Thandar Aye-zheng

I read that Anti-Vel(not sure) react stronger with D+ cells then D- cells. could this be it?

I am sorry to find out patient is expired as soon as i got to work today

Yes Malcolm, I had an Anti Lea positive woman in pre op work up for her C section while her prenatal screening was negative. So may be the same thing is happening to this patient. Yesterday, I also found out that patient never had remission since he started in our hospital. Patient was transferred to ICU yesterday. I am also suspecting platelet refractoriness in this patient (post tx count is lower than pre tx count by 1000 increment everyday, while he is receiving 1 unit per day) Galvania- Yes patient has been receiving 1 platelet per day or every other day for a couple of week. We have been transfusing non type specific irr cmv neg. We tried our best to give A platelet since the patient typed A (even thou a couple of O might be tx). So chances of getting Anti A1 is very unlikely. Liz – patient has been typing A pos since mid 2010 without any discrepancy in typing, until last month while the forward typing was changed to O. and 2 week ago I started seeing positive A1 cell reaction. So I don’t think the patient is subgroup of A. I am suggesting patient is developing anti A1 even thou he was initially typed as A. I think patient blood type has changed to O from A. Even thou I have eliminated as much “cold” antibodies that may interfere with my reverse typing, my supervisor kept insisting that it was non specific cold and not to change the historical blood type. Being a fresh out of school blood banker, I do not have confident to argue with her.

I also did 4'C incubation for 3 screen cells and turned out negative. Therefore, I was able to rule out "cold" antibodies such as Lewis, M, N, P1. I am scrtching my head whether it could be Anti A1 or not.

Today I came across a case with AML patient in the lab. Patient was dx with AML when admitted in mid 2010 and typed as A pos. Pt has been multiply transfused with irradiated O pos RBC (and non-type specific platelets) throughout the year. 2 months ago patient forward typing was changed to O while the reversed typing remains A (I understand that patient was volume replaced due to repeated transfusion with O pos cells). Just last week patient was re-admitted and both forward and reversed typing demonstrated O. Forward typing was AntiA-0, Anti B-0 at both Immediate Spin and 10 min RT incubation. Reverse typing was 1+s immediated spin, 2+s 10' incubation and 2+ at 37C, 10' incubation. Antibody screen was negative with Liss AHG 10'. I also did a "mini cold panel" using patient serum O cord cell, O adult cells, A1 adult cells, A2 adult cells and auto control, at IS, 10'RT and 10' 4C. Everything turned up negative except A1 Adult cells. So I ruled out non specific cold agglutinins and cold auto antibodies. I called the floor and asked whether patient had BM transplant at some point of his life and the answer was NO. I understand that Antigens can be weaken and forward typing can change in oncology patients. What I dont understand is if the patient is intrinsically capable of producing ABH antibody while his antigens are weaken. Or Am I typing some "junk" as Anti A1? ?

New Blood Banker here. Please bare with me if I am not making sense. I am thinking panagglutinin on eluate with non-specific cold. Try 4C incubation with pt's serum on the panel and prewarm crossmatch with these 2 incompatible units? see if the panel turned up pos and prewarm xm turn up comp? ?

I got one "real insufficiency" instead of "renal insufficiency"

Fresh off school blood banker here. So, please bare with me if my technical terms are wrong. Re: post tx mix field Intermediate Spin D+ Use 6% albumin as Rh Control to see if it is positive at immediate spin. If it is, this can be due to cold antibody coating the cells. Re: Weak D+ Use Rh control when performing weak D?? If Rh control is positive, the positive result is due to antibodies coating on the red cells.

thanks!

Fresh out of school blood banker here, so please bare with me if I am not getting the technical terms correctly Does the platelet refractoriness to transfusion refer to as poor recovery or shortern survival of transfused platelet? I wonder what are the chance of refractoriness due to alloimmunity(Anti-HLA etc)? If I see a patient who has been transfused over and over again with shortern platelet life (i think, after 2-3 day she is back to her low 5-10) should i be bringing it to pathologist's attention? ?