High Altitude Cerebral Oedema During Adventure Training on Mount Kenya

2012 ◽  
Vol 158 (3) ◽  
pp. 245-247 ◽  
Author(s):  
S Raitt
2016 ◽  
Vol 6 (3) ◽  
pp. 126-128 ◽  
Author(s):  
K.V.S. Hari Kumar ◽  
K.P. Shijith ◽  
Dalbara Singh

2017 ◽  
Vol 26 (143) ◽  
pp. 160096 ◽  
Author(s):  
Andrew M. Luks ◽  
Erik R. Swenson ◽  
Peter Bärtsch

At any point 1–5 days following ascent to altitudes ≥2500 m, individuals are at risk of developing one of three forms of acute altitude illness: acute mountain sickness, a syndrome of nonspecific symptoms including headache, lassitude, dizziness and nausea; high-altitude cerebral oedema, a potentially fatal illness characterised by ataxia, decreased consciousness and characteristic changes on magnetic resonance imaging; and high-altitude pulmonary oedema, a noncardiogenic form of pulmonary oedema resulting from excessive hypoxic pulmonary vasoconstriction which can be fatal if not recognised and treated promptly. This review provides detailed information about each of these important clinical entities. After reviewing the clinical features, epidemiology and current understanding of the pathophysiology of each disorder, we describe the current pharmacological and nonpharmacological approaches to the prevention and treatment of these diseases.


1988 ◽  
Vol 134 (2) ◽  
pp. 98-101 ◽  
Author(s):  
J. P. North

The Lancet ◽  
1975 ◽  
Vol 306 (7945) ◽  
pp. 1154 ◽  
Author(s):  
N.A. Lassen ◽  
A.M. Harper

1988 ◽  
Vol 09 (02) ◽  
pp. 170-174 ◽  
Author(s):  
C. Clarke

Trials ◽  
2019 ◽  
Vol 20 (1) ◽  
Author(s):  
O. Fisher ◽  
R. A. Benson ◽  
S. Wayte ◽  
P. K. Kimani ◽  
C. Hutchinson ◽  
...  

Abstract Background Acute mountain sickness (AMS) is a cluster of symptoms that commonly occur in those ascending to high altitudes. Symptoms can include headaches, nausea, insomnia and fatigue. Exposure to high altitude can also lead to high-altitude cerebral oedema (HACE), which is a potential cause of death whilst mountaineering. Generally, AMS precedes the development of HACE. Historical studies have demonstrated the effectiveness of regular dexamethasone administration in reducing the symptoms of AMS. However, the mechanism by which dexamethasone works to reduce symptoms AMS remains poorly understood. Further studies, simulating altitude using hypoxic tents, have characterised the effect of prolonged exposure to normobaric hypoxia on cerebral oedema and blood flow using MRI. This randomised trial assesses the effect of dexamethasone on hypoxia-induced cerebral oedema in healthy adult volunteers. Methods/design D4H is a double-blind placebo-controlled randomised trial assessing the effect of dexamethasone on hypoxia-induced cerebral oedema. In total, 20 volunteers were randomised in pairs to receive either 8.25 mg dexamethasone or normal saline placebo intravenously after 8 h of hypoxia with an FiO2 of 12%. Serial MRI images of the brain and spinal cord were obtained at hours 0, 7, 11, 22 and 26 of the study along with serum and urinary markers to correlate with the severity of cerebral oedema and the effect of the intervention. Discussion MRI has been used to identify changes in cerebral vasculature in the development of AMS and HACE. Dexamethasone is effective at reducing the symptoms of AMS; however, the mechanism of this effect is unknown. If this study demonstrates a clear objective benefit of dexamethasone in this setting, future studies may be able to demonstrate that dexamethasone is an effective therapy for oedema associated with brain and spinal cord ischaemia beyond AMS. Trial registration Clinicaltrials.gov, NCT03341676. Registered on 14 November 2017.


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