HYPOCALCEMIA IN DOES AND SOWS Parturient paresis in pregnant lactating does & sows is a disturbance of metabolism characterized by acute hypocalcemia & rapid development of hyperexcitability , ataxia , paresis , coma & death. It is also called as milk fever but it is not really a fever at all. Hypocalcemia may be termed as deficiency disease but since the deficiency of Calcium in feed is not the main factor of the disease & there are other causal factors too, the disease is termed as metabolic disease rather than deficiency disease. Etiopathogenesis
The bulk of evidence points to hypocalcemia as the cause of the signs of classical milk fever with hypophosphatemia and variations in levels of serum magnesium playing subsidiary role. Skeletal muscles and plain muscles atony are known physiological effects of hypocalcemia. In experimental hypocalcemia in doe the blood flow was reduced by about 60% to all tissues examined except kidney , heart , lung and bladder in which reduction was not as high. In prolonged cases the blood flow to skeletal muscles and alimentary tract may be reduced to 60-70% of normal blood flow. It results in significant increase in PO2 which suggest s an impairment of oxygen uptake by pulmonary blood flow and an impairment of peripheral tissue uptake of oxygen. Hypocalcemia in late pregnant ewes and sows could induce neonatal hyperthyroidism, hypoinsulinemia and metabolic alterations in their progeny. When hypomagnesemia coexists then relaxation, muscle weakness, depression and coma supervene. Ratio of Ca:Mg may change from 6:1 to 2:1 in hypermagnesemia. Normally serum Mg level rises at kidding and farrowing but in those cases of parturient paresis in which tetany is a feature serum Mg levels are low. Some cases don’t respond to Ca injections even though serum Ca level return to normal but do recover when the udder is inflated and serum P level rise.Low concentration of serum calcium in heavily lactating animals or those with multiple fetuses.Some cases are also complicated by hypophosphataemia & hyper or hypomagnesemia. The disease occurs at any time from 6 weeks before parturition to 10 weeks after due to calcification of fetal bones. The greatest demand for Ca for non dairy animals occurs 3-4weeks prepartum , particularly if more than 1 fetus is present in uterus. Whenever an abrupt calcium demand occurs , the body requires 24-72 hours to activate the metabolic machinery necessary to metbolize stored Ca. High intake of Ca , P or some cations .(Na , K) may decrease the production of parathyroid hormone(PTH).During decreased parathyroid function , less 1-25-dihydroxy cholecalciferol is produced result in lowered absorption & mobilization of Ca from the intestine and bones , respectively. Estrogen also inhibites Ca mobilization. It is antagonist to PTH. Vit.D3 ( cholecalciferol ) is a very important factor. This Vit.D3 is 1st converted to 1, 25 dihydroxy cholecalciferol by enzymes of kidney. The whole process is influence by PTH 1-25 dihydroxy cholicalciferol as activated form of Vit.D3, this activated form acts on the gut cells and helps in absorption from intestine and resorption of Ca from bone. In this way positive Ca balance is maintain in blood. So due to this physiochemical properties Vit.D3 is recently considered as hormone. The normal ratio of Ca and P level in blood is 2.3:1. If this ratio is upset hypo or hypercalcemia may takes place. Some time milk fever is associated with low level of Ca and P in blood. Occasionally , It is associated with low level of Mg++ when the milk fever is associated with hypocalcamia , hypophosphatemia and hypomagnesemia. It is known as “ Milk fever syndrome ” or “ Milk fever complex” Anion-Cation Balance (ACB):
The anion-cation dietary balance exerts a strong, linear effect on the incidence of milk fever. Recent studies indicate that the anion-cation balance in the prepartum diet may be more...
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