Acclimatization improves submaximal exercise economy at 5533 m.

We tested whether the better subjective exercise tolerance perceived by mountaineers after altitude acclimatization relates to enhanced exercise economy. Thirty-two mountaineers performed progressive bicycle exercise to exhaustion at 490 m and twice at 5533 m (days 6-7 and day 11), respectively, during an expedition to Mt. Muztagh Ata. Maximal work rate (W(max)) decreased from mean ± SD 356 ± 73 watts at 490 m to 191 ± 49 watts and 193 ± 45 watts at 5533 m, days 6-7 and day 11, respectively; corresponding maximal oxygen uptakes (VO2max ) were 50.7 ± 9.5, 26.3 ± 5.6, 24.7 ± 7.0 mL/min/kg (P = 0.0001 5533 m vs 490 m). On days 6-7 (5533 m), VO(2) at 75% W(max) (152 ± 37 watts) was 1.75 ± 0.45 L/min, oxygen saturation 68 ± 8%. On day 11 (5533 m), at the same submaximal work rate, VO(2) was lower (1.61 ± 0.47 L/min, P < 0.027) indicating improved net efficiency; oxygen saturation was higher (74 ± 7%, P < 0.0004) but ratios of VO(2) to work rate increments remained unchanged. On day 11, mountaineers climbed faster from 4497 m to 5533 m than on days 5-6 but perceived less effort (visual analog scale 50 ± 15 vs 57 ± 20, P = 0.006) and reduced symptoms of acute mountain sickness. We conclude that the better performance and subjective exercise tolerance after acclimatization were related to regression of acute mountain sickness and improved submaximal exercise economy because of lower metabolic demands for non-external work-performing functions.

Effect of hypoxia and dexamethasone on inflammation and ion transporter function in pulmonary cells.

Dexamethasone has been found to reduce the incidence of high-altitude pulmonary oedema. Mechanisms explaining this effect still remain unclear. We assessed the effect of dexamethasone using established cell lines, including rat alveolar epithelial cells (AEC), pulmonary artery endothelial cells (RPAEC) and alveolar macrophages (MAC), in an environment of low oxygen, simulating a condition of alveolar hypoxia as found at high altitude. Inflammatory mediators and ion transporter expression were quantified. Based on earlier results, we hypothesized that hypoxic conditions trigger inflammation. AEC, RPAEC and MAC, pre-incubated for 1 h with or without dexamethasone (10(-7) mol/l), were subsequently exposed to mild hypoxia (5% O(2), or normoxia as control) for 24 h. mRNA and protein levels of cytokine-induced neutrophil chemoattractant-1, monocyte chemoattractant protein-1 and interleukin-6 were analysed. mRNA expression and functional activity of the apical epithelial sodium channel and basolateral Na(+)/K(+)-ATPase were determined using radioactive marker ions. In all three types of pulmonary cells hypoxic conditions led to an attenuated secretion of inflammatory mediators, which was even more pronounced in dexamethasone pretreated samples. Function of Na(+)/K(+)-ATPase was not significantly influenced by hypoxia or dexamethasone, while activity of epithelial sodium channels was decreased under hypoxic conditions. When pre-incubated with dexamethasone, however, transporter activity was partially maintained. These findings illustrate that long-term hypoxia does not trigger an inflammatory response. The ion transport across apical epithelial sodium channels under hypoxic conditions is ameliorated in cells treated with dexamethasone.

Aliskiren-associated acute renal failure with hyperkalemia.

We report the first case of acute renal failure with hyperkalemia associated with the recently marketed direct renin inhibitor aliskiren. To optimize blood pressure control, the antihypertensive medication of a 76-year-old hypertensive female patient was changed from the angiotensin II receptor antagonist irbesartan to aliskiren. Spironolactone was continued, as serum creatinine and potassium levels were initially normal. Two weeks later the patient presented with acute oliguric renal failure, symptomatic hyperkalemia and metabolic acidosis, necessitating emergency dialytic treatment. Unrecognized pre-existing renal insufficiency (CKD Stage 2 - 3) and the continuation of spironolactone were identified as predisposing risk factors.

Patterns of alcohol consumption and acute myocardial infarction: a case-crossover analysis.

BACKGROUND: Alcohol consumption has been causally related to the incidence of coronary heart disease, but the role of alcohol before the event has not been explored in depth. This study tested the hypothesis that heavy drinking (binge drinking) increases the risk of subsequent acute myocardial infarctions (AMI), whereas light to moderate drinking occasions decrease the risk. METHODS: Case-crossover design of 250 incident AMI cases in Switzerland, with main hypotheses tested by conditional logistic regression. RESULTS: Alcohol consumption 12 h before the event significantly increased the risk of AMI (OR 3.1; 95% CI 1.4-6.9). Separately, the effects of moderate and binge drinking before the event on AMI were of similar size but did not reach significance. In addition, AMI patients showed more binge drinking than comparable control subjects from the Swiss general population. CONCLUSIONS: We found no evidence that alcohol consumption before the event had protective effects on AMI. Instead, alcohol consumption increased the risk.

Platelet count and function at high altitude and in high-altitude pulmonary edema.

Platelet aggregation is the key process in primary hemostasis. Certain conditions such as hypoxia may induce platelet aggregation and lead to platelet sequestration primarily in the pulmonary microcirculation. We investigated the influence of high-altitude exposure on platelet function as part of a larger study on 30 subjects with a history of high-altitude pulmonary edema (HAPE) and 10 healthy controls. All participants were studied in the evening and the next morning at low altitude (450 m) and after an ascent to high altitude (4,559 m). Platelet count, platelet aggregation (platelet function analyzer PFA100; using epinephrine and ADP as activators), plasma soluble P (sP)-selectin, and the coagulation parameters prothrombin fragments 1+2 and thrombin-antithrombin complex were measured. High-altitude exposure decreased the platelet count, shortened the platelet function analyzer closure time by approximately 20%, indicating increased platelet aggregation, increased sP-selectin levels to approximately 250%, but left plasma coagulation unaffected. The HAPE-susceptible subjects were prophylactically treated with either tadalafil (a phosphodiesterase 5 inhibitor), dexamethasone, or placebo in a double-blind way. Subgroup analyses between these different treatments and comparisons of the seven placebo-treated individuals developing HAPE and controls revealed no differences in platelet count, platelet aggregation, or sP-selectin values. We conclude that exposure to high altitude activates platelets, which leads to platelet aggregation, platelet consumption, and decreased platelet count. These effects are, however, not more pronounced in individuals with a history of HAPE or actually suffering from HAPE than in controls and therefore may not be a pathophysiological mechanism of HAPE.

Effects of low flow on pulmonary vascular flow-pressure curves and pulmonary vascular impedance.

OBJECTIVE: Flow-pressure curves and vascular impedance are commonly used to investigate pulmonary circulation, but they may be affected at low flow by reflex neurohumoral activation. We therefore investigated the mechanical effects and the reflex effects of decreased flow on pulmonary vascular resistance and impedance. METHODS: In ten anaesthetized dogs, we compared flow-pressure curves generated in less than 10 s to prevent sympathetic activation (fast curves), or generated over 20-30 min to allow neurohumoral equilibration (slow curves), in hyperoxia (inspired oxygen, 40%) and in hypoxia (inspired oxygen, 10%), before and after adrenergic blockade by phentolamine and propranolol. Resistance was assessed from the flow-pressure relationship. Impedance was computed from instantaneous flow and pressure obtained with an ultrasonic flowmeter and a micromanometer-tipped catheter. RESULTS: At baseline, fast flow-pressure curves were steeper and had a lower pressure intercept. Transient low flow did not affect heart rate or pulmonary arterial elastance. Sustained low flow increased heart rate, resistance and elastance, suggesting baroreceptor-induced sympathetic stimulation. After adrenergic blockade, no difference persisted between effects of transient and sustained low flow. In hypoxia, slow and fast flow-pressure curves were similar. Hypoxia increased heart rate and resistance but did not decrease elastance, suggesting chemoreceptor-induced sympathetic stimulation. In hypoxia, differences between transient and sustained low flow were no longer significant, and were completely suppressed by adrenergic blockade. In two additional dogs, epinephrine infusion increased pulmonary vascular resistance and elastance. CONCLUSIONS: We conclude that (1) compared to transient low flow, sustained low flow is associated with increases in distal resistance and proximal elastance due to sympathetic stimulation and (2) these differences between the effects of transient and sustained low flow do not persist in hypoxia, because of an already present chemoreceptor-induced sympathetic stimulation.

Irreversibility of cyclosporine-induced renal function impairment in heart transplant recipients.

The use of cyclosporine therapy for heart transplant recipients has been associated with a significant improvement of graft survival. Renal function impairment is a frequent finding in patients chronically treated with cyclosporine. The purpose of this prospective randomized study was to establish renal function in a group of heart transplant recipients receiving chronic cyclosporine treatment and to test the hypothesis of reversibility of cyclosporine-induced nephropathy by late reduction of cyclosporine. A total of 28 patients who underwent operation at least 18 months before this study began were randomly assigned to either group A (n = 14), in which the whole-blood polyclonal cyclosporine target trough level was reduced from 400 to 600 micrograms/L to 200 to 400 micrograms/L, and group B (n = 14), in which the level was maintained at 400 to 600 micrograms/L. Renal and cardiac function were assessed by paraaminohippuric acid, inulin and lithium clearances and heart catheterization, respectively, at entry and 4 months later. Cellular rejection in the transplanted heart was monitored by at least four endomyocardial biopsies every 14 days with the histologic Texas scale (grading: 0 to 10). In heart recipients renal blood flow (592 +/- 202 ml/min/1.73 m2) and glomerular-filtration rate (74 +/- 33 ml/min/1.73 m2) were significantly lower (p < 0.01), and mean arterial blood pressure (109 +/- 13 mm Hg) and renal vascular resistance (22.4 +/- 9 mm Hg/dl/min/1.73 m2) were significantly higher than the corresponding values in normal controls (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Orthotopic heart transplantation: an efficient treatment in a young boy with doxorubicin-induced cardiomyopathy.

We present the case of a boy who underwent orthotopic heart transplantation at the age of 14 years because of doxorubicin-induced cardiomyopathy 9 years after treatment of a Wilms tumor of the left kidney. Three years after heart transplantation the patient enjoys a normal daily life. Invasive studies show normal cardiac hemodynamic results and in spite of previous nephrectomy and long-term cyclosporine treatment, renal function is only slightly impaired. So far no secondary neoplasia has occurred under chronic immunosuppression.

Acute mountain sickness is not related to cerebral blood flow: a decompression chamber study.

To evaluate the pathogenetic role of cerebral blood flow (CBF) changes occurring before and during the development of acute mountain sickness (AMS), peak mean middle cerebral artery flow velocities () were assessed by transcranial Doppler sonography in 10 subjects at 490-m altitude, and during three 12-min periods immediately (SA1), 3 (SA2), and 6 (SA3) h after decompression to a simulated altitude of 4,559 m. AMS cerebral scores increased from 0. 16 +/- 0.14 at baseline to 0.44 +/- 0.31 at SA1, 1.11 +/- 0.88 at SA2 (P < 0.05), and 1.43 +/- 1.03 at SA3 (P < 0.01); correspondingly, three, seven, and eight subjects had AMS. Absolute and relative at simulated altitude, expressed as percentages of low-altitude values (%), did not correlate with AMS cerebral scores. Average % remained unchanged, because % increased in three and remained unchanged or decreased in seven subjects at SA2 and SA3. These results suggest that CBF is not important in the pathogenesis of AMS and shows substantial interindividual differences during the first hours at simulated altitude.

Effects of pulmonary embolism on pulmonary vascular impedance in dogs and minipigs.

Pigs have been reported to present with a stronger pulmonary vascular reactivity than many other species, including dogs. We investigated the pulmonary vascular impedance response to autologous blood clot embolic pulmonary hypertension in anesthetized and ventilated minipigs (n = 6) and dogs (n = 6). Before embolization, minipigs, compared with dogs, presented with higher mean pulmonary arterial pressure (Ppa; by an average of 9 mmHg), a steeper slope of Ppa-flow (Q) relationships, and higher 0-Hz impedance (Z0) and first-harmonic impedance (Z1), without significant differences in characteristic impedance (Zc), and a lower ratio of pulsatile hydraulic power to total hydraulic power. Embolic pulmonary hypertension (mean Ppa: 40-55 mmHg) was associated with increased Z0 and Z1 in both species, but the minipigs had a steeper slope of Ppa/Q plots and an increased Zc. At identical Q and Ppa, minipigs still presented with higher Z1 and Zc and a lower ratio of pulsatile hydraulic power to total hydraulic power. The energy transmission ratio, defined as the hydraulic power in the measured waves divided by the hydraulic power in the forward waves, was better preserved after embolism in minipigs. No differences in wave reflection indexes were found before and after embolism. We conclude that minipigs, compared with dogs, present with a higher pulmonary vascular resistance and reactivity and adapt to embolic pulmonary hypertension by an increased Zc without earlier wave reflection. These differences allow for a reduced pulsatile component of hydraulic power and, therefore, a better energy transfer from the right ventricle to the pulmonary circulation.

Enhanced exercise-induced rise of aldosterone and vasopressin preceding mountain sickness.

A possible contribution of exercise to the fluid retention associated with acute mountain sickness (AMS) was investigated in 17 mountaineers who underwent an exercise test for 30 min on a bicycle ergometer with a constant work load of 148 +/- 9 (SE) W at low altitude (LA) and with 103 +/- 6 W 4-7 h after arrival at 4,559 m or high altitude (HA). Mean heart rates during exercise at both altitudes and during active ascent to HA were similar. Exercise-induced changes at LA did not differ significantly between the eight subjects who stayed well and the nine subjects who developed AMS during a 3-day sojourn at 4,559 m. At HA, O2 saturation before (71 +/- 2 vs. 83 +/- 2%, P less than 0.01) and during exercise (67 +/- 2 vs. 72 +/- 1%, P less than 0.025) was lower and exercise-induced increase of plasma aldosterone (617 +/- 116 vs. 233 +/- 42 pmol/l, P less than 0.025) and plasma antidiuretic hormone (23.8 +/- 14.4 vs. 3.4 +/- 1.8 pmol/l, P less than 0.05) was greater in the AMS group, whereas exercise-induced rise of plasma atrial natriuretic factor and changes of hematocrit, potassium, and osmolality in plasma were similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Enhanced fibrin formation in high-altitude pulmonary edema.

Blood coagulation, fibrinolysis, and arterial blood gases were examined in 66 nonacclimatized mountaineers at 4,557 m. Subjects were classified according to a clinical score as healthy (n = 25), having mild acute mountain sickness (AMS) (n = 24), showing severe AMS (n = 13), and suffering from high-altitude pulmonary edema (HAPE) (n = 4). Coagulation times, euglobulin lysis time, and fibrin(ogen) fragment E were normal in all groups without significant changes. Fibrinopeptide A (FPA), a molecular marker of in vivo fibrin formation, was elevated in HAPE to 4.2 +/- 2.7 ng/ml (P less than 0.0001) compared with the other groups showing mean values between 1.6 +/- 0.4 and 1.8 +/- 0.7 ng/ml. FPA was normal in one patient with HAPE, however. Severe AMS was accompanied by a significant decrease in arterial PO2 due to an increase in alveolar-arterial O2 difference, whereas arterial PCO2 did not change significantly. We conclude that activation of blood coagulation is not involved in the pathogenesis of AMS and the impairment of gas exchange in this disease. Fibrin generation occurring in HAPE is probably an epiphenomenon of edema formation.

Pulmonary vascular impedance response to hypoxia in dogs and minipigs: effects of inhaled nitric oxide.

The pig has been reported to present with a stronger hypoxic pulmonary vasoconstriction (HPV) than many other species, including dogs. We investigated [pulmonary arterial pressure (Ppa)-pulmonary arterial occluded pressure (Ppao)] vs. pulmonary blood flow (Q) relationships and pulmonary vascular impedance (PVZ) spectra in nine minipigs and nine weight-matched dogs. The animals were anesthetized and ventilated in hyperoxia [inspired O2 fraction 0.4] or hypoxia (inspired O2 fraction 0.12). PVZ was computed from the Fourier series for Ppa and Q. In hyperoxia, the pigs had a higher Ppa (26 +/- 1 vs. 16 +/- 1 mmHg), a higher first-harmonic impedance (Z1), and a more negative low-frequency phase angle but no different characteristic impedance (Zc) compared with the dogs at the same Q. Hypoxia in the dogs increased (Ppa-Ppao) at all levels of Q studied by an average of 2 mmHg but did not affect Z1 or Zc. Hypoxia in the pigs increased (Ppa-Ppao) at all levels of Q by an average of 13 mmHg and increased Z1 and Zc. Inhaled NO (150 ppm) reversed the hypoxia-induced changes in (Ppa-Ppao)/Q plots and PVZ in the dogs and pigs. However, differences in (Ppa-Ppao)/Q plots and PVZ between the dogs and pigs in hyperoxia and hypoxia were not affected by inhaled NO. We conclude 1) that minipigs present with an elevated pulmonary vascular resistance and impedance in hypoxia more than in hyperoxia and 2) that baseline differences in pulmonary hemodynamics between dogs and minipigs are structural rather than functional.

Should cardiac transplantation for congenital heart disease be delayed until adult age?

The number of pediatric heart transplantations for complex congenital heart disease has increased over the last years, but little experience has been reported in adolescent and adult populations. Between 1987 and 1992, 14 patients (mean age 33.2 years, range 14 to 51 years) were transplanted in our institution because of structural congenital heart disease (n = 9) or other rare disorders of the endomyocardial morphogenesis (n = 5). The main diagnosis included transposition of the great arteries, congenitally corrected transposition of the great vessels, left superior vena cava, tricuspid atresia with right ventricular hypoplasia, double outlet right ventricle with transposition, left ventricular sinusoidal malformation and right ventricular dysplasia. In several cases there were additional intracardiac malformations, including ventricular septum defect, atrial septum defect as well as different forms of pulmonary stenosis. Seven patients had undergone one or more palliative repairs that consisted of modified Blalock-Taussig shunts, Glenn's cavopulmonary anastomosis, Waterstone shunt, Blalock-Hanlon atrioseptectomy and Brock pulmonary valvotomy. Two patients had undergone Senning procedure for transposition of the great arteries. The donor cardiectomy was modified in order to include complete inflow and outflow tissue in the explant and transplantation could be performed without prosthetic material in all patients; deep hypothermic cardiac arrest was never necessary in this series. There was no early or late mortality after a mean follow-up of 37 months (range 4 to 74 months); postoperative echocardiography and cardiac catheterization demonstrated perfect anatomical and functional results in all patients. Adolescent and adult patients with complex congenital cardiac diseases can be transplanted with a very low perioperative risk, even after several prior operative procedures.(ABSTRACT TRUNCATED AT 250 WORDS)

Update: High altitude pulmonary edema.

Recent high altitude studies with pulmonary artery (PA) catheterization and broncho-alveolar lavage (BAL) in early high altitude pulmonary edema(HAPE) have increased our understanding of the pathogenetic sequence in HAPE. High preceding PA and pulmonary capillary pressures lead to a non-inflammatory leak of the alveolar-capillary barrier with egress of red cells, plasma proteins and fluid into the alveolar space. The mechanisms accounting for an increased capillary pressure remain speculative. The concept that hypoxic pulmonary vasoconstriction (HPV) is uneven so that regions with less vasoconstriction are over-perfused and become edematous remains compelling but unproved. Also uncertain is the role and extent of pulmonary venoconstriction. With disruption of the normal alveolar-capillary barrier, some individuals may later develop a secondary inflammatory reaction. A high incidence of preceding or concurrent respiratory infection in children with HAPE has been used to support a causative role of inflammation in HAPE. However, alternatively even mild HPV may simply lower the threshold at which inflammation-mediated increases in alveolar capillary permeability cause significant fluid flux into the lung. Other major questions to be addressed in future research are: 1.) What is the mechanism of exaggerated hypoxic pulmonary vasoconstriction? Is there a link to primary pulmonary hypertension? Several observations suggest that susceptibility to HAPE is associated with endothelial dysfunction in pulmonary vessels. This has not yet been studied adequately. 2.) What is the nature of the leak? Is there structural damage, i. e. stress failure, or does stretch cause opening of pores? 3.) What is the pathophysiologic significance of a decreased sodium and water clearance across alveolar epithelial cells in hypoxia? 4.) What is the role of exercise? Do HAPE-susceptible individuals develop pulmonary edema when exposed to hypoxia without exercise? Answers to these questions will increase our understanding of the pathophysiology of HAPE and also better focus research on the genetic basis of susceptibility to HAPE.

Enhanced cerebral blood flow in acute mountain sickness.

Mean blood flow velocity (v) of both middle cerebral arteries (MCA) was assessed by transcranial Doppler sonography (TCD) in 23 subjects at an altitude of 490 m, as well as after a rapid ascent to a high altitude research laboratory at 4559 m, and daily during a continued 72-h stay at this altitude. Relative changes of mean blood flow velocities (v) of both MCA at high altitude were expressed as percentages of low altitude values and correlated with the development of signs and symptoms of acute mountain sickness (AMS) and changes of arterial PO2, PCO2, and hemoglobin. After ascent to 4559 m, overall MCA-v (mean of all measurements obtained in each subject at high altitude) increased significantly to 148 +/- 16% of baseline values in the subjects with AMS (AMS+) and to 127 +/- 24% in the subjects without AMS (AMS-) (mean +/- SD). This v increase was higher in subjects with AMS and reached statistical significance on day 1 (+50 +/- 19%) and on day 2 (+48 +/- 23%) as compared to the healthy subjects (+27 +/- 24% and +21 +/- 26% on days 1 and 2, respectively). The rise of MCA-v correlated inversely with arterial PO2 on days 2 (r = -0.62, p < 0.005), 3 (r = -0.67, p < 0.025) and 4 (r = -0.69, p < 0.025) and from days 1 to 4 (r = -0.51, p < 0.001). MCA-v did not correlate with blood pressure, arterial PCO2 or hemoglobin. Our results suggest that subjects with AMS have a higher MCA-v increase due to a lower arterial PO2 than healthy subjects.

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.

Cognitive changes at high altitude in healthy climbers and in climbers developing acute mountain sickness.

We report the cognitive functions of 17 non-acclimatized mountaineers who ascended from low lands to an altitude of 4,559 m in 24 h and were studied there within 6 h. We found that this rapid ascent to high altitude had small, but differential effects upon cognitive performance depending upon the later development of acute mountain sickness (AMS). Subjects who developed AMS within a 24-48-h stay at high altitude were mildly impaired in short term memory, but improved in conceptual tasks, while subjects who remained healthy had a better short term memory performance but no improvement in cognitive flexibility. Possible explanations for these unexpected effects of high altitude are discussed.

Prevalence of acute mountain sickness in the Swiss Alps.

OBJECTIVE: To assess the prevalence of symptoms and signs of acute mountain sickness of the Swiss Alps. DESIGN: A study using an interview and clinical examination in a representative population of mountaineers. Positive symptoms and signs were assigned scores to quantify the severity of acute mountain sickness. SETTING: Four huts in the Swiss Alps at 2850 m, 3050 m, 3650 m, and 4559 m. SUBJECTS: 466 Climbers, mostly recreational: 47 at 2850 m, 128 at 3050 m, 82 at 3650, and 209 at 4559 m. RESULTS: In all, 117 of the subjects were entirely free of symptoms and clinical signs of acute mountain sickness; 191 had one or two symptoms and signs; and 158 had more than two. Those with more than two symptoms and signs were defined as suffering from acute mountain sickness. At 4559 m 11 climbers presented with high altitude pulmonary oedema or cerebral oedema, or both. Men and women were equally affected. The prevalence of acute mountain sickness correlated with altitude: it was 9% at 2850 m, 13% at 3050 m, 34% at 3650 m, and 53% at 4559 m. The most frequent symptoms and signs were insomnia, headache, peripheral oedema, and scanty pulmonary rales. Severe headache, vomiting, dizziness, tachypnoea, and pronounced pulmonary rales were associated with other symptoms and signs and therefore characteristic of acute mountain sickness. CONCLUSION: Acute mountain sickness is not an uncommon disease at moderately high altitude--that is, above 2800 m. Severe headache, vomiting, dizziness, tachypnoea, and pronounced pulmonary rales indicate severe acute mountain sickness, and subjects who suffer these should immediately descend to lower altitudes.

Simulated descent v dexamethasone in treatment of acute mountain sickness: a randomised trial.

OBJECTIVE: Evaluation and comparison of the therapeutic efficacy of a portable hyperbaric chamber and dexamethasone in the treatment of acute mountain sickness. DESIGN: Randomised trial during the summer mountaineering season. SETTING: High altitude research laboratory in the Capanna Regina Margherita at 4559m above sea level (Alps Valais). SUBJECTS: 31 climbers with symptoms of acute mountain sickness randomly assigned to different treatments. INTERVENTIONS: One hour of treatment in the hyperbaric chamber at a pressure of 193 mbar or oral administration of 8 mg dexamethasone initially, followed by 4 mg after 6 hours. MAIN OUTCOME MEASURES: Symptoms of acute mountain sickness (Lake Louise score, clinical score, and AMS-C score) before one and about 11 hours after beginning the different methods of treatment. Permitted intake of mild analgesics before treatment and in the follow up period. RESULTS: After one hour of treatment compression with 193 mbar caused a significantly greater relief of symptoms of acute mountain sickness than dexamethasone (Lake Louise score: mean (SD) -4.6 (1.9) v -2.5 (1.8); clinical score: -4.0 (1.2) v -1.5 (1.4); AMS-C score: -1.24 (0.51) v -0.54 (0.59)). In contrast after about 11 hours subjects treated with dexamethasone suffered from significantly less severe acute mountain sickness than subjects treated with the hyperbaric chamber (-7.0 (3.6) v -1.6 (3.0); -4.1 (1.9) v -1.0 (1.5); -1.78 (0.73) v -0.75 (0.82) respectively). Intake of analgesics was similar in both groups. CONCLUSION: Both methods were efficient in treatment of acute mountain sickness. One hour of compression with 193 mbar in the hyperbaric chamber, corresponding to a descent of 2250 m, led to short term improvement but had no long term beneficial effect. On the other hand, treatment with dexamethasone in an oral dose of 8 mg initially followed by 4 mg every 6 hours resulted in a longer term clinical improvement. For optimal efficacy the two methods should be combined if descent or evacuation is not possible.