Submitted to: Submitted by:

Dr. S.P. Madhira Krunal Patel, No. 37

Priyank Patel, No. 38
Shiven Patel, No. 39
 KETOSIS

Ketosis is a common disease of dairy cattle. It typically occurs in early lactation & is
most consistently characterized by partial anorexia & depression.
In addition to inappetence, signs of nervous dysfunction, including pica, abdominal
licking, incoordination & abnormal gait, bellowing & aggression occasionally are
seen.
This condition is worldwide in distribution, but it is most common where dairy cows
are bred & managed for high production.
 ETIOLOGY & PATHOGENESIS

High glucose demand & intense adipose mobilization are causes ketosis.
Both these condition are present in early lactation, at which time negative energy
balance leads to adipose mobilization & milk synthesis creates high glucose demand.
Adipose mobilization is accompanied by high blood serum concentration of
nonesterified fatty acids(NEFA)
During period of intense gluconeogenesis, a large portion of serum NEFA is directed to
ketone body synthesis in the liver.
Ketone bodies are acetone, acetoacetate & -hydroxy butyrate (BHB).
Thus, clinicopathologic characterization of ketosis include high serum concentration of
NEFA & ketone bodies & low concentrations of glucose.
 FACTORS ATTRIBUTABLE TO KETOSIS
1. Lack of nutritive feed
2. Adreno-cortical insufficiency
3. Hypothyroidism
4. Role of insulin
5. Lack of exercise
6. Hepatic insufficiency
7. Deficiency of co-enzyme A
 CLINICAL FINDINGS

Animals may suffer from sub acute, acute or chronic ketosis.

There are four types of disease.
1. Sub-clinical type where urine & blood contain ketone bodies in excess amounts but
there is no obvious symptoms of ketosis
2. The digestive form of ketosis : There is digestive upset, decrease in milk yeild &
depression.
3. Nervous form of ketosis
4. Milk fever type whre hypocalcaemia accompanies hypoglycaemia
 Digestive form:--
Decrease in appetite for 2-4 days
Milk production sharply decreased
Faeces are dry & covered with mucous
Temperature, Pulse & respiration remain with in normal range but in last stage of ketosis
there may be subnormal temperature due to hypoglycaemia
Ruminal motility is decreased
Characteristic odour of ketone bodies (sweet to vinegary smell) is detectable on breath &
in milk
 Nervous form:--
The syndrome stimulates delirium
Characteristic sign include circling movement, crossing of legs, blindness, aimless
wandering & vigorous licking of skin & unusual inanimate objects.
Deprived appetite with profuse salivation
Moderate tremors & tetany may be present & gait is staggery
 CLINICAL PATHOLOGY

Hypoglycaemia, ketonaemia & ketouria are characteristics of disease.

1. Blood sugar level:--

In normal animal (cow) In ketosis

40mg/dl blood Reduced

2. Ketone bodies in blood

Ketone bodies Normal value In ketosis

Acetoacetic acid 0.1mg/dl Increase up to 7mg/dl
BHB 8 mg/dl Increase up to 30mg/dl
Free fatty acids 9 mg/dl Increase up to 28 mg/dl
3. Ketone bodies in milk:--
Normally ketone bodies are not excreted in milk but in ketosis, It may go as high
40mg/100ml of milk. So, sweet odour of ketone bodies can be detected in milk
4. Ketone bodies in urine :--
In ketosis level of ketone bodies may go up to 500-1000mg/100 ml of urine
 BIOCHEMICAL TESTS FOR DETECTION OF
KETONE BODIES IN URINE
Rotheras test:--
For positive diagnosis of ketosis, ketone bodies should be demonstrated in the urine &
milk & this is a test which can be carried out in field.
Reagents required:-
Ammonium sulphate 100 g
Anhydrous sodium carbonate 50 g
Sodium nitropruside 3g
 DIAGNOSIS

History
Clinical sign
Biochemical examination
Subclinical ketosis can be detected by estimation of BHB in milk. Value excess of 1-2
mg/dl will indicate about subclinical ketosis which ultimately may turn into clinical
ketosis.
 DIFFERENTIAL DIAGNOSIS

Digestive form :--

Simple indigestion, Traumatic reticulitis, Abomasal displacement, Metritis & cystic ovaries,
Vagus indigestion, Pleurisy, Pneumonia, Peritonitis, Diabetes mellitus.

Nervous form :--

Rabies, Lead poisoning, Nitrate poisoning, Milk fever
 LINE OF TREATMENT

1. Replacement therapy:--
The only rational treatment in ketosis is to relieve the need of glucose formation from
tissue & allow ketone body utilisation to continue normally.
The simplest means of doing this is by administration of glucose replacement
therapy.
Generally 500-800 c.c of a 40-50% solution of glucose (Dextrose solution) should be
given intravenously at once.
Oral hyperglycaemic agents should be given which maintain glucose level in blood.
 ORAL HYPERGLYCAEMIC AGENTS

Oral hyperglycaemic agents Dose

Glycerol or Glycerine Adult cattle: 100 mg twice daily for 2-3 days
Small cattle: 50mg twice daily for 2-3 days
Propylene gylcol 2 folds of glycerine
Sodium propionate 100-200 g once daily 3 days
Na-lactate & Ca-lactate 1 kg initially followed by 0.5kg daily for 7 days
as maintenance dose
 2. Hormonal therapy
Injection with adrenal corticoids is the successful treatment in field cases
(A) Betamethasone or Dexamethasone are very much effective & can be given upto
30mg I/m
(B) Triamcinolone (Vetalog) is very much active against ketosis. Generally available
in 1 ml vial. Dose is 1 ml I/m for small animal & 5ml I/m for large animal
(C( Prednisolone available in 10 ml vial & concentration is 10mg/ml. Dose for small
animal is 5 ml & for large anima 5ml I/m.
 KETOACIDOSIS

It is a serious complication of diabetes mellitus in dogs.

An absolute or relative lack of insulin leads to diabetic metabolic
decompensation with hyperglycaemia and ketoacidosis.
A precipitating factor (eg infection, stress) which causes an excess of
stress hormones (which antagonise the actions of insulin).
 The major switch in hepatic lipid metabolism occurs by rise in levels of
the stress hormones (glucagon, corticosteroids, catecholamines,
growth hormone).
The hepatic effects of a fall in the insulin:glucagon ratio are:
Increased glycogenolysis
Increased gluconeogenesis
Increased ketogenesis

DKA leads to decrease the production and level of malonyl CoA Which
inhibits fatty acid oxidation
A fall in malonyl CoA levels leads to excessive fatty acid oxidation with
excessive production of acetyl CoA and excess acetoacetate.
 Acetoacetic acid and beta-hydroxybutyric acid dissociate
producing H+ which is buffered by HCO3- in the blood.
For each anion produced there is a loss of one bicarbonate.
The increase in the anion gap (representing the increase in the
unmeasured acid anions) should approximately equal the
decrease in the [HCO3-].
SO A pure high anion gap metabolic acidosis results.
Complication
Hyperchloraemic metabolic acidosis develops during the treatment phase.
Acetoacetate and beta-hydroxybutyrate are moderately strong acids and
even at the lowest urinary pH are significantly ionised. They are excreted with
a cation (usually Na+ or K+) to maintain electroneutrality.
The net effect is the loss of potential bicarbonate equal to the level of urinary
ketone body loss.
The HCO3- is replaced in the blood by Cl- derived from renal reabsorption,
gut absorption or (particularly) IV saline administered during treatment.
 MANAGEMENT OF DKA
DKA can be treated with potent but regular short-acting crystalline
insulin injections to help get the serum glucose levels back under
control.
Phosphate supplementation
Bicarbonate to correct acid-base disturbances
If the serum bicarbonate concentration falls below 10 mEq/l, or the pH
is less than 7.15, specific treatment with sodium bicarbonate is
necessary
 IDENTIFY AND TREAT PRECIPITATING
FACTORS
Antibiotics therapy can be useful to prevent secondary Bacterial
infection.
Pancreatitis and Hyperadrenocorticism treatment also initiated to
prevent so that DKA does not recur.
Reference:-- The merck veterinary manual
Textbook of clinical veterinary medicine by Amalendu chakrabarti