Immersion Pulmonary Edema
(Swimming-Induced Pulmonary Edema; SIPE)
(See also Overview of Diving Injuries.)
Immersion pulmonary edema has become more common over the past 2 decades. Abnormal left ventricular systolic or diastolic function may contribute. Immersion pulmonary edema is not related to pulmonary barotrauma or decompression sickness. Risk factors include exposure to cold water, a history of hypertension, lung disorders, and other cardiac disorders that could contribute to elevated left ventricular end-diastolic pressure (including valvular disorders and cardiomyopathy). This syndrome occurs in divers and especially competitive open water swimmers.
Severe dyspnea develops. Divers usually ascend rapidly and have cough, frothy sputum, scattered crackles throughout both lung fields, and sometimes cyanosis. Hypoxia is often present.
Chest x-ray shows typical pulmonary edema. Cardiac evaluation usually shows normal right and left ventricular function and normal coronary arteries, but wall motion abnormalities, valvular dysfunction, and cardiomyopathies have been reported. Diastolic dysfunction can be documented by echocardiography.
Oxygen administration to treat hypoxemia, and sometimes inhaled beta-2 agonists are usually sufficient to allow immersion pulmonary edema to resolve. Diuretics are rarely required. Mechanical ventilation may be necessary for severe cases. Recompression therapy is not indicated.
Prevention efforts aim to identify people at high risk. Individuals who have experienced immersion pulmonary edema should be screened for predisposing conditions such as hypertension, valvular heart disease, cardiomyopathy, and lung disorders. Silent coronary artery disease should be considered in individuals at risk.