Cases reported "Brain Edema"

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1/79. Bilateral sphenoid wing metastases of prostate cancer presenting with extensive brain edema.

    A 76-year-old man insidiously developed diffuse neurological symptoms: cognitive decline, dysphagia, dysphasia and mental disturbance. Computed tomography of the cranium revealed widespread bilateral brain edema and symmetrical bilateral sphenoid wing hyperostosis. Adjacent to the hyperostosis that resembled skull base meningiomas, two separate parenchymatous temporal lobe lesions enhancing with contrast medium were observed. The patient had earlier been diagnosed to have prostatic carcinoma. dexamethasone therapy resulted in discontinuation of the neurological symptoms. The diagnosis of metastasized adenocarcinoma of the prostate was confirmed histologically on autopsy after a sudden death from pneumonia. Intracranial metastases of prostate cancer may have a predilection site at the sphenoid wing, and can mimic a skull base meningioma. Intracranial spread of prostatic adenocarcinoma should be considered in elderly men as a treatable cause of gradual neurological deterioration, especially if cranial malignancy or hyperostosis is found.
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2/79. Lethal encephalopathy complicating childhood shigellosis.

    A 6-year-old girl is described who died following rapid neurological deterioration, ending in lethal cerebral oedema. Despite the absence of severe intestinal and metabolic derangement, shigella was cultured from the stool. Toxic encephalopathy is responsible for death following this rare complication of childhood shigellosis in developed countries. The pathophysiology is unknown. CONCLUSION: Lethal toxic encephalopathy can be caused by shigella despite the absence of severe intestinal and metabolic derangement. If shigelllosis is suspected, headache may be a first significant sign for the development of toxic encephalopathy. Early recognition and rapid measures to prevent brain oedema may improve outcome.
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3/79. Fatal toxic effect of bleomycin on brain tissue after intracystic chemotherapy for a craniopharyngioma: case report.

    OBJECTIVE AND IMPORTANCE: Craniopharyngiomas are benign neoplasms of epithelial origin that arise from the remnants of Rathke's pouch and are located in the sellar, parasellar, and third ventricular regions. Despite major advances in microsurgical techniques, total removal of these tumors is associated with a high risk of death, long-term endocrinological dependence, cognitive dysfunction, and behavioral disorders. For patients with monocystic craniopharyngiomas, encouraging postoperative survival rates and high rates of cyst regression after intracavitary administration of bleomycin have been reported. Moreover, only a few side effects have been reported for this treatment method. We report a patient with a cystic craniopharyngioma who was treated using intracavitary bleomycin administration and died as a result of the direct toxic effects of bleomycin on deep brain structures and the brainstem. CLINICAL PRESENTATION AND INTERVENTION: A 47-year-old woman with a cystic craniopharyngioma underwent stereotactic insertion of a catheter attached to a subcutaneous reservoir. Five months after the procedure, positive-contrast computed tomographic cystography was performed to confirm the absence of fluid leakage. Daily intracavitary injections of bleomycin were administered through the reservoir into the cyst, until a total dose of 56 mg had been administered in 8 days. After the treatment, the cystic cavity regressed but the patient exhibited neurological deterioration; magnetic resonance imaging scans revealed diffuse edema in the diencephalon and brainstem. The patient died 45 days after completion of the treatment. CONCLUSION: Intracavitary administration of bleomycin is not a treatment protocol without risks or side effects, even if there is no fluid leakage into the cerebrospinal fluid. Although this is known to be an effective treatment for cystic craniopharyngiomas, previous reports cannot be used to establish a standard treatment method, and more research is needed to yield a safer effective protocol.
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4/79. The care of students with insulin-treated diabetes mellitus living in university accommodation: scope for improvement?

    Concern has been expressed about the welfare of young adults with Type 1 diabetes mellitus who leave home to attend university or college for tertiary education. This has been highlighted by the local experience in Edinburgh of two male students with Type 1 diabetes, both of whom died from metabolic complications of diabetes during their first term at universities distant from their homes. One student died following the development of cerebral oedema secondary to diabetic ketoacidosis, which was probably precipitated by prolonged coma after an episode of severe hypoglycaemia. Another student, who was found 'dead in bed', had a history of previous severe hypoglycaemia. At a Fatal Accident Inquiry in Edinburgh, held following the death of the first student, recommendations were made to improve the care and personal safety of students with diabetes living in university accommodation. Despite the report being circulated to all Scottish universities, the second student died within three years of the inquiry. Further efforts to protect the welfare of students with Type 1 diabetes who are attending centres for tertiary education away from their home environment may require the more active participation by diabetes healthcare professionals.
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5/79. Successful treatment of a patient suffering from severe acute potassium dichromate poisoning with liver transplantation.

    BACKGROUND: Oral ingestion of potassium dichromate produces a complex spectrum of complications. It has an extremely poor prognosis and usually leads to rapid death. methods: We report the case of a 16-year-old male patient who was admitted to hospital after oral ingestion of potassium dichromate with suicidal intention. RESULTS: The patient's condition deteriorated, and he became comatose within 5 days in spite of immediate attempts at detoxification. Because of irreversible liver failure, which occurred within 2 days after admission, and because of cerebral edema, the decision to perform a liver transplantation was made. On day 6 after admission, a compatible donor liver was transplanted. The course of liver transplantation and the patient's subsequent recovery were uneventful. CONCLUSION: The rationale for the delayed transplantation was to avoid damage of the new organ because of high serum chromium levels. Despite severe organ damage, the chromium content of the liver was increased. To the authors' knowledge, this is the first case report of acute toxic liver failure, caused by potassium dichromate poisoning, treated successfully by means of liver transplantation.
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6/79. Massive cerebral edema after I.V. cyclosporin overdose.

    We describe a patient who accidentally received an infusion of cyclosporin at a rate of 30 mg/hr during 13 hr instead of the prescribed dose of 3 mg/hr and who concomitantly developed massive intracerebral edema with brainstem compression and death. A cyclosporin level as high as 1700 ng/ml could have been reached before the drug was withdrawn. To the best of our knowledge, this is the first case of fatal cyclosporin overdose reported in an adult patient.
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7/79. Cerebral atrophy and convulsive seizures after recovery from cerebral edema and coma in a patient with fulminant hepatitis b.

    We report a 48-year-old woman who developed convulsive seizures and cerebral atrophy after recovery from fulminant hepatitis b with coma and cerebral edema at the acute stage. Neurological disturbances and cerebral signs are rare sequelae of fulminant hepatic failure (FHF); only a few cases have reported in the literature. Cortical laminar necrosis secondary to cerebral edema or delayed neuronal death due to toxic substances may have caused delayed brain atrophy and epileptogenesis.
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8/79. Fatal progression of posttraumatic dural arteriovenous fistulas refractory to multimodal therapy. Case report.

    The authors report the case of a man who suffered from progressive, disseminated posttraumatic dural arteriovenous fistulas (DAVFs) resulting in death, despite aggressive endovascular, surgical, and radiosurgical treatment. This 31-year-old man was struck on the head while playing basketball. Two weeks later a soft, pulsatile mass developed at his vertex, and the man began to experience pulsatile tinnitus and progressive headaches. magnetic resonance imaging and subsequent angiography revealed multiple AVFs in the scalp, calvaria, and dura, with drainage into the superior sagittal sinus. The patient was treated initially with transarterial embolization in five stages, followed by vertex craniotomy and surgical resection of the AVFs. However, multiple additional DAVFs developed over the bilateral convexities, the falx, and the tentorium. Subsequent treatment entailed 15 stages of transarterial embolization; seven stages of transvenous embolization, including complete occlusion of the sagittal sinus and partial occlusion of the straight sinus; three stages of stereotactic radiosurgery; and a second craniotomy with aggressive disconnection of the DAVFs. Unfortunately, the fistulas continued to progress, resulting in diffuse venous hypertension, multiple intracerebral hemorrhages in both hemispheres, and, ultimately, death nearly 5 years after the initial trauma. Endovascular, surgical, and radiosurgical treatments are successful in curing most patients with DAVFs. The failure of multimodal therapy and the fulminant progression and disseminated nature of this patient's disease are unique.
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9/79. Severe hypernatremic dehydration and death in a breast-fed infant.

    breast milk is acknowledged as the best source of nutrition for neonates. We present the case of a full-term newborn who was fed solely breast milk and developed severe dehydration and hypernatremia. The patient developed cerebral edema, transverse sinus thrombosis, and died. The literature on the uncommon entity of breast-feeding hypernatremia and dehydration is reviewed, and management strategies are presented.
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10/79. Sudden death from fulminant acute cerebellitis.

    Acute cerebellitis is postulated to result from viral and/or autoimmune etiologies. This disease has been reported to have a variable course. We report a case of sudden death from acute fulminant cerebellitis in a 13-year-old ballet dancer. Serial CT and MRI demonstrated rapid progression of the disease. Histopathologic correlation is provided. The etiologies, clinical course, therapeutic interventions and postmortem evaluation of this potentially life-threatening condition are briefly reviewed.
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ranking = 5
keywords = death
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