Milk fever

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Bovine 'milk fever' (or parturient paresis) is an acute to subacute, afebrile paralysis of mature dairy cows that occurs most commonly at or soon after parturition.

Cause

Milk fver is triggered by a sudden loss of circulatory calcium due to sudden losses into the colostrum and milk. Serum calcium levels decline from a normal of 8.5–10 mg/dL to 2–7 mg/dL. Commonly, serum phosphorus is decreased, and cows are hyperglycemic. The disease may be seen in cows of any age but is most common in high-producing dairy cows entering their third or greater lactation. Incidence is higher in the Jersey breed[1].

Most dairy cows exhibit different degrees of hypocalcaemia around calving because the gestational Ca requirements shift to the disproportionately high Ca requirements of lactation. Ca homeostasis is a robust system that effectively adapts to changes in Ca demand or supply. However, these adaptations often are not rapid enough to avoid hypocalcaemia. A delay in the reconfiguration of intestinal Ca absorption and bone resorption is probably the underlying cause of this transient hypocalcaemia[2].

Clinical signs

Milk fever can be confused with other causes of downer cow syndrome, toxic mastitis, toxic metritis, other systemic toxic conditions, traumatic injury (eg, stifle injury, coxofemoral luxation, fractured pelvis, spinal compression), calving paralysis syndrome (damage to the L6 lumbar roots of sciatic and obturator nerves), or compartment syndrome. Some of these diseases, in addition to aspiration pneumonia, may also occur concurrently with parturient paresis or as complications.

Affected cows are often reluctant or unable to stand, show visible grunting noises and are often inappetant.

Diagnosis

Although most cases can be diagnosed based on historical evidence of recent parturition and breed predisposition, confirmation usually requires demonstration of reduced serum calcium.

Treatment

Recommended treatment, at least in cases that are diagnosed quickly, involves intravenous administration of calcium gluconate salt, although SC and IP routes are also used. Doses of 1 g calcium/45 kg body wt are usually sufficient. Most solutions are available in single-dose, 500 mL bottles that contain 8–11 g calcium. In large, heavily lactating cows, a second bottle given SC may be helpful because it is thought to provide a prolonged release of calcium into the circulation. Subcutaneous calcium treatment alone may not be adequately absorbed because of poor peripheral perfusion and should not be the sole route of therapy. Note that calcium is cardiotoxic; therefore, calcium-containing solutions should be administered slowly (10–20 min) while cardiac auscultation is performed. If severe dysrhythmias or bradycardia develop, administration should be stopped until the heart rhythm has returned to normal. Endotoxic animals are especially prone to dysrhythmias caused by IV calcium therapy.

Cases where the cow has been recumbent for more than 24 hours requires more intensive supportive therapy including additional feeding, moving the cow to prevent pressure neuropathy and crane lifting to improve circulation in the limbs. Cows that have been recumbent for more than 7 days have a poorer prognosis due to secondary complications.

Prevention of hypocalcaemia is implemented during the dry period. Dry cows should not receive feeds high in calcium such as lush spring grass, kale, sugar beet pulp. However feeding low-calcium diets prior to parturition to stimulate intestinal absorption and enhance skeletal reabsorption is not as effective as once thought.

References

  1. Merck Vet Manual
  2. Martín-Tereso J & Verstegen MW (2011) A novel model to explain dietary factors affecting hypocalcaemia in dairy cattle. Nutr Res Rev 24(2):228-243