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Metabolic acidosis occurs frequently in small children. The most common causes are hypoxia, sepsis, gastroenteritis and hypovolaemia. Calculation of the anion gap is useful in establishing the cause. An increased anion gap represents unmeasured anions, e.g. lactate in lactic acidosis. Metabolic acidosis was diagnosed in two boys aged one year and six weeks respectively. The first patient had a normal, the second an increased anion gap in blood. By determining the pH and the anion gap in urine it is possible to distinguish between a proximal and a distal tubular disease. The first patient had distal renal tubular acidosis; he recovered after correction of the acidosis. The second patient had a defect in the mitochondrial respiratory chain; he died at the age of seven months.

A 2-year-old Friesian mare was examined because she had been sluggish for a few weeks. Blood biochemistry showed that concentrations of creatinine (136 mumol.L-1) and urea nitrogen (6.1 mmol.L-1) in plasma were within their normal limits. Severe metabolic acidosis was apparent; the venous pH was 7.154 and the bicarbonate concentration was 13 mmol.L-1. The base excess amounted to -15.3 mmol.L-1 and the venous pCO2 measured 5.1 kPa. Plasma sodium was normal (135 mmol.L-1) and plasma chloride (113 mmol.L-1) was slightly elevated, but there was a hypokalaemia (2.9 mmol.L-1). The urine had a specific gravity of 1.040 and a pH of 5. These findings indicated type 2 renal tubular acidosis. The blood values returned to normal 3 days after treatment with sodium bicarbonate as a 4.2 per cent solution (3.2 mol in total) and additional bicarbonate (125 g) and potassium chloride (100 g) administered orally.