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FEBRILE SEIZURES and status epilepticus 2022.ppt
1. FEBRILE SEIZURES
DR. OMAR NAFI AJARMAH MRCP
PEDIATRIC NEUROLOGIST
PROFESSOR OF PEDIATRICS
MUTAH UNIVERSITY
2. DEFINITION & CRITERIA
Age 6 months 5 years old
Associated with fever
No evidence of CNS infection
3. CLASSIFICATION
Simple febrile seizure
Complex febrile seizure
Duration > 15 minutes
Multiple in 24 hours
Focal
Symptomatic febrile seizures
The child has a preexisting neurologic
abnormality
4. EPIDEMIOLOGY
Febrile seizures are the most common
seizure disorder in childhood
Occur in 2-4% of children
In 20% of cases first FEBRILE
SEIZURE IS COMPLEX
The most common age of onset is the
SECOND year
Male > Female
5. Pathophysiology
This is a unique form of epilepsy that
occurs in early childhood and only in
association with an elevation of
temperature. The underlying
pathophysiology is unknown, but
genetic predisposition clearly
contributes to the occurrence of this
disorder.
6. RECURRENCE
33% will experience one or
more after the first
9% will have 3 or more
GENETICS
Tends to occur in families
Exact inheritance not
known
Risk for siblings
10-20%
7. RISK FACTORS FOR
RECURRENCE
Young age
Family history of febrile seizures
Short duration of fever before the onset
of seizures
Low grade fever at the time of initial
seizures
Complex febrile seizures are not likely to
have more recurrence
8. RISK FACTORS FOR
EPILEPSY
Abnormal development
Complex first febrile seizures
Family history of a febrile seizures
No risk factor 2%
1 one or more risk 3%
2 or more 13% a febrile
seizure
9. ETIOLOGY
Most case are due to common infections
Tonsillitis URTI OM
HHSV – 6 +ve culture in 19% of cases
+ve for serology in 26%
cases
10. CLINICAL ASPECTS
Febrile seizure occur early in the course of
febrile illness
Rate of increment of fever
important trigger!?
Tonic-clonic is the most common
Most seizures last < 6 minutes
< 8% of seizures > 15 minutes
11. HISTORY
Symptoms of infection
Drugs
Trauma
Developmental Level
Family history of febrile or a Febrile
seizures
13. INVESTIGATION
LUMBAR PUNCTURE
if Meningitis or Encephalitic
Age less than 18 months
+ OM does not roll out Meningitis
+ should not be omitted on the sole basis
of age
EEG
Not helpful to predict recurrence
After 1 week of seizures
ROUTINE LAB TEST
Only as a part of evaluation of fever source
SKULL X-RAY, CT, MRI
Seldom helpful
Should not be performed routinely
14. HOSPITALIZATION
Decision for Admission
- specific clinical situation
- family circumstances
Admission
- clinically unstable
- questionable meningitis
- unreliable parents
16% may experience another febrile
seizures in 24 hours
15. PARENTAL COUNSELING
Parents must be reassured
Given instruction to manage possible
recurrence
A written handout is helpful
Vigorous control of fever has not been
proven to lower the risk of Febrile
Seizure recurrence
16. IMMUNIZATION
Seizures following childhood
immunization are not different from
other febrile seizures
Seizures most common occur following
prevention/immunization of DPT. The
period of greater risk is:
48 hours DPT
7-10 days Measles
17. LONG TERM MANAGEMENT
Rx to prevent recurrence (no evidence)
prevent Epilepsy
CONCLUSIONS
Benign syndrome
Determined largely by genetics
Manifested by age related susceptibility
to seizure that eventually overgrown
19. Status Epilepticus (SE)
Definition
Continuous convulsion lasting longer than 5 minutes or
occurrence of serial convulsions between which there is no
return of consciousness
It is medical emergency
Associated morbidity and mortality
Need skillful approach
20. Definitions
Impending SE 5-10 minutes
Established SE 10-30 minutes
Refractory SE 30-60 minutes
Super refractory more than 60 minutes
22. Etiology
3 major subtypes
Febrile status epilepticus
idiopathic status epilepticus
symptomatic status epilepticus
23. Etiology
Idiopathic status
sudden withdrawal of treatment
treatment on irregular bases
initial presentation of epilepsy
sleep deprivation
24. Pathophysiology
SE results from a failure of the inhibitory
mechanisms to stop seizures.
Gamma-aminobutyric acid (GABA) is the most
prevalent inhibitory neurotransmitter in the
brain
Glutamate is the primary excitatory amino acid
neurotransmitter .
25. Pathologic Changes Secondary to
SE
After approximately 20 to 40 minutes, there is a
progressive failure of the compensatory mechanisms.
Glucose, blood pressure, and cerebral perfusion and
oxygenation decrease.
Associated respiratory acidosis occurs as a result of
hypoventilation, and hypoxia and pulmonary edema
contribute to the already developing lactic acidosis.
An increase in the peripheral blood cell count frequently
occurs in the absence of infection.
Rhabdomyolysis may compromise renal function and
worsen the electrolyte imbalances.
Severe acidosis and/or hyperkalemia may lead to
cardiac arrest.
26. Pathophysiology
Relation between duration and neuronal damage
Cell death excessive relies of excitatory mediators as
glutamate
Vulnerable area in the brain hippocampus ,amygdale,
cerebellum middle cortical area and hypothalamus
Characteristic changes venous congestion small
petechial hemorrhage and edema
Neuronal concentration of calcium arachidonic acid
prostaglandin promote cell death
27. Physical examination and neurological assessment
Evidence of trauma
Papilledema
Bulging ant fontanel's
Lateralizing neurological signs
Signs of sepsis or meningitis
Retinal hemorrhage
Kusmmual breathing +dehydration M Acidosis
FTT skin odor skin pigmentations IEM
Pupils
28. Laboratory Testing
glucose
calcium
electrolytes
and complete blood count.
blood gases
Medication levels
toxicology screens
blood cultures and a
lumbar puncture have a high yield in children with SE
and a clinical suspicion of infection
In some children, neuroimaging may be needed before
lumbar puncture.
29. EEG Monitoring
EEG monitoring allows optimal management
of SE and should be used whenever available
and feasible
30. Time to Treatment
There are three major determinants of
prognosis in SE:
Age; is a nonmodifiable factor
etiology; Etiology is usually not modifiable
SE duration; might be modified with
appropriate and timely management.
31. Stabilization
A. Secure airway. Blood pressure. Nasal O. Be prepared to intubate.
B. Secure intravenous access.
1. Draw blood for CBC, electrolytes, drug levels, calcium, magnesium,
toxic screen,
glucose. (Also perform a dextrostix immediately.)
2. Start intravenous infusion with 5% dextrose in normal saline.
3. Administer 50% glucose, I gm/kg, if indicated by dextrostix or if
dextrostix is not available.
4. Blood gas for O2 pH. Give bicarbonate ifpH <7.10.
32. Treatment Guidelines for SE
secure the airway and ensure adequate breathing and
circulation.
Importantly, most seizures resolve spontaneously in less
than 5 minutes and will not require rescue medication.
when seizures last more than 5 minutes, they should be
considered as impending SE and treatment should be
initiated immediately.
Benzodiazepines are the first-line treatment, and among
them, intravenous lorazepam is frequently the preferred
option. When intravenous access is not available,
intramuscular, rectal, intranasal, or buccal medication
administration are potential alternatives.
The first dose of benzodiazepines can be repeated if
seizures persist.
33. Thus after 10 minutes switch
Benzodiazepines ------------ nonbenzodiazepine.
Nonbenzodiazepine
phenytoin
Phenobarbiton .
Other nonbenzodiazepine
valproate and
levetiracetam
34. Refractory SE
SE is considered refractory when it has not been controlled with
appropriate doses of benzodiazepines and 1 or 2 doses of
nonbenzodiazepines.
Initiation of treatment with anesthetic medications such as
midazolam or pentobarbital may lead to respiratory depression
and hypotension,
One of the most frequently used initial continuous infusions is
midazolam. Administration often involves a 0.2 mg/kg loading
dose followed by 0.2 to 0.6 mg/kg/h infusion rate
Another common option is pentobarbital infusion.
Administration often involves a 5 mg/kg loading dose followed
by 1 to 5mg/kg/h infusion rate
35. Refractory SE
A third option for continuous infusion is propofol.
Administration often involves 2 mg/kg loading
dose followed by 2 to 5 mg/kg/h infusion rate. it
may cause propofol infusion syndrome
The main clinical features of propofol infusion
syndrome are cardiovascular collapse with lactic
acidosis, hypertriglyceridemia, and
rhabdomyolysis. As this syndrome is frequently
lethal, propofol infusions with doses of at least 5
mg/kg/h are not recommended for more than 48
hours, especially in children
36. Super-Refractory SE
When SE continues despite one to two
continuous infusions, it is considered super-
refractory SE
“status epilepticus that continues for 24 hours or
more after the onset of anesthesia, including
those cases in which the SE recurs on the
reduction or withdrawal of anesthesia”
Thiopental, Ketamine, Inhaled anesthetics,
Lidocaine.
37. Prognosis
mortality rate 5%
most mortality symptomatic group
hemiplegia
extra pyramidal syndrome
mental retardation
More common in those less than 1 yr
Status FSC mesial temporal sclerosis
