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