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STATUS EPILEPTICUS AND
FEBRILE SEIZURES
STATUS EPILEPTICUS
• It is a medical emergency that should be anticipated in any pt who presents
with an acute seizure
• It implies prolonged simple seizure or multiple episodes of seizures lasting
for more than 30 min without regaining consciousness in between
• Impending SE refers to any seizure lasting more than 5 min
• SE can be
1. Convulsive [tonic-clonic, clonic ,tonic , or myoclonic
2. Non-convulsive[absence , complex partial ,speech sensorial alteration]
• Convulsive SE is the most common and is associated with significant
mortality and morbidity
• Neurological residua – mental retardation, focal neurological deficits,
behavioural disorders and chronic epilepsy
• The neurological sequelae depend upon etiology, age and duration of SE
• The risk of complications increases substantially with duration[>60 min]
• Mortality rate is 10% ; most deaths are attributable to pt’s underlying
pathology
• Seizures recur in 25-75% of pts
• 50% cases- pt’s first seizure
• 25% of childhood epilepsy- idiopathic
• 25% - associated with fever or meningoencephlitis
• 50% cases – neurodevelopmental abnormality, head trauma ,
stroke , drug intoxication , subarachnoid bleed, pyridoxine
deficiency , metabolic abnormality
• PATHOPHYSIOLOGY
• SE results from excessive and persistant excitation or ineffective recruitment of
inhibition
• Excitatory neurotransmitters- glutamate , aspartate and Ach
• GABA is the dominant inhibitory neurotransmitter
• Blockage of NMDA receptors by magnesium ions seems to be important in the
pathogenesis of neuronal damage
• SE can produce both neuronal necrosis and apoptosis
• Cytokines [interleukin 1 𝝰 ] can modify neuronal excitability by rendering NMDA
receptors more permeable for calcium influx
• Prostaglandins can increase glutamate release and reduce potassium currents
leading to increased excitability
EVALUATION IN EMERGENCY DEPARTMENT
• History is taken for description of the event , associated symptoms, duration and
the post ictal period, prior history of seizures, non compliance with antiepileptic
drugs or change of antiepileptic drugs and history of prior neurological
development
• If post ictal confusion doesn’t resolve , search for other causes like hypoglycemia ,
dyselectrolemia ,CNS infection , CNS vascular event ,drug toxicity ,psychiatric
disorders and non convulsive SE
• Non convulsive SE manifests as confusional state, dementia , hyperactivity with
behavioural problems, fluctuating impairment of consciousness, fluctuating
mental status ,paranoia ,aggressiveness , catatonia ,psychotic symptoms. It can
be diagnosed by EEG monitoring
• INVESTIGATIONS
• Pts who are in convulsive SE require comprehensive diagnostic testing
which includes – serum glucose, electrolyte, urea, creatinine , calcium,
magnesium,complete blood cell count,malarial parasite and culture,arterial
blood gas analysis, determination of anticonvulsant level[if the pt is on
anticonvulsants], RFT and LFTs
• If meningitis is suspected but LP cannot be done, antibiotics should be
administered immediately .
• NEUROIMAGING- the yield is higher in developing countries because of
neuroinfections and neuricysticercosis. A head CT is informative for acute
head trauma, malignancy, meningoencephalitis ,neurometabolic
disorders,persistant headache or in presence of focal neurological signs
• EEG-an urgent EEG recommended for pts with SE especially when non-
convulsive SE is suspected.
MANAGEMENT
• 4 goals of therapy
• ensure adequate vitals , systemic and cerebral oxygenation
• terminate seizure activity
• prevent seizure recurrence
• establish the diagnosis and treat the underlying disorder
Emergency supportive treatment
• Secure the airway, maintain oxygenation, ensure per fusion, obtain intravenous
access and protect the patient from hypoglycemia, hyperthermia and injury.
• Head and neck should be positioned to keep the airway open. If necessary, airway
should be suctioned. Oxygen by nasal cannula or mask, if needed, is administered,
endotracheal intubation may be required.
• Two IV access should be established. Blood samples should be sent for laboratory
studies, and 10-25% dextrose (2 ml/kg) should be given empirically.
• Systolic BP should be maintained at normal levels.
• Hyperthermia occurs frequently in SE; temperature should be recorded and
treated promptly.
• ANTICONVULSANTTREATMENT
• The goal of treatment is rapid termination of clinical and electrical seizure activity
by the prompt administration of appropriate drugs in adequate doses, with
attention to the possibility of complicating apnea, hypoventilation and other
metabolic abnormalities.
• Early and effective treatment is essential to prevent a refractory status and
longterm neurological sequela.
• DOMICILIARYTREATMENT- Prehospital treatment with anticonvulsants is
advocated for all children with recurrent prolonged seizures to reduce
hospitalization episodes and complications. Drugs used are oral or intranasal
midazolam or rectal diazepam
HOSPITALTREATMENT
• Any child who Presents actively convulsing to emergency room is assumed
to be in SE and managed aggressively
• The drug recommended is IV lorazepam, midazolam and diazepam
• If diazepam is used when treating SE, a long acting anticonvulsant such as
phenytoin must be administered concurrently with diazepam to prevent
recurrent convulsions.
• Seizure control occurs within 5 min of benzodiazepine administration in
80% of patients.
• The usual IV dosage for diazepam is 0.1 to 0.3 mg/kg given at a rate of 1
mg/min.This dose can be repeated two times every 5 to 10 min if seizures
persist up to a maximum dose of 10 mg.
• Lorazepam (0.05-0.1 mg/kg IV) is the preferred first line
anticonvulsant as it has a longer duration of action (12-24 hr), less
respiratory depression and repeated doses are less often required
than with diazepam
• A second long-acting anticonvulsant is also not required because of
longer duration of action
• Maintenance drugs should be added to control further seizures.
• If IV access cannot be immediately obtained, then other routes of
administration (rectal, oral) should be considered.
• Midazolam is an important drug for the initial management of acute seizure. It
can be used IM or intranasal if IV access is not available at a dose of 0.1 to 0.2
mg/kg.
• Phenytoin is used for maintaining a prolonged antiseizure effect after rapid
termination of seizures with a benzo diazepine.The loading dose is 20 mg/kg
infused at a rate of 0.5-1 mg/kg/min (maximum 50 mg/min).
A therapeutic effect can be seen in 20 min.
Saline solution should be used for dilution as phenytoin precipitates in dextrose.
Side effects include hypotension, cardiac dysarrhythmia, phlebitis and tissue
necrosis from extravasation, movement disorder and cerebellar ataxia.
• Fosphenytoin is a water-soluble ester of phenytoin that is rapidly
converted to phenytoin by systemic phosphatases and can be
administered intramuscularly.
The dose of fosphenytoin is expressed in phenytoin equivalents
(PE) and is 15-20 mg/kg, infused at a rate of no more than 3
mg/kg/min (maximum 150 mg/min).
Phlebitis is less common with fosphenytoin but its primary
disadvantage is high cost.
• If no response to benzodiazepines and phenytoin,
phenobarbitone is administered at a loading dose of 10 to 20
mg/kg at a rate of 1 to 2 mg/kg/min
• Potential side effects include hypotension, respiratory depression
and sedation.
• Phenobarbitone is the drug of choice in neonatal seizures,
hypersensitivity to phenytoin and cardiac conduction abnormality.
• In patients on oral phenytoin or phenobarbitone, 5-10 mg/kg of
the drug should be given if drug with drawal is the likely cause of
SE.
REFRACTORY STATUS EPILEPTICUS
• When the seizure do not respond to at least two doses of
benzodiazepines, followed by phenytoin/valproate and
phenobarbitone or midazolam infusion beyond 60 min after
treatment has been started, it is labeled as refractory SE
• must be ideally managed in a tertiary health care center with ICU
where facility for artificial ventilation is available
• Treatment of refractory SE include barbiturate coma, midazolam
infusion, lignocaine, intra venous valproate, propofol and
inhalation anesthesia.
• midazolam infusion is a good choice for initial treatment of
refractory SE with fewer hemodynamic consequences and lesser
need for invasive monitoring and mechanical ventilation.
• The optimum rate of infusion at which seizure control is achieved is
maintained for a period of 48 hr.
• Subsequently the infusion rate is gradually decreased with
frequent EEG review
• Any seizure activity during the weaning period requires an
immediate resumption of the infusion to achieve again a seizure-
free period of 48 hr.
• Both pentobarbital and thiopental have been used for barbiturate coma.
Patients requiring barbiturate coma must be intubated and mechanically
ventilated with close hemodynamic and continuous EEG monitoring
• Pento barbital is given in a loading dose of 5 mg/kg followed by an infusion of
0.5-3 mg/kg/hr.The patient is monitored for a burst suppression pattern by
EEG.The patient remains in barbiturate coma for 12 to 24 hr.
• The patient is then weaned and observed for recurrence of seizure activity. If
seizure recurs, the patient is placed back into the barbiturate coma and
weaning is again tried after another 24 hr.
• Barbiturate coma is advantageous over the use of general anesthesia.
Continuous EEG is necessary to ensure that burst suppression has occurred.
• Longterm anticonvulsant drugs- The decision for therapy is based on the
underlying cause and predicted risk of seizure.When no etiology is identified
and the EEG is normal, the recurrence risk is 24% at 2 yr.
• Patients with abnormal neuroimaging/EEG or focal seizures have a 65% risk of
recurrence and should receive longterm anti convulsant therapy.
• FEVER-INDUCED REFRACTORY EPILEPTIC ENCEPHALOPATHY-[FIRES] It
is a syndrome of refractory SE in school aged children that is associated with
acute febrile infections and para infectious in nature. It is highly drug resistant
but responsive to ketogenic diet.
FEBRILE CONVULSIONS
• Febrile convulsions are the commonest provoked seizures
affecting 3-5% children
• seizures during fever occurring between 6 months and 5 yr age in
the absence of infection of the central nervous system in a
neurologically normal child
• Febrile seizures are frequently genetically determined.
• The convulsions are not related to the degree of temperature,
but are frequent if temperature rises abruptly.
• Febrile convulsions may be (i) simple, benign; or (ii) atypical,
complex.
• SIMPLE FEBRILE SEIZURES -The seizure occurs within 24 hr of the onset of fever,
last less than 15 min and are usually single per febrile episode. Convulsions are
generalized.There is no postictal neurological deficit.
• ATYPICAL FEBRILE SEIZURES- Atypical or complex febrile convulsions should be
distinguished from simple febrile convulsions. Presence of family history of
epilepsy, neuro developmental retardation and atypical episodes increase
recurrence risk of febrile seizures and subsequent epilepsy.
• Convulsions in developmentally challenged children may be precipitated by fever,
as the cerebral threshold for seizures is reduced with the elevation of temperature.
These are distinct from febrile convulsions, which occur in a neurodevelopmentally
normal child.
• Differentiation from meningitis- Infections of the central nervous system
such as meningitis or encephalitis, are important causes of convulsions
associated with fever and can be easily confused with simple febrile
convulsions.
• Lumbar puncture should be performed in the first episode of febrile seizure,
in infants below 1 yr who are not immunized with Hib and pneumococcal
vaccine, or if immunization status is not known and where meningitis is
suspected
• In all patients with febrile convulsions, a lumbar puncture is not required
routinely.
• EEG and neuroimaging have no role in febrile seizures.
• TREATMENT- Febrile convulsions are managed by prompt
reduction of temperature with antipyretics or hydro therapy to
comfort the patient
• Maintenance of airway, breathing and circulation should be
ensured
• In case of prolonged febrile seizures, IV access should be
established to maintain adequate hydration and to administer
anticonvulsant medication.
• Injection of midazolam or diazepam (0.2--0.3 mg/kg/dose) is
given for control of seizures.
FEBRILE SEIZURE PROPHYLAXIS
• Prophylaxis may be continuous or intermittent.
• Intermittent prophylaxis of febrile convulsions is indicated if 3 or more
febrile seizures in 6 months, or 6 or more in 1 yr, febrile seizures lasting
more than 15 min or requiring pharmacological therapy to control seizures.
• Intermittent prophylaxis is currently prescribed during episodes of fever. A
drug that attains drug levels quickly and prevents febrile convulsions should
be used.
• Oral clobazam (0.75-1 mg/kg/day) is an effective prophylactic and is given
for 3 days during fever episodes. Antipyretics, hydrotherapy and meticulous
temperature recording should be advocated for all patients. Domiciliary
care is recommended.
• Continuous prophylaxis with antiepileptic drugs is advocated in the event
of failure of intermittent therapy, recurrent atypical seizures and in
particular, when parents are unable to promptly recognize the onset of
fever.
• Only sodium valproate (10-20 mg/kg/day) or phenobarbitone (3-5
mg/kg/day) are effective for febrile seizure prophylaxis.
• Carbamazepine and phenytoin are ineffective.
• The duration of therapy should be for 1-2 yr or until 5 yr of age
prognosis
• RISK FACTORS FOR RECURRENCE OF FEBRILE SEIZURES-
• Major- age <1 yr, duration of fever <24 hr, fever- 38 -39 °C
• Minor- family H/O febrile seizures, family H/O epilepsy, complex
febrile seizure, day care , male gender, lower serum sodium at
time of presentation
RISK FACTORS FOR OCCURRENCE OF
SUBSEQUENT EPILEPSY
Status epilepticus and febrile convulsions

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Status epilepticus and febrile convulsions

  • 2. STATUS EPILEPTICUS • It is a medical emergency that should be anticipated in any pt who presents with an acute seizure • It implies prolonged simple seizure or multiple episodes of seizures lasting for more than 30 min without regaining consciousness in between • Impending SE refers to any seizure lasting more than 5 min • SE can be 1. Convulsive [tonic-clonic, clonic ,tonic , or myoclonic 2. Non-convulsive[absence , complex partial ,speech sensorial alteration]
  • 3. • Convulsive SE is the most common and is associated with significant mortality and morbidity • Neurological residua – mental retardation, focal neurological deficits, behavioural disorders and chronic epilepsy • The neurological sequelae depend upon etiology, age and duration of SE • The risk of complications increases substantially with duration[>60 min] • Mortality rate is 10% ; most deaths are attributable to pt’s underlying pathology • Seizures recur in 25-75% of pts
  • 4. • 50% cases- pt’s first seizure • 25% of childhood epilepsy- idiopathic • 25% - associated with fever or meningoencephlitis • 50% cases – neurodevelopmental abnormality, head trauma , stroke , drug intoxication , subarachnoid bleed, pyridoxine deficiency , metabolic abnormality
  • 5. • PATHOPHYSIOLOGY • SE results from excessive and persistant excitation or ineffective recruitment of inhibition • Excitatory neurotransmitters- glutamate , aspartate and Ach • GABA is the dominant inhibitory neurotransmitter • Blockage of NMDA receptors by magnesium ions seems to be important in the pathogenesis of neuronal damage • SE can produce both neuronal necrosis and apoptosis • Cytokines [interleukin 1 𝝰 ] can modify neuronal excitability by rendering NMDA receptors more permeable for calcium influx • Prostaglandins can increase glutamate release and reduce potassium currents leading to increased excitability
  • 6. EVALUATION IN EMERGENCY DEPARTMENT • History is taken for description of the event , associated symptoms, duration and the post ictal period, prior history of seizures, non compliance with antiepileptic drugs or change of antiepileptic drugs and history of prior neurological development • If post ictal confusion doesn’t resolve , search for other causes like hypoglycemia , dyselectrolemia ,CNS infection , CNS vascular event ,drug toxicity ,psychiatric disorders and non convulsive SE • Non convulsive SE manifests as confusional state, dementia , hyperactivity with behavioural problems, fluctuating impairment of consciousness, fluctuating mental status ,paranoia ,aggressiveness , catatonia ,psychotic symptoms. It can be diagnosed by EEG monitoring
  • 7. • INVESTIGATIONS • Pts who are in convulsive SE require comprehensive diagnostic testing which includes – serum glucose, electrolyte, urea, creatinine , calcium, magnesium,complete blood cell count,malarial parasite and culture,arterial blood gas analysis, determination of anticonvulsant level[if the pt is on anticonvulsants], RFT and LFTs • If meningitis is suspected but LP cannot be done, antibiotics should be administered immediately . • NEUROIMAGING- the yield is higher in developing countries because of neuroinfections and neuricysticercosis. A head CT is informative for acute head trauma, malignancy, meningoencephalitis ,neurometabolic disorders,persistant headache or in presence of focal neurological signs • EEG-an urgent EEG recommended for pts with SE especially when non- convulsive SE is suspected.
  • 8. MANAGEMENT • 4 goals of therapy • ensure adequate vitals , systemic and cerebral oxygenation • terminate seizure activity • prevent seizure recurrence • establish the diagnosis and treat the underlying disorder
  • 9. Emergency supportive treatment • Secure the airway, maintain oxygenation, ensure per fusion, obtain intravenous access and protect the patient from hypoglycemia, hyperthermia and injury. • Head and neck should be positioned to keep the airway open. If necessary, airway should be suctioned. Oxygen by nasal cannula or mask, if needed, is administered, endotracheal intubation may be required. • Two IV access should be established. Blood samples should be sent for laboratory studies, and 10-25% dextrose (2 ml/kg) should be given empirically. • Systolic BP should be maintained at normal levels. • Hyperthermia occurs frequently in SE; temperature should be recorded and treated promptly.
  • 10. • ANTICONVULSANTTREATMENT • The goal of treatment is rapid termination of clinical and electrical seizure activity by the prompt administration of appropriate drugs in adequate doses, with attention to the possibility of complicating apnea, hypoventilation and other metabolic abnormalities. • Early and effective treatment is essential to prevent a refractory status and longterm neurological sequela. • DOMICILIARYTREATMENT- Prehospital treatment with anticonvulsants is advocated for all children with recurrent prolonged seizures to reduce hospitalization episodes and complications. Drugs used are oral or intranasal midazolam or rectal diazepam
  • 11.
  • 12. HOSPITALTREATMENT • Any child who Presents actively convulsing to emergency room is assumed to be in SE and managed aggressively • The drug recommended is IV lorazepam, midazolam and diazepam • If diazepam is used when treating SE, a long acting anticonvulsant such as phenytoin must be administered concurrently with diazepam to prevent recurrent convulsions. • Seizure control occurs within 5 min of benzodiazepine administration in 80% of patients. • The usual IV dosage for diazepam is 0.1 to 0.3 mg/kg given at a rate of 1 mg/min.This dose can be repeated two times every 5 to 10 min if seizures persist up to a maximum dose of 10 mg.
  • 13. • Lorazepam (0.05-0.1 mg/kg IV) is the preferred first line anticonvulsant as it has a longer duration of action (12-24 hr), less respiratory depression and repeated doses are less often required than with diazepam • A second long-acting anticonvulsant is also not required because of longer duration of action • Maintenance drugs should be added to control further seizures. • If IV access cannot be immediately obtained, then other routes of administration (rectal, oral) should be considered.
  • 14. • Midazolam is an important drug for the initial management of acute seizure. It can be used IM or intranasal if IV access is not available at a dose of 0.1 to 0.2 mg/kg. • Phenytoin is used for maintaining a prolonged antiseizure effect after rapid termination of seizures with a benzo diazepine.The loading dose is 20 mg/kg infused at a rate of 0.5-1 mg/kg/min (maximum 50 mg/min). A therapeutic effect can be seen in 20 min. Saline solution should be used for dilution as phenytoin precipitates in dextrose. Side effects include hypotension, cardiac dysarrhythmia, phlebitis and tissue necrosis from extravasation, movement disorder and cerebellar ataxia.
  • 15. • Fosphenytoin is a water-soluble ester of phenytoin that is rapidly converted to phenytoin by systemic phosphatases and can be administered intramuscularly. The dose of fosphenytoin is expressed in phenytoin equivalents (PE) and is 15-20 mg/kg, infused at a rate of no more than 3 mg/kg/min (maximum 150 mg/min). Phlebitis is less common with fosphenytoin but its primary disadvantage is high cost.
  • 16. • If no response to benzodiazepines and phenytoin, phenobarbitone is administered at a loading dose of 10 to 20 mg/kg at a rate of 1 to 2 mg/kg/min • Potential side effects include hypotension, respiratory depression and sedation. • Phenobarbitone is the drug of choice in neonatal seizures, hypersensitivity to phenytoin and cardiac conduction abnormality. • In patients on oral phenytoin or phenobarbitone, 5-10 mg/kg of the drug should be given if drug with drawal is the likely cause of SE.
  • 17.
  • 18. REFRACTORY STATUS EPILEPTICUS • When the seizure do not respond to at least two doses of benzodiazepines, followed by phenytoin/valproate and phenobarbitone or midazolam infusion beyond 60 min after treatment has been started, it is labeled as refractory SE • must be ideally managed in a tertiary health care center with ICU where facility for artificial ventilation is available • Treatment of refractory SE include barbiturate coma, midazolam infusion, lignocaine, intra venous valproate, propofol and inhalation anesthesia.
  • 19.
  • 20. • midazolam infusion is a good choice for initial treatment of refractory SE with fewer hemodynamic consequences and lesser need for invasive monitoring and mechanical ventilation. • The optimum rate of infusion at which seizure control is achieved is maintained for a period of 48 hr. • Subsequently the infusion rate is gradually decreased with frequent EEG review • Any seizure activity during the weaning period requires an immediate resumption of the infusion to achieve again a seizure- free period of 48 hr.
  • 21. • Both pentobarbital and thiopental have been used for barbiturate coma. Patients requiring barbiturate coma must be intubated and mechanically ventilated with close hemodynamic and continuous EEG monitoring • Pento barbital is given in a loading dose of 5 mg/kg followed by an infusion of 0.5-3 mg/kg/hr.The patient is monitored for a burst suppression pattern by EEG.The patient remains in barbiturate coma for 12 to 24 hr. • The patient is then weaned and observed for recurrence of seizure activity. If seizure recurs, the patient is placed back into the barbiturate coma and weaning is again tried after another 24 hr. • Barbiturate coma is advantageous over the use of general anesthesia. Continuous EEG is necessary to ensure that burst suppression has occurred.
  • 22. • Longterm anticonvulsant drugs- The decision for therapy is based on the underlying cause and predicted risk of seizure.When no etiology is identified and the EEG is normal, the recurrence risk is 24% at 2 yr. • Patients with abnormal neuroimaging/EEG or focal seizures have a 65% risk of recurrence and should receive longterm anti convulsant therapy. • FEVER-INDUCED REFRACTORY EPILEPTIC ENCEPHALOPATHY-[FIRES] It is a syndrome of refractory SE in school aged children that is associated with acute febrile infections and para infectious in nature. It is highly drug resistant but responsive to ketogenic diet.
  • 23. FEBRILE CONVULSIONS • Febrile convulsions are the commonest provoked seizures affecting 3-5% children • seizures during fever occurring between 6 months and 5 yr age in the absence of infection of the central nervous system in a neurologically normal child • Febrile seizures are frequently genetically determined. • The convulsions are not related to the degree of temperature, but are frequent if temperature rises abruptly. • Febrile convulsions may be (i) simple, benign; or (ii) atypical, complex.
  • 24. • SIMPLE FEBRILE SEIZURES -The seizure occurs within 24 hr of the onset of fever, last less than 15 min and are usually single per febrile episode. Convulsions are generalized.There is no postictal neurological deficit. • ATYPICAL FEBRILE SEIZURES- Atypical or complex febrile convulsions should be distinguished from simple febrile convulsions. Presence of family history of epilepsy, neuro developmental retardation and atypical episodes increase recurrence risk of febrile seizures and subsequent epilepsy. • Convulsions in developmentally challenged children may be precipitated by fever, as the cerebral threshold for seizures is reduced with the elevation of temperature. These are distinct from febrile convulsions, which occur in a neurodevelopmentally normal child.
  • 25. • Differentiation from meningitis- Infections of the central nervous system such as meningitis or encephalitis, are important causes of convulsions associated with fever and can be easily confused with simple febrile convulsions. • Lumbar puncture should be performed in the first episode of febrile seizure, in infants below 1 yr who are not immunized with Hib and pneumococcal vaccine, or if immunization status is not known and where meningitis is suspected • In all patients with febrile convulsions, a lumbar puncture is not required routinely. • EEG and neuroimaging have no role in febrile seizures.
  • 26. • TREATMENT- Febrile convulsions are managed by prompt reduction of temperature with antipyretics or hydro therapy to comfort the patient • Maintenance of airway, breathing and circulation should be ensured • In case of prolonged febrile seizures, IV access should be established to maintain adequate hydration and to administer anticonvulsant medication. • Injection of midazolam or diazepam (0.2--0.3 mg/kg/dose) is given for control of seizures.
  • 27. FEBRILE SEIZURE PROPHYLAXIS • Prophylaxis may be continuous or intermittent. • Intermittent prophylaxis of febrile convulsions is indicated if 3 or more febrile seizures in 6 months, or 6 or more in 1 yr, febrile seizures lasting more than 15 min or requiring pharmacological therapy to control seizures. • Intermittent prophylaxis is currently prescribed during episodes of fever. A drug that attains drug levels quickly and prevents febrile convulsions should be used. • Oral clobazam (0.75-1 mg/kg/day) is an effective prophylactic and is given for 3 days during fever episodes. Antipyretics, hydrotherapy and meticulous temperature recording should be advocated for all patients. Domiciliary care is recommended.
  • 28. • Continuous prophylaxis with antiepileptic drugs is advocated in the event of failure of intermittent therapy, recurrent atypical seizures and in particular, when parents are unable to promptly recognize the onset of fever. • Only sodium valproate (10-20 mg/kg/day) or phenobarbitone (3-5 mg/kg/day) are effective for febrile seizure prophylaxis. • Carbamazepine and phenytoin are ineffective. • The duration of therapy should be for 1-2 yr or until 5 yr of age
  • 29. prognosis • RISK FACTORS FOR RECURRENCE OF FEBRILE SEIZURES- • Major- age <1 yr, duration of fever <24 hr, fever- 38 -39 °C • Minor- family H/O febrile seizures, family H/O epilepsy, complex febrile seizure, day care , male gender, lower serum sodium at time of presentation
  • 30. RISK FACTORS FOR OCCURRENCE OF SUBSEQUENT EPILEPSY