Abstracts

Rationale: The ketogenic diet has been used since the 1920’s as treatment for various types of epilepsy. Mechanism of action with regards to anticonvulsant and antiepileptic properties are not fully understood. Recently, use of the ketogenic diet has become more widespread for the management of intractable epilepsy. We present two cases of refractory status epilepticus successfully treated with the initiation of the ketogenic diet. Methods: Two cases of refractory status epilepticus successfully managed with the initiation of the ketogenic diet were identified via retrospective chart review. Both patients were initially treated with standard intravenous agents without success. Results: (Case 1) A 10 year-old female with a history of symptomatic generalized epilepsy characterized by atypical absence and generalized tonic-clonic seizures presented to the hospital with mental status changes. Long-term video EEG monitoring confirmed non-convulsive status epilepticus. The EEG showed nearly continuous generalized spike and slow wave discharges (1.5-2Hz) with a bifrontal predominance. The patient did not respond to intravenous phenobarbitol, valproate, levetiracetam or pentobarbital. Initiation of the ketogenic diet via nasogastic tube (KetoCal, ratio 4:1) improved the EEG findings within 36 hours. Clinically, the patient became responsive in 48 hours. The patient has been maintained on the ketogenic diet and antiepileptic drugs without recurrence of status epilepticus for nine months. (Case 2) A 9 year-old female with progressive myoclonic epilepsy of mitochondrial origin presented to the hospital in status epilepticus with a concurrent influenza A infection. The EEG showed continuous high amplitude bursts of generalized polyspike and spike and slow wave discharges (2.5-3Hz). Intravenous valproate, levetiracetam, phenobarbitol, fosphenytoin and midazolam did not significantly alter the continuous EEG findings. Propofol was not given secondary to the patient’s mitochondrial disease. Pentobarbitol was not administered due to multi-organ system failure associated with the patient’s influenza A infection. The ketogenic diet was started via nasogastic tube (KetoCal, ratio 4:1). Electographic and clinical seizures decreased 48 hours later. With one month follow up the patient has been successfully managed on the ketogenic diet and antiepileptic drugs. Conclusions: The ketogenic diet may be a successful alternate treatment option for patients with status epilepticus refractory to standard therapies.