3. Refractory Status Epilepticus
Definition:
o status epilepticus that continues despite
first and second line therapies(typically a
benzodiazepine followed by phenytoin
&valproate.
o benzodiazepine and one antiepileptic
medication, failure of benzodiazepine and
2 antiepileptic medications.
4. Refractory Status Epilepticus
• the mortality in RSE is three times that of
status epilepticus that is not refractory.
• Refractory status epilepticus is a
potentially life- threatening medical
emergency.
• Nearly 40% of status epilepticus are
refractory.
5.
6. pathophysiology
• Loss of GABA-mediated inhibitory synaptic transmission in hippocampus.
• Glutaminergic excitatory synaptic transmission, important for sustaining
SE.
7. Treatment
• As in any emergency situation, the first priority
should be assessment and management of
airway, breathing, and circulation.
• continuous EEG monitoring should be initiated to
observe the patient for ongoing sub-clinical
seizure activity.
8. Treatment
• There are three main agents in treatment of
RSE. These include; pentobarbital or
thiopental, midazolam, and propofol.
All three have GABA-A agonistic action.
Pentobarbital and propofol have NMDA
antagonistic and Ca+ channel modulatory effects
as well.
9. Treatment
• Midazolam is one of the first line agents in treatment
of RSE.
• is a fast-acting, short half-life benzodiaze.pine
• The drug's elimination half-life is approximately 4 to
6 hours. It is metabolized through liver and excreted
in urine.
• Treatment is initiated with an intravenous loading
dose of 0.2 mg/kg followed by an IV infusion
initiated at 0.1to 0.4 mg/kg/hr, and titrated to the
goal of seizure suppression on EEG.
10. Treatment
• Propofol is another option for RSE treatment.
• CNS depressant used in anesthesia.
• It activates GABA receptors and inhibits the
NMDA receptors.
• It is started with a loading dose of 1 to 2 mg/kg
and then infused at 2 to 5 mg/kg/min, titrated to
seizure suppression on EEG.
11. Treatment
• The third commonly used agent in RSE is
Pentobarbital
• The initial dose is 5 mg/Kg IV followed by
and infusion of 0.5-9 mg/kg/hour.
• The half life is about 80 hours.
• Elimination is chiefly by liver and excreted
in urine.
12. Defenition;
• status epilepticus that continues or recurs 24hours
or more after the onset of anaesthetic therapy.
• status epilepticus that doesn’t respond to anesthetic
drugs.
• status epilepticus that recurs after reducing the
anesthetic drugs.
13. etiology
1. it occurs in patients with severe acute brain injury
or infection
1. in patients with no history of epilepsy in whom status
epilepticus (SE) develops from no overt cause
referred to as NORSE (new-onset refractory status
epilepticus).
3. Other conditions presenting with super-refractory status in
which the aetiology of the problem is unknown include
• ;
• DESC (devastating epileptic encephalopathy in school-
age children)
• FIRES (febrile related epilepsy syndrome)
.
14. risk factors
Some risk factors for developing status
epilepticus such as;
• intracranial space-occupying lesions,
• cerebrovascular disease
• sudden cessation of antiepileptic drugs
have also been implicated