Post on 19-Jan-2016
STATUS EPILEPTICUS IN CHILDRENDr:Abdelwhab M EL Sadany
MD PhD Pediatrics Mansoura G hospital
Definition of SE
The 30 minute definitionIt is a prolonged seizure that last more
than 30 minutes, orRecurrent seizures during which the
patient does not regain consciousness within a 30 min period.
The theory is that neuronal damage may begin after 30 minutes
Classification of SE
According to the presence or absence of motor activity:
Convulsive status epilepticus Nonconvulsive status epilepticusAccording to the cause Symptomatic, when there is a definite
cause Remote symptomatic with acute
precipitant. Idiopathic with unknown cause.
Convulsive SE
Convulsions that are associated with rhythmic jerking of extremities.
Generalized tonic clonic Focal seizures Myoclonic seizures Absence seizures
Non-Convulsive Status Epilepticus (NCSE)
Defined as seizure activity seen on electroencephalogram (EEG) without clinical findings associated with GCSE.
This patient presents with: Tonic eye deviation that often occurs in
the setting of acute brain injury). Prolonged post-ictal state Complex partial seizures without
recovery of consciousness
Refractory Status Epilepticus (RSE)
Patients who continue to experience either clinical or electrographic seizures after receiving adequate doses of an initial benzodiazepine followed by a second acceptable antiepileptic drug (AED) will be considered refractory.
Refractory Status Epilepticus
Super-refractory SE: SE that continues 24 hours or more after the onset of anesthesia, including those cases in which the SE recurs on reduction or withdrawal of anesthesia.
Etiology of SE
Febrile convulsion is the most common cause in children 52%
Epilepsy: First presentation Difficult seizure control Subtheraputic anticonvulant levels
Cerebrovascular disease Metabolic abnormalities Idiopathic Hypoxia CNS infections Trauma Poisoning
Investigations
Basic lab investigations CBC Blood gases Blood: Magnesium, electrolytes,
calcium, glucose, and creatinine
Investigations
Advanced lab investigations Metabolic investigations: ammonia Toxicology screening Anti-convulsants level ESR, RF, antineutrophil cytoplasmic
antibodies ANCA, serum complement. Lumbar puncture
Investigations
Brain imaging CT MRI MR angiography to diagnose CNS
vascultitis EEG PET CT to diagnose epileptogenic zone
Cortical hyperperfusion frontal right during NCSE. Bottom left: EEG shows right frontal spike-and-wave activity.
Prognosis of SE
MortalityConvulsive status epilepticusMortality ranges from 3 to 11 %Mortality in the first year is 17.8% and
24% in the first six months.NCSE: mortality is higher in those
diagnosed after 24 hours reaching 75%RSE: the mortality rate is high in
symptomatic SE 20%
Morbidity Of SE
Convulsive SE Severe neurological or cognitive sequelae:
11–16 %.RSE A new deficit occurrs in 36 Motor and visual deficits may be seen at 1
year after SE. Morbidity and mortality is highest in those
with symptomatic SE or a progressive encephalopathy
Pathophysiology of SE
The exact mechanism is still unknown Theoretically it is either failure of
phyisologic neuronal inhibition or an excess of excitation.
Clinically demonstrated by poor response of prolonged seizures to the GABA agonists benzodiazepines and barbiturates, a phenomenon called time-dependant pharmaco-resistance
Complications of SE
Cardiovascular compromise and hypotension
Hyperpyrexia Rhabdomyolysis that may lead to renal
failure Raised intracranial pressure Risk of hospital acquired infection Cardiac arrhythmias are also common
with higher mortality in these patients
Complications of SE
Lactic acidosis Stress cardiomyopathy Neurogenic pulmonary edema Fractures
Guidelines for the treatment of SE
Initially Assessment Management of airway, breathing, and
circulation: Secure the airways Administer O2 Obtain IV access
ABC
Maintain air way Intubate if
necessary Supplement oxygen Continuous
cardiovascular monitoring
Find vascular access
Treatment of SE
All protocols take a staged approach to treatment.
Typically, in Stage 1 (early status Epilepticus),therapy is with benzodiazepines.
If seizures continue despite this therapy, the patient is said to be in Stage 2 (established status Epilepticus) and therapy is with intravenous anti-epileptic drugs such as phenytoin, Phenobarbital or valproate.
Treatment of SE
If seizures continue despite this treatment for up to 1 h, the patient is said to be in Stage 3 (refractory status Epilepticus) and GA is indicated .
If seizure continue despite GA for >24h the patient is said to be in Super Refractory SE.
support ABC and give oxygenestablish IV access
rapid glucose check and consider critical lab Na, Ca Mgproceed with AED
5 minute
s Diazepam or Midazolam
IV 0.3mg/kg intranasal: 0.2 mg/kg
pr 0.5MG/KG buccal : 0.5mg/kg
IV max < 5 years 5mg/dose Max 5mg/nostril
> 5 years 10 mg/dose buccal max 10 mg5
minutes
phenytoin IV 20mg/kg in NS only over 5-10 minutes
max 1000 mg
5 minutes
phenobarbitalIV 20 mg.kg in NS or D5W over 20 minutes
or IV push over 5- 10 minutesmax 1000 mg
10minutes
RSE intubate if needed
arrange for admission to ICU
Midazolam continuous infusion
IV 0.15 mg/kg bolus then 2mic/kg/min infusion
Increase as need 2 mic/kg/min q5 min
Bolus 0.15 mg/kg with each increase
Max infusion 25mic/kg/min
Midazolam continuous infusion
IV 0.15 mg/kg bolus then 2mic/kg/min infusion
Increase as need 2 mic/kg/min q5 min
Bolus 0.15 mg/kg with each increase
Max infusion 25mic/kg/min
If no seizures within for 48 hrs
Taper midazolam
Decrease by 1 mic/kg/min q 15 min
If seizures persist
Thiopental continuous infusion via CVL2- 4 mg/kg bolus then2-4 mg/kg/hr Increase as needed by 1 mg/kg/hr every 30 minutesBolus 2 mg/kg with each increase Max infusion 6 mg/kg/hr Discontinue midazolam and phenobarbitone
If seizure recur, reinstate midazolam for another 48 hr
If no seizures for 48 hrs
Taper thiopenatal
Decrease rate by 25% q3 hrs
Reinstitute phenobarbitone while tapering
if seizures persist If seizures recur
Individualized therapy
Management of SE
Treat the underlying condition; meningitis, or increased intracranial pressure
Start AED to abort the electrical activityBenzodiazepine is the first line therapy Routes of administration IV, IM, buccal,
nasal, and rectalLorazepam preferred IVMidazolam preferred IM, can be given buccal
and nasalDiazepam preferred rectal
Management of SE
Urgent control therapy is required after short acting benzodiazepine
For patients who respond to emergent initialtherapy and have complete resolution of SE,
the goal is rapid attainment of therapeutic levels of an AED and continued dosing for maintenance therapy.
For patients who fail emergent initial therapy, the goal of urgent control therapy is to stop SE.
2nd stage of management
The preferred top tier agents that are generally used for urgent control of SE are
IV fosphenytoin/phenytoin valproate sodium phenobarbital Levetiracetam continuous infusion midazolam
Treatment of RSE
Treatment of RSE is extremely difficult
Continuous infusion of benzodiazepines Propofol Phenobarbitone General anasthetics Surgical treatment
High dose benzodiazepines
Midazolam infusion 2-24Mic/kg/min Advantages Rapid onset of action Short half life Lower incidence of cardiovascular
depression Disadvantage Tachyphylaxis High dose diazepam is also an alternative
Propofol
Advantage Rapid onset of action Short half life Disadvantage Rapid tapering can precipitate seizures Respiratory depression Prolonged usage produce “propofol
infusion syndrome” (metabolic acidosis, rhabdomyolysis, bradyrhythmias, lipemia, death”
Valproic acid
Intravenous valproic acid Caution with hepatic patientsDisadvatage Hyperammonemia in predisposed child Thrombocytopenia Fatal hepatotoxicity
Ketamine and lidocaine
Ketamine is NMDA antagonist that has anticonvulsants and neuroprotective properties
Lidocaine is another option although not commonly uses
Pyridoxine
Pyridoxine (vitamin B6) is a cofactor for both glutamic acid decarboxylase and GABA transaminase
Pyridoxine dependency is a rare disorder it presents in neonatal or infantile period but may present as lates as age 2.5 years.