Cases reported "Coma"

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1/322. Acute hemorrhagic leukoencephalitis in patients with acute myeloid leukemia in hematologic complete remission.

    The authors describe the cases of three patients affected by acute myeloid leukemia, in complete remission, who rapidly developed neurologic symptoms leading to death. Neither clinical characteristics, nor radiological or microbiological procedures, allowed an etiological diagnosis of the neurologic syndrome. Post-mortem examination of the brain showed both macroscopic and microscopic findings compatible with acute hemorrhagic leukoencephalitis. The difficulty in distinguishing this entity from other CNS disease-related complications (e.g. leukemia infiltration, drug toxicity, hemorrhages) should not lead to an underestimation of the true incidence of this complication. We believe that with more attention to the possibility of this complication there would probably be both a greater possibility of collecting clinical informations about the real impact of this dramatic disease and a stronger hope of finding the right treatment for it.
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2/322. Successful use of alternate waste nitrogen agents and hemodialysis in a patient with hyperammonemic coma after heart-lung transplantation.

    BACKGROUND: Lethal hyperammonemic coma has been reported in 2 adults after lung transplantation. It was associated with a massive elevation of brain glutamine levels, while plasma glutamine levels were normal or only slightly elevated. In liver tissue, glutamine synthetase activity was markedly reduced, and the histologic findings resembled those of reye syndrome. The adequacy of therapy commonly used for inherited disorders of the urea cycle has not been adequately evaluated in patients with this form of secondary hyperammonemia. OBJECTIVE: To determine whether hemodialysis, in conjunction with intravenous sodium phenylacetate, sodium benzoate, and arginine hydrochloride therapy, would be efficacious in a patient with hyperammonemic coma after solid-organ transplantation. DESIGN: Case report. SETTING: A children's hospital. PATIENT: A 41-year-old woman with congenital heart disease developed a hyperammonemic coma with brain edema 19 days after undergoing a combined heart and lung transplantation. methods: Ammonium was measured in plasma. amino acids were quantitated in plasma and cerebrospinal fluid by column chromatography. The effectiveness of therapy was assessed by measuring plasma ammonium levels and intracranial pressure and performing sequential neurological examinations. RESULTS: The patient had the anomalous combination of increased cerebrospinal fluid and decreased plasma glutamine levels. To our knowledge, she is the first patient with this complication after solid-organ transplantation to survive after combined therapy with sodium phenylacetate, sodium benzoate, arginine hydrochloride, and hemodialysis. Complications of the acute coma included focal motor seizures, which were controlled with carbamazepine, and difficulty with short-term memory. CONCLUSIONS: The aggressive use of hemodialysis in conjunction with intravenous sodium phenylacetate, sodium benzoate, and arginine hydrochloride therapy may allow survival in patients after solid-organ transplantation. An acute acquired derangement in extra-central nervous system glutamine metabolism may play a role in the production of hyperammonemia in this illness that resembles reye syndrome, and, as in other hyperammonemic disorders, the duration and degree of elevation of brain glutamine levels may be the important determining factors in responsiveness to therapy.
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3/322. Successful plasmapheresis in the not-so-benign Bickerstaff's brain stem encephalitis associated with anti-GQ1b antibody.

    A patient with Bickerstaff's brain stem encephalitis (BBE) associated with anti-GQ1b antibody developed coma, severe weakness, and respiratory distress. The patient required ventilatory support. After having failed to improve on steroids, she was treated with plasmapheresis. She improved concomitantly with the plasmapheresis treatment and made a complete recovery. BBE associated with anti-GQ1b antibody is generally considered to be benign, and specific treatments have not been established. The results with this patient suggest that the condition is not always benign, and plasmapheresis may be beneficial in this disorder.
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4/322. Right median nerve electrical stimulation to hasten awakening from coma.

    Electrical stimulation of the right median nerve may hasten the awakening of closed head injured, comatose patients. A series of 25 comatose patients have been treated. These patients made better recoveries than similar individuals reported in the literature. In a double-blind pilot project patients in the treated group scored better on interval glasgow coma scale scores, spent fewer days in the intensive care unit, and showed better Glasgow Outcome Scores at 1 month post-injury. Peripheral electrical stimulation of the right median nerve, through activation of the ascending reticular activating system, may be sufficient to arouse the moderate to severely comatose patient.
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5/322. Fatal subarachnoid hemorrhage after endoscopic third ventriculostomy. Case report.

    In recent years, endoscopic third ventriculostomy has become a well-established procedure for the treatment of various forms of noncommunicating hydrocephalus. Endoscopic third ventriculostomy is considered to be an easy and safe procedure. Complications have rarely been reported in the literature. The authors present a case in which the patient suffered a fatal subarachnoid hemorrhage (SAH) after endoscopic third ventriculostomy. This 63-year-old man presented with confusion and drowsiness and was admitted in to the hospital in poor general condition. Computerized tomography scanning revealed an obstructive hydrocephalus caused by a tumor located in the cerebellopontine angle. An endoscopic third ventriculostomy was performed with the aid of a Fogarty balloon catheter. Some hours postoperatively, the patient became comatose. Computerized tomography scanning revealed a severe perimesencephalic-peripontine SAH and progressive hydrocephalus. Despite emergency external ventricular drainage, the patient died a few hours later. Although endoscopic third ventriculostomy is considered to be a simple and safe procedure, one should be aware that severe and sometimes fatal complications may occur. To avoid vascular injury, perforation of the floor of the third ventricle should be performed in the midline, halfway between the infundibular recess and the mammillary bodies, just behind the dorsum sellae.
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6/322. Sudden death and cerebral anoxia in a young woman with congenital ostial stenosis of the left main coronary artery.

    We report a 36-year-old woman with ventricular fibrillation, subsequent sudden clinical cardiac death, and a prolonged brain anoxia. After a successful resuscitation coronary angiography revealed congenital ostial left main coronary artery (LMCA) stenosis. Surgical anastomosis of the left internal mammary artery (LIMA) to LAD led to a complete recovery. Postoperative electrophysiological examination, mainly programmed ventricular stimulation, failed to excite any rhythm disturbances. Cathet. Cardiovasc. Intervent. 48:67-70, 1999.
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7/322. Acute encephalopathy and intractable seizures in a 10-year-old boy.

    We report a 10-year-old child with Robinow's syndrome who had a 2-week history of headaches and dizziness. On the day of admission, he developed a focal onset seizure with rapid secondary generalization. The seizures were intractable despite adequate doses of benzodiazepine, phenytoin, and phenobarbital, requiring a pentobarbital drip. Continuous electroencephalogram (EEG) monitoring showed persistence of the epileptiform discharges for 13 days. cerebrospinal fluid and brain biopsy studies were unrevealing. Mycoplasma pneumonia titers showed elevation of both immunoglobulins G and M that doubled during the tenth hospital day. High-dose methylprednisolone was begun, and within 12 hours of initiation the patient sat up and began to follow commands appropriately. The overall EEG background markedly improved. central nervous system mycoplasma pneumoniae infection should be suspected in patients with an encephalopathy of unclear etiology.
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8/322. Hypoglycemic coma masquerading thyrotoxic storm.

    A 59-year-old woman was hospitalized in hypoglycemic coma. Although hypoglycemia was promptly reversed, she was in a somnolent, restless state with tachycardia, tremor, profuse sweating, and high body temperature. Thyrotoxic storm was highly suspected and vigorous antithyroid regimens gradually brought her up to normal mental and cardiovascular states in several days. However, profound generalized myopathy necessitated the maintenance with a respirator. One month later, an episode of angina pectoris was followed by generalized convulsion, coma, and death in a few days. neuroimaging study disclosed posterior leukoencephalopathy syndrome. This case is instructive in that hypoglycemic coma may masquerade the major symptomatology of thyrotoxic storm, and that profound myopathy and angiopathic or angiospastic processes of the brain and the heart may interfere with the outcome.
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9/322. Normal pressure hydrocephalus in diabetic patients with recurrent episodes of hypoglycemic coma.

    The pathophysiology of brain damage induced by severe hypoglycemia is still unknown. We experienced a case with type 1 diabetes and recurrent severe hypoglycemic coma who showed a central brain atrophy and an abnormal cerebrospinal fluid flow, suggesting normal pressure hydrocephalus. Following this case, the CSF flow was studied using 111In-DTPA cisternography in six consecutive diabetic patients admitted for repeated episodes of hypoglycemic coma. All the patients showed the central brain atrophy on computed tomography and four of them (67%) had the ventricular reflux, with delayed clearance of 111In-DTPA. Two patients with abnormal CSF flow showed cognitive dysfunction by WAIS or WAIS-R. In contrast, none of five randomly selected diabetic patients, without hypoglycemic coma showed abnormal CSF flow. Our results suggest the presence of normal pressure hydrocephalus in diabetic patients with recurrent hypoglycemic coma. It may associate with the cognitive dysfunction.
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10/322. Acute isoniazid neurotoxicity during preventive therapy.

    OBJECTIVE: To describe rare side effects of treatment with isoniazid. DESIGN: Descriptive case report. SETTING: Medical intensive care unit in a university medical center. PATIENT: A 14-yr old previously healthy girl receiving preventive isoniazid therapy who suddenly developed generalized tonic-clonic seizures and coma. INTERVENTIONS: Patient was sedated and mechanically ventilated. She also received pyridoxine intravenously. MEASUREMENTS AND MAIN RESULTS: An isoniazid overdose was not confirmed. Computed tomography of the brain and electroencephalogram revealed nothing abnormal. seizures gradually disappeared within 2 hrs after sedation and treatment with pyridoxine. The patient was discharged on day 14 without consequences and has been well for 10 mos. No seizures reappeared after isoniazid was discontinued. CONCLUSIONS: We caution against possible isoniazid neurotoxicity in healthy individuals using recommended preventive doses.
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