Postparturient hemoglobinuria is a sporadic condition present worldwide that most commonly affects individual high-yielding dairy cows at the onset of lactation. It is characterized by development of acute intravascular hemolysis, often associated with hemoglobinuria and leading to potentially life-threatening anemia. Although the condition is widely held to be caused by hypophosphatemia and phosphorus deficiency, other etiologies such as copper deficiency and excessive consumption of rapeseed, turnips, and sugar-beet pulp were also found to cause hemoglobinuria. Clinical signs can include a drop in milk production, anorexia, lethargy, and pale, icteric mucous membranes. However, these might not be apparent until the disease is well advanced. Diagnosis is often by clinical signs and ruling out other causes of intravascular hemolysis. Transfusion of whole blood is the only treatment known to be effective. However, this is only indicated for severe cases.
Etiology and Pathogenesis of Postparturient Hemoglobinuria in Dairy Cows
The exact cause of postparturient hemoglobinuria is unknown; however, phosphorus depletion or hypophosphatemia, as well as copper deficiency and possibly hemolyzing substances contained in certain feeds (such as Brassica spp, sugar beets, or green forage) have been incriminated as potential causative or predisposing factors.
Phosphorus deficiency associated with depletion of intracellular phosphorus stores of RBCs is assumed to result in insufficient availability of ATP in these cells, which can increase their osmotic fragility, possibly predisposing to intravascular hemolysis. Although marked hypophosphatemia appears to be the most consistent laboratory result of blood biochemical analysis in affected animals, many dairy cows experience pronounced transient hypophosphatemia in early lactation and do not develop postparturient hemoglobinuria, suggesting that hypophosphatemia is not the sole causative factor. Cases of postparturient hemoglobinuria observed in New Zealand have been linked to copper deficiency, which is thought to increase the susceptibility of RBCs to oxidative stress (1).
Clinical Findings and Lesions of Postparturient Hemoglobinuria in Dairy Cows
Clinical cases of postparturient hemoglobinuria are rare. However, when they occur, the fatality rate is considerable (10–30%) (2). In general, the disorder remains clinically inapparent until the PCV drops below 20%. As intravascular hemolysis continues, affected cows display a drop in milk production, anorexia, and lethargy. Clinical signs of marked hemolytic anemia, such as pale and icteric mucous membranes, tachycardia, tachypnea, and hemoglobinuria with dark brown or red urine, become readily apparent. Cases of spontaneous recovery in which intravascular hemolysis stops without therapeutic intervention are frequent. Cows that survive the hemolytic crisis can take several weeks to recover completely.
Diagnosis of Postparturient Hemoglobinuria in Dairy Cows
Clinical evaluation
History of recent parturition
History of exposure to diets low in phosphorus or containing large amounts of beet pulp, rapeseed, or turnips
Exclusion of other causes of intravascular hemolysis
Diagnosis of postparturient hemoglobinuria is usually made by recognition of clinical signs, particularly dark urine and anemia, during the characteristic stage of lactation. Hemoglobinuria can best be diagnosed by noting failure of the urine to clear with centrifugation (excluding hematuria) and presence of concurrent severe anemia.
Jaundice becomes apparent after a few days of hemolysis. Intravascular hemolysis caused by babesiosis or theileriosis can be excluded by blood smear analysis, and standard laboratory methods can be used to exclude leptospirosis or bacillary hemoglobinuria.
Diagnostic testing and feed or pasture analysis can be performed to identify toxic plants and deficiency of phosphorus, copper, and other antioxidants. Blood phosphorus concentrations are unreliable indicators for diagnosis of this condition, because cases with normal or even elevated blood phosphorus concentrations can be observed. Normal or high blood phosphorus concentrations in animals with postparturient hemoglobinuria have been explained by massive intravascular hemolysis releasing large amounts of phosphorus from the intracellular space into plasma.
Treatment and Prevention of Postparturient Hemoglobinuria in Dairy Cows
Transfusion of whole blood in severe cases
Transfusion of 4–6 L of whole blood is the only effective treatment for postparturient hemoglobinuria (3). Blood transfusion, however, is only indicated in the most severe cases, with PCV < 15%. Affected cows should be restrained in a calm environment, avoiding physical stress as much as possible and allowing easy access to water and feed. Color of urine, demeanor of the animal, and PCV should be followed closely to identify animals requiring blood transfusion. Oral drenches with fluids to maintain hydration might be needed in depressed animals.
Oral treatment with 200–300 g of sodium-phosphate salts every 12 hours (which can be preceded by IV infusion with monosodium dihydrogen phosphate, 60 g in 300 mL of sterile water, is suitable to rapidly correct hypophosphatemia. However, it does not stop hemolysis (4).
The efficacy of these treatments in preventing further hemolysis is not documented. No sodium-phosphate or copper-glycinate solution approved for parenteral administration by the FDA is currently available for use in ruminants. The use of these compounds in dairy cows is therefore extralabel. Correction of mineral deficiencies and elimination of plant toxins from the diet can help prevent recurrence.
Key Points
Postparturient hemoglobinuria is most commonly found in high-producing dairy cows at the onset of lactation.
The exact cause is unknown. However, hypophosphatemia, copper deficiency, toxic plant exposure, and presence of hemolyzing substances in certain feeds have been proposed as predisposing factors.
Many cows do not display clinical signs until the PCV falls below 20%. Once that occurs, mortality risk can be 10–30%.
Transfusion of whole blood is indicated for severe cases.
For More Information
Macwilliams PS, Searcy GP, Bellamy JE. Bovine postparturient hemoglobinuria: a review of the literature. Can Vet J. 1982;23(11):309-312.
Van den Brink LM, Cohrs I, Golbeck L, et al. Effect of dietary phosphate deprivation on red blood cell parameters of periparturient dairy cows. Animals. 2023;13(3):404.
References
Smith B, Woodhouse D, Fraser A. The effects of copper supplementation on Stockhealth and production. 2. The effect of parenteral copper on incidence of disease, haematological changes and blood copper levels in a dairy herd with hypocuprosis. N Z Vet J. 1975;23(6):109-112. doi:10.1080/00480169.1975.34210
Macwilliams PS, Searcy GP, Bellamy JE. Bovine postparturient hemoglobinuria: a review of the literature. Can Vet J. 1982;23(11):309-312. https://pmc.ncbi.nlm.nih.gov/articles/PMC1790234/
Van den Brink LM, Cohrs I, Golbeck L, et al. Effect of dietary phosphate deprivation on red blood cell parameters of periparturient dairy cows. Animals. 2023;13(3):404. doi:10.3390/ani13030404
Cohrs I, Grunberg W. Suitability of oral administration of monosodium phosphate, disodium phosphate, and magnesium phosphate for the rapid correction of hypophosphatemia in cattle. J Vet Intern Med. 2018;32(3):1253-1258. doi:10.1111/jvim.15094
