gagpinks

You are well deserved for this. 

Another expensive but possibly effective approach would be to use one of the complement activation inhibitors, such as eculizamab, that is used to treat paroxysmal nocturnal hemoglobinuria, a disease with inadequate inactivation of complement components.  

This could be due to anti c IgM in nature. I have seen this many time especially in pregnant lady. 

I just answered this question.


My Score PASS  

Could the Daily/Day of Use QC for the ABO Plasma Grouping Cells ( A1 and B ) be considered a positive and negative control for the saline crossmatch?  In both cases these tests use patient serum/plasma added to donor red cells, the only difference being that the ABO Plasma Grouping cells are stored in solution designed to maintain agglutinability  while the donor cells are stored in a solution designed to maintain oxygen transport.

DTT SOP.pdf
 
This procedure is based on the HemoBioscience SOP and the AABB SOP.  Works for us.
Prior threads on this topic have indicated that the DTT treated cells will not last long, so we do this only at need.

I have a question about the "newborn card".  I am not familiar with this card, so forgive me if this is the case.  Does this card contain IgG, and is it incubated at 37 prior to centrifugation?  And when you perform the testing in tube, do you incubate and carry it through AHG phase?  This is how we detect weak D.

Another strategy, which works for ABO incompatible kidney transplants in some cases, is a combination of immunosuppressive drug therapy, IVIgG and plasma exchange.   If it works for ABO, one would guess that it could work for Inb (or anything else, for that matter).  One also guesses that the antibody might be wholly or largely IgM if it only causes HTR and not HDN. If that were the case, plasma exchange could be particularly effective.

She very possibly can (although two things; it would most certainly depend on the titre of the anti-Inb prior to EACH transfusion [and that would have to be 1) a doctor's decision and 2) a bit of a guess, as anti-Inb is so rare) and also, I would suggest IvIgG, rather than methylprednisolone (or, possibly, both).  However, having said all this, there is NO DOUBT that anti-Inb is clinically significant in terms of haemolytic transfusion reactions, although the same is not the same for HDFN.

This could be due to anti c IgM in nature. I have seen this many time especially in pregnant lady. 

Below is the exact text from the guidelines.    I agree that potentiators added to the reverse group may detect non ABO antibodies in addition to the ABO antibodies but who adds potentiators to reverse group routinely?   One reason that anti c is mentioned may be that reverse group cells are usually Rh neg.   I have seen strong IgG anti c react in reverse group with no potentiators. 
 
 
Other reverse grouping anomalies: Potentiators in the reverse grouping reagents may cause IgG antibodies such as anti-c to be detected in the reverse group.

Hope this is okay to post administrators, but I have been asked to publicise the MHRA Discussion Forum, especially for members of PathLabTalk who are either UK citizens, or who are working in a laboratory inspected by the MHRA.  The address is forums.mhra.gov.uk/forumdisplay.php?60-Blood-Forum.
You can go on there anonymously and ask virtually any questions you like concerning their inspections, quality, haemovigilance and SABRE, and a whole lot of other subjects.
This will also help the UK TLC group (of which I am currently a member) formulate their standards.
Lastly, you have to remember that despite both the MHRA and UK TLC being rather regarded as "sticks" with which to "beat" Biomedical Scientists, both are actually there to help.

I dont think you need special state licenses for these states. CLIA (Clinical laboratory improvement amendment) defines most tests performed in hematology and immunohematology as moderate to high complexity testing, therefore needs specific education/experiences or accreditation. The easiest way to achieve it is to challenge accreditation exams conducted by ASCP (american society for clinical laboratory science). I have the link to their website below. You can go ahead and make an account free of charge and start looking through education/experience requirements and paperworks needed to challenges the exams. As you have 17 years of prior experience, recommend you to look into BB(work in blood bank), MLS (can work in every area of the lab except for cytology), H (can work in hematology)which are technoligist licenses. Also, specialized licenses SBB (specialist in blood bank, which majority of blood bank lab leadership personnel are certified for) or SH (specialist in hematology, which majority of hematology lab leaderships are certified for). 
https://www.ascp.org/content/board-of-certification/get-credentialed
Please do not hesitate to ask us questions here. We are all here to help you with your transition. 

Hi dothandar and Malcolm
These are the card we use in our lab as part of DAT protocol.  
Malcolm , I guess this finding is not clinically significant then. Is there any particular reason for DAT to be positive in C3d or cause is unknown?

Well, the first thing I would say is that you would be wasting time and reagents to cross-match at the hospital, for the precise reason you quote; of course the units will be incompatible, so just perform an "immediate spin" cross-match (if you must) or perform an electronic issue, as you say that you trust RCI results.  As far as antibodies directed against low prevalence antigens are concerned (the antibodies are usually quite common, it is the antigen that is usually quite rare), I would advise you to read Garratty G.  How concerned should we be about missing antibodies to low incidence antigens?  Transfusion 2003; 43 (7): 844-847, which, basically says what I said above - i.e.  that NO TRANSFUSION IS 100% SAFE, but such antibodies are low down on the list of risks.
Just before I retired, there was a move that all RCI Departments would go over to electronic issue, when there was a positive DAT and no detectable underlying atypical alloantibodies, but whether or not this ever went through, I don't know; you would have to contact your local RCI Department.

There are two ways gagpinks.
Either you can believe your local RCI Laboratory when they say that there are no atypical alloantibodies detected (and why send them there if you don't believe their results?), or do the work yourself with DTT-treated panel cells.  NO TRANSFUSION IS 100% SAFE.

Dear God, you have my deepest sympathy. 
1.  Push the company to give details on their benchmark standards and where they come from.  Chances are, you are not in the same boat.  We had a similar problem here because our Micro and BB staffing for the weekends did not meet corporate standards (desires), but we were unable to cut staff because of the physical layout of our facility and the distance between the departments. 
2.  Your situation matches one hospital I know of, if you could contact them - University Medical Center, El Paso, TX.  The Blood Bank is in the Main hospital and the main lab is way across the parking lot.  They are a level 1 trauma center and a big surgical hospital, but the NICU is in a separate hospital next to them and did have it's own Blood Bank staff.
3.  Do you have current FTE numbers that justify your current staffing?  What is the difference in the "factors" in the staffing equations that are being used that lead to this new company coming up with their figures vs. your current FTE figures?
Good luck.  Patient safety arguments sometimes sway Administrations when nothing else will.  If you can make a case for how dangerous it is for the staff of a Trauma center to be too little, too late - maybe it could help.
 

Oh, you mean that they have suddenly woken up to the realisation that their figures don't add up, but are too embarrassed to admit it.  

It looks to me that there are 12 states in the US with licensure requirements, including Florida, California and New York.  You will want to check the state government website for more information for the state you wish to move to. 
As for certification, which is required for any clinical lab science position in the US, check out the ASCP website as Cliff suggested.  You will have to take a national certifying exam.  You can google that also, here is one resource: https://study.com/articles/ASCP_Certification_Requirements_and_Information.html
Scott

Most states in the US do not require a license.  I suspect after that it is up to the individual facility on what the requirements are.  We require our techs to be ASCP certified, you might want to look into that.

This doesn't fit the pattern for an antibody to a low incidence antigen - in this case, all 7 group A units are incompatible and the 4 group O units are compatible.

Might be a rare IgG anti-A1 - you may not see in in the Reverse (presumably IS or buffer-only gel card), but is detected when you do anything with an antiglogulin reagent. You could try doing the Reverse by IAT. The DAT may just be a red herring, but it might represent a weird autoantibody that favors group A cells.

If RhIg not given in this pregnancy than it might be silent fetomaternal haemorrhage and lady might developing allo anti-D in this pregnancy. We had a similar case where antibody screen was negative at booking blood and all of sudden antiD level shoot up at 28 weeks.  

In many ways I do agree with what you write, but, however rare K+k- individuals may be, they are considerably more common than are either Kp(b-) and Js(b-) individuals.  It would seem reasonable, therefore, to test for such individuals, in the knowledge that, nationally, and, perhaps, internationally, K+k- blood can be supplied reasonably easily, whereas the search for a reasonable supply of either Kp(b-) or Js(b-) donations could prove fruitless.
Again, with regard to Dombrock antibodies, although undeniably these can be clinically significant, such clinically significant antibodies are incredibly rare - so much so that they are often still written up as posters or abstracts, even in patients who are not on Dara, or similar monoclonal antibody treatment.

here is a fun case along with a question that I cannot wrap my head around it. 
Mother:
Anti-D and anti-G identified (both strongly reactive by PeG and saline-IAT), Anti-C ruled out by differential adsorption and elution with R2R2 cells and r'r cells.
All other common alloantibodies ruled out. She was not previously transfused or pregnant. 
TITER with R2R2 cells = 1024, titer with r'r cells - 128 (I know this titer is so unhelpful since expression on each of our indicator cells are different) 
Baby: (here is the fun part.. ready?) - on the birthday
D typing negative with MoAb anti-D reagent at room temperature with untreated cells, EGA treated cells, twice EGA treated cells.  DAT 4+ with untreated cells, EGA treated cells and twice EGA treated cells. 
Baby is fine (dont need transfusion, not hemolysing). Plasma and eluate reactive with D+ and C+ cells. insufficient sample to perform adsorption/Elution to differential anti-D from anti-G. 
eluate- reactive with D+ cells and C+ cells/ we assume it was anti-D and anti-G in there. 
Genotyping result. RHD*DAU0. Homozygote D deletion detected. So baby is heterogygote DAU-0 without a normal D gene. 
1 month later, baby came back hemolysing. 
DAT 4+ with untreated cells. Anti-D typing 4+ with EGA treated and untreated cells. DAT on EGA treated cells is negative. 
plasma and eluate reactive with C+ and D+ cells. all other alloabs ruled out. Not enough sample to perform adsorption/Elution
 
My question is.. 
The baby's red cells were clearly coated with anti-G and/or anti-D why did it not hemolyse at birth but 1 month after. 
I have heard of blocking mechanism serologically as in this case
 Does the heavy coating of antibodies makes Fc receptor inaccessible for macrophages for hemolysis? 
Could it be anti-G alone (not anti-D) coating on the red cells protecting the red cells from hemolysis by anti-D?