Abstracts

Rationale: The ketogenic diet (KD) is a well-established non-pharmacologic treatment for patients with epilepsy. The diet can be associated with various side effects, including constipation, mineral deficiencies, and acidosis. Information regarding the safety and efficacy of the KD for patients with type 1 diabetes is lacking. This case study evaluates a patient who developed type 1 diabetes while being actively treated with the KD.  Methods: Case report and Literature Review Results: Epilepsy onset was status epilepticus at 5 months of age after developing Influenza A, septic shock, and DIC, which resulted in moderate-severe, multifocal hypoxic ischemic encephalopathy, cerebral palsy with spastic quadriparesis, and cognitive impairment.  Focal seizures were initially treated with Phenobarbital and Levetiracetam, but became medically refractory and epilepsy evolved to include infantile spasms. Infantile spasms persisted despite adequate trials of ACTH & Vigabatrin. After counseling available treatment options tailored to the patient’s multifocal epilepsy and structural abnormalities, parents selected KD over presurgical evaluation.  He was continued on Levetiracetam, Vigabatrin, and Topiramate during KD therapy initiation. He was started on the KD 3.5:1 ratio on March 15, 2016 (4 years old). Diet was advanced due to lack of seizure control to a 4:1 ratio of RCF and Microlipids. Focal seizures completely resolved and infantile spasms frequency was reduced by >90%. Isolated spasms (0 – 3 per 24 hr video EEG study) were observed, whose intensity was >90% improved and mostly subclinical. Development also improved, with gains in cognitive function, speech and gross motor milestones. He was diagnosed with diabetes mellitus (DM) type 1 on May 2, 2017 (5 years old; autoantibodies positive). Despite meticulous blood sugar/diabetes management by Endocrinology while on the KD, blood sugars were erratic and, within 12 months, he experienced 5 episodes of ketoacidosis (blood sugars ranging from 250 – 450), each requiring hospital admissions.  Urine & blood ketones were also high (up to 6.7 mg/dl). Because of the significant morbidity and mortality associated with DKA in children with type 1 diabetes mellitus, a multidisciplinary decision was made to conclude ketogenic dietary therapy. Since being weaned off, overt epileptic spasms have recurred daily, independently and in clusters. Although the KD was efficacious for the patient’s epilepsy by clinical report and with electroencephalographic confirmation, it significantly exacerbated his diabetes and had to be discontinued. Since that time, the patient’s diabetes has been better controlled, with no further episodes of diabetic ketoacidosis nor hospital admission.  Conclusions: The KD was an efficacious treatment option for a child with medically refractory epilepsy including infantile spasms who also had diabetes type I.  However, blood sugars were too labile while on the diet despite close monitoring by Endocrinology, resulting in several hospital admissions for ketoacidosis and eventual diet discontinuation. If KD is initiated with DM type 1, ndocrine management is recommended to manage blood sugars. Funding: None