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(See also Overview of Diving Injuries.)

Immersion pulmonary edema has become more widely recognized over the past 2 decades. Immersion pulmonary edema is not related to pulmonary barotrauma or decompression sickness. Instead, in susceptible individuals it involves development of hemodynamic pulmonary edema due to excessively high pulmonary vascular pressures due to blood redistribution from the periphery into the pulmonary vessels. Risk factors include exposure to cold water, a history of hypertension, lung disorders, and other cardiac disorders that involve abnormal left ventricular systolic or diastolic function (including valvular disorders and cardiomyopathy). This syndrome occurs in divers and, when occurring at the surface, most commonly in competitive open water swimmers.

Severe dyspnea develops, usually while the diver is at depth. Divers usually ascend rapidly and have cough, frothy sputum, scattered crackles throughout both lung fields, and sometimes cyanosis. Hypoxia is often present and may result in death.

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 (including Takotsubo cardiomyopathy) have been reported as causes. 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.