The Incidence of Subclinical High-altitude Pulmonary Oedema at High Altitude

The high-altitude pulmonary edema (HAPE) is the leading cause of death from high altitude sickness. At moderate altitude (2500-4500m) the incidence (0.2-6%) may be underestimated because only clinical HAPE leads to symptoms and motivates the patient to seek medical advice. Cremona et al. [Cremona et al. Pulmonary extravascular fluid accumulation in recreational climbers: a prospective study. Lancet 2002;359:303-09] suggested that a silent interstitial pulmonary edema arises in most recreational climbers at moderate altitude. Recently, chest sonography has been shown to effectively detect pulmonary edema and quantify extravascular lung water through the sign of "ultrasound lung comets" (ULCs) originating from water-thickened interlobular septa [Lichtenstein D et al. The comet-tail artifact. An ultrasound sign of alveolar-interstitial syndrome. Am J Respir Crit Care Med;156:1640-46]. The technique requires only basic twodimensional technology and has been applied in extreme, out-of-hospital setting, showing in recreational climbers a high prevalence of clinically silent interstitial pulmonary edema at high-altitude [Pratali L et al. Frequent subclinical high-altitude pulmonary edema detected by chest sonography as ultrasound lung comets in recreational climbers. Crit Care Med 2010;38:1818-23]. However, data for moderate altitude remain scarce, despite that mountaineers are increasing in age and comorbidities and could be more prone to high altitude emergencies. Prospective, non-randomised, observational study. Study participants are recruited from a scientific research group lead by the Ohio State University during a glaciology study on the Ortles Glacier in South Tyrol (3905m). Patients are tested for a baseline measure, during a permanent stay on the glacier camp (3h, 9h, 24h, 48h, 72h, 7d ). Parameters include chest ultrasound, Lake Louise score, cerebral sensitive score, non-invasive haemodynamic parameters (i.e. US) and markers of hypoxia responses, endothelial damage and inflammation.