Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “acute mountain sickness”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1990

[Acute mountain sickness].

Acute mountain sickness is a pathologic reaction as a result of bad adaptation to high altitudes (greater than 2.500 meters). The main symptoms are headache, nausea, vomits, and insomnia. When severe it can produce oliguria, retinal hemorrhage, ataxia and sometimes coma. Its etiology is not well known. It is considered that the first producer factor of the disease is tissular hypoxia secondary to low partial oxygen pressure existing in areas of high sea level. The treatment consists of descent and the use of dexametasone and acetazolamide.

Acute Disease↗
PubMed1995

A trek to the top: a review of acute mountain sickness.

Acute mountain sickness (AMS) affects, to varying degrees, all travelers to high altitudes (elevations greater than 5280 feet). In a small percentage of patients, AMS can lead to high-altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE). Symptoms of AMS range from a combination of headache, insomnia, anorexia, nausea, and dizziness, to more serious manifestations, such as vomiting, dyspnea, muscle weakness, oliguria, peripheral edema, and retinal hemorrhage. Although the primary cause of these symptoms is related to the reduced oxygen content and humidity of the ambient air at high altitudes, the physiologic pathway relating hypoxemia to AMS and its sequelae remains unclear. Tips on self-diagnosis and symptom recognition are critical elements to be included in educating patients who are contemplating a trip to high altitudes. Preventive strategies include allowing 2 days of acclimatization before engaging in strenuous exercise at high altitudes, avoiding alcohol, and increasing fluid intake. Conditioning exercise for patients older than 35 years is also recommended before departure. A high-carbohydrate, low-fat, low-salt diet can also aid in preventing the onset of AMS. Acetazolamide (125 mg two or three times daily, or once at bedtime) has also been shown to reduce susceptibility to AMS and the incidence of HAPE and HACE. Although effective in treating cerebral symptoms of AMS, dexamethasone is not routinely recommended as a prophylactic agent for AMS.

Acute Disease↗
PubMedDate not supplied

Current prevention and management of acute mountain sickness.

Acute mountain sickness was known to the Chinese in ancient times, as they traversed mountain passes between the Great Headache and Little Headache mountains into present-day Afghanistan. The Jesuit priest, Father Joseph Acosta, lived in Peru during the sixteenth century; he described both this syndrome and deaths which occurred in the high Andes. The incidence of high-altitude illness will rise as previously remote sites become more accessible to trekkers and skiers. Prevention and treatment are important concerns for those physicians who wish to advise their more adventuresome patients properly. This article incorporates a selected review of pertinent investigations, in the English-language literature over the past five years, into material previously presented at travel symposia for clinicians managing the prophylaxis and treatment of acute mountain sickness.

Altitude Sickness↗
PubMed2004

Pulse oximetry in the diagnosis of acute mountain sickness.

Acute mountain sickness (AMS) is a common condition in individuals who travel to altitudes over 2000 m. While AMS is an important public health problem, no measurements can reliably support or predict the diagnosis with any degree of confidence. We therefore set out to study whether pulse oximetry data are associated with AMS. We studied 169 subjects who had recently arrived by foot at 3080 m. Subjects completed a demographic survey, which collected data on ascent profiles and AMS symptoms. Resting arterial oxygen saturation and pulse rate were then measured using finger pulse oximetry. Forty-six subjects (27%) had AMS, using the Lake Louise score. Only pulse rate was significantly associated with the presence of AMS (OR: 1.4; 95% CI, 1.1 to 1.9; p < 0.05, backwards stepwise logistical regression). A trend showed worse AMS diagnoses were associated with higher mean pulse rates (p < 0.05, ANOVA linear weighted analysis). While some previous studies have shown an association between decreased oxygen saturation and acute mountain sickness at altitude, our results did not demonstrate such an association. The utility of pulse oximetry remains limited in the diagnosis of AMS. We recommend further study to determine the possible utility of pulse rate in the diagnosis and prediction of AMS.

Acute Disease↗
PubMed2005

Statistical models of acute mountain sickness.

Acute mountain sickness (AMS) is caused by exposure to altitudes exceeding 2500 m and often resolves by acclimatization without further ascent. Statistical models of AMS score and the probability of an AMS diagnosis were developed to allow the combination of dissimilar exposures for simultaneous analysis. The study population was 302 trekkers from a previous investigation who provided self-reported symptoms upon arrival at 3840 m during hikes through altitudes of 1500 to 6200 m. AMS score (Hackett scale) was estimated by linear regression and the probability of an AMS diagnosis (Lake Louise criteria) by logistic regression. AMS score or probability was significantly associated with exposure day and altitude. Increased altitude over the prior 3 days resulted in higher estimated AMS score or probability and decreased altitude in lower score or probability. The odds ratio (OR) of AMS was 3.6 if not on acetazolamide. Females appeared slightly more susceptible than males (1.5 OR). The approach offers the advantages of (1) improved statistical power by combining exposures, (2) insight into the dose-response relationship of altitude exposure and AMS risk, (3) quantitative tests for the significance of factors that might affect AMS susceptibility, and (4) practical tools to track individual climbers and plan operational ascents.

Acclimatization↗
PubMed1989

Relationship of cerebral blood flow regulation to acute mountain sickness.

Acute mountain sickness (AMS) is a prevalent illness seen in humans exposed to high altitudes. An increase in cerebral blood flow as a result of cerebrovasodilatation is felt by many to be responsible for its occurrence. Using the recently developed transcranial Doppler (TCD), it has become possible to detect and quantify flow velocity in the large cerebral vessels. By this method, intracranial arterial blood flow velocities and vasodilatation were measured at high altitude and correlated with clinical symptoms. Mean middle cerebral artery velocity (MCA-V) showed a significant increase from 55 +/- 7 cm/s at sea level to 71 +/- 13 cm/s at 13,500 feet. The pulsatility index (PI) and vasomotor reactivity (VMR) both decreased (.71 +/- .11 at sea level to .53 +/- .12 at 13,500 and 45 +/- 17% sea level to 23 +/- 15% at 8,000 feet, respectively). These preliminary studies indicated that TCD technique is a viable tool for measurement of cerebral blood flow velocities and cerebral arterial vasodilatation at altitude.

Acute Disease↗
PubMed1976

The incidence, importance, and prophylaxis of acute mountain sickness.

Acute mountain sickness (A.M.S.) and its severe complications, high-altitude pulmonary oedema (H.A.P.O.) and cerebral oedema (C.O.), were studied in 278 unacclimatised hikers at 4243 m altitude at Pheriche in the Himalayas of Nepal. The overall incidence of A.M.S. was 53%, the incidence being increased in the young and in those who flew to 2800 m, climbed fast, and spent fewer nights acclimatising en route. It was unrelated to sex, to previous altitude experience, to the load carried, and to recent respiratory infections. The severity of A.M.S. was inversely related to age (independent of rate of ascent) and the highest altitude attained, and was highly ocrrelated with speed of ascent. There were 7 cases of H.A.P.O. and 5 with the more intractable C.O. and, of these 12, 11 had flown in, 9 had spent only one night at Pheriche, and none were on acetazolamide. 11 required evacuation. Acetazolamide, compared in a double-blind study with a placebo and also compared with no tablets at all, reduced both the incidence and the severity of A.M.S. in those who flew to 2800 m but not in those who hiked up to that altitude. Prevention consists in slow ascent, rapid recognition of warning signs, and prompt descent to avoid progression.

Acetazolamide↗
PubMed1997

The illness of ascent: acute mountain sickness.

Acute mountain syndrome, although common, is preventable. Even after its development, progression into life-threatening HAPE and HACE is avoidable through prompt recognition and treatment. Although there are medical treatment modalities, the simplest and surest solution remains descent. The nurse practitioner has a responsibility to advise clients of the ramifications of AMS, and to counsel skiers, tourists, hunters, trekkers, and mountaineers considering travel to high altitudes in prevention, self-diagnosis, and treatment of this condition.

Acclimatization↗
PubMed2002

Glucocorticoids as prophylaxis against acute mountain sickness.

OBJECTIVE: Acute mountain sickness (AMS) characterized by presence of symptoms including headache, nausea, excessive fatigue, loss of appetite, irritability and insomnia is a major impediment to work performance in human subjects who are rapidly inducted to high altitude (HA) during the initial phase of induction. The present study aims at to evaluate the efficacy of prophylactic administration of low dose glucocorticoids in prevention of AMS in normal healthy men who are inducted to HA by air. DESIGN: Fifty healthy men were randomly divided into five groups of 10 each. Group I received prednisolone (Pred) 10 mg, Group II Pred 20 mg, Group III Pred 40 mg, Group IV dexamethasone 0.5 mg, Group V received placebo once a day in the morning for 2 days at sea level (SL) and for 3 days on arrival at an altitude of 3450 m by air. MEASUREMENTS: The severity of AMS was assessed using Lake Louise AMS scoring system. Physiological parameters like blood pressure, respiratory rate, peripheral blood O2 saturation and heart rate were measured at sea level and on arrival at HA. Circulatory levels of cortisol and adrenocorticotropic hormone (ACTH) were measured by radioimmunoassay (RIA) and immunoradiometreic assay (IRMA), respectively. RESULTS: In the placebo group, significant AMS could be detected at 12 h of arrival at HA, peaked by day 1 or 2 of stay and started declining thereafter. As compared to the placebo group, the steroid treated groups showed a significant (P < 0.01) reduction in daily AMS score. When compared with prednisolone 10 mg, 40 mg and dexamethasone groups, the prednisolone 20 mg group showed an optimal response in reduction of AMS symptoms. The O2 saturation showed a significant decline (P < 0.001) on arrival at HA, but the pattern of O2 saturation in placebo and glucocorticoid groups was identical. Similarly, the rise in heart rate and blood pressure and on day 3 of stay at HA was similar in placebo and glucocorticoid-treated groups. An increase in plasma cortisol in placebo group was observed on day 3 of stay at HA and continued to rise till day 8 of observations. The cortisol levels in Pred 10 mg and Pred 20 mg groups on day 1 and 3 of arrival at HA were not significantly different than the SL post-treatment values but were found to be significantly higher on day 8 of stay. Plasma cortisol in Pred 40 mg and dexamethasone groups was significantly lower (P < 0.01) on day 1 and 3 of stay but showed an increase by day 8 of stay. The ACTH levels were increased at HA in placebo group but did not show any significant change till day 3 of stay in steroid treated subjects and were found to be higher in all groups on day 8 of observations. CONCLUSION: These observations suggest that administration of low-dose glucocorticoids can curtail acute mountain sickness significantly without influencing the normal adreno cortical response to hypoxia.

Acute Disease↗
PubMed1983

Procedures for the measurement of acute mountain sickness.

Although acute mountain sickness (AMS) has been studied for well over a century, a standard measure or index of the degree of illness for use in experimental research does not exist. This paper outlines a definition and procedures for an operational measurement of AMS using the Environmental Symptoms Questionnaire (ESQ). After 58 men completed over 650 ESQs during a stay of 1-3 weeks atop Pike's Peak (4300 m), factor analysis produced nine distinct symptom groups, with two factors representing AMS. The first factor contains symptoms indicative of cerebral hypoxia and is labeled AMS-C. The second reflects respiratory distress and is called AMS-R. Signal detection theory was used to establish a criterion score value for each factor. Standard deviation values were used to derive indices of sickness severity. Discussion is given to the possible relationships between the two types of AMS and the more serious conditions of cerebral and pulmonary edema.

Acute Disease↗
PubMed1998

Arterial oxygen saturation for prediction of acute mountain sickness.

BACKGROUND: Acute mountain sickness (AMS) is a usually self-limiting syndrome encompassing headache, nausea and dizziness. AMS is seen in those that go from low to high altitudes too quickly, without allowing sufficient time to acclimatize. At present, susceptibility to AMS cannot be predicted. One feature of AMS noted in some studies is impaired gas exchange. If impaired gas exchange presages AMS then those individuals with exaggerated hypoxemia at high altitude may be more likely to develop AMS. If true, then monitoring of arterial oxygen saturation (SaO2%) may differentiate AMS-resistant individuals from those with impending AMS. METHODS: To test this hypothesis, we measured SaO2% and AMS symptom scores in 102 healthy asymptomatic climbers at 4200 m on Denali (Mt. McKinley) prior to their further ascent toward the summit at 6194 m, and on their return from higher altitudes to 4200 m. RESULTS: The results show that exaggerated hypoxemia in asymptomatic climbers prior to further ascent correlates with subsequent AMS (r = -0.48, p < 0.001). Criteria are presented for identification of 80-100% of those climbers who later become ill with AMS. CONCLUSION: We conclude that resting arterial hypoxemia is related to later development of clinical AMS, and can exclude the occurrence and caution those at risk for development of subsequent AMS. Likely mechanisms are hypoventilation relative to normally acclimatizing individuals and/or abnormalities of gas exchange. Thus, non-invasive oximetry provides a simple, specific indicator of inadequate acclimatization to high altitudes and impending AMS.

Acclimatization↗
PubMed2004

Cysteinyl leukotriene blockade does not prevent acute mountain sickness.

BACKGROUND: Acute Mountain Sickness (AMS) is a multi-system disorder that is characterized by headache, anorexia, nausea, vomiting, insomnia, lassitude, and malaise. The syndrome is common in unacclimatized low altitude residents who rapidly ascend to terrestrial elevations exceeding 2,500 m. AMS may be a manifestation of hypoxia-induced cerebral edema resulting, in part, from increased capillary permeability. HYPOTHESIS: We hypothesized that cysteinyl leukotrienes (CysLTs) may be involved in the pathogenesis of AMS, as these compounds are known to increase endothelial permeability. METHODS: To test this hypothesis, we orally administered a CysLTs type-1 receptor antagonist (montelukast) to 11 subjects prior to and during exposure to high altitude (4,300 m) in a hypobaric chamber in a randomized, placebo-controlled, crossover design. We measured the resulting prevalence and/or severity of AMS, plasma CysLTs levels and urinary CysLTE4, and associated physiological responses. RESULTS: At 12 h exposure, AMS prevalence and symptom severity was lower (p = 0.002) during montelukast administration compared with placebo, but not different at 22 h exposure. Plasma CysLTs and urinary LTE4 levels were not significantly elevated at 22 h exposure, nor did these CysLTs levels correlate with AMS severity. Compared with placebo, montelukast administration was not associated with any significant differences in physiologic measures at sea level or high altitude. CONCLUSIONS: These results do not support a role for the CysLTs mediating the early development of AMS through the CysLT-1 receptor.

Acetates↗
PubMed1984

Prevention of acute mountain sickness by dexamethasone.

Acute mountain sickness is a syndrome that occurs when unacclimatized persons ascend rapidly to high altitudes. It is postulated that cerebral edema causes its symptoms. Since dexamethasone is useful in treating some forms of cerebral edema, we investigated its role in the prevention of acute mountain sickness. Using a double-blind crossover design, we exposed eight young men to a simulated altitude of 4570 m (15,000 ft) on two occasions. By random assignment, each subject received dexamethasone (4 mg every 6 hours) or placebo for 48 hours before and throughout the 42-hour exposure. The presence of symptoms of acute mountain sickness was established by two methods: a questionnaire and an interview by a physician. Dexamethasone significantly reduced the symptoms of acute mountain sickness. During dexamethasone treatment, the cerebral-symptom score (mean +/- S.E.) decreased from 1.09 +/- 0.18 to 0.26 +/- 0.08, and the respiratory-symptom score decreased from 0.64 +/- 0.09 to 0.31 +/- 0.06 (both, P less than 0.05). As judged by the interviewing physician, the symptom score decreased from 1.10 +/- 0.11 to 0.28 +/- 0.07 (P = 0.01). We conclude that dexamethasone may be effective in preventing the symptoms of acute mountain sickness.

Acute Disease↗
PubMed1990

Mountain sickness.

Acute mountain sickness (AMS) is a failure to adapt to high altitude. Although some people may be at increased risk, most cases are unpredictable. Much can be done, however, to prevent AMS or limit its severity. Staging ascent, sleeping low, and avoiding overexertion and respiratory depressants are all helpful. For some, drug prophylaxis should be considered. Treatment is based on clinical severity, with descent remaining the primary treatment for severe cases.

Acetazolamide↗
PubMed1988

Hypoxic ventilatory response and acute mountain sickness.

The acute ventilatory response to hypoxia (HVR) and to hypercapnia (CO2VR) was measured in 32 members of two mountaineering expeditions prior to their departure. Both teams made rapid ascents to their base camps at 5200 m and 4300 m and remained there for at least four days. Symptom scores for acute mountain sickness (AMS) were collected daily for these four days. There was a range of AMS from the unaffected to severe sickness requiring evacuation, but there was no correlation between AMS scores and HVR or CO2VR. When ascent to altitude takes a day or more, HVR (measured at sea level) is probably not the major determinant of ventilation and from our studies does not predict susceptibility to AMS. The rate of respiratory acclimatization is probably more important.

Acute Disease↗
PubMed1980

Intravascular hemolysis in acute mountain sickness.

A case of acute mountain sickness (AMS) is described of a fit young man while on a climbing expedition in Mexico. The subject exhibited intravascular hemolysis in addition to normal AMS symptoms. This case is reported in the hope that others will look for and report the presence or absence of intravascular hemolysis on climbing expeditions.

Acute Disease↗
PubMed1993

Pressurization and acute mountain sickness.

Numerous cases of acute mountain sickness (AMS) during trekking were reported to have been successfully treated with portable pressure chambers. The effect of early pressurization during acute altitude exposure in the Alps had not been previously studied. In order to test the hypothesis that an early pressurization of unacclimatized subjects for 3 h could prevent or delay the appearance of symptoms of AMS, 51 previously healthy subjects climbed from 1,030 to 4,360 m within 12 h. Upon arrival at 4,360 m, AMS scores (Lake Louise Consensus Questionnaire '91), oxygen saturation (SaO2), and heart rate (HR) were determined at rest. The subjects were then randomly divided in two groups; one group was pressurized to 200 mBar for 3 h while the other rested. AMS score, HR, and SaO2 were similar in both groups before treatment. AMS score had decreased (from 2.44 +/- 0.41 (S.E.) to 0.89 +/- 0.26, p < 0.05) and SaO2 had increased (from 75.22 +/- 1.32% to 79.07 +/- 1.27%, p < 0.05) in the treatment group 15 min after leaving the pressure chamber whereas the control group had unchanged AMS score (2.50 +/- 0.40 vs. 2.40 +/- 0.40, N.S.) and SaO2 (77.83 +/- 1.41 vs. 76.67 +/- 1.24, N.S.). The next morning, however, AMS score, HR, and SaO2 were similar for both groups. It is concluded that during acute ascent in the Alps, an early 3-h pressurization of unacclimatized subjects does slightly delay the onset of AMS but does not prevent the illness nor does it attenuate its severity upon appearance.

Acute Disease↗