118:'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." '"It was like I was very drunk," Kruse recollects. "I couldn't walk without stumbling, and completely lost the ability to think or speak. It was a really strange feeling. I'd have some word in my mind, but I couldn't figure out how to bring it to my lips. So Scott and Neal had to get me dressed and make sure my harness was on correctly, then Scott lowered me down the fixed ropes." By the time Kruse arrived in Base Camp, he says, "it was still another three or four days before I could walk from my tent to the mess tent without stumbling all over the place."'
336:. 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). It is not definitely established whether they had HACE or acute decompression sickness. MRI has been used to study the effects of high altitude on the brain, providing the best evidence about the condition. A 1998 MRI study of nine climbers with HACE clearly demonstrated vasogenic edema.
283:) can by used as a temporary measure in the treatment of HACE. These devices simulate a decrease in altitude of up to 7000 ft, but they are resource intensive and symptoms will often return after discontinuation of the device. Portable hyperbaric chambers should not be used in place of descent or evacuation to definitive care.
154:(oxygen deprivation). This occurs after the body is exposed to a low-oxygen environment and before it acclimatizes. The rate of change from a normal oxygen environment and how little oxygen is in the new environment can be used to predict the chance of developing HACE. Prolonged exertion in low oxygen also causes serious
101:, and an altered mental state. Those affected generally attempt to cease physical activities, regardless of their necessity for survival. Severe headaches develop and people lose the ability to sit up. Retinal venous dilation occurs in 59% of people with HACE. Rarer symptoms include brisk deep tendon reflexes,
339:
Data about HACE are lacking because it generally occurs in remote areas, far from hospitals and is generally rare. It is uncommon for doctors to be able to study victims within six days of the condition's development. Animal models of HACE have not been developed. Several genes are being examined for
313:
Recovery varies between days and weeks, but most recover in a few days. After the condition is successfully treated, it is possible for climbers to reascend. Dexamethesone should be discontinued, but continual acetazolamide is recommended. In one study, it took patients between one week and one month
181:
While there is strong evidence that vasogenic edema plays a major role in HACE, cytotoxic edema, cellular retention of fluids, may contribute as well. Cytotoxic edema may be caused by the failure of cellular ion pumps, which results from hypoxia. Then intracellular sodium and osmolarity increase, and
322:
HACE occurs in 0.5% to 1% of people who climb or trek between 4,000 metres (13,000 ft) and 5,000 metres (16,000 ft). In some unusual cases, up to 30% of members of expeditions have had the condition. The condition is seldom seen below 3,000 metres (9,800 ft), but in some rare cases it
177:
may cause the vascular permeability at the root of HACE. 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.
304:
Although AMS is not life-threatening, HACE is usually fatal within 24 hours if untreated. Without treatment, the patient will enter a coma and then die. In some cases, patients have died within a few hours, and a few have survived for two days. Descriptions of fatal cases often involve climbers who
258:
are administered. Generally, the use of acetazolamide is preferred, but dexamethasone can be used for prevention if there are side effects or contraindications. Some individuals are more susceptible to HACE than others, and physical fitness is not preventive. Age and sex do not by themselves affect
249:
HACE is generally preventable by ascending gradually with frequent rest days while climbing or trekking. Not ascending more than 1,000 metres (3,300 ft) daily and not sleeping at a greater height than 300 metres (980 ft) more than the previous night is recommended. The risk of developing
193:
It is not known why some are more vulnerable to HACE than others. One theory is that variations in brain size play a role, but the increase in brain volume from edema does not likely cause cranial vault impingement. The presence of large sulci indicate the condition may be influenced by the brain
76:
also helps prevent the condition. Untreated patients usually die within 48 hours. Those who receive treatment may take weeks to fully recover. It is a rare condition, occurring in less than one percent of people who ascend to 4,000 metres (13,000 ft). Although it was first described in 1913,
267:
Patients with HACE should be brought to lower altitudes and provided supplemental oxygen, and rapid descent is sometimes needed to prevent mortality. Early recognition is important because as the condition progresses patients are unable to descend without assistance. Dexamethasone should also be
275:
If available, supplemental oxygen can be used as an adjunctive therapy, or when descent is not possible. FiO2 should be titrated to maintain arterial oxygen saturation of greater than 90%, bearing in mind that oxygen supply is often limited in high altitude clinics/environments.
125:
and cell counts but an increase in pressure. In one study, CT scans of patients with HACE exhibited ventricle compression and low density in the cerebellum. Only a few autopsies have been performed on fatal cases of HACE; they showed swollen
65:), although cytotoxic edema (cellular retention of fluids) may play a role as well. Individuals with the condition must immediately descend to a lower altitude or coma and death can occur. Patients are usually given supplemental oxygen and
331:
HACE was first described by a medical officer stationed in Chile in 1913, but few took note of it. Later, access to air travel made the condition more common because it allowed more people access to high mountains, such as those in the
158:, lower carbon dioxide in the bloodstream, which may play a role in HACE. These factors cause the brain to swell with fluid, resulting in severe impairment. If the swelling is untreated, it causes death by brain herniation.
268:
administered, although it fails to ameliorate some symptoms that can be cured by descending to a lower altitude. It can also mask symptoms, and they sometimes resume upon discontinuation. Dexamethasone's prevention of
1275:
208:
synthase. Vasodilation is caused by the release of nitric oxide and adenosine. This in turn can increase vascular permeability and causes edema. This may combine with low levels of cytokines to cause HACE.
169:
in the brain. The leaking may be caused by increased pressure, or it may be caused by inflammation that makes the endothelium vulnerable to leaking. An MRI study found microhemorrhages in the
343:
Increased education and helicopter capabilities have combined to cut the number of deaths from the condition. Symptoms of HACE have been reported in many cases of deaths while descending
225:, hallucinations, and stupor. In some situations, however, AMS progresses to HACE without these symptoms. HACE must be distinguished from conditions with similar symptoms, including
178:
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.
323:
has developed as low as 2,500 metres (8,200 ft). The condition generally does not occur until an individual has spent 48 hours at an altitude of 4,000 metres (13,000 ft).
194:
tightly fitting. Elevated intracranial pressure is generally accepted to be a late effect of HACE. High central venous pressure may also occur late in the condition's progression.
121:
Patients with HACE have an elevated white blood cell count, but otherwise their blood count and biochemistry are normal. If a lumbar puncture is performed, it will show normal
54:) 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
58:
and involves disorientation, lethargy, and nausea among other symptoms. It occurs when the body fails to acclimatize while ascending to a high altitude.
927:
Luks, Andrew; Scott E. Macintosh; Colin K. Grissom; Paul S Auerbach; George W Rodway; Robert B Schoene; Ken Zafren; Peter H Hackett (June 2010).
879:
Luks, Andrew; Scott E. Macintosh; Colin K. Grissom; Paul S Auerbach; George W Rodway; Robert B Schoene; Ken Zafren; Peter H Hackett (June 2010).
116:, 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:
272:
may explain why it treats HACE well. Three studies that examined how mice and rat brains react to hypoxia gave some credence to this idea.
1108:
Imray, Chris; Wright, Alex; Subudhi, Andrew; Roach, Robert (2010). "Acute
Mountain Sickness: Pathophysiology, Prevention, and Treatment".
241:, or ingestion of toxic substances. It should be the first diagnosis ruled out when sickness occurs while ascending to a high altitude.
221:(HAPE) or AMS precede HACE. In patients with AMS, the onset of HACE is usually indicated by vomiting, headache that does not respond to
201:
does not cause HACE. What role the sympathetic nervous system plays in determining who gets HACE is unclear, but it may have an effect.
147:
165:
by fluids. This process has been observed in MRI studies. Hypoxia increases extracellular fluid, which passes through the vasogenic
150:. Acclimatization precludes the development of HACE by maintaining adequate levels of cerebral oxygen. The primary cause of HACE is
1204:
1150:
222:
1079:
1311:
174:
368:
186:
form and cause damage that complicates the edema. Evidence against cytotoxic edema includes the high levels of
218:
929:"Wilderness Medical Society Consensus Guidelines for the Prevention and Treatment of Acute Altitude Illness"
881:"Wilderness Medical Society Consensus Guidelines for the Prevention and Treatment of Acute Altitude Illness"
347:, although HACE may not be the only problem they experienced. HACE also posed a threat to workers on the
1214:
Wilson, Mark; Newman, Stanton; Imray, Chris (2009). "The
Cerebral Effects of Ascent to High Altitudes".
173:
of HACE patients, and hypoxia may also cause microvascular permeability. It has been hypothesized that
348:
138:. There was some variation between individuals, and the results may not be typical of HACE deaths.
182:
there is an influx of water that causes cellular swelling. After the failure of the ATPase pumps,
1142:
162:
86:
77:
little was known about the cause of the condition until MRI studies were performed in the 1990s.
72:
HACE can be prevented by ascending to heights slowly to allow the body more time to acclimatize.
62:
55:
135:
122:
17:
89:(AMS). Initial symptoms of HACE commonly include confusion, loss of consciousness, fever,
8:
1279:
198:
1241:
102:
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1200:
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878:
151:
1225:
1216:
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892:
1245:
1162:
170:
161:
The brain swelling is likely a result of vasogenic edema, the penetration of the
1121:
106:
945:
897:
1300:
372:(2011), with the precision that the spelling in the United States is 'edema'.
344:
255:
251:
205:
183:
85:
Early symptoms of HACE generally correspond with those of moderate to severe
73:
66:
1237:
1183:
1129:
1100:
954:
906:
298:
269:
131:
109:, and ocular paralysis. Cranial nerve palsies occur in some unusual cases.
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1077:
Bärtsch, Peter; Swenson, Erik (2013). "Acute High-Altitude
Illnesses".
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238:
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Schoene, Robert; Milledge, James; Luks, Andrew; West, John (2012).
820:
818:
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747:
745:
234:
1007:
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may be helpful, but pose risks outside of a hospital environment.
204:
Another theory about the cause of HACE is that hypoxia may induce
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305:
continue ascending while experiencing the condition's symptoms.
473:
461:
297:
may help HACE, but there is little evidence of their efficacy.
226:
90:
1031:
857:
830:
619:
279:
In addition to oxygen therapy, a portable hyperbaric chamber (
928:
880:
409:
375:
114:
Into Thin Air: A Personal
Account of the Mt. Everest Disaster
61:
It appears to be a vasogenic edema (fluid penetration of the
340:
the role they may play in the development of the condition.
676:
674:
672:
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607:
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583:
581:
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127:
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395:
1139:
Molecular
Physiology and Metabolism of the Nervous System
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763:
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661:
570:
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534:
505:
455:
392:
1160:
Schoene, Robert (2008). "Illnesses at High
Altitude".
720:
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703:
197:One study demonstrated that normal autorelation of
1213:
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1076:
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866:
836:
640:
424:
386:
366:'Oedema' is the standard form defined in the
190:(low bloodstream oxygen) needed to cause it.
314:to display a normal CT scan following HACE.
1136:
1013:
944:
896:
680:
613:
589:
403:
301:is also theorized to help the condition.
146:Most people who travel to high altitudes
112:In the bestselling 1996 non-fiction book
1159:
933:Wilderness & Environmental Medicine
885:Wilderness & Environmental Medicine
724:
14:
1299:
1193:High Altitude Medicine and Physiology
223:non-steroidal anti-inflammatory drugs
80:
41:High-altitude cerebral oedema (HACO)
1110:Progress in Cardiovascular Diseases
1080:The New England Journal of Medicine
24:
175:vascular endothelial growth factor
25:
1323:
1253:
369:Concise Oxford English Dictionary
1070:
1062:Wilson, Newman & Imray 2009
1026:Wilson, Newman & Imray 2009
1002:Wilson, Newman & Imray 2009
975:Wilson, Newman & Imray 2009
920:
872:
825:Wilson, Newman & Imray 2009
752:Wilson, Newman & Imray 2009
737:Wilson, Newman & Imray 2009
602:Wilson, Newman & Imray 2009
485:Wilson, Newman & Imray 2009
468:Wilson, Newman & Imray 2009
317:
360:
13:
1:
1230:10.1016/S1474-4422(09)70014-6
354:
244:
219:high-altitude pulmonary edema
308:
262:
212:
141:
105:, blurred vision, extension
48:High-altitude cerebral edema
33:High-altitude cerebral edema
7:
10:
1328:
1122:10.1016/j.pcad.2010.02.003
1038:Bärtsch & Swenson 2013
867:Bärtsch & Swenson 2013
837:Bärtsch & Swenson 2013
641:Bärtsch & Swenson 2013
425:Bärtsch & Swenson 2013
387:Bärtsch & Swenson 2013
326:
1312:Mountaineering and health
1261:
1016:, pp. 146 & 150.
946:10.1016/j.wem.2010.03.002
898:10.1016/j.wem.2010.03.002
37:
32:
1137:Rosenberg, Gary (2012).
1143:Oxford University Press
259:vulnerability to HACE.
87:acute mountain sickness
56:acute mountain sickness
250:HACE is diminished if
1176:10.1378/chest.07-0561
1093:10.1056/NEJMcp1214870
349:Qinghai–Tibet Railway
123:cerebral spinal fluid
97:, rapid heart beat,
793:Schoene et al. 2012
698:Schoene et al. 2012
662:Schoene et al. 2012
535:Schoene et al. 2012
506:Schoene et al. 2012
456:Schoene et al. 2012
199:cerebral blood flow
163:blood–brain barrier
103:retinal hemorrhages
63:blood–brain barrier
616:, pp. 146–50.
81:Signs and symptoms
1294:
1293:
1206:978-1-4441-5432-0
1152:978-0-19-539427-6
1050:Imray et al. 2010
990:Imray et al. 2010
852:Imray et al. 2010
808:Imray et al. 2010
776:Imray et al. 2010
764:Imray et al. 2010
571:Imray et al. 2010
559:Imray et al. 2010
547:Imray et al. 2010
134:, and compressed
45:
44:
27:Medical condition
16:(Redirected from
1319:
1259:
1258:
1249:
1217:Lancet Neurology
1210:
1187:
1156:
1133:
1104:
1087:(24): 2294–302.
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1059:
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229:, intoxication,
130:, spongiosis of
107:plantar reflexes
30:
29:
21:
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1207:
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1073:
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1056:
1048:
1044:
1040:, p. 2300.
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1008:
1000:
996:
988:
981:
973:
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925:
921:
911:
909:
877:
873:
869:, p. 2299.
865:
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850:
843:
839:, p. 2298.
835:
831:
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643:, p. 2295.
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491:
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431:
427:, p. 2294.
423:
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389:, p. 2296.
385:
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365:
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329:
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247:
215:
171:corpus callosum
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117:
83:
28:
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22:
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5:
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1262:Classification
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1254:External links
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1141:(5 ed.).
1134:
1116:(6): 467–484.
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1064:, p. 180.
1054:
1052:, p. 475.
1042:
1030:
1028:, p. 184.
1018:
1014:Rosenberg 2012
1006:
1004:, p. 176.
994:
992:, p. 478.
979:
977:, p. 179.
967:
939:(2): 146–155.
919:
891:(2): 146–155.
871:
856:
854:, p. 471.
841:
829:
827:, p. 175.
812:
810:, p. 467.
797:
795:, p. 307.
780:
778:, p. 472.
768:
766:, p. 474.
756:
754:, p. 181.
741:
739:, p. 183.
729:
702:
700:, p. 305.
685:
683:, p. 148.
681:Rosenberg 2012
666:
664:, p. 306.
645:
618:
614:Rosenberg 2012
606:
604:, p. 182.
594:
592:, p. 147.
590:Rosenberg 2012
575:
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563:
561:, p. 468.
551:
549:, p. 470.
539:
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510:
508:, p. 303.
489:
487:, p. 177.
472:
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460:
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406:, p. 146.
404:Rosenberg 2012
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1224:(2): 175–91.
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217:Generally,
167:endothelium
148:acclimatize
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1301:Categories
355:References
291:Sildenafil
245:Prevention
239:meningitis
237:symptoms,
156:hypocapnia
1197:CRC Press
334:Himalayas
309:Prognosis
295:tadalafil
287:Diuretics
281:Gamow bag
263:Treatment
231:psychosis
213:Diagnosis
188:hypoxemia
142:Mechanism
99:lassitude
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1307:Cerebrum
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327:History
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293:and
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