癲癇持續(xù)狀態(tài)nicu課件

Statusepilepticus

SE

首都醫(yī)科大學(xué)宣武醫(yī)院神經(jīng)內(nèi)科N-ICU宿英英BackgroundStatusepilepticus(SE)isacommonlife-threateningneurologicaldisorder.Itisessentiallyanacute,prolongedepilepticcrisis.ThefirstdescriptionofSEinthemedicalliteraturewasaBabyloniantextfromthefirstmillenniumBC.

“Ifanepilepsydemonfallsmanytimesuponhimonagivenday,heseventimespunisheshimandpossesseshim,hislifewillbespared.Ifhefallsuponhimeighttimes,hislifemaynotbespared.“（WilsonandReynolds,1990）

Definition

AusefulworkingdefinitionwasformulatedbytheEpilepsyFoundationofAmerica'sworkinggrouponSE.

“Morethan30minutesofcontinuousseizureactivityortwoormoresequentialseizureswithoutfullrecoveryofconsciousnessbetweenseizures.”（Dodsonetal,1993

）Frequency

IntheUSExtrapolatingfromapopulation-basedstudyinRichmond,estimatedthat50,000-200,000ofstatusepilepticus

casesoccurannuallyintheUnitedStates.（DeLorenzoetal1996）

Mortality

Inthe1998VeteransAdministration（VA）study,theSECooperativeStudyGroupquantitatedmortalityrateat27%forovertgeneralizedconvulsiveSEand65%forsubtlegeneralizedconvulsiveSE.DeLorenzoetal（1995）reportedamortalityrateof21%inpatientswithgeneralizedSE,definingmortalityasdeathoccurringwithin30days.AicardiandChevrie（1970）studied239childrenwithgeneralizedconvulsiveSEthatlastedmorethananhour.11%diedand37%sufferedpermanentneurologicaldamage.MortalityThemortalityratesofSEhavedecreasedoverthepast60yearswhichprobablyisrelatedtofasterdiagnosisandmoreaggressivetreatment.deathcauseddirectlybySEoccursinnomorethan2%ofcases.BothseveresystemicdiseaseandanacuteCNSinsultassociatedwiththeSEpredictapooroutcome.（Hauser1990）

MortalityInprospectivepopulation-basedstudies（DeLorenzoetal）mortalityratefortheentirepopulationwas22%

inyoungadults,itwas13%

perinatalhypoxicinsultsormetabolicdisordersintheelderly,38%inthoseolderthan80years,greaterthan50%hypoxicorischemiccentralnervoussystem（CNS）insultsSystemicchanges

systemicarterialpressuredecreasestolevelsthatarebelowbaseline.

（1961）

MarkedacidosisoccurswithSE（1980

）33%patientshadapHoflessthan

7.0

（AminoffandSimon,1980）acidosisdoesnotcorrelatewiththedegreeofneuronalinjuryacidosisisknowntobeananticonvulsantsystemicchangesHyperthermiamotoractivity.

centralsympatheticdrive.83%patients

hadhyperthermiawithtemperaturesreaching42℃.（AminoffandSimon,1980）poorneurologicaloutcomeandshouldbetreatedaggressively.Marginatingleukocytesarecommon.withoutevidenceofinfectionhadWBCelevationsfrom12,700-28,800.Bandsshouldnotbeseen.Cerebrospinalfluid（CSF）pleocytosisiscommonbutthecellcountelevationsareusuallymodest.Only4of65patientshadgreaterthan30cellsintheCSF

（AminoffandSimon,1980）.

GCSE

ClinicalandEEG（２）

Iftheconditionisnottreatedoristreatedinadequately,theSEpersistsandthemotormanifestationsbecomelessandlessdramatic.Eventually,onlysubtlemovementssuchasnystagmoidjerksoftheeyesortwitchingoftheshouldermaybeseen（ie,subtlestatus）.IfSEcontinues,allmotoractivitymaystop,althoughelectrographicseizurespersist（ie,electricalgeneralizedconvulsiveSE）.GCSE

ClinicalandEEG（3）Theparadoxicalevolutionofapparentclinicalimprovementisimportanttounderstand.Theclinicianunfamiliarwiththisphenomenonmaystoptreatmentbecauseoftheapparentimprovement.Treatmentshouldbecontinueduntiltheelectrographicseizureactivityhasresolvedcompletely.Insomepatients,theunderlyingencephalopathicinsultissoseverethatonlyafew(orno)generalizedconvulsionsoccurbeforesubtleconvulsiveactivitydevelops.Finally,asthepatientevolvesfromgeneralizedtonic-clonicstatusintosubtleandthenelectricalgeneralizedtonic-clonicSE,themanifestationsbecomelessintermittentandmorecontinuous.PsychogenicseizuresPsychogenicseizuresmay,attimes,beindistinguishablefromGCSEbyappearancealone.unresponsivenesswithoutmovementwasthemostcommonpresentation.asynchronousextremitymovement,forwardpelvicthrusting,andgeotropiceyemovementstheeyesdeviatingtowardthegroundinanonphysiologicmannerwhethertheheadisturnedleftorright.MyoclonusRepetitivemyoclonusinacomatosepatientfollowingdiffusehypoxicbraininjurymaysimulategeneralizedseizures.Thephysiologicoriginofthemyoclonicjerksmaynotbecortical.Themyoclonususuallyislimitedindurationtoseveralhours.Causes（1groups

）

Inroughlyonethirdofcases,anexacerbationofanidiopathicseizuredisorderisthoughttobethecause.（thisisadiagnosisofexclusion）Inpeoplewithknownepilepsy,themostcommoncauseisachangeinmedicationthechangemaybeeitherunderthedirectionofaphysicianorduetononcompliance.NoncomplianceisthemostcommoncauseofSEinpatientswithknownepilepsy.Causes（3）

Amyriadofotherconditionsmayprecipitatestatusepilepticus,includingtoxicormetaboliccausesandanythingthatmightcausecorticalstructuraldamage.Stroke(remoteoracute)HypoxicinjuryTumorSubarachnoidhemorrhageTraumaToxicologic(eg,cocaine,theophylline,isoniazid,alcoholwithdrawal)Electrolyteabnormalities(eg,hyponatremia,hypernatremia,hypercalcemia,hepaticencephalopathy)Infectiousetiology(eg,meningitis,brainabscess,encephalitis)CausesInchildrenyoungerthan16years,themostcommoncausewasfever/infection（36%）;incontrast,thisaccountedforonly5%inadults

（DeLorenzoetal,1995）.Thesamestudyrevealedthatthemostcommonprecipitantforadultswascerebrovasculardisease（25%）,whereasthisfactorcausedonly3%ofpediatriccases.Inamorerefinedstudythatfocusedonchildrenfoundthatmorethan80%ofchildrenyoungerthan2yearshadSEoffebrileoracutesymptomaticorigin,whereascryptogenicandremotesymptomaticcausesweremorecommoninolderchildren（Shinnaretal，1997）

Laboratoryelectrolytestoxicologyscreeningglucoseanticonvulsantlevelscompletebloodcount(CBC)BloodculturesrenalfunctiontestsurinalysisarterialbloodgaseslumbarpunctureImaging

BrainCT/MRIisoftenhelpfultoevaluateforastructurallesionunderlyingSEbraintumor,infarction,abscess,hemorrhage.

Aneuroimagingstudyshouldnotbeallowedtoimpedetherapidandaggressivetreatmentofthedisorder.TreatmentPrehospitalCareSupportivecare,includingABCsHistoriccluesmaybeevidenttoEMSproviders.anticonvulsantsintravenously(IV)orperrectum(PR)diazepam(Valium)

TreatmentEmergencyDepartmentCarepromptterminationofelectricalseizureactivityarethegoals.nasopharyngealairwayplacementforsomepatientsendotrachealintubationforsomepatientsshort-actingneuromuscularparalysisEEGmonitoringInitiaterapidglucosedeterminationandcorrection.EstablishIVaccess,ideallyinalargeveinanticonvulsantmedicationEstablishcardiacandotherhemodynamicmonitoring.TreatmentNoprospective,double-blindstudiesontheofSEhavebeenpublishedrecently.Therefore,thechoiceofthebestinitialdrugtreatmentremainsuncertain.Treimanetal（1998）publishedatreatmentcomparisonforgeneralizedconvulsiveSE,investigatingtheuseofdiazepamfollowedbyphenytoin,lorazepam,phenobarbital.

Anticonvulsantagents

StartanIVline,administer50ccof50%dextroseIVpush,thenstarttheanticonvulsant.Administerdiazepamorlorazepam0.15mg/kgIVover5minutes,followedbyfosphenytoin15-20mgphenytoinequivalents(PE)/kgatamaximumrateof150mg/minorless.IntubateifnecessaryandcontrolhyperthermiaIfseizurescontinueafter20minutes,giveanadditional10mgPE/kgoffosphenytoin.Ifseizurescontinueafter20minutes,giveanadditional10mgPE/kgoffosphenytoin.Ifseizurescontinue,administergeneralanesthesia.GCSE

系統(tǒng)性病理生理兒茶酚胺大量釋放，血壓增高、心率加快、心律失常、血糖升高。GCSE持續(xù)發(fā)作不止，最終血壓下降，心率下降，心功能失代償機(jī)械性呼吸運(yùn)動停止、急性肺水腫、抗癲癇藥物的呼吸中樞抑制作用，呼吸功能障礙，呼吸性酸中毒（有人認(rèn)為酸中毒可結(jié)束癲癇發(fā)作，因此，當(dāng)PH值下降時(shí)，無需加以糾正）肌肉強(qiáng)烈收縮，乳酸鹽增多，代謝性酸中毒，體溫過高體溫中樞受累，體溫＞41℃，神經(jīng)細(xì)胞繼發(fā)損傷多數(shù)癲癇發(fā)作自行終止，終止原因不清；少數(shù)自行終止失敗，原因也不清。Generalizedconvulsivestatusepilepticus陣發(fā)性或持續(xù)性肌肉節(jié)律性強(qiáng)直、陣攣、強(qiáng)直-陣攣意識障礙，發(fā)作間期意識障礙不恢復(fù)GCSE發(fā)作3個(gè)階段顯而易見的GCSE，肌肉節(jié)律性強(qiáng)直、陣攣、強(qiáng)直-陣攣微小而不意識別的GCSE，肌肉運(yùn)動越來越小，甚至變得十分微細(xì)而不易被發(fā)現(xiàn)，如眼皮的眨動或肩的肌肉顫動（twitch）肌肉運(yùn)動停止的電GCSE，異常電活動仍然繼續(xù)伴隨外傷，包括舌咬傷，肩關(guān)節(jié)脫位，頭顱外傷和面部創(chuàng)傷GCSE未予治療或治療不充分，癲癇發(fā)作繼續(xù)AbsencestatusepilepticusEEG雙側(cè)同步節(jié)律性3Hz棘慢復(fù)合波或彌散棘波臨床表現(xiàn)與EEG變化不同步，持續(xù)時(shí)間數(shù)min~數(shù)d突發(fā)意識障礙程度輕，嗜睡或意識混濁自主運(yùn)動減少，語言緩慢伴或不伴其他臨床征象，如定向力障礙，記憶力障礙（癲癇性失記憶），復(fù)雜的自動癥或精神癥狀Complexpartialstatusepilepticus意識障礙程度和EEG異常電活動多樣性、周期性、長久性意識障礙從朦朧狀態(tài)到完全無反應(yīng)EEG從一側(cè)性癲癇樣發(fā)放（PLED）到彌漫性棘慢復(fù)合波節(jié)律異常電發(fā)放的起源通常在顳葉伴隨癥狀與ASE相似，但更豐富Simplepartialstatusepilepticus意識基本正常感覺異常發(fā)作：軀體感覺的、視覺的、聽覺的、嗅覺的、味覺的運(yùn)動異常發(fā)作：軀體運(yùn)動、眼球陣攣、軟腭震顫、語言障礙或失語發(fā)作自主神經(jīng)異常發(fā)作和其它奇異發(fā)作少見

EEG異常電活動（如3Hz棘慢復(fù)合波）具有周期性、局限性、不擴(kuò)展性，異常電活動的部位與臨床感覺或運(yùn)動異常一致，有時(shí)大腦皮層病變非常局限而EEG無異常發(fā)現(xiàn)診斷與鑒別診斷診斷內(nèi)容癲癇的識別癲癇持續(xù)狀態(tài)的確認(rèn)癲癇持續(xù)狀態(tài)類型的區(qū)分癲癇持續(xù)狀態(tài)病因的確定實(shí)驗(yàn)室、影像學(xué)、或其它輔助檢查幫助尋找病因和判斷繼發(fā)損害治療原則積極支持性醫(yī)療與護(hù)理無論是容易判斷的SE，如肢體肌肉連續(xù)大幅度抽動；還是難以識別的SE，如非驚厥性或微小的肌肉顫動；迅速終止癲癇發(fā)作“Seizuresbegetseizures”已經(jīng)成為公認(rèn)的警句。癲癇發(fā)作4min~5min不停止，應(yīng)迅速給予antiepilepticdrug（AED）終止發(fā)作。支持性醫(yī)療與護(hù)理呼吸支持開放通氣道，鼻咽通氣道、氣管插管、機(jī)械通氣建立大靜脈通道矯正異常生理生化指標(biāo)降溫昏迷與氣道護(hù)理用藥原則首