jnadeau

After being cited by a NYS inspector a few years ago for vital signs not being documented as described in the blood administration policy (some pre- and post vitals were documented with the same time as the start and end times) I searched through numerous P&P's and regulations from around the world (English speaking anyway) to find a fix.  The citing was legitimate (pre=BEFORE START, post....) and I wanted the corrective action to reflect the most up-to-date best practice I could find.  There was an almost universal policy/regulation for pre-, 15 min and post vital signs.  The variations in the timing of vital signs (other than the 15 min ) was all over the map.  The multitude of situations patients are in make it difficult to be cut and dry in a P&P.  Decided to go with pre- and post within 30 min of start and stop;  must stay with patient first 15 min so that was easy.  More frequent vitals if provider indicated (almost never) or transfusionist deems patient requires - or if I recommend with my knowledge of the patient history / lab results.   You know though, that as soon as there's an incident they'll "fix" it by requiring more frequent vitals and the loop continues...keep your old policy handy.

I am sorry, but this rather proves to me that the FDA should take more advice, if they are going to claim to be the "be all and end all" in terms of ultimate authority.

I, and many people much more expert in the field than me (to name one, Dr Geoff Daniels), would agree with Dr Gandhi that serological ABO typing is far superior to molecular typing, BUT, the same cannot be said for RHD typing, where molecular typing is vastly superior to serological typing (not least because no blend of monoclonal anti-D reagent can detect all weak and partial D types, and no monoclonal anti-D has yet to be found that will not react with a Partial DIII).
It is also disappointing that Dr Gandhi is unable to use the internationally accepted terminology for the D antigen.  Many, many moons ago, Dr Patricia Tippett, who, you will recall, did the original work on partial D categorisation, which, to a large extent, is still used,not least by the International Society of Blood Transfusion.  Patricia pointed out that the correct terminology for the first of the Rh antigens was "D", and certainly not Rh(D).  Obviously, Dr Gandhi is one of those who feel they are above and beyond the reaches of those who really know.
Turning to Dr Park, I would again say that ABO typing is, almost universally, better done serologically (I doubt anyone would argue with that), but that the molecular testing of the RHD gene and, by inference, the fact that they are far more accurate than is D typing by serological techniques.  If this were not so, people with partial D types would not still be making allo-anti-D in the numbers that they are.
Similarly to the misuse of terminology by Dr Gandhi, I also note that Dr Park writes, "We use molecular-based testing for a lot of blood bank phenotyping now."  Since when has a "molecular technique" in the world of blood transfusion been "phenotyping", rather than "genotyping".  This is not just a mistake in terms of "blood grouping terminology", this is a very basic mistake in terms of biological science.
This brings me back to my question, do these "experts" make up their rules as they go along, or do they actually take any advice from the experts in the field, who wrote those two papers I cited in my earlier post?  I must say that they don't seem to be that "expert" to me.

I have NO idea who are HFAP, but I would say that, whoever they may be, they are complete idiots.
Your way of treating the patients as D Negative until proven otherwise (i.e. the patient is D Positive or is Weak D Type 1, 2 or 3) is EXACTLY what is suggested by people who actually know about the subject on both sides of the Atlantic (Daniels G.  Variants of RhD – current testing and clinical consequences.  British Journal of Haematology 2013; 161: 461-470, and Sandler SG, Flegel WA, Westhoff CM, Denomme GA, Delaney M, Keller MA, Johnson ST, Katz L, Queenan JT, Vassallo RR, Simon CD.  It’s time to phase in RHD genotyping for patients with a serological weak D phenotype.  Transfusion 2015; 55: 680-689).
I have, as I said above, no idea whether this was an HFAP ruling, or the ruling of a rogue inspector from HFAP, but, either way, I would be appealing against the citation, or changing the organisation who inspects my laboratory, if the appeal is rejected.  From my point-of-view (and I have a bit of experience) you have done no wrong, but the inspector/inspectors have not got a clue about the Rh Blood Group System, and, in particular, the vagaries of the RHD gene.
My own wife is D Negative, and if this lot forced her to be assigned as D Positive on such minimal reactions, I would be suing immediately.
Sorry about the rant!

We do this test on all Rh (weak D) negative cord blood specimens from babies with Rh negative moms -- just to make sure that it is baby blood and that mom doesn't need RhIG.

If you put a drop of blood on something like a filter paper, and then add a drop of 1M NaOH, if it is adult blood, after a couple of minutes it will turn a sort of yellow/brown colour, as the Hb is denatured by the alkaline, whereas, if it is blood derived from the baby (including cord blood), the red cells will stay red, as HbF is not denatured by the alkaline for much longer.
It is rather like doing a Kleihauer, but by "bucket chemistry", as it is known!  

Our stuff is stored for 10 years, with a set of notebooks for each year.  The patient's records are stored alphabetically within each year, with the current year's set is found in the Blood Bank.  We do not collate individual patient's records from year-to-year.   We do not search for expired patients in order to clean our printed records.  We just toss a year's worth when it is 10 years old.
Scott

Yes...we've seen this phenomenon at our facility as well. Am not certain if it's a problem with centrifugation or if it could be remedied by pre-spinning the gel cards prior to use. I vaguely recall some facilities having pre-spun the cards on receipt but never got an explanation of this practice. Upon getting a positive reaction on the 3-cell screen, I always set up a new card and repeat prior to running a panel to avoid this problem. Have not seen anything from Ortho to suggest that others have this problem and/or explanations to this.
Also...I like the Immucor cells myself, and do often reduce them to 0.8% and run them in gel as you do ... does Immucor sell 0.8% panels? If not, they should...have found their cells to have a stronger antigen expression than the Ortho cells.

I have never seen a need for an exclusive blood bank arm band.  If the universal hospital arm band provides the needed info and is used appropriately then why needlessly complicate a process with a blood bank exclusive arm band? Complicating process never makes it better. 
To answer the original question we required Patient's full name, DOB, and MR # along with the phlebotomist's initials and date/time of the collection.  Utilizing the biologics arm band system (pre barcode tech) the 1st three were provided on the label made directly from the patient's armband.  The last 3 were hand written by the phlebotomist.  I'm certain the technology has changed but I'm confident the bar code systems function very much the same.  
As far as regulations go I believe that CAP or maybe JACHO required 3 identifiers and 2 of them had to be full name and DOB.  I may be mistaken in this but that's what I seem to remember.    

Well, yes and no (I realise that is not helpful, so I will expand!).
The patient's do wear arm bands that have both eye readable identification (full name, hospital number, date of birth, etc), but also a bar code that can be read by a scanner, with the same information (at least, if not more).  The bar code can be used to produce sticky labels at the bedside that can be used to label sample tubes for blood bank - but no pre-printed sticky labels are allowed.  The blood bank also can produce labels for the units of blood/blood components and blood products, and so these can be scanned at the bedside (against the arm band) before administration.  This is the "yes" bit!
Having said all that, the arm bands are not exclusive to blood bank; they can also be used to identify the patient for the administration of, for example, medication, to ensure correct patient identification.  Therefore, the arm bands are not exclusive to the blood bank.  This is the "no" bit!

WOW; a real can of worms!
Just for fun and off the top of my head here is my opinion. PPE is by definition to protect the techs. The lab lay out should allow a transition location to don lab coat. When entering lab proper; add gloves and safety glasses (ask anyone who has had their head in the eyewash for 15min). Gloves should be changed when visibly soiled and periodically as they loose their impermeability over time (I remember reading either vinyl or latex in ~20min). Wash hands when changing gloves. Put face shields in key locations. Small reagent/blood smudges on paperwork are taped over, if larger spill occurs put in plastic folder and photocopy. If this is followed the tech is protected and contamination throughout the lab minimized/contained. Gloves are prohibited but lab coats required in labeled "Clean" areas of the lab that are used for issuing blood products and manager/Sr. tech paperwork. Blood products worked on in the lab are handled with gloves but products are issued without gloves and placed in Ziploc bags so that if dropped leaks are contained. The RBC will be taken out of the bag and hung by an RN wearing gloves.
Yes I know that it is purely semantically that if working on a RBC I wear gloves but when issuing the same unit I do not. It does however provide a clear distinction as far as writing and interpreting policy.  
The last thought is that whatever you decide is your policy; it must be practical and enforceable or will not be followed by the techs and therefore only an academic exercise.

In the US we have been doing what you say is going to be the new policy for many years, except we only would do a DAT if the autocontrol was positive.  I think that approach is pretty common.  Orthos' panel A is for the ijnitial assessment.  Most of the time, you will have a pretty good idea what you are dealing with with those results.  Then, going by the 3 x 3 rule, w use other panels for rule-outs / rule-ins.  Also, if there is no history, we antigen-type the patient for those antibodies that are being made.
Scott

Most developing clinically significant alloantibodies still react at 37oC, and so trying to detect them at room temperature is more or less futile as, in most cases, all you will detect are antibodies that  you do not want to detect, such as cold-reacting anti-M, anti-N, anti-P1, etc, which would be a waste of time, reagents and, most importantly these days it would seem, money.
Most polyspecific or broad-spectrum AHG reagents these days are a mixture of anti-IgG and anti-C3d (particularly in the UK).  They do not contain anything but the merest hint of an anti-IgM (certainly, they would not be CE-marked for anti-IgM).  The other thing is that I am prepared to bet quite a lot of money that your laboratory is using EDTA-anti-coagulated samples.  This means that the Ca++, Mg++ and Mn++ ions are all chelated from the plasma, which means that the complement pathway cannot be initiated in vitro, so, even if the de novo antibody was capable of "fixing" complement, the anti-C3d would not detect such an antibody anyway.
Therefore, as the number of recently transfused patients who are developing antibodies not yet detected by normal serological techniques who have been fatally affected by a further transfusion hasn't been great (zero in fact) and the same applies to pregnant ladies, stick to trying to detect clinically significant antibodies at 37oC using monospecific anti-IgG.
GOOD QUESTION THOUGH - SHOWS YOU ARE THINKING!

I agree with Neil and Mabel about the bureaucracy, but I agree with pbaker.  The number of times I have had a doctor change his or her mind about uncross-matched blood when I have told them that THEY take full responsibility if there is any nasty reactions, and wait for the fully cross-matched blood, is not huge; it is enormous.

I have seen uncrossmatched be able to wait for crossmatched.  It is amazing how the need becomes much less urgent when they have to put their name on something.

Right, good point.  The previously ID'd antibody does NOT need to be "reproved" (even if it is not showing up you will be screening units for it anyway).  But any newly developed (i.e. de novo - Spanish for "not vocal" BTW) must be ruled out each time.  Assuming they do not exist because a screen panel of 2 or 3 cells "matches' previous screen results just isn't adequate as far as appropriate "additional testing" that "must be performed".
Scott

Congratulations Malcolm and well deserved.  Very happy that you chose to share this with us.  It's gratifying when some one in our profession is truly recognized.  

To address this question of safety, I would like to see hard data from the AABB community as to the frequency of events where an ABO discrepancy was detected in the second ABO determination that was not detected in the first ABO determination.  More importantly, did the detection of an ABO discrepancy (missed by the first ABO determination) prevent the transfusion of ABO incompatible red blood cells? 
My responses above assume that the ABO discrepancy was demonstrable by repeat testing of the first blood sample.

You use a less sensitive assay method to reduce interference with cold and warm auto antibodies that you have shown or proven are not clinically significant, with the idea that a clinically significant allo antibody like Kell, if present, will shine through.  It's a balancing act.  

Thank you very much Malcolm.  I'm going to read this over again at home - maybe with a cold beverage in hand - and let it sink in.  I appreciate the time you take to answer these questions and my student will be very pleased with your compliments.

If it was a "cold" antibody, we would perform the ABO and D type by tube technique at strictly 37oC.  If the antibody has an exceptionally wide thermal amplitude (still interferes with the ABO and D type at 37oC, we would give group O, D Negative blood - unless of course, the antibody is a saline reacting anti-c or anti-e).
If the "cold" antibody does not interfere with the ABO and D type at 37oC, we would probably test to see if the antibody can be detected at 30oC (which means that it could be a clinically-significant "cold" auto-antibody), but we wouldn't bother to try to find the specificity, unless we were so bored that we had nothing else to do, because, under these circumstances, the antibody would not be clinically significant in terms of a transfusion.

I feel your pain! So much for evidence based medicine

Whether you call yourselves Lean (or Six Sigma or some other facetious productivity name) or not, the reality for many labs these days is that generalists are more and more necessary to keep things going in light of personnel shortages,
We are a 250 bed level 2 trauma hospital, with a fair amount of Lab work on the type of patient population we see, including BB.  The only real "dedicated"  techs we have are in Micro (and of course, Histology). About a quarter of the techs on first shift are generalists that can work on a regular basis in BB (in addition to the main Lab area).  On second and third shift, virtually all of the techs work BB in addition to the main lab area.
Whether one has BB with all dedicated staff or no, the key is to have adequate training and competency, along with extensive references, including having good P&Ps available.  This is true for all areas of the Lab (and in health care in general!).  It requires a sharp and dedicated management model and staff.
Scott
 

Unfortunately, NHSBT RCI reports now use "coded comments", rather than free text.  The "coded comments" are, almost universally, ungrammatical, reflect poor scientific (in particular, blood group) nomenclature, are frequently clinically inaccurate and are totally confusing, so I am not surprised you are not familiar with the term, because, in reality, it shouldn't exist, especially in a report from a Reference Laboratory.
The reason "canned comments" are used are two-fold.  Firstly, they can be put in quickly (striking one key can put in a complete sentence - although, as I said above, most of them are far from grammatically correct sentences - and, of course, hit the wrong key, and you have a comment that is even less relevant than hitting the correct key), so this is "LEAN".  Secondly, and much more insulting, is that one of the senior managers thinks that, if a CORRECT free text report is provided, the poor souls who work in a hospital laboratory will not be able to understand it.  How would you feel about that applejw?
Of course, in this case, there is probably an auto-antibody, directed against an antigen within the Rh Blood Group System, such as anti-Rh17 or anti-Rh18, that mimics more "common" Rh antibody specificities, such as anti-c and anti-E.  In this case, the antibody reacts with all antibody panel cells, but reacts more strongly with those cells expressing the c and the E antigen, hence the inaccurate, and scientifically poor (appalling) comment about "non-specific anti-E and anti-c".
I hope you are sufficiently intelligent to understand this.
THAT LAST SENTENCE IS MEANT AS A JOKE (although, not necessarily, if the person reading this happens to be the senior NHSBT manager who thinks hospital staff are thick)!

Plasma is hard to keep track of just by temperature alone.  If you are in a hurry - there is a good chance the plasma is going to be warmer that 1-6C when it leaves the Blood Bank to start with.  Even in a separate cooler, that means the temperature monitoring tabs won't work and there is no way to know what happens to the plasma that way.  Data loggers wouldn't work either.  Difficult situation. 
We will only accept plasma back if it is cold and in it's own cooler and will only keep it for 24 hours.  We do not extend FFP (any type) that was issued and returned into a Thawed Plasma product either.
 

@SMILLER, we have always been able to determine who received our products, including all emergency release products.  We have a form the physician signs that lists the units.  The blood bank issues those products (when they have time) to that patient and we can track where every product goes.
What I take exception to is the inspector insisting that we also put the patients name and MRN on the product.  They again insisted this made the process safer.  It does not in any way make it safer, especially if it's a system assigned name / MRN and more importantly, when it takes a modest amount of time to generate these labels.
We have done a tremendous amount of planning to ensure we can give out emergency release coolers, almost on demand.  It takes us very little time to give the requester their products, these labeled units have put a significant delay on that, and in my opinion, has deceased patient safety.