Ketosis

Definition and Etiology

Ketosis is a multifactorial disorder of energy metabolism in high yielding dairy animals after calving. The negative energy balance (NEB) results in hypoglycaemia, ketonemia (accumulation of acetoacetate, β-hydroxybutyrate and acetone in blood) and ketonuria. The causal factors of ketosis are (i) dietary factors (starvation/loss of appetite or feeding of low carbohydrate diet/excess feeding of protein-rich diet and silage), (ii) animal factors (heavy drain of lactose (45 g/kg milk) in high yielding animals through milk leads to NEB along with hepatic insufficiency), and (iii) hormonal factors (absence of glucocorticoids/gluconeogenesis in stress conditions such as pregnancy and parturition).

Predisposing Factors

It is the disease of lactating crossbred (high-yielding) stall-fed cows and buffaloes. Incidence is higher during third to fifth lactation between two weeks to two months after calving.

Clinical Signs

The two clinical forms of ketosis are (i) Wasting form – common form, refusal to eat grain, decrease in milk yield, loss of body weight (woody appearance), depression, abdominal pain, hangdog appearance and odour of ketones in breath and milk, and (ii) Nervous form – encircling straddling, head pushing, blindness and vigorous licking of skin or inanimate objects and hyperesthesia.

Diagnosis

Diagnosis is based on history, clinical signs, milk and urine cow-side tests (Rothera’s test), and milk fat to protein ratio. Milk and urine ketone concentrations are detected by the reaction of acetoacetate with sodium nitroprusside. Milk fat concentration tends to increase and milk protein concentration tends to decrease during post-partum NEB.

Differential Diagnosis

Wasting form of ketosis should be differentiated from diseases characterized by wasting such as traumatic reticulitis/pericarditis/diaphragmatic hernia, vagus indigestion, pneumonia, metritis/ cystitis/pyelonephritis and abomasal displacement. Nervous form of ketosis should be differentiated from tetanus, rabies, encephalitis, lead poisoning and lactation tetany/ hypomagnesemia.

Treatment

Treatment includes: Replacement therapy – Dextrose (25 percent, 500-1,000 mL, IV for 2-3 days), Propylene glycol (@ 225 g PO every 24 hours for 3-5 days) and sodium propionate (@ 110-225 g PO for 3-6 days); hormonal therapy – glucocorticoids such as dexamethasone sodium phosphate (@ 40 mg, IV, 4 to 6 days) along with IV glucose therapy; long-acting insulin (@ 200-300 U, SC) along with IV glucose and supportive therapy (vitamin B1 / B-complex @ 10 ml IM on alternate day; feeding of mineral mixture containing phosphorus and cobalt).

Prevention and Control

Avoid starvation or overfeeding at calving, give extra concentrate ration (1.5 kg/day) during advanced pregnancy. In late lactation cows, increase the energy supply from digestible fibres and reduce the energy supply from starch. Early lactation rations should be relatively high in non-fibre carbohydrates (38-41 percent). Monensin sodium (@ 300 mg/head/day) throughout the transition period may be used in preventing subclinical ketosis.

Source: STANDARD VETERINARY TREATMENT GUIDELINES FOR LIVESTOCK AND POULTRY

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