Biomedical subjects
Publications and source records attributed to B Basnyat.
High-altitude pulmonary edema (HAPE) is a well-recognized disease entity in trekkers to the Nepal Himalayas. We present the case of a patient who had clinical features consistent with HAPE but did not descend the mountain on time, which contributed to his death. The important factors of the diagnosis, the descent, and the follow-up in Kathmandu are examined.
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We report the case of a 60-year-old European man with myocardial infarction at high altitude (4000 m). Myocardial infarction is an uncommonly encountered problem in high-altitude trekking in the Himalayas. The paucity of coronary artery disease at high altitude (hypoxia, exercise, and age not-withstanding) is discussed. Finally, the importance of recognizing disease entities that mimic acute mountain sickness in this environment is emphasized.
At a travel clinic in Kathmandu we reviewed the vaccination records from March 1997 to March 1998 for all travelers to developing countries like Nepal, for two important vaccines, namely, typhoid and hepatitis A. These travelers visited the clinic for various medical problems. One of the reasons for doing this study was that in previous years we saw a disproportionate number of Japanese travelers with hepatitis A, who had not taken the hepatitis A vaccine or immune gamma globulin for prevention of this illness. We hypothesized, therefore, that one of the reasons that Japanese patients visiting our clinic had higher rates of hepatitis A was because they were not vaccinated against this disease. There were 765 tourists for that time period out of which about 10% were Japanese. The rest were Americans, British, Israelis, Canadians, Australians, Danish and a small miscellaneous group from other countries.
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BACKGROUND: Acute mountain sickness (AMS), High altitude pulmonary edema (HAPE) and High Altitude Cerebral Edema (HACE) are well known problems in the high altitude region of the Nepal Himalayas. To assess the proportion of AMS, HAPE, and HACE from 1983 to 1995 in the Himalaya Rescue Association (HRA) aid posts' patients at the Everest (Pheriche 4,243 m) and Annapurna (Manang 3,499 m) regions, the two most popular trekking areas in the Himalayas. A retrospective study was conducted at the HRA medical aid posts in Manang (3,499 m) and Pheriche (4,243 m) in the Himalayas, where 4,655 trekkers (tourists, mostly Caucasians) and 4,792 Nepalis (mostly porters and villagers) were seen at the two high-altitude clinics from 1983 to 1995, for a variety of medical problems, including AMS. METHODS: The number of trekking permits issued for entering the two most popular regions in the Himalayas was calculated and referenced to the proportion of trekkers with medical conditions. Well established guidelines like the Lake Louise Diagnostic Criteria were used in the assessment of AMS, HAPE and HACE. Linear regression analyses were performed on data collected from the two aid posts to determine the effect of time on each variable. For comparison between the aid posts, angular transformation (arcsine) and analysis of variance (ANOVA) were performed on all proportional (incidence) data. RESULTS: Approximately 20% of all visitors (Nepali plus trekkers) who visited the higher Pheriche aid post were diagnosed with AMS compared to around 6% at the lower Manang aid post. There was a linear increase over time in the number of trekkers entering the Everest (r=0.904, p<.001) and the Annapurna (r=0.887, p<.001) regions. The proportion of trekker patients with any medical condition visiting the two HRA aid posts at Manang and Pheriche, expressed as a function of the total number of trekkers entering the Everest and Annapurna regions, was not significantly different between Pheriche (average 4%) and Manang (average 1%). However, the proportion of AMS, HAPE and HACE in patients (Nepali plus trekkers) to the aid posts was greater in those visiting the higher Pheriche aid post compared to the lower Manang aid post (f=56.74, n=13; p<. 001). Importantly, only the proportion of AMS (r=0.568; p<.05) and not HAPE or HACE increased over time in Pheriche, alongside an unchanged proportion of trekker patients, amongst all Pheriche aid post patients. There was no increase of AMS, HAPE or HACE in Manang. CONCLUSIONS: HAPE and HACE are the life-threatening forms of AMS and although there is a linear increase of trekkers entering the Himalayas in Nepal, the findings revealed that HAPE and HACE have not increased over time. One possible explanation may be that awareness drives by organizations like the Himalayan Rescue Association may be effective in preventing the severe forms of AMS.
The purpose of this study was twofold: 1) to determine whether at high altitude cerebral blood flow (CBF) as assessed during CO2 inhalation and during hyperventilation in subjects with acute mountain sickness (AMS) was different from that in subjects without AMS and 2) to compare the CBF as assessed under similar conditions in Sherpas at high altitude and in subjects at sea level. Resting control values of blood flow velocity in the middle cerebral artery (VMCA), pulse oxygen saturation (SaO2), and transcutaneous PCO2 were measured at 4,243 m in 43 subjects without AMS, 17 subjects with AMS, 20 Sherpas, and 13 subjects at sea level. Responses of CO2 inhalation and hyperventilation on VMCA, SaO2, and transcutaneous PCO2 were measured, and the cerebral vasomotor reactivity (VMR = DeltaVMCA/PCO2) was calculated as the fractional change of VMCA per Torr change of PCO2, yielding a hypercapnic VMR and a hypocapnic VMR. AMS subjects showed a significantly higher resting control VMCA than did no-AMS subjects (74 +/- 22 and 56 +/- 14 cm/s, respectively; P < 0.001), and SaO2 was significantly lower (80 +/- 8 and 88 +/- 3%, respectively; P < 0.001). Resting control VMCA values in the sea-level group (60 +/- 15 cm/s), in the no-AMS group, and in Sherpas (59 +/- 13 cm/s) were not different. Hypercapnic VMR values in AMS subjects were 4.0 +/- 4.4, in no-AMS subjects were 5.5 +/- 4. 3, in Sherpas were 5.6 +/- 4.1, and in sea-level subjects were 5.6 +/- 2.5 (not significant). Hypocapnic VMR values were significantly higher in AMS subjects (5.9 +/- 1.5) compared with no-AMS subjects (4.8 +/- 1.4; P < 0.005) but were not significantly different between Sherpas (3.8 +/- 1.1) and the sea-level group (2.8 +/- 0.7). We conclude that AMS subjects have greater cerebral hemodynamic responses to hyperventilation, higher VMCA resting control values, and lower SaO2 compared with no-AMS subjects. Sherpas showed a cerebral hemodynamic pattern similar to that of normal subjects at sea level.
BACKGROUND: Thousand of tourists trek in the Himalayas every season and risk acute mountain sickness (AMS). Prior studies have shown that the rate of ascent is one of the primary risk factors for the development of AMS but the role of body hydration, age, gender, alcohol and medication usage, body weight, and altitude of residence continues to be in question. This study estimates the incidence of AMS at 4234 m at Pheriche in the Everest region, explores a number of risk factors predisposing trekkers to a diagnosis of AMS and attempts to quantify the relationship between the Lake Louise AMS diagnostic criteria and oxygen saturation. METHODS: Demographic data and information about risk factors felt to place trekkers at increased risk of AMS was collected from 550 trekkers for 1 mo in the fall of 1996 at 4234 m in the Everest region. RESULTS: Diagnosis of AMS was made in 29.8% (159 trekkers) of the study population. Low water intake (odds ratio 1.57; 95% confidence interval,1.02-2.40), the presence of respiratory symptoms (odds ratio 2.21; 95% confidence interval, 1.43-3.40), and an oxygen saturation below 85% at 4243 m (odds ratio 2.35; 95% confidence interval, 1.55-3.56) were identified as independent risk factors for AMS diagnosis in this sample. In addition, AMS risk decreased 18.7% (95% confidence interval, 3.8-31.2%) for each additional night spent between Lukla (2804 m) and the study site at 4243 m. CONCLUSION: Increased reported fluid intake decreased the risk of AMS in this cross sectional prospective study. Further studies need to be done to confirm this finding before recommendations can be made. In addition the rise in the risk of AMS as the rate of ascent increased along this popular Everest trek was quantified for the first time. Finally, AMS was also associated with respiratory symptoms and with a lower oxygen saturation.
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A 35-year-old healthy Dutch woman went on a trek (Lang Tang) in Nepal up to an approximate altitude of about 3800 meters. She had no prior history of any medical problems except attacks of generalized epilepsy when she was 19 years old, which had been controlled with antiepileptic medications. She had had no attacks after the age of 20. A CT scan done around that time had apparently been normal. On this trek she had developed diarrhea which had been cured with norfloxacin 400 mg two times per day for 3 days. Two days later, while descending, she developed a grand mal seizure at an altitude of 3300 meters, after which she developed a classic postictal phase but gradually recovered. She developed grand mal seizures again the next day, but when she went to a travel clinic in Kathmandu, she had been seizure free for 72 hours. She also revealed that she had not suffered from acute mountain sickness on the trek. She also had a prior history of gastroenteritis at high altitude which improved significantly with norfloxacin, a quinolone antibiotic. This was corroborated by her party. Upon examination she was fully conscious and oriented to person, place and time. Her pulse was 70 beats per minute and her BP was 110/80 mm of Hg. Her fundi and cranial nerves exam were completely normal. Her abstract thinking, gait, power, tone, reflexes and other facets of her neurologic exam revealed absolutely no abnormalities. Her cardiovascular exam revealed a normal rhythm with no murmurs or bruits. The rest of her exam was also normal. She revealed that she played tennis on a regular basis and was an outdoor person. She had not trekked before in the Himalayas and it was uncertain if she had been to high altitude before. She was on no medications at the time. There was no history of drug abuse. She did not smoke and consumed few alcoholic beverages. She had not consumed any alcohol on the trek. She was advised to get a CT scan (she declined as she was going home to Holland in 2 days) and she was prescribed a loading dose of phenytoin 1 g orally spread over several hours and it was recommended she take 300 mg of phenytoin per day. She was going to see her neurologist in Holland on arrival there. She went to her hotel in Kathmandu while her friends went to fill the prescription of phenytoin. When her friends returned to the hotel she was having another grand mal seizure. Medical help was sought, but she died before the doctor arrived to control her seizures. When the doctor did arrive and carried out CPR for half an hour it was to no avail as she continued to have no pulse or blood pressure.
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The mountain climate can modify respiratory function and bronchial responsiveness of asthmatic subjects. Hypoxia, hyperventilation of cold and dry air and physical exertion may worsen asthma or enhance bronchial hyperresponsiveness while a reduction in pollen and pollution may play an important role in reducing bronchial inflammation. At moderate altitude (1,500-2,500 m), the main effect is the absence of allergen and pollutants. We studied bronchial hyperresponsiveness to both hyposmolar aerosol and methacholine at sea level (SL) and at high altitude (HA; 5,050 m) in 11 adult subjects (23-48 years old, 8 atopic, 3 nonatopic) affected by mild asthma. Basal FEV1 at SL and HA were not different (p = 0.09), whereas the decrease in FEV1 induced by the challenge was significantly higher at SL than at HA. (1) Hyposmolar aerosol: at SL the mean FEV1 decreased by 28% from 4.32 to 3.11 liters; at 5,050 m by 7.2% from 4.41 to 4.1 liters (p < 0.001). (2) Methacholine challenge: at SL PD20-FEV1 was 700 micrograms and at HA > 1,600 micrograms (p < 0.005). In 3 asthmatic and 5 nonasthmatic subjects plasma levels of cortisol were also measured. The mean value at SL was 265 nmol and 601 nmol at HA (p < 0.005). We suppose that the reduction in bronchial response might be mainly related to the protective role carried out by the higher levels of cortisol and, as already known, catecholamines.