Bedside detection of urine β-hydroxybutyrate in diagnosing metabolic acidosis

Objectives: While critically important, the rapid identification of the etiology of metabolic acidosis (MA) may be labor-intensive and time-consuming. Alcoholic, starvation, and severe diabetic ketoacidosis (AKA, SKA, and DKA, respectively) may produce beta-hydroxybutyrate (BOHB) in marked excess of acetone (ACET) and acetoacetate (AcAc). Unfortunately, current urine dipstick technology poorly detects ACET and cannot measure BOHB. The inability to detect BOHB might delay therapy for ketoacidoses or provoke unnecessary evaluation or empiric treatment of other causes of MA, such as toxic alcohol poisoning. The authors tested the previous assertion that commonly available hydrogen peroxide (H(2)O(2)) would improve BOHB detection. The effectiveness of alkalinization and use of a silver nitrate (AgNO(3)) catalyst was also assessed. Methods: Control and urine test specimens containing from 0.5 to 800 mmol/L ACET, AcAc, and BOHB were prepared. Urine specimens were oxidized with H(2)O(2) (3%) 1:9 (H(2)O(2):urine), alkalinized with potassium hydroxide (KOH; 10%), exposed to AgNO(3) sticks, or altered with a combination of these methods in a random fashion. Three emergency physicians (EPs) blinded to the preparation technique evaluated urine dipsticks (Multistix, Bayer Corp.) placed in the specimens for ketones. Results: Multistix detected AcAc appropriately; ACET was detected only at high concentrations of >= 600 mmol/L. Multistix failed to measure BOHB at all concentrations tested. H(2)O(2) improved urinary BOHB detection, although not to clinically relevant levels (40 mmol/L). Alkalinization and AgNO(3) sticks did not improve BOHB detection beyond this threshold. Conclusions: Addition of H(2)O(2) (3%), alkalinization, or AgNO(3) sticks did not improve clinically meaningful urine BOHB detection. Clinicians should use direct methods to detect BOHB when suspected.