PSUN242 Severe Hypernatremia in a patient with combined Hyperosmolar Hyperglycemic State and Diabetic Ketoacidosis

Abstract

Abstract Introduction Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are the complications of diabetes with highest morbidity. In both, there are fluid shifts and osmotic diuresis with electrolyte disturbances that result in hyponatremia. With high glucose levels, sodium become falsely decreased due to dilutional effects of water shifting from intracellular to extracellular space. Hypernatremia is an uncommon electrolyte abnormality in this setting, with unclear exact etiology. We present a 35-year-old gentleman who was found to have severe hypernatremia in the setting of combined DKA and HHS. Clinical Case A 35-year-old male with class III obesity presented to the emergency department with altered sensorium and lethargy. Patient was having nausea and vomiting, along with polyuria, polydipsia and nocturia, prior to worsening encephalopathy. Physical exam showed rapid shallow breathing and lethargy. No focal neurologic deficits noted.Initial labs revealed severe hyperglycemia and hypernatremia with sodium at 164 mmol/L, severe metabolic acidosis, and acute kidney injury. Hemoglobin A1C was 9.8%. Ketonuria and ketonemia were present. Given the high osmolality, he was diagnosed with DKA and HHS.Free water deficit was 15.4 L. Insulin drip was started, along with 5 liters of intravenous Lactated Ringer's boluses. As blood glucose improved, patient was placed on dextrose-5% water infusion at 200 mL/hour.Encephalopathy improved approximately 48 hours after admission. His glucose stabilized, renal function improved, acidosis resolved, and sodium returned to normal. Sodium was corrected at a rate of 8 mmol/L daily. He was transitioned to general wards and started on an oral carbohydrate-restricted diet and subcutaneous insulin regimen containing long- and short-acting insulin analogs. Conclusion During severe hyperglycemia, glucose increases extracellular osmolality, creating a gradient for water to move from intracellular to extracellular compartments, leading to hyponatremia. As the renal threshold is reached, glucosuria ensues, causing osmotic diuresis and water loss. If this process continues, excess water loss can cause dehydration, further increase serum osmolality, and lead to hypernatremia.A previous study evaluated patients who present with hypernatremia during DKA. It was found that patients with new-onset diabetes are more likely to present with hypernatremia (1).Several etiologies contribute to altered sensorium in such patients, including cerebral hypoperfusion in the setting of dehydration and excess water loss, acidosis, and direct effect of ketone bodies on brain cells (2). As electrolyte abnormalities are corrected with adequate fluid selection, patients return to baseline mentation. It is best to correct hypernatremia at a rate of 6-8 mmol/L daily to prevent the complications of rapid correction. References KW Monroe, WD King, MH Nichols, JA Atchinson. Hypernatremia in diabetic ketoacidosis. Practical Diabetes Int 1997;14(6): 159-61. Elias Estifan, Sushant M. Nanavati, Vinod Kumar, et al. Salty diabetes: a case series of hypernatremia presenting with diabetic ketoacidosis. AME Case Rep 2019;3: 27. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.