An update on hypocalcaemia control

The lactational demands on the dairy cow make it almost unique in its inability to maintain calcium (Ca) homeostasis at parturition. The incidence of clinical hypocalcaemia (milk fever) in the field generally ranges from 0 to 10%, but may exceed 25% of cows calving (Garis and Lean, 2008). Data from a UK retailer scheme showed that the recorded incidence decreased from 5.8 to 2.7% from 2009 to 2017 (Sainsburys plc., Press briefing, 2017) but up to date UK wide data are not available.

A clinical target incidence of less than 3% is realistic. It is easier to achieve these targets in larger herds where dedicated groups of cows with carefully controlled dietary macromineral concentrations are more feasible (seeBox 1).

Box 1.Dietary micromineral recommendations for control of hypocalcaemia

Calcium containing drenches and boluses

The use of Ca salt containing drenches around calving is popular and is reasonably effective at controlling clinical hypocalcaemia. The most soluble salts are the most effective; calcium chloride is the most soluble and carbonate is the least making it almost useless as a treatment/prevention in drenches and boluses. Calcium chloride drenches may be the most rapidly absorbed but can damage the oesophageal lining; mixtures with propylene gycol gels were formulated to mitigate this risk (Goff and Horst, 1994). Calcium propionate is more slowly absorbed but the duration of a serum blood Ca rise is slightly longer. However, it should be borne in mind that most proprietary salts and drenches contain between 40 and 50 g of Ca and these will only lead to a 2 hour rise in serum Ca. Higher quantities of calcium can give longer responses, Martinez (2016) observed a maximum of an 8 hour rise when using a Ca bolus containing 86 g of Ca.

Supplementation effects are variable depending on the animal; Oetzel and Miller (2012) dosed animals aft er calving with 43 g of Ca salts and found that supplementation was only worthwhile in multiparous cows. Analysing the effect on multiparous cows more closely, use in higher yielding animals was most beneficial from a yield increase perspective and most beneficial in lame cows from a prevention of negative health events perspective.

Leno et al (2018) also saw that Ca supplementation with a single bolus containing 54 to 64 g Ca in the first 24 hours post calving was most effective when it was targeted at certain cows. Multiparous cows with a low serum Ca at enrolment had a reduced risk of one or more health disorders when supplemented, and cows with a body condition score >3.5 showed higher milk production over the first four milk recordings when supplemented. Despite the observed beneficial responses in certain groups of cows there was no significant difference in serum Ca in the 24 hours after enrolment, but it is worth noting that the cows were not supplemented at calving but within 19 hours of calving.

Domino et al (2017) compared oral bolusing at calving and again 12 hours later with a bolus containing 43 g Ca with a single subcutaneous injection of 500 ml of 23% Ca gluconate given at calving. Compared with control cows, the subcutaneous injection gave higher serum Ca levels until between 24 and 48 hours. The cows that received boluses had lower serum Ca concentrations than the subcutaneously injected cows until between 12 and 24 hours but higher concentrations than the control cows until 48 hours when the sampling ended.

Martinez et al (2014) found that Ca drenches did not reverse the decrease in neutrophil function observed in experimentally induced hypocalcaemic animals. This observation, combined with the short duration of action of boluses and drenches, shows that Ca dosing can be useful but is no substitute for a proper dietary prevention strategy.

Subclinical hypocalcaemia

Subclinical hypocalcaemia in the 72 hours post calving has a high incidence. The incidence depends on the definition used but using a standard definition of serum Ca being <2.2 mmol/litre, it is not uncommon for more than 50% of animals in a herd to be affected (Rheinhardt et al, 2011).

Many papers have shown associations between periparturient hypocalcaemia and the incidence of displaced abomasums, ketosis, retained placenta and metritis. Rodriguez et al (2017) identified different serum Ca cut offs at 24 to 48 hours when looking at associations with different diseases. The thresholds for the different diseases were 1.93 mM/litre for ketosis, 2.05 for retained placenta and metritis and 2.10 for displaced abomasum. In the same study, it was observed that normocalcaemic animals were more likely to have an earlier first oestrus than ones that had suffered hypocalcaemia in the first 72 hours.

Neves et al (2018) found that different serum Ca thresholds should be adopted for different cows depending on the day of assessment and the parity of the cows. Serum Ca concentrations less than 2.15, 2.10 and 2.15 mmol at days 2, 3 and 4 post calving respectively in second lactation animals were associated with a greater risk of metritis in second lactation animals, and a serum concentration less than 1.97 mmol/l at day 2 was associated with an increased risk of displaced abomasum.

Monitoring hypocalcaemia — convenience versus interpretation of results

A one-off serum Ca test after calving can provide cheap monitoring information. Timing is important as the serum concentration of Ca changes rapidly in the first 72 hours after calving, normally hitting its nadir at approximately 24 hours. In reality, blood sampling is not often routinely carried out. If herds are prepared to sample cows, the easiest method is to take the sample as soon as possible after calving even though there is perhaps a better rationale for doing so 2 days post calving (see below).

If taking samples as soon as possible, a workable target (in the author's experience) is that >75% of multiparous animals in the first 12 to 24 hours should achieve serum Ca levels >1.8 mmol/litre. However, the Neves et al (2018) study mentioned above would suggest that this is too early to sample as they saw no link between serum Ca in the first 24 hours and clinical disease outcomes. Their study would suggest that it is better to assess the blood Ca concentration at 2 days post calving and set a target of >2 mmol/litre for second lactation animals and to test at day 4 and have a target of >2.2 mmol/litre for older animals. The duration of hypocalcaemia may have a greater effect than its depth, meaning that one off sampling may not be very useful and that serial sampling over the first 72 hours is required. However, the practical demands of this make it near impossible to achieve on farm.

Prediction rather than monitoring

A simple means of prediction may be more useful than monitoring. There are three main areas that can be examined: herd; diet; and animals.

Herd

Breed and age structure of the herd is important and previous history at an individual and herd level. Channel Island breeds are particularly susceptible to hypocalcaemia and older cows are also more susceptible.

Diet

The potassium (K) content of the ration in the transition period prior to calving is a major driver for herd hypocalcaemia susceptibility. The forage dry matter intake in a typical transition dry cow diet is approximately 70% of the total intake. Hence, it is important to decrease the K content of the forage portion of the diet as much as possible. This is usually the number one consideration when trying to address problems on farm (seeBox 2).

Box 2.Approximate risk from high K from different foragesHigh risk

• Spring grass
• First cut grass silage
• Lush September grass

Medium risk

• Later cut grass silage-June/July
• Late summer ‘standing hay’
• Maize silage

Low risk

• Whole crop silages
• Barley straw
• Wheat straw

The K content of forages is very variable. Box 2 gives an indication of the milk fever risks associated with different forages but the safest method is to test the mineral content of the forages that are available for the dry cows (Figure 1). Practical points to remember are that the predisposing effects of high K wear off over a week so the mineral content of the forages in the ‘far off’ dry cow ration, if two rations are being used in the dry period, will not be relevant if cows are moved to the transition ration for long enough prior to calving.

High quality grass silage tends to carry the highest risk (Figure 1). Silage cut in June and July, especially when there has been a big gap (6 weeks or more) between that cut and the previous one will be lower risk. Maize silage, whole crop cereal silage and straw also tend to be lower risk. A ration without grass silage or hay can be unpalatable especially if a high straw inclusion is being used; the use of more than one forage and mixing with water can help. Brewers' grains have a negative dietary cation–anion balance (DCAB) (see Box 3) and cause a beneficial metabolic acidosis for hypocalcaemia control. Hence, the use of 5 to 10 kg of brewers' grains is recommended if available.

Box 3.Explaining the dietary cation–anion difference/balance (DCAD/B)The DCAB equation gives an indication of the metabolic acidogenic or alkalogenic properties of a diet.DCAB (mEq/kg DM) = (Sodium + Potassium) + (Chlorine + Sulphur)Anionic salts are higher in chlorine and sulphur than sodium and potassium, while cationic salts are higher in sodium and potassium than chlorine and sulphur.Cow diets are almost invariably high in strong cations relative to anions due to the high K content of grass-based forages. This means that cows are metabolically alkalotic unless the diet is manipulated by the addition of anionic salts.The DCAB of a diet can be calculated easily if the percentage concentrations (in terms of DM) of sodium, potassium, chlorine and sulphur ions are known. These are then multiplied by their appropriate conversion factors (derived from the reciprocals of the molecular weights of the elements; see Table below) and added together to derive a positive or negative value.

In practical terms, high DCAB feedstuffs increase milk fever susceptibility and the low DCAB or negative DCAB feedstuffs decrease the risk.Example: What is the DCAB of MgCl₂.7H₂O?The molecular weight is 24 + (35.5 × 2) + (18 × 7) = 221Using the DCAB equation, the concentration of Na and K (strong cations) is 0% as is the S, however, the % of Cl is 71/221 x 100 = 32%The DCAB of MgCl₂.7H₂0 is therefore (435 × 0) + (255.7 × 0) + (32 × −282) + (−623.8 × 0) = −9062 meq/kg DM

Animals

Cows are normally metabolically alkalotic with a urine pH >8 due to the high potassium concentration of normal diets (see Box 3). Excessive metabolic alkalosis coupled with hypomagnesaemia disrupts parathyroid hormone (PTH) binding to its receptor thus affecting vitamin D activation and release of Ca from bone stores and active uptake from the gut (Goff, 2014). Metabolic alkalosis also reduces the proportion of serum Ca that is ionized and hence biologically active and reduces the Ca that is available in the bone canaliculi. Urine analysis can be very useful to check the acid–base status of a group of animals. When cows are less metabolically alkalotic, the following changes are seen in the urine:

• pH decreases
• Ca excretion increases
• Strong-ion difference (SID= Na+K-Cl) decreases
• Carbon dioxide decreases.

These changes are beneficial for better control. It is also very easy to check the Mg status in urine.

Control of clinical hypocalcaemia is often straightforward and can usually be effectively achieved by removing or decreasing the quantity of high K forages fed in transition and adding 100 to 150 g of magnesium chloride to the total mixed ration (TMR) or mixing it with water and adding it with a watering can. It should be noted that magnesium chloride is not palatable and to avoid drops in feed intake it is best to limit its supplementation to 150 g. The magnesium chloride works by decreasing the DCAB and improving the Mg status. Decreasing the DCAB of a ration by the addition of anionic salts such as ammonium chloride or magnesium sulphate is still the mainstay of most prevention techniques. In the author's experience, it is often not necessary to decrease the urine pH to much less than 8, but in herds where greater acidification seems to be necessary dropping the pH to 7 across a group usually works well (Figure 2).

There is still considerable debate over whether dietary Ca needs to be supplemented to 1.2% of dry matter when strongly acidifying, but at pH 7 this does not appear to be necessary and if any Ca is added it is better to use calcium chloride to achieve a dietary Ca level of 0.5 to 0.7% dry matter (DM) rather than using calcium carbonate (limestone) and increasing it to 1.2% DM. The chloride salt has acidifying capacity whereas carbonate is mildly alkalinising which is counterproductive.

Calcium binding

It has been known for a long time that placing cows in true negative Ca balance pre calving can upregulate the homeostatic mechanisms early, prior to colostrogenesis. In practical terms this was impossible due to the relatively high background Ca contents of most feeds. By restricting Ca using a Ca binder the cow can be placed into true negative Ca balance.

Zeolite A is a Ca binder and when mixed with starch to try to mitigate the adverse taste can be extremely effective in controlling hypocalcaemia. However, it is considerably more expensive than the methods already mentioned. A recent study from Cornell (Kerwin et al, 2019) showed a significantly lower prevalence of hypocalcaemia in the immediate post-calving period using the Ca binding technique compared with a traditional DCAB technique. Zeolite A also binds phosphorus (P) and serum P is often low at calving with this technique and can be low enough to cause periparturient haemoglobinuria unless dietary P precalving is kept at 0.35% DM (without using zeolite A it should be 0.3 to 0.32%).

Both anionic salts and zeolite A are unpalatable (but zeolite A more so) and both need to be well disguised in blends and meals and cannot be easily ‘top dressed’ on a ration.

Conclusion

Controlling subclinical and clinical hypocalcaemia is a key veterinary area on dairy farms due to its often high incidence and the knock on effects it has on health and fertility.

A degree of control can be gained using calcium supplements but must be underpinned by preventative dietary strategies.

KEY POINTS

• Clinical hypocalcaemia target incidences should be low, preferably < 3%.
• Calcium drenches and boluses are useful but have a short duration and need to be focused on the right cows. There is little evidence for their use in heifers.
• Serum testing for subclinical hypocalcaemia is a useful monitoring exercise. The timing relative to calving is important, day 2 post calving is probably the most effective but perhaps not the most convenient.
• Risk analysis can be carried out using the breed and age of the herd but dietary analysis, especially concentrating on the forages, is the most predictive.
• Ca binding is very effective but significantly more expensive than other milk fever control methods. Beware of the dietary P concentration of the diet and make sure the palatability of the ration is good.