Acute Respiratory Distress Syndrome

CXR findings in ARDS: Diffuse bilateral alveolar infiltrates without cardiomegaly or pleural effusion, consistent with non-cardiogenic pulmonary oedema.

ARDS is an acute, diffuse, inflammatory lung injury leading to failure of gas exchange. It is characterised by:

• Hypoxaemia
• Decreased lung compliance
• Bilateral diffuse pulmonary infiltrates on chest X-ray
• Non-cardiogenic pulmonary oedema
• Normal PAWP: PAWP ≤ 18 mmHg
• PaO₂/FiO₂ < 26.7 kPa or < 300 mmHg

ARDS has two phases: an acute exudative phase and a later proliferative/fibrotic phase.

Acute exudative phase

1. Widespread destruction of the capillary endothelium, extravasation of protein-rich fluid into the interstitium and alveoli → interstitial and alveolar oedema
2. Migration of neutrophils into the lungs → Extensive release of cytokines, proteases, oxidants
3. Damage to the alveolar basement membrane → Fluid enters the alveoli → loss of surfactant, alveolar collapse, stiff lungs → Reduced lung compliance → Ventilation–perfusion mismatch and refractory hypoxaemia

Proliferative fibrotic phase

4. Fibroproliferation with organisation of lung tissue
5. If resolution does not occur → disordered collagen deposition → extensive fibrosis and long-term scarring → produce stiff, non-aerated lungs and impaired oxygenation

The Berlin criteria provides the diagnostic criteria for ARD based on timing, chest imaging, origin of oedema, and oxygenation and classifies the severity of the ARDS into mild, moderate or severe.

The patient must have all three of the following:

1. Onset: Within 1 week of a known clinical insult or new/worsening respiratory symptoms
2. Chest X-ray: Bilateral opacities not explained by effusions, lung/lobar collapse, or nodules
3. Pulmonary oedema not fully explained by cardiac failure or fluid overload (normal PAWP of ≤ 18 mmHg)

The severity is graded based on the 𝑃𝑎𝑂2/𝐹𝑖𝑂2 ratio, using at least 55 cmH₂O of PEEP:

• Mild: 𝑃𝑎𝑂2/𝐹𝑖𝑂2 ≤ 300 mmHg
• Moderate: 𝑃𝑎𝑂2/𝐹𝑖𝑂2 ≤ 200 mmHg
• Severe: 𝑃𝑎𝑂2/𝐹𝑖𝑂2 ≤ 100 mmHg 

• Sepsis
• Diffuse pulmonary infections: Vital, Mycoplasma, pneumocystis peneumonia, miliary tuberculosis
• Gastric aspiration
• Mechanical trauma including head injuries
• Burns
• Pancreatitis
• TRALI
• DIC
• Chemical injury: Heroin overdose, barbiturate overdose, acetylsalicylic acid, paraquat
• Hypersensitivity reactions to solvents and drugs
• Inhaled irritants
• Pulmonary contusions
• Fractures with fat embolism

• Admit to ICU and treat underlying cause, most commonly: sepsis, trauma, aspiration, pancreatitis, burns
• Low tidal volume: 6 mL/kg ideal body weight
• Aim for low plateau pressure: < 30 cmH₂O
• High respiratory rate to compensate
• PEEP 5–15 cmH₂O prevents alveolar collapse
• Prone positioning, recruits posterior lung units
• High-frequency oscillation ventilation → Low pressure with very high rate, prevents ventilator-induced lung injury
• ECMO for refractory severe ARDS
• Replace fluids but avoid overload; finer assessment may be necessary using a Swan Ganz catheter to measure the PAWP
• Furosemide 40-120 mg per 24 hours IV if fluid overloaded
• Consider low-dose dopamine as a renal arterial dilator, and dobutamine for its positive inotropic action, if falling BP or UOP despite adequate hydration
• Find and treat infection; empirical broad-spectrum antibiotics if sepsis suspected
• Avoid nephrotoxic agents
• Low-dose steroids may improve morbidity and mortality when used early
• Nutritional support with early enteral feeding
• Stress ulcer prophylaxis with PPI
• DVT prophylaxis with pLMWH

ALI and ARDS are on the same spectrum of inflammatory lung injury. ARDS is simply a more severe form of ALI with more profound hypoxaemia, worse compliance, higher mortality.

Pulmonary sequelae

• Impaired gas exchange with refractory hypoxaemia due to persistent V/Q mismatch
• Decreased lung compliance: “Stiff lungs” from fibrosis and scarring
• Pulmonary hypertension from hypoxic vasoconstriction and vascular remodelling

Structural lung changes

• Fibrosis and scarring of previously injured lung regions
• Persistent non-aerated lung segments

Functional limitations

• Reduced exercise tolerance
• Chronic breathlessness
• Fatigue

Systemic sequelae (important in viva)

• ICU-acquired weakness
• Neuromuscular wasting
• Psychological effects: PTSD, depression, anxiety
• Cognitive impairment after prolonged ICU stay