Incidence and outcomes of childhood status epilepticus in Kano, northern Nigeria.

How to Cite this Article: Fallah R, Yadegari Y, Salmani Nodushan M. Efficacy and Safety of Intravenous Sodium Valproate in Convulsive Status Epilepticus in Children in Shahid Sadoughi Hospital. Iran. J. Child. Neurol 2012;6(2):39-44. Objective Status epilepticus (SE) is the most common pediatric neurologic emergency with high mortality and morbidity. There is no consensus on the drug of choice in the treatment of children. The purpose of this study was to evaluate the clinical efficacy and safety of intravenous sodium valproate as a third-line drug in the treatment of generalized convulsive SE of children. Materials & Methods In a retrospective study, medical records of those children who were admitted to Shahid Sadoughi Hospital of Yazd due to refractory generalized convulsive SE and were treated by intravenous sodium valproate as a third-line drug from 2009 to 2011 were evaluated. Results Six girls and five boys with a mean age of 5.12 ± 1.2 years (range: 3 - 9.6 years) were evaluated. Intravenous valproate was effective for cessation of seizures in seven patients (63.6 %). The mean dose of valproate for stopping seizures was 27.1 ± 1.4 mg/kg/day. Children whose seizures were controlled by sodium valproate were older than non- responsive children (mean± SD: 4.8 ± 1.2 years vs. 3.1 ± 0.43 years, p= 0.03) and they also had shorter ICU stay days (mean± SD: 2.6 ± 1.4 days vs. 5.6 ± 2.8 days, p= 0.01). Two children had mild and transient nausea and vomiting. None of them had cardiopulmonary or severe paraclinical side effects. Conclusion Intravenous sodium valproate may be used as an effective and safe third-line antiepileptic drug in the treatment of pediatric generalized convulsive status epilepticus. References Raj D, Gulati S, Lodha R. Status epilepticus. Indian J Pediatr 2011;78(2):219-26. Shearer P, Riviello J. Generalized convulsive status epilepticus in adults and children: treatment guidelines and protocols. Emerg Med Clin North Am 2011;29(1):51-64. Mikati MA. Status epilepticus. In: Kliegman RM, Stanton BF, Schor NF, St. Geme JW, Behrman RE. Nelson textbook of pediatrics. 19th ed. Philadelphia: Saunders; 2011. P. 2013-7. Nair PP, Kalita J, Misra UK. Status epilepticus: Why, what, and how. J Postgrad Med 2011;57(3):242-52. Saz EU, Karapinar B, Ozcetin M, Polat M, Tosun A, Serdaroglu G et al. Convulsive status epilepticus in children: etiology, treatment protocol and outcome. Seizure 2011;20(2):115-8. Nam SH, Lee BL, Lee CG, Yu HJ, Joo EY, Lee J et al. The role of ketogenic diet in the treatment of refractory status epilepticus. Epilepsia 2011;52(11):e181-4. Shiloh-Malawsky Y, Fan Z, Greenwood R, Tennison M. Successful treatment of childhood prolonged refractory status epilepticus with lacosamide. Seizure 2011;20(7):586-8. Abend NS, Monk HM, Licht DJ, Dlugos DJ. Intravenous levetiracetam in critically ill children with status epilepticus or acute repetitive seizures. Pediatr Crit Care Med 2009;10(4):505-10. Chang YC, Lin JJ, Wang HS, Chou ML, Hung PC, Hsieh MY. Intravenous valproate for seizures in 137 Taiwanese children - valproate naive and non-naive. Acta Neurol Taiwan 2010;19(2):100-6. Wheless JW, Vazquez BR, Kanner AM, Ramsay RE, Morton L, Pellock JM. Rapid infusion with valproate sodium is well tolerated in patients with epilepsy. Neurology 2004;63(8):1507-8. Sofou K, Kristjansdottir R, Papachatzakis NE, Ahmadzadeh A, Uvebrant P. Management of prolonged seizures and status epilepticus in childhood: a systematic review. J Child Neurol 2009;24(8):918-26. Visudtibhan A, Bhudhisawadi K, Vaewpanich J, Chulavatnatol S, Kaojareon S. Pharmacokinetics and clinical application of intravenous valproate in Thai epileptic children. Brain Dev 2011;33(3):189-94. Kalviainen R, Eriksson K, Parviainen I. Refractory generalised convulsive status epilepticus: a guide to treatment. CNS Drugs 2005;19(9):759-68. Arif H, Hirsch LJ. Treatment of status epilepticus. Semin Neurol 2008;28(3):342-54. Misra UK, Kalita J, Patel R. Sodium valproate vs phenytoin in status epilepticus: A pilot study. Neurology 2006;67(2):340-2. Kwan SY. The role of intravenous valproate in convulsive status epilepticus in the future. Acta Neurol Taiwan 2010;19(2):78-81. Aldenkamp A, Vigevano F, Arzimanoglou A, Covanis A. Role of valproate across the ages. Treatment of epilepsy in children. Acta Neurol Scand Suppl 2006;184:1-13. Limdi NA, Shimpi AV, Faught E, Gomez CR, Burneo JG. Efficacy of rapid IV dministration of valproic acid for status epilepticus. Neurology 2005;64(2);353-535. Morton LD, O’Hara KA, Coots BP, Pellock JM. Safety of rapid intravenous valproate infusion in pediatric patients. Pediatr Neurol 2007;36(2):81-83. Yu KT, Mills S, Thompson N, Cunanan C. Safety and efficacy of intravenous valproate in pediatric status epilepticus and acute repetitive seizures. Epilepsia 2003;44(5):724-6. Trinka E. The use of valproate and new antiepileptic drugs in status epilepticus. Epilepsia 2007;48 Suppl 8:49-51. Chen L, Feng P, Wang J, Liu L, Zhou D. Intravenous sodium valproate in mainland China for the treatment of diazepam refractory convulsive status epilepticus. J Clin Neurosci 2009;16(4):524-6. Mehta V, Singhi P, Singhi S. Intravenous sodium valproate versus diazepam infusion for the control of refractory status epilepticus in children: a randomized controlled trial. J Child Neurol 2007;22(10):1191-7. Jha S, Jose M, Patel R. Intravenous sodium valproate in status epilepticus. Neurol India 2003;51(3):421-2. Kanner AM. Intravenous valproate for status epilepticus. An effective, yet still merely empirical alternative! Epilepsy Curr 2008;8(3):66-7. Russell S. Carnitine as an antidote for acute valproate toxicity in children. Curr Opin Pediatr 2007;19(2):206- 10. Gilad R, Gilad R, Izkovitz N, Dabby R, Rapoport A, Sadeh M, et al. Treatment of status epilepticus and acute repetitive seizures with i.v. valproic acid vs. phenytoin. Acta Neurol Scand 2008;118(5):296-300.

We have not identified any new high-quality evidence on the efficacy or safety of an anticonvulsant in stopping an acute tonic-clonic convulsion that would inform clinical practice. There appears to be a very low risk of adverse events, specifically respiratory depression. Intravenous lorazepam and diazepam appear to be associated with similar rates of seizure cessation and respiratory depression. Although intravenous lorazepam and intravenous diazepam lead to more rapid seizure cessation, the time taken to obtain intravenous access may undermine this effect. In the absence of intravenous access, buccal midazolam or rectal diazepam are therefore acceptable first-line anticonvulsants for the treatment of an acute tonic-clonic convulsion that has lasted at least five minutes. There is no evidence provided by this review to support the use of intranasal midazolam or lorazepam as alternatives to buccal midazolam or rectal diazepam.

The etiology and prognosis of super-refractory convulsive status epilepticus in children

This paper is written from a pediatric perspective. The starting point in trial design is the identification of important questions, particularly those about therapeutic purposes. The main justification for clinical trials is that status epilepticus is harmful and therefore needs to be treated. In terms of permanent CNS damage and epilepsy following status epilepticus, the rates in published studies vary between 4% and 40% depending on their quality (Raspall-Chaure et al., 2006) and none have looked for subtle cognitive impairments which might be suggested by the finding of acute hippocampal edema following febrile convulsive status epilepticus (CSE) (Scott et al., 2002, 2003). Thus, we are left with a general view that it would be better if we could safely reduce the time that children are convulsing. However, the expense and effort of a randomized controlled trial (RCT) needs to be justified as alternative approaches for example, well-designed epidemiological studies may also provide useful therapeutic information for achieving this goal. The types of questions requiring clinical trial fall into two groups: drug related and clinical approach related.

Incidence, cause, and short-term outcome of convulsive status epilepticus in childhood: prospective population-based study

SummaryBackgroundConvulsive status epilepticus (CSE) is the most common neurological emergency in childhood and is often associated with fever. In sub-Saharan Africa, the high incidence of febrile illnesses might influence the incidence and outcome of CSE. We aimed to provide data on the incidence, causes, and outcomes of childhood CSE in this region.MethodsBetween March, 2006, and June, 2006, we studied all children who had been admitted with CSE to a Kenyan rural district hospital in 2002 and 2003. Confirmed CSE had been observed directly; probable CSE was inferred from convulsions on arrival, requirement for phenobarbital or phenytoin, or coma with a recent history of seizures. We estimated the incidence with linked demographic surveillance, and risk factors for death and neurological sequelae were analysed by multivariable analysis.FindingsOf 388 episodes of CSE, 155 (40%) were confirmed CSE and 274 (71%) were caused by an infection. The incidence of confirmed CSE was 35 (95% CI 27–46) per 100 000 children per year overall, and was 52 (21–107) and 85 (62–114) per 100 000 per year in children aged 1–11 months and 12–59 months, respectively. The incidence of all CSE was 268 (188–371) and 227 (189–272) per 100 000 per year in these age-groups. 59 (15%) children died in hospital, 81 (21%) died during long-term follow-up, and 46 (12%) developed neurological sequelae. Mortality of children with confirmed CSE while in hospital was associated with bacterial meningitis (adjusted relative risk [RR]=2·6; 95% CI 1·4–4·9) and focal onset seizures (adjusted RR=2·4; 1·1–5·4), whereas neurological sequelae were associated with hypoglycaemia (adjusted RR=3·5; 1·8–7·1) and age less than 12 months (adjusted RR=2·5; 1·2–5·1).InterpretationPrevention of infections and appropriate early management of seizures might reduce the incidence and improve the outcome of CSE in children in sub-Saharan Africa.

Purpose: We studied the detailed practical procedures and management of the complications of pentobarbital (PTB) therapy for convulsive status epilepticus (C‐SE) in children with epilepsy. Methods: Eighty‐six episodes of C‐SE in 24 children with epilepsy that could not be abolished by intravenous administration (i.v.) of diazepam (DZP) and phenytoin (PHT) were given i.v. PTB. If C‐SE continued, lidocaine was given i.v. followed by drip infusion (d.i.v.). When C‐SE still continued, d.i.v. PTB was started under continuous EEG monitoring, and the dosages were increased until a burst suppression pattern (BSP) on the EEG, consisting of one burst per 10 s of suppression, or complete EEG suppression (CS) was obtained. The subjects included diagnoses of frontal lobe epilepsy (15 cases). other localization‐related epilepsies (two cases), Lennox‐Gastaut syndrome (four cases), and other symptomatic generalized epilepsies (three cases). Results: Seventy‐one episodes were terminated with i.v. PTB alone. C‐SE was completely abolished by one or more doses of PTB. 2.5–12.0 (mean, 4.6) mg/kg. during 61 episodes, and incompletely terminated by one or more doses of PTB, 1.5–10.0 (4.5) mg/kg, during 10 episodes. Mild respiratory depression developed during one episode with i.v. PTB, 5.4 mg/kg; however, this seemed to he caused by the previous administration of high doses of DZP, PHT, and phenobarbital (PB). Fifteen episodes required div. PTB. C‐SE was completely abolished by one d.i.v. course in 10 episodes and by two d.i.v. courses in two episodes; however, three episodes in three patients could not be stopped by two to four d.i.v. courses. The initial and maximal d.i.v. dosages were 0.5–2.0 (1.1) mg/kg/h and 0.5–4.0 (2.4) mg/kg/h in the successful cases, and 1.0–3.0 (1.8) mg/kg/h and 2.0–5.0 (3.4) mg/kg/h in the unsuccessful cases. Among 14 trials of d.i.v in 12 successful episodes, attempt of PTB discontinuation started based on BSP for 13–45 (30) h in nine trials, CS for 3348 (40) h in two trials, cessation of C‐SE for 9–17 (13) h in two trials, and hypotension in one trial. Among nine trials of PTB in three unsuccessful episodes, PTB could not be discontinued despite BSP for 17–82 (39) h in four trials and CS for 37–81 (56) h in three trials, and PTB was discontinued owing to poor general condition, administration of prednisolone, and surgical intervention. During PTB discontinuation, 10 of 15 episodes needed supportive therapy including i.v. PHT, DZP, or PTB, intramuscular PB. or rectal DZP or PB. Complications with d.i.v. PTB included respiratory depression requiring mechanical ventilation in 13 of 15 episodes, hypotension treated with vasopressors in 11 of 15, PTB precipitation and occlusion of the d.i.v. line in 10 of 15, markedly increased the C‐reactive protein (CRP) value in 13 of 15, decreased bowel movement or ileus in six of 15, and vasculitis in five of 15. Mechanical ventilation and vasopressors were not required until >1.5 mg/kg/h and >2.0 mg/ kg/h of PTB. PTB precipitation could be prevented by undiluted PTB or >10 times diluted PTB. Central venous line placement or highly diluted PTB solution could prevent vasculitis. Conclusions: PTB was effective and safe even by i.v., and d.i.v. was not mandatory in the treatment of C‐SE. Tapering of PTB in d.i.v. could be started after 30–40 h of BSP or CS. Mechanical ventilation and vasopressors were not needed until >1.5 mg/kg/h and >2.0 mg/kg/h of PTB. PTB precipitation could be prevented by using >I0 times diluted PTB or undiluted PTB. Caution must be paid to increased CRP, vasculitis, and ileus.

Intravenous levetiracetam in Thai children and adolescents with status epilepticus and acute repetitive seizures.

Background: Present study was undertaken to study the clinical profile, immediate outcome and possible risk factors for mortality in children with convulsive status epilepticus, admitted in pediatric intensive care unit in a tertiary care centre.Methods: This retrospective descriptive study included children between 1 month and 12 years of age admitted in pediatric intensive care unit with convulsive status epilepticus from April 2016 to March 2017. They were evaluated for their clinical presentation, laboratory parameters and immediate outcome. Data were gathered on 52 patients with convulsive status epilepticus. Factors were analysed using univariate and multivariate analyses.Results: Among the 52 patients, the observations made were, common age group1-5years (51%), males (63%), wih fever (62%), idiopathic seizures (41.5%), febrile status epilepticus (22.7%) abnormal eeg (9.4%), leuocytosis (54.7%), csf abnormalities (33%), prolonged seizures (33%), need for intubation (31%), shock (29%), mortality (9.4%).Conclusions: Clinical profile of children with convulsive status epilepticus is described. Presence of shock, need for intubation and prolonged seizures are significantly associated with mortality.

Status epilepticus is common in patients admitted to hospitals in resource poor countries (RPC). However, there appear to be differences in the epidemiology, aetiology and outcome of status epilepticus in these regions compared to the West, although there is little data from the former regions. RPC countries are those classified by the World Bank as low income or middle-low income countries encompass those situated in the tropical and subtropical regions. The International League Against Epilepsy (ILAE) definition of status epilepticus (ILAE, 1993) is problematic in these areas, since patients often present to health facilities, without adequate documentation of the duration of convulsion. Thus more pragmatic definitions have been developed (Sadarangani et al., 2008). Most studies on status epilepticus in RPC describe convulsive status epilepticus (CSE) (Misra et al., 2008;Sadarangani et al., 2008), since non-convulsive epilepticus is rarely detected in these regions. Although one study non-convulsive status epilepticus was detected in 11% of adults with altered mental status (Narayanan and Murthy, 2007). The incidence of convulsive status epilepticus appears to be higher in RPC than the West, but there has been only one epidemiological study conducted. In this study, the incidence of children fulfilling the ILAE definition of CSE who presented to a Kenyan District General Hospital was 35/100,000/year, with 268/100,000/year in children aged 1-11 months old. The incidence is higher if those with probable epilepsy are also included (35/100,000/year, with 268/100,000/year). These figures are likely to be an underestimate; since many children with CSE are not admitted hospital, either because convulsions are thought to be caused by traditional causes or the children die before they reach hospital. Thus the rate in this area of Kenya is 2-5 times that of similar study in London, United Kingdom (Chin et al., 2006). CSE appears to be more common in children than adults; mainly because acute symptomatic seizures or febrile status epilepticus are more common, particularly in RPC(Sadarangani et al., 2008;Tabarki et al., 2001). A significant proportion of people with epilepsy in RPC have an episode of CSE, usually in childhood and often as the first reported seizure. Thus in a cross-sectional study of active convulsive epilepsy in Kenya, 35% of those identified with active convulsive epilepsy had a history of prolonged seizures (probable CSE), of which 75% were associated with a febrile illness(Edwards et al., 2008). Thus, the high incidence of acute symptomatic epilepsy in many RPC may account for the increased incidence and prevalence of epilepsy in these regions. Most CSE is symptomatic, with the increased incidence attributed to the increased incidence of infections (Misra et al., 2008;Sadarangani et al., 2008). In malaria endemic areas, malaria is an important cause of CSE in children (Sadarangani et al., 2008), whist bacterial meningitis and viral encephalitis are important causes in other areas (Murthy et al., 2007). Patients appear to be in status for longer periods, although there is little reliable data on the duration of CSE in patients presenting to hospital. The increase duration may be due to the lack of treatment prior to admission to hospital, inadequate treatment on admission to hospital and/or a reduction in the responsiveness to the benzodiazepines. The mortality associated with CSE in RPC is greater (11-15%), both in adults (Murthy et al., 2007) and children (Sadarangani et al., 2008); but the long-term outcome in terms of premature mortality and neurocognitive sequelae is undetermined. Risk factors for mortality i.e. young age (< 1 years), aetiology (particularly bacterial meningitis), focal seizures and duration of seizure, are similar to the West. The neuro-cognitive outcome of CSE appears worse with 36% of Tunisian children having intellectual disability or epilepsy (Tabarki et al., 2001). The risk factors for neuro-cognitive impairment include young age (<1 year), focal seizures. Many hospitals in RPC, particularly those in rural areas have few drugs to treat CSE, and many hospitals do not have intensive care facilities such as ventilators or sufficient staff to provide optimal management. The antiepileptic drugs are limited to benzodiazepines, particularly Diazepam and Phenobarbital. However, the response to diazepam appears poorer in many areas, either because the patients present with seizures lasting many hours or possibly the aetiology such as malaria makes them more resistant to these compounds. The treatment of CSE in RPC is further complicated by the lack of rectal preparations of diazepam (parenteral preparation is often used, but has erratic absorption (Ogutu et al., 2002)) and lack of supply of parenteral Phenobarbital (Wilmshurst and Newton, 2005). These issues may affect the outcome. Thus, CSE appears to be more common, with a worse outcome in RPC than in the West; but at present, there is little data on which to base the burden and recommendations of treatment in these countries.

Convulsive status epilepticus in children: Etiology, treatment protocol and outcome

The prognosis of convulsive status epilepticus (CSE), a common childhood medical neurological emergency, is not well characterised. We aimed to investigate the long-term outcomes in a cohort of participants who previously had CSE. In this prospective study, we followed up a population-based childhood CSE cohort from north London, UK (the north London convulsive status epilepticus surveillance study cohort; NLSTEPSS). We collected data from structured clinical neurological assessment, neurocognitive assessment (Wechsler Abbreviated Scale of Intelligence), brain MRI, medical records, and structured interviews with participants and their parents to determine neurological outcomes, with adverse outcome defined as presence of one or more of epilepsy (active or in remission), motor disability, intellectual disability, or statement of special educational needs. We applied multiple imputation to address missing data and performed binary logistic regression analyses on complete-case and imputed datasets to investigate sociodemographic and CSE factors associated with adverse outcomes. Of 203 survivors (90% of inception cohort), 134 (66%) were assessed at a median follow-up of 8·9 years (IQR 8·2-9·5). The cumulative incidence of epilepsy was 24·7% (95% CI 16·2-35·6), with most (89%) emerging within 18 months after CSE. The cumulative incidence of epilepsy was lower in patients with prolonged febrile seizures (14·3%, 6·3-29·4) and survivors of acute symptomatic CSE (13·3%, 3·7-37·9) than in those of remote symptomatic CSE (45·5%, 21·3-72·0) and unclassified CSE (50·0%, 25·4-74·6). One participant (2·9%, 0·5-14·5) in the prolonged febrile seizures group developed temporal lobe epilepsy with mesial temporal sclerosis. The absence of fever at CSE was the only predictor of incident epilepsy (odds ratio [OR] 7·5, 95% CI 2·25-25·1). Motor and intellectual disability was seen predominantly in participants who had idiopathic and cryptogenic CSE (seven [36·8%, 95% CI 19·1-59·0] and 16 [84·2%, 62·4-94·5] of 19, respectively) and remote symptomatic CSE (33 [62·3%, 48·8-74·1] and 40 [75·5%, 62·4-85·1] of 53), and most of these participants had pre-existing disabilities. Pre-existing epilepsy was the only predictor of intellectual disability (OR 8·0, 95% CI 1·1-59·6). 51·5% (95% CI 43·1-59·8) of those followed up had a statement of special educational needs. Childhood CSE is associated with substantial long-term neurological morbidity, but primarily in those who have epilepsy, neurological abnormalities, or both before the episode of CSE. Survivors without neurological abnormalities before CSE have favourable outcomes. BUPA Foundation, The Academy of Medical Sciences, Wellcome Trust, National Institute for Health Research, and Young Epilepsy.

The risk of long-term mortality and its predictors following convulsive status epilepticus in childhood are uncertain. We report mortality within 8 years after an episode of convulsive status epilepticus, and investigate its predictors from a paediatric, prospective, population-based study from north London, UK. In the current study, we followed-up a cohort previously ascertained during a surveillance study of convulsive status epilepticus in childhood. After determining the survival status of the cohort members, we defined cause of death as that listed on their death certificates. We estimated a standardized mortality ratio to compare mortality in our cohort with that expected in the reference population. Multivariable Cox regression analysis was used to investigate any association between the clinical and demographic factors at the time of status epilepticus and subsequent risk of death. The overall case fatality was 11% (95% confidence interval 7.5-16.2%); seven children died within 30 days of their episode of convulsive status epilepticus and 16 during follow-up. The overall mortality in our cohort was 46 times greater than expected in the reference population, and was predominantly due to higher mortality in children who had pre-existing clinically significant neurological impairments when they had their acute episode of convulsive status epilepticus. Children without prior neurological impairment who survived their acute episode of convulsive status epilepticus were not at a significantly increased risk of death during follow-up. There were no deaths in children following prolonged febrile convulsions and idiopathic convulsive status epilepticus. A quarter of deaths during follow-up were associated with intractable seizures/convulsive status epilepticus, and the rest died as a complication of their underlying medical condition. On regression analysis, presence of clinically significant neurological impairments prior to convulsive status epilepticus was the only independent risk factor for mortality. In conclusion, there is a high risk of death within 8 years following childhood convulsive status epilepticus but most deaths are not seizure related. Presence of pre-existing clinically significant neurological impairments at the time of convulsive status epilepticus is the main risk factor for mortality within 8 years after the acute episode. The attributable role of convulsive status epilepticus on mortality remains uncertain, but appears less than is generally perceived.

Tonic-clonic (grand mal) convulsions and convulsive status epilepticus (currently defined as a grand mal convulsion lasting at least 30 minutes) are medical emergencies and demand urgent and appropriate anticonvulsant treatment. Diazepam, lorazepam, phenobarbitone, phenytoin and paraldehyde may all be regarded as drugs of first choice. To review the evidence comparing diazepam, lorazepam, phenobarbitone, phenytoin and paraldehyde in treating acute tonic-clonic convulsions and convulsive status epilepticus in children. We searched the Cochrane Epilepsy Group's specialized register (4 July 2002); the Cochrane Controlled Trials Register (Cochrane Library Issue 2, 2002); MEDLINE (28 May 2002) and EMBASE (January 2002). Randomized controlled trials comparing lorazepam and other anticonvulsant drugs used for the treatment of convulsive status epilepticus in children. This was a review of published, aggregate data. The main outcome measures included cessation of the presenting tonic-clonic convulsion/episode of convulsive status epilepticus; the number of additional drugs required to stop the convulsion; people demonstrating respiratory depression and people requiring admission to the intensive care unit because of respiratory depression. Only one trial was found, in which children were allocated lorazepam or diazepam. The main results are as follows. (1) One or two intravenous doses stopped the convulsion in 19 of 27 (70%) lorazepam and 22 of the 34 (65%) intravenous diazepam-treated children. The relative risk (RR) with 95% confidence intervals (CIs) was 1.09(95% CI 0.77 to 1.54). A single dose of rectal lorazepam stopped the convulsion in six of six, compared to six of 19 children treated with rectal diazepam, RR 3.17(95% CI 1.63 to 6.14). (2) Six of the 27 (22%) intravenous lorazepam and 12 of the 34 (35%) intravenous diazepam-treated children respectively, experienced a further convulsion within 24 hours after presentation RR 0.63(95% CI 0.27 to 1.46). (3) Only one of 27 children (4%) who received intravenous lorazepam compared to five of 34 children (15%) who received intravenous diazepam required additional antiepileptic drugs to terminate the presenting seizure RR 0.25(95% CI 0.03 to 2.03). (4) A lower incidence of respiratory depression occurred in the lorazepam-treated group: one of 27 (4%) children compared to seven of 34 in the diazepam-treated group (21%), RR 0.21(95% CI 0.02 to 1.37). This review provides no evidence to suggest that intravenous lorazepam should be preferred to diazepam as the first-line drug in treating acute tonic-clonic convulsions including convulsive status epilepticus in children. There was some evidence from this review that rectal lorazepam may be more effective and safer than rectal diazepam, but the data were insufficient to indicate that lorazepam should replace diazepam as the first choice rectal drug in treating acute tonic-clonic convulsions and convulsive status epilepticus.

Convulsive status epilepticus (CSE) is a common neurological emergency. Our objectives were to study children with recurrent nonfebrile CSE to assess the evidence for focal origin. Series of 18 children with recurrent CSE and intractable epilepsy were identified by chart review. Clinical, radiological, and EEG data were reviewed. Focal structural abnormalities were identified on MRI and CT images by one neuroradiologist who was unaware of the clinical details. The patient's ages ranged between 6-22 years (mean 15.3, SD 4), and 67% were males. Most children (89%) had a severe cognitive and / or behavioural disorder. Most patients (89%) had multiple seizure types and 95% of these were partial seizures. Twelve (67%) children had at least one episode of CSE with focal features identified clinically. Focal brain abnormalities were detected on 18% and 55% of CT and MRI films respectively. Overall, 53% had a focal abnormality on structural neuroimaging. Interictal EEG revealed focal or multifocal abnormalities on at least one occasion in 94% and 22% of patients respectively. Overall, 17 patients had focal features on at least one EEG. Thirteen ictal EEGs were recorded on 11 (61%) patients. Ten (91%) of these recordings revealed a focal onset. Many handicapped children with recurrent CSE have focal clinical, radiological, or electrographic features. This supports a focal origin for CSE in most children with intractable epilepsy.