Emily K. Thomas,     Philadelphia, Pennsylvania

Lori S. Waddell,     Philadelphia, Pennsylvania

Risk Factors

ARDS has many potential causes. It may result either from direct pulmonary insult or from a generalized inflammatory response such as systemic inflammatory response syndrome (SIRS) or sepsis. Box 9-1 lists many of the risk factors proposed in dogs, but this list is not exhaustive. Sepsis of either pulmonary or nonpulmonary origin is the most common predisposing cause of ARDS identified in dogs. Risk factors have not been characterized in cats, but the few available reports suggest similar underlying etiologies. A single patient may have multiple precipitating causes.

Pathophysiology

The pathogenesis of ARDS is similar regardless of the underlying etiology and is characterized by an overwhelming inflammatory process that leads to epithelial damage in the lung. Macrophages, neutrophils, and proinflammatory cytokines such as tumor necrosis factor and interleukin-1β interact to cause alveolar and vascular epithelial injury.

Three overlapping phases of inflammation are typically described. The exudative phase begins as a diffuse vascular leak syndrome, with infiltration of erythrocytes and inflammatory cells and effusion of protein-rich fluid into the alveoli; progressive pulmonary edema and hemorrhage result. Activation of inflammatory cells causes release of harmful mediators that contribute to ongoing lung injury. Synthesis of surfactant is impaired, with consequent alveolar collapse. Hyaline membranes (organized proteinaceous debris) form within the alveoli.

In the proliferative phase that follows, a proliferation of type II pneumocytes and fibroblasts occurs in an attempt to repair damaged tissue. This leads to interstitial fibrosis. Lastly, the fibrotic phase is characterized by collagen deposition and the development of varying degrees of fibrosis before eventual resolution.

Historical Findings and Clinical Features

The hallmark sign of ARDS is an acute history of severe respiratory distress. It is most commonly seen in intensive care unit patients with other underlying diseases but may affect any animal with a predisposing risk factor. The earliest signs, tachypnea and increased respiratory effort, rapidly progress to severe respiratory distress. Signs may develop within hours or up to 4 days after an inciting event.

Clinical examination usually reveals severe respiratory distress with cyanosis. Dogs may expectorate a pink, foamy fluid from the lungs. In the early stages harsh airway or loud bronchial sounds are heard on thoracic auscultation, but these rapidly progress to crackles. If the animal is intubated, sanguineous fluid may drain from the endotracheal tube. Tachycardia is common secondary to severe hypoxemia, with poor oxygen delivery to the tissues. Evidence of other underlying or systemic disease may be found.

Diagnosis

In small animal veterinary medicine four criteria are required to diagnose ARDS (Wilkins et al, 2007). Respiratory distress should be acute in onset (< 72 hours), with one or more known risk factors present (see Box 9-1). Evidence of inefficient gas exchange is required, together with evidence of pulmonary capillary leak without increased pulmonary capillary pressure. Evidence of pulmonary inflammation is an optional fifth criterion. Other differential diagnoses should be considered if the above criteria are not met in a patient (Box 9-2).

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