exlimey

What, precisely, are the "H&S" risks?

Anything is possible, but the screening cells are designed with the intent to detect all (common) antibodies, including the antibodies traditionally considered "colds" - MN, Lea/b, P1, etc. It is remotely possible that the frequencies/incidences of an antigen have come together perfectly to yield these results, but you'd have to be very lucky or unlucky, depending upon your point of view.

If the screen is negative by IS, it rules out the presence of a generic "cold". Are you only seeing this phenomenon during an IS crossmatch ? Are you only crossmatching group A units ? Does the same "incompatibility" happen if you crossmatch group O units ? Typically antibodies detected prior to an antiglobulin phase are IgM. These do not necessarily "carry through" to the antiglobulin phase, especially if they have limited thermal amplitude.

I don't know why the Control is positive, but the actual test is negative. In theory, the anti-D and control should be a matched set - they should be formulated exactly the same, except for the presence of the anti-D. Every manufacturer has "secret ingredients" - potentiators and other chemicals that stabilize and enhance the antibody reactivity. The controls, if supplied, should include the same ingredients. If you are using a control from a different manufacturer or product line, it might explain your findings. Are you saying that a monospecific anti-complement reagent is reactive with the patient's cells? It's not unheard of for warm-autos to bind complement, but since this looks like an autoanti-e, it would be highly unusual.

Nicely done. Often, a little strategic word-smithing will save the time and effort of revising a procedure or policy.

"Hens' teeth" is a phrase that comes to mind.

Your point is well taken. My comment above to natalynn was perhaps poorly composed, but your experience emphasizes the point I was trying to make: Many, many, many examples of anti-K will be identified before one anti-k is found. Certainly the rarities should not be ignored, but they should not be the focus of everyday work.

I wasn't questioning the immunology, merely the fact that the average hospital/blood bank is rarely going to encounter a K+k- patient. If "we" are going be really concerned about k- patients in the Dara scenario, shouldn't "we" also be worried about Kp(b-) and Js(b-) patients ? And what about patient with antibodies to Dombrock system antigens ? I agree that emphasis on giving K- blood to K- patients is well founded, but it appears that a unduly disproportionate amount of concern is being applied to other, rare blood types. I guess we blood bankers are always looking for zebras ? ☺

I understand your position on (big) K antigen, but how many patients are you treating that are (little) k-negative ? That's a fairly rare phenotype.

That fits with my thinking, too. I suspected we were having "communication problems". Ain't the English language grand ?

At first glance, it sounds like a good idea, but at the very least, it would contradict with the manufacturer's instructions (if it's a commercial preparation). I'm quite sure the stability is based on storage at RT. And SMILLER's point about bug growth is well taken.

Fair enough. Just to clarify......your (and Anna's opinion is that a 37C test using enzyme-treated cells and no antiglobulin phase will detect anti-D better than a test using the same enzyme-treated cells and an antiglobulin reagent ?

I disagree. I would not expect enzyme-treated cells used in a direct agglutination test to react better than those same cells used in a technique using an antiglobulin reagent.

Most typically Screening Cells will be treated. If that screen is negative, then no further action is required (except perhaps antigen-typing the patient). If the DTT-treated screen is positive, it may be necessary to DTT-treat a reagent red cell panel (or selected cells).

I understand. Do you phenotype all eligible patients (un-transfused or not recently transfused), or just those that you expect to see again ?

I agree with Malcolm - a typical FMH involves a very small volume of cells. Their presence should not interfere with antigen typing of the mother, especially if using reagents that are IgM. Just curious.....what would you do if the mother typed c+? Would you "ignore" the anti-c? I know we've all been programmed to antigen type when we identify an antibody, but sometimes it seems pointless.

Just curious: Other than common sense, is there a regulation that says coolers or blood boxes/transports need to be cleaned? Obviously, if there is some overt issue, they should be cleaned, but in practical terms, the OUTSIDE of blood bags do not claim to be clean/sterile. I can't imagine that the coolers themselves are taken into "clean" areas like ORs, but if they are, that's a different story - they should be clean INSIDE and OUT. While the Blood Bank is probably cleaner than the "smoking" shack, I'm sure it's not claimed to be clean in the clinical sense. As a parallel.....how often are blood storage refrigerators and freezers cleaned? Certainly not every time they are used. Perhaps more focus should be on coolers returned with noticeable blood contamination: where did it come from?, was the blood inside compromised?, did a unit of blood with a hole in it get transfused? Of course, that still implies an inspection process, but doesn't necessarily mandate cleaning. Just a few brain drippings, no soap box or intent to offend.

Presumably the operators check that the troublesome reactivity that they are trying to circumvent is actually present in the unpotentiated test ?

I agree with David - DTT-treatment is not difficult and any semi-competent operator should be able to manage it. "matched blood" can mean many things. If you are supplying red cells matched to avoid immunization to the "common" antigens (Rh[C, E, c, e], S/s, K, Fya/Fyb and Jka/Jkb), one could consider a longer period between testing. Perhaps a policy similar to the way some facilities treat patients with warm autoantibodies? After all, they shouldn't be making any antibodies, in theory. This process doesn't help for antibodies to the lower-incidence antigens, but neither does repeated testing of DTT-treated screening cells. On another track: In your facility, what percentage of Dara patients need transfusion and how many of those have the reported serological problems ?

I am not familiar with the British regulations, but I imagine that said compatibility testing must include a technique to detect IgG antibodies. The enzyme test you describe may detect them but not always - exactly the situation you outline. It still sounds like a weak anti-D. The variability in reactivity over time from sample to sample might just be because the patient is pregnant - their immune systems are doing very strange things, including exhibiting a fine-tuned tolerance for the "not-me / parasite" that they are carrying. Can you do an antiglobulin test using enzyme-treated cells ? If you can, it would be wise to include an enzyme-treated autocontrol.

Am I to understand that the enzyme test is NOT an antiglobulin test ? Am i correct in thinking that's what "neutral cards " mean ? If that is the case, you are not comparing like assays. One has an antiglobulin reagent, the other does not. Use of enzyme-treated cells may enhance detection of anti-D before the antiglobulin phase, but not always. My interpretation of your results is that you have a weak IgG anti-D, only reliably detected by IAT.

One can use any of the manual tube techniques, as long as one is comparing apples to apples - if one's basic (normal) test uses a potentiator, one must use it in the pre-warmed verison. As Malcolm suggests, sometimes a plain vanilla saline antiglobulin test is the way to go, provided the "cold" reacts in that phase.

Perhaps some clarification is in order. I'm in the US but am not subject to the clinical regulations that apply to hospitals and blood centers that do clinical work on patients (or donors). Those regulations, often with the addition of local/state riders, are "enforced" by a number of government entities and surrogates. My facility is not "accredited" by any agency, but instead we are licensed by the FDA for the specific work that we do. The FDA inspect us (as well as our internal auditors) using a completely different set of criteria.

Don't do any. I use panels, but I don't work in a clinical laboratory.

Apologies in advance, I don't have Ortho package inserts handy. Does the insert actually suggest using an Fy(a+b-) panel cell?