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Introduction

Acute respiratory distress syndrome (ARDS) is a life-threatening condition marked by widespread alveolar damage, inflammation, and noncardiogenic pulmonary edema.  It was first described in Vietnam War–era combat soldiers who survived their initial injury (eg, burns, trauma) but later developed bilateral alveolar infiltrates and severe hypoxemia in the subsequent hours to days.

Pathophysiology and pathology

ARDS involves an identifiable clinical event that induces a massive inflammatory response ( Figure 1).  Damage can originate from within the lungs (direct) or outside of the lungs (indirect).

  • Direct lung injury, which includes pneumonia, inhalation (eg, smoke), and aspiration (eg, gastric contents)
  • Indirect lung injury, which includes trauma, sepsis, and pancreatitis

The resulting inflammation causes disruption of the alveolar air-blood barrier (endothelial leakiness, epithelial sloughing), neutrophil migration/activation, and exudation of fluid into the airspaces.  Microscopically, the alveoli are flooded with proteinaceous debris and necrotic cells and are lined with a fibrinous (hyaline) membrane (

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