PARTURIENT PARESIS
(milk fever)
DEFINITION
This metabolic disorder occurs around parturition in mature dairy cows and is characterised by general muscle weakness and circulatory collapse.
AETIOLOGY
In every cow and heifer the concentration of calcium in the blood falls at or just after calving. When this fall is excessive, milk fever develops. Only about 50 per cent of the calcium in the blood is immediately available. During gestation the gradual increased demand for calcium by the calf is met by an increased absorption from the gut. At calving there is a sudden increase in the demand for available calcium as colostrum/milk is produced. The calcium in the blood suddenly drops as a result of a temporary inability by the newly calved cow to replace this calcium. It is when this drop is excessive that clinical signs of milk fever become apparent.
During the first day of lactation, the demand for calcium is about three times the total available. However, it takes about two days for the calcium homeostatic mechanisms to adjust to this sudden demand associated with the onset of lactation
Around calving, there is stasis of the intestinal tract for a short period and the animal*s appetite is decreased. While the food intake of heifers drops only slightly, that of a mature cow may decrease to only 20 per cent of her normal intake. This period of reduced calcium intake, which can persist from 8 to 20 hours, is crucial in determining the degree of hypocalcaemia because absorption from the gut constitutes the dominant or only source of calcium.
Furthermore, as a cow gets older the amount of calcium which can be mobilised quickly from the bones decreases progressively. This means that there is an increased dependence on diet as a major source of calcium and this makes the individual increasingly susceptible to hypocalcaemia when her food intake is suddenly decreased. Cattle fed a diet high in calcium during the last few weeks before calving are particularly susceptible to the development of milk fever because they become entirely dependent on absorption from the gut with resorption from the bones almost nil. Conversely, when cows are fed very little calcium before calving, active bone resorption is stimulated and susceptibility to clinical milk fever is reduced presumably because such individuals are not solely dependent upon dietary sources.
EPIDEMIOLOGY
Milk fever is a modern disease and almost invariably affects high yielding dairy cows. There is no doubt that within breeds, the condition occurs regularly in certain families. This disorder is rare in heifers, uncommon in second calvers with the highest incidence being in 5 to 6 year old cows. Although cases arise throughout the year, the incidence is highest in Britain in the late summer and autumn. About 10 per cent of the cases occur during the two days before calving while 80% occur in the 3 days following calving.
CLINICAL SIGNS
A cow with milk fever can progress to death through three clinically recognisable stages:
Prodromal stage. The cow is apprehensive tending to paddle especially with her hind legs. There are widespread muscle tremors and slight hyperaesthesia. There is smooth muscle paralysis which results in an inability to swallow, consequently inappetance and low thirst, ruminal stasis with the passing of small amounts of dry faeces or none or all, and the suspension of urination. These signs can regress spontaneously or they can become more severe. In the latter instance, the cow falls down and, after trying to get to her feet several times, she will lie in sternal recumbency with her hind legs stuck out awkwardly
Sternal recumbency. Once an individual has become recumbent, spontaneous recovery is very unlikely. The cow becomes increasingly hypoaesthetic and tends to lie with her head tucked into her flank. Her temperature is subnormal, her muzzle dry and, because of ruminal stasis, ruminal tympany becomes obvious. The degree of hypoaesthesia becomes worse and eventually the cow goes into lateral recumbency.
Lateral recumbency. The respiratory rate decreases (10/minute) and groaning respirations may be heard. The heart rate increases but the heart sounds become increasingly more difficult to hear. The papillary reflex is absent and the pupils become more and more dilated. There is a worsening of the above signs and the affected individual eventually dies.
In the few cases which occur before calving, there is the added complication of uterine inertia. Therefore, in those cases which develop immediately after calving, it is advisable to check that there is not another calf in the uterus. Other complications include uterine prolapse and retained placenta.
TREATMENT
Any individual suspected of being hypocalcaemic should be treated promptly and, if possible, before she becomes recumbent. Before milk fever is diagnosed and drug therapy instituted, other causes of recumbency such as physical injury and infectious diseases should be considered and ruled out as far as is possible. Therapy is based upon the parenteral administration of a warmed solution of calcium salts with calcium borogluconate being the most frequently used. Optimal responses have been obtained alter the administration of the equivalent of about 8g calcium. Since one bottle (400m1) of a 20 per cent solution of calcium borogluconate supplies the equivalent of 6.8g calcium, it is better to use the 40 per cent solution in which there is the equivalent of 13.5g calcium in 400m1. It is common practice to give half the volume intravenously and half subcutaneously but this has not been shown in Britain to improve the recovery rate. Calcium salts should be given slowly (400ml over 10-15 minutes) because of the effect of overdosage on the heart.
Following treatment, many cows will then eructate, defaecate and get to their feet within 15 minutes. Those in lateral recumbency will first rise into sternal recumbency and then stand up after about two hours. Cows with milk fever should be allowed to get to their feet in their own time because if forced to by to get up, they can easily injure themselves particularly on slippy concrete floors.
The recovery rate in uncomplicated cases is about 75 per cent with about 15 per cent of the total having to be culled or dying because of complications. About 20 per cent of apparently successfully treated cases will relapse and require a second course of therapy. If a cow does not get to her feet within three days the prognosis is poor because of the development of muscle necrosis.
A small proportion of cases remain recumbent (downer cows) following calcium therapy. It has been shown that the longer therapy is delayed after the onset of clinical signs the lower is the recovery rate.
PREVENTION
Nutritional management. A high calcium diet before calving increases the incidence of milk fever by increasing the individual*s dependence on diet as a source of calcium and reduces skeletal mobilisation. Conversely, a low calcium diet reduces the incidence of milk fever. However, in Britain where a large proportion of a normal dairy cow*s diet is grass-based, it is difficult to devise a diet which will supply less than 50g calcium per day. Cereals are relatively low in calcium and therefore the feeding of barley for 3-4 weeks before parturition is to be recommended. Feeding cereals also reduces the pH of the rumen content and it has also been shown that an acid diet also reduces the incidence of milk fever by increasing the calcium absorption.
In the U.S.A. the feeding of a high phosphorus/low calcium ration to cows during the last month of pregnancy reduced the incidence of milk fever. However, such diets tend to be unpalatable and expensive although the addition of 5 per cent monosodium phosphate in the concentrate ration may be useful. Cows should not be overfed especially with energy to prevent the development of the fatty liver syndrome.
Administration of Vitamin D and metabolites or analogues.
A single injection of 10 million units of Vitamin D from 2~to 8 days before calving will significantly reduce the incidence of milk fever in susceptible cows. If the cow then does not calve this regime can be repeated every eighth day until calving does occur.
Vitamin D3 preparations are very effective at increasing serum calcium concentrations. Dosing is recommended at 24 to 48 hours before calving in order to produce protection from milk fever. A second injection can also be given 72-96 later but it is recommended that this is followed by corticosteroid treatment to ensure that the cow calves within 48 hours. Its disadvantages are twofold: firstly the date of parturition may be uncertain and secondly it depresses serum magnesium concentrations and it is advised that it is important to ensure that the magnesium intake of cows in late pregnancy is adequate.
On farms where previous experience has shown that the incidence of milk fever is likely to be high, every cow may be given 400ml of calcium borogluconate subcutaneously after calving.
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