Chapter 14: Acute Respiratory Distress Syndrome

DEFINITION AND ETIOLOGY

Acute respiratory distress syndrome (ARDS) develops rapidly and includes severe dyspnea, diffuse pulmonary infiltrates, and hypoxemia; it typically causes respiratory failure. Key diagnostic criteria for ARDS include (1) diffuse bilateral pulmonary infiltrates on CXR; (2) PaO₂ (arterial partial pressure of oxygen in mmHg)/FIO₂ (inspired O₂ fraction) ≤200 mmHg; and (3) absence of elevated left atrial pressure (pulmonary capillary wedge pressure ≤18 mmHg). Acute lung injury is a related but milder syndrome, with less profound hypoxemia (PaO₂/FIO₂ ≤300 mmHg), that can develop into ARDS. Although many medical and surgical conditions can cause ARDS, most cases (>80%) result from sepsis, bacterial pneumonia, trauma, multiple blood transfusions, gastric acid aspiration, and drug overdose. Individuals with more than one predisposing factor have a greater risk of developing ARDS. Other risk factors include older age, chronic alcohol abuse, metabolic acidosis, and overall severity of critical illness.

CLINICAL COURSE AND PATHOPHYSIOLOGY

There are three phases in the natural history of ARDS:

1. Exudative phase: Characterized by alveolar edema and neutrophil inflammation, with subsequent development of hyaline membranes from diffuse alveolar damage. The alveolar edema, which is most prominent in the dependent portions of the lung, causes atelectasis and reduced lung compliance. Hypoxemia, tachypnea, and progressive dyspnea develop, and increased pulmonary dead space can also lead to hypercarbia. Respiratory failure frequently develops during this phase. CXR reveals bilateral, diffuse alveolar, and interstitial opacities. The differential diagnosis is broad, but common alternative etiologies to consider are cardiogenic pulmonary edema, pneumonia, and alveolar hemorrhage. Unlike cardiogenic pulmonary edema, the CXR in ARDS rarely shows cardiomegaly, pleural effusions, or pulmonary vascular redistribution. The exudative phase duration is typically up to 7 days in length and usually begins within 12–36 h after the inciting insult.

2. Proliferative phase: This phase typically lasts from approximately days 7 to 21 after the inciting insult. Although most pts recover, some will develop progressive lung injury and evidence of pulmonary fibrosis. Even among pts who show rapid improvement allowing removal of mechanical ventilatory support, dyspnea and hypoxemia often persist during this phase.

3. Fibrotic phase: Although the majority of pts recover within 3–4 weeks of the initial pulmonary injury, some experience progressive fibrosis, necessitating prolonged ventilatory support and/or supplemental O₂. Increased risk of pneumothorax, reductions in lung compliance, and increased pulmonary dead space are observed during this phase.