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

2021 ◽  
Author(s):  
Rachel E.F. Turner ◽  
Hannes Gatterer ◽  
Marika Falla ◽  
Justin Stevan Lawley
Keyword(s):  
High Altitude ◽  
Cerebral Edema ◽  
Vasogenic Edema ◽  
Acute Mountain Sickness ◽  
Edema Formation ◽  
Intracellular Space ◽  
High Altitude Cerebral Edema ◽  
Mountain Sickness ◽  
Cerebral Vasodilation ◽  
End Stage

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.

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

2021 ◽  
Author(s):  
Gustavo Zubieta-Calleja ◽  
Natalia Zubieta-DeUrioste
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Cerebral Edema ◽  
Acute Mountain Sickness ◽  
Point Of View ◽  
La Paz ◽  
Mountain Climbing ◽  
High Altitude Pulmonary Edema ◽  
High Altitude Cerebral Edema ◽  
Mountain Sickness

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;

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

2021 ◽  
Author(s):  
Gustavo Zubieta-Calleja ◽  
Natalia Zubieta-DeUrioste
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Cerebral Edema ◽  
Acute Mountain Sickness ◽  
Healthy Children ◽  
Number Of Children ◽  
High Altitude Pulmonary Edema ◽  
High Altitude Cerebral Edema ◽  
Potential Risks ◽  
Mountain Sickness

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.

scholarly journals The cerebral venous system and hypoxia

2016 ◽  
Vol 120 (2) ◽  
pp. 244-250 ◽  
Author(s):  
Mark H. Wilson ◽  
Christopher H. E. Imray
Keyword(s):  
Intracranial Pressure ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Venous Outflow ◽  
Edema Formation ◽  
Care Environment ◽  
Fluid Production ◽  
High Altitude Cerebral Edema ◽  
Blood Inflow ◽  
Mountain Sickness

Most hypobaric hypoxia studies have focused on oxygen delivery and therefore cerebral blood inflow. Few have studied venous outflow. However, the volume of blood entering and leaving the skull (∼700 ml/min) is considerably greater than cerebrospinal fluid production (0.35 ml/min) or edema formation rates and slight imbalances of in- and outflow have considerable effects on intracranial pressure. This dynamic phenomenon is not necessarily appreciated in the currently taught static “Monro-Kellie” doctrine, which forms the basis of the “Tight-Fit” hypothesis thought to underlie high altitude headache, acute mountain sickness, and high altitude cerebral edema. Investigating both sides of the cerebral circulation was an integral part of the 2007 Xtreme Everest Expedition. The results of the relevant studies performed as part of and subsequent to this expedition are reviewed here. The evidence from recent studies suggests a relative venous outflow insufficiency is an early step in the pathogenesis of high altitude headache. Translation of knowledge gained from high altitude studies is important. Many patients in a critical care environment develop hypoxemia akin to that of high altitude exposure. An inability to drain the hypoxemic induced increase in cerebral blood flow could be an underappreciated regulatory mechanism of intracranial pressure.

Acute Mountain Sickness

2018 ◽  
pp. 36-39
Author(s):  
Nathaniel R. Mann
Keyword(s):  
Carbon Monoxide ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Cerebral Edema ◽  
Carbon Monoxide Poisoning ◽  
Acute Mountain Sickness ◽  
Practical Management ◽  
High Altitude Cerebral Edema ◽  
Mountain Sickness

Altitude-related illness takes many forms, including cerebral edema, pulmonary edema, mountain sickness, and other conditions. Fatigue, dehydration, carbon monoxide poisoning, infections, and other illnesses can mimic or confound these processes. This chapter discusses common symptoms and treatments for high altitude cerebral edema, with a focus on practical management in field environments.

scholarly journals Microhemorrhages in Nonfatal High-Altitude Cerebral Edema

2008 ◽  
Vol 28 (9) ◽  
pp. 1635-1642 ◽  
Author(s):  
Kai Kallenberg ◽  
Christoph Dehnert ◽  
Arnd Dörfler ◽  
Peter D Schellinger ◽  
Damian M Bailey ◽  
...  
Keyword(s):  
Corpus Callosum ◽  
High Altitude ◽  
Cerebral Edema ◽  
Imaging Techniques ◽  
Vasogenic Edema ◽  
Acute Mountain Sickness ◽  
Characteristic Finding ◽  
High Altitude Cerebral Edema ◽  
Magnetic Resonance Imaging Mri ◽  
Hemosiderin Deposits

Vasogenic edema in the corpus callosum is a characteristic finding in high-altitude cerebral edema (HACE). Furthermore, microhemorrhages have been found at autopsies in brains of HACE victims. The objective of this study was to determine if microhemorrhages also occur in nonlethal HACE. Consequently, magnetic resonance imaging (MRI) was performed in patients who had suffered from HACE and in patients who had suffered from severe acute mountain sickness (AMS) by applying imaging techniques highly susceptible to blood or blood remnants. Two experienced neuroradiologists independently evaluated the exams blinded to clinical data. The MRI was performed 2 to 31 months after the event. The MRI of the HACE patients revealed multiple hemosiderin depositions in the brain—predominantly found in the corpus callosum—indicative of microhemorrhages. These changes were not present in the three AMS patients. In summary, hemosiderin deposits detectable by MRI predominantly in the corpus callosum indicate that microhemorrhages occur in nonlethal HACE, which may serve as a novel diagnostic MRI sign for HACE even many months after the event.

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