1. Status epilepticus
By
NANCY MOHAMMED ALAA
Assistant lecturer of pediatrics
Assiut university

2. 1-definition
2-epidemiology
3-classification
4-pathophysiology
5-consequences
6-differential diagnosis
5-management
A-prehospital
B-at hospital

3. status epileptics is
defined as more than 30 minutes of either
1) continuous seizure activity clinically or
subclinical (EEG)
Or
2) two or more sequential seizures without full
recovery of consciousness inbetween.

4. EPIDEMIOLOGY
1-the annual incidence of SE in pediatrics is
10-73 episode/100,000 children and is highest in
children < 2 years old
2-the higher incidence in vulenrable populations
with acute or chronic neurological conditions
3 -75% of cases of SE may be the first seizure of
life, and they will have 30% risk of later diagnosis of
epilepsy

5. 4-The overall mortality of children is less than in
adult, it has been reported to be 2-8% .
10-20%The morbidity is estimated to be

6. Classification
According to
A-TIME
B-SEIZURE TYPE
C-ETIOLOGY

7. A-TIME
1-The first five minutes of a seizure have been
termed “prodromal” or “incipient status
epilepticus” .
2-Continued seizure activity can be further
subdivided into early status epilepticus (5–30
min),
3-established status epilepticus (>30 min),
4-refractory status epilepticus (ongoing status
epilepticus clinical or electrographic) despite
administration of 2–3 appropriately dosed anti-
seizure medications).

8. 5-super-refractory status epilepticus is defined as
recurrent seizures in spite of anticonvulsants
and anaesthetic therapy beyond the 24-hour.

9. B-SEIZURE TYPE
1) convulsive status epileptics consisting of repeated
A-generalized tonic–clonic (GTC) seizures
B-myoclonus,tonic,clonic,atonic
2) Non convulsive :impairment of conscious level
withoutconvulsive movement but with EEG finding
3) repeated partial seizures partial seizures without
impairment of consciousness or secondary
generalisation, manifested as focal motor signs
(epilapsia partia;is continua ), focal sensory
symptoms, or focal impairment of speech (aphasia)

10. C-ETIOLOGY

11. Pathophysiology
1-decrease inhibitory neurotransmitter
At the transition from single seizures to status, GABA
receptors move from the synaptic membrane to the
cytoplasm, where they are functionally inactive.
This reduces the number of GABA receptors available
for binding GABA or GABAergic drugs,
This explain the development of time-dependent
pharmacoresistance to benzodiazepines

12. 2-increase excitatory neurotransmitter
.
At the same time, 'spare' subunits of AMPA (alpha-
amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) and
NMDA (N-methyl-D-aspartic acid) receptors move from
subsynaptic sites to the synaptic membrane,
causing further hyperexcitability and possibly
explaining the preserved sensitivity to NMDA
blockers(ketamine) late in the course of SE.

13. Consequences

15. •DIFFERENTIAL DIAGNOSIS

16. A-seizure and pseudoseizure
.
2-pseudoseizure1-seizure
Often closed or flutteringUsually open, or with clonic
blinking or nystagmus
Eye
noyesRhythmic
movement
yesnoPelvic thrust
nondilatedPupil
Increase movementnonrestrain
Decrease movementnonreassurance
noconfusedDirect after attack
Crying/screaming occasionaGrunt with generalized
convulsions;
VOCALIZATIONS
absentpresentcyanosis
Waxes and wanes, some
memory for event
Lost suddenly, regained
gradually; no memory
RESPONSIVENESS
Gradual, from waking or
“pseudosleep,
Abrupt, from waking or
sleep,
ONSET

17. B-Generalized Convulsive Status Epileptics
CHARACTERESTIC FEATURES
NORMAL CONSCIOUS LEVEL
rhythmic oscillation (back and forth movement) about a
central point.
INCREASE WITH STRESS DECREASE WITH SLEEP
Tremor
FIXED ABNORMAL POSITION
Increase with voluntary action ,stress
decrease at rest ,sleep
BUT NORMAL CONSCIOUS LEVEL
Dystonia
FACIAL MUSCLE LOCK WITH OPISTHOTONUS POSITIONTetanus
THE MOVEMENT IS EASILY ELICITED AND STOPPED WITH
RAPID LIMB MOVEMENT
Clonus

18. (C-non convulsive status epileptics (NCSE
Hallucinations
Hypoglycemia
Drug effects
Psychosis
POST ICTAL

19. EEG OF NCSE

20. D-Partial Convulsive (MOTOR)
CHARACTERESTIC FEATURES
Usually at onset of sleep ,involve legs ,rarely repeat over long
periods
Hypnic Myoclonic
jerks
Rapid ,stereotyped involuntary movement usually involve face
and neck. They disappear in sleep ,increase with stress
Tic disorder
Focal dystonia
Focal dystonia involve eyes that increase with bright light and
activity
Blepharospasm

21. •E-PARTIAL SENSORY
1-Ocular disorders
2-Hearing disorders
3-Migraine and its attendant neurologic phenomena
(eg, sensory, visual)

22. Management
A-pre hospital
B-At hospital

23. A-prehospital

25. B-At hospital

27. •2-at hospital

29. 2-termination of seizures and prevention of
recurrence
disadvantageadvantageDose ,routeDrugs
hypotension,
respiratory depression
-If used within the
first 20 min of seizure
onset, termination
rates of seizures can
be as high as 70-85%
.
1-LONGER
DURATION
0.1mg/kg/IV UP TO
4 mg/dose repeat in 5
Min
0.15-0.2mg/kg IV up to
10mg/DOSE repeat in 5
min
0.2-0.5mg/kg PR up to
20mg/dose
1-benzodiazepine
A-lorazepam
B-diazepam

30. •-
disadvantageadvantageDose,routedrug
IM 5mg(13-40kg)
10mg( >40kg)
IV 0.3mg/kg
Buccal 0.5mg/kg
Nasal 0.2mg/kg
C-midazolam

31. 3-diagnosis and treatment of the life threatening
causes of SE
A- HISTORY
Has the child ever had a seizure before?
History of trauma? Fever? Ingestion?
What medications (including nonprescription) does the
child take?
Any medical problems?
Any neurologic/developmental problems?
If child has known epilepsy
–Name and dosage of medications
–Has the child missed dosage of medication
–Be aware of paradoxical side effects of AEDs
•Phenytoin and carbamazepine toxicity may precipitate SE

32. B-EXAMINATION
Head to toe examination aiming to determine
underlying etiology
General examination
:
vital signs: pulse, BP, RR,Temperature
Anthropometric measures: HC(canavan)
•Examination of the head: ant. fontanel ,skull shape and eyes
(including fundus examination)
•Abnormal facies(metabolic disorders)
•Skin abnormality(neurocutaneous diseases)
•Search for evidence of trauma.
•Evidence of failure to thrive, particular body odour or hair
pigmentation (in born error of metabolism)
•Cardiac examination: Congenital heart diseas

33. Chest examination: specially for accumulated
secretions
Abdominal examination:
Hepatosplenomegaly
Examination of the back
Neurological examination:
1-Conscious level: AVPU system
2-Motor system.
3-Sensory system
4- tests of coordination
5- cranial nerves
6- Superficial reflexes
7- Gait
8- Meningeal signs

34. C-INVESTIGATIONS
A- Lab investigations:
1.CBC: in patients who looks like ill, suspect sepsis
2.Serum electrolytes (Na, Ca ,Mg): Because 6% of pts
with convulsions showing electrolyte and blood
glucose disturbance
3.Serum level of anti epileptic drugs (AEDs): to detect
compliance or toxcicity
4. Toxicology screen: if clinically suspected
5. Metabolic screen: depends upon history and
examination
6-liver function test

35. B.lumbar puncture:
•it is indicated in:
a-Any convulsions with fever below age of one year
b-Convulsions with fever+ manifestations of CNS
affection
c-Atypical febrile convulsions after age of one year
d-diagnosis of demyelinating disease or inflammatory (MS,
GBS)

36. CONTRAINDICATIONS
A-ABSOLUTE
1-signs of ICP (papilledema,
2-local skin infections
3-Imaging show (midline shift, posterior fossa mass,
4-clinically unstable
B-RELATIVE
1-bleeding tendency (DIC,PLT < 50,000)

37. •C-indication for CT:
1-Any convulsions below age of one year except
febrile convulsions
2-Focal convulsions except simple focal convulsions
3-Covulsions with focal neurological deficit,
4- disturbed conscious level or increased intracranial
pressure"
5-Intractable convulsions
6-Status epileptics with unknown cause.
7-Abnormal fundus examination
8-History of trauma
9-EEG with focal source

38. D-MRI
It is indicated if:
-Auspect neurodegenrative disease
- Areas not well visualized by CT
-Uncertain lesion in CT

39. •E - EEG
1-continuous EEG monitoring if the patient is not waking up
after clinical seizures cease((15–60minutes
2-critically ill encephalopathic child
3-Patients who ultimately require continuous infusion
with a barbiturate or benzodiazepine should undergo EEG
monitoring
It is helpful in defining the limits of therapy by the
occurrence of burst suppression.
.

40. 4-MANAGEMENT OF REFRACTORY STATUS EPILPTICS
If the convulsive activity does not stop:
1.Fosphenytoin and phenytoin:the2nd line medication:
*Fosphenytoin is a prodrug of phenytoin has advantages of being water soluble, less
irritating after IV injection and well absorbed after IM injection.
*The loading dose :15 -20mg/kg IV at the rate of 1 mg/kg/min added to normal saline
given up to three loading doses.
*The maintenance dose of 3-6 mg/kg divided into two equal doses daily is begun 12-
24 hr later
*Side effects:
1-the undiluted drug can cause pain,
irritation, and phlebitis of the vein
2- Arrhythmias and bradycardia
3- Systemic hypotension

41. 2.Phenobarbital is the 3rd line medication:
is initiated before phenytoin in some centers and in neonates.
Loading dose :
20 mg/kg in neonates IV during 10-30 min.
::5-10mg/kg Infant and children
Side effects:
Respiratory depression
It is given up to three doses
,
the maintenance dose is 3-5 mg/kg/24 hr divided into two equal doses

42. 4-valproic acid
Dose: 20-40 mg/kg/IV May give additional 20 mg/kg
Side effects:
1-hyperammonemia
2-thrombocytopenia
3-hepatotoxicity
3-levitracetam
Dose :20-60 mg/kg/IV
Precaution
1-dose adjustment in renal failure

43. 5. Induction of pharmacological coma:

44. 1-monitoring
A-mechanical ventilation for airway protection
ventilation
B-central line (control BP, frequent sampling)
C-EEG monitor
D-temperature management
2-goal
A-termination of seizure
B-EEG; burst suppression
3-time of withdrawal :
24-48 hrs of seizure, EEG control