Cases reported "Pulmonary Edema"

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1/89. A case of McLeod syndrome with chronic renal failure.

    A 50-year-old man with the rare McLeod syndrome, associated with glomerular lesion to the end stage of chronic renal failure and death, is reported. McLeod syndrome is an X-linked recessive disorder on the basis of abnormal expression of the Kell blood group antigens and absence of erythrocyte surface Kx antigen. Most often the clinical and pathological findings are retinitis pigmentosa to blindness, progressive chronic neuropathy, cortical atrophy, dilated cardiomyopathy, and glomerular lesion with chronic renal failure. Among the laboratory parameters the most important are very low level of cholesterol and triglycerides, then various numbers of acanthocytes in peripheral blood smears and sometimes in urine (as in our case).
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2/89. Pelvic abscess in the second half of pregnancy after oocyte retrieval for in-vitro fertilization: case report.

    We describe a very late manifestation of pelvic abscesses after oocyte retrieval for in-vitro fertilization (IVF). In a twin pregnancy achieved after intracytoplasmic sperm injection, rupture of bilateral ovarian abscesses occurred at the end of the second trimester. An emergency laparotomy was necessary because of an acute abdomen. This complication led to severe maternal and neonatal morbidity, preterm birth and neonatal death. The rare occurrence of acute abdomen in pregnancy due to pelvic infection and the non-specific symptoms of a pelvic abscess after oocyte retrieval for IVF are discussed.
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3/89. 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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4/89. Fatal acute alcohol intoxication in an ALDH2 heterozygote: a case report.

    On an evening in November, a 25-year-old man was found dead in his bedroom. There were many empty snap-out sheets for flunitrazepam tablets in the trash at his bedside. He had been beaten by a gang of young people earlier in the morning of the same day. At the medico-legal autopsy, although there were many bruises and/or abrasions on the whole body, only slight subdural hemorrhage was observed, and none of them was thought to be the cause of death. flunitrazepam and its metabolites were not detected in his body fluid by gas chromatography-mass spectrometry (GC-MS). Marked lung edema and a severe congestion of organs were observed. His blood alcohol concentration from the femoral vein was 2.00 mg/ml. Fatal cases of acute alcohol intoxication usually have shown higher alcohol concentration (2.25-6.23 mg/ml). Although the genotype of aldehyde dehydrogenase 2 (ALDH2) has not previously been mentioned as a contributing factor in determining the cause of death, in this case the genotype of ALDH2 was ALDH2*1/2 and thus is important. Those who possess the ALDH2*2 gene show high concentrations of acetaldehyde (AcH) at even comparatively lower alcohol levels. Consequently, the cause of death was considered to be acute alcohol intoxication including AcH poisoning.
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5/89. Contralateral reexpansion pulmonary edema.

    Reexpansion pulmonary edema (RPE) is an unusual complication of thoracentesis. Significant morbidity can result, and death is reported in 20% of cases. It is typically manifested as edema within a lung that has recently been reexpanded. Few reports document contralateral edema formation. We present a case of recurrent left-sided pulmonary edema after repeated drainage of a right-sided pleural effusion due to hepatic hydrothorax. We believe this is the first reported case of recurrence and only the fifth overall case of contralateral RPE. We also review the pathophysiology, treatment, and case reports of contralateral RPE. physicians should be aware of the complications of thoracentesis, particularly RPE, given the significant morbidity and mortality associated with it.
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6/89. Respiratory failure after liver transplantation.

    A rapidly growing haemangioendothelial sarcoma of the liver in a twenty-two year old woman was treated by liver transplantation. disseminated intravascular coagulation resulted in massive blood loss during surgery, and contributed to the death of the patient from respiratory failure on the fourth post-operative day, despite continuous post-operative intermittent positive-pressure ventilation. Other factors leading to her respiratory failure are discussed. There was no evidence of dysfunction in the transplanted liver.
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7/89. Re-expansion pulmonary edema following puncture of a giant bulla.

    Ipsilateral pulmonary edema may occur in a lung that has been rapidly reinflated after a period of collapse. The syndrome of re-expansion pulmonary edema is associated with variable degrees of hypotension and hypoxemia. In its extreme form, it may result in cardiac arrest and death. The initial cause of uninflated pulmonary parenchyma described with re-expansion pulmonary edema has typically been either a large undrained pleural effusion or a pneumothorax. The authors describe a patient in whom re-expansion pulmonary edema developed when inadvertent puncture of large emphysematous bullae released previously atelectatic lung.
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8/89. Acute pulmonary edema as a complication of anti-snake venom therapy.

    Polyvalent Anti-snake Venom (ASV) is a life-saving antivenin for severe envenomation due to snake bite in india. ASV infusion is occasionally associated with severe allergic reactions, i.e. anaphylaxis and death. We report a rare instance of non-cardiogenic pulmonary edema due to ASV infusion in an eleven years old boy.
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9/89. pulmonary edema in the neuroradiology suite: a diagnostic dilemma.

    PURPOSE: To present the case of an initially unexplained complication of sudden pulmonary edema in a patient during stenting of the carotid artery in the interventional neurology suite. CLINICAL FEATURES: A 46-yr-old woman (ASA III) having an intracavernous carotid artery angioplasty and stenting procedure under neurolept anesthesia developed sudden pulmonary edema on completion of an otherwise uneventful stenting procedure. The patient responded well to initial management of pulmonary edema although the cause of the edema remained unclear. On retrospective examination of data and with the evolution of clinical signs it became apparent that the patient had suffered a subarachnoid hemorrhage which eventually resulted in her death. CONCLUSIONS: Clinical signs of intracerebral events may be slow to evolve. The cause of sudden pulmonary edema in patients undergoing an interventional neuroendovascular procedure is likely to be neurogenic in origin despite the initial lack of neurological signs.
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10/89. Management of severe decompression sickness with treatment ancillary to recompression: case report.

    Recompression remains the primary form of treatment in decompression sickness, but severe cases require ancillary treatment. The case of a compressed air worker with decompression sickness is presented who, in addition to recompression, required 5.5 of I.V. fluids in the first 8 h, heparin, digitalis, steroids, and respiratory support, to prevent death. The report includes a description of the precipitation causes, the course during recompression, the drugs and dosages used, and comments on respirator treatment.
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