Role of acid-base physiology on the pathogenesis of parturient hypocalcaemia (milk fever)--the DCAD theory in principal and practice.

Abstract

The hypocalcemia associated with the clinical disease known as milk fever is due to a failure of the calcium homeostatic mechanisms in the cow to restore normal blood calcium concentration in a timely manner at the onset of lactation. The defect in calcium homeostasis appears to reside in the sensitivity of bone and kidney tissues to parathyroid hormone (PTH) stimulation. Evidence suggests the acid-base status of the cow dictates the sensitivity of the tissues to PTH stimulation, and that metabolic alkalosis is responsible for blunting tissue PTH responsiveness. Hypomagnesemia can also reduce tissue PTH responsiveness but hypomagnesemia can be corrected in most rations. Excessive dietary potassium is very common and is the most important factor causing metabolic alkalosis in dairy cows. Formulation of rations to reduce metabolic alkalosis and/or induce a compensated metabolic acidosis in the pre-partal cow has proved a useful strategy for prevention of milk fever. The concept of dietary cation-anion difference manipulation and the physiologic effects this can have in the cow are presented, with special emphasis on the Strong Ion Difference theory of acid-base physiology.