THU379 A Case Of Hyperglycemia With Severe Anion Gap Metabolic Acidosis: HHS Vs DKA

Disclosure: M. Shrivastava: None. B.J. Armendariz: None. U. Asija: None. A. Shah: None. M. Levy-kern: None. D. Klamp: None. Background: DKA is more profoundly associated with metabolic acidosis secondary to excessive ketones production in the setting of low insulin. Whereas HHS is associated with hyperglycemia with mild acidemia because ketone production is not as severe, as insulin is high/normal. We present a case of hyperglycemic state which challenged this stereotype. Clinical Case: 57 YO male with no prior history of DM or CKD presented with altered mental status, abdominal pain, 15lbs weight loss. As per wife, patient had URI and his condition had been deteriorating since then. Initial labs revealed leukocytosis, BUN 105, serum creatinine 5.8, Anion gap 37, and blood glucose (BG) 1433mg/dl. Blood Gas significant for pH 7.1, PCO2 20, PO2 138, bicarbonate 7.8, and Lactic acid 1.5. Further testing revealed Urine ketone 15, Serum beta-hydroxybutyrate 0.5 mmol/l, HbA1c 13%, serum Osmolarity 391mOsm/kg. Treatment was initiated with 0.9% NS, electrolyte replacement, and IV insulin infusion. Serum glucose corrected at 50-75mg/dl/hr unmasked underlying hypernatremia. Fluid was switched to 0.45% NS with dextrose 5%. Despite BG correction, patient’s mentation remained altered. Further imaging including MRI brain was negative for osmotic demyelination syndrome. Eventually, BG came below 200mg/dl, and acidemia resolved. Pt was transitioned to subcutaneous insulin. Mentation started improving. Clinical Lesson: T1DM and T2DM are Insulin deficient vs insulin resistant states respectively[1]. Insulin deficiency causes decreased intracellular consumption of glucose, triggering intracellular starvation, promoting lipolysis in presence of stress hormones like glucagon, Norepinephrine, and cortisol[2]. Free fatty acids, produced from lipolysis undergo beta-hydroxylation forming ketones. Hence, metabolic acidosis in DKA is secondary to ketoacidosis. HHS is seen in insulin-resistant states, with normal/high serum insulin. Insulin promotes lipogenesis, hence HHS has minimal ketoacidosis, and is rarely associated with AGMA. Both DKA and HHS are hyperosmolar states most commonly triggered by infections[3], but in HHS, osmolarity generally exceeds 320mmol/l, free water deficit is more profound. This reflects severe dehydration, decreased intravascular volume, tissue hypoperfusion, possibly end organ damage including AKI[4], and in severe cases present as Acute renal failure(ARF)[4][5][6]. Hyperosmolarity can itself induce rhabdomyolysis and thus AKI[5][6]. In our case, ARF caused elevated BUN, decreased acid secretion from renal tubule, worsened acidosis, and presented as AGMA, mimicking DKA. In such situations measuring serum beta-hydroxybutyrate and C-Peptide can differentiate the two conditions. Hypernatremia and dysregulated osmolarity pose risk of osmotic demyelination syndrome. It is pertinent to correct AGMA, osmolarity, and hyperglycemia concurrently. Presentation: Thursday, June 15, 2023