An outlook of Postparturient Hemoglobinuria (PPH) in Buffalo

 An outlook of Postparturient Hemoglobinuria (PPH) in Buffalo

  Akshay Kumar¹*, Deeksha Bharti²

                                      1*- Division of Veterinary Surgery and Radiology, ICAR-IVRI

                          2- Department of Veterinary Medicine, GBPUAT, Pantnagar

Introduction

Parturient hemoglobinuria also known as red water or hypophosphatemia or post parturient hemoglobinuria or Lahu mutna or Rakth mutna”. It  is an acute  life threatening metabolic disorder of high producing dairy animals and an endemic disease in buffalo, which is characterized by intravascular haemolysis, haemoglobinuria and anemia. Since last more than 45 years back it has been recognized and considered to be the most periodic metabolic ailment of parturient buffaloes. The disorder is immenseky fatal owed  to intravascular haemolysis and severe anemic anoxia. In buffaloes a higher incidence rate has been recorded as  compared to cattle. In cattle the condition is widely prevalent during the post partum period however, in buffaloes the condition is mostly observed during advanced pregnancy or within a month of parturition.

Etiology

• A consistently low serum phosphorous in affected buffaloes
• Dietary deficiency of phosphorous
• Feeding of sugar cane tops, sugar beet, kale, mustard, cabbage and lucerne or berseem , cabbage and turnip leaves  precipitate deficiency of phosphorous
• Addition of maize husk and barley grit caused an outbreak of nutritional hemoglobinuria in recently calved buffaloes at a farm.
• The dietary cation/anion ratio is an important aspect in maintaining the homeostasis of phosphorous and calcium in the serum.

Pathogenesis

Hypophosphatemia, a low dietary intake of phosphorus and drain of  phosphorus in lactation causes further depletion of phosphorus reserves. The mammalian red blood cells are dependent  on glucose metabolism as the main source of energy for its  viable function and structure. Owing to the above  the RBCs are highly vulnerable to factors inhibitory to the glycolytic pathways. The deficiency of phosphorous causes depletion of ATP. There is a remarkable drop in red blood cell adenosine triphosphate (ATP) and 2,3 diphosphoglycerate (2,3-DPG) synthesis in RBC’s because of insufficient availability of intracellular phosphate.

Without sufficient ATP to power sodium pumps, the intracellular sodium concentration rises and the cells become more rigid and, as a result, rupture as they pass through capillary beds. The reduced ATP levels along with decreased membrane phospholipids (which help in maintaining the shape and integrity of red cells) were considered responsible for the change in the shape of red blood cells with resultant echinocytosis/ sphero-echinocytosis which are prone to hemolysis.

Clinical findings

• Red to coffee colored urine
• The pulse rate, temperature and respiratory rates are increased in PPH affected buffaloes. Enlarged lymph nodes, pale mucous membranes, decreased capillary refill time (1-2 per sec), dyspnoea, weak pulse, tachycardia, panting and mild salivation
• Pale mucous membrane, tachycardia, tachypnea
• The urine from hemoglobinuria affected buffaloes produces moderately stable foam when it falls on the ground.
• Milk yield is significantly reduced and anorexia is marked as the disease progresses.
• Ruminal movement are reduced in affected buffaloes.
• With the progression of the disease jaundice and weakness may be evident with recumbency. Laboured breathing and jugular pulsation can be observed during the terminal stages of the disease.

Clinical pathology

• Lactating buffaloes in an affected herd may have moderately low levels of phosphorous below 4 mg/dL without any clinical sign. Buffaloes with hemoglobinuria evidence extremely low levels of 0.97-2.6 mg/dL of phosphorous.
• The blood glucose, bilirubin, creatinine and serum alkaline phosphatase are elevated in affected buffaloes suggesting jaundice due to intravascular hemolysis.
• The serum enzymes AST, ALT and ALP are significantly elevated in buffaloes with parturient hemoglobinuria .
• A marked decrease in the PCV, hemoglobin and total erythrocyte count has been recorded in hemoglobinuria affected buffaloes along with Howell Jolly bodies.
• Affected buffaloes evidence macrocytic hypochromic anemia with neutrophilia.

Diagnosis

• The presence of haemoglobin in the urine can be verified by the Benzidine test or using commercially available dip stick strips.
• On centrifugation of the dark coffee colored urine the red blood cells settle at the bottom in hematuria whereas in hemoglobinuria the color remains unchanged.
• The lecithin cholesterol acyltransferase (LCAT) was found to be low in hemoglobinuria in buffaloes.
• Estimation of phosphorus level is done for diagnosis for hypophosphatemia

Treatment

• Sodium acid phosphate 60-80 g dissolved in 300 mL of distilled water as a 20% solution administered IV is the usual therapy administered to affected buffaloes. This is followed by a similar dose administered SC and oral supplementation of phosphorous (60 gm), copper sulfate (3-5 gm) and cobalt sulfate (100 mg) for a period of 7-10 days. Two to four IV therapies are required for complete recovery.
• The intravenous injection of phosphorus in the form of monobasic sodium phosphate (60g) in 300 ml of sterile distilled water followed by oral administration of the same dose, twice daily for 3 days, has often been effective.
• Epsilon amino caproic (EACA) (20 g dissolved in 540 mL of 5% dextrose and administered IV till recovery) and para-amino methyl benzoic acid (300 mg dissolved in 540 mL of 5% dextrose and administered IV till recovery) have been shown to be 90-92% effective for treating hemolysis
• Antioxidants have been suggested for therapy of hemoglobinuria in buffaloes because of the possible oxidative stress that may be present in affected buffaloes, antioxidants like vitamin A and E have also been suggested to be helpful.
• Supportive therapy includes Liver tonics, Anti-inflammatory drugs (Dexamethasone 4.4 mg/ml), Calcium borogluconate together with Magnesium and Phosphorous in organic combination and Dextrose (Mifex), 300 ml slow IV and reset subcutaneously, Nicinamide, Folic acid, Vit. B₁₂and B₆ Glycinated iron copper and cobalt, vitamin E.
• The best treatment for severely affected cows in PPH is transfusion of large quantity of whole blood

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