Cases reported "Coma"

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1/64. 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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2/64. 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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3/64. Extensive subdural empyema treated with drainage and barbiturate therapy under intracranial pressure monitoring: case report.

    In subdural empyema (SDE), if the mass effect and vasogenic edema are not controlled, the brain can be fatally damaged. Massive SDE over the skull base often requires repeated surgical drainage for removal of accumulated pus. intracranial pressure (ICP) management until obliteration of the empyema is important to the improvement of clinical outcome. An 18-year-old man was admitted to our center in a nearly comatose state and with a mild fever. CT scan showed massive SDE extending to the skull base and parafalx. ICP was measured with a pressure transducer through an intraventricle tube. Repeated surgical drainage was performed while ICP was controlled with barbiturate therapy. He was discharged with no neurological deficits. In patients with an extensive SDE over the cerebral hemisphere, ICP control with barbiturate therapy may enhance the therapeutic effect of surgical drainage.
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4/64. Isolated medulla oblongata function after severe traumatic brain injury.

    The objective was to report the first pathologically confirmed case of partly functionally preserved medulla oblongata in a patient with catastrophic traumatic brain injury.A patient is described with epidural haematoma with normal breathing and blood pressure and a retained coughing reflex brought on only by catheter suctioning of the carina. Multiple contusions in the thalami and pons were found but the medulla oblongata was spared at necropsy. In conclusion, medulla oblongata function may persist despite rostrocaudal deterioration. This comatose state ("medulla man") closely mimics brain death.
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5/64. Ventriculopleural shunt obstruction and positive-pressure ventilation. Case report.

    The authors report an unusual case of a patient with low-pressure hydrocephalus and a ventriculopleural shunt, in whom routine respiratory management performed using positive-pressure ventilation caused shunt obstruction and coma. While the patient received positive-pressure ventilation with external cerebrospinal fluid (CSF) drainage at subatmospheric pressure, the ventricles returned to normal size and the coma rapidly reversed. After the authors' recognition of the effect of positive-pressure ventilation on intrapleural pressure and ventriculopleural shunt function, and the subsequent removal of positive-pressure ventilation, CSF flow through the shunt resumed and the patient's coma resolved.
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6/64. Reversible coma with raised intracranial pressure: an unusual clinical manifestation of cadasil.

    A 50-year-old woman presented with recurrent episodes of headache, nausea and disturbed consciousness that were fully reversible within a few days. Clinical and radiological findings suggested raised intracranial pressure, which on one occasion was confirmed by intracranial pressure monitoring. magnetic resonance imaging performed in the asymptomatic interval disclosed a diffuse leukoencephalopathy. Brain biopsy surprisingly revealed the typical vascular changes of cadasil and subtle endothelial alterations. The white matter showed edematous changes and reactive gliosis. Mutational analysis of the Notch3 gene revealed a previously unreported mutation. We suggest that a transient disturbance of the blood-brain barrier related to the underlying vascular pathology may have caused this unusual presentation of cadasil.
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7/64. A survival case of acute mitral regurgitation and cardiogenic shock caused by subtotal occlusion of the first diagonal branch.

    An 80-year-old woman was admitted with cardiogenic shock; she arrived in a deep coma with systolic blood pressure of 44 mmHg. An electrocardiogram showed ST elevation in I, aVL, V5 and V6, suggesting myocardial infarction in the lateral area of the left ventricle. A chest roentgenogram showed right pulmonary edema without cardiomegaly. Transthoracic and transesophageal echocardiograms revealed severe mitral regurgitation and a flailing anterior mitral valve leaflet, suggesting a ruptured papillary muscle. The patient was initially treated with high-dose dopamine, dobutamine and norepinephrine. Intraaortic balloon pumping was initiated after the patient's condition stabilized. She underwent emergency mitral valve replacement with a prosthetic valve. Complete rupture of the anterior papillary muscle was confirmed. Histological examination revealed necrosis of the anterior papillary muscle with inflammatory changes. She recovered uneventfully. Postoperative coronary angiography demonstrated subtotal occlusion of the first diagonal branch, and left ventriculography demonstrated akinesis of the lateral segment. This was a rare case in which subtotal occlusion of the first diagonal branch caused rupture of an anterior papillary muscle leading to severe mitral regurgitation.
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8/64. Intrathecal saline infusion in the treatment of obtundation associated with spontaneous intracranial hypotension: technical case report.

    OBJECTIVE AND IMPORTANCE: Spontaneous intracranial hypotension is an increasingly recognized cause of postural headache. However, appropriate management of obtundation caused by intracranial hypotension is not well defined. CLINICAL PRESENTATION: A 43-year-old man presented with postural headache followed by rapid decline in mental status. Imaging findings were consistent with the diagnosis of spontaneous intracranial hypotension, with bilateral subdural hematomas, pachymeningeal enhancement, and caudal displacement of posterior fossa structures and optic chiasm. INTERVENTION: Despite treatment with lumbar epidural blood patch, worsening stupor necessitated intubation and mechanical ventilation. Contrast-enhanced magnetic resonance imaging and computed tomographic myelography of the spine failed to demonstrate the site of cerebrospinal fluid fistula. The enlarging subdural fluid collections were drained, and a ventriculostomy was performed. Postoperatively, the patient remained semicomatose. To restore intraspinal and intracranial pressures, intrathecal infusion of saline was initiated. After several hours of lumbar saline infusion, lumbar and intracranial pressures normalized, and the patient's stupor resolved rapidly. Repeat computed tomographic myelography accomplished via C1-C2 puncture demonstrated a large ventrolateral T1-T3 leak, which was treated successfully with a thoracic epidural blood patch. Follow-up magnetic resonance imaging demonstrated resolution of intracranial hypotension, and the patient was discharged in excellent condition. CONCLUSION: Spontaneous intracranial hypotension may cause a decline of mental status and require lumbar intrathecal saline infusion to arrest or reverse impending central (transtentorial) herniation. This case demonstrates the use of simultaneous monitoring of lumbar and intracranial pressures to appropriately titrate the infusion and document resolution of intracranial hypotension. Maneuvers aimed at sealing the cerebrospinal fluid fistula then can be performed in a less emergent fashion after the patient's mental status has stabilized.
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9/64. coma blisters in a case of fatal theophylline intoxication.

    A case of fatal poisoning caused by theophylline toxicity (serum level 127 micro g/ml) is presented. At external examination, skin blisters on regions exposed to pressure were distinctive. Histologic examination demonstrated subepidermal bullae with eosinophilic necrosis of the eccrine sweat gland coil but no epidermal necrosis, vascular changes, or inflammatory infiltrate. To the authors' knowledge, this is the first description of coma blisters in a case of theophylline intoxication.
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10/64. life-threatening hyperkalaemia following therapeutic barbiturate coma.

    OBJECTIVE: To report the occurrence of life-threatening hyperkalaemia following treatment with therapeutic thiopentone coma. SETTING: The neurosurgical intensive care units of Royal North Shore Hospital and Liverpool Hospital, Sydney, australia. patients: Three patients treated with theraputic thiopentone coma. One patient with raised intracranial pressure secondary to a severe traumatic brain injury and two patients with refractory vasospasm secondary to subarachnoid haemorrhage. Two of the three patients developed hypokalaemia on starting thiopentone, which was resistant to potassium supplementation. All three patients developed severe hyperkalaemia during the recovery phase of coma. This was life-threatening in all three patients and fatal in one. CONCLUSIONS: Severe hypokalaemia refractory to potassium therapy may occur during therapeutic thiopentone coma. Severe rebound hyperkalaemia may occur after cessation of thiopentone infusion. Protocols for the management of patients with therapeutic barbiturate coma should recognise this potentially serious complication.
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