Pediatric Status Epilepticus Differential Diagnoses

  • Author: Rajesh Ramachandrannair, MBBS, MD, FRCPC; Chief Editor: Timothy E Corden, MD   more...
 
Updated: Jan 19, 2012
 
 

Diagnostic Considerations

Always consider the possibility of infections in pediatric patients presenting with generalized tonic-clonic status epilepticus (GTCSE). Sources of infection often, but not always, are obvious (eg, otitis media, pneumonia). Treat these infections appropriately because they contribute to lowering the seizure threshold in predisposed patients.

Infections can be the precipitating factor for both GTCSE and nonconvulsive status epilepticus (NCSE). Patients with CNS infections and mental status changes should not be assumed to have infection-related neurologic dysfunction before EEG findings rule out NCSE.

Catscratch disease

Consider catscratch disease, particularly in a school-aged child with a cat or kitten at home who presents with a history of unexplained mental status changes, status epilepticus (SE) of unknown etiology, prolonged seizures, or persistent fatigue. Catscratch fever is an infection acquired from cats (often from kittens) infected with Bartonella henselae via the cat flea. Although the disease may be transmitted by any close contact with a cat, scratches or bites cause 75% of cases.

Psychogenic seizures

Occasionally, nonepileptic seizures can be confused with GTCSE. They may occur in patients with a previous diagnosis of epilepsy.[12]

Patients with nonepileptic seizures can reproduce an outward clinical seizure pattern as a manifestation of an unresolved psychological conflict (psychogenic seizure), or the seizure may be a manifestation of malingering, providing the patient with a clear secondary gain. Pediatric patients rarely fake a seizure, however. Symptoms of true psychogenic seizures resemble conversion symptoms.

In many cases, details of the presentation can help differentiate nonepileptic seizures from GTCSE. Features suggesting nonepileptic seizures include the following:

  • No loss of consciousness in the presence of bilateral movements
  • Asynchronous, side-to-side, and out-of-phase movements
  • Pelvic thrusting
  • Inconsistency of movement patterns and waxing and waning patterns
  • Persistent eye closure
  • Crying during the seizure

On the other hand, no loss of consciousness in the presence of bilateral movements, pelvic thrusting, and asynchronous and thrashing movements can also be part of frontal lobe seizures, which may lead to SE in some cases. Only careful observation of the patient (eg, video) with simultaneous EEG (ie, EEG video monitoring) allows the physician to differentiate between sustained nonepileptic seizures and GTCSE.

Differential Diagnoses

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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 and American Epilepsy Society

Disclosure: Novartis Salary Speaking and teaching; Cyberonics Salary Speaking and teaching; Athena diagnostics Salary 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, and 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, and Wisconsin Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

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.

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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/kgIf 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.



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