3 Third stage Milk Fever

Transcript

Welcome to lesson-3, before that just recall what we have dealt with in the previous class that is Pathogenesis and the Clinical signs of Hypocalcemia. Mainly how the reduced level of calcium has influenced the skeletal and smooth muscle contractility, causing reduced cardiac function, as well as nerve cell membrane instability, and we have seen the stage-1 Hypocalcemia characterized by a stage of excitement and stage-2 that’s the main stronghold recumbency, flaccidity of all the skeletal muscle, and there is loss of muscular tone an animal becomes sternal recumbency and there will be lateral twitching of head and neck and in addition there will be bloat and reduced defecation and there is tachycardia, but the poor intensity of cardiac sound and weak pulse are all the signs we have seen in stage-2 Milk fever.

And today we have that is a third-stage milk fever, and we are going to see about the complications of Milk fever and How to diagnose Hypocalcemia at the field level as well as Differential diagnosis.

Stage-3 really is a challenging one for the veterinarian because most of the animal dies at this stage. See what happens there is a severe reduction in the Calcium level and the animal is in the sternal recumbency if it is not properly treated it will be going for lateral recumbency and almost you can say it is a comatose stage and the animal there will be lots of complete loss of skeletal muscle and it is unable to raise its head and neck.

So in the sternal recumbency, you could see you can appreciate the lateral kicking of the head and neck. Now in the lateral recumbency, it is unable to raise the head and neck, it is unable to maintain the sitting posture, so now it is on lateral recumbency and there is a severe tachycardia, it is very very difficult to raise the jugular vein and there is abnormal temperature and the animal is comatose and there is reduced defecation, urination and there is bloat.

So if the animal is left in that stage, it will die within 12 to 24 hours of lateral recumbency. So most of the time the hypercalcemic animal will have a concurrent ailment.

Sometimes you may give specific treatment to Hypercalcemia but it will fail because there will be concurrent hypomagnesemia and then hypophosphatemia and in Hypocalcemia, there is reduced rumen activity and intake also reduces.

So, there will be a negative energy balance, and the animal is predisposed to Ketosis. And recumbent animal with additional reduced immune activity, it is highly predisposed to Mastitis, especially Peracute Toxic Mastitis.

And then finally the animal’s Sternal recumbency, if there are more than four hours the animal is on recumbent without any treatment it highly predisposes the animal to go for downer cow syndrome and it’s a main/major complication of Hypocalcemia.

How to Diagnose Hypocalcemia in Cattle:

Usually the classical, clinical signs of different stages, apart from that to confirm the disease we need to go for Blood analysis, that is a Serum Calcium level, either total calcium or Ionized Calcium.

Total calcium is easy to estimate in any laboratory and will give the value of calcium if the sample is given. There is Ionized calcium, it will be estimated in a referral center, that is based on either the blood gas analyzer or electrolyte analyzer, high-end laboratory facilities are needed to estimate the Ionized calcium level.

Apart from Calcium concurrently you need to measure the Magnesium level as well as a Phosphorous level. There will be less Magnesium and Serum Phosphorus also, so in the clinical[1]pathological analysis, apart from the estimation of calcium in the blood, other components to be estimated are Inorganic Phosphorus, there will be Hypophosphatemia.

Apart from that most animals will have a negative energy balance, so we need to estimate the blood glucose level, if it is less than 50 milligram/deciliter, then we need to give a dextrose treatment also.

Apart from this recumbent animal, there will be the release of muscle enzyme-like Creatine kinase(CK) and Aspartate aminotransferase.

And in blood hematological alterations there will be Neutrophilia, Lymphopenia, and Eosinopenia. These are all but they are not specific for Hypocalcemia but there are changes you can observe.

So apart from clinical signs due to Hypocalcemia Calcium exerts its major effect on skeletal and cardiac muscle contractility. So there will be in ECG you can appreciate prolongation of the acute interval, which is a major change in cardiac activity.

Another important field test to diagnose the Hypercalcemia is Sulkowitch test. In the homeostasis I have clearly mentioned that in a normal animal there is excess calcium is excreted in the urine, so by adding urine with Sulkowitch reagent, a normal animal you will get a white color discoloration or precipitation.

Whereas in Hypocalcemic animals due to the action of Parathamron hormone and vitamin D3, there will be complete resorption of calcium from the urine, so there will no or less Hypocalcemia in the urine analysis. So the clear color there is no white precipitation indicates there is hypocalcemia in animals. So always we need to differentiate the similar disease condition that occurs during the periparturient period, that is a downer cow syndrome following a Milk fever and usually, the animal is recumbent, so immediately after calving common disease or acute carbohydrate engorgement and hip dysplasia, then that is degenerative myopathy and Obturator nerve paralysis, fat cow syndrome and even severe toxemia like your peritonitis due to foreign body or else coliform mastitis or materials causing the animal to become recumbent. So the common differential diagnosis as we discussed earlier mainly downer cow syndrome, then a hip dysplasia, then a pelvic fracture, then Obturator nerve paralysis, the common fatty cow syndrome, and toxic menstrual mastitis, these are all the common differential diagnosis.

So in this lesson-3 of a module, we had seen about

• How to diagnose the hypocalcemia mainly based on clinical signs and
• then laboratory technique and
• then complications of Hypoglycemia and
• Differential diagnosis and Diagnosis.