Hyperchloraemic metabolic acidosis
hyperchloraemic acidosis, the anion-gap is normal (in most cases).
But normal anion-gap acidosis is NOT hyperchloraemic acidosis.
e.g. when Na+ is low
1. One possibility is the increase in anions may be too low to push the anion gap out of the reference range
2. Another possibility is intracellular movement of acid anions in exchange for chloride
In lactic acidosis, the movement of lactate intracellularly in exchange for chloride occurs via an antiport.
3. The situation may also be due to the wide normal range of the anion gap
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In general then the diagnosis of a normal anion gap acidosis is just to look for evidence of one of only two mechanisms:
* GIT loss of base
* Renal loss of base
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GIT Bicarbonate Loss
Secretions into the large and small bowel are mostly alkaline with a bicarbonate level higher than that in plasma. Excessive loss of these fluids can result in a normal anion gap metabolic acidosis.
Some typical at risk clinical situations are:
* severe diarrhoea
* villous adenoma
* external drainage of pancreatic or biliary secretions (eg fistulas)
* chronic laxative abuse
* administration of acidifying salts
Severe diarrhoea
This can cause either a metabolic acidosis or a metabolic alkalosis. Development of a significant acid-base disturbance requires a significant increase in stool water loss above its normal value of 100 to 200 mls/day. The more fluid and anions lost, the more marked the problem.
Hyperchloraemic metabolic acidosis tends to be associated with acute infective diarrhoea. This is the classical finding in patients with cholera. The problem is an excessive loss of bicarbonate in the diarrhoeal fluid. Diarrhoeas which are caused by predominantly colonic pathology may cause a metabolic alkalosis: this includes chronic diarrhoeas due to ulcerative colitis, colonic Crohn’s disease and chronic laxative abuse.
The acid-base situation with severe diarrhoea can be complicated by other factors (see Table below) and it may not be possible to completely sort out all the factors in the acid-base disturbance in an individual case.