new up date in Management of status epilepticus in children 2017

2. • Definition
• EPIDEMIOLOGY
• Pathology
• Classification
• Risk factors
• Immediate assessment
• Immediate Treatment
• Laboratory studies
• Stabilization
• Monitoring
• PHARMACOLOGIC
AGENTS
• Prognosis

3. Definition
Status Epilepticus:
 The International League Against Epilepsy (ILAE) and the World
Health Organization currently define SE as a
“condition characterized by an epileptic seizure that is
so frequently repeated or so prolonged as to create a
fixed and lasting condition”

4. Definition
practical definition of SE
has emerged as any seizure that lasts
more than 5 minutes
 continuous seizure activity or recurrent seizure activity
without regaining of consciousness lasting for more than
5 min

5. Definition
practical definition of SE
has emerged as any seizure that lasts
more than 5 minutes
Nonconvulsive SE (NCSE) refers to
 ongoing EEG seizure activity without associated clinical
signs.

6. Definition
Refractory Status Epilepticus :
failed to respond to therapy, usually with at least 2 (such as a
benzodiazepine and another medication) medications.
New-onset refractory status
epilepticus (NORSE):
refractory status epilepticus in a patient without prior epilepsy

7. ILAE Definitions of Status Epilepticus
Time after which if seizures do not
terminate patient is considered in
status epilepticus (t1)
Time after which ongoing
seizures have long term
consequences (t2)
Convulsive status epilepticus 5 min 30 min
Focal status epilepticus with
impaired consciousness
10 min 60 min
Absence status epilepticus 10–15 min unknown
Other Definitions of Status Epilepticus
Established statusepilepticus
Status epilepticus that persists after treatment with a benzodiazepine
(1st line treatment)
Refractory status epilepticus
Status epilepticus that persists after a 1st line agent (benzodiazepine)
and 2nd lines
agent (additional agent such as levetiracetam, phenytoin, valproic
acid) have failed

8. Definition
 New-onset refractory status epilepticus (NORSE):
 refractory status epilepticus in a patient without prior epilepsy
 fever-induced refractory epileptic encephalopathy in school age children
(FIRES)
is a syndrome of refractory status epilepticus that is associated with
acute febrile infections, appears to be parainfectious in nature, and to
be highly drug resistant but responsive to the ketogenic diet.

10. Definition*
several clinical studies have been published
using durations of 5 minutes
More information is needed to clarify and
allow acceptance of a standard operational
definition for SE.

11. • incidence of status epilepticus ranges between 10
and 60 per 100,000 population
• Status epilepticus is most common in children
younger than 5 yr of age, with an incidence in
this age group of >100 per 100,000 children.
EPIDEMIOLOGY

12. • Approximately 30% of patients presenting with
status epilepticus are having their first seizure,
and approximately 40% of these later develop
epilepsy
EPIDEMIOLOGY

13. • Febrile status epilepticus is the most common type of
status epilepticus in children.
• In the 1950s and 1960s, mortality rates of 6-18% were
reported after status epilepticus; currently, with the
recognition of status epilepticus as a medical emergency, a
lower mortality rate of 4-5% is observed, most of it
secondary to the underlying etiology rather than to the
seizures.
• Status epilepticus carries an approximately 14% risk of
new neurologic deficits, most of this (12.5%) secondary to
the underlying pathology.
EPIDEMIOLOGY

14. 1. convulsive SE (CSE)
2. nonconvulsive SE (NCSE) : There are
10-20%

15. 1. Neuronal (Cerebral)
2. Systemic Effects.

16. Cerebral Injury
DISTURBANCE EQUALIBRIM
Excitation >inhibitory mechanisms
PROLONGED : SE
Systemic
Complications.
+vE
Precipitating factors
+vE

17. 1. Downregulation Of GABAA Receptors May Reduce
The Efficacy Of Benzodiazepines In RSE
2. Extrusion Of Anticonvulsants Across The Blood-brain
Barrier (BBB) May Limit Anticonvulsant Activity.
3. Over Expression Of The Transporter's Multidrug
Resistance Gene

19. 1. Ensure adequate brain oxygenation , cardiorespiratory function
2. Terminate clinical , electrical seizure activity as rapidly as possible
3. Prevent seizure recurrence
4. Identify precipitating factors such as hypoglycemia, electrolyte
imbalance, lowered drug levels, infection, and fever
5. Correct metabolic imbalance
6. Prevent systemic complications
7. Further evaluate and treat the etiology of SE

20.  Out of hospital management
– Community education
– Patients must be brought to the hospital at the earliest
 Hospital emergency management
 PICU management
– It is helpful to have a protocol in every hospital.

22. 1. Look for medical identification.
2. Protect the person from nearby hazards.
3. Loosen ties or shirt collars.
4. Protect the head from injury.
5. Turn the person on his side to keep the airway clear.
6. Time record
7. Reassure when consciousness returns.
8. Ask whether hospital evaluation is wanted, call an ambulance

23. 1. Do not put any hard implement in the mouth.
2. Do not try to hold the tongue. It cannot be swallowed.
3. Do not try to give liquids during or just after the seizure.
4. Do not use artificial respiration unless breathing is absent after muscle
jerks subside, or unless water has been inhaled.
5. Do not restrain the person.
6. The person should be transferred to a medical center as soon as
possible if their
– seizure continues beyond 5 minutes
– if after ceasing, it begins again

24. • The therapeutic window
– for most effective treatment with benzodiazepines may have already passed
by the time that hospital treatment starts, which is usually more than 20
min after the onset of GTC-SE.
• administer drugs by
1. Buccal
2. Rectal
3. Nasal
4. other non-invasive routes
• if appropriately instructed and if proper “rescue medications” are
available for emergency use

25. 1. Rectal diazepam (0.5 mg/ kg for children )
2. Buccal midazolam (0.4–0.5 mg/kg in children )
3. Intranasal midazolam (0.2 mg/Kg in children )
 For any of these medications a repeat dose can be
given at least 10 min after the first dose.

26. 1. the seizure has happened in water.
2. there's no medical I.D., and no way of knowing whether the seizure is caused
by epilepsy.
3. the person is
1. Pregnant
2. Injured
3. diabetic.
4. the seizure continues for more than five minutes.
5. a second seizure starts shortly after the first has ended.
6. consciousness does not start to return after the shaking has stopped.

27. DEFINITION
Continuous tonic-clonk seizure activity lasting more than 5 minutes or
Two or more seizures without regaining consciousness in between seizures
This gaud line in india
AT CLINIC OR OUTSIDE HOSPHAL
Maintain airways and assess cardio-respiratory function
Brief history and examination
Inject rectal diazepam -0.5 mg/kg (children) or
Give buccal midazolam - 0.2 mg/kg (children)
If seizures persist, shift the patient to the nearest hospital
IN HOSPITAL SETTING
•A.B.C and assess cardio-respiratory function , take history , physical exam
•Take blood samples for glucose, urea, AED levels and others as appropriate
•Inject PHT: 15 - 20 mg/kg IV at maximum rate of 50 mg/min
•CT scan,lumbar puncture if indicated ,Consult neurologist if seizures persist

32. OVERVIEW OF ASSESSMENT
 The evaluation includes:
1. General assessment(ABC);
the pediatric assessment triangle
 appearance
 work of breathing
 circulation
2. Primary assessment:
 rapid evaluation of
1. Cardiopulmonary
2. Neurologic function
2. Secondary assessment :
 focused medical history and thorough head to toe physical exam
2. Tertiary assessment :
1. Laboratory
2. Radiographic
3. other ancillary studies 32
Appearance (TICLS)
1. Tone : abnormal tone
2. Interactiveness : decreased
interactiveness
3. Look/gaze : poor color
4. Consolability : abnormal stare
Consolability
5. Speech/cry : weak cry.
Breathing:
1. Abnormal airway sounds
2. position of comfort that
maximizes airway opening
3. use of accessory muscles
Circulation Assessment
1.Heart rate
2.Pulse
3.capillary refill
4.Blood pressure
5.End organ profusion
•Urine output
•Level of consciousness
•Muscle tone
Primary assessment
rapid sequence assess (ABCDE):
1.Airway:
 Patent
 patent with maneuvers/adjuncts
 partially or completely obstructed
2.Breathing:
 respiratory rate
 Effort
 tidal volume
 lung sounds
 pulse oximetry
3.Circulation:
4)Disability
 CNS function Level of conscious ;
 AVPU pediatric response scale:
 Dextrose hypoglycemia :
rapid bedside glucose or response to empiric
administration of dextrose
6.Exposure :
fever or hypothermia, skin findings, trauma

36.  Has the child ever had a seizure before?
 History of :
 Trauma?
 Fever?
 Ingestion?

37.  Was the child his usual self prior to this event?
 What medications child take?
 Past- History:
 Any medical problems?
 Any neurologic ?
 developmental problems?

38.  If child has known epilepsy
 Name and dosage of medications!!! Calculate if this is appropriate dosage.
 Has the child missed dosage of medication
 If so, consider loading with that medication
 Be aware of paradoxical side effects of ACDS
• Phenytoin and carbamazepine toxicity may precipitate SE

39. 1. Serum glucose and a rapid "finger-stick" glucose
2. Serum electrolytes, calcium, and magnesium levels
3. Arterial blood gases and pH , RFT , LFT
4. A complete blood count and general chemical screen
5. Urine and blood toxicology
6. Serum antiepileptic drug (AED) levels
7. Other testing in specific clinical
circumstances may include
1. Blood cultures and lumbar puncture (LP)
2. Metabolic studies for inborn errors of
metabolism
3. Neuroimaging is generally deferred until the
patient is stabilized.

40. Ancillary studies in children with status epilepticus
Patient
population Studies
All patients
Serum electrolytes
Serum calcium, phosphate, and
magnesium
Brain imaging (CT or MRI)
EEG
Patient
population Studies
Epilepsy pts on
anticonvulsants
Anticonvulsant level
Patient
population Studies
Febrile
patients
CBC with differential , Blood culture
Urinalysis, urine culture
CSF culture (once seizures stopped and
if brain imaging excludes increased
intracranial pressure)
Patient population Studies
Poisoned patient Urine screen for cocaine, amphetamines,
and PCP
Aspirin level
Venous or arterial pH and pCO2
ECG once seizures stop
Patient Studies
Infants <6
months of
age*
Blood gas , Plasma ammonia , Plasma amino acids
PT, PTT
Serum AST, ALT, LDH, Alkaline phosphatase
Blood lactate and pyruvate
Urinalysis ,Urine for reducing substances
Urine organic acids ,Urine amino acids
Check newborn urine screening results if infant from
country where instituted

41. C. Electrocardiographic (ECG)
D. EEG monitoring

42. At 0 min
On presentation to hospital, initiate ABCs:
A – support airway
B – 100% oxygen, assess ventilation, SpO2 monitor
C – cardiorespiratory monitor, check pulses, do IV access
• History (SAMPLE) , Examination
• Investigations
• Suspect and treat raised ICP as needed, CT scan when warranted
• Keep normothermic, acetaminophen/ibuprofen as appropriate
At 5 min IV access?

43. Mistake Made In The Treatment Of SE
inadequate doses of drugs are given
initially
physicians wait for more seizures to
occur before administering the necessary
total dose

44. 1. Previous response
2. Missed medication
3. Paradoxical effects
4. Nonprescription medications
5. Alternative routes of administration
6. Nonepileptic seizures

45. 1. Rapid Onset Of Action
2. Broad Spectrum Of Activity
3. Ease Of Administration Including Intravenous (IV) And
Intramuscular (IM) Preparations
4. Minimal Redistribution From The CNS
5. Wide Therapeutic Safety Margin

46. Lorazepam vs. Diazepam ,Midazolam
Lorazepam Diazepam Midazolam
Duration of
action
6-8 hours 20-30 minutes Mean: 2 hours
Onset of action 5 minutes 1-3 min 3-5 minutes
Sedation + ++ +++

47. • Mechanism of Action
– Depresses all levels of the CNS, including the
limbic and reticular formation, by binding to the
benzodiazepine site on the gamma-aminobutyric
acid (GABA) receptor complex and modulating
GABA, which is a major inhibitory
neurotransmitter in the brain

48. • Dose :
– 0.05-0.1 mg/kg
– (maximum: 4 mg/dose)
• Rate :
– slow I.V. over 2-5 minutes
– (maximum rate: 2 mg/minute)
• Frequency :
– may repeat every 10-15 minutes if needed
• Onset of action:
– Oral: Within 60 minutes
– I.M.: 30-60 minutes
– I.V.: 15-30 minutes
• Duration:
– 8-12 hours
• more effective than diazepam
• Longer duration of action (6-12 hours vs. <1 hour)
• Less respiratory depression than diazepam
• Not available rectally

49. • dose:
• Loading dose: 0.15-0.2 mg/kg
• Continuous I.V. infusion:
• Initial rate: 0.06-0.12 mg/kg/hour (1-2 mcg/kg/minute);
• increase rate every 5-15 minutes in increments of 0.06-0.24
mg/kg/hour (1-4 mcg/kg/minute) until seizure activity ceases
• maximum dose: 3 mg/kg/hour (50 mcg/kg/minute)
• Onset of action:
– Oral: Children: Within 10-20 minutes
– I.M.:
• Children: Within 5 minutes
• Adults: Within 15 minutes
– I.V.: Within 1-5 minutes
– Intranasal: Within 5 minutes
Maximum effect:
–I.M.:
• Children: 15-30 minutes
• Adults: 30-60 minutes
–I.V.: 5-7 minutes
–Intranasal: 10 minutes
• Duration:
– I.M.: Mean: 2 hours, up to 6 hours
– I.V.: 20-30 minutes
– Intranasal: 30-60 minutes
– Note: Full recovery may take more than 24
hours

50. – Dose
– Children 2-5 years: 0.5 mg/kg
– Children 6-11 years: 0.3 mg/kg
– Children ≥12 years and Adults: 0.2 mg/kg
– Infants >30 days and Children: I.V: 0.1-0.3
mg/kg/dose given over 3-5 minutes, every 5–10
minutes
– (maximum: 10 mg/dose)
–Onset of action:
–I.V.: 1-3 minutes
–Rectal: 2-10 minutes
–Duration:
–15-30 minutes
– Highly effective in rapidly terminating seizures
– However, redistribution into adipose tissue limits
anticonvulsant effect to less than 20 minutes
– Available in rectal gel, which can be given outside
the ED

52. At 0 min
On presentation to hospital, initiate ABCs:
A – support airway
B – 100% oxygen, assess ventilation, SpO2 monitor
C – cardiorespiratory monitor, check pulses, do IV access
• History (SAMPLE) , Examination
• Investigations
• Suspect and treat raised ICP as needed, CT scan when warranted
• Keep normothermic, acetaminophen/ibuprofen as appropriate
At 5 min IV access?

53. At 10 min
At 15 min Phenytoin 20 mg/kg IV/IO,
max 1 g, over 20 minutes, in
0.9% NaCl (NS)
Phenobarbital 20 mg/kg
IV/IO, max 1 g, over 5-10mins
At 25 min
• The order of Phenytoin and Phenobarbital
may be interchanged
• Phenytoin should be used in head trauma
• Phenobarbital should be used 1st if patient
already on phenytoin maintenance
• Rapid Sequence Intubation if compromised
airway at any point
• Ventilate to normal parameters
• Sedation and muscle relaxants only if
necessary to ventilate or protect airway
At 35 min
Early referral to PICU if any of following:
• airway/ventilation/cardiovascular
compromise
• seizure refractory to 2nd line
medications
• seizure >30 minutes
• initiating Midazolam or Thiopental infu
Midazolam 0.15 m g/k g IV
bolus, then 2 mcg/kg/min
by IV infusion

54. o seizure refractory
o prevent recurrance
If seizures continue for 10 minutes after at least two injections
of lorazepam, begin treatment with fosphenytoin
 dose of 20 mg phenytoin equivalents (PE)/kg IV
 at a rate of 3 mg/kg per minute (maximum rate 150 mg/min).
 The maximum dose in 24 hours is 1500 mg PE
 General rule of thumb: for each 1 mg/kg phenytoin (or 1PE/kg
fosphenytoin) expect level to rise by 1)
Alternative to second Line drugs
Phenobarbital
phenytoin
Third Line medication
1. Valproic acid
2. Levetiracetam

55.  Alternative to second Line drugs
1. phenytoin (If fosphenytoin is unavailable)
 dose :18 to 20 mg/kg IV , give in large vein, dilute with N/S
 rate of 1 mg/kg per minute
 maximum rate 50 mg/min.
 Maximum dose 1500mg/day
 onset of action: 10 - 30 min
 duration of action: 12 - 24 hr
2. Phenobarbital
 dose : 20 mg/kg
 rate 2 mg/kg per minute or 50 mg/min
 followed by repeated increments of approximately 8 to 10 mg/kg
every 30 minutes
 Maximum dose 1500mg/d

57. • Loading dose:
– 15-18 mg/kg in a single or divided doses
• Maintenance dose :
– usually starts 12 hours after the loading dose:
– Infants and Children: Initial: 5-10 mg/kg/day in 2-3 divided
doses
• onset of action may be delayed for 10 to 30 minutes
• Mechanism of Action
• Stabilizes neuronal membranes and decreases seizure
activity by increasing efflux or decreasing influx of
sodium ions across cell membranes in the motor cortex
during generation of nerve impulses; prolongs effective
refractory period and suppresses ventricular pacemaker
automaticity, shortens action potential in the heart
• S/E - (most avoided if slower administration)
1. hypotension
2. arrhythmias - (must monitor)
3. respiratory depression
4. venous irritation
5. extravasation -->tissue injury / necrosis
6. “purple glove syndrome”: progressive limb edema,
discoloration and pain 2-12 hr post IV admin

58. • a prodrug of Phenytoin
– it has no anticonvulsant action itself, but is
rapidly converted to Phenytoin
– Dosage: in “Phenytoin Equivalents” to
attempt to avoid confusion
– can safely give at 3x rate of Phenytoin,
resulting in 2x amount of Phenytoin
delivered

59. • Advantages over Phenytoin:
– does not require solvent (Phenytoin is dissolved in
propylene glycol)
• can give IM when no IV access
• IV: - less potential for irritation - can give faster
- no risk of tissue necrosis if goes
interstitial - does not precipitate in IV
solutions
– lower risk of hypotension and dysrhythmias

60. • Negative considerations:
– COST Approx 20x that of Phenytoin

61. Third Line Medication :if necessary
1. Valproic acid
2. Levetiracetam

62. Valproic acid
third-line treatment.
loading dose of 20 to 40 mg/kg IV (diluted 1:1 with normal
saline or 5 percent dextrose in water) over 5 to 10 minutes
may be repeated after 10 to 15 minutes
This is followed by an IV infusion of 5 mg/kg per hour

63.  continued seizures after 2 or 3 line antiepileptic drugs have failed
 Will usually need EEG monitoring at this point
 The goal is to stop electrographic seizure activity before reducing
the therapy
Usually this implies achievement of complete flattening of the
EEG.
a burst suppression pattern may be enough, and the periods of
flattening in such a case need to be >8-20 sec

64.  hemodynamically stable
1. pentobarbital : Short acting barbiturate with a rapid onset of action
oRequires
1. intubation
2. mechanical ventilation
3. vasopressor agents.
oDose
 initial bolus infusion of 5 to 15 mg/kg IV
 followed by a continuous infusion of 0.5 to 5.0 mg/kg per hour .
• Maintenance of pentobarbital anesthesia is continued for
approximately 4 h by an infusion of 1–3 mg/kg/hr.
• The patient is then checked for the seizure activity
– If clinical seizures and/or generalized discharges persist on EEG, the
procedure is repeated;
– if not, the pentobarbital is tapered over 12–24 hours.
 Significant side effects:
1. respiratory depression
2. Hypotension
3. myocardial depression
4. reduced cardiac output
5. pulmonary edema
6. ileus
2. Midazolam

65. • Dose: 2-5 mg/kg IV
• rapid onset: 30 - 60 sec
• short duration: 20 - 30 min
• S/E:
– CV depression, hypotension, arrhythmias
– resp depression, apnea
• Thiopental - negative aspects:
– accumulates in fatty tissues
– an active metabolite - Pentobarbital
– long recovery time after infusion
– hemodynamic instability

66.  hemodynamically unstable
Midazolam may be better tolerated
 Dose
 initial bolus infusion of 0.15 to 0.2 mg/kg IV
 followed by continuous infusion of 1 mcg/kg per min
 the infusion is increased by 1 mcg/kg per min every 15 minutes until
seizures are controlled or max dose
(50 mcg/kg/minute)
 3 mg × body wt (in kg), added to diluent to make 50 mL→ 1 mL/h
delivers 1 μg/kg/min

67.  hemodynamically unstable
Propofol :Intravenous anesthetic
• Dose: 1-2 (3-5) mg/kg
• Rate: 5-10 mg/min (1-15 mg/kg/hr)
• Onset: 2-4 min
• Half-life: 30-60 min
• does not accumulate --> rapid recovery
• Mechanism:
– stimulates GABA receptors
– suppresses CNS metabolism
Risk of
1. Hypotension
2. Apnea
3. Bradycardia
4. Fatal Acidosis
5. Rhabdomyolysis of the skeletal and cardiac muscles
6. Contraindicated in child on ketogenic diet
 Advantages over Barbiturates
– less hypotension
– more rapid onset of action
– rapid elimination
• “Pro-convulsant effect” - is now thought to be
myoclonus, unlikely a significant problem

68.  Inhalational anesthesia :-
isoflorane is preferable because
 halothane can increase intracranial pressure
 enflurane can induce seizures

69.  Valproic acid
 Levetiracetam Keppra
 Consider IV pyridoxine if age <18 month

70. nelson2016
• After the emergent therapy usually with a benzodiazepine,
the subsequent urgent therapy medication is usually
fosphenytoin,
• The subsequent medication is ofen phenobarbital.
• Ideally, emergent and urgent therapies should have been
received within less than 30 min so as to initiate the
subsequent therapy soon,

71. nelson2016
• Currently, the level of the evidence for refractory treatment
is strongest for midazolam and valproate, followed by
propofol and pentobarbital/thiopental, followed by
levetiracetam, phenytoin/fosphenytoin, lacosamide,
topiramate, and phenobarbital.

72. nelson2016
• Current evidence for the urgent therapy is strongest for
valproate, followed by phenytoin/fosphenytoin and
midazolam continuous infusion, followed by phenobarbital
and levetiracetam, the last of which are currently being
increasingly used

73. Tim Assessment Supportive care Seizure treet
0 to 5
minutes
prehospi
tal
Obtain initial vital signs,
including temperature
Lateral position, Open airway
Suction secretions
Administer 100 percent O2
Benzodiazepine (first
line):Lorazepam 0.05 to
0.1 mg/kg IV or IO,
maximum 4 mg IV or IO
access not achieved
within 3 minutes:
Rectal diazepam
(Diastat® gel or injection
solution given rectally)
0.5 mg/kg, maximum 20
mg OR Buccal midazolam
0.2 mg/kg, maximum 10
mg OR IM midazolam
0.1-0.2 mg/kg, maximum
10 mg
Identify airway obstruction and
hypoxemia
Place continuous
cardiorespiratory monitors and
pulse oximetry
Identify impaired oxygenation
or ventilation
Perform bag-valve-mask
ventilation, as needed
Prepare for RSI*
Obtain rapid bedside blood
glucose and other studies
Establish IV or IO access
Evaluate for signs of
sepsis/meningitis
Treat hypoglycemia (IV
dextrose 0.25 to 0.5 gm/kg)
Evaluate for signs of head
trauma
Treat fever (acetaminophen 15
mg/kg rectally)

74. Tim Assessment Supportive care Seizure treet
5 to 10
minutes
ER
Reevaluate vital signs,
airway, breathing, and
circulation
Maintain monitoring, ventilatory
support, and vascular access
Benzodiazepine: second dose
Evaluate for signs of
trauma, sepsis, meningitis,
encephalitis
Give antibiotics if signs of sepsis or
meningitisΔ
10 to 15
minutes
Reevaluate vital signs,
airway, breathing, and
circulation
Maintain monitoring, ventilatory
support, and vascular access
Fosphenytoin (second line):20
mg PE per kg IV or IO◊
OR
Phenobarbital:
20 mg/kg IV or IO, maximum
1 gram, if toxin-induced
seizure (expect respiratory
depression with apnea)§
Place second IV
RSI potentially indicated*

75. Tim Assessment Supportiv
e care
Seizure treet
15 to 30
minutes
PICU
Reevaluate vital signs,
airway, breathing, and
circulation
Maintain
monitoring,
ventilatory
support, and
vascular
access
Phenobarbital (third line):
20 mg/kg IV or IO, maximum 1 gram, (10
mg/kg if phenobarbital given as second line)§
OR
Valproic acid 20 to 40 mg/kg IV or IO
AND
Pyridoxine 100 mg IV or IO in infants <1
year of age
Pyridoxine 70 mg/kg IV or IO, maximum 5
grams, if INH poisoning suspected
Obtain pediatric neurology consultation (see
Refractory status epilepticus algorithm)
Obtain continuous
EEG monitoring, if
available

76. Tim Assessment Supportive
care
Seizure treet
>35 to
30
minute
s
PICU
Reevaluate vital signs,
airway, breathing, and
circulation
Maintain
monitoring,
ventilatory
support, and
vascular access
Pentobarbital anesthesia (patient
already intubated)
Loading dose: 5-7 mg/kg; may repeat
1- to 5-mg/kg boluses until EEG
exhibits burst suppression
Maintenance dose: 0.5-3 mg/kg/h;
monitor EEG to keep burst
suppression pattern at 2-8 bursts per
min
Obtain continuous
EEG monitoring, if
available

77. Tim Assessment Supportive care Seizure treet
>35 to
30
minutes
PICU
Reevaluate
vital signs,
airway,
breathing, and
circulation
Maintain
monitoring,
ventilatory support,
and vascular access
Midazolam* infusion loading dose is
100-300 mcg/kg followed by infusion of
1-2 mcg/kg/min; increase by 1-2
mcg/kg/min q15min if seizures persist
(effective range 1-24 mcg/kg/min).
When seizures stop and/or burst
suppression is achieved, continue same
dose for 48 h then wean by decrements
of 1-2 mcg/kg/min q15min.
Propofol* initial bolus is 2 mg/kg IV;
repeat if seizures continue and follow by
infusion of 5-10 mg/kg/h, if necessary,
guided by EEG monitoring. Taper dose
12 h after seizure activity stops.
Obtain
continuous
EEG
monitoring, if
available

78. At 0 min
On presentation to hospital, initiate ABCs:
A – support airway
B – 100% oxygen, assess ventilation, SpO2 monitor
C – cardiorespiratory monitor, check pulses, do IV access
• History (SAMPLE) , Examination
• Investigations
• Suspect and treat raised ICP as needed, CT scan when warranted
• Keep normothermic, acetaminophen/ibuprofen as appropriate
At 5 min IV access?

79. At 10 min
At 15 min Phenytoin 20 mg/kg IV/IO,
max 1 g, over 20 minutes, in
0.9% NaCl (NS)
Phenobarbital 20 mg/kg
IV/IO, max 1 g, over 5-10mins
At 25 min
• The order of Phenytoin and Phenobarbital
may be interchanged
• Phenytoin should be used in head trauma
• Phenobarbital should be used 1st if patient
already on phenytoin maintenance
• Rapid Sequence Intubation if compromised
airway at any point
• Ventilate to normal parameters
• Sedation and muscle relaxants only if
necessary to ventilate or protect airway
At 35 min
Early referral to PICU if any of following:
• airway/ventilation/cardiovascular
compromise
• seizure refractory to 2nd line
medications
• seizure >30 minutes
• initiating Midazolam or Thiopental infu
Midazolam 0.15 m g/k g IV
bolus, then 2 mcg/kg/min
by IV infusion

80. Midazolam
increase by 2 mcg/kg/min q 5 min,
0.15 mg/kg bolus as needed,
Max50 mcg/kg/min
If stops x 48 hrs
Midazolam taper by
1 mcg/kg/min q 30 minAt 90 min
Thiopental 4 mg/kg IV bolus,
then 1 mg/kg/hr IV infusion
Discontinue Midazolam Infusion
Thiopental increase by 1 mg/kg/hr q 30
min,
2 mg/kg bolus as needed, max 6 mg/kg/hr
Thiopental taper by 25%
q 12 hrs
If stops x 48 hrs
At 35 min

81. Initial assessment
Neurologic examination
General evaluation with attention to
respiratory and circulatory status
02 *-/- mechanical ventilation PRN
IV catheters inserted (at least two)
Blood work: electrolytes, glucose, toxicology, CBC, LFTS, Ca, Mg,
ABG, Flngerstfck glucose
Cardiac monitoring with pulse oximetry
Frequent vital signs
Consider glucose + thiamine IV
Initial therapy
In first IV:
Lorazepam 0.02-0.03 mg/kg IV
Alternatives: Diazepam 0.1 mg/kg IV
Midazolam 0.05 mg/kg IV
Wait l minute for response then additional
Lorazepam PRN: max dose 0.1 mg/kg;max rate 2 mg/min
in second IV:
Phenytoin 20 mg/kg at 25-50 mg/min* OR
Fosphenytoin 20 mg/kg PE at 50-125 mg PE/min*
Correct metabolic abnormalities if present
Second-line therapy Phenytoin or Fosphenytoin dose: 10 mg/kg PE
intubate, mechanical ventilation ,Continuous blood pressure, cardiac monitoring
Risk for prolonged ventilation
Propofol infusion l to 2 mg/kg
per hour, titrated to seizure free
state. Rates may be as high as
10 to 12 mg/kg per hour
After seizures controlled, maintain
for 24 hours, then taper at 5
percent per hour
If seizures persist after
45 to 60 minutes, then
pentobarbital infusion
Maintain therapeutic levels of

82. • Patients who are at high risk for prolonged
mechanical ventilation (eg, those with severe
COPD, severe debilitation, or cancer) should
be treated with propofol in an attempt to
minimize the duration of sedation

83. • The term "malignant" status epilepticus has been
introduced to refer to status epilepticus that either
fails to respond to the therapies discussed above or
recurs quickly on tapering these medications
• It has been reported that as many as 20 percent of
patients with refractory status epilepticus evolve into
malignant status epilepticus, a transition that is
associated with a very poor prognosis

84. • SE can be
1. fatal ( mortality)
2. Morbidity associated with long-term morbidity,
including:
seizure recurrence
neurologic problems.
Prognosis
OUTCOME

85. Depend on
Age, etiology, and duration correlate directly
with mortality
The highest mortality is seen in the elderly;
fortunately, children have a far lower mortality
rate than do adults
Prognosis

86. OUTCOME
Mortality :can result from
1. Underlying condition
2. Respiratory
3. Cardiovascular
4. metabolic complications of SE
 mortality rates of SE in children varies between 3 and 9
percent
 The underlying etiology is the main predictor of mortality
 mortality rates of SE in adult 20 percent

87. OUTCOME Morbidity
 Neurologic sequelae of SE include;
1. focal motor deficits
2. mental retardation
3. behavioral disorders
4. chronic epilepsy.
 morbidity other than epilepsy occurred in 15 percent of patients Neurologic
sequelae are usually caused by the underlying condition rather than the
seizures
 rates of neurologic sequelae are
 increased in younger patients with a longer duration of seizures,
 Patients with cryptogenic SE and those with febrile SE do not have an increased
incidence of recurrent seizures or other neurologic sequelae over baseline

88. OUTCOME-Morbidity
Recurrent seizures
The risk for having future seizures of any type :
 Is high when SE is the child's first seizure, up to 50 percent in two reports
 Recurrent SE also was more likely to occur in children who presented with
SE (21 versus 1 percent in those with a brief initial seizure.
 Other risk factors for recurrence include :
1. Remote symptomatic etiology
2. Abnormal electroencephalogram
3. Seizure during sleep
4. History of prior febrile seizures
5. Focal post-ictal deficits, including Todd's paresis

89. OUTCOME
Neurologic sequelae more with :
prolonged
inadequately treated

90. OUTCOME
 Refractory status epilepticus
 high mortality and morbidity.
 mortality ; 33% to 52%
 More in :
 Younger patients (<5 years)
 multifocal abnormalities on EEG
 generalized abnormalities on EEG
 Morbidity In survivors,
 recurrent seizures were common (31 to 97 percent)
 new neurologic deficits (71 to 100 percent).

91. Treatment
posttreatment subtle SE is
identical to that of refractory SE
central theme to improving outcome is early
recognition
intensive EEG monitoring.

93. Neonatal Status EpilepticusTreatment
• Phenobarbital
– Usually used first
– Prolonged half life—100 hours after day 5-7; therefore watch for toxicity
– 20 mg/kg IV (up to 40 mg); repeat 10/kg every 15-30 minutes times two
• Phenytoin/Fosphenytoin
– 20 mg/kg (over 30-45 minutes)
– Half-life 100 hours
– Nonlinear kinetics; redistribution, variable rate hepatic metabolism require
individuallization of maintenance dosing
• Benzodiazepine
– Diazepam
• 0.25mg/kg IV bolus or 0.5 mg/kg PR
– Lorazepam
• 0.05 mg/kg IV over2-5 minutes
• Midazolam infusion

94. References
1. UpToDate 21.6
2. Text book of pediatric_epilepsy-diagnosis_and_therapy_3rd
3. CLINICAL PEDIATRIC NEUROLOGY: A SIGNS AND SYMPTOMS APPROACH ; 2009
4. Pediatric Neurology ;2010
5. Neurocrit Care society
6. EPILEPSY: GLOBAL ISSUES FOR THE PRACTICING NEUROLOGIST
7. Atlas of Pediatric EEG
8. eMedicine Medical
9. A Clinical Guide to Epileptic Syndromes and their Treatment
10. Current Management in Child Neurology, Third Edition
11. Nelson_Textbook_of_Pediatrics__19th_Edition
12. Rudolph's Pediatrics
13. epilepsyfoundation.org
14. Nelson_Textbook_of_Pediatrics__20th_Edition
15. Child Neurology 6th edition : by John H. Menkes (Editor), Harvey B. Sarnat, Samat By
Lippincott, Williams & Wilkins