A. Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) represent a continuum of severity for the same pathologic condition of acute, diffuse alveolar damage (DAD) and pathophysiologically are defined by the presence of increased capillary permeability, pulmonary edema, and refractory hypoxemia due to progressively more severe ventilation-perfusion mismatch and right-to-left shunting.

B. ARDS has an estimated annual incidence in the United States of approximately 79 cases per 100,000 person-years.

C. As of June 2012, the clinical definition ALI and ARDS has changed. This new definition addresses some of the limitations of the previous classification (American-European Consensus Conference, 1994) including clarification of exclusion of hydrostatic edema and provides an increased accuracy of prediction for mortality and duration of mechanical ventilation. There are 4 components of the new Berlin Classification of ARDS.

1. Timing: development of ARDS within 1 week of a known clinical insult or appearance of new or worsening of previous respiratory symptoms.

2. Chest imaging: bilateral opacities not fully explained by effusions, lobar/lung collapse, or nodules. These findings may be demonstrated on either computed tomography (CT) scan of the chest or simple chest radiograph (CXR).

3. Origin of pulmonary edema: Due to the decline in use of pulmonary artery catheters, the pulmonary artery wedge pressure criterion <18 mm Hg was removed from the definition. If there is no risk factor identifiable for ARDS, an objective evaluation with echocardiogram is required to assist in elimination of a possible hydrostatic edema.

4. Oxygenation: ARDS has three categories based on severity of hypoxemia.

a. Mild ARDS (formerly ALI): 200 mm Hg < PaO₂/FIO₂ < 300 mm Hg.

b. Moderate ARDS: 100 mm Hg < PaO₂/FIO₂ < 200 mm Hg.

c. Severe ARDS: <100 mm Hg PaO₂/FIO₂.

A. ARDS may be caused by conditions eliciting lung injury directly (gastric aspiration, pulmonary contusion, pneumonia, or other toxic inhalational injury) and those that induce lung injury indirectly (sepsis, trauma, burns, drug ingestion, pancreatitis, plasma-containing blood products causing transfusion-related acute lung injury [TRALI]). Indirect mechanisms are responsible for most cases of ARDS.

B. Systemic inflammatory response syndrome (SIRS) or sepsis syndrome is responsible for up to 50% of ARDS cases.

C. The risk of ARDS increases as the number of potential causes (risk factors) increases.

A. The initial pathology of ARDS is defined by DAD including interstitial and proteinaceous intra-alveolar edema and fibrin deposition. Alveolar flooding typically occurs in only some alveoli; others appear to be normal.

B. Deposition of hyaline membranes within alveoli and degenerative cellular changes occur within 1 to 2 days of the initial insult.

C. Most of the alveolar edema usually resolves after approximately 1 week. Some patients seem to resolve lung injury with little if any fibrosis, whereas others go on to develop severe parenchymal fibrosis. The reason that outcomes are so variable is unknown.

D. The extensive right-to-left shunt in ARDS (up to 25% to 50% of the cardiac output) results from persistent perfusion of atelectatic and fluid-filled alveoli.