Last week I posted a list of topics that we discussed during a 5 day period of rounding.  I was asked to share my teaching points.

We had 2 patients, one who had a normal gap acidosis and one who had an increased anion gap acidosis at admission.  The team did not treat the normal gap acidosis, but did treat the increased anion gap acidosis.  They got it backwards.

This is actually quite straightforward.  Normal gap acidosis always deserves treatment, while increased anion gap rarely requires bicarbonate. Sabatini, S. and Kurtzman, N.A., 2009. Bicarbonate therapy in severe metabolic acidosis. Journal of the American Society of Nephrology, 20(4), pp.692-695.

Metabolic acidosis results from a loss of bicarbonate from the body (e.g., diarrhea) or from its titration to an anionic base that often can be converted back to bicarbonate, such as seen in diabetic ketoacidosis or lactic acidosis (Table 1). This nonbicarbonate base anion is commonly termed “potential” bicarbonate. Giving bicarbonate to a patient with a true bicarbonate deficit is not controversial. Controversy arises when the decrease in bicarbonate concentration is the result of its conversion to another base, which, given time, can be converted back to bicarbonate. If one knew that the timely and efficient conversion of acetoacetate and ?-hydroxybutyrate or lactate back to bicarbonate would occur without morbidity or mortality, then there would be no reason even to contemplate giving bicarbonate.

Rule #1 – bicarbonate deficiency from diarrhea or most renal tubular acidoses will require bicarbonate replacement with a goal bicarbonate of 22 mEq/ml

Rule #2 – try to avoid bicarbonate replacement with anion gap acidoses unless the pH < 7.0  then you provide enough bicarbonate to prevent harm to the patient while you treat the underlying reason for the increased anion gap.