EXCESS FEEDING OF CALCIUM OR HYPERCALCEMIA IN DAIRY CATTLE

Calcium requirements of lactating dairy cows are high relative to other species or to nonlactating cows because of the high calcium concentration in milk. Thus, inorganic sources of calcium, such as calcium carbonate or dicalcium phosphate, must be added to the rations of lactating dairy cows. For the first 6–8 wk of lactation, most dairy cows are in negative calcium balance, ie, calcium is mobilized from bone to meet the demand for milk production. This period of negative calcium balance does not appear to be detrimental so long as there is sufficient dietary calcium such that bone reserves can be replenished in later lactation. The availability of dietary calcium for absorption varies with dietary source. Dietary calcium from inorganic sources is generally absorbed with greater efficiency than that from organic sources. Furthermore, cows in negative calcium balance absorb calcium more efficiently than cows in positive calcium balance.

When calculating calcium requirements, newer nutritional models take into account the variability in calcium availability from different sources. This availability generally ranges from 75%–85% for inorganic calcium supplements to a low of 30% for forage sources of calcium. This approach makes it difficult to generate general recommendations for total dietary calcium concentrations across various diets. Generally, diets with large portions of forage from legume sources will have minimum calcium concentration requirements in the range of 0.71%–0.75%, while diets with forages from primarily grass (including corn silage) sources will have minimum calcium concentration requirements in the range of 0.42%–0.47%.

Two approaches are taken with respect to the calcium supply for dry cows, each with the objective of preventing milk fever, or parturient paresis .

One approach is to place cows in a calcium-deficient state during the last 2–3 wk of gestation; the rationale is to stimulate parathyroid hormone secretion and skeletal calcium mobilization before calving. This makes calcium homeostatic mechanisms more responsive at the time of parturition, allowing cows to maintain serum calcium concentrations during lactation. This approach requires diets with calcium concentrations near 0.3% of dry matter. Such diets are difficult to formulate with available feedstuffs while still meeting other nutritional requirements. Another approach is to feed an acidifying diet, usually referred to as a diet with a low or negative dietary cation-anion difference (DCAD). The low-calcium diet approach is not additive with the DCAD approach to milk fever prevention. When low-DCAD diets are fed, total dietary calcium concentrations should be near 0.9%, which is substantially greater than the requirement for a dry cow on a conventional diet.

Phosphorus nutrition for lactating dairy cows has dynamics similar to those of calcium. The efficiency of phosphorus absorption is affected by physiologic state and dietary source. As is the case with calcium, most dairy cows in early lactation are in negative phosphorus balance. Phosphorus mobilized from bone early in lactation is replaced during later lactation when feed intakes are higher. Young animals and animals in negative phosphorus balance absorb phosphorus more efficiently than do older animals or animals in positive phosphorus balance. Phosphorus from inorganic sources is more available than that from organic feed sources.

Judiciously balancing diets to meet, but not exceed, phosphorus requirements is important for dairy cow performance and environmental stewardship. Excess phosphorus excreted in feces is one of the major pollutant risks associated with livestock production. Newer nutritional models account for variation in phosphorus availability from different sources, but there is less variation in availability among phosphorus sources than among calcium sources. In general, concentrates when fed to ruminants have a phosphorus availability of 70%, and forages close to 64%. Inorganic mineral supplements are usually rated at 75%–80% availability, but rock phosphate is very low, ~30%. Total dietary phosphorus concentration requirements for most dairy diets will be in the range of 0.35%–0.4%, and for dry cows, 0.3%–0.35%. Phosphorus supplementation for dry cows is seldom necessary.

The dietary calcium:phosphorus ratio is not of particular importance in ruminants. Ratios from 7:1 to 1:1 are acceptable, so long as the total amount of each element meets the dietary requirements.

Serum concentrations of calcium and inorganic phosphorus are of value in assessing the short-term homeostasis of these minerals but of little value in assessing longterm nutritional status. Bone ash concentrations are the best way to assess longterm calcium and phosphorus nutritional status.

Usually hyper calcemia in the dairy cattle occur after multiple treatments by quacks/ paravets/ vets to recently calved cows leading to increased serum calcium concentration.

Animal recumbent, lies the head to the ground, unable to get up, cessation of rumination and urination, highly depressed or semi comatosed. Auscultation revealed MUFFLED HEART SOUND and 32-40 BEATS PER MINUTE, shallow respiration.

Based on symptoms, and history of having treated with many bottles of calcium intravenously and/or oral to milk fever condition.

Usually misdiagnosed as ketosis, toxaemia and non-responding milk fever.

Good.

Carefully drench 750 ml and after 2 hours 400 ml of Antacid (Digene). Antacid inhibit calcium absorption from gut. Observe the animal every hour. Within 6 hours the animal get up and urinate.

In cattle, major source of calcium is from alimentary tract absorption. Even though there is more serum calcium, the absorption from GI tract is also simultaneously occurring. The drenched antacid forms a coating over the mucosal layer of GI tract and thus prevents the calcium absorption. Within 6 hours of oral antacid, the serum calcium level is spontaneously reduced by deposition in bone and physiological elimination through urine.

Hypercalcemia is a total serum calcium concentration > 10.4 mg/dL (>2.60 mmol/L) or ionized serum calcium > 5.2 mg/dL (> 1.30 mmol/L). Principal causes include hyperparathyroidism, vitamin D toxicity, and cancer. Clinical features include polyuria, constipation, muscle weakness, confusion, and coma. Diagnosis is by measuring serum ionized calcium and parathyroid hormone concentrations. Treatment to increase calcium excretion and reduce bone resorption of calcium involves saline, sodium diuresis, and drugs such as zoledronate

In mild hypercalcemia, many patients are asymptomatic. Clinical manifestations of hypercalcemia include constipation, anorexia, nausea and vomiting, abdominal pain, and ileus. Impairment of the renal concentrating mechanism leads to polyuria, nocturia, and polydipsia. Elevation of serum calcium > 12 mg/dL (>3.00 mmol/L) can cause emotional lability, confusion, delirium, psychosis, stupor, and coma. Hypercalcemia may cause neuromuscular symptoms, including skeletal muscle weakness. Hypercalciuria with nephrolithiasis is common.

Less often, prolonged or severe hypercalcemia causes reversible acute kidney injury or irreversible kidney damage due to nephrocalcinosis (precipitation of calcium salts within the kidney parenchyma).

In severe hypercalcemia a shortened QTcinterval is shown on ECG, and arrhythmias may occur, particularly in patients taking digoxin. Hypercalcemia >18 mg/dL (> 4.50 mmol/L) may cause shock, renal failure, and death.