What are the serum chemistry findings in alcoholic ketoacidosis (AKA)?

Updated: Aug 27, 2020
  • Author: George Ansstas, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
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The anion gap is elevated. Lactate levels may be elevated. An elevated lactate level (usually does not exceed 3 mmol/L) may result from dehydration or seizure or could be the direct metabolic effect of alcohol.

Hyponatremia and hypokalemia are common laboratory findings in patients with AKA. Vomiting and extracellular volume depletion may cause hyponatremia. Hypokalemia is often associated with hypomagnesemia.

Hypomagnesemia may be caused by poor nutrition, decreased renal absorption of magnesium, or nasogastric suctioning. Serum magnesium levels are not reliable indicators of total body magnesium stores, however. Due to the linked excretion between potassium and magnesium, the presence of hypokalemia is a strong indicator of hypomagnesemia and can be used as a surrogate test to determine if magnesium replacement is needed.

True hypocalcemia associated with hypomagnesemia may be present. Concomitant pancreatitis also may contribute to true hypocalcemia. Factitious hypocalcemia can result from a markedly decreased serum albumin level following prolonged malnutrition with alcoholism.

Phosphate levels may be low, normal, or elevated. Ethanol-enhanced urinary excretion, emesis, and antacid use may contribute to hypophosphatemia in people who have chronic alcoholism.

Hyperuricemia is commonly observed; it results from decreased renal perfusion, tissue catabolism, competitive inhibition of renal uric acid excretion by ketone bodies, and direct ethanol enhancement of adenine nucleotide degradation. In a study of alcoholic Japanese men aged 40 years or older, Yokoyama et al suggested that the development of hyperuricemia was associated with quicker ethanol and acetaldehyde metabolism by those who had both the ADH1B*2 allele and the ALDH2*1/*1 genotype and with greater levels of ketosis. [25]

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