Bovine Hypocalcaemia (Milk Fever): In-Depth Welfare Guide

Key Facts

• Milk fever results from calcium mobilization failure at the onset of lactation — demands exceed supply
• Clinical signs progress from early trembling and unsteadiness to recumbency and coma within 6-12 hours
• High-yielding dairy cows in their 3rd+ lactation are most at risk — over 50% of Holstein cows over 7 may be affected
• IV calcium borogluconate treatment reverses signs dramatically — most cows are standing within 20-30 minutes
• Sub-clinical hypocalcaemia (no visible signs) affects many more cows and impairs immune function, fertility, and production

Welfare Considerations

Milk fever causes severe welfare suffering through rapid neurological deterioration. Recumbent cows are unable to rise, pass urine, or avoid injury. Without treatment, progression to coma and death occurs within hours. The welfare window for effective treatment is narrow — prolonged recumbency causes secondary muscle damage (downer cow syndrome) that may be irreversible even after calcium replacement. Sub-clinical hypocalcaemia affects the majority of transition cows to some degree and impairs immune function, making it both a welfare and health risk. Prevention through DCAD (dietary cation-anion difference) management is highly effective and eliminates most clinical cases.

What You Can Do

• Ensure a calcium drench is available on farm for immediate administration at any signs of hypocalcaemia
• Administer IV calcium borogluconate promptly for any cow down after calving — do not delay
• Implement DCAD diets in the dry period to prevent sub-clinical hypocalcaemia across the transition herd
• Monitor all fresh cows for sub-clinical signs: reduced feed intake, dullness, reduced rumen motility
• Target body condition score 3.0-3.25 at calving — over-conditioned cows have higher hypocalcaemia risk