Acidosis-induced hypochloremic alkalosis in diabetic ketoacidosis confirmed by the modified base excess method

Abstract

Context and Objective: Diabetic ketoacidosis (DKA) is associated with a metabolic alkalosis, which is thought to be due to vomiting. However, alkalosis can occur in DKA without vomiting. We retrospectively reviewed the acid-base disturbances in DKA admissions without vomiting. Participants and Methods: We included admissions of the patients with blood glucose and betahydroxybutyrate (βOHB) levels≥250 mg/dL and≥1.0 mmol/L, respectively. Admissions without vomiting were classified into a group with a βOHB ≥3.0 mmol/L (DKA group) and a group with βOHB of 1.0-3.0 mmol/L (pre-DKA group). The acid-base status was analyzed by the modified base excess (BE) method. BE effects were calculated by changes in sodium (BE free water, [BEFW]), and chloride (BECl). Positive and negative values for each parameter suggested alkalosis and acidosis, respectively. Results: Forty-five included admissionsweredivided intoDKA(n=34)andpre-DKA(n=11) groups. Sodium-corrected chloride level and the chloride/sodium ratio were significantly lower in the DKA group than in the pre-DKA group. In both groups, BEFW values were modestly negative. The mean BECl values were positive in both groups, but significantly higher in theDKAgroup. The alkalinizing effects by hypochloremia diminished the base deficit in theDKAgroup by approximately 25%. The BECl value significantly correlated with serum total ketone levels (r =0.66; P ≤.0001). Conclusion: The modified BE method successfully proved the presence of hypochloremic alkalosis in DKA without vomiting. This suggests the direct participation of serum ketoacids in the pathogenesis of hypochloremic alkalosis.