Swimming-Induced Pulmonary Edema Masquerading as Acute Respiratory Distress Syndrome: A Case Report.

Immersion pulmonary edema, also known as swimming-induced pulmonary edema (SIPE), manifests with cough, dyspnea, hemoptysis, and hypoxemia from flash pulmonary edema after surface swimming, often in healthy young individuals with no predisposing conditions. SIPE commonly resolves spontaneously within 24-48 hours but can be fatal. Post-mortem findings demonstrate heavy, edematous lungs and frothy airways. Although these pathologic findings are like those seen in patients with drowning, SIPE, by definition, is associated with pulmonary edema that develops with a closed glottis without drowning/aspiration. However, patients who develop SIPE during swimming could lose consciousness and drown. Its pathophysiology is poorly understood, and the medical literature infrequently describes SIPE. Due to the multifactorial and complex pathophysiology and the scarcity of medical literature describing SIPE, the diagnosis could be difficult at presentation. This case report elaborates on diagnosing and treating swimming-induced pulmonary edema in a hypertensive and obese female who presented to our emergency room with an acute onset of shortness of breath after recreational swimming in a pool.

Symptom Duration, Recurrence, and Long-Term Effects of Swimming-Induced Pulmonary Edema: A 30-Month Follow-Up Study.

BACKGROUND: Swimming-induced pulmonary edema (SIPE) has been reported to subside within 24 to 48 h, but comprehensive follow-up studies on symptom duration and long-term effects are missing. RESEARCH QUESTION: What are 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 at admission. Telephone interviews at 10 days and 30 months were performed to explore symptom duration, recurrence of SIPE symptoms, need for 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 patients were women, and their mean age was 48 years. At the 10-day follow-up, symptom duration > 2 days after the swimming race was reported by 38%. The most common symptoms were dyspnea and cough. In patients at 30-month follow-up, 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 = .045 and P = .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 < 48 h, whereas 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.

Swimming-Induced Pulmonary Edema found in a U.S. Navy Basic Underwater Demolition/SEAL Recruit.

A rare condition that can potentially be fatal, immersion pulmonary edema (also known as swimming-induced pulmonary edema, SIPE) occurs when the lungs fill with fluid during a physically exerting swim not associated with aspiration. This case study illustrates the diagnosis and treatment of swimming-induced pulmonary edema in a healthy young male recruit undergoing training at the United States Naval Special Warfare Basic Underwater Demolition/SEAL (BUD/S) course. This case report explores the clinical presentation, pathophysiology, and management of SIPE.

Swimming-Induced Pulmonary Edema: An Underrecognized Cause of Triathlon-Associated Medical Emergencies.

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.).

Immersion-Induced Mitral Regurgitation: A Novel Risk Factor for Swimming-Induced Pulmonary Edema.

Immersion pulmonary edema, more commonly referred to as swimming-induced pulmonary edema (SIPE), is a well-documented condition believed to be a result of immersion physiologic condition that is characterized by a peripheral-to-central redistribution of blood volume. It disproportionally affects young, healthy athletes with no clinically overt cardiovascular or pulmonary conditions. We present four cases of healthy athletes with previously documented SIPE, who participated in Institutional Review Board-approved clinical studies that examined the pathophysiologic condition and prevention of SIPE. During standard recumbent echocardiography, trivial mitral regurgitation was observed in all four individuals. Acute exacerbation of their mitral regurgitation was observed during immersion with both immersed resting and immersed exercise echocardiography, contributing to the development of SIPE. These observations demonstrate that the occurrence of subclinical or trivial mitral valve regurgitation during dry rest is a novel risk factor for SIPE. We propose the use of immersion echocardiography as a useful investigative tool for otherwise healthy individuals with SIPE and no previously explainable cause.

Swimming-Induced Pulmonary Edema: Evaluation of Prehospital Treatment With CPAP or Positive Expiratory Pressure Device.

BACKGROUND: Swimming-induced pulmonary edema (SIPE) occasionally occurs during swimming in cold open water. Although 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, from 2017 through 2019. Swimmers with a diagnosis of SIPE and with peripheral oxygen saturation (Spo2) of ≤ 95%, persistent respiratory symptoms, or both were eligible for the study. NPPV was administered on site as CPAP by facial mask or as positive expiratory pressure (PEP) by a PEP device. Discharge criteria were Spo2 of > 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 received treatment with a PEP device, and one required tracheal intubation. In total, 108 individuals (91%) were discharged after NPPV for a median of 10 to 20 min and 11 individuals (9%) required hospital transfer. NPPV resulted in increased Spo2 from a median of 91% to 97% (P < .0001) together with improvement of six patient-reported respiratory symptoms (median numerical rating scales, 1-7 to 0-1; P < .0001). No significant decrease in auscultation of crackles (93% vs 87%; P = .508) or pulmonary edema on LUS (100% vs 97%; P = .500) was seen during NPPV treatment. INTERPRETATION: NPPV administered as CPAP or via a 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 findings did not.

Incidence of Swimming-Induced Pulmonary Edema: A Cohort Study Based on 47,600 Open-Water Swimming Distances.

BACKGROUND: Despite increasing awareness of swimming-induced pulmonary edema (SIPE), large population-based studies are lacking and the incidence is unknown. RESEARCH QUESTION: What is the incidence of SIPE in a mixed group of competitive and recreational swimmers during a large open-water swimming event? METHODS: In four consecutive years (2016-2019), a prospective cohort study was conducted during Sweden's largest open-water swimming event, Vansbrosimningen. All swimmers seeking medical care with acute respiratory symptoms were eligible for the study. SIPE diagnosis was based on clinical findings in 2016 and 2017 and pulmonary edema assessed by lung ultrasound in 2018 and 2019. Data on patient characteristics, clinical findings, and information about the race were collected. RESULTS: Based on 47,573 consecutive swimming distances, 322 patients with acute respiratory symptoms (0.68%; CI, 0.61%-0.75%) were treated at the mobile medical unit. Of these, 211 patients (0.44%; CI, 0.39%-0.51%) received a diagnosis of SIPE. The annual incidence of SIPE was 0.34%, 0.47%, 0.41%, and 0.57%, respectively, from 2016 through 2019. Most patients diagnosed with SIPE were women (90%), despite about equal percentages of men and women participating (47% men and 53% women). The incidence of SIPE overall was 0.75% in women and 0.09% in men. The incidence increased with age, from 0.08% in the youngest age group (18-30 years) to 1.1% in the oldest age group (≥ 61 years). Based on multiple logistic regression analysis, the adjusted odds for SIPE occurring was 8.59 times higher for women compared with men and 12.74 times higher for the oldest age group compared with the youngest age group. INTERPRETATION: The incidence of SIPE over 4 years during a large open-water swimming event in Sweden was 0.44%. The incidence was higher in women than in men and increased with age.

Swimming-Induced Pulmonary Edema: Diagnostic Criteria Validated by Lung Ultrasound.

BACKGROUND: Despite the increasing popularity of open water swimming worldwide, swimming-induced pulmonary edema (SIPE) is a poorly recognized condition lacking established diagnostic criteria. RESEARCH QUESTION: The aim of this study was to identify diagnostic criteria of SIPE during a large open water swimming event. STUDY DESIGN AND METHODS: In this cross-sectional study, 17,904 individuals swam 1,000, 1,500, or 3,000 m in cold open water during Sweden's largest open water swimming event in 2018 and 2019. Of 166 swimmers seeking medical attention for acute respiratory symptoms, 160 were included in the study. Medical history, symptoms, and clinical findings were collected. On-site lung ultrasound (LUS) was performed to verify pulmonary edema. RESULTS: Pulmonary edema was confirmed by LUS in 102 patients (64%); findings were unilateral in 11 (7%). Peripheral oxygen saturation was identified as a strong independent diagnostic test for pulmonary edema, with ≤ 95% as the suggested cut off based on receiver-operating characteristic curve analysis (area under the curve, 0.893; P < .0001). Crackles on lung auscultation, predominantly over the anterior chest, identified 88% of patients with edema. Peripheral oxygen saturation ≤ 95% or auscultation findings of crackles identified pulmonary edema with a sensitivity of 97% and a specificity of 86%. A specificity of 98% and a positive predictive value of 99% for LUS-verified pulmonary edema were reached if patients presented with both oxygen saturation ≤ 95% and auscultation of crackles. INTERPRETATION: We suggest a clinical algorithm for diagnosis of SIPE for swimmers with acute respiratory symptoms during swimming in cold open water. Novel features of focally distributed edema in the anterior parts of the lungs, sometimes unilateral, add to this unique dataset of an underreported condition.

Late-Presenting Swimming-Induced Pulmonary Edema: A Case Report Series from the Norseman Xtreme Triathlon.

Swimming-induced pulmonary edema (SIPE) may develop during strenuous physical exertion in water. This case series reports on three cases of suspected late-presenting SIPE during the Norseman Xtreme Triathlon. A 30-year-old male professional (PRO) triathlete, a 40-year-old female AGE GROUP triathlete and a 34-year-old male AGE GROUP triathlete presented with shortness of breath, chest tightness and coughing up pink sputum during the last part of the bike phase. All three athletes reported an improvement in breathing during the first major uphill of the bike phase and increasing symptoms during the downhill. The PRO athlete had a thoracic computed tomography, and the scan showed bilateral ground glass opacity in the peripheral lungs. The male AGE GROUP athlete had a normal chest x-ray. Both athletes were admitted for further observation and discharged from hospital the following day, with complete regression of symptoms. The female athlete recovered quickly following pre-hospital oxygen treatment. Non-cardiogenic pulmonary edema associated with endurance sports is rare but potentially very dangerous. Knowledge and awareness of possible risk factors and symptoms are essential, and the results presented in this report emphasize the importance of being aware of the possible delayed development of symptoms. To determine the presence of pulmonary edema elicited by strenuous exercise, equipment for measuring oxygen saturation should be available for the medical staff on site.

Swimming induced pulmonary oedema in athletes - a systematic review and best evidence synthesis.

BACKGROUND: Swimming induced pulmonary oedema is an uncommon occurrence and usually presents during strenuous distance swimming in cold water. The prevalence is most likely underreported and the underlying mechanisms are controversial. The purpose of this study was to summarize the evidence with regards to prevalence, pathophysiology and treatment of swimming induced pulmonary oedema in endurance athletes. METHODS: Medline, Embase, Scopus and Google Scholar were searched and level I-IV from 1970 to 2017 were included. For clinical studies, only publications reporting on swimming-induced pulmonary oedema were considered. Risk of bias was assessed with the ROBINS-I tool, and the quality of evidence was assessed with the Cochrane GRADE system. For data synthesis and analysis, a best evidence synthesis was used. RESULTS: A total of 29 studies were included (174 athletes). The most common symptom was cough, dyspnoea, froth and haemoptysis. The risk of bias for the clinical studies included 13 with moderate risk, 3 with serious, and 4 with critical. Four of the pathophysiology studies had a moderate risk, 3 a serious risk, and 1 a critical risk of bias. A best evidence analysis demonstrated a strong association between cold water immersion and in increases of CVP (central venous pressure), MPAP (mean pulmonary arterial pressure), PVR (peripheral vascular resistance) and PAWP (pulmonary arterial wedge pressure) resulting in interstitial asymptomatic oedema. CONCLUSION: The results of this study suggest a moderate association between water temperature and the prevalence of SIPE. The presence of the clinical symptoms cough, dyspnoea, froth and haemoptysis are strongly suggestive of SIPE during or immediately following swimming. There is only limited evidence to suggest that there are pre-existing risk factors leading to SIPE with exposure to strenuous physical activity during swimming. There is strong evidence that sudden deaths of triathletes are often associated with cardiac abnormalities.

Pulmonary Aspects of Exercise and Sports.

Although the lungs are a critical component of exercise performance, their response to exercise and other environmental stresses is often overlooked when evaluating pulmonary performance during high workloads. Exercise can produce capillary leakage, particularly when left atrial pressure increases related to left ventricular (LV) systolic or diastolic failure. Diastolic LV dysfunction that results in elevated left atrial pressure during exercise is particularly likely to result in pulmonary edema and capillary hemorrhage. Data from race horses, endurance athletes, and triathletes support the concept that the lungs can react to exercise and immersion stress with pulmonary edema and pulmonary hemorrhage. Immersion in water by swimmers and divers can also increase stress on pulmonary capillaries and result in pulmonary edema. Swimming-induced pulmonary edema and immersion pulmonary edema in scuba divers are well-documented events caused by the fluid shifts that occur with immersion, elevated pulmonary venous pressure during extreme exercise, and negative alveolar pressure due to inhalation resistance. Prevention strategies include avoiding extreme exercise, avoiding over hydration, and assuring that inspiratory resistance is minimized.