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


Pediatric Status Epilepticus Clinical Presentation

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


In the initial presentation of status epilepticus (SE), a directed history suffices. Obtain a more detailed history after stabilization, including the following details about the current seizure activity:

  • Time and nature of onset of seizure activity
  • Involvement of extremities or other body parts
  • Nature of movements (eg, eye movements, flexion, extension, stiffening of extremities)
  • Incontinence
  • Cyanosis (perioral or facial)
  • Duration of seizure activity prior to medical attention
  • Mental status after cessation of seizure activity
  • Postictal neurologic deficit

Other important information to elicit in the history includes the following:

  • Fever or intercurrent illnesses
  • Prior history of seizures - If present, specify medications, anticonvulsant use, and compliance.
  • Head injury (recent and remote)
  • Central nervous system (CNS) infection or disease (eg, meningitis, neurocutaneous syndrome)
  • Intoxication or toxic exposure (see Etiology for examples)
  • Other CNS abnormality (eg, ventricular-peritoneal shunt, prior CNS trauma)
  • Birth history and developmental delay (eg, anoxic encephalopathy, cerebral palsy)
  • Other medical history (eg, acquired immunodeficiency syndrome, systemic lupus erythematosus, type 1 diabetes mellitus)

Phases of convulsive status epilepticus

Generalized tonic-clonic SE (GTCSE) has 3 phases. In phase 1, discrete partial seizures or, less frequently, generalized seizures can be observed both clinically and on electroencephalography (EEG). Blood pressure usually remains within the reference range, but metabolic acidosis may be observed in association with elevated serum lactate and glucose levels.

In phase 2, discrete SE events fuse and partial seizures become secondarily generalized. The main outward manifestation of continuous clinical and EEG seizure activity consists of a tonic phase (sustained muscle contraction) followed by clonic jerks (alternating contraction and relaxation of the 4 limbs). Phase 2 may include altered blood pressure.

In phase 3, clinical seizures may become quite subtle, with brief rhythmic clonic or myoclonic movements often restricted to a single part of the body. During this period, the patient's EEG findings start to show slow-frequency discharges similar to periodic lateralizing epileptiform discharges (PLEDs). Rhythmic activity may be observed as myoclonus that affects only the feet, hands, facial muscles, or eyes (as nystagmus).

As the episode progresses, a motionless patient's EEG may reveal generalized or PLED-like discharges. This type of activity is thought to represent a burned-out form of SE. This conclusion is supported by cases in which positron emission tomography (PET) scanning revealed hypermetabolism of the mesiotemporal region in patients with abnormal mental status and PLED-like discharges after an episode of SE.

Hyperthermia, respiratory compromise, hypotension, and hypoglycemia may be observed. If not promptly treated, these metabolic, cardiovascular, and respiratory complications can exacerbate the patient's clinical condition and neurologic deficit.

Nonconvulsive status epilepticus

Patients with nonconvulsive SE are described as appearing forgetful and sleepy, behaving as if deaf and blind (“like a zombie”), or having the appearance of being drugged. In more severe cases, patients are described as unresponsive. Sometimes parents describe the motor component of frequent falls, poor motor control, or abnormal balance.


Physical Examination

Perform a rapid, directed physical and neurologic examination during SE, followed by a detailed examination when the child is stabilized. During the initial physical examination, seek signs of sepsis or meningitis and of head trauma or CNS injury.

Signs of sepsis or meningitis include the following:

  • Temperature above 38.5°C; in patients younger than 2-3 months, above 38.0°C
  • Respiratory distress
  • Cyanosis
  • Poor peripheral perfusion
  • Bulging fontanelles in infant
  • Meningismus (in children >12-18 mo)
  • Presence of petechiae or purpura, herpetic vesicles

When the patient's situation stabilizes, look for lymphadenopathy, which suggests catscratch fever.

Evidence of head or other CNS injury includes the following:

  • Bradycardia, tachypnea, and hypertension (Cushing triad for signs of increased intracranial pressure)
  • Poor pupillary response
  • Asymmetry on neurologic examination
  • Abnormal posturing
  • Gross deformity or soft tissue injury to head

Hallmarks of neurocutaneous syndromes (eg, port wine stain) may also be found.

Patients with GTCSE usually have bilateral and synchronous movements of the extremities. Although asynchronous alternating movements of the extremities are often thought to be caused by pseudoseizures, a similar pattern can be observed in cases of frontal lobe epilepsy. Epilepsia partialis continua manifests by unilateral and, at times, focal (eg, one hand or even one finger) clonic activity (ie, twitching).

Patients with absence SE present with altered consciousness, with or without clonic movements of the eyelids or upper extremities, and automatisms involving the hands and face. A child may sometimes continue to perform a motor act that he or she was engaged in before onset of the absence seizure (eg, bouncing a basketball). In some cases, the patient may answer simple questions, but detailed examination reveals slowed mentation and poor processing of complex information. Episodes of absence SE may last 12 hours or longer.

In patients who present to the emergency department (ED) after an episode of prolonged seizure, carefully observe for signs of subtle seizures or SE, such as clonic or myoclonic rhythmic movements involving the limbs or face and eyes. These movements often are easy to recognize in overt generalized tonic-clonic seizures and in SE. Clonic activity may start focally then spread to the hemibody and finally become generalized. Focal clonic activity may assume the form of rhythmic facial muscle contractions, or it may involve the limbs.


The most feared complication of GTCSE is brain damage associated with neuronal loss mediated by sustained electrical seizure activity in the brain. Other complications of prolonged seizures may include the following:

  • Aspiration
  • Fluid, electrolyte, and metabolic disturbances
  • Trauma
  • Cardiopulmonary problems
  • Complications as a result of the underlying cause

Fluid, electrolyte, and metabolic complications include lactic acidosis, dehydration, and hypotension. Myoglobinuria caused by muscle breakdown during a seizure may lead to renal dysfunction.

Traumatic complications of SE include oral trauma, both internal (eg, biting the tongue or oral mucosa) and external (eg, hitting the lips). Many patients incur closed head or facial injuries during the clonic phase of seizures. Posterior shoulder dislocation is a classic complication and is difficult to diagnose in the unconscious patient

Pulmonary edema and cardiac arrhythmias may be complications of SE or its treatment.

Disseminated intravascular coagulation in association with significant leukocytosis and mild cerebrospinal fluid pleocytosis may produce a clinical picture similar to sepsis or CNS infection. In these cases, patients are often treated for a severe infection until sepsis or meningitis/encephalitis can be safely ruled out.

Contributor Information and Disclosures

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

Disclosure: Nothing to disclose.


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.


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.

  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 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].

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.

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