Status Epilepticus

PICU Resident Lecture SeriesLucile 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

• Penicillins• Isoniazid• Metronidazole• Antihistamines• Narcotics• Ketamine• Halothane/Enflurane

• Tricyclic antidepressants• Antipsychotics• Phencyclidine• Cocaine

Physiologic Consequences of SE

• 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

• 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 non-convulsive 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