Understanding Downer Cow Syndrome (DCS) in Cattle

Downer Cow Syndrome
                (DCS)
The common clinical sign :The 
inability to rise
They do not respond to treatment for
hypocalcemia
It can be seen at all stages of the production
cycles
Most are affected between 2 days before and
10 days after parturation
They are high producers
They suffer from 
parturient paresis 
i.e.
partially paralyzed during labor
Etiology and pathogenesis
A sequela to parturient paresis :
1.
Metabolic disorders
2.
Physical injuries during parturition
3.
Traumatic muscular injuries associated with
attempts to rise from prolonged recumbency
contribute to the Downer condition
The risk factors associated with the
development of DCS
1.
Parturient paresis
        As a result of delayed or incomplete treatment for hypocalcemia
        It may lead to ischemic muscle necrosis and nerve paralysis when the
cow may be lying on one hind limb for 6-12 hrs. 
2.
Poor housing conditions
        Hard and slippery floors predispose them to traumatic bone, ligament,
joint, tendon, muscle and nerve injuries when they attempt to stand 
3.
Excess fat
        Lead to traumatic nerve injury at parturition and muscle degeneration
during prolonged recumbency
       More susceptible to incidences of Downer cow in herds
4.
Septic conditions
        Mastitis, metritis, and traumatic pericarditis
5.
Malnutrition
        During periods of prolonged starvation, malnutrition contributes to the
development of the DCS
Clinical signs
:
Cows may appear
Bright and or alert
Dull and depressed
Hyper excited
After treatment for hypocalcemia
The cows usually appear alert and normal in
most respects but are weak in the limbs or
make no effort to rise
Clinical pathology
1. Cows have 
hypocalcemia
 (< 8mg Ca/ 100 ml) and
hypophosphatemia 
(< 3mg P / 100ml)
Serum Mg conc. may be low (< 1.5mg /100ml) showing
muscle tremors or excitability
2. Serum aspartate transaminase (
AST
) and creatine
phosphokinase (
CPK
) are elevated indicating muscle
damage
3. Urinalysis:
      Animal shows proteinuria 2-3 days after extensive muscle
damage
     
Myoglobinuria: 
Should be differentiated from
haemoglobinuria
          Ketonuria
    
May also be present in complicated cases
Bilirubinuria
Necropsy:
No specific lesions
Hemorrhage and degeneration of the upper
hind limb musculature and nerves
Myocarditis in some cases
Diagnosis
:
1.
Clinical signs is the basis of diagnosis
2.
Clinical exam for differential diagnosis by paying
special attention to the caudal part of the spine,
including the tail, the pelvic ring and the hind legs.
Rectal examination should be done
3.
Painful reaction to manipulation, abnormal mobility,
lack of motor and sensory responses, or audible
crepitation may reveal the site and nature of
physical injuries responsible for prolonged
recumbency
4.
AST > 200mU /ml indicates guarded prognosis,
>500mU /ml indicates hopeless prognosis; increased
CPK
5.
Hypoglycemia, proteinuria, ketosis
Differential Diagnosis
:
 Some conditions causing prolonged
recumbency are bone fracture of pelvis,
luxation of hip joints, and rupture of major
muscles
Treatment:
1.
Basic aim to get the cow onto her feet i.e.
Hoisting a cow with hip clamps
2. Cow that show relapses after treatment with
calcium alone are given 
more calcium
intravenously or solution containing 
Ca, P, Mg,
glucose 
and 
K
3. 
Phosphorus
 (30 gm sodium acid phosphate in
300 ml water intravenously) or ‘
Tonophosphan
’ is
given as downer cow show persistent
hypophosphatemia
4. CNS stimulants e.g. 
tripelennamine HCl 
@ 0.5
mg/kg body weight by slow intravenous injection
5. Serum potassium and skeletal muscle
potassium conc. are found to be low in downer
cows. 10 liters of water containing 80gm NaCl
and 20gm KCl are given by stomach tube and a
similar solution is provided in a bucket for the
cows to drink. Another container with fresh
water is provided
6. Treatment of septic conditions like mastitis and
metritis with broad-spectrum antibiotics
7. Provision of shelter, bedding and food to cows
without obvious bone fractures and joint
dislocations
8. Cows should be turned frequently (every 4-6 hr)
from one side to other side
Preventions:
Attention to nutrition to avoid excessively fat cows
Low calcium intake in the preparturient period
Early treatment of PP with sufficient calcium. At least
8 gm calcium is required for complete cure. Close
observation should be made after treatment for
relapses
Provision of adequate bedding for cows during
parturition and supervision of cows to minimize
prolonged dystocia to prevent traumatic nerve and
muscular damage
 
 
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Downer Cow Syndrome (DCS) is characterized by the inability of cows to rise, commonly seen around calving. It is associated with metabolic disorders, physical injuries, and prolonged recumbency. Risk factors include poor housing conditions and health issues like mastitis. Clinical signs range from dullness to hyperexcitability. Clinical pathology reveals hypocalcemia, muscle damage, and proteinuria. Necropsy findings may include muscle degeneration. Early recognition and appropriate management are crucial in addressing DCS in cattle.


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  1. Downer Cow Syndrome (DCS)

  2. The common clinical sign :The inability to rise They do not respond to treatment for hypocalcemia It can be seen at all stages of the production cycles Most are affected between 2 days before and 10 days after parturation They are high producers They suffer from parturient paresis i.e. partially paralyzed during labor

  3. Etiology and pathogenesis A sequela to parturient paresis : 1. Metabolic disorders 2. Physical injuries during parturition 3. Traumatic muscular injuries associated with attempts to rise from prolonged recumbency contribute to the Downer condition

  4. The risk factors associated with the development of DCS Parturient paresis As a result of delayed or incomplete treatment for hypocalcemia It may lead to ischemic muscle necrosis and nerve paralysis when the cow may be lying on one hind limb for 6-12 hrs. 1. 2. Hard and slippery floors predispose them to traumatic bone, ligament, joint, tendon, muscle and nerve injuries when they attempt to stand Poor housing conditions 3. Lead to traumatic nerve injury at parturition and muscle degeneration during prolonged recumbency More susceptible to incidences of Downer cow in herds Excess fat 4. Mastitis, metritis, and traumatic pericarditis Septic conditions 5. During periods of prolonged starvation, malnutrition contributes to the development of the DCS Malnutrition

  5. Clinical signs: Cows may appear Bright and or alert Dull and depressed Hyper excited After treatment for hypocalcemia The cows usually appear alert and normal in most respects but are weak in the limbs or make no effort to rise

  6. Clinical pathology 1. Cows have hypocalcemia (< 8mg Ca/ 100 ml) and hypophosphatemia (< 3mg P / 100ml) Serum Mg conc. may be low (< 1.5mg /100ml) showing muscle tremors or excitability 2. Serum aspartate transaminase (AST) and creatine phosphokinase (CPK) are elevated indicating muscle damage 3. Urinalysis: Animal shows proteinuria 2-3 days after extensive muscle damage Myoglobinuria: Should be differentiated from haemoglobinuria Ketonuria Bilirubinuria May also be present in complicated cases

  7. Necropsy: No specific lesions Hemorrhage and degeneration of the upper hind limb musculature and nerves Myocarditis in some cases

  8. Diagnosis: 1. Clinical signs is the basis of diagnosis 2. Clinical exam for differential diagnosis by paying special attention to the caudal part of the spine, including the tail, the pelvic ring and the hind legs. Rectal examination should be done 3. Painful reaction to manipulation, abnormal mobility, lack of motor and sensory responses, or audible crepitation may reveal the site and nature of physical injuries responsible recumbency for prolonged 4. AST > 200mU /ml indicates guarded prognosis, >500mU /ml indicates hopeless prognosis; increased CPK 5. Hypoglycemia, proteinuria, ketosis

  9. Differential Diagnosis: Some conditions causing prolonged recumbency are bone fracture of pelvis, luxation of hip joints, and rupture of major muscles

  10. Treatment: 1. Basic aim to get the cow onto her feet i.e. Hoisting a cow with hip clamps 2. Cow that show relapses after treatment with calcium alone are intravenously or solution containing Ca, P, Mg, glucose and K given more calcium 3. Phosphorus (30 gm sodium acid phosphate in 300 ml water intravenously) or Tonophosphan is given as downer hypophosphatemia cow show persistent 4. CNS stimulants e.g. tripelennamine HCl @ 0.5 mg/kg body weight by slow intravenous injection

  11. 5. Serum potassium and skeletal muscle potassium conc. are found to be low in downer cows. 10 liters of water containing 80gm NaCl and 20gm KCl are given by stomach tube and a similar solution is provided in a bucket for the cows to drink. Another container with fresh water is provided 6. Treatment of septic conditions like mastitis and metritis with broad-spectrum antibiotics 7. Provision of shelter, bedding and food to cows without obvious bone fractures and joint dislocations 8. Cows should be turned frequently (every 4-6 hr) from one side to other side

  12. Preventions: Attention to nutrition to avoid excessively fat cows Low calcium intake in the preparturient period Early treatment of PP with sufficient calcium. At least 8 gm calcium is required for complete cure. Close observation should be made after treatment for relapses Provision of adequate bedding for cows during parturition and supervision of cows to minimize prolonged dystocia to prevent traumatic nerve and muscular damage

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