Cases reported "Altitude Sickness"

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1/9. Superior sagittal sinus thrombosis occurring at high altitude associated with protein c deficiency.

    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.
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ranking = 1
keywords = thrombosis, venous thrombosis
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2/9. pulmonary embolism presenting as high-altitude pulmonary edema.

    High-altitude pulmonary edema (HAPE) is a recognized risk of rapid ascent to high altitude. Since the recognition of this entity more than 30 years ago, most pulmonary deaths at high altitude have been attributed to HAPE. However, as the bodies can almost never be recovered for postmortem examination, rare diagnoses that appear clinically similar to HAPE will not be recognized. A 33-year-old woman climbing on Mt. Everest, and taking oral contraceptive pills, developed what seemed to be severe HAPE. Examination after she was evacuated from the mountain revealed a deep venous thrombosis in her left leg and multiple pulmonary emboli. We propose that multiple pulmonary emboli at high altitude can mimic HAPE, and fatal pulmonary embolism may be an explanation for some alleged victims of HAPE who died despite what should have been adequate descent.
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ranking = 0.20492118766398
keywords = thrombosis, venous thrombosis, deep
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3/9. An unusual swelling in the neck.

    venous thrombosis is a fundamental pathological entity. Our patient provides an opportunity to consider etiology in terms of Virchow's classic triad. We also draw attention to the effort syndrome, in which recurrent, vigorous exertion of an upper extremity is thought to produce venous thrombosis by virtue of local endothelial trauma.
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ranking = 0.31826721547557
keywords = thrombosis, venous thrombosis
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4/9. Pulmonary blood vessels and endocrine cells in subacute infantile mountain sickness.

    A male infant of 16 months, of the Han race, died from subacute infantile mountain sickness in Lhasa (3600 m). At necropsy there was right ventricular hypertrophy secondary to muscularization of the pulmonary arteries and arterioles thought to have been induced by hypobaric hypoxia. In addition, there was intimal proliferation of myofibroblasts in the pulmonary arterioles, venules and veins. There were increased numbers within the bronchioles of pulmonary endocrine cells, containing calcitonin and bombesin, which could be related to hypoxia or trophic effects on the pulmonary vasculature. The relation of delayed effects of hypoxia to primary pulmonary hypertension is considered in this study.
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ranking = 0.0001574804641409
keywords = vein
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5/9. A case of high altitude pulmonary edema followed by brain computerized tomography and electroencephalogram.

    A case of high altitude pulmonary edema with high altitude cerebral edema was reported. A young Japanese male complained of severe palpitation and shortness of breath on the third day of climbing at 3,000 m above sea level. During the next 2 d at altitude, the following symptoms occurred: cough with foamy sputum, cyanosis, and loss of consciousness. Soon after evacuation, he showed severe hypoxemia and deep coma with decerebrate rigidity; electroencephalogram showed diffuse alpha waves, indicating "alpha wave coma." Brain computerized tomography revealed brain edema, showing small compressed ventricles and diffuse low density of the cerebrum. pulmonary edema on chest roentgenogram disappeared by the fifth hospital day, and his consciousness recovered gradually during the next 2 weeks after the admission. He was examined serially by electroencephalography and brain computerized tomography. He recovered fully, but there were transient psychological abnormalities soon after discharge and mild brain atrophy was observed by brain computerized tomography 6 years later.
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ranking = 0.00027610294247883
keywords = deep
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6/9. Cerebral venous thrombosis due to high-altitude polycythemia. Case report.

    A case of cerebral venous thrombosis due to polycythemia secondary to adaptation to a high altitude is reported. A 27-year-old previously healthy man developed severe neurological symptoms after climbing 8511 m. Computerized tomography and cerebral angiography suggested hemorrhagic infarction or intratumoral hemorrhage, and a craniotomy was performed. Pathological examination confirmed the diagnosis of hemorrhagic infarction secondary to cortical venous thrombosis. The etiology and incidence of cerebral venous thrombosis secondary to polycythemia are discussed.
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ranking = 1.4325155930505
keywords = thrombosis, venous thrombosis
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7/9. Cerebral thrombosis at altitude: its pathogenesis and the problems of prevention and treatment.

    In analyzing cerebral thrombosis at altitude--own case and in the literature--we anatomically confirmed that cerebral thrombi in mountain sickness were all of venous origin. All climbers went higher than 5,000 m and most stayed in that altitude longer than 3 weeks. Hemoconcentration was confirmed in two cases, including our own patient. It was suspected that hemoconcentration resulting from secondary polycythemia and dehydration at altitude, as well as cerebral circulatory disturbance produced by high-altitude cerebral edema, played a major role in the development of cerebral thrombosis. The problems of prevention and treatment of cerebral thrombosis at altitude are discussed.
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ranking = 0.7953549152785
keywords = thrombosis
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8/9. altitude-related deaths in seven trekkers in the Himalayas.

    The clinical features and necropsy findings are described for seven trekkers in the Himalayas whose deaths were related to high altitude. The fatal outcome was due to serious pulmonary and cerebral disease. Oedema of the lungs and brain was prominent but so was thrombosis and haemorrhage, features of acute mountain sickness that have received insufficient recognition in the past. Most of the men were middle aged. Some began their trekking soon after flying to high altitude before becoming acclimatised and some remained at high altitude or climbed even higher despite the development of vomiting, breathlessness, and exhaustion. In one case death occurred despite prompt recognition and treatment of symptoms by administration of oxygen and swift evacuation to low altitude.
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ranking = 0.11362213075407
keywords = thrombosis
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9/9. High altitude retinal hemorrhage: a clinical and pathological case report.

    Retinal hemorrhages may occur at high altitudes. They occur more commonly in association with acute mountain sickness and particularly with high-altitude cerebral edema. We describe a 27-year-old man who experienced retinal hemorrhages as well as papilledema and coma at 5,330-m altitude and who died four days later, one day after evacuation to 1,300-m altitude. At autopsy, we found papilledema and hemorrhages in the nerve fiber layer. These were sometimes distant from areas where there were arterioles and venules. There was perivascular red cell infiltration. Deeper layers of the retina were intact. We conclude that the hemorrhages were form both retinal capillaries and veins and we speculate that hypoxia, with or without the Valsalva effect, was the cause of the endothelial damage.
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ranking = 0.0001574804641409
keywords = vein
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