SUN-LB031 An Atypical Case of Diabetic Keto-Alkalosis with Severe Hypernatremic Hyperosmolarity in a Patient with Amphetamine Abuse

Introduction- Acid base disturbances have a complex interplay in Diabetic Ketoacidosis (DKA). Substance abuse in DKA is associated with more severe metabolic acidosis with higher acidosis-ketosis gap. Severe hypernatremia and alkalosis are rare in DKA but were exhibited in our case. Case- A 31-year-old female with Type 1 diabetes and schizophrenia was hospitalized after she was found to be minimally responsive at home. She had abdominal pain and polyuria since few days and wasn’t compliant with her medications. There was no history of vomiting, diarrhea, alkali ingestion, laxative or diuretic use. On admission, she was severely dehydrated, obtunded and only responsive to painful stimuli. Initial biochemical findings: serum glucose 1323 mg/dl (n 70-140 mg/dl), sodium 135 mEq/L (n 136-148 mEq/L, corrected sodium 154, bicarbonate 32 mEq/L (n 22-28 mEq/L), serum osmolality 379 (n 275-295 mOsm/Kg), beta hydroxybutyrate 62.56 mg/dl (n <=4.17 mg/dl), anion gap 30 (n 12-16) and delta gap of 24. Venous blood gas showed: pH-7.40 (n 7.31-7.41), pCO2-62 (n 41-51), HCO3-38.4 (23-27). She was adequately managed and was fully awake and alert with closed anion-gap within 24 hours of admission. Serum sodium initially peaked to 163 but normalized over the next 36-42 hours. She was also admitted with HHS (Hyperglycemic Hyperosmolar State) 3 months before and 1 month after this admission. Urine drug screen was positive for amphetamines in all 3 admissions. Discussion- Our patient exhibited mixed metabolic acidosis (elevated anion gap, ketonemia), metabolic alkalosis (elevated bicarbonate, elevated delta gap) and compensatory respiratory acidosis. Osmotic diuresis due to glycosuria and amphetamine abuse led to severe volume depletion and bicarbonate reabsorption leading to severe contraction alkalosis. Studies have shown that methamphetamine use leads to elevated plasma cortisol and corticosterone levels via hyper-activation of the hypothalamic-pituitary-adrenal axis. Ecstasy use has been shown to cause an acute increase in cortisol levels of around 150% in sedentary humans and 800% in dance clubbers. Excess glucocorticoids promote Hᶧ secretion from kidneys via mineralocorticoid receptors contributing to alkalosis. DKA/HHS patients usually present with eunatremia/hyponatremia. Adult schizophrenics who receive psychostimulants have been shown to develop polydipsia and hyponatremia. Ecstasy intoxication can precipitate both DKA and hyponatremia in Type1 diabetics. Combined DKA/HHS and hypernatremic hyperosmolarity has been reported due to huge intake of sugar-rich carbonated beverages to quench thirst especially in pediatric population. There is frequent association between decompensated diabetes and illicit drug use. Substance abuse should be suspected in young Type 1 diabetics presenting with recurrent hyperglycemic emergencies especially with atypical biochemical features. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. Abstracts presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.