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A fit, competitive long-distance swimmer in her 50s was rushed to the hospital from her regular open water swimming event with acute shortness of breath, coughing up pink frothy sputum, a group detailed in .

The water she swam in was around 17°C (62.6 °F) and she was wearing a wet-suit.

At the hospital, she denied any chest discomfort, heart palpitation, dizziness, or preceding viral symptoms. On clinical examination, she was breathless, coughing, and had a heart rate of 100 beats per minute. Oxygen saturation was 96%, blood pressure 138/69 mm Hg, and body temperature 36.5°C (97.7°F), reported James Willis, PhD, cardiac ultrasound specialist of Royal United Hospitals Bath NHS Foundation Trust in England, and colleagues.

The group noted that the woman's symptoms and tachycardia resolved on their own within 2 hours of her arrival at the hospital.

Her cardiovascular system was normal except for the presence of fine bi-basal crepitations. The admission ECG revealed sinus rhythm with T wave inversion in leads I, AvL, and V2 with a normal cardiac axis and corrected QT interval. CT of the thorax ruled out large vessel pulmonary embolism and demonstrated perihilar ground-glass consolidation bilaterally, with more significant changes in the lower lobes.

Blood tests initially revealed elevations in white cell count (14.7 × 10⁹/L), neutrophils (12.6 × 10⁹/L), troponin T (23 and 32 ng/L), and N-terminal pro-brain natriuretic peptide (NT-Pro BNP; 974 ng/L).

Based on her history of acute shortness of breath when swimming in cold water while wearing a wet suit, along with pulmonary edema without evidence of aspiration or structural cardiac disease, and her quick recovery, she was diagnosed with swimming-induced pulmonary edema (SIPE), a subtype of immersion pulmonary edema.

Clinicians also learned that she had received her Pfizer COVID-19 booster vaccination 6 hours before her group's nighttime swim. Given the timing of the symptoms, however, they ruled out the COVID-19 booster as a contributing factor.

"Interestingly, cardiac MRI demonstrated prolonged T2 relaxation time of the basal to mid anterior, anterolateral and inferior-lateral segments, indicative of myocardial edema," noted Willis and colleagues. They added that there was evidence of basal inferolateral non-ischemic mid-wall late gadolinium enhancement which suggested possible fibrosis. Left ventricular diameter and systolic and diastolic function were all normal.

The patient told clinicians that she had experienced similar but milder symptoms while swimming in the sea just 2 weeks previously, and she had also had problems with running and pool swimming training, but assumed she was just "a bit under the weather."

The patient was monitored and discharged from hospital the next day, with laboratory and ECG findings returned to normal.

"Interval cardiac MRI demonstrated resolution of myocardial edema as well as basal cavity inferior lateral fibrosis," Willis and colleagues reported. They also observed residual basal inferior myocardial fibrosis and normal left ventricular size and function.

About 8 weeks later, the patient underwent CT coronary angiography, which showed normal coronary anatomy "with a minor burden of non-flow-limiting atheromatous plaque, along with resolution of pulmonary edema," the group noted.

Discussion

Since it was initially reported in 1989, the pathophysiology for SIPE remains unknown, but is hypothesized to be related to stress cardiomyopathy akin to Takotsubo, cold-induced coronary vasospasm or ventricular pressure overload, or an inflammatory process. SIPE likely remains under-reported, with an estimated incidence of 1.1% to 1.8% among swimmers.

People affected are frequently fit and healthy. Risk factors include advanced age, female sex, high blood pressure, long-distance swimming, cooler water temperature, and pre-existing heart disease.

of SIPE is based on acute onset of dyspnea and/or hemoptysis during or immediately after swimming in the absence of water aspiration, laryngospasm, or preceding infection; hypoxia; x-ray evidence of pulmonary edema; and a quick resolution within 2 days, the case authors detailed.

On presentation, CT angiography helps rule out coronary artery abnormalities; cardiac MRI may be used to better define cardiac structure and function, and MRI renal angiography and 24-hour urinary catecholamines may be performed to rule out less common causes of pulmonary edema, the authors explained.

Pre-existing reductions in lung volumes and expiratory flow, and elevated mean pulmonary artery pressure (PAP) and pulmonary arterial wedge pressure (PAWP) at rest, have also been with SIPE.

Affected individuals should be removed from water, remain seated in an upright position, and stop activity. Treatment is largely supportive, but often involves oxygen therapy, and in some cases, diuresis, bronchodilators, and continuous positive airway pressure. As in this case, patients typically recover fully within 1 to 2 days of leaving the water, according to the authors.

Importantly, SIPE has been implicated in about 10% of scuba-diving deaths, with left ventricular hypertrophy confirmed in all cases. Between 13% and 22% of those affected have recurring episodes, and patients should be informed of this and considered to be predisposed to SIPE. Accordingly, they are instructed to modify their swimming and diving activities -- especially in cold water -- as needed.

Case authors advised avoidance of non-steroidal anti-inflammatory drugs (NSAIDs) following an episode of SIPE, and optimization of any comorbidity that worsens diastolic function. "Prophylactic has been shown to lower PAP and PAWP, and this appears to be an effective measure in those with a history of recurrent SIPE," they added.

Case authors noted that their aim was to raise awareness among doctors and swimmers of a relatively under-recognized condition. The U.K. Diving Medical Committee has published for divers. However, "there are no formal national medical guidelines concerning the recognition and management of this complex condition," they said, urging a high level of suspicion in any patient with dyspnea following immersion.

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