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HYPOCALCEMIA

HYPOCALCEMIA

Pathophysiology

The normal blood calcium concentration in adult cows is between 8.5 and 10 mg/dl, which translates into a total plasma pool of only about 3 g in a 600-kg individual. It is evident that to meet the calcium needs of colostrums production, fetal maturation, and incipient lactation at the end of gestation (collectively these requirements may reach 30 g/day), adult cows will need to mobilize substantial amounts of calcium from bone and increase the efficiency of gastrointestinal tract absorption. Intestinal absorption of calcium is heavily dependent on the production of 1,25-dihydroxyvitamin D3 by the kidney in response to parathormone (PTH) secretion. The third component of calcium homeostasis, namely, enhanced renal absorption of calcium, is quantitatively very small in terms of its contribution to increased calcium availability in the transitioning adult cow. Regulation of calcium homeostasis within plasma levels that maintain critical muscular, nervous, and other cellular functions is achieved through the action of PTH. The normal physiologic response to decreasing calcium levels is to produce PTH, which acts to increase osteoclastic bone resorption (direct PTH effect), increase intestinal absorption (via 1,25-dihydroxyvitamin D3), and enhance renal tubular resorption of calcium. PTH secretion is exquisitely sensitive to small decreases in plasma calcium, but the response can be blunted by hypomagnesemia, partly explaining the well-documented link between clinical hypomagnesemic tetany and hypocalcemia, even in nonlactating cattle. There are several other important factors that interfere with PTH activity at a tissue level that can serve to blunt the individual’s ability to respond efficiently to the increased demands of lactation, despite appropriate PTH secretion. Perhaps the most important factor, and one that has been the subject of a great deal of interest and research in recent years, is the role that acid-base status plays. Metabolic alkalosis predisposes to both milk fever and subclinical hypocalcemia principally because it interferes with skeletal calcium resorption and intestinal absorption by conformationally altering the PTH-receptor interaction at the tissue level. By altering this interaction, downstream signaling events that should result in increased plasma calcium do not occur despite PTH secretion. The first observations that dietary acidification could reduce the incidence of hypocalcemia by Ender and Dishington in 1971, and the subsequent exploitation of this paradigm by many researchers such as Oetzel and Goff, have led to the widespread practice of anionic salt supplementation to the diets of dry cows as a means by which milk fever and subclinical hypocalcemia rates can be reduced because of relative acidification of cattle in late gestation. It is worth noting that strong univalent cations, such as potassium and sodium, probably influence the development of milk fever via their alkalinizing effects and subsequent diminished tissue responsiveness to PTH, far more than does calcium in the diet during the late dry and early lactational period. Low calcium diets can theoretically be fed as a means of reducing milk fever incidence because prolonged exposure to high PTH levels can overcome the negative effects of alkalinization on tissue responsiveness; however, these prolonged and low calcium diets are impractical to formulate and deliver.

 

There are other factors that contribute to the development of hypocalcemia in dairy cattle, specifically age, breed, and endocrinologic factors such estrogen levels. With increasing age there is a reduced pool of calcium available for absorption from bone as a result of diminishing numbers of bone cells, and this is a reason why heifers, in whom osteoblastic activity is high, do not suffer from clinical milk fever. A further age-related change is the reduction in PTH receptors in peripheral tissues of older cattle. It has long been observed by practitioners that the incidence of milk fever is higher in Jersey cattle than in Holsteins, and although the absolute explanation for this is uncertain, two factors that likely contribute to this breed predilection are the higher calcium concentration in colostrum and milk from Jerseys and the lower number of intestinal receptors for 1,25-dihydroxyvitamin D3 within the breed compared with Holsteins. Although estrogens increase predictably in the last few days of gestation and this hormone has a negative effect on calcium mobilization from bone, it does not appear to be a significant contributor to the incidence of milk fever nor the severity of hypocalcemia.

Clinical Signs

Parturient hypocalcemia or milk fever may occur from about 24 hours before to 72 hours after parturition. The initial signs are restlessness, excitability, and anorexia.

Many cows at this stage will protrude their tongue when stimulated around the head. This activity otherwise only occurs in cows as a displacement activity when they would rather kill you or run away but cannot. The ability to regulate core temperature is gradually lost. Therefore rectal temperature will be either high or low depending on ambient temperature. Cutaneous circulation is depressed, leading to cool extremities when the ambient temperature is less than 68.0° F/20.0° C. Rumen contractions will progress from weak to absent. Skeletal muscle weakness develops over several hours. Cows may stagger or fall but more commonly are found down and unable to rise. Heart rate increases during the development of hypocalcemia, yet cardiac output decreases as a result of reduced venous return and weaker cardiac muscle. Bloat occurs because of failure to eructate. Death may occur within 12 hours of the onset of signs caused by suffocation secondary to bloat or cardiovascular collapse. Historically texts have divided hypocalcemia into three stages, with stage 1 characterized by the cow still being able to stand, stage 2 by recumbency, and stage 3 by coma and unresponsiveness.

Treatment

Parenteral administration of calcium borogluconate has been the most common treatment of hypocalcemia for many years worldwide. Concentrations of calcium, calcium salt formulations, and other elemental and carbohydrate components within the infusion solution vary widely according to personal preference and the perceived needs of the cow. There is no doubt that treatment with calcium borogluconate solutions IV or SQ leads to rapid recovery of skeletal muscle tone and smooth muscle function in the gastrointestinal tract. Cows often will eructate, defecate, or urinate during the IV administration of calcium, and many truly uncomplicated cases of stage 2 hypocalcemia are capable of standing before or shortly after the infusion is finished. Individuals with stage 3 hypocalcemia may take longer to generate the ability to stand unassisted but are still frequently able to stand within minutes of receiving IV calcium. Cattle that are recumbent on slippery surfaces such as concrete free stall alleys should be moved or slid to good footing. This procedure may help prevent exertional myopathy and other musculoskeletal injuries that are common to hypocalcemic cows that struggle to rise on slippery surfaces.

Serum calcium concentration is normally between 8.5 and 10 mg/dl. The degree of hypocalcemia that develops at parturition is not perfectly correlated with the clinical signs. At a level of 7 mg/dl, most cows will be able to stand but have moderate bloat and anorexia. At a level of 5 mg/dl, most cows will be down. At levels less than 4 mg/dl, most cows will be comatose. A standard 500-ml bottle of 23% calcium borogluconate contains 10 g of calcium. A mature Holstein in good condition weighing 700 kg will have about 210 L of extracellular fluid. If her calcium level is 5 mg/dl, her calcium deficit is 10.5 g. Thus one standard bottle of calcium will increase serum calcium to 10 mg/dl. Most practitioners will give all or part of a second bottle of calcium, perhaps giving it SQ, to provide extra calcium for anticipated ongoing losses. The heart rate normally decreases to some degree during infusion of IV calcium solutions to hypocalcemic cows. A sudden increase in heart rate or arrhythmia that develops during infusion may require slowing or stopping the infusion.

Calcium solutions to be administered IV should be warmed to body temperature before administration. SQ treatment alone is inadequate for down cows because of the slow rate of absorption with impaired circulation.

Oral gels and liquids have become increasingly available and utilized by producers for treatment and/or prevention

of hypocalcemia. Among the simple calcium salts, only calcium chloride has proven to be adequately bioavailable for therapy of clinical milk fever. Liquid forms of calcium chloride, when given as a drench to down cows, tend to be highly caustic and have caused aspiration pneumonia and death. The use of oral calcium supplements requires functional swallowing reflexes to prevent these caustic materials from entering the trachea such that the severity of hypocalcemia and muscle weakness should be assessed in an individual before their use.

Increasingly, calcium propionate has been incorporated into drench mixtures given to early lactation cows that are off feed. A total of 1.5 lb of calcium propionate administered orally provides approximately 140 g of calcium, whereas 1 lb provides approximately 90 g of calcium and calcium propionate has the advantage of also providing an energy source (propionate) and not being caustic. Evidence-based research suggests that the relapse rates and clinical response of true milk fever cases to oral calcium administration compare favorably with those seen with conventional IV therapy. However, personal clinician and farm experience often dictates that IV calcium administration is elected for the treatment of recumbent milk fever cases, but on many dairies, calcium administration to anorectic cows that may only be mildly hypocalcemic has moved completely to the oral route.

In the majority of uncomplicated cases of milk fever, a single treatment is all that is required. Should relapse occur, consideration should be given to supplementing magnesium in addition to calcium. A convenient method for supplementing magnesium for an individual is to use magnesium hydroxide rumen laxative boluses or magnesium oxide for a few days after parturition. Excessive use may cause systemic alkalosis and decrease ionized calcium.

Practitioners vary in their advice of complete milk out of mature cows at risk of milk fever. Partial milk removal may lessen the development of hypocalcemia.

However, cows not fully milked out may leak milk and be predisposed to environmental mastitis.

 

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HYPOCALCEMIA

The normal blood calcium concentration in adult cows is between 8.5 and 10 mg/dl, which translates into a total plasma pool of only about 3 g in a 600-kg individual. It is evident that to meet the calcium needs of colostrums production, fetal maturation, and incipient lactation at the end of gestation (collectively these requirements may reach 30 g/day), adult cows will need to mobilize substantial amounts of calcium from bone and increase the efficiency of gastrointestinal tract absorption.

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