Assessment of metabolic acidosis

The presence of metabolic acidosis is a clue to the possible existence of several underlying medical conditions. Arterial pH <7.35 defines acidosis. Metabolic acidosis is indicated by a decrease in the plasma bicarbonate level and/or a marked increase in the serum anion gap (AG).

Metabolic acidosis may occur due to the following reasons:

1. Addition of strong acid that is buffered by and consumes bicarbonate ion

2. Loss of bicarbonate ion from the body fluids, usually through the GI tract or kidneys

3. Rapid addition to the extracellular fluid of a non-bicarbonate solution.

Differentiating between the causes of metabolic acidosis begins with calculation of serum AG. Serum AG is calculated by subtracting the sum of major measured anions, chloride (Cl-) and bicarbonate (HCO₃-), from the major measured cation, sodium (Na+).

• AG = Na+ - (Cl- + HCO₃-)

Normal serum AG is due to the difference between unmeasured anions such as sulfate (SO₄2-), phosphate (PO₄-), albumin, and organic anions, and unmeasured cations such as potassium (K+), magnesium (Mg+), and calcium (Ca2+). Plasma proteins also play a role in maintaining normal serum AG.[1]Dubin A, Menises MM, Masevicius FD, et al. Comparison of three different methods of evaluation of metabolic acid-base disorders. Crit Care Med. 2007 May;35(5):1264-170. http://www.ncbi.nlm.nih.gov/pubmed/17334252?tool=bestpractice.com

Acute metabolic acidosis, lasting minutes to several days, is relatively common among critically ill patients with reported incidence varying from 6% for more severe acidosis (plasma pH <7.20) to up to 64%.[1]Dubin A, Menises MM, Masevicius FD, et al. Comparison of three different methods of evaluation of metabolic acid-base disorders. Crit Care Med. 2007 May;35(5):1264-170. http://www.ncbi.nlm.nih.gov/pubmed/17334252?tool=bestpractice.com [2]Jung B, Rimmele T, Le Goff C, et al. Severe metabolic or mixed acidemia on intensive care unit admission: incidence, prognosis and administration of buffer therapy. A prospective, multiple-center study. Crit Care. 2011;15(5):R238. https://www.doi.org/10.1186/cc10487 http://www.ncbi.nlm.nih.gov/pubmed/21995879?tool=bestpractice.com [3]Kraut JA, Madias NE. Treatment of acute metabolic acidosis: a pathophysiologic approach. Nat Rev Nephrol. 2012 Oct;8(10):589-601. https://www.doi.org/10.1038/nrneph.2012.186 http://www.ncbi.nlm.nih.gov/pubmed/22945490?tool=bestpractice.com [4]Gunnerson KJ, Saul M, He S, et al. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit Care. 2006 Feb;10(1):R22. https://www.doi.org/10.1186/cc3987 http://www.ncbi.nlm.nih.gov/pubmed/16507145?tool=bestpractice.com Chronic metabolic acidosis, lasting weeks to years, is much less common but its frequency is likely to increase with a rise in chronic kidney disease among older people.[5]Kraut JA, Madias NE. Metabolic acidosis: pathophysiology, diagnosis and management. Nat Rev Nephrol. 2010 May;6(5):274-85. https://www.doi.org/10.1038/nrneph.2010.33 http://www.ncbi.nlm.nih.gov/pubmed/20308999?tool=bestpractice.com