I’ve been learning about swimming induced pulmonary edema (SIPE) and I thought I’d offer an introduction here based on my reading and conversations with experts in the field as well as affected athletes.

The problem of SIPE, or immersion pulmonary edema (IPE) as it was first known, was recognized at least as far back as the mid-1990s. Early reports in the scientific literature focused primarily on a small number of healthy scuba divers who experienced problems with unusual breathlessness (dyspnea), particularly when diving in cold water. Medical evaluation for the problem showed that the divers had low levels of oxygen in the blood (hypoxemia), often reported coughing up frothy, blood-tinged secretions, and had findings on chest x-ray that suggested pulmonary edema. In the setting of immersion in cold water, this collection of difficulties–dyspnea, hypoxemia, excess lung secretions, and pulmonary edema–became known as IPE.

Interestingly, the victims of IPE were often very experienced swimmers who had difficulties only with swimming and/or diving in cold water (~50-60 degrees Fahrenheit).

It’s worth taking a moment to review a few important facts about the anatomy and physiology of the lungs. We have two lungs, each about the size and shape of a 2-liter soda bottle. Healthy lungs are extraordinarily light and very spongy. For our discussion today, it will help to think of the lungs as sponges. The lungs are ordinarily almost colorless, but take on a pink hue because of blood that flows throughout the lung tissue.

The right ventricle of the heart pumps blood to the lungs through the pulmonary arteries which branch into smaller and smaller branches and eventually into miscrosopically small capillaries which come into contact with the air-filled spaces in the lungs. It’s here where the blood unloads carbon dioxide and picks up oxygen. The blood then flows into increasingly larger veins and eventually into the pulmonary veins that carry the blood back to the left side of the heart where it is pumped to the rest of the body.

Like I mentioned, the lungs are usually extraordinarily light. But when fluid escapes the bloodstream and collects in the spongy lung tissue outside the blood vessels, the lungs become water-logged, much the way that a sponge becomes heavy once it soaks up water. One of the consequences is that it is much more difficult for oxygen to get into the bloodstream and much more difficult for carbon dioxide to get out. We call this situation pulmonary edema.

There are many causes of pulmonary edema. The most commonly encountered cases are due to heart problems of one sort or another (eg, heart valve problems, weakness of the left ventricle), but other causes include: reactions to blood transfusion, direct injury to the lungs, infection, and perhaps various inflammatory conditions.

The exact cause of pulmonary edema with SIPE is not completely understood, but experts suspect that a combination of increased bloodflow into the lungs due to immersion combines with increased pressure in the pulmonary arteries and veins (because of exercise) to cause a leak of fluid out of the bloodstream and into the lung tissue.

It is not clear if exercise-induced pulmonary edema occurs on land.

SIPE and Triathlon

As many readers here will know, there have been a number of episodes of sudden cardiac death (SCD) in triathlons in recent years, and these episodes have occurred with a preponderance during the swim portion of triathlon events. The cause of most of these deaths appears to be typical sports-related SCD due to a sudden arrhythmia, but some have wondered if SIPE could have played a role. There have been a handful of thoughtful opinion pieces about this possibility and I’d refer you to one such article by Rudy Dressendorfer in a recent edition of Sports Medicine Bulletin, entitled “Triathlon Swim Deaths: Initial Steps Toward Prevention.” This article lays out one view on the issue. In my opinion, though, it is not at all clear that SIPE has had a role in triathlon-related swim deaths.

Charles Miller and colleagues at Texas Tech University Health Sciences Center published an interesting report in 2009 that dealt with the possibility of SIPE in triathletes. During late 2008, they distributed a questionnaire to the membership of USA Triathlon asking about athletes’ experiences with “swim-related breathing problems.” The response rate to the survey was tiny–at only 1.3%–and it’s important to remember that the low response rate might have tremendous bias with the results. Nonetheless, about 1.4% of respondents reported having a swim-related episode of “pink frothy or blood-tinged secretions” that was suggestive of pulmonary edema. Moreover, the authors identified several risk factors for this occurrence, including high blood pressure, female gender, increasing length of the swim, and use of fish oil supplements. Only a minority of reported episodes suggestive of SIPE occurred in the absence of one or more of these 4 risk factors.

I’ve heard from several triathletes about their personal experiences with SIPE and I thought I’d share their stories here.

Nathan Farrugia, an avid runner and triathlete from Malta, shares his story at his blog. He describes his experience of discovering the problem in 2009 and then learning about SIPE and eventually traveling to Duke University for detailed physiologic testing. He’s very thoughtful about the physiology of the condition and the factors that might promote SIPE while racing.

Katherine Calder-Becker, a triathlete from Montreal, wrote to me to share stories about her struggle with SIPE. You can read about her discovery of the problem, how it’s affected her triathlon racing, her visit to Duke University for testing, and her recipe for heading off the problem now at her website. In addition to her personal story, she shares useful links to additional scientific articles and press reports for those who might want to do some additional reading. Those of you with a physiology background, in particular, will enjoy reading about her visit to Duke Dive Medicine to participate in a study of athletes with SIPE.

I gather that Nathan’s and Katherine’s stories are typical. I know of other athletes who have experienced similar symptoms during open water swimming, particularly during races, who received medical attention, at the scene or the hospital, who were suspected of having pulmonary edema. Supportive care with rest and oxygen, if needed, resulted in a resolution of the symptoms. I’m not aware of any triathlon-related death where clinical or autopsy findings specifically suggested SIPE as a cause.

Athletes who have been bothered by SIPE have offered a variety of suggestions for how to avoid trouble. These are also summarized in the article by Dressendorfer:

1. Avoid overhydration on race morning (to limit the immersion-related increase in bloodflow to the lungs).

2. Become acclimated to the water conditions, and particularly the water temperature, immediately before a race with a gentle warm-up swim.

3. Avoid using a wetsuit that has a restrictive fit at the neck.

4. Think to signal and request assistance during the swim if symptoms of unusual breathlessness develop.

SIPE is an area of ongoing basic investigation. One prominent group of investigators is headed by Dr. Richard E. Moon at the Duke University Center for Hyperbaric Medicine and Environmental Physiology. This group continues to study (in human subjects) the various physiologic changes that accompany SIPE, trying to identify the causative mechanisms that are responsible. I’ve had a chance to speak with Dr. Moon recently and I’m encouraged that his team’s work will be productive in defining this condition more precisely, identifying the causes and risk factors, and suggesting ways to avoid or alleviate the problem among triathletes.

That’s what I can offer in the way of an introduction to this topic. It would be great to hear from readers who can share their experiences with SIPE so that we might all learn more about this condition.