Immersion Pulmonary Edema

Pulmonary edema is an abnormal leakage of fluid from the bloodstream into the alveoli, the microscopic air sacs in the lungs. It is most often the result of heart failure or other cardiac problems. Sometimes, however, pulmonary edema is observed in swimmers and divers when no underlying medical cause is apparent. This condition, immersion pulmonary edema (IPE), presents as a rapid onset of shortness of breath, cough and sometimes blood-tinged, frothy sputum. Because the fluid builds up in the air-containing spaces of the lungs and interrupts gas exchange, IPE resembles drowning. The important difference is that the obstructing fluid comes from within the body rather than from inhalation of surrounding water.

The DAN Medical Information department receives a few calls each month in which divers report symptoms suggestive of IPE. Anyone who experiences sudden shortness of breath or persistent cough while diving should abort the dive in as safe a manner as possible and breathe 100 percent oxygen on the surface. Further diving should be postponed until a physician can be consulted. Although IPE often resolves quickly once a diver has exited the water, respiratory distress in the diving environment can be extremely dangerous.

Why does IPE occur?
Douglas Ebersole: IPE is an uncommon condition first reported in 1989. It was originally described in cold-water diving and called "cold-induced pulmonary edema." However, it has now been reported in warm-water diving as well. An absence of chest pain helps differentiate IPE from pulmonary decompression sickness ("chokes"). The exact mechanism is not known, but it is thought to be due to a combination of the increased hydrostatic pressure in the pulmonary capillaries that occurs with immersion in water and the presence of a gradient between the hydrostatic pressure at mouth level and at chest level when a diver is upright. Additionally, diving causes increased negative pressure in the alveoli due to denser breathing gas and when using a poorly tuned regulator.

Immersion in water causes a number of physiologic effects including a rapid distribution of blood from the legs to the thorax, which can increase blood volume in the thorax by up to 700 ml. This additional blood causes an increase in pressure in the right atrium by 16-18 mm Hg, a 30-percent increase in cardiac output and a slight increase in blood pressure. Divers with conditions such as hypertension or underlying cardiovascular disease, especially those with weakened heart muscle function, are less able to tolerate these physiologic changes and are thus more prone to pulmonary edema. No large studies have been performed, but review of the medical literature shows several small case studies of patients with IPE. In these, a high percentage of subjects had hypertension or cardiovascular disease. Most of them also report a higher proportion of women.

Alfred Bove: There are several scenarios that provoke IPE. High-intensity surface swimming causes it; this has been reported in triathletes and U.S. Navy SEALs. Divers get IPE when swimming on the bottom without clear evidence of stress. In some cases, the diver relates a tight-breathing regulator, and in others no evident stress or equipment problems are noted. In most cases, cardiac evaluation is normal. Reduced diastolic relaxation (usually a result of long-standing hypertension) can lead to increased venous pressure in the lungs — the usual cause of pulmonary edema from cardiac problems. Measurements of both systolic and diastolic heart function can be readily obtained from an echocardiogram. IPE is not a manifestation of decompression sickness and does not require recompression. The treatment is oxygen and diuretics to remove water from the lungs.

Pete Witucki: We don't know, and this is the dilemma. There have been multiple proposed theories, but none seems completely satisfactory. One theory suggests that prolonged immersion in cold water causes peripheral blood vessels to constrict and shunt blood to the heart and central circulation, which then leads to fluid leaking into the lungs. However, one would think that otherwise healthy individuals should be able to compensate for this fluid shift. Not to mention, IPE has been documented to occur in warm water. Another theory, similar to the first, is that hydrostatic pressure from the water causes blood to be shunted to the core. Yet again, one would think this volume would not be enough to overwhelm a young, healthy circulatory system. None of these theories explains why IPE may occur in an individual during a particular dive while other divers diving the same profile and wearing the same thermal protection remain unaffected.

Yet another theory suggests IPE is the result of respiratory mechanics. This idea is that a strong, forced inhalation against resistance (essentially overbreathing a snorkel or regulator) may cause the lungs to respond by leaking fluid out of the capillaries and into the alveoli (pulmonary edema). This may explain why young, healthy swimmers with strong lungs may develop IPE especially during particularly strenuous swims. There may also be a genetic component to IPE. In other words, some individuals may have the potential to develop IPE under certain conditions, yet others may never develop IPE even under the same stress. Though there may be a genetic predisposition, I have seen and treated cases of IPE and then returned the diver to full duty with no recurrence. The diver went on to complete identical dive profiles, wearing the same thermal protection and breathing the same regulator, but never again developed IPE. Of course, it may be that the circumstances of the subsequent dives never matched identically the IPE trigger (or triggers) of the culprit dive.

Under what circumstances can someone who experienced IPE return to diving?
Bove: One common problem is excess hydration coupled with rapid onset of heavy swimming exercise on the surface. In triathletes who develop IPE, excess hydration and rapid onset of extreme exercise while immersed should be avoided. Military divers are instructed to avoid overhydration before high-energy swimming. Divers are advised to ensure normal regulator function and not to use regulators that allow breathing resistance to be increased. The majority of divers can return to diving with proper precautions and confirmation their cardiac evaluation is normal.

Ebersole: Unfortunately, very little is known about the likelihood of recurrent IPE once a diver has had an episode. After an episode of IPE, there is often spontaneous recovery once the diver leaves the water. If not, it tends to respond to standard therapy for pulmonary edema, such as diuretics. Whether or not a diver should return to diving after an episode of IPE should be determined on a case-by-case basis. The decision should be based on the physical condition of the diver, a history of hypertension or cardiovascular disease and the type of diving being considered. Obviously, shallow warm-water diving in a young, healthy diver who suffered a mild case of IPE is less concerning than a middle-aged diver with multiple medical problems who wants to return to cold-water diving after a severe episode of IPE that required hospitalization.

Witucki: An otherwise healthy person who has experienced a single, isolated episode of IPE may return to diving once all symptoms have resolved. This person should be counseled that futures dives should be aborted if they again develop signs of IPE. Again, I have treated many cases and subsequently returned these divers to full duty without recurrence. A person who has known or potential cardiac disease (hypertension, advanced age, diabetes) and develops IPE is a different matter. These people should have further cardiac evaluation prior to diving to make sure they do not have heart valve problems or underlying blockages in their coronary arteries. The results of this further testing should dictate return to diving. A person who experiences recurrent episodes of IPE should probably refrain from diving again in the future.

What do we not understand about IPE — in what ways is it still a mystery?
Bove: The mechanisms of IPE are not well understood. The phenomenon of negative-pressure pulmonary edema is well known in anesthesia and likely contributes to IPE in divers. The development of pulmonary edema in swimmers is better understood and has a model in the well-known pulmonary edema problem found in highly motivated racehorses. However, there are still a number of divers and swimmers who get IPE who don't have a good explanation for why it occurred.

Ebersole: Despite the best efforts of many investigators, the medical community does not know much about IPE. Until we better understand the mechanism of the disorder and who is predisposed to it, it is difficult to make recommendations to divers as to how to avoid it or when to return to diving after an episode.

Witucki: The cause! We do not know what causes IPE nor can we currently predict which people are at increased risk of developing this condition. We know how to identify and treat IPE. We know the disease involves fluid leaking out of pulmonary capillaries and into the alveoli. What we do not know is why it occurs. It is hoped the research that is currently under way will answer this question or at least begin to lead us in the right direction.

Meet the Experts
Alfred Bove, M.D., Ph.D., is professor emeritus of medicine at the Temple University School of Medicine in Philadelphia, Pa. He is board certified in cardiology, internal medicine, and undersea and hyperbaric medicine. Bove is a National Association of Underwater Instructors (NAUI) lifetime scuba instructor, course director for Temple University Underwater Medicine and author of the textbook Diving Medicine.

Douglas Ebersole, M.D., is an invasive and interventional cardiologist at Watson Clinic and director of the cardiac catheterization laboratories at Lakeland Regional Medical Center in Lakeland, Fla. He is a cave and technical diver, a Scuba Schools International (SSI) instructor and an International Association of Nitrox and Technical Divers (IANTD) and Technical Diving International (TDI) rebreather and trimix instructor.

Pete Witucki, M.D., is a faculty member in the Department of Emergency Medicine at University of California San Diego Medical Center. He is board certified in emergency medicine as well as undersea and hyperbaric medicine. He served as a Diving Medical Officer (DMO) in the U.S. Navy for four years and continues to serve as a DMO in the U.S. Navy Reserves.

Current Research
Dr. Richard Moon of the Duke Center for Hyperbaric Medicine and Environmental Physiology, in collaboration with DAN, is currently conducting research on IPE. The goal of the study is to identify susceptible individuals and develop methods to prevent the condition. DNA samples from participants who have experienced IPE will be compared with samples from those who have not, and the effects of cold-water immersion on blood pressure, cardiac output and pulmonary artery pressures will be compared between the two groups. Volunteers with a history of IPE are still needed for the study. For more information, contact

© Alert Diver — Fall 2011