Swimming Induced Pulmonary Oedema – raising awareness about this potentially life-threatening condition

Sport and Exercise Medicine: The UK trainee perspective – A BJSM blog series


By Dr Ralph Smith, Dr Jim Kerss & Dr Daniel Brooke

With the new season approaching, Triathlon is one of the fastest growing participation sports in the United Kingdom (UK). The swim component of a triathlon is usually held in open water (fresh water lakes, rivers or sea based). Alongside triathlon, there has been a recent surge in participation in open water swimming events. Both events attract competitors varying in age, ability and fitness levels. There are risks in addition to significant health benefits of participation, and there is a growing requirement for on-site medical care. Event medical staff must be aware of and prepared for the specific illnesses and injuries that present in these sports.

In 2014, whilst providing medical cover at UK based open water triathlons, we (the authors) encountered two cases of Swimming Induced Pulmonary Oedema (SIPE). This is a rare and potentially life-threatening condition which is increasing in frequency with the sport’s growing popularity. Thus, our aim in writing this blog is to raise awareness and improve the recognition of SIPE amongst athletes and event medical staff.



SIPE is also known as immersion pulmonary oedema. It was first described in the 1980s in healthy scuba divers1. Since then, there have been over three hundred reported cases in triathletes, swimmers and divers2 which include fatalities3.


Typically affected patients usually present during or shortly after swimming (or diving) with:

  • Acute Shortness of Breath
  • The absence of water aspiration
  • Cough which is often productive of copious pink frothy sputum
  • Examination signs consistent with acute pulmonary oedema

Investigation & Management

In the pre-hospital setting, it is paramount appropriate resources are available for a safe water evacuation to prevent drowning. After an initial assessment (using an ABCDE approach including oxygen saturations +/- supplementary oxygen if clinically indicated) the patient will likely require transfer to hospital for further investigations and management.

In the acute hospital setting, investigations should include a chest radiograph (CXR), 12 Lead Electrocardiogram (ECG), Echocardiogram and measurements of cardiac enzymes. There is often evidence of hypoxia on oxygen saturations, pulmonary oedema on CXR, and raised cardiac enzymes. However, it is important to note that these tests can be normal.

The symptoms of SIPE usually resolve within 24-48 hours of presentation – sometimes without the need for any treatment such as Oxygen or diuretics. Despite this prompt evaluation of cardiac and pulmonary function one must exclude any underlying pathological cause. Investigations usually show normal underlying cardiac and pulmonary function, however, Peacher et al recently suggested that the role of cardiopulmonary dysfunction in SIPE may be underestimated, particularly in the older athlete, and that an episode of SIPE may unmask subclinical disease2. Rates of recurrence are as high as twenty two percent4 and are unpredictable. The medical team should advise that further episodes can occur and explain appropriate safety precautions. Indeed in one of our cases the patient suffered a further episode whilst open water swimming.


Due to the sporadic nature of SIPE and the inability to reproduce it under experimental conditions the exact pathophysiology remains somewhat elusive and debated5. The prevailing hypothesis is that cold water immersion leads to peripheral vasoconstriction, central blood pooling and increased cardiac preload2. In combination with the increased cardiac output from exercise this results in an elevated pulmonary artery pressure, increased hydrostatic pressure and alveolar oedema. Tight fitting wetsuits may exacerbate the situation through compression of peripheral blood vessels, further increasing central blood pooling and cardiac preload6.

Is the condition more common than we think?

As symptoms tend to resolve spontaneously, those with a milder episode of SIPE may not always seek medical attention as their symptoms could resolve when exiting the water and resting. Indeed Miller et al surveyed 1400 triathletes and found 1.4% of athletes had experienced symptoms that were suggestive of SIPE, suggesting significant under reporting7. Such an incidence would have resulted in almost 20 presentations at Ironman UK 2014 (1,982 competitors).

Future suggestions

Medical staff working at mass participation sporting events that include an open water swim component should suspect SIPE in competitors who are unusually short of breath, particularly if they have a cough productive of pink frothy sputum. Investigation is necessary to exclude any underlying cardiopulmonary dysfunction but this may be normal. Communication about the potential diagnosis of SIPE should be made when transferring affected patients to hospital to alert colleagues of this condition. Race organisers, athletes and medical staff should be educated in the recognition of SIPE and its management, particularly considering the rapid raise in popularity in triathlon and open water swimming.


  1. Wilmshurst PT, Nuri M, Crowther A et al. Cold-induced pulmonary oedema in scuba divers and swimmers and subsequent development of hypertension. Lancet 1989 Jan;14;1(8629):62-5.
  2. 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. 2014 Sep 12. [Epub ahead of print]
  3. Scuba divers’ pulmonary oedema:recurrences and fatalities. Diving Hyperb Med. 2012;42(1):40-4.
  4. Adir Y, Shupak A, Gil A, Peled N, Keynan Y, Domachevsky L, Weiler-Ravell D. Swimming-induced pulmonary edema. Chest. 2004;126(2):394-9.
  5. Wenger M, Russi EW. Aqua jogging-induced pulmonary oedema. Eur Respir J. 2007;30(6):1231-2
  6. Spiteri DB, Debono R, Micallef-Stafrace K, Xuereb RG. Recurrent swimming-induced pulmonary oedema (SIPE) in a triathlete. ISMJ. 2011;12(3):141-4.
  7. Miller C, Calder-Becker K, Modave F. Swimming-induced pulmonary oedema in triathletes. Am J Emerg Med 2010 Oct;28(8):941-6.





About the Authors


Ralph Smith is an ST3 SEM trainee in the Thames Valley Deanery. Prior to entering the training programme, he completed an MSc in SEM and his General Practice training. He is currently works in rugby union with Henley Hawks and Wasps Academy. He has keen interest in endurance sports and started open water swimming and triathlons last year.


Jim Kerss is an ST5 SEM trainee in the North West Deanery based at the English Institute of Sport in Manchester and is the British Para-Swimming Team Doctor. He has a keen interest in medical education and is currently undertaking a NW Deanery Medical Education Fellowship. He is the current Trainee representative on the SEM SAC and co-ordinates the UK SEM Speciality Trainee teaching days.


Daniel Brooke is a GP ST2 working in Surrey with a keen interest in pursuing SEM. He has extensive experience covering a wide range of sports across the UK.


Dr Farrah Jawad co-ordinates the BJSM Trainee Perspective blog.

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