In recent years, doctors and television advertisements have made older women aware of the risks of osteoporosis, a disease resulting from chronic, excessive bone resorption. This cellular "mining" of bone calcium deposits occurs normally and out of necessity in all mammals to support milk production. Most dairy producers do not realize, however, that preventative strategies for milk fever usually require temporary inducement of osteoporosis in their cows.

Here's how milk fever is caused, and how you can manipulate the cow's system to produce more calcium.

Cause of milk fever
The cow adapts to increased calcium needs for lactation by mobilizing more calcium from bones, absorbing more calcium from the gut, and losing less calcium in the urine. As a cow ages and her milk production increases, she cannot absorb calcium from the gut or resorb calcium from bone as efficiently as younger animals. At calving, a typical dairy cow unloads her entire blood pool of calcium into the udder to produce colostrum. When her body cannot "mine" the bone deposits quickly enough, muscles and nerves fail.

Muscles that fail without calcium include those in the uterus, gastrointestinal and urinary tracts, skeletal system, and the heart. A hypocalcemic cow (low in calcium) does not push out calves well, may prolapse the uterus, and often retains the placenta. She may bloat and cease defecation and urination. As blood calcium levels decrease, she cannot stand. In severe cases or when the condition is corrected too quickly, her heart can stop.

As a result of milk fever, other conditions, such as a retained placenta metritis and displaced abomasum, can occur.

Prevention strategies
To limit milk fever on your dairy, help the cows to gear up their blood calcium supplies prior to calving.

During the close-up period (two to three weeks prior to calving), feeding diets that are deficient or low in calcium can stimulate body mechanisms to generate calcium reserves.

Many dairy producers have tried feeding anionic salts. Feeding anionic minerals, such as sulfur and chloride, and limiting cationic minerals, such as sodium and potassium, will lower the cow's blood pH, which sets the calcium-generating process into motion. Among these is acidification of blood which induces a state of bone resorption - just like osteoporosis in women, only temporary.

To measure cations and anions in the ration, nutritionists have designed the dietary cation-anion difference, or DCAD. Because potassium levels vary between forage batches, ration DCAD can swing dramatically. Generally, if the ration DCAD is greater than 25 milliequivalents per 100 grams dry matter or varies above and below this level, anionic salts are recommended. Your nutritionist should re-balance the DCAD every time a new forage is used.

Your role is to monitor urine pH in close-up cows to see how the ration is affecting the DCAD. Using pH paper or a pH meter, test 10 cows every week that have been on the close-up ration for at least three days. The pH should average 6.0, indicating that blood pH has freed up calcium reserves. If not, verify the identity of forages actually used, check feed mixing and sorting, check the ration on paper and monitor feed intake.

In the worst outbreak of milk fever I've seen, 95 percent of mature cows had clinical signs that lasted for days. Everything checked out on paper. Then, we looked at feed inventory. Far-off dry mineral was disappearing faster than expected and close-up mineral had not been used. When the correct mineral was added, the problem took several days to resolve itself.

Marguerita B. Cattell is a consulting veterinarian in Loveland, Colo.

Effect of high potassium levels

The following example shows how the dietary cation-anion difference (DCAD) in a close-up ration without anionic salts can change when the potassium levels (a cation) in the 10 pounds of alfalfa used in the ration varies. Remember, when the base ration is above 25 milliequivalents (meq) per 100 grams of dry matter, a DCAD diet is recommended.

Ration 1 Ration 2
Potassium in hay (percent dry matter) 3.5 2.1
DCAD(meq/100 grams dry matter) 34 23