HACE is a clinical diagnosis with the patient typically presenting with signs of encephalopathy, preceeded by signs and symptoms of Acute Mountain Sickness. Neither theory is considered the standard by which HACE is fully understood.
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In this model, hypoxia induces free radical formation causing damage/failure of the Na+/K+ ATPase Pump with resultant astrocyte swelling from osmotic-oxidative stress, with subsequent cytotoxic edema. The “revised theory” to the development of HACE argues against volume overload and intracranial hypertension as the leading cause. This theory would help to explain the seemingly random nature of AMS that can evolve into HACE.
The “tight fit” hypothesis suggests that one’s susceptibility to AMS/HACE is dependent upon the individual’s intracranial space available to compensate for increasing edema. The disruption of the blood-brain barrier from these stressors leads to subsequent cerebral edema. This leads to intracranial hypertension with elevated capillary pressure and capillary leakage. Hypoxia at altitude elicits neuro-hormonal (VEG-F, Nitric Oxide, reactive cytokines, free radicals) and hemodynamic responses resulting in hypoxia-induced cerebral vasodilation leading to over perfusion of microvascular cerebral beds. Although the exact mechanism of development of HACE is not fully understood, it is thought to be the extreme form/end-stage of AMS.
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