Status Epilepticus
PICU Resident Lecture Series
Lucile Packard Children’s Hospital
(Updated: April 2011)
Objectives
• What are common causes of SE
• Learn the physiologic sequela of SE
– (Why do these patients need to be in the PICU?)
• Learn what tests/labs are needed acutely
• Acute management of SE
– Including procedures, medications, and
“pentobarb” comas
Definitions
• No absolute definition of Status Epilepticus (EP)
• Generally accepted definition is
– Greater than 30 minutes OR
– Frequent seizures without returning to baseline
• Treatment if seizure lasts >5 minutes
– High risk of lasting >30 minutes
– Delayed treatment can lead to permanent sequela
Common etiologies
Common drugs related to seizures
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Penicillins
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Isoniazid
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Metronidazole
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Antihistamines
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Narcotics
Ketamine
Halothane/Enflurane
Tricyclic antidepressants
Antipsychotics
Phencyclidine
Cocaine
Physiologic Consequences of SE
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Phases of SE
Respiratory Effects
Hyperpyrexia
Metabolic derangements
Laboratory changes
Summary
Phases of SE
• Hyperdynamic Phase
– Increased cerebral metabolic demand
– Massive catecholamine/autonomic discharge
– Increased CBF, HTN, tachycardia
• Exhaustive Phase (with persistent SE)
– Catecholamine depletion
– Hypotension, decreased CBF
– Can lead to neuronal damage (ongoing metabolic
demand with tissue hypoxia)
Respiratory Effects
• Hypoxia and Hypercarbia are common
– Chest wall rigidity (muscle spasms, oral secretions)
– Hypermetabolic state with increased 02 demand
and increased C02 production
– Neurogenic pulmonary edema is rare complication
• Marked increased in pulmonary vascular pressure is
presumed etiology
Hyperpyrexia
• Can lead to seizures or be a result of SE
• Exacerbates mismatch of cerebral metabolic
demand and substrate delivery
• Therefore fevers should be treated
aggressively
– Antipyretics/cooling
Metabolic derangements
• Acidosis
– Lactic acidosis due to poor tissues oxygenation
with inc energy expenditure
– Respiratory acidosis may also develop
• Glucose
– Initial hyperglycemia from catecholamine surge
followed by hypoglycemia
– Can be detrimental to the brain, and can further
worsen lactic acidosis
Metabolic derangements (cont’d)
• Rhabdomyolysis
– Protracted tonic-clonic activity can have extensive
muscle breakbdown
– Leads to hyperkalemia, myoglobinuria
• Leukocytosis
– Stress response causes demarginalization of SBCs
– In 15% of children, this leukocytosis can be seen in
the CSF
Summary of complications
Treatment
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ABCs
Venous access
Labs
Other diagnostic
Meds
ABCs
• Avoid hypoxia by providing oxygen (facemask
or NC)
• Oral airway can be helpful (but difficult to
place)
• Nasal trumpet is good alternative
• Optimize position, jaw thrust
• If poor respiratory effort, begin bag-mask
ventilation and consider intubation
Intubation
• Some indications:
– Difficult to maintain airway
– Unable to manage oral secretions
– Ineffective respiration
– Hypoxia
– Hypercarbia
– CNS pathology, unequal pupils
– SE >30 minutes despite appropriate treatments
• REMEMBER: paralytics DO NOT control CNS
epileptiform discharges
Venous access
• Obtain IV/IO access
– Can give IM or Rectal meds but venous access is
necessary
• Blood pressure management
– Hypertension likely to resolve with sz control
– Some cases need tx (like inc BP with renal failure)
– Start volume resuscitation if hypotensive with
bolus of NS (20ml/kg)
• Labs required in ALL pts with SE:
– CBC, Chem panel (with LFTs, glucose, ca, mg)
• Hyponatremia and hypocalcemia are readily treatable
– Stat beddside glucose (*especially in neonates and
infants)
– Ammonia
– Anticonvulsant levels
– Tox screen
• LP: defer in pts with signs of increased ICP or if
unstable (but do not delay therapy i.e. abx)
Other diagnostics
• CT scan
– Focal seizures or deficits; History of trauma
– Non-contrast: mass lesions, hemorrhage,
hydrocephalus
– Contrast: meningitis, abscess, encephalitis
• EEG- indicated in ALL pts with SE
– Standard: one time study in SE that has resolved
– Continuous: difficult to control SE, burst
suppresion, subclinical seizures
– Video: can be used in conjunction for seizures that
are difficult to characterize
Medications
• Initiate antiepileptic therapy early
• With delayed treatment, pt will also have
delayed response to treatment
– Thus requiring higher doses
• Combine rapid acting to control with long
acting to prevent recurrence
Rapid Acting Anticonvulsants
Long Acting Anticonvulsants
Persistent SE
• “Pentobarb” coma
– CNS electrical quiescence by continuous infusion
– Pentobarbital: 1-3mg/kg/hr after bolus (10mg/kg)
– Midazolam: 1-10mcg/kg/min after bolus (0.15mg/kg)
– Propofol 20-70 mcg/kg/min
• Normal physiologic activity also suppressed
– Intubation necessary
“Pentobarb” coma (cont’d)
• Central line placement
– For delivery of continuous infusion
– May cause hypotension so pt may require rapid
fluid bolus or inotropes
• Treat hypotension aggressively in these pts
• Continuous EEG
– “Burst suppression” is the specific electric pattern
noted on EEG once in a successful coma.
Electrical activity is only noted once per screen
(15-20sec)
“Pentobarb” coma (cont’d)
• Pt must be started on a long acting
anticonvulsant
– Check for therapeutic levels
• Burst suppression for 24-48 hrs
– Coma gradually lifted while monitoring for seizure
activity
Non-convulsive SE
• Up to 20% of children with SE have nonconvulsive SE after tonic-clonic activity
• If no response to painful stimulation within
20-30 min of tonic-clonic activity
• Urgent EEG
• Must maintain High Index of Suspicion
• Often difficult to assess (i.e. previous medications,
post-ictal state)
• Neurology consult is imperative