1. Status Epilepticus
Dr. Ravindra K. Sharma
Pediatric Specialist
Fujairah Hospital, UAE
drravindrakr@yahoo.co.in

2. TAJ MAHAL, AGRA, INDIA

3. “Status
epilepticus is a medical
emergency that requires an organized
and skillful approach to minimize the
associated mortality and morbidity”

4.  Status epilepticus (SE)
presents in a multitude
of forms, dependent on etiology and patient
age (myoclonic, tonic, subtle, tonic-clonic,
absence, complex partial etc.)
 Generalized, tonic-clonic SE is the most
common form of SE.

5. Definition:
 Conventional definition:
 Single
 Series
seizure > 30 minutes
of seizures > 30 minutes without
full recovery

6. Definition:….
“If appropriate therapy is delayed, SE can
cause permanent neurologic sequelae or
death …”
thus


“ … any child who presents actively convulsing
should be assumed to have SE.”
Haafiz A. Pediatr Emerg Care 1999;15(2):119-29

7. The longer SE persists,
the lower is the likelihood of spontaneous
cessation
the harder is it to control
the higher is the risk of morbidity and mortality
Treatment for most seizures needs to be
instituted after > 5 minutes of seizure activity
Bleck TP. Epilepsia 1999;40(1):S64-6

8. But
 This is
not practical operational definition.
 Longer periods with uncontrolled seizure
activity, more likely to develop a RSE
syndrome.
 More practical guidelines needed to draw that
arbitrary ‘line in sand’, beyond which
substantial risk of developing clinical SE exists.

9. Operational Definition:
“Continuous seizures lasting at least 5 minutes
or two or more discrete seizures between which
there is an incomplete recovery of
consciousness”

10. Causes.







Fever
Medication change
Unknown
Metabolic
Congenital
Anoxic
Other (trauma, vascular,
infection, tumor,
drugs,endocrine)
DeLorenzo RJ. Epilepsia 1992;33 Suppl 4:S15-25
36 %
20 %
9 %
8%
7 %
5 %
15 %

11. Pathophysiology
GLUTAMATE = the major excitatory AA
neurotransmitter in brain
 Any factor increases Glutamate activity can lead to
seizures
 NMDA(N-methyl-D-aspartic acid) is an AA derivative
which acts as a specific agonist at the NMDA receptor
mimicking the action of glutamate
 GABA = main inhibitory neurotransmitter, ; GABA
antagonists can cause SE


12. Drugs which can cause seizures


Antibiotics
 Penicillins
 Isoniazid
 Metronidazole
Anesthetics, narcotics
 Halothane, enflurane
 Cocaine, fentanyl
 Ketamine

Psychopharmaceuticals
 Antihistamines
 Antidepressants
 Antipsychotics
 Phencyclidine
 Tricyclic antidepressants
 List of drugs

13. Mortality


Adults
Children
15 to 22%
3 to 15%
Reviewed in: Fountain NB. Epilepsia 2000;41 Suppl 2:S23-30

14. Prolonged seizures
Temporary
systemic
changes
Life
threatening
systemic
changes
Duration of seizure
Death

15. Respiratory

Hypoxia and hypercarbia
-
ventilation (chest rigidity from muscle spasm)
Hypermetabolism ( O2 consumption, CO2 production)
Poor handling of secretions
-
Neurogenic pulmonary edema?
-

16. Hypoxia


Hypoxia/anoxia markedly increase the risk of
mortality in SE
Seizures (without hypoxia) are much less dangerous
than seizures and hypoxia
Towne AR. Epilepsia 1994;35(1):27-34

17. Neurogenic pulmonary edema
Rare
complication
Likely occurs as
consequence of marked
increase of pulmonary
vascular pressure
Johnston SC. Postictal pulmonary edema requires pulmonary vascular pressure
increases. Epilepsia 1996;37(5):428-32

18. Acidosis


Respiratory
Lactic


Impaired tissue oxygenation
Increased energy expenditure

19. Hemodynamics

Sympathetic overdrive
 Massive
catecholamine /
autonomic
discharge
 Hypertension
 Tachycardia
 High CVP
0 min
60 min

Exhaustion
 Hypotension
 Hypoperfusion

20. COMMON WEALTH GAMES, DELHI 2010.

21. Cerebral blood flow - Cerebral O2 requirement

Hyperdynamic phase

O2 requirement

Exhaustion phase


Blood flow

Blood pressure
Seizure duration
CBF meets CMRO2
CBF drops as
hypotension sets in
Autoregulation
exhausted
Neuronal damage ensues

22. Glucose
Glucose

Hyperdynamic
phase


SE
Exhaustion phase


30 min
SE + hypoxia

Seizure duration
Hyperglycemia
Hypoglycemia
develops
Hypoglycemia appears
earlier in presence of
hypoxia
Neuronal damage
ensues

23. Hyperpyrexia
 Hyperpyrexia may develop during protracted
SE, and aggravate possible mismatch of
cerebral metabolic requirement and substrate
delivery
 Treat hyperpyrexia aggressively
 Antipyretics, external cooling

24. Other alterations
 Blood leukocytosis
(50% of children)
 Spinal fluid leukocytosis (15% of children)

K+

creatine kinase
 Myoglobinuria

25. Boring!

26. Acute Management of Seizures
0-5 min
5-15 min
15-35 min
45 min
60 min

27. Common Sense:0-5 minutes
Stabilize the patient-
A
Oxygen, oral airway. Avoid hypoxia!
B
Consider bag-valve mask ventilation. Consider
intubation
C
IV/IO access. Treat hypotension, but NOT
hypertension

28. (0-5 minutes)…
 Arterial blood gas?
 All children in SE have acidosis. It often resolves rapidly with
termination of SE
 Intubate?
 It may be difficult to intubate the actively seizing child
 Stop or slow seizures first, give O2, consider BVM ventilation
 If using paralytic agent to intubate, assume that SE continues

29. 0-5 minutes….
 Give glucose (2-4 ml/kg D25%, infants 5 ml/kg D10%), unless
normo- or hyperglycemic
 Hyperglycemia has no negative effect in SE
(as long as significant hyperosmolality is being avoided)
 Adoloscent-Thiamin
100 mg IV first

30. Initial investigations(0-5 minutes)….

Labs







Na,K, Ca, Mg, PO4 , BUN, Cret, glucose
CBC
Liver function tests, ammonia
Anticonvulsant level
Toxicology
Blood C/S
Initial screening history and Physical examination

31. Work-Up (when stable)

Lumbar puncture


CT scan/MRI scan


Always defer LP in unstable patient, but never delay
antibiotic/antiviral rx if indicated
Indicated for focal seizures or deficit, history of trauma or
bleeding d/o
EEG

32. Treatment (Pharmacotheraqpy)
5-15 minutes..
 The longer
we wait with anticonvulsant, the
more anticonvulsant we will need to stop SE
 Most common
mistake is ineffective dose

33. Anticonvulsants

Rapid acting
plus

Long acting

34. Anticonvulsants - Rapid acting

Benzodiazepines





Lorazepam 0.05- 0.1 mg/kg i.v.(rectal dose same) upto 4-6
mg over 1-2 minutes
or
Diazepam 0.2- 0.5 mg/kg i.v. upto 6-10mg over 1-2 minutes
Diazepam 0.5 mg/kg rectally
Midazolam 0.15-0.3 mg/kg IV ; nasal or Buccal (0.5 mg/kg)
is used if no IV line
If SE persists, repeat every 5-10 minutes

35. Benzodiazepines

Lorazepam




Low lipid solubility
Action delayed 2 minutes
Anticonvulsant effect 6-12 hrs
Less respiratory depression than
diazepam
Midazolam
for brief seizures
May be given i.m.
 to treat refractory SE

Diazepam





High lipid solubility
Thus very rapid onset
Redistributes rapidly
Thus rapid loss of
anticonvulsant effect
Adverse effects are
persistent:


Hypotension
Resp. depression

36. Anticonvulsants :15-35 minutes
(If seizures persists)

Phenytoin





15-20 mg/kg i.v. over 15-20
min
pH 12
Extravasation causes severe
tissue injury
Onset 10-30 min
May cause
hypotension, dysrhythmia
Cheap

Fosphenytoin

15-20 mg PE/kg i.v./i.m. over 57 min PE = phenytoin equivalent

Fosphenytoin 150 mg is equal to 100
mg phenytoin

pH 8.6
Extravasation well tolerated
Onset 5-10 min
May cause hypotension
Expensive




37. Anticonvulsants :(15-35 minutes)
 Phenobarbital
 15-20
mg/kg (neonate 20-30 mg/kg)i.v.
over 15-20 min
 Onset 15-30 min
 May cause hypotension, respiratory
depression

38. Initial choice of long acting
anticonvulsants in SE
Is patient an infant?
Is patient already receiving phenytoin?
No
At high risk for extravasation ?
(small vein, difficult access etc.)?
No
Phenytoin
Yes
Fosphenytoin
Yes
Phenobarbital

39. If SE persists (45 minutes)





Phenobarbital if Phenytoin used
Additional phenytoin or FP 5 mg/kg (Nelson 10 mg/kg
increment) max upto 30 mg ,
Additional phenobarbital 5 mg/kg/dose every 15–30
min (max total dose of 30 mg/kg)
be prepared to support respirations
Consider IV valproate, especially for partial status
epilepticus

40. Seizures Persists (60 minutes)
 Consider
Diazepam infusion, pentobarbital
(Barbiturate coma), midazolam, paraldehyde
or general anesthesia infusion in PICU
 Midazolam 0.2 mg/kg bolus & 20-400
mcg/kg/hr infusion
 Propofol 1-2 mg/kg then 2-10 mg/kg/hr
infusion
 Avoid paralytics

41. Still Seizures Persists….




Induction of Barbiturate coma for 48 hrs
IV loading thiopental 2–4 mg/kg till a burst
suppression EEG pattern till 48 hrs
check phenobarbital level to be normal.
Paraldehyde :loading 150–200 mg/kg IV for 15–20
min, then 20 mg/kg/hr in a 5% concentration in a
glass bottle freshly prepared

42. Still Seizures Persists….

General anesthesia: if barbiturate coma is not
option.
 halothane and Isoflurane.
 Acts by reversing cerebral anoxia and metabolic
abnormalities, allowing the previously
administered anticonvulsants to exert their
effect.

43. Possible new drugs for Status





Lidocaine - some positive trials
Valproate - IV form available
 10-15 mg/kg IV.
Gabapentin / Vigabatrin / Lamotrigine
Felbamate - blocks NMDA receptors
Ketamine - blocks NMDA receptors
Use of AED after status episode is controversial especially
idiopathic or febrile seizure.

44. Non - convulsive status epilepticus?
 NCSE
is a term used to denote a range
of conditions in which electrographic
seizure activity is prolonged and results
in non convulsive clinical symptoms.

45. Non - convulsive SE ?

Up to 20 % of children with SE have non convulsive SE after tonic - clonic SE

46. Non - convulsive SE ?
 If child does
not begin to respond to painful
stimuli within 20 - 30 minutes after tonic clonic SE, suspect non - convulsive SE
 Urgent EEG

47. Summary
Status Epilepticus is >5 min of seizures or two seizures
without return to consciousness
 Status Epilepticus is common
 Delay in therapy makes SE harder to rest
 Mortality and morbidity is increased in prolonged SE
 BZD, Pheny/Pheno, Call for PICU
 Status Epilepticus needs a DIAGNOSIS


48. Take-Home points 




Better outcome if seizure stopped earlier, so no need to
wait
Always ABC D FIRST
Lorazepam - best 1st line Rx
Fosphenytoin - surpasses Phenytoin for SE, and can be
given IM in difficult situation
Propofol - advantages over barbiturates for resistant SE,
low toxicity , quick action, and fast recovery upon
discontinuation