Swimming-Induced Pulmonary Edema

• Yonghoon Lee, MD
  PGY-2, Mount Sinai Medical Center, Miami Beach, FL
• C. Michael Lee, DO CAQSM
  Core Faculty, Kaiser Permanente Central Valley, Modesto, CA

Case:

You are working the medical tent at a triathlon when a 52 year old female is rushed in complaining of shortness of breath. She had been doing well until the swimming portion of the race when she began to have difficulty breathing. She began to cough and gasp with each breath and, despite trying to continue, she eventually had to be rescued by lifeguards.

On your evaluation, her vital signs demonstrated a blood pressure of 142/94, heart rate of 115 beats/min, respiratory rate of 30 breaths/min, and an oxygen saturation of 91% on room air. She appears anxious and in moderate respiratory distress. She is leaning forward, coughing up pink frothy sputum, and only able to speak very short sentences with diffuse rales on lung auscultation.

You place her on two liters of oxygen via nasal cannula, improving her oxygen saturation to  98%, and send her to the emergency department where a chest x-ray demonstrates bilateral increased bronchial wall visibility, central perihilar haziness, alveolar filling, and Kerley B lines consistent with mild pulmonary edema.

A Brief Introduction to Swimming-Induced Pulmonary Edema:

Swimming-induced pulmonary edema (SIPE) is a rare but serious condition that is characterized by the accumulation of fluid in the lungs without water aspiration during a physically demanding swim.^1,2 It can happen to healthy and active athletes who are training or competing in swimming events as well as military personnel, scuba divers, and snorkelers.^3,4 One comprehensive review estimates a prevalence between 1.1% and 1.8% among triathletes and military combat swimmers.3

Symptoms of SIPE may include cough, dyspnea, hypoxemia, hemoptysis, hypoxemia, and even altered mental status secondary to the hypoxemia.^1,2,4 Although SIPE can be fatal, over 80% cases resolve within 48 hours.⁴

Risk Factors:

Although there are case reports of SIPE in warm water immersion, swimming in cold water is suggested to be a major risk factor for developing SIPE^.2,5 Additional risk factors may include a history of systemic or pulmonary hypertension, anxiety, asthma, diabetes, exertion level, age > 50, female sex, obesity, left ventricular hypertrophy, overhydration, inadequate warm-up, and tight wetsuits with full-length leg coverage.^1,3,5 However, the biggest risk factor for SIPE is a previous episode of SIPE as recurrence rate is estimated to be between 13-22%.³

Pathophysiology:

The exact pathophysiology of SIPE is not entirely clear, but it is thought that a mixture of factors leads to physiological changes resulting in an increased pulmonary capillary pressure that overcomes alveolar air pressure and thus leakage into the alveolar space.^2,3

Immersion in water leads to increased venous return to the heart and thus central blood pooling and increased cardiac preload.² In particular, head-above-water immersion leads to a 32% increase in cardiac output and increase in mean arterial pressure.² Both cold water immersion and wetsuit usage leads to increased peripheral vasoconstriction and thus increased central pooling.^2,3 Exertion, like that required in a triathlon, race, or military exercises, leads to increased cardiac output and thus higher pulmonary arterial pressure.^3,4. Any conditions, such as hypertension, that increase preload also contributes to this pathophysiology.₃

Another potential factor is the autonomic response to exercise resulting in a mismatch between left ventricle (LV) and right ventricle (RV) afterload. Although both RV and LV afterload increase with exertion, RV afterload does not increase as much due to pulmonary vasodilation which subsequently results in a higher RV stroke volume. In a scenario where cardiac output is near its maximum, the LV cannot adequately compensate and thus pulmonary congestion results.³

Diagnostics and Imaging:

Despite being a potentially life-threatening condition, diagnosis of SIPE can be quite difficult, and it is felt to be frequently misdiagnosed or underdiagnosed.⁴

Diagnostic criteria vary and some findings suggestive of pulmonary edema, such as desaturations, rales on auscultation, or radiographic findings, are not always present.⁷ Furthermore, many of the symptoms and signs of SIPE are not specific and can be present in other conditions such as aspiration, infection, asthma exacerbation.⁴

In 2006, Ludwig et al proposed four criteria for the diagnosis of SIPE including 1) acute onset of dyspnea or hemoptysis during or immediately after swimming, 2) hypoxia with oxygen saturation of < 92% or an alveolar-arterial gradient > 30 mmHg, 3) no history of water aspiration, laryngospasm, or preceding infections, and 4) radiographic opacities consistent with an alveolar filling process or interstitial pulmonary edema that resolves within 48 hours.⁶

In 2020, Hardstedt et al proposed an algorithm for diagnosing SIPE which begins with the acute onset of cough/dyspnea immediately after swimming in cold open water. If spO2 < 95%, crackles are present on auscultation, and there is excessive sputum production or hemoptysis, SIPE should be diagnosed. If spO2 < 95% and there are no crackles OR if spO2> 95% and there are crackles with excessive sputum production and hemoptysis present in either scenario, lung ultrasound is suggested to be used to aid in diagnosis. In this proposed algorithm, SIPE is not excluded in the presence of water aspiration.⁷

In terms of imaging, chest x-ray is a practical imaging modality to assess for SIPE. Radiographs may demonstrate signs of pulmonary edema such as cephalization of pulmonary vessels, loss of vascular definition, peribronchial cuffing, and Kerley B lines. Airspace opacities and pleural effusions may also be appreciated. It should be noted that there are cases of SIPE with a normal chest x-ray.4 Additional imaging modalities may include ultrasound or computed tomography (CT), which both are very sensitive in visualizing pulmonary edema or pleural effusions.⁴

Radiograph demonstrating pulmonary edema.
Radiograph courtesy of Dr. Jeremy Jones, Radiopaedia.org, rID-6463

Management and Prevention:

As the hallmark of SIPE is relatively rapid resolution of symptoms (24-48 hours), treatment is predominantly supportive. Actions taken may include immediate removal from water, placing the keeping the individual warm, and removal of a constrictive wetsuit if present. Supplemental oxygenation or non-invasive positive pressure ventilation may also be required depending on the level of hypoxemia and respiratory distress. Beta 2-agonists may help with symptomatic relief and alveolar fluid clearance.² In some instances, diuretics may also be tried. However, the role and efficacy of pharmacological treatment is not well studied.²

As SIPE is not correlated with level of fitness, experience, or training, it is recommended that athletes focus more on their race day approach with a warm up of at least 15 minutes, starting the race at an easy pace, avoid races that are held in cold water, and being mindful of overhydration or salt loading prior to the race.³  

Pre-medication with sildenafil has been shown to be beneficial in mitigating risk of SIPE as it reduces pulmonary arterial and wedge pressures.⁸ Nifedipine has been shown to reduce the vasoconstriction in SIPE and thus Wilmshurst recommends 5 mg of nifedipine before the activity.9 For athletes who are fluid overloaded, furosemide or other diuretics may be considered although these medications may be banned at certain levels of competition.³

Summary:

• Consider SIPE in athletes in swimming competitions who experience sudden onset shortness of breath and hypoxia.
• Individuals with prior episodes of SIPE, older age, female sex, and underlying cardiac and/or pulmonary diseases may be at greater risk.
• Risk factors include cold water, increased exertion, tight swimwear, and overhydration or fluid retention.
• Imaging may demonstrate signs of pulmonary edema or pleural effusion.
• Treatment is predominantly supportive, and symptoms should resolve within 48 hours.

References:

1. Paz P, Makram J, Mallah H, Mantilla B, Ball S, Nugent K. Swimming-induced pulmonary edema. Proc (Bayl Univ Med Cent). 2020;33(3):409-412. Published 2020 Mar 9. doi:10.1080/08998280.2020.1735236
2. Borza ML, Blonien NE. Swimming-Induced Pulmonary Edema found in a U.S. Navy Basic Underwater Demolition/SEAL Recruit. Cureus. 2022;14(9):e29417. Published 2022 Sep 21. doi:10.7759/cureus.29417
3. Barouch LA. Swimming-Induced Pulmonary Edema: An Underrecognized Cause of Triathlon-Associated Medical Emergencies. JACC Case Rep. 2022;4(17):1094-1097. Published 2022 Sep 7. doi:10.1016/j.jaccas.2022.05.019
4. Grünig H, Nikolaidis PT, Moon RE, Knechtle B. Diagnosis of Swimming Induced Pulmonary Edema-A Review. Front Physiol. 2017;8:652. Published 2017 Aug 31. doi:10.3389/fphys.2017.00652
5. Hageman SM, Chakraborty RK, Murphy-Lavoie HM. Immersion Pulmonary Edema. [Updated 2023 Jul 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available here.
6. Ludwig B. B., Mahon R. T., Parrish J. S., Lamb C., Kerr S. (2004). Pulmonary edema in combat swimmers: clinical and bronchoalveolar lavage description demonstrating stress failure of the pulmonary capillaries. Hyperb. Med. 31:318.
7. Hårdstedt M, Kristiansson L, Seiler C, Braman Eriksson A, Sundh J. Incidence of Swimming-Induced Pulmonary Edema: A Cohort Study Based on 47,600 Open-Water Swimming Distances. Chest. 2021;160(5):1789-1798. doi:10.1016/j.chest.2021.06.034
8. Moon RE, Martina SD, Peacher DF, et al. Swimming-induced pulmonary edema: pathophysiology and risk reduction with sildenafil. Circulation 2016;133:988-96.
9. Wilmshurst PT. Immersion pulmonary oedema: a cardiological perspective. Diving Hyperb Med. 2019;49(1):30-40. doi:10.28920/dhm49.1.30-40