Causes

• Tissue hypoperfusion, e.g. heart failure, hypovolaemia, sepsis. The anion gap is related to production of lactic and other organic acids. Anaerobic metabolism contributes in part to this metabolic acidosis although other cellular mechanisms are involved.

• Hyperchloraemia, e.g. excessive saline infusion.

• Ketoacidosis — high levels of p-hydroxybutyrate and acetoacetate related to uncontrolled diabetes mellitus, starvation and alcoholism.

• Renal failure — accumulation of organic acids, e.g. sulphuric.

• Drugs — in particular, aspirin (salicylic acid) overdose, acetazolamide (carbonic anhydrase inhibition), ammonium chloride. Vasopressor agents may be implicated, possibly by inducing regional ischaemia or, in the case of epinephrine, accelerated glycolysis.

• Ingestion of poisons, e.g. paraldehyde, ethylene glycol, methanol.

• Bicarbonate loss, e.g. severe diarrhoea, small bowel fistulae, large ileostomy losses.

• Type B lactic acidosis — no evidence of tissue hypoperfusion.

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