Dr Arjun Tandon's First Seminar

1. Status epilepticus
By Dr Arjun TandonModerator- DR SS PRASAD

2. OBJECTIVES
 Ability to define status using practical approach
 Probable causes
 Understading pathophysiology
 Management

3. What is status epilepticus?
 Emergency
 True defintion-acc to international league against
epilepsy “a seizure which shows no clinical signs of
arresting after 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”

4. Operational definition
 Continuos seizure activity for more than 5 mins
 Recurrent seizure activity without regaining
conciousness in between
BY DICTUM
Any patient presenting to us in casuality with ongoing seizure
shud be treated as status
Earlier the cutoff time was 30 min
This has been reduced to emphasise the risks involved with longer
durations

5. Incidence
 10-60 per 1 lakh population in vvarious studies
 Most common in children younger than 5 years
 Incidence In this age group >100 per 1 lakh children
 30% present to us with first seizure
 40% later develop epilepsy

6. types
status
convulsive
Gerneralised
tonic
Clonic Tonic clonic
Non
convulsive
Complex
partial
absence

7. Misc types
 Myoclonic status
 Epilepsia partialis continua
 Neonatal status epilepticus

8. Etiology

9. others
 Melas- mitochondrial encephalopathy with lactic
acidosis in infants
 Folinic acid , pyridoxine and pyridoxal phosphate
deficiency
 Rare disease-
Hemiconvulsion hemiplegia epilepsy syndrome
prolonged febrile status
caused by focal acute encephalitis

10. •Infections causing status
• those causing acute encephalitis
• bartonella{non convulsive}
•Herpes simplex[complex partial and convulsive]
• ebstein barr virus
• mycoplasma
•Hhv6 also causes status

11. Mechanism
Ampa
receptors
• Failure of desensitisation of ampa receptors
• So persistance of increased excilitibilty
Gaba a
• Reduction of gaba mediated inhibition
• Also there is internalisation of gaba a receptors
• So benzodiazapene appear to be less effective in
longer seizure

12. Pathophysiology

14. status
Neuronal
necrosis
Apostosis
Due to incresed
intracellar ca
Proapoptaotic
factors like bax,
ceramide
Cytokine like interleukin 1b can also modify
neuronal activity . This is released during seizure

15. Approach to status
in casuality

16. Early intervention
Left lateral
postion
Maintian abc
Check
hypoglycemia

17. Protocol

18. Refractory status epilepticus?
 Defined as the status that has failed to respond to
therapy,, usually with atleast 2
medications(benzodiazapine+some other)
 Treatment includes—
1. intravenous bolus followed by contonuous
infusion of midazolam, phenobarbital, thiopental
2. Done in icu
3. Choice is based on experience due drastic side effects
of these agents

20. Newer drug
 Lacosamide– iv loading 4mg/kg then 4-12mg/kg/24hr
 Levetiractam-iv 20-60mg/kg
 Topiramate- enterally 5-10 mg/kg/24hr then same for
maintenence

21. Diazepam and lorazepam

24. Early investigations
 Serum electrolytes
 Anti epeleptic drug levels
 Liver function test
 Glucose level
 Lumbar puncture
 Eeg and ct scan

25. Evaluation in emergency
department
 History taken for description of event
 Duration of post ictal period
 Prior history of seizures
 Non compliance with anti epileptic drugs
 If post ictal confusion does not resolve then think of
hypoglycemia , cns infections,drug toxicity
 Most imp think of non convulsive status

26. Some points to remember

28. Take home message
 Status is an emergency
 More is the time more is the brain damage
 Early intervention is good
 Take proper history to get the probable etiology of
status
 Try to make difference between convulsive and non
convulsive status
 Manage accordingly

29. THANK
YOU