| A 42-year-old male presented with right-sided weakness, dysphasia and seizures while climbing the French Alps at an approximate altitude of 3,000 m. Imaging studies were consistent with superior sagittal sinus thrombosis with hemorrhage. Laboratory testing for thrombophilic states, 18 days after presentation at our hospital, showed a low protein C level (0.32 U/ml, normal 0.80-1.60 U/ml). A family member was also found to have protein c deficiency without a history of thrombosis. The patient gradually improved and was discharged on warfarin and valproic acid. This is the first reported case of cerebral venous thrombosis in a patient with congenital protein c deficiency who ascended to high altitude. We postulate that the ascent to high altitude represented an additional prothrombotic risk factor to the congenital protein c deficiency leading to cerebral thrombosis. ( info) |
2/84. Serial scintigraphic assessment of iodine-123 metaiodobenzylguanidine lung uptake in a patient with high-altitude pulmonary edema. iodine-123 metaiodobenzylguanidine ((123)I-MIBG) can be considered an indicator of pulmonary endothelial cell function. Serial (123)I-MIBG images of the chest were acquired in a patient with high altitude pulmonary edema (HAPE). The initial evaluation was performed 7 days after admission. The lung to upper mediastinum ratios (LMRs) of (123)I-MIBG uptake were 1.33 (for the right lung) and 1.12 (for the left lung). The second examination of (123)I-MIBG lung uptake, which was performed 2 months later, showed LMRs of 1.39 (right lung) and 1.33 (left lung). We speculated that the decreased lung uptake of (123)I-MIBG at the early recovery stage could reflect an impairment in pulmonary endothelial cell metabolic function in the development of HAPE. ( info) |
3/84. Alveolar haemorrhage in a case of high altitude pulmonary oedema. A case of high altitude pulmonary oedema (HAPE) in a climber who made a rapid ascent on Mt McKinley (Denali), alaska is described. The bronchoalveolar lavage (BAL) fluid contained increased numbers of red blood cells and an abundance of haemosiderin laden macrophages consistent with alveolar haemorrhage. The timing of this finding indicates that alveolar haemorrhage began early during the ascent, well before the onset of symptoms. Although evidence of alveolar haemorrhage has been reported at necropsy in individuals dying of HAPE, previous reports have not shown the same abundance of haemosiderin laden macrophages in the BAL fluid. These findings suggest that alveolar haemorrhage is an early event in HAPE. ( info) |
| High-altitude illness may occur after recent pulmonary infection, but high-altitude illness after root canal therapy has not been described previously. A 44-year-old man is presented who skied to a 3333 m high peak in the Eastern Alps one day after he had undergone root canal therapy because of a tooth root infection. After 4 hours above 3000 m severe symptoms of high-altitude illness, including pulmonary oedema, developed. His condition improved after immediate descent. The next day he presented with local and general signs of infection which were successfully treated with gingival incisions and antibiotics. In conclusion, acute tooth root infection and root canal therapy may induce high-altitude illness at an altitude just above 3000 m. ( info) |
5/84. Experimental use of a transportable hyperbaric chamber durable for 15 psi at 3700 meters above sea level. A transportable hyperbaric chamber durable for 15 psi of pressure was used to treat a patient suffering from moderate acute mountain sickness at 3700 m above sea level. The symptoms were ameliorated a few minutes after pressurization in the chamber. After a 20-minute stay in the chamber, the patient was completely free of symptoms. Since the chamber can be inflated by using compressed air from a cylinder, no strenuous work was required of the operators. This transportable chamber seems to be useful for the treatment of high-altitude disorders at around 3000 m above sea level. ( info) |
| A variety of transient focal neurological signs presenting at high altitude have been described without associated acute mountain sickness or other concurrent illness. We report a case series of transient global amnesia at high altitude. The term high-altitude global amnesia (HAGA) is introduced to indicate this condition, and the pathophysiology is discussed. We hypothesize that because of the highly variable ventilatory response to hypoxia and to individual cerebral vasomotor reactivity, individuals with a marked hyperventilatory response could experience significant hypocapnic cerebral vasoconstriction that in turn could cause local hypoxia or ischemia to particular regions of the brain and resulting transient focal neurological impairment. ( info) |
7/84. A tragic report of probable high-altitude pulmonary edema in the Himalayas: preventive implications. 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. ( info) |
8/84. High-altitude cerebral edema (HACE): the Denver/Front Range experience. High-altitude cerebral edema (HACE) is a potentially fatal metabolic encephalopathy associated with a time-dependent exposure to the hypobaric hypoxia of altitude. Symptoms commonly are headache, ataxia, and confusion progressing to stupor and coma. HACE is often preceded by symptoms of acute mountain sickness and coupled, in its severe form, with high-altitude pulmonary edema. Although HACE is mostly seen at altitudes above that of the Denver/Front Range visitor-skier locations, we report our observations over a 13-year period of skier-visitor HACE patients. It is believed that this is a form of vasogenic edema, and it is responsive to expeditious treatment with a successful outcome. ( info) |
| 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. ( info) |
10/84. Reascent following resolution of high altitude pulmonary edema (HAPE). There is an absence of information in the literature regarding reascent to high altitude following resolution of HAPE (high altitude pulmonary edema). This report presents three cases of HAPE that are notable for later reascent to a high summit (up to 8,850 m) within the time course of each expedition. These cases illustrate that careful, gradual reascent following recovery and acclimatization after an episode of HAPE precipitated by rapid ascent may be considered. The pathophysiology of HAPE is reviewed with a focus on the evidence for rapid reversibility of pulmonary vascular injury. The evidence for protective pulmonary vascular remodeling is discussed to further support such a recommendation for cases of uncomplicated HAPE. ( info) |