Hypocalcemia, or milk fever, occurs when there is not enough calcium in the blood to meet demand. Normal blood calcium levels are between 8.5 and 10 mg/dL and are maintained at those levels through a balance between dietary absorption, bone demineralization, and urinary excretion. After calving, the calcium requirement of the cow increases dramatically due to the increased demand for milk production. To meet this demand, the rates of calcium release from bone and intestinal absorption from the diet are elevated substantially in early lactation. However, milk fever can occur if this adaptation occurs too slowly after calving and blood calcium levels are depleted faster than they are replenished. Milk fever generally occurs within 48 hours after calving and is more common in cows entering their second or greater lactation. Jerseys are also at a greater risk for developing milk fever than Holsteins.
Calcium is required for milk synthesis as well as a host of other normal body functions, such as muscle contraction and nerve-impulse conduction. It is for this reason that the tell-tale clinical symptoms of milk fever include weakness and difficulty standing or walking. However, milk fever can also present in a subclinical form, in which blood calcium levels are low, but cows do not exhibit outward signs of deficiency. Even if incidence of clinical milk fever is low in the herd, the rate of subclinical milk fever is usually much greater. Research suggests that up to half of all cows may be affected by subclinical milk fever. Milk fever (both clinical and subclinical) is considered a “gateway” disease in that its occurrence often precedes other metabolic conditions such as metritis, displaced abomasum, and mastitis.
“Even if incidence of clinical milk fever is low in the herd, the rate of subclinical milk fever is usually much greater.”
Clinical milk fever is often diagnosed through observation of clinical symptoms, such as lethargy, wobbly gait, and difficulty standing. Cows with clinical milk fever may also lay in the sternal position with their head tucked to the side. These cows should be treated with IV calcium and/or oral calcium to reverse symptoms as directed by the herd veterinarian. Unfortunately, on-farm detection of subclinical milk fever is difficult because methods for measuring blood calcium concentration are best-suited for a laboratory setting and are not easily applied on-farm. Blood samples can be collected and submitted to a diagnostic laboratory for analysis of mineral concentrations but it can be several days before results are available.
The concept of dietary cation anion difference, or DCAD, was first studied in dairy cattle in the 1980s. It is defined as the difference between the negatively-charged anions, sulfur and chloride, and the positively-charged cations, potassium and sodium. Researchers in the 1980s learned that increasing the difference between these positively- and negatively-charged ions in favor of negatively-charged anions reduced the occurrence of milk fever in dairy cows. Thus the concept of feeding a negative DCAD diet, or a diet that has a greater concentration of sulfur and chloride relative to sodium and potassium, was born.
Subsequent research has shown that feeding a negative DCAD diet induces mild metabolic acidosis which increases the rate of calcium absorption from the digestive tract and release from bone. Therefore, feeding a negative DCAD diet can actually help prime the cow’s body to begin the naturally-occurring shifts in calcium metabolism before she calves so that she has ready access to sufficient calcium supplies when demands for milk production increase.
A negative DCAD diet should be fed beginning at least 3 weeks before calving to ensure sufficient time for these adaptations in calcium metabolism to occur. If dry cows are all managed as one group, then feeding a negative DCAD diet for the duration of the dry period is acceptable. It can be very difficult implement a negative DCAD diet through manipulation of many common forages, which typically contain high levels of potassium. Because of this, anionic salts, which contain greater levels of sulfur or chloride, are utilized to formulate a negative DCAD diet. One drawback to feeding anionic salts is that they can be unpalatable at high feeding rates and may reduce feed intake if care is not taken.
To be effective, dry cow diets should contain DCAD levels that are between -23 and -68 mEq/lb of dry matter. When anionic salts are used to formulate a negative DCAD diet, monitoring urine pH of cows after they have consumed the diet for 7-10 days can indicate whether it is inducing mild metabolic acidosis as intended. Target urine pH is between 5.5 and 6.0. If urine pH is greater than 6.0, the diet formulation and feeding methods should be reevaluated.
Additional approaches to minimize milk fever occurrence involve increasing calcium intake after calving. Providing cows with an oral calcium supplement, such as a bolus or paste, within a few hours after calving is a common practice that can help restore blood calcium levels. However, this approach may only provide temporary relief from low blood calcium if cows are not yet able to efficiently utilize calcium stores from bone, so several treatments may be necessary.
The old adage, an ounce of prevention is worth a pound of cure definitely holds true here. As with approaches for the management of other metabolic diseases, prevention of milk fever begins during the dry period. Clinical and subclinical milk fever can both pose a substantial threat to long-term cow health, productivity, and profitability. Feeding an effective, negative-DCAD diet during the last 3 weeks of pregnancy remains one of the most effective and widely accepted strategies for reducing milk fever risk after calving.
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