Cerebral Injury in Pediatric Diabetic Ketoacidosis

First Author(s)

• RP

  Rachel Palting, DO

  Physician
  n/a

  Disclosure information not submitted.

  Slides and Audio

Co-Author(s)

• CJ

  Christopher Jenkins, MS

  Medical Student
  Loma Linda University School of Medicine, United States

  Disclosure information not submitted.
• CK

  Chieko Kimata, PhD, MPH, MBA

  Lead Biostatistician/Operations Researcher
  Hawai‘i Pacific Health | Patient Safety & Quality Services, United States

  Disclosure information not submitted.
• MY

  Melissa Yamauchi, MD

  Pediatric Cardiologist
  Kapiolani Medical Center for Women and Children, United States

  Disclosure information not submitted.
• AS

  Andrea Siu, MPH, RAC

  Regulatory Coordinator
  Hawai‘i Pacific Health | Research Institute, United States

  Disclosure information not submitted.
• BM

  Barry Mizuo, MD

  Pediatric Hospitalist
  Kapiolani Medical Center for Women and Children, United States

  Disclosure information not submitted.
• AB

  Andras Bratincsak, MD PhD

  Pediatric Cardiologist
  Kapiolani Medical Center for Women and Children, United States

  Disclosure information not submitted.
• SL

  Sian Yik Lim, MD

  Rheumatologist
  Hawaii Pacific Health Medical Group, United States

  Disclosure information not submitted.
• RW

  Russell Woo, MD

  Pediatric Surgeon
  Kapiolani Medical Center for Women and Children, United States

  Disclosure information not submitted.
• PP

  Prashant Purohit, MD FAAP

  Pediatric Intensivist
  Kapiolani Medical Center for Women and Children, Hawaii, United States

  Disclosure information not submitted.

Title: Cerebral Injury in Pediatric Diabetic Ketoacidosis Patients

Objective: Identify the factors affecting outcomes of cerebral injury (CI) in pediatric diabetic ketoacidosis (DKA) patients.

Methods: Pediatric patients (< 18 years) receiving DKA treatment at a single center PICU were included in the study. They were divided into study group (developed CI) and control group (didn’t develop CI). CI was identified based on the International Society of Pediatric and Adolescent Diabetes definition of cerebral edema or clinical features prompting hyperosmolar therapy. Fisher Exact, Wilcoxon, T-test and logistic regression analysis were applied using SAS 9.4.

Results: We found 1429 pediatric diabetic patients in our system, of which 571 (40%) were admitted with DKA in 11 years, of which 21 patients developed CI (3.68% incidence). Variables were compared between the study group (n=21) and control group (n=146).
The patients in CI group were older (14 years versus 11 years), heavier (51.6 kg versus 32.5 kg), had lower initial blood pH (7.0 versus 7.10), lower HCO3 (5 versus 8), lower venous CO2 (4 versus 8), higher hemoglobin (16.1 versus 15), and higher anion gap (30 versus 26). These variables were statistically significant on univariate analysis (p< 0.05). The other baseline characteristics including new-onset versus known diabetic, initial glucose, BUN, sodium, beta-hydroxybutyrate and glycosylated hemoglobin were not significantly different between two groups. The treatment variables including treatment at pediatric versus non-pediatric ED, number of initial fluid boluses, fluid bolus volume > 20 mL/kg or < 20 mL/kg, receiving insulin or sodium bicarbonate bolus were not significantly different between two groups. On multivariable logistic regression analysis, older age and bicarbonate < 6 mEq/L were significantly different (aOR 1.32, 9.69). Mean CI onset was at 7 hours (2-16). Eleven patients received mannitol, four received hypertonic saline, and six received both. There was no mortality. All patients returned to their baseline neurologic exam by the time of discharge.

Conclusions: Patients with older age, and sodium bicarbonate < 6 mEq/L were associated with the development of CI but treatment variables including fluid, insulin or bicarbonate boluses were not. The outcomes of CI were encouraging with no mortality and return of baseline neurologic exam in all the patients.