HYPOCALCEMIAIN

DAIRY CATTLESophie RosevearJess Neal

Tara HallAlex Doddridge

Introduction 99% of a cow’s calcium is stored in the skeleton. Calcium is essential for many physiological processes;

neuromuscular function, blood clotting and hormonal secretion. Failure to maintain calcium homeostasis (hypocalcaemia, milk

fever, parturient paresis) affects productivity of the cows and profitability of the dairy industry.

Calcium homeostasis is stressed in dairy cattle as their main function is to produce high milk yields. Also, during the transition period the demand for calcium dramatically increases.

Calcium Homeostasis Cows can only obtain calcium from dietary sources

and absorb calcium through the epithelial cells of the small intestine.

Calcium is removed from the body through: Urine Faeces, and Milk production.

Plasma calcium levels should be 8.5-10 mg/dL for a healthy adult cow. This is regulated by intestinal and renal absorption, and bone turnover.

Calcium is removed from the body via urine and faeces and is also lost through milk production.

Calcium Homeostasis II A decline in calcium levels stimulates the

parathyroid gland to release parathyroid hormone (PTH). This increases calcium reabsorption from the glomerular filtrate.

PTH also triggers production of 1 α-hydroxylase which converts circulating vitamin D to 1,25-dihydroxyvitamin D.

Calcium Homeostasis III When the calcium levels return to normal, the

secretion of PTH decreases via a negative feedback loop.

Calcitonin is secreted by the thyroid in response to calcium levels increasing beyond the ‘setpoint’.

Osteocytic osteolysis is stimulated if both the demand for calcium and the PTH levels remain high.

Calcium Homeostasis IIII

Development of hypocalcaemia

Dairy cows: Lactate for 10 months of the year. Pregnant from about 3 months into lactaction (3 monthas after last

calving). Calve once a year, 8 weeks into their dry period.

During the ‘dry period’, calcium levels required for foetal growth are quite low compared to the demands of lactation.

The onset of lactation requires a high level of calcium, this can cause an imbalance from the high output of calcium in the colostrums and the influx of calcium to maintain the plasma levels.

Development of hypocalcaemia II

~50% of adult dairy cows develop subclinical hypocalcaemia within the first few weeks of lactation.

5-20% of dairy cows each year will not adapt and recover calcium balance.

This is a severe metabolic disease known as milk fever and normally occurs 12-24 hours after parturition, but can occur several weeks before and after.

Prolonged release of PTH increases reabsorption of calcium (intestinal, renal and bone).

Clinical signs and pathology of disease

Initially: Anorexia Listlessness Muscle weakness

Body temperature declines

Sternal recumbancy

Clinical signs and pathology of disease II

“Crush Syndrome” If parturient, the birthing process is suspended. Weak pulse and heart sounds, tachycardia. Loss of consciousness with body temperature as

low as 32°C. Death can occur within hours without treatment.

Predisposing factors

Age

Breed

Metabolic Alkalosis

Hypomagnesia

Control (Prevention)

The Dietry Cation-Anion Difference (DCAD) Method Reduce dietry cations, increase anions Lowers blood

pH Feed a calcium deficient diet

Decreases plasma calcium Higher dietry magnesium

Maintains adequate levels of Magnesium in the blood.

Effect of DCAD

Source: Horst et al. 2005 (full ref in reference list)

TreatmentTreat as early as possible. Fastest: IV injection of Calcium salts  (commonly Ca

borogluconate). Administer the Ca at a rate of 1 g/min

Subcutaneous injection Blood flow is often compromised, so absorption is

variable A single subcutaneous site should be limited to 1–

1.5 gCa (50–75 mL).  Intramuscular administration

Limited to 0.5–1.0 g Ca/injection site to avoid tissue necrosis.

Oral treatments are not reccomended.

Conclusion Hypocalcaemia in dairy cows is an economically

important disease. Loss of production Cost of control Treatment measures.

It reduces a dairy cow’s productive life. Prevention is better than cure complications are

difficult to prevent once the clinical signs are present.

Future research will bring a greater understanding of the regulatory mechanisms and control of calcium homeostasis in the dairy cow.

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