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CURRICULUM VITAE
dr. Imam Rusdi,Sp S (K)
Lahir : Yogyakarta, 16 September 1952 Pekerjaan : Dosen /dokter Alamat : Jl Sisingamangaraja 76 Jogja
Riwayat PendidikanSpesialis Saraf UGM (1997)
Riwayat Jabatan / pekerjaan- KepalaSMF Saraf/BagianSarafRS Sardjito/FK UGM- Anggota PERDOSSI- AnggotaPokdiNyeri&NyeriKepala- AnggotaPokdiEpilepsi
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Neuro-Emergency
Update
Imam rusdi, Neuro-Emergency Update,FK UGM/RS Dr Sardjito, 26-27 Maret 2011
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Status Epilepticus in Children Adult Pregnancy
Childbearing
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Status Epilepticus (SE) The term status epilepticus may be used to describe any
continuing type of seizure.
Status epilepticus is a common, life-threatening
neurologic disorder. It is essentially an acute, prolongedepileptic crisis.
In early studies, SE was defined by its duration, that is,as continuous seizures occurring for longer than 1 hour .
Clinical and animal experiences later showed thatpathologic changes and prognostic implications occurredwhen SE persisted for 30 minutes. Therefore, the timefor the definition was shortened.
EFNS guideline on the management of status epilepticus in adultsEuropean Journal of Neurology 2010, 17: 348 355 3
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More than 30 minutes of continuous seizureactivity ortwo or more sequential seizureswithout full recovery of consciousness between
seizures. More recently, SE be defined as any seizure
lasting longer than 5 minutes based on naturalhistory data that show typical generalizedconvulsive seizures that resolve spontaneouslyafter 3-5 minutes.
Status Epilepticus (SE)-cont
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Diagnosis Children (%) Adults (%)Stroke 3 25
Drug change/noncompliance 20 20
Alcohol/other drugs 2 15CNS infection 5 10
Hypoxia 5 10
Metabolic 10 10
Tumor
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o Low blood concentrations of AED (34%)o Remote symptomatic causes (24%)o Cerebrovascular accidents (22%)o Anoxia or hypoxia (10%)o Metabolic causes (10%)o Alcohol and drug withdrawal (10%)
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Causes of SE
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SE Classification
Generalized convulsive SE (GCSE)Subtle SE
Non-Convulsive SE (NCSE) Absence SE Complex partial SE
Simple Partial SE
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Non ColvulsiveStatus Epilepticus
NCSE refers to continuous seizure activitywithout predominant motor activity.
This should not be confused with subtlestatus epileptics which refers to GCSE inwhich the motor findings have diminished
either through high doses of administeredmedications or from muscular fatigue dueto prolonged seizure activity
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Aktifitas serangan yang berlangsung terus akanmengurangi secara bertahap reseptor2 GABA Apada synaptic membrane diikuti denganinternalisasi reseptor ke dalam vesikel2endositotik dan degradasi berikutnya.
Proses ini berakibat pada erosi endogen GABA
ergic inhibisi yang akan meningkatkann aktifitasepileptic berkepanjangan.
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Patomekanisme Status Epilepticuscont.
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Hilangnya reseptor GABA A post sinaptikmerupakan factor patofisiologik yg relevansehingga terjadi farmakoresisten terhadap obat2seperti benzodiazepine, barbiturate dan propofol.
Sebaliknya, selama aktifitas epileptic berlangsung,reseptor NMDA secara progresif berpindah kesynaptic membrane, sehingga menambahreseptor NMDA exitatorik presynaps. Proses inimemudahkan exitabilitas neuron dan berikutnyamemperpanjang SE.
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Patomekanisme Status Epilepticuscont.
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Namun sebaliknya, meningkatnya expressireseptor Glutamat dapat merupakan target yang
dipakai pada farmakological management dariSE advanced stage. Absance SE with 3-Hz spike wave discharge
akan menginduksi dengan excessive inhibition.Bentuk SE spt ini tdk menyebabkan neuronalinjury dengan excitasi yang excessive.
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Patomekanisme Status Epilepticuscont.
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Seizures produce a number ofphysiologic consequences.
During a generalized convulsion transientapnea and hypoxia .
Initially, brain compensatory mechanisms mayprevent neuronal injury from seizures hypertension with increased cerebral blood flow.Normal physiological response includes anincrease in body temperature with up to 43%
Temperature >100 F
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Glucose levels also increase, and lactic acidosis(occurs within 60 seconds of a convulsive event and
normalizes within one hour after ictus). A rise in the peripheral white blood cell count withoutan increase in bands is often seen.
If the seizure persists, at approximately 30 minutesthe homeostatic mechanisms begin to deteriorate.
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Seizures produce a number ofphysiologic consequences. Cont.
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Animal models suggest that, even if systemic factors,such as acidosis and hypoxia are controlled,prolonged status epilepticus results in direct neuronaldamage from neurotoxic amino acids and calciuminflux.
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Seizures produce a number ofphysiologic consequences. Cont.
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Management ofStatus Epilepticus
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o Prehospital Concernso Emergency Departemento
ICU
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Prehospital Concerns
Managing the airwayMaintainingoxygenationObtainingIntra Venous accessProtecting the patient from injury.(The use of a padded tongue blade
is contraindicated since it may induceemesis or break a tooth )
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When IV access is not immediately available, rectaldiazepam is an option.One prospective study reported that there were no
significant differences betweenrectal andintravenous diazepam therapy with regard to SEduration, intubation, or recurrent seizures in theemergency department (ED).
These data suggest that prehospital administrationof diazepam may shorten the duration of SE inchildren and simplify the subsequent management.
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Prehospital Concerns cont..
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In a retrospective study on prehospital seizuremanagement in children, rectal diazepam (5 mg/kg),was compared to IM midazolam(15 mg /kg).
Over the 4 year study period,2566 children presented with seizures and107 children were eligible for entry into the study.Of these 107 patients received diazepamand 45 received midazolam.
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Prehospital Concerns cont..
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Both drugs were effective in stopping seizures within5 minutes of drug administration; however, fewerpatients in the midazolam group suffered apnea.
In a study comparing IV diazepam to IM midazolam,Chamberlain et al concluded that IM midazolam isan effective anticonvulsant for children with motor
seizures and an important alternative when IVaccess is not easily available.
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Prehospital Concerns cont..
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Vilke et al compared IM to IV midazolam andreported that IV delivery was more effective:47/49 in the IV group vs 20/25 with IM
administration (p less than 0.05).Four patients (three treated IM and one IV) hadrespiratory compromise necessitating field airwaymanagement. In light of the Chamberlain and Vilke
studies, some experts recommend IV midazolam asthe agent of choice in the prehospital managementof seizures.
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Prehospital Concerns cont..
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Tests include a determination of :serum glucose
electrolytesurea nitrogen, creatininemagnesium, phosphate, calciumcomplete blood count
pregnancy testsanti-epileptic drug levelsliver function testsdrugs of abuse screening.
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Diagnostic TestingLaboratory
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Status EpilepticusClinical manifestations
Convulsive SERelated to acutely elevated serumcatecholamine levelsRespiratory interferenceCardiovascular system adversely affected
Acidosis and rhabdomyolysis Hyperkalemia Myoglobinuria
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Status EpilepticusClinical manifestations
Nonconvulsive SE (10-15%) Obtundation
underlying systemic or neurological disorder sedating or paralyzing medication
Alterations in behavior Slow mentation
Confusion Stupor coma Unexplained, prolonged coma
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Protocol for Convulsive SEMinutes 0-5
100% O2 by mask or canulaHead position for airway patency
Assist ventilation if necessaryCardiac monitoringRecord vital signs: BP, temperature, etc.Check glucose
Establish IVDraw blood for glucose, chemistry, CBC, toxicology,antiseizure medication level, etc.
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Protocol for Convulsive SE Minutes 5-15
Thiamine 100 mg IV and 50 ml D50W if indicated Sedatives
Lorazepam (ativan) 0.1 mg/kg IV, 2 mg/min, OR
Diazepam (valium) 0.2 mg/kg IV, 5 mg/min, OR Diazepam (valium) 0.5 mg/kg per rectum (if no IV) Anticonvulsant
Fosphenytoin 15-20 mg/kg IV, 150 mg/min, OR Phenytoin (dilantin) 15-20 mg/kg IV, 50 mg/min, OR Valproic acid (depakin) 800 mg IV
Monitor BP and cardiac rhythm Do not infuse phenytoin through a line containing
glucose
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Protocol for Convulsive SE Minutes 15-30
Repeat lorazepam or diazepam if seizure continues Additional fosphenytoin or phenyoin in increments dose of
5 mg/kg to total 30 mg/kg
Minutes 30-60 Monitor respirations because patient may require assistedventilation (intubation). Monitor EEG.
If status persists, give phenobarbital 20 mg/kg, 100 mg/min Midazolam (dormicum) IV infusion (0.2 mg/kg slow bolus;
0.1-2.0 mg/kg/hr) Propofol 1-5 mg/kg bolus over 5 min, then 2-4 mg/kg/hr
Minutes 60 or more If status remains refractory, consider pentobarbital 5 mg/kg
load, then 1-4 mg/kg/h infusion30
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Seizures continuing stage ofRefractory Status Epilepticus
General anesthesia should be induced Propofol : 2mg/kg IV bolus, Repeat if necessary, followed byinfusion (5mg/kg/hr)
Thiopental : 100-250mg IV bolus over 20 sec. with further50mg bolus every 2-3 min.until seizure control followed by IVinfusion(3-5mg/kg/hr) Midazolam : 0.1-0.3mg/kg IV bolus dose at the rate of 4mg/minfollowed by infusion(0.05-0.4mg/kg/hr) If seizures have been controlled for 12hrs., reduce the doseover further 12hrs. If seizure recurs again GA agent should be given
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Lancet Neurol 2006; 5: 252
Diff ti l Di i Of Alt d
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Differential Diagnosis Of AlteredMental Status In The Patient
Who Has Seized
Post-ictal state
NCSE or subtle convulsive status
Hypoglycemia
CNS infection
CNS vascular event
Drug toxicity
Psychiatric disorder
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NonconvulsiveStatus Epilepticus (NCSE)
NCSE, like convulsive status epilepticus, is a state ofcontinuous or intermittent seizure activity lasting morethan thirty minutes without a return to baseline function.
NCSE can be either a primary generalized process(absence status) or secondary generalized (complexpartial status).
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NCSEThough the distinction is not clear in theliterature, NCSE in general should bedistinguished from subtle GCSE, which is the
end stage of GCSE, associated with anoxicbrain injury, and has a very poor prognosis.
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Special Situations Alcohol Withdrawal Seizures (AWS)
Of special concern to any emergency physician is the relationof alcohol to seizures. Twenty to 40% of seizure patientspresenting to an ED will have their seizures related to
alcohol abuse, and alcohol is reported as a causative factorin 15 to 24% of patients with status epilepticus.
Diagnostic yield for CT after first alcohol related seizure is high,mainly because patients who overuse alcohol have a high
incidence of structural intracranial lesions, such as subduralhematomas or other intracranial hemorrhages.
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EclampsiaEclampsia is the major consideration in pregnantpatients of more than 20-week gestation and up to23 days postpartum who present with new onsetseizures . Magnesium has been demonstrated tobe the therapy of choice in the treatment of acuteeclamptic seizures and for prevention of recurrenteclamptic seizures. A systematic review of fourgood quality trials involving 823 women found
magnesium sulfate to be substantially moreeffective than phenytoin with regards to recurrenceof convulsions and maternal death.
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Complications, such as respiratory depressionand pneumonia, were also less for magnesiumthan for phenytoin.
Magnesium showed a trend towards increasedincidence of renal failure when compared tophenytoin; however, this was not statisticallysignificant. Magnesium sulfate was alsoassociated with benefits for the baby, includingfewer admissions to the NICU.
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Eclampsia
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Ten to 50% of cases of status epilepticus in childrenare associated with febrile seizures; status in thisgroup is a consistent predictor of increased risk forsubsequent seizures.Simple febrile seizures are a benign process.When they occur in children older than 18 monthswho have not been on antibiotics, they do notrequire any particular diagnostic work-up, even for afirst time event. Management focuses on a carefulhistory and physical, and on parental education.
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Febrile Seizures
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Two to four percent of all children will have a simplefebrile seizure. Children who have had a febrile seizurehave a 25 to 50% chance of having a second event,usually within a year. Children at highest risk forrecurrence are those with a first degree relative who hashad a febrile seizure, complex first febrile seizure, or ageyounger that one year when the first event occurred.There is an increased incidence of developing epilepsy inchildren who have had a simple febrile seizure (2.4%versus a .4% incidence in the general population).
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Febrile Seizures
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Patients with simple febrile seizures require no specialworkup or treatment. Reassuring the parents is often themost Herculean task. Nearly half of parents think thattheir child is dying during the seizure. Such concernsneed to be addressed; simply suggesting the child bedischarged on acetaminophen is not appropriate.
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Febrile Seizures
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S E il i
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Both phenytoin and phenobarbital are often effective inpediatric status if a bolus administration of a benzodiazepinefails. However, as in adults, continuous infusion ofbenzodiazepines have been reported as successful. Infection
has been reported as a more common cause of status inchildren than in adults. Therefore, many physicians willempirically cover such children with broad-spectrumantibiotics, usually ceftriaxone (or the combination of
ceftriaxone and amoxicillin in neonates). The routine use ofempiric acyclovir to treat presumed herpes encephalitis in theneonate remains unstudied.
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Status Epilepticusin Children
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Causes
Fever Medicationchange. Unknown.. Metabolic. Congenital Anoxic... Other (trauma, vascular, infection,tumor, drugs)...
36%20%9%8%7%5%
15%
DeLorenzo RJ. Epilepsia 1992;33 Suppl 4:S15-25
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Drugs which can cause seizures
Antibiotics Penicillins Isoniazid Metronidazole
Anesthetics, narcotics Halothane, enflurane Cocaine, fentanyl Ketamine
Psychopharmaceuticals Antihistamines Antidepressants Antipsychotics Phencyclidine Tricyclic antidepressants
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Respiratory Hypoxia and hypercarbia
ventilation (chest rigidity from muscle spasm)Hypermetabolism ( O2 consumption, CO2 production)Poor handling of secretions - Neurogenic pulmonary edema?
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Hypoxia Hypoxia/anoxia markedly increase the risk
of mortality in SE Seizures (without hypoxia) are much less
dangerous than seizures and hypoxia
Towne AR. Epilepsia 1994; 35(1): 27-34
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Neurogenic pulmonary edema
Rare complicationLikely occurs as
consequence of markedincrease of pulmonaryvascular pressure
Johnston SC. Postictal pulmonary edema requires pulmonary vascularpressure increases. Epilepsia 1996; 37(5):428-32
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Acidosis
Respiratory
Lactic Impaired tissue oxygenation Increased energy expenditure
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Hemodynamics
Sympathetic overdrive Massive catecholamine /
autonomic discharge Hypertension Tachycardia High CVP
0 min 60 min
Exhaustion Hypotension hypoperfusion
Cerebral blood flow
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Cerebral blood flow Cerebral O2 requirement
Blood pressure
Blood flow
O2 requirement
Seizure duration
Hyperdynamic phase CBF meets CMRO2
Exhaustion phase CBF drops as
Hypotension sets in Autoregulation
exhausted Neuronal demage
ensue
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Glucose
G l u c o s e
Seizure duration
30 min
SE
SE + hypoxia
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Hyperpyrexia
Hyperpyrexia may develop during protractedSE, and aggravate possible mismatch ofcerebral metabolic requirement and substratedelivery
Treat hyperpyrexia aggressively Antipyretics, external cooling Consider intubation, relaxation, ventilation
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Initial investigations
Labs Na, Ca, Mg, PO 4 , glucose
CBC Liver function tests, ammonia Anticonvulsant level
Toxicology
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Initial investigations
Lumbar puncture Always defer LP in unstable patient, but never
delay antibiotic/antiviral rx if indicated
CT scan Indicated for focal seizures or deficit, history of
trauma or bleeding d/o
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Treatment
Hyponatremia: Give 5 cc/kg of 3% (hypertonic saline)
Hypocalcemia: Give 20-25 mg/kg of Calcium Chloride
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Treatment
The longer you wait with anticonvulsant, themore anticonvulsant you will need to stop SE
Most common mistake is ineffective dose
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Anticonvulsants
Rapid acting
plus
Long acting
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Anticonvulsants - Rapid acting
Benzodiazepines Lorazepam 0.1 mg/kg i.v. over 1-2 minutes Diazepam 0.2 mg/kg i.v. over 1-2 minutes
If SE persists, repeat every 5-10 minutes
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Benzodiazepines
Diazepam High lipid solubility Thus very rapid onset Redistributes rapidly Thus rapid loss of
anticonvulsant effect
Adverse effects are
persistent: Hypotension Respir depression
Lorazepam Low lipid solubility Action delayed 2 minutes Anticonvulsant effect 6-12 hrs Less respiratory depression than
diazepam
Midazolam May be given i.m.
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Anticonvulsants - Long acting
Phenobarbital 20 mg/k g i.v. over 10 - 15 min
Onset 15-30 min May cause hypotension, respiratory depression
Initial choice of long acting
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Initial choice of long actinganticonvulsants in SE
Is patient an infant?Is patient already receiving phenytoin?
Yes No
At high risk for extravasation?
(small vein, difficult access etc.)?
Phenobarbital
YesNo
Phenytoin Fosphenytoin
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NCSE?
Neurologic signs after terminationof SE are common: Pupillary changes Abnormal tone Babinski Posturing
Clonus May be asymmetrical
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NCSE?
Up to 20% of children with SE have
NCSE after GCSE
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Management of a pregnant
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Management of a pregnantpatient in status epilepticus
Establish the ABCs, and check vital signs, includingoxygenation. Assess the fetal heart rate or fetal status.Rule out eclampsia.
Administer a bolus of lorazepam (0.1 mg/kg, ie, 5-10 mg) atno faster than 2 mg/min.Load phenytoin (20 mg/kg, ie, 1-2 g) at no faster than 50mg/min, with cardiac monitoring.If this is not successful, load phenobarbital
(20 mg/kg, ie, 1-2 g) at no faster than 100 mg/min.Check laboratory findings, including electrolytes, AED levels,glucose, and toxicology screen.If fetal testing results are nonreassuring, move to emergentdelivery.
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