A 60 year old man presented to the urgent care clinic complaining of several hours of shortness of breath, a gurgling sensation in his chest, and a cough productive of frothy, blood stained sputum. Earlier that day he had been kitesurfing, and after crashing had not been able to raise his kite. He was forced to swim for 15 min to reach the shore. He had been wearing a wetsuit. The water temperature was 12 deg C.
He appeared mildly dyspneic. t – 36.3 HR 63 BP 133/67 RR 18 O2sat =98%
His chest was resonant to percussion with vesicular breath sounds and no crepitations or wheeze.
The history suggested the possibility of swimming induced pulmonary oedema (SIPE), however without auscultation findings to support this.
Next stop – ultrasound…
Disposition
The ultrasound findings of bilateral B lines (B profile) with normal LV systolic function supported the presumtive diagnosis of swimming induced pulmonary oedema. After discussion with the on call emergency physician the patient was referred to hospital and admitted to the observation ward overnight. His symptoms improved suficiently to be discharged the following morning. A CXR taken in hospital is shown below.
Interestingly, he reported that he had had a similar episode 7 years previously. On that occasion he had also been admitted to hospital and told that he had suffered from “dry drowning”.
Discussion
- Swimming induced pulmonary oedema (SIPE) typically affects young, otherwise healthy individuals involved in vigorous water sports such as swimming and diving.
- The presence of cough, dyspnoea, froth and haemoptysis are strongly suggestive of SIPE, when occuring during or immediately following swimming. (1)
- Risk factors may include strenuous exertion, cold water temperatures, prior fluid loading, and the use of compressive wetsuits.
- Pathophysiology is not completely understood, but is thought to be caused by pulmonary over-perfusion, with high pulmonary capillary pressures leading to extravasation of fluid into the interstitium. This overperfusion is caused by the increase in ambient pressure, peripheral vasoconstriction from cold immersion, and increased pulmonary blood flow from exercise. (2)
- Those with a past history suggestive of SIPE have been shown to have higher MPAP and PAWP when performing submerged exercise in cold water, compared to subjects with no past history of SIPE. (3)
- In a 3 year study of healthy male recruits involved in an open water swimming training program, the incidence of SIPE was 1.8%, and the risk of recurrence was 22.9% amongst those affected. (4)
- While the ultrasound “B Profile” is non-specific for the aetiology of pulmonary oedema, this is yet another example where lung ultrasound can be a useful bedside adjunct in urgent care, to aid in rapidly establishing a diagnosis.
References
- Hohmann E, Glatt V, Tetsworth K. Swimming induced pulmonary oedema in athletes – a systematic review and best evidence synthesis BMC Sports Sci Med Rehabil. 2018; 10(1). [pubmed]
- Koehle MS, Lepawsky M, McKenzie DC. Pulmonary oedema of immersion. Sports Med. 2005; 35(3):183-90. [<a href=”https://pubmed.ncbi.nlm.nih.gov/15730335/” target=”_blank”>pubmed</a>]
- Moon RE, Martina SD, Peacher DF, et al. Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil. Circulation. 2016; 133(10):988-96. [<a href=”https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5127690/pdf/main.pdf” target=”_blank”>PDF</a>]
- Adir Y, Shupak A, Gil A, et al. Swimming-induced pulmonary edema: clinical presentation and serial lung function. Chest. 2004; 126(2):394-9. [<a href=”https://pubmed.ncbi.nlm.nih.gov/15302723/” target=”_blank”>pubmed</a>]
Header Photo by uniqsurface on Unsplash
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