(699) Parasympathetic Response Is Altered During Diabetic Ketoacidosis-Induced Encephalopathy

Introduction: Diabetic ketoacidosis encephalopathy (DKAe) and associated cerebral edema have a complex pathobiology that has not been completely elucidated. The impact of DKAe in the pupillary light reflex (PLr) has not been described in pediatric patients. In preliminary studies, we noticed an alteration of the parasympathetic component (initial response) of the PLr. In this project, we focused on assessing the impact of DKAe on the components of the PLr affected by the parasympathetic system.

Methods: We performed a retrospective chart review from 7/2021 to 7/2023 of patients aged 5 years to 18 years admitted to the PICU at Wolfson Children’s Hospital, Jacksonville with the diagnosis of DKA who did not have optic neuropathy. Demographics, presence of encephalopathy and pupillometry findings on admission (T0) and after the DKA was resolved (>12 hours) (T1) were retrieved. 20 patients were included and divided into 2 groups based on presence of encephalopathy upon admission. We utilized the NPi-300 Pupillometer by NeurOptics, California for pupillary assessment.
Constriction velocity (CV) and maximum constriction velocity (MCV) of both eyes were documented and the readings at T0 were compared between groups. We calculated CV and MCV percent changes between T0 and T1 for each eye and compared the percent changes between groups as a secondary measure. In addition, the median difference between two measurements of each eye was compared.

Results: DKAe was found to slow the CV and MCV by approximately 70%; at T0 (median (m)CV 1.7mm/s (IQR 1.86) and (m)MCV 2.81mm/s (IQR 2.98) vs T1 (m)CV 3.14mm/s (IQR 1.05) and (m)MCV 4.87mm/s (IQR 1.73), p < 0.01 for CV and MCV, which corrected once the encephalopathy resolved. A significant difference between measurements at T0 and T1 was observed only in patients with encephalopathy.

Conclusions: We found a transient alteration of the parasympathetic component of the PLr associated with the presence of DKAe. The results suggest that the slowing of the CV and MCV resolves once the encephalopathy subsides. This study provides data that introduce intriguing questions as to the impact of the parasympathetic response in the pathobiology of DKAe.
Is the altered parasympathetic response responsible for the DKAe or a “surrogate metric” of disease severity?