Ketotic cows: treatment and prognosis (Proceedings)


An absolute requirement for treating ketosis in cattle is to identify and treat the primary cause for the negative energy balance. Symptomatic treatment for ketosis without attacking the primary cause is doomed to failure.

An absolute requirement for treating ketosis in cattle is to identify and treat the primary cause for the negative energy balance. Symptomatic treatment for ketosis without attacking the primary cause is doomed to failure.

Propylene glycol is a routine treatment for ketosis. Only 2 oral formulations are approved for use in cattle as a treatment and the dose rate is 8 oz, q 12 h, for up to 10 days (2 other formulations labeled for use as preventive treatment). Research suggests that 296 ml once/day as on oral drench is just as effective as 887 ml once/day. Propylene glycol is absorbed from the rumen as propylene glycol, some propylene glycol is metabolized to propionate in the rumen, but most is absorbed intact and metabolized to glucose in liver. Propylene glycol increases serum [glucose], decreases serum β-OH butyrate & NEFA concentrations but only if a functional liver as propylene glycol must be metabolized. Propylene glycol is only beneficial if rumen motility to aid mixing and absorption.

Glycerol (same dose rate as propylene glycol) and sodium propionate (uncertain dose rate) also reported to be of use but are both considered inferior to propylene glycol. Sodium propionate may have palatability problems. Calcium propionate has been examined, but the evidence is not convincing that it is superior to propylene glycol, even though it also has calcium. Not very soluble, and large volumes need to be administered.

500 ml of 50% Dextrose IV is also a routine treatment (one time administration of 250 g). Numerous approved products for treating ketosis in cattle. A cow uses 50-70 g glucose/hour for maintenance and 200 g glucose/hour high production, from a total blood glucose pool <40 g. Milk is 4.5% lactose, 50 kg of milk contains 2.25 kg lactose (glucose and galactose), which is equivalent to 4.5 kg of glucose (18 bottles of 50% dextrose). A rough rule of thumb is 1.6 bottles of 50% glucose / 10 pounds of milk.

Dextrose suppresses NEFA release and hepatic ketogenesis for a few hours which is beneficial. There is a low renal threshold of 150 mg/dl glucose, serum glucose concentrations are back to normal after 2 to 4 hours. Hyperglycemia inhibits rumen and abomasal motility for at least two hours after administration, the effect appears to be insulin-mediated so not a problem in early lactation (dairy cows have very low serum insulin concentrations early in lactation).

Only two glucocorticoid products are currently approved for treataing ketosis, dexamethasone and isoflupredone acetate. Glucocorticoids promote release of amino acids from muscle and may be gluconeogenic. Glucocorticoids promotes conversion of amino acids in liver to glucose. Careful in cattle with concurrent infectious disease, as immunosuppressive dose of dexamethasone is 0.04-0.05 mg/kg, IM. Experimentally, 10-20 mg IM dexamethasone ester increases blood glucose concentration, decreases blood ketone concentration. Be carefeul with repeated injections of isoflupredone acetate as clinical hypokalemia may result.

B Vitamins are theoretically of benefit, are inexpensive, and come in pretty colors. There is no data to support use for treatment, but B vitamins are recommend as a routine administration to all prolonged cases of ketosis. Probably need at least B1 and B12. Recent studies strongly support the effectiveness of B12 in improving energy homeostasis in periparturient dairy cattle.

Decrease milk production is an underutilized treatment for ketosis. The energy loss through milk is a major drive for ketogenesis. One of the mechanisms for effectiveness of glucocorticoids is that they decrease milk production. May want to consider not completely milking cow; milking out 50 to 75 % q 12 h better than milking q 24 h and can probably do for 5 days without significantly impacting lactation curve. Force-feeding is clinically useful in valuable cattle but efficacy not documented. Make slurry by dissolving alfalfa cubes and pelleted concentrate in warm water, pump slurry into rumen using bilge pump and large diameter stomach tube. In valuable animals, place rumen fistula to facilitate feeding.

A summary of treatments is: 1) mild to moderate ketonuria (producer treated) - oral propylene glycol; 2) severe ketonuria, initial treatment (veterinarian treated) - oral propylene glycol, IV 500 ml 50% dextrose, IM dexamethasone & B vitamins; 3) severe ketonuria, subsequent treatments (referral veterinarian treated) - oral propylene glycol, IM dexamethasone & B vitamins, decreased milk removal, forced feeding (slurry pumped into rumen), and possible continuous IV slow drip glucose. Ancillary treatments include insulin, nicotinic acid, and bypass protected choline and L-methionine (in an attempt to enhance lipoprotein production and facilitate fat export from the liver).

The best prognostic tests are increased appetite following initial treatment and liver biopsy with quantification of fat %.


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