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Year : 2013  |  Volume : 7  |  Issue : 4  |  Page : 488-489

High altitude cerebral edema with a fatal outcome within 24 h of its onset: Shall acclimatization be made compulsory?

1 Department of Neuroanaesthesiology and Critical Care, Jai Prakash Narayan Apex Trauma Centre, All India Institute of Medical Sciences, New Delhi, India
2 Department of Neurosurgery, Max, Patpargang, New Delhi, India

Correspondence Address:
Keshav Goyal
Department of Neuroanaesthesiology and Critical Care, Jai Prakash Narayan Apex Trauma Centre, All India Institute of Medical Sciences, New Delhi 110 029
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1658-354X.121070

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Date of Web Publication7-Nov-2013

How to cite this article:
Bhutia M, Goyal K, Rai A, Kedia S, Kumar N, Mitra R. High altitude cerebral edema with a fatal outcome within 24 h of its onset: Shall acclimatization be made compulsory?. Saudi J Anaesth 2013;7:488-9

How to cite this URL:
Bhutia M, Goyal K, Rai A, Kedia S, Kumar N, Mitra R. High altitude cerebral edema with a fatal outcome within 24 h of its onset: Shall acclimatization be made compulsory?. Saudi J Anaesth [serial online] 2013 [cited 2022 Jun 28];7:488-9. Available from:


High altitude cerebral edema (HACE) is a rare clinical condition which occurs as a result of travelling to high altitude without acclimatization, causing significant morbidity, and mortality. Clinically and pathophysiologically, HACE has been considered extension of acute mountain sickness (AMS), characterized by features of encephalopathy. Generally, it takes 3-5 days to develop HACE after AMS. We present a case of a 39-year-old healthy male patient who developed HACE with fatal out-come within 24 h of travelling to a height of 3524 meters above sea level.

A 39-year-old male patient with no co-morbidity, residing at 560 meters above sea-level decided to go on a vacation by air to an altitude of 3524 m without any prior acclimatization. He started having generalized headache associated with vertigo, nausea, and vomiting, progressively worsening within 14 h of arrival at his destination. He was soon admitted to a local hospital with respiratory distress and altered sensorium. There he was intubated and put on mechanical ventilation. Non-contrast computed tomography (NCCT) of head revealed bilateral thalamic and brain stem infarct. After having received symptomatic and supportive care he was referred to our center.

Thirty-six hour after onset of symptoms; he was received in our casualty with a Glasgow coma scale of E 1 V T M 1 and no cardiac activity. Patient was resuscitated within 10 min using Advanced Cardiac Life Support (ACLS) guidelines. Repeat NCCT head here showed same infarcts with diffuse brain edema and hydrocephalus [Figure 1]. Patient had two more incidence of cardiac arrest from which he was successfully resuscitated. His pupils were fixed dilated, absent corneal, conjunctival, cough, and gag reflex with negative Dolls eye movement although with spontaneous respiration. He was put on mechanical ventilation and could be given only symptomatic and supportive care. Following day, apnea and calorie test was done which was positive and patient was declared brain dead. The relatives of the patient took the patient home against medical advice.

HACE has a lesser incidence than high altitude pulmonary edema (HAPE) and acute mountain sickness (AMS) and occurs commonly in conjunction with HAPE. [1] At an altitude of 3000 m, it can occur in unacclimatized persons, lowest reported altitude of occurrence being 2100 m. [2] Here, the patient had rapidly ascended to an altitude of 3343 meters and went into coma within 3 h of developing symptoms of AMS (headache, nausea, and vomiting). The recommended ascent is 300 m/day while the ascent in our case was almost 10 times the recommended ascent. Space-occupying intracranial masses or cysts is perhaps the only identified risk factor. [3] This patient was a middle-aged healthy person with no risk factors.
Figure 1: Non.contrast computed tomography head showing holocranial infarct with diffuse brain edema and hydrocephalus

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Typically, HACE is preceded by AMS for a period of 24-36 h. Although initial symptoms are subtle psychological changes, patient may present with altered sensorium or ataxic gait. Anorexia and nausea is a consistent symptom while seizure is rare. [4] With delay in diagnosis, patient slowly progresses to coma. [5],[6] Computed tomography scans of the brain reveal attenuation of signals in the white matter along with compression of sulci and flattening of gyri as was observed in our case. Although magnetic resonance imaging (MRI) findings are more confirmatory, [7] patient here was too critical to be taken up for MRI. Pathophysiology of HACE involves raised intracranial pressure with vasogenic cerebral edema. [7] Terminal stage findings from brain autopsy include venous sinus thrombosis and small petechial hemorrhages and thrombosis in other parts of the brain. [4] Mechanical factors leading to break-down of blood brain barrier, biochemical factors leading to increased permeability of blood brain barrier or both are the possible mechanism. [8]

Timely treatment is the key to success and the treatment consists of proper oxygenation and descent to lower altitude. HACE requires greater descent as compared to AMS and HAPE. [6] Other modalities of treatment include large dose steroids and cerebral decongestants, but care must be taken to maintain adequate intravascular volume to maintain cerebral perfusion pressure. Prolonged recovery time and permanent impairment are common.

Prevention is better than cure; people who plan to ascent to high altitude must be properly acclimatized and should have a fair knowledge regarding this clinical entity to recognize the symptoms to institute therapy at the earliest. Ascent should be in steps with rest/halt at some place of lower height for optimum time. Acetazolamide 125 mg twice daily may be started a day before the ascent to accelerate acclimatization and avoid complications.

HACE presents a serious threat to the life hence, graded, reasonable rate of ascent to high altitude must be done in order to prevent HACE. Early recognition of the symptoms and its treatment, proper oxygenation and descent to lower altitude is the key to surviving this clinical entity. Acclimatization should be made compulsory or a word of caution is warranted to the young, healthy, and enthusiastic tourists to high altitude to hold their nerves before indulging in recreational activities and should give time to adjust to the environment.

  References Top

1.Basnyat B, Subedi D, Sleggs J, Lemaster J, Bhasyal G, Aryal B, et al. Disoriented and ataxic pilgrims: An epidemiological study of acute mountain sickness and high-altitude cerebral edema at a sacred lake at 4300 m in the Nepal Himalayas. Wilderness Environ Med 2000;11:89-93.  Back to cited text no. 1
2.Dickinson J. Severe acute mountain sickness. Postgrad Med 1979;55:454-8.  Back to cited text no. 2
3.Hackett PH. Subarachnoid cyst and ascent to high altitude - A problem? High Alt Med Biol 2000;1:337-9.  Back to cited text no. 3
4.Dickinson JG. High altitude cerebral edema: Cerebral acute mountain sickness. Semin Respir Med 1983;5:151-8.  Back to cited text no. 4
5.Norboo T, Angchuk ST. High altitude cerebral edema in Ladakh, in: Progress in Mountain Medicine and High Altitude Physiology. The 3 rd World Congress on Mountain Medicine and High Altitude Physiology, Matsumoto, Japan, Japanese Society of Mountain Medicine. 1994. p. 210-1.  Back to cited text no. 5
6.Hackett PH, Roach RC. High altitude cerebral edema. High Alt Med Biol 2004;5:136-46.  Back to cited text no. 6
7.Hackett PH, Yarnell PR, Hill R, Reynard K, Heit J, McCormick J. High-altitude cerebral edema evaluated with magnetic resonance imaging: Clinical correlation and pathophysiology. JAMA 1998;280:1920-5.  Back to cited text no. 7
8.Krasney JA. A neurogenic basis for acute altitude illness. Med Sci Sports Exerc 1994;26:195-208.  Back to cited text no. 8


  [Figure 1]

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