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The aim of the study was to examine the efficacy and safety of temazepam on nocturnal oxygenation and next-day performance at altitude. A double-blind, randomized, cross-over trial was performed in Thirty-three healthy volunteers. Volunteers took 10 mg of temazepam and placebo in random order on two successive nights soon after arrival at 5000 m, following a 17-day trek from 410 m. Overnight SaO(2) and body movements, and next-day reaction time, maintenance of wakefulness and cognition were assessed. Compared with placebo, temazepam resulted in a reduction in periodic breathing from a median (range) of 16 (0-81.3)% of the night to 9.4 (0-79.6)% (P = 0.016, Wilcoxon's signed-rank test), associated with a small but significant decrease in mean nocturnal SaO(2) from 78 (65-84)% to 76 (64-83)% (P = 0.013). There was no change in sleep latency (P = 0.40) or restlessness (P = 0.30). Temazepam had no adverse effect on next-day reaction time [241 (201-380) ms postplacebo and 242 (204-386) ms post-temazepam], maintenance of wakefulness (seven trekkers failed to maintain 40 min of wakefulness postplacebo, and four post-temazepam), cognition or acute mountain sickness. At high altitude temazepam reduces periodic breathing during sleep without an adverse effect on next-day reaction time, maintenance of wakefulness or cognition. The 2% reduction in mean SaO(2) post-temazepam is likely to be predominantly because of acclimatization, as by chance more trekkers took temazepam on the first night (19 versus 14). We conclude that at high altitude temazepam is effective in reducing periodic breathing, and is safe to use, without any adverse effect upon next-day performance.

In 1853, Stanhope Templeman Speer published a two-part paper in The Association Medical Journal on Mountain Sickness. Speer was a physician who had worked at the Brompton Hospital for Chest Diseases in London and had been Professor of Medicine in Dublin. He was also an Alpine climber and had made the first ascent of one of the Wetterhorn peaks. His article ran to ten and a half pages in the Journal and to 50 pages in a reprint. It consists of anecdotal accounts of symptoms suffered at altitude from the literature and from his own experiences in the European Alps. He asks three pertinent questions. Is there a condition of mountain sickness? Are these symptoms felt by all persons alike and at the same height? What are the causes, and whence the explanation of such phenomena? In the course of the article, he answers the first two questions but, like us, 162 years later, is unable to answer the third. This article seeks to present Speer's original work and such facts about his life as I have been able to discover.

AFTER TWO SYMPOSIA at Jasper, Hypoxia returned to Banff, the town in the front ranges of the Canadian Rockies where Charlie Houston started the meetings 24 years ago. We were not, however, at the Edwardian Banff Springs Hotel, where the first conferences were lodged, but at the Banff Conference Center on the opposite bank of the Bow River. This is a campus of buildings including lecture theaters, dining hall, accommodation blocks, and leisure center. The facilities were excellent, especially the lecture room allotted to us with adjacent rooms for poster presentations, coffee lobby, and the like. The ski slopes of Sunshine and Norquay were a 20-minute bus ride away, and we had the use of the swimming pool and gym in the Center. Access to Banff is much easier than to Jasper, with direct flights to Calgary from many cities in North America and Europe and a transfer from the airport of only about 90 minutes. However, some 40 registrants were delayed by a very severe storm affecting New York, Boston, and other U.S. East Coast airports and arrived up to 2 days late. There were a total of 190 people registered from 32 countries, including about 40 students. It is good to see so many younger participants as they bode well for the future of our specialty. There was the usual mix of people from Europe and North America, though we would like to see more from other countries.

Lewis Griffith Cresswell Evans Pugh (1909-1994), best known as the physiologist on the successful 1953 British Everest Expedition, inspired a generation of scientists in the field of altitude medicine and physiology in the decades after World War II. This paper details his early life, his introduction to exercise physiology during the war, and his crucially important work in preparation for the Everest expedition on Cho Oyu in 1952. Pugh's other great contribution to altitude physiology was as scientific leader of the 1960-1961 Himalayan Scientific and Mountaineering Expedition (the Silver Hut), and the origins and results of this important expedition are discussed. He had a major and continuing interest in the physiology of cold, especially in real-life situations in Antarctica, exposure to cold wet conditions on hills in Britain, and in long distance swimming. He also extended his interest to Olympic athletes at moderate altitude (Mexico City) and to heat stress in athletes. Pugh's strength as a physiologist was his readiness to move from laboratory to fieldwork with ease and his rigor in applying the highest standards in both situations. He led by example in both his willingness to act as a subject for experiments and in his attention to detail. He was not an establishment figure; he was critical of authority and well known for his eccentricity, but he inspired great loyalty in those who worked with him.

Anecdotal evidence surrounding Tibetans' and Sherpas' exceptional tolerance to hypobaric hypoxia has been recorded since the beginning of high-altitude exploration. These populations have successfully lived and reproduced at high altitude for hundreds of generations with hypoxia as a constant evolutionary pressure. Consequently, they are likely to have undergone natural selection toward a genotype (and phenotype) tending to offer beneficial adaptation to sustained hypoxia. With the advent of translational human hypoxic research, in which genotype/phenotype studies of healthy individuals at high altitude may be of benefit to hypoxemic critically ill patients in a hospital setting, high-altitude natives may provide a valuable and intriguing model. The aim of this review is to provide a comprehensive summary of the scientific literature encompassing Tibetan and Sherpa physiological adaptations to a high-altitude residence. The review demonstrates the extent to which evolutionary pressure has refined the physiology of this high-altitude population. Furthermore, although many physiological differences between highlanders and lowlanders have been found, it also suggests many more potential avenues of investigation.

The aims of the present study were to determine the changes in forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1) and peak expiratory flow (PEF), during an ascent to 5,300 m in the Nepalese Himalayas, and to correlate the changes with arterial oxygen saturation measured by pulse oximetry (SpO2) and symptoms of acute mountain sickness (AMS). Forty-six subjects were studied twice daily during an ascent from 2,800 m (mean barometric pressure 550.6 mmHg) to 5,300 m (mean barometric pressure 404.3 mmHg) during a period of between 10 and 16 days. Measurements of FVC, FEV1, PEF, SpO2, and AMS were recorded. AMS was assessed using a standardized scoring system. FVC fell with altitude, by a mean of 4% from sea level values [95% confidence intervals (CI) 0.9% to 7.4%] at 2,800 m, and 8.6% (95% CI 5.8 to 11.4%) at 5,300 m. FEV1 did not change with increasing altitude. PEF increased with altitude by a mean of 8.9% (95% CI 2.7 to 15.1%) at 2,800 m, and 16% (95% CI 9 to 23%) at 5,300 m. These changes were not significantly related to SpO2 or AMS scores. These results confirm a progressive fall in FVC and increase in PEF with increasing hypobaric hypoxia while FEV1 remains unchanged. The increase in PEF is less than would be predicted from the change in gas density. The fall in FVC may be due to reduced inspiratory force producing a reduction in total lung capacity; subclinical pulmonary edema; an increase in pulmonary blood volume, or changes in airway closure. The absence of a correlation between the spirometric changes and SpO2 or AMS may simply reflect that these measurements of pulmonary function are not sufficiently sensitive indicators of altitude-related disease. Further studies are required to clarify the effects of hypobaric hypoxia on lung volumes and flows in an attempt to obtain a unifying explanation for these changes.

Acetazolamide is the standard carbonic anhydrase (CA) inhibitor used for acute mountain sickness (AMS), however some of its undesirable effects are related to intracellular penetrance into many tissues, including across the blood–brain barrier. Benzolamide is a much more hydrophilic inhibitor, which nonetheless retains a strong renal action to engender a metabolic acidosis and ventilatory stimulus that improves oxygenation at high altitude and reduces AMS. We tested the effectiveness of benzolamide versus placebo in a first field study of the drug as prophylaxis for AMS during an ascent to the Everest Base Camp (5340 m). In two other studies performed at sea level to test side effect differences between acetazolamide and benzolamide, we assessed physiological actions and psychomotor side effects of two doses of acetazolamide (250 and 1000 mg) in one group of healthy subjects and in another group compared acetazolamide (500 mg), benzolamide (200 mg) and lorazepam (2 mg) as an active comparator for central nervous system (CNS) effects. At high altitude, benzolamide‐treated subjects maintained better arterial oxygenation at all altitudes (3–6% higher at all altitudes above 4200 m) than placebo‐treated subjects and reduced AMS severity by roughly 50%. We found benzolamide had fewer side effects, some of which are symptoms of AMS, than any of the acetazolamide doses in Studies 1 and 2, but equal physiological effects on renal function. The psychomotor side effects of acetazolamide were dose dependent. We conclude that benzolamide is very effective for AMS prophylaxis. With its lesser CNS effects, benzolamide may be superior to acetazolamide, in part, because some of the side effects of acetazolamide may contribute to and be mistaken for AMS.

The 1960-1961 Himalayan Scientific and Mountaineering Expedition, commonly known as the Silver Hut Expedition, was a unique project to study the physiology of acclimatization in human lowlander subjects at extreme altitude over a prolonged period and also to make an attempt on Makalu, an 8470-m peak. The leader was Sir Edmund Hillary, and Dr. Griffith Pugh was the scientific leader. Studies were conducted at a Base Camp in the Everest region of Nepal at 4500 m and at the Silver Hut at 5800 m on the Mingbo Glacier. Simpler physiology was continued on Makalu, in camps at 6300 and 7400 m. The expedition left Kathmandu at the end of the monsoon in 1960 and spent the autumn setting up the Base Camp and the Silver Hut. Some members also spent time making a study of the evidence for the existence of the Yeti. The winter was spent on physiological studies at Base Camp and in the Silver Hut, and the nearby peak of Ama Dablam was climbed. In the spring the expedition moved over to Makalu and made an unsuccessful attempt to climb it without supplementary oxygen. The 9-month expedition ended at the start of the 1961 monsoon. An ambitious program of studies was successfully completed. It was a very happy and, scientifically, a successful expedition. Many of the findings were not repeated for many years, and none has been refuted. On the mountaineering side, we were unsuccessful on Makalu owing to a combination of weather and illness, but the ascent of Ama Dablam was considerable compensation.

To demonstrate that the Snow Snorkel can be used safely by healthy volunteers buried in snow for up to 1 hour.Nine healthy male volunteers were placed in a shoulder-width trench and buried with snow to a depth of 30 to 40 cm. The study was divided into 2 stages. The first stage (Stage 1) was performed with the Snow Snorkel in operation (60-minute duration) and was then followed by a second stage (Stage 2) (15-minute duration) when the device was removed. Arterial oxygen saturation (SaO2), heart rate (HR), respiratory rate (RR), axillary temperature (T), and 3-lead electrocardiography (ECG) were monitored throughout the study.Of the 9 volunteers who were enrolled, 7 were able to complete Stage 1, while only 3 were able to complete Stage 2. In those who completed Stage 1, the mean HR fell by 14.1 beats/min (P = .002), while RR (P = .5) and SaO2 (P = .7) remained unchanged compared to baseline measurements. There were no changes in T or ECG.Simple systems such as the Snow Snorkel are effective during snow burial and warrant further investigation.

Objective and importance The "tight-fit" hypothesis and subsequent current understanding of acute mountain sickness (AMS) is that individuals with less compliant cerebrospinal fluid systems (smaller ventricles and cerebrospinal fluid spaces) have a greater increase in intracranial pressure (ICP) for a given increase in brain volume as a result of hypoxic cerebral edema. There has only been 1 study of direct (telemetric) ICP measurement at high altitude. This was performed in 1985 on 3 subjects by Brian Cummins up to a maximum height of 16,500 ft (5030 m). The group also investigated the "tight-fit" hypothesis by correlating computed tomographic scans that measured ventricular size (read blindly) with headache score and AMS symptomatology in 10 subjects. Unfortunately, the data were thought to have been destroyed by fire, and, hence, the findings were not published. The data have now been rediscovered, and this article reviews the methodology and findings of this unique piece of work. Results The ICP monitoring study demonstrated that ICP remained normal at rest at all altitudes; however, in the single subject with AMS, there was a dramatic increase in ICP even on minimal exertion. The computed tomographic scan analysis of brain compliance demonstrated an inverse correlation between ventricular size and headache score. Conclusion This unique research, which is unlikely to ever be repeated, is the only report of direct ICP measurement at high altitude. This and the computed tomographic study provide the first objective evidence supporting the "tight-fit" hypothesis of AMS.

This study examines the potential for a ventilatory drive, independent of mean Pco2, but depending instead on changes in Pco2 that occur during the respiratory cycle. This responsiveness is referred to here as “dynamic ventilatory sensitivity.” The normal, spontaneous, respiratory oscillations in alveolar Pco2 have been modified with inspiratory pulses approximating alveolar Pco2 concentrations, both at sea level and at high altitude (5,000 m, 16,400 ft.). All tests were conducted with subjects exercising on a cycle ergometer at 60 W. The pulses last about half the inspiratory duration and are timed to arrive in the alveoli during early or late inspiration. Differences in ventilation, which then occur in the face of similar end-tidal Pco2 values, are taken to result from dynamic ventilatory sensitivity. Highly significant ventilatory responses (early pulse response greater than late) occurred in hypoxia and normoxia at sea level and after more than 4 days at 5,000 m. The response at high altitude was eliminated by normalizing Po2 and was reduced or eliminated with acetazolamide. No response was present soon after arrival (2 oscillations provide a feedback signal for respiratory control, independent of changes in mean Pco2, suggesting that natural Pco2 oscillations drive breathing in exercise.

Oxygen delivery (DO2) calculated from cardiac output, haematocrit (Hct) and arterial oxygen saturation (SaO2), has been obtained on six subjects at sea level (London) and after slow ascent to 5000 meters (Chamlang base camp) at rest and during mild exercise (25 watts and 50 watts). Haematocrit was increased in all six subjects at 5000 m and expressed as haemoglobin (Hb) rose from a mean (+/- standard error; SEM) of 13.8 +/- 0.1 g (100 ml)(-1) to 15.8 +/-0.3 g (100 ml)(-1) (t = 6.3, p = 0.0014). SaO2 was almost constant with exercise at sea level (rest 98.5%, 25 w 98.3% and 50 w 98.3%) but declined more steeply with exercise at 5000 m (rest 88.8 +/-0.6%, 25 w 85.4 +/-0.4% and 50 w 84.4 +/- 0.5%). Arterial oxygen content (CaO2) was very similar for 25 watts exercise at altitude (5000 m, 18.1 ml per decilitre--dl) as at sea level (London, CaO2 18.2 ml dl(-1)). At rest CaO2 was higher at altitude (18.8 +/-0.2 ml dl(-1)) than at sea level (18.3 +/- 0.4 ml dl(-1)) and at 50 w CaO2 was lower at altitude (17.9 +/- 0.4 ml dl(-1)) than at sea level (18.2 +/- 0.2 ml dl(-1)). Hence, similar cardiac output values at rest (sea level, 5.0 +/- 0.4 litres min(-1) l min(-1); altitude, 5.6 +/- 0.31 min(-1)-) and at 25 w exercise (sea level, 8.2 +/-0.7 1 min(-1); altitude, 8.3 +/-0 .9 1 min'(-1) resulted in similar values for DO2 at rest (sea level, 0.9 +/-0.1 l min(-1) altitude, 1.0 +/-0.1 l min(-1) and 25 w exercise (sea level, 1.5 +/-0.1 l min(-1) altitude, 1.5 +/- 0.2 l min(-1). For 50 w exercise cardiac output and oxygen delivery were greater at altitude in one subject but were significantly reduced for the remaining five (cardiac output mean difference 3.0 +/- 0.91 min(-1), p = 0.015; DO2 mean difference, 0.56 +/- 0.21 l min(-1) p = 0.028). Acclimatization was therefore adequate to sustain a normal value for oxygen delivery for rest and 25 watts exercise (via compensatory erythropoiesis) but insufficient for 50-watt exercise in five of the six subjects.

Oxygen delivery (DO 2 ) calculated from cardiac output, haematocrit (Hct) and arterial oxygen saturation (SaO 2 ), has been obtained on six subjects at sea level (London) and after slow ascent to 5000 meters (Chamlang base camp) at rest and during mild exercise (25 watts and 50 watts). Haematocrit was increased in all six subjects at 5000 m and expressed as haemoglobin (Hb) rose from a mean (+/- standard error; SEM) of 13.8 +/-0.1 g (100 ml) -1 to 15.8 +/-0.3 g (100 ml) -1 (t = 6.3, p = 0.0014). SaO 2 was almost constant with exercise at sea level (rest 98.5%, 25 w 98.3% and 50 w 98.3%) but declined more steeply with exercise at 5000 m (rest 88.8 +/-0.6%, 25 w 85.4 +/-0.4% and 50 w 84.4 +/-0.5%). Arterial oxygen content (CaO 2 ) was very similar for 25 watts exercise at altitude (5000 m, 18.1 ml per decilitre - dl) as at sea level (London, CaO 2 18.2 ml dl -1 ). At rest CaO 2 was higher at altitude (18.8 +/-0.2 ml dl -1 ) than at sea level (18.3 +/-0.4 ml dl -1 ) and at 50 w CaO 2 was lower at altitude (17.9 +/-0.4 ml dl -1 ) than at sea level (18.2 +/-0.2 ml dl -1 ). Hence, similar cardiac output values at rest (sea level, 5.0 +/-0.4 litres min -1 l min -1 ; altitude, 5.6 +/-0.3 l min -1 ) and at 25 w exercise (sea level, 8.2 +/-0.7 l min -1 ; altitude, 8.3 +/-0.9 l min -1 ) resulted in similar values for DO 2 at rest (sea level, 0.9 +/-0.1 I min -1 ; altitude, 1.0 +/-0.1 I min -1 ) and 25 w exercise (sea level, 1.5 +/-0.1 l min -1 ; altitude, 1.5 +/-0.2 l min -1 ). For 50 w exercise cardiac output and oxygen delivery were greater at altitude in one subject but were significantly reduced for the remaining five (cardiac output mean difference 3.0 +/-0.9 1 l min -1 , p = 0.015; DO 2 mean difference, 0.56 +/-0.2 1 1 min -1 , p = 0.028). Acclimatization was therefore adequate to sustain a normal value for oxygen delivery for rest and 25 watts exercise (via compensatory erythropoiesis) but insufficient for 50―watt exercise in five of the six subjects.

John West is well known to the “Hypoxia” community for his many contributions to the physiology and Pathophysiology of high altitude and for his leadership of the 1981 American Medical Research Expedition to Everest. He is known to the wider medical world for his researches into respiratory physiology especially gas exchange in the lung and perhaps even more for his numerous books on these topics. His publication list numbers over 400 original papers. His research career started in the UK but since 1969 he has been Professor of Medicine at UCSD, leading a very productive team at La Jolla. He has been honoured by numerous prizes and named lectureships, the latest honour being to be elected to the Institute of Medicine, National Academies (USA).

I am honoured to be asked to give this talk to the Hypoxia Symposium. I have been fortunate to have attended all but one of the 15 symposia up to now including the first one in 1979. I feel inadequate to follow the illustrious names of Houston, Rahn, Pugh, Grover, Hultgren, Reeves, Severinghaus and West. I decided I should, like last time’s Honoree, talk about my own experience of research in high altitude medicine and physiology. There will be some overlap with John West’s talk of last time since we have been on two major expeditions together but that is a consequence of choosing us one after the other#

With increasing numbers of people travelling to high altitude destinations for recreation or work, there is a need for practitioners of Travel Medicine to be familiar with altitude illnesses and the physiology of altitude. In mountainous areas travellers may also be exposed to problems of heat and cold. This article reviews these topics and gives practical advice on the management of the clinical problems involved, together with a discussion of underlying mechanisms, as far as they are understood at present.

The aims of the present study were to measure the satiety neuropeptide cholecystokinin (CCK) in humans at terrestrial high altitude to investigate its possible role in the pathophysiology of anorexia, cachexia, and acute mountain sickness (AMS). Nineteen male mountaineers aged 38 +/- 12 years participated in a 20 +/- 5 day trek to Mt. Kanchenjunga basecamp (BC) located at 5,100 m, where they remained for 7 +/- 5 days. Subjects were examined at rest and during a maximal exercise test at sea-level before/after the expedition (SL1/SL2) and during the BC sojourn. There was a mild increase in Lake Louise AMS score from 1.1 +/- 1.2 points at SL1 to 2.3 +/- 2.3 points by the end of the first day at BC (P0.05). A marked increase in resting plasma CCK was observed on the morning of the second day at BC relative to sea-level control values (62.9 +/- 42.2 pmol/L(-1) vs. SL1: 4.3 +/- 8.3 pmol/L(-1), P0.05 vs. SL2: 26.5 +/- 25.2 pmol/L(-1), P0.05). Maximal exercise increased CCK by 78.5 +/- 24.8 pmol/L(-1), (P0.05 vs. resting value) during the SL1 test and increased the plasma concentration of non-esterified fatty acids and glycerol at BC (P0.05 vs. SL1/SL2). The CCK response was not different in five subjects who presented with anorexia on Day 2 compared with those with a normal appetite. While there was no relationship between the increase in CCK and AMS score at BC, a more pronounced increase in resting CCK was observed in subjects with AMS (or =3 points at the end of Day 1 at BC) compared with those without (+98.9 +/- 1.4 pmol/L(-1) vs. +67.6 +/- 37.2 pmol/L(-1), P0.05). Caloric intake remained remarkably low during the stay at BC (8.9 +/- 1.4 MJ.d(-1)) despite a progressive decrease in total body mass (-4.5 +/- 2.1 kg after 31 +/- 13 h at BC, P0.05 vs. SL1/SL2), which appeared to be due to a selective loss of torso adipose tissue. These findings suggest that the satiogenic effects of CCK may have contributed to the observed caloric deficit and subsequent cachexia at high altitude despite adequate availability of palatable foods. The metabolic implications of elevated CCK in AMS remain to be elucidated.

BACKGROUND: Portable peak flow meters are used in clinical practice for measurement of peak expiratory flow (PEF) at many different altitudes throughout the world. Some PEF meters are affected by gas density. This study was undertaken to establish which type of meter is best for use above sea level and to determine changes in spirometric measurements at altitude. METHODS: The variable orifice mini-Wright peak flow meter was compared with the fixed orifice Micro Medical Microplus turbine microspirometer at sea level and at Everest Base Camp (5300 m). Fifty one members of the 1994 British Mount Everest Medical Expedition were studied (age range, 19-55). RESULTS: Mean forced vital capacity (FVC) fell by 5% and PEF rose by 25.5%. However, PEF recorded with the mini-Wright peak flow meter underestimated PEF by 31%, giving readings 6.6% below sea level values. FVC was lowest in the mornings and did not improve significantly with acclimatisation. Lower PEF values were observed on morning readings and were associated with higher acute mountain sickness scores, although the latter may reflect decreased effort in those with acute mountain sickness. There was no change in forced expiratory volume in one second (FEV1) at altitude when measured with the turbine microspirometer. CONCLUSIONS: The cause of the fall in FVC at 5300 m is unknown but may be attributed to changes in lung blood volume, interstitial lung oedema, or early airways closure. Variable orifice peak flow meters grossly underestimate PEF at altitude and fixed orifice devices are therefore preferable where accurate PEF measurements are required above sea level.

Consultant surgeon Stamford and Peterborough Hospitals 1969-93 (b India 1931; q Cambridge/The London Hospital 1957; MA, FRCS), d 22 May 2003.​2003. Figure 1 Terry did house jobs at The London Hospital and then went into the Royal Army Medical Corps for three years. He volunteered for parachute training and on leaving the army continued this interest as medical officer to the 10th Territorial Battalion. On becoming a consultant he realised there was a need for specialisation among general surgeons and took up peripheral vascular surgery. He had a passion for mountaineering, climbing to a good standard into his 70s. He completed the London marathon six times and was training for the 2003 event when struck by an aggressive mesothelioma. He leaves a wife, Elizabeth; two daughters; and a granddaughter.

Ed Paul M O'Byrne, Neil C Thomson Saunders, £29.95, pp 851 ISBN 0 7020 1781 7 To provide “comprehensive yet practical and easily accessed advice on …asthma management” is the aim of the editors of Manual of Asthma Management. With 49 chapters by 69 authors from around the world the book is certainly comprehensive and well referenced. Is the advice practical? Parts of it are very good indeed - for instance, the chapters on bronchodilators and on steroids. Also the final …

the effect of altitude and hypoxia on the renin-angiotensin-aldosterone system is interesting for many reasons. As a physician and mountaineer I have been puzzled for many years by the etiology of acute mountain sickness, especially high-altitude pulmonary edema (HAPE). A derangement of fluid homeostasis produced indirectly by hypoxia appeared to be one characteristic. The time lag of 6–24 h between exposure to hypoxia and the onset of symptoms suggests that hypoxia may stimulate a hormonal response which over this time course could upset fluid homeostasis enough to cause symptoms. For a time we considered the antidiuretic hormone, but, although levels are raised in cases of HAPE (4), this is more likely a result than a cause of the condition. Case reports of HAPE persistently stress the importance of strenuous exertion in the formation of this condition. We therefore decided to first study the effect of exercise typical of mountaineers on fluid balance.

Following the successful use of hyperbaric oxygen in Clostridium welchii infections, occasional cases of tetanus were treated by this method. The first series published was by Pascale et al 1 who reported dramatic improvement in most of their nine patients. Treatment consisted of one to three treatments of two hours' duration. No complications or difficulties were encountered and all except one patient appeared to make a rapid recovery. Other workers had rather less favorable experience. Winkel and Kroon 2 treated seven patients and considered the therapy to be moderately successful. Brummelkamp, 3 with seven patients, could not see any definite effect on their condition except for some relaxation of trismus. We report our experience of treating eight patients with tetanus: three neonates, three children, and two adults. These cases were all of severe tetanus, ie grade 4 or 5 of Patel and Joag's 4 classification, the spasms of which were