slight Serum And Urine Ketones Normal Breath Shallow Respirations

Serum pH Normal
Severe Dehydration

DKA vs HHNK
DKA

HHNK

Faster Onset Glucose 300-800 Acidosis Fruity Breath

Slower Onset Glucose 600-2000 No Acidosis Normal Breath

Kussmaul Respirations

Shallow Respirations

Treatment of DKA & HHNK

Reverse Dehydration
NS, then NS

Restore Glucose Levels

D5 NS When Glu 250

Restore Electrolytes

Diabetes Insipitus

What is Diabetes Insipitus?

A Condition resulting from too little ADH

Why is it called Diabetes Insipitus?

The term Diabetes refers to polyuria

Diabetes Insipitus

SIGNS & SYMPTOMS

Polyuria Severe Hypovolemia Severe Dehydration Elevated Serum Osmolality Elevated Serum Sodium Shock

Diabetes Insipitus

CAUSES
Decreased ADH Neurological Surgery Head Trauma Dilantin or Lithium

Diabetes Insipitus

TREATMENT
Fluid Resuscitation

ADH Replacement

Vasopressin, Pitressin, DDAVP

Treat The Cause

SIADH

What is SIADH?
Syndrome of Inappropriate ADH

Too much ADH

SIADH

SIGNS & SYMPTOMS

Hyponatremia Low Serum Sodium

Elevated ADH Level Weight Gain Without Edema Elevated CVP, PAP, PAWP Hypertension Concentrated And UOP Headache

Serum NA < 135

Low Serum Osmolality High Urine Osmolality Elevated Specific Gravity

Urine specific gravity > 1.030

Altered LOC
Seizures

Elevated Urine Osmolality

SIADH

CAUSES
Head Trauma Oat Cell Carcinoma Other Cancers Viral Pneumonia Medications Stress Mechanical Ventilation

SIADH

TREATMENT
Monitor Fluid Balance, Monitor I & O Restrict Fluids

Replace Na+ loss when necessary

May Give 3% (Hypertonic) Saline May Give Dilantin or Lithium May require PA Catheter For Monitoring May Give Diuretics

DI vs SIADH
DI

SIADH

Too Little ADH Dehydration High Serum Sodium High Serum Osmolality

Too Much ADH Water Intoxication Low Serum Sodium Low Serum Osmolality

Low Urine Osmolality

High Urine Osmolality

DI vs SIADH Treatment
DI

SIADH

Lots of Fluids

Fluid Restriction

Hold Dilantin
Hold Lithium Give ADH

May Give Dilantin

May Give Lithium 3% Saline

DIC

What is DIC?
Disseminate Intravascular Coagulation

A clotting disorder that ultimately causes bleeding

DIC

Caused by over-activation of the clotting pathways Causes widespread fibrin deposits

Bleeding and renal failure are most common manifestations

Treating the underlying disease is the most important step

Disseminated Intravascular Coagulation

Systemic activation of coagulation

Intravascular deposition of fibrin

Depletion of platelets and coagulation factors

Thrombosis of small and midsize vessels with organ failure

BLEEDING

DIC

SIGNS & SYMPTOMS

Bleeding

Thrombosis
Organ Failure

DIC

DIC

CAUSES
Massive Tissue Injuries Obstetric Emergencies

Septicemia
Cancers Vascular Disorders

Systemic Disorders
Many More Causes

DIC Lab Results

CLOTTING TESTS ELEVATED

PT aPTT Fibrin degradation products (D-dimer)

CLOTTING FACTORS DEPLETED

Platelets Fibrinogen Protein Activated C Antithrombin

DIC

TREATMENT
Treat the Cause

Replace Clotting Factors

Anticoagulation Therapy (Heparin)

CCRN REVIEW

THE END
PART 2

CCRN REVIEW PART 2

THANK YOU!

CCRN REVIEW

GOOD LUCK!

References

American Stroke Association. (2007). Acute and Preventative Treatments. Retrieved March 4, 2007 from http://www.strokeassociation.org/presenter.jhtml?identifier=2532.
Block, C., and Manning, H. (2002). Prevention of acute renal failure in the critically ill. American Journal of Respiratory and Critical Care Medicine; (165)320-324.

Brenner, B. M., and Rector, F.C. (2000). The kidney (6th ed), Vol I. Philadelphia: W.B. Saunders Company; (1)399-416.
Brettler S. (2005). Endovascular coiling for cerebral aneurysms. AACN Clinical Issues; (16)515-525.

Britz, G. W. (2005). ISAT trial: Coiling or clipping for intracranial aneurysms? Lancet; (366)783-785.
Campbell, D. (2003). How acute renal failure puts the breaks on kidney function. Nursing 2003; (33)59-63.

References Continued

Campbell, D. (2003). How acute renal failure puts the breaks on kidney function. Nursing 2003; (33)59-63.
Carlson, K. (2009) Advanced Critical Care Nursing. Philadelphia, Pa: Saunders/Elsevier. Guyton, A. C., and Hall, J. E. (2000). Unit V: The kidneys and body fluids. In A. C. Guyton & J. E. Hall. Textbook of medical physiology (10th ed.). Philadelphia: W.B. Saunders Company; pg. 264-379. Impact of Stroke. (2007). American Stroke Association. Retrieved March 4, 2007 from http://www.strokeassociation.org/presenter.jhtml?identifier=1033. Lynn-Mchale Wiegand, D. J. (ed.). (2011). AACN Procedure Manual for Critical Care. 6th ed. St. Louis, MO: Saunders. Pagana, K. D. & Pagana, T. J. (2008). Mosbys Diagnostic and Laboratory Test Reference. 9th ed. St. Louis, MO: Mosby/Elsevier. Stillwell, S. (2006). Mosbys Critical Care Nursing Reference. 4th ed. St. Louis, MO: Mosby/Elsevier.: Diagnosis and Management (5th ed).