The Adult Respiratory Distress Syndrome: Mechanisms and Management

Abstract

The term “adult respiratory distress syndrome”, abbreviated ARDS, was coined less than 20 years ago to describe adult patients with a specific form of acute respiratory failure (1). As implied by the name, ARDS is a syndrome characterized by a group of clinical and pathophysiologic features which indicate severe lung injury that results from a variety of underlying disease processes. The key pathophysiologic feature that differentiates ARDS from other forms of acute respiratory failure in adults is diffuse injury to the alveolar capillary membrane (2). The injury can result from insults delivered via the airway (as in gastric acid aspiration or diffuse bacterial pneumonia), via the bloodstream (as in ARDS associated with gram negative bacteremia, or endotoxemia, resulting from an infectious focus distant from the lung), or via both routes. There is no single clinical feature that defines the syndrome of ARDS. Furthermore, a laboratory test that identifies diffuse alveolar capillary injury, and differentiates it from other disease processes, does not exist. Therefore the syndrome is recognized by a constellation of clinical and pathophysiologic findings (1,3) (Table 1). Each of the features listed in Table 1 can occur in association with other causes of acute respiratory failure, but together they define the clinical syndrome of ARDS. In addition to the classic findings listed in Table 1, pulmonary hypertension is a common feature in patients with this syndrome (16,17).