Cases reported "Coma"

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11/68. Ulcerative colitis, status epilepticus and intractable temporal seizures.

    Three patients with ulcerative colitis (UC) and without any other risk factors, developed intractable status epilepticus de novo. Intractable temporal lobe seizures followed and were investigated 7-19 years later. Two had bi-temporal abnormalities and catastrophic memory loss and the third, severe temporoparietal damage. Status occurred in the context of steroid taper, fasting and abdominal surgery respectively, and it is unlikely that it was merely due to coincidence. encephalitis or vasculitis were suspected in all cases, but without evidence; metabolic factors may have been present. status epilepticus in UC may lead to catastrophic sequelae.
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12/68. 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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13/68. Use of an anesthesia cerebral monitor bispectral index to assess burst-suppression in pentobarbital coma.

    A seven-year-old child with generalized status epilepticus who was placed in a barbiturate coma was monitored with the bispectral index monitor in addition to the standard full channel electroencephalogram. This child had a low bispectral index number and high suppression ratio on the bispectral index monitor when the desired level of pentobarbital coma was induced. There was excellent correlation of the bispectral index monitor to the suppression ratio. The burst rate also correlated well to the bispectral index number and to the suppression ratio. Therefore the bispectral index monitor could allow the patient in barbiturate coma to leave the intensive care unit for diagnostic or therapeutic procedures and may one day replace the full-channel electroencephalogram in the management of patients in barbiturate coma.
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14/68. Case report: hypoglycemia and diffusion-weighted imaging.

    The effect of severe hypoglycemia on the brain is well known, ranging from alterations of mental status to profound coma and death. We describe a case of global diffusion abnormalities eventually resulting in death. This otherwise healthy patient presented with seizures and a serum glucose level less than 20 mg/dL. Testing suggested that the hypoglycemia was likely caused by exogenous insulin or perhaps insulin receptor antibodies. magnetic resonance imaging on the day after admission showed regions of restricted diffusion in the temporal and occipital lobes as well as in the basal ganglia. Despite the large body of literature concerning the pathophysiology of hypoglycemia and its clinical implications, little is known regarding its radiologic correlations.
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15/68. Ingestion of tea tree oil (melaleuca oil) by a 4-year-old boy.

    A 4-year-old boy ingested a small quantity of tea tree oil. Within 30 minutes, he became ataxic and shortly thereafter progressed to unresponsiveness; he was endotracheally intubated by paramedics. His neurologic status improved gradually over 10 hours, and he remains well on follow-up. tea tree oil is an increasingly popular topical antiseptic that is available in a wide variety of products, often without warning labels. Healthcare providers should be aware of the common uses of tea tree oil, as well as its potential toxicity.
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16/68. ammonia induced encephalopathy from valproic acid in a bipolar patient: case report.

    valproic acid is widely used as a mood stabilizer. We report a case of an adult with bipolar disorder taking therapeutic doses of valproic acid, who presented to the emergency department with coma related to hyperammonemia as a complication of valproic acid treatment. valproic acid was discontinued which resulted in rapid clinical recovery. valproic acid induced coma was likely related to a urea cycle enzymopathy. Clinicians should consider hyperammonemia in all patients who present with coma and other mental status changes while on valproic acid. In such patients, ammonia level should be obtained in addition to liver function tests.
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17/68. Acute postpartum mental status change and coma caused by previously undiagnosed ornithine transcarbamylase deficiency.

    BACKGROUND: Acute postpartum mental status change usually represents postpartum blues or depression. Psychosis and coma are rare. This is a case report of a patient with previously undiagnosed ornithine transcarbamylase deficiency presenting as postpartum acute mental status change and coma. CASE: A 28-year-old multipara developed acute mental status change and coma 3 days after cesarean delivery. A metabolic profile and neurologic workup were unrevealing. An electroencephalogram revealed diffusely slow brain activity. She developed hyperammonemia and hyperglutaminemia and was diagnosed with ornithine transcarbamylase deficiency. Her newborn son was diagnosed with ornithine transcarbamylase deficiency on the previous day. Treatment with oral lactulose resulted in normalization of her ammonia level and resolution of her coma within 48 hours. She suffers no long-term sequelae. Dietary avoidance of protein was advised; outpatient treatment with sodium benzoate, sodium phenylacetate, and lactulose was initiated. A pedigree analysis is ongoing. CONCLUSION: ornithine transcarbamylase deficiency should be included in the differential diagnosis of acute postpartum coma. hyperammonemia, hyperglutaminemia, and orotic aciduria are diagnostic, facilitate early treatment, and mitigate the risk of permanent neurologic impairment or death.
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18/68. Accidental clozapine intoxication in a ten-year-old child.

    clozapine is a tricyclic dibenzodiazepine derivative used commonly in the treatment of schizophrenia. Severe side effects of overdose have been described in children. This report describes the unintentional ingestion of clozapine by a 10-y-o girl, presenting dramatic changes of mental status and progressive alteration of consciousness with a glasgow coma scale drop from 12 to 7. urine analysis revealed 500 microg clozapine/L 24 h after ingestion. Full resolution of symptoms occurred after approximately 55 h with no sequels or alterations at follow-up. awareness must be taken when administering atypical antipsychotics such as clozapine to children because of the severe intoxication effects cases reported.
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19/68. Reversible coma secondary to cefepime neurotoxicity.

    OBJECTIVE: To describe a case of cefepime neurotoxicity associated with acute renal failure that resulted in nonconvulsive status epilepticus. CASE SUMMARY: A 66-year-old woman with acute myeloid leukemia had fever on the third day of the initial chemotherapy cycle. Empiric antibiotic treatment with cefepime 2 g every 8 hours was started; fluconazole and vancomycin were subsequently added due to the persistence of fever. Ten days after initiation of cefepime, the patient developed acute renal failure followed by altered consciousness (glasgow coma scale 6) associated with nonconvulsive status epilepticus. Cefepime was discontinued. Epileptiform activity in the electroencephalogram disappeared with clonazepam, and the patient regained consciousness 48 hours after cefepime withdrawal. DISCUSSION: Acute renal impairment combined with the use of cefepime may account for nonconvulsive status epilepticus. An objective causality assessment revealed that the adverse event was probably due to cefepime. Cefepime's neurotoxic effects derive from high serum concentrations resulting from decreased renal clearance, increased unbound antibiotic, and blood-brain barrier dysfunction during uremia. CONCLUSIONS: The combination of cefepime treatment and acute renal failure may induce drug-related neurotoxicity. Nonconvulsive status epilepticus frequently passes unnoticed in severely ill patients without a history of epilepsy. This disorder should be included in the list of potential causes of coma. In this patient, early detection of nonconvulsive status epilepticus and withdrawal of the antibiotic resulted in full recovery.
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20/68. Myoclonic status epilepticus following repeated oral ingestion of colloidal silver.

    The authors report a case of a 71-year-old man who developed myoclonic status epilepticus and coma after daily ingestion of colloidal silver for 4 months resulting in high levels of silver in plasma, erythrocytes, and CSF. Despite plasmapheresis, he remained in a persistent vegetative state until his death 5.5 months later. silver products can cause irreversible neurologic toxicity associated with poor outcome.
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