Leaderboard

We start with one panel (or cells 1-10 of Immucor's Panel 20 if doing tube testing). If a specificity is apparent when crossouts are done/the pattern of reactivity is reviewed, then we use selected cells (negative for the antigen the antibody reacts with) to complete rule outs OR if a number of rule outs are needed, run another panel on the Echo. If the patient has a more complex history or the antibody screen looks more complicated, we might choose to run 2 panels on the Echo right away. I require 3 antigen positive cells which are reactive and 3 antigen negative cells which are non-reactive to 'prove' specificity. The patient is antigen typed for the specificity identified if not previously typed for that antigen and if not recently transfused. Other common clinically significant alloantibodies are ruled out with 2 cells. This works well with straight forward, single specificity samples with antibodies like anti-K, anti-E, anti-Fya, etc., which are the majority of what we see. If the antibody screen on the Echo is positive in all three cells, which happens occasionally, we run a tube/PeG screen with an autocontrol plus one panel on the Echo with some questions in mind - is it an autoantibody? is it solid phase speficific? is it multiple antibodies? is it directed against a high incidence antigen? could there be a drug involved (anti-CD38, I'm looking at you!). If the auto is positive, we do a DAT. If the specificity is not readily apparent, then we run another panel, or two, or three as needed, based on what the first panel looks like. Almost all of our IDs start on the Echo and those panels are pretty well designed for rule outs of the common offenders. It is not uncommon to use only one panel for some specificities. I encourage everyone to look at the big picture, then narrow their search based on what they see. In the long run that will save them time (and reagents). And I will admit that on a busy day, we may put 2 panels on the Echo and push GO to expedite things a bit. If we are doing tube testing, running extra panels we may not need up front, is probably going to use more time and effort. Change is uncomfortable, especially for blood bankers, but give it shot. Think the steps through and work smart. You'll start to see problem solving in a way that you hadn't seen it before. Ask your work buddies for a second opinion if you're not comfortable. Review some cases with your supervisor to really get a good feel for what he/she is asking you to do. Once you've worked through the process it a few times, you'll feel better about it. And for those ugly case - the folks at the reference lab are your best friends!

I like the way your new supervisor has you performing antibody ID and panels. Why would you continue running full panels after the first if you can start narrowing down the specificity after the first panel and run selected cells? For example, if you suspect the patient has anti e, why run any more e+ cells? Not sure I agree with the DAT if auto control is negative. I think many transfusion services do not do this but I imagine that reference labs do. There may be times when running a DAT is advised when autocontrol is negative but running DATs routinely when an auto control is negative will just take you down a path that will delay blood transfusion IMO

In the US we have been doing what you say is going to be the new policy for many years, except we only would do a DAT if the autocontrol was positive. I think that approach is pretty common. Orthos' panel A is for the ijnitial assessment. Most of the time, you will have a pretty good idea what you are dealing with with those results. Then, going by the 3 x 3 rule, w use other panels for rule-outs / rule-ins. Also, if there is no history, we antigen-type the patient for those antibodies that are being made. Scott

Most developing clinically significant alloantibodies still react at 37oC, and so trying to detect them at room temperature is more or less futile as, in most cases, all you will detect are antibodies that you do not want to detect, such as cold-reacting anti-M, anti-N, anti-P1, etc, which would be a waste of time, reagents and, most importantly these days it would seem, money. Most polyspecific or broad-spectrum AHG reagents these days are a mixture of anti-IgG and anti-C3d (particularly in the UK). They do not contain anything but the merest hint of an anti-IgM (certainly, they would not be CE-marked for anti-IgM). The other thing is that I am prepared to bet quite a lot of money that your laboratory is using EDTA-anti-coagulated samples. This means that the Ca++, Mg++ and Mn++ ions are all chelated from the plasma, which means that the complement pathway cannot be initiated in vitro, so, even if the de novo antibody was capable of "fixing" complement, the anti-C3d would not detect such an antibody anyway. Therefore, as the number of recently transfused patients who are developing antibodies not yet detected by normal serological techniques who have been fatally affected by a further transfusion hasn't been great (zero in fact) and the same applies to pregnant ladies, stick to trying to detect clinically significant antibodies at 37oC using monospecific anti-IgG. GOOD QUESTION THOUGH - SHOWS YOU ARE THINKING!