SUN-277 Severe Hyperglycemia in the Setting of Hypernatremic Dehydration

Abstract

Background: Hypernatremic dehydration associated with hyperglycemia in non-diabetic infants has a potential to cause serious metabolic derangement. Review of limited literature available on this condition reveals pathogenesis of hyperglycemia is likely multi-factorial. We present a case of extreme hyperglycemia in a 10 months old infant with severe hypernatremic dehydration with possible mechanisms discussed. Case Report: Our patient was a 10 months old Caucasian male former 25 weeks premature infant (birth weight: 0.79 kg) with chronic lung disease on furosemide and potassium supplements (KCl) presenting with lethargy, respiratory failure, severe hypovolemic shock and acute kidney injury (AKI) requiring intubation and aggressive fluid resuscitation with pressor support. Initial labs showed blood glucose (BG)> 750 mg/dl, repeat BG 1438 mg/dl, pH 7.09, PCO2 80 mm Hg, sodium 194 mmol/L, BUN 197 mg/dl, Cr 2.6 mg/dl, potassium 11 mmol/L, chloride 155 mmol/L, bicarb 22 mmol/L, POC ketones 4.7 mmol/L, beta hydroxybutyrate 0.58 mmol/L. Possibility of diabetic ketoacidosis was considered. Regular insulin drip was started at 0.05 units/kg/hour. Glucose levels normalized after approximately 17 hours. He remained euglycemic off insulin for rest of hospitalization on glucose containing fluids. C-peptide 17.99 ng/ml indicated endogenous insulin production. HbA1C was 6.2% with negative pancreatic autoantibodies. Associated risk factors were identified to include viral URI, 1 week of watery diarrhea and potential administration of inappropriately diluted (increased solute) formula and/or KCl overdose. Septic work up was negative. Hypernatremia slowly corrected over 10 days. AKI resolved and patient had no metabolic abnormalities prior to discharge. Conclusion: Hypernatremic dehydration is associated with significant morbidity and mortality and requires carefully controlled rehydration due to risk of cerebral edema. Hyperglycemia in such cases is typically transient, associated with normal insulin/C-peptide levels, negative pancreatic autoantibodies and often resolves with fluid resuscitation alone. However, extreme hyperglycemia as in our case may warrant initiation of insulin. The pathogenesis is unclear but related to a combination of insulin resistance induced by counter-regulatory hormones like cortisol, glucagon and growth hormone with increased endogenous glucose production and decreased peripheral glucose utilization. This may be compounded by altered renal glucose threshold in sick infants.