Rescue Emergencies Due to High-Altitude Illnesses Are Rare in Switzerland

Background: Despite a potential high risk of acute mountain sickness (AMS) in the Swiss Alps, there is a lack of analyses concerning its relevance over longer periods. In consequence, the aim of this study is to analyze the prevalence of AMS in comparison to other causes of mountain emergencies in recent years in Switzerland. Material and Methods: Based on the central registry of mountain emergencies of the Swiss Alpine Club (SAC), all cases in the period between 2009 and 2020 were analyzed for AMS including the most severe forms of high-altitude pulmonary edema (HAPE) and high-altitude cerebral edema (HACE). Emergencies were assessed for the severity of the event with a National Advisory Committee for Aeronautics (NACA) score. Results: From a total of 4596 high-altitude mountaineering emergencies identified in the observational period, a total number of 352 cases of illnesses were detected. Detailed analysis revealed 85 cases of AMS, 5 cases of HAPE, and 1 case of HACE. The average altitude was 3845 ± 540 m. Most cases were in the canton of Valais, especially in the Monte Rosa region and the mountains of the Mischabel group (Täschhorn, Dom, Südlenz, Nadelhorn, Hohberghorn). There were only three deaths related to high-altitude illnesses; all the other events could be identified as moderate to severe but not life-threatening. Discussion: An emergency due to AMS that requires rescue is unlikely in the Swiss Alps. This does not imply that AMS is not a concern. However, the facts that the maximal altitude is relatively low and that fast self-descents often seem possible probably minimize the likelihood that mountaineers with symptoms contact emergency services.

The impact of hypoxia on blood-brain, blood-CSF and CSF-brain barriers

The blood-brain barrier (BBB), blood-cerebrospinal fluid barrier (BCSFB) and CSF-brain barriers (CSFBB) are highly regulated barriers in the central nervous system comprising of complex multi-cellular structures that separate nerves and glia from blood and cerebrospinal fluid, respectively. Barrier damage has been implicated in the pathophysiology of diverse hypoxia-related neurological conditions including stroke, multiple sclerosis, hydrocephalus and high-altitude cerebral edema. Much is known about damage to the BBB in response to hypoxia but much less is known about the BCSFB and CSFBB. Yet it is known that these other barriers are implicated in damage after hypoxia or inflammation. In the 1950s, it was shown that the rate of radionucleated human serum albumin passage from plasma to CSF was 5-times higher during hypoxic than normoxic conditions in dogs, due to blood-CSF barrier disruption. Severe hypoxia due to administration of the bacterial toxin, lipopolysaccharide (LPS) is associated with disruption of the CSFBB. This review discusses the anatomy of the BBB, BCSFB and CSFBB, and the impact of hypoxia and associated inflammation on the regulation of those barriers.

High altitude cerebral edema - its own entity or end-stage acute mountain sickness?

High-altitude cerebral edema (HACE) and acute mountain sickness (AMS) are neuro-pathologies associated with rapid exposure to hypoxia. However, speculation remains regarding the exact etiology of both HACE and AMS and whether or not they share a common mechanistic pathology. This mini-review outlines the basic principles of HACE development, highlighting how edema could develop from 1) a progression from cytotoxic swelling to ionic edema, or 2) permeation of the blood brain barrier (BBB) with or without ionic edema. Thereafter, discussion turns to the available neuroimaging literature in the context of cytotoxic, ionic or vasogenic edema in both HACE and AMS. While HACE is clearly caused by an increase in brain water of ionic and/or vasogenic origin, there is very little evidence that this type of edema is present when AMS develops. However, cerebral vasodilation, increased intracranial blood volume and concomitant intracranial fluid shifts from the extracellular to the intracellular space, as interpreted from changes in diffusion indices within white matter, are observed consistently in persons acutely exposed to hypoxia and with AMS. Therefore, herein we explore the idea that intracellular swelling occurs alongside AMS, and is a critical pre-cursor to extracellular ionic edema formation. We propose that this process produces a subtle modulation of the BBB, which either together with or independent of vasogenic edema provides a transvascular segue from the end-stage of AMS to HACE. Ultimately, this mini-review seeks to shed light on the possible processes underlying HACE pathophysiology, and thus highlight potential avenues for future prevention and treatment.

Acute Mountain Sickness, High Altitude Pulmonary Edema, and High Altitude Cerebral Edema: An enhanced view from the High Andes

Background: Travelling to high altitude for entertainment or work is sometimes associated with acute high altitude pathologies. In the past, scientific literature from the lowlander point of view was mostly based on mountain climbing. Nowadays, altitude descent and evacuation are not mandatory in populated highland cities. Methods: We present how to diagnose and treat acute high altitude pathologies based on 50 years of high altitude physiology and medical practice in hypobaric hypoxic diseases in La Paz, Bolivia (3,600m; 11,811ft), at the High Altitude Pulmonary and Pathology Institute (HAPPI – IPPA) altitudeclinic.com.Results: Acute Mountain Sickness, High Altitude Pulmonary Edema, and High Altitude Cerebral Edema are all medical conditions faced by some travelers. These can occasionally present after flights to high altitude cities, both in lowlanders or high-altitude residents during re-entry, particularly after spending more than 20 days at sea level.Conclusions: Acute high altitude ascent diseases can be adequately diagnosed and treated without altitude descent. Traveling to high altitude should not be feared as it has many benefits;

Acute Mountain Sickness, High Altitude Pulmonary Edema, and High Altitude Cerebral Edema: A view from the High Andes

Healthy children and those with pre-existing conditions traveling to high altitude may experience diverse physiologic changes. Individuals who are not acclimatized and ascend rapidly are at risk of developing acute high altitude illnesses (HAI), which may occur within a few hours after arrival at high altitudes, being acute mountain sickness (AMS) the most common. In very few cases, serious complications may occur, including High Altitude Pulmonary Edema (HAPE) and very rarely High Altitude Cerebral Edema (HACE). Moreover, the number of children and adolescents traveling on commercial aircrafts is growing and this poses a need for their treating physicians to be aware of the potential risks of hypoxia while air traveling. In this article we present 50 years of medical practice at high altitude treating these pathologies succesfully with no casualties.