Presence Of Acute Mountain Sickness Research Articles

Mitochondrial DNA Variation Correlated With the High Altitude Intolerance in Chinese Young Han Males.

ObjectiveAcute exposure to hypobaric hypoxia can trigger acute mountain sickness (AMS), while the exact mechanism has not been fully revealed. The role of genetic factors in the susceptibility of various high-altitude diseases has also gained much interest. Previous studies have provided evidence for the link between AMS and certain nuclear genes or mitochondrial haplogroup. The correlation between point mutations of mitochondrial DNA (mtDNA) and AMS was further explored in the present study.MethodsA total of 84 young Han males residing at low altitude were taken to an elevation of 4,000 m within 40 h. We collected data of their heart rate, blood pressure, peripheral oxygen saturation (SaO2), and obtained blood samples, at sea level and at high altitude. AMS was diagnosed using the revised version of the Lake Louise Questionnaire Score. Sequencing was utilized to identify the association between mtDNA alleles and the occurrence of AMS. We also assessed the association between the presence of AMS and physiological variables, and provided a preliminary discussion of the association between genotypic and phenotypic variation.ResultsThe percentage of neutrophils [Odds ratio (OR): 1.06, 95% confidence interval (CI): 1.01–1.12, P = 0.034) and SaO2 level (OR: 0.87, 95% CI: 0.79–0.95, P = 0.004) were independently associated with the development of AMS. A4576G was a risk factor for AMS (OR: 6.27, 95% CI: 1.2–32.7). T11613C (OR: 0.10, 95% CI: 0.01–0.83), A8923G (OR: 0.15, 95% CI: 0.03–0.76), and T5543C (OR: 0.19, 95% CI: 0.04–0.95) were protective factors for AMS. The level of SaO2 was significantly lower in the individual with A4576G mutation as compared with the individual without A4576G mutation (68.1 ± 7.9 vs. 75.8 ± 6.1, P = 0.001). The level of serum sodium was significantly higher in the individual with A8923G mutation as compared to the individual without A8923G mutation (144.6 ± 1.9 vs. 143.2 ± 1.9, P = 0.027).ConclusionsThe increase in neutrophils and the disability to preserve oxygen saturation may be associated with the high altitude intolerance in young Chinese Han males. A4576G is the risk factor for AMS. T11613C, A8923G, and T5543C are protective factors for AMS. The role of A8923G mutation may correlate with the sodium and water balance and the role of the A4576G mutation may be related to the disability to maintain blood oxygen level after quickly entering the plateau.

Association of Genes of the NO Pathway with Altitude Disease and Hypoxic Pulmonary Hypertension.

Chronic intermittent hypoxia leads to high-altitude pulmonary hypertension, which is associated with high asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthesis. Therefore, we aimed to understand the relation of single nucleotide polymorphisms in this pathway to high-altitude pulmonary hypertension (HAPH). We genotyped 69 healthy male Chileans subjected to chronic intermittent hypoxia. Acclimatization to altitude was determined using the Lake Louise Score and the presence of acute mountain sickness. Echocardiography was performed after six months in 24 individuals to estimate pulmonary arterial pressure. The minor allele of dimethylarginine dimethylaminohydrolase (DDAH)1 rs233112 was associated with high-baseline plasma ADMA concentration, while individuals homozygous for the major allele of DDAH2 rs805304 had a significantly greater increase in ADMA during chronic intermittent hypoxia. The major allele of alanine glyoxylate aminotransferase-2 (AGXT2) rs37369 was associated with a greater reduction of plasma symmetric dimethylarginine (SDMA). Several genes were associated with high-altitude pulmonary hypertension, and the nitric oxide synthase (NOS)3 and DDAH2 genes were related to acute mountain sickness. In conclusion, DDAH1 determines baseline plasma ADMA, while DDAH2 modulates ADMA increase in hypoxia. AGXT2 may be up-regulated in hypoxia. Genomic variation in the dimethylarginine pathway affects the development of HAPH and altitude acclimatization.

Incidence of Mild Cognitive Impairment with Ascending Altitude.

Background: This study aimed to longitudinally quantify the prevalence of mild cognitive impairment (MCI) in individual trekkers at three different ascending altitudes (Site 1: ∼3500 m, Site 2: ∼4400 m, and Site 3: ∼5100 m). We correlated these findings with the presence of acute mountain sickness (AMS). Materials and Methods: We performed serial assays using the environmental quick mild cognitive impairment (eQMCI) score on 103 English-speaking 18- to 65-year-old volunteers trekking to Everest Base Camp in Nepal during spring 2016. We defined MCI as a score less than 67 (lower scores indicating more cognitive impairment). Additional data collected included the Lake Louise Score, demographics, and other possible confounders. Results: eQMCI scores significantly decreased with ascent from Site 1 to 2 (a score of 78.95 [SD = 7.96] to 74.67 [SD = 8.8] [Site 1-2 p = 0.04]), but then increased on ascent to Site 3 to 83.68 (SD = 8.67) (Site 1-3 p = <0.0001, Site 2-3 p = <0.0001). However, subjects who fulfilled eQMCI criteria for MCI increased despite the overall improvement in score: 6.8% (N = 7) at Site 1, 18.7% (N = 14) at Site 2, and 3.3% (N = 2) at Site 3. Incidence of AMS at Sites 1, 2, and 3 was 22.3% (N = 23), 21.3% (N = 16), and 48.3% (N = 29), respectively. Of those with MCI, 1.94% met criteria for AMS at Site 1 (p = 0.0017), 2.67% at Site 2 (p = 0.6949), and 3.33% at Site 3 (p = <0.0001). Conclusions: There is a significant incidence of MCI at high altitude, even in those without subjective findings of AMS. Interestingly, subjects with a decline in cognitive function show an increasing trend for developing AMS at higher altitude. Future research on the clinical impact of MCI on a subject's health, judgment, and performance remains to be elucidated.

Association between ACTN3 and acute mountain sickness

BackgroundDuring the process of acclimatization, when our organism needs to adjust several metabolic processes in the attempt of establishing a better oxygenation, it is normal that individuals present some symptoms that can lead to the disease of the mountain. However, not everyone presents such symptoms and individuals native of high altitudes regions present genetic differences compared to natives of low altitudes which can generate a better acute adaptation. One of these differences is the higher proportion of type I muscle fibers, which may originate from the R577X polymorphism of the ACTN3 gene. The aim of this study was to compare the response of individuals with different ACTN3 genotypes at simulated 4500 m altitude on the presence of Acute Mountain Sickness (AMS) symptoms. Twenty-three volunteers (RR = 7, RX = 8, XX = 8) spent 4 hours exposed to a simulated altitude of 4500 m inside a normobaric hypoxia chamber. Lactate and glucose concentrations, SpO2, heart rate and the symptoms of AMS were analyzed immediately before entering the chamber and at each hour of exposure. Statistical analysis was performed using IBM SPSS Statistics 21 software.ResultsOur results point to an association between AMS symptoms and the presence of R allele from R577X polymorphism.ConclusionWe conclude that individuals with at least one R allele of the R577X polymorphism seems to be more susceptible to the effects of hypoxia during the acclimatization process and may develop AMS symptoms.

P6480Asymmetric dimethylarginine (ADMA) predicts altitude-associated hypoxic pulmonary arterial hypertension

Abstract Prolonged exposure to altitude-associated chronic hypoxia (CH) may cause high altitude pulmonary hypertension (HAPH). Chronic intermittent hypobaric hypoxia (CIH) occurs in individuals who commute between sea level and high altitude. CIH is associated with repetitive acute hypoxic acclimatization and conveys the long-term risk of HAPH. As nitric oxide (NO) is an important regulator of systemic and pulmonary vascular tone and asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthesis that increases in hypoxia, we aimed to investigate whether ADMA predicts the incidence of HAPH among Chilean frontiers personnel exposed to six months of CIH. We performed a prospective study of 123 healthy male subjects who were subjected to CIH (5 days at appr. 3,550 m, followed by 2 days at sea level) for six months. ADMA, SDMA, L-arginine, arterial oxygen saturation, systemic arterial blood pressure, and haematocrit were measured at baseline and at months 1, 4, and 6 at high altitude. Acclimatization to high altitude was determined using the Lake Louise Score and the presence of acute mountain sickness (AMS). Echocardiography was performed after six months of CIH in a subgroup of 43 individuals with either good (n=23) or poor (n=20) aclimatization to altitude, respectively. Logistic regression was used to assess the association of biomarkers with HAPH. 100 study participants aged 18.3±1.3 years with complete data sets were included in the final analysis. Arterial oxygen saturation decreased upon the first ascent to altitude and plateaued at about 90% during the further course of the study. Haematocrit increased to about 47% after one month and remained stable thereafter. ADMA continuously increased and SDMA decreased during the study course, whilst L-arginine levels showed no distinct pattern. The incidence of AMS and the Lake Louise Score were high after the first ascent (53 and 3.1±2.4, respectively) and at one month of CIH (47 and 3.0±2.6, respectively), but decreased to 20 and 1.4±2.0 at month 6, respectively (both p&lt;0.001 for trend). In echocardiography, 18 participants (42%) showed a mean pulmonary arterial pressure (mPAP) greater than 25 mm Hg (mean ± SD, 30.4±3.9 mm Hg), out of which 9 (21%) were classified as HAPH (mPAP ≥30 mm Hg; mean ± SD, 33.9±2.2 mm Hg). Baseline ADMA, but not SDMA, was significantly associated with mPAP at month 6 in univariate logistic regression analysis (R = 0.413; p=0.007). In ROC analysis, a cut-off for baseline ADMA of 0.665 μmol/l was determined as the optimal cut-off level to predict HAPH (mPAP &gt;30 mm Hg) with a sensitivity of 100% and a specificity of 63.6%. ADMA concentration increases during long-term CIH. It is an independent predictive biomarker for the incidence of HAPH. SDMA concentration decreases during CIH and shows no association with HAPH. Our data support a role of impaired NO-mediated pulmonary vasodilation in the pathogenesis of high altitude pulmonary hypertension. Acknowledgement/Funding CONICYT/FONDEF/FONIS Sa 09I20007; FIC Tarapaca BIP 30477541-0; BMBF grant 01DN17046 (DECIPHER); Georg &amp; Jürgen Rickertsen Foundation, Hamburg

Asymmetric Dimethylarginine at Sea Level Is a Predictive Marker of Hypoxic Pulmonary Arterial Hypertension at High Altitude.

Background: Prolonged exposure to altitude-associated chronic hypoxia (CH) may cause high-altitude pulmonary hypertension (HAPH). Chronic intermittent hypobaric hypoxia (CIH) occurs in individuals who commute between sea level and high altitude. CIH is associated with repetitive acute hypoxic acclimatization and conveys the long-term risk of HAPH. As nitric oxide (NO) regulates pulmonary vascular tone and asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthesis, we investigated whether ADMA concentration at sea level predicts HAPH among Chilean frontiers personnel exposed to 6 months of CIH. Methods: In this prospective study, 123 healthy army draftees were subjected to CIH (5 days at 3,550 m, 2 days at sea level) for 6 months. In 100 study participants with complete data, ADMA, symmetric dimethylarginine (SDMA), L-arginine, arterial oxygen saturation (SaO2), systemic blood pressure, and hematocrit were assessed at months 0 (sea level), 1, 4, and 6. Acclimatization to altitude was determined using the Lake Louise Score (LLS) and the presence of acute mountain sickness (AMS). Echocardiography was performed after 6 months of CIH in 43 individuals with either good (n = 23) or poor (n = 20) acclimatization. Results: SaO2 acutely decreased at altitude and plateaued at 90% thereafter. ADMA increased and SDMA decreased during the study course. The incidence of AMS and the LLS was high after the first ascent (53 and 3.1 ± 2.4) and at 1 month of CIH (47 and 3.0 ± 2.6), but decreased to 20 and 1.4 ± 2.0 at month 6 (both p < 0.001). Eighteen participants (42%) showed a mean pulmonary arterial pressure (mPAP) >25 mm Hg, out of which 9 (21%) were classified as HAPH (mPAP ≥ 30 mm Hg). ADMA at sea level was significantly associated with mPAP at high altitude in month 6 (R = 0.413; p = 0.007). In ROC analysis, a cutoff for baseline ADMA of 0.665 μmol/L was determined to predict HAPH (mPAP > 30 mm Hg) with a sensitivity of 100% and a specificity of 63.6%. Conclusions: ADMA concentration increases during CIH. ADMA at sea level is an independent predictive biomarker of HAPH. SDMA concentration decreases during CIH and shows no association with HAPH. Our data support a role of impaired NO-mediated pulmonary vasodilation in the pathogenesis of HAPH.

Physiological Variables Associated with the Development of Acute Mountain Sickness.

Objective To identify the physiological variables associated with the development of acute mountain sickness (AMS).Methods Eighty four young Chinese men residing at low altitude were taken to an altitude of 4000 m within 40 hours. At sea level and at high altitude, we measured the heart rate, blood pressure, and peripheral oxygen saturation (SpO2) respectively. We also collect blood samples from each participants before and after the altitude elevation. The blood routine and biochemical examinations were performed for all blood samples. The revised Lake Louise Criteria was adopted to diagnose AMS after the subjects arrived at the target high altitude. The association between the presence of AMS and subjects' physiological variables were analysed statistically.Results Of 84 participants, 34 (40.5%) developed AMS. Compared with non AMS group, in the AMS group, the percentage of neutrophils was significantly higher (64.5%±11.2% vs. 58.1%±8.8%, P =0.014), while the level of SpO2 was significantly lower (79.4%±5.4% vs. 82.7%±5.6, P=0.008). Binary logistic regression analyses emphasized the association of neutrophils (OR: 1.06, 95% CI: 1.01-1.12, P=0.034) and SpO2 level (OR: 0.87, 95% CI : 0.79-0.95, P=0.004) with the development of AMS.Conclusion The ability to sustain SpO2 after altitude elevation and the increase of neutrophils were associated with the development of AMS in young males.

Three-Minute Step Test for Predicting Acute Mountain Sickness: A Post Hoc Analysis of Rhodiola Crenulata Extract for Prevention of Acute Mountain Sickness, a Randomized, Double-Blind, Placebo-Controlled, Crossover Trial.

Acute mountain sickness (AMS) often occurs in individuals who rapidly travel above 2,500 m. As the convenience of traveling and the development of mountain sports increase, AMS will become an increasingly important public health problem. However, no method to effectively predict AMS before it occurs is currently available. This post hoc study investigated whether the 3-Minute Step Test (3MST), which evaluates physical fitness, is predictive of AMS development. The data collected in "Rhodiola crenulata extract for prevention of AMS: a randomized, double-blind, placebo-controlled, crossover trial" was used in the analysis. This study collected 204 observations of 102 participants who made two ascents of Hehuan Mountain (3,100 m) by bus within a 3-month period. Participants completed the 3MST at 250 m (before ascent) and 3,100 m (on Hehuan Mountain). The presence of AMS was accessed using the Lake Louise scoring system. AMS was identified in 124 observations (60.78%). In the univariate analysis, the pre-departure 3MST score (at 250 m) was not significantly associated with AMS (p = 0.498), but the 3MST score measured at 3,100 m, ascent number, pulse rate at 3,100 m, and saturation of peripheral oxygen (SpO2) measured at 3,100 m were significantly correlated with the occurrence of AMS (p = 0.002, 0.039, 0.005, < 0.001, respectively). In a further multivariate analysis, only SpO2 measured at 3,100 m had a significant association with AMS (p = 0.016 and 0.006, respectively). The trend analysis showed that for every 1-point increase in the 3MST score at 3,100 m, the AMS decreased by 4% (adjusted odds ratio [AOR] = 0.96, 95% confidence interval [CI] = 0.92-1.01). The 3MST score cannot be a predictor of AMS, but it may have a potential role in predicting ascent safety in high-altitude areas.

Comparison of Spontaneous versus Paced Breathing on Heart Rate Variability at High Altitude

© 2018, Journal of Clinical and Diagnostic Research. All rights reserved. Introduction: There is conflicting data at sea-level to suggest that Paced Breathing (PB) versus Spontaneous Breathing (SB) during short-term Heart Rate Variability (HRV) measurement improves data reliability. Aim: This study sought to examine the effects of SB versus PB on HRV, at High Altitude (HA). Materials and Methods: This was a prospective observational study on thirty healthy adult men who were investigated over nine days at altitudes of 800-4107 m. Cardiac inter-beat interval data were measured over 55 seconds, twice daily, using an ithlete finger sensor linked to a mobile phone to generate a HRV score. Agreements in the paired (SB vs PB) HRV scores were examined using paired t-tests, correlation coefficients and F-Testing. A factorial repeated measures ANOVA was used to examine the main effect of altitude and breathing method on the paired differences in HRV scores. Results: HA led to a significant reduction in SpO2 and increase in Acute Mountain Sickness (AMS) Scores. HRV scores (511 paired scores) were consistently higher with PB versus SB (mean difference +6.0; 96.1% within 95% agreement limit), though the variance was lower (F=1.2; p=0.04) and the scores strongly correlated (r=0.78; p<0.0001). HRV scores were lower with AMS (versus without AMS), but this difference was only significant with SB (68.1±12.1 vs. 74.3±11.4 vs; p=0.03) but not PB (76.3±11.8 vs. 80.3±10.4 vs; p=0.13). There was a significant main-effect for altitude (F=5.3; p<0.0001) and breathing (F=262.1; p<0.0001) on HRV scores but no altitude-x-breathing interaction (F=1.2; p=0.30). Conclusion: Ithlete HRV scores obtained with PB and SB strongly correlate at moderate HA but are consistently higher and the variance lower with PB. Whilst the actual per se does not affect this difference, the presence of AMS may be an important confounder.

Understanding of Altitude Illness and Use of Pharmacotherapy Among Trekkers and Porters in the Annapurna Region of Nepal.

We surveyed Nepali porters and guides as well as English- and non-English-speaking trekkers on their knowledge of altitude illness and its treatment during trekking expeditions to the Annapurna region of Nepal. From March 15 to April 15, 2014, Nepali porters and visiting trekkers were surveyed regarding their ability to recognize and treat altitude illness in Manang, Nepal (3540 m). Their personal use of medications and home remedies and presence of acute mountain sickness (AMS) symptoms were also assessed. 504 subjects were surveyed, including 108 Nepalis. Overall incidence of AMS symptoms was 16%, 5% among Nepalis, and 21% among trekkers. Subjects recognized that headache (88%) was one of the symptoms of AMS, however many reported not knowing the symptoms of high altitude pulmonary edema (40%) or high altitude cerebral edema (42%). 58% of subjects reported carrying and 16% reported taking acetazolamide, while only 2 (0.4%) respondents took dexamethasone. The majority of subjects reported that they would be able to recognize (67%) and treat (62%) altitude illness. Trekkers reported a higher incidence of AMS symptoms than Nepalis. Although most respondents recognized symptoms of AMS, both Nepalis and trekkers lacked knowledge regarding more serious presentations of altitude illness, thus both groups were overconfident in their ability to recognize and treat altitude illness.

Cardiac biomarkers at high altitude.

Classically, biomarkers such as the natriuretic peptides (NPs) BNP/NT-proBNP are associated with the diagnosis of heart failure and hs-cTnT with acute coronary syndromes. NPs are also elevated in pulmonary hypertension. High pulmonary artery systolic pressure (PASP) is a key feature of high altitude pulmonary edema (HAPE), which may be difficult to diagnose in the field. We have previously demonstrated that NPs are associated with high PASP and the presence of acute mountain sickness (AMS) in a small cohort at HA. We aimed to investigate the utility of several common cardiac biomarkers in diagnosing high PASP and AMS. 48 participants were assessed post-trekking and at rest at three altitudes: 3833 m, 4450 m, and 5129 m. NPs, hs-cTnT and hsCRP, were quantified using immunoassays, PASP was measured by echocardiography, and AMS scores were recorded. Significant changes occurred with ascent in NPs, hs-cTnT, hsCRP (all p<0.001) and PASP (p=0.006). A high PASP (≥40 mm Hg) was associated with higher NPs, NT-proBNP: 137±195 vs. 71.8±68 (p=0.001); BNP 15.3±18.1 vs. 8.7±6.6 (p=0.001). NPs were significantly higher in those with AMS or severe AMS vs. those without (severe AMS: NT-proBNP: 161.2±264 vs. 76.4±82.5 (p=0.008)). The NPs correlated with hsCRP. cTnT increased with exercise at HA and was also higher in those with a high PASP (13.8±21 vs. 7.8±6.5, p=0.018). The NPs and hs-cTnT are associated with high PASP at HA and the NPs with AMS.

Heart rate variability during two sequential mountaineering expeditions

This study was undertaken to assess the duration of altitude acclimatization retention in individuals after initial exposure to a maximum altitude of 5360m during a mountaineering expedition. Spectral heart rate variability analysis accompanied by an assessment of acute mountain sickness using the Lake Louise Scoring System was performed during two sequential mountaineering expeditions to altitudes of 5360m and 5642m, with a period of 30 days between each expedition. Subjects displayed varying degrees of alterations in heart rate variability during the initial expedition, which indicated differing degrees of dysadaptation and stress development. Their Lake Louise Scores accounted for the presence of acute mountain sickness throughout the trip. During the subsequent expedition, the subjects' heart rate variability measures were within the normal range, and there were no signs of acute mountain sickness. All three subjects who underwent step-by-step exposure to altitudes of 5360m displayed differing degrees of alterations in heart rate variability in conjunction with differing degrees of acute mountain sickness. All subjects also developed acclimatization to hypoxic conditions at this altitude, which was preserved for 30 days, and was sufficient to prevent them from showing any significant alterations in heart rate variability when re-exposed to the same altitude.

Carbon Monoxide Exposure on Denali: Comparing the 2004 and 2005 Climbing Seasons

This study assessed a potential relationship between elevated carboxyhemoglobin (COHb) levels and the presence of acute mountain sickness (AMS) at 4300 m on Denali and evaluated the relationship between COHb levels, AMS, and climber characteristics and behaviors. Building on our research done in 2004, in this article we report further data gathered during the 2005 climbing season and evaluate the combined results. Participants were screened for AMS using the Lake Louise Self-Report Questionnaire and answered questions focusing on AMS symptoms, AMS prevention, and previous history of altitude illness. Carboxyhemoglobin levels were measured by serum co-oximetry. Additional questions assessed stove practices, climbing practices, and climber behaviors. Nonparametric statistical analyses were performed to examine potential relationships between COHb levels, AMS symptoms, and climber behaviors across the 2 years and with years combined. Overall, 317 climbers participated in the 2-year study. As in 2004, the combined data demonstrated no relationship between positive carbon monoxide (CO) exposure and positive criteria for AMS (P = .276). Climbers in 2005 were 1.92 times more likely to meet positive criteria for AMS, compared to climbers in 2004 (P = .028). On the contrary, climbers in 2004 were 3.93 times more likely to be CO exposed than climbers in 2005 (P = .003). Overall, climbers descending the mountain were more likely to be positive for CO exposure (5.56 times more likely than ascending climbers, P = .002) and to have higher overall mean COHb levels (2.26% descending vs 0.93% ascending, P = .006). The previous association between increased stove use and climbers who met positive criteria for AMS was not observed in the 2005 or in the combined data (P = .715). A relationship was observed between increased hours of operating stoves and increased COHb levels (P = .002). Female climbers were 2.041 times more likely to meet criteria for AMS (P = .043). No relationship between AMS symptoms and CO exposure was observed. As found in our initial study, descending climbers had higher overall COHb levels and an increased risk of CO exposure (COHb of >3% in nonsmokers and >10% in smokers). Also, increased hours of stove operation was linked to climbers who had elevated COHb levels.

Hypoxia-Induced Acute Mountain Sickness is Associated with Intracellular Cerebral Edema: A 3 T Magnetic Resonance Imaging Study

Acute mountain sickness is common among not acclimatized persons ascending to high altitude; the underlying mechanism is unknown, but may be related to cerebral edema. Nine healthy male students were studied before and after 6-h exposure to isobaric hypoxia. Subjects inhaled room air enriched with N(2) to obtain arterial O(2) saturation values of 75 to 80%. Acute mountain sickness was assessed with the environmental symptom questionnaire, and cerebral edema with 3 T magnetic resonance imaging in 18 regions of interest in the cerebral white matter. The main outcome measures were development of intra- and extracellular cerebral white matter edema assessed by visual inspection and quantitative analysis of apparent diffusion coefficients derived from diffusion-weighted imaging, and B0 signal intensities derived from T2-weighted imaging. Seven of nine subjects developed acute mountain sickness. Mean apparent diffusion coefficient increased 2.12% (baseline, 0.80+/-0.09; 6 h hypoxia, 0.81+/-0.09; P=0.034), and mean B0 signal intensity increased 4.56% (baseline, 432.1+/-98.2; 6 h hypoxia, 450.7+/-102.5; P<0.001). Visual inspection of magnetic resonance images failed to reveal cerebral edema. Cerebral acute mountain sickness scores showed a negative correlation with relative changes of apparent diffusion coefficients (r=-0.83, P=0.006); there was no correlation with relative changes of B0 signal intensities. In conclusion, isobaric hypoxia is associated with mild extracellular (vasogenic) cerebral edema irrespective of the presence of acute mountain sickness in most subjects, and severe acute mountain sickness with additional mild intracellular (cytotoxic) cerebral edema.

Ataxia at Altitude Measured on a Wobble Board

To establish a simple measure of ataxia for use at high altitude. Twenty healthy subjects took part in a trek to 5005 m. At 5 different altitudes on the route, they undertook a balance test using a wobble board. The primary objectives were to investigate disturbances of ataxia at altitude and to correlate any observed disturbances with acute mountain sickness (AMS) scores. Secondary outcomes were correlations with cerebral regional oxygenation, pulse oximetry, and age. After a short learning curve, the wobble board test was found to be reproducible. Subjects over 31 years of age were significantly less steady than younger subjects. Subjects suffering acute mountain sickness scored significantly worse on the wobble board test, although scores did not correlate with a specific question on unsteadiness. A positive test defined as equal to or more than 2.5 contacts over 2 minutes gave a predictive value for acute mountain sickness of 66.7% at 4650 m and 100% at 5005 m. Cerebral regional oxygenation in 9 subjects at 5005 m correlated with the wobble board test (r = 0.73; p < .05), whereas pulse oximetry did not. The wobble board may be a useful adjunct in quantitating ataxia in the field. A positive result may indicate the presence of AMS and may be a useful clinical measure of cerebral hypoxia but should be correlated with other clinical features.

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.

Physiologic response to moderate altitude exposure among infants and young children.

Substantial numbers of children are exposed to moderate altitude while traveling to mountain resorts with their families. Although there has been extensive study of the adult physiologic response to altitude exposure, few studies of infants and young children exist. This investigation examines the acute physiologic responses to moderate altitude exposure among young children and the relationship of these responses to the development of acute mountain sickness (AMS). Children 3 to 36 months old participated in the prospective observational study, which included baseline measurements at 1610 m and measurements after a 24-h exposure to 3109 m. Measurements included pulse and respiratory rate, end-tidal CO(2), arterial oxygen saturation (pulse oximetry), cerebral tissue oxygenation (St(O2)) by near-infrared spectroscopy, middle cerebral artery resistive index by transcranial Doppler, lateral ventricle volumes (ultrasound), and clinical evaluation for the presence of acute mountain sickness (Children's Lake Louise Score). Twenty-four children (13 girls and 11 boys, age 14.5 +/- 10.2 months) participated. After acute exposure to 3109 m, these children showed an increase in respiratory rate from 45 +/- 13 to 51.9 +/- 15 breaths/min (p < 0.008), accompanied by a decrease of end-tidal CO(2) from 31 +/- 3 to 28 +/- 2 mm Hg (p < 0.001) and a reduction of arterial oxygen saturation from 95 +/- 2 to 91 +/- 2% (p < 0.001). St(O2) also decreased from 78 +/- 8 to 67 +/- 13% (p < 0.001), and this reduction appeared to be related to age (r = 0.58, p < 0.05), with lower saturations found in younger children. No evidence of increased intracranial pressure, as assessed by middle cerebral artery resistive index, was seen during ascent. Seven subjects developed symptoms of AMS; however, no relationship was found between the physiologic changes observed and the presence of symptoms. Ascent from 1610 to 3109 m resulted in tachypnea, relative hypoxia, hypocapnia, and a reduction in cerebral tissue oxygenation (St(O2)). The reduction in St(O2) appeared to be related to age, with infants appearing to be the most susceptible to cerebral tissue oxygen desaturation at high altitude. No relationship appears to exist between the presence of AMS and the physiologic measurements.

Acute Mountain Sickness in Tourists with Children at Lake Chungará (4400 m) in Northern Chile

To evaluate the presence of acute mountain sickness (AMS) and cardiorespiratory responses in adult and pediatric tourists exposed to high altitude (Putre and Chungará). The study was performed during a tourist expedition to Lake Chungará (4400 m) with an overnight stay in the town of Putre (3500 m). The study group included 15 adults (21-44 years), 10 teenagers (13-18 years), and 6 children (6-48 months). We evaluated AMS symptoms in adults with the Lake Louise questionnaire and in children with the modified Children's Lake Louise Score for preverbal subjects. Cardiorespiratory measurements included heart rate and oxygen saturation on arrival at Putre and Chungará. Values were expressed as mean +/- SD; significance was tested by analysis of variance, followed by the Newman-Keuls test (P < .05). Significantly lower hemoglobin saturation was found among the children in Putre (74.8% +/- 5.2%) and Chungará (65.3%+/-1.3%) than among the teenagers (82.2%+/-3.2% and 78.6% 2.5%) and adults (83.9%+/-3.3% and 79.7%+/-5.5%) at a similar altitude. A higher incidence of AMS was observed in children (100%) in Putre than in teenagers (50%) and adults (27%). Our results indicate that children are extremely sensitive to hypoxia, as expressed by symptoms of AMS and significant desaturation. Our findings add to the available information regarding the problems encountered when ascending to high altitude with children and support the importance of close monitoring of young children during ascent to high altitude.