There's been alot of talk lately about triathlon deaths and injuries. I discovered something else that may account for some of this.
SIPE is Swimming Induced Pulmonary Edema. It seems to only happen in open water. It starts as shortness of breath or the onset of a panic attack. It can then proceed to spitting up a pink frothy foam. That's blood from your lungs. But this is not a cardiac event.
The reason I'm bringing it up is because last summer I think I experienced it. Originally I thought it might have been an asthma attack, but now I'm not completely sure. Since it often involves open water swimming, I thought it might have happened to someone else from the forums. Whether it has or not, I thought it should be brought up so people are aware.
There is also a website that has explanations and some links. SIPE
JIM
I was skeptical and decided to check it out on Medline. I came across two citations:
: Clin J Sport Med. 2006 Jul;16(4):348-51.www.ncbi.nlm.nih.gov/.../http:--www.lwwonline.com-pt-pt-core-template-journal-lwwgateway-images-pmlogo.gif
Cardiopulmonary function after recovery from swimming-induced pulmonary edema.
Ludwig BB, Mahon RT, Schwartzman EL.
National Naval Medical Center, Division of Pulmonary and Critical Care, Bethesda, MD, USA.
OBJECTIVE: This study aimed to compare cardiopulmonary function in patients with a history of swimming-induced pulmonary edema (SIPE) with controls by measuring pulmonary function tests, oxygen consumption with exercise, and the pulmonary arterial pressure response to hypoxemia. DESIGN: Case control study. SETTING: Tertiary Military Medical Center. PATIENTS: US Navy Special Warfare members who had previously suffered SIPE. INTERVENTIONS: Measurement of pulmonary function tests, cardiopulmonary exercise test, pulmonary artery pressure by echocardiography at rest on room air and with hypoxia. MAIN OUTCOME MEASUREMENTS: Pulmonary function testing, carbon monoxide diffusing capacity, maximal oxygen consumption, and pulmonary arterial pressure response to hypoxemia. RESULTS: Subjects who previously had SIPE did not demonstrate differences in pulmonary function tests, carbon monoxide diffusing capacity, maximal oxygen consumption, or pulmonary arterial pressure response to hypoxemia. CONCLUSIONS: Subjects with a history of SIPE do not have abnormal pulmonary function tests, abnormal exercise capacity, or abnormal pulmonary arterial pressure response to hypoxemia when tested in dry conditions.
1: Chest. 2004 Aug;126(2):394-9.www.ncbi.nlm.nih.gov/.../http:--highwire.stanford.edu-icons-externalservices-pubmed-standard-chest_final_free.gif Links
Swimming-induced pulmonary edema: clinical presentation and serial lung function.
Adir Y, Shupak A, Gil A, Peled N, Keynan Y, Domachevsky L, Weiler-Ravell D.
IDF Medical Corps, Israel Naval Medical Institute, Haifa. adir-sh@zahav.net.il
BACKGROUND: Acute pulmonary edema has been noted in swimmers and divers, and has been termed swimming-induced pulmonary edema (SIPE). The mechanisms and consequences of SIPE are unknown, and there are currently no series of carefully evaluated patients with this condition. Herein we report the clinical presentation, incidence of recurrence, findings on physical examination, chest radiography, and oxygen saturation in 70 trainees with a diagnosis of SIPE. We also report the results of forced spirometry in a subgroup of 37 swimmers. METHODS: SIPE was diagnosed when severe shortness of breath and cough were reported during or after swimming, and were associated with evidence of pulmonary edema. During the years from 1998 to 2001, 70 cases of SIPE were documented in young healthy male subjects participating in a fitness-training program. Physical examination and pulse oximetry were performed immediately. Chest radiographs were obtained in all cases 12 to 18 h following onset of symptoms. In 37 swimmers, spirometry was performed at the time of chest radiography and again after 7 days. RESULTS: All subjects complained of severe shortness of breath. Sixty-seven of the 70 subjects (95.7%) had a prominent cough; in 63 subjects (90%), there was significant sputum production. Hemoptysis was observed in 39 subjects (55.7%). Mean arterial oxygen saturation after swimming was 88.4 +/- 6.6% breathing air, compared with 98 +/- 1.7% breathing air at rest before the start of the swimming trial (mean +/- SD) . Chest radiographs obtained 12 to 18 h after swimming were normal in all cases. Sixteen trainees (22.9%) had a recurrence of SIPE. Spirometry demonstrated restrictive lung function, which persisted for a week. CONCLUSIONS: In our trainee population, SIPE is a not uncommon, often recurrent phenomenon that significantly influences performance. It is not clear what predisposes to its occurrence or recurrence and what, if any, are its long-term effects.
Nothing in medical literature since 2006. I wonder if it could be allergy related. Or perhaps something to do with panic and water aspiration. Anyhow who has swum the Chesapeake Bay swim knows how nasty open water can be (brackish nightmare laced with blue crab urine and dripped motor oil from the traffic driving overhead!) Plus if the waters are choppy enough, it's very hard to avoid swallowing and/or inhaling a few mouth and/or lungfulls.
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Good luck. You might want to go to the journals, find out the name of the lead investigator, and email him or her for advice and the latest updates on the phenomenon.
Armchair SIPE theory of the "you read it first here" variety
The other sports related pulmonary edema I have heard about is HAPE, or high altitude pulmonary edema. What happens in thin air is that the blood pressure to the lungs gets higher, and in essence causes the capillaries to leak a little, almost like a soaker hose.
In cold water, blood is shunted to the core and away from the periphery in order to keep the vital organs warm as long as possible. The capillaries in the periphery, meantime, constrict, plus the external water pressure aids this constriction, almost as if your body were wrapped in a large blood pressure cuff.
Thus the original total volume of a cold water swimmer's blood is thus confined to a smaller space, increasing blood pressure. One of the ways the body deals with this is increased urination to reduce the fluid content.
I wonder if there is any correlation between SIPE occurrence and water temperature. My hypothesis is that SIPE would become more common as water temperature decreases because this would increase the internal blood preessure, which, in turn, might cause the pulmonary arterioles to start acting like soak hoses, a la HAPE.
Note: my armchair theory is probably wrong, but if you are an exercise physiologist looking for a new topic to research, I gladly bequeathe my amateur ruminations for you to either kibosh or validate!
Former Member
That's pretty scary, any ideas why this happens?
Former Member
Very interesting articles, Jim. Thanks!
Here's an armchair SIPE theory I have:
I think there could be some kind of allergy involved. After all, I have not heard of any cases happening in a chlorine pool. They all happen outdoors in open water. Temperature sensitivity could be a factor as well.
JIM