Perspective: Transient postparturient hypocalcemia—A lactation-induced phenomenon of high-producing dairy cows

Abstract

Milk fever is one of the most historically relevant diseases of dairy cows. It is caused by tremendous calcium (Ca) expenditure at the initiation of lactation, so severe that cows can no longer stand and, if left untreated, die. Fortunately, through prepartum nutritional improvements, this version of clinical hypocalcemia is rare in the United States. Nonetheless, the opinion that all versions of postpartum hypocalcemia are detrimental remains pervasive, which is particularly significant given that 50% of cows are subclinically hypocalcemic after calving. This has led to a variety of available management and treatment strategies, ranging from prepartum dietary programs to postpartum Ca gels and boluses, targeted at preventing hypocalcemia in dairy cows. Recent research has determined that postpartum dairy cows can experience different types of subclinical hypocalcemia: transient, persistent, or delayed. We now know cows experiencing transient hypocalcemia as part of the homeorhetic adaptation to lactation are the highest milk producers in modern dairy herds, whereas cows with hypocalcemia several days after calving experience disease and losses in milk production. Therefore, it is wrong to assume all postpartum hypocalcemia is detrimental and that treatment of all cases is considered necessary and beneficial. Research indicates that milk synthesis at the onset of lactation contributes to immediate postpartum hypocalcemia, and that the mammary gland is a critical factor in management of Ca homeostasis. However, cows differ in their ability to manage this phenomenon, and it is possible that immediate postpartum influences such as dry matter intake, inflammation, and immune activation affect appropriate Ca regulation in the days following calving.