Milk fever

[7] In this stage, lateral recumbency,[8] muscle flaccidity,[5] unresponsiveness to stimuli, and loss of consciousness progressing to coma are observed.

When the mammary drain of plasma calcium causes hypocalcemia severe enough to compromise neuromuscular function, the cow is considered to have clinical milk fever.

It is believed that hypocalcemia causing milk fever is due to a lower level of responsiveness of the cow's tissues to circulating parathyroid hormone.

This generally involves close attention to mineral and fiber levels in the diet prior to calving, as well as improving cow comfort to eliminate other problems that may interfere with appetite (and so trigger hypocalcemia).

[9] A synthetic analogue of 25-hydroxycholecalciferol can be given by injection in the days leading up to calving, although the timing of this prophylaxis makes it difficult to use.

[10] An orally administered bolus containing a much higher concentration of calcium than the injectable solutions can also be given so long as the cow is standing or sitting up.

Defecation, urination and eructation are frequent during the treatment, due to pharmacological effect of calcium on the smooth muscles.

[13] In 1901, Anderson and Evers trialled a treatment of udder inflation with air, which reduced mortality rates to just 1%.

[16] Although this was an effective treatment (and is still used as a backup today),[11] it was not understood at the time why it worked, and remains the source of some debate.

[17] Other scientists suggested that udder inflation prevented milk secretion, reducing calcium loss overall.

[18] The true cause of milk fever was first suggested by Prof John Russell Greig and Henry Dryerre in March 1925,[13] at the Moredun Research Institute in Scotland.