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Acute Mountain Sickness (acute + mountain_sickness)

Distribution by Scientific Domains
Medical Sciences71%

Selected Abstracts

AGE AND ACUTE MOUNTAIN SICKNESS: EXAMINING THE DATA

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 4 2005
Jeremy Graham DO
No abstract is available for this article. [source]

Neck Irradiation or Surgery May Predispose to Severe Acute Mountain Sickness

JOURNAL OF TRAVEL MEDICINE, Issue 2 2002
Buddha Basnyat
No abstract is available for this article. [source]

Acute mountain sickness is associated with sleep desaturation at high altitude

RESPIROLOGY, Issue 4 2004
Keith R. BURGESS
Objective: This study was intended to demonstrate a biologically important association between acute mountain sickness (AMS) and sleep disordered breathing. Methodology: A total of 14 subjects (eight males, six females aged 36 ± 10 years) were studied at six different altitudes from sea level to 5050 m over 12 days on a trekking route in the Nepal Himalaya. AMS was quantified by Lake Louise (LL) score. At each altitude, sleep was studied by 13 channel polysomnography (PSG). Resting arterial blood gases (ABG) and exercise SaO2 were measured. Ventilatory responses (VR) were measured at sea level. Individual data were analysed for association at several altitudes and mean data were analysed for association over all altitudes. Results: ABG showed partial acclimatization. For the mean data, there were strong positive correlations between LL score and altitude, and periodic breathing, as expected. Strong negative correlations existed between LL score and PaO2, PaCO2, sleep SaO2 and exercise SaO2, but there was no correlation with sea level VR. There were equally tight correlations between LLs/PaO2 and LL score/sleep SaO2. The individual data showed no significant correlations with LL score at any altitude, probably reflecting the non-steady state nature of the experiment. In addition, mean SaO2 during sleep was similar to minimum exercise SaO2 at each altitude and minimum sleep SaO2 was lower, suggesting that the hypoxic insult during sleep was equivalent to or greater than walking at high altitude. Conclusions: It is concluded that desaturation during sleep has a biologically important association with AMS, and it is speculated that under similar conditions (trekking) it is an important cause of AMS. [source]

Extreme altitude mountaineering and Type 1 diabetes; the Diabetes Federation of Ireland Kilimanjaro Expedition

DIABETIC MEDICINE, Issue 9 2001
K. Moore
Abstract Aims To examine the effects of extreme altitude mountaineering on glycaemic control in Type 1 diabetes, and to establish whether diabetes predisposes to acute mountain sickness (AMS). Methods Fifteen people with Type 1 diabetes and 22 nondiabetic controls were studied during the Diabetes Federation of Ireland Expedition to Kilimanjaro. Daily insulin requirements, blood glucose estimations and hypoglycaemic attacks were recorded in diaries by the people with diabetes. The performance of blood glucose meters at altitude was assessed using standard glucose solutions. Symptoms of acute mountain sickness were recorded daily by people with diabetes and by the nondiabetic controls using the Lake Louise Scoring Charts. The expedition medical team recorded the incidence of complications of altitude and of diabetes. The final height attained for each individual was recorded by the expedition medical team and verified by the expedition guides. Results The final altitude ascended was lower in the diabetic than the nondiabetic group (5187 ± 514 vs. 5654 ± 307 m, P= 0.001). The mean daily insulin dose was reduced from 67.1 ± 28.3,32.9 ± 11.8 units (P < 0.001), but only 50% of recorded blood glucose readings were within the target range of 6,14 mmol/L. There were few hypoglycaemic attacks after the first two days of climbing. Both blood glucose meters tested showed readings as low as 60% of standard glucose concentrations at high altitude and low temperatures. The Lake Louise questionnaires showed that symptoms of AMS occurred equally in the diabetic and nondiabetic groups. There were two episodes of mild diabetic ketoacidosis; two of the diabetic group and three of the nondiabetic group developed retinal haemorrhages. Conclusions People with Type 1 diabetes can participate in extreme altitude mountaineering. However, there are significant risks associated with this activity, including hypoglycaemia, ketoacidosis and retinal haemorrhage, with the additional difficulties in assessing glycaemic control due to meter inaccuracy at high altitude. People with Type 1 diabetes must be carefully counselled before attempting extreme altitude mountaineering. Diabet. Med. 18, 749,755 (2001) [source]

Acute mountain sickness is associated with sleep desaturation at high altitude

RESPIROLOGY, Issue 4 2004
Keith R. BURGESS
Objective: This study was intended to demonstrate a biologically important association between acute mountain sickness (AMS) and sleep disordered breathing. Methodology: A total of 14 subjects (eight males, six females aged 36 ± 10 years) were studied at six different altitudes from sea level to 5050 m over 12 days on a trekking route in the Nepal Himalaya. AMS was quantified by Lake Louise (LL) score. At each altitude, sleep was studied by 13 channel polysomnography (PSG). Resting arterial blood gases (ABG) and exercise SaO2 were measured. Ventilatory responses (VR) were measured at sea level. Individual data were analysed for association at several altitudes and mean data were analysed for association over all altitudes. Results: ABG showed partial acclimatization. For the mean data, there were strong positive correlations between LL score and altitude, and periodic breathing, as expected. Strong negative correlations existed between LL score and PaO2, PaCO2, sleep SaO2 and exercise SaO2, but there was no correlation with sea level VR. There were equally tight correlations between LLs/PaO2 and LL score/sleep SaO2. The individual data showed no significant correlations with LL score at any altitude, probably reflecting the non-steady state nature of the experiment. In addition, mean SaO2 during sleep was similar to minimum exercise SaO2 at each altitude and minimum sleep SaO2 was lower, suggesting that the hypoxic insult during sleep was equivalent to or greater than walking at high altitude. Conclusions: It is concluded that desaturation during sleep has a biologically important association with AMS, and it is speculated that under similar conditions (trekking) it is an important cause of AMS. [source]

Altered free radical metabolism in acute mountain sickness: implications for dynamic cerebral autoregulation and blood,brain barrier function

THE JOURNAL OF PHYSIOLOGY, Issue 1 2009
D. M. Bailey
We tested the hypothesis that dynamic cerebral autoregulation (CA) and blood,brain barrier (BBB) function would be compromised in acute mountain sickness (AMS) subsequent to a hypoxia-mediated alteration in systemic free radical metabolism. Eighteen male lowlanders were examined in normoxia (21% O2) and following 6 h passive exposure to hypoxia (12% O2). Blood flow velocity in the middle cerebral artery (MCAv) and mean arterial blood pressure (MAP) were measured for determination of CA following calculation of transfer function analysis and rate of regulation (RoR). Nine subjects developed clinical AMS (AMS+) and were more hypoxaemic relative to subjects without AMS (AMS,). A more marked increase in the venous concentration of the ascorbate radical (A,,), lipid hydroperoxides (LOOH) and increased susceptibility of low-density lipoprotein (LDL) to oxidation was observed during hypoxia in AMS+ (P < 0.05 versus AMS,). Despite a general decline in total nitric oxide (NO) in hypoxia (P < 0.05 versus normoxia), the normoxic baseline plasma and red blood cell (RBC) NO metabolite pool was lower in AMS+ with normalization observed during hypoxia (P < 0.05 versus AMS,). CA was selectively impaired in AMS+ as indicated both by an increase in the low-frequency (0.07,0.20Hz) transfer function gain and decrease in RoR (P < 0.05 versus AMS,). However, there was no evidence for cerebral hyper-perfusion, BBB disruption or neuronal,parenchymal damage as indicated by a lack of change in MCAv, S100, and neuron-specific enolase. In conclusion, these findings suggest that AMS is associated with altered redox homeostasis and disordered CA independent of barrier disruption. [source]