ACUTE RESPIRATORY
DISTRESS SYNDROME
DR Aishwarya R
AP, Internal Medicine
DEFINITION
Clinical syndrome of severe dyspnea of rapid onset, hypoxemia and
diffuse pulmonary infiltrates leading to respiratory failure
BERLIN DEFINITION: Revised in 2012
INCIDENCE
5-7 per 1 lakh population per annum
India: 4.5 per 1 lakh population
COVID: Approximately 1/3rd of the patients admitted.
PRECIPITATING CAUSES
Sepsis- 40-60%
Multiple trauma- 20-35%
Pneumonias and gastric aspiration- 20-35%
Massive multiple transfusions- 9%
CLINICAL VARIABLES FOUND TO BE ASSOCIATED WITH INCREASED RISK OF
ARDS
Chronic alcohol abuse
Hypoproteinemia
Advanced age
Hypertransfusion of blood products
Cigarette smoking
Higher BMI
Note: Diabetes and prehospitalisation platelet therapy appears to
decrease the risk of ARDS.
PATHOPHYSIOLOGY
3 PHASES
Exudative
Proliferative
Fibrotic
EXUDATIVE PHASE
First 7 days of illness
Usually present within 12-36h of initial insult.
Alveolar capillary endothelial cells and Type 1
pneumocytes are injured
Loss of tight alveolar barrier to fluid and macromolecules
Edema fluid rich in protein accumulates in the interstitial and alveolar
spaces
Proinflammatory cytokines(IL-1, IL-8< TNF-alfa) and lipid
mediators( LTB4) are increased leading to recruitment of leukocytes in
to pulmonary interstitium and alveoli
Formation of hyaline membrane
Alveolar edema involves dependant portion of the lung with diminished
aeration.
Collapse of large section of dependent lung-----decreased lung compliance
Intrapulmonary shunting and hypoxia develops and work of breathing
increases------Dyspnea.
Microvascular occlusion----pulmonary hypertension
Thus in addition to severe hypoxia, hypercapnea secondary to an increase in
pulmonary dead space can be prominent in early ARDS.
REFRACTORY HYPOXEMIA
PaO2 < 50 on an Fio2=1
Due to increased right to left
shunt
PROLIFERATIVE PHASE
Lasts from 7 to 21 days.
1st sign of resolution evident in this phase.
Organisation of alveolar exudates
Shift from neutrophil to lymphocyte predominant pulmonary infiltrates
Type 2 pneumocytes proliferate
Synthesize pulmonary surfactant
Type 1 pneumocytes
FIBROTIC PHASE
Alveolar edema and inflammatory exudates of earlier phase convert to
extensive alveolar duct and interstitial fibrosis.
Emphysema like changes with large bullae
Intimal fibroproliferation----pulmonary hypertension
Increased risk of pneumothorax, decreased lung compliance and increased
pulmonary dead space.
May require long term support on mechanical ventilators/supplemental
oxygen.
DIFFERENTIAL DIAGNOSIS
INVESTIGATIONS
CHEST RADIOGRAPH:
Diffuse, bilateral alveolar infiltrates consistent with pulmonary edema
Infiltrates maybe variable: mild or dense, interstitial or alveolar, patchy or
confluent
To differentiate from cardiogenic pulmonary edema
Cardiomegaly
Increased width of vascular pedicle
Septal lines
Perihilar distribution of edema
ARTERIAL BLOOD GAS ANALYSIS: Pao2/Fio2 < 300
BRAIN NATRIURETIC PEPTIDE:
BNP< 100 pg/ml rules out heart failure
2D ECHO:
INVASIVE HEMODYNAMIC MONITORING: PAWP< 18
mmHg
BRONCHOALVEOLAR LAVAGE- To look for specific cause of ARDS
LUNG BIOPSY- Should be reserved for a highly selective group of
patients where alternative diagnosis are possible and would
significantly change management and prognosis.
APPROACH TO TREATMENT
GOALS OF MANAGEMENT
Treat the precipitating cause
Maintain oxygenation- Fio2<0.7
Prevent ventilator induced lung injury
Keep pH in normal range
Enhance patient ventilator synchrony and patient comfort
VENTILATOR MANAGEMENT IN ARDS
LUNG PROTECTIVE VENTILATION
Goal is to prevent ventilator induced lung injury
VENTILATOR INDUCED LUNG INJURY
Excessive inflation of the distal airspaces
Stress fractures in the alveolar capillary interface
Infiltration of the lung parenchyma and distal airspaces
VOLUTRAUMA-
Overexpansion of alveoli during inspiration
ATELECTRAUMA-
Decreased lung distensibility---->collapse of small airways at the end of
expiration.
Cyclic opening and closing of small airways during inspiration and expiration.
PROTOCOL FOR LUNG PROTECTIVE VENTILATION
1ST STAGE-
1) Calculate patient’s predicted body weight
2) Males: PBW= 50+ {2.3 x (height in inches-60)}
3) Females: PBW= 45.5 + {2.3 x (height in inches -60)}
4) 2) Set initial tidal volume at 8ml/kg PBW
5) 3) Add PEEP of 5 cm H2o
6) 4) Select the lowest Fio2 that achieves an Spo2 of 88-95%
7) 5) Reduce TV by 1ml/kg every 2 hours until TV= 6ml/kg
2nd STAGE
1. When TV= 6ml/kg, measure plateau pressure
2. If plateau pressure >30 cm H20, decrease TV in 1ml/kg until Ppl <30 cm H20
or VT = 4ml/kg
3rd STAGE:
1. Monitor ABG for respiratory acidosis
2. If pH=7.15-7.3-----> increase RR until pH>7.3 or RR=35 bpm
3. If pH is still <7.15, increase TV in 1ml/kg increaments until pH>7.15
OPTIMAL GOALS
1. TV=6ml/kg
2. Plateau pressure< 30 cm of H2o
3. Spo2= 88-95%
4. pH= 7.3-7.45
LUNG PROTECTION DUE TO HIGHER PEEP
Goal is to prevent the cyclic opening and closing of small airways
Higher PEEP levels have been associated with shorter duration of
mechanical ventilation and a borderline increase in survival in ARDS,
but only when Pao2/Fio2 ratio is < 200 mmHg
PEEP >5 cm H20 can be used to reduce the Fio2 to safer levels
Increase in PEEP can reduce the cardiac output
PERMISSIVE HYPERCAPNEA
Low tidal volume ventilation results in decrease in CO2 elimination
Due to benefits of low tidal volume, hypercapnia is allowed to persist
Pco2 of 60-70mm Hg and pH 0f 7.2-7.25 are safe for most patients
CONTRAINDIACTIONS TO PERMISSIVE HYPERCAPNIA
Increased intracranial pressure from any cause
Acute cerebrovascular accident
Acute myocardial ischemia
Severe pulmonary hypertension
Right ventricular failure
Uncorrected severe metabolic acidosis
Sickle cell anemia
Tricyclic antidepressants
Pateints taking beta-blockers
Pregnancy
RESCUE OR SALVAGE INTERVENTIONS
Prone positioning
High frequency oscillatory ventilation
Inhaled nitric oxide or prostacyclin
Pressure controlled inverse ratio ventilation
Recruitment maneuvers
Tracheal gas insufflation
Fluid management
Corticosteroids
Extracorporeal CO2 removal
Extracorporeal membrane oxygenation
PRONE POSTIONING
MECHANISMS
Increased functional residual capacity
Change in regional diaphragmatic motion
Perfusion redistribution
Improved clearance of secretions
Considered only in patients with PaO2/Fio2< 150
Done for atleast 16 hours a day
Adverse outcomes-
Pressure necrosis of nose, face and ears
Dislodgement of catheters and endotracheal tubes
Retinal ischemia and cardiac arrhythmias
HIGH FREQUENCY OSCILLATORY VENTILATION
Mode of ventilation with rapid pressure oscillations that generate
very small tidal volumes.
Commonly used in respiratory distress in new borns
RECRUITMENT MANEUVERS
Defined as application of CPAP aimed at recruiting or opening totally
or partially collapsed alveoli.
Alveoli are kept inflated during expiration using high level of PEEP
INHALED NITRIC OXIDE:
Vasodilates pulmonary capillaries and arterioles that serve ventilated
alveoli
FLUID MANAGEMENT:
Maintaining low left atrial filling pressure minimizes pulmonary edema
Target CVP < 4mm Hg
NEUROMUSCULAR BLOCKING AGENTS:
To promote ventilator synchrony
EXTRACORPOREAL LIFE SUPPORT
Based on hypothesis that more patients will survive if the lung is
allowed to recover from its injury by resting using extracorporeal
membrane oxygenation.
PROGNOSIS
CAUSES OF DEATH
Approximately one-third deaths occur in the first 7 days-underlying disease
or injury.
Majority die after 7 days- most common cause being sepsis
LONG TERM SEQUELAE
PULMONARY:
Usually recover maximal lung function within 6 months.
Diffusion capacity is mildly impaired, but it may return to normal by 2-5
years.
PHYSICAL AND NEUROMUSCULAR SEQUELAE
Low exercise capacity, weakness and decreased physical quality of life.
Abnormalities
Critical illness polyneuropathy
Critical illness myopathy
Entrapment neuropathy
Heterotopic ossification
COGNITIVE AND PSYCHOLOGICAL SEQUELAE
Cognitive dysfunction appears to be worse in first 3 months
Depression and anxiety
PTSD
REFERENCES
HARRISON’S PRINCIPLES OF INTERNAL MEDICINE ; 20TH EDITION
FISHMAN’S PULMONARY DISEASES AND DISORDERS; 5TH EDITION
MILLER’S ANESTHESIA; 9TH EDITION
PAUL MARINO’S ICU BOOK; 4TH EDITION
CROFTON AND DOUGLAS RESPIRATORY DISEASES; 5TH EDITION
