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Biomedical subjects

O Oelz

Publications and source records attributed to O Oelz.

At least 37 records · Page 2Linked to original sources
PubMed1995

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.

Acute Disease↗
PubMed1995

Endothelin-1 in pulmonary hypertension associated with high-altitude exposure.

BACKGROUND: Endothelin-1 is involved in chronic pulmonary hypertension. Its role in acute pulmonary hypertension due to hypoxia in humans is not clear. We therefore studied the influence of hypoxia caused by exposure to high altitude on plasma endothelin-1 levels, arterial blood gases, and pulmonary arterial pressure in subjects taking nifedipine or placebo. METHODS AND RESULTS: Twenty-two healthy volunteers were investigated at low altitude (490 m) and high altitude (4559 m). Arterial blood gases were analyzed immediately, endothelin-1 was measured by radioimmunoassay, and pulmonary artery pressure was assessed by Doppler echocardiography. After baseline investigations, the mountaineers were allocated in a randomized double-blind fashion to receive either placebo or nifedipine (20 mg TID) during rapid ascent to high altitude within 22 hours. Tests were repeated at the high-altitude research laboratories located in the Capanna "Regina Margherita" (Italy, 4559 m). Plasma endothelin-1 was increased twofold at high altitude (5.9 +/- 2.2 pg/mL compared with 2.9 +/- 1.1 pg/mL, P < .05), was inversely related to arterial PO2 (r = -.46, P < .001), and correlated with pulmonary artery pressure (r = .52, P < .002). At high altitude, arterial endothelin-1 was lower (4.3 +/- 1.6 pg/mL) than venous endothelin-1 (5.9 +/= 2.2 pg/mL, P < .001), indicating either predominant production in the venous vasculature or pronounced clearance in the pulmonary circulation. The calcium antagonist nifedipine, which lowered pulmonary artery pressure at high altitude (32 +/- 5 versus 42 +/- 11 mm Hg, P < .05), had no influence on plasma endothelin-1 levels. The administration of 35% O2 at high altitude normalized arterial PO2, tended to decrease endothelin-1, and decreased pulmonary artery pressure accordingly. CONCLUSIONS: We conclude that plasma endothelin-1 is increased at high altitude, but whether or not it represents an important pathogenetic factor for pulmonary hypertension remains to be investigated.

Adult↗
PubMed1994

Nifedipine does not prevent acute mountain sickness.

Nifedipine has been shown effective for prevention and treatment of high altitude pulmonary edema (HAPE). Because acute mountain sickness (AMS) and HAPE may share common pathophysiologic mechanisms, we evaluate the prophylactic effect of nifedipine on the development of AMS in 27 mountaineers not susceptible to HAPE. They were randomly assigned to receive in a double-blind manner either nifedipine or placebo during rapid ascent to 4559 m and a subsequent three-day sojourn at this altitude. Nine of 14 subjects on nifedipine and eight of 13 subjects on placebo felt ill at high altitude. Pulmonary artery pressures (PAP) estimated by Doppler echocardiography were significantly lower with nifedipine, but arterial PO2, oxygen saturation, and alveolar-arterial oxygen pressure gradient were not significantly different between groups at high altitude. This study demonstrates that lowering PAP has no beneficial effect on gas exchange and symptoms of AMS in subjects not susceptible to HAPE. Therefore, nifedipine cannot be recommended for prevention of AMS, and its use in high altitude medicine should be limited to prevention and treatment of HAPE.

Acute Disease↗
PubMed1994

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.

Acute Disease↗
PubMed1993

[Should the obligation to feed continue until death? Viewpoint and conflict of the treating physician].

At first it is pointed out that artificial nutrition is an unphysiological measure. Its indication is part of the problem that we find it hard to accept the reality of death. In the course of his studies, a physician learns that it is his task to help and to heal. Preservation of life is seen as the equivalent of successful medicine. The conflict arises when palliative measures in an incurable illness may consist in the prolongation of life as well as in the shortening of suffering. The solution is easy, if the intent of the patient is known. If not, the physician has to act according to the presumed intent. In a terminally ill patient unable to express himself, artificial nutrition may be withheld, if the patient shows no signs of being hungry or thirsty and if there is general consent on the issue among physicians, family members and nursing staff. Truly difficult is the situation if we deal with a not terminally ill, yet permanently unconscious patient whose former views on the subject are not known. In such a case, the ultimate moral decision lies with the physician.

Attitude to Death↗
PubMed1993

Treatment of acute mountain sickness by simulated descent: a randomised controlled trial.

OBJECTIVE: To evaluate the therapeutic efficacy of a portable hyperbaric chamber for treatment of acute mountain sickness. DESIGN: Controlled randomised trial over two mountaineering seasons. SETTING: High altitude research laboratory at 4559 m above sea level. SUBJECTS: 64 climbers with acute mountain sickness randomly allocated to different treatments. INTERVENTIONS: One hour of treatment in the hyperbaric chamber at a pressure of 193 mbar or 20 mbar as control or bed rest. MAIN OUTCOME MEASURES: Symptoms of acute mountain sickness before, immediately after, and 12 hours after treatment. Permitted intake of analgesic and antiemetic drugs in the follow up period. RESULTS: Treatment with 193 mbar caused greater relief of symptoms than did control treatment or bed rest. During the 12 hour follow up period intake of analgesics was similar (58-80% of subjects in each group). Symptom scores had improved in all subjects after 12 hours with no significant differences between groups. CONCLUSIONS: One hour of treatment with 193 mbar in a portable hyperbaric chamber, corresponding to a descent of 2250 m, leads to a short term improvement in symptoms of acute mountain sickness but has no beneficial long term effects attributable to pressurisation.

Acute Disease↗
PubMed1993

Interactions between Hb, Mg, DPG, ATP, and Cl determine the change in Hb-O2 affinity at high altitude.

Ascent to high altitude (HA) causes an increase in erythrocyte 2,3-diphsophoglycerate (DPG) and standard PO2 at 50% O2 saturation, PCO2 40 Torr, and blood pH 7.4 (P50,st). We studied the early phase of acclimatization to HA of mountaineers without and with a history of HA pulmonary edema. Tests were performed before ascent and after arrival at HA (4,559 m), approximately 22 h after the departure from low altitude (HA1) and on the following 3 days at HA (HA2-HA4). We investigated the relation between changes in DPG and P50,st, since at moderate altitude P50,st increases more rapidly than DPG, indicating that other factors may contribute to the change in P50,st. Combined effects of interaction between allosteric effectors of hemoglobin (Hb) (DPG, ATP, Cl) and Mg, which competes with Hb for DPG and ATP binding, might explain that phenomenon. Therefore concentrations of liganded Hb species were calculated from the total erythrocyte concentrations of the ligands by use of published binding constants and were related to changes in Hb-O2 affinity. P50,st increased at HA by approximately 4.5 Torr; the concentration of total DPG and ATP increased by 28 and 19%, respectively. Whereas P50,st reached a plateau already at HA1, the concentration of DPG reached its highest value at HA4. The erythrocyte Cl concentration decreased, whereas cellular Hb and Mg concentrations increased slightly. The sum of concentrations of all liganded Hb species increased, reaching 79% of its total change within 22 h after ascent; this can mainly be attributed to the change in the concentration of Hb[DPG] (+77% of total increase).(ABSTRACT TRUNCATED AT 250 WORDS)

2,3-Diphosphoglycerate↗
PubMed1993

IgA nephropathy and hypercalcemia in Whipple's disease.

In 2 patients an IgA nephropathy was found 2 and 5 years before gastrointestinal symptoms led to the diagnosis of Whipple's disease. One patient additionally presented with hypercalcemia. Subsequently 1 patient died, whereas treatment with trimethoprim/sulfamethoxazole resulted in an improvement of IgA nephropathy and in a complete recovery from hypercalcemia and all the manifestations of Whipple's disease in the other patient. IgA nephropathy and hypercalcemia may be considered as early manifestations of Whipple's disease.

Adult↗
PubMed1993

[An analysis of overstrain injuries in rock climbing].

Between spring and autumn 1990 a study was performed with the goal of recording and classifying overstrain injuries due to rock-climbing and to define their causes. Of the 332 climbers participating in the study, 114 (34.4%) had suffered from at least one overstrain injury. The degree of climbing skill proved to be the main risk factor; with increasing climbing skills of the observed persons the percentage of injuries increased very substantially. The degree of climbing skill also was the only significant difference between injured and non-injured persons--injured persons had a climbing skill which was 1.3 degrees (UIAA) higher. Warming up was unable to prevent most overstrain injuries. A total of 237 injuries were described. 34.6% of these were long-term defects such as foot deformations and nail dystrophies of the toes. 65.4% were overstrain injuries; 90.3% of these cases concerned the upper part of the body and the upper extremities including the thoracic girdle, areas which are particularly strained in climbs of high degrees of difficulty. The areas affected were almost exclusively tendons, joint capsules and ligaments. By far the most frequent injury of the upper extremity was the proximal interphalangeal joint injury, followed by injuries to the proximal phalanx, the flexor tendons of the forearm and the distal interphalangeal joint. With regard to training injuries, finger injuries occurred most frequently in addition to elbow injuries. 51% of the overstrain injuries were severe, with healing times of months to years. Only 30% of the injured persons consulted a physician.

Athletic Injuries↗
PubMed1993

[High altitude sojourn in heart diseases].

Altitude exposure may cause a number of events in patients with cardiovascular diseases. In patients with coronary heart disease, an increase in the intensity of angina pectoris or a new onset of angina pectoris may be seen most frequently. This happens mainly in the first few days of altitude exposure. Blood pressure may rise, particularly in patients with known hypertension. These changes are caused by increased activity of the sympathetic nervous system. In patients with pulmonary hypertension, additional hypoxic pulmonary vasoconstriction aggravates the degree of pulmonary hypertension.

Altitude Sickness↗
PubMed1993

[Does drinking protect against mountain sickness?].

This paper summarizes the main findings of 3 publications of our group [2-4] examining fluid balance at high altitude. Of 57 mountaineers ascending from 1170 m to 4559 m within 22 to 77 hours, 24 developed acute mountain sickness (AMS) and 16 developed high altitude pulmonary edema (HAPE). In 14 cases HAPE was preceded by symptoms of AMS. Independently of the amount of fluid intake, which varied from 2 to 4 l/24 h in these studies, subjects developing AMS showed decreased diuresis and natriuresis compared to healthy controls with similar fluid intake. Higher fluid intake resulted in greater urine output but did not prevent AMS. Higher plasma levels of aldosterone at rest and greater exercise-induced rises of plasma aldosterone and vasopressine may explain the increased water and salt retention in subjects with AMS. Whether these hormonal changes are secondary to a more severe hypoxemic stress or present a primary cause of AMS remains to be determined.

Adult↗
PubMed1992

[Pathophysiology, prevention and therapy of altitude pulmonary edema].

Alveolar hypoxia and resulting tissue hypoxia initiates the pathophysiological sequence of high altitude pulmonary edema (HAPE). Very rapid ascent to high altitude without prior acclimatization results in HAPE, even in subjects with excellent tolerance to high altitude. Upon acute altitude exposure, HAPE-susceptible individuals react with increased secretion of norepinephrine, epinephrine, renin, angiotensin, aldosterone and atrial natriuretic peptide. In response to exercise at high altitude, subjects developing acute mountain sickness and HAPE secrete more aldosterone and antidiuretic hormone than subjects who remain well. This results in sodium and water retention, reduction of urine output, increase in body weight and development of peripheral edemas. The hypoxic pulmonary vascular response is enhanced in HAPE-susceptible subjects, thus favouring the development of severe pulmonary hypertension on exposure to high altitude. It has been postulated that uneven pulmonary vasoconstriction enhances filtration pressure in non-vasoconstricted lung areas, leading to interstitial and alveolar edema. The high protein content of the edema fluid in HAPE characterizes this edema as a permeability edema. The prophylactic administration of nifedipine prevents the exaggerated pulmonary hypertension of HAPE-susceptible subjects upon rapid ascent to 4559 m and thus prevents HAPE in most cases. This finding illustrates the crucial role of hypoxic pulmonary hypertension in the development of HAPE. The causal treatment of HAPE is descent, evacuation and administration of oxygen. Treatment of HAPE patients with nifedipine results in a reduction of pulmonary artery pressure, clinical improvement, increased oxygenation, decrease of the alveolar arterial oxygen gradient and progressive clearing of pulmonary edema on chest x-ray. Thus nifedipine offers a pharmacological tool for the treatment of HAPE.

Aldosterone↗
PubMed1992

Prevention and treatment of high altitude pulmonary edema by a calcium channel blocker.

High altitude pulmonary edema (HAPE) is characterized by marked pulmonary hypertension. Treatment of 6 subjects suffering from radiographically documented HAPE with the calcium channel blocker nifedipine, lowered pulmonary artery pressure and resulted in clinical improvement, better oxygenation, reduction of alveolar-arterial oxygen gradient and a progressive clearing of alveolar edema on chest x-ray. This amelioration occurred despite continued exercise at an altitude above 4000 m and without supplementary oxygen. Prophylactic application of nifedipine slow release preparation, 20 mg every 8 hours, prevented HAPE in 9 out of 10 subjects with a history of radiographically documented HAPE upon rapid ascent and subsequent stay to an altitude of 4559 m. Seven of 11 comparable subjects who received placebo developed pulmonary edema at 4559 m. As compared with the subjects who received placebo, those who received nifedipine had a significantly lower mean systolic pulmonary artery pressure, alveolar-arterial pressure gradient of oxygen and symptom score of acute mountain sickness at 4559 m. Thus nifedipine offers a potential emergency treatment of HAPE when descent or evacuation is impossible and oxygen is not available. Prophylactic administration of nifedipine prevents HAPE in susceptible subjects. High pulmonary artery pressure has an important role in the pathogenesis of HAPE.

Acute Disease↗
PubMed1991

Prevention of high-altitude pulmonary edema by nifedipine.

BACKGROUND: Exaggerated pulmonary-artery pressure due to hypoxic vasoconstriction is considered an important pathogenetic factor in high-altitude pulmonary edema. We previously found that nifedipine lowered pulmonary-artery pressure and improved exercise performance, gas exchange, and the radiographic manifestations of disease in patients with high-altitude pulmonary edema. We therefore hypothesized that the prophylactic administration of nifedipine would prevent its recurrence. METHODS: Twenty-one mountaineers (1 woman and 20 men) with a history of radiographically documented high-altitude pulmonary edema were randomly assigned to receive either 20 mg of a slow-release preparation of nifedipine (n = 10) or placebo (n = 11) every 8 hours while ascending rapidly (within 22 hours) from a low altitude to 4559 m and during the following three days at this altitude. Both the subjects and the investigators were blinded to the assigned treatment. The diagnosis of pulmonary edema was based on chest radiography. Pulmonary-artery pressure was measured by Doppler echocardiography and the difference between alveolar and arterial oxygen pressure was measured in simultaneously sampled arterial blood and end-expiratory air. RESULTS: Seven of the 11 subjects who received placebo but only 1 of the 10 subjects who received nifedipine had pulmonary edema at 4559 m (P = 0.01). As compared with the subjects who received placebo, those who received nifedipine had a significantly lower mean (+/- SD) systolic pulmonary-artery pressure (41 +/- 8 vs. 53 +/- 16 mm Hg, P = 0.01), alveolar-arterial pressure gradient (6.6 +/- 3.8 vs. 11.8 +/- 4.4 mm Hg, P less than 0.001), and symptom score of acute mountain sickness (2.0 +/- 0.7 vs. 3.9 +/- 1.9, P less than 0.01) at 4559 m. CONCLUSIONS: The prophylactic administration of nifedipine is effective in lowering pulmonary-artery pressure and preventing high-altitude pulmonary edema in susceptible subjects. These findings support the concept that high pulmonary-artery pressure has an important role in the development of high-altitude pulmonary edema.

Adult↗