STATUS EPILEPTICUS

IN CHILDREN
CHANIKHAN SATTAPORN, MD
PEDIATRIC DEPARTMENT,
NEUROLOGICAL INSTITUTE OF THAILAND
3RD MARCH,2023
 OUTLINE
• DEFINITION
• STAGE OF STATUS EPILEPTICULS
• PATHOPHYSIOLOGY
• ETIOLOGY
• TREATMENT & PITFALL OF TREATMENT
• OUTCOME
 Definition of SE (ILAE 2015)

• A condition resulting either from the failure of the

mechanisms responsible for seizure termination or from
the initiation of mechanisms, which lead to abnormally,
prolonged seizures (after time point t1)
• It is a condition, which can have long-term consequences
(after time point t2), including neuronal death, neuronal
injury, and alteration of neuronal networks, depending on
the type and duration of seizures.
 GTC sz

Focal
status
with
impaired
conscious

Absence
SE

25 years of advances in the definition, classification and treatment of status epilepticus ; seizure 44 (2017) 65-73
 2.STAGE OF SE

• Acute repetitive seizure, Sz <5 min : Prodrome SE

• Seizure 5-30 min : Impending SE or Early SE

• Seizure 30-60 min : Established SE
• Seizure > 60 min : Refractory SE

Pediatric status epilepticus , Current Opinion of Pediatric 2014, 26 : 655-661

 CLASSIFICATION OF SE

The presence or absence of prominent motor

symptoms
1. Convulsive SE
2. Non-convulsive SE (NCSE)

A definition and classification of SE. Epilepsia, 56 (10) : 1515-1523 , 2015

 EPIDEMIOLOGY
• 10-40 cases / 100,000 population.
• Peak incidence : younger than 10 years , older than 50 years.
• Highest mortality : elderly population.
• Present in epilepsy pt : up to 30%, acute symptomatic : 40-50%
• Incidence : increased in past 10 years esp. elderly in ICU
(increased detect NCSE in ICU & increase using Cont EEG
monitoring )
• NCSE in ICU : up to 34% of pt with alter mental status in ICU.
Epilepsy Emergencies. Continuum 2016 ; 22 (1) : 173-190
 PATHOPHYSIOLOGY
Inhibitory Excitatory
Neurotransmitter Neurotransmitter
 3. PATHOPHYSIOLOGY
• Change in gamma-aminobutyric acid (GABA) receptor composition
• Loss of benzodiazepine efficacy
 PATHOPHYSIOLOGY
• Prolonged seizure are associated with
• Cerebral hypoxia
• Hypoglycemia
• Hypercarbia
• Progressive lactic and respiratory acidosis
• Result -> Neuronal injury and may be irreversible.
 PATHOPHYSIOLOGY

• Systemic changes may cause secondary brain injury.

• Early SE, brain glucose and oxygen requirements increase. If
cerebral autoregulation is preserved then substrate delivery also
increases.
• Later SE hypotension and respiratory compromise may occur as a
result of SE itself and anticonvulsant administration, leading to
subsequent brain hypoxia, hypoglycemia, and acidosis.
• Hyperthermia and rhabdomyolysis (and secondary renal failure) may
develop with prolonged convulsions.
Pedaitric SE Management, Curr Opin Pediatr. 2014 December ; 26(6): 668–674.
4. ETIOLOGY OF SE
 ETIOLOGY OF CHILDHOOD SE
• PROLONGED FEBRILE • NEURODEGENERATIVE DISEASE
SEIZURE • PARANEOPLASTIC
• CNS INFECTION • AUTOIMMUNE ENCEPHALITIS
• METABOLIC/ TOXIC • HASHIMOTO’S ENCEPHALITIS
• HYPOXIA
• VASCULAR
• DRUG WITHDRAWAL
• EPILEPSY
4.1 EVALUATING FOR PRECIPITATING & ETI0LOGY

• CBC • Rare infection, metabolic,

• Electrolyte, Ca, Mg, PO4, Autoimmune, Paraneoplastic
• DTX / BS • IBM
• H/C
• LP
• Neuroimaging (CT/ MRI)
• EEG

1.Practice Parameter: Diagnostic assessment of the child with status epilepticus (an evidence-based review) , Neurology 2006
2.Prospective study of new-onset seizures presenting as status epilepticus in childhood , Neurology 2010
 LUMBAR PUNCTURE (LP)
• CNS infections are a common cause for acute symptomatic SE.
• LP should be performed if there is a clinical suspicion for
infection.
• There are insufficient data to support or refute whether LP should
be done on a routine basis in children in whom there is no clinical
suspicion of a CNS infection (Level U). (1)
• Precaution : postictal CSF pleocytosis (WBC up to 12 cell/mm3) may
be found.

1.Practice Parameter: Diagnostic assessment of the child with status epilepticus (an evidence-based review) , Neurology 2006
2.Prospective study of new-onset seizures presenting as status epilepticus in childhood , Neurology 2010
 EEG
• 1.An EEG may be considered in a child presenting with new onset SE
• determine whether there are focal or generalized abn. -> may influence
diagnostic and treatment decisions (Level C, class III evidence).
• 2. Although NCSE occurs in children who present with SE, there are
insufficient data to support or refute recommendations regarding
whether an EEG should be obtained to establish this diagnosis (Level U).
• 3. An EEG may be considered in a child presenting with SE if the
diagnosis of pseudo-status epilepticus is suspected (Level C, class III
evidence).

Practice Parameter: Diagnostic assessment of the child with status epilepticus (an evidence-based review) , Neurology 2006
 CONTINUOUS EEG MONITORING
• 1.The use of CEEG is usually required for the treatment of SE.
• 2. CEEG should be initiated within 1 h of SE onset if ongoing seizures
are suspected.
• 3. The duration of CEEG monitoring should be at least 48 h in comatose
patients to evaluate for non-convulsive seizures.
• 4. The person reading EEG in the ICU setting should have specialized
training in CEEG interpretation, including the ability to analyze raw EEG
as well as quantitative EEG tracings.
 NEUROIMAGING
• 1. Neuroimaging may be considered
• child with SE if there are clinical indications or if the
etiology is unknown (Level C, class III evidence)
• 2. There is insufficient evidence to support or refute
recommending routine neuroimaging (Level U).

1.Practice Parameter: Diagnostic assessment of the child with status epilepticus (an evidence-based review) , Neurology 2006
 NEUROIMAGING
• Neuroimaging abnormalities have been reported in 30% of children
with SE and described to alter acute management in 24%.
• CT is more widely available, rapid, and does not require sedation, but it
may not detect some smaller lesions which can be identified by MRI.
• 44 children who underwent head CT and MRI, 14 -normal CT but abn MRI.
• Conclusion : MRI had a superior yield and should be considered whenever
available if head CT is non-diagnostic.

Prospective study of new-onset seizures presenting as status epilepticus in childhood , Neurology 2010
 EVALUATING FOR PRECIPITATING & ETIOLOGY
• Insufficient data to support or refute whether blood cultures
should be done on a routine basis (Level U).
• AED levels should be considered when a child with epilepsy on AED
prophylaxis
• Toxicology testing : if no apparent etiology is identified, yield 3.6%
• Inborn errors of metabolism may be considered if there is a
preceding history suggestive of a metabolic disorder.
• There are insufficient data to support or refute whether genetic
testing should be done routinely in children with SE .
1.Practice Parameter: Diagnostic assessment of the child with status epilepticus (an evidence-based review) , Neurology 2006
PRINCIPLE OF TREATMENT OF SE

Stabilize pt.

Prevent
Stop seizure further
seizure

Find out
Prevent & Rx
Etiology
complication
&Precipitating
 TREATMENT

• Pre-hospital Rx
• Emergency Department
• Inpatient Rx
 PRE-HOSPITAL TREATMENT
• Diazepam IV (0.2-0.3 mg/kg) (max 10mg/dose),
• Diazepam rectum (0.5 mg/kg) (max 20 mg/dose)
• Midazolam IM (0.2 mg/kg) (max 10 mg/dose)
 EMERGENCY ROOM TREATMENT
• Step 1 : Stabilized patient : ABCDE
• A : Airway : Maintain airway (pt has risk to aspiration)
• B : Breathing : Place O2, be ready to intubate
• C : Circulation : IV access if possible
• D : Dextrose : check glucose
• E : Electrolyte : check electrolyte (including Ca Mg PO4),
CBC, (Anticonvulsant level and other lab if need)
 EMERGENCY ROOM TREATMENT
• STEP 2 : STOP SEIZURE
Diazepam Midazolam Lorazepam
Route and Dose 0.2-0.3 mg/kg IV 0.2 mg/kg IV, IM, 0.1-0.2 mg/kg IV
0.5 mg/kg PR IN
Max dose 10 mg/dose IV 10 mg 4 mg
20 mg/dose PR
Onset of action 1-3 min 3-5 min 6-10 min
Duration of 15-30 min 15-30 min 12-24 hr
action
Disadvantage Prolong sedation Risk to seizure Rapid tolerance
And respiratory relapse
depression
 EMERGENCY ROOM TREATMENT

• Step 3 prevent and treatment further seizure

• ***all patients present with status epilepticus need urgent
antiepileptic drugs unless definite cause is treated ex.
Hypoglycemic seizure. ***
• Step 3 prevent and Rx further seizure with IV AED
Drugs Dose & Rate Max Dilution with Precaution
dose
Phenytoin 20 mg/kg 1500 mg With NSS Resp depress
< 1mg/kg/min only Arrhythmia
Phebitis (pH11-12)
Fosphenytoin 20 mg/kg NA All solutions CNS depress
< 3 mg/kg/min CVS failure
hypotension
Phenobarbital 20 mg/kg 1000 mg All solutions Resp depress
< 3 mg/kg/min Hypotension
Valproic acid 20-40 mg/kg NA All solutions Liver disease
<1-3 Pancreatitis
mg/kg/min Hyperammonia
Levetiracetam 30-40 mg/kg 4000 mg All solutions Can give in liver dis.
 •Step 3 prevent and treatment further seizure
with IV AED
Drugs Dose & Rate Max Dilution with Precaution
dose
Topiramate 5-10 mg/kg - Metabolic acidosis
NG feed then
MT 5 MKD
Lacosamide 200-4oo mg All solutions PR prolong
< 3 mg/kg/min hypotension
(no ped dose)
GUIDELINE TREATMENT OF SE(EPILEPSY SOCIETY OF THAILAND 2010)
Stage of status General measures AED Treatment
1 Premonitory ABC evaluation Diazepam (IV or PR)
(0-5 min) Seizure evaluation
2 Early SE Monitor VS, seizure Diazepam (IV bolus) then followed by
(5-30 min) DTX, CBC , Electrolyte, BUN, LFT and other lab Phenytoin IV loading OR
following patient condition (AED level, C/S, Phenobarbital IV loading OR
toxicology) Levetiracetam
Given 50% glucose and Vit B1 (if have indication)
Given 25% glucose 2ml/kg (in children ,if have
indication)
Given Vit B6 100 mg (<18 months)
If seizure is still persist, transfer patient to ICU.
3 Established SE Evaluation etiology and treatment complication, Give half dose of previous first AED.
(30-60 min) Add drugs increasing BP if hypotension present. If seizure continue, give additional another
AED (phenobarbital IV OR phenytoin IV
OR sodium valproate IV OR Levetiracetam
IV
4 Refractory SE Continuous EEG monitoring Propofol IV OR Midazolam IV OR
GUIDELINE TREATMENT OF SE(EPILEPSY SOCIETY OF THAILAND 2010)
Stage of status General measures AED Treatment
1 Premonitory ABC evaluation Diazepam (IV or PR)
(0-5 min) Seizure evaluation
2 Early SE Monitor VS, seizure Diazepam (IV bolus) then followed by
(5-30 min) DTX, CBC , Electrolyte, BUN, LFT and other lab Phenytoin IV loading OR
following patient condition (AED level, C/S, Phenobarbital IV loading OR
toxicology) Levetiracetam
Given 50% glucose and Vit B1 (if have indication)
Given 25% glucose 2ml/kg (in children ,if have
indication)
Given Vit B6 100 mg (<18 months)
If seizure is still persist, transfer patient to ICU.
3 Established SE Evaluation etiology and treatment complication, Give half dose of previous first AED.
(30-60 min) Add drugs increasing BP if hypotension present. If seizure continue, give additional another
AED (phenobarbital IV OR phenytoin IV OR
sodium valproate IV OR Levetiracetam IV
4 Refractory SE Continuous EEG monitoring Propofol IV OR Midazolam IV OR
(>60 min) Neurological and seizure evaluation Pentobarbital (IV bolus or Inf) OR
Thiopental (IV bolus or inf) OR topiramate
 REFRACTORY STATUS EPILEPTICUS
Drugs Loading dose Maintainance Solution Precaution

Midazolam 0.2 mg/kg/dose 0.02-0.4 All solutions Resp depression

Repeated q 5 min mg/kg/hr Hypotension
< 4 mg/min

Pentobarbit 2-10 mg/kg 0.5-1 mg/kg/hr NSS or SW Resp depression

al < 25 mg/min To Conc 2- Hypotension
2.5%
Thiopental 5 mg/kg 3-5 mg/kg/hr ALL solutions Resp depressin
To Conc 2.5 % Hypotension

Propofol 1-2 mg/kg 2-3 mg/kg/hr NSS or 5% Hyperlipidemia

< 50 mcg/kg/min Dextrose Acidosis
ALTERNATIVE RX FOR REFRACTORY SE
 OUTCOME
• Morbidity and mortality are largely related to SE etiology.
• Children with febrile SE or epilepsy related SE have a 0–2% mortality
while children with acute symptomatic SE have a 12–16% mortality.
• Mortality may also be higher in younger children (relate to the high
occurrence of CNS infections causing SE in this group)
• In a prospective study of children with SE, 9% of survivors were found
to have new neurologic deficits, Additionally, younger children were more
likely to have new neurologic deficits (29% in <1 year, 6% in >3 years).
• Of children without prior epilepsy, 30% had subsequent seizures.

Pediatric SE Management, Curr Opin Pediatr. 2014 December ; 26(6): 668–674.

 OUTCOME
• Outcome may be at least partially dependent on SE duration.
• RSE is associated with higher mortality and morbidity (both new
neurological deficits and subsequent epilepsy) as compared to
SE episodes aborted by the initial two anticonvulsants.
• SE recurrence occurs in 3–67% of children, and is rare with
febrile or idiopathic etiologies but common with acute
symptomatic or progressive etiologies.

Pediatric SE Management, Curr Opin Pediatr. 2014 December ; 26(6): 668–674.

 PITFALL IN TREATMENT SE
• Delay in diagnosis and initiation of Rx
• Too many doses of benzodiazepine
• Inadequate dose of anticonvulsant
• Delay and inadequate maintainance dose of AED
• Do not treat underlying condition and precipitating
causes
 CASE 1
• 2 YR NO UNDERLYING DISEASE
• FEVER 1 DAY WITH GTC SEIZURE -> VALIUM 1 DOSE AT ER + ADMIT
15.00 CBC + ELECTROLYTE +DTX -
• AT IPD : 19.00 GTC SZ 1 TIME -> RX – VALIUM 1 DOSE
• 24.00 GTC 1 TIME -> VALIUM 1 TIME
• 3.00 GTC SZ -> VALIUM 1 DOSE + ON ET TUBE +REFER
 CASE 1 : PITFALL

• 1. MUST FIND OUT THE CAUSE

• 2. MULTIPLE OF VALIUM XXX
• 3. PREVENT SEIZURE WITH ANTIEPILEPTIC DRUGS
 CASE 2 : 5 YR ,20 KG
• UNDERLYING EPILEPSY 1 YR ,ON DEPAKIN 400 MG/DAY (20 MKDAY)
• GTC SEIZURE 1O MIN PTA
• AT ER STILL HAS SEIZURE -> RX VALIUM 1 DOSE + METABOLIC W/U
• AT 10 MIN LATER, DEVELOP GTC SZ AGAIN RX : VALIUM 1 DOSE + LOAD
DILANITN 20 MKDOSE
• STILL HAS SEIZURE + NOT GAIN CONSCIOUS
 CASE 2 : NEXT APPROPRIATE MX?

• A : VALIUM 1 DOSE
• B : LOAD DILANTIN 10 MKDOSE
• C : LOAD PHENOBARBITAL 20 MKDOSE
• D : LOAD DEPAKIN 2O MKDOSE
 CASE 2
• IF STILL HAS SEIZURE : NEXT MX?

• A : LOAD DILANTIN 10 MKDOSE

• B : LOAD PHENOBARBITAL 20 MKDOSE
• C : LOAD DEPAKIN 2O MKDOSE
• D : LOAD LEVETIRACETAM 30 MKDOSE