What are miscellaneous etiologies of 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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The administration of calcium chloride (CaCl2) or cholestyramine (cationic resin that is given as its chloride salt) may cause acidosis because of the formation of calcium carbonate or the bicarbonate salt of cholestyramine in the lumen of the intestine, which is then eliminated in the stool.

Ureteral-GI connections, such as ureterosigmoidostomy for urinary diversion, also cause a potentially severe acidosis in virtually all patients. [10] This acidosis results from the retention of urinary ammonium across the colonic mucosa and from the stool losses of bicarbonate. Because of this complication, ileal conduits have now largely replaced the procedure. However, hyperchloremic metabolic acidosis still occurs in approximately 10% of patients with ileal conduits, especially if obstruction is present.

The occurrence of metabolic acidosis with a normal AG is common in the late phase of diabetic ketoacidosis (DKA). This results from urinary loss of ketoanions with sodium and potassium. This external loss is equivalent to a loss of potential bicarbonate because each ketoanion, if retained and metabolized, would consume a proton and generate a new molecule of bicarbonate.

Infusion of large volumes of solutions containing sodium chloride and no alkali can cause a hyperchloremic metabolic acidosis. This is due to a dilution of the preexisting bicarbonate and to decreased renal bicarbonate reabsorption as a result of volume expansion.

In patients with a chronic respiratory alkalosis, renal acid secretion is decreased but endogenous acid production and chloride reabsorption are normal, resulting in a decreased plasma bicarbonate concentration and elevated chloride concentration. When the hypocapnia is repaired, the return of the PaCO2 to normal unveils a transient metabolic acidosis, which will self-correct shortly.

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