咪达唑仑治疗儿童癫痫持续状态的临床分析

目的观察咪达唑仑治疗儿童癫痫持续状态的疗效及副作用。方法本组所有病儿均在使用安定、鲁米那无效后改用咪达唑仑。建立咪达唑仑专用静脉通道，首次按0．1—0．3mg／kg剂量静脉推注，随之以1μg·kg^-1·min^-1速度持续静脉滴注。如发作不缓解，每15分钟以1μg·kg^-1·min^-1幅度加量，直到缓解为止。对患儿的发病年龄、抽搐控制情况、控制抽搐的用药量、药物起效时间、用药后病儿恢复清醒状态时间和药物的毒副作用进行系统观察。结果本组发病年龄跨度为0．02～14岁，平均年龄为4．55岁，1-3岁为发病高峰（占总发病的48．0％）；控制发作的药物有效范围是1～6μg·kg^-1·min^-1,平均为2．69μg·kg^-1·min^-1；控制抽搐时间最短15min以内，最长90min，平均时间为40．34min；癫痫控制，停止药物输注，病人完全恢复神志的时间最短2h，最长6．5h，平均3．6h；1例出现瞳孔轻微缩小，其余病例均未发现血压、心率、血氧饱和度和呼吸状态的变化，更未出现肝肾功能异常。结论咪达唑仑治疗癫痫持续状态起效快，效果好，毒副作用小，应首选用于治疗难控制癫痫持续状态。     

咪达唑仑对成人癫痫持续状态的疗效观察

目的探讨咪达唑仑静脉持续输注治疗成人癫痫持续状态的疗效。方法选择23例成人癫痫持续状态作为研究对象,先予咪达唑仑0．1mg／kg静脉注射后予0．1mg／（kg·h）静脉持续输注,如癫痫再发作,加用咪达唑仑0．1mg／kg静脉注射并以0．05mg／（kg·h）幅度加量,直到惊厥控制,如果给药剂量达0．6mg／（kg．b）时,癫痫未控制考虑无效,不再加大用药剂量。如持续24h无癫痫发作,予逐渐减量,每12h以0．05～0．1mg／（kg·h）减量直至停用。所有患者同时胃肠道给予其他1至3种抗癫痫药物,并积极治疗原发病和并发症等处理。结果13例显效,7例有效,3例无效,总有效率为86．96％,3例出现低血压,经小剂量多巴胺升压及适当补液后纠正;2例出现呼吸减慢,血氧饱和度尚维持90％以上,未予特殊处理。结论静脉持续输注咪达唑仑是治疗癫痫持续状态的安全有效方法,值得推广。     

咪哒唑仑治疗成人癫痫持续状态的研究

目的:探讨咪哒唑仑治疗癫痫持续状态(SE)的疗效和副作用.方法:将2007年1月-2010年6月收治SE患者70例随机分为治疗组(n＝35)和对照组(n＝35),治疗组和对照组分别应用咪达唑仑和地西泮治疗,方法:(0.15-0.2) mg/kg静脉推注,(0.1-0.6)mg/(kg·h)速度持续静脉泵入,不缓解者以(0.1-0.5)μg/( kg·min)的速度加量,直至完全缓解,最大量不超过3 μg/( kg·min);发作控制24 h后开始减量,48 h后停药.结果:治疗组起效时间明显短于对照组,疗效明显优于对照组,P均＜0.05.结论:咪哒唑仑治疗SE起效快,疗效好,副作用小,可作为SE的首选治疗方法,建议临床推广应用.     

咪达唑仑联合苯巴比妥、地西泮治疗小儿惊厥性癫痫持续状态的临床研究

目的探讨咪达唑仑联合苯巴比妥、地西泮治疗小儿惊厥性癫痫持续状态(convulsive status epilepticus,CSE)的临床效果及安全性。方法选取我院2016年10月—2017年10月收治的103例小儿CSE,根据治疗方法的不同分为观察组(n=56)和对照组(n=47)。两组均予地西泮、苯巴比妥及常规治疗,在此基础上,观察组加用咪达唑仑。比较两组临床疗效,记录治疗前后癫痫持续状态严重程度评分量表(status epilepticus severity score,STESS)评分变化以评估预后,观察不良反应发生情况及出院后1年后遗症发生情况。结果观察组、对照组治疗总有效率分别为91. 07%、72. 34%,不良反应总发生率分别为14. 29%、31. 91%,后遗症总发生率分别为14. 29%、31. 91%,比较差异均有统计学意义(P 0. 05)。与对照组比较,观察组治疗后STESS评分降低,差异有统计学意义(P 0. 05);与本组治疗前比较,两组治疗后STESS评分下降,差异有统计学意义(P 0. 05)。结论咪达唑仑联合苯巴比妥、地西泮治疗小儿CSE可显著提高临床疗效,减轻脑损伤,改善预后,且安全性较好。     

硫喷妥钠和咪达唑仑治疗难治性癫痫持续状态的疗效比较

难治性癫痫持续状态是神经内科常见的疾病,及时控制难治性癫痫持续状态可有效减少死亡率和致残率,目前难治性癫痫持续状态的治疗是临床最棘手的问题之一。本研究采用硫喷妥钠治疗难治性癫痫持续状态,并与咪达唑仑进行效果比较,现报告如下。
　　1资料与方法
　　1．1一般资料
　　选取2010年4月-2014年4月在本院住院治疗的难治性癫痫持续状态患者40例。本组难治性癫痫持续状态的诊断符合以下标准：①癫痫持续发作超过2h以上,或2h内反复发作,间歇期意识未恢复正常;②均为强直-阵挛发作,有意识障碍;③经反复静脉推注安定、苯巴比妥、氯硝安定无效。排除标准：①单纯部分发作持续状态,无意识障碍;②有继发性头部外伤,无法行脑电图监测。本组患者发作时昏迷、发绀、呼吸加快或呼吸不规则,心动过速或心律失常,甚至出现高热、酸中毒、脑水肿和呼吸、循环衰竭等濒危状态。将40例患者分为咪达唑仑组21例,其中男12例,女9例,平均年龄为（44．7±16．7）岁;病因：脑外伤16例,急性细菌性脑膜炎2例,急性病毒性脑膜炎1例,颅内出血2例;硫喷妥钠组19例,其中男10例,女9例,平均年龄为（45．7±17．1）岁;病因：脑外伤14例,急性病毒性脑膜炎2例,颅内出血3例。2组患者采用ApacheII 评分：咪达唑仑组（23．2±7．8）分,硫喷妥钠组（24．1±6．9）分。2组患者的临床资料具有可比性（P＞0．05）。     

咪达唑仑治疗小儿癫痫持续状态的疗效观察

癫痫持续状态（status epilepticus SE）是指癫痫发作30分钟以上或反复发作间期意识不能恢复。目前大多数学者认为成年人及5岁以上儿童SE的诊断指全身性惊厥性癫痫发作,持续5分钟或5分钟以上,或两次或更多次的发作,发作间期意识仍不能恢复。将SE定在5分钟,有利于全身性强直-阵挛性发作时尽早抢救。惊厥持续可产生不可逆的脑损伤,惊厥时间越长,脑损伤就越严重,甚至危及生命。     

硫喷妥钠和咪达唑仑治疗难治性癫痫持续状态的疗效观察

难治性癫痫持续状态(refractory status epilepticus, RSE)通常是指经足量一线、二线抗癫痫药物(简称AEDS,如安定、劳拉西泮、苯巴比妥及苯妥英钠等)治疗不能控制持续的癫痫发作且持续1 h以上者.     

持续静脉泵入咪达唑仑治疗小儿癫痫持续状态的护理

本文探讨应用持续静脉泵入咪达唑仑治疗小儿癫痫持续状态的护理。应用持续静脉泵入咪达唑仑治疗22例小儿癫痫持续状态,观察其疗效、副作用,并对其副作用采取相应的护理措施。应用持续静脉泵入咪达唑仑能维持有效的血药浓度,治疗过程顺利,控制癫痫持续状态有效率达90．9％,副作用少,无严重并发症。同时密切观察患儿生命体征,保持静脉通道通畅。     

系统护理干预在持续静脉泵入咪达唑仑治疗小儿癫痫持续状态的临床护理应用

目的研究和探讨系统护理干预在持续静脉泵入咪达唑仑治疗小儿癫痫持续状态中的护理效果和应用价值。方法选择本院2014年11月~2016年11月收治的应用持续静脉泵入咪达唑仑治疗的癫痫患儿90例,随机分为对照组和观察组各45例。对照组患儿采用常规护理,观察组患者使用护理干预模式,对比和分析两组患儿临床治疗情况。结果观察组患儿临床治疗有效率为93.33%明显高于对照组的71.11%,且临床不良反应发生率为8.89%明显低于对照组的24.44%。结论应用持续静脉泵入咪达唑仑治疗小儿癫痫持续状态的同时采用系统干预护理措施,能够显著提高患儿的临床治疗效果,降低不良反应发生率,具有推广价值。     

持续性静脉泵入咪达唑仑治疗癫痫持续状态的护理干预效果分析

目的探讨持续性静脉泵入咪达唑仑治疗癫痫持续状态的护理干预效果。方法选取2013年8月至2014年8月本院收治的癫痫患者70例,按照随机数字表法分为研究组和对照组各35例,两组均给予咪达唑仑持续性静脉泵入,研究组给予护理干预,对照组给予常规护理,比较两组临床疗效和不良反应。结果研究组总有效率94.3%(33/35)明显高于对照组的71.4%(25/35),差异有统计学意义(P0.05);研究组不良反应发生率明显低于对照组,差异有统计学意义(P0.05)。结论持续静脉泵入咪达唑仑加护理干预治疗癫痫持续状态具有较好的临床疗效,能明显降低不良反应的发生。     

小儿癫(癎)持续状态36例临床分析

目的总结不同类型小儿癫持续状态(SE)的临床、脑电图特点及治疗反应,提高诊断及治疗水平。方法对36例临床发作及脑电图监测符合SE的患儿按发作类型进行分类,分析不同类型发作特点、病因、脑电图变化及治疗反应。结果症状性癫19例,隐源性癫14例,特发性癫3例。既往SE史14例,4例为首次发作。10例发病前智力、运动发育落后,5例发病后倒退。12例诊断为癫综合征。不同发作类型脑电图改变不同。非惊厥性癫持续状态(NCSE)患儿脑电图均表现为背景活动差,慢波多,其中4例伴有睡眠中癫性电持续状态。12例给予氯硝西泮,11例有效控制。结论不同类型的SE发作形式及脑电图表现不同,NCSE更为复杂,早期诊断和处理可提高生存率,减少神经后遗症的发生。     

全面性癫痫持续状态的治疗现状

全面性癫痫持续状态是癫痫持续状态中最严重的类型，是神经科一种急诊。本文就近年来有关全面性癫痫持续状态的流行病学、病因、药物治疗的研究现状进行阐述。     

万可松联合呼吸机辅助呼吸治疗顽固性癫痫持续状态

目的 探讨万可松联合呼吸机辅助呼吸治疗6例顽固性癫痫持续状态患者的疗效。方法 对于采用常规抗癫痫治疗12h后无效的顽固性癫痫持续状态的6例患者,均应用静脉注射万可松联合气管切开、呼吸机辅助呼吸治疗7～15d以控制癫痫发作。结果 6例患者癫痫发作症状得到明显控制,药物起效时间3～6h,停药后平均自动转复时间为30～60min;疗程中未出现与治疗相关的呼吸、循环功能障碍,患者均安全出院。结论 万可松联合呼吸机辅助呼吸治疗顽固性癫痫持续状态是安全、有效、可行的。     

High-dose midazolam therapy for refractory status epilepticus in children

Objective To assess the efficacy of high-dose midazolam in the treatment of refractory status epilepticus in children.Setting Paediatric intensive care unit (PICU).Design Audit of clinical experience.Subjects Seventeen consecutive patients treated for episodes of refractory status epilepticus.Interventions Algorithm-driven administration of intravenous midazolam to control RSE. Regular, mandatory, patient evaluation to avoid delay in the appropriate escalation of therapy. Our target was the abolition of clinical seizures within 30 min of initiating treatment and early confirmation of cessation of all seizure activity using EEG. The algorithm had failed if clinical seizures persisted beyond 30 min despite the administration of midazolam at 24 μg/kg/min or if administration of a further acute anti-epileptic drug was required to achieve seizure control.Measurements The midazolam infusion rate, cumulative midazolam dose and duration of midazolam therapy at time of clinical seizure control were recorded. Haemodynamic parameters were recorded continuously. Episodes of algorithm failure, breakthrough seizures and seizure relapses were identified. Patient outcome was measured in terms of survival to PICU discharge.Results In 13 patients (76%) midazolam achieved clinical seizure control within 30 min of treatment initiation. Midazolam was eventually successful in treating 15 seizure episodes (88%). Breakthrough seizures occurred in 8 patients (47%). Relapse after discontinuation of therapy occurred in 1 patient (6%). No significant adverse effects attributable to the use of midazolam occurred. There were 3 deaths (18%) related to underlying CNS pathology.Conclusions Midazolam can offer control of refractory status epilepticus without significant morbidity.This article is discussed in the editorial available at:     

Pathophysiology and definitions of seizures and status epilepticus

The pathophysiology of seizures is multifactorial and incompletely understood. Experimental work demonstrates that prolonged, abnormal, and excessive neuronal electrical activity in itself is injurious through several mechanisms independent of systemic acidosis and hypoxia. Population survival studies and laboratory investigations support the idea that brain injury and epileptogenesis result from status epilepticus. The basic distinction in seizure types is that of generalized and partial seizures. Correct classification of seizure types will aid in clinical communications and guide correct therapies. Revised definitions of generalized convulsive status epilepticus suggest making this diagnosis with as few as 5 minutes of continuous seizure activity.     

Nonconvulsive status epilepticus

A 49-year-old man presented with dizziness and altered behavior associated with a nonconvulsive seizure. He had a long history of well-controlled tonic-clonic seizures and daily episodes of 10-second staring spells. Despite normal neurological and laboratory examinations, an emergent electroencephalogram showed changes consistent with nonconvulsive generalized status epilepticus.     

Generalized convulsive status epilepticus in adults and children: treatment guidelines and protocols

Generalized convulsive status epilepticus (GCSE) has a high morbidity and mortality, such that the rapid delivery of anticonvulsant therapy should be initiated within minutes of seizure onset to prevent permanent neuronal damage. GCSE is not a specific disease but is a manifestation of either a primary central nervous system (CNS) insult or a systemic disorder with secondary CNS effects. It is mandatory to look for an underlying cause. First-line therapies for seizures and status epilepticus include the use of a benzodiazepine, followed by an infusion of a phenytoin with a possible role for intravenous valproate or phenobarbital. If these first-line medications fail to terminate the GCSE, treatment includes the continuous infusion of midazolam, pentobarbital, or propofol.     

Fulminant hepatic failure associated with status epilepticus in children: Three cases and a review of potential mechanisms

Fulminant hepatic failure is a rare complication of status epilepticus. Although many of the anticonvulsants used to treat the seizures are known to have hepatotoxic properties, the exact mechanism leading to massive destruction of the liver following a prolonged seizure remains unclear. Three children are presented who developed fulminant hepatic failure following status epilepticus and subsequently died of multiple organ failure. The literature is reviewed with particular attention to the possible interaction between the anticonvulsants and the metabolic consequences of status epilepticus. We postulate that it is a combination of hypoxia and ischemia that occurs during a prolonged seizure with altered metabolism of free radicals secondary to the anticonvulsant drugs which leads to widespread hepatocyte membrane damage.     

Outcomes in 140 critically ill patients with status epilepticus

Objective Despite recent management guidelines, no recent study has evaluated outcomes in ICU patients with status epilepticus (SE). Design and setting An 8-year retrospective study. Subjects and intervention Observational study in 140 ICU patients with SE, including 81 (58%) with continuous SE and 59 (42%) with intermittent SE (repeated seizures without interictal recovery). Measurements and results The 95 men and 45 women had a median age of 49 years (IQR 24–71). Median seizure time was 60 min (IQR 20–180), and 58 patients had seizures longer than 30 min. The SE was nonconvulsive in 16 (11%) patients and convulsive in 124 (89%), including 89 (64%) with tonic-clonic generalized seizures, 27 (19%) with partial seizures, 7 (5%) with myoclonic seizures, and 1 with tonic seizures. The most common causes of SE were cerebral insult in 53% and anticonvulsant drug withdrawal in 20% of patients. No cause was identified in 35% of patients. Median time from SE to treatment was 5 min (IQR 0–71). The SE was refractory in 35 (25%) patients. Mechanical ventilation was needed in 106 patients. Hospital mortality was 21%. By multivariate analysis, independent predictors of 30-day mortality were age (OR 1.03/year; 95% CI 1.00–1.06), GCS at scene (OR 0.84/point; 95% CI 0.72–0.98), continuous SE (OR 3.17; 95% CI 1.15–8.77), symptomatic SE (OR 4.08; 95% CI 1.49–11.10), and refractory SE (OR 2.83; 95% CI 1.06–7.54). Conclusion Mortality in SE patients remains high and chiefly determined by seizure severity. Further studies are needed to evaluate the possible impact of early maximal anticonvulsant treatment on outcomes. An erratum to this article can be found at