Mo.Shahid SaiyedRakesh KumarDevang BhattAshish Mehra

Hypocalcemia in Goat & female pig

Hypocalcemia in goats&sowsHypocalcemia in goats&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 it is metabolic disease rather than deficiency disease.

Etiopathogenesis:Etiopathogenesis:

•Low concentration of serum calcium in heavily lactating animals or those with multiple fetuses.

•Some cases are also complicated by hypophosphataemia & hyper or hypomagnesemia.

•Decreased parathyroid function.

•Estrogen also inhibits Ca mobilization.

•Vit.D3 ( cholecalciferol ) is a very important factor. This Vit.D3 is 1st converted to 1, 25 dihydroxy cholecalciferol by enzymes of kidney.

The normal ratio of Ca and P level in blood is 2.3:1.

• It is associated with low level of Mg++ when the milk fever is associated with hypocalcaemia, hypophosphatemia and hypomagnesemia. It is known as “ milk fever syndrome “ or “ milk fever complex “

Anion-Cation balance (ACB):Anion-Cation balance (ACB):

•The anion-cation dietary balance exerts a strong, linear effect on the incidence of milk fever. •Prepartum diet high in cation•while diets high in anion especially chloride or sulphur are associated with a decrease in incidence of diseases.

•Most forages such as legumes and grasses are high in K and are alkaline.

•When hypocalcaemia is linked with normal Mg the patient When hypocalcaemia is linked with normal Mg the patient paddles with the hind legs, becomes recumbent, may or may paddles with the hind legs, becomes recumbent, may or may not get up, finally, becomes paretic and coma supervenes.not get up, finally, becomes paretic and coma supervenes.

•When the hypocalcaemia is linked with a hypomagnesemia When the hypocalcaemia is linked with a hypomagnesemia the patient shows tetany of fore leg and hind legs, the patient shows tetany of fore leg and hind legs, hyperesthesia and may become recumbent followed by hyperesthesia and may become recumbent followed by convulsion. Hypomagnesaemia inhibits mobilization of Ca convulsion. Hypomagnesaemia inhibits mobilization of Ca from bone.from bone.

CLINICAL FINDINGSCLINICAL FINDINGS

•The onset is sudden and almost invariably follows within 24 hour an abrupt change of feed , a sudden change in weather or short period of fasting imposed by circumstances such as shearing, crutching or transportation.

•Early signs include a stilty, propy gait and tremor, Particularly of shoulder muscles. Recumbency follows with the tetany of limbs•The charecteristic posture is sternal recumbency with the legs under the body or stretched out behind

•Mental depression is evidence by drowpy appearance and depression of corneal reflexes

•Response to parentral injection of Ca salts is rapid, the doe being normal 30 minutes after a subcutaneous injection. Death after occur within 6-12 hour if treatment is not administered.•The syndrome is usually more severe in pregnant does than in lactating ones, possible because of the simultaneous occurance of pregnancy toxemia or hypomagnesaemia

•Fat late pregnant does on high grain diet indoors or in feedlots. Show a similar syndrome accompanied by prolapse of vagina and intestine

Clinical Pathology:•Total serum Ca level in does 3.8 ± 0.6 mg/dl ( 0.94 ± 0.15 m.mol/lit.) is reduce to bellow 2 mg/dl.

•The sulkowitch test based on detection of Ca in the urine, is not an accurate guide to the ca status of the animal. A rapid semi-quantitative test based upon the amount of sodium ethylene diamine tetra acetate ( EDTA ) required to prevent clotting of blood sample and hence the approximate Ca concentration seems worthy a trial as field test for Ca concentration in serum. •Clinico-pathological findings are not described in details except for depression of total serum Ca level.

•Blood glucose level is usually normal although this may be depressed if ketosis occurs constantly. Higher than blood glucose level are libery to occur in case of long duration and all therefore an indication of a poorer than normal prognosis.

•Serum inorganic P level is usually depressed. Some times there is no change in it.

•Change in leucocyte count include eosinophilia, lymphopenia, neutrophilia suggestive of adrenal cortical hyperactivity. High plasma cortisol levels and PCV occurs.

Swine : Swine :

•Signs develops within a few hour of farrowing. There is restlessness, a normal temperature, and anorexia followed by inability to rise and later lateral recumbency and coma.

•The signs may stimulate a condition known as mastitis, metritis, agalactia complex

•The signs of such complex will include swollen mammary glands, uterine discharge and loss of appetite followed by toxemia.

Diagnosis: Diagnosis:

•Diagnosis is based on history and clinical science.

•A tentative diagnosis of acute hypocalcemia can be confirmed readlly by a dramatic and usually lasting response to Ca therapy.

•Biochemical examination of blood is also helpful.

•TreatmentTreatment Replacement therapy Replacement therapy ::•CBG i/v (50-150 ml of 23% solution) ( 1 g/45 kg body weight)

•Ca gel p.o. or s/c administration of Ca solution prevent relapse.

•During treatment the heart should be monitored, and therapy slower or stopped if arrhythmia. •An alternative mode of therapy would be to add 50-150 ml of 23% CBG solution to 1 liter of 5% dextrose solution.

•The more hypoglycemia an animal is ( i.e. the worse the clinical signs are) the more cardiotoxic the I/v administered Ca becomes. So in this case 10% MgSO4 solution (100-400 ml) is injected S/C.

•CBG is given when hypocalcemia is associated with hypomagnesemia and hypophosphatemia.

•Supplimentation therapy : Supplimentation therapy :

•Given complete full dose of Ca along with Iodide of sodium acid phosphate +4 oz glucose I/V. sodium acid phosphate lowers the blood pH and thus helps in the absorption of Ca.

Some preparation available to cure Some preparation available to cure hypocalcemiahypocalcemia

•Corrective therapy Corrective therapy • If the animal is recumbent for a considerable period of time there will be ruminal bloat resulting in to cardiac trouble and asphyxia. In this case antihistaminic should be given.

•Hormonal therapy Hormonal therapy :• PTH, thyroxin, thyrocalcitonin hormone are necessary but hormonal therapy is not done.

•Udder inflation :Udder inflation :• Udder inflation act by preventing the further secretion of milk slowing down the excretion of Ca and P. thus it raises blood plasma Ca

•Miscellaneous therapy : Miscellaneous therapy :

•Sancal vet injection : 2 ml thrice/week. I/M at 6-8hrs before parturition and 3ml I/M after parturition.

•Ammonia chloride : It prevents reoccurrence of hypocalcemia in animal which suffered previously. Dose:- 2-3 g over last few week of pregnancy increasing to 10 g/day at kidding or farrowing orally t.i.d.

Prevention1.Dietary modification.2. Immidiately after parturition the calcium level in diet should be increased.3. Movement , periods of inadequate dietary intake , heavy parasitic burden or other forms of stress should be minimized during final 8 weeks of gestation.4. Administration of ammonium chloride 3 weeks before parturition is usefull.5. Use of vit.D3 and its metabolites.6. Oral calcium gel dosing ( 50% calcium chloride is to be given to prevent milk fever)7. Parathormone -60 hours before parturition i/v or 6 days before parturition i/m.

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