Introduction

• Cause: the blood accumulates high levels of ketones, usually when the cow is trying to release energy from her body fat and muscle reserves.
• Signs: weight loss, reduced appetite, ketonuria, nervous signs, vocalizing.
• Diagnosis: clinical signs in a recently calved cow, cow side blood test, ketonuria, response to treatment.
• Treatment: glucose and/or glucocorticoids.
• Prognosis: good.
• Clinical disease is often an indicator of more widespread subclinical ketosis in the herd.

Pathogenesis

Etiology

• Modern dairy cows have been bred to produce extremely high milk yields.
• In early lactation, these huge milk yields can put an enormous strain on the cow and her body reserves, as her dry matter intakes of food are unable to match the energy output required for her production.
• The Krebs cycle of energy metabolism is illustrated in this simple diagram A simple guide to energy metabolism.
• In periods of high energy demand, fat is mobilized and pathways resulting in the formation of 'ketone bodies' are upregulated.
• The diagrams, links below, illustrate the cycle whereby negative energy balance results in the formation of ketone bodies:
  • Early lactation: using fat stores.
  • What happens when a cow mobilizes fat?.
• The formation of ketone bodies can be illustrated in further detail Ketone body formation.
• Glucose (from proprionate metabolism) is 'spared' as an energy source for the brain as this is the only form of energy that the brain can utilize.

Predisposing factors

• Anything that limits dry matter/energy intake in freshly calved cows will act as a potential predisposing factor for ketosis:
  • Management factors ie insufficient access to feed (lack of feed space, food running out/not 'pushed up', inappropriate ration composition/balance/palatability for stage of lactation.
  • Cow factors ie reduced intake capability (excessive body condition/internal fat deposition, reduced rumen volume due to space occupied by calf and insufficient intakes when dry), heat stress.
  • Disease/health factors eg, Hypocalcemia Hypocalcemia (milk fever), Dystocia Dystocia and sequelae eg, retained fetal membranes RFM, Metritis, mastitis, lameness, etc (all affect dry matter intake - DMI).
  • Genetic predisposition.

Timecourse

• Clinical disease can appear to have a sudden onset, although this is often preceeded by a period of subclinical disease.
• Response to treatment is usually rapid, although relapse may occur without 'maintenance therapy'.

Epidemiology

•  Acetonemia is essentially a disease caused by an imbalance between energy intake and output, for maintenance and milk production.
• Acetonemia is likely to affect 20% or more of cows, calved up to 3 weeks, in many herds with yields over 8,000 liters. 
• These cows may have sub optimal production but are not necessarily affected by clinical ketosis.
• A proportion are likely to develop clinical disease.
• As production is reduced, energy balance is restored, and so in many cows this is a self curing condition and may go unnoticed.

Diagnosis

Treatment

Prevention

Outcomes