Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Pediatric Status Epilepticus Treatment & Management

  • Author: Rajesh Ramachandrannair, MBBS, MD, FRCPC; Chief Editor: Timothy E Corden, MD  more...
 
Updated: Oct 06, 2014
 

Approach Considerations

Status epilepticus (SE) treatment should follow a logical sequence of interventions. Every institution dealing with this problem should design a plan, such as the one outlined below, that is based on current information derived from authoritative sources, as well as on recent reviews of the literature, and the protocol should be communicated to the medical staff. Review the protocol at least annually.

The lack of a structured protocol has been blamed for increased morbidity from SE.[16] Litigation involving patients suffering sequelae of SE is often based on perceptions that treatment deviated from established standards of practice.

Physicians should become familiar with the pharmacology of the drugs used to treat SE. Prudence calls for doses of these drugs to be placed in visible locations within emergency departments (EDs), pediatric units, and nursing stations.

Treatment for generalized SE should be part of a continuum of the management for seizures of shorter duration. Any algorithm for treating seizures should consider the time of onset of the ictal activity (continuous or intermittent without recovery of consciousness) and the number and type of drugs that did not control the seizures, despite appropriate dosages and routes of administration. Remember that seizures of longer duration tend to be more difficult to treat.

Next

Prehospital Care

Supportive care, including management of airway, breathing, and circulation (the ABCs), must be addressed in the prehospital setting. Emergency medical system (EMS) personnel should proceed as follows:

  • Secure the airway
  • Administer supplemental 100% oxygen
  • Infuse isotonic intravenous fluids and dextrose
  • Immobilize the cervical spine in patients with possible trauma

If the seizure fails to stop within 4-5 minutes or if the patient is continuing to seize at the time of EMS arrival, prompt administration of anticonvulsants may be indicated, if permitted by local protocols. Consider rectally administered diazepam (0.5 mg/kg/dose) or intramuscularly administered midazolam (0.1-0.2 mg/kg/dose; not to exceed a cumulative dose of 10 mg).[17]

If persons who know the patient, or who witnessed the onset of the seizures, are present at the scene, EMS providers may be able to collect information that offers clues to the cause of the SE.

Previous
Next

Patient Stabilization

As in any medical emergency, attend to the ABCs first, before starting any pharmacologic intervention. Place patients in the lateral decubitus position to avoid aspiration of emesis and to prevent epiglottis closure over the glottis. Further adjustments of the head and neck may be necessary to improve patency of the airways (use care in the setting of potential neck trauma without full radiographic evaluation). Immobilize the cervical spine if trauma is suspected.

Administer 100% oxygen by facemask. Assist ventilation and use artificial airways (eg, endotracheal intubation) as needed. Suction secretions and decompress the stomach with a nasogastric tube.

Respiratory depression is a common complication of the management of prolonged seizures. Ensure that equipment is available to deliver supplemental oxygen and positive pressure ventilation when initiating anticonvulsant therapy.

Carefully monitor the patient's vital signs, including blood pressure. Carefully monitor the patient's temperature because hyperthermia may worsen brain damage caused by seizures.

In the first 5 minutes of seizure activity, before starting any medications, try to establish intravenous (IV) access and to obtain samples for laboratory tests and for seizure medication levels (see Workup). Infuse isotonic intravenous fluids plus glucose at a rate of 20 mL/kg/h (eg, 200 mL dextrose 5% in normal saline [D5NS] over 1 h for a 10-kg child).

In children younger than 6 years, use intraosseous (IO) infusion if intravenous access cannot be established within 5-10 minutes . Most available anticonvulsants may be administered intravenously or intraosseously.

If serum glucose is low or cannot be measured, give children 2 mL/kg of 25% glucose. Adults should receive 50 mL of 50% glucose, along with 100 mg of thiamine to avoid Wernicke- Korsakoff syndrome.

Other specific treatments may be indicated if the clinical evaluation identifies precipitants of the seizures. Selected agents and indications are as follows:

  • Naloxone - 0.1 mg/kg/dose intravenously preferably (if needed may administer intramuscularly/subcutaneously) for narcotic overdose
  • Pyridoxine - 50-100 mg intravenously/intramuscularly for possible dependency, deficiency, or isoniazid toxicity
  • Antibiotics - If meningitis is strongly suspected, initiate treatment with antibiotics prior to cerebrospinal fluid (CSF) analysis or CNS imaging

If the onset of the seizure was witnessed, initiate anticonvulsant treatment only after 5 minutes of seizure duration. Most seizures stop without intervention.

Obtain a history of the prehospital treatment of the seizures. Cumulative doses of benzodiazepine medication (prehospital included) increase the risk of respiratory failure.

In cases of repetitive convulsions without recovery of consciousness, the duration of the seizure is defined as the time elapsed from the onset of the first seizure to the termination of the last.

Call for the pediatric intensive care unit (PICU) service and respiratory therapists (or anesthesiologists) if seizures persist for more than 20 minutes.

The Table below is based on the Emergency Management Guidelines of Children's Hospital and Regional Medical Center. Step 1, which encompasses the first 0-5 minutes of care and thus precedes the actions outlined in this table, consists of addressing the patient's ABCs.

Table 1. Medical Treatment of Seizures and Status Epilepticus Based on Time Elapsed Since Seizure Onset (Steps 2-4) (Open Table in a new window)

Step Medication Dose Alternatives
Step 2 (6-15 min) Diazepam (Valium) 5-20 mg IV slowly; not to exceed infusion rate of 2 mg/min; pediatric dose is 0.3 mg/kg If IV line is unavailable, use rectally administered (PR) diazepam at 0.5 mg/kg (not to exceed 10 mg) or midazolam (Versed) at 0.2 mg/kg intramuscularly (IM)*, IV, or intranasally*
Lorazepam* (Ativan) 2-4 mg IV slowly*; not to exceed infusion rate of 2 mg/min or 0.05 mg/kg over 2-5 min; pediatric dose is 0.05-0.1 mg/kg
Step 3 (16-35 min) Phenytoin (Dilantin) or fosphenytoin (Cerebyx)† 20 mg/kg IV over 20 min; not to exceed infusion rate of 1 mg/kg/min; do not dilute in 5% dextrose in water (D5W)



If seizures persist, administer 5 mg/kg for 2 doses (if blood pressure is within the reference range and no history of cardiac disease is present)



If unsuccessful, administer phenobarbital 10-20 mg/kg IV (not to exceed 700 mg IV); increase infusion rate by 100 mg/min; phenobarbital may be used in infants before phenytoin; be prepared to intubate patient; closely monitor hemodynamics and support blood pressure as indicated
Step 4 (45-60 min)‡ Pentobarbital anesthesia (patient already intubated) Loading dose: 5-7 mg/kg IV; may repeat 1-mg/kg to 5-mg/kg boluses until EEG exhibits burst suppression; closely monitor hemodynamics and support blood pressure as indicated



Maintenance dose: 0.5-3 mg/kg/h IV; monitor EEG to keep burst suppression pattern at 2-8 bursts/min



Midazolam* infusion loading dose: 100-300 mcg/kg IV followed by IV infusion of 1-2 mcg/kg/min; increase by 1-2 mcg/kg/min every 15 min if seizures persist (effective range 1-24 mcg/kg/min); closely monitor hemodynamics and support blood pressure as indicated; when seizures stop, continue same dose for 48 h then wean by decrements of 1-2 mcg/kg/min every 15 min



Propofol* initial bolus: 2 mg/kg IV; repeat if seizures continue and follow by IV infusion of 5-10 mg/kg/h, if necessary, guided by EEG monitoring; taper dose 12 h after seizure activity stops; closely monitor hemodynamics and support blood pressure as indicated



With phenobarbital-induced anesthesia, repeated boluses of 10 mg/kg are administered until cessation of ictal activity or appearance of hypotension; closely monitor hemodynamics and support blood pressure as indicated



*Not approved by the FDA for the indicated use.



†Doses for fosphenytoin administered in phenytoin equivalents (PE).



‡An alternative third step preferred by some authors is midazolam



administered by continuous IV infusion with a loading dose 0.1-0.3 mg/kg followed by infusion at a rate of 0.1-0.3 mg/kg/h.



Previous
Next

Anticonvulsant Selection

The optimal protocol for management of SE begins with a benzodiazepine, either lorazepam or diazepam.[18] In the United States, lorazepam is the drug of choice in patients with intravenous or intraosseous access. Lorazepam (0.05-0.1 mg/kg IV or IO slowly infused over 2-5 min) has rapid onset and long duration of anticonvulsant action. It is preferred over diazepam,[19, 20] although one review found lorazepam and diazepam equally effective for controlling SE in children.[21, 22]

If an IV line cannot be established rapidly in a child who is too old for IO infusion, use per rectum (PR) diazepam. Midazolam (0.1-0.2 mg/kg IM) is the most effective choice when IV or IO access is not immediately available, but IM midazolam is not approved by the US Food and Drug Administration (FDA) for that indication.

Midazolam is the only benzodiazepine that can be administered safely intramuscularly while providing rapid onset equivalent to that of intravenous agents and a moderate duration of action. Intranasal midazolam may also be an option in children with prolonged seizure without an IV access.

In one study, no difference in efficacy was observed between caregiver-administered intranasal midazolam and rectal diazepam for terminating sustained seizures (ie, >5 minutes) in children at home. Caregiver's satisfaction was higher with the inhaled midazolam (easier to administer) and the median time from medication administration to seizure cessation was 1.3 minutes less for inhaled midazolam compared with rectal diazepam.[23]

If the seizures cease, no further drugs are immediately necessary. The etiology of SE epilepticus should then be investigated.

If benzodiazepine therapy proves ineffective, IV or IO fosphenytoin or phenytoin is used. These agents are effective for most idiopathic generalized seizures and for posttraumatic, focal, or psychomotor SE. Fosphenytoin offers the advantage of a potentially rapid rate of administration with less risk of venous irritation and vascular compromise of the infused limb (eg, purple-glove syndrome).

The loading dose of phenytoin is 20 mg/kg IV or IO; for fosphenytoin, it is 20 mg/kg PE IV or IO. A full loading dose should be delivered unless the patient is known to have a current therapeutic level. With phenytoin, use a slow rate of infusion (< 1 mg/kg/min or < 50 mg/min) to avoid hypotension or cardiac arrhythmias. Although respiratory depression that requires endotracheal intubation may occur at any time during treatment of GTCSE, it is especially common during administration of phenytoin/fosphenytoin.

If fosphenytoin or phenytoin is not effective, phenobarbital (20 mg/kg IV/IO) is the third-line therapy. In many pediatric institutions, phenobarbital is the second-line choice, rather than fosphenytoin or phenytoin, especially for febrile and neonatal SE. Phenobarbital's major disadvantages are that it significantly depresses mental status and causes respiratory difficulty. Obtain serum anticonvulsant levels prior to administering additional long-acting anticonvulsants such as phenytoin or fosphenytoin.

For more information, see the Medscape Reference article Antiepileptic Drugs.

Refractory status epilepticus

The term refractory GTCSE has been used when seizures do not respond to benzodiazepines, phenytoin/fosphenytoin, and phenobarbital. Several options are presently available for these patients.

Barbiturate anesthesia is among the most popular treatments, although midazolam infusions (neither is approved by the FDA) have gained growing acceptance in the United States over the past 5 years. In the United States, barbiturate anesthesia is commonly performed with pentobarbital infusions. Pentobarbital is given in a loading dose of 5-10 mg/kg IV or IO, followed by 0.5-3 mg/kg/hr. In the United Kingdom, thiopental (thiopentone) is often used rather than pentobarbital. High-dose phenobarbital has been used in patients with GTCSE. All barbiturates used in anesthetic doses have been associated with such complications as hypotension, cardiac depression, and infections.

Midazolam and propofol are gaining increasing acceptance throughout the world as alternative treatments for refractory GTCSE, thanks to the comparative ease of handling these drugs in a continuous infusion.[24] However, propofol is not currently recommended for long-term control of SE, due to reports of severe acidosis and movement disorder after prolonged use. Also worrisome is the association of propofol-related metabolic acidosis in patients on the ketogenic diet.

Midazolam has been used, even in neonates, and has a reasonably predictable pharmacology, although movement disorders have been reported from prolonged use of midazolam for sedation.[25] Midazolam is given in a loading dose of 0.2 mg/kg IV or IO, followed by 0.75-10 mcg/kg/min.

In a few cases, adding a maintenance anticonvulsant medication to the patient’s regimen may help wean the patient off a continuous barbiturate infusion. Although the experience is still very limited, both IV valproic acid and topiramate via nasogastric tube have been used with that goal.

High-dose topiramate has been used in adults with SE, at doses as high as 1600 mg/day.[26] One pediatric study used relatively lower initial doses of 2-3 mg/kg/day before proceeding within 48-72 hours to a maintenance dose of 5-6 mg/kg/day (in 2 divided doses daily), which terminated the episode of SE.[27] Another study reported a loading dose of 10 mg/kg followed by 5 mg/kg/day maintenance (in 2 divided doses daily).[28] Treatment of SE with topiramate is suggested by the neuroprotective action of this drug in animal models. Nonetheless, further data are necessary to show similar action in humans.

Intravenous valproic acid is used for 3-Hz spike and wave stupor (absence SE) and myoclonic SE in cases of juvenile myoclonic epilepsy and postanoxic myoclonus.[29, 30] Treatment of convulsive status (ie, GTCSE) with IV valproic acid after failure of other drugs (eg, benzodiazepines, phenytoin, phenobarbital) has been rarely reported. Both secondary and primary GTCSE seem to equally respond to IV valproic acid.

A loading dose of 15-20 mg/kg is used, followed by 10 mg/kg every 6 hours. Alternatively, Uberall et al recommend a loading dose of 20-40 mg/kg over 5 minutes, followed by an infusion at a rate of 5 mg/kg/h.[31] After 12 hours of clinical and EEG cessation of seizures, the dose is reduced to 1 mg/kg every 2 hours.

Reports have shown the efficacy of levetiracetam as an add-on therapy in adults with refractory SE, with reported loading doses of 500-3000 mg/day and a maintenance dose of 2000-3000 mg/d. In children, the reported loading dose is 30-40 mg/kg.[32, 33, 34]

In Europe, alternative agents such as paraldehyde, lidocaine (Sweden and United Kingdom), and chlormethiazole (mostly United Kingdom) have been used. Paraldehyde is no longer commercially available in the United States, whereas chlormethiazole is not approved by the FDA. Lidocaine is unpopular in the United States because of its narrow therapeutic index and proconvulsant effect at toxic levels.

Paraldehyde is a very effective drug, despite problems (eg, sterile abscess, pulmonary edema), but was discontinued from the US market in 2008. Respiratory failure and hypotension of sudden onset has been described. Shorvon recommends pediatric doses of 0.07-0.35 mL/kg.[35] The adult dose is 5 mL PR diluted on the same volume of water.

Exposure to air and light causes conversion of paraldehyde to acetaldehyde and then to acetic acid, with subsequent metabolic acidosis when administrated. Paraldehyde dissolves some plastic syringes and tubing if not used immediately.

Approximately 80% of the paraldehyde is absorbed after a single rectal dose. Because of the high solubility of paraldehyde in lipids, the passage through the blood brain barrier may depend more on the cerebral blood flow; this is an attractive quality because of the possibility of a differential absorption concentration of the drug by the regions of the cortex involved in the epileptiform activity because they have higher blood flow than the rest of the brain during seizures.

A therapeutic trial with folinic acid (0.5-1 mg/kg) and enteral pyridoxine (up to 30 mg/kg/day) for a week is worth considering in prolonged refractory status epilepticus.

Previous
Next

Further Inpatient Care

Most children with an episode of SE should be admitted for inpatient observation, evaluation, and treatment. Any child with persistent altered mental status (despite cessation of seizure activity) or with prolonged status epilepticus should be admitted to a pediatric critical care unit.

Treat patients with status epilepticus (SE) who have suspected herpes encephalitis with acyclovir until the diagnosis can be confirmed. Suspect herpes virus encephalitis in all patients with fever, mental status changes, and de novo onset of partial seizures, with or without secondary generalization.

Treatment of catscratch disease is not universally efficacious. Rifampin, ciprofloxacin, and trimethoprim-sulfamethoxazole have been successfully used.

Electrolyte disturbances may cause or perpetuate seizures; hypocalcemia and hyponatremia are the most common. Efforts to correct hyponatremia should be performed carefully because quick shifts in serum osmolality may cause irreversible brain damage from central pontine myelinolysis. Correction of hypocalcemia with IV calcium gluconate should be performed under electrocardiographic (ECG) monitoring because of the possibility of cardiac arrhythmias.

Previous
Next

Long-Term Antiepileptic Therapy

Although a complete guide for outpatient management of epilepsy is beyond the scope of this article, the Epilepsy Foundation Working Group on Status Epilepticus recommends starting some patients, including those with a history of epilepsy or brain lesion, on long-term antiepileptic therapy after an episode of SE.

No long-term therapy is indicated for SE caused by transient problems (eg, metabolic disturbances such as hyponatremia, intoxications). No consensus has been reached regarding the need for treatment after an instance of febrile SE or when a first unprovoked seizure is an SE episode.

Although many studies have shown that recurrent seizure risk is unrelated to seizure duration, a recurring GTCSE episode is more likely to be a prolonged seizure.

Knowledge of the seizure type and EEG pattern can help confirm the diagnosis of an epileptic syndrome and guide the selection of anticonvulsant medication. Patients with partial seizures respond better overall to carbamazepine, phenytoin, and phenobarbital (infants).

Valproic acid and phenobarbital are better treatments for patients with generalized tonic-clonic seizures, although carbamazepine and phenytoin can also be administered for patients with secondary generalized seizures. Valproic acid carries a higher risk of liver failure in patients younger than 2 years and those on polypharmacy.

Previous
Next

Consultations

After initial emergency stabilization, consider consultation with the following specialists:

  • Pediatric emergency or critical care specialist or general pediatrician
  • Pediatric neurologist
  • Pediatric neurosurgeon if needed

Transfer is prudent unless the hospital facility has a pediatric critical care unit and staff familiar with the risks and complications of SE in children.

A child who has a single generalized tonic-clonic seizure for the first time often does not receive long-term anticonvulsant therapy. Consult a pediatric neurologist.

Previous
 
 
Contributor Information and Disclosures
Author

Rajesh Ramachandrannair, MBBS, MD, FRCPC Associate Professor, McMaster University School of Medicine; Staff Neurologist, McMaster Children's Hospital, Canada

Disclosure: Nothing to disclose.

Coauthor(s)

Marcio Sotero de Menezes, MD Clinical Associate Professor, Department of Neurology, Division of Pediatric Neurology, Seattle Children's Hospital, University of Washington School of Medicine; Director, Pediatric Neuroscience Center and Genetic Epilepsy Clinic, Swedish Neuroscience Institute

Marcio Sotero de Menezes, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society

Disclosure: Received salary from Novartis for speaking and teaching; Received salary from Cyberonics for speaking and teaching; Received salary from Athena diagnostics for speaking and teaching.

Ednea Simon, MD Consulting Staff, Swedish Pediatric Neuroscience Center

Ednea Simon, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Child Neurology Society

Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Acknowledgements

G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami, Leonard M Miller School of Medicine; Medical Director, Palliative Care Team, Director, Pediatric Critical Care Transport, Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Manager, FEMA, Urban Search and Rescue, South Florida, Task Force 2; Pediatric Medical Director, Tilli Kids – Pediatric Initiative, Division of Hospice Care Southeast Florida, Inc

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Garry Wilkes MBBS, FACEM, Director of Emergency Medicine, Calvary Hospital, Canberra, ACT; Adjunct Associate Professor, Edith Cowan University; Clinical Associate Professor, Rural Clinical School, University of Western Australia

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Wayne Wolfram, MD, MPH Associate Professor, Department of Emergency Medicine, Mercy St Vincent Medical Center

Wayne Wolfram, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Grace M Young, MD Associate Professor, Department of Pediatrics, University of Maryland Medical Center

Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians

Disclosure: Nothing to disclose.

References
  1. De Novo Mutations in Synaptic Transmission Genes Including DNM1 Cause Epileptic Encephalopathies. Am J Hum Genet. 2014 Sep 24. [Medline].

  2. Mitchell WG. Status epilepticus and acute serial seizures in children. J Child Neurol. 2002 Jan. 17 Suppl 1:S36-43. [Medline].

  3. Tassinari CA, Daniele O, Michelucci R, Bureau M, Dravet C, Roger J. Benzodiazepines: efficacy in status epilepticus. Adv Neurol. 1983. 34:465-75. [Medline].

  4. Meldrum BS, Horton RW, Brierley JB. Epileptic brain damage in adolescent baboons following seizures induced by allylgycine. Brain. 1974 Jun. 97(2):407-18. [Medline].

  5. Meldrum BS, Vigouroux RA, Brierley JB. Systemic factors and epileptic brain damage. Prolonged seizures in paralyzed, artificially ventilated baboons. Arch Neurol. 1973 Aug. 29(2):82-7. [Medline].

  6. Chin RF, Neville BG, Scott RC. Meningitis is a common cause of convulsive status epilepticus with fever. Arch Dis Child. 2005 Jan. 90(1):66-9. [Medline]. [Full Text].

  7. Raspall-Chaure M, Chin RF, Neville BG, Bedford H, Scott RC. The epidemiology of convulsive status epilepticus in children: a critical review. Epilepsia. 2007 Sep. 48(9):1652-63. [Medline].

  8. Maytal J, Shinnar S, Moshé SL, Alvarez LA. Low morbidity and mortality of status epilepticus in children. Pediatrics. 1989 Mar. 83(3):323-31. [Medline].

  9. zz. zz.

  10. Sahin M, Menache CC, Holmes GL, Riviello JJ Jr. Prolonged treatment for acute symptomatic refractory status epilepticus: outcome in children. Neurology. 2003 Aug 12. 61(3):398-401. [Medline].

  11. Pohlmann-Eden B, Gass A, Peters CN, Wennberg R, Blumcke I. Evolution of MRI changes and development of bilateral hippocampal sclerosis during long lasting generalised status epilepticus. J Neurol Neurosurg Psychiatry. 2004 Jun. 75(6):898-900. [Medline]. [Full Text].

  12. Pujar SS, Neville BG, Scott RC, Chin RF. Death within 8 years after childhood convulsive status epilepticus: a population-based study. Brain. 2011 Oct. 134:2819-27. [Medline]. [Full Text].

  13. Haffey S, McKernan A, Pang K. Non-convulsive status epilepticus: a profile of patients diagnosed within a tertiary referral centre. J Neurol Neurosurg Psychiatry. 2004 Jul. 75(7):1043-4. [Medline]. [Full Text].

  14. Riviello JJ Jr, Ashwal S, Hirtz D, Glauser T, Ballaban-Gil K, Kelley K, et al. Practice parameter: diagnostic assessment of the child with status epilepticus (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology. 2006 Nov 14. 67(9):1542-50. [Medline].

  15. Epilepsy Foundation of America's Working Group on Status Epilepticus. Treatment of convulsive status epilepticus. Recommendations of the Epilepsy Foundation of America's Working Group on Status Epilepticus. JAMA. 1993 Aug 18. 270(7):854-9. [Medline].

  16. Chin RF, Verhulst L, Neville BG, Peters MJ, Scott RC. Inappropriate emergency management of status epilepticus in children contributes to need for intensive care. J Neurol Neurosurg Psychiatry. 2004 Nov. 75(11):1584-8. [Medline]. [Full Text].

  17. Brevoord JC, Joosten KF, Arts WF, van Rooij RW, de Hoog M. Status epilepticus: clinical analysis of a treatment protocol based on midazolam and phenytoin. J Child Neurol. 2005 Jun. 20(6):476-81. [Medline].

  18. [Guideline] Meierkord H, Boon P, Engelsen B, Göcke K, Shorvon S, Tinuper P, et al. EFNS guideline on the management of status epilepticus. Eur J Neurol. 2006 May. 13(5):445-50. [Medline].

  19. Lang ES, Andruchow JE. Evidence-based emergency medicine. What is the preferred first-line therapy for status epilepticus?. Ann Emerg Med. 2006 Jul. 48(1):98-100. [Medline].

  20. Prasad K, Al-Roomi K, Krishnan PR, Sequeira R. Anticonvulsant therapy for status epilepticus. Cochrane Database Syst Rev. 2005 Oct 19. CD003723. [Medline].

  21. Choudhery V, Townend W. Best evidence topic reports. Lorazepam or diazepam in paediatric status epilepticus. Emerg Med J. 2006 Jun. 23(6):472-3. [Medline]. [Full Text].

  22. Chamberlain JM, Capparelli EV, Brown KM, Vance CW, Lillis K, Mahajan P, et al. Pharmacokinetics of Intravenous Lorazepam in Pediatric Patients with and without Status Epilepticus. J Pediatr. 2011 Nov 1. [Medline].

  23. Holsti M, Dudley N, Schunk J, Adelgais K, Greenberg R, Olsen C, et al. Intranasal midazolam vs rectal diazepam for the home treatment of acute seizures in pediatric patients with epilepsy. Arch Pediatr Adolesc Med. 2010 Aug. 164(8):747-53. [Medline].

  24. Morrison G, Gibbons E, Whitehouse WP. High-dose midazolam therapy for refractory status epilepticus in children. Intensive Care Med. 2006 Dec. 32(12):2070-6. [Medline].

  25. Tasker RC. Midazolam for refractory status epilepticus in children: higher dosing and more rapid and effective control. Intensive Care Med. 2006 Dec. 32(12):1935-6. [Medline].

  26. Tarulli A, Drislane FW. The use of topiramate in refractory status epilepticus. Neurology. 2004 Mar 9. 62(5):837. [Medline].

  27. Kahriman M, Minecan D, Kutluay E, Selwa L, Beydoun A. Efficacy of topiramate in children with refractory status epilepticus. Epilepsia. 2003 Oct. 44(10):1353-6. [Medline].

  28. Perry MS, Holt PJ, Sladky JT. Topiramate loading for refractory status epilepticus in children. Epilepsia. 2006 Jun. 47(6):1070-1. [Medline].

  29. Chez MG, Hammer MS, Loeffel M, Nowinski C, Bagan BT. Clinical experience of three pediatric and one adult case of spike-and-wave status epilepticus treated with injectable valproic acid. J Child Neurol. 1999 Apr. 14(4):239-42. [Medline].

  30. Sheth RD, Gidal BE. Intravenous valproic acid for myoclonic status epilepticus. Neurology. 2000 Mar 14. 54(5):1201. [Medline].

  31. Uberall MA, Trollmann R, Wunsiedler U, Wenzel D. Intravenous valproate in pediatric epilepsy patients with refractory status epilepticus. Neurology. 2000 Jun 13. 54(11):2188-9. [Medline].

  32. Abend NS, Dlugos DJ. Treatment of refractory status epilepticus: literature review and a proposed protocol. Pediatr Neurol. 2008 Jun. 38(6):377-90. [Medline].

  33. Patel NC, Landan IR, Levin J, Szaflarski J, Wilner AN. The use of levetiracetam in refractory status epilepticus. Seizure. 2006 Apr. 15(3):137-41. [Medline].

  34. Gallentine WB, Hunnicutt AS, Husain AM. Levetiracetam in children with refractory status epilepticus. Epilepsy Behav. 2009 Jan. 14(1):215-8. [Medline].

  35. Shorvon S. Emergency treatment of epilepsy. Handbook of Epilepsy Treatment. Oxford, UK: Blackwell Science; 2000. 173-93.

  36. Parke TJ, Stevens JE, Rice AS, Greenaway CL, Bray RJ, Smith PJ, et al. Metabolic acidosis and fatal myocardial failure after propofol infusion in children: five case reports. BMJ. 1992 Sep 12. 305(6854):613-6. [Medline]. [Full Text].

  37. Bray RJ. Propofol infusion syndrome in children. Paediatr Anaesth. 1998. 8(6):491-9. [Medline].

  38. Coetzee JF, Coetzer M. Propofol in paediatric anaesthesia. Curr Opin Anaesthesiol. 2003 Jun. 16(3):285-90. [Medline].

  39. Corbett SM, Montoya ID, Moore FA. Propofol-related infusion syndrome in intensive care patients. Pharmacotherapy. 2008 Feb. 28(2):250-8. [Medline].

  40. Hill M, Peat W, Courtman S. A national survey of propofol infusion use by paediatric anaesthetists in Great Britain and Ireland. Paediatr Anaesth. 2008 Jun. 18(6):488-93. [Medline].

  41. Fodale V, La Monaca E. Propofol infusion syndrome: an overview of a perplexing disease. Drug Saf. 2008. 31(4):293-303. [Medline].

  42. Anderson P. Convulsive Status Epilepticus Has Prolonged Cognitive Effect. Medscape Medical News. April 10, 2013. Available at http://www.medscape.com/viewarticle/782293.. Accessed: April 22, 2013.

  43. Baumeister FA, Oberhoffer R, Liebhaber GM, Kunkel J, Eberhardt J, Holthausen H, et al. Fatal propofol infusion syndrome in association with ketogenic diet. Neuropediatrics. 2004 Aug. 35(4):250-2. [Medline].

  44. Brooks M. Lorazepam, diazepam similar in pediatric status epilepticus. Medscape Medical News. April 30, 2014. [Full Text].

  45. Chamberlain JM, Capparelli EV, Brown KM, Vance CW, Lillis K, Mahajan P, et al. Pharmacokinetics of Intravenous Lorazepam in Pediatric Patients with and without Status Epilepticus. J Pediatr. 2011 Nov 1. [Medline].

  46. Chamberlain JM, Okada P, Holsti M, et al. Lorazepam vs diazepam for pediatric status epilepticus: a randomized clinical trial. JAMA. 2014 Apr 23-30. 311(16):1652-60. [Medline].

  47. Krishnamurthy KB, Drislane FW. Depth of EEG suppression and outcome in barbiturate anesthetic treatment for refractory status epilepticus. Epilepsia. 1999 Jun. 40(6):759-62. [Medline].

  48. Martinos MM, Yoong M, Patil S, Chong WK, Mardari R, Chin RF, et al. Early developmental outcomes in children following convulsive status epilepticus: A longitudinal study. Epilepsia. 2013 Apr 8. [Medline].

  49. Mathews HM, Carson IW, Lyons SM, Orr IA, Collier PS, Howard PJ, et al. A pharmacokinetic study of midazolam in paediatric patients undergoing cardiac surgery. Br J Anaesth. 1988 Sep. 61(3):302-7. [Medline].

  50. Neville BG, Chin RF, Scott RC. Childhood convulsive status epilepticus: epidemiology, management and outcome. Acta Neurol Scand Suppl. 2007. 186:21-4. [Medline].

 
Previous
Next
 
Treatment algorithms for convulsive status epilepticus.
Table 1. Medical Treatment of Seizures and Status Epilepticus Based on Time Elapsed Since Seizure Onset (Steps 2-4)
Step Medication Dose Alternatives
Step 2 (6-15 min) Diazepam (Valium) 5-20 mg IV slowly; not to exceed infusion rate of 2 mg/min; pediatric dose is 0.3 mg/kg If IV line is unavailable, use rectally administered (PR) diazepam at 0.5 mg/kg (not to exceed 10 mg) or midazolam (Versed) at 0.2 mg/kg intramuscularly (IM)*, IV, or intranasally*
Lorazepam* (Ativan) 2-4 mg IV slowly*; not to exceed infusion rate of 2 mg/min or 0.05 mg/kg over 2-5 min; pediatric dose is 0.05-0.1 mg/kg
Step 3 (16-35 min) Phenytoin (Dilantin) or fosphenytoin (Cerebyx)† 20 mg/kg IV over 20 min; not to exceed infusion rate of 1 mg/kg/min; do not dilute in 5% dextrose in water (D5W)



If seizures persist, administer 5 mg/kg for 2 doses (if blood pressure is within the reference range and no history of cardiac disease is present)



If unsuccessful, administer phenobarbital 10-20 mg/kg IV (not to exceed 700 mg IV); increase infusion rate by 100 mg/min; phenobarbital may be used in infants before phenytoin; be prepared to intubate patient; closely monitor hemodynamics and support blood pressure as indicated
Step 4 (45-60 min)‡ Pentobarbital anesthesia (patient already intubated) Loading dose: 5-7 mg/kg IV; may repeat 1-mg/kg to 5-mg/kg boluses until EEG exhibits burst suppression; closely monitor hemodynamics and support blood pressure as indicated



Maintenance dose: 0.5-3 mg/kg/h IV; monitor EEG to keep burst suppression pattern at 2-8 bursts/min



Midazolam* infusion loading dose: 100-300 mcg/kg IV followed by IV infusion of 1-2 mcg/kg/min; increase by 1-2 mcg/kg/min every 15 min if seizures persist (effective range 1-24 mcg/kg/min); closely monitor hemodynamics and support blood pressure as indicated; when seizures stop, continue same dose for 48 h then wean by decrements of 1-2 mcg/kg/min every 15 min



Propofol* initial bolus: 2 mg/kg IV; repeat if seizures continue and follow by IV infusion of 5-10 mg/kg/h, if necessary, guided by EEG monitoring; taper dose 12 h after seizure activity stops; closely monitor hemodynamics and support blood pressure as indicated



With phenobarbital-induced anesthesia, repeated boluses of 10 mg/kg are administered until cessation of ictal activity or appearance of hypotension; closely monitor hemodynamics and support blood pressure as indicated



*Not approved by the FDA for the indicated use.



†Doses for fosphenytoin administered in phenytoin equivalents (PE).



‡An alternative third step preferred by some authors is midazolam



administered by continuous IV infusion with a loading dose 0.1-0.3 mg/kg followed by infusion at a rate of 0.1-0.3 mg/kg/h.



Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.