Hyperchloremic acidosis

Hyperchloremic acidosis
Specialty	Endocrinology, nephrology

Hyperchloremic acidosis is a form of metabolic acidosis associated with a normal anion gap, a decrease in plasma bicarbonate concentration, and an increase in plasma chloride concentration^[1] (see anion gap for a fuller explanation). Although plasma anion gap is normal, this condition is often associated with an increased urine anion gap, due to the kidney's inability to secrete ammonia.

Causes[]

In general, the cause of a hyperchloremic metabolic acidosis is a loss of base, either a gastrointestinal loss or a renal loss.

• Gastrointestinal loss of bicarbonate (HCO⁻
  ₃)
  • Severe diarrhea (vomiting will tend to cause hypochloraemic alkalosis)
  • Pancreatic fistula with loss of bicarbonate rich pancreatic fluid
  • Nasojejunal tube losses in the context of small bowel obstruction and loss of alkaline proximal small bowel secretions
  • Chronic laxative abuse
• Renal causes
  • Proximal renal tubular acidosis with failure of HCO⁻
    ₃ resorption
  • Distal renal tubular acidosis with failure of H⁺
    secretion
  • Long-term use of a carbonic anhydrase inhibitor such as acetazolamide
• Other causes
  • Ingestion of ammonium chloride, hydrochloric acid, or other acidifying salts
  • The treatment and recovery phases of diabetic ketoacidosis
  • Volume resuscitation with 0.9% normal saline provides a chloride load, so that infusing more than 3-4L can cause acidosis
  • Hyperalimentation (i.e., total parenteral nutrition)

See also[]

• Anion gap
• Metabolic acidosis
• Pseudohypoaldosteronism

References[]

Further reading[]

• Kellum JA (February 2002). "Fluid resuscitation and hyperchloremic acidosis in experimental sepsis: improved short-term survival and acid-base balance with Hextend compared with saline". Crit. Care Med. 30 (2): 300–5. doi:10.1097/00003246-200202000-00006. PMID 11889298.

External links[]

• Diseases Database (DDB): 11673
• NIH - Renal Tubular Acidosis