X hits on this document

Word document

Adverse Outcomes in Blood and Blood Component Therapy - page 4 / 19





4 / 19

been implicated as causing DHTR. Rothman et al9, described a patient who developed a DHTR 11 days after receiving a transfusion, that was caused by anti-U. The case was a good illustration of the difficulty that can occur in differentiating a delayed transfusion reaction from autoimmune hemolytic disease when the antibody involved is directed against a high incidence blood group antigen.9 In another case, Moheng et al10, described the case of a 27-year-old, gravida 3, para 2 woman who experienced a DHTR caused by anti-Dob. She had anti-Dob in both her serum and eluate 8 days after transfusion of 6 units of Dob positive red cells. No antibody had been detected prior to transfusion however, by the 15th day posttransfusion, there was no evidence of survival of red cells from any of the 6 units. Anti-Dob are IgG, red cell stimulated antibodies that react primarily in indirect antiglobulin test (IAT) with polyethylene glycol (PEG) or enzyme enhancement.2 Anti-C and anti-M were also demonstrated later, but 29 months after transfusion, no atypical antibodies were detectable. This evidence suggests that anti-Dob should be considered an antibody of potential clinical significance until contrary evidence becomes available.10

Squires et al11, described a DHTR that was precipitated by anti-Cob in a multiple transfused primigravida woman with sickle-cell disease. Sixteen days after the prophylactic transfusion of the first of 4 units of red cells, the patient was reported to have experienced a fall in hemoglobin concentration accompanied by a newly positive antibody screen and direct antiglobulin test (DAT). Anti-Cob was identified both in her serum and in an eluate prepared from her red cells.11 Anti-Cob is encountered rarely but they is IgG, red cell stimulated and reactive in IAT. It binds complement weakly and has been known to cause DHTR. Anti-M has also been shown to cause DHTR, as was the case reported by Alperin et al.12, of a 52-year-old gravida 1, para 1 woman with M- red cells who experienced a DHTR and exhibited an anti-M antibody following the infusion of four units of M+ red cells. Measurements of erythrocyte survival using 51Cr-labeled donor M+ and M- red cells and in vitro studies of monocyte-macrophage phagocytosis of sensitized reagent red cells implicate anti-M in the pathogenesis of the hemolysis.12 Chandeysson et al13, reported the case of a 67-year-old white woman who received a total of 87 units of whole blood and red blood cells transfusions during and within 48 hours following a pneumonectomy. Even though she had previously been transfused, unexpected antibodies were not detectable by routine screening. On the second postoperative day, she is said to have developed fever, hemoglobinemia, hemoglobinuria, and oliguria. However, the DAT and the antibody screen were negative. On the eighth postoperative day, an IgM anti-P1 antibody was detected for the first time. This anti-P1 antibody is reported to have increased in thermal amplitude from 22 to 37 C, but remained IgM. The circulating transfused P1-positive cells decreased progressively without evidence of bleeding. Testing of the patient's preoperative blood at 15 C found her serum to be weakly reactive with P1 cells, while her own cells were P2. Thus, an anamnestic response to the P1 antigen was most probably responsible for her DHTR.13 A 39-year-old multiparous woman who developed a mixed field positive DAT within 15 days of receiving four units of crossmatch compatible red blood cells was described by Waheed et al14 as later demonstrating anti-Jsb in both her serum and an eluate prepared from her red cells. The case was complicated by the fact that the patient's pretransfusion red blood cells typed as Jsb positive. Serologic studies demonstrated that this was a case of allo-anti-Jsb in a Jsb positive patient, which provides evidence of heterogeniety of the Js locus.14

Garraty et al15 reported the case of a 92-year-old group A, Rh-negative man with diverticulitis who was mistyped as group AB with the use of a monoclonal anti-B reagent. Anti-B was not detected in the patient's serum and after a negative antibody screen blood was issued through an immediate-spin crossmatch. The patient received 3 units of group AB blood and 1 unit of group A blood and no problems were noted. After a fourth unit of AB blood was transfused, the patient had a severe HTR, which resulted in kidney failure and death 10 days later. After the transfusion reaction, the patient's pretransfusion red cells were discovered to be group A with an acquired B antigen. A sample of the patient's serum taken before the transfusion was later found to contain a weak anti-B, detectable most obviously by the antiglobulin test, which was not performed at the crossmatch stage.15

In order to investigate the use of immediate-spin crossmatch procedures in preparing blood for transfusion to patients in whom unexpected clinically significant antibodies have not been found by antibody screening by the

Document info
Document views78
Page views94
Page last viewedThu Oct 27 13:10:07 UTC 2016