MANAGEMENT OF

CONVULSIVE STATUS EPILEPTICUS

IN CHILDREN

Yazid Dimyati
Child Neurology Division
Department of Child Health, Medical Faculty
University of Sumatera Utara, H Adam Malik Hospital Medan
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▪ 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
Definition

▪ Conventional “textbook” definition of status

epilepticus:

▫ Single seizure > 30 minutes

▫ Series of seizures > 30 minutes without full

recovery
More practical: Mechanistic
definition

▪ GCSE is a condition which most likely will not

terminate rapidly and / or spontaneously
▪ GCSE is a condition which requires prompt
intervention

Lowenstein DH. Epilepsia 1999

Typical seizure 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

Reviewed in: Lowenstein DH. It's time to revise the definition of status epilepticus. Epilepsia
1999;40(1):120-2.
 Revised Definition

▪ 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
Lowenstein DH, Bleck T, Macdonald RL. It's time to revise the definition of status
epilepticus. Epilepsia 1999;40(1):120-2.
Causes

▪ Fever 36%
▪ Medication change 20%
▪ Unknown 9%
▪ Metabolic 8%
▪ Congenital 7%
▪ Anoxic 5%
▪ Other (trauma, vascular, 15%
infection, tumor, drugs)

DeLorenzo RJ. Epilepsia 1992;33 Suppl 4:S15-25

Drugs which can cause seizures

▪ Antibiotics ▪ Psychopharmaceuticals
▫ Penicillins ▫ Antihistamines
▫ Isoniazid ▫ Antidepressants
▫ Metronidazole ▫ Antipsychotics
▪ Anesthetics, narcotics ▫ Phencyclidine
▫ Halothane, enflurane ▫ Tricyclic antidepressants
▫ Cocaine, fentanyl
▫ Ketamine
Mortality

▪ Adults 15 to 22%
▪ Children 3 to 15%

Reviewed in: Fountain NB. Epilepsia 2000;41 Suppl

2:S23-30
 Mortality

▪ 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)

Mitchell WG. J Child Neurol 2002;17 Suppl 1:S36-43.

Prolonged seizures

Life
Temporary
threatening
systemic Death
systemic
changes
changes

Duration of seizure
Respiratory

▪ Hypoxia and hypercarbia

▫ Ventilation
 (chest rigidity from muscle spasm)
▫ Hypermetabolism
 ( O2 consumption, CO2 production)

▫ Neurogenic pulmonary edema

Hypoxia

▪ Hypoxia/anoxia markedly increase (triple?) 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

 Neurogenic Pulmonary Edema

▪ Rare complication of SE
in children
▪ Likely occurs as
consequence of marked
increase of pulmonary
vascular pressure during
SE

Johnston SC. Postictal pulmonary edema requires pulmonary vascular pressure

increases. Epilepsia 1996;37(5):428-32
Acidosis

▪ Respiratory
▪ Lactic
▫ Impaired tissue oxygenation
▫ Increased energy expenditure
 Hemodynamics

▪ Sympathetic
overdrive
▫ Massive catecholamine / ● Exhaustion
autonomic discharge
❖ Hypotension
▫ Hypertension
❖ Hypoperfusion
▫ Tachycardia
▫ High CVP

0 min 60 min
Cerebral blood flow - Cerebral O2 requirement

▪ Hyperdynamic
phase
O2 requirement
▫ CBF

▪ Exhaustion phase
▫ CBF drops as
Blood flow hypotension sets in
▫ Autoregulation
Blood pressure
exhausted
Hyperdynamic Exhaustion ▫ Neuronal damage
Seizure duration ensues

Lothman E. Neurology 1990;40(5 Suppl

2):13-23.
 Glucose

▪ Hyperdynamic
phase
▫ Hyperglycemia
Glucose

▪ Exhaustion phase
SE ▫ Hypoglycemia
develops
▫ Hypoglycemia
appears earlier in
30 min presence of hypoxia
SE + hypoxia
▫ Neuronal damage
ensues
Seizure duration

Lothman E. Neurology 1990;40(5 Suppl 2):13-23.

Hyperpyrexia

▪ Hyperpyrexia may develop during protracted

SE

▪ Treat hyperpyrexia aggressively

▫ Antipyretics, external cooling
▫ Consider intubation, relaxation, ventilation
Other alterations

▪ Blood leukocytosis (50% of children)

▪ Spinal fluid leukocytosis (15% of children)
▪ K+
▪ creatine kinase
▪ Myoglobinuria
A Oxygen, oral airway. Suction. Avoid
hypoxia!

B Consider bag-valve mask ventilation.

Consider intubation

IV/IO access. Treat hypotension, but NOT

C hypertension
Treatment

▪ 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
Initial investigations

▪ Labs
▫ Na, Ca, Mg, PO4 , glucose
▫ CBC
▫ Liver function tests, ammonia
▫ Anticonvulsant drug level
▫ Toxicology
 Initial investigations

▪ 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

Treatment of convulsive status epilepticus. Recommendations of the Epilepsy Foundation

of America's Working Group on Status Epilepticus. JAMA 1993;270(7):854-9.
Treatment

▪ Give glucose (2-4 ml/kg D25%, infants 5 ml/kg D10%),

unless normo- or hyperglycemic

▪ Hyperglycemia has no negative effect in SE

(as long as significant hyperosmolality is being avoided)
Treatment

▪ 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 - Intramuscular

▪ 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
Chamberlain JM. Pediatr Emerg Care 1997;13(2):92-4.
Towne AR. J Emerg Med 1999;17(2):323-8.
Anticonvulsants - Long acting

▪ Phenytoin ▪ Fosphenytoin
▫ 20 mg/kg i.v. over 20 min ▫ 20 mg PE/kg i.v. over 5-7 min
PE = phenytoin equivalent

▫ Onset 10-30 min ▫ Onset 5-10 min

▫ May cause hypotension, ▫ May cause hypotension
dysrhythmia ▫ Expensive
▫ Cheap
If in doubt, measure 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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