Abstract
Avalanche burial occasionally precipitates pulmonary edema, yet its pathogenesis remains poorly understood. Two male back-country skiers (aged 39 and 53 years) were completely buried for 30 min and 20 min, respectively, by the same avalanche, and immobilized in a right-lateral posture without safety devices. They arrived 2 h post-extrication, conscious but hypothermic (32.4 °C and 34.2 °C, respectively), tachycardic, tachypneic, and hypoxemic (SpO2 88% and 83%, respectively). Chest radiography and computed tomography demonstrated extensive infiltrates or ground-glass opacities confined predominantly to the gravity-dependent right lung and no cardiomegaly. C-reactive protein and N-terminal pro-B-type natriuretic peptide values were within normal limits, and transthoracic echocardiography showed preserved biventricular function. Low-flow oxygen and passive rewarming corrected hypoxia and hypothermia; the pulmonary infiltrates resolved within 24 h, permitting discharge without sequelae. Classical mechanisms, such as negative-pressure pulmonary edema from airway obstruction, hypoxia-induced left ventricular failure, and edema secondary to regional hypoxic pulmonary vasoconstriction, do not fully explain the unilateral dependent pattern observed. We propose that excessive sympathetic nervous system activation and fluid distribution changes caused by extreme emotional stress, cold exposure, systemic hypoxia, whole-body compression by snow, and head-down posture led to an excessive cardiac load increase, resulting in gravity-enhanced cardiogenic edema despite normal intrinsic cardiac function. These cases suggest a previously unrecognized hemodynamic pathway for avalanche-related pulmonary edema. Awareness of cardiac overload as a potential contributor may refine field triage and postrescue management. Additional clinical and experimental studies are warranted to validate this hypothesis and inform preventive strategies.
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