After all standard therapy has failed or has been determined to have unacceptable side effects most neurology textbooks recomend consulting an anesthesiolo
gist for administration of general anesthesia to manage SE.Under these situations what anesthetic should be given ?
Unfortunately no controlled clinical studies have been conducted to adequately answer this question.
Anesthetic drugs that have been used successfully to stop SE include barbitutates,benzodiazepine,propofol,etomidate ketamine,isoflurane,enflurane,and halothane.
If general anesthesia is needed to manage SE a patient outcome is thought to corelate more with the underlying diseases than the success in terminating seizures.
One factor in this is the delay in beginning general anesthesia caused by the need to first try less potent drugs and the logistic problems in starting an anesthetic in an intensive care unit.
Prolonged used of high dose of barbiturate (i.e.for days or weeks) has been associated with barbiturate tolerance which may exacerbate the underlying seizure problem.
In one case report,isoflurane was used to facilitate the withdrawal of barbiturate.In addition,the neurochemical effects of such prolonged anesthetic used can result in substantial increases in brain glycogen after only a few hours. Moreover the potential for prolonged volatile anesthesia to be organotoxic or to induce tolerance is unknown.
The effects of isoflurane,thiopental,ketamine and midazo
lam were assessed in rats undergoing mercaptopropionic acid induced or flurothyl induced seizures.
Midazolam resulted in less damaged in the substantia nigra after seizures.
No protective effect was suggested with isoflurane or thiopental and although a protective effect was suggested with ketamine,it was statistically unsignificant.
Unfortunately this study revealed nothing about the anes
thetic effects or seizure induce damage in the lymbic system.The ketamine data however are supported by other reports of anticonvulsant or neuroprotective of ketamine in the lymbic system during seizures in rodents.
For the reasons previously given the therapeutic approach in choosing an anesthetic agent for SE should first involve increasing dosis of benzodiazepine or barbiturate.
Only after this therapy failed should volatile anesthetic drugs be considered.
Volatile anesthetics have the advantage of allowing continuous realtime titration to maintain a spesific blood anticonvulsant level based on entidal gas monitoring.
In one patient the monitoring of end tidal volatile anesthetic concentration facilitated titration of the anti
convulsant anesthetic against EEG.
In another patient,isoflurane use facilitated withdrawal of a prolonged barbiturate infusion on which the patient was thought to be dependent.
Thus volatile anesthetics may have a role in closely titrating anticonvulsant therapy for seizures in situation where a general anesthesia is to use as little as possible while observing the patient closely for cessation of seizure and for hemodynamic compromise.
Such patient must be intubated and mechanical ventilated .
Optimally continuous EEG shoul be monitored through anesthetic procedure.If thiopental is used 50 to 500 mg iv can be given as a loading dose in adult,followed by an iv infusion,the infusion rate initially should be higher
and then should be decreased as indicated by EEG.
After the loading dose the infusion rate could be set initially at 500-1000 mg/h and then decreased as indicated to the lowest rate feasible.
Repeated boluses,100-500 mg,might be needed initially to mantain close titration.
If isoflurane is used it should be started at 0,2-0,3% inspired concentration (6L/min gas flow initially) and inreased over 10 to 20 min as indicated by EEG and hemodynamic tolerance.
Determining the end point to guide drug titration can be difficult. For example,burst occuring within a burst suppression pattern on EEG can resemble epileptic discharges.
The decision about seizure control and EEG interpretation should be jointly with the refering neurologist or epileptologist.
After seizures are controlled and if the source is still unclear reversible causes should be sought and corrected,
after which,anesthesia should be stopped.
Otherwise the anesthetic dose should be decreased periodically to permit assessment.
If seizures continue to recur on anesthetic discontinuation the next decision is wether to continue anesthesia considering the many unknown effects,bioethical concerns and logistic and economic issues of prolonged anesthetic administration compared with drawing life support. Nothing,the trend toward end tidal concentrations at which seizures recur,a real time seizure thresold,over such
assessment may contribute to such decision.
Summary :
Status epilepticus can be defined as a condition in which prolonged or recurrent seizures or epileptic events persist for more than 30 minutes.
SE is most often seen with drug withdrawal (including antiepilepticmedication and alcohol),drug intoxication
metabolic disarray and structural lesion from stroke,tumor,
abscess and trauma.
Morbidity and mortality from SE are related to three factors
1.the damage to the CNS caused by the acute insult
precipitating the SE.
2.systemic stress from repeated seizures.
3.the injury from repetitive electrical discharges with the
CNS.
The most important clinical factors determining outcome are etiology, and the time from onset of SE until treatment is initiated.
The worst prognosis is found in those in whom status results from a serious intracranial process such as encephalitis,
stroke or cerebral hemorhage.The best prognosis is seen in patients without structural lesions.
Generalized convulsive status epilepticus is considered
a neurologic emergency.
To prevent brain damage seizure must be stopped as soon as possible optimally within 30 minutes of onset.
Initial treatment of SE starts with basic life support.
In addition the management of SE is best carried out using a predetermined protocol.
After all standard therapy has failed or has been deter mined unacceptable side effects neurology textbooks recomend consulting anesthesiologist for administration of general anesthesia to manage status epilepticus.
Reference :
1.Koffke Andrew W et all: Status Epilepticus,Anesthesia for
Epileptic Patients ;Cottrell E James;Anesthesia and
Neurosurgery;4th edit,Mosby Company,St Louis,
London,Philadelphia,2001,pp 477-8.
2.Trop Davy,Oliver Andre:The Problem of Status Epilepti
cus,Albin S M;Textbook of Neuroanesthesia ,The McGraw
Hill Company,Newyork,1997,pp.684-7.
3.Chang JW,Bleck P Thomas:Status epilepticus;Stone DJ
Sperry JR;the Neuroanesthesia Handbook,Mosby,St louis
Baltimore,1966.pp.452-5
4.Namara MC Brian,Boniface J Simon:The EEG in Status
Epilepticus;Matta F Basil;Textbook of Neuroanesthesia
and Critical Care,Greenwich Medical Media Ltd,London
2000,pp.78-80.
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