STATUS EPILEPTIKUS

EPILEPSYEPILEPSY- A CRITICAL BALANCE

EXCITATION INCREASE

INHIBITION DECREASE SEIZURE SEIZURE

Na+ channel antagonists Ca2+ channel antagonists Glutamate receptor antagonists GABAA agonists Enhanced GABA levels K+ channels modulatorsFeb 4, 2005

STATUS EPILEPTIKUS. EPILEPTIKUS.Bangkitan yang berlangsung lebih dari 30 mnt atau adanya dua bangkitan/lebih dimana di antara bangkitan tersebut tidak terdapat pemupemulihan kesadaran. Penyebab : . Penghentian obat tiba-tiba. tiba. Kelelahan. . Adanya penyakit sistemik. . Adanya kelainan neurologi yang progresif.

Definition - Status Epilepticuscontinuous or rapidly repeating seizures no consensus on exact definition - abn prolonged no recovery between attacks 20-30 min --> injury to CNS neurons 20--> more practical definition: since isolated tonic clonic seizures rarely last > few minutes ... consider Status if sz > 30 min or 2 discrete sz with no regaining of consciousness between

vs. serial sz - close together - regained consciousness in between

Epidemiology - SElife threatening USA: -102,000 -152,000 cases / year - 52,000 deaths / year of new cases of epilepsy, 12 -30% present in Status generalized Status is most common form - and subject of this review

Pathophysiology - SEnumerous mechanisms - poorly understoodexcess excitation or ineffective inhibition there are excitatory and inhibitory receptors in the brain - activity is usually in balance

Pathophysiology - SE cont dGLUTAMATE = the major excitatory AA neurotransmitter in brainany factor which increases Glutamate activity can lead to seizures e.g. 1987- contaminated with Domoic acid, a 1987glutamate analog --> profound SE / deaths -->

Pathophysiology - SEGABA = main inhibitory neurotransmitter

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GABA antagonists can cause SE eg Penicillins, other antibiotics prolonged sz can desensitize GABA receptors

Pathophysiology - SE

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CNS damage can occur - mechanism:uncontrolled neuronal firing -> excess glutamate -> this sustained high influx of calcium ions into neurons leads to cell death ( excitotoxicity ) GABA released to counteract this, but GABA receptors eventually desensitize these effects worsened if hyperthermia, hypoxia, or hypotension

KLASIFIKASI:1. STATUS EPILEPTIKUS KONVULSIF ( BANGKITAN UMUM TONIK-KLONIK). TONIK2. STATUS EPILEPTIKUS NON KONVULSIF ( BANGKITAN LENA,PARSIAL KOMPLEKS)

Status epilepticusIt is a medical emergency requires prompt and aggressive treatment Therapy should be aimed at:Rapid termination of status epilepticus Prevention of seizure recurrence Treatment of underlying cause

Management of SEABC s (+ monitor / O2 / large IV s) START PHARMACOTHERAPY Metabolic acidosis common - if severe, severe, give Bicarb if intubating / ventilating - avoid longlongacting n-m blockers - sz activity nbeware hyperthermia 2 sz - in 30-80% 30--> passive cooling -->

Management of SE

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consider.... Thiamine Glucose Pyridoxine 5 gm IV (70 mg/kg kids)reverses INH action inhibiting GABA synthesis now recommended routinely by NYC Poison Control in REFRACTORY SE d/t frequency of INH OD

Management of SE

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consider underlying causes:infection (systemic / CNS) structural: trauma, CVA, IC bleed CNS malformations metabolic - hypoxia, abn electrolytes, hypoglycemia toxic - alcohol, other drugs drug withdrawal - AED s, benzos

Management of SE

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LAB: gluc, electrolytes, creat, BUN, Mg,Phos, LFT s, AED levels, toxicology, PTT / INR , ( Blood Gase Analyse/ AGD )

Status Epilepticus TreatmentImmediate treatment 1. Secure IV line draw blood for analysis (including anticonvulsant levels). 2. Push 50 cc of 50% Dextrose i.v., i.v., 100mg thiamine i.v. i.v. 3. Monitor vital signs. 4. Examine patient. 5. Protect airway, tongue, head, never leave patient alone 6. Intubate all patients if first line drugs fail.

Status Epilepticus-Definitive Treatment EpilepticusDiazepam - 10mg IV push over 30-60 seconds 30repeat after 10-15mins upto 30mg 10(5mg/min). Repeat after 2-4hrs. 100mg/day 2i.Good results, easy to administer. (fast acting, short lasting) ii. If two doses fail to stop status, then further doses probably won't work either. iii. Side effects -- hypotension, iii. bradycardia, bradycardia, respiratory depression, cardiac arrest, depresses mental status.

PENANGANAN STATUS EPILEPTIKUS.0-10 mnt: 0-60 mnt: ABC.dan Pasang Infus. Pemberian OAE Short action : Diazepam 1010-20 IV ( maksimal 60 mg). Glukosa 40% 25 -50 cc dan thiamine 250 mg. Pemeriksaan status neurologi.

0-60/90 mnt: Bila terus kejang Phenitoin 15-18 mg/kg pelan 15(kecepatan 50 mg/mnt.) 90 mnt masih kejang rawat dengan pemberian anestesi.

STATUS EPILEPTIKUS REFRAKTER.80% SE KONVULSIKUS DAPAT DIHENTIKAN DENGAN DIAZEPAM DAN PHENYTOIN. BILA BANGKITAN MASIH BERLANGSUNG KITA SEBUT : SE REFRAKTER. HARUS RAWAT ICU DILAKUKAN TINDAKAN ANESTESI.

OBAT YANG DAPAT DIBERIKAN:MIDAZOLAM: 0,1 mg/kgBB KECEPATAN INFUS 4 mg/mnt.DILANJUTKAN DOSIS 0,05-0,4mg/kgBB/JAM INFUS. THIOPENTHONE: 100-250 mg BOLUS PELAN. SELANJUTNYA 3-5 mg/kgBB/JAM. PENTOBARBITAL: 10-20mg/kgBB KECEPATAN 25 mg/mnt.DILANJUTKAN 1-3mg/kgBB/JAM. PROPOFOL: 2 mg/kgBB DITINGKATKAN 5-10mg/kgBB/JAM.

SE NON KOVULSIKUS:1/3 DARI KASUS. PILIHAN OBAT : SE LENA : BENZODIAZEPINE IV VALPROAT IV. PARSIAL KOMP : CLOBAZAM LORAZEPAM/IV PHENYTOIN/IV. PADA PASIEN KOMA: PHENYTOIN/IV ANESTESI.

EPILEPSI REFRAKTER/INTRACTABLE EPILEPSY. BANGKITAN YANG TIDAK BISA DATASI WALAU DENGAN OAE YANG MAKSIMAL. ETILOGI : BIASANYA OLEH KARENA ADANYA SKLEROSIS PADA HIPOKAMPUS.

PENANGANAN EPILEPSI REFRAKTER.1. TERAPI BEDAH. 2. STIMULASI NERVUS VAGUS. 3. MODIFIKASI TINGKAH LAKU. 4. RELAKSASI. 5. MENGURANGI DOSIS OAE.

ComaConsciousness requires arousal (coming from the brainstem reticular formation) and content (the cerebral hemispheres) Alterations in consciousness stem from: Disorders affecting the reticular formation Disorders affecting both cerebral hemispheres Disorders affecting the connections between the brainstem and the hemispheres

Anatomic correlation of consciousnessWidespread damage in both hemispheres Global suppression of cerebral function

Conscious level less severe

Conscious level--severe

Brainstem lesions that cause proximate damage to RAS

Glasgow Coma ScaleThree components. Score derived by adding the score for each component.Eye opening (4 points) Verbal response (5points) Best motor response (6 points)

Glasgow Coma ScaleEye opening4 3 2 1 spontaneous to speech to pain none

Best Motor Response6 - obeys 5 - localizes 4 - withdraws 3 - abnormal flexion 2 - abnormal extension 1 - none

Verbal Response5 - oriented 4 - confused conversation 3 - inappropriate words 2 - incomprehensible sounds 1 - none

EXAMINE ComaFour domains to examine: examine: Pupillary responses Extraocular movements Respiratory pattern Motor responses

Herniasi unkus, std. N III lanjut

Approach to the Comatose Patient

Initial TreatmentAirway Breathing Circulation ABC - identify and address life threatening inadequacies Treat rapidly progressive metabolic disorders -- hypoglycemia Evaluate for intracranial hypertension and imminent herniation and treat

AirwayIntubate (protecting neck) anyone who will let youAny of the following are adequate criteriaGCS < 9 Airway not secure or open Respiration not adequate Any significant respiratory failure Uncertainty regarding direction or rate of mental status changes, particularly if constant observation not available (during CT scans, etc..)

BreathingEvaluate - is patient moving adequate air, is respiratory rate appropriate, is gas exchange adequate, are breath sounds adequate and symmetrical Must assure oxygenation and ventilation If intubated don t forget to ventilate Identify and immediately treat problems - pneumothorax, airway pneumothorax, obstruction, etc..

CirculationIs patient in shock?Check pulses, heart rate, blood pressure, perfusion Remember hypotension is late sign of shock

Start treatment for shockDo not restrict fluids in comatose patient with inadequate intravascular volume. Cardiac output and cerebral perfusion are much more important than fluid restriction

CirculationUse isotonic solutions and blood, as indicated. Do not use hypotonic solutions to treat shock, particularly patients with coma or possible cerebral edema Identify life threatening hemorrhage and control it.