Noncardiogenic Pulmonary Edema: A Complication of Salicylate Toxicity

Abstract

The course of patients with salicylate intoxication is commonly complicated by non-cardiogenic pulmonary edema. Salicylate intoxication causes pulmonary edema through an increase in the alveolar-capillary membrane permeability to fluids and proteins, although the mechanism by which this occurs has not been determined. Salicylate pulmonary edema, a potentially lethal disorder, especially when the underlying salicylism is undiagnosed or when its diagnosis is delayed, develops most commonly in persons who are middle-aged, smoke cigarettes, and have salicylate intoxication from chronic use of aspirin compounds. The presence of respiratory failure, in addition to the patients' depressed mental functioning, which often prevents their giving a clear drug history, can obscure the presence of salicylate intoxication. Clinical clues of salicylate toxicity are proteinuria, prolonged prothrombin time, and a mixed acid-base disturbance (metabolic acidosis and respiratory alkalosis). A serum salicylate level above 40 mg/dl provides the only certain basis for the diagnosis of salicylate pulmonary edema. In addition, a ferric chloride test of the urine can quickly detect the presence of salicylates. Many patients have been successfully managed by forced alkaline diuresis, and those in severe respiratory failure have required intubation and mechanical ventilation with PEEP. Most patients survive, with clearing of the chest radiograph within 1-7 days and extubation within 4-7 days.