LAUSR

A physically fit 56-year-old experienced dyspnoea and haemoptysis after starting the swim leg of a half triathlon, forcing him to terminate the swim within 8minutes. Noteworthy, his wetsuit felt constrictive and he had taken ibuprofen prior to the race to ease an aching knee. Physical examination revealed marked hypoxaemia with bilateral rales. CT scan excluded pulmonary embolism and showed diffuse ground-glass opacifications, in the absence of increased CRP or BNP. Troponin T was mildly elevated; however, resting ECG and left ventricular regional wall motion (as evaluated by bedside TTE) were normal. A diagnosis of swimming-induced pulmonary oedema (SIPE) was made. Endurance exercise elicits profound cardiorespiratory stresses, which can be particularly high in water-based sports as a result of simultaneous exertion, voluntary apnoea, cold-water exposure and bodily immersion. In susceptible individuals, pulmonary vascular pressures rise up to a point of capillary breach, leading to high-permeability pulmonary oedema. Known predisposing factures include arterial hypertension, long event distance, female gender and fish oil consumption. Treatment is supportive: immediate evacuation from the water, removal of cold compressive clothing, supplemental oxygen if clinically indicated and longacting inhaled b2-agonist for symptomatic relief and improved alveolar fluid clearance. Although SIPE is rare (1–2% of triathletes) and largely self-limiting, early diagnosis is still paramount as it can be life-threatening. Moreover, up to one-third of patients experience repeat episodes on re-exposure, during emotional stress or at high altitude. Raising awareness of this disorder among athletes, race organisers and supervising physicians is therefore mandatory.