This schematic depicts the steps taken to type, screen, and crossmatch blood. To determine ABO group and rhesus type, commercial anti-A, anti-B, anti-Rh(D)

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This schematic depicts the steps taken to type, screen, and crossmatch blood. To determine ABO group and rhesus type, commercial anti-A, anti-B, anti-Rh(D) agglutinate patient cells. This direct agglutination test and hemolysis is visible.3 Antibody screening test: A panel of commercial red cells of known antigen type (each cell carries numerous antigens) are incubated with patient plasma. In North America, a typical panel of 3 cells (eg, Immunor Gamma, Immunocor Inc, Norcross, GA) will detect alloantibodies to rhesus (C, c, E, e, f, V, CW), Kell (K, k, Kpa, Kpb, Jsa, Jsb), Kidd (Jka, Jkb), Duffy (Fya, Fyb), Lewis (Lea, Leb), MN (M, N, S, s), Lutheran (Lua, Lub), P1, and Xga antigens. The mostly IgG alloantibodies that bind cells then need rabbit antihuman IgG (antiglobulin reagent or Coombs serum) to agglutinate (indirect agglutination test).2 Electronic or computer crossmatch requires no history of a positive antibody screen; a previous group, type, and negative antibody screen from bloodbank records; a current group, type, and negative antibody screen. An immediate spin is a final check of ABO compatibility, looking for direct agglutination (visible clumping or hemolysis) on mixing patient plasma with donor cells.4 Antibody identification: A more extensive panel of up to eight commercial red cells of known antigen type (eg, Ortho Clinical Diagnostics Inc, Raritan, NJ) are tested against patient plasma to identify which antigens are responsible for the agglutination. This process may need to be extended to panels expressing rarer antigens not listed above (such as anti-U seen in some sickle cell patients) to identify alloantibodies. Occasionally, this process may take days for multiply transfused patients such as those with sickle cell disease. However, current US practice is to antigen-match patients needing repeat transfusions for all rhesus and Kell antigens to prevent common alloantibody formation, and to reduce the development of subsequent “rarer” alloantibodies and the need for difficult crossmatching. Source: Blood and Blood Component Therapy, Anesthesiology, 3e Citation: Longnecker DE, Mackey SC, Newman MF, Sandberg WS, Zapol WM. Anesthesiology, 3e; 2017 Available at: http://accessanesthesiology.mhmedical.com/DownloadImage.aspx?image=/data/books/2152/longnecker3_ch78_f004.png&sec=164241137&BookID=2152&ChapterSecID=164240980&imagename= Accessed: November 05, 2017 Copyright © 2017 McGraw-Hill Education. All rights reserved