This document summarizes hypocalcemia in goats and sows. It describes the condition as acute hypocalcemia around the time of parturition, characterized by nervous system signs like ataxia and recumbency. Causes include low serum calcium due to heavy lactation demands, low parathyroid function, and estrogen effects. Treatment involves calcium supplementation, such as calcium borogluconate intravenously. Prevention focuses on dietary calcium intake and vitamin D supplementation in the weeks before parturition.

1. Mo.Shahid Saiyed
Rakesh Kumar
Devang Bhatt
Ashish Mehra

2. Hypocalcemia in Goat &
female pig

3. Hypocalcemia 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.

4. 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.

5. •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 “

6. 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.

7. •When hypocalcaemia is linked with normal Mg the patient
paddles with the hind legs, becomes recumbent, may or may
not get up, finally, becomes paretic and coma supervenes.
•When the hypocalcaemia is linked with a hypomagnesemia
the patient shows tetany of fore leg and hind legs,
hyperesthesia and may become recumbent followed by
convulsion. Hypomagnesaemia inhibits mobilization of Ca
from bone.

8. CLINICAL 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

9. •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

10. 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.

11. •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.

12. 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.

13. 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.

14. •Treatment
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.

15. •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 :
•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.

16. Some preparation available to cure
hypocalcemia

17. •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 :
• PTH, thyroxin, thyrocalcitonin hormone are necessary but
hormonal therapy is not done.
•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

18. •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.

19. Prevention
1.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.

20. Thank You
Questions??