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)

As the anticonvulsant plasma level of diazepam (DZP) after intravenous injection is maintained only for a short period, it is profitable to administer DZP as an intravenous infusion. It has, however, been claimed that DZP cannot be mixed with dextrose injection as DZP would precipitate. As this is in contrast to our clinical experience we added DZP of various brands to dextrose injections. A precipitate was in fact found in dextrose injections containing Valium and Stesolid whereas Diazepam A.L. was not only slightly cloudy. The concentration of DZP was, however, the same in all the samples and corresponded to the calculated concentration. The precipitate in the solutions with Valium and Stesolid which did not pass the filter must therefore be due to additives, most probably benzoates. On the basis of these findings and our clinical experience of this mode of administration we recommend the infusion method as one of the most effective in the acute treatment of status epilepticus.
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PMID:Diazepam: intravenous infusion in the treatment of status epilepticus. 96 79

Paraldehyde is used in the treatment of status epilepticus, alcohol withdrawal, and delirium tremens. Because it is a solvent, concerns have been raised about infusing it through plastic intravenous tubing sets. In a three-phase study, 4% paraldehyde in 5% dextrose solution was analyzed over 24 hours for photodegradation, adsorption to polyvinylchloride- (PVC) and polyethylene- (PE) lined intravenous tubing, and the presence of di(2-ethylhexyl) phthalate (DEHP). Paraldehyde and DEHP samples were quantified by gas chromatography, and DEHP was confirmed by mass spectral analysis. On exposure to light for 24 hours, the concentration of paraldehyde decreased from 100 to 97%. This decrease is statistically significant but clinically insignificant. A 24-hour continuous infusion of paraldehyde through the two types of tubing revealed a decrease in concentration attributable to adsorption of 4% with PE and 13% with PVC tubing at 2 hours. In addition, there was no appreciable leaching of DEHP over 24 hours with either type of tubing. Concerns about paraldehyde's light instability and effects on tubing integrity appear to be unwarranted with commercially available intravenous administration sets.
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PMID:The effect of paraldehyde on intravenous tubing sets. 261 53

The effect of bicuculline-induced status epilepticus (SE) on local cerebral metabolic rates for glucose (LCMRglc) was studied in 2-wk-old ketamine-anesthetized marmoset monkeys, using the 2-[14C]-deoxy-D-glucose autoradiographical technique. To estimate LCMRglc in cerebral cortex and thalamus during SE, the lumped constant (LC) for 2-deoxy-D-glucose (2-DG) and the rate constants for 2-DG and glucose were calculated for these regions. The control LC was 0.43 in frontoparietal cortex, 0.51 in temporal cortex, and 0.50 in thalamus; it increased to 1.07 in frontoparietal cortex, 1.13 in temporal cortex, and 1.25 in thalamus after 30 min of seizures. With control LC values, LCMRglc in frontoparietal cortex, temporal cortex, and dorsomedial thalamus appeared to increase four to sixfold. With seizure LC values, LCMRglc increased 1.5- to 2-fold and only in cortex. During 45-min seizures, LCMRglc in cortex and thalamus probably increases 4- to 6-fold initially and later falls to the 1.5- to 2-fold level as tissue glucose concentrations decrease. Together with our previous results demonstrating depletion of high-energy phosphates and glucose in these regions, the data suggest that energy demands exceed glucose supply. The long-term effects of these metabolic changes on the developing brain remain to be determined.
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PMID:Local cerebral glucose utilization during status epilepticus in newborn primates. 273 93

The regional influx of glucose across the blood-brain barrier and regional blood flow were studied simultaneously in conscious and restrained rats using the single pass bolus injection of [14C]butanol and [3H]D-glucose method. Glucose extraction by the cerebellum was about twice that of other brain regions. Thus, despite the lower cerebellar blood flow, the influx of glucose into the cerebellum was equivalent to that of the cerebral cortex and higher than that of the hippocampus over a wide range of plasma glucose concentrations. Because the local metabolic rate for glucose is higher in the cerebral cortex than in the cerebellum, the equal influx of glucose in these two regions means a relative oversupply of glucose to the cerebellum. In vivo analysis of blood to brain glucose transport kinetics showed similar plasma glucose concentrations at half-maximal transport (Kt) in brain regions that were studied. The values for Kt ranged between 4.4 and 5.1 mM. Maximal transport capability (Tmax), on the other hand, was similar in the cerebral cortex and cerebellum but significantly lower in the hippocampus (P less than 0.05). The higher ratio of glucose influx to glucose utilization in the cerebellum may explain the clinical and experimental findings of relative resistance of the cerebellum to hypoglycemia while the lower Tmax in the hippocampus may be the mechanism underlying its selective vulnerability during pathophysiologic conditions associated with marked increments in brain oxidative metabolism, such as status epilepticus.
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PMID:Regional comparisons of brain glucose influx. 397 Nov 56

The pharmacokinetic parameters controlling paraldehyde elimination were determined in nine infants infused with paraldehyde at the rate of 150 mg/kg/hr in a 5% solution in 5% dextrose for the treatment of status epilepticus. The mean +/- SEM values for the observed parameters were as follows: rate constant for the disposition of paraldehyde 0.0680 +/- 0.0071 hr,-1 half-life 10.2 +/- 1.0 hr; volume of distribution 1.73 +/- 0.20 L/kg; clearance 0.121 +/- 0.023 L/hr/kg. Phenobarbital administration prior to or within 24 hours of the cessation of paraldehyde infusion decreased both paraldehyde clearance and volume of distribution in a manner linearly related to the logarithm of the phenobarbital dose. The rate constant for paraldehyde elimination was decreased as a linear function of the logarithm of the combined dose of administered phenobarbital and phenytoin. No acetaldehyde was detected in any blood samples. Paraldehyde administration was not correlated with any adverse reactions or toxicities.
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PMID:Pharmacokinetics of paraldehyde disposition in the neonate. 669 30

A 2-month-old girl survived a lethal serum level of paraldehyde after being given the drug intravenously (IV) for status epilepticus. On the basis of known pharmacokinetic data in man, a slow IV infusion, over a period of five minutes, of 200 mg/kg of paraldehyde followed by a drip of 20 mg/kg/hr should result in safe, rapid control of status epilepticus when first-line anticonvulsant drugs have failed. The paraldehyde should be diluted to a 10% solution with 5% dextrose water.
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PMID:Paraldehyde toxicity during treatment of status epilepticus. 708 Nov 59

The substantia nigra pars reticularis (SNPR) of rats is highly susceptible to both seizure- and ischaemia-mediated damage. Hyperglycaemic exacerbation of brain damage similar to that observed after global brain ischaemia may also occur in rats with status epilepticus. We tested the hypotheses that hyperglycaemia exacerbates seizure-induced SNPR damage in rats and that SNPR lesions develop rapidly post-seizure. Halothane-anaesthetized, paralysed, and mechanically ventilated rats were prepared for haemodynamic and EEG monitoring. Halothane was discontinued, and mechanical ventilation on 30% oxygen/70% nitrous oxide was continued for 1 h. Three treatment groups (20 rats each) were studied: (1) control, lactated Ringer's solution; (2) equiosmolar control, 40% mannitol; and (3) hyperglycaemia, 50% dextrose. Infusions were started 5 min before seizures were induced with flurothyl 3% administered for either 45 (n = 10) or 75 (n = 10) min. Immediately after seizures, half of the animals underwent cerebral perfusion-fixation with formalin and half were allowed to recover for 2 h post-seizure and then perfused. Brain histology was assessed by light microscopy and scored 0-5 (0 = no damage) for the percentage of eosinophilic neurons and vacuolation in the SNPR. Glucose administration decreased the severity of SNPR damage in rats subjected to 75 min of seizures and 2 h recovery (pathology scores: control, eosinophilic neurons = 3.6, vacuolation = 4.0; hyperglycaemia, eosinophilic neurons = 3.0, vacuolation = 2.75; p < 0.05). SNPR damage was worse after 2 h of recovery (pathology scores: 0 h recovery, eosinophilic neurons = 0.9, vacuolation = 0.1; 2 h recovery, eosinophilic neurons = 3.9, vacuolation = 3.8; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Substantia nigra damage after fluorothyl-induced seizures in rats worsens after post-seizure recovery: no exacerbation with hyperglycaemia. 790 8

Status epilepticus remains a life-threatening condition associated with a high mortality. In order to understand the pathophysiological mechanisms underlying sustained seizures, the identification of structures involved in seizure activity allowing to define epileptic networks may be important. Thus, local cerebral metabolic rate for glucose (LCMR(glc)) was measured in a rat model of self-sustaining status epilepticus (SSSE) induced by a brief intermittent perforant path stimulation of 30 min, using the quantitative [(14)C]2-deoxyglucose autoradiographic technique. SSSE induced a generalized bilateral increase in LCMR(glcs) affecting 27 of the 42 structures studied. Largest metabolic increases (>250%) were recorded in the hippocampus, amygdala, entorhinal and piriform cortices, and lateral septum. Marked metabolic activation was also seen in basal ganglia areas such as the substantia nigra, globus pallidus and accumbens nucleus. LCMR(glcs) in brainstem, some midbrain structures, and in the neocortex were not affected by SSSE. In conclusion, a brief stimulation of the hippocampus induced a reproducible limbic SSSE in 100% of the rats, characterized by the metabolic activation of limbic and extralimbic structures, known to be involved in this type of seizures. Therefore, this new model allowing the development of a well-defined SSSE, appears to be particularly suitable for further studies on the mechanisms involved in status epilepticus.
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PMID:Self-sustaining status epilepticus after a brief electrical stimulation of the perforant path: a 2-deoxyglucose study. 1044 23

Status epilepticus (SE) is a potentially life-threatening condition that requires prompt and aggressive treatment. Prolonged status seizures are associated with significant physiological sequelae and neurological deficits. Although systemic events such as hyperthermia and anoxia contribute to neuronal damage, SE in and of itself can induce cell death. In general, the sooner it is brought under control, the more favourable is the prognosis. Benzodiazepines, as a group, are the most frequently used anticonvulsants in the management of status seizures. Midazolam, a water-soluble benzodiazepine, is a potent anticonvulsant that offers many advantages over typical benzodiazepines. Because of its stability in aqueous media, midazolam dissolves in common diluents such as normal saline or dextrose water. Consequently, midazolam both intravenously (i.v.) and intramuscularly (i.m.) is well tolerated locally and is associated with less venoirritation than benzodiazepines or antiepileptics that require organic solvents. The water solubility of midazolam also allows rapid and reliable absorption of the drug from the i.m. injection site. Because it is rapidly metabolised and its metabolites are pharmacologically inactive, midazolam has a short duration of action. Most patients regain full conscious state and can be evaluated soon after the cessation of treatment. Midazolam by continuous i.v. infusion and by the i.m. route has been successfully used in the treatment of SE. Although some respiratory and haemodynamic side-effects have been associated with midazolam, no clinically significant side-effects were observed with its use for the indication of SE. It is suggested that midazolam is a safe and rapidly effective treatment option in the management of SE in the critical care setting.
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PMID:Treatment of status epilepticus with midazolam in the critical care setting. 1075 Feb 57

Cases of N-acetylcysteine overdose have been reported before. In some cases, these overdoses have led to death if an anaphylactoid reaction was present. A healthy 30-month-old girl allegedly ingested acetaminophen at 418 mg/kg. Because the emergency physician feared the time of ingestion might not be accurate, he decided to start the 20.5-hour intravenous N-acetylcysteine protocol 8 hours after ingestion. He mistakenly prescribed the maximum milliliter-per-kilogram volume of the dextrose 5% diluent for the milliliter-per-kilogram volume of N-acetylcysteine 20% to be administered. Five hours after the error was detected (19.5 hours postingestion), the patient started developing myoclonus on the left side of her body, with left eye deviation. This condition persisted intermittently for 3 hours despite treatment with diazepam, lorazepam, and phenytoin. A first computed tomographic scan result was normal. A few hours later, she sustained shorter recurrences of the myoclonus. At 30 hours after ingestion, she started to have irregular breathing and became unresponsive to pain. A repeated computed tomographic scan showed diffuse cerebral edema. A postmortem examination showed the presence of acute anoxic encephalopathy with marked cerebral edema and the beginning of uncal herniation that confirmed the clinical diagnosis of intracranial hypertension and brain death. A cumulative intravenous dose of 2,450 mg/kg of N -acetylcysteine was associated with status epilepticus, intracranial hypertension, and death in a child.
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PMID:Status epilepticus after a massive intravenous N-acetylcysteine overdose leading to intracranial hypertension and death. 1545 24


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