For prdiatrics postgraduates

2.  It is defined as continuous seizure activity or
recurrent seizure activity without regaining of
consciousness lasting for more than 5 min as part
of an operational definition put forth within the
past few years.
 In the past, the cutoff time was 30 min, but this
has been reduced to emphasize the risks involved
with the longer durations.

3. The ILAE defines status epilepticus
as “a seizure which shows no clinical
signs of arresting after a duration
encompassing the great majority of
seizures of that type in most patients or
recurrent seizures without resumption
of baseline central nervous system
function interictally.”

5.  The incidence of status epilepticus ranges
between10 and 60 per 100,000 population in
various studies.
 Status epilepticus is most common in children
younger than 5 yr of age, with an incidence
in this age group of >100 per 100,000 children.
Incidence is highest among in children younger
than 1 year cause being febrile seizure.

6.  Etiologies include new-onset epilepsy of any type;
 drug intoxication (e.g., tricyclic antidepressants) in
children and drug and alcohol abuse in
adolescents;
 drug withdrawal or overdose in patients on AEDs;
 hypoglycemia; hypocalcemia; hyponatremia;
hypomagnesemia;
 Acute head trauma; encephalitis; meningitis;
autoimmune encephalitis (such as anti-NMDA
receptor and anti–voltage-gated potassium
channel complex antibody syndromes);
 ischemic (arterial or venous) stroke intracranial
hemorrhage;

7.  folinic acid and pyridoxine and pyridoxal
phosphate dependency (these usually present in
infancy but childhood onset is also possible);
 inborn errors of metabolism.
systemic conditions (such as hypertensive
encephalopathy, posterior reversible
encephalopathy,
renal or hepatic encephalopathy)
 brain tumors;
 any other disorders that can cause epilepsy (such
as brain malformations, neurodegenerative
disorders, different types of progressive myoclonic
epilepsy, storage diseases).

9.  (1) failure of desensitization of AMPA
glutamate receptors, thus persistence of
increased excitability, and
 (2) reduction of GABA-mediated inhibition as
a result of intracellular internalization of GABA
A receptors.

14.  There is no clear evidence to guide therapy in
this phase (level u)
 Choices include ;
 Repeat second line therapy or anesthetic dose
of either, midazolam(0.2mg/dl bolus then
infusion @ 1microgm/kg/min increasing to 1
microgm/kg/min every 5 -10min max. upto 30
ugm/ kg/min),
 Phenobarbital( boluses of 5-10mg/kg every 30
min upto 120 mg/kg /min in 24 hrs)

15.  Ketamine ( loading dose 1.5mg/kg followed by
10-50 ugm/kg/min
 Propofol ( initial boluses of 1-2 mg/ kg
followed by infusion of 1-2mg/kg /min max.
upto 5mg/kg)
 Thiopentone( loading dose 5mg/kg followed
by 3-5 mg/kg/min
( with continous eeg monitoring)

16.  Topiramate loading dose 2-5 mg/kg followed
by 5-10mg/kg/day upto 25mg/kg/d
 Inhaled anaesthetics : isoflurane and desflurane
 Ketogenic diet
 Epilepsy surgery
 Controlled hypothermia 32 to 35 degree celcius
 Immunotherapy : steroid ,IVIg ,plasma
exchangr
 Magnesium infusion
 Electroconvulsive therapy