Status epilepticus (SE) is defined as continuous seizure activity lasting more than 5 minutes or 2 or more seizures within 5 minutes without regaining consciousness. SE is a medical emergency that requires rapid stabilization, seizure termination through pharmacotherapy, and treatment of the underlying cause. First-line drugs for seizure termination include benzodiazepines, phenytoin, and valproate. For refractory SE that does not respond to initial treatment, additional options include midazolam infusion, barbiturates, propofol, ketamine, or inhaled anesthetics. Prolonged SE can cause complications and is associated with higher mortality and long-term neurological deficits.

1. STATUS EPILEPTICUS

2. DEFINITION:
• SE is a common neurological emergency.
• SE is defined as continues seizure activity
lasting more than 30 min or 2 or more seizures
in this duration without gaining consciousness
between them.
• However the operational definition has brought
the time down to 5 min.
• Recent data suggests that neuronal damage
starts much early than 30 minuts.

3. TERMINOLOGY:
• IMPENDING SE : Term used for seizures
between 5 and 30 minuts.
• CONVULSIVE SE : Manifests as GTCS, clonic
or tonic-clonic seizures.
• NON-CONVULSIVE SE : Manifests as
confusional state,dementia,hyperactivity with
behavioral problems, fluctuating impairment of
consciousness with at times unsteady sitting
and walking (absence status), hallucinations,
paranoia.

4. TERMINOLOGY Contd..
• REFRACTORY SE: SE that has failed to
respond to therapy, usually with at least 2
(some have specified 3) medications.
• NEW-ONSET REFRACTORY SE (NORSE) : A
distinct entity that can be caused by almost any
of the causes of SE in a patient without prior
epilepsy. It is often of unknown etiology,
presumed to be encephalitic or post-encephalitic,
can last for several weeks or
longer and often has a poor prognosis.

5. ETIOLOGY:
• New onset epilepsy of any type.
• Drug intoxication (eg. TCA’s), drug withdrawl and
abuse.
• Electrolyte imbalance,
• Acute head trauma.
• Encephalitis, Meningitis,Stroke.
• HIE, Brain tumors.
• IEM (nonketotic hyperglycenemia, MELAS).
• Neurodegenerative diseases.

6. ETIOLOGICAL CLASSIFICATION OF SE:
• CRYPTOGENIC: SE in absence of an acute precipitating CNS
insult or metabolic dysfunction in a patient without a pre-existing
neurologic abnormality.
• REMOTE SYMPTOMATIC: SE in a patient with a known
history of a neurologic insult asociated with an increased risk
of seizures(Stroke,TBI,static encephalopathy).
• FEBRILE: THE MOST COMMON TYPE IN CHILDREN. SE
provoked solely by fever in a patient without a history of
afebrile seizures.
• ACUTE SYMPTOMATIC: SE during an acute illness involving
a known neurologic insult or metabolic dysfunction.
• PROGRESSIVE ENCEPHALOPATHY: SE in a pt. with a
progressive neurologic disease.

7. MECHANISM OF SE:
• Desensitization of AMPA glutamate receptors, thus
persistant electrical activity.
• Reduction of GABA mediated inhibition due to
intracellular internalization of GABA-A receptors, thus
SE is often refractory to BZD’s.
• SE can cause both neuronal necrosis and apoptosis.

8. MANAGEMENT PROTOCOL:
• Initial stabilization.
• Seizure termination.
• Pharmacotherapy.

9. MANAGEMENT:
• INITIAL STABILIZATION:
• Airway,Breathing,Circulation.
• Rapid sequence intubation to be don when- GCS<8
or respiratory failure develops.
• SEIZURE TERMINATION:
• Achieved by pharmacotherapy.
• Diagnostic evaluation and seizure termination should
be achieved simultaneously.

10. PHARMACOTHERAPY:
• BENZODIAZEPINES:
• First line drugs.
• Acts on GABA-a receptors and inhibit neuronal
transmission.
• However as seizure progresses, these receptors
are internalized resulting in lower efficacy of
these drugs in prolonged seizures.
• Eg. Lorazepam (0.1mg/kg IV), Diazepam (0.2-0.5
mg/kg IV or 0.5 mg/kg rectal), Midazolam (0.15-
0.2 mg/kg IV; 0.2 mg/kg IM; 0.3 mg/kg buccal or
nasal).
• BZD’s may be repeated after 3-5 min. if required.

11. PHARMACOTHERAPY contd..
• PHENYTOIN:
• Second line agent.
• Indicated when seizures are not controlled by one or more
dose of BZD’s.
• Acts by slowing the rate of recovery of voltage gated
sodium channels.
• Phenytoin – LD 20 mg/kg (NOT compatible with dextrose);
additional 10mg/kg may be required.
• Phosphenytoin- water soluble phosphate ester of
phenytoin hence can be administered 3 times faster than
phenytoin. LD- 20 mg/kg Phenytoin equivalent.

12. PHARMACOTHERAPY contd..
• PHENOBARBITONE:
• First line agent in neonatal seizures.
• A potent AED, acts by enhancing GABA-A activity.
• Dose- 20 mg/kg infused at no more than 30 mg/min.
• Unacceptably high incidence of sedation and respiratory
depression and it may be difficult to perform neurological
assesment upto 24-36 hrs.

13. PHARMACOTHERAPY contd..
• VALPROATE:
• Acts through several mechanisms including modulation of
sodium and calcium currents and increasing inhibitory
GABA transmission.
• Variable doses ranging from 20-40 mg/kg have been used
with success.
• Rare side effects- Hepatotoxicity, Encephalopathy,
hyperammonemia.
• Broad spectrum, low incidence of adverse effects, ability
to administer rapidly and ease of conversion to oral
therapy makes it a good choice as second line AED after
BZD’s.

14. PHARMACOTHERAPY contd..
• LEVETIRACETAM:
• New broad spectrum anticonvulsant, recently been used
with success in acute seizures and SE.
• Renal excretion, free from any significant drug
interactions, neuroprotective effects demonstrated.
• Multiple sites of action- Ca, glutamate receptors and
GABA modulation.
• LD- 20-30 mg/kg @ 5 mg/kg/min.

15. PHARMACOTHERAPY contd..
• MIDAZOLAM INFUSION:
• Effective both as bolus dose in initial m/g and refractory
SE when second line drugs have failed.
• Water soluble BZD with rapid action and short halflife.
• Started at 1mcg/kg/min increasing by 1mcg/kg/min every
5 min, max dose upto 32mcg/kg/min have been used with
no serious side effects.

16. REFRACTORY SE (RSE) :
• Various definitions used- some suggests duration of
seizures> 1 or 2 hrs but a widely acceptable definition is
saizure (clinical or electrographic) persisting despite use
of two or more AED.
• Often have systemic complications of SE, require hemo-dynamic-
respiratory support, continous EEG monitoring
and have poor outcome.
• Drugs used in m/g of RSE- Levetiracitam, Valproate,
Midazolam infusion, Anaesthetic agents (phenibarbital,
thiopentone,propofol, inhaled anesthetics). High dose
phenobarbitone, Ketamine and Topiramate.

17. BARBITURATE COMA:
• THIOPENTAL AND PHENOBARBITAL:
• Good efficacy in RSE, short half-life, penetrates CNS
quickly, gets deposited in fat and released slowly.
• Thiopental - LD- 3-5 mg/kg f/b further boluses of 1-2
mg/kg within 3-5 min till seizure cessation.
• Phenobarbital – 10-15 mg/kg initial bolus f/b further 2-5
mg/kg boluses q 5 min till seizure control f/b infusion of 1-
3 mg/kg/hr.
• Serious side-effects – hypotension, respiratory depression
and decreased cardiac contractility, suppression of
lymphocyte activation.

18. PROPOFOL:
• An IV GA- acts through GABA-A receptors via a
mechanism probably different from BZD’s and
barbiturates.
• Short half life and does not gets accumulated in fat so
rapid awakening after discontinuation.
• Can cause “Propofol infusion syndrome” in children
characterized by cardiac failure,rhabdomyolysis,
metabolic acidosis, RF, death.
• Hence NOT recommended in children <16 yrs of age.
• Dose- bolus 1-2 mg/kg f/b infusion of 1-2 mg/kg/hr to a
max of 5mg/kg/hr.

19. INHALED ANAESTHETICS:
• Used when all other drugs fail.
• Desflurane and Isoflurane are preferred.
• Side effects- hypotension requiring fluids and
vasopressors.

20. HIGH DOSE PHENOBARBITINE:
• Phenobarbitone has significantly longer half life as
compared to phenobarbital and thiopental.
• In RSE doses upto 80mg/kg have been used resulting in
serum levels >1000 mcg/ml.

21. KETAMINE:
• Acts independent of GABA pathway.
• Non- competitive NMDA receptor antagonist with
additional neuro-protective effect.
• In RSE give IV. Dose- Bolus 1.5 mg/kg f/b infusion @
0.01-0.05 mg/kg/hr.
• Caution in patients with increased ICP. Ketamine
increases ICP.
• Rule out SOL.

22. TOPIRAMATE:
• Oral novel anticonvulsant.
• Multiple sites of action- potentiates GABA activity, reduces
Glutamate release and blockade of voltage sensitive
sodium and calcium channels.
• Effective in controlling seizures while weaning of coma
inducing drugs is being done.
• Side effects- lethargy, ataxia and metabolic acidosis.

23. IAP Convulsive Status Epilepticus M/g Protocol
CONVULSIVE STATUS EPILEPTICUS
- Convulsions for > 5 min
- Not regained consciousness b/w two
episodes of seizures
STABILIZE
- Airway, Breathing,
Circulation
0 min
10 min
30 min
- IV ascess
- Blood sugar level
- Take samples
- Inj. Lorazepam 0.05-0.1 mg/kg, or
- Diazepam 0.2 mg/kg or
Midazolam 0.2 mg/kg
- Repeat Inj. Lorazepam,
Diazepam or Midazolam at same
doses
- Inj. Phenytoin 20 mg/kg @ 1
mg/kg/min; or
- Inj. Phosphenytoin 30 mg/kg @
3 mg/kg/min
ABC STABILIZED
SEIZURES CONTROLLED
- Place the child in recovery position
- Monitor Vitals
- Shift to ward
- Inv. Cause – EEG
RULE OUT NON-CONVULSIVE SE

24. - Inj. Phenytoin 10 mg/kg 2nd dose or;
- Inj. Phosphenytoin 15 mg/kg 2nd
dose
- Intubate – Put on Ventilator
- Start Midazolam infusion @ 1-24
mcg/kg/min
- Increase dose every 15 min
- Shift to PICU
- Order EEG
REFRACTORY FURTHER OPTIONS
STATUS
EPILEPTICUS
Inj. Sod. Valproate
ICU SETTING
- Inj. Propofol 2.5-3.5
mg/kg stat
- Infusion 7.5-15
mg/kg/hr
- Bolus Inj. Thiopentone
2-5 mg/kg
- Infusion 1-5 mg/kg/hr
Topiramate or
Leveteracitam

25. NO CONTROL
CONSIDER
- Ketamine infusion
- Inhalational Anaesthesia

26. EVALATION AND T/T OF UNDERLYING
CAUSE:
• A good history and general physical examination gives
important clues to diagnosis.
• S.electrolytes, Blood sugar, BUN, toxic screen, CBC, LP,
Neuroradiological examinations are warrented if required.

27. COMPLICATIONS OF SE:
• Initial phase- tachycardia, hypertension and increased
cardiac output are present due to increased sympathetic
discharge.
• With ongoing seizure hypotension develops.
• Hypoxia, metabolic acidosis,hyperpyrexia,hyperglycemia
and later hypolycemia.
• Less common- neurogenic pulmonary edema, renal
failure due to rhabdomyolysis, aspiration pneumonia and
shock.

28. OUTCOME:
• Prolonged SE is associated with higher mortality and
morbidity.
• Long term neurological sequele- Epilepsy, behavioural
problems, cognitive decline and focal neurological deficits.