janet

Left out 3 hours then refrozen -do we need to recollect?

I had my student work on our two patients some more - both women we thought had Anti-K along with their Passive D's have had K negative babies - they have not been transfused and pre-RhIg injection screens were negative! I too looked at all the cells that were reacting and they are Bg positive. 3 more K+Bg- cells are negative. BUT a couple K-Bg+ cells are not reacting!?!?!

We have had two reactions similar to this!?!?! Our gel reactions were not 2+ mind-you......weak 1+ and testing on other K+ cells show weak reactions also but not with all K+ cells (2 out of 3). When the patient typed as K- (I know, odds are they would) we felt safest to call it an Anti-K but were a bit puzzled when one of the baby's was K- (will have test the other baby Monday!). Baby's DAT was negative so doesn't fit that it was false negative due to antigen sites being coated. I have seen once and found support in "Applied Blood Group Serology" by Issett that Anti-K has been found naturally occurring but now I am thinking more about the HLA antibodies as we have seen this so many times with gel testing in certain screen/panel cells We give WinRho brand RhIg .... I have detected and Anti-C a couple days after giving it but would be surprised this Anti-K would still be detected a month plus later (as with you our ladies had their RhIg at 28 weeks and are presenting now at delivery.

Anyone use the DiaCent-12 Centrifuge for Tubes .... from BioRad?

Under what conditions would you NOT perform the Rosette test and do a Kleihauer instead.....from what I've read there are the obvious times like either Mom or Baby are Weak D positive or mom has a positive DAT that is interferring. What about if Mom was givien RHIg prior to the sample being drawn .... ??one might worry the antigen sites of any Rh;Pos are covered by the RHIg and won't be detected by the kit Anti-D?? If you agree with this scenario how long would you consider the RHIg to interfere?

We have a new hematologist with a set panel she orders on all her new patients (with initial diagnosis varying from thrombosis .... hypogamaglobinemia ....low WBC/high plt ..... high WBC/low plt). Every patient has CBC,retic,DAT,TSH,free T4, chemistry panel and serogy (HIV, all hepatitis'). Needless to say my department has been effected by a doubling of DAT requests all from this doctor. Does anyone know of a paper or journal to help me discourage this kind of shot gun testing? Most have good hemoglobins and only one of 28 last month were positive! Any words of wisdom would be appreciated

I was told it was to prevent post transfusion purpura but I can't find any supporting papers, articles or journals!?

Do you wash red cells for transfusion in these patients? References?

There are a couple studies I know of; ABLE - global but most are in Canada (&US?) started in 2008 and hope to have enough patients by end of this year - synopsis: http://www.controlled-trials.com/ISRCTN44878718/ one out of McMaster University in Toronto - link to vidio presentation when just beginning http://mediasite.otn.ca/Mediasite/Play/03201e7ac63d42e7a32c6d41704e9e441d?catalog=fd668812-d87c-47f9-b1ba-6d979fed9af4 One completed on babies - I believe did not show a benefit ARIPI - I can find info at work if you'd like

What about a unit that is started but IV site lost just before it reaches patient .... so filter and tubing are full of blood - still okay if given within 4 hours or would you worry that the stagnant blood in the tubing and filter might have bacteria proliferate??

THANKS Malcolm!!!! - you say transfusion can "exacerbate ab auto-antibody" - do you try hard to prevent transfusion in these patients? We have an oncologist who orders to transfuse below 90, she signs a release form but these patients seem to continue to be transfusion dependent for months before Prednisone does anything to stop the antibody production. I have read many articles stating transfusion should be avoided but that does not seem to be her practice!? - I appreciate the reference to BCSH Guidelines stating the IAT crossmatch can be omitted. Our practice is to send the initial sample to our reference lab 8 hours away for autoabsorbtion and full phyenotype, they often send compatible units based on the negative absorbed plasma workup. Our policy is to do a tube IAT crossmatch with full phenotypically matched units from then on, which are never compatible How often is a workup done on your auto-antibody patients? Seems silly to repeat every 96 hours when everything reacts and you've given phenotypically matched!?

We had a group A MDS patient have a hemolytic reaction to a group O platelet - so we starting titering our platelets before issuing incompatible. He came in a year later and all we had were O's again. Titre was okay so they were issue = hemolytic reaction AGAIN Dr. tested for PNH and he was positive..... a high percentage of MDS patients transform to PNH and since their cells are primed with complement from the disease there is a risk of hemolysis if incompatible products are given. The Canadian Blood Services area Medical Director prepared a poster for AABB - I will try to post it when I'm back at work tomorrow, recommendation was to watch for these MDS patients!

Our oncologist pre-medicate. This often causes a decrease in temperature and can confuse nurses when the tylenol wears off and temperature increases one degree but isn't abnormal! We also may have missed a hemolytic reaction - patient was pre-treated so did not have a temperature increase. He was prone to cardiac complications so presented as that ... I wonder if the hematuria would have been ignored without the temp. increase. Dr. clued into it right away. We had given group O pooled platelets to a group A patient (he was later diagnosed with PNH and the physician explains it as his cells were primed with complement all ready to burst when the Anti-A was introduced

Does anyone use a "p value" when identifying antibodies. I've seen the following and wonder if anyone uses this or similar? (A+! x (C+D)! x (A+C)! x (B+D)! N! x A! x B! x C! x D A = number of pos. reactions observed with antigen-positive RBC B = number of pos. reactions observed with antigen-negative RBC C = number of neg. reactions observed with antigen-positive RBC D = number of neg. reactions observed with antigen-negative RBC N = total number of RBC tested (panel or screening cells "0.05 is the accepted minimum statistical value." Thanks!

We have history comments on this 92Y Caucasion female patient stating she had an Anti-HRb identified by our reference lab in May 1989 (screen was negative April 1989 prior to giving her 3 packed cells). Methodology then was saline IAT. Antibody screens were negative on July 24th, August 2nd and August 14th of this year (gel technology). We gave her 2 packed cells each of these occasions. Yesterday we received a request for 2 more packed cells, after a night of testing we think she has formed an Anti-S (1+ reactions with Ss, 2+ with SS), E (2+)and an "unidentified" that reacted weakly with 5 of 9 E-S- panel cells and 3 of 4 E-S- units. Does the historical antibody seem plausible - should I worry?

My two cents about worrying about what we might be missing: -- all antibody screen methods have there good and bad qualities (eg. you may pick up an autoantibody in gel but when using less sensitive tube IAT the auto is gone and you still hope you have the sensitivity to pick up an alloantibody possibly underneath that auto -- one method may be better for one antibody than another (eg. LISS and Anti-K .... I have suspected an anti-K in gel, increased the incubation time to 40 minutes and had those weak? reactions a 1+ eg. Anti-Jka in gel not detected by reference lab using PEG) -- I recall "before my time" when screens were set up at 4, 20 and 37 degrees - looking for ANY possible antibody (in time it was realized these were a waste of resource for the rare time they might be significant) -- progression to I.S. and now Computer Xmatch - we realize there may be units we would have had incompatible by IAT testing are being transfused but are more patients reacting since we went to these time/resource saving methods?? I recall a quote from a while back "medicine is not a perfect science and if you expect it to be you will be disappointed....we do the best we can with the resources we have" (or something like that).

Us too .... staff feel this is going backwards ,my concern is years of missing information! Caught us totally off guard - who'd think a computer system wouldn't want to help you retain all patient records! How are you moving forward? How do you plan to explain missing patient records if asked (I realize there's debate on how long this type of record is to be retained)?

I thought we had permanent storage of our antigrams in Meditech (it was so handy to print a patient's panel from years ago and compare it to reactions we were getting today.) I now realize we were one of the few using this feature, as Meditech decided not to move it forward into the 5.6 update. Seems bizarre that a computer system would not work toward keeping and making it easier for facilities using their system to have easy, permanent access to this important patient information. I am wondering if any others in this same predicament would share how they plan to move forward and how they plan to explain years of missing antibody work-ups if asked.

There is a standard in Canada that states cord samples cannot be used for typing in transfusion cases. Some techs argue that we trust that type for giving the mom RhIG

We have a few surgeons who order G&S on EVERYTHING they do (OBG inserting IUD's!! Orthopod doing knee scopes!!! ENT doing ear tubes!!!). How can we change this type of over-ordering!?

Yesterday we did a work up on a 52YF going for completion of thyroid. This was follow-up to the partial thyroidectomy done in October. She was transfused "many years ago" and has 3 children. October we detected an Anti-K - she was not and has not been transfused since. Yesterday we detected the Anti-K again what appears to be an Anti-Fya showing dosage (reacts with homozygous cells only + patient is Fya negative). We use gel - Anti-K was 3+ for both samples. Any thoughts of what could have stimulated this Anti-Fya ... the Thyroidectomy?? No notes of lymph nodes being taken - thought the manipulation may stimulate T-cells to become active again??

Any one have a list or know of resources? Our physicians continually order anemia panels AFTER the patient has been transfused .... how reliable are results - RBC folate or retic couldn't be too accurate could they?

56 years old

Like I didn't write enought already .... a couple other facts forgotten: DAT postive (C3d only) Auto control positive I.S. and warmed I.S. but negative at prewarm tube IAT

We had a patient transferred to us from an outlying facility. Hgb 64, diagnosis query mantle cell lymphoma. We were unable to get a valid blood group due to interferring cold antibodies: Anti-A 3+ Anti-B neg Anti-D 3+ Rh Control neg A Cell 3+, warmed 2+, cells and plasma warmed then tested 2+, washed and prewarmed1+ B Cell 4+ Historical group from 10 years earlier was APos ...... only way we could get a negative reaction with the A cell was to let it settle at 37 and resuspend WITHOUT spinning (is this valid with all the talk of these IgM antibodies not being detected at 37c??) Futher testing to identify cold antibody (which strangly did not seem to interfere with obtaining CBC results!): O screening cell: 3+ room temp, 2+ warmed (thinking of HI) A Cord cell: 4+ room temp, 4+ warmed (less H,i) O Cord cell: 4+ room temp, 3+ warmed (Hi) Gel antibody screen had typical 'cold-mixed field' look, prewarm tube IAT was negative. We transfused 2 group A units and hgb showed no real increase (to 69). They held off further transfusion until hgb was 46 three days later and gave 2 more A units warmed during infusion this time. Hgb rose to 55!? Droped again to 47 and 2 warmed A units given = 57 hgb. Droped again to 47 and A washed cells with warmer given (thinking if complement was a problem washing the cells would deplete the complement in the unit). Hgb up to 57, then few days later back to 47, more washed/warmed A units gave hgb rise to 62....only to drop the next day to 47. Decided washed cells were not the answer and resumed transfusion of A units with warmer, started him on Prednisone and hgb stayed around 75 (anytime Prednisone was weaned the hgb would drop and retics would fall!). His final diagnosis is high grade B cell lymphoma - Waldenstrom's. IgA, IgG normal,IgM elevated (3.53 (Normal 0.4 to 2.3)). Hemociderin was normal. Haptoglobin less than 0.12 (low) LDH 1200 (elevated) Total Bilirubin 41 (sl. elevated) There did not seem to be intense intravascular clearance (no hemolysis/icteris in sample) but the patients spleen was grossly enlarged and our pathologist thought the red cells were being sequestered here and then removed. Hematologist said the marrow showed erythroid hyperplasia. The hematologist called me months later stating she had read an article that Waldenstroms can develop anti-I antibodies, she would really like to figure out specificity to learn from this case. ANY THOUGHTS ..... I feel it's a pan-agglutinin, we did all we could to figure out specificity!