Status epilepticus is a medical emergency that requires prompt treatment to prevent neurological damage or death. It is defined as continuous seizure activity lasting more than five minutes or two or more discrete seizures between which there is incomplete recovery of consciousness. The document discusses the definition, causes, pathophysiology, treatment approach, and medications used to treat status epilepticus in children. Treatment involves stabilizing the patient, administering rapid-acting anticonvulsants like lorazepam followed by long-acting medications like fosphenytoin if seizures persist, with progression to anesthetic treatments in refractory cases to stop seizures.

1. Status Epilepticus
Dr. Ravindra K. Sharma
Pediatric Specialist
Fujairah Hospital,UAE

2. TAJ MAHAL, AGRA, INDIA
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
0 min High CVP


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

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
Dilute with Dext. free solution
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 ?
Yes
Phenobarbital
(small vein, difficult access etc.)?
No
Phenytoin
Preffered in Cardiac patient,
Head trauma,
Yes
Fosphenytoin

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