Depending on the severity and underlying cause of liver disease, a nonregenerative or regenerative anemia may develop. Severe or acute anemia can impact the liver as a result of hypoxia, causing alterations in hepatocyte membranes, leading to release of transaminases and induction of ALP. Altered RBC morphology (poikilocytes, irregularly irregular RBCs) is common in cats with cholangiohepatitis and hepatic lipidosis (HL). Cats with HL, severe cholangiohepatitis, and EHBDO also may develop Heinz bodies, reflecting oxidative injury that may lead to hemolysis. Severe hypophosphatemia in HL may develop secondary to a re-feeding syndrome and cause hemolysis severe enough to require a blood transfusion; this can be avoided by providing fluid therapy supplemented with potassium phosphate when nutritional support is implemented. In dogs with diffuse necroinflammatory liver disease (altered sinusoidal perfusion), RBCs with microvascular shearing (eg, schistocytes, acanthocytes) may be seen. RBC microcytosis is common in congenital or acquired portosystemic shunting, although the pathologic mechanism remains unclear.
Change in WBC count or distribution are variable. Leukocytosis may reflect inflammatory, infectious, necrolytic, or diffuse infiltrative hepatic disorders, or release of endogenous glucocorticoids or administration of glucocorticoids. Leukopenia can reflect sepsis or toxicosis. In severe diffuse necroinflammatory liver injury, damaged sinusoidal microvasculature can provoke platelet aggregation, contributing to thrombocytopenia and disseminated intravascular coagulation.