A coagulation panel is justified to investigate blood loss as a cause of anemia or as an indicator of disseminated intravascular coagulation (DIC).²⁴ Elevations in coagulation times, however, have not been shown to predict thromboembolism or mortality in patients with IMHA. In one study in dogs with IMHA, no statistical difference was noted in survival times in patients with or without baseline coagulation abnormalities.²⁵

An antinuclear antibody (ANA) test is occasionally performed in patients with IMHA to investigate systemic lupus erythematosus; but to truly have this condition, patients must have high ANA titers and two or more manifestations of autoimmunity (e.g. dermatomyositis, vasculitis, polyarthropathy) in addition to IMHA.²⁶ False positive results can occur with certain underlying infections and neoplastic diseases.

A bone marrow aspirate or core biopsy may be helpful in an ongoing nonregenerative anemia to search for underlying diseases such as RBC aplasia or hypoplasia, immune destruction of RBC precursors, or neoplastic infiltration.²⁴

The decision to hospitalize a patient with IMHA depends largely on the severity of clinical signs. If the disease is caught early and the patient is stable, close outpatient management can be a reasonable option. More often, patients presenting with IMHA are already quite sick and need hospitalization for monitoring, supportive care, and treatment.

The treatment of IMHA is extremely case-specific but generally involves four principles: 1) preventing hemolysis with immunosuppressive therapy, 2) treating tissue hypoxia, 3) deterring the formation of thromboemboli, and 4) providing supportive care.

Immunosuppressive therapy

Numerous drugs have been described to treat IMHA (Table 3). The first line of treatment in IMHA is immunosuppressive corticosteroids. The addition of secondary and tertiary immunosuppressants may be indicated when patients present with severe IMHA (very low hematocrits, severe autoagglutination, intravascular hemolysis, or thrombocytopenia), when glucocorticoids do not adequately control the hemolysis, or when the side effects of glucocorticoids become unacceptable. The use of multiple cytotoxic drugs in combination requires careful monitoring, however, as there is a risk of severe immunosuppression and danger of infection.²⁷

Table 3: Immunosuppressive Drugs Used to Treat IMHA in Dogs

Corticosteroids. Dexamethasone (0.1 to 0.3 mg/kg intravenously once or twice daily) can be given initially if oral medications cannot be tolerated. Prednisone or prednisolone (2 mg/kg orally once or twice daily) is the oral drug of choice. Glucocorticoids are thought to prevent hemolysis by decreasing the clearance of antibody-coated RBCs by macrophages, reducing the amount of antibody binding and complement activation on RBCs, and, in the long-term, minimizing autoantibody production.¹ Side effects include polyuria, polydipsia, polyphagia, increased panting, gastrointestinal ulceration, and increased susceptibility to infection.

Azathioprine. In cases of severe IMHA (low RBC counts, autoagglutination, or intravascular hemolysis), the second drug usually added in dogs is azathioprine (2 mg/kg orally once daily or every other day). Studies have shown increased survival times in dogs treated with glucocorticoids and azathioprine.^13,28 Drawbacks to this medication are that it is only available in oral form and it can take weeks to take effect.

Azathioprine is a purine analogue antimetabolite that disrupts DNA and RNA synthesis and is effective in limiting cell-mediated immunity (T-lymphocyte function).²⁴ Side effects can include gastrointestinal upset, bone marrow suppression, pancreatitis, and hepatotoxicity. Regular physical examinations and complete blood counts and serum chemistry profiles (weekly at first, then monthly) will help to monitor for the more serious complications of this medication. Azathioprine can cause severe bone marrow and hepatic toxicosis in cats and is not recommended.²⁴