The typical reaction will be a generalized tremor of the skeletal muscles, and sometimes cardiac arrhythmia. Defecation, urination and eructation are frequent during the treatment, due to pharmacological effect of calcium on the smooth muscles. Prognosis
The prognosis is generally good, even in advanced cases. However, some cows can relapse the following day, and even a third time the day after. Without treatment, between 60% and 80% of cows usually die, although death rates as high as 90% have been recorded. History
It is thought that milk fever has existed for a very long time in dairy cattle. The first reports in veterinary literature can be traced to around 1793. Early Theories
Early treatments involved venesection, but this proved ineffective. Potassium Iodide
In the late 1800s, Jurgens Schmidt proposed the use of an infused solution of potassium iodide for treatment. A follow-up study of this treatment by Danish veterinarians showed that 90% of cows recovered after use of the treatment, compared with only 20-40% survival without. A study in Iowa showed that 76.5% of cows recovered after use of the treatment. However, the premise of the Schmidt treatment was misleading, as later veterinarians used water alone to the same success rate. Udder Inflation
In 1901, Anderson and Evers trialled a treatment of udder inflation with air, which reduced mortality rates to just 1%. although with the added complication of mastitis. Although this was an effective treatment (and is still used as a backup today), it was not understood at the time why it worked, and remains the source of some debate.
Cause
During the dry period (late gestation, non-lactating), dairy cattle have relatively low calcium requirements, with a need to replace approximately 30 g of calcium per day due to utilization for fetal growth and fecal and urinary losses. At parturition, the requirement for calcium is greatly increased due to initiation of lactation, when mammary drainage of calcium may exceed 50g per day. Due to this large increase in demand for calcium, most cows will experience some degree of hypocalcemia for a short period following parturition as the metabolism adjusts to the increased demand. When the mammary drain of plasma calcium causes hypocalcemia severe enough to compromise neuromuscular function, the cow is considered to have clinical milk fever. Mechanism
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. It is believed that hypocalcemia causing milk fever is due to a lower level of responsiveness of the cows 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. Prevention
Diet
Proper dietary management will prevent most cases of milk fever.