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Healthcare workers run the risk of contracting COVID-19 during the course of their work if required precautions and usage of appropriate personal protective equipment is not adhered to In the transfusion testing laboratory, indirect exposure to COVID-19 may result from environmental contamination that may occur through surface contact or be airborne Handling of potentially contaminated surfaces such as sample tubes and sample packaging, and subsequent self-inoculation through the mucous membranes of mouth, nose and eyes may occur Information on the risk of indirect contact transmission of COVID-19 from such surfaces is limited When risk assessments are conducted in the laboratory, assumptions often need to be based on studies derived from other coronaviruses and respiratory viruses such as HCoV-229E, SARS-CoV, MERS-CoV and Influenza The other mode of potential indirect transmission is through aerosols generated from certain laboratory processes The risk of inhaling aerosolized blood containing COVID-19 viral RNA is unresolved Laboratories need to perform risk assessment of their activities before appropriate decisions can be made with regards to COVID-19 exposure risk reduction or elimination

The majority of allelic variants conferring red cell blood group antigens are attributable to single nucleotide polymorphisms, which are immensely amenable to routine genotyping methods such as PCR-RFLP, SSP, SSO and fluorescent-based real-time PCR assays. These techniques are feasible in a low- to medium-throughput setting. Multiplexing and use of solid surfaces or beads for probe capture have further improved the throughput and turnaround time allowing multiple alleles to be interrogated simultaneously. Novel approaches, as in the use of MALDI-TOF mass spectrometry, appear as an attractive option for accurate, cost-effective, high-throughput SNP genotyping within major blood centres. Massively parallel targeted sequencing is likely the next step in the evolution of RBC genotyping. In the hospital setting, genotyping is unlikely to supplant serological typing but would rather be complementary to it. Scenarios where it would play an important role would be in the transfusion management of transfusion dependant patients such as in sickle cell anaemia or in situations where RBC phenotyping cannot be reliably undertaken as in auto-immune haemolytic anaemia and haemolytic disease of foetus and newborn. Genotyping would also be useful where anti-sera are not readily available or are of weak potency. Molecular typing is likely to, however, show its greatest potential in donor genotyping to establish pools of fully typed donors as well as identify donors with rare blood groups. Such an exercise will facilitate prompt and efficient delivery of best-matched blood for patients.

Despite the large number of serologically identified red cell antigens to date, it is reassuring to note that in the common clinical scenario, the transfusion laboratory would only likely deal with a narrow range of clinically significant antibodies to specific antigens of blood group systems. Accurate ABO and RhD typing still remains the most crucial step in pretransfusion testing followed by the antibody screen. The correct identification of single antibodies or multiple antibodies and whether they are alloantibodies or autoantibodies is necessary so that corresponding antigen-negative red cells can be supplied. Clinically insignificant antibodies or what some would denote as ‘nuisance’ antibodies would need to be differentiated from clinically significant antibodies. When discrepancies occur between forward and reverse ABO typing, it is crucial that laboratories resolve the discrepancy before a specific ABO blood group is assigned. The inclusion of O cells in reverse grouping, anti-H and anti-A1 lectins in the forward, performing the typing on a range of temperatures using washed red cells and careful interpretation of agglutination patterns, would usually provide an answer. On occasions, a saliva test may be necessary and rarely molecular typing. With regard to RhD typing, test systems should identify RhD-negative and D-variant individuals so that D-negative units can be issued to them. Testing with antisera from different clones, the use of adsorption–elution techniques and RhD.CcEe typing aids in coming to a conclusion, before molecular testing becomes necessary. Extended red cell phenotyping is indicated if the patient is at risk for developing a red cell antibody.

Autoimmune haemolytic anaemia (AIHA) occurs as a result of antibodies directed against self-red blood cell (RBC) antigens, leading to the premature destruction of RBC. RBC destruction may occur within the vasculature, often mediated by the membrane-lysing complex, which is generated upon complement activation or occur extravascularly, within the reticulo-endothelial system that expresses FcγR and C3 receptors that bind antibody and complement coated RBC. The laboratory hallmark of AIHA is a positive direct antiglobulin test (DAT) although it has to be recognized that occasional cases of DAT-negative AIHA may occur. Secondary causes for AIHA such as an underlying autoimmune disorder, infections or malignancies should be considered as part of the investigation process for AIHA. Immunohaematology investigations for AIHA should always include a DAT using monospecific anti-IgG and anti-C3d. On occasions, further testing with anti-IgA or -IgG subtypes may be necessary. While the DAT provides information on bound RBC antibodies, the indirect antiglobulin test (IAT) using screening and antibody identification cells will provide information on the specificity of circulating antibody. Often this will give a pan-reactive pattern although it is not unusual to identify coincident autoantibodies with defined red cell specificity. Negative IAT with screening and identification cells in the presence of a positive DAT should raise suspicion of drug-induced AIHA. In patients who may have been potentially alloimmunized, further procedures should be performed to exclude the coincident presence of alloantibodies as failure to recognize alloantibodies may result in an immediate or delayed haemolytic transfusion reaction if red cell transfusions are initiated. Elution and auto- or allo-adsorbtion techniques are useful to separate allo- and autoantibodies. Complete red cell phenotyping should be concurrently performed to aid in identifying antibody specificities. Heavily antibody-coated red cells may be difficult to phenotype with some anti-sera, in which case, molecular based red cell genotyping should be initiated. Molecular based red cell typing is also particularly useful where the patient has recently been transfused and the initial red cell phenotype of the patient is not known. The primary management of the patient with AIHA is amelioration of the underlying condition and suppression of immune mediated haemolysis. This is usually achieved with administration of steroids or immunosuppressive agents. Splenectomy may be an effective second line treatment. Rituximab is increasingly becoming an effective treatment option in patients who are steroid-refractory and not suitable for splenectomy. Red cell transfusions in patients with AIHA should be undertaken carefully although they should never be denied blood transfusions because of inability to find compatible units. As far as possible, phenotype matched red cells, cross-match compatible with the patient's autoadsorbed serum should be transfused. If coincident alloantibodies are identified, antigen-negative red cells will need to be selected.