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Frostbite is a common injury in high altitude medicine. Intravenous vasodilators have a proven efficacy and, recently, have been proposed as a safe outpatient treatment. Nevertheless, the lack of availability and consequently delayed application of this treatment option can result in poor clinical outcomes for patients. We present the case of a 60-year-old Chilean man with severe frostbite injuries suffered while climbing Mount Everest. The patient was initially given field treatment to the extent permitted by conditions and consensus guidelines. Unfortunately, advanced management was delayed, with iloprost administered 75 hours after the initial injury. The patient also underwent 5 days of hyperbaric and analgesic/antibiotic therapies. An early bone scan predicted a poor clinical outcome, and five of the patient's fingers, between both hands, were incompletely amputated. We present this case to exemplify the importance of advanced in-field management of frostbite injuries.

Hypothermia and frostbite occur when there is a significant decrease in central and peripheral body temperature in individuals exposed to cold windy conditions, often at high altitude or in a mountain environment. Portable hyperbaric chambers increase the barometric pressure and thereby the partial pressure of oxygen inside the chamber, and their use is a well-known treatment for altitude illness. This study aims to show that a portable hyperbaric chamber could also be used to treat hypothermia and frostbite in the field, when rescue or descent is impossible or delayed.During a European research program (SOS-MAM, Flow Pulse study) measurements were taken from 27 healthy nonacclimatized voluntary subjects (21 men, 6 women, mean age 41 ± 17) at an altitude of 3800 m (Chamonix Mountain Lab, Aiguille du Midi, France) right before and immediately after spending 1 hour in a portable hyperbaric chamber at 300 mbar. We measured digital cutaneous temperature (Tcut), digital cutaneous blood flow (Fcut), digital tissue oxygenation (TWe observed significant increases in Tchamb: 9.3°C compared with the outside temperature, Tcut: +7.5°C (±6.2°C 71%), Fcut: +58This study shows that a portable hyperbaric chamber can be used to treat frostbite and/or hypothermia in the field at altitude when descent or rescue is impossible or even simply delayed.

Brustia, Raffaele, Giulia Enrione, Bruna Catuzzo, Luca Cavoretto, Massimo Pesenti Compagnoni, Enrico Visetti, Emmanuel Cauchy, Stefanie Ziegler, and Guido Giardini. Results of a prospective observational study on mountaineering emergencies in Western Alps: mind your head. High Alt Med Biol. 17:116-121, 2016.-In the northern Italian district Valle d'Aosta district during winter and summer season the population can increase up to 170% of the resident population. A prospective monocentric observational registry was held to obtain a precise picture of seasonal mountain-related medical and traumatic major events.From 1st January 2012 to 31st December 2013 all patients admitted to the Aosta Regional Hospital Emergency Room for any event occurred above 2500 m were screened: all those affected by High Altitude Illness, Acute Illness in High Altitude, Trauma, or Cold disease were prospectively included. Activity incidence rate is expressed as the occurrence of mountain-related events per 1000 hours of mountain activity. Event Incidence rate is expressed as the occurrence of new cases per 1000 hours of mountain activity.Two hundred two patients were included during the study period. Trauma (65.1% vs. 24.6%, p 0.001) and head commotive injury (48.1% vs. 15.1%, p 0.001) were more frequent during winter compared to the summer season. High altitude illness (36.9% vs. 9.3%, p 0.001) and cold pathologies (15.1% vs. 0.1%, p 0.001) occurred more frequently in summer than in winter. Patients (51.4%) were immediately discharged from emergency room, 8.4% after a 24-hour observation period, and 30.6% required hospitalization. During summer, the event risk is 0.013 per person and 1000 hours of mountain activity, while in winter, event risk amounts to 0.005 per person and 1000 hours of mountain activity.High altitude medical events or trauma represent1% of pathologies observed in the emergency room department of a mountain district in the western Alps. Head commotive injury is the most observed mountain-related event in high altitude, in winter and during ski practice. High altitude illness and cold injuries are observed more frequently in summer, during trekking or climbing activities.

Purpose: The aim of this study is to explore the physiological vascular adaptation to exposure to high altitude and to test the hypothesis that its impairment might play a role in the pathophysiology of acute mountain sickness (AMS). Methods: 34 healthy volunteers (age 38±11years, 13 women) were studied at the sea-level and after passive ascent to 3842 m (Aguille du Midi, France). Blood pressure (BP), O2 saturation (SO2), endothelial function (flow-mediated dilation, FMD), carotid distensibility coefficient (DC), carotid-femoral pulse wave velocity (PWV), peak systolic velocity in the middle cerebral artery (MCA-PSV) were performed at sea level (T0) and after 4-h hypobaric hypoxia (T1). AMS was defined as a Lake-Louise Score>5 after 24-h hypobaric hypoxia (T2). Results: At T2 12 individuals developed AMS (AMS+). AMS+ had a greater SO2 worsening at T1 as compared to AMS- (AMS+: 97.2±1.2 to 79.3±5.8%; AMS-: 97.3±1.2 to 83.1 ± 5.7%, p=0.03), with similar heart rate increase and unchanged BP. FMD was significantly reduced in AMS+ (5.75±3.01 to 3.27±1.87%, p=0.04), but not in AMS- (4.74±2.47 to 4.02±2.36%). Mean carotid diameter was increased at T1 in both groups. DC tended to be increased in AMS- but not in AMS+, while PWV was unchanged. MCA-PSV was increased in AMS-, but not in AMS+. Conclusions: In healthy asymptomatic individuals exposed to high altitude, conduit artery endothelial function is preserved in the cerebral district vasodilatation, increased elasticity and blood flow occurs. This compensatory response is early blunted in AMS+, before symptoms onset, thus suggesting a pathogenetic role.

This study tested the hypothesis that a prolonged decrease in arterial oxygen pressure in resting or contracting skeletal muscles alters their ability to develop force through an impairment of energy-dependent metabolic processes and also through an alteration of electrophysiological events. The experiment was conducted during a 32-day simulated ascent of Mt. Everest (8848 m altitude) (Everest III Comex '97), which also allowed testing of the effects of re-oxygenation on muscle function. Maximal voluntary contractions (MVCs) of the flexor digitorum, and static handgrips sustained at 60% of MVC, were performed by eight subjects before the ascent (control), then during the stays at simulated altitudes of 5000 m, 6000 m and 7000 m, and finally 1 day after the return to 0 m. The evoked muscle compound action potential (M-wave) was recorded at rest and during the manoeuvres at 60% of MVC. The changes in median frequency of electromyographic (EMG) power spectra were also studied during the contraction at 60% of MVC. In four individuals, transient re-oxygenation during the ascent allowed us to test the reversibility of hypoxia-induced MVC and M-wave changes. At rest, a significant decrease in M-wave amplitude was noted at 5000 m. This effect was associated with a prolonged M-wave conduction time at 6000 m and an increased M-wave duration at 7000 m, and persisted after the return to 0 m. Re-oxygenation did not modify the changes in M-wave characteristics. A significant decrease in MVC was measured only during the ascent (-10 to -24%) in the non-dominant forearm of subjects who underwent re-oxygenation; this intervention slightly improved muscle strength at 6000 m and 7000 m. During the ascent and after the return to 0 m, there was a significant reduction of the median frequency decrease throughout contraction at 60% of MVC compared with the EMG changes measured before the ascent. It is concluded that prolonged exposure to hypoxia slows the propagation of myopotentials and alters sensorimotor control during sustained effort. Re-oxygenation did not affect the hypoxia-induced EMG changes and had a modest influence on muscle strength.

To the Editor: Many alternatives have been proposed for the treatment of frostbite: hemodilution, platelet-aggregation inhibitors, low-molecular-weight heparin, alpha-adrenergic vasodilators, calcium-channel inhibitors, nonsteroidal antiinflammatory agents, prostacyclin analogues, fibrinolytic agents, and hyperbaric oxygen. None have been assessed in prospective randomized trials. Small retrospective studies1–3 suggest the efficacy of thrombolysis or prostacyclin analogues against spasm and thrombosis. Between 1996 and 2008, we randomly assigned 47 patients (44 men and 3 women) with severe frostbite to one of three treatment regimens in an open-label study. Severe frostbite was defined as having at least one digit (finger or toe) with frostbite stage 3 . . .