Cases reported "Coma"

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1/43. 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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2/43. 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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3/43. Treatment of amitriptyline poisoning with ovine antibody to tricyclic antidepressants.

    We report clinical improvement with the use of an ovine antibody (Fab fragment) to tricyclic antidepressants for the treatment of toxic effects of amitriptyline on the central nervous system and heart in a 48-year-old man.
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4/43. coma and respiratory depression following the ingestion of GHB and its precursors: three cases.

    Gamma hydroxybutyrate (GHB) is a product of the metabolism of both gamma butyrolactone (GBL) and 1,4-butanediol (1,4-BD). Gamma hydroxybutyrate (GHB) is an illegal agent that causes central nervous system depression. Chemical precursors of GHB, such as GBL and 1,4-BD, have been available for purchase from many health food stores and internet websites for mood-enhancement, sleep-induction, and stimulation of growth hormone release. We report three cases of ingestion of products containing GHB and chemical precursors of GHB. All three patients had severe presentations followed by full recoveries. Some products containing GBL were withdrawn from the market after the FDA issued a warning regarding these products. Products containing 1,4-butanediol remain on the market today.
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5/43. ethylene glycol ingestion resulting in brainstem and midbrain dysfunction.

    INTRODUCTION: ethylene glycol toxicity has produced central nervous system abnormalities including coma, cerebral edema, and cranial nerve dysfunction. CASE REPORT: A 26-year-old male developed widespread brainstem and midbrain dysfunction with corresponding cranial computed tomography findings after ingesting ethylene glycol. The computed tomography scan which was obtained 3 days after ethylene glycol ingestion showed low density areas in the basal ganglia, thalami, midbrain, and upper pons. The neurologic findings in our patient reflected dysfunction of all the areas of hypodensity on the cranial computed tomography scan. A magnetic resonance imaging of the brain obtained 24 days after ingestion revealed bilateral putamen necrosis. The patient's neurologic sequelae resolved over the following 4 months.
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6/43. Gamma-hydroxybutyrate (GHB): a newer drug of abuse.

    Gamma-hydroxybutyrate (GHB) is an illicitly marketed substance that has recently gained popularity among body builders and party attendees as a drug of abuse. GHB is a depressant that acts on the central nervous system. It is purported as a strength enhancer, euphoriant and aphrodisiac and is one of several agents reported as being used as a "date rape" drug. Because of its central nervous system depressant effects, GHB can be lethal when combined with alcohol or other depressants. Currently, there is no accepted medical use for GHB, and the U.S. Food and Drug Administration has prohibited its manufacture and sale. Clinicians should be familiar with the typical clinical presentation of GHB and its adverse effects. In addition, patients should be warned of its potential toxicity and be cautioned to avoid the use of GHB.
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7/43. Prolonged coma and loss of brainstem reflexes following amitriptyline overdose.

    Severe tricyclic antidepressant (TCA) overdose is generally manifested by cardiovascular and/or central nervous system toxicity. Although the majority of patients who are comatose following these overdoses regain consciousness within 24 h, this case had 5-days of coma with associated loss of brainstem reflexes. Severe central nervous system depression can occur as a sole manifestation of TCA overdose without concomitant cardiovascular toxicity.
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8/43. miller fisher syndrome with transient coma: comparison with Bickerstaff brainstem encephalitis.

    We herein report a 4-year-old boy with miller fisher syndrome (MFS) who presented with transient coma in addition to the typical triad of internal and external ophthalmoplegia, cerebellar ataxia and areflexia after an influenza type B infection. The electroencephalogram findings revealed intermittently generalized slow wave bursts. The cerebrospinal fluid revealed high protein and a lack of any cellular response. The serum anti-GQ1b IgG antibody was elevated in the acute phase and disappeared in the convalescent phase. The transient coma with the triad of MFS in this patient indicated an extended brainstem lesion including a reticular formation, which is also the responsible lesion of Bickerstaff brainstem encephalitis (BBE), but the magnetic resonance imaging repeatedly showed no abnormal finding. Our patient suggested the involvement of central nervous system in addition to the peripheral nerve injury in MFS. He also suggested that MFS and BBE may belong to the same group of disorders as syndrome of ophthalmoplegia, ataxia and areflexia (SOAA).
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9/43. Episodic coma in a new leukodystrophy.

    Among the leukodystrophies of a hypomyelinating nature, childhood ataxia with diffuse central nervous system hypomyelination exhibits the unique feature of rapid decrease in mental status after relatively minor head injuries or otherwise noncomplicated febrile illnesses. This article reports the case of a child with progressive spastic quadriparesis in whom unconsciousness developed repeatedly as a result of minor head trauma and required prolonged critical-care nursing. Although cognition is believed to be relatively preserved in this disorder, this child developed progressive cognitive decline. A detailed review of the literature is presented along with discussion of the potential mechanisms of neurologic deterioration.
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10/43. Reversible coma caused by risperidone-ritonavir interaction.

    Medications that act on the central nervous system are frequently used in people infected with human immunodeficiency virus (hiv). Actually, drug interactions are an important factor in the treatment of patients with (hiv) infection and because of the complexity of the current drug regimens, clinicians should be trained in order to recognize and manage drug interactions. Herein, we present an hiv infected male admitted for manic behavior and treated with risperidone who developed a profound coma secondary to increased levels of risperidone because of a possible drug interaction with ritonavir and indinavir. Subsequently, we discuss this interaction, rarely described in the literature. risperidone is a cytochrome P450 (CYP2D6) enzyme substrate and weak inhibitor and a CYP3A4 substrate. Possible interactions with CYP2D6 inhibitors (amiodarone, fluoxetine or ritonavir) and CYP3A4 inhibitors (indinavir and ritonavir) can increase its serum concentrations and produce significant adverse effects. In conclusion, this drug combination should be administered with caution and routinely examined for signs and symptoms of risperidone toxicity. Dosages should be reduced as needed. Finally, we think that in patients taking multiple medications, plasma levels of risperidone should be monitored especially if drug interactions are possible.
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