Pediatric Emergency Conference

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 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 Duration of seizure Werner, MD; GTC SE in Children; University of Kentucky Hospital

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.

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

Etiopathogenesis