Postparturient hemoglobinuria is a sporadic condition seen worldwide that most commonly affects individual high-yielding dairy cows at the onset of lactation. It is characterized by development of peracute intravascular hemolysis and anemia with potentially fatal outcome. Beef and nonlactating cattle are rarely affected. The exact cause is unknown, but phosphorus depletion or hypophosphatemia has been incriminated as a major predisposing factor. Severe intracellular phosphorus depletion of RBCs is known to increase osmotic fragility of the RBCs, possibly predisposing to intravascular hemolysis. Although marked hypophosphatemia is commonly diagnosed in affected animals, most cases of severe hypophosphatemia are not associated with intravascular hemolysis, suggesting that hypophosphatemia is not the sole causative factor responsible for postparturient hemoglobinuria. A similar condition reported in New Zealand was associated with copper deficiency, potentially making RBCs more susceptible to oxidative stress. Other potential causes are hemolytic or oxidative plant toxins (often from Brassica spp, sugar beets, or green forage).
Clinical cases are rare, but when they occur the case fatality rate is high (10%–30%). With clinical disease, rapid intravascular hemolysis leads to severe anemia, tachycardia, weakness, hemoglobinuria with dark brown or red urine, and pallor over several days. Milk production drops rapidly. Affected cows also may have fever, diarrhea, and tachypnea. Cows that survive the hemolytic crisis may take several months to recover completely. Convalescent cows and cows with subclinical disease develop icterus and evidence of increased erythropoiesis.
Diagnosis is usually made by recognition of clinical signs, particularly dark urine and anemia during the characteristic stage of lactation. Hemoglobinuria may best be diagnosed by noting failure of the urine to clear with centrifugation (excluding hematuria) and presence of concurrent severe anemia. Intravascular hemolysis caused by Babesia (see Babesiosis) or Theileria (see Theileriases) may be excluded by blood smear analysis, and standard laboratory methods can be used to exclude leptospirosis (see Leptospirosis) or bacillary hemoglobinuria (see Bacillary Hemoglobinuria). Diagnostic testing and feed or pasture analysis can be performed to identify toxic plants and deficiency of phosphorus, copper, and other antioxidants.
Transfusion of large quantities of whole blood is the best treatment for severely affected cows. Crystalloid fluids may be beneficial if blood is not available and may protect the kidneys against toxic and anoxic damage, but monitoring the PCV and the total protein concentration is required to prevent third spacing due to the decreased intravascular oncotic pressure. Parenteral treatment with monosodium dihydrogen phosphate (60 g in 300 mL of sterile water) IV followed by oral treatment with 200–300 g of sodium phosphate salts every 12 hr is suitable to rapidly correct hypophosphatemia. Copper glycinate (120 mg available copper) has been recommended in cases in which copper deficiency is suspected as the underlying cause. The efficacy of these treatments to prevent 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 extra-label. Correction of mineral deficiencies and elimination of plant toxins from the diet may help prevent recurrence.
Last full review/revision April 2014 by Walter Gruenberg, DrMedVet, MS, PhD, DECAR, DECBHM