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Do you have a plan for your little patient when he just won’t stop seizing?  What do you do when your typical treatment is not enough? Get up-to-date in the understanding and management of pediatric status epilepticus. Definition of status epilepticus:Continuous seizure activity of 5 minutes or greater – OR – Recurrent activity without recovery between intervals.  (This definition includes clinically apparent seizures as well as those seen only on EEG.) During a seizure, GABA receptors in the neuron’s membrane are internalized and destroyed.  Seizure activity itself starts this self-defeating process – this is the first reason we need to act as quickly as possible and take advantage of the GABA receptors that are still recruitable. Excitatory receptors – the NMDA receptors – are acutely upregulated and mobilize to the neuron’s surface.  This is the second reason to act quickly and avoid this kindling effect. In other words – time is brain. Or… is it something else as well? Pediatric status epilepticus is analogous to the multi-organ dysfunction syndrome in severe sepsis.  Status epilepticus affects almost every organ system.  Cardiac – dysrhythmias, high output failure, and autonomic dysregulation resulting in hypotension or hypertension.  Respiratory – apnea and hypoxia, ARDS, and potentially aspiration pneumonia.  Renal – rhabdomyolysis, myoglobinuria, and acute renal failure. Metabolic – lactic acidosis, hypercapnia, hyperglycemia, sometimes hypoglycemia, hyperkalemia, and leukocytosis. Autonomic – hyperpyrexia and breakdown of cerebral circulation.  DeLorenzo et al.: Mortality correlated with time seizing.  Once the seizure has met the 30 min mark, Delorenzo reported a jump from 4.4% mortality to 22%!  If the seizure lasts greater than 2 hours, 45%.  Time spent seizing is a vicious cycle: it’s harder to break the longer it goes on, and the longer it goes on, the higher the mortality. Think about treatment of pediatric status epilepticus in terms of time: prehospital care, status epilepticus (greater than 5 min), initial refractory status epilepticus (greater than 10 min), later refractory status (at 20 min), and coma induction (at 25 minutes). Case 1: Hyponatremic Status Epilepticus Give 3 mL/kg of 3% saline over 30 min. Stop the infusion as soon as the seizure stops. Case 2: INH toxicity Empiric treatment -- you are the test.  If we know the amount of ingestion in adults or children, we give a gram-for-gram replacement, up to 5 grams.  If a child under 2 years of age arrives to you in stats epilepticus, give 100 mg of IV pyridoxime for potentially undiagnosed congenital deficiency. Case 3: Headache and Arteriovenous Malformation Unlike in adults, stroke in children is divided evenly between hemorrhagic and ischemic etiologies.  The differential is vast: cardiac, hematologic, infectious, vascaulr, syndromic, metabolic, oncologic, traumatic, toxic.  Treatment: stabilization, embolization by interventional radiology, elective extirpation when more stable.  Other options for stable patients include an endovascular flow-directed microcatheter using cyanoacrylate. Radiosurgery is an options for others. Non-convulsive Status Epilepticus Risk factors include age SUMMARY POINTS The longer the seizure lasts, the harder it is to break – act quickly Have a plan for normal escalation of care, and Search for an underlying cause Recognize when the routine treatment is not enough.Before You Go “Healing is a matter of time, but it is sometimes also a matter of opportunity.” “Extreme remedies are very appropriate for extreme diseases.”  – Hippocrates of KosSelected References Abend NS et al. Nonconvulsive seizures are common in critically ill children. Neurology. 2011; 76(12):1071-7 Baren J. Pediatric Seizures and Strokes: Beyond Benzos and Brain Scans. ACEP Scientific Assembly. October 8th, 2009. Boston, MA. Brophy et al. Guidelines for the Evaluation and Management of Status Epilepticus. Neurocrit Care. 2012; DOI 10.1007/s12028-012-9695-z Capovilla G et al. Treatment of convulsive status epilepticus in childhood: Recommendations of the Italian League Against Epilepsy. Epilepsia. 2013; 54 Suppl 7:23-34 Chin RFM et al., for the NLSTEPSS Collaborative Group. Incidence, cause, and short-term outcome of convulsive status epilepticus in childhood: prospective population-based study. Lancet. 2006; 368: 222–29. Chen JW, Chamberlain CG. Status epilepticus: pathophysiology and management in adults. Lancet Neurol. 2006; 5:246-256. DeLorenzo RJ. Comparison of status epilepticus with prolonged seizure episodes lasting from 10 to 29 minutes. Epilepsia. 1999 Feb;40(2):164-9. LaRoche SM, Helmers SL. The New Antiepileptic Drugs: Scientific Review. JAMA. 2004;291:605-614. Minns AB, Ghafouri N, Clark RF. Isoniazid-induced status epilepticus in a pediatric patient after inadequate pyridoxine therapy. Pediatr Emerg Care. 2010; 26(5):380-1. Ogilvy CS et al. Recommendations for the Management of Intracranial Arteriovenous Malformations: A Statement for Healthcare Professionals From a Special Writing Group of the Stroke Council, American Stroke Council. Stroke. 2001; 32: 1458-1471 Rosati A et al. Efficacy and safety of ketamine in refractory status epilepticus in children. Neurology. 2012; 79:2355-2358. Schwartz ID. Hyponatremic seizure in a child using desmopressin for nocturnal enuresis.  Arch Pediatr Adolesc Med. 1998 Oct;152(10):1037-8 Trommer BL, Pasternak JF.  NMDA receptor antagonists inhibit kindling epileptogenesis and seizure expression in developing rats. Brain Res Dev Brain Res. 1990 May 1;53(2):248-52. Waterhouse EJ et al. Prospective population-based study of intermittent and continuous convulsive status epilepticus in Richmond, Virginia. Epilepsia. 1999 Jun;40(6).