Acute mountain sickness in the Southern Alps of New Zealand

AIM: To assess the incidence and impact of acute mountain sickness in the Southern Alps of New Zealand. METHODS: Over a 22 month period, mountaineers in the Mount Cook region were asked to complete a questionnaire at the completion of their climbing excursions. The questionnaire recorded demographic data and incorporated the Lake Louise scoring system to assess the presence of acute mountain sickness. RESULTS: Of the 114 subjects who completed the questionnaire, 30 (26%) developed acute mountain sickness. The incidence was higher amongst those who slept above 2500 m (50%). Of those with acute mountain sickness, 33% reported that their symptoms resulted in no reduction in activity, while 13% reported a moderate or severe reduction in activity. CONCLUSION: Mountaineers climbing in New Zealand's Southern Alps should be aware of the risk of acute mountain sickness, especially for those sleeping above 2500 m.     

Assessment of acute mountain sickness by different score protocols in the Swiss Alps

INTRODUCTION: Purpose of the present study was to evaluate the Lake Louise acute mountain sickness (AMS) score questionnaire at different altitudes and to compare it with the currently used clinical score and the environmental symptoms questionnaire AMS-C score. METHODS: We investigated 490 climbers who stayed over night at 4 huts in the Swiss Alps, located at the altitudes of 2850 m, 3050 m, 3650 m, and 4559 m. AMS was assessed using our previously described clinical score, the Lake Louise consensus AMS score questionnaire and the environmental symptoms questionnaire III. RESULTS: Below 4000 m, the prevalence of AMS, defined by symptoms that force a reduction in activity, was 7%; when assessed with the clinical score (score > or = 3) it was 22%; with the AMS-C score (score > or = 0.7) 4% and with the Lake Louise score (score > 4) 8%. At the altitude of 4559 m, the prevalence of AMS was 30%, 38%, 40%, and 39%, respectively. The standardized regression coefficients from multiple regression analysis (adjusted R2 0.65, p < 0.001) were 0.45 (p < 0.001) for the self-reported Lake Louise score, 0.48 (p < 0.001) for the sum of the points assigned in the clinical section of the Lake Louise questionnaire, and 0.05 (p = 0.27) for the AMS-C score. The sensitivity and specificity of the Lake Louise score > 4 was 78% and 93%, respectively. CONCLUSIONS: The Lake Louise consensus score is adequate and, compared with the AMS-C score, more effective for the assessment of acute altitude illness at different altitudes.     

Mountain sickness, retinal haemorrhages, and acclimatisation on Mount Everest in 1975

During the 1975 British Everest Expedition, which made the first ascent of the south-west face, observations were made in relation to mountain sickness and the appearance of retinal changes. Two Sherpas with cerebral oedema and one Briton with pulmonary oedema were treated. Retinal haemorrhages occurred in four out of six Britons who were newcomers to altitudes over 6000 m (19 685 ft) but in only two out of 14 Britons who had previously visited these altitudes. Intraocular pressures during ascent to 6000 m were within normal limits. The relevance of the ocular findings to acclimatisation in previous years was examined, the results supporting the hypothesis of a "carry-over" effect from previous visits to high altitude.     

Changes of cerebral blood flow during short-term exposure to normobaric hypoxia

Decreased arterial partial oxygen pressure (PaO2) below a certain level presents a strong stimulus for increasing cerebral blood flow. Although several field studies examined the time course of global cerebral blood flow (gCBF) changes during hypoxia at high altitude, little was known about the regional differences in the flow pattern. Positron emission tomography (PET) with [(15)O]H2O was used on eight healthy volunteers to assess regional cerebral blood flow (rCBF) during short-term exposure to hypoxia corresponding to simulated altitudes of 3,000 and 4,500 m. Scans at the simulated altitudes were preceded and followed by baseline scans at the altitude of Zurich (450 m, baseline-1 and baseline-2). Each altitude stage lasted 20 minutes. From baseline to 4,500 m, gCBF increased from 34.4 +/- 5.9 to 41.6 +/- 9.0 mL x minute(-1) x 100 g(-1) (mean +/- SD), whereas no significant change was noted at 3,000 m. During baseline-2 the flow values returned to those of baseline-1. Statistical parametric mapping identified the hypothalamus as the only region with excessively increased blood flow at 4,500 m (+32.8% +/- 21.9% relative to baseline-1). The corresponding value for the thalamus, the structure with the second largest increase, was 19.2% +/- 16.3%. Compared with the rest of the brain, an excessive increase of blood flow during acute exposure to hypoxia is found in the hypothalamus. The functional implications are at present unclear. Further studies of this finding should elucidate its meaning and especially focus on a potential association with the symptoms of acute mountain sickness.     

Biomechanical evaluation of a crimp clamp system for loop fixation of monofilament nylon leader material used for stabilization of the canine stifle joint

Exposure to high altitude results in significant physiologic changes and may precipitate mountain sickness, ranging from mild symptoms above 2,500 m to severe symptoms above 4,000 m. In a previous study, changes in the pharmacokinetics of meperidine were observed after exposure to high altitude. This study was conducted to investigate whether similar changes occur for acetazolamide, which is prescribed for prophylaxis of acute mountain sickness. Acetazolamide 250 mg was administered orally to young, healthy male volunteers in groups of 12 each: those residing at sea level (group L), these same volunteers on the day after arrival at high altitude (4,360 m, group HA), and volunteers living at high altitude for 10 months or longer (group HC). Serial blood samples were collected for 24 hours and acetazolamide concentrations were measured in whole blood, plasma, and plasma water. The elimination rate constant (lambda z) was significantly increased in group HA compared with group L. Clearance uncorrected for bioavailability (Cl/F) increased significantly in group HA compared with group L, and further increased in group HC. Apparent volume of distribution (Vz/F) was decreased by 17% in group HA compared with group L, and increased by 37% in group HC compared with group HA. Mean residence time (MRT) was significantly decreased in group HA compared with groups L and HC. Erythrocyte (RBC) uptake increased significantly after a significant increase in RBC count in group HC compared with group L. The extent of protein binding (EPB), however, was significantly decreased in group HA compared with groups L and HC. Free acetazolamide concentrations were significantly lower in group HC than in group L 12 hours after administration. Based on these observations, it is suggested that patients travelling to high altitude, especially altitudes above 4,000 m, should be closely monitored and acetazolamide dosage adjusted as necessary.     

Influence of simulated altitude on the performance of five blood glucose meters

OBJECTIVE: To determine the reliability of five blood glucose meters (BGMs) at various simulated altitudes using a hypobaric chamber. RESEARCH DESIGN AND METHODS: Blood glucose levels (ranged from 1.5 to 26.3 mmol/l, according to the reference method) were measured in 18 venous blood samples by each BGM at 200, 1,000, and every 500 m up to 4,000 m in a hypobaric chamber, where temperature and humidity were held constant. RESULTS: Four BGMs underestimated and one overestimated blood glucose concentration while barometric pressure decreased. The average percent error varied in relation to simulated altitude from 0.26 +/- 4.8% (SD) at 200 m to -28.9 +/- 4.5% at 4,000 m (Glucometer 3; P < 0.05), from 28.4 +/- 5.7 to 49.3 +/- 5.9% (Accu-Chek Easy; P < 0.05), from -10.5 +/- 2.6 to 19.8 +/- 4.3% (Tracer, P < 0.05), from -5.5 +/- 2.6 to -11.2 +/- 3.0% (Reflolux; NS), and from 17.8 +/- 4.3 to 14.8 +/- 3.6% (One Touch; NS). The most accurate seemed to be the Reflolux, except for high blood glucose levels at simulated high altitudes. The One Touch II showed a good agreement, whatever the barometric pressure and the range of blood glucose concentrations. The highest underestimation was seen with the Glucometer 3. CONCLUSIONS: Except for the Accu-Chek Easy, low barometric pressure underestimated the BGM results in comparison with measurements taken at simulated low altitudes. The lack of accuracy and consistency of performance > 2,000 m should be known by diabetic patients practicing sports activities, such as trekking or skiing at high altitudes.     

Altitude-related illnesses

Altitude-related illnesses are a frequent cause of morbidity and occasional mortality in travelers to high altitudes in the United States and throughout the world. The primary altitude illnesses are acute mountain sickness, high-altitude pulmonary edema, and high-altitude cerebral edema. The pathogenesis of these syndromes remains unclear despite considerable research. Altitude also has potential deleterious effects on common medical conditions including coronary artery disease, pulmonary disease, hemoglobinopathies, and pregnancy. Most of these problems are primarily preventable with appropriate information before travel. Education should include information about rate of ascent, diet, alcohol intake, physical activity, and preventive medications, including acetazolamide, nifedipine, and dexamethasone in selected circumstances.     

Pulmonary gas exchange in acute mountain sickness

The severity of acute mountain sickness (AMS) was investigated in healthy volunteers, airlifted to high altitude (5,360 m). Blood gases were measured at 2,990 m and 5,360 m. Symptoms of AMS were found in all subjects, but ranged from malaise to vomiting with intractable headache. The clinical severity of AMS was directly related to the arterial PCO2 and inversely to pH, but unrelated to the PO2 on arrival at high altitude. However, PO2 fell and was lowest 48 h after arrival at high altitude in those subjects with the most severe AMS. These were the only subjects to show an increase in the alveolar-arterial PO2 difference and in the venous admixture ratio during the first 48 h. These abnormalities in gas exchange, which developed in the subjects with the most marked cerebral symptoms, suggest that the manifestations of cerebral and pulmonary dysfunction at altitude develop simultaneously, a finding that suggests coexisting cerebral and pulmonary edema.     

Physical fitness influences water turnover and body water changes during trekking

PURPOSE: This study was performed to assess water turnover and changes of body water during a trekking tour at moderate altitude. METHODS: Fifteen healthy normally trained adults participated in a 7-d backpack trek tour in the Swiss Alps (total walking distance: 120.5 km; cumulated altitude difference: 6990 m (uphill) and 7550 m downhill; lowest point: 1285 m; highest point: 3317 m). Total body water and water turnover were measured using deuterium dilution and elimination (oral load of 0.33 g 99.8% D2O per kg body weight, overnight equilibration period, pre- and postdose saliva samples immediately before and after sleep, analysis of D2O concentrations in saliva using Fourier-transform infrared spectroscopy, CV < 1%). Physical training state was assessed after the tour using the lactate-exercise intensity relationship obtained by performing 50-W increments every 3 min on a cycle ergometer. RESULTS: Body water decreased from the evening of day 0 to the evening of day 4 (from 45.3 +/- 7.3 L to 43.4 +/- 7.6 L, P < 0.05), and did not significantly decrease (43.5 +/- 7.9 L) until the evening of day 5 (maximum of trekking exercise intensity). Mean daily water turnover was 5.7 +/- 1.8 L x d(-1) corresponding to 78.7 +/- 17.5 mL x kg(-1) x d(-1). Body water changes and water turnover were significantly related to the exercise intensity obtained at the lactate threshold as well as at the level of 4 mM lactate. CONCLUSIONS: This correlation may be in part explained by differing glycogen content of muscle tissue.     

Effects of ramipril and spironolactone on ventricular remodeling after acute myocardial infarction: randomized and double-blind study

BACKGROUND: Studies have shown that angiotensin converting enzyme (ACE) inhibition prevents left ventricular remodeling and cardiovascular events after an acute myocardial infarction. The role of aldosterone in ventricular remodeling after a myocardial infarction has not been addressed. AIM: To compare the effects of an ACE inhibitor, an aldosterone receptor antagonist and placebo on left ventricular remodeling after a first episode of transmural acute myocardial infarction. PATIENTS AND METHODS: Patients hospitalized for a first episode of acute myocardial infarction were blindly and randomly assigned to receive ramipril (2.5 mg bid), spironolactone (25 mg tid) or placebo. Ejection fraction, left ventricular end diastolic and end systolic volumes were measured by multigated radionuclide angiography, at baseline and after six months of treatment. RESULTS: Twenty four patients were assigned to placebo, 31 to ramipril and 23 to spironolactone. Age, gender, Killip class, treatment with thrombolytics, revascularization procedures and use of additional medications were similar in the three groups. After six months of treatment, ejection fraction increased from 34.5 +/- 2.3 to 40.2 +/- 2.4% in patients on ramipril, from 32.6 +/- 2.9 to 36.6 +/- 2.7% in patients on spironolactone, and decreased from 37 +/- 3 to 31 +/- 3% in patients on placebo (ANOVA between groups p < 0.05). Basal end systolic volume was similar in all three groups, increased from 43.4 +/- 3.4 to 61.4 +/- 6.0 ml/m2 in patients on placebo and did not change in patients on spironolactone or ramipril (ANOVA p < 0.05). End diastolic volume was also similar in the three groups, increased from 70.6 +/- 4.3 to 92.8 +/- 6.4 ml/m2 in patients on placebo and did not change with the other treatments. CONCLUSIONS: Ramipril and spironolactone had similar effects on ventricular remodeling after acute myocardial infarction, suggesting that aldosterone contributes to this phenomenon and that inhibition of its receptor may be as effective as ACE inhibition in its prevention.     

A patient with Wegener''s granulomatosis presenting with a subarachnoid hemorrhage: case report and review of CNS disease associated with Wegener''s granulomatosis

1. Travellers to high altitude often complain of paroxysmal cough, which has not been previously investigated. We recorded overnight cough frequency and cough-receptor sensitivity to inhaled citric acid in a group of climbers travelling to 5300 m or higher. 2. Cough frequency, monitored in ten subjects, increased from a median of 0 coughs at sea level (range 0-1) to 5 coughs at 5000 m (range 0-13) and to over 60 coughs in subjects ascending to 7000 m. Citric acid cough threshold, measured in 42 subjects, was unchanged on arrival at 5300 m compared with sea level (geometric mean difference 1.26, 95% confidence intervals 0.84-1.89, P = 0.25), but was significantly reduced after 6 days, or more, at altitude compared with sea level (geometric mean difference 2.2, 95% confidence intervals 1.54-3.15, P = 0.0002). Cough threshold was not related to symptoms of acute mountain sickness, oxygen saturation, carbon dioxide tension or lung function. 3. These results indicate an increase in cough and cough-receptor sensitivity after some days at altitude. This may be due to respiratory tract damage from breathing cold dry air at increased ventilatory rates. Other explanations, such as sub-clinical pulmonary oedema or an effect on the cough centre of acclimatization to altitude, cannot be excluded.     

Quantitative EEG in acute mountain sickness

OBJECTIVES: To investigate if the EEG response at moderate altitude may predict a person's tolerance to acute mountain sickness (AMS). MATERIALS AND METHODS: Frequency analysis (QEEG) of tape-recorded ambulatory EEG was performed in 6 climbers during a mountaineering expedition to 7546 m above sea level. The QEEG response in climbers, measured at sea level, at 4500 m, and at 1800 m 1-4 days after maximal altitude exposure, was compared to the change observed during consecutive sea level recordings in 10 control subjects. RESULTS: Three climbers experienced slight (grade 1) AMS symptoms both at 4500 m and at maximal altitude exposure (Group 1). Three other climbers (Group 2) had no symptoms at 4500 m, but they developed AMS (grades 1, 2, or 3) at maximal altitude. Alpha amplitudes were higher at 4500 m in group 1 climbers, while it was lower in group 2 climbers compared to the sea level recording. Significant time x group interactions in ANOVA were found for delta (P = 0.005), theta (P = 0.001) and alpha (P = 0.001) amplitude, indicating that QEEG amplitudes decreased significantly at high altitude in group 2 climbers. CONCLUSION: The QEEG response to moderate hypobaric hypoxia is not uniform, but the direction of QEEG amplitude change, particularly in the alpha band, may possibly predict the risk of developing AMS.     

Acute high altitude sickness--medical experiences from Mount Everest during the spring season 1996

In April-May 1996 a Norwegian expedition climbed Mount Everest from the Tibetan side, Eight out of the ten members reached the summit. The expedition did not experience any serious incidents but took part in the rescue and treatment of climbers from other expeditions. Eleven cases are reported. Four of these were fatal. Cerebral oedema and frostbite were the most common problems in addition to hypothermia and exhaustion. The author also discusses acute mountain sickness, including clinical features, treatment and prophylaxis.     

Spontaneous aorta and coronary lesions in mountain mammals. II. The chamois (Rupicapra rupicapra)

The study of the aorta and coronary arteries from 25 chamois shot in their mountain natural habitat allowed the observation that this animal is more exposed to liposclerotic lesions than other wild herbivorous mammals which live in the plain or at low altitudes. This observation is supported by both the frequency of the lesions (found in the coronary arteries of 14 animals and in the aorta of 10) and their morphologic and histochemical features. The author discusses the possible role of the relatively hypoxic condition, in which this animal lives at high altitudes, on the etiopathogeny of the above mentioned lesions.     

High-altitude pulmonary edema: a clinical crisis

High-altitude pulmonary edema is a serious clinical condition observed in individuals participating in mountain climbing and skiing at high altitudes. High-altitude pulmonary edema is an oncardiogenic form of pulmonary edema. Atrial natriuretic factor and endothelin are implicated and ventilatory support is important in preventing fatalities.     

Endothelial selectins in acute mountain sickness and high-altitude pulmonary edema

STUDY OBJECTIVES: Mechanical or inflammatory injury to pulmonary endothelial cells may cause impaired pulmonary gas exchange in acute mountain sickness (AMS) and noncardiogenic pulmonary edema in high-altitude pulmonary edema (HAPE). This study was designed to determine whether markers of endothelial cell activation or injury, plasma E- and P-selectin, were increased after ascent to high altitude, in AMS or in HAPE. DESIGN: We collected clinical data and plasma specimens in control subjects at sea level and after ascent to 4,200 m, and in climbers with AMS or HAPE at 4,200 m. Data analysis was performed using standard nonparametric statistical methods, and results reported as mean+/-SD. SETTING: National Park Service medical camp at 4,200 m on Mt. McKinley (Denali), Alaska. PATIENTS: Blood samples and clinical data were collected from 17 healthy climbers at sea level and again after ascent to 4,200 m, and from a different group of 13 climbers with AMS and 8 climbers with HAPE at 4,200 m. Climbers with AMS were divided into normoxic (n=7) and hypoxemic (n=6) groups. MEASUREMENTS AND RESULTS: Using an enzyme immunoassay technique, plasma E-selectin concentrations were found to be increased in the 17 control subjects after ascent to 4,200 m (17.2+/-8.2 ng/mL) as compared to sea level (12.9+/-8.2 ng/mL) (p=0.001). Plasma E-selectin concentrations were also increased in subjects with hypoxemic AMS (30.6+/-13.4 ng/mL) and HAPE (23.3+/-9.1 ng/mL) compared to control subjects at sea level (p=0.009). Increased plasma E-selectin concentration significantly correlated with hypoxemia (p=0.006). Plasma P-selectin concentrations were unchanged after ascent to 4,200 m and in subjects with AMS and HAPE. CONCLUSION: Because E-selectin is produced only by endothelial cells, increased plasma E-selectin after ascent to high altitude and in hypoxemic climbers with AMS and HAPE provides evidence that endothelial cell activation or injury is a component of hypoxic altitude illness.     

Cognition and metacognition at extreme altitudes on Mount Everest.

The FACTRETRIEVAL2 test battery, which assesses both retrieval of general information from memory and metacognition about that retrieval, was administered to people before and after a recent expedition to Mount Everest and at extreme altitudes above 6,400 m (higher than any mountain in North America or Europe). Major findings were as follows: First, the same extreme altitudes known to impair learning did not affect accuracy or latency of retrieval, and this robustness of retrieval occurred for both recall and forced-choice recognition. Second, extreme altitude did affect metacognition: Climbers showed a decline in their feeling of knowing both while at extreme altitude and after returning to Kathmandu (i.e., both an effect and an aftereffect of extreme altitude). Third, extreme altitude had different effects than alcohol intoxication (previously assessed by T. O. Nelson et al [see PA, Vol 73:29460]). Alcohol intoxication affected retrieval without affecting metacognition, whereas extreme altitude affected metacognition without affecting retrieval; this different pattern for extreme altitude versus alcohol intoxication implies that (a) hypoxia does not always yield the same outcome as alcohol intoxication and (b) neither retrieval nor metacognition is strictly more sensitive than the other for detecting changes in independent variables. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Acclimatization at high altitude in gradual and acute induction

The study assessed physiological responses to induction to high altitude first to 3,500 m and then to 4,200 m and compared the time course of altitude acclimatization in two groups of male volunteers. The acutely inducted group was transported by aircraft (AI) to 3,500 m in 1 h, whereas the gradually inducted group was transported by road (RI) in 4 days. Baseline recordings of basal cardiovascular, respiratory, and blood gas variables were monitored at sea level as well as at 3,500 m on days 1, 3, 5, and 7. Blood gases were measured on day 10 also. After 15 days at 3,500 m, the subjects were inducted to 4,200 m by road, and measurements were repeated on days 1, 3, and 5, except blood gas variables, which were done on day 10 only. Acute mountain sickness symptoms were recorded throughout. The responses of RI were stable by day 3 of induction at 3,500 m, whereas it took 5 days for AI. Four days in transit for RI appear equivalent to 2 days at 3,500 m for AI. Acclimatization schedules of 3 and 5 days, respectively, for RI and AI are essential to avoid malacclimatization and/or high-altitude illness. Both groups took 3 days at 4,200 m to attain stability for achieving acclimatization.     

High altitude retinal hemorrhages in the expeditions to 8,000 meter peaks. A study of 10 cases

BACKGROUND: Retinal haemorrhages are common at high altitude. Their pathogenesis is unknown. It has been suggested that they are less frequent in sherpas, and that possible predisposing factors might be the abscence of previous high-altitude experience, the extent of the high-altitude hypoxic exposure, polycythemia (because of hyperviscosity), history of cough and Valsalva manoeuvres during the expedition, existence of severe forms of mountain sickness (high-altitude pulmonary oedema and high-altitude cerebral oedema) and use of antiinflammatory drugs. The aim of this study is to know the incidence of retinal haemorrhages in the expeditions to mountains higher than 8.000 m and their relationship to the previously referred possible predisposing factors. SUBJECTS AND METHODS: Funduscopy was performed on 17 healthy subjects taking part in expeditions to Cho-Oyu (8.201 m) and to Shisha Pangma (8.046 m) and on six of their Nepali coworkers. RESULTS: Retinal haemorrhages were found in 10 of the European (59%) and in none of the Nepali mountaineers (p = 0.019). Other 2 Spanish climbers had tortuosity and engorgment of the retinal veins. No statistical association was found between retinal haemorrhages and maximal altitude attained prior to the expedition, maximal altitude reached during the present expedition, number of nights spent at extreme altitude, weight loss as an expression of chronic exposure to hypoxia, haemoglobin, history of cough or Valsalva manoeuvres during the expedition, existence of severe forms of mountain sickness or use of drugs. CONCLUSIONS: These results do not allow us to state that the mentioned factors predispose to high-altitude retinal haemorrhages.     

Diving at diminished atmospheric pressure: air decompression tables for different altitudes

Fifty subjects performed 106 simulated dives at a final ambient pressure of 0.7 at (3000 m above sea level). One hundred and forty-three subjects performed 278 actual controlled dives at altitudes 900-1700 m above sea level. From the experience of these dives, air-decompression tables for altitudes 0-3200 m above sea level were calculated. Tables up to 2000 m above sea level were tested on humans under wet conditions.