Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied the availability of parenteral solutions of diazepam in glass bottles or polyethylene (PE) containers during infusion through polyvinyl chloride (PVC) administration sets. Diazepam solutions in concentration of 1000 mg/500 ml in 0.9% sodium chloride (NS) and 5% glucose (G5W) injection were infused at a flow rate of 30 ml/h, and samples were taken from the bottle and at the end of the administration set, till 12 hours of infusion. The samples were tested in triplicate using ultraviolet spectrophotometry. The greatest loss of diazepam was observed in all solutions at 30 minutes of infusion (63.5% G5W glass, 60.5% NS glass, 55% G5W PE and 58% NS PE from the original concentration of 200 micrograms/ml). The diazepam concentrations in the containers did not significantly changed. The loss of diazepam from solutions infused through PVC administration sets should be kept in mind in severe clinical situations as status epilepticus, tetanus and eclampsia.
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PMID:Factors affecting diazepam availability from intravenous admixture solutions. 261 6

The treatment of status epilepticus can be improved by using recent developments in the pharmacokinetics and method of intravenous (IV) administration of phenytoin sodium. While diazepam, administered IV, remains the drug of choice for the short-term control of seizures associated with compromised respiratory exchange, phenytoin is effective in preventing recurrence of such seizures and in treating most other forms of status epilepticus. A loading dose of 18 mg/kg given by IV infusion in either 0.45% or 0.9% sodium chloride at a rate no greater than 50 mg/min results in therapeutic serum levels for up to 24 hours in most patients. Maintenance therapy with phenytoin should start at 4 to 7 mg/kg/day and be adjusted to both clinical response and serum levels.
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PMID:Status epilepticus. The role of intravenous phenytoin. 742 Jun 42

The child who presents with acute coma runs a high risk of cardiopulmonary insufficiency, direct brain injury or even cerebral herniation. The case-management of such child requires a coma-specific emergent evaluation, immediate treatment of any hypoxicischemic insults and of the underlying cause. The coma-specific examination includes performance of child-adapted Glasgow Coma Score, the evaluation of brain stem functions such as pupillary response to light, cough- and gag reflex, and determination of all vital signs including body temperature. Treatment of hypoxicischemic insults includes control of airways and ventilation in patient with coma defined as GCS <8; liberal treatment of impaired cardiovascular states with isotonic fluids such as 0.9% sodium chloride; and treatment of cerebral herniation with head elevation, mannitol, hypertonic sodium chlorid fluids, steroids and hyperventilation. Immediately treatable causes are hypoglycemia, meningitis/encephalitis, opioid overdose and status epilepticus. Exclusion of rapidly progressive intracranial lesions almost always requires referral to the tertiary centre with head CT-scan facilities. Finally, an extensive etiology search of the stable coma is performed by looking for disease or trauma of the brain, for metabolic causes, for intoxications and for cardiopulmonary problems.
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PMID:[The comatose child]. 1613 15

The treatment of status epilepticus may require in certain situations the concurrent administration of lorazepam or midazolam with fosphenytoin. Simulated Y-site fosphenytoin/lorazepam and fosphenytoin/midazolam hydrochloride admixtures, respectively, in 0.9% sodium chloride injection were analyzed using a stability-indicating high-performance liquid chromatography (HPLC) method. Each drug was analyzed for stability by HPLC from three simulated Y-site samples over an eight-hour period. The HPLC assay results indicate that both fosphenytoin and lorazepam are stable together at a Y site over an eight-hour period. In addition, there was neither a change in sample clarity nor a change in pH over the same period. The results indicate that, when medically necessary, fosphenytoin and lorazepam in 0.9% sodium chloride injection can be administered via the same intravenous (IV) line. Midazolam free base was precipitated upon admixture of midazolam hydrochloride and fosphenytoin solutions. Therefore, midazolam hydrochloride and fosphenytoin should not be given via the same IV line.
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PMID:Fosphenytoin y-site stability studies with Lorazepam and midazolam hydrochloride. 2398 22

To investigate the expressions of Nav1.5 mRNA at different time points in a rat model of temporal lobe epilepsy (TLE), and to assess the potential contribution of Nav1.5 to epileptogenesis. Male Sprague-Dawley rats (72) weighing 230 to 250 g were used for this study. They were randomly assigned to six groups (12 rats/group): control and five TLE groups. The TLE groups were day 1 (acute period), days 7 and 14 (latent period), and days 30 and 60 (chronic period). With the exception of control, epilepsy was induced in the rats with an intraperitoneal (i.p.) injection of aqueous solution of lithium chloride 18 h prior to pilocarpine injection (i.p.) at a dose of 125 mg/kg body weight (b.wt). Rats in the control group were injected i.p. with 0.9 % sodium chloride (125 mg/kg b.wt.) in place of pilocarpine. A total of 84 out of 112 rats developed status epilepticus (SE). The expression of Nav1.5 in the brains of rats was assessed using quantitative real-time polymerase chain reaction (qRT-PCR), immunohistochemistry and Western blot analysis. The expressions of Scn5a mRNA in the hippocampus during the latent and chronic periods were significantly higher than in the control group (p &lt; 0.05), but there were no significant differences in the corresponding expressions between the two different time points in the latent and chronic period groups (p &gt; 0.05). The expression peaked 30 days post-SE, and was sustained for 60 days. There was no significant difference in the expression of Scn5a mRNA in the acute group, when compared to control. Immunohistochemical staining showed that expression levels of Nav1.5 in the CA3 region during latent and chronic periods were significantly higher than those in control group (p &lt; 0.05), and the expressions peaked at day 30. However, there was no significant difference in the expression of Nav1.5 in the latent group, relative to the chronic period group. These results show that Nav1.5 might be involved in the pathogenesis of TLE.
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PMID:Expression of Nav1.5 in the pathogenesis of temporal lobe epilepsy. 3086 Apr 72