Immersion pulmonary edema (IPE) in a new, healthy diver


A 56-year-old male diver was participating in a shore dive for his entry-level diving certification. He had no significant medical history except borderline hypertension which was regularly monitored, and he maintained good physical fitness. Water temperature was 65°F (18°C) and he was wearing a 7mm wetsuit, gloves and a hood. The diver and his group swam approximately 50 yards (46 meters) alternating between regulator and snorkel. Upon reaching the surface buoy he experienced severe dyspnea (shortness of breath) and fatigue. The diver communicated this to the divemaster who then towed him to shore. During the tow the diver developed hemoptysis (coughing up blood) and audible respiratory crackles. Within approximately ten minutes of exiting the water his symptoms began to improve. The diver rested for two hours prior to driving home. Cough and hemoptysis persisted for an additional six hours and crackles lasted until the next day. Lung soreness lingered for approximately one week. Medical follow-up revealed no cardiopulmonary abnormalities and immersion pulmonary edema was suspected.


Immersion pulmonary edema (IPE), or swimming-induced pulmonary edema, is a condition that presents with dyspnea, hemoptysis and respiratory distress during in-water activity. It has been reported during scuba diving, triathlons, military swimming and snorkeling.

The mechanism for IPE is multifactorial. Immersion results in redistribution of blood from the periphery to the core resulting in a greater thoracic blood volume. With increased breathing resistance pressures in the pulmonary vasculature elevate. In susceptible individuals, pulmonary artery and capillary pressures can become too great and cause loss of integrity of the blood-gas barrier (pulmonary capillary stress failure). This can result in fluid leaking out of the pulmonary vasculature and into the lungs.1

In this case, possible contributing factors include cold water, augmenting blood volume, exercise and increased breathing resistance from the regulator and snorkel. Furthermore, hypertension is a known contributing factor to susceptibility and could have conceivably contributed in this case. It has been proposed that a tight-fitting wetsuit may be a compounding variable but this remains to be proven.

Onset and severity of IPE can vary from mild to life threatening. While typically cases resolve within 24-48 hours, fatalities have been reported. Symptoms will worsen with continued exposure, thus early recognition and removal from the water is integral to managing IPE. In this scenario, the diver was wise to report symptoms promptly. When asked if he could swim to shore on his own, the diver requested assistance. Had the diver disregarded the symptoms as exertional fatigue or attempted to swim back to shore alone, the outcome may have been much less favorable. After exiting the water, oxygen should be administered if available and medical attention should be sought. As many conditions can present similarly, such as an acute cardiac event, appropriate evaluation is warranted as well as discussing return to activity since IPE can sometimes reoccur.

-Stefanie D. Martina, BS

1. Ludwig BB, Mahon RT, Schwartzman EL. Cardiopulmonary function after recovery from swimming induced pulmonary edema. Clin J Sport Med. 2006;16(4):348-51.