1. Pediatric Emergency Conference

3. Speiser, et al. New England Journal of Medicine, 2003

4. Seizures
result from rapid abnormal electrical discharges from cerebral neurons
presents clinically as involuntary alterations of consciousness or motor activity
Consumption of oxygen, glucose, and energy substrates (e.g, ATP, phosphocreatine) is significantly increased in cerebral tissue during seizures.
Optimal delivery of these metabolic substrates to cerebral tissue requires adequate cardiac output and intravascular fluid volume.
Pediatric, Status Epilepticus; emedicine 2008

5. Important points in the History
The course of 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), including any focal movements and details of postictal neurologic deficit
Incontinence
Cyanosis (perioral or facial)
Duration of seizure activity prior to medical attention
Mental status after cessation of seizure activity
Fever or intercurrent illnesses
Prior history of seizures - If present, specify medications, anticonvulsant use, and compliance.
Pediatric, Status Epilepticus; emedicine 2008

6. Important points in the History
Head injury (recent and remote)
CNS infection or disease (eg, meningitis, neurocutaneous syndrome)
Intoxication or toxic exposure
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)
Pediatric, Status Epilepticus; emedicine 2008

7. Important points in the PE
Signs of sepsis or meningitis
Temperature more than 38.5°C; in patients younger than 2-3 months, more than 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
Evidence of head or other CNS injury
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 (e.g., port wine stain)
Pediatric, Status Epilepticus; emedicine 2008

8. Monitoring of Vital Functions
Respiratory rate, blood pressure, cardiac rate
Observation of seizure activity
Skin bruises, petechiae or needle marks
Papilledema, retinal hemorrhages
Organomegaly and abdominal tenderness

9. Factors that lower Seizure Threshold
Sleep deprivation
Hyperventilation
Photic stimulation
Infection
Metabolic disturbances
Head trauma
Cerebral ischemia
Kindling
Handbook of Neurosurgery by Greenberg

10. Status Epilepticus
Continuous clinical or electroencephalographic seizures lasting for at least 30 minutes or recurrent seizures without return of consciousness during interictal period: the series lasting for 30 minutes or more. It is a medical emergency.
Handbook of Medical & Surgical Emergencies, 6th edition

11. Clinical Classification of Status Epilepticus
Overt generalized convulsive status epileptus
Subtle generalized convulsive status epilepticus
Simple status epilepticus
Nonconvulsive status epilepticus
Continuous convulsive activity and intermittent convulsive activity without regaining full consciousness
Convulsive (tonic-clonic)
Tonic
Clonic
Myoclonic
Coma following generalized convulsive status epilepticus with or without motor activity
Consciousness preserved
Simple motor status epilepticus
Sensory status epilepticus
Aphasic status epilepticus
Consciousness impaired; twilight or fugue state
Petit mal status (absence status)
Complex partial status epilepticus
Handbook of Medical & Surgical Emergencies, 6th edition

12. Types of Status Epilepticus
Generalized Status
Convulsive: generalized convulsive tonic-clonic status epilepticus (SE) is the most frequent type
Absence
Secondarily generalized: accounts for ~75% of generalized SE
Myoclonic
Atonic (drop attack): especially in Lennox-Gastaut syndrome
Partial Status (usually related to anatomic abnormality)
Simple (Epilepsy Partialis continuans)
Complex
Secondarily generalized
Handbook of Neurosurgery by Greenberg

13. Etiologies Febrile seizures Cerebrovascular accidents CNS infection
Idiopathic
Epilepsy
Subtherapeutic antiepileptic drug
Electrolyte imbalance
Drug intoxication
Alcohol withdrawal
Traumatic brain injury
Anoxia
Tumor
Handbook of Neurosurgery by Greenberg

14. Children and adolescents (>6 y)
DIFFERENTIAL DIAGNOSIS
Neonates
(first month of life)
Early childhood
(<6 y)
Children and adolescents (>6 y)
Birth injury (eg, anoxia, hemorrhage) and congenital abnormalities
Birth injury
Metabolic disorders (eg., hypoglycemia, hypocalcemia, hyponatremia) and inborn errors of metabolism (eg., lipidoses, amino acidurias)
Febrile convulsions (3 mo to 6 y)
Trauma
Infection (eg, meningitis)
Infection
Metabolic disorders
Epilepsy with inadequate drug levels
Cerebral degenerative disease
Neurocutaneous syndromes
Tumor
Cerebral degenerative diseases
Toxins
Tumors
Idiopathic
Toxins and medications
Topical anesthetics (eg, lidocaine)
Anticonvulsant overdose
Camphor
Hypoglycemic agents (eg, insulin, ethanol)
Carbon monoxide
Cyanide
Heavy metals (eg, lead)
Pesticides (eg, organophosphate)
Cocaine
Phencyclidine
Belladonna alkaloids
Nicotine
Sympathomimetics (eg, amphetamines, phenylpropanolamine [recalled from US market])
Tricyclic antidepressants
Pediatric, Status Epilepticus; emedicine 2008

15. In children < 1year age 75% acute cause 30% electrolyte disorders 28% secondary to CNS infection 19% associated with fever
Handbook of Neurosurgery by Greenberg

16. Prolonged seizures are associated with cerebral hypoxia, hypoglycemia, and hypercarbia and with concurrent and progressive lactic and respiratory acidosis. When cerebral metabolic needs exceed available oxygen, glucose, and metabolic substrates (especially during status epilepticus), neuronal destruction can occur and may be irreversible. Hypoxia, hypercarbia, hyperthermia, tachycardia, hypertension, hyperglycemia, hyperkalemia, and lactic acidosis result from massive sympathetic discharge.
Pediatric, Status Epilepticus; emedicine 2008

17. Prolonged seizures Life threatening systemic changes Temporary
Death
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 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
Duration of seizure
Werner, MD; GTC SE in Children; University of Kentucky Hospital

18. Mortality
The primary determinant of mortality and morbidity of SE in children is its etiology
The greatest mortality and highest rate of neurological deficits occurs when SE is caused by an acute neurological condition (infection, trauma, stroke)
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.
Mitchell WG. J Child Neurol 2002;17 Suppl 1:S36-43.

19. Mean duration of SE in patients without neurologic sequelae is 1
Mean duration of SE in patients without neurologic sequelae is 1.5hours. Mortality is lowest among children (~6%) subtherapeutic AEDs unprovoked SE Highest Mortality elderly patients SE due to anoxia or CVA
Handbook of Neurosurgery by Greenberg

20. Etiopathogenesis