Ketosis is a metabolic disease common in high-yielding dairy cows in early lactation characterized by hypoglycemia, ketonemia, and ketonuria. It occurs when cows cannot produce enough glucose to meet energy demands and instead produce ketone bodies from fat metabolism. Risk factors include negative energy balance, low carbohydrate intake, excess protein intake, and other health issues. Treatment involves glucose therapy to restore blood glucose and reduce ketone bodies along with supportive care. Prevention focuses on proper nutrition and management around calving to meet energy needs and avoid ketosis.

1. Ketosis (Acetonemia)
By-Dr.Suman Kumar Singh
Asst.Professor,IAAS, Tribhuvan University

2. Ketosis is a common metabolic disease of high
yielding animal. It typically occurs in dairy cows in
early lactation and is most consistently characterized
by, hypoglycemia, Ketonaemia and ketonuria.
or
ketosis means accumulation of abnormal amount of
ketone-bodies in the tissues and tissue fluids.
-ketosis is a multifactorial disorder of energy
metabolism in ruminants.
-The disease in cattle respod to treatment and is sef-
limiting.

3. Primary ketosis
-It occurs in high yielding animals,having
well to excellent body condition and fed
quality rations.
It is uncomplicated ketosis.
Heavy body condition and high dietary
protein may lead to excessive mobilization
of fat.

4. Starviation ketosis
-It ocur in animal having poor body
conditions and fed poor quality ration(low
propionate and protein)
-It is due to deficiency of propionate in the
diet and limited capacity of
gluconeogenesis from body reserves.
Alimentary ketosis
-It results from excessive feeding of silage
which is rich in butyrate.

5. -Secondary ketosis
It is caused by various systemic or
infectious disease eg.mastitis, pneumonia,
And complicated ketosis:Responsible for
inadequate feed due to loss of appetite.
Epidemiology
Species-Cows and buffaloes are affected.
Breeds:Buffaloes and crossbred cows are
more suspectible than indigenous cows.
Age-cows of any age may be affected but the
disease appears more common in later
lactations peaking at about the fourth
lactation.

6.  Body condition at calving - over fatness at
calving has been associated with increased
levels of ketosis.
 Physiological status – It is a disease of
lactating cows buffaloes.
 Stage of lactation-It is commonly occur in
between 10 days to 2 months of calving.
 Season –Incidence is higher during calving
season.i.e september to December.

7. Predisposing factor-Genetic susceptibility,
cold stress.

8. Dietary factors:
Under nutriotion/Starviation of feeding of
low carbohydrate diet
-This leads to decreased production of
propionate,hypoglycemia,increased in fat
metabolism and ketone body formation.
Feeding of excess amount of protein
rich diet-This is responsible for increased
production of ketogenic acid like butyric
acid.

9. Excess feeding of sillage-Silage
produces more butyrate and sometimes
silage itself contain 2-4% butyric acid.
Animal factors:
High milk yield-Heavy drain of lactose
through milok mlead negative energy
balance.
Lack of exercise:This leads to decreased
oxidation i.e. Utilization of ketone bodies
by muscle

10. Hepatic insufficiency- The glycogen is
stored in the liver and it is converted to
glucose in emergencies by hepatic
cells.But in hepatic insufficiency there is
insufficient conversion of glycogen to
glucose leading hypoglycemia
Insulin deficiency-It leads to decresed
utilization of glucose and increased
lipolysis.

11. Ketone bodies can be regarded as water-
soluble, transportable form of acetyl units.
Fatty acids are released by adipose tissue
and converted into acetyl units by the liver,
which then exports them as ketone bodies.
• Acetoacetate, D(-3) –hydroxy butyrate
(Beta hydroxy butyrate), and acetone are
often referred to as ketone bodies

12. Low feed intake during late pregnancy and
early lactation
 large amounts of body fat are utilised as
an energy source to support production,
Negative energy balance in the body

13. Drop in blood glucose level
Decrease production of insulin from
pancrease and liver enzyme
Excess fatty acids/other energy sources
from body store will rush to liver
Liver fails to convert the fatty acids and
others into glucose. Due to partial
metabolism of body lipids,ketone bodies
are produced in liver.
Ketosis

15. Digestive/Wasting form
It is most common form of ketosis (about
90% case)
Reduce feed intake
Drop in milk production.
Emaciation/woody apperance due to rapid
loss of body weight.
Depression and reluctant to move.
Dull and rough skin coat.

16. Sweetish smell of breath,milk and urine
Body tempreture usually become normal.
If not treated,few animals may die.In
remaining animals the milk yield falls and
spotaneous recovery(self limiting) occurs
within a month but milk yield is not
regained.

17. Nervous form
Less common form of ketosis
Aimless wandering
Staggering gait,crossing of legs
Circling movement
Head pressing
Vigorous licking of skin and inanimate
objects.
Chewing movement and profuse
salivation.

18. Nervous sign like
hyperasthesia,tremor,convulsions may
occur in short episodes at an interval of
about 8-12 hrs.
Sub-Clinical/Spotaneous ketosis
It occurs in high milk producing cattle due
to excessive production of aceto-acetic
acid in mammary gland.
It may regress or remain as such turn into
clinical form.

19. Drop in milk yield.
Reduce fertility.

20. History-Recent calving (2-8 weeks post-
partum),high milk yield,underfeeding of
CHO,excess feeding of protein rich
concentrates,exposure to cold climate.
Clinical finding-Selective appetite,drop in
milk production,Rapid emaciation and
sweetish smell to breath,urine and milk.
Clinicalpathology:hypoglycemia(<40mg%),
Ketoanemia(>

21. Blood glucose-Decreased to 20-40
mg/dl(Normal:50-60mg/dl)
Blood ketone :increased 20-100mg/dl
(Normal:<10mg/dl)
Urinanlysis
Urine samples are positive for ketone
bodies.
Response to treatment-glucose therpay.

22. Traumatic reticulitis
Metritis
Polynephritis
Surra
Theleriosis
Diabetes mellitus
Tetanus
Rabies
Lactation tetany
Lead poisoning

23.  Treatment is aimed at reestablishing
normoglycemia and reducing serum ketone body
concentrations.
 Administration of 500 ml of 50% dextrose solution
is a common therapy. This solution is very
hyperosmotic and, if administered perivascularly,
results in severe tissue swelling and irritation, so
care should be taken to assure that it is given IV.
 glucose therapy generally results in rapid
recovery, especially in cases occurring near peak
lactation. However, the effect frequently is transient
and relapses are common.

24.  Administration of glucocorticoids including
dexamethasone or isoflupredone acetate at 5-20
mg/dose, IM, generally results in a more sustained
response.
 Glucose and glucocorticoid therapy may be
repeated daily as necessary. Propylene glycol
(250-400 g/dose, PO, [~8-14 oz]) acts as a
glucose precursor and may be effective as ketosis
therapy, especially in mild cases or in combination
with other therapies. This dose may be
administered twice per day. Overdosing propylene
glycol leads to CNS depression.

25. long-acting insulin preparation given IM at
150-200 IU/day(0.5U/kg) may be
beneficial. Insulin suppresses both adipose
mobilization and ketogenesis, but should
be given in combination with glucose or a
glucocorticoid to prevent hypoglycemia.
Glucose orally 500 gm drench with 30 gm
sodium bicarbonate solution.

26. Niacin @ 8 gm orally daily for 5-6 days.
-Niacin is antilipolytic.
Vitamin B12 1-2 mg/kg IM or Iv
-Vit B12 convert propionate to glucose.
Supportive treatment
-INJ.liver extract Feroliv with B complex @5-
10 ml IM on alternate days
Mineral mixture.

27.  It is important to prevent ketosis from occurring,
rather than treating cases as they
appear.Prevention depends on adequate feeding
and management practices.
 Should not be starved or over fat at calving.
 Adequate calorie intake in early lactation.
 Highly fermentable feed such as molasses help
to check the ketosis
 Provide ration contain adequate amount of
phosphorus,cobalt and iodine.


28. Perform rothera’s test on urine and milk
sample at weekly interval till 6-8 wks after
calving.
Avoid wet silage or mouldy hay or dusty
hay asthey increase the level of butyrate
Blood glucose and milk ketone estimation
during 6th week of lactation.

29. Occasionally, very high-producing cows
will be susceptible to ketosis every year. In
these cases a preventive drenching
program of propylene glycol immediately
after calving may avert ketosis in individual
problem cows.