management of status epilepticus an update
TRANSCRIPT
Status Epilepticus-An update
Dr.W.A.P.S.R.WEERARATHNARegistrar in Medicine
Ward 10/02
Objectives…Current definition of status epilepticusClassificationEpidemologyEtiologyClinical manefestations-convulsive/nonconvulsiveDiagnosisTypes of status epilepticusCurrent guidelines for the management of status
epilepticus-Neurocritical care society guide lines-2013
Refferences
Definition-2012 Neurocritical care society Guidelines5 minutes or more of 1.continuous clinical and/or
electrographic seizure activity or 2. recurrent seizure activity without
recovery(returning to baseline) between seizures
classsificationBased on1.Age of onset2.Etiology3.Clinical features4.EEG features
Ictal EEG activity
Motor Activity Conciousness
Genaralized Focal/Lareralized
Intense(convulsive)
Markedly to severely impaired
Tonic-clonic,tonic,clonic,myoclonic
hemiconvulsive
Normal to mildly impaired
Myoclonic(primarily gen.epi.)
Epilepsia partialis continua
Absent or subtle (nonconvulsive)
Markedly to severely impaired
Absence( including typical,atypical, late onsetSubtle or purely electrographic
Complex partialSubtle or purely electrographic
Normal to mildly impaired
Absence (including typical,atypical, late onset)
Simple partial(including aura continua)or mild or int.complex partial
Status epilepticus-EpidemiolodyUS-20-40/100 000Bimodal-< 1 year & >60 yearsNonconvulsive status epilepticus- 10% - an altered level of conciousness 16% - confused elderly patients
Status epilepticus –common etiology1.stroke,including haemorrhagic - 20%2.low AED levels - 35%3.alcohol withdrawal - 15% 4.anoxic brain injury - 15%5.Metabolic disturbances - 15%6.remote brain injury/congenital malformations -
20%
7.infections - 5%8.brain neoplasms - 5%9.Idiopathic - 5%
Clinical featuresGenaralized convulsive status epileptics-Self-perpetuating genaralized tonic-clonic seizure
or of a series of genaralized tonic-clonic seisures without return to consciousness in between seizures.
Initial compensatory phase-sympathatic overdrive
increased C.O increased BP increased BS increased blood lactate levels
Decompensation –homeostatic faliure Redused C.O/ BS/lactate/O2 levels leading
to 1. Cardiorespiratory collapse2. Electrolyte imbalance 3. Rhabdomyolysis & delayed tubular necrosis4. Hyperthermia5. MOF6. Raised ICP & cerebral oedaema
Nonconvulsive status epilepticusDiverse-severe impairment of consciousness to
subtle phenomena.Motor manifestations if any –needs careful CNS
exam.Prolonged subjective sensory phenomena(ie.
aura continua), negative S/S, changes in cognition or behavior-simple partial status epilepticus.
Often mistaken for psychogenic/psychiatric disorders.
DiagnosisDiagnosis of nonconvulsive status
epilepticus in critically ill patients.Correlate with poorer outcomeEEG patterns are difficult to interpret(equivocal
patterns)-criteria is not validated.A trial of rapidly acting IV AED is used to
observe improvement in both clinical EEG by several hours.
Other available modalitiesCont….
Brain imaging.( perfusion/metabolic imaging)Intracranial monitoring with intra cortical
EEG.Brain tissue O2 monitoring.Cerebral micro dialysis.
Other forms or status epilepticusRefractory status epilepticus Status epilepticus that fails to respond to 2
AED.Nearly 40% of status epilepticus are
refractory!Predictors- encephalitis/nonstructural
causes(HIE)/delayed diagnosis & treatment/subtle status epilepticus.
Malignant/super- refractory status epilepticus
Status epilepticus that does not respond to a course of anesthetic drug.
20% of refractory status epilepticus patients.Needs combination therapy (AED &
Anesthetic drugs) /immune therapy.
Management of status epilepticus-convulsive/nonconvulsiveInitial management- (first 5 min)Stabilize A/B/C etc…Peripheral IV accessContinuous Monitoring &
support-SpO2/BP/PR etc…Labs-ABG/AED levels/BS/Metabolic profile-
(Ca/Mg/Po4) FBC/LFT/RFT-BUN & S.Cr, cTnI,toxicology screening etc…
Give Dextrose-D50W 50 ml-unknown glucoseThiamine 100 mg IV prior to dextrose
Benzodiazepines are the treatment of choice followed by IV AED’s!! (SR-HQ)-strong recc./high qua)
Lorazepam 4 mg IV push over 2 min(evidence I-A)
If still seizing-after 5 min rpt once –consult neurology
If NO IV access-Diazepam 20 mg using IV solution RECTALLY (evidence IIa-A) or
Midazolam 10 mg IN/IM/buccal IV solution(evidence I-A) -consult Neurology
If sseizures continue-rapid sequence(RSI) ETT(you may use succinylcholine/avoid etomidate!
Within 30 min.. Midazolam load-0.2 mg/Kg IV push-rpt 0.2-
0.4mg/Kg untill seizure stops ( max.2.0 mg)IVI-initial 0.1mg/Kg/hr: maintenance 0.05-
2.9mg/Kg/hr)-(evidence-IIb-B)Simultaneous
fosphenytoin/phenytoin(evidence IIa-B)/valproate(evidence IIa-A)/phenobarbital(evidence Iib-C)/levetiracetam(evidence Iib-C)
Fosphenytoin: 20mg PE/Kg IV, may give as slower rate(50-150mg/min)
If still seizing-additional 5mg/Kg PRNValproate:40mg/Kg IV, may give @ a slower
rate(over 10-30 min)If still seizing-additional 20 mg/Kg PRNAlternative IVI: Propofol-load 1-2 mg/Kg IV
push, rpt every 3-5 mins untill seizure stops.(max10 mg/kg)
>30 min…Give at least 1 continuous IVI with boluses of either
phenobarbital/propofol/midazolam Phenobarbital: load 5mg/Kg IV at 50 mg/min ,rpt
untill seizure stops, IVI-1mg/Kg/hrPerform neuroimaging when convulsive activity is
controlled.Begin continous EEG,if pt.doesn’t awaken rapidly or
if continuous IV Rx is used.Treat hypothermia.Consider LP & or AB if clinical suspicion of infection.
Management of refractory status epilepticus & subtle status epilepticusIn the ICU that can provide cEEG(evidence
SR-VLQ)Additional treatment-(switch to or start a new
AED) preferred over rebolouses of AED used initially. (evidence SR-LQ)
Continuous IV midazolam ,propofol,phenobarbital +/- intermittent bolouses or
Intermittent IV AED in nonintubated patients(evidence SR-VLQ)
Use maintenance AEDs for the transition from continuous IV.(evidence SR-VLQ WR –VLQ)
Titrate to seizure suppression or burst suppression (evidence WR-VLQ)
Electrographic control for 24-48 hrs before weaning.
Nonpharmacologic approaches used in status epilepticus.ECT-dose-1 session daily for 3-8 days.Duration-up to 2/52.Mechanism-not knownAED doses reduced before ECT.A/E- due to short anesthesia Hypothermia-decrease brain metabolism which
is neuroprotective.Acid-base, electrlyte imbalance ,thrombosis,
infection arrythmias may occur.Resective surgery.Ketogenic diet.
Refferences.Review article-Status Epilepticus-Lawrence
J .Hirsch,MD,FAAN: Nicolas Gaspard,MD,Phd-2013