Cases reported "Pulmonary Edema"

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1/41. 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.
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2/41. 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.
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3/41. High-altitude illness induced by tooth root infection.

    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.
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4/41. 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.
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5/41. 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.
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6/41. myocardial infarction or high-altitude pulmonary edema?

    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.
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7/41. 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.
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8/41. Unilateral high-altitude pulmonary edema (HAPE): a case report and discussion of pathophysiology.

    High-altitude pulmonary edema (HAPE), a potentially life-threatening altitude adaptation disorder, is considered to be caused by an exaggerated increase in pulmonary blood pressure and a non-cardiogenic rise in pulmonary vascular permeability subsequent to alveolar hypoxia. A 40-year-old male mountaineer was affected by an advanced stage of HAPE at high altitude (Monte rosa plateau, 4000 m). The symptoms abated immediately after the patient descended from the altitude. However, six hours after the symptoms had resolved, radiographic signs of pulmonary edema, confined to the right lung, were seen. This rarely described unilateral radiological pattern of HAPE resolved completely within two days. We suggest that aspiration events of nasal secretion, the right sleeping position at night and an elevated right diaphragm reduced the patient's compensatory hyperventilation capacity of the right lung. The resulting increased alveolar hypoxia in the right lung was responsible for unilateral edema. The pathophysiological mechanism underlying unilateral HAPE is discussed.
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9/41. Recurrent high altitude pulmonary edema with blunted chemosensitivity.

    A young man who had had two episodes of high-altitude pulmonary edema in the absence of any respiratroy distress was noted to have a depression of his hypoxic and hypercapnic ventilatory drives. It is postulated that because of his blunted ventilaory drives, the patient progessed to coma on exposure to low ambient oxygen tensions (i.e., high altitude) without ever increasing his ventilation. The importance of including highaltitude pulmonary edema in the differential diagnosis of any patient who is admitted with coma after a sojourn at high altitude is stressed.
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10/41. pulmonary edema in 6 children with down syndrome during travel to moderate altitudes.

    OBJECTIVE: Children with down syndrome (DS) are living longer and are increasingly participating in recreational activities. When a child with DS was diagnosed with high-altitude pulmonary edema (HAPE), this study was undertaken to determine whether and under what circumstances children with DS develop HAPE. DESIGN: A retrospective review of the medical records of Children's Hospital, Denver, colorado was performed for children with a discharge diagnosis of HAPE. Diagnostic criteria for HAPE included the presence of crackles or frothy sputum production on examination, hypoxemia, chest radiograph findings consistent with pulmonary edema, and rapid clinical improvement after descent or oxygen therapy. RESULTS: A total of 52 patients with HAPE were found of whom 6 also had DS. The age range of the children with DS was 2 to 14 years. HAPE developed at altitudes ranging from 1738 to 3252 m. Four children developed HAPE within 24 hours of arrival to altitude. Three children had chronic pulmonary hypertension, and 4 had either an existing cardiac defect with left-to-right shunt or previously had a defect with left-to-right shunt that had been repaired. One child had Eisenmenger syndrome with chronic right-to-left shunting of blood. Five children had preexisting illnesses before travel to altitude. CONCLUSION: Children with DS often have medical problems such as chronic pulmonary hypertension, frequent infections, and pulmonary vascular overperfusion and injury from existing or previous cardiac defects. These problems all may be viewed as risk factors for HAPE and thus result in the rapid development of HAPE at low altitudes. Care should be taken when traveling to even moderate altitudes with children with DS.
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