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.
- Send pretreatment samples when safe, including group and screen and a detailed transfusion history, but never delay resuscitation or essential transfusion for a complete antibody work-up.
- Prednisolone is the supported initial treatment for warm AIHA, commonly 1 mg/kg once daily under haematology supervision, followed by a response-led taper rather than abrupt cessation.
- Cold-antibody disease responds poorly to corticosteroids in many patients. Keep the patient and infused fluids warm, treat a reversible trigger and use specialist B-cell-directed therapy when indicated.
- Investigate secondary causes through history, examination, FBC and film, immunoglobulins or protein studies, infection tests, autoimmune assessment and imaging or marrow testing selected by the phenotype.
- Monitor thrombosis, infection, glucose, blood pressure, bone and gastric risks during treatment as well as haemoglobin and haemolysis; relapse may occur before anaemia becomes severe.
Key red flags
Haemoglobinuria, rapid haemoglobin decline, kidney injury, back pain, shock or marked LDH elevation indicates dangerous destruction and urgent organ support.
Low reticulocytes despite active haemolysis suggests early disease, infection, renal or nutrient limitation, marrow pathology or immune targeting of erythroid precursors.
Recent transfusion, new antibody, fever or an unexpected post-unit haemoglobin fall requires a haemolytic-reaction pathway even when the DAT is positive.
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.
- Escalate to critical care for organ compromise and begin subtype-appropriate immunotherapy with specialist oversight while monitoring renal function, thrombosis and the haemoglobin trajectory.