Something also that is gaining a lot of popularity for super refractory status epilepticus and refractory status epilepticus is the early use of ketamine. Going back into the pathophysiology, our brain lives in a harmonious state between GABA and glutamate, inhibition and excitation. We have animal data that shows that within 20 minutes of having a status epilepticus, there is a downregulation of the GABA receptors that are in the synaptic cleft and upregulation of the excitatory receptors such as NMDA and AMPA...
Something also that is gaining a lot of popularity for super refractory status epilepticus and refractory status epilepticus is the early use of ketamine. Going back into the pathophysiology, our brain lives in a harmonious state between GABA and glutamate, inhibition and excitation. We have animal data that shows that within 20 minutes of having a status epilepticus, there is a downregulation of the GABA receptors that are in the synaptic cleft and upregulation of the excitatory receptors such as NMDA and AMPA. Ketamine is one of the drugs, a drip, that has NMDA antagonism properties. So early use of ketamine in these patients may be beneficial for seizure cessation. There are case reports and case series that show that upon starting ketamine, seizures can reduce up 68% and seizure burden can reduce up to 80% in the patients. However, these case series normally have a wide timing on when they start ketamine: within 12-24 hours to 27 days. So early on in the stages, within minutes or hours of the presentation to our hospital (because if we think about it, the patient takes about 20 to 30 minutes to come to us and this disbalance is already occurring), if the patient has failed the first and second line and we’re thinking about using anesthetics, ketamine might be also a good medication to start using.