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With the growing popularity of water-based sports, cases of swimming-induced pulmonary edema (SIPE) are becoming increasingly recognized. SIPE, a potentially life-threatening condition, is an acute cause of breathlessness in athletes. It has been described frequently in scuba divers, swimmers, and triathletes and is characterized by symptoms and signs of pulmonary edema following water immersion. It is important to recognize that athletes’ symptoms can present with a spectrum of severity from mild breathlessness to severe dyspnea, hemoptysis, and hypoxia. In most cases, there is rapid resolution of symptoms within 48 hours of exiting the water. Recent advances in the understanding of the pathophysiology of SIPE, particularly regarding exaggerated pulmonary vascular pressures, have begun to explain this elusive condition more clearly and to distinguish its predisposing factors. It is essential that event organizers and athletes are aware of SIPE. Prompt recognition is required not only to prevent drowning, but also to implement appropriate medical management and subsequent advice regarding return to swimming and the risk of recurrence. This manuscript provides a current perspective on SIPE regarding the incidence rate, the current understanding of the pathophysiology, clinical presentation, medical management, recurrence rates, and advice on return to sport.
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Swimming-induced pulmonary edema: current
Ralph Smith1
Julian O M Ormerod2
Nikant Sabharwal2
Courtney Kipps3
1Department of Sport and Exercise
Medicine, Nuffield Orthopaedic
Centre, Oxford University Hospitals
NHS Trust, Oxford, UK; 2Department
of Cardiology, John Radcliffe Hospital,
Oxford University Hospitals NHS
Trust, Oxford, UK; 3Institute of Sport,
Exercise and Health, Division of
Surgery and Interventional Sciences,
UCL, London, UK
Abstract: With the growing popularity of water-based sports, cases of swimming-induced pul-
monary edema (SIPE) are becoming increasingly recognized. SIPE, a potentially life-threatening
condition, is an acute cause of breathlessness in athletes. It has been described frequently in
scuba divers, swimmers, and triathletes and is characterized by symptoms and signs of pulmo-
nary edema following water immersion. It is important to recognize that athletes’ symptoms can
present with a spectrum of severity from mild breathlessness to severe dyspnea, hemoptysis,
and hypoxia. In most cases, there is rapid resolution of symptoms within 48 hours of exiting
the water. Recent advances in the understanding of the pathophysiology of SIPE, particularly
regarding exaggerated pulmonary vascular pressures, have begun to explain this elusive condi-
tion more clearly and to distinguish its predisposing factors. It is essential that event organizers
and athletes are aware of SIPE. Prompt recognition is required not only to prevent drowning, but
also to implement appropriate medical management and subsequent advice regarding return to
swimming and the risk of recurrence. This manuscript provides a current perspective on SIPE
regarding the incidence rate, the current understanding of the pathophysiology, clinical presenta-
tion, medical management, recurrence rates, and advice on return to sport.
Keywords: triathletes, open water swimming, diving, immersion, breathing difficulties
With the increasing popularity of water-based events, such as triathlon and open
water swimming, cases of swimming-induced pulmonary edema (SIPE) have become
more frequently recognized. This rare cause of acute and occasionally fatal breath-
lessness was first described in the 1980s in apparently healthy scuba divers.1 Since
then, over 300 cases have been described in scuba divers, military and recreational
swimmers, and triathletes.2 Cases range from young, fit, military swimmers,3,4 who
have undergone careful medical screening, to older recreational athletes and divers
with preexisting cardiopulmonary disease.5 SIPE is characterized by acute onset of
dyspnea, cough, and occasionally hemoptysis, and is associated with water immer-
sion.2 A key feature in the majority of cases is a rapid resolution of symptoms within
48 hours. Initial management requires safe water evacuation to prevent drowning and
to perform a preliminary assessment. Symptoms usually begin to resolve after exiting
the water and management may be supportive. Supplementary oxygen is important.
Oxygen saturations are often low (<92%), and there are often audible crepitations on
auscultation of the chest. The affected individual is often transferred to hospital for
further investigations and management. The prognosis is generally excellent when
Correspondence: Ralph Smith
Department of Sport and Exercise
Medicine, Nufeld Orthopaedic Centre,
Oxford University Hospitals NHS Trust,
Windmill Road, Oxford OX3 7LD, UK
Tel +44 (0) 1865 738109
Fax +44 (0)1865 738058
Journal name: Open Access Journal of Sports Medicine
Article Designation: Review
Year: 2018
Volume: 9
Running head verso: Smith et al
Running head recto: Swimming-induced pulmonary edema: current perspectives
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Smith et al
treated, though fatal cases have been reported.6 Recurrent
episodes are unpredictable and are not uncommon.2 It has
been proposed as a probable cause of unexplained death
during swimming training in triathletes.7 While the exact
pathophysiology remains elusive, a recent study suggests
that there is an exaggerated rise in pulmonary artery and
pulmonary artery wedge pressures (PAWPs) during exer-
cise in SIPE susceptible individuals.8 It has been suggested
that Sildenafil may play a role as an effective prophylactic
agent against SIPE.8,9 Medical professionals and event
organizers should be aware of SIPE in order to manage
cases safely and avoid a delay in diagnosis. Furthermore,
advice should be given on returning to activity and the risk
of recurrence.
This manuscript provides a current perspective on SIPE
regarding the incidence rate, the latest understanding of the
pathophysiology, clinical presentation and management,
recurrence rates, and advice on return to sport.
Incidence and prevalence
SIPE, also known as immersion pulmonary edema, has been
described in a variety of water-based sporting activities
predominantly in scuba divers, military and recreational
swimmers, and triathletes. However, there are also cases
described during snorkeling10 and aqua jogging.11
While there is now a considerable body of reported cases,
relatively few studies have examined the incidence and preva-
lence. Estimates vary considerably; this is partly explained
by the varying study methods and populations studied, which
can make direct comparison challenging (Table 1).
Pons et al estimated the incidence of SIPE among scuba
divers to be 1.1%. Eighteen of the 460 scuba divers who
responded to a questionnaire-based survey reported symp-
toms which were consistent with an episode of pulmonary
edema.12 These suspected cases were then interviewed and
five cases were confirmed.12 In a similar population, in an
unpublished study, Keuski attempted to quantify the cumula-
Table 1 Shows the incidence and details of SIPE in reported cases
Study Context Method and duration No of
Age (years),
mean (range)
Comorbidities N=Subjects with
recurrent episodes
Smith et al16 Triathletes Retrospective study of
medical records over a
5 year period
5 (2M, 3F) 5/68,557
42 (21–58) 1 subject = Ischemic
heart disease,
and hypertension
(details in Table 2)
Ma and
Triathletes Retrospective study of
medical records from
one Ironman triathlon
(3.8 km swim, 180 km
bike and 42.2 km run)
1 (M) 1/1594
Data not available
Miller et al14 Triathletes Online self-reported
20 20/1400
(20–59)bData not available Data not available
Keuski et al13 Divers
Survey medical
completed by medical
(1-year period)
Data not
Data not available Data not available
et al4
Field study over a
3-year period
70 (M) 70 cases
Nil 16 (22%)
All recurrent episodes
occurred at least 3
months following rst
Shupak et al3 Surface
Field study
(2-month period)
21 (M) 21/35
Nil 6 (28%)
Pons et al12 Divers/ surface
Survey with follow-up
medical review
5 (4M, 1F) 5/460
Nil 1 female (20%) had
4 recurrent episodes:
1 episode while scuba
diving and 3 while
surface swimming
Notes: aOnly one athlete with conrmed SIPE. bMean value was not given in this study.
Abbreviations: SIPE, swimming-induced pulmonary edema; M, male; F, female.
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Swimming-induced pulmonary edema: current perspectives
tive incidence of SIPE at two US Navy diving training facili-
ties. Surveys were completed by diving medical officers as
cases presented over the course of year. Unfortunately, key
information was missing in many data sheets. Thirty-one
lacked complete chest radiograph data. Only two collected
sheets were marked as positive for all five predetermined
case criteria used yielding a 0.085% incidence of SIPE.13
During a 2-month field study of 35 male military swim-
mers who were participating in an open water (sea) training
program (2.4 km–3.6 km), Shupak et al reported a consider-
ably higher incidence rate.3 In this study, a clinical diagnosis
of SIPE was made in swimmers who reported shortness of
breath accompanied by cough. They encountered 29 events
of SIPE in 21 individuals, and reported an incidence rate
of 60%. Twenty-one episodes were categorized as “mild”
and eight as “severe”. Episodes were categorized as mild
when the swim trial was completed despite the appearance
of symptoms, and severe when the participant had to stop
swimming due to symptoms. There was a significant dif-
ference in oxygen saturations between symptomatic and
asymptomatic individuals (91–96% in symptomatic group vs
98% in asymptomatic group P<0.001). However, in a similar
population, Adir et al reported an incidence of 1.8% in a series
of 70 cases of SIPE in military swimmers participating in
sea-based time trials between 2.4 and 3.6 km (30–45 minutes
in duration).4 The diagnostic criteria included acute onset of
dyspnea, cough, and/or expectoration of frothy sputum, with
evidence of pulmonary edema on physical examination and
with no history of water aspiration. Miller et al, in 2010,
found a similar rate of 1.4% in a survey of 1400 triathletes
who had self-reported symptoms suggestive of SIPE.14 Ma
and Dutch published a case series of five triathletes, who
presented with dyspnea and hemotypsis during or following a
long-distance race. The race included 1594 competitors with
a total of 147 encounters to the onsite medical team. Follow-
ing clinical assessment, one case of SIPE was suspected.
The patient was transported to the hospital for further care.
Follow-up information was not available.15
More recently, authors from this paper conducted a retro-
spective analysis of 68,557 competitors’ medical records from
two large UK-based triathlon competitions over 5 consecu-
tive years.16 Competitors were a mix of elite and non-elite
triathletes who raced in a variety of triathlon distances from
Super Sprint to Olympic Plus. We found an incidence of SIPE
of 0.73/10,000 triathletes, using the diagnostic criteria of
Adir et al.4 These cases of SIPE accounted for 1.2% (5/429)
of the presentations to the triathlon medical team.16 All were
non-elite athletes competing in a variety of race distances;
one patient had preexisting cardiac comorbidities, and three
were competing in their first triathlon (Table 2). Each case
failed to complete their race, and the majority (4/5) withdrew
during/after the swim phase with one retiring during the bike
phase. Supplementary oxygen and transfer to hospital for
definitive management were required in all cases.
Possible explanations for these discrepancies in incident
rate include:
1. Athletes may suffer a minor episode of SIPE which resolves
quickly after exiting the water, and which they do not
report to the medical teams. Hence, only the more severe
episodes are documented. However, prospective studies
actively seeking SIPE will detect these mild episodes.
2. Variations in diagnostic criteria used and populations
Predisposing factors
Typical cases of SIPE demonstrate normal underlying cardiac
and pulmonary function on further investigation.17 However,
this may be less likely in older swimmer/divers, as an episode
of SIPE may unmask other subclinical diseases. In a group
Table 2 Details of competitors presenting with SIPE during mass-participation triathlon races
Gender Race
Presenting symptoms Comorbidities
30 Female Super sprint Yes Breathlessness Mild respiratory symptoms (cough)
1 week prior to race
55 Female Sprint No Breathlessness Taking anti-depressants
Subsequence recurrence of symptoms
47 Male Sprint Yes Hemoptysis Previous myocardial infarction, hypertension, raised cholesterol
21 Female Olympic No Breathlessness + hemoptysis None
57 Male Olympic No Breathlessness Recent long haul ight
Similar previous episodes not investigated
Note: Data from Smith et al.16
Abbreviation: SIPE, swimming-induced pulmonary edema.
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Smith et al
of 36 subjects (mean age 48 years) with a history of SIPE,
Peacher et al found that 72% had at least one significant
concurrent medical condition (e.g., hypertension; cardiac
dysrythmia, dysfunction, or structural abnormality; asthma,
diabetes mellitus, or overweight). In contrast, the same authors
found no obvious preexisting co-morbidities or cardiac risk
factors in a literature review of 136 published cases of SIPE
in military swimmers/divers. The patients in this review were
much younger (mean age of 23 years) than the 36 cases.5
More recently, Moon et al7 investigated 23 triathlon
deaths that occurred during the swim leg. They compared
the postmortem findings to a control group of living triath-
letes who were assessed by echocardiography. The authors
reported that a greater proportion of the 23 triathletes who
had died compared to the control group had left ventricular
hypertrophy (LVH; which can cause a stiffer heart and might
predispose to SIPE). On the basis of this result, the authors
propose that SIPE may have been a significant cause of death
in this group.7 This is an interesting finding but there are
several possible pitfalls in its interpretation. Increased wall
thickness and cardiac mass are common findings in trained
athletes and are not necessarily pathological. Additionally,
measurements of left ventricular (LV) wall thickness and
heart mass do not reliably correlate with echocardiographic
measures taken in life. Measurements of wall thickness post-
mortem are challenging as it is not possible to determine the
phase of the cardiac cycle with any accuracy. The phase of
contraction also determines the amount of mass attributable
to blood at postmortem; echocardiographic measures are
intended to estimate bloodless mass only.
Cases of SIPE are usually linked to exertion.3,18,19
Exercise- induced pulmonary edema has been reported in
land athletes,20 and is a well-known phenomenon seen in thor-
oughbred racehorses.21 Although exertion itself is a common
factor, the onset of symptoms in SIPE does not seem to cor-
relate with the duration of exertion, as many cases have been
reported to occur soon after entering the water and it seems
that immersion itself is the common etiological factor.22–24
Other proposed risk factors include cold water,1 overhydra-
tion,18 wetsuit use,14,23 and female gender.14 Cold water immer-
sion causes an increase in central venous blood pooling and a
subsequent increase in cardiac preload secondary to peripheral
vasoconstriction; however, it should be noted that there have
been reported cases in warm or tropical environments.25,26
Over-hydration exacerbates central venous pooling due to an
increase in circulating plasma volume.18 Tight-fitting wetsuits
may also cause external compression of peripheral vessels
and limb deep veins, leading to central venous pooling and a
subsequent increase in cardiac preload.27 Nevertheless, there
are several cases of SIPE where a wetsuit was not worn.3,4,18
Cases are commonly but not exclusively seen in open water
swimming/immersion; however, to the best of our knowledge,
there has been at least one reported case. Gnadinger et al
described a case of SIPE in a scuba diver in a swimming pool.28
Current views on the pathophysiology of SIPE are discussed
in more detail in the following section.
The exact pathophysiology of SIPE still remains elusive; this
is partly attributed to its sporadic nature and the difficulty in
replicating it under experimental conditions. It is likely to
be a combination of simultaneously occurring factors that
together create a “perfect storm”.
Predominant theories suggest the fundamental importance
of redistribution of blood from the extremities, which occurs
with immersion,29 leading to central blood pooling.30 This is
enhanced further by peripheral vasoconstriction from cold
water or a tight wetsuit. As a result, there is engorgement of
the central veins leading to an increase in cardiac preload,
reflected in an increase in left atrial pressure (usually estimated
using the PAWP). 8,31 This, in combination with an increased
cardiac output from strenuous exercise, gives rise to elevated
pulmonary artery pressures. Subsequently, the increased
hydrostatic pressure results in alveolar edema and breakdown
of the capillary–alveolar barrier.32,33 The prone horizontal
swimming position may further exacerbate central pooling.
Interestingly, there are a few cases of unilateral SIPE (in the
submerged/dependent lung) in individuals swimming in the
lateral decubitus position, suggesting either a mechanical effect
or an effect of differential (external) pressure.19,34 Individuals
with pathological LVH, and hence a stiffer heart, are less able
to cope with increases in preload. Additionally, those with
conditions that increase afterload, e.g., hypertension, aortic
valve stenosis, or hypertrophic obstructive cardiomyopathy,
would be expected to have a higher left atrial pressure at a
given level of preload and would also be at greater risk of SIPE.
Casey et al propose a modification to this theory, arguing
that athletes may augment their right ventricular (RV) stroke
volume (SV) to a greater degree than their LV SV. They sug-
gest that both ventricles can increase cardiac work to a very
high degree, but that peripheral vasoconstriction (and perhaps
external compression) increases LV afterload during exercise.
Pulmonary vasodilatation means that RV afterload is increased
to a substantially lesser degree and therefore there is a stroke
volume difference (RV > LV), leading to congestion in the
lungs. Such a mismatch would usually be compensated by
increased LV work on the Frank–Starling curve, but if cardiac
output is already maximal this may not be possible.35
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Swimming-induced pulmonary edema: current perspectives
A recent study has advanced our understanding by measur-
ing mean pulmonary artery pressure (MPAP) and PAWP in
cases and controls exercising submerged in cold water. They
found a statistically significant exaggerated rise in MPAP (34.0
mmHg vs 22.5 mmHg [P=0.004]) and PAWP (11.0 mmHg
vs 18.8 mmHg [P=0.028]) in the 10 athletes with a previous
history of SIPE compared to the control group,8 which they
interpreted as confirming the central importance of hemody-
namics (as opposed to capillary failure) in the development
of SIPE.9 They suggest the mechanism for these elevated
pressures is multifactorial, including higher blood volume,
elevated venous tone, and reduced diastolic LV compliance.8
Clinical presentation and
SIPE is characterized by the clinical features of pulmonary
edema induced by immersion water and is related to vigor-
ous physical activity.2 Grünig et al’s recent review of 38 cases
confirmed the most common presenting symptoms were
dyspnea (79%), cough (71%), and hemoptysis (68%).2 Water
aspiration is a common differential diagnosis in this setting
and may present with comparable features. Prompt clinical
examination is invaluable as abnormal signs are frequently
detected on auscultation, specifically basal crepitations and/
or rhonchi. Hypoxia is a common finding.2 A prompt accurate
measurement of oxygen saturations in the pre-hospital setting,
while nonspecific, adds objective information which may aid in
monitoring and response to treatment. Clinicians should con-
duct an appropriate primary assessment and maintain a broad
differential diagnosis when assessing the acutely unwell athlete.
In the pre-hospital setting, it is vital that appropriate
resources are available for a safe water evacuation to prevent
drowning, and minimum standard supplementary oxygen
should be available, as oxygen was required in 77% of cases.2
Appropriate medical equipment and facilities should also
be available at training locations as SIPE is not confined to
competitions. Patients are likely to require transfer to hospital
for further investigations and management. Clear communi-
cation regarding the potential diagnosis of SIPE should be
made when transferring patients to alert colleagues of this
relatively rare condition.22
Pulmonary edema in the emergency department setting
is most often confirmed by the use of chest X-ray (CXR).
CXR was abnormal in 71% of cases reviewed.2 Point-of-care
ultrasound (POCUS) is now frequently used in the pre-
hospital setting, and could potentially be used to assess for
SIPE at the waterside during events. It can confirm the pres-
ence of abnormal interstitial fluid in the lung to distinguish
pulmonary edema from other causes of breathlessness. With
a greater level of operator training, POCUS may be used to
evaluate the heart and exclude major cardiac causes of pul-
monary edema such as stress cardiomyopathy or myocardial
infarction. POCUS was recently used to confirm pulmonary
edema in the emergency department in a case of a highly
trained young female swimmer who developed acute SIPE
during open water training.36
Immediate removal from water is vital and can initiate
symptoms resolution due the reverse of the hemodynamics
promoting lung edema. In most cases, supplementary oxygen
therapy is required. In combination with oxygen therapy,
beta-2 agonists are used in some cases (37%), 2 perhaps due to
the presence of rhonchi. However, there is also rationale that
beta-2 agonists may accelerate the resolution of pulmonary
edema.37,38 Intravenous/oral diuretics are sometimes used.
It is recommended that those who suffer with an episode
of SIPE should have prompt evaluation of their cardiac and
pulmonary physiology.5 Electrocardiography, echocardiog-
raphy, stress echocardiography, measurement of cardiac
enzymes, and coronary angiography may be indicated to
rule out coronary disease or structural heart disease causing
pulmonary edema. If clinically indicated, further investiga-
tions such as MRI renal angiogram and a 24-hour urinary
collection for catecholamines may be required to rule out
rare causes of flash pulmonary edema.
In most cases of SIPE, there is a rapid resolution of signs
and symptoms within 48 hours (82% of cases). This often
starts from simply exiting the water and providing supportive
treatment.2 Regular monitoring and follow-up examination
will ensure that patients are following this trajectory. It is
important to recognize that there is a spectrum of severity
of symptoms. This poses several challenges:
1. Triathletes/swimmers with mild symptoms may not seek
help from medical teams as their symptoms improve on
exiting the water and as they enter the bike phase adopting
a more supine position. They may attribute their relative
poor performance to various training factors.
2. They may be reluctant to attend hospital if symptoms are
mild or have quickly resolved.
3. Lack of awareness among the admitting team may result
in the patient being discharged without a formal diagnosis
if symptoms have resolved by the time of assessment.
SIPE should be suspected in athletes who are unusually
short of breath during or after swimming. Grünig et al identi-
fied that there were variations in the diagnostic pathways in
reviewed cases. They proposed a checkpoint list to improve
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Smith et al
diagnostic accuracy.2 Athlete governing bodies, race orga-
nizers, and clinicians have a duty to promote awareness and
ensure appropriate standards of care are being delivered.
Athlete education programs will play a role in publicizing
the recognition of SIPE.
Recurrence rates and return to
Recurrent episodes are common, and rates have been reported
to be between 13% and 22% among scuba divers and
swimmers.2–5,18 Authors from this manuscript found in their
report that 40% (2/5) of triathletes had prior or subsequent
episodes (Table 1).16 Recurrence of SIPE appears to be unpre-
dictable and is not limited by age, sport, or environmental con-
ditions. Adir et al found 16 of the 70 military swimmers had
a recurrence of SIPE. All cases took place at least 3 months
after the first incident.4 Furthermore, a fatal case of SIPE
was described in a 51-year-old female recreational diver who
logged 54 dives over the course of a year between episodes
of SIPE.31 Carter and Koehle highlight that two of the three
female triathletes in their group suffered with recurrence of
SIPE. Among them, a 58-year-old female suffered at least four
episodes over a 4-year period. On each occasion, symptoms
started within 15 minutes of commencing swimming. How-
ever, not all of these episodes required hospitalization and in
between the episodes she successfully completed two open
water triathlons and multiple lake training sessions, further
confirming the variable nature of this condition.23
It is of paramount importance that athletes are warned
about recurrent episodes and should be emphasized that it
is essential that a thorough evaluation of their cardiac and
pulmonary physiology has been performed to look for any
underlying causes of SIPE.5 Authors from this manuscript
described a case of a 55-year-old female recreational triath-
lete who suffered with recurrent episodes of SIPE. The risk
of potential recurrence was not highlighted to her during her
hospital admission and she subsequently suffered a life-threat-
ening episode when she returned to open water swimming.22
Athletes with a history of SIPE should be presumed to have
a predisposition to recurrence. Although it is acknowledged that
episodes of recurrence are unpredictable, these athletes should
take care to swim in controlled environments to reduce the risk
of drowning if a repeat episode was to occur. Spiteri et al suggest
that starting swimming at a slower pace may be appropriate to
reduce the recurrence rate.39 A gradually progressive step-wise
return to swimming is a sensible approach. Prophylaxis has
been suggested. New developments have shown that a single
oral dose of sildenafil 50 mg can lower PAP and PAWP.8 In
clinical practice, Martina et al illustrated a case of a 46-year-
old female ultra-triathlete with a history of at least five SIPE
episodes who had no further recurrences during 20 subsequent
triathlons while taking 50 mg of sildenafil before each swim.9
These findings require sufficiently powered controlled studies
to support this prophylactic use. Sildenafil is currently not on
the prohibited list of the World Anti-Doping Code.40
Cases of SIPE will continue to occur as the popularity of open
water swimming and similar water-based activities increase.
Recent developments in the understanding of pulmonary
vascular pressures have started to unravel the pathophysiology
of this elusive condition. Further research to establish the inci-
dence of SIPE for specific activities using appropriate common
diagnostic criteria will help to define the extent of this condi-
tion. This in turn will help to distinguish predisposing factors.
Increased awareness among athletes, event medics, and
emergency departments can assist in a prompt diagnosis
and ensure optimum management, which includes advice
regarding the return to activities and risk of recurrence. Fur-
ther research is required to establish the role of prophylactic
sildenafil in recurrent cases.
Author contributions
RS collected all studies and drafted the manuscript. JOMO,
NS, and CK helped in drafting the manuscript. All authors
approved the final version. All authors contributed toward
data analysis, drafting and critically revising the paper and
agree to be accountable for all aspects of the work.
The authors report no conflicts of interest in this work.
1. Wilmshurst PT, Nuri M, Crowther A, Webb-Peploe MM. Cold-induced
pulmonary oedema in scuba divers and swimmers and subsequent
development of hypertension. Lancet. 1989;1(8629):62–65.
2. Grünig H, Nikolaidis PT, Moon RE, Knechtle B. Diagnosis of swimming
induced pulmonary edema – a review. Front Physiol. 2017;8:652.
3. Shupak A, Weiler-Ravell D, Adir Y, Daskalovic YI, Ramon Y, Kerem
D. Pulmonary oedema induced by strenuous swimming: a field study.
Respir Physiol. 2000;121(1):25–31.
4. Adir Y, Shupak A, Gil A, et al. Swimming-induced pulmonary
edema: clinical presentation and serial lung function. Chest.
5. Peacher DF, Martina SD, Otteni CE, Wester TE, Potter JF, Moon RE.
Immersion pulmonary edema and comorbidities: case series and updated
review. Med Sci Sports Exerc. 2015;47(6):1128–1134.
6. Edmonds C. The evolution of scuba divers pulmonary edema. Undersea
Hyperb Med. 2016;43(2):83–91.
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7. Moon RE, Martina SD, Peacher DF, Kraus WE. Deaths in triathletes:
immersion pulmonary oedema as a possible cause. BMJ Open Sport
Exerc Med. 2016;2(1):e000146.
8. Moon RE, Martina SD, Peacher DF, et al. Swimming-induced pulmonary
edema: pathophysiology and risk reduction with sildenafil. Circulation.
9. Martina SD, Freiberger JJ, Peacher DF, et al. Sildenafil: possible pro-
phylaxis against swimming-induced pulmonary edema. Med Sci Sports
Exerc. 2017;49(9):1755–1757.
10. Cochard G, Henckes A, Deslandes S, et al. Swimming-induced immer-
sion pulmonary edema while snorkeling can be rapidly life-threatening:
case reports. Undersea Hyperb Med. 2013;40(5):411–416.
11. Wenger M, Russi EW. Aqua jogging-induced pulmonary oedema. Eur
Respir J. 2007;30(6):1231–1232.
12. Pons M, Blickenstorfer D, Oechslin E, et al. Pulmonary oedema in
healthy persons during scuba-diving and swimming. Eur Respir J.
13. Keuski BM. The incidence of swimming-induced pulmonary edema
(SIPE) in trainees at U.S. Navy dive training facilities. 2011. Available
from: Accessed
April 10, 2108.
14. Miller CC, Calder-Becker K, Modave F. Swimming-induced pulmonary
edema in triathletes. Am J Emerg Med. 2010;28(8):941–946.
15. Ma JL, Dutch MJ. Extreme sports: extreme physiology. Exercise-induced
pulmonary oedema. Emerg Med Australas. 2013;25(4):368–371.
16. Smith R, Parkin J, Knight N, Kipps C. The incidence of swimming-
induced pulmonary oedema during mass-participation triathlon races:
optimising athlete safety. Br J Sports Med. 2017;51(4):391–391.
17. Slade JB, Hattori T, Ray CS, Bove AA, Cianci P. Pulmonary edema asso-
ciated with scuba diving: case reports and review. Chest. 2001;120(5):
18. Weiler-Ravell D, Shupak A, Goldenberg I, et al. Pulmonary oedema and
haemoptysis induced by strenuous swimming. BMJ. 1995;311(7001):
19. Mahon RT, Kerr S, Amundson D, Parrish JS. Immersion pulmonary
edema in special forces combat swimmers. Chest. 2002;122(1):383–384.
20. Bates ML, Farrell ET, Eldridge MW. The curious question of exercise-
induced pulmonary edema. Pulm Med. 2011;2011:361931.
21. West JB, Mathieu-Costello O, Jones JH, et al. Stress failure of pulmonary
capillaries in racehorses with exercise-induced pulmonary hemorrhage.
J Appl Physiol (1985). 1993;75(3):1097–1109.
22. Smith R, Brooke D, Kipps C, Skaria B, Subramaniam V. A case of
recurrent swimming-induced pulmonary edema in a triathlete: the need
for awareness. Scand J Med Sci Sports. 2017;27(10):1130–1135.
23. Carter EA, Koehle MS. Immersion pulmonary edema in female triath-
letes. Pulm Med. 2011;2011:261404.
24. Deady B, Glezo J, Blackie S. A swimmer’s wheeze. CJEM. 2006;8(4):
281, 297–288.
25. Kwek W, Seah M, Chow W. Swimming-induced pulmonary
edema in a tropical climate: a case report. Undersea Hyperb Med.
26. Yamanashi H, Koyamatsu J, Nobuyoshi M, Murase K, Maeda T.
Exercise-induced pulmonary edema in a triathlon. Case Rep Med.
27. Lundgren CEG, Miller JN. The Lung at Depth. New York: Dekker;
28. Gnadinger CA, Colwell CB, Knaut AL. Scuba diving-induced pulmo-
nary edema in a swimming pool. J Emerg Med. 2001;21(4):419–421.
29. Arborelius M, Ballidin UI, Lilja B, Lundgren CE. Hemodynamic
changes in man during immersion with the head above water. Aerosp
Med. 1972;43(6):592–598.
30. Wester TE, Cherry AD, Pollock NW, et al. Effects of head and body
cooling on hemodynamics during immersed prone exercise at 1 ATA.
J Appl Physiol (1985). 2009;106(2):691–700.
31. Edmonds C, Lippmann J, Lockley S, Wolfers D. Scuba divers’ pulmonar y
oedema: recurrences and fatalities. Diving Hyperb Med. 2012;42(1):
32. Tsukimoto K, Mathieu-Costello O, Prediletto R, Elliott AR, West JB.
Ultrastructural appearances of pulmonary capillaries at high transmural
pressures. J Appl Physiol (1985). 1991;71(2):573–582.
33. West JB, Tsukimoto K, Mathieu-Costello O, Prediletto R. Stress failure
in pulmonary capillaries. J Appl Physiol (1985). 1991;70(4):1731–1742.
34. Lund KL, Mahon RT, Tanen DA, Bakhda S. Swimming-induced pul-
monary edema. Ann Emerg Med. 2003;41(2):251–256.
35. Casey H, Dastidar AG, MacIver D. Swimming-induced pulmonary
oedema in two triathletes: a novel pathophysiological explanation. J R
Soc Med. 2014;107(11):450–452.
36. Alonso JV, Chowdhury M, Borakati R, Gankande U. Swimming-induced
pulmonary oedema an uncommon condition diagnosed with POCUS
ultrasound. Am J Emerg Med. 2017;35(12):1986.e1983–1986.e1984.
37. Licker M, Tschopp JM, Robert J, Frey JG, Diaper J, Ellenberger C.
Aerosolized salbutamol accelerates the resolution of pulmonary edema
after lung resection. Chest. 2008;133(4):845–852.
38. Groshaus HE, Manocha S, Walley KR, Russell JA. Mechanisms of
beta-receptor stimulation-induced improvement of acute lung injury
and pulmonary edema. Crit Care. 2004;8(4):234–242.
39. Spiteri D DR, Micallef-Stafrace K, Xuereb RG. Recurrent swimming-
induced pulmonary oedema (SIPE) in a triathlete: case report. Int Sports
Med J. 2011;12(3):141–144.
40. Agency WA-D. The World Anti-Doping Code: International Standard
2017. 2017. Available from: Accessed
December 2017.
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... Tis fnding does not appear to be true for younger athletes. Risk factors include cold water immersion, overhydration, wetsuit use, hypertension, and female gender [23,24]. All three cases described, occurred in older athletes swimming in cold, open-water, which likely predisposed them to developing SIPE. ...
... Point-of-care ultrasound (POCUS) of the lung has been used to verify pulmonary oedema in the feld [21],and in conjunction with a feld echocardiography to evaluate cardiac function, this may help confrm the isolated diagnosis of SIPE. Nevertheless, those who sufer with an episode of SIPE should have prompt evaluation of their cardiac and pulmonary physiology to rule out coronary disease or structural heart disease causing pulmonary oedema [10,23]. ...
... Athletes with a history of SIPE should be presumed to have a predisposition to recurrence, especially if they are found to have an underlying cause. Swimming in controlled environments, starting swimming at a slower pace and prophylactic sildenafl have all been suggested as methods for reducing recurrence rate [8,23]. ...
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Objectives. To report three cases of triathletes who presented with swimming-induced pulmonary edema (SIPE) following water immersion. They were subsequently diagnosed with Takotsubo cardiomyopathy (TCM). Design. Retrospective case series. Method. All cases were recreational athletes competing in mass participation triathlons between June 2018 and 2019. They were initially managed by the event medical team and subsequently at the local tertiary level hospital. Written consent was gained from all the subjects. Results. The three triathletes were aged between 50 and 60 years, two were females, and all presented with acute dyspnoea on exiting the water. Two also presented with chest pain and haemoptysis. A diagnosis of SIPE was suspected by the medical event team on initial presentation of low oxygen saturations and clinical signs of pulmonary oedema. All were transferred to the local emergency department and had signs of pulmonary oedema on chest radiographs. Further investigations led to a diagnosis of TCM with findings of T wave inversion in anterolateral electrocardiogram leads and apical hypokinesia on transthoracic echocardiogram and unobstructed coronary arteries. Conclusions. This case series presents triathletes diagnosed with SIPE and TCM following the open water swim phase. It is unclear whether the myocardial dysfunction contributed to causation of SIPE or was the result of SIPE. Mass participation race organizers must be prepared that both SIPE and TCM can present in this population. Those presenting with an episode of SIPE require prompt evaluation of their cardiac and pulmonary physiology. Further research is required to ascertain the exact nature of the relationship between TCM and SIPE.
... 1 It is a rare but serious condition that typically occurs in otherwise healthy athletes competing in triathlon or open water swimming events. 2 SIPE is associated with cold water events and presents with rapid onset of shortness of breath, cough, and rales. 3 Another proposed mechanism is that there may be a mismatch between the right ventricle (RV) and LV at the onset of exercise. Both LV and RV afterload increase with exertion, but RV afterload increases less due to pulmonary vasodilation, resulting in RV>LV stroke volume. ...
... 7 It is unknown why there is a female predominance.PATHOPHYSIOLOGY. The exact pathophysiology is not fully understood; however, a combination of factors that lead to a "perfect storm" of increased pulmonary capillary pressure ultimately overwhelms the alveolar air pressure, resulting in pulmonary edema.3 Water immersion with supine positioning increases central blood pooling, augmented by peripheral vasoconstriction due to cold temperatures and leg compression from a wetsuit. ...
... This increases cardiac preload, left atrial pressure, and pulmonary capillary wedge pressure. Combined with increased cardiac output, these factors result in higher pulmonary artery pressure.3 They are further exacerbated by any condition that increases preload, such as hypertension, or any condition that increases pulmonary vascular pressure. ...
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Swimming-induced pulmonary edema is a leading cause of triathlon-associated emergencies and death. Cold water immersion, female sex, age>50, and wetsuit compression are associated risk factors. Pathophysiology is due to increased central blood pooling, leading to increased pulmonary capillary wedge pressure. Treatment is focused on prevention; however, recurrence is common. (Level of Difficulty: Intermediate.)
... Decreased P O2 ultimately affects all aspects of the oxygen transport system to the tissues and as a result complications arise, most commonly acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). 1 While the etiology of HAPE is fairly well understood, the pathophysiology of pulmonary edema resulting from diving or swimminginduced pulmonary edema (SIPE) has been ambiguous. 2,3 Diving at altitude can confound the symptoms presented for both HAPE and SIPE. ...
... Similarities exist between the pathophysiologic mechanisms believed to underlie both HAPE and SIPE; water immersion and exertion lead to centralized pooling of blood in the cardiovascular unit, elevating pulmonary artery pressure. 2,3 Patchy or nonuniform areas of pulmonary vasoconstriction lead to some capillaries experiencing higher pressure and subsequent leakage. 12 Exertion exacerbates both the work of breathing and airway pressures, resulting in further capillary permeability 14 (Fig. 4). ...
... Most common symptoms such as dyspnea, cough, and hemoptysis with hypoxia are also reported. 3,12 A further commonality between HAPE and SIPE is that athletes or service members may retrospectively minimize and attribute symptoms to their conditioning and environmental factors. Because SIPE resolves rapidly upon cessation of activity, many cases go unexamined. ...
Military diving operations occur in a wide range of austere environments, including high-altitude environments and cold weather environments; however, rarely do both conditions combine. Ice diving at altitude combines the physiologic risks of diving, a hypothermic environment, and a high-altitude environment all in one. Careful planning and consideration of the potential injuries and disease processes affiliated with the aforementioned physiologic risks must be considered. In this case report, we describe a Navy diver who became obtunded secondary to hypoxia during an ice dive at 2,987 m (9,800 ft) elevation and was subsequently diagnosed with high-altitude pulmonary edema. Further consideration of the environment, activities, and history does not make this a clear case, and swimming-induced pulmonary edema which physiologically possesses many overlaps with high-altitude pulmonary edema may have contributed or been the ultimate causal factor for the diver's acute response.
... Swimming-induced pulmonary edema (SIPE), also called immersion pulmonary edema (IPE), is a medical condition, seen in various water-based activities such as scuba diving, swimming, snorkeling, breath-holding diving, surface swimming, military swimming, aqua jogging and triathlete competition [1,2]. In 1981, was the first reported case of SIPE in scuba diving [2]. ...
... The signs and symptoms of SIPE can range from mild breathlessness to severe dyspnea, pink-tinged sputum, cough, hemoptysis, hypoxia, wheeze and chest tightness [1,6,7]. To the best of our knowledge, to date, a couple of case reports of immersion pulmonary edema due to snorkeling [8,9] and two cases of snorkeling-induced pulmonary hemorrhage have been reported [10,11]. ...
... SIPE, is an acute cause of breathlessness in athletes with potentially life-threatening consequences, seen commonly in scuba divers, swimmers and triathletes, characterized by signs and symptoms of immersion pulmonary edema following water immersion [1]. Immersion pulmonary edema (IPE) can be used as an umbrella term for Swimming induced pulmonary edema (SIPE) and Scuba divers pulmonary edema (SDPE) [12]. ...
Full-text available
Swimming-induced pulmonary edema (SIPE), also called immersion pulmonary edema (IPE), is a medical condition seen in various water-based activities such as scuba diving, swimming, aqua jogging, triathlete competition and snorkeling. It occurs when transcapillary filtration of low protein fluid collects in the lungs, in the absence of water aspiration during an aquatic activity, causing acute dyspnea, cough and/or hemoptysis. The hallmark of this entity is the complete resolution of symptoms within 48 hours. SIPE in snorkeling is an under-reported and understudied subject. The true prevalence of SIPE is unknown with an estimated range from 1.8-60% among combat swimmers trainee and 1.4% in triathletes. Recent developments have been done in elucidating the pathophysiology of SIPE with regards to pulmonary capillary pressure so that the predisposing factors and potential causes can be targeted. SIPE can be a potentially life-threatening condition, which needs to be recognized by the swimmers, divers, supervising physicians in order to diagnose and manage it promptly. We report a rare case of SIPE in snorkeling which presented with acute respiratory symptoms and managed with supportive measures in the hospital.
... 5 Individuals with left ventricular hypertrophy, hypertension or structural heart disease typically have higher atrial pressures and are therefore less likely to tolerate further increases in preload, predisposing to SIPE. 11 Clinical examination typically demonstrates bi-basal crepitations, and radiological investigations frequently display changes consistent with alveolar oedema. It is recommended that those presenting with SIPE undergo detailed evaluation of their cardiovascular physiology. ...
... Treatment is primarily supportive and involves immediate removal from water and cessation of exercise while sitting upright. 11 Oxygen therapy is frequently required. Diuresis, bronchodilators and continuous positive airway pressure may be necessary in some instances, while invasive mechanical ventilation with haemodynamic support is reserved for the most severe cases. ...
Immersion pulmonary oedema (IPE) is an under-reported and poorly understood phenomenon thought to be related to exercise-induced haemodynamic changes while submersed in water. Previous work has demonstrated reversible myocardial dysfunction during acute episodes. We present a case of IPE with concomitant, transient, left ventricular myocardial oedema characterised via MRI. This is a novel finding and may be evidence of left ventricular strain due to pressure overload or secondary to a subclinical myocarditis.
... 9,[12][13][14][15][16][17] An important aspect of prehospital care for SIPE is the growing popularity of open water swimming competitions that challenges the surrounding health care organizations. 15,18 Vansbrosimningen is the largest open water swimming event in Sweden and attracts approximately 11,000 participants yearly. A considerable number of patients with SIPE seeking medical care during the swimming event each year, together with a 78-km distance to the nearest hospital, puts pressure on the on-site prehospital medical service. ...
... The rationale for b 2 -agonist inhalation can be increased alveolar fluid absorption of pulmonary edema or comorbidity of SIPE and acute asthma. 2,18,30,33 Simultaneously, reports have been published of patients with SIPE and immersion pulmonary edema with reversible myocardial dysfunction or Takotsubo cardiomyopathy. 12,34,35 In such cases, safety using b 2 -agonist inhalation may be uncertain, and more knowledge about adrenergic activation as a trigger of SIPE is required. ...
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Background Swimming-induced pulmonary edema (SIPE) occasionally occurs during swimming in cold open water. While optimal treatment for SIPE is unknown, non-invasive positive pressure ventilation (NPPV) is an option for prehospital treatment. Research question Is NPPV a feasible and safe prehospital treatment for SIPE, and which outcome measures reflect recovery after treatment? Study design and methods A prospective observational study was conducted at Vansbrosimningen, Sweden’s largest open water swimming event, in 2017-2019. Swimmers diagnosed with SIPE and with peripheral oxygen saturation (SpO2) ≤95% and/or persistent respiratory symptoms were eligible for the study. NPPV was administered on-site as continuous positive airway pressure (CPAP) by facial mask or as positive expiratory pressure device (PEP-device). Discharge criteria were SpO2 >95% and clinical recovery. Four outcome measures were evaluated: SpO2, crackles on pulmonary auscultation, pulmonary edema on lung ultrasound (LUS) and patient-reported respiratory symptoms. Results Of 119 treated individuals, 94 received CPAP, 24 PEP-device and one required tracheal intubation. In total, 108 (91%) individuals were discharged after NPPV for median 10-20 minutes, 11 (9%) required hospital transfer. NPPV resulted in increased SpO2 from median 91% to 97% (p<0.0001) together with improvement of six patient-reported respiratory symptoms (median numerical rating scales 1-7 to 0-1; p<0.0001). No significant decrease in auscultation of crackles (93% vs 87%, p=0.508) or pulmonary edema on LUS (100% vs 97%, p=0.500) was seen during NPPV-treatment. Interpretation NPPV administered as CPAP or PEP-device proved feasible and safe as prehospital treatment for SIPE with a vast majority of patients discharged on-site. SpO2 and patient-reported respiratory symptoms reflected recovery after treatment, whereas pulmonary auscultation or LUS did not.
... Der erhöhte pulmonalarterielle Druck und pulmonale Wedge-Druck führen zur Dysfunktion der Kapillar-alveolar-Barriere und zum Lungenödem. Die fast flache Körperlage im Wasser, Hypertonus und linksventrikuläre Hypertrophie können ebenfalls zur Ausprägung des Krankheitsbilds beitragen [9]. Untersuchungen aus 2016 legen nahe, dass vor allem die Hämodynamik zum Lungenödem führt und Sildenafil eine Rolle in der Prävention dieses Krankheitsbilds spielen könnte [5]. ...
After an uneventful dive, a 55-year-old man developed a massive pulmonary edema requiring rapid sequence induction (RSI) and endotracheal intubation performed by helicopter emergency medical service (HEMS) personnel. We present swimming-induced pulmonary edema (SIPE), which must be considered as a further relevant differential diagnosis in addition to drowning or a dive accident.
Background: Swimming-induced pulmonary edema (SIPE) has been reported to subside within 24-48 hours, but comprehensive follow-up studies on symptom duration and long-term effects are missing. Research question: What is the symptom duration, recurrence, and long-term effects of SIPE? Study design and methods: A follow-up study was conducted based on 165 cases of SIPE from Sweden's largest open water swimming event with 26,125 individuals participating during 2017-2019. Data on patient characteristics, clinical findings and symptoms were collected upon admission. Telephone interviews at 10 days and 30 months were performed to explore symptom duration, recurrence of SIPE symptoms, need of medical evaluation and long-term effects of self-assessed general health and physical activity level. Results: Follow-up at 10 days was performed for 132 cases and at 30 months for 152 cases. Most of the cases were women and mean age was 48 years. At the 10-day follow-up, symptom duration >2 days after the swimming race were reported by 38%. The most common symptoms were dyspnea and cough. In patients followed for 30 months, recurrence of respiratory symptoms during open water swimming was reported by 28%. In multivariable logistic regression, asthma was independently associated with both symptom duration >2 days and recurrence of SIPE symptoms (p =0.045 and p =0.022 respectively). Most participants reported equal or improved general health (93%) and physical activity level (85%) after experiencing SIPE, but 58% had not swum in open water since the event. Interpretation: The present large cohort study challenges the established hallmark of SIPE symptom duration of <48 hours, while SIPE recurrence was in the previously reported range. At 30 months, most patients reported unchanged self-assessed general health and physical activity level. These findings add to our understanding of the course of SIPE and can provide evidence-based information to swimmers and health care professionals.
Pulmonary physiology is significantly altered during underwater exposure, as immersion of the body and increased ambient pressure elicit profound effects on both the cardiovascular and respiratory systems. Thoracic blood pooling, increased breathing gas pressures, and variations in gas volumes alongside ambient pressure changes put the heart and lungs under stress. Normal physiologic function and fitness of the cardiovascular and respiratory systems are prerequisites to safely cope with the challenges of the underwater environment when freediving, or diving with underwater breathing apparatus. Few physicians are trained to understand the physiology and medicine of diving and how to recognize or manage diving injuries. This article provides an overview of the physiologic challenges to the respiratory system during diving, with or without breathing apparatus, and outlines possible health risks and hazards unique to the underwater environment. The underlying pathologic mechanisms of dive-related injuries are reviewed, with an emphasis on pulmonary physiology and pathophysiology.
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Swimming induced pulmonary edema (SIPE) is a complication during exercise with the possibility of misdiagnosis and can quickly be life threatening; however, it is infrequently described in the medical literature. Therefore, the aim of this review was to analyse all individual cases diagnosed with SIPE as reported in scientific sources, with an emphasis on the diagnostic pathways and the key-facts resulting in its diagnosis. Due to a multifactorial and complicated pathophysiology, the diagnosis could be difficult. Based on the actual literature, we try to point out important findings regarding history, conditions, clinical findings and diagnostic testing helping to confirm the diagnosis of SIPE. Thirty-eight cases from seventeen articles with the diagnosis of SIPE were selected. We found remarkable differences in the individual described diagnostic pathways. A total of 100 % of the cases suffered from an acute onset of breathing problems, infrequently accompanied by haemoptysis. A total of 73 % showed initial hypoxemia. In most of the cases (89%), an initial chest X-Ray or chest CT was available, of which one-third (71%) showed radiological signs of pulmonary edema. The majority of the cases (81%) experienced a rapid resolution of signs and symptoms within 48 hours, the diagnostic hallmark of SIPE. Due to a foreseeable increase in participation in swimming competitions and endurance competitions with a swimming component, diagnosis of SIPE will be important, especially for medical teams taking care of these athletes.
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Background/aim To address the question as to whether immersion pulmonary oedema (IPO) may be a common cause of death in triathlons, markers of swimming-induced pulmonary oedema (SIPO) susceptibility were sought in triathletes' postmortem examinations. Methods Deaths while training for or during triathlon events in the USA and Canada from October 2008 to November 2015 were identified, and postmortem reports requested. We assessed obvious causes of death; the prevalence of left ventricular hypertrophy (LVH); comparison with healthy triathletes. Results We identified 58 deaths during the time period of the review, 42 (72.4%) of which occurred during a swim. Of these, 23 postmortem reports were obtained. Five individuals had significant (≥70%) coronary artery narrowing; one each had coronary stents; retroperitoneal haemorrhage; or aortic dissection. 9 of 20 (45%) with reported heart mass exceeded 95th centile values. LV free wall and septal thickness were reported in 14 and 9 cases, respectively; of these, 6 (42.9%) and 4 (44.4%) cases exceeded normal values. 6 of 15 individuals (40%) without an obvious cause of death had excessive heart mass. The proportion of individuals with LVH exceeded the prevalence in the general triathlete population. Conclusions LVH—a marker of SIPO susceptibility—was present in a greater than the expected proportion of triathletes who died during the swim portion. We propose that IPO may be a significant aetiology of death during the swimming phase in triathletes. The importance of testing for LVH in triathletes as a predictor of adverse outcomes should be explored further.
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. Family physicians have more opportunities to attend athletic competitions as medical staff at first-aid centers because of the increasing popularity of endurance sports. Case . A 38-year-old man who participated in a triathlon race experienced difficulty in breathing after swimming and was moved to a first-aid center. His initial oxygen saturation was 82% and a thoracic computed tomography scan showed bilateral ground glass opacity in the peripheral lungs. His diagnosis was noncardiogenic pulmonary edema associated with exercise or swimming: exercise-induced pulmonary edema (EIPE) or swimming-induced pulmonary edema (SIPE). Treatment with furosemide and corticosteroid relieved his symptoms of pulmonary edema. Discussion . Noncardiogenic pulmonary edema associated with endurance sports is not common, but knowledge about EIPE/SIPE or neurogenic pulmonary edema associated with hyponatremia, which is called Ayus-Arieff syndrome, is crucial. Knowledge and caution for possible risk factors, such as exposure to cold water or overhydration, are essential for both medical staff and endurance athletes. Conclusion . To determine the presence of pulmonary edema associated with strenuous exercise, oxygen saturation should be used as a screening tool at a first-aid center. To avoid risks for EIPE/SIPE, knowledge about these diseases is essential for medical staff and for athletes who perform extreme exercise.
Swimming Induced Pulmonary Edema, or SIPE, is an emerging condition occurring in otherwise healthy individuals during surface swimming or diving that is characterized by cough, dyspnea, hemoptysis, and hypoxemia. It is typically found in those who spend time in cold water exercise with heavy swimming and surface swimming, such as civilian training for iron Man, triathalon, and military training. We report the case of a highly trained young female swimmer in excellent cardiopulmonary health, who developed acute alveolar pulmonary oedema in an open water swimming training diagnosed in the emergency department using POCUS ultrasound.
Background Swimming Induced Pulmonary Edema (SIPE) is life-threatening condition that can affect healthy triathletes. There have been several reported cases amongst triathletes, however the current estimation of incidence is derived from a survey of triathletes with self-reported symptoms suggestive of SIPE. Objective To investigate the incidence of SIPE and associated risk factors in mass participation Triathlon Competitions (TC). Design A retrospective analysis of Competitors' Medical Records (CMR). Setting 11 consecutive UK-based TCs between 2011 and 2016. The competitions involved elite and non-elite competitors who raced Super Sprint, Sprint, Olympic and Olympic Plus distances. Participants CMR of patients presenting to Triathlon Medical Team (TMT) with medical complaints/injuries were analysed. Those diagnosed with SIPE were included. Diagnostic criteria included absence of water aspiration, acute onset of dyspnoea, cough and/or expectoration of frothy sputum, with evidence of pulmonary oedema on physical examination. Assessment of Risk Factors Patients' Age, gender, race distance, co-morbidities and medical management were recorded. Main Outcome Measurements The incidence of SIPE in TCs. Results 68557 competitors started the TCs and 429 competitors presented to the TMT. Five case of SIPE were recorded, giving rise to an incidence of 0.73/10,000 competitors and 1.2% of all presentations to the TMT. Mean age was 42 (21–58) and a third were female. All were non-elite athletes competing in a variety of race distances; one patient had pre-existing cardiac comorbidities; and in 3 cases participants were competing in their first triathlon. All required supplementary oxygen and transfer to hospital for definitive management. Conclusion This report is the first to describe the incidence of SIPE in mass participation triathlon competitions. Event organisers and TMTs should be prepared for competitors developing SIPE which appears not to be bound by age, gender, race distance or co-morbidities. Further research is required to identity those who are at risk of SIPE.
Introduction: Swimming-induced pulmonary edema (SIPE) occurs during strenuous physical exertion in cold water and has been reported in scuba divers, free-diving competitors, combat swimmers, and triathletes. We describe a case of SIPE in a combat swimmer in warm tropical waters. Case report: A 21-year old diver trainee developed dyspnea, chest discomfort and hemoptysis after performing a 2-km sea swim in water temperatures of around 30°C. Over a two-hour period, his oxygen saturations deteriorated. Chest X-ray showed pulmonary edema. He was admitted to the general ward for observation and was given supportive treatment. His symptoms resolved over two days. Repeat CXR was normal. He was reviewed and certified fit to continue with diver training. Discussion: Much of the earlier literature on SIPE describes the development of symptoms after exposure to temperate waters as one main risk factor. This case highlights the risk of development of SIPE in warm tropical waters. With a low reported incidence of SIPE in warm waters, this condition is likely to be underdiagnosed. There is therefore a need to increase local awareness of SIPE in the medical community. A deliberate effort to collate data on SIPE in our local community will help us to better understand the pathophysiology of SIPE in the context of a tropical climate. Conclusion: Development of SIPE in tropical waters suggests that other risk factors may be predominant. There should be a high index of suspicion when any strenuous in-water activity is conducted so that timely treatment may be instituted.
Swimming-induced pulmonary edema (SIPE) occurs during swimming and scuba diving, usually in cold water, in susceptible healthy individuals, especially military recruits and triathletes. We have previously demonstrated that pulmonary artery pressure (PAP) and pulmonary artery wedge pressure (PAWP) are higher during immersed exercise in SIPE-susceptible individuals vs. controls, confirming that SIPE is a form of hemodynamic pulmonary edema. Oral sildenafil 50 mg 1 hour before immersed exercise reduced PAP and PAWP, suggesting that sildenafil may prevent SIPE. We present a case of a 46-year old, female ultra-triathlete with a history of at least five SIPE episodes. During a study during exercise submerged in 20°C water, physiological parameters before and after sildenafil 50 mg orally were: O2 consumption 1.75, 1.76 L.min-1; heart rate 129, 135 bpm; arterial pressure 189/88 (mean 121.5), 172/85 (mean 114.3) mmHg; mean pulmonary artery (PA) pressure 35.3, 28.8 mmHg; PA wedge pressure 25.3, 19.7 mmHg. She has had no recurrences during 20 subsequent triathlons while taking 50 mg sildenafil before each swim. This case supports sildenafil as an effective prophylactic agent against SIPE during competitive surface swimming.
This report discusses a rare case of a 55-year-old female triathlete who developed recurrent episodes of swimming-induced pulmonary edema (SIPE). She had two hospital admissions with pulmonary edema after developing breathlessness while swimming, including a near-drowning experience in an open water swim. With increasing popularity of triathlon and open water sports, this case highlights the importance of a greater awareness of SIPE among health professionals, event organizers, and athletes. This report explores the previous reported cases in triathletes and those who have suffered recurrent episodes. It is paramount that an accurate diagnosis is made as these individuals may be at an increased risk of future life-threatening episodes.
The evolution of scuba divers pulmonary edema is described. When discovered in 1981, it was believed to be a cold-induced response in a submerged, otherwise healthy, scuba diver. The clinical features are described and discussed, as are the demographics. An alleged prevalence of 1.1% was complicated by problematic statistics and an apparent increase in reported cases. Recurrences both while diving and swimming or snorkeling were common. More recent case reports and surveys are described, identifying predisposing factors and associations, including cardiac pathology. Stress cardiomyopathies, reversible myocardial disorder or Takotsubo cardiomyopathy, may complicate the presentation, especially in older females. Relevant cardiac investigations and autopsy findings are reviewed. Disease severity and potential lethality of scuba divers pulmonary edema became more apparent early this century, and these influence our current recommendations to survivors. First aid and treatment are also discussed.
Background: -Swimming-induced pulmonary edema (SIPE) occurs during swimming or scuba diving, often in young individuals with no predisposing conditions, and its pathophysiology is poorly understood. This study tested the hypothesis that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise compared to the general population and are reduced by sildenafil. Methods and results: -Ten study subjects with a history of SIPE (mean age 41.6 years) and 20 control subjects (mean age 36.2 years) were instrumented with radial artery and pulmonary artery catheters and performed moderate cycle ergometer exercise for 6-7 minutes while submersed in 20°C water. SIPE-susceptible subjects repeated the exercise 150 minutes after oral administration of 50 mg sildenafil. Work rate and mean arterial pressure during exercise were similar in controls and SIPE-susceptibles. Average VO2 and cardiac output (CO) in SIPE-susceptibles and controls were: VO2 2.42 L.min(-1) vs. 1.95 L.min(-1), P=0.2; CO 17.9 L.min(-1) vs. 13.8 L.min(-1), P=0.01). Accounting for differences in CO between groups, mean pulmonary artery pressure (MPAP) at CO=13.8 L.min(-1) was 22.5 mmHg in controls vs. 34.0 mmHg in SIPE-susceptibles (P=0.004) and the corresponding pulmonary artery wedge pressure (PAWP) 11.0 mmHg vs. 18.8 mmHg (P=0.028). After sildenafil, there were no statistically significant differences in MPAP or PAWP between SIPE-susceptibles and controls. Conclusions: -These observations confirm that SIPE is a form of hemodynamic pulmonary edema. The reduction in pulmonary vascular pressures after sildenafil with no adverse effect on exercise hemodynamics suggests that it may be useful in SIPE prevention. Clinical Trial Registration Identifier: NCT00815646.