ODP225 Mixed Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Syndrome with recent diagnosis of Diabetes Mellitus.

Abstract

Abstract Background Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemia syndrome (HHS) are often discussed as two distinct clinical entities but can present in the same patient. Combined DKA and HHS is associated with higher mortality than either DKA or HHS alone. Clinical case: A 68 years old female diagnosed with type 2 diabetes 3 months prior to hospitalization was brought into the hospital with severe hyperglycemia and altered mental status. On exam she was unresponsive with grimace only to sternal rub. Pulse was elevated at 113, RR 31, temperature 100.3, and blood pressure 130/80. Initial labs showed severe hyperglycemia with glucose of 1454 (74-106 mg/dL), elevated beta-hydroxybutyrate of 8.6 (0. 02-0.27 mmol/L), sodium 138 (135-145 mmol/L), potassium 5.3 (3.6-5.2 mmol/L), serum bicarbonate 16 (21-32 mmol/L), anion gap 31 (6-18), plasma osmolality 353 (273-304 osm/kg), pH 7.33 (7.35-7.45) and lactic acid 4 (0.7-1.9 mmol/L). DKA protocol with normal saline, intravenous insulin infusion, and potassium replacement initiated and patient was transferred to ICU for further management. Sequential labs revealed development of hypernatremia with calculated free water deficit of 8.8 liters. Fluids changed to ½ normal saline. On Day 2 of hospitalization, she became responsive. She had resolution of acidosis but continued to have severe hypernatremia with peak sodium level of 163 on day 3. Urine studies showed urine osmolality of 700 mOsm/kg ruling out diabetes insipidus; urine sodium level was 5 mmol/L. Fluids were again changed to ¼ Normal saline with careful monitoring of serum sodium and glucose at 2 hour intervals. Hypernatremia resolved with aggressive fluid resuscitation. Her A1c prior to discharge was found to have increased to 13.3% from 6.5% (< 5.6%), 3 months prior. Prior to discharge she had measurable C-peptide, insulin autoantibodies and negative GAD antibodies making autoimmune diabetes unlikely. Conclusion Individuals with concomitant DKA and HHS may have normal sodium or even hyponatremia at presentation due to the pseudo-hyponatremia induced by severe hyperglycemia. However, actual sodium concentration may be markedly elevated due to the osmotic diuresis induced by severe hyperglycemia. Aggressive fluid resuscitation is required to treat the profound dehydration found in HHS but the serum sodium concentration must be monitored carefully. A switch from normal saline to hypotonic fluids may be necessary to treat hypernatremia in HHS but overly rapid correction of serum sodium must be avoided for volume overload especially in elderly, owing to heart failure and due to higher mortality. The incidence of hypernatremia is noted in 14% of children and 27% of adults, however degree of hypernatremia is variable from mild to moderate and in rare instances is severe. Presentation: No date and time listed