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Altitude sickness is a clinical syndrome that occurs with abrupt ascents to altitudes of 3000 metres and above. Symptoms include headache, malaise, fatigue, dizziness, anorexia, nausea and vomiting, and oliguria. At higher altitudes more severe illness resulting from pulmonary oedema or cerebral oedema can occur.
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PMID:Altitude sickness. 232 86

A clinical syndrome identical to the chronic mountain sickness of the Andes occurs commonly in Lhasa, Tibet. It affects, almost exclusively, the immigrant Han population and develops after an average of 15 years' residence at high altitude. The early symptoms are attributable to polycythaemia--headache, dizziness, loss of memory and fatigue being prominent. In the later stages of the disease, dyspnoea and peripheral oedema develop. Haemodynamic investigations show pulmonary hypertension with a normal cardiac output and dilatation of the right ventricle in the long-established case. Respiratory gas studies provide evidence of alveolar underventilation and ventilation: perfusion inhomogeneity. Both clinical and investigatory data suggest that the earlier stages of the disease are dominated by polycythaemia, while cardiopulmonary involvement increases with the duration of the disease. The disease is rare in women and uncommon in Tibetans. Cigarette smoking appears to be a contributory factor.
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PMID:Chronic mountain sickness in Tibet. 251 94

Forty-seven climbers participated in a double-blind, randomized trial comparing acetazolamide 250 mg, dexamethasone 4 mg, and placebo every eight hours as prophylaxis for acute mountain sickness during rapid, active ascent of Mount Rainier (elevation 4,392 m). Forty-two subjects (89.4 percent) achieved the summit in an average of 34.5 hours after leaving sea level. At the summit or high point attained above base camp, the group taking dexamethasone reported less headache, tiredness, dizziness, nausea, clumsiness, and a greater sense of feeling refreshed (p less than or equal to 0.05). In addition, they reported fewer problems of runny nose and feeling cold, symptoms unrelated to acute mountain sickness. The acetazolamide group differed significantly (p less than or equal to 0.05) from other groups at low elevations (1,300 to 1,600 m), in that they experienced more feelings of nausea and tiredness, and they were less refreshed. These drug side effects probably obscured the previously established prophylactic effects of acetazolamide for acute mountain sickness. Separate analysis of an acetazolamide subgroup that did not experience side effects at low elevations revealed a prophylactic effect of acetazolamide similar in magnitude to the dexamethasone effect but lacking the euphoric effects of dexamethasone. This study demonstrates that prophylaxis with dexamethasone can reduce the symptoms associated with acute mountain sickness during active ascent and that acetazolamide can cause side effects that may limit its effectiveness as prophylaxis against the disease.
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PMID:A randomized trial of dexamethasone and acetazolamide for acute mountain sickness prophylaxis. 333 64

A double-blind randomized study of 45 climbers on Mt. Rainier was conducted to test the effectiveness of antacids in preventing acute mountain sickness. All 45 climbed to 3353 m, and 31 continued to the summit. Ten climbers listed acute mountain sickness as the reason for not attaining the summit. Of symptoms monitored throughout the climb, neither headache, nausea, dizziness, pounding heart, nor shortness of breath differed in severity between antacid-treated and placebo-treated groups. In both groups vital capacity decreased significantly with ascent (p less than 0.05), while peak flow (p less than 0.005) and minute ventilation (p less than 0.001) increased significantly. The 7 climbers with the most severe AMS symptom scores above 4000 m had significantly lower peak flow at sea level prior to ascent compared with the other 25 climbers who completed sea level tests (p less than 0.005). The results of this study fail to document efficacy for antacid use for the prevention of acute mountain sickness.
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PMID:Acute mountain sickness, antacids, and ventilation during rapid, active ascent of Mount Rainier. 634 73

Phenytoin sodium was evaluated for its effect on the development and intensity of acute mountain sickness (AMS) because of its ability to reduce intracellular Na+ concentrations in brain and thereby minimize any tendency to increase cellular volume, a hypothetical cause of AMS. Six men aged 19-35 were exposed to approximately 4600 m altitude in a hypobaric chamber for 52 h on two occasions separated by 10 d at sea level. Subjects received wither phenytoin or placebo for 18 h before (700 mg, divided dose) and throughout (100 mg t.i.d.) each altitude exposure in a double-blind, repeated-measures (crossover) design. Phenytoin serum concentrations ranged from 4.4-13.9 micrograms/ml during altitude exposure. Twice daily questionnaires and clinical evaluations showed no marked benefit from phenytoin on the occurrence, severity, or duration of AMS symptoms: headache, nausea, insomnia, and general malaise. Overall, 1 subject felt better, 2 felt worse, 1 felt the same; 2 were not suitably comparable. There was no observed relationship between serum levels and symptoms of AMS. Moderate degrees of weakness and dizziness were each reported by 3 subjects with phenytoin but not with placebo, however. Resting pulmonary ventilation, end-tidal PO2 and PCO2, map reading abilities and respiratory mask donning times were not affected by phenytoin. Under the conditions of this trial, phenytoin did not appear to be useful in managing AMS.
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PMID:Phenytoin: ineffective against acute mountain sickness. 676 69

Sixty-four climbers participated in a randomized clinical trial of acetazolamide prophylaxis for acute mountain sickness (AMS) during rapid, active ascent of MT Rainier. Twenty-nine (93.6%) of 31 climbers receiving acetazolamide and 25 (75.8%) of 33 receiving placebo attained the summit. Time spent ascending from sea level to the summit (4,394 m) averaged 33.5 hours (range, 23 to 48 hours). On the summit AMS was less common in climbers receiving acetazolamide, and they experienced less headache, nausea, drowsiness, shortness of breath, and dizziness and a greater sense of satisfaction and psychological well-being. Minute ventilation on the summit was significantly greater in subjects taking acetazolamide (24.9 +/- 2.0 L/min compared with 16.9 +/- 3.8 L/min). Expired vital capacity was also greater on the summit in the acetazolamide group (6.9 +/- 0.4 L compared with 5.8 +/- 0.4 L). We conclude that acetazolamide is effective in the prophylaxis of AMS for climbers attempting rapid, active ascent. Increased ventilation at altitude, producing an increased alveolar oxygen tension, may be related to the observed amelioration of symptoms.
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PMID:Acute mountain sickness and acetazolamide. Clinical efficacy and effect on ventilation. 704 33

The effect of previous physical conditioning on young well-conditioned mountaineers in relationship to acquiring acute mountain sickness is controversial. Data show both increased and decreased effects on the incidence of altitude illness. How general tourists at moderate altitudes are affected is unknown. To determine the influence of sea-level habitual physical activity on the incidence of mountain sickness, we surveyed 205 participants in a scientific conference at 3,000 m (9,840 ft). A 36-item questionnaire was distributed to the subjects 48 hours after arrival at altitude. Their sea-level physical activity (SLPA) was measured by a published and validated instrument that included questions about patterns of work, sporting, and leisure-time activities. Acute mountain sickness was defined as the presence of 3 or more of the following symptoms: headache, dyspnea, anorexia, fatigue, insomnia, dizziness, or vomiting. Most of the respondents were male (62%) from sea level (89%) with a mean age of 36 +/- 8.7 (standard deviation) years (range, 22 to 65). Nearly all (94%) were nonsmokers, and 28% had acute mountain sickness. The mean SLPA score was 8.0 +/- 1.3 (range, 5.1 to 12.0). No statistically significant difference in mean SLPA scores was found between those with and without acute mountain sickness (8.1 versus 7.8), nor in the individual indices (work, 2.5 versus 2.4; sport, 2.9 versus 2.7; leisure, 2.8 versus 2.7). We conclude that habitual physical activity performed at sea level does not play a role in the development of altitude illness at moderate altitude in a general tourist group.
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PMID:Sea-level physical activity and acute mountain sickness at moderate altitude. 757 57

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
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PMID:[Mountaineering and altitude sickness]. 1144 1

Acute mountain sickness and high altitude cerebral edema are specific pathologies of high altitude exposure. The usual symptoms of acute mountain sickness are headache, nausea, vomiting, insomnia, lassitude, dizziness and ataxia. High altitude cerebral oedema is a severe state of acute mountain sickness with, in addition, alteration of mental status and consciousness. The pathophysiology of these 2 diseases are essentially due to an increase of intracranial pressure directly dependent of an increase of cerebral volume. Molecular and cellular mechanisms underlying acute mountain sickness and high altitude cerebral oedema are still poorly understood. The regulation of cerebral blood flow by nitric oxide seems to play a major role.
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PMID:[High altitude cerebral oedema]. 1281 24


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