Intravenous calcium infusion in a calving protocol disrupts calcium homeostasis compared with an oral calcium supplement.

Hypocalcaemia, which may lead to parturient paresis or milk fever, is a common post-calving metabolic condition in dairy cows, which negatively affects health and production. To prevent the condition, intravenous calcium (Ca) infusions are sometimes introduced at calving to prevent or mitigate the effect of hypocalcaemia in multi-lactation cows. However, intravenous infusion is drastic and not always practical and therefore the question can be posed whether an ordinary Ca supplement cannot be similarly effective. Thus, Dr J. Wilms and colleagues sought to contrast the effect of intravenous Ca infusion against voluntary oral Ca intake on Ca metabolism. There results were published in the Journal of Dairy Science, Volume 102 of 2019, page 6056 to 6064, the title being: Intravenous calcium infusion in a calving protocol disrupts calcium homeostasis compared with an oral calcium supplement.

Serum total Ca (tCa) and whole-blood ionized Ca (iCa) were monitored in 24 multi-lactation Holstein cows after parturition. Pre-calving diets were formulated with a positive dietary cation-anion difference of 172 mEq per kg of DM and contained 4.1 g of Ca per kg of DM. At calving, cows were blocked by calving sequence and blood Ca status as either normo-calcaemic (cut-off threshold of iCa equal or more than 1.10 mmol per L) or hypocalcaemic (cut-off threshold of iCa less than 1.10 mmol per L). Twelve cows in each block were randomly assigned to one of two treatments: either an oral source of Ca (Ca-Oral) or an intravenous source of Ca (Ca-IV). Cows in the Ca-Oral group were offered a 20-L commercial Ca suspension (48 g of Ca) for voluntary consumption. The supplement contained Ca carbonate, Ca formate, Ca propionate, and other minerals and vitamins. Cows in the Ca-IV group received a 450-mL intravenous Ca solution (13 g of Ca) that contained 298 mg per mL of Ca gluconate, 33 mg per mL of magnesium chloride and 82 mg per mL of boric acid. Both treatments were initiated within 25 ± 10 minutes after calving. The oral Ca suspension was offered to cows in a 25-L bucket and was available for 10 minutes. All cows in the Ca-Oral group voluntarily consumed the entire 20 L of the Ca suspension within 5 minutes. Blood samples for Ca analyses were collected at 0 (before treatment initiation), 1, 3, 10 and 18 hours relative to treatment, and at 07:00 and 19:00 hours for the next two consecutive days, to represent the 24-, 36-, 48-, and 60-hour sampling time points. 

In Ca-IV cows, both iCa and tCa concentrations peaked at one hour (1.54 mmol per L for iCa and 2.85 mmol per L for tCa) and declined to a low at 24 hours (0.94 mmol per L for iCa and 1.74 mmol per L for tCa) following treatment initiation. Although whole-blood iCa and serum tCa were higher at one and three hours in Ca-IV cows, concentrations of iCa were greater for Ca-Oral cows at 18, 24, and 36 hours and for tCa at 24 and 36 hours. The data, therefore, indicate that intravenous Ca infusion immediately induced a state of hypercalcaemia followed by lower whole-blood iCa and serum tCa concentrations 24 hours later compared with oral Ca.

In conclusion: The intravenous infusion of Ca at calving induced a marked increase in blood Ca concentration, disrupting Ca homeostasis, whereas administration of oral Ca (from Ca carbonate) did not. Intravenous Ca should therefore not be administered to all animals immediately after calving but should be restricted to severe cases of clinical hypocalcaemia, when animals experience parturient paresis. Further research performed on a larger number of cows is however needed to do a thorough evaluation.