SN3 SHORT NOTE 5M ★ High-yield

Describe acute respiratory distress syndrome with its causes, pathogenesis and morphology.

Pathology · 2nd Professional — Para-Clinical

Definition

Acute respiratory distress syndrome (ARDS) is acute, diffuse, inflammatory lung injury causing increased alveolar-capillary permeability, non-cardiogenic pulmonary oedema and severe hypoxaemia refractory to oxygen. Its histological counterpart is diffuse alveolar damage.

Berlin definition

Acute onset within 1 week of a known insult
Bilateral opacities on chest imaging, not fully explained by effusion, collapse or nodules
Not fully explained by cardiac failure or fluid overload — hence the term non-cardiogenic
Impaired oxygenation — PaO2/FiO2 ratio 300 or less (mild 200–300, moderate 100–200, severe under 100)

Causes

Direct lung injury	Indirect (systemic) injury
Pneumonia	Sepsis — the commonest cause overall
Aspiration of gastric contents	Severe trauma with shock; multiple fractures
Inhalation of smoke or toxic gases	Acute pancreatitis
Near-drowning	Massive transfusion; TRALI
Pulmonary contusion	Burns; DIC; drug overdose; fat embolism
Oxygen toxicity; radiation	Cardiopulmonary bypass; eclampsia

Pathogenesis

The insult activates alveolar macrophages → Release of IL-1, IL-8 and TNF → neutrophils are recruited and sequestered in the pulmonary capillaries → They release proteases, reactive oxygen species and leukotrienes → Damage to both the endothelium and the alveolar epithelium → Increased permeability → protein-rich exudate floods the alveoli → Loss of type II pneumocytes → surfactant deficiency → widespread collapse → hyaline membranes form from fibrin and necrotic cell debris → Severe ventilation–perfusion mismatch and shunting → refractory hypoxaemia

Morphology — Diffuse Alveolar Damage

Phase	Timing	Features
Exudative	First week	Heavy, red, boggy, airless lungs; congestion, interstitial and intra-alveolar oedema, fibrin, and the characteristic hyaline membranes lining the alveolar ducts; necrosis of type I pneumocytes
Proliferative (organising)	1–3 weeks	Type II pneumocyte hyperplasia attempting repair; fibroblast proliferation; organisation of the exudate
Fibrotic	After 3–4 weeks	Interstitial fibrosis; honeycombing in survivors

CLINICAL PEARL

ARDS and cardiogenic pulmonary oedema look alike on the radiograph and are treated in opposite ways. ARDS is a permeability problem: the pulmonary capillary wedge pressure is normal, the fluid is protein-rich, and diuresis alone does not fix it. Cardiogenic oedema is a pressure problem: the wedge pressure is raised, the fluid protein-poor, and diuretics work. Getting this wrong is dangerous in both directions.

Applied Aspects

Treat the underlying cause — nothing else alters the outcome; source control in sepsis is the priority
Lung-protective ventilation saves lives — low tidal volume (about 6 mL/kg predicted body weight) and limited plateau pressure, accepting some hypercapnia. Large tidal volumes cause ventilator-induced lung injury by overdistending the few remaining normal alveoli
PEEP recruits collapsed alveoli and improves oxygenation
Prone positioning improves survival in severe ARDS by improving ventilation–perfusion matching
Conservative fluid management once shock is corrected shortens ventilation
Mortality remains about 30 to 40%, usually from multi-organ failure rather than from hypoxaemia; survivors may have long-term impairment of lung function and quality of life

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