Status epilepticus is a medical emergency that requires prompt treatment to prevent irreversible brain damage. It is defined as continuous seizure activity lasting more than five minutes, or two or more seizures between which consciousness is not regained. Status epilepticus can be classified as generalized convulsive or non-convulsive and has various etiologies including low anti-epileptic drug levels, stroke, electrolyte imbalances, and infections. Treatment involves airway protection, treatment of underlying causes, administration of benzodiazepines or phenytoin to stop seizures, and induction of anesthesia with thiopental or propofol if seizures persist. Outcomes depend on factors like age, etiology, and degree of impaired consciousness,

1. Dr.V.NAGARJUNA
Fellow Critical Care
AWARE GLOBAL HOSPITAL

2. STATUS EPILEPTICUS

3. STATUS EPILEPTICUS
•Medical emergency
•Requires prompt intervention to
prevent irreversible brain
damage

4. DEFINITION
Seizure activity more than 30
minutes.
OR
Intermittent seizures with no
regaining of consciousness
between seizures

5. ACCEPTED DEFINITION
>5 minutes of continuous seizure activity.
or
2 or more discrete seizures with no intervening recovery of
consciousness
Seizures persisting beyond this duration are unlikely to cease
spontaneously & more likely to cause irreversible brain
damage

6. CLASSIFICATION OF STATUS
EPILEPTICUS
•Status epilepticus is classified in to
two categories
1.Generalized Convulsive Status
Epilepticus(GCSE)
2.Non Convulsive Status
Epilepticus(NCSE)

7. GCSE
•Seizures are primary or
secondarily generalised
•Patient has generalised tonic &/or
clonic convulsive movements with
loss of consciousness

8. NCSE
Altered consciousness and EEG
evidence of seizures without
convulsive movements
May evolve from GCSE when
electrical seizure activity continues
with loss of motor manifestations

9. PATHOPHYSIOLOGY
•Imbalance between inhibitory &
excitatory mechanisms
•GABA(A) receptor mediated
inhibition
•NMDA receptor mediated
excitation

11. INHIBITORY MECHANISM
Major inhibitory mechanism is
GABA acting on GABA(A) receptor
Causes:
Cl- influx
Hyperpolarization

12. EXCITATORY MECHANISM
•Major excitatory mechanism is
glutamine acting on N-methyl-D-
aspartate(NMDA) receptors
Causes:
Calcium influx
Depolarization

13. NEURONAL CIRCIUT INJURY
•Pathophysiological effects of
seizures on the brain are directly
due to excito- toxic effect &
mitochondrial dysfunction &
secondary to systemic
complications such as hypoxia ,
hyperthermia.

14. ETIOLOGY
•Status epilepticus may occur de
novo(approximately 60% of
presentations) or less commonly
in a previously diagnosed
epileptic.

15. CAUSES OF SE IN ADULTS
• Low antiepileptic drug levels
• Stroke-Ischemic/haemorrhagic
• Electrolyte
disturbances(Hyponatraemia,hypocalcemia,hypomagnesemia)
• Hypoglycaemia/Hyperglycaemia
• Cerebral hypoxia
• Alcohol-withdrawal
• Head trauma
• Organ failure-uraemia/hepatic encephalopathy

16. CAUES OF SE IN ADULTS
•Drug toxicity—
cephalosporins,isoniazid,tranexamic
acid,cocaine,theophylline)
•CNS tumors-primary/secondary
•Hypertensive encephalopathy/eclampsia
•Immunological disorders-Hashimotos
encephalopathy,cerebral lupus

17. GENERALISED CONVULSIVE STATUS
EPILEPTICUS
GCSE is the most common &
dangerous type accounts for
approximately 75%

18. GCSE CLINICAL PRESENTATION
•May range from overt GTCS to subtle convulsive
movements in a profoundly comatose patient
.May be tonic or clonic
Symmetrical or asymmetrical
.Late GCSE may show only small amplitude
twitching movements of the face ,hands , or feet
and also nystagmoid jerking of the eyes

19. EEG CHANGES
Predictable sequence of EEG changes during
untreated GCSE
1.Waxing & waning pattern
2.Continuous monomorphic discharges
3.Increasing periods of electrographic silence
4.Periodic epileptiform discharges on a
relatively flat background

20. PHYSIOLOGICAL EFFECTS IN GCSE
• Hypoxia
• Respiratory acidosis
• Lactic acidosis
• Hyperpyrexia
• Hypertension(early)/Hypotension (late)
• Hyperglycemia (Early)
• Hypoglycemia (Late)
• Tachycardia
• Intracranial hypertension
• Aspiration pneumonitis
• Rhabdomyolysis
• Neurogenic pulmonary edema

21. GCSE Vs PSEDOSEIZURES
•Differentiate between true
seizures & pseudoseizures
•Pseustatus misdiagnosed as true
SE is often refractory to initial
therapy & can lead to patients
receiving GA & MV

22. Features suggestive of pseudoseizures
.Lack of sustained convulsions(on-off)
.Increase in movement if restrained is applied
.Abolition of motor movements with reassurance or
suggestion
.Resistance to eye opening & gaze aversion
.Absence of pupillary dilatation
Normal tendon reflexes & plantar responses immediately
after convulsion
.Lack of metabolic consequences

23. NCSE
• Accounts for 25% of SE
• Diagnosis of NCSE requires an altered conscious state, no
overt seizure activity and EEG with epileptiform discharges
• A response to intravenous antiepileptic drugs(Eg:BZDs)
with clinical improvement & resolution EEG epileptic
activity is helpful in confirming the diagnosis
• NCSE should be considered in any patient with an
unexplained altered conscious state , particularly those
with CNS injury , metabolic disturbance , hepatic
encephalopathy or sepsis

24. DD of NCSE includes
•Metabolic encephalopathy
•Drug intoxication
•Cerebrovascular disease
•Psychiatric syndromes(Acute
psychosis)
•Post-ictal confusion

25. INVESTIGATIONS IN SE
•Initial studies include
glucose,electrolytes Na+,K+,calcium ,
magnesim),urea
ABG analysis
Anticonvulsant drug levels
Full blood count
Urine analysis

26. Further investigations after
stabilization
•LFT
•Lactate
•Creatine kinase
•Toxicology screen
•Lumbar puncture
•Electroencephalogram
•Brain imaging with CT or MRI

27. OTHER FORMS OF STATUS
EPILEPTICUS
•Refractory SE:Failure of initial therapy
such as BZDs & phenytoin, usually
necessitating treatment with agents
that induce general anaesthesia
•It develops in about 1 in 5 patients
with an SE
•Associated with a worse prognosis

28. OTHER FORMS OF SE
•SUPER REFRACTORY SE:
Continuation or recurrence of SE
beyond 24 hours of anaesthetic
therapy

29. MANAGEMENT
1.Initial resuscitation
Assess A,B,C,sensorium
Initial priority in an ongoing seizure patient is airway
protection
This can be achieved by proper positioning,oral suctioning &
oral/nasopharyngeal airway devices
If necessary, the patient should be intubated
Obtain IV access & draw blood for investigations
Blood glucose should be checked

30. MANAGEMENT
•If patient is hypoglycaemic give
glucose
•Adults: Give thiamine 100mg IV
& 100ml of 25% glucose IV

31. SEIZURE CONTROL
A.Give BZDs
Diazepam:0.2 mg/kg i.v at 5
mg/min
OR
Lorazepam:0.1 mg/kg i.v at
2mg/min

32. SEIZURE CONTROL
•If seizures persist:
Phenytoin:15-20mg/kg at
</=50mg/min
OR
Fosphenytoin:15-20mg/kg at
</=150mg/min

34. SEIZURE CONTROL
• If seizures persist(refractory SE) intubate & ventilate patient
Thiopental:Slow bolus 3-5mg/kg i.v followed by infusion 1-5mg/kg
per hour
OR
Propofol:Slow bolus 1-2mg/kg i.v followed by infusion 2-5mg/kg per
hour
Titrate doses based on clinical & electrographic evidence of seizures,
targeting electrographic suppression of seizures.
Monitor BP>maintain normo-tension by reducing infusion
rates/giving fluids/pressor agents if required

35. SEIZURE CONTROL
.Start reducing propofol or thiopental,
approximately 12 hours after resolution of
seizures
.Continuous EEG monitoring is required
Observe for further clinical /electrographic
seizures.If seizures recur,reinstate the infusion
as long as the patients seizures remain
refractory

36. In addition
•Look for & treat cause &
precipitant
•Look for & treat complications
like hypotension,hyperthermia
& rhabdomyolysis

37. SURGERY IN REFRACTORY SE
•Procedures based on standard
epilepsy surgery
Success has been reported with
focal resections,subpial
transections,corpus
callosotomy,hemispherectomy

38. OUT COME
•Depends on age,etiology,degree of
impairment of consciousness
•Refractory & super refractory>>worse
prognosis
•No irreversible brain damage>>Good
recovery is possible even after weeks
of Status epilepticus

39. THANK YOU