Extreme hyperglycemia and hyperosmolar state in new onset type 1 diabetes: are sugar- and salt-containing beverages at fault?

The hyperglycemic hyperosmolar state (HHS) is an acute complication of diabetes mellitus generally thought to occur in individuals with type 2 diabetes mellitus (T2DM) and usually in older patients who are dependent on others for support.1 Although HHS is infrequently encountered in children, it is associated with a mortality rate of approximately 15%.2 Some reports have implicated high-carbohydrate-containing beverages in causing exaggerated hyperglycemia and hyperosmolarity, resembling the clinical and laboratory picture of HHS, in the acute presentation of type 1 diabetes mellitus (T1DM).3,4 With the high case fatality rates associated with HHS, patients with diabetes presenting in a similar manner require prompt identification to ensure adequate fluid replacement and gradual correction of serum osmolarity.5 The following cases describe 3 children seen at our institution with new onset T1DM and severe hyperglycemia, hypernatremia, and hyperosmolarity. Although these cases are not classic for HHS due to the presence of ketones,5 the clinical presentation and other biochemical abnormalities are comparable. Each child required a prolonged hospital stay and intensive fluid management to correct fluid and electrolyte abnormalities. The clinical and biochemical characteristics of all 3 cases are described in Table 1. The potential influence of high-carbohydrate- and high-sodium-containing beverages is discussed. Table 1 Clinical and Biochemical Characteristics of 3 Boys at Presentation With New Onset Type 1 Diabetes Mellitus Case Reports Case 1 A 9.6-year-old prepubertal white male presented with a week history of flu-like symptoms. Parents noted polydipsia, polyuria, and vomiting 2 days prior to admission. He drank 4 liters of soft drinks in a 14-hour period, resulting in consumption of approximately 217 g of carbohydrates and 392 mg of sodium. He was noted to have hyperglycemia, hypernatremia, hyperosomolarity, and acidosis (Table 1). He initially received 1 liter of normal saline and was then started on 5% dextrose in half normal saline at maintenance. He was also placed on an insulin drip at 0.1 U/kg/h and transported to our medical center. At our hospital, his serum glucose was 756 mg/dL and serum sodium was 159 mEq/L. He had acute neurologic changes, including decreased activity, impaired cognition, and incoherent speech. One dose of mannitol was administered, and a head computed tomography showed no intracranial abnormalities or cerebral edema. After 16 hours of IV fluids (IVF), he was switched to 5% dextrose in quarter normal saline at 1.5 times maintenance to correct his hypernatremia. After his neurologic status returned to baseline, he was transferred to the pediatric floor. Serum sodium was 156 mEq/L, serum glucose was 163 mg/dL, and acidosis had resolved. He was started on subcutaneous insulin and allowed to eat but was maintained on IVF for another 24 hours. IVF were discontinued on the fourth day of admission when his serum sodium was 137 mEq/L. In total, he received 6100 mL (175 mL/kg) of IVF. At his follow-up clinic visit, he did not demonstrate any neurologic sequelae.