High-altitude cerebral edema (HACE) is a medical condition in which the brain swells with fluid because of the physiological effects of traveling to a high altitude.
It generally appears in patients who have acute mountain sickness and involves disorientation, lethargy, and nausea among other symptoms.
Early symptoms of HACE generally correspond with those of moderate to severe acute mountain sickness (AMS).
[2] Initial symptoms of HACE commonly include confusion, loss of consciousness,[3] fever, ataxia,[4] photophobia, rapid heart beat,[5] lassitude, and an altered mental state.
Everest Disaster, Jon Krakauer describes the effects of HACE upon Dale Kruse, a forty-four-year-old dentist and one of the members of Scott Fischer's team: 'Kruse was having an incredibly difficult time simply trying to dress himself.
He put his climbing harness on inside out, threaded it through the fly of his wind suit, and failed to fasten the buckle; fortunately, Fischer and Neal Beidleman noticed the screwup before Kruse started to descend.
"If he'd tried to rappel down the ropes like that," says Beidleman, "he would have immediately popped out of his harness and fallen to the bottom of the Lhotse Face."
If a lumbar puncture is performed, it will show normal cerebral spinal fluid and cell counts but an increase in pressure.
[8] In one study, CT scans of patients with HACE exhibited ventricle compression and low density in the cerebellum.
[8] Only a few autopsies have been performed on fatal cases of HACE;[9] they showed swollen gyri, spongiosis of white matter, and compressed sulci.
[12] Prolonged exertion in low oxygen also causes serious hypocapnia, lower carbon dioxide in the bloodstream,[13] which may play a role in HACE.
[9] An MRI study found microhemorrhages in the corpus callosum of HACE patients,[16] and hypoxia may also cause microvascular permeability.
[17] MRI scans of patients with HACE showed increased T2 in the corpus callosum, although grey matter was unchanged.
This demonstrated that the blood-brain barrier was broken by cerebral blood vessels, thus interfering with white matter metabolism.
[18] Another study looked at the brains of people with HACE several months after their recovery; it showed hemosiderin deposits in the corpus callosum, evidence of vascular permeability.
[9][19] After the failure of the ATPase pumps, free radicals form and cause damage that complicates the edema.
[13] Evidence against cytotoxic edema includes the high levels of hypoxemia (low bloodstream oxygen) needed to cause it.
[3] In patients with AMS, the onset of HACE is usually indicated by vomiting, headache that does not respond to non-steroidal anti-inflammatory drugs, hallucinations, and stupor.
[5] Patients with HACE should be brought to lower altitudes and provided supplemental oxygen,[18] and rapid descent is sometimes needed to prevent mortality.
[17] Three studies that examined how mice and rat brains react to hypoxia gave some credence to this idea.
[31] In addition to oxygen therapy, a portable hyperbaric chamber (Gamow bag) can by used as a temporary measure in the treatment of HACE.
[5] Descriptions of fatal cases often involve climbers who continue ascending while experiencing the condition's symptoms.
[3] One early description of HACE may have been published in 1969 after a group of Indian soldiers made a rapid ascent to almost 6,000 metres (20,000 ft).