PATHOPHYSIOLOGICAL ASPECTS OF ACIDOSIS IN DIARRHEIC CALVES

Diarrhoea of moderate to severe intensity in calves of 2 to 28 days pr oduced a marked acidosis with a venous pH <7.30. In very severe cases the pH reduced to life threatening values below 6.85. The causes of ac idosis in calves with diarrhoea are dominated by metabolic disturbance s in acid-base balance. The values for base-excess dropped below -20 m mol/l. The anion gap increased significantly as diarrhoea intensified from 2 to 20 mmol/l, the normal range, to 33+/-10 mmol/l. This indicat ed there was an addition-acidosis and/or a retention-acidosis in these diarrhoeic calves. Lactate played an insignificant or no role in the observed rise in the anion group; the normal plasma lactate concentrat ion is 0.8-1.8 mmol/l and in cases of severe diarrhoea 3.6+/-1.9 mmol/ l. Almost two thirds of 34 calves in the study showed no respiratory c ompensation for their metabolic acidosis. In addition one quarter of t he calves had a mixed respiratory-metabolic acidosis, with a reduced b ase excess and an increased pCO(2). No obvious signs of respiratory di sease were present on clinical examination. Under these conditions of disturbed acid-base equilibrium in diarrhoea, buffers traditionally us ed in veterinary practice such as lactate, acetate or equivalent bases are of no or only limited use compared with sodium bicarbonate. In co ntrast, buffers without production of CO2 in the body are advantageous for the effective treatment of acidosis.