MON-549 - Not All Is Needed: Diabetic Ketoacidosis Masked by Hemodialysis and Vomiting

Introduction:
Diabetic ketoacidosis (DKA) is an endocrine emergency and remains a significant cause of morbidity and mortality worldwide. Despite advances in diabetes management, DKA continues to pose diagnostic and therapeutic challenges, underestimating the importance of early recognition and prompt treatment. Here, we highlight an interesting case of normal bicarbonate in the setting of DKA.

Case Presentation:

We present this case of a 48-year-old woman with a history significant for type 1 diabetes mellitus status post pancreatic transplant (2010), end-stage renal disease due to diabetic nephropathy status post failed renal transplant 2010, on three times weekly hemodialysis, and hypertension, who presented with acute altered mental status. The patient was lethargic and unresponsive (AAOx0). She had several days of nonbilious vomiting, with over 10 episodes on the day prior to presentation, accompanied by lower abdominal pain. Similar prior episodes had been associated with hypoglycemia; however, home glucose readings this time were in the 400s. She had been using short-acting insulin without taking her basal insulin for two days. She is anuric and missed two dialysis sessions the prior week. She was reportedly alert on arrival to dialysis but became acutely altered one hour into treatment. In the Emergency Department, the patient was found to be in DKA with a B-hydroxy of 3.38 mmol/L, glucose 270 mg/dl, venous blood gas pH of 7.38, and a normal bicarbonate of 24mmol/L with an elevated anion gap of 30. The patient was emergently dialyzed and started on an insulin drip. Although formal diagnostic criteria for DKA (blood glucose >200 mg/dl, pH < 7.3/ bicarbonate < 18 mmol/L, and beta-hydroxybutyrate >3 mmol/L/ urine ketones >2) were not met, the patient’s overall clinical picture warranted prompt recognition and management. Given the history of recent vomiting and dialysis session on the day of presentation, acidosis was likely normalized with these two factors.



Conclusion:
This case illustrates masked acidosis in the presentation of DKA, attributable to recent hemodialysis and vomiting. Dialysate fluid itself carries a higher concentration of bicarbonate than blood itself. Therefore, when blood flows past the semi-permeable dialysis membrane, bicarbonate diffuses from the dialysate into the blood while hydrogen ions and other acidic waste products diffuse into the dialysate. This increases serum bicarbonate and raises blood pH, therefore correcting metabolic acidosis. Vomiting will also increase pH by the excretion of hydrogen ions, inducing a metabolic alkalosis with a higher-than-expected serum bicarbonate. Recognition of DKA in this setting requires a high index of suspicion and careful evaluation of the overall clinical picture, rather than reliance on diagnostic criteria alone.

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