Background
The acute respiratory illness designated coronavirus disease 2019 (COVID‐19) was first reported in Wuhan, China, in December 2019 and caused a worldwide pandemic. Concerns arose about the impact of the COVID‐19 pandemic on blood donations and potential significant blood transfusion needs in severely ill COVID‐19 patients. Data on blood usage in hospitalized COVID‐19 patients are scarce.
Study Design and Methods
We performed a retrospective observational study of blood component transfusions in the first 4 weeks of COVID‐19 ward admissions. The study period began 14 days before the first COVID‐19 cohort wards opened in our hospital in March 2020 and ended 28 days afterward. The number of patients and blood components transfused in the COVID‐19 wards was tabulated. Transfusion rates of each blood component were compared in COVID‐19 wards versus all other inpatient wards.
Results
COVID‐19 wards opened with seven suspected patients and after 4 weeks had 305 cumulative COVID‐19 admissions. Forty‐one of 305 hospitalized COVID‐19 patients (13.4%) received transfusions with 11.1% receiving red blood cells (RBCs), 1.6% platelets (PLTs), 1.0% plasma, and 1.0% cryoprecipitate (cryo). COVID‐19 wards had significantly lower transfusion rates compared to non‐COVID wards for RBCs (0.03 vs 0.08 units/patient‐day), PLTs (0.003 vs 0.033), and plasma (0.002 vs 0.018; all p < 0.0001). Cryo rates were similar (0.008 vs 0.009, p = 0.6).
Conclusions
Hospitalized COVID‐19 patients required many fewer blood transfusions than other hospitalized patients. COVID‐19 transfusion data will inform planning and preparation of blood resource utilization during the pandemic.
Background: We instituted RHD genotyping in our transfusion service for obstetrical patients and transfusion candidates. We sought to examine how RHD genotyping resolved weak or discrepant automated microplate direct agglutination (MDA) RhD phenotypings and impacted needs for Rh Immune Globulin (RhIG) and D-negative RBCs.Study Design and Methods: We investigated RhD phenotypes with equivocal or reagent-discrepant automated MDA (Immucor, Norcross, GA), weak-2+ immediate-spin tube typings, historically discrepant RhD typings, or D+ typings with anti-D. We performed microarray RHD genotyping (RHD BeadChip, Immucor BioArray Solutions, Warren, NJ). Patients were managed as D+ with weak-D types 1, 2, and 3, and as D-negative with all other results. Results: Our weak-D prevalence was 0.14%. Among 138 patients (73 obstetrics, 65 transfusion candidates), 38% had weak-D types 1, 2 or 3, 25% weak partial type 4.0, 21% other partial-D variant alleles, and 15% no variant detected. One novel allele with weak partial type 4.0 variants plus c.150T>C (Val50Val) was discovered. Weak D types 1, 2 or 3 were identified in 66% (48/73) of Whites versus 3% (2/62) of diverse ethnic patients (p < .0001). RHD genotyping changed RhD management in 60 patients (43%) (49 to D+, 11 to D-negative), resulting in net conservation of D-negative RBCs (98 avoided, 14 given) and RhIG (8 avoided, 3 given).
Conclusion:In our patient population, equivocal or reagent-discrepant MDA RhD phenotypes were highly specific for weak-D or partial-D RHD genotypes.Resolution of RHD genotype status reduced our use of D-negative RBCs and RhIG.
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