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If you're up for a little more discussion (and a little entertainment ) may I suggest this thread, from 2012? Saline incubation...why is this SOP still allowed?

We use regular blood bank saline or whatever suspension the reagent RBCs are in (as long as it isn't a LISS suspension). The procedure is just doing a screen/panel/xm don't add enhancement media, and incubate for 30min@ 37C

We see this fairly often from our hospitals. Often the reactions have an abnormal appearance, as in they have mixed field or uniform haze through entire column, but the auto-control is negative. Usually we run a converted panel from another manufacturer and 4-6 random units. All of this testing is usually negative.

Cannot post the entire article due to copyright restrictions, but most institutions have access to NEJM through their library. If not, shoot me an email at neil_blumberg@urmc.rochester.edu and I'll send along the .pdf. If you are transfusing 40-60 platelets a day, giving ABO identical to group O and A individuals should be relatively easy. When patients are changing ABO blood group it becomes more difficult. We avoid transfusion ABO antigen and/or antibody that is incompatible with either original recipient type or donor type. Usually means washed group O red cells and platelets. That's the bad news. It does require time and effort, and as you say, med techs are in short supply. Here's the good news. If you transfuse ABO identical or washed compatible platelets you will use between 30-50% fewer platelets per patient, increasing your supply and decreasing your cost/problems. You will also use next to no HLA matched platelets (we used 3 out of 6,000 one recent year), you will have fewer febrile and allergic transfusion reactions, you will have fewer red cell as well as HLA antibodies made in recipients, and you may reduce TRALI and TACO. Obviously you have to have universal leukoreduction to start with. Selective leukoreduction misses about 50% of the patients who will become refractory, probably due to missed or delayed diagnosis of hematologic malignancy, aplastic anemia, etc. But the big attraction is you will have less bleeding, although that mainly affects the patients and the docs and nurses at the bedside. When you transfuse ABO major incompatible, which seems to be the default due to fear of hemolysis from minor incompatible, you don't get any increments, you use lots of platelets and the patients bleed more. (see references below) Bleeding causes lots of harm, but also impacts the blood transfusion service for obvious reasons. So figure out a way to start giving patients with aplastic anemia and acute myeloid leukemia who are newly diagnosed only ABO identical platelets and that will be a great start for the patients and the transfusion service. Those patients will bleed less, need fewer platelet transfusions, have fewer transfusion reactions, will not have positive DATs, and will likely survive their hospitalization and disease at higher rates if our experience is typical. And if you cannot give ABO identical or washed platelets free of incompatible cellular and soluble antigen and free of incompatible ABO antibody, start out with minor incompatible platelets (e.g., O to A) rather than ABO major incompatible (e.g., A to 0). The risks of hemolysis are not negligible (about 1 in 800) but are less serious and severe than having life threatening bleeding or refractoriness which occur more rapidly with ABO major incompatible in all likelihood. There's a ton of antibody that is incompatible with antigen transfused when we give A platelets to O recipients which means each antigen winds up with a ton of antibody making huge immune complexes. When we transfuse antibody incompatible we are transfusing a small amount of antibody into a recipient with huge amounts of antigen, so the size and number of immune complexes is probably smaller. These are my best guesses that we've been making exactly the wrong decision when we give ABO mismatched platelets. Best to avoid any, but major mismatched provides no hemostasis, minimal to no increment and is associated with increased bleeding mortality in the study from Columbia (David Roh and colleagues https://pubmed.ncbi.nlm.nih.gov/33649761/). But ABO identical is not that hard for larger centers for the 85% of patients who are group O or A. You just have to start small, get the hang of it, and then extend to other blood groups and other diseases than leukemia, MDS and aplastic anemia (including transplants, particularly allo--transplants). All those tables of how to select ABO mismatched platelets for transplant recipients are well intentioned but scientifically without evidence. Avoid infusing incompatible antigen and antibody as much as possible, and delay transfusion when ABO identical will be available within hours. Give priority to patient well being over inventory management. Give reduced doses, which work just as well. Get a Terumo or Haemonetics washing device and wash with PAS. It's a big set of changes, but neither terribly expensive nor rocket science. The dogmas and expert opinion about universal leukoreduction and ABO matching of transfusions are now proven to be tragically mistaken. https://www.ashclinicalnews.org/news/from-the-blood-journals/written-in-blood/outcomes-abo-incompatible-platelet-transfusions-patients-intracerebral-hemorrhage/ https://pubmed.ncbi.nlm.nih.gov/11399821/ https://pubmed.ncbi.nlm.nih.gov/21414009/

The prediluted cells from Ortho contain the antibiotic nitrofurantoin as I recall. I think that contributes to why they are to be kept in the dark as that drug is always dispensed in a brown bottle. Patients make antibodies to the antibiotic and thus react in the prediluted cells. Diluent 2 lacks preservatives because we can't store the suspensions over 24 hours so 3% cells suspended in it don't react with antibodies to the antibiotic because the antibiotic isn't present. In my experience, the antibiotic doesn't seem to wash off of the cells but rather adheres to them. What you are doing is a great way to prove that this is the problem rather than a cold antibody etc. Most of our patients who have this, continue to have it for years to come.

I retired recently so I do not have access to the product insert but I do remember that cells stored in LISS for longer periods can give some false positive reactions. Also, cold antibodies are enhanced by LISS so by diluted your 3% screen cells there is less time in LISS so less chance of false positives that can be experienced with older cells stored in LISS and also less chance of picking up a non specific cold antibody.

We stop the transfusion and initiate the transfusion reaction procedure. And until the workup is complete (minus any micro), the patient is unable to receive any other products. Normally it is just something with the donor plasma and Benadryl should cover and propholactically thereafter prior to transfusion. Normally the physicians order Tylenol before the transfusions, so adding Benadryl is not an issue.

Well labgirl153, there was a little paper written in 1945 by Coombs et al (Coombs RRA, Mourant AE, Race RR. Detection of weak and “incomplete” Rh agglutinins. Lancet 1945; ii: 15-16) that rather contradicts your theory of this SOP being "bogus". I think that you should remember that, before we had enhancement, this was the ONLY indirect antiglobulin technique that was available and that, although a few patients may have been "lost" due to incubation period, none were "lost" due to antibodies not being detected, as long as the test was performed correctly. If you do not acknowledge,remember and learn from history, you are doomed to live through it again.