9-7-12. Updated in 2013 and 2014 (see updates at the end of this post)
Every heard of it? Swimming Induced Pulmonary Edema – SIPE. I had not. But after reading an article written by a triathlete in this year’s NY City Ironman Triathlon (link below), I was sufficiently alarmed. This is something every open water swimmer and triathlete should learn about. This condition can affect even healthy, well-conditioned and highly trained athletes.
SIPE is a form of pulmonary edema first discovered in the mid 1990s. Athletes most affected are divers, swimmers, and triathletes. From Wikipedia:
SIPE occurs when fluids from the blood leak abnormally from the small vessels of the lung (pulmonary capillaries) into the airspaces (alveoli)…
As with other forms of pulmonary edema, the hallmark of SIPE is cough productive of pink, frothy or blood-tinged sputum. Symptoms include (from Wikipedia):
Shortness of breath out of proportion to effort being expended.
Crackles, rattling or ‘junky’ feelings deep in the chest associated with breathing effort – usually progressively worsening with increasing shortness of breath.
Cough, usually distressing and productive of copious pink, frothy or blood-tinged sputum
Contributing factors to SIPE are the temperature of the water, constriction from wetsuits, and even pre-race adrenaline. Other factors may include: direct injury to the lungs; heart problems, infection, hypertension and even fish oils.
Here are some articles I reviewed to learn more about SIPE:
- This is the article that initially caught my eye: Why I Also Almost Died During the 2012 New York City Ironman Triathlon
- Here is an article from an Endurance Triathlete website: http://www.endurancetriathletes.com/sipe.html
- This article is written by a triathlete who also happens to be a heart surgeon: http://athletesheart.blogspot.com/2012/04/swimming-induced-pulmonary-edema-sipe.html
- In this American Journal of Emergency Medicine article, the authors note potential contributing factors of hypertension and fish oils in athletes who have experienced SIPE. http://www.journals.elsevierhealth.com/periodicals/yajem/article/PIIS0735675709004021/abstract
As the first article indicates, an athlete must find that balance between pushing hard and wanting to finish a race with understanding and recognizing signs of what could be a serious problem. The triathlete in the NY marathon did not want to stop, but he did know that something wasn’t quite right. He may be alive today because he stopped. No race or event is worth dying for. There will always be another opportunity to compete. Listen to your body, and when it gives you warning signs, heed them.
Update 9-7-12. In an email today from usopenwaterswimming.org, they had a great section on S.I.P.E. I’ve copied and pasted their posting (not yet showing on their website).
Swimming Induced Pulmonary Edema (SIPE)
This month we are going to partially reprint an article which appeared 4 years ago in our newsletter. This reprint is prompted by a recent post titled “Why I almost Died During the New York City Ironman Triathlon” at http://ht.ly/djjoE. It is written by a triathlete about her experience with SIPE.
Swimming Induced Pulmonary Edema or SIPE is a rare condition which occurs sometimes in open water swimming. The following is an e-mail interview conducted with Dr. Jolie Bookspan who has studied condition.
1. What is pulmonary edema and why should swimmers know or be concerned about it?
Edema means too much fluid accumulation. Fluid suddenly fills the lungs. The left side of the heart is not pumping properly. It can cause athletes to have to stop a race. Sometimes it can cause serious illness and death.
2. Is it more likely to occur in cold water?
It seems to be more likely in cold water. It has occurred in surface swimmers and scuba divers in both cold and warm water. Cold is only one of the several proposed causes.
Causes or contributors seem to be things that increase cardiac preload and afterload, including immersion in water, cold water, heavy exercise, negative pressure breathing (like breathing with a snorkel, and swimming with the chest below the surface and even the slight elevation of the head to breathe in), and drinking too much water or other fluids before swimming. Don’t drink lots of water before swimming.
3. What are the signs and symptoms?
Unusually shortness of breath (not just fatigue) and coughing bloody froth. No chest pain. With a stethoscope you can hear rales, an abnormal rattling breathing sound. Chest x-rays show the classic pattern of pulmonary edema. When blood oxygen in the arteries is checked, arterial O2 may be lowered.
4. Do wet suits provide any measure of protection against PE?
Difficult to say since it has occurred in people with and without wet suits. I haven’t seen charts where the numbers of each predisposing possibility, like protective garments and temperature, were compared.
5. Can medical personnel easily detect PE?
Pulmonary edema is not subtle. The person is usually gasping and spitting pink froth, and asking for help with a worried look. A swimmer who develops shortness of breath and cough in a race may have something else like exercise induced asthma.
6. What is the first aid if PE is suspected?
Get them out of the water. Sit them up to elevate the head, if conscious. Give them 100% oxygen by mask, and get them to the emergency facility.
6. If PE is untreated and the athlete continues to the race/swim, what could happen?
Depends how serious. Symptoms can resolve on their own, or they can get worse. There have been deaths. We wonder how many people who suddenly went under were not drowning but developed pulmonary edema? There is no way yet to tell. Drowning also produces pulmonary edema (after the fact). Repeat cases of pulmonary edema can occur in the same person.
Interestingly, the frothing pulmonary edema occurs in racehorses after hard races. They are blowing bloody nose froth all over, but veterinarians have reassured me that the horses are fine. If it is a person who is frothing, get help.
Although SIPE seems to be a rare condition, open water swimmers and race organizers should be aware of its existence and plan accordingly. A doctor on site will be able to hear the “rales” condition by listening to lungs/breathing with a stethoscope. Also, it is recommended to have oxygen available to administer for anyone suspected of SIPE.
The following excerpt is written by Regan Scheiber and her personal experience with the SIPE after the 40K Memphremagog Marathon swim in Canada.
“It was the summer of 2000 that I experienced my first and only episode of pulmonary edema. I don’t know exactly what combinations of events caused the edema, but I do know this: A week prior to the Magog race, I swam the Atlantic City marathon. It was a close, intense, eight hour race that tested my will to win. I was very dehydrated at the end of the race, but that was normal. That night I started to develop what I thought was a cold or allergic reaction to the water. I had a stuffy nose and felt very rundown. The next day, I drove to Maine to do some lake training in preparation for the Magog race, now less than a week away. I could not shake the sinus cold and would feel the need to cough every time I was horizontal and swimming. A little something would come up, but I thought nothing of it, and just hoped I would be 100% for the race.
I arrived in Magog, Quebec, three to four days before race day. The day before the marathon, all the swimmers participate in a short competition swim for the public, I was definitely not 100%, but my upper respiratory irritation seemed to have calmed down. On race day, the water was a cold 64-65 degrees; it was cloudy, and windy. Not good for someone like me, who was relatively thin, and, as I was about to find out, did not do well in long term cold water conditions. After the first two hours of the race, I started to feel noticeably uncomfortable. I was drinking warm feeds, but it wasn’t enough. My hip flexors cramped up and I had to drag my legs for the remainder of the race. My stroke count went from 84-86 to 76-80 and maintained that pace. I remained fully lucid. Other than a slower stroke rate, I did not show any other alarming signs of hypothermia. (I think at least 4-5 swimmers were pulled from the race that day for hypothermia.)
The last kilometer, I slipped into third place, with nothing left to give. I wasn’t in any respiratory distress, just weak. When I finished the 10 hour swim (one hour longer than the previous year), I stood up in the shallow water and felt fine, just tired. Since my hip flexors were so cramped, I had to pull myself up onto the dock. I landed on my belly. Instantly, I started coughing up fluid that came from my lungs. Within a minute I was shivering so severely, I was put on a stretcher and later sent to the hospital. It took an hour of warm I.V. fluids and a warm blanket to raise my body temperature from 88 degrees to 98 degrees. All the while, I was having trouble catching my breath and was periodically coughing to clear my lungs. Once I was comfortable, I told the doctor about my lungs and he did a chest x-ray. It showed fluid in the lungs, also known as pulmonary edema. My body had started to clear the fluid on its own, but it needed the help of Lasex, a diuretic, to speed the process along. A few hours later, I signed myself out; my only ongoing injury was now the hip flexors.
I took two weeks off to heal and do some light training. I then swam Long Island Sound, winning the women’s race in record breaking time. A year later, I swam the elusive English Channel. The water temperature was 64-66 degrees, and again, my hip flexors cramped up. I dragged my legs, shivered and swam with a slower stroke rate, all the way to France. I did not have pulmonary edema. I was fine, and so was Jane, my daughter, with whom I was three months pregnant.
Did the sinus cold and upper respiratory problem I got after Atlantic City compromise my immune system and make me more susceptible to pulmonary edema, given the right conditions? I don’t know the answer.”
Regan was swimming a very long 9 hour race, but the condition has occurred in swimmers with only 15 – 30 minutes of immersion.
The following article appeared in the American Family Physician, March 1, 2004 issue. It details an incident of SIPE and discusses proper treatment for the condition.
“A healthy 20-year-old United States Navy search and rescue swimmer trainee, who was equipped with only a mask and fins, developed hemoptysis, sharp substernal chest pain, and shortness of breath after performing a dive to a depth of 12 feet. He immediately surfaced and began to cough up pink, frothy sputum and have persistent shortness of breath. His initial oxygen saturation was 70 percent on room air and improved to 86 percent on three liters of oxygen via nasal cannula during ambulance transfer. On arrival at the emergency department, the patient had an oxygen saturation of 100 percent on three liters of oxygen with improved shortness of breath and resolved hemoptysis.
Auscultation of the lungs revealed bilateral rhonchi. The remainder of the physical examination was unremarkable with all vital signs being normal. Electrocardiogram, complete blood count, electrolytes, creatine kinase, troponin, and coagulation studies were all within normal limits. A chest radiograph showed fluffy perihilar infiltrates bilaterally. A chest radiograph taken several hours later showed resolving infiltrates. The patient was diagnosed with swimming-induced pulmonary edema (SIPE) and discharged.
While the exact pathophysiology of SIPE remains uncertain, it is believed to be related to exertion, immersion in cold water, and overhydration. The body’s normal response to exercise is to increase cardiac output to meet the increased oxygen demand. Although an increased cardiac output is known to cause pulmonary edema in racehorses, this increase is rarely enough to produce such an effect in humans.
(1) Cold-water immersion is instrumental in this process because the peripheral vasculature constricts to divert blood away from the extremities in an effort to maintain the core body temperature. This results in a central pooling of blood, leading to an increased preload, increased pulmonary artery pressure, and an increased cardiac output. The vasoconstriction also causes an increase in afterload, which leads to an increase in pulmonary vasculature resistance. The increased cardiac output from exertional activities coupled with an increased preload and afterload from immersion appear to be sufficient to rupture the pulmonary capillary membranes, thus resulting in pulmonary edema. In several documented cases of SIPE, it has been noted that the patients consumed anywhere from two to four liters of water in the hours leading up to their swim in an effort to remain well hydrated.
(2) It is believed that this degree of hydration led to a fluid overload that contributed to the onset of pulmonary edema by increasing the pulmonary capillary pressure.
(3) Patients may present with symptoms, such as cough, dyspnea, hemoptysis, tachypnea, and confusion with hypoxia, after exertional cold water activity such as swimming and scuba diving.
(4) Treatment for patients with SIPE consists primarily of supportive measures such as removing the patient from the wet and/or cold environment and providing supplemental oxygen. Although useful in treating pulmonary edema in racehorses, diuretics are typically not necessary because patients tend to show relief of symptoms soon after being placed on supplemental oxygen.
(5) Full resolution of radiographic findings typically occurs within 24 to 48 hours.”
JASON A. YODER, MS3, ENS, MC, USNR
Uniformed Services University of the Health Sciences, 4301 Jones Bridge Rd.Bethesda, MD 20814 ANTHONY J. VIERA, LCDR, MC, USNR. Naval Hospital Jacksonville. 2080 Child St. Jacksonville, FL 32214
(1.) Hopkins SR, Schoene RB, Henderson WR, Spragg RG, Martin TR, West JB. Intense exercise impairs the integrity of the pulmonary blood-gas barrier in elite athletes. Am J Respir Crit Care Med 1997; 155:1090-4.
(2.) Weiler-Ravell D, Shupak A, Goldenberg I, Halpern P, Shoshani O, Hirschhorn G, et al. Pulmonary oedema and haemoptysis induced by strenuous swimming. BMJ 1995;311:361-2.
(3.) Pons M, Blickenstorfer D, Oechslin E, Hold G, Greminger P, Franzeck UK, et al. Pulmonary oedema in healthy persons during scuba-diving and swimming. Eur Respir J 1995;8:762-7.
(4.) Lund KL, Mahon RT, Tanen DA, Bakhda S. Swimming-induced pulmonary edema. Ann Emerg Med 2003; 41:251-6.
Update 6-25-14. So many have written in about seeing this blog post and sharing their own incredibly scary S.I.P.E. experiences. I received an email from Elaine Howley, Asst. Editor of the U.S. Masters Swimming publication SWIMMER Magazine this month. She wrote an article on S.I.P.E. in the March/April 2013 publication of SWIMMER. We’ve corresponded on the topic, and she shared with me a Duke study that you might be interested in.
Elaine spoke with Dr. Moon from Duke last spring. They had been exploring the use of Viagra as a treatment in Immersion Pulmonary Edema (also known as S.I.P.E). When Elaine spoke with Dr. Moon, they were in the study phase, so results should be out or forthcoming. According to the study’s site, however, it looks like it’s still ongoing: http://dukedivemedicine.org/?p=724.
If you have had Immersion Pulmonary Edema and would like more information about it, or if you would like to participate in the project (Duke pays travel expenses and gives a participation stipend), please contact Dr Moon or Dr. Freiberger at 919-684-6726 or email firstname.lastname@example.org