What is hyperchloremic acidosis?

Updated: Oct 18, 2018
  • Author: Sai-Ching Jim Yeung, MD, PhD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
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Answer

This article covers the pathophysiology and causes of hyperchloremic metabolic acidoses, in particular the renal tubular acidoses (RTAs). [1, 2, 3, 4] It also addresses approaches to the diagnosis and management of these disorders.

A low plasma bicarbonate (HCO3-) concentration represents, by definition, metabolic acidosis, which may be primary or secondary to a respiratory alkalosis. Loss of bicarbonate stores through diarrhea or renal tubular wasting leads to a metabolic acidosis state characterized by increased plasma chloride concentration and decreased plasma bicarbonate concentration. Primary metabolic acidoses that occur as a result of a marked increase in endogenous acid production (eg, lactic or keto acids) or progressive accumulation of endogenous acids when excretion is impaired by renal insufficiency are characterized by decreased plasma bicarbonate concentration and increased anion gap without hyperchloremia.

The initial differentiation of metabolic acidosis should involve a determination of the anion gap (AG). This is usually defined as AG = (Na+) - [(HCO3- + Cl-)], in which Na+ is plasma sodium concentration, HCO3- is bicarbonate concentration, and Cl- is chloride concentration; all concentrations in this formula are in mmol/L (mM or mEq/L) (see also the Anion Gap calculator). The AG value represents the difference between unmeasured cations and anions, ie, the presence of anions in the plasma that are not routinely measured.

An increased AG is associated with renal failure, ketoacidosis, lactic acidosis, and ingestion of certain toxins. It can usually be easily identified by evaluating routine plasma chemistry results and from the clinical picture.

A normal AG acidosis is characterized by a lowered bicarbonate concentration, which is counterbalanced by an equivalent increase in plasma chloride concentration. For this reason, it is also known as hyperchloremic metabolic acidosis.

This finding suggests that plasma HCO3- has been effectively replaced by plasma Cl-; hyperchloremic metabolic acidosis arises from one of the following conditions [5, 6] :

  • Bicarbonate loss from body fluids through the GI tract or kidneys, with subsequent chloride retention
  • Defective renal acidification, with failure to excrete normal quantities of metabolically produced acid (whereby the conjugate base is excreted as the sodium salt and sodium chloride is retained)
  • Addition of hydrochloric acid to body fluids
  • Addition or generation of another acid with rapid titration of bicarbonate and rapid renal excretion of the accompanying anion and replacement by chloride
  • Rapid dilution of the plasma bicarbonate by saline

Go to Metabolic Acidosis, Pediatric Metabolic Acidosis, and Emergent Management of Metabolic Acidosis for complete information on these topics.


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