Metabolic acidosis is an acid-base imbalance in the body due to increased hydrogen ion concentration and a reduction in bicarbonate concentration. Patients will have an acidotic, or low, pH (< 7.35), although in cases of mixed acid-base disturbances, patients with an underlying metabolic acidosis may have low, normal, or high pH values. The development of a metabolic acidosis occurs in 1 of the following 4 ways:
Increased acid generation – Lactic acidosis from decreased perfusion or sepsis, ketoacidosis due to poorly controlled diabetes, excess alcohol ingestion or starvation, medication or ingestion adverse effect (eg, methanol, ethylene glycol, diethylene glycol, propylene glycol, aspirin, chronic use of acetaminophen, and toluene).
Increased bicarbonate loss – Profuse diarrhea, proximal renal tubular acidosis (RTA), or loss of ketoacid anions in the urine during ketoacidosis.
Diminished renal acid excretion – Reduced acid secretion in the setting of reduced glomerular filtration rate. This occurs in chronic kidney disease, distal RTA, and type 4 RTA due to tubular dysfunction.
Dilution acidosis – A decrease in serum bicarbonate concentration due to extracellular fluid volume expansion with alkali-free isotonic intravenous (IV) fluid. This only occurs with large-volume infusion of alkali-free isotonic fluid (ie, 5% dextrose solution [D5W]).
Metabolic acidosis can be classified as either normal anion gap or increased anion gap. To calculate the anion gap: [Na] - ([Cl] + [HCO3]) with normal values ≤ 12 mEq/L. To evaluate possible causes of metabolic acidosis with a normal anion gap or hyperchloremic metabolic acidosis, remember the acronym HARDASS:
Below is a list of drugs with literature evidence indicating an adverse association with this diagnosis. The list is continually updated through ongoing research and new medication approvals. Click on Citations to sort by number of citations or click on Medication to sort the medications alphabetically.
