sshel55

How many allo adsorptions do you perform before becoming concerned about diluting an allo-antibody to the point of non-reactivity?

Did you consider anti-LW?

I have a related question. Let's say you get a new sickle cell patient who has been transfused regularly at another facility. You call the facility and are given a list of antibodies identified and a RBC phenotype. What do you do with the phenotype information? Do you transfuse RH and K matched blood based on this information? Do you "try" to get a RBC phenotype even though patient has been transfused? Do you hypowash? How do you handle these cases? I'm writing a case study and would love to get some data on this. Thanks!

Crossmatch compatible group A RBC would be transfused in our facility.

I was going to post this very observation. The ITP patients given RHIG are D+ and therefore there will be an immune reaction to the anti-D and the D+ RBC. It isn't severe in most cases, and possibly non-hemolytic, but there is likely extra-vascular destruction of some D+ RBC that might account for the flu-like symptoms. This should be less likely in the D- post-partum recipient.

I hesitate to respond but here goes. You might want to look at the anti-A titer in the platelets the patient received. There are numerous papers (including ours) that address hemolysis from group O apheresis platelets transfused to group A recipients. The fact that he is negative with A1 lectin is suspect, especially if he has been receiving A RBC as `80% would be expected to be A1. That would mean he has cleared most of the transfused cells. Does he show clinical evidence of hemolysis? Regardless of the reason, group O RBC should be given until or if, group A RBC are crossmatch compatible again.

Agree with Dwharrell, the indicators are not dosimeters. They simply show that the unit was exposed to irradiation. So the placement on the unit should not matter. I believe the indications for use states this.

Good luck to you, Jana. Looking forward to the publication.

So I was answering the question. About titering an auto-antibody in a pregnant female. My concern is discerning an auto-D from an allo-D in a pregant female. I wasn't trying to cover every feasible option and lecture on partial and weak D phenotypes and resolving warm autos although our reference lab does all these techniques but we prefer EGA to CPD (yes it denatures Kell group antigens). Unfortunately, it seems that new opinions are not welcome here so I will refrain from posting and those of you who own the board can have at it.

Not each time, Malcolm. But for patients who have complicated serology that includes Warm Autos along with allo-antibodies or for African American patients with D-CE hybrid genes, it is well worth the cost. Many patients we see have been multi-transfused before we get them, so sometimes phenotyping is not an option and genotyping fits the need perfectly. We are in the process of genotyping all of our repeat donors.

Titers may be helpful in discerning allo vs auto antibodies when there is apparent blood group specificity. Also, keep in mind that some apparent auto-anti D may in fact be allo if the mom is a D variant.

I believe there is a parameter setting where you enter all your "ABO" tests so that Soft knows what test codes qualify as an ABO type for confirmation purposes. I agree that your implementation specialist should be a valuable resource for these questions.

Once an initial workup has been done and the patient is being chronically transfused, we perform an adsorption one every two weeks. We also utilize phenotypically and genotypically similar antigens matching of transfused units, particularly in patients who have formed antibodies.

That is my question as well (retype on unit). It is known that some ABO incompability will not be detected by the crossmatch test. That is why we have so many other checks in place including the confirmation of the blood group of units after labeling. Perhaps the unit was a subgroup of A which may help explain the compatibility especially if the anti-A titer in the patient was low.

Done! Which program are you affiliated with, Jana?

Elin, I would report this to your blood supplier and ask them to see if this particular donor had ever been implicated in a hemolytic reaction previously and to perform an isotiter at both room temperature and AHG phases. High titer isoagglutinins can indeed cause brisk hemolysis and if the titers are high enough (some are well over 1000), they would react with A subgroups. There are numerous case reports and articles that demonstrate hemolysis caused by ABO incompatible platelet transfusions. Given the fact that the patient experienced fever and hemolysis during the platelet infusion, it is prudent to look at the platelet. If the high titer isoagglutinin was in fact primarily IgM, it could cause intravascular hemolysis and might not be detected by the DAT.

This is a CMS regulation, not FDA. What happens if you get a CLIA citation? Is one citation enough to hold up your CLIA approval status? I think we need to INSIST on some logic and reasonable judgment on this. It says that the ABO compatible status must be assured. If you demonstrate that your computer system is designed to disallowed ABO incompatible units to be selected, and you show that you confirm the ABO of all donor units received, and you reconfirm the ABO of all patients, then I would argue (hard) that this is demonstrating ABO compatibility. There are many ways to do so and ISXM is but one. Also, if you have validation data on the GEL implementation where you have tested AB (including A2B) units with group A and B recipients, and demonstrated incompatibility, you have additional data to prove that your Gel method detects ABO incompatibility. One thing is for certain. If we all kill ourselves to implement something that does not add to patient safety but does add to health care costs, things will just get more rediculous. I vote for civil disobedience on this one.

If the A cells are serologically compatible, I suggest switching back to A.

I'm wondering how many of you are using a blast freezer to freeze FFP prior to storage at <18C? We had been using an ultra low freezer to quick freeze our FFP since we have a relatively small batch each day (<20 units) and then moved it to a -30C freezer for storage. We just purchased a new ultra low freezer and we are having problems with it spiking temp each day when FFP is put in and then taking hours to recover (and driving us crazy with the alarm):cool:. I am curious how others handle freezing FFP. If you do use a special blast freezer for this purpose, would you mind sharing the brand name and your experience with it (good or bad). Thanks!

In the case of the trauma scenario we have elected to do as you suggest, CKCheng, and save the antigen negative units until the patient's blood loss has slowed. This has worked remarkably well for us on several occasions with rapid blood loss in the OR. Patients who are rapidly bleeding may exhibit immune tolerance over patients who are given units to manage chronic anemia. This is a medical judgment call that should be made by the medical director of the blood bank. As for the initial question that started this thread. AABB Standard 5.14.3 says it all.

You could also submit a request for a variance from FDA, especially is this was your entire inventory.

The key here is "for a possible hemolytic reaction" and if your clerical check, DAT and observation for hemoglobinemia are all negative then some would say you have ruled out an immediate hemolytic reaction. This question was answered in AABB Standards Source in 2005 where it says that "there is no reason to perform an ABO/Rh on a post transfusion specimen unless there is reason to suspect that a hemolytic reaction has occurred" and that "the evaluation and tests used to evaluate whether a hemolytic reaction had occurred could be defined by the medical director." In our facility the ABO is part of the tier II testing.

Thanks for the reply, Heather. What is the protein content that you all consider acceptable in the final wash supernatant and how did you determine the lacceptable level? I'll check out the refractometer. It might come in handy for protein levels for serial plasmapheresis donors. Sherry Sheldon

To all of you who do dipsticks for protein. Do you have an SOP for that and do you run controls? Just wondering as I can anticipate the next question from the assessor. Did any of you "validate" the process to show that it consistently resulted in a protein below detectable levels? If so, did that not fly with the assessor?

If you dip stick, do you QC the dip stick? I've been chastised for that. So you have to buy dipsticks and controls for the dip sticks. Whatever happened to "a method known to result......."? Personally I would "validate" my method if forced to. Perform protein measurement on 11 or so units and then keep that for the inspectors rather than having to do each one.