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) ≤300 mmHg; (3) absence of elevated left atrial pressure; and (4) acute onset within 1 week of a clinical insult or new or worsening respiratory symptoms. Although many medical and surgical conditions can cause ARDS, most cases (>80%) result from sepsis, 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, pancreatitis, and overall severity of critical illness.
Clinical Course and Pathophysiology 
There are three phases in the natural history of ARDS:
- 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 opacities consistent with pulmonary edema. The differential diagnosis is broad, but common alternative etiologies to consider are cardiogenic pulmonary edema, bilateral 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.
- 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.
- 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.
| TREATMENT | ||
ARDSProgress in recent therapy has emphasized the importance of general critical care of pts with ARDS in addition to lung protective ventilatory strategies. General care requires treatment of the underlying medical or surgical problem that caused lung injury, minimizing iatrogenic complications, prophylaxis to prevent venous thromboembolism and GI hemorrhage, prompt treatment of nosocomial infections, and adequate nutritional support. An algorithm for the initial management of ARDS is presented in Fig. 16-1. Algorithm for the Initial Management of ARDS. MECHANICAL VENTILATORY SUPPORTPts with ARDS typically require mechanical ventilatory support due to hypoxemia and increased work of breathing. A substantial improvement in outcomes from ARDS occurred with the recognition that mechanical ventilator-related overdistention of normal lung units with positive pressure can produce or exacerbate lung injury, causing or worsening ARDS. Currently recommended ventilator strategies limit alveolar distention but maintain adequate tissue oxygenation. It has been clearly shown that low tidal volumes (≤6-mL/kg predicted body weight) provide reduced mortality compared with higher tidal volumes (12-mL/kg predicted body weight). In ARDS, alveolar collapse can occur due to alveolar/interstitial fluid accumulation and loss of surfactant, thus worsening hypoxemia. Therefore, low tidal volumes are combined with the use of positive end-expiratory pressure (PEEP) at levels that strive to minimize alveolar collapse and achieve adequate oxygenation with the lowest required FIO2. Use of PEEP levels higher than necessary to optimize oxygenation has not been proven to reduce ARDS mortality. Measurement of esophageal pressures to estimate transpulmonary pressure may help to identify an optimal level of PEEP. Other techniques that may improve oxygenation include placing the pt in the prone position; however, experience in repositioning critically ill pts is required. ANCILLARY THERAPIESPts with ARDS have increased pulmonary vascular permeability leading to interstitial and alveolar edema. Therefore, they should receive IV fluids only as needed to achieve adequate cardiac output and tissue O2 delivery as assessed by urine output, acid-base status, and arterial pressure. A randomized, placebo-controlled clinical trial suggested that neuromuscular blockage with cisatracurium for 48 h could potentially reduce mortality in severe ARDS. Lung-replacement therapy with extracorporeal membrane oxygenation (ECMO) may have utility in selected adult pts with severe ARDS. There is not convincing evidence currently to support the use of glucocorticoids or nitric oxide in ARDS. |
Mortality from ARDS has declined with improvements in general critical care treatment and with the introduction of low tidal volume ventilation. Current mortality from ARDS is 35-46%, with most deaths due to sepsis and nonpulmonary organ failure. Increased risk of mortality from ARDS is associated with advanced age, preexisting organ dysfunction (e.g., chronic conditions of liver disease, alcohol abuse, immunosuppression, or renal disease). Increased mortality has also been associated with ARDS related to direct lung injury (e.g., pneumonia, pulmonary contusion, and aspiration) compared with indirect lung injury (e.g., sepsis, trauma, and pancreatitis). Most surviving ARDS pts do not have significant long-term pulmonary disability.