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    Epilepsy

    Uploaded by

    JENIFER KARINA PUTZ LORENZI

    Copyright:

    © All Rights Reserved
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    58. EPILEPSY Maryam Jowza and Dominika James INTRODUCTION Scizures are often related to other underlying conditions, such as trauma, tumor, or metabolic abnormality, with 10% risk of lifetime occurrence. In comparison, epi lepsy is a congenital condition affecting approximately 196 of the population and involving recurrent seizure disorder. Epilepsy is mose common at extremes of age and in those with structural brain abnormalities. Seizures can be classi- fied as “focal” if the seizure arises from one hemisphere or “generalized” if the seizure arises from both hemispheres. Scizuresare considered as “simple” when no lossofconscious- ness is involved and “complex” with loss of consciousness. Seizures can arise as a result of dysfunctional parox- ysmal neuronal discharge resulting from dysregulation of neuronal circuits and imbalance between excitatory and in- hibitory central nervous system (CNS) modulatory centers Although the precise mechanism leading to seizures is not known, seizures can be congenital, caused by struc tural CNS abnormality (tumor, scar), or associated with transient metabolic dysregulation, such as hypoglyeemia, hyponatremia, medication toxicity or withdrawal (with- drawal of medications that inhibit neuronal transmission, eg» as benzodiazepines or antiepileptic drugs [AEDs] may lead to unopposed neuronal excitation, leading to seizure). THERAPEUTIC OPTIONS As epilepsy is thought to be due to an imbalance between excitatory and inhibitory neuronal activity, AEDs act by either increasing inhibitor neurotransmiteer activity (y aminobutyric acid [GABA]), decreasing excitatory neu- rotransmitter activity (glutamate, aspartate) or reducing inward voltage-gated positive currents (sodium channels, calcium channels). Partial seizures are treated with carba- mazepine, valproate, or phenytoin, For generalized seinures, ‘medications such as barbieurates, gabapentin, or lamotrigine reused Phenytoin, barbiturates, and carbamazepine cause hepatic enzyme induction. AEDs are also associated with dose-dependent toxicity. Phenytoin may cause intraoperative hypotension and dysthythmias, and valproate is associated. with liver toxicity and increased bleeding) Surgical options for treatment of refractory epilepsy in clude left vagal nerve stimulator implantation (right vagus nerve is not recommended due to significane cardiac inner vation) or seizure site surgical resection (most often em: poral lobectomy) “The most favorite candidates for surgical resection are patients wich complex partial seizures, unilateral temporal lobe focus, normal intelligence quotient, motivation, no diffuse brain damage, seizures that were uncontrolled by medications, and a seizure focus that is resectable without causing major neurologic damage. Scatus epilepticus is defined as 30 minutes or more of continuous seizure activity without complete recovery or with incomplete recovery of consciousness.® This is a med- ical emergency as it can lead to cerebral damage and can be faral. In the event of status epilepticus, one should secure the airway, ventilate the patient with oxygen, and monitor and support the cardiovascular function with establish- ‘ment of intravascular access and administration of seizure- suppressing medications. Intubation should be performed usinga short-acting muscle relaxant, suchas uccinylcholine oor mivacurium, as continuous monitoringof tonic activity is essential for evaluating the efficacy of treatment. Use of thi opental or propofol is preferred over other sedatives due to their transient seizure-suppressing effects, Benzodiazepines remain the firstline therapy for status epilepticus, followed by fosphenytoin, levetiracetam, or valproate if the seizure is not resolved. Alternatively, use of intravenous phenobar- bital may be considered. ANESTHETIC CONSIDERATIONS. Many ofthe antiepileptic medications tend to alter the phar rmacokineties and pharmacodynamics of anesthetic drugs by enzyme function alterations, such as enzyme induction or inhibition (Table 58.1) In turn, some anesthetic agents are known to affect the seizure threshold and may induce an intraoperative epileptic event. As such, these interactions 154 + CENTRAL NERVOUS SYSTEM Table $8.1 SUMMARY OF COMMONLY USED AEDS, SIDE EFFECTS, AND ANESTHETIC CONSIDERATIONS, CONSIDERATIONS, Phenytoin Gingival hyperplasia Dysthythmias Induction Accelerated metabolism ofbenzodiazepines, Hiesutiom Hypotension CyP3A4 ‘buprenorphine, meperidine, methadone, Aplastic anemia duction and feneanyl CYP2CI9. Resistance to NMBDs Accelerated metabolism of diszepam Fosphenytoin etter No clfcet side-effect profile than phenytoin) ‘Valptoic acid Hepatic failure Increased surgical bleeding Induction Resistance o NMBDs Pancreat “Thrombocytopenia CYP2CI9 Accelerated metabolism of diazepam D.C Inhibition Decreased methadone elimination cyP2p6 Carbamazepine __Diplopia Revitanceto NMBDs Induction _ Accelerated metabolism of benzodiazepines, Ageanulocytosis ‘Hyponatremia cypsas buprenorphine, meperidine, methadone, sis Induction snd fentanyl D.C.S CYP2CI9 Resistance to NMBDs Accelerated metaholism of diazepam Oxycarbazepine Hypersensitivity, rash Hyponatremia D.C, Phenobarbital Withdrawalsyndrome/ Hypotension (venous Induction Accelerated metabolism ofbenzodiazepines, addiction ppoolingand negative CYP3A4 ‘buprenorphine, meperidine, methadone, D.C.S fonotropic effets) Induction and fentanyl NS depression CYP2B6 Enhanced methadone metabolism Lamotrigine SIS, diplopia No lfect Insomnia, D, C,S ‘Topiramate ‘Weight loss, Renally excreted 65% No effect. nephrolithias Metabolic acidosis DCS Gabapentin ‘Weight gain,D,C,S —Renally excreted 100% Noeffect Tevetiracetam D.CS Renallyexcreted 100% No effect ‘Cyconfasion:D, deanes Sedan: 9S sJohasonsydvom must be taken into consideration when establishing the an- esthetie plan. ANESTHETIC CONSIDERATION PREOPERATIVE, It is important to determine preoperatively if the patient hasa known diagnosis of epilepsy orf they are experiencing, new onset seizures. Those with a new onset of symptoms te {quirean evaluation to determine the etiology of the seizures. As seizures can be caused by a variety of issues, including trauma, medication toxicity or withdrawal, fevers, tumors, ‘or metabolic abnormalities, it is best thar the presence of such conditions be determined prior to an anesthetic.’ In the review of medical history its also important to deter mine the degree of control of seizures, triggers (fasting sleep 15 MAC in epileptic patients and inthe presence ofhypocapnia [NMBD,neuromutslar blocking drag: MAC, minimal sola concentration. ape fom Baja J Jindal R.Fplepeyandnoneplepey sarge Recent avancemensin anesthesia management. dnt Exe ee 201370) 10-17 4:10 4103/0059-162.1139| commonly used AEDS, their side effects and interactions with anesthetics, and their effect on enzymes, Some anestherie agents can have proconvulsant properties. For example, methohexital, alfentanil, and remifentanil can lower the seizure threshold, Agents such as benzodiazepines, propofol, and thiopental lower the seizure threshold, Table 58,2 summarizes medications and their known effeets on seizures In order to avoid reduction of the seizure threshold intraoperatively, hypoxia, hypotension, hypocapnia, and hyponatremia should be avoided. Regional anesthesia can bbe employed safely in an epileptic patient.*® POSTOPERATIVE Patients should resume AED treatment as soon as pos- sible postoperatively. If multiple doses may be missed, medications should be administered using either the oral route if possible or the intravenous route. Phenytoin, so- dium valproate, and levetiracetam are available in intra venous form with oral and intravenous doses equivalent.’ Patients with preexisting poorly concrolled epilepsy are at highest risk for a seizure in the postoperative period and will require special attention and timely administration of AEDs, 156 + CENTRAL NERVOUS SYSTEM REFERENCES. 1, GlauserT, tal. Evidence based guideline treatment of convulsive os epilepsics in and adults repore of the Guideline wmmitee of the American Epilepey Sociry. Fpilepiy Carn 2016 16(1):48-61 2. Maranhio MY, et al. Eplepay and anesthesia. Rev Bras Anestesiol. 2011;61(2)232-236 3. Bajora SJ, Jindal R. Epilepsy and nonepilepsy surgery: recent sdvancements in anesthesia management, cnet Lisayt Ret. 2013:70}:10-17 4, Perks A, etal. Anaesthesia an 562-571, Kofke WA. Anesthesic management of che paient with

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