Hypobaric Hypoxia and the Failing Brain: High-altitude Cerebral Edema in the Nepalese Himalayas
Govinda Bhandari1, Neeharika Balla2, Raghabendra Kumar Mahato3
1Tribhuvan University, Institute of Medicine, 2Maharajah’s Institute of Medical Sciences, 3Gandaki Medical College Teaching Hospital and Research Centre
Background:
High-altitude cerebral edema (HACE) represents a severe form of hypobaric hypoxic encephalopathy encountered at elevations typically above 2,500 meters.HACE, though less common, is the most life-threatening, characterised by altered mental status, gait ataxia, varying degrees of psychiatric changes, and neurological deficit, which could progress to coma or even death within 24 hours of onset if untreated.
Design/Methods:
Case Presentation: A 32-year-old male developed acute neurological deterioration during descent from Tilicho Lake (4,919 m) in the Annapurna region of Nepal. After rapid ascent from Besisahar (760 m) to Khangsar (3,750 m) in one day and further ascent to Tilicho Base Camp (4,140 m), he experienced severe headache, vomiting, dizziness, and progressive disorientation. While descending, he became ataxic, lost consciousness, and had urinary incontinence.
At the aid post, his oxygen saturation was 35% on room air and GCS was 8 (E2V2M4). He had no fever, pulmonary findings, or focal neurological deficits. Based on rapid ascent history, neurological signs, and absence of pulmonary edema, HACE was clinically diagnosed. Immediate treatment with supplemental oxygen and intramuscular dexamethasone (8 mg) resulted in gradual recovery of consciousness within 4–5 hours. His transient visuospatial disorientation and slurred speech resolved completely with descent and continued oxygen therapy.
Results:
Discussion: This case exemplifies the neurocritical spectrum of altitude induced hypoxic encephalopathy, demonstrating that rapid ascent and hypobaric hypoxia can precipitate reversible cerebral dysfunction even in healthy individuals. Recognition and management of HACE in resource limited setting are vital to prevent fatal outcomes.The rapid reversibility after descent highlights the critical importance of early recognition and altitude descent over drugs alone.
Conclusions:
HACE represents a preventable but potentially fatal hypoxic encephalopathy. Neurologists should recognize it as a neurocritical emergency, particularly as high-altitude exposure becomes more common through rapid vehicular ascent. Rapid descent, prompt administration of dexamethasone and oxygen can be lifesaving.
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