This sporadic condition that commonly affects only individual high-yielding dairy cows at the onset of lactation is characterized by the development of peracute intravascular hemolysis and anemia with a potentially fatal outcome. Beef and nonlactating cattle are rarely affected. It is seen worldwide. The exact cause is unknown, but phosphorus depletion or hypophosphatemia is believed to be a major predisposing factor. Severe intracellular phosphorus depletion of RBC is known to increase cellular fragility and, therefore, the risk of cellular lysis. A similar condition reported in New Zealand was associated with copper deficiency, potentially making RBC more susceptible to oxidative stress. Other potential causes are hemolytic or oxidative plant toxins (often from Brassica spp, sugar beets, or green forage). Clinical disease is rare but, when it occurs, 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 erythrogenesis.

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 (ruling out hematuria) and presence of concurrent severe anemia. Intravascular hemolysis caused by Babesia (see Blood Parasites: Babesiosis) or Theileria (see Blood Parasites: Theileriases) may be ruled out by blood smear analysis, and standard laboratory methods can be used to rule out leptospirosis (see Leptospirosis) or bacillary hemoglobinuria (see Clostridial Diseases: 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 the decreased intravascular oncotic pressure. Treatment with sodium phosphate (60 g in 300 mL of sterile water, IV followed by SC, every 12 hr) or copper glycinate (120 mg available copper) has been used but frequently is not effective in preventing further hemolysis. 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 July 2011 by Walter Gruenberg, DrMedVet, MS, PhD, DECAR, DECBHM