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PharmD May 28 2014 UW Medicine Status Epilepticus Definition Status Epilepticus SE 5 minutes of more of continuous clinical andor electrographic seizure activity OR Recurrent seizure activity without recovery between seizures ID: 248737

seizure status epilepticus patients status seizure patients epilepticus etiology convulsive neurological cns fosphenytoin duration aed activity uptodate control treatment

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Slide1

Ives Hot, PharmDMay 28, 2014UW Medicine

Status

EpilepticusSlide2

DefinitionStatus Epilepticus

(SE)

5 minutes of more of continuous clinical and/or electrographic seizure activity

-OR-

Recurrent seizure activity without recovery between seizures Slide3

Epidemiology Estimated 100,000 to 200,000 episodes of SE in the United States annually

Mortality: 17-26%

Additional 10-23% of patients have disabling neurological deficits Slide4

CategorizationConvulsive

Associated with rhythmic jerking of extremities

Findings: tonic-

clonic

movements, mental status impairment, focal neurological deficits

Non-convulsive

Seen on electroencephalogram (EEG) without clinical findings

Refractory (RSE)

Patients who DO NOT respond to standard treatment

Received adequate doses of initial benzodiazepine

Second acceptable antiepileptic drug (AED)Slide5

Etiology Acute: Metabolic disturbances

Sepsis

CNS infection: meningitis, encephalitis, abscess

Stroke

Head trauma

Pharmacologic

Hypertensive encephalopathy

Autoimmune encephalitis Slide6

Etiology Chronic: Pre-existing epilepsy

Breakthrough seizure

Discontinuation/non-adherence to AED

Chronic ethanol abuse

CNS tumors

Remote CNS pathology ( stroke, abscess, TBI, cortical

dysplasia

)Slide7

Diagnostic Work-upAll Patients

Finger-stick glucose

Vital Signs

Head computed tomography

Lab:

CBC

, BMP, Ca, Mg, AED levels

Continuous EEG monitoring

Consider

Brain MRI

Lumbar puncture

Toxicology panel

Other lab testsSlide8

Prognosis

Convulsive

Non-convulsive

RSE

Mortality

-Discharge:

9-21%

-30-day: 19-27%

-Discharge: 18-52%

-30-day: 65%

-Discharge: 23-61%

Morbidity

-Severe neurological

sequealae

: 11-16%

-Return to functional baseline 39% at

3 months

Factors associated with poor outcome

-Underlying etiology

-De novo

-Duration

-Focal

neurological signs present at onset

-Impaired consciousness

-Age

-Underlying etiology

-Severe mental status impairment

-Duration

-Underlying etiology

-Age

-Duration

-High APACHE-2

scale scores Slide9

Treatment Goals

Emergently stop both clinical and electrographic seizure activity

Definitive control of SE should occur within 60 minutes Slide10

TreatmentAirway protectionEstablish and support baseline vital signs

Establish medication route (Peripheral IV access), in order to:

Stop seizure

Establish

euvolemia

Reverse thiamine deficiency/treat hypoglycemia

Other: labs, EEG, diagnostic testing, neurologic exam

Determine patient’s historySlide11

Drugs That Can Lower Seizure Threshold

Antibiotics

Imipenem

,

penicillins

,

cephalosporins

,

metronidazole

,

isoniazid

Antihistamines

Antipsychotics

Antidepressants

Bupropion

Tricyclics

Baclofen

Fentanyl

Ketamine

Lidocaine

Lithium

Meperidine

Propoxyphene

TheophyllineSlide12

Emergent Initial Therapy Agent of choice = Benzodiazepines

IV:

lorazepam

(Class I, Level A)

IM:

midazolam

(Class I, Level A)

PR: diazepam (Class

IIa

, Level A)

MOA:

increase frequency of

chloride

channel opening in

CNS GABA(A) receptors—decreasing neuronal

excitability

-VERSUS-

MOA of Phenobarbital: enhances GABA (A) chloride currents by increasing duration of chloride channel opening

First-line medications control SE in 80% of patients when initiated within 30 minutes, but in only 40% if started after 2 hours of onset Slide13
Slide14

Intranasal Midazolam

Administration

Use of atomizer

Use 5mg/mL

injectable

solution

Higher concentration

injectable

solution to minimize volume

Maximum dose is 1

mL

per

nare

Adverse effects

Burning/irritation Slide15

Urgent Control Therapy Required following benzodiazepine administration in all patients who present with SE

UNLESS known cause of SE is identified and corrected

Goal 1: Rapid attainment of therapeutic levels of an AED and continued dosing for maintenance

Goal 2: To stop SE, if the patient failed emergent control Slide16
Slide17

Fosphenytoin versus Phenytoin

MOA: stabilizes neuronal membranes and decreases seizure activity by increasing efflux or decreasing influx of Na ions across cell membranes in the motor cortex during generation of nerve impulses

Dosing difference

Fosphenytoin

is converted to

phenytoin

on a 1:1 molar basis

Molecular weight

fosphenytoin

> Molecular weight of

phenytoin

Greater weight of

fosphenytoin

must be givenSlide18

Questions? Slide19

References Brophy GM, Bell R,

Claassen

J, et al. Guidelines for the evaluation and management of status

epilepticus

.

Neurocrit

Care.

2012;17(1):3-23.

Arif

H, Hirsch LJ. Treatment of status

epilepticus

.

Semin

Neurology

. 2008;28(3):342-354.

Stecker

MM. Status

epilepticus

in adults.

UpToDate

Web site. http://www.uptodate.com/. Accessed May 23, 2014.

UpToDate

Web site. http://

www.uptodate.com

/. Accessed May 24, 2014.