Description

• Acute respiratory distress syndrome (ARDS) is defined as the onset of acute hypoxemia within 7 days of a known clinical insult or new or worsening respiratory symptoms with bilateral opacities (patchy, diffuse, or homogenous) consistent with pulmonary edema on imaging.
• Severity of ARDS is measured with a ratio of partial pressure of arterial oxygen (PaO₂) to fraction of inspired oxygen (FiO₂) at a positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) of at least 5 cm H₂O.
  • Mild—200 mm Hg < PaO₂/FiO₂ ≤300 mm Hg
  • Moderate—100 mm Hg < PaO₂/FiO₂ ≤200 mm Hg
  • Severe—PaO₂/FiO₂ ≤100 mm Hg
• Synonym(s): acute lung injury; increased permeability pulmonary edema; noncardiac pulmonary edema
• Systems affected: pulmonary, cardiovascular

Epidemiology

Incidence

• Incidence of ARDS is highly variable and underrecognized.
• Incidence rate varies from 10 to 86 cases per 100,000 persons.

Etiology and Pathophysiology

• ARDS is a response to direct or indirect alveolar injury leading to diffuse alveolar damage.
  • Direct
    • Pneumonia (bacterial, viral, fungal, or opportunistic)
    • Aspiration of gastric contents
    • Near drowning
    • Pulmonary contusion
    • Inhalation injury
  • Indirect
    • Sepsis (nonpulmonary)
    • Shock
    • Transfusion of blood products
    • Major burn injury
    • Nonthoracic trauma
    • Drug overdose
    • Cardiopulmonary bypass
    • Reperfusion edema after lung transplant or embolectomy
• Progression of the diffuse alveolar damage in ARDS is divided into three phases.
  • Exudative phase—The initial highly inflammatory phase when alveolar macrophages are activated due to lung injury, leading to complement activation, release of proinflammatory mediators, and activation of neutrophils. This causes epithelial–endothelial barrier disruption, leading to intra-alveolar and extra-alveolar flooding with fluid. This is followed by hyaline membrane formation leading to alveolar collapse.
  • Proliferative phase—The second phase characterized by fibroblasts, myofibroblasts, and alveolar epithelial cell (ACE) II mediated repair. Formation of new matrix, differentiation into ACE I, and formation of cellular junctions begins which leads to expression of aquaporin and ion channels, aiding in the reabsorption of fluid.
  • Fibrotic phase—The final phase, not experience by every patient, is characterized by prolonged mechanical ventilation and associated with increased mortality.

Genetics
No single gene has been identified for clinical use.

Risk Factors

Increased levels of markers of systemic inflammation have been associated with adverse outcomes.

General Prevention

Early identification of sepsis with appropriate resuscitation and antibiotic use

Commonly Associated Conditions

• Pneumonia, sepsis, and aspiration of gastric contents cause 85% of ARDS cases.
• Other causes can include:
  • Trauma
  • Burns
  • Cardiothoracic surgery
  • Pancreatitis
  • Inhalational injuries and near drownings
  • Transfusion-related acute lung injury (TRALI)
  • Shock
  • Medication toxicity