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Status Epileptikus
Status Epileptikus
Status epilepticus 2
Definition
• No consensus on exact definition
20-30 min : injury to CNS neurons
• Conventional definition:
– Single seizure > 30 minutes
– Series of seizures > 30 minutes without full recovery
Status epilepticus 3
Definition
– “If appropriate therapy is delayed, SE can cause
permanent neurologic sequelae or death …”
thus
Status epilepticus 4
The longer SE persists,
Status epilepticus 5
Epidemiology - SE
• life 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
Status epilepticus 6
Mortality
• Adults 15 to 22%
• Children 3 to 15%
Status epilepticus 7
Pathophysiology - SE
• numerous mechanisms - poorly understood
– excess excitation or ineffective inhibition
– there are excitatory and inhibitory receptors in the brain -
activity is usually in balance
Status epilepticus 8
Pathophysiology - SE
• GLUTAMATE = the major excitatory AA
neurotransmitter in brain
– any factor which increases Glutamate activity can lead to
seizures
– e.g. 1987- mussels contaminated with Domoic acid, a
glutamate analog --> profound SE / deaths
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Pathophysiology - SE
• GABA = main inhibitory neurotransmitter
– GABA antagonists can cause SE - eg Penicillins,
other antibiotics
– prolonged sz can desensitize GABA receptors
Status epilepticus 10
Pathophysiology - SE
• 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
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Pathophysiology - SE
• PHASE 1 (0-30 min) -- compensatory mechanisms
remain intact
– adrenaline or noradrenaline release ++
– increased CBF & metabolism
– hypertension, hyperpyrexia
– hyperventilation, tachycardia
– lactic acidosis
Status epilepticus 12
Pathophysiology - SE
• PHASE 2 (>30 min) -- compensatory mechanisms
failing
– cerebral autoregulation fails / cerebral edema
– respiration depressed
– cardiac arrhythmias
– hypotension
– hypoglycemia, hyponatremia
– renal failure, rhabdomyolysis, hyperthermia
– DIC
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Physiological Changes in GTCSE-
Compensation
Status epilepticus 14
Physiological Changes in GTCSE-
Decompensation
Seizure duration
Status epilepticus 16
Glucose
• Hyperdynamic
phase
Glucose
– Hyperglycemia
• Exhaustion phase
SE
– Hypoglycemia develops
– Hypoglycemia appears
earlier in presence of
30 min hypoxia
SE + hypoxia
– Neuronal damage ensues
Seizure duration
Status epilepticus 17
Status epilepticus 18
Imaging Evidence of SE Damage
Status epilepticus 19
Causes
• Fever 36%
• Medication change 20%
• Unknown 9%
• Metabolic 8%
• Congenital 7%
• Anoxic 5%
• Other (trauma, vascular, infection, 15%
tumor, drugs)
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Prolonged seizures
Life
Temporary
threatening
systemic Death
systemic
changes
changes
Duration of seizure
Status epilepticus 22
OUTLINE - Management of SE
• General approach & management
1. Maintenance of oxygenation and circulation
2. Assessment of etiology and lab evaluations
3. Obtaining intravenous access and initiation of therapy
Status epilepticus 23
General Measures in
SE Management
• Maintenance of oxygenation and circulation
(ABC’s : monitor / O2 / large IV’s)
- Metabolic Acidosis : give bicarbonat
- if intubating/ventilating : avoid muscle relaxan :
mask seizure activity
Status epilepticus 24
Assessment of etiology and lab evaluations
• Labs
– Na, Ca, Mg, PO4 , glucose
– CBC
– Liver function tests, ammonia
– Anticonvulsant level
– Toxicology
• 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
Status epilepticus 25
Obtaining intravenous access and initiation of
therapy
• Ideal Antiepileptic Drug
1. Intravenous routes
2. Few adverse effects
3. High CNS penetrance
4. Easy pharmacokinetics
5. Rapid efficacy : prompt onset, long-acting
6. No depression of cardio-resp function /mental
status
Status epilepticus 26
AEDs for Status epilepticus
• Benzodiazepines
– Diazepam
– Lorazepam
– Midazolam
• Phenytoin ( Fosphenytoin)
• Valproic acid
• Phenobarbital
Status epilepticus 27
Benzodiazepines
• Diazepam (Valium, Diastat)
• Lorazepam (Ativan)
• Midazolam (Versed)
Status epilepticus 28
Benzodiazepines
• Lorazepam • Diazepam
– Low lipid solubility – High lipid solubility
– Action delayed 2 minutes – Thus very rapid onset
– Anticonvulsant effect 6-12 hrs – Redistributes rapidly
– Less respiratory depression than – Thus rapid loss of
diazepam anticonvulsant effect
– Adverse effects are
persistent:
• Midazolam • Hypotension
– May be given i.m. • Respir depression
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Lorazepam vs. Diazepam
Lorazepam Diazepam
Status epilepticus 30
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
– pH 8.6
– pH 12
Extravasation well tolerated
Extravasation causes severe
tissue injury – Onset 5-10 min
– Onset 10-30 min – May cause hypotension
– May cause hypotension,
dysrhythmia – Expensive
– Cheap
Status epilepticus 31
Anticonvulsants - Long acting
• Phenobarbital
– 20 mg/k g i.v. over 10 - 15 min
– Onset 15-30 min
– May cause hypotension, respiratory depression
Status epilepticus 32
Drug Rx - Refractory SE
• Anesthetic doses of:
– Midazolam (0.2 mg/kg slow IV bolus) - ->continuous IV infusion @
.4 - 6.0 mcg/kg/min OR .1 - 2.0 mg/kg/hr
– Propofol (1-2 mg/kg)
– Barbiturates (Thiopental, Phenobarbital, Pentobarbital)
– Inhalational anesthetics (Isoflurane)
• General Anesthetic can suppress immune system --
>infection
• Bleck TP. Management approaches to prolonged seizures and status epilepticus. Epilepsia 1999;40(1):S64-6.
Status epilepticus 33
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
Status epilepticus 34
Non - convulsive SE ?
• How do you tell that patient’s seizures have stopped?
• Neurologic signs after termination of SE are common:
– Pupillary changes
– Abnormal tone, Babinski
– Posturing, clonus
– May be asymmetrical
• Up to 20% of children with SE have non - convulsive SE after
tonic - clonic SE
• If child does not begin to respond to painful stimuli within 20 -
30 minutes after tonic - clonic SE, suspect non - convulsive SE
– Urgent EEG
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TERIMA KASIH
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