Warm autoimmune hemolytic anemia (AIHA) is caused by IgG autoantibodies that bind red blood cells (RBCs) optimally at body temperature (37 degrees C), opsonizing them for destruction by splenic macrophages via Fc-receptor-mediated phagocytosis (extravascular hemolysis). The direct antiglobulin test (Coombs test) is positive for IgG and/or C3 on the RBC surface, confirming immune-mediated hemolysis. The pathophysiology involves autoantibodies coating RBCs, which are then recognized by Fc-gamma receptors on splenic macrophages; partial phagocytosis removes portions of the RBC membrane, creating spherocytes (small, dense cells lacking central pallor) that are trapped and destroyed in the spleen. Laboratory hallmarks include anemia, reticulocytosis (bone marrow compensation), elevated LDH and indirect bilirubin (from hemoglobin catabolism), decreased haptoglobin (consumed binding free hemoglobin), spherocytes on peripheral smear, and positive direct Coombs test. Warm AIHA may be primary (idiopathic) or secondary to lymphoproliferative disorders (CLL, lymphoma), autoimmune diseases (SLE), medications, or infections. The nurse monitors hemoglobin levels, assesses for worsening anemia symptoms (fatigue, dyspnea, tachycardia, pallor), monitors LDH, bilirubin, and reticulocyte count as hemolysis markers, administers corticosteroids (first-line) as prescribed, administers rituximab for steroid-refractory disease, ensures blood bank...