Parturient hypocalcaemia (milk fever)

What it is

At the onset of lactation the mammary gland draws a large amount of calcium from the blood for colostrum and milk. The cow compensates by increasing calcium resorption from bone and its absorption from the intestine, under the control of parathyroid hormone and active vitamin D (1,25-dihydroxyvitamin D). These mechanisms take several days to come into play; if they do not respond in time, blood calcium falls in the hours or days around calving.

There are two forms:

• Clinical hypocalcaemia (milk fever, parturient paresis): calcium falls far enough to impair muscle contraction and nerve function, and the cow weakens until she becomes recumbent. Despite its name, it does not cause fever: body temperature is usually normal or low.
• Subclinical hypocalcaemia: calcium is below normal without visible signs. It is far more common than the clinical form and is associated with other postpartum diseases, although not every transient fall has consequences.

A key factor is acid-base balance: prepartum diets rich in potassium and sodium (high-potassium forages) cause a metabolic alkalosis that reduces tissue responsiveness to parathyroid hormone. Prevention with diets of negative dietary cation-anion difference (DCAD) is based on this.

Who it affects

Mainly high-producing multiparous dairy cows, within 72 hours after calving; the risk rises with the number of lactations. Jersey cows are more susceptible than Holsteins. First-calf heifers rarely develop the clinical form, although they can have subclinical hypocalcaemia. Other risk factors are prepartum diets high in potassium or calcium, overconditioning and a history of milk fever.

Anatomy involved

• Udder: colostrum secretion is the cause of the fall in calcium. Hypocalcaemia also reduces the tone of the teat sphincter, which stays open longer after milking and favours mastitis.
• Uterus: uterine smooth muscle needs calcium to contract. Hypocalcaemia is associated with uterine inertia and dystocia, retained fetal membranes, metritis and uterine prolapse.
• Rumen: the forestomach musculature loses strength; ruminal hypomotility or atony and bloat appear, especially in a cow in lateral recumbency, which cannot eructate. Reduced feed intake worsens energy balance and the dietary supply of calcium.

Clinical signs

Clinical hypocalcaemia progresses through three stages:

• Stage 1 (standing): excitability, hypersensitivity, muscle tremors, stiff hind limbs and a staggering gait; the cow stops eating.
• Stage 2 (sternal recumbency): the cow cannot rise and often rests her head on her flank, with an S-shaped neck. There is depression, cold extremities, a dry muzzle, dilated pupils, tachycardia with weak heart sounds, ruminal stasis, constipation and low body temperature.
• Stage 3 (lateral recumbency): complete muscle flaccidity, bloat, stupor and coma. Without treatment, the cow dies.

A cow that stays recumbent for a long time can suffer compressive muscle and nerve damage and become a "downer cow" that does not rise even after calcium is corrected. Subclinical hypocalcaemia has no signs of its own.

Diagnosis

• Clinical: the typical picture in a freshly calved cow and a rapid response to calcium treatment support the diagnosis.
• Blood calcium: confirms hypocalcaemia; the sample is best taken before treatment. Hypophosphataemia is common, and magnesium is sometimes abnormal as well.
• Differential diagnosis of the downer cow: calving injuries (obturator nerve paralysis, fractures, hip luxation), toxic mastitis or metritis, hypomagnesaemia, ketosis and other causes.
• Subclinical hypocalcaemia: detected only by measuring calcium; it is most meaningfully assessed at herd level, in several cows in the days after calving.

Treatment and prevention

• Recumbent cow: intravenous calcium, given slowly with cardiac auscultation, because a rapid infusion can cause severe arrhythmias. The cow should be kept in sternal recumbency, prevented from lying on her side and watched for relapse.
• Standing cow or mild hypocalcaemia: oral calcium; it should not be given by mouth to a cow that does not swallow well or is recumbent, because of the risk of aspiration.
• Herd-level prevention:
  • Prepartum diets with a negative DCAD (anionic salts) in the last weeks of gestation, checking their effect through urine pH.
  • Avoiding excess calcium, phosphorus and potassium in the prepartum diet and ensuring adequate magnesium.
  • Oral calcium around calving in the cows at highest risk.
  • Controlling body condition during the dry period.

Drug use in food-producing animals is subject to each country's regulations and to withdrawal periods for milk and meat.

Key studies

• Lean et al. (2006), meta-analysis of 137 trials with 2545 calvings. It confirmed that a higher prepartum DCAD increases the risk of milk fever and that the only DCAD equation with statistical support was (Na + K) − (Cl + S). Jersey cows had 2.25 times the risk of Holsteins. A higher magnesium content in the prepartum diet reduced the risk, a higher phosphorus content increased it, and risk peaked at 1.35% calcium in the prepartum diet.
• Santos et al. (2019), meta-analysis of 42 randomised experiments with 1803 cows. According to the model, reducing DCAD from +200 to −100 mEq/kg would raise total blood calcium on the day of calving from 1.86 to 2.04 mM and increase postpartum intake by 1.0 kg/d and milk by 1.7 kg/d in multiparous cows. Lowering DCAD reduced the risk of milk fever in multiparous cows and that of retained placenta and metritis. In heifers it did not improve production, and experiments with them were few.
• Reinhardt et al. (2011), national sampling of 1462 cows from US herds within 48 hours after calving. Subclinical hypocalcaemia (below 2.0 mM) increased with the number of lactations: 25% in first-lactation cows and 41%, 49%, 51%, 54% and 42% from the second to the sixth lactation. It is a cross-sectional study with a single sample per cow, which did not assess whether hypocalcaemia caused other diseases.
• McArt and Neves (2020), prospective cohort of 407 Holstein cows from 2 herds. Transient subclinical hypocalcaemia (only on the first day) did not clearly increase the risk of disease or removal from the herd, and those cows produced more milk. In contrast, persistent hypocalcaemia multiplied the risk by 4.1 in first-lactation and 1.8 in multiparous cows, and delayed hypocalcaemia by 3.2 and 1.9. A single low value just after calving does not by itself indicate a problem; it is an observational study in only two herds.
• Oetzel and Miller (2012), randomised trial in 927 cows in their second or later lactation from 2 large herds already fed anionic diets. Oral calcium boluses after calving did not change mean ionised calcium, and clinical milk fever was rare (0.6% of calvings). Benefit was seen only in subgroups: lame cows had 0.34 fewer health events in the first 30 days, and cows with higher previous production gave 2.9 kg more milk at the first test. These are subgroup analyses; the evidence does not support giving oral calcium to all cows alike.