1. Status Epilepticus PICU Resident Lecture Series Lucile Packard Children’s Hospital (Updated: April 2011)

2. 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

3. 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

4. Common etiologies

5. Common drugs related to seizures Penicillins Isoniazid Metronidazole Antihistamines Narcotics Ketamine Halothane/Enflurane Tricyclic antidepressants Antipsychotics Phencyclidine Cocaine

6. Physiologic Consequences of SE Phases of SE Respiratory Effects Hyperpyrexia Metabolic derangements Laboratory changes Summary

7. 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)

8. 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

9. 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

10. 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

11. 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

12. Summary of complications

13. Treatment ABCs Venous access Labs Other diagnostic Meds

14. 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

15. 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

16. 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)

17. 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)

18. 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

19. 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

20. Rapid Acting Anticonvulsants

21. Long Acting Anticonvulsants

22. 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

23. “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)

24. “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

25. 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