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Background
Febrile seizures are the most common type of seizures observed
in the pediatric age group.
Although described by the ancient Greeks, it was not until this
century that febrile seizures
were recognized as a distinct syndrome separate from epilepsy.
In 1980, a consensusconference held by the National Institutes of
Health described a febrile seizure as, "An event
in infancy or childhood usually occurring between three months
and five years of age,
associated with fever, but without evidence of intracranial
infection or defined cause."[1] It
does not exclude children with prior neurological impairment and
neither provides specific
temperature criteria nor defines a "seizure." Another definition
from the International League
Against Epilepsy (ILAE) is "a seizure occurring in childhood
after 1 month of age associated
with a febrile illness not caused by an infection of the central
nervous system (CNS), without
previous neonatal seizures or a previous unprovoked seizure, and
not meeting the criteria for
other acute symptomatic seizures".[2]
For other information, see Medscape's Pediatrics
Specialtypage.
Pathophysiology
Febrile seizures occur in young children at a time in their
development when the seizure
threshold is low. This is a time when young children are
susceptible to frequent childhood
infections such as upper respiratory infection, otitis media,
viral syndrome, and they respond
with comparably higher temperatures. Animal studies suggest a
possible role of endogenous
pyrogens, such as interleukin 1beta, that, by increasing
neuronal excitability, may link fever
and seizure activity.[3] Preliminary studies in children appear
to support the hypothesis that the
cytokine network is activated and may have a role in the
pathogenesis of febrile seizures, butthe precise clinical and
pathological significance of these observations is not yet
clear.[4, 5]
Febrile seizures are divided into 2 types: simple febrile
seizures (which are generalized, last 20 mcg/mL
Vd: Adults (0.12 L/kg), febrile children
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Mechanism of Action
Sedative hypnotic with short onset of effects and relatively
long half-life
By increasing the action of gamma-aminobutyric acid (GABA),
which is a major inhibitory
neurotransmitter in the brain, may depress all levels of CNS,
including limbic and reticular
formation
AbsorptionBioavailability: 90%
Onset: IV 1-5 min; IM 15-30 min
Peak plasma time: 2 hr
Peak plasma concentration: 20 ng/mL
Duration: 12-24 hr (IV/IM)Distribution
Protein Bound: 85%Metabolism
Glucuronic acid conjugation
Metabolites: inactive
EliminationHalf-Life: unconjugated lorazepam, 12hr; major
metabolite lorazepam glucuronide, 18hr
Excretion: Urine
http://emedicine.medscape.com/article/801500-overview
http://emedicine.medscape.com/article/801500-overviewhttp://emedicine.medscape.com/article/801500-overview
