Status Epilepticus


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  • SE and GCSE are the only abbreviations used during this presentation
  • This definition has been repeated in most articles and textbooks. However, there is nothing magic about 30 minutes. In fact, the likelihood for a tonic-clonic seizure to stop spontaneously decreases dramatically after 5 minutes. Where did the initial definition of 30 minutes come from?
  • This information however is not very helpful when trying to formulate a rational approach to the treatment of a child with GCSE.
  • The key questions for the physician treating a child with GCSE should be: - When does treatment for GCSE need to be initiated? - After what length of GCSE is it unlikely to stop spontaneously? - Should I wait ? How long?
  • The above statements are reviewed and referenced in the papers by Bleck and by the (British) Status Epilepticus Working Party. Bleck TP. Management approaches to prolonged seizures and status epilepticus. Epilepsia 1999;40(1):S64-6 Appleton R, Choonara I, Martland T, et al. The treatment of convulsive status epilepticus in children. The Status Epilepticus Working Party, Members of the Status Epilepticus Working Party. Arch Dis Child 2000;83(5):415-9
  • Lowenstein and Bleck review (with references) average duration of tonic-clonic seizures in children, i.e. usual length of seizure with high chance of spontaneous cessation. Lowenstein DH, Bleck T, Macdonald RL. It's time to revise the definition of status epilepticus. Epilepsia 1999;40(1):120-2.
  • They consequently present a revised definition of status epilepticus. They essentially use the term status epilepticus for GCSE in a child which - is unlikely to stop by itself, and - will require active intervention.
  • The fact that infants with SE have a higher mortality is likely due to the different etiologies of SE in infants, when compared to older children.
  • Nicely reviewed in : Fountain NB. Status epilepticus: risk factors and complications. Epilepsia 2000;41 Suppl 2:S23-30 Marked systemic and neurologic changes occur after about 30-60 minutes of seizure activity (see Fountain) and also: DeLorenzo RJ, Towne AR, Pellock JM, et al. Status epilepticus in children, adults, and the elderly. Epilepsia 1992;33 Suppl 4:S15-25 Bassin S, Smith TL, Bleck TP. Clinical review: status epilepticus. Crit Care 2002;6(2):137-42 Neurologic injury is likely to occur after 60 minutes of SE ( reviewed in: DeLorenzo.) There is also a nice graph with probable time relationship in: Haafiz A, Kissoon N. Status epilepticus: current concepts. Pediatr Emerg Care 1999;15(2):119-29
  • The priority is oxygenation! All actively seizing children have a significant respiratory (and usually moderate metabolic) acidosis. Most practitioners feel that, intubation (and ABG sampling) can be deferred until the seizures have been stopped, as long as the patient remains well oxygenated and is not completely apneic. See: Treatment of convulsive status epilepticus . Recommendations of the Epilepsy Foundation of America's Working Group on Status Epilepticus. JAMA 1993;270(7):854-9 Aminoff MJ, Simon RP. Status epilepticus. Causes, clinical features and consequences in 98 patients. Am J Med 1980;69(5):657-66 Any NMB agent given during SE should be very short acting, so that ongoing SE can be observed if it occurs. Termination of convulsive activity by muscular paralysis alone does not protect the brain from seizure induced hypermetabolism and risk of neuronal injury!
  • CT indications clearly are not exclusive. Other patients also need to be considered. On the other hand, not every child with established seizure disorder need a CT for each episode of GCSE. MRI will give a more detailed image, and may show changes not seen on CT.
  • Lorazepam is for most practitioners the preferred benzodiazepine in SE, mostly because it has a longer lasting anticonvulsant effect. Both midazolam and lorazepam can be given i.m. . Although some reviews suggest i.m. medications in case of impossible i.v. access, rectal diazepam followed by intraosseus access are recommended by most
  • Rectal administration of undiluted diazepam was simple, safe, and effective in the treatment of seizures when intravenous access could not be obtained (Seigler, 1990). A 1 cc disposable insulin syringe, inserted 4 to 5 cm into the rectum was recommended as the means to administer the 0.5 to 1 milligram/kilogram diazepam dose. Alternatively, a small feeding tube attached to the syringe can be absorbed rectally. Prior to the advent of Diastat (quite expensive!!), many practitioners routinely used iv diazepam rectally with excellent results. Seigler RS. The administration of rectal diazepam for acute management of seizures. J Emerg Med 1990;8(2):155-9.
  • Chamberlain JM, Altieri MA, Futterman C, et al. A prospective, randomized study comparing intramuscular midazolam with intravenous diazepam for the treatment of seizures in children. Pediatr Emerg Care 1997;13(2):92-4. Towne AR, DeLorenzo RJ. Use of intramuscular midazolam for status epilepticus. J Emerg Med 1999;17(2):323-8.
  • The main difference between phenytoin and fosphenytoin in children is the pH. Fosphenytoin will not cause the severe tissue damage seen with phenytoin in case of infiltration. In most markets, fosphenytoin is significantly more expensive
  • Phenobarbital is usually the preferred long-acting anticonvulsants in infants , as it can be easily maintained later with oral administration. Intestinal phenytoin absorption is very erratic in infants. Otherwise, many recommend phenytoin as first choice, as it may alter mental state less severely.
  • The finding of any of the above does not necessarily suggest non-convulsive SE. Clonus, Babinski and some posturing are often found just after termination of SE, especially when touching/handling the patient
  • Oxygen Airway (suction, position, listen, consider oral airway) Breathing? (consider BVM) Monitor IV access
  • Reasonable indication to give intramuscular midazolam (0.2 mg/kg) or rectal diazepam (0.3 - 0.5 mg/kg), either as gel or iv solution, using a tuberculin syringe, r a small syringe with attached feeding tube. Continue attempts at iv access.
  • Continue oxygen and airway maintenance Labs, including rapid blood sugar Lorazepam 0.1 mg/kg i.v., readily repeat after 5 minutes if still seizing Needs long-acting anticonvulsant, phenytoin probably preferred over phenobarb in this 3 year old. As he has a small peripheral iv catheter only, he has a good indication to use the more expensive fosphenytoin. Give 20 mg/kg phenytoin-equivalent Start glucose containing iv fluid
  • Respiratory and metabolic acidosis very common while actively seizing. ABG does not help with management. There is no indication to intubate, as pt is now oxygenating well, and is not apneic. Unresponsiveness likely will improve soon, as his postictal state lightens. No need to repeat ABG. No indication for bicarbonate.
  • The usual: Oxygen, airway, circulation Monitor Start iv access Possible causes include hyponatremia/ - glycemia, and/or viral encephalitis or bacterial meningitis. Important to check electrolytes and blood sugar early.
  • First intervention should be manual ventilation with a bag. As it is - quite likely for the chest wall rigidity/hypoventilation to resolve as the seizure stops, and as - intubation of the actively seizing child is near impossible without significant trauma, Intubation should be postponed if possible. If oxygenation can not be maintained with manual ventilation, the patient should be intubated using a short acting muscle relaxant (rocuronium, or even succinylcholine).
  • Assume ongoing electrical seizure activity, treat seizures as urgently as if there were ongoing, visible convulsions. Waiting for blood sugar and sodium.
  • SE is likely due to acute, severe hyponatremia. SE is persisting, pt has only received one dose of lorazepam so far! Give more lorazepam. Load with 20 mg/kg phenobarbital (or phenytoin; but phenobarb is probably preferred drug for this age) As hyponatremia is symptomatic (and history suggests recent development), need to treat hyponatremia with hypertonic saline. Would suggest to raise Na rapidly to about 125 mEq/L. 125 - 118 = 7 In order to raise serum Na by 1 mEq/L, 0.6 mEq/kg Na are required 3% NaCl contains 0.5 mEq/ml 7 x 1.2 x weight (kg) = ml of 3% NaCl required
  • Status Epilepticus

    1. 1. Generalized, Tonic-Clonic Status Epilepticus in Children Heinrich Werner, MD Pediatric Critical Care University of Kentucky Children’s Hospital
    2. 2. Objectives <ul><li>The participant will increase her/his </li></ul><ul><ul><li>ability to define status epilepticus using a practical, mechanistic approach </li></ul></ul><ul><ul><li>ability to list probable causes for status epilepticus in children </li></ul></ul><ul><ul><li>understanding of the pathophysiologic events </li></ul></ul><ul><ul><li>knowledge of treatment strategies for pediatric status epilepticus </li></ul></ul>
    3. 3. <ul><li>Status epilepticus (SE) presents in a multitude of forms , dependent on etiology and patient age (myoclonic, tonic, subtle, tonic-clonic, absence, complex partial etc.) </li></ul><ul><li>Generalized, tonic-clonic SE (GCSE) is the most common form of SE </li></ul><ul><li>The following presentation refers to generalized, tonic-clonic SE </li></ul>
    4. 4. Definition <ul><li>Conventional “textbook” definition of status epilepticus: </li></ul><ul><ul><li>Single seizure > 30 minutes </li></ul></ul><ul><ul><li>Series of seizures > 30 minutes without full recovery </li></ul></ul>
    5. 5. Why 30 minutes ? <ul><li>Animal experiments in the 1970s and 1980s had shown that ... </li></ul><ul><li>… neuronal injury could be demonstrated after 30 min of seizure activity, even while maintaining respiration and circulation </li></ul><ul><li>Nevander G. Ann Neurol 1985;18(3):281-90. </li></ul>
    6. 6. More practical: Mechanistic definition <ul><li>GCSE is a condition which most likely will not terminate rapidly and / or spontaneously </li></ul><ul><li>GCSE is a condition which requires prompt intervention </li></ul><ul><li>Lowenstein DH. Epilepsia 1999 </li></ul>
    7. 7. <ul><li>The longer SE persists, </li></ul><ul><ul><li>the lower is the likelihood of spontaneous cessation </li></ul></ul><ul><ul><li>the harder it is to control </li></ul></ul><ul><ul><li>the higher is the risk of morbidity and mortality </li></ul></ul><ul><li>Bleck TP. Epilepsia 1999;40(1):S64-6 </li></ul><ul><li>The Status Epilepticus Working Party. Arch Dis Child 2000;83(5):415-9. </li></ul>
    8. 8. Typical seizure duration <ul><li>Children > 5 years: </li></ul><ul><li>Typical, generalized tonic-clonic seizure lasts < 5 minutes </li></ul><ul><li>Young children and infants: </li></ul><ul><li>Paucity of data. Suggested time frame for typical tonic-clonic seizure : < 10-15 minutes </li></ul><ul><li>Reviewed in: Lowenstein DH. It's time to revise the definition of status epilepticus. Epilepsia 1999;40(1):120-2. </li></ul>
    9. 9. Revised Definition <ul><li>Generalized, convulsive status epilepticus in older children (> 5 years) refers to > 5 minutes of continuous seizure or > 2 discrete seizures with incomplete recovery of consciousness </li></ul><ul><li>Patients with generalized seizure activity at arrival in the ER are treated promptly regardless of prior duration </li></ul><ul><li>Lowenstein DH, Bleck T, Macdonald RL. It's time to revise the definition of status epilepticus. Epilepsia 1999;40(1):120-2. </li></ul>
    10. 10. Causes <ul><li>Fever </li></ul><ul><li>Medication change </li></ul><ul><li>Unknown </li></ul><ul><li>Metabolic </li></ul><ul><li>Congenital </li></ul><ul><li>Anoxic </li></ul><ul><li>Other (trauma, vascular, infection, tumor, drugs) </li></ul><ul><li>36% </li></ul><ul><li>20% </li></ul><ul><li>9% </li></ul><ul><li>8% </li></ul><ul><li>7% </li></ul><ul><li>5% </li></ul><ul><li>15% </li></ul>DeLorenzo RJ. Epilepsia 1992;33 Suppl 4:S15-25
    11. 11. Drugs which can cause seizures <ul><li>Antibiotics </li></ul><ul><ul><li>Penicillins </li></ul></ul><ul><ul><li>Isoniazid </li></ul></ul><ul><ul><li>Metronidazole </li></ul></ul><ul><li>Anesthetics, narcotics </li></ul><ul><ul><li>Halothane, enflurane </li></ul></ul><ul><ul><li>Cocaine, fentanyl </li></ul></ul><ul><ul><li>Ketamine </li></ul></ul><ul><li>Psychopharmaceuticals </li></ul><ul><ul><li>Antihistamines </li></ul></ul><ul><ul><li>Antidepressants </li></ul></ul><ul><ul><li>Antipsychotics </li></ul></ul><ul><ul><li>Phencyclidine </li></ul></ul><ul><ul><li>Tricyclic antidepressants </li></ul></ul>
    12. 12. Mortality <ul><li>Adults </li></ul><ul><li>Children </li></ul><ul><li>15 to 22% </li></ul><ul><li>3 to 15% </li></ul>Reviewed in: Fountain NB. Epilepsia 2000;41 Suppl 2:S23-30
    13. 13. Mortality <ul><li>The primary determinant of mortality and morbidity of SE in children is its etiology </li></ul><ul><li>The greatest mortality and highest rate of neurological deficits occurs when SE is caused by an acute neurological condition (infection, trauma, stroke) </li></ul>Mitchell WG. J Child Neurol 2002;17 Suppl 1:S36-43.
    14. 14. Prolonged seizures Duration of seizure Life threatening systemic changes Death Temporary systemic changes
    15. 15. Respiratory <ul><li>Hypoxia and hypercarbia </li></ul><ul><ul><li>Ventilation </li></ul></ul><ul><ul><ul><li>(chest rigidity from muscle spasm) </li></ul></ul></ul><ul><ul><li>Hypermetabolism </li></ul></ul><ul><ul><ul><li>(  O 2 consumption,  CO 2 production) </li></ul></ul></ul><ul><ul><li>Poor handling of secretions </li></ul></ul><ul><ul><li>Neurogenic pulmonary edema? </li></ul></ul>
    16. 16. Hypoxia <ul><li>Hypoxia/anoxia markedly increase (triple?) the risk of mortality in SE </li></ul><ul><li>Seizures (without hypoxia) are much less dangerous than seizures and hypoxia </li></ul><ul><li>Towne AR. Epilepsia 1994;35(1):27-34 </li></ul>
    17. 17. Neurogenic Pulmonary Edema <ul><li>Rare complication of SE in children </li></ul><ul><li>Likely occurs as consequence of marked increase of pulmonary vascular pressure during SE </li></ul>Johnston SC. Postictal pulmonary edema requires pulmonary vascular pressure increases. Epilepsia 1996;37(5):428-32
    18. 18. Acidosis <ul><li>Respiratory </li></ul><ul><li>Lactic </li></ul><ul><ul><li>Impaired tissue oxygenation </li></ul></ul><ul><ul><li>Increased energy expenditure </li></ul></ul>
    19. 19. Hemodynamics <ul><li>Sympathetic overdrive </li></ul><ul><ul><li>Massive catecholamine / autonomic discharge </li></ul></ul><ul><ul><li>Hypertension </li></ul></ul><ul><ul><li>Tachycardia </li></ul></ul><ul><ul><li>High CVP </li></ul></ul><ul><li>Exhaustion </li></ul><ul><ul><li>Hypotension </li></ul></ul><ul><ul><li>Hypoperfusion </li></ul></ul>0 min 60 min
    20. 20. Cerebral blood flow - Cerebral O 2 requirement <ul><li>Hyperdynamic phase </li></ul><ul><ul><li>CBF meets CMRO 2 </li></ul></ul><ul><li>Exhaustion phase </li></ul><ul><ul><li>CBF drops as hypotension sets in </li></ul></ul><ul><ul><li>Autoregulation exhausted </li></ul></ul><ul><ul><li>Neuronal damage ensues </li></ul></ul>Blood pressure Blood flow O 2 requirement Seizure duration Hyperdynamic Exhaustion Lothman E. Neurology 1990;40(5 Suppl 2):13-23.
    21. 21. Glucose <ul><li>Hyperdynamic phase </li></ul><ul><ul><li>Hyperglycemia </li></ul></ul><ul><li>Exhaustion phase </li></ul><ul><ul><li>Hypoglycemia develops </li></ul></ul><ul><ul><li>Hypoglycemia appears earlier in presence of hypoxia </li></ul></ul><ul><ul><li>Neuronal damage ensues </li></ul></ul>Lothman E. Neurology 1990;40(5 Suppl 2):13-23. Glucose Seizure duration 30 min SE SE + hypoxia
    22. 22. Hyperpyrexia <ul><li>Hyperpyrexia may develop during protracted SE, and aggravate possible mismatch of cerebral metabolic requirement and substrate delivery </li></ul><ul><li>Treat hyperpyrexia aggressively </li></ul><ul><ul><li>Antipyretics, external cooling </li></ul></ul><ul><ul><li>Consider intubation, relaxation, ventilation </li></ul></ul>
    23. 23. Other alterations <ul><li>Blood leukocytosis (50% of children) </li></ul><ul><li>Spinal fluid leukocytosis (15% of children) </li></ul><ul><li> K + </li></ul><ul><li> creatine kinase </li></ul><ul><li>Myoglobinuria </li></ul><ul><li>Blood leukocytosis (50% of children) </li></ul><ul><li>Spinal fluid leukocytosis (15% of children) </li></ul><ul><li> K + </li></ul><ul><li> creatine kinase </li></ul><ul><li>Myoglobinuria </li></ul>
    24. 24. <ul><li>Oxygen, oral airway. Suction. Avoid hypoxia! </li></ul><ul><li>Consider bag-valve mask ventilation. Consider intubation </li></ul><ul><li>IV/IO access. Treat hypotension, but NOT hypertension </li></ul>A B C
    25. 25. Treatment <ul><li>Arterial blood gas? </li></ul><ul><ul><li>All children in SE develop acidosis. It often resolves rapidly with termination of SE </li></ul></ul><ul><li>Intubate? </li></ul><ul><ul><li>It may be difficult to intubate a child with active seizures </li></ul></ul><ul><ul><li>Stop or slow seizures first, give O 2 , consider BVM ventilation </li></ul></ul><ul><ul><li>If using paralytic agent to intubate, assume that SE continues </li></ul></ul>
    26. 26. Initial investigations <ul><li>Labs </li></ul><ul><ul><li>Na, Ca, Mg, PO 4 , glucose </li></ul></ul><ul><ul><li>CBC </li></ul></ul><ul><ul><li>Liver function tests, ammonia </li></ul></ul><ul><ul><li>Anticonvulsant drug level </li></ul></ul><ul><ul><li>Toxicology </li></ul></ul>
    27. 27. Initial investigations <ul><li>Lumbar puncture </li></ul><ul><ul><li>Always defer LP in unstable patients, but never delay antibiotic/antiviral treatment if indicated </li></ul></ul><ul><li>CT scan </li></ul><ul><ul><li>Indicated for focal seizures or focal deficit or focal EEG, history of trauma or bleeding disorder </li></ul></ul>Treatment of convulsive status epilepticus. Recommendations of the Epilepsy Foundation of America's Working Group on Status Epilepticus. JAMA 1993;270(7):854-9.
    28. 28. Treatment <ul><li>Give glucose (2-4 ml/kg D25%, infants 5 ml/kg D10%), unless normo- or hyperglycemic </li></ul><ul><li>Hyperglycemia has no negative effect in SE </li></ul><ul><li>(as long as significant hyperosmolality is being avoided) </li></ul>
    29. 29. Treatment <ul><li>The longer you wait to administer anticonvulsants, the more anticonvulsants you will need to stop SE </li></ul><ul><li>Most common mistake is ineffective dose </li></ul>
    30. 30. Anticonvulsants <ul><li>Rapid acting </li></ul><ul><li>plus </li></ul><ul><li>Long acting </li></ul>
    31. 31. Anticonvulsants - Rapid acting <ul><li>Benzodiazepines </li></ul><ul><ul><li>Lorazepam 0.1 mg/kg i.v. over 1-2 minutes </li></ul></ul><ul><ul><li>Diazepam 0.2 mg/kg i.v. over 1-2 minutes </li></ul></ul><ul><ul><li>If SE persists, repeat every 5-10 minutes </li></ul></ul>
    32. 32. Benzodiazepines <ul><li>Diazepam </li></ul><ul><ul><li>High lipid solubility </li></ul></ul><ul><ul><li>Thus very rapid onset </li></ul></ul><ul><ul><li>Redistributes rapidly </li></ul></ul><ul><ul><li>Thus rapid loss of anticonvulsant effect </li></ul></ul><ul><ul><li>Adverse effects are persistent: </li></ul></ul><ul><ul><ul><li>Hypotension </li></ul></ul></ul><ul><ul><ul><li>Respiratory depression </li></ul></ul></ul><ul><li>Lorazepam </li></ul><ul><ul><li>Low lipid solubility </li></ul></ul><ul><ul><li>Action delayed 2 minutes </li></ul></ul><ul><ul><li>Anticonvulsant effect 6-12 hrs </li></ul></ul><ul><ul><li>Less respiratory depression than diazepam </li></ul></ul><ul><li>Midazolam </li></ul><ul><ul><li>May be given i.m. </li></ul></ul>
    33. 33. Benzodiazepine - Rectal <ul><li>Rectal diazepam </li></ul><ul><ul><li>0.3 to 0.5 mg/kg rectal gel, typically reaches anticonvulsant levels within 5-10 minutes </li></ul></ul><ul><ul><li>Intravenous solution given rectally is equally effective </li></ul></ul><ul><ul><li>(and much cheaper) </li></ul></ul><ul><ul><li>Seigler RS. J Emerg Med1990;8(2):155-9. </li></ul></ul><ul><ul><li>Cost : </li></ul></ul><ul><ul><ul><li>5 mg Diastat rectal gel $ 78.00 </li></ul></ul></ul><ul><ul><ul><li>5 mg diazepam intravenous solution $ 1.40 </li></ul></ul></ul>
    34. 34. Benzodiazepine - Intramuscular <ul><li>Intramuscular midazolam </li></ul><ul><ul><li>0.2 mg/kg i.m. </li></ul></ul><ul><ul><li>Aqueous solution is rapidly absorbed, anticonvulsant effect begins after 2 minutes </li></ul></ul><ul><li>Intramuscular lorazepam </li></ul><ul><ul><li>Can be given, but lacks water solubility, thus later onset than midazolam </li></ul></ul><ul><ul><li>Chamberlain JM. Pediatr Emerg Care 1997;13(2):92-4. </li></ul></ul><ul><ul><li>Towne AR. J Emerg Med 1999;17(2):323-8. </li></ul></ul>
    35. 35. Anticonvulsants - Long acting <ul><li>Phenytoin </li></ul><ul><ul><li>20 mg/kg i.v. over 20 min </li></ul></ul><ul><ul><li>pH 12 </li></ul></ul><ul><ul><li>Extravasation causes severe tissue injury </li></ul></ul><ul><ul><li>Onset 10-30 min </li></ul></ul><ul><ul><li>May cause hypotension, dysrhythmia </li></ul></ul><ul><ul><li>Cheap </li></ul></ul><ul><li>Fosphenytoin </li></ul><ul><ul><li>20 mg PE/kg i.v. over 5-7 min PE = phenytoin equivalent </li></ul></ul><ul><ul><li>pH 8.6 </li></ul></ul><ul><ul><li>Extravasation well tolerated </li></ul></ul><ul><ul><li>Onset 5-10 min </li></ul></ul><ul><ul><li>May cause hypotension </li></ul></ul><ul><ul><li>Expensive </li></ul></ul>
    36. 36. If in doubt, measure free phenytoin! <ul><li>Phenytoin is largely protein bound </li></ul><ul><li>(> 90%, varies with serum protein concentration) </li></ul><ul><li>Free phenytoin = active phenytoin </li></ul><ul><li>(anticonvulsant and toxic effects) </li></ul><ul><li>Toxicity more likely with hypoalbuminemia (usually if < 2 g/dL) </li></ul><ul><li>Therapeutic levels </li></ul><ul><ul><li>Total phenytoin: 10 - 20 mcg/ml </li></ul></ul><ul><ul><li>Free phenytoin: 0.8 - 1.6 mcg/ml </li></ul></ul>
    37. 37. Anticonvulsants - Long acting <ul><li>Phenobarbital </li></ul><ul><ul><li>20 mg/kg i.v. over 10 - 15 min </li></ul></ul><ul><ul><li>Onset 15-30 min </li></ul></ul><ul><ul><li>May cause hypotension, respiratory depression </li></ul></ul>
    38. 38. Initial choice of long acting anticonvulsants in SE Is patient an infant? Is patient already receiving phenytoin? Yes No At high risk for extravasation ? (small vein, difficult access etc.)? Phenobarbital Yes No Phenytoin Fosphenytoin
    39. 39. If SE persists <ul><li>Propofol infusion 5-10 mg/kg/hr after bolus 2 mg/kg </li></ul><ul><li>Midazolam infusion 1 - 10 mcg/kg/min after bolus 0.15 mg/kg </li></ul><ul><li>Pentobarbital infusion 1-3 mg/kg/hr after bolus 10 mg/kg </li></ul><ul><li>Paraldehyde: no longer allowed for human use </li></ul><ul><li>Isoflurane </li></ul>
    40. 40. Non - convulsive status epilepticus <ul><li>How do you tell that patient’s seizures have stopped? </li></ul>
    41. 41. Non - convulsive SE ? <ul><li>Neurologic signs after termination of SE are common: </li></ul><ul><ul><li>Pupillary changes </li></ul></ul><ul><ul><li>Abnormal tone </li></ul></ul><ul><ul><li>Abnormal Babinski reflex </li></ul></ul><ul><ul><li>Posturing </li></ul></ul><ul><ul><li>Clonus </li></ul></ul><ul><ul><li>May be asymmetrical </li></ul></ul>
    42. 42. Non - convulsive SE ? <ul><li>Up to 20% of children with SE have non - convulsive SE after tonic - clonic SE </li></ul><ul><li>Particularly common in infants < 2 months </li></ul>Mitchell WG. J Child Neurol 2002;17 Suppl 1:S36-43.
    43. 43. Non - convulsive SE ? <ul><li>If child does not begin to respond to painful stimuli within 20 - 30 minutes after tonic - clonic SE stops, suspect non - convulsive SE </li></ul><ul><ul><li>Urgent EEG </li></ul></ul>
    44. 44. Case Scenario (1a) <ul><li>A 2 y.o. boy arrives in your ER via ambulance, with active seizures. Parents had called 911, crew found pt having generalized, tonic-clonic seizure </li></ul><ul><li>No drugs given yet </li></ul><ul><li>What are your priorities? </li></ul>
    45. 45. Case Scenario (1b) <ul><li>A,B,C. Stopping seizure. </li></ul><ul><li>With supplemental O 2 , saturation signal comes and goes, but reads 100% when plethysmographic tracing looks acceptable. Lips are pink. Child is moving air with proper head positioning and jaw thrust </li></ul><ul><li>HR 145/min, BP 130/85 </li></ul><ul><li>Several unsuccessful i.v. attempts, still trying after 5 minutes. Continued seizure activity </li></ul><ul><li>What next? </li></ul>
    46. 46. Case Scenario (1c) <ul><li>Use alternate route for initial dose of benzodiazepine </li></ul><ul><li>A few minutes after midazolam 7.5 mg im, seizures stop, but then start again. There was time enough for one of your best nurses to insert a 24g iv catheter into the pt’s hand. </li></ul><ul><li>Vital signs unchanged </li></ul><ul><li>Everybody looks to you for new orders </li></ul>
    47. 47. Case Scenario (1d) <ul><li>After two doses of lorazepam and initiation of 20 mg/kg fosphenytoin, the child stops convulsing </li></ul><ul><li>He currently is unresponsive, RR 12/min, O 2 Sat 100% in oxygen, HR 115/min, BP 105/60 </li></ul><ul><li>ABG drawn earlier (sent by RN, you had not asked for it): pH 7.02 pCO 2 76 pO 2 95 BE - 8 </li></ul><ul><li>What will you do ? Intubate (mental state, pCO 2 )? Give bicarb? Repeat ABG? </li></ul>
    48. 48. Case Scenario (1e) <ul><li>Combined metabolic/respiratory acidosis to be expected during SE. Does not dictate intubation, does not require HCO 3 </li></ul><ul><li>As long as pt is oxygenating well, can wait for post-ictal state to resolve, without further ABG </li></ul><ul><li>If pt remains completely unresponsive 30 minutes after cessation of GCSE, suspect non-convulsive SE </li></ul>
    49. 49. Case Scenario (2a) <ul><li>3 month old infant with a 4 day history of vomiting and diarrhea. Parents tried to maintain hydration using diluted formula , soda and now rice water </li></ul><ul><li>Lethargic all day, then started convulsing </li></ul><ul><li>Active, generalized tonic-clonic seizure on arrival in ER </li></ul><ul><li>Your initial actions? </li></ul><ul><li>Possible cause? </li></ul>
    50. 50. Case Scenario (2b) <ul><li>Meningo-encephalitis? Sepsis? Electrolyte disturbance? </li></ul><ul><li>After you start high flow oxygen via a partial rebreather mask, suction the airway and position the head in mild hyperextension with jaw thrust, O 2 saturation reads around 60%, and the child looks blue. He is still seizing . You see no chest rise and hear no air entry. </li></ul><ul><li>What is your plan of action? </li></ul>
    51. 51. Case Scenario (2c) <ul><li>Saturation improves to about 85% with BVM ventilation, the pt looks less blue but not pink. Fairly violent seizure activity continues. </li></ul><ul><li>Per your order, the first dose of lorazepam is going into the IV, but pt continues to seize and is cyanotic </li></ul><ul><li>You give rocuronium 1 mg/kg rapidly iv, and expertly intubate the child. He is now being ventilated, pink and not seizing any more </li></ul><ul><li>Good job! Anything else to be done? What information are you eagerly waiting for? </li></ul>
    52. 52. Case Scenario (2d) <ul><li>Have to assume ongoing electrical seizures. What is the sodium? </li></ul><ul><li>Blood sugar is 180 mg/dL, Na is 118 mEq/L </li></ul><ul><li>Neuromuscular blockade is beginning to wear off, there is still seizure activity </li></ul><ul><li>What now? </li></ul>
    53. 53. Case Scenario (2e) <ul><li>After 20 mg/kg phenobarbital, and halfway into an infusion of 3% NaCl, seizure activity slows, and then stops </li></ul><ul><li>You consider a CT, plan an LP, start antibiotics </li></ul><ul><li>You have a high index of suspicion for ongoing electrical seizures (non-convulsive SE) in this infant </li></ul>
    54. 54. Suggested Reading 1. Fountain NB. Status epilepticus: risk factors and complications. Epilepsia 2000;41 Suppl 2:S23-30. 2. Treatment of convulsive status epilepticus. Recommendations of the Epilepsy Foundation of America's Working Group on Status Epilepticus. JAMA 1993;270(7):854-9. 3. Bassin S, Smith TL, Bleck TP. Clinical review: status epilepticus. Crit Care 2002;6(2):137-42. 4. Bleck TP. Management approaches to prolonged seizures and status epilepticus. Epilepsia 1999;40(1):S64-6. 5. DeLorenzo RJ, Towne AR, Pellock JM, et al. Status epilepticus in children, adults, and the elderly. Epilepsia 1992;33 Suppl 4:S15-25. 6. Haafiz A, Kissoon N. Status epilepticus: current concepts. Pediatr Emerg Care 1999;15(2):119-29. 7. Lowenstein DH, Bleck T, Macdonald RL. It's time to revise the definition of status epilepticus. Epilepsia 1999;40(1):120-2. 8. Orlowski JP, Rothner DA. Diagnosis and treatment of status epilepticus. In: Fuhrman BP, Zimmerman JJ, editors. Pediatric Critical Care. St. Louis: Mosby; 1998. p. 625-35.