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)

In a retrospective survey of mortality among the first 1000 unselected patients referred to the Epilepsy Research Unit at the Western Infirmary in Glasgow between 1985 and 1990, a total of 18 deaths were identified. Three patients had committed suicide and one each had died of status epilepticus in hospital, a subdural haematoma and a myocardial infarction. The remaining 12 deaths (67%) were sudden (median age 32 years; range 22-68 years). Poor seizure control and poor compliance with antiepileptic drug therapy were recorded in only three (25%) of these patients. There was a change in antiepileptic drug regimen in five (28%) in the month before death. Only two (17%) underwent postmortem examination. In nine of the 12 patients dying suddenly, the primary cause of death was not listed as epilepsy but as asphyxia (3), aspiration (2) and one each of ischaemic heart disease, myocardial infarction, asystole and drowning (in the bath). 'Status epilepticus' was assumed to have been responsible for the other three deaths, two of which were unwitnessed. Sudden death in people with epilepsy is an entity of great concern. Appropriate death certification and mandatory postmortem examination are essential to provide a truer picture of this neglected phenomenon.
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PMID:Sudden death in epilepsy: an avoidable outcome? 143 37

The etiology of sudden death in patients with epilepsy remains unclear. Previous studies in a well-established sheep model of status epilepticus showed that more than one-third of the unsedated animals died within 5 minutes of seizure onset due to hypoventilation. The relative contributions of airway obstruction and central hypoventilation could not be determined because airway flow and respiratory effort were not monitored. In this study, status epilepticus was induced in unsedated sheep with tracheostomies monitored by electrocardiography, electroencephalography, arterial line, serial blood gases, and airway flowmeter. All 8 animals demonstrated central apnea and hypoventilation, which resulted in the death of 1 and contributed to the death of another. A third animal died of acute heart failure within 2 minutes of seizure onset, accompanied by a large septal myocardial hemorrhage, contraction bands, and signs of global cardiac ischemia. More subtle contraction bands, subendocardial hemorrhage, and signs of acute myocardial ischemia were seen in other animals as well, none of which died of cardiac causes. Malignant arrhythmia was not seen in any of the sheep. Central hypoventilation and apnea accompany generalized status epilepticus and may be an important cause of sudden death in epileptics. Acute cardiac failure may also be a cause of epileptic sudden death.
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PMID:Central apnea and acute cardiac ischemia in a sheep model of epileptic sudden death. 938 70

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

Carbon monoxide (CO) poisoning is one of the most serious medical emergencies causing life-threatening conditions, including cardiovascular and neurological sequelae. Acute CO poisoning can lead to myocardial ischemia, ventricular arrhythmia, syncope, seizures, and coma. Seizures and other neurological complications in the early stages of presentation are related to severe intoxication in CO poisoning. In such situations, aggressive hyperbaric oxygen therapy is recommended. In CO poisoning, non-convulsive status epilepticus has rarely been observed following hyperbaric oxygen therapy (HBO2). We report a case of CO poisoning presenting as non-convulsive status epilepticus treated with HBO2. Mechanisms and implications for non-convulsive status epilepticus provocation during HBO2 treatment are discussed.
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PMID:Carbon Monoxide Poisoning Presenting as Non-Convulsive Status Epilepticus Treated with Hyperbaric Oxygen Therapy. 3080 6