Milk Fever (Etiology, pathogenesis, clinical signs, diagnosis, treatment, and control)

A disease of adult female bovine occurring around the parturition and caused by hypocalcemia, characterized by weakness, recumbency, paresis, shock, and death.

Incidence of milk fever

• 5-10 yrs age group most commonly affected

• High prevalence during 3 rd – 7th calving

• Jerseys breed is the most susceptible than other breeds.

• High susceptibility when animals are fed with high protein diet before and after calving.

• No specific seasonal occurrence 

• Complete milking in first 48 hrs- precipitating factor 

• Certain families within the breed – more susceptible

• Cases may occur during the last few days of pregnancy and immediately after parturition. 

• Majority cases occur within 72 hours postpartum 

• Acid – diet decreases the incidences 

• Alkaline diet increases the incidence

Factors precipitating occurrence of milk fever

• Failure of mobilization of Ca to circulation from body reserves 

• Depletion of reserves by the development of negative Ca balance in late pregnancy

• Increased estrogen levels – interfere with Ca mobilization from bone 

• Hypomagnesaemia – decrease Ca mobilization from bone 

• Coliform mastitis – toxin decreases serum Ca and P levels


In normal calcium regulation, a decrease in plasma calcium levels causes the parathyroid glands to secrete parathyroid hormone(PTH), which regulates the activation of vitamin D3 in the kidney. These two compounds act to increase blood calcium levels by increasing absorption of dietary calcium from the intestine, increasing renal tubular reabsorption of calcium in the kidney, and increasing resorption of calcium from bones.

It has been found that tissue is less responsive to parathyroid hormone prepartum, compared to postpartum and the hypocalcemia causing milk fever is due to a lower level of responsiveness of the cow’s tissues to circulating parathyroid hormone.

The resultant decreased plasma calcium causes hyperexcitability of the nervous system and weakened muscle contractions, which result in both tetany and paresis.

Clinical signs

Clinical signs of milk fever vary with the stage of the disease

I Stage – prodromal stage 

• Excitement and tetany 

• Hypersensitiveness 

• Muscular tremor of head and limbs 

• Disinclined to eat and move 

• Grinding of teeth 

• Protruding tongue 

• Stiff hind limb 

• Animals ataxic and falls easily

II Stage – Sternal recumbency 

• Sternal recumbency with lateral kink 

• No tetany but unable to get up 

• Muzzle – dry 

• Skin and extremities – cold 

• Temperature – Subnormal (97-101ºF)

• Pupil – dilated – no reflex 

• Eyes – disparity in the size of pupils staring and dry – pupillary light reflex decrease or absent 

• Relaxation of anus and loss of anal reflex-dung in the rectum 

• Circulatory system – decrease heart sound – veins cannot be raised 

• Weak pulse, ruminal stasis, forced expiratory grunt

III Stage – Lateral recumbency

• Lateral recumbency 

• Coma 

• Limbs – flaccid, unable to get up 

• Pulse – impalpable 

• Heart sounds – inaudible 120/min 

• Unable to raise the vein 

• Bloat if without treatment – animal dies within a period of 12 – 24 hrs 

• Milk fever with hypomagnesemia and hyperphosphatemia 

• Tetany and hypersensitiveness beyond 1st stage 

• Excitement and fibrillary and twitching of the eyelids 

• Tetanic convulsion by touch or sound 

• Trismus 

• Heat and respiratory rate-accelerated 

• Heart sound – increased 

• Death occurs  due to respiratory failure

Reproductive tract

• Dilated cervix, normal presentation of fetus, uterine prolapse, dystocia, retained placenta


• Characteristic clinical signs

• Sign related with serum levels of Ca, Mg, P

• Estimation of serum levels of Ca, Mg, P

• Ketosis (concurrent) – animal rise  after Ca therapy but continue to have  signs of ketosis

• Ischemic muscle necrosis (Degenerative myopathy)

  • Post mortem – pale muscle surrounded by normal color
  • SGOT increase

• History of access to plants rich in oxalates


• Treatment during I stage – ideal

• Longer the interval between recumbency and treatment, the greater the incidence of downer cow due to ischemic muscle necrosis

• Temperature > 39ºC – an indication of existing complication – the higher mortality rate

• To be placed in sternal recumbency until the treatment ends to avoid aspiration pneumonia. 

• Calborogluconate 500 ml to 1 liter – 3 g/10 lb,  50% i/v,  50% s/c 

• Shifting to the non-slippery ground or pure rubber mat 

• Do not milk for 6 hours. 

• Do not urge the cow to stand too soon


Dose of Calcium 

• 1 gm Ca / 45kg (100 lb) 

• 25 % calcium borogluconate = 10.4 gm /500ml 

• Cattle – 400-500ml i/v , 100-200 gm s/c

• Goat- 15-20 gm i/v, 5-10 g s/c

Response to Calcium  therapy 

• Belching

• Muscle tremor – flanks→ whole body

• Pulse rate   decreases and amplitude improves

• Heart sound intensity is increased 

• Sweating of muzzle

• Defecation – firm stool with mucous

• Urination does not follow until the cow rises

• Wait for 5-8 hrs until it stands. If not repeat the dose 

• If it doesn’t stand after 24 hrs – use hip lifters.

Unfavorable Response to Calcium therapy

• Cardiac irregularities

• Heart rate increased

• Shallow respiration.


Dietary management during the transition period

• Feed low Ca (<20 g Ca /day) and  normal level of P for 2 weeks before parturition

• Avoid drastic change in the diet (3 or 4 days for a change)

• Dietary cation-anion difference program

Parenteral vitamin D and analogs

• Vitamin D2 20-30 million units/day for 3-7 days antepartum (predicting the date of parturition is a problem)

• 1, 25 (OH2)D3 – 10,000 IU i/m / 24 hrs prior to parturition. If no delivery repeat at 24 hrs interval 270 mg until delivery

Calcium gel oral dosing before calving, at calving, and 12 and 24 h after calving 

• CaCl2 40-50 g