Blood Banking and Immunohematology
ABO typing has two independent arms
Forward (cell) typing uses anti-A and anti-B reagents against the patient's red cells; reverse (serum) typing uses A1 and B reagent cells against the patient's plasma. In a healthy adult the two must agree, so the first response to any discrepancy is to repeat the test and rule out a clerical or wrong-patient error.
Reverse typing depends on antibody that takes months to develop and can fade, so cord bloods, the elderly, and immunosuppressed or heavily transfused patients may show weak or absent isohemagglutinins. Other classic discrepancy causes: rouleaux from excess protein (resolves with saline replacement), cold autoagglutinin such as anti-I (reacts below 37 °C), weak A or B subgroups, acquired B, and chimerism after transplant.
Rh and antibody detection
D is the most immunogenic red cell antigen; weak D and partial D variants explain why some D-negative patients must receive D-negative units. Antibody screening uses 2–3 group O donor cells at immediate spin and AHG (IAT); a positive screen leads to a panel where you rule out specificities using cells homozygous for the antigen (dosage) and compare enzyme-treated versus untreated cells (ficin destroys Duffy and MNS, enhances Rh, Kidd, Lewis).
Traps and a worked example
Questions love phase-of-reactivity: reactivity only at immediate spin that disappears at AHG points to a cold-reactive IgM, not an alloantibody. Remember O red cells and AB plasma for emergency release.
Worked example: a patient's screen is positive at room temperature only, panreactive, and negative at AHG. The workup is a cold autoantibody (anti-I); prewarm technique and, if transfusion is needed, ABO-compatible units that are crossmatch-compatible at 37 °C/ AHG are appropriate.