Emergency Medicine Myths: Cerebral Edema in Pediatric Diabetic Ketoacidosis and Intravenous Fluids

• Published in: The Journal of emergency medicine 2017-08, Vol.53 (2), p.212-221
• Main Authors: Long, Brit, MD, Koyfman, Alex, MD
• Format: Article
• Language: English
• Subjects: Administration, Intravenous - methods; Administration, Intravenous - standards; Adolescent; Brain Edema - etiology; Brain Edema - therapy; cerebral edema; Child; Child, Preschool; dehydration; diabetic ketoacidosis; Diabetic Ketoacidosis - complications; Diabetic Ketoacidosis - therapy; Emergency; Emergency Service, Hospital - organization & administration; fluid infusion; Fluid Therapy - adverse effects; Fluid Therapy - standards; Humans; pediatric; Pediatrics - methods; Pediatrics - trends
• ISSN: 0736-4679; 2352-5029
• DOI: 10.1016/j.jemermed.2017.03.014

Abstract Background Pediatric diabetic ketoacidosis (DKA) is a disease associated with several complications that can be severe. One complication includes cerebral edema (CE), and patients may experience significant morbidity with this disease. Objective This review evaluates the myths concerning CE in pediatric DKA including mechanism, presentation of edema, clinical assessment of dehydration, and association with intravenous (i.v.) fluids. Discussion Multiple complications may occur in pediatric DKA. CE occurs in < 1% of pediatric DKA cases, though morbidity and mortality are severe without treatment. Several myths surround this disease. Subclinical CE is likely present in many patients with pediatric DKA, though severe disease is rare. A multitude of mechanisms likely account for development of CE, including vasogenic and cytotoxic causes. Clinical dehydration is difficult to assess. Literature has evaluated the association of fluid infusion with the development of CE, but most studies are retrospective, with no comparator groups. The few studies with comparisons suggest fluid infusion is not associated with DKA. Rather, the severity of DKA with higher blood urea nitrogen and greater acidosis contribute to CE. Multiple strategies for fluid replacement exist. A bolus of 10 mL/kg of i.v. fluid is likely safe, which can be repeated if hemodynamic status does not improve. Conclusions Pediatric CE in DKA is rare but severe. Multiple mechanisms result in this disease, and many patients experience subclinical CE. Intravenous fluids are likely not associated with development of CE, and 10-mL/kg or 20-mL/kg i.v. bolus is safe.