Low Blood Calcium Equals High Production

Mark Thomas, DVM, DA BVP

As we continue to generate new data on transition cow metabolism, low blood calcium and clinical milk fever continue to be areas where we gain more knowledge.  However, some of the results don’t necessarily follow our first principle thoughts that low blood calcium at calving is bad.

The definition of milk fever is pretty simple.  It is a down cow suffering from low blood calcium, generally very soon after calving. Clinically these cows will respond rapidly to treatment with IV calcium.  Cows suffering from subclinical hypocalcemia are the cows with low calcium that look normal.  They do not have clinical signs so are therefore “subclinical”.  So how do we define the reference range of what is normal and abnormal for blood calcium?  Many of the reference ranges historically used were just based on average blood calcium readings of “normal, healthy” fresh cows.  We now know that there is room to fine tune these ranges as we gather data from modern, high production cows.

NOT EVERY COW IS THE SAME In practice we can find cows with blood calcium so low they shouldn’t be standing and others that may be considered subclinical that actually show signs of weakness.  Obviously, as we work with the physiology of the cows, there are many variables.  What we do know is that low calcium immediately after calving is not correlated with future disease.  This is contrary to what we thought.  Based on first principles we would think that low calcium is bad, but actually the data shows that the cows with low blood calcium (in the subclinical, not clinical down cow range) immediately after calving produce the most milk.

So low calcium equals high production.  If we think about this a bit, it actually makes sense.  There is lots of calcium in milk (about 56 grams in 100 pounds of milk), so the highest production cows mobilize that calcium from the body to supply the milk.

Low calcium is bad only when the cow can’t recover calcium levels to normal within a few days of calving.  So, if she freshens with low calcium but can increase her dry matter intake (and intake of calcium) and quickly recover blood levels to normal there are no negative consequences.  The cows that fail to return to normal calcium levels in a day or two are a different story.  These are the cows that are at a greater risk of transition diseases such as metritis and DA and also lower lactation milk production.

So how do we prevent low blood calcium in the first place?  There are a number of successful strategies that can be used that have also been proven to be cost effective.

-DCAD rations:  The use of anionic salts is a feeding strategy that has been researched and used successfully for many years.  Of course, it takes additional management in the form of routine close-up cow urine pH measurement and potential ration adjustments, but the benefits are well proven in most herds.  These rations prevent milk fever by acidification of the cow which makes body stores of calcium more available at the time of calving.

-Low-calcium/calcium binder rations:  With the availability of newer calcium binding feed supplements, this appears to be a successful alternative to the DCAD approach.  The concept here is that by feeding low calcium during the close-up period the cow’s metabolism is already in a state of drawing calcium from body stores.  This process is functional right at calving with little to no adaptation and therefore it helps prevent of low blood calcium.

-Oral calcium supplementation: Results of a number of large field trials have shown the health, production and overall economic benefits of calcium bolus use.  In general, the protocol with the greatest economic return is to dose all adult (lactation>1) cattle at freshening and first lactation heifers that are either high body condition (>3.5) or longer days carried calf (>277 DCC).  If this strategy is implemented in a herd, the calculated net benefit is $72/cow/lactation.

DON’T IV STANDING COWS The evaluation of blood calcium status following oral, subcutaneous and intravenous calcium supplementation in subclinical (standing) cows has been evaluated in a few studies.  From this data it is obvious we should not give a standing cow injectable calcium as it provides an oversupply and the cow actually increases her excretion of calcium to get rid of the excess. Blood calcium actually drops lower than it was prior to treatment.  Oral calcium supplements have not been shown to have this effect.  Of course, the down milk fever cow does need IV calcium.

As we continue to research and gain more data, we will be able to fine tune the recommendations and identification of cows that will benefit most from intervention.

But utilizing existing strategies to prevent versus treat hypocalcemia such as ration balancing, feed supplement use and routine oral calcium supplementation, we can reduce the risk of this important and often under-recognized transition cow disease.