Synopsis
Confirm immune red-cell destruction, distinguish warm, cold and mixed patterns, identify secondary causes and deliver urgent transfusion support and subtype-specific immunotherapy with specialist monitoring.
- Diagnose autoimmune haemolytic anaemia from active destruction plus immune evidence: reticulocytes, bilirubin, LDH, haptoglobin, film and DAT must be interpreted together.
- Warm AIHA is usually IgG-mediated and predominantly extravascular, with spherocytes and splenic clearance; cold-antibody disease is commonly complement-mediated and may show agglutination and cold-triggered symptoms.
- A positive DAT is not synonymous with AIHA. Recent transfusion, medicines and immunoglobulin treatment can produce coating without sufficient haemolysis, while occasional immune haemolysis is DAT negative by routine methods.
Key red flags
Haemoglobinuria, rapid haemoglobin decline, kidney injury, back pain, shock or marked LDH elevation indicates dangerous destruction and urgent organ support.
Investigation priorities
Measure severity, tempo, marrow compensation and other lineage changes.
Management branches
Haemolysis is rapid or causes chest pain, syncope, heart failure, shock, neurological change or kidney injury.
- Use ABCDE, obtain haemolysis, DAT, group and antibody samples, involve senior haematology and the transfusion laboratory immediately, and treat precipitating infection or another reversible driver.
- Preferred support is clinically indicated red-cell transfusion using the safest units the laboratory can provide; incompatibility from an autoantibody must not create harmful delay when oxygen delivery is failing.
Key medicines
PrednisoloneA common BSH initial regimen for warm AIHA is 1 mg/kg by mouth once daily, followed by a gradual haematology-directed taper after response.
RituximabA commonly used off-label specialist regimen is 375 mg/m² intravenously once weekly for four doses; follow the haematology protocol and current product guidance.