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)

Acute bacterial meningitis (ABM) in children is associated with a high rate of acute complications and mortality, particularly in the developing countries. Most of the deaths occur during first 48 hours of hospitalization. Coma, raised intracranial pressure (ICP), seizures, shock have been identified as significant predictors of death and morbidity. This article reviews issues in critical care with reference to our experience of managing 88 children with ABM in PICU. Attention should first be directed toward basic ABCs of life-support. Children with Glasgow Coma Scale (GSC) score < 8 need intubation and supplemental oxygen. Antibiotics should be started, even without LP (contraindicated if focal neuro-deficit, papilledema, or signs of raised ICP). Raised ICP is present in most of patients; GCS < 8 and high blood pressure are good guides. Mannitol (0.25 gm/Kg) should be used in such patients. If there are signs of (impending) herniation short-term hyperventilation is recommended; prolonged hyperventilation (> 1 hour) must be avoided. Any evidence of poor perfusion, hypovolemia and/or hypotension needs aggressive treatment with normal saline boluses and inotropes, if necessary, to maintain normal blood pressure. Empiric fluid restriction is not justified. Seizures may be controlled with intravenous diazepam or lorazepam. Refractory status epilepticus may be treated with continuous diazepam (0.01-0.06) mg/kg/min) or midazolam infusion. Ventilatory support may be needed early for associated pneumonia, poor respiratory effort and/or coma, and occasionally to reduce work of breathing in shock. Provision of critical care to children with ABM may reduce the mortality significantly as experienced by us.
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PMID:Bacterial meningitis in children: critical care needs. 1156 52

Status epilepticus is a life-threatening condition requiring emergent medical attention. Although initial therapies with antiepileptic drugs generally terminate seizures within 30 to 60 minutes, patients with refractory status epilepticus require additional intervention. High-dose pentobarbital has been the most commonly prescribed agent for the management of refractory status epilepticus in children. The objective of this research was to evaluate the association between the response of pentobarbital coma and neurologic outcomes in refractory status epilepticus. Twenty-three subjects were treated with pentobarbital coma for at least 48 hours. Medical records were reviewed to collect patient demographic information, responses to treatment, and neurologic outcomes. Among the 23 patients reviewed, 12 patients were controlled with pentobarbital (responders), six were unresponsive to pentobarbital (nonresponders), and five patients relapsed after discontinuation or during tapering of pentobarbital (relapser). The mortality rate among the relapser and nonresponder groups combined was 90.9%, but no deaths occurred among the responder group (P < 0.001). The survival rate was greater among toddlers compared with neonates or older children. Failure of seizure control after pentobarbital coma was associated with a poor prognosis. The potential for serious complications of pentobarbital therapy among neonates highlights the need for careful dosing in this age group.
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PMID:Neurologic outcomes of pediatric epileptic patients with pentobarbital coma. 1158 76

The clinical profile of neurotoxicity caused by immunosuppression has changed. When toxic levels are reached, both cyclosporine and tacrolimus may produce a clinical spectrum that varies from tremor and acute confusional state to status epilepticus and major speech or language abnormalities. Coma has become an unusual manifestation. Magnetic resonance imaging has been better defined, and abnormalities may be more widespread than those in the posterior lobes. These white matter lesions are caused by vasogenic edema, but may lead to apoptosis and cytotoxic edema if exposure is prolonged. Recent evidence suggests inhibition of a drug-efflux pump and dysfunction of the blood-brain barrier by enhanced nitric oxide production.
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PMID:Neurotoxicity of immunosuppressive drugs. 1169 28

We report a 14-year-old girl with carbamazepine intoxication who developed alpha coma and status epilepticus. She fell into deep coma and developed frequent generalized convulsions. The EEG during coma showed diffuse alpha activity predominantly in the frontal area. Serum carbamazepine concentration was 42.8 micrograms/ml. The convulsions were suppressed by diazepam only transiently, and by midazolam completely. Although half a day had passed since carbamazepine ingestion, we could wash out much of drug remnants by gastric lavage. Thereafter, the serum concentration of carbamazepine decreased efficiently and the patient recovered dramatically without complication. Early diagnosis and appropriate treatments should improve the prognosis of carbamazepine intoxication.
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PMID:[A case of carbamazepine intoxication with alpha coma and status epilepticus]. 1172 22

A previously healthy, 29-year-old man developed generalized convulsion with disturbed consciousness 3 days after the flu-like symptoms. On the next day, his convulsion evolved into generalized status epilepticus (GSE) that was unresponsive to administration of various anticonvulsants. Then, intravenous anesthetic agents, including midazolam, propofol and vecuronium sodium, were continuously infused. During the following 9 days, despite of high-dose infusion of these anesthetic agents, his GSE could not be suppressed, and complex partial seizure with secondary generalization frequently occurred. The patient was comatose and mechanically ventilated, whereas the brainstem reflexes were preserved. Electroencephalogram revealed a diffuse slowing of the background activity and occasional focal spike and wave complexes with secondary generalization. Cerebrospinal fluid analysis showed pleocytosis and elevated protein concentration. Cranial CT scans obtained on day 8 demonstrated brain edema. On day 10, his GSE ceased with abolition of the brainstem reflexes, and he lapsed into brain death resulting from the progressive brain edema. Over the following six days, his systemic circulation gradually worsened, and he died on day 16. On postmortem examination, the brain was markedly edematous and showed the findings consistent with acute anoxic encephalopathy with extensive circulatory stasis. Mild gliosis was observed in the insular cortex, yet no evidence of inflammatory disease was found throughout the brain. This patient was characterized by acutely progressive severe brain edema without inflammatory changes, suggesting that his primary disease was acute toxic encephalopathy presumably induced by viral infection. His GSE was refractory and unresponsive to the intensive treatment with the intravenous anesthetic agents. This case epitomizes the difficulties in controlling refractory seizures in some patients with encephalopathy or encephalitis.
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PMID:[Acute edematous encephalopathy presenting with refractory generalized status epilepticus: an autopsy case]. 1176 16

Sedatives continue to be used on a routine basis in critically ill patients. Although many agents are available and some approach an ideal, none are perfect. Patients require continuous reassessment of their pain and need for sedation. Pathophysiologic abnormalities that cause agitation, confusion, or delirium must be identified and treated before unilateral administration of potent sedative agents that may mask potentially lethal insufficiencies. The routine use of standardized and validated sedation scales and monitors is needed. It is hoped that reliable objective monitors of patients' level of consciousness and comfort will be forthcoming. Each sedative agent discussed in this article seems to have a place in the ICU pharmacologic armamentarium to ensure the safe and comfortable delivery of care. Etomidate is an attractive agent for short-term use to provide the rapid onset and offset of sedation in critically ill patients who are at risk for hemodynamic instability but seem to need sedation or anesthesia to perform a procedure or manipulate the airway. Ketamine administered through intramuscular injection or intravenous infusion provides quick, intense analgesia and anesthesia and allows patients to tolerate limited but painful procedures. The risk/benefit ratio associated with the use of this neuroleptic agent must be weighed carefully. Ketamine is contraindicated in patients who lack normal intracranial compliance or who have significant myocardial ischemia. Barbiturates are reserved mainly to induce coma in patients at risk for severe CNS ischemia, which frequently is associated with refractory intracranial hypertension, or in patients with status epilepticus. When administered in high doses, these drugs have prolonged sedative and depressant effects. Judicious hemodynamic monitoring is required when barbiturate coma is induced. Haloperidol is indicated in the treatment of delirium. Patients should be monitored for extrapyramidal side effects and, when they require higher doses, for potential electrocardiographic prolongation of the QT interval. Dexmedetomidine may evolve into an agent with qualities comparable with midazolam and propofol, and it may even become a drug of choice in select patients. Further study is required, however. Propofol has many of the qualities of an ideal sedative agent. Benzodiazepines and narcotics often are used in concert with propofol to provide reliable amnesia and to relieve pain, respectively. Propofol frequently causes hypotension when administered as a bolus or infusion, particularly in patients with limited cardiac reserve or hypovolemia. More data must be obtained to identify potential deleterious effects of hypertriglyceridemia, and further evaluation of the potential benefits in certain patient populations, such as neurosurgical patients, is needed.
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PMID:Use of propofol and other nonbenzodiazepine sedatives in the intensive care unit. 1176 65

Periodic lateralized epileptiform discharges (PLEDs) are typically associated with encephalitis, cerebral abscess, cerebral infarct, and status epilepticus. There is considerable debate as to whether this pattern is ictal or interictal when seen in association with status epilepticus. We present a patient with complex partial status epilepticus who developed PLEDs and remained comatose despite optimal drug therapy. Technetium 99m single-photon emission computed tomography (SPECT) showed hyperperfusion that resolved with further aggressive antiepileptic drug therapy, indicating that this pattern may indeed be ictal. Further studies are needed to define the significance of PLEDs in patients with status epilepticus. The role of SPECT in differentiating PLEDs as an interictal or ictal pattern also requires further study.
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PMID:Periodic lateralized epileptiform discharges after complex partial status epilepticus associated with increased focal cerebral blood flow. 1177 70

A 7-year-old Chinese boy with steroid-resistant nephrotic syndrome developed thalamic stroke secondary to straight sinus thrombosis. He was hospitalized due to status epilepticus and coma. The child recovered after treatment by low-molecular-weight heparin (LMWH) and warfarin. This case highlights the importance of magnetic resonance imaging with venography in the early diagnosis of cerebral sinus thrombosis (CST) in nephrotic children and the effectiveness of anticoagulation therapy in improving the neurological outcome.
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PMID:Thalamic stroke secondary to straight sinus thrombosis in a nephrotic child. 1268 64

Japanese encephalitis (JE) causes at least 10 000 deaths each year. Death is presumed to result from infection, dysfunction and destruction of neurons. There is no antiviral treatment. Seizures and raised intracranial pressure (ICP) are potentially treatable complications, but their importance in the pathophysiology of JE is unknown. Between 1994 and 1997 we prospectively studied patients with suspected CNS infections referred to an infectious disease referral hospital in Ho Chi Minh City, Vietnam. We diagnosed Japanese encephalitis virus (JEV), using antibody detection, culture of serum and CSF, and immunohistochemistry of autopsy material. We observed patients for seizures and clinical signs of brainstem herniation, measured CSF opening pressures (OP) and, on a subset of patients, performed EEGs. Of 555 patients with suspected CNS infections, 144 (26%) were infected with JEV (134 children and 10 adults). Seventeen (12%) patients died and 33 (23%) had severe sequelae. Of the 40 patients with witnessed seizures, 24 (62%) died or had severe sequelae, compared with 26 (14%) of 104 with no witnessed seizures [odds ratio (OR) 4.50, 95% confidence interval (CI) 1.94-10.52, P < 0.0001]. Patients in status epilepticus (n = 25), including 15 with subtle motor seizures, were more likely to die than those with other seizures (P = 0.003). Patients with seizures were more likely to have an elevated CSF OP (P = 0.033) and to develop brainstem signs compatible with herniation syndromes (P < 0.0001). Of 11 patients with CSF OP > or =25 cm, five (46%) died, compared with seven (9%) of 80 patients with lower pressures [OR 8.69, 95% CI 1.73-45.39, P = 0.005). Of the 50 patients with a poor outcome, 35 (70%) had signs compatible with herniation syndromes (including 19 with signs of rostro-caudal progression), compared with nine (10%) of those with better outcomes (P < 0.0001). Of 11 patients with CSF OP > or =25 cm, five (46%) died, compared with seven (9%) of 80 patients with lower pressures (OR 8.69, 95% CI 1.73-45.39, P = 0.005). The combination of coma, multiple seizures, brainstem signs and illness for 7 or more days was an accurate predictor of outcome, correctly identifying 42 (84%) of 50 patients with a poor outcome and 82 (87%) of 94 with a better outcome. These findings suggest that in JE, seizures and raised ICP may be important causes of death. The outcome may be improved by measures aimed at controlling these secondary complications.
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PMID:Seizures and raised intracranial pressure in Vietnamese patients with Japanese encephalitis. 1196 Aug 97

Continuous EEG (CEEG) monitoring allows uninterrupted assessment of cerebral cortical activity with good spatial resolution and excellent temporal resolution. Thus, this procedure provides a means of constantly assessing brain function in critically ill obtunded and comatose patients. Recent advances in digital EEG acquisition, storage, quantitative analysis, and transmission have made CEEG monitoring in the intensive care unit (ICU) technically feasible and useful. This article summarizes the indications and methodology of CEEG monitoring in the ICU, and discusses the role of some quantitative EEG analysis techniques in near real-time remote observation of CEEG recordings. Clinical examples of CEEG use, including monitoring of status epilepticus, assessment of ongoing therapy for treatment of seizures in critically ill patients, and monitoring for cerebral ischemia, are presented. Areas requiring further development of CEEG monitoring techniques and indications are discussed.
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PMID:Continuous EEG monitoring in the intensive care unit. 1206 13


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