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
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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.
Hinweis der Redaktion
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
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
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