The HAF RESEARCH data show that the number of cases of acetonaemia (or ketosis) increase significantly during the winter, and the number of cases continue to increase until turnout. So it is particularly important to look out for acetonaemia until at least a month after turn-out.

Like most metabolic diseases it is important to remember that for every cow that shows clinical signs, there will be several more which are affected sub-clinically.

What is acetonaemia?

Acetonaemia occurs when the cow’s energy intake does not match its requirement and the cow is unable to compensate and mobilises its body reserves too quickly. In the beef cow, this is most likely to occur in late pregnancy when the cow’s appetite is at its lowest and the energy requirement of the growing calf near its peak. In the dairy cow, the mismatch between input and output usually occurs in the first few weeks of lactation, because the cow is not able to eat enough to match the energy lost in the milk.

Clinical Signs

  1. Reduced milk yield: Initially a moderate decline, eventually a sudden drop
  2. Body condition and weight loss
  3. Reduction in appetite (initially non-forage feeds)
  4. Dull, stary coat
  5. Firm, ‘waxy’ dung
  6. Acetone (pear drop) smell of breath or milk – not always detectable
  7. Temperature, pulse rate and respiratory rate usually normal
  8. A few develop nervous signs including excess salivation, licking, incoordination, aggression.

Acetonaemia is more common in the dairy cow, probably because the energy difference of the lactating cow is more difficult to overcome than that of the pregnant cow, which means that most dairy cows in the UK are in negative energy balance during the first few weeks of lactation. Acetonaemia occurs when the cow is not able to cope with this energy deficit, either because it is too great or if it continues for too long.

If it occurs in one cow, it usually indicates that although the other cows in the herd are currently compensating, many are suffering from an energy deficit that is significantly reducing their productivity. A clinical case of acetonaemia is the tip of the iceberg, and therefore it is advisable to discuss blood testing other cows in the same lactation group, for the subclinical form of the disease.


Each treated cow is the tip of the iceberg, so prevention is very important. The aim of any prevention regime is to maximise dry matter intake during the critical period. This can be achieved by:

  1. Avoiding over-fat and over-thin cows: Aim to calve cows at condition score (CS) 3.0. Fat cows have lower appetites and mobilise more fat and so are more prone to ketosis Dry-off cows at CS 3.0. Cows should not gain or lose weight during the dry period. Thin cows should be fed to gain condition during late lactation. Fat cows should be fed to lose condition during late lactation.
  2. Preventing disease around calving. Cows with calving difficulties, retained membranes, endometritis, milk fever, toxic mastitis, and hypomagnesaemia all have an increased risk of acetonaemia, so preventing these diseases reduces the risk of acetonaemia.
  3. Feeding correctly Introduce the milking ration to the dry cows from two weeks before calving. This allows the rumen time to adapt to the milking diet Maximise palatability. Good quality forage and feeding as a total mixed ration both increase intake and thus reduce the energy deficit Maximise feeding time. Increasing the feeder space, particularly for self-fed silage, can increase intake and thus reduce energy deficit Keep the diet consistent. Avoid sudden changes to the diet even if only batch changes of concentrate.
  4. Reduce stress Keep freshly-calved cows separate from the milking herd for at least two weeks after calving. Acetonaemia is a significant cause of economic loss, but these losses can be reduced by good management and attention to detail.
  5. Early treatment leads to early recovery, so treat as soon as possible Veterinary advice should be sought to ensure that displaced abomasum is ruled out as a cause of the acetonaemia.

If acidosis occurs in one cow, it usually indicates that although the other cows in the herd are currently compensating, many are suffering from sub-clinical acidosis that is significantly reducing their productivity. A clinical case is the tip of the iceberg, and therefore solutions have to be for the whole herd not the individual animal.

Many diseases have been linked to acidosis. For some, such as liver abscesses, the evidence is very strong. For others, such as sole ulcer and white-line disease, the link is not so strong.


Difficult as signs are non-specific
Ketosis (acetonaemia) must be ruled out
Reduced milk fat is strongly indicative of excess starch feeding
Most diagnoses are based on eliminating other causes of reduced appetite and yield


Most treatment is supportive to allow the rumen to return to normal
Ruminal stimulants are of little value
Feeding of buffers such as sodium bicarbonate can help in the short term, particularly in animals in the same group.


Every treated cow is the tip of the iceberg, so prevention is vital. The aim of any prevention regime is to give the cow time to adapt to change and not to expect the rumen to be able to adapt to whatever is thrown at it.

There are two types of sub-acute acidosis. The first occurs in freshly calved cows (up to 20 days after calving). This occurs because of a failure to adapt the rumen to the lactation diet before calving. In this case, dry cow management is the key to prevention. In particular, feeding a transition diet and minimising calving stress are important.

The second type of acidosis affects cows from peak to mid-lactation. At this time rumen adaptation to the diet should have occurred, so acidosis in these cows occurs as a result of feeding diets that are low in fibre and high in starch (or which allow for feed selection).

In all herds with an acidosis problem there needs to be a full assessment of the feeding, with attention paid to what the cows are being fed and to what they are eating. Each individual situation will be different and require a different range of solutions. Nevertheless there are several factors which are likely to be of importance in most situations:

  • Forage to concentrate ratio. Except in very high yielding cows a ratio of 60:40 will significantly reduce the risk of acidosis
  • Feeding total mixed rations with forage and concentrates mixed can significantly reduce acidosis, provided selection of the concentrate portion doesn’t occur
  • Feeding space: If there is insufficient space average meal size will increase, increasing the risk of acidosis (even with a TMR). (This can also occur if feeding time is restricted or if feeding times are irregular).


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