Hyperchloremic acidosis
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| 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[edit]
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
- Proximal renal tubular acidosis with failure of HCO−
- 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[edit]
References[edit]
- ^ "Hyperchloremic Acidosis: Practice Essentials, Etiology, Patient Education". 2017-10-19.
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Further reading[edit]
- 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. S2CID 24375350.
External links[edit]
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