HYPOCALCEMIA

IN
DAIRY CATTLE
Dr A. Murondoti (BVSc,
MSc,PhD
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
 .
PREDISPOSING FACTORS
 Breed-Jersey, Swedish red and white and
Channel Island are more susceptible
 Susceptibility linked to fewer intestinal
receptors
 Milk production level
 Lactation number
 Age
 Feeding regime
ASSOCIATION WITH OTHER DAIRY DISEASES

 LDA and RDA

 Mastitis
 Retained fetal membranes
 Uterine prolapse
 Ketosis
 Dystocia
 Metritis, Endometritis (Immunosuppresion)
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
 Definition & Mechanism
 Ca homeostasis
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 SIGNSchanism
 Signs
 Low milk
 Excitement stage
 Restlessness, hypersensitivity, tremors, S-shape neck, teeth
grinding, stiff gait, and fall easily, protrude tongue,
salivation
 Sternal recumbancy
 Recumbancy, neck turned into flank, hypothermia, increased
heart rate but with decreased intensity, dry muzzle, dilated
pupil, ruminal stasis and constipation
 Lateral recumbancy
 Limbs stuck out, hypothermic, die within 12-24 hrs
Treatment
Treat 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.
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.
Prevention
Calcium Chloride
Acidogenic salt which lowers blood ph and
make issue more responsive to PTH
Calcium propionate
Propionate part useful in hepatic
Gluconeogenesis
Hydrochloric acid
Source of anions which have acidifying effects
Prevention contd
Vit D and Parathyroid hormone
Not helpful because of negative
feedbackmechanisms and cow may fail to
recover from hypocalcemia
DCAD
Effect of DCAD

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

 Dietary Management
1. DCAD
 How it affects milk fever?
 If anions > cations  acidic blood 
 ↑ PTH
 ↑ responsiveness to PTH
 ↑1, 25(OH)2D3 (↑ intestinal absorption)
 ↑ ostoclast resorption

 If cations > anions  alkaline blood 

 Opposite to above
 Dietary Management
2. Adding dietary anions
 Used when it is hard to decrease dietary Ca
 Do not use when Ca intake is low (< 100 g)
 Palatability problems
 Cl- and SO4- salts of Ca, ammonium, Mg
 S is not recommended (why? Toxicity, not
documented)
 Phosphate salts is not recommended (why? Weak
acidifier, weak absorption, inhibit renal synthesis of
1,2(OH)2D3)
 Dietary Management
1. DCAD
 Dietary Management
3. Removing dietary cations
 Be careful not to go below requirements
 Support: diet low in Na & K prevented milk fever
 Alfalfa use should be limited if it contains high K
 Dietary Management
1. DCAD
 http://ahdairy.com/our-products/dcad-balancers/dcad-calculator.aspx

 Target
 Transition period: -50 to -100 meq/kg DM
 Fresh, lactation: +200-300+ meq/kg DM
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.
References
Bigras-Poulin, M. & Tremblay, A. 1998, ‘An epidemiological study of calcium metabolism in non-paretic
postparturient Holstein cows’, Preventive Veterinary Medicine vol. 35, pp. 195-207
El-Samad, H., Goff, J.P. and Khammash, M. 2002, ‘Calcium homeostasis and parturient hypocalcaemia:

An integral feedback perspective’, Journal of Theoretical Biology vol. 214, pp. 17-29

Goff, J.P. 2008, ‘The monitoring, prevention, and treatment of milk fever and subclinical hypocalcaemia

in dairy cows’, The Veterinary Journal vol. 176, pp. 50-57

Goff, J.P., Reinhardt, T.A. and Horst, R.L. 1991, ‘Enzymes and factors controlling vitamin D metabolism

and action in normal and milk fever cows’, Journal of Dairy Science vol. 74, no. 11, pp. 4022-4032
Goff, J.P., Ruiz, R. and Horst, R.L. 2004, ‘Relative acidifying activity of anionic salts commonly used to

prevent milk fever’, Journal of Dairy Science vol. 87, pp. 1245-1255

Hamali, H. 2008, 'Post estrus hypocalcemia in a repeat breeder half-breed holstein cow', Journal of

Animal and Veterinary Advances vol. 10, pp. 1301-1304

Horst, R.L. (1986), ‘Regulation of calcium and phosphorus homeostasis in the dairy cow’, Journal of

Dairy Science vol. 69, pp. 604-616

Horst, R.L., Goff, J.P. and Reinhardt, T.A. 1994, ‘Calcium and vitamin D metabolism in the dairy

cow’,Journal of Dairy Science vol. 77, pp. 1936-1951

Horst, R.L., Goff, J.P. and Reinhardt, T.A. 2005, ‘Adapting to the transition between gestation and

lactation: Differences between rat, human and dairy cow’, Journal of Mammary Gland Biology and
Neoplasia vol. 10, no. 2, pp. 141-156
 Kimura, K., Reinhardt, T.A. and Goff, J.P. 2006, ‘Parturition and hypocalcaemia blunts calcium signals in immune
cells of dairy cattle’, Journal of Dairy Science vol. 89, pp. 2588-2595
 Lean, I. J., DeGaris, P. J., McNeil, D. M. and Block, E. 2006, 'Hypocalcemia in dairy cows: meta-analysis and
dietary cation anion difference theory revised', Journal of Dairy Science vol. 89, pp. 669-684
 Oba, M., Oakley, A.E. and Tremblay, G.F. 2011, ‘Dietary Ca concentration to minimise the risk of hypocalcaemia
in dairy cows is affected by the dietary cation-anion difference’, Animal Feed Science and Technology  vol. 164,
pp. 147-153
 Peacock, M. 2010, ‘Calcium Metabolism in Health and Disease’, Clinical Journal of the American Society of
Nephrology vol.5, pp. s23-s30
 Radositis, O.M., Gay, C.C., Hinchcliff, K.W. and Constable, P.D. (2007), 'Veterinary Medicine - A textbook of the
diseases of cattle, horses, sheep, pigs and goats,' Saunders Elsevier, worldwide (Sydney)
 Reinhardt, T. A., Lippolis, J. D., McCluskey, B. J., Goff, J. P. and Horst, R. L. 2011, 'Prevalence of subclinical
hypocalcemia in dairy herds', The Veterinary Journal vol. 188, pp. 122-124
 Ramberg, C.F., Johnson, E.K., Fargo, R.D. and Kronfeld, D.S. 1984, ‘Calcium homeostasis in cows, with special
reference to parturient hypocalcaemia’, America Journal of Physiology vol. 246, no. 15, pp. R698-R704
 Schenck, P. A. and Chew, D. J. 2008, 'Hypocalcemia: A Quick Reference', Veterinary Clinic Small Animal vol. 38,
pp. 455-458
 Shahzad, M. A. and Mahr-un-Nisa, M. S. 2008, 'Influence of varying dietary cation anion difference on serum
minerals, mineral balance and hypocalcemia in Nili Ravi buffaloes', Livestock Science vol. 113, pp. 52-61