mrmic

I am curious to find out what methods other Microbiology Labs are using for investigating Transfusion Reactions for the Blood Bank Transfusion Service? Limited verbal communications suggest there are a lot of variations out there. Based on product, how do you screen for Salmonella, etc., Staph aureus, Yeast or Yersinia? Currently, the ways its has been handed down for X years, is that we inoculate three Thio broth tubes and incubate them at 4C, 22C, and 35-37C for 5 days. If there is any growth we, gram stain and sub to appropriate media plates. I am a little concerned if this is still adequate, esp for Yersinia spp. What does your Blood Bank Transfusion Service "think" you are screening for? Thanks

History History History pregnancies, transfusions, daddies, medications, High BP? Early autoantibody, early autoantibody mimicking anti-D? One pathologist I have worked with considered pregnancy a disease, you may have some non-red cell stimulated mimicking antibody specificities due to a hyped up immune system. We have seen an Anti-K titer rise during the pregnancy only to find the subsequent child and daddy to be Kell negative. Would be nice to be able to follow patient, antibody detections, titers, Rh-hr typing of infant, etc................... make a good abstract case presentation at a meeting.....

If I remember from many moons ago, there was a reference paper indicating the optimal time for antibody-antigen complexes in saline was 60 minutes. I believe there were subsequent papers/abstracts suggesting that shorter incubation times using saline and "pre-warm" methods allo-antibodies were being missed, however, the warm reactive autoantibody was not interfering and the crossmatches were "compatible". Hence, once allo-antibodies are ruled out through other immunohematological testing methods, issuing "least incompatible" crossmatches are ok as well thereby reflecting what is really happening.

Warm autos are a curious bunch. Are antibodies present truly auto or are the allo? Are they really allo or mimicking specificities of the autoantibody(ies) present. Once you start transfusions you should be doing allo-absorptions since transfused red cells may be present. Do multiple adsorptions have a dillutional effect with the absorbed serum which may cause a weak significant allo antibody be missed? Maybe the crossmatch is of little use in these situations so whatever you do is ok? In these situations the focus is on the cause and resolution of the warm autoantibody production by the patient and the determination of the benefits/risks of transfusion. We had seen little differences with utilizing "absorbed" sera crossmatchs vs "least incompatible" crossmatches with regards to patient outcome. However, it is a technically challenging/interesting when we get these cases sent to us and then to try to follow up of the patients as long as we can.

God is Great, Beer is Good, Some Regulations are Crazy... Why not use outdated sera and cells for screening and then use the 1 in-date bottle to retest and use as test of record? What about rare red cells and sera from commercial or patients that may be frozen in liquid nitrogen and used to help with antigen and antibody problems? Of course you would run controls. Where have all the blood bankers gone? Who is writing these regs.? Have they been out of the lab too long? There are patients waiting for us and our results..... I will step off my soapbox now. Good Luck to all and to all Good Luck.

Blood Bank procedures still have a lot of manual testing, much like Micro. The Gram stain is the most basic but most important test in Micro just like ABO/RH typing is for Blood Bank. Complex antibody identifications in Blood Bank require focus and skillful hands on testing and interpretations just like reading culture plate colonies in Micro and antibiotic susceptibilities in Micro. You communicate with Physicians and Nurses regarding specimen requirements and help with interpretation of clinical significance of antibodies in Blood Bank and with antibiotics in Micro. As long as you have good communication skills and work ethic and are proficient in Blood Bank you should be a fast learner in Micro................and visa-versa........ hope that helps a little.......

We are thinking about reporting as follows: Any comments or other suggestions welcomed. (Drug Name) (Methodology) MIC: xx mcg/ml (Drug Name): No CLSI guidelines available for test methodology or antibiotic susceptibility interpretation for this drug/organism combination.

Consider for the sake of discussion, E-tests, automated micro-dilution, Kirby-Bauer methods for antibiotic susceptibility testing. If there are no CLSI guidelines for reporting a particular drug/organism combination (therefore no in-vitro to in-vivo validation); If a physician requests the MIC value only or Kirby-Bauer measurement; Can this be reported? If yes, does anyone have a comment they post with the result? If yes, how do you justify which method you utilize to report and how do you justify the in-vitro/in-vivo correlation? Since there are no CLSI guidelines or data?

Does anyone still utilzie this broth with routine cultures? If you have specific sources/sites that you use or don't use what are they? Has there been a recent paper published regarding the use of thio? We have had a increasing number of physicians requesting how the organism was growing in the broth, i.e., at the top, at the bottom, etc.... We have been trying to limit our use of Thio broth because of getting so much contaminating flora being picked up, especially from swab specimens.... Just would like to hear where everyone else is with this. mic

Don't you love warm autos??? Is it real or is it mimicking? The joys of BB. Why transfusing this patient?

How did patients survive prior to Typenex??? It would be interesting to hear about real transfusion errors due to the lack of or because of additional armbands. Both numbers small no doubt. The cases I have observed really didn't matter whether there were more ID armbands or not. ie. the nurse gave the blood to the patient because they were expecting the blood to be for the patient (wrong patient); next ie, the room was darker than normal and the patient's looked alike, I didn't know they switched beds; Even the classic about what does the SOP say?, at the sentinel meeting the nurse said that's SOP not practice.....AAAAAHHHHHH! Accountabilty of who IDs and bands the patient and then who identifies the patient at the time of transfusion is needed. The "its nobody's fault, it is a process error" is overated. I agree with KISS....

what? While it is not uncommon to find autoantibodies with non-Rh specificities it is also not common. As long as the last wash from the washing of the patient's rbcs for the eluate is tested for the presence of antibody, then the eluate represents what is eluted from the red cells. It may be an autoantibody showing preference for K1 or it may be one of the units were actually Kell positive. Transfused rbcs may last longer in the circulation than 3 months. Thoroughly check the transfusion history and recheck K1 typings. Would the patient have been transfused elswhere? There was a abstract written in the past about red cell and HLA antibody development due to sharing needles for drugs. History is important documentation. Colaboration is nice too. Some labs check to see if actually more than one cell population is present and if the "autoantibody" is actually an "alloantibody" coating transfused cells. Orrrrr it could just be a new autoantibody problem starting. You should be able to discuss specifics with your Immunohematology Reference Lab and get some answers. These are interesting and fun things to investigate!

I would agree with Malcolm. If the patient does need transfusion then rr units can be selected. The underlying cause of the autoantibody could be investigated clinically to deternine if treatment is warranted to deal with any anemia the patient may be experiencing. The transfused red cells may or may not have normal survival in the presence of autoantibody, even if the in-vitro crossmatch is compatible. The laboratory investigation of the autoantibody (ies) specificities may be best done at a Immunohematology Reference Lab. They can be complex with very unique specificities or mimicking specificities or may just show preference for certain antigens. That the fun of working in a Reference Lab!

In Oklahoma, anti-K has not been that frequently encountered with severe HDN. In fact, we have seen in some cases the titer of the antibody rise to 1:32/64 levels and the baby turns out to be Kell negative. I think the comments made concerning the relatively low frequency of K+ in the population (at least in OKLA). It will be interesting to follow the work done with the HLA alleles and the association with HDN. I also wonder if the blood transfusion triggers are different for different regions. Sometime UV lights work well.....

With all the abstracts and posters at AABB annual meetings I probably did see something there about the low titers and prenatal RhIg. We report that titers less than 1:8 are consistent with prenatal RhIg but it is up to the clinician to decide the significance since we rarely have the patient's history or clinical data. Any titer result may be important during a pregnancy and should be evaluated on a case by case basis. IgG crosses the placenta at any titer. Also, the clinical significance of the antibody specificity and literature references with regards to HDN are as well important to investigate. Titers are what they are. Given the consequences, any anti-D should be investigated during a pregnancy. This case, again, Mr. Needs said it best, absolutely immune anti-D and monitor it.