Ketosis

Source: msdvetmanual.com

Overview

• The pathogenesis of bovine ketosis is incompletely understood, but it requires the combination of intense adipose mobilization and a high glucose demand. Both of these conditions are present in early lactation, at which time negative energy balance leads to adipose mobilization, and milk synthesis creates a high glucose demand. Adipose mobilization is accompanied by high blood serum concentrations of nonesterified fatty acids (NEFAs). During periods of intense gluconeogenesis, a large portion of serum NEFAs is directed to ketone body synthesis in the liver. Thus, the clinicopathologic characterization of ketosis includes high serum concentrations of NEFAs and ketone bodies and low concentrations of glucose. In contrast to many other species, cattle with hyperketonemia do not have concurrent acidemia. The serum ketone bodies are acetone, acetoacetate, and β-hydroxybutyrate (BHB).
• All dairy cows in early lactation (first 6 wk) are at risk of ketosis. The overall prevalence in cattle in the first 60 days of lactation is estimated at 7%–14%, but prevalence in individual herds varies substantially and may exceed 14%. The peak prevalence of ketosis occurs in the first 2 wk of lactation.
• Ketosis cases occurring closer to peak milk production, which usually occurs at 4–6 wk postpartum, may be more closely associated with underfed cattle experiencing a metabolic shortage of gluconeogenic precursors than with excessive fat mobilization. Ketosis at this time is sometimes described as type I ketosis.
• Ketosis in the immediate postpartum period is sometimes described as type II ketosis. Such cases of ketosis in very early lactation are usually associated with fatty liver (see Fatty Liver Disease of Cattle ). Both fatty liver and ketosis are probably part of a spectrum of conditions associated with intense fat mobilization in cattle.

Clinical signs

• In cows maintained in confinement stalls, reduced feed intake is usually the first sign of ketosis. If rations are offered in components, cows with ketosis often refuse grain before forage. In group-fed herds, reduced milk production, lethargy, and an “empty” appearing abdomen are usually the signs of ketosis noticed first. On physical examination, cows are afebrile and may be slightly dehydrated. Rumen motility is variable, being hyperactive in some cases and hypoactive in others. In many cases, there are no other physical abnormalities. CNS disturbances are noted in a minority of cases. These include abnormal licking and chewing, with cows sometimes chewing incessantly on pipes and other objects in their surroundings. Incoordination and gait abnormalities occasionally are seen, as are aggression and bellowing. These signs occur in a clear minority of cases, but because the disease is so common, finding animals with these signs is not unusual.

Diagnosis and differentials

• The clinical diagnosis of ketosis is based on presence of risk factors (early lactation), clinical signs, and ketone bodies in urine or milk.

Treatment and control

• Treatment of ketosis is aimed at reestablishing normoglycemia and reducing serum ketone body concentrations. Bolus IV administration of 500 mL of 50% dextrose solution is a common therapy.
• Administration of glucocorticoids, including dexamethasone or isoflupredone acetate at 5–20 mg/dose, IM, may result in a more sustained response, relative to glucose alone. Glucose and glucocorticoid therapy may be repeated daily as necessary. Propylene glycol administered orally (250–400 g/dose [8–14 oz]) once per day acts as a glucose precursor and is effective as ketosis therapy. Indeed, propylene glycol appears to be the most well documented of the various therapies for ketosis. Overdosing propylene glycol leads to CNS depression.
• Prevention of ketosis is via nutritional management. Body condition should be managed in late lactation, when cows frequently become too fat.
• Modifying diets of late lactation cows to increase the energy supply from digestible fiber and reduce the energy supply from starch may aid in partitioning dietary energy toward milk and away from body fattening.

Summary

• high milk production during the early lactation causes negative energy balance which leads to intense fat mobilization and glucose demand. Production of glucose from liver leads to increased ketone bodies in the blood which is called ketosis. cattles with excess fat and BCS above 3.75 are highly susceptible.
• Off feed, lethargic, anorexia, decreased milk production, and could be CNC incoordination are common signs.
• Dx is based upon signs and ketone bodies in urine.
• Treatment includes blous IV 50% dextrose, dexamethasone, propylene glycol to normalize the blood glucose level and reduce serum ketone bodies concentration.
• Control by nutritional management, energy supply from digestible fibers and reduce energy supply from starch.
• A 3-year old Holstein dairy cow, 3 weeks post partum, is presented with the complaint that she has dropped in milk production over the last several days. You perform a physical exam and the only abnormality you note is a large amount of ketone bodies in the milk and urine. You decide to administer glucose IV and insulin SQ. What else should this cow be administered?
• The oral propylene glycol will serve as a precursor for glucose production, and will help with the demands of lactation that are causing increased fat mobilization and ketosis. A fourth treatment that is sometimes used is corticosteroids, as they decrease milk production and increase gluconeogenesis.
• IV glucose i. Typically associated with marked improvement when administered. b. Oral propylene glycol. i. Glucose precursor will also support gluconeogenesis. c. Corticosteroids. i. I.E. - Dexamethasone. ii. Used to prolong hyperglycemia because of their gluceoneogenic and appetite stimulating effects. d. Insulin may be used as an adjunctive therapy to IV glucose. e. Force feeding (tube feeding).
• Other primary diseases that may result in secondary ketosis include displaced abomasum, metritis, peritonitis and mastitis, among others. ● Ketosis is characterized by elevated concentrations of the ketone bodies: a. Acetoacetic acid b. Acetone c. B-hydroxybutyric acid
• Ketosis occurs most commonly in lactating cows because the energy (glucose) necessary to support heavy milk production exceeds caloric and nutrient intake. The increased mammary uptake and utilization of glucose in high producing animals is not adequately offset by increased gluconeogenesis in the liver. The body attempts to increase energy production/precursors by mobilizing adipose stores in the form of free fatty acids (FFAs) to contribute to gluconeogenesis in the liver. ● Ketosis is also known as pregnancy toxemia in ewes and does; it occurs during the last 2-4 weeks of gestation when there is increased energy demands from rapidly growing fetuses (i.e. twins) combined with insufficient feed intake.