Parturient paresis (milk fever, hypocalcaemia)
Parturient paresis is an acute to peracute non-febrile disease, which occurs in diary cows and buffaloes usually around the time of parturition. The name ‘milk fever’ is a misnomer as the disease is an outcome of disruption of calcium metabolism and rise in body temperature is not a consistent finding. The disease is clinically manifested by weakness, recumbency and circulatory collapse. Milk fever also occurs in pregnant ewes and lactating does and is characterized by hypocalcaemia, hyperexcitability, ataxia, paresis, coma and death.
Aetiology: Sudden loss of calcium into milk during onset of lactation at parturition or near the parturition, resulting in low levels of ionized calcium in tissue fluids causes onset of hypocalcaemia. The plasma calcium in milk fever is reduced to a level of 2-7 mg/dl. Commonly, the phosphorous level is also decreased, and cows are hypoglycaemic while the magnesium level in plasma is increased. Mature high producing cows and buffaloes in the age group of 5-10 years and at their 3 rd to 7th lactation are relatively more susceptible. Cows of Jersey breed are thought to be more prone to milk fever, but the breed difference appears to be insignificant. Composition of diet during dry and prepartum periods, and environmental factors influence occurrence of milk fever. Feeding of calcium rich diet (more than 100 g of calcium daily) during the dry period increases the chances of the disease, whereas feeding of diets high in calcium just before parturition may lower the incidence. High levels of dietary phosphorous and cation-anion balance in prepartum diet may also increase the risk for parturient paresis. Alkaline diet with an excess concentration of sodium and potassium increase incidence of hypocalcaemia. Since most of the leguminous fodder and grasses are alkaline and rich in potassium, the chances of milk fever are more when legumes rich diet is fed during pre-partum period.
Sheep and goats also suffer from hypocalcaemia. In ewes, the condition occurs in the form of an out-break. Mature ewes that are put to forced exercise or those transported for long distance or deprived of feed are more likely to suffer. The period from 6 weeks prior to and 10 weeks after lambing is usually considered as most critical. Hypocalcaemia ewes develop hypoglycaemia due to depressed endogenous glucose production, which precipitates pregnancy toxaemia. Milking goats, commonly in the age group of 4-6 year, are more susceptible to the diseases. The hypoglycaemic condition occurs usually before and during kidding in does.
Clinical findings: Three discernible stages of milk fever are reported in cows. In the first stage, the animal remains standing but is disinclined to move and becomes anorectic. Rumen stasis, agalactia and a brief stage of excitement and tetany with hypersensitivity, shaking of head, protrusion of tongue, grinding of teeth and tremors of head and limbs are the common signs. The rectal temperature is normal or slightly above normal.In the second stage, cows and buffaloes are unable to stand and suffer from prolonged recumbency with lateral kink in the neck or head tucked into their flank. The muzzle and eyes are dry, extremities are cold and temperature is subnormal. There are signs of bloat, rumen stasis and constipation. Inability of animals to urinate is reflected by distended bladder.
The third stage is marked by lateral recumbency, and the animals are almost comatose. Severe bloat, low temperature, increased heart rate with almost inaudible heart sounds and impalpable pulse are seen during this stage. Untreated cows in third stage may survive only for few hours. Clinical outcome in milk fever may be complicated by concurrent hypomagnesaemia or hypophosphataemia.Clinical signs of milk fever in buffaloes are similar to that in cattle. In ewes, early signs of the disease include proppy gait and tremors of shoulder muscles followed by recumbency. Goats also show similar signs. They assume characteristic posture with the legs under the body or stretched out behind and head rested on the ground. Constipation, ruminal stasis and tympani are also seen.
Diagnosis: The disease needs to be differentiated from hypophosphatemia, hypomagnesaemia, downer cow syndrome, carbohydrate engorgement, mastitis, toxic metritis and other systemic toxaemias, aspiration pneumonia, and injuries to pelvis and pelvic limbs in cattle and buffaloes, and pregnancy toxaemia and enterotoxaemia in sheep and goats. The diagnosis of milk fever is confirmed by marked decrease in calcium and phosphorous concentration in serum, and a favourable response to the treatment with calcium borogluconate.
Treatment and Prevention: Animals respond favourably to early treatment with intravenous administration of calcium borogluconate salt. The usual dose for cows and buffaloes is 1 g calcium per 45 kg body weight, which is calculated to 400-800 ml of 25% solution depending upon their body weight. Under dosing increases chances of incomplete response and downer cow syndrome. However, rapid intravenous administration of total dose of calcium may be detrimental due to cardiotoxic effect of calcium. Therefore solution containing calcium should be administered slowly over a period of 10-15 minutes and heart should be auscultated throughout calcium administration for the evidence of gross arrhythmia. In large-heavy body weight animals, half of the total dose may be given by subcutaneous route after initial intravenous infusion. Magnesium tends to protect myocardial irritation caused by calcium. As such, administration of solutions containing magnesium and phosphorous in addition to calcium may be advantageous. Oral administration of calcium solution avoids cardiotoxicity in mild cases of milk fever.
Majority of cows respond to the treatment within 2 hours, and those not responding should be re-evaluated to decide further course of treatment. Standard intravenous dose of calcium borogluconate (23% solution) for treatment of hypocalcaemia is 50-150 ml in sheep and goats.Various methods are available for prevention and control of hypocalcaemia. Feeding low calcium diet during dry period was thought to prevent milk fever in dairy cows and buffaloes by stimulating intestinal absorption and enhancing skeletal resorption of calcium prior to its sudden demand at the onset of lactation. However, doubts have been raised on the effectiveness and practical aspects of this method. Use of dietary cation-anion difference (excess of anions over cations) has been recently introduced as more effective preventive method. Excess anions in the diet are thought to enhance intestinal absorption and skeletal resorption of calcium. Vitamin D (20-30 million unit) given in the feed for 5-7 days before parturition or as a single intravenous/ subcutaneous dose of 10 million IU of crystalline Vitamin D given 8 days before calving is effective in preventing milk fever.