Background and definitions

The acute respiratory distress syndrome (ARDS) is an inflammatory lung condition with associated noncardiogenic pulmonary edema and impairment of gas exchange. ARDS is a major cause of respiratory failure in patients in the intensive care unit (ICU). In the perioperative period, patients who are undergoing major surgical procedures, who are seriously ill, or who aspirate are susceptible to developing ARDS. In 2012, ARDS was redefined according to the Berlin definition (Table 227-1) in an effort to overcome some of the inadequacies of the previously used American-European Consensus definition, which dated from 1994 (Table 227-2). Compared with the prior definition, the Berlin definition defines “acute,” clarifies the methods to exclude hydrostatic edema, adds minimal ventilator-setting requirements, drops the term “acute lung injury,” and classifies ARDS into three categories of severity.

ARDS may result from a direct insult to the lung, such as from pneumonia or from aspiration of gastric contents. Direct injury may also be related to pulmonary contusion, fat embolus, inhalation or drowning injury, or transfusion of blood products. Secondary ARDS occurs as part of a systemic illness or may be related to trauma and may be thought of as the lung manifestation of the systemic inflammatory response, just as oliguria, mental status changes, and hypotension are manifestations of sepsis in the kidney, brain, and cardiovascular systems, respectively.

ARDS manifests as noncardiogenic pulmonary edema with hypoxemia. An alteration in the relationship between the alveolar epithelium and the capillary endothelium allows influx of protein-rich edema fluid into the alveoli. Injury to type II alveolar cells results in disruption of epithelial fluid transport, impairs removal of alveolar fluid, and alters surfactant production. These changes lead to abnormalities in gas exchange. Pulmonary neutrophils play a key role in the generation of an inflammatory response, and this inflammatory process may be augmented by inappropriate mechanical ventilation (see later discussion).

A prospective study in 1999 to 2000 estimated an incidence of ARDS in the United States of almost 200,000 adult patients per year. The incidence appears to have decreased over the subsequent decade, probably because of the use of lung-protective ventilation, more conservative use of blood products, and a reduction in nosocomial infections. ARDS remains, however, a major ICU disease entity. Approximately 10% to 15% of patients admitted to the ICU and up to 20% of those requiring mechanical ventilation have ARDS.

ARDS has been divided into a number of pathologic stages. Diffuse alveolar damage seen in the initial “exudative” stage gives way over the first week to a “proliferative” stage, during which type II alveolar cells predominate and interstitial inflammation develops. A later “fibrotic” stage occurs in some patients, during which normal lung architecture is disrupted by deposition of collagen.

Clinical manifestations of ARDS include rapidly worsening dyspnea, tachypnea, and hypoxemia with diffuse rales on lung auscultation. Arterial blood gas analysis shows an elevated alveolar-arterial O₂ gradient with severe hypoxemia, consistent with right-to-left shunt physiology. Pulmonary hypertension may develop. Although a respiratory alkalosis may be present in early ARDS, respiratory acidosis usually develops later in the course of the condition. Diffuse “fluffy” bilateral infiltrates are apparent on chest radiography. A computed tomography scan will show areas of alveolar filling, consolidation, and atelectasis, especially in the dependent lung zones. Despite the heterogeneity of the computed tomographic findings, the whole lung is involved in the inflammatory process, and bronchoalveolar lavage of even the relatively spared areas will show inflammatory changes.

Patients with ARDS almost invariably need mechanical ventilation, which is the mainstay of supportive therapy. Noninvasive ventilation, such as continuous positive airway pressure or biphasic positive airway pressure, may be sufficient in some patients, but most patients with moderate or severe ARDS require tracheal intubation. Although oxygenation tends to improve over the course of the first few days as pulmonary edema resolves, the presence of continued hypoxemia, high minute ventilation requirements, and poor lung compliance necessitate prolonged ventilation in a significant number of patients. Large doses of sedative agents and, on occasion, the use of infusions of neuromuscular blocking agents may be required to enable appropriate ventilation of the patient with ARDS. Current guidelines (2012) from the Society of Critical Care Medicine, based on the results of one prospective study, advocate a short course (≤48 h) of a neuromuscular blocking agent for septic patients with ARDS.

Ventilator-associated lung injury is a major concern (Figure 227-1). Inspired gas flows preferentially to relatively uninvolved alveoli, potentially causing overdistention and lung injury due to volutrauma and barotrauma. Constant opening and closing of derecruited lung units can lead to shear stress (atelectrauma). These physical forces can lead to an increase in the injurious inflammatory response (biotrauma). Laboratory investigations have suggested that a “safe zone” exists on the pulmonary pressure-volume curve defined by lower and upper “inflection points” in which ventilation should occur. At the lower end of the pressure-volume curve, lung units are susceptible to derecruitment and atelectasis, and, at the upper end of the pressure-volume curve, overdistention leads to lung injury (Figure 227-2).