Maha Salah A*, Hanaa Y. Hashem B, Mahmoud M.

Alsagheir C, Mohammed Salah D

Acute Respiratory Distress Syndrome (ARDS)
Developed Clinical Pathway: Suggested
Protocol

health. They provide opportunities for collaborative practice
Abstract—Acute respiratory distress syndrome (ARDS) represents a and team approaches that can maximize the expertise of
complex clinical syndrome and carries a high risk for mortality. The multiple disciplines. Clinical pathways have four main
severity of the clinical course, the uncertainty of the outcome, and the components; a timeline, the categories of care or activities and
reliance on the full spectrum of critical care resources for treatment their interventions, intermediate and long term outcome
mean that the entire health care team is challenged. Researchers and criteria, and the variance record (to allow deviations to be
clinicians have investigated the nature of the pathological process and
documented and analyzed). They differ from practice
explored treatment options with the goal of improving outcome.
Through this application of research to practice, we know that some guidelines, protocols and algorithms as they are utilized by a
previous strategies have been ineffective, and innovations in multidisciplinary team and have a focus on the quality and co-
mechanical ventilation, sedation, nutrition, and pharmacological ordination of care [1].
intervention remain important research initiatives. Developed
Clinical pathway is multidisciplinary plans of best clinical practice Acute respiratory distress syndrome (ARDS)
for this specified group of patients that aid in the coordination and represents a complex clinical syndrome and carries a high risk
delivery of high quality care. They are a documented sequence of for mortality. The severity of the clinical course, the
clinical interventions that help a patient to move, progressively uncertainty of the outcome, and the reliance on the full
through a clinical experience to a desired outcome. Although there is
a lot of heterogeneity in patients with ARDS, this suggested protocol
spectrum of critical care resources for treatment mean that the
for developed clinical pathway with alternatives was built depended entire health care team is challenged. Since the 1960s,
on a lot of researches and evidence based medicine and nursing researchers and clinicians have investigated the nature of the
practices which may be helping these patients to improve outcomes, pathological process and explored treatment options with the
quality of life and decrease mortality. goal of improving outcome. Through this application of
Keywords— Clinical pathway - Acute respiratory distress research to practice, we know that some previous strategies
syndrome (ARDS). have been ineffective, and innovations in mechanical
ventilation, sedation, nutrition, and pharmacological
I. INTRODUCTION intervention remain important research initiatives [2].

C linical pathways are multidisciplinary plans (or blueprint

for a plan of care) of best clinical practice for specified
groups of patients with a particular diagnosis that aid in the
Acute Lung Injury (ALI)/ Acute Respiratory Distress
Syndrome (ARDS) are affecting both medical and surgical
coordination and delivery of high quality care. They are a patients. Despite great advances in understanding the
documented sequence of clinical interventions that help a pathogenesis of disease mortality rate is still high. Mortality
patient with a specific condition or diagnosis move, rates ranges between (30-50 %), although some trials had
progressively through a clinical experience to a desired demonstrated lower mortality rates (25 -30 %). Prevention of
outcome. Predominantly, they are management tools and long-term disabilities must be a priority of care. Even
clinical audit tool that are based on clinical information survivors of ARDS usually experience long ICU stay, hospital
developed in other guidelines or parameters. They are specific stay and several co-morbidities & require prolonged
to the institution using them. Originally, critical pathways rehabilitation time until of full recovery. Restoration of normal
began with admission and ended with discharge from the activities ranges between 6 months to 12 months. Nearly half
hospital. Today, they are usually interdisciplinary in focus, of survivors had neurocognitive impairment & decrease
merging the medical and nursing plans of care with those of quality of life that persist at least 2 years. ALI/ARDS not only
other disciplines, such as physical therapy, nutrition, or mental represent great impact on ICU but on nation's economics as
well [3].

F.A Author, Assistant Lecturer of Critical Care and Emergency Nursing
Faculty of Nursing, Cairo University, Egypt. (e-mail: metcy A key role for the critical care nurse is early detection
2004@yahoo.com) and prevention of ARDS. Therefore, with respect to ARDS, it
S. B. Author, Assistant Professor of Medical-Surgical Nursing & Director is essential that critical care nurses be knowledgeable about
of the Quality Assurance Unit Faculty of nursing, Cairo University, Egypt.
T. C. Author, Lecturer of Anesthesia and Intensive Care, Faculty of risk factors, assessment tools and protocols, and prevention
Medicine - Al- Azhar University, Egypt strategies. ARDS is at the extreme end of a continuum of
F.D. Author, Resident of Anesthesia and Intensive Care Assigned Doctor hypoxic acute lung injury (ALI) that results in respiratory
for Pain Management, Nizwa Hospital – Sultanate Oman. failure. In 1994, the American-European Consensus
Conference members issued definitions of ALI and ARDS that • Oxygen saturation by pulse oximetry
are widely used by researchers today [2]. • Vital signs (Temperature, pulse, blood pressure and
respiratory rate).
II.SUBJECT & METHODS • Ventilator parameters according to lung protective
AIM: The aim of this study is to evaluate the effect of applying strategies conventional therapy (ARDSNET).
a suggested protocol from developed clinical pathway on
patients with severe acute respiratory distress syndrome.
III. SUGGESTED PROTOCOL
MEDICAL AND NURSING MANAGEMENT
RESEARCH HYPOTHESES: To fulfill the aim of this study the
Objectives:
following research hypotheses was formulated:
• Control the original cause
1- Applying a suggested protocol from developed
• Achieve adequate oxygenation
clinical pathway will improve clinical outcomes of
• Improve lung function
patients with severe acute respiratory distress
• Decrease probability of development of ventilator
syndrome.
associated lung problems
2- Applying a suggested protocol from developed
• Decrease days of mechanical ventilator and length of
clinical pathway will reduce mortality rate of patients
ICU stay
with severe acute respiratory distress syndrome.
• Prevent other organ failure
• Reduce mortality
RESEARCH DESIGN: This study will conducted using a quasi-
experimental design.
ARDS Already Diagnosed
SETTING: The study will be carried out at Critical Care Units, 1. Control of original cause
affiliated to Cairo University Hospitals which had patients 2. Non-invasive O2 therapy
diagnosed with ARDS. • Face mask
• Non-rebreathing face mask
SAMPLE: Convenience sample of all male and female adult • CPAP mask
patients had severe ARDS will be admitted to the selected 3. Continuous monitoring of ABG and chest x-ray
critical care units within 1year. • If abnormalities start Mechanical ventilation
CRITERIA OF INCLUSION: • If normal ranges continue Non-invasive O2 therapy
1. On 1st 48 hours after mechanical ventilation (Low
tidal volume ventilation strategy) Methods of Therapy:
2. Severe ARDS as diagnosed by the following 1- Conventional therapy (Lung Protective Strategy)
criteria: 2- Supportive therapy
• Time: Acute onset within one week of respiratory 3- Non-conventional therapy (Rescue therapy)
event
• Chest X-ray: Bilateral opacities 1. Conventional Therapy (Lung Protective Strategy)
• Origin of edema: Respiratory failure, non-cardiac ARDSNET(5)
• Oxygenation: PaO2/FiO2< 100 mmHg with PEEP Lung Protective Strategy
> 5 mmHg • Low tidal volume (VT)
3. Pao2< 60 mmHg or Sao2< 88% or FiO2> 60% • Low plateau pressure (P Plat)
• Fio2 at non-toxic level (< 60 %)
TOOLS: to achieve the aim, data pertinent to this study will • Positive end expiratory pressure (PEEP)
collect utilizing the suggested protocol. These protocol was
constructed by the researcher then revised by a panel of 5 PART I: VENTILATOR SETUP AND ADJUSTMENT
critical care & emergency nursing and medical experts.
These tools are: Ventilator Mode
Tool (1) A mechanically ventilated patients characteristics • Any mode can be used
questionnaire: • Choose mode & parameters according to severity and
A- Socio-demographic data sheet: covers age, gender, patient condition
educational level, and occupation. • Start with Controlled Mandatory Ventilation (CMV)
B- Medical data sheet: consists of items such as: admission • Change according to patient response
date, past medical and surgical history, height, weight, BMI, • Always we use Volume control modes
diagnosis, duration of stay in Critical Care Unit, • Some cases need Pressure control modes [4]
pharmacological treatment and physiological parameters. 1. Calculate predicted body weight (PBW)
Tool (2) Clinical outcomes sheet: it includes a following: Males = 50 + 2.3 [height (inches) - 60]
• Berlin definition criteria for ARDS. Females = 45.5 + 2.3 [height (inches) -60]
• Glasgow coma score (GCS). 2. Select any ventilator mode
• Arterial blood gases values (ABGs)
 3. Set ventilator settings to achieve initial VT = 8 ml/kg 3. Patient has acceptable spontaneous breathing efforts. (May
PBW decrease vent rate by 50% for 5 minutes to detect effort.)
4. Reduce VT by 1 ml/kg at intervals ≤ 2 hours until VT 4. Systolic BP ≥ 90 mmHg without vasopressor support.
= 6ml/kg PBW. 5. No neuromuscular blocking agents or blockade.
5. Set initial rate to approximate baseline minute
ventilation (not > 35 bpm). B. SPONTANEOUS BREATHING TRIAL:
6. Adjust VT and RR to achieve pH and plateau If all above criteria are met and subject has been in the study
pressure goals below. for at least 12 hours, initiate a trial of UP TO 120 minutes of
spontaneous breathing with FiO2 < 0.5 and PEEP < 5:
OXYGENATION GOAL: PaO2 55-80 mmHg or SpO2 88- 1. Place on T-piece, trach collar, or CPAP ≤ 5 cm H2O with
95% PS < 5
Use a minimum PEEP of 5 cm H2O. Consider use of 2. Assess for tolerance as below for up to two hours.
incremental FiO2/PEEP combinations such as shown below a. SpO2 ≥ 90: and/or PaO2 ≥ 60 mmHg
(not required) to achieve goal. b. Spontaneous VT ≥ 4 ml/kg PBW
c. RR ≤ 35/min
d. pH ≥ 7.3
e. No respiratory distress (distress= 2 or more)
 Heart Rate > 120% of baseline
 Marked accessory muscle use
 Abdominal paradox
 Diaphoresis
 Marked dyspnea
3. If tolerated for at least 30 minutes, consider extubation.
4. If not tolerated resume pre-weaning settings[5].

Other Medical Strategies for ARDS Management

PLATEAU PRESSURE GOAL: ≤ 30 cm H2O A. Permissive Hypercapnia
• Hypercapnia and respiratory acidosis are a
 Check Pplat (0.5 second inspiratory pause), at least q
consequence of this strategy due to low alveolar
4h and after each change in PEEP or VT.
pressure and low tidal volume.
 If Pplat > 30 cm H2O: decrease VT by 1ml/kg steps
• Hypercapnia can be minimized by using the highest
(minimum = 4 ml/kg).
respiratory rate and shortening the ventilator tubing to
 If Pplat < 25 cm H2O and VT< 6 ml/kg, increase VT decrease dead space.
by 1 ml/kg until Pplat > 25 cm H2O or VT = 6 ml/kg. • Help to preserve minute volume in acceptable range
 If Pplat < 30 and breath stacking or dis-synchrony and prevent increase of P plat.
occurs: may increase VT in 1ml/kg increments to 7 or • May give Hco3
8 ml/kg if Pplat remains < 30 cm H2O.
Stop Permissive Hypercapnia If:
PH GOAL: 7.30-7.45 • Increase intracranial pressure
Acidosis Management: (pH < 7.30)
• Myocardial infarction
 If pH 7.15-7.30: Increase RR until pH > 7.30 or • Metabolic acidosis
PaCO2 < 25 (Maximum set RR = 35). • Pregnant
 If pH < 7.15: Increase RR to 35. • Renal failure
 If pH remains < 7.15, VT may be increased in 1 ml/kg • Cardiovascular problems/Arrhythmia
steps until pH > 7.15, (Pplat target of 30 may be
exceeded). May give NaHCO3 B. Open Lung Ventilation
A strategy that combines low tidal volume ventilation and
Alkalosis Management: (pH > 7.45) Decrease vent rate if high PEEP to maximize alveolar recruitment by:
possible. • Mitigate alveolar overdistension
• Minimize atelectasis
I: E RATIO GOAL: Recommend that duration of inspiration • Together, decrease the risk of ventilator-associated
be < duration of expiration. lung injury
PART II: WEANING C. Recruitment Maneuvers
A. Conduct a SPONTANEOUS BREATHING TRIAL daily • Application of a high level of PEEP (35 to 40
when: cmH2O) for 40 seconds
1. FiO2 ≤ 0.40 and PEEP ≤ 8.
• To open the collapsed alveoli [6]
2. PEEP and FiO2 ≤ values of previous day.
Adverse effects:
 • Hypotension Evidence:
• Desaturation • Clinical trials show no survival benefits, two small
RCT’s show improvement in oxygenation and lung
2- Supportive Management injury

A. Hemodynamic management 3- B2 Agonist

• Decreases alveolar-capillary permeability in patients
Early management of any abnormalities in vital signs and with ARDS, possibly by simulating alveolar wound
hemodynamics. repair.
• Reduces the incidence pulmonary edema
B. Fluid Management
Conservative fluid strategy 4- Lasix
• Negative balance is preferred unless in hypotension 5- Albumin
and hypovolemia. 6- Low molecular weight Heparin ( Anticoagulant effect &
• Give colloid or vasopressor rather than crystalloid Prophylaxis against deep venous thrombosis {DVT})
• Preliminary data suggests that combination therapy 7- Omeprazole – Zantac (Prophylaxis against stress ulcer
with albumin and furosemide may improve fluid & gastrointestinal (GI) bleeding) [11]
balance, oxygenation, and hemodynamics [7]- [8].

C. Nutritional support 3- Non – Conventional Therapy (Alternative Therapy)

Aim: (Rescue Therapy)
• To provide adequate nutrition to meet the patient’s
level of metabolism & reduce morbidity. A. Surfactant Replacement Therapy
Specialized Formula:  Numerous randomized trials have found no clinical
• Eicosapentaenoic acid, Gama-linolenic acid & benefit from recombinant surfactant protein C,
elevated antioxidant. synthetic surfactant, or freeze-dried natural animal
Effect: surfactant in patients with ARDS, despite its benefit in
• Reduce mortality animal models.
• Improve oxygenation secondary to reduce pulmonary  No effect on duration of mechanical ventilation and
inflammation mortality. The exogenous surfactant was generally
• Fewer day on mechanical ventilator well tolerated.
B. Refractory Hypoxemia
D. Control of blood glucose levels  Increasing the I: E ratio by prolonging inspiratory time
E. Treatment of nosocomial pneumonia may improve oxygenation.
F. Pharmacological Management  When the inspiratory time is increased, there is an
1- Sedatives and neuromuscular block obligatory decrease in the expiratory time. This can
Sedatives lead to air trapping, auto-PEEP, barotrauma,
• Aim: to minimize patient – ventilator asynchrony, hemodynamic instability, and decreased oxygen
prevent self extubation, promote rest/sleep & delivery.
decrease anxiety. Also, use in treatment of  A prolonged inspiratory time may require significant
hypercapnia sedation or neuromuscular blockade.
• Assess: Sedation assessment scale & Delirium C. High Frequent Oscillation
assessment scale  Patient fully sedated and paralyzed
 Increase respiratory rate till 35br/min with low tidal
Neuromuscular Block (Therapeutic Paralysis): volume
• Aim: To control ventilation, promote adequate  To open collapsed lung and improve lung recruitment
oxygenation, & decrease O2 consumption [9] D. Selective Pulmonary Vasodilators Inhaled Nitric
• Hazardous: Increase risk of prolonged myopathy oxide (INo)
• N.B.: NBA improve survival in ARDS patient,  Improves Oxygenation
decrease ventilator time & didn’t increase muscle - Selective vasodilatation of vessel leading to
weakness in some population better ventilation
2- Corticosteroids:  Improves v/q mismatch.
Rationale & Risks:
 Reduction in pulmonary artery pressure
• Helps by inhibiting neutrophil activation, fibroblast
- Improves oxygen
proliferation, and collagen deposition.
- direct smooth muscle relaxation
• May increase incidence of severe neuromyopathic
- Improved RV Fn.
events. Subjects started on steroids 14 days after
- Reduced capillary leak.
diagnosis had increased mortality rates [10].
 Inhibit platelet aggregation and neutrophil adhesion.
  Mortality Benefits – None • Fast entry criteria: PaO2 <50 mmHg for >2 h at FiO2
1.0; PEEP > 5 cmH2O
E. Partial Liquid Ventilation (Perfluorocarbon ) • Slow entry criteria: PaO2 <50 mmHg for >12 h at
Mechanism of action FiO2 0.6; PEEP > 5 cmH2O
• Reduces surface tension • Maximal medical therapy >48 h
• Alveolar recruitment – liquid PEEP. Selective
distribution to dependent regions. ECMO Complication:
• Increases surfactant phospholipid synthesis and a) Mechanical Problem:
secretion. • Oxygenator failure
• Anti-Inflammatory Properties. • Circuit disruption
• Improve gas exchange • Pump or heat exchanger mal functioning
• Open the dependent alveoli • Cannula placement /removal
b) Patient related:
F. Prone Position: • Bleeding
Effect on gas exchange: • Neurological complications
• Improve oxygenation • Additional organ failure
• Allow decrease Fio2; PEEP ( Variable - not • Barotrauma, infection, metabolic
predictable )
• Response rate – 50-70% Post ARDS:
How prone position improve oxygenation After ARDS, patient may has:
• Increase in Functional Residual Capacity • Depression (43%)
• Improve ventilation of previously dependent regions. • Anxiety (48%)
• Improve in Cardiac output • Post-Traumatic Stress Syndrome (35%)
• Facilitate clearance of chest secretions • Myopathy, neuropathy & cognitive impairment
• Decrease quality of live
• Improve lymphatic damage [12]
Contraindications
• Unresponsive cerebral hypertension
• Unstable bone fractures
• Left heart failure
• Hemodynamic instability
• Active intra-abdominal pathology or surgery
• Facial fracture
• Spinal instability
TIMING ARDS > 24 hrs. / 2nd Day
FREQUENCY Usually One Time per Day
DURATION 16 to 20 hrs. /Day. Alternatively, 48h. Prone -
24h. Supine
Outcome:
 Improvement Of Oxygenation
 No Improvement of Survival.
Complications
• Pressure Sore Fig. 1 Clinical Pathway general view from admission to
• Accident Removal Of ETT; Catheters ; lines discharge [13]-[14]-[15]-[18].
• Arrhythmia
• Reversible Dependent edema (Face, Anterior Chest
Wall)

G. Extracorporeal Membrane Oxygenation (ECMO)

• Adaptation of conventional cardiopulmonary bypass
technique. Oxygenate blood and remove CO2
extracorporally.

TYPES
• High-flow venoarterial bypass system.
• Low-flow venovenous bypass system.

Criteria for treatment with extracorporeal gas exchange

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