Introduction

• May be primary immune-mediated or secondary, eg drugs, infections, lymphoproliferative disease. Common cause of regenerative anemia Anemia: overview.
• Cause: antibodies (IgG or IgM) or complement bound to erythrocyte → intravascular or extravascular hemolysis.
• Signs: lethargy, tachypnea, tachycardia.
• Diagnosis: hematology, Coombs' test.
• Treatment: cytotoxic drugs Chemotherapy: general principles : azathioprine, cyclosporine, prednisone.
• Prognosis: fair for chronic cases, 50% mortality for acute cases.

Pathogenesis

Etiology

Primary AIHA

• Cause not known.
• ?Genetic influences in certain breeds.

Secondary AIHA

• Secondary AIHA may be triggered by:
  • Neoplasia, eg lymphoproliferative Lymphoproliferative disease and myeloproliferative Acute myeloid leukemia diseases, hemangiosarcoma Hemangiosarcoma.
  • Infections, eg bacterial endocarditis Endocarditis: bacterial.
  • Auto-immune diseases, eg systemic lupus erythematosus Systemic lupus erythematosus (SLE).
  • Drug induced, eg potentiated sulfonamides Trimethoprim , penicillins.
  • Increased incidence following vaccination may be a cause - not proven.

Predisposing factors

General

• Breed predispositions.

Specific

• ?Increased incidence in following estrus in female.

• Increased incidence in month following vaccination - suggested but not proven.

Pathophysiology

• Auto-antibodies to red cell membrane components → removal of red cells from circulation → anemia.

• Antibodies on red cells prompt the mononuclear phagocyte system to remove the red cells mainly in the spleen and liver, ie extravascular hemolysis → acute or chronic form of disease; chronic form more common.
• Partially phagocytosed cells become spherocytes.
• If antibodies fix complement on the red cell surface in sufficient quantities, intravascular hemolysis results → acute form of disease.
• Increased red cell breakdown results in hyperbilirubinemia.
• Hyperbilirubinemia → jaundice if bilirubin formation exceeds ability of liver to remove and conjugate it. Jaundice common with intravascular hemolysis, rare with extravascular hemolysis.
• Cold hemagglutin disease → antibodies preferentially bind to red blood cells in blood colder than normal body temperatures, eg in peripheral capillary beds in cold weather. Agglutination → occlusion of capillary beds → ischemic necrosis.

Timecourse

• Acute form 1-4 days.
• Chronic form days to weeks.

Diagnosis

Treatment

Prevention

Outcomes