Metabolic disorders in dairy animals can occur around the time of calving due to hormonal and dietary changes. Common disorders include displaced abomasum, bloat, grain overload, ketosis, milk fever, and pregnancy toxemia. Clinical signs may include decreased appetite, milk production, weakness, and low blood glucose or calcium levels. Treatment involves fluid therapy, anti-acid drugs, calcium supplements, and glucose to correct electrolyte and energy imbalances. Changing diets gradually and meeting nutritional needs can help prevent some metabolic disorders.

1. METABOLIC DISORDERS
AND THEIR
MANAGEMENT
PRESENTED BY
HAMZA JAWAD
PRESENTED TO
DR. HUSSAIN AHMAD

2. Metabolic disorders relates to
disturbances of one or more
metabolic processes in the
animal
In dairy animals the time of
disease is important from 3
weeks before and after
parturition

3. Influencing factors are
1.Hormonal changes
2.Moving from non-
lactating to lactating
stage
3.Changing of diet
from roughages to
highly fermentable
CHO

4. DISORDERS
1. Abomasal Displacement
2. Bloat or Ruminal Tympany
3. Grain overload (Rumen Acidosis)
4. Ketosis (Acetonemia)
5. Parturient paresis (Milk fever)
6. Pregnancy toxemia
7. Urolithiasis
8. Subacute Ruminal Acidosis

5. •1. Abomasal Displacement
NORMAL POSITION OF ABOMASUM
lies ventral to the rumen suspended
loosely by the greater and lesser omenta.

6. Left displaced abomasum or right displaced abomasums
(LDA or RDA) and abomasal volvulus occur when it rotates
on its mesenteric axis.

7.  Factors related to
a) Decreased motility of the abomasum
b) Displacement of the abomasum
1. High-
concentrate
and low-
roughage
diets,
2. Hypoc-
alcemia,
3.
Concurrent
diseases
(mastitis,
metritis, and
ketosis),
4. Changes in
position of
intra-
abdominal
organs,
5. Genetic
predisposition

8. Diagnosis & CLINICAL SYMPTOMS
1. Diagnosis The spontaneous
fluid splashing

Or gas tinkling
sounds on the area
of the ping 
Or on
simultaneous
ballottement,

rule out other
causes of left-
or right-sided
pings
2. Clinical
symptoms
Anorexia Decreased milk
production
Ping
Characteristic
Rectal
Examinations
with LDA include
a medially
displaced rumen
and left kidney.
Abomasum is rarely
palpable in LDA and
only occasionally in
RDA.

9. Ping
• Ping sounds like coin sounds produce
• On simultaneous auscultation & percussion of the abdomen
• Between ribs 9 and 13, middle to upper third of the abdomen
• Which should be performed in the area are marked by a line
• From the tuber coxae to the point of the elbow, and from the elbow
toward the stifle.

10. Treatment
3. TREATMENT
Non-drug treatment
Rolling through a 70° arc after casting on her
right side corrects most LDA. Recurrence is
likely
Surgical
Right Omasal-abomasal volvulus is
corrected only surgically.
TREATMENT
Fluid therapy
Initial treatment:
• Balanced Electrolyte Solution (BES), 8 L
(Ringers or isotonic sodium chloride
solution) administered rapidly.
150 g of sodium chloride & 30 g
potassium chloride dissolved in 10
L of water. Administer 40 L per os
MAINTENANCE
TREATMENT
BES, 5L/h until normal hydration is restored (ca.
20 liters).
Precautions  Sodium
bicarbonate and/or sodium
lactate should not be used
Chemotherapy Antibiotics could be administered if surgery is
applied.
4. PREVENTION • Proper feeding is required for dry cows.

11. SURGERY…

12. •2. Bloat or Ruminal Tympany
An over distension of the rumenoreticulum with the
gases of fermentation,
1. Persistent foam mixed with the ruminal contents called
primary or frothy bloat,
2. Free-gas separated from the ingesta called secondary
or free-gas bloat.

14. Condition is very
common
During the rainy
season when legumes
(that have high
percentage of soluble
proteins) grow
abundantly.

15. Bloat-producing pastures include
Legume or legume-dominant pastures
Particularly alfalfa, ladino, and red and white
clovers
But also occur with grazing of young green cereal
crops

16. Alfalfa Ladino Red clovers

17. Secondary ruminal Tympany
Esophageal obstruction caused by
A
foreign
body
Stenosis
Pressure
from
enlargement
outside the
esophagus,
Acute onset of
ruminal atony
due to
anaphylaxis,
Grain overload
and
hypocalcemia.

19. 1. CLINICAL
SYMPTOMS
1.Distensio
n of the
left flank
2.Protrusion
of the
paralumbar
fossa above
the ventral
column
3.Enlarged
abdomen
4.Dyspnea and
granting
5.Mouth
breathing
6.Protrusio
n of the
tongue
7.Extension
of the head
8.Occasionall
y vomition
are observed
2.
DIAGNOSIS
In frothy
bloat,
clinical
diagnosis
is obvious
The causes of
secondary
bloat must be
ascertained
by
clinical
examination to
determine the
cause of the
failure of
eructation

20. 3.Non-surgical
Non-drug treatment
Surgical  Plus
Free gas bloat:
Remove free-gas by
passing a stomach
tube.
Frothy bloat:
Oil, 226-454 g, PO per
stomach tube, stat.
In life-threatening cases:
Emergency rumenotomy or
use a trocar and cannula with
a bore of 2.5cm
Antifoaming agents e.g.
vegetable or mineral oils
80-250 ml/animal

21. Treatment
.Monensin300mg daily protects against pasture bloat.

22. • 3. Grain overload (Rumen Acidosis)
An acute disease of ruminants characterized by
Indigestion
Rumen
stasis
Dehydration Acidosis ToxemiaIncoordination
collapse,
and
frequently
death.

23. It is most common in cattle

25. CLINICAL
SYMPTOMS
Body temperature is
usually below normal
(36.5-38.5°C)
It may be
increased to
41°C if
animals are
exposed to
the sun in hot
weather.
Respirations
tend to be
shallow and
rapid, up to
60-90/min and
heart rate may
be as high as
120-140/min
In severe
cases, rumen
motility is
completely
absent, the
contents of
the rumen
may feel firm
and doughy.
Diagnosis The diagnosis is from the
history if available
A low ruminal
pH (5.5-6)
and
examining the
microflora of
the rumen
Where the
number of
protozoa per
field will be
reduced from
its usual value
of 6-7.
A pH of <5
indicates
severe
acidosis.

26. Dynamic MAPPING Of Rumen Acidity
( How a bolus measures acidosis- red to blue )

27. Non-drug treatment Antiacids Fluid therapy
Initial
Remove the rumen
contents & replace with
ingesta taken from
healthy animals e.g.
animals slaughtered in
the abattoir
Magnesium carbonate or
magnesium hydroxide 1g/kg, PO
mixed in 8 to 12 liters of warm
water, repeated every 6 to 12 h; if
the rumen is evacuated, do not
exceed 225g/ 450kg cow
Activated charcoal 2g/kg to
inactivate endotoxemia
Sodium bicarbonate 5%
solution, 5 L/450 kg IV
within ~30 min
S/E: Excess dose may cause
systemic alkalosis especially
if renal function is impaired
resulting in muscle
weakness and shortness of
breath.
Excessive sodium may
cause diarrhea, abdominal
cramp, tachycardia, and
pulmonary edema.

28. MAINTENANCE S/E: Precaution
Balanced electrolyte solution (BES), or a 1.3%
solution of sodium bicarbonate in saline, 60
L/450 kg, IV for the next 6- 12 hr
see above. Restrict water intake for 18-24 hr
Restrict animals from accessing
grain and the feed should contain
at least 10% of roughage
In feedlot, give ionophore
compounds e.g. monensin to
maintain the rumen pH at higher
level.
PROPHYLAXIS & CONTROL
Avoid sudden and drastic ration changes

29. •4. Ketosis
It occurs in dairy cows that are
• Weak, low glucose level
• provide high milk yield
 In cows at pasture and less frequently with rations of inadequate
calorie content.
 It is generally a result of negative energy balance.

32. CLINICAL SYMPTOMS CLINICAL SYMPTOMS
It occurs with in a week time after calving
1. Inappetance,
2. Constipation,
3. Mucus covered feces,
4. Depression,
5. Staring expression,
6. Drop in milk production,
7. Hump back posture,
8. Weight loss,
9. Circling,
10.Staggering,
11.Licking,
12.Chewing and bellowing,
13.Hyperstesia,
14.Compulsive walking,
15.Head pressing.
16.The breath has acetone odour

33. DIAGNOSIS History on the length of dry
period
Level of nutrition during the dry
period and after parturition
Daily milk production records, if
available.
Blood glucose levels drops from the
normal levels of 400-600 mg/ liter to
250 mg/liter in clinical
Ketone bodies in urine increases from
a maximum of 500 mg/liter up to
12000 mg/liter

34. Non-drug treatment Side effect
Fluid therapy
Initial
Glucose, 500ml , IV
Propylene glycol may cause
hyperosmolarity, lactic acidosis, CNS
depression and adrenal suppression
and ataxia if given parenterally
Plus
Propylene glycol (glucose precursor) 125-250g
mixed with an equal volume of water, PO q12h
for 2 days
D/F :Glucose in 40 or 50% solution;
Propylene glycol as aqueous
solution

35. Prophylaxis
Cows at calving should not be too fat or in very poor condition;
Avoid sudden change of feed; add sufficient protein to the ration

36. •5.Parturient paresis (Milk fever)
Metabolic disease of
mature high producing
dairy cows (>5 years age)
predominantly during the
first 48 hours of parturition.
The disease is associated
with hypocalcemia

39. Characterized by
General
muscle
weakness,
Circulatory
collapse,
Depression
contributes
to dystocia,
Uterine
prolapse
retained
fetal
membranes

40. 3 clinical stages related to the severity of hypocalcemia
Stage 1: Inappetence, Lethargy,
Dullness,
Cold ears, Pupil might be
dilated
Stage 2: Cow stands the
hocks straight and
paddles from one
hind foot to the
other.
Tremors of
muscle,
particularly
of the head
and limbs,
grinding of
teeth, and
incoordination
may occur
Sometimes,
hyperexcitability
and
hypersensitivity
might occur
Stage 3: Cow becomes
recumbent,
drowsy
appearance and
flaccid paralysis
At first lies on
the sternum,
with curvature
of the neck,
and may
struggle to
stand
Then lies on
her side and
becomes
comatose, with
dilated pupil
and a dry
muzzle
Urine and feces not
pass, ruminal
tympany occurs,
body temperature
decreases but heart
beat remains
normal
At last, the
heart rate
and
breathing
becomes
irregular;
dystocia is
common

41. DIAGNOSIS Clinical signs Particularly paresis
in cows close to
calving
And quick response
to calcium
borogluconate
solution are
sufficient

42. Drug treatment
INITIAL
Maintenance S/E:
General rule for fluid therapy is
to give 1 g calcium /45 kg body
wt.
Calcium borogluconate single IV
dose of between 8 and 10 g
Ca; 400 ml of 40% solution will
give 12 g of available Ca.
The drug is infused within 5 to
10 minutes
It may also be concurrently
administered SC
Propylene glycol
125 – 250 g PO q 12
h mixed with an
equal volume of
water prevents
relapse
plus
Calcium
borogluconate as
above
Excessive amount of calcium salts
may lead to hypercalcemia
Symptoms include anorexia,
abdominal pain, constipation,
muscle weakness, mental
disturbance, renal calculi, cardiac
arythmia and coma.
Too rapid administration of
calcium IV is also associated with
many symptoms of hypercalcemia,
particularly cardiac symptoms,
thus administer slowly (at least
over 10-20 min) and monitor
heartbeat

43. Precaution Caution Prevention S/E: (CONT.)
Store in a
controlled
temperature at
15-30oC
Follow strict
sterile
procedures
During the dry
period,
maintain low
level calcium in
feed
(<50g Ca/day),
supply Mg (>50
g per day).
Hypercalcemia is
usually associated
with the parenteral
route of
administration but
also if there is renal
insufficiency.
Administration of
oral calcium avoids
these side effects.

44. •6. Pregnancy toxemia
It is the result of fetal carbohydrate or energy demand
exceeding maternal supply during the last trimester of
pregnancy.
It is precipitated by large or multiple fetuses, low energy
or protein feeds, and health conditions that increase
energy demand or decreased ability to take in feed.

45. CLINICAL SIGNS
Mild cases
CLINICAL SIGNS
Severe cases
DIAGNOSIS
Decreased appetite,
rumination, fecal
production, and nose
licking are general signs of
illness.
cows become depressed,
weak, ataxic, and
recumbent.
Opisthotonus, seizures, or
coma may be seen
terminally.
The history,
Stage of pregnancy
Nutritional status give
tentative diagnosis.
Elevated ketone and
decreased calcium levels
in blood are confirmatory.

46. Supportive
treatment
Mild cases
Supportive
treatment
Severe cases
Drug treatment S/E:
Glucose 500 ml, IV
or
Calcium
borogluconate
combined with
phosphorus,
magnesium, and
20% glucose 500 ml,
IV, PO
Propylene glycol
180-240 ml q 12 h
and fluids 20-60
L/day, PO or IV.
Anabolic steroids
like
dihydrotestester
one
undecyclenate,
200-300
mg/animal, IM,
stat.
Dihydrotesterone may
give rise to adverse
effects related to its
androgenic or anabolic
effect.
These include
increasing in retention
of nitrogen, sodium,
and water,
hypercalcemia,
increased bone growth
and skeletal muscle.

47. •Simple indigestion or ruminal atony
Characterized by
accumulation of indigestible
feed in the rumen.
It is caused by a sudden
change of the feed, such
as

48. 1. Addition of
urea to a ration,
2. Turning cattle
onto a lush cereal
grain pasture,
3. Introducing
feedlot cattle to a
high-level grain
ration
4. Which may lead to
excessive fermentation
or putrefaction and
impairs rumen function
for 24-48 hours

49. CLINICAL SYMPTOMS
Silage over
feeding
CLINICAL SYMPTOMS
Excessive feeding of
grain
DIAGNOSIS
Anorexia
Rumen becomes full, firm,
doughy
Primary ruminal contractions are
absent,
But secondary contractions may
be present..
Anorexia and ruminal
stasis;
The rumen is not necessarily
full and may contain
excessive fluid;
The feces is usually soft and
foul smelling
This is based largely
on elimination of
other possibilities
History of a change
in the nature or
amount of the diet.

50. Non-drug
treatment
Drug treatment S/E: Drug treatment
Warm water or
saline, 20-40 L,
PO, followed by
vigorous kneading
of the rumen.
Indigestion due to
excessive high-energy
feeds intake:
Magnesium
hydroxide, 0.5mg/kg
in a 10% aqueous
suspension, PO or by
stomach tube.
Magnesium
hydroxide may
cause diarrhea
and may interfere
with absorption of
drugs
administered PO
Indigestion due to
too much urea or
protein intake:
Acetic acid 5% or
vinegar PO by
stomach tube. Or
4-8 L of ruminal
fluid from a healthy
cow in case of
reduced ruminal
microbes.

51. •7. Urolithiasis
Uroliths are
common in cattle
resulting from
urinary tract
obstruction by
mineral-protein
calculin.
It is common in
males than
females.

52. In the bull, the sigmoid flexure is the most common site
for uroliths to lodge.
Early castration predisposes to urolith-induced urethral
obstruction by removing hormonal influences necessary
for mature development of the penis and urethra.

54. CLINICAL SIGNS CLINICAL SIGNS CLINICAL SIGNS DIAGNOSIS
In partial
obstruction
animals dribble
blood-tinged
urine, pain on
urination
On complete
obstruction
tenesmus,
Tail twitching,
weight shifting,
and signs
consistent with
colic are
observed.
Inappetence, depression,
and rectal prolapse may also
be seen
Affected steers may elevate
the tail and show urethral
pulsations just ventral to the
rectum.
Complete occlusion results
in urethral perforation or
urinary bladder rupture and
animals die of uremia.
History,
Clinical signs,
Physical
examination
are sufficient

55. Non-drug treatment Plus Plus
Establish patent urethra
plus
Correct fluid imbalance
In severe uremic animals
Rehydration and correction of
acid-base and electrolyte
abnormalities
Conservative therapy
involving administration of
antispasmodics and
tranquilizers to straighten
the sigmoid flexure
PREVENTION Adjust Calcium to
phosphorus ratios of
1.2 to 2:1 of the feed
Sodium chloride
may be raised to 4%
together with
sufficient water
intake;
Feeding urine
acidifers such as
ammonium chloride
(45 g/steer/day).

56. 8. Subacute Ruminal Acidosis
• One consequence of feeding excessive amounts of rapidly
fermentable carbohydrates in conjunction with inadequate fiber to
ruminants is subacute ruminal acidosis.
• Characterized
by periods of low ruminal pH that resolve without
treatment and is rarely diagnosed
• Dairy cows, feedlot cattle, and feedlot sheep are at risk of developing
this condition.

58. Etiology and Pathophysiology:
• Ruminal pH fluctuates considerably during a 24–hr period (typically
between 0.5–1 pH units)
• Determined by the dynamic balance between the intake of
fermentable carbohydrates, buffering capacity of the rumen, and rate
of acid absorption from the rumen.
• SARA is caused by ingestion of diets high in rapidly fermentable
carbohydrates and/or deficient in physically active fiber.

59. • Ruminal VFAs are absorbed passively across the rumen wall
• Absorption of VFA inherently increases as ruminal pH drops.
• These acids are absorbed only in the protonated state.
• They have a pKa of ~4.8, the proportion of these acids that is
protonated increases dramatically as ruminal pH decreases below 5.5

60. Clinical Findings:
• Reduced or cyclic feed intake
• Decreased milk production
• Reduced fat
• Poor body condition score despite adequate feed intake
• Unexplained diarrhea.
• High rates of culling or unexplained deaths may be noted in the herd

61. Clinical Findings:
• Sporadic cases of caudal vena cava syndrome may also be seen.
• The clinical signs are delayed and insidious.
• Actual episodes of low ruminal pH are not identified; in fact, by the
time an animal is observed to be off-feed, its ruminal pH has probably
been restored to normal.
• Diarrhea may follow periods of low ruminal pH
• however, this finding is inconsistent and may be related to other
dietary factors as well.

62. Diagnosis
• Diagnosed on a group rather than individual basis.
• Measurement of pH in the ruminal fluid of a
representative portion of apparently healthy animals
in a group
• Animal selection should be from highest-risk groups:
cows between ~15–30 days in milk in component-fed
herds and cows between ~50–150 days in milk in
herds fed total mixed rations

63. Diagnosis
• Ruminal fluid is collected by rumenocentesis, and its pH is
determined on a pH meter.
• Twelve or more animals are typically sampled at ~2–4 hr after a grain
feeding (in component-fed herds) or 6–10 hr after the first daily
feeding of a total mixed ration

64. Diagnosis
• If >25% of the animals tested have a ruminal pH <5.5, then the group
is considered to be at high risk of subacute ruminal acidosis.
• This type of diagnostic tool should be used in conjunction with other
factors such as ration evaluation, evaluation of management
practices, and identification of health problems on a herd basis.
• Milk fat depression is a poor and insensitive indicator of subacute
ruminal acidosis in dairy herds.

65. Treatment and Prevention
• Because subacute ruminal acidosis is not detected at the time of depressed
ruminal pH, there is no specific treatment for it.
• Secondary conditions may be treated as needed.
• The key to prevention of subacute ruminal acidosis is allowing for ruminal
adaption to high-grain diets, as well as limiting intake of readily fermentable
carbohydrates.
• This requires both good diet formulation (proper balance of fiber and non fiber
carbohydrates) and excellent feed bunk management.

66. Treatment and Prevention
• Animals consuming well-formulated diets remain at high risk of this
condition if they tend to eat large meals because of excessive
competition for bunk space or after periods of feed deprivation.

67. Treatment and Prevention
• Field recommendations to feed component-fed concentrates to dairy cattle
during the first 3 wk of lactation are usually excessive.
• Feeding excessive quantities of concentrate and insufficient forage results in a
fiber-deficient ration likely to cause subacute ruminal acidosis.
• The same situation may be seen during the last few days before parturition if the
ration is fed in separate components; as dry-matter intake drops before calving,
dry cows preferentially consume concentrates instead of forage and develop
acidosis

68. Treatment and Prevention
• Supplementing the diet with direct-fed microbials that enhance
lactate utilization in the rumen may reduce the risk of subacute
ruminal acidosis.
• Yeasts, propionobacteria, lactobacilli, and enterococci have been
used for this purpose.
• Ionophore (eg, monensin sodium) supplementation may also reduce
the risk by selectively inhibiting ruminal lactate producers and by
reducing meal size.

70. Protecting cow from mastitis

71. A perfect calcium balance at calving