Hyperchloremic acidosis
From Wikipedia, the free encyclopedia
Hyperchloremic acidosis | |
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Classification and external resources | |
ICD-10 | E87.2 |
ICD-9 | 276.2 |
eMedicine | med/1071 |
Hyperchloremic acidosis is a form of metabolic acidosis associated with a normal anion gap, a decrease in plasma bicarbonate concentration, and in an increase in plasma chloride concentration (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
- Renal tubular acidosis failure of HCO3- resorption(i.e., proximal renal tubular acidosis, or overdose of carbonic anhydrase inhibitor) or failure of H+ secretion (i.e. in distal renal tubular acidosis)
- Renal failure
- Gastrointestinal loss of HCO3- with diarrhea (vomiting will tend to cause hypochloraemic alkalosis).
- Ingestions
- Ammonium chloride, Hydrochloric acid
- Hyperalimentation fluids (i.e., total parenteral nutrition)
- Zonisamide [1]
- Acetazolamide
- Alcohol (such as ethanol) can affect anion gap by inducing alcohol dehydrogenase enzyme.
- Volume Resuscitation 0.9% Normal Saline provides a chloride load such that infusing more than 3-4L causes acidosis.
See also
References
- ↑ "Zonegran (Zonisamide) Drug Information: Warnings and Precautions - Prescribing Information at RxList". Rxlist.com. Retrieved 2012-08-21.
External links
- DDB 11673
- NIH - Renal Tubular Acidosis
- 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.
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