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Acute respiratory distress syndrome (ARDS)

{Acute lung injury = Shock lung = Diffuse Alveolar Damage}


(Non cardiogenic pulmonary oedema)

  1. ARDS is a clinical syndrome caused by diffuse alveolar capillary damage.
  2. It is characterized clinically by the rapid onset of severe life-threatening respiratory insufficiency, cyanosis, and severe arterial hypoxemia that is refractory to oxygen therapy and that may progress to extrapulmonary multisystem organ failure.
  3. Chest radiographs shows diffuse alveolar infiltration.
  4. Diffuse alveolar damage (DAD) (LQ 2012) is the histologic manifestation. (Robins, 7th edi, pg no 715)
  5. ARDS, or acute lung injury, caused by direct lung injury or occur secondary to severe systemic illness.
  6. Lung damage and release of inflammatory mediator cause increased capillary permeability and non-cardiogenic pulmonary edema often accompanied by multiorgan failure. 

Causes (Ref. Hari. 18th ed., Table 268.1 Pg- 2205)


Pulmonary: (Direct lung injury)
  1. Pneumonia;             
  2. Gastric aspiration         
  3. Toxic gas inhalation         
  4. Lung injury;
  5. Vasculitis;                
  6. Lung Contusion.

: (Indirect lung injury)

  1. Shock;
  2. Septicaemia;
  3. Haemorrhage;
  4. Multiple transfusions:
  5. DIC;
  6. Pancreatitis;
  7. Acute liver failure;
  8. Trauma Q;
  9. Head injury;
  10. Malaria Q;
  11. Fat embolism;
  12. Burns;
  13. Obstetric events Q (eclampsia; amniotic fluid embolus);
  14. Drugs/toxin (heroin) Q.
  15. Cardiopulmonary bypass with heart lung machine

Clinical physiology

  1. Clinical history of insult known to cause ARDS there is sudden onset of dyspnea
  • Accumulation of proteinaceous pulmonary edema in the interstitium.

The diagnosis of ARDS is made on clinical grounds on the following criteria.

  1. Acute onset
  2. Bilateral pulmonary infiltrate on chest X-ray.
  3. Pulmonary artery wedge pressure < 18mm/Hg (i.e. LA pressure is normal).
  4. A partial pressure of arterial oxygen to fractional inspired oxygen concentration (PaO2/FiO2) <200mmHg.


Extra Edge:

Left atrial (LA) pressure is normal in ARDS, (LA pressure is high in cardiac pulmonary edema) (MCQ)


Pathophysiology of ARDS ­

  1. Diffuse alveolar damage.
  2. Reduced surfactant (Injury to type II pneumocytes) 
  3. Increased permeability of alveolar capillary membrane.
  4. Due to damage to the normally tight alveolar barrier, edema fluid rich in protein, accumulates, in the interstitial and alveolar spaces (non cardiogenic pulmonary edema).
  5. The proteins then aggregate in air spaces with cellular debris and dysfunctional pulmonary surfactant to form hyaline membrane whorls.
  6. It leads to O2 diffusion from alveolus to capillary but CO2 being a water soluble gas can diffuse from capillary to alveolus. It leads to acute type I respiratory failure.
  7. Pulmonary edema + Hyaline membrane (fibrin + coagulated cell debris)
  8. Reduced compliance (stiff lung) (LQ 2012)
  9. Diminished tidal volume
  10. Hypoxemia (Worsened gas exchange d/t pulmonary shunting) (LQ 2012)
  11. Hypocapnia (CO2 washout) (LQ 2012)
Extra Edge: Pulmonary Shunting:
  1. Significant shunt occurs in ARDS where pulmonary arterial blood shunts past flooded and collapsed Alveoli into pulmonary veins.
  2. Shunting of the poorly oxygenated venous blood into arterial circulation significantly contributes to arterial hypoxemia.
  3. Reduced compliance: Reduced lung compliance and stiff lung are characteristic features of ARDS
  4. Hypoxemia: Arterial hypoxemia is a characteristic feature of ARDS and may be caused by reduced lung compliance and pulmonary shunting.


HAPE: (High Altitude pulmonary edema)

  1. Pulmonary vasoconstriction is as the prime mechanism
  2. May occur in both acclimatized and unacclamatized individuals
  3. HAPE is exacerbated by exercise and is associated with high cardiac output. 

Clinical features

  1. Tachypnea; tachycardia; peripheral vasodilatation.
  2. There may not be any clinical sign on chest auscultation.
  3. 'Acute Lung Injury' (ALI) is a milder disorder than ARDS and is characterized by PaO2/FiO2 of less than 300 mmHg.
  4. ALI is a less severe disorders than ARDS but has the potential to evolve into ARDS. ALI can be differentiated from ARDS by the arterial PO2/FiO2 (Inspiratory O2 fraction) ratio. 
(Ref. Hari. 18th ed.,  Table 268.2 Pg- 2205)

Diagnostic Criteria



PaO2 / FiO2

300 mm Hg

200 mm Hg




Chest Radiograph

Bilateral alveolar or interstitial infiltrates

Bilateral alveolar or interstitial infiltrates

Absence of left atrial hypertension

PCWP â 18 mmHg

No Clinical evidence of increased left atrial pressure

PCWP â 18 mmHg

No Clinical evidence of increased left atrial pressure


Extra Edge:
  1. ALI is associated with a PaO2/FiO2 300
  2. Bilateral alveolar interstitial infiltrates on Radiographs along with, hypoxemia and pulmonary shunting due to intra alveolar filling are characteristic features of both ALI and ARDS.


Important Points:


Diagnostic criteria:

  1. Acute onset.
  2. CXR: bilateral infiltrates.
  3. PCWP <18mmHg or a lack of clinical congestive heart failure.
  4. Total thoracic compliance <30ml/cm H2O.  

Important Points:


Management Admit to ICU; give supportive therapy; treat the underlying cause.

  1. Respiratory support In early ARDS, continuous positive airway pressure (CPAP Q) with 40-60% oxygen may be adequate to maintain oxygenation. But most patients need mechanical ventilation Q.  

Complications of endotracheal intubation and positive pressure mechanical ventilation include:


Pulmonary complications

Gastrointestinal complications


1. Barotrauma

2. Nosocomial pneumonia

3. Oxygen toxicity

4. Tracheal stenosis

5. Deconditioning of respiratory muscles

1. Stress ulceration

2. Mild to moderate cholestasis



1. Malnutrition

2. Decubitus ulcers

3. Venous thrombosis

4. Depression

  1. For Sepsis Give antibiotic
  2. Nutritional support: with high fat, antioxidant formulations.
  3. Steroids protect those at risk of fat embolization and with pneumocystosis and may improve outcome in subacute ARDS.
  4. Prognosis Overall mortality is 50%-75%.

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