M A N A G EM EN T O F

C O N V U LS IV E S TATU S
EP ILEP TIC U S IN C H ILD R EN
Yazid Dimyati
Child Neurology Division
Department of Child Health, Medical Faculty
University of Sumatera Utara, H Adam Malik Hospital
Medan

 Status epilepticus (SE) presents in a

multitude of forms, dependent on

etiology and patient age (myoclonic,
tonic, subtle, tonic-clonic, absence,
complex partial etc.)

Generalized, tonic-clonic SE (GCSE) is the

most common form of SE

D efi
nition
Conventional textbook definition of

status epilepticus:
Single seizure > 30 minutes
Series of seizures > 30 minutes without

full recovery

M ore practical:M echanistic

defi
nition
GCSE is a condition which most likely will

not terminate rapidly and / or spontaneously

GCSE is a condition which requires prompt
intervention
LowensteinDH.Epilepsia1999

Typicalseizure duration
Children > 5 years:

Typical, generalized tonic-clonic seizure lasts

< 5 minutes
Young children and infants:

Paucity of data. Suggested time frame for

typical tonic-clonic seizure : < 10-15 minutes
Reviewedin:LowensteinDH.It'stimetorevisethedefinitionofstatusepilepticus.Epilepsia
1999;40(1):1202.

Revised D efi
nition
Generalized, convulsive status

epilepticus in older children (> 5

years) refers to > 5 minutes of
continuous seizure or >2 discrete
seizures with incomplete recovery of
consciousness
LowensteinDH,BleckT,MacdonaldRL.It'stimetorevisethedefinitionofstatus
epilepticus.Epilepsia1999;40(1):1202.

Causes
Fever
Medication change
Unknown
Metabolic
Congenital
Anoxic
Other

(trauma, vascular,
infection, tumor, drugs)

36%
20%
9%
8%
7%
5%
15%

DeLorenzoRJ.Epilepsia1992;33Suppl4:S1525

D rugs w hich can cause seizures

Antibiotics

Psychopharmaceuti

Penicillins

cals

Isoniazid

Antihistamines

Metronidazole

Antidepressants

Anesthetics,

narcotics
Halothane,

enflurane
Cocaine, fentanyl
Ketamine

Antipsychotics
Phencyclidine
Tricyclic

antidepressants

M ortality
Adults
Children

15 to 22%
3 to 15%

Reviewedin:FountainNB.Epilepsia2000;41Suppl
Reviewedin:FountainNB.Epilepsia2000;41Suppl
2:S2330
2:S2330

M ortality
The primary determinant of mortality and

morbidity of SE in children is its etiology

The greatest mortality and highest rate

of neurological deficits occurs when SE is

caused by an acute neurological
condition (infection, trauma, stroke)
MitchellWG.JChildNeurol2002;17Suppl1:S3643.

Prolonged seizures
Temporary
systemic
changes

Life
threatening
systemic
changes

Durationofseizure

Death

Respiratory
Hypoxia and hypercarbia

Ventilation
(chest rigidity from muscle spasm)

Hypermetabolism
( O2 consumption, CO2
production)
Neurogenic pulmonary edema

H ypoxia
Hypoxia/anoxia markedly increase

(triple?) the risk of mortality in SE

Seizures (without hypoxia) are much
less dangerous than seizures and
hypoxia
TowneAR.Epilepsia1994;35(1):2734

N eurogenic Pulm onary Edem a

Rare complication

of SE in children
Likely occurs as
consequence of
marked increase of
pulmonary vascular
pressure during SE
JohnstonSC.Postictalpulmonaryedemarequirespulmonaryvascularpressure
JohnstonSC.Postictalpulmonaryedemarequirespulmonaryvascularpressure
increases.Epilepsia1996;37(5):42832
increases.Epilepsia1996;37(5):42832

Acidosis
Respiratory
Lactic
Impaired tissue oxygenation
Increased energy

expenditure

H em odynam ics
Sympathetic

overdrive
Massive catecholamine /

autonomic discharge
Hypertension
Tachycardia
High CVP

0min

Exhaustio

60min

Hypotension
Hypotension
Hypoperfusion
Hypoperfusion

Cerebralblood fl
ow -CerebralO 2 requirem ent

Hyperdynamic

phase

O2requirement

CBF

Exhaustion
Bloodflow
Bloodpressure
Hyperdynamic

Exhaustion

Seizureduration
LothmanE.Neurology1990;40(5Suppl
2):1323.

phase
CBF drops as

hypotension sets in
Autoregulation
exhausted
Neuronal damage
ensues

G lucose
Hyperdynamic

phase

Glucose

Hyperglycemia

Exhaustion
SE

30min

SE+hypoxia
Seizureduration

LothmanE.Neurology1990;40(5Suppl2):1323.

phase

Hypoglycemia

develops
Hypoglycemia
appears earlier in
presence of
hypoxia
Neuronal damage
ensues

H yperpyrexia
Hyperpyrexia may develop during

protracted SE
Treat hyperpyrexia aggressively
Antipyretics, external cooling
Consider intubation, relaxation, ventilation

O ther alterations
Blood leukocytosis (50% of children)
Spinal fluid leukocytosis (15% of

children)
K+
creatine kinase
Myoglobinuria

Oxygen, oral airway. Suction.

Avoid hypoxia!

Consider bag-valve mask

ventilation. Consider intubation

IV/IO access. Treat hypotension,

but NOT hypertension

Treatm ent
Arterial blood gas?
All children in SE develop acidosis. It often

resolves rapidly with termination of SE

Intubate?
It may be difficult to intubate a child with

active seizures
Stop or slow seizures first, give O2
If using paralytic agent to intubate, assume
that SE continues

Initialinvestigations
Labs
Na, Ca, Mg, PO4 , glucose
CBC
Liver function tests,

ammonia
Anticonvulsant drug level
Toxicology

Initialinvestigations
Lumbar puncture
Always defer LP in unstable patients, but

never delay antibiotic/antiviral treatment if

indicated

CT scan
Indicated for focal seizures or focal deficit or

focal EEG, history of trauma or bleeding

disorder
Treatmentofconvulsivestatusepilepticus.RecommendationsoftheEpilepsyFoundation
ofAmerica'sWorkingGrouponStatusEpilepticus.JAMA1993;270(7):8549.

Treatm ent
Give glucose (2-4 ml/kg D25%, infants 5

unless normo- or
hyperglycemic
ml/kg D10%),

Hyperglycemia has no negative effect

in SE
(as long as significant hyperosmolality is being
avoided)

Treatm ent
The longer you wait to administer

anticonvulsants, the more

anticonvulsants you will need to
stop SE
Most common mistake is

ineffective dose

Anticonvulsants
Rapid

acting

plus
Long acting

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

Benzodiazepines
Lorazepam
Low lipid solubility
Action delayed 2 minutes
Anticonvulsant effect 6-12

hrs
Less respiratory
depression than diazepam

Midazolam
May be given i.m.

Diazepam
High lipid solubility
Thus very rapid

onset
Redistributes rapidly
Thus rapid loss of
anticonvulsant effect
Adverse effects are
persistent:
Hypotension
Respiratory depression

Benzodiazepine -Rectal
Rectal diazepam
Diazepam IV

Benzodiazepine -Intram uscular

Intramuscular midazolam
0.2 mg/kg i.m.
Aqueous solution is rapidly absorbed,

anticonvulsant effect begins after 2

minutes

Intramuscular lorazepam
Can be given, but lacks water solubility,

thus later onset than midazolam

ChamberlainJM.PediatrEmergCare1997;13(2):924.
TowneAR.JEmergMed1999;17(2):3238.

Anticonvulsants -Long acting

Phenytoin
20 mg/kg i.v. over 20

min
Onset 10-30 min
May cause

hypotension,
dysrhythmia
Cheap

Fosphenytoin
20 mg PE/kg i.v. over 5-7

min

PE = phenytoin equivalent

Onset 5-10 min

May cause hypotension
Expensive

Ifin doubt,m easure free phenytoin!

Phenytoin is largely protein bound
(> 90%, varies with serum protein concentration)

Free phenytoin = active phenytoin

(anticonvulsant and toxic effects)

Toxicity more likely with

hypoalbuminemia (usually if < 2 g/dL)

Therapeutic levels
Total phenytoin: 10 - 20 mcg/ml
Free phenytoin: 0.8 - 1.6 mcg/ml

Anticonvulsants -Long acting

Phenobarbital
20 mg/kg i.v. over 10 - 15 min
Onset 15-30 min
May cause hypotension, respiratory

depression

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