Synopsis
Confirm accelerated red-cell destruction, separate intravascular from extravascular and immune from non-immune mechanisms, and recognise fragmentation, transfusion reactions and inherited disorders requiring urgent action.
- Confirm haemolysis with a pattern, not a solitary LDH: falling haemoglobin, raised absolute reticulocytes, unconjugated bilirubin and LDH, reduced haptoglobin and supportive film findings should be reconciled with timing and liver function.
- A low reticulocyte response does not exclude dangerous haemolysis early in the episode or when infection, marrow disease, renal failure, iron, B12 or folate deficiency limits compensation.
- The direct antiglobulin test detects immunoglobulin or complement on red cells; it supports immune classification but does not by itself prove that active haemolysis is occurring.
Key red flags
Dark urine, haemoglobinaemia or haemoglobinuria, markedly consumed haptoglobin, renal injury and rapid symptoms indicate free haemoglobin released within the circulation.
Investigation priorities
Quantify anaemia, compensation and tempo across all lineages.
Management branches
There is shock, severe symptomatic anaemia, haemoglobinuria with kidney injury, thrombocytopenia with fragments, or a suspected transfusion reaction.
- Use ABCDE, stop any transfusion, maintain venous access, check identity and send urgent FBC, film, reticulocytes, haemolysis, renal, coagulation, group and blood-bank reaction samples while supporting circulation and urine output.
- The preferred emergency route is immediate senior haematology and transfusion discussion, with a TTP pathway for high-probability microangiopathy and the local transfusion-reaction pathway for temporally related haemolysis.
Anaemia, jaundice, reticulocytosis, dark urine or an abnormal film raises red-cell destruction in a stable patient.