Post-Parturient Haemoglobinuria in Dairy Cows

Post-parturient Haemoglobinuria
Synonyms: Hypophosphataemia/
 
       Red Water disease/
                     Nutritional Haemoglobinuria
It is a metabolic disease of high producing dairy cows occuring soon
after calving (2-4 weeks after calving),  is characterised by intravascular
haemolysis, haemoglobinuria and profound anaemia.
It May affect buffaloes before or after parturition
Buffaloes are more susceptible than Cattle
3rd – 6th calving cattle/cows are more susceptible.
 
Etiology:
Deficiency of Phosphorus in diet :
       a) Forages grown on Phosphorus Deficient soil:
          
Natural Deficiency in soil.
         Constant removal by cropping.
          Leaching by rains.
 
Reduced availability due to extreme pH or high levels of AI, Fe,Ca,
in soil.
Drought conditions reduces ‘ P ’ content in the forage
b)
 Heavy feeding on hemolytic or oxidative plant toxins(e.g Brassica
spp , sugar beets, or green forage)and plants low in P(cruciferous
plants& Barseem) may predispose to the case
c) Impaired absorption
:
Vitamin ‘ D ’ Deficiency
Improper Ca : P ratio
Intestinal diseases – diarrhoea
Ruminal stasis / dysfunction
d) Increased requirement of phosphorus :
Heavy drain of ‘ P ’ throudh milk ( 0.93 - 1 gm / kg ) in recently
              calved animals.
Increased requirement for development of foetus during advance
               pregnancy.
 
d) 
Very cold drinking water
Normal function of Phosphorous:
Intracellular functions(Glycolysis, o2 transport, muscle
contractions)
Cell membrane from oxidative damage.
Demineralization of bone
Pathogenesis:
 
Decreased Phosphorous
Inhibit the Glycolytic Pathway of RBCs
Decrease Glycolysis and ATP Synthesis
Haemolysis and
Haemoglobinuria
Altered structural and functional changes, and increased fragility of RBCs
Clinical signs:
Partial to complete anorexia
Marked drop in milk yield
Temperature usually normal but
    heart rate is increased
Tachycardia, loud heart sounds
Rapid breathing in early stage and dysponea (anoxic anoxia) in
later stages
secondary ketosis
Light to dark coffee coloured urine
Pale mucous membranes with  Jaundice is seen in very late stage
of disease
Usually have firm and dry faeces
Death occur due to anaemic anoxia
 
Clinical Pathology
Serum level of P 0.5-1.5mg/dl(Normal 4-7mg/dl)
 
Haemoglobin drop to 6-8 gm% (Normal 10-12 gm%)
 
TEC drop to 2-3 millions/cumm of blood (Normal 5-8
millions /cumm of blood )
 
PCV drop to 2.5-15 (N= about 35)
 
Serum bilirubin and BUN raised.
 
Low Cu level of  blood
Diagnosis:
(I) History
(II) Clinical signs
(III) Laboratory diagnosis
Quick response to replacement therapy of P
Enlargement of liver & spleen
Differential diagnosis:-
Babesiosis
Leptospirosis
Bacillary haemoglobinuria(Clostridium haemolyticum)
 Treatment:
a. 
Specific treatment
Sodium acid phosphate (60g in 300 ml DW, IV, ) followed by S/C
dose after 12 hr for  3-5 days, and also , oral dose (60 gm ) / daily /
till 3 days after recovery
Inj. Ascorbic acid (Vit. C)@ 15 - 20 mg / kg IV daily for 2- 4 days can
also be used. Ascorbic aid is antioxidant and hence it relives
oxidatives stress on RBCs.
Anti fibrinolytic drugs (Inj. Botropase 10 ml in  20 ml Normal
Saline  IV daily for 1 - 3 days)
b. Supportive treatment:
 Blood transfusion in severe cases. A minimum of 5 L of blood to a
450 kg cow is recommended. This will usually suffice for up to 48
h by which time an additional transfusion may be necessary if the
cow is weak and the mucous membranes pale.
Fluid therapy for both supportive therapy and to minimize the
danger of haemoglobinuric nephrosis
Oral dosing with bone meal (120 g twice daily) or dicalcium
phosphate or a suitable source of Ca & P daily for 5 days is
recommended
 
Mineral mixtures @ 50 gm daily orally to maintain serum
inorganic phosphorous  levels.
Haematinic like Feritas inj. during convalescence may be given
 
Prevention & Control
Mineral mixture @30-40gm/animal/day
Preparation containing Ca, P & Vit. D
Protect recently calved & advance pregnant animals from cold
stress
Do not have the access to kale, beets, turnips, alfa-alfa in excess
while grazing in the pasture
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Post-Parturient Haemoglobinuria (PPH) is a metabolic disease affecting high-producing dairy cows after calving, characterized by hemolysis, hemoglobinuria, and anemia. Common in buffaloes and cows, it is caused by phosphorus deficiency in diet, affecting intracellular functions and leading to clinical signs like anorexia, drop in milk yield, and dark urine. Diagnosis involves measuring serum phosphorus levels, hemoglobin, and total erythrocyte count. Treatment includes addressing the underlying deficiency and managing clinical symptoms.

  • PPH
  • Dairy Cows
  • Metabolic Disease
  • Hemoglobinuria
  • Phosphorus Deficiency

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  1. POST-PARTURIENT HAEMOGLOBINRURIA(PPH) VCM-609 (Medicine) Asst. Professor Dr. Anil Kumar Dept. of VCC

  2. Post-parturient Haemoglobinuria Synonyms: Hypophosphataemia/ Red Water disease/ Nutritional Haemoglobinuria It is a metabolic disease of high producing dairy cows occuring soon after calving (2-4 weeks after calving), is characterised by intravascular haemolysis, haemoglobinuria and profound anaemia. It May affect buffaloes before or after parturition Buffaloes are more susceptible than Cattle 3rd 6th calving cattle/cows are more susceptible. Etiology: Deficiency of Phosphorus in diet : a) Forages grown on Phosphorus Deficient soil: Natural Deficiency in soil. Constant removal by cropping. Leaching by rains.

  3. Reduced availability due to extreme pH or high levels of AI, Fe,Ca, in soil. Drought conditions reduces P content in the forage b) Heavy feeding on hemolytic or oxidative plant toxins(e.g Brassica spp , sugar beets, or green forage)and plants low in P(cruciferous plants& Barseem) may predispose to the case c) Impaired absorption: Vitamin D Deficiency Improper Ca : P ratio Intestinal diseases diarrhoea Ruminal stasis / dysfunction d) Increased requirement of phosphorus : Heavy drain of P throudh milk ( 0.93 - 1 gm / kg ) in recently calved animals. Increased requirement for development of foetus during advance pregnancy.

  4. d) Very cold drinking water Normal function of Phosphorous: Intracellular functions(Glycolysis, o2 transport, muscle contractions) Cell membrane from oxidative damage. Demineralization of bone Pathogenesis: Decreased Phosphorous Inhibit the Glycolytic Pathway of RBCs Decrease Glycolysis and ATP Synthesis Altered structural and functional changes, and increased fragility of RBCs Haemolysis and Haemoglobinuria

  5. Clinical signs: Partial to complete anorexia Marked drop in milk yield Temperature usually normal but heart rate is increased Tachycardia, loud heart sounds Rapid breathing in early stage and dysponea (anoxic anoxia) in later stages secondary ketosis Light to dark coffee coloured urine Pale mucous membranes with Jaundice is seen in very late stage of disease Usually have firm and dry faeces Death occur due to anaemic anoxia

  6. Clinical Pathology Serum level of P 0.5-1.5mg/dl(Normal 4-7mg/dl) Haemoglobin drop to 6-8 gm% (Normal 10-12 gm%) TEC drop to 2-3 millions/cumm of blood (Normal 5-8 millions /cumm of blood ) PCV drop to 2.5-15 (N= about 35) Serum bilirubin and BUN raised. Low Cu level of blood

  7. Diagnosis: (I) History (II) Clinical signs (III) Laboratory diagnosis Quick response to replacement therapy of P Enlargement of liver & spleen Differential diagnosis:- Babesiosis Leptospirosis Bacillary haemoglobinuria(Clostridium haemolyticum) Treatment: a. Specific treatment Sodium acid phosphate (60g in 300 ml DW, IV, ) followed by S/C dose after 12 hr for 3-5 days, and also , oral dose (60 gm ) / daily / till 3 days after recovery

  8. Inj. Ascorbic acid (Vit. C)@ 15 - 20 mg / kg IV daily for 2- 4 days can also be used. Ascorbic aid is antioxidant and hence it relives oxidatives stress on RBCs. Anti fibrinolytic drugs (Inj. Botropase 10 ml in 20 ml Normal Saline IV daily for 1 - 3 days) b. Supportive treatment: Blood transfusion in severe cases. A minimum of 5 L of blood to a 450 kg cow is recommended. This will usually suffice for up to 48 h by which time an additional transfusion may be necessary if the cow is weak and the mucous membranes pale. Fluid therapy for both supportive therapy and to minimize the danger of haemoglobinuric nephrosis Oral dosing with bone meal (120 g twice daily) or dicalcium phosphate or a suitable source of Ca & P daily for 5 days is recommended

  9. Mineral mixtures @ 50 gm daily orally to maintain serum inorganic phosphorous levels. Haematinic like Feritas inj. during convalescence may be given Prevention & Control Mineral mixture @30-40gm/animal/day Preparation containing Ca, P & Vit. D Protect recently calved & advance pregnant animals from cold stress Do not have the access to kale, beets, turnips, alfa-alfa in excess while grazing in the pasture

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