jnadeau

We're moving to eliminating the saline bag and using a 50cc saline flush (syringe) at the end of the transfusion.  A bag of saline will be at the bedside in case of a transfusion reaction.  This has been prompted by the saline shortage - the pharmacy is very happy with the move.  The saline flush was suggested because the nurses said patients notice if they don't get all of the blood they're paying for...not worth the argument.

We're moving to eliminating the saline bag and using a 50cc saline flush (syringe) at the end of the transfusion.  A bag of saline will be at the bedside in case of a transfusion reaction.  This has been prompted by the saline shortage - the pharmacy is very happy with the move.  The saline flush was suggested because the nurses said patients notice if they don't get all of the blood they're paying for...not worth the argument.

Someone reminded me that saline is used to keep the line open until it is certain that there is not going to be any need for it --- like in the case of a delayed transfusion reaction.  (Although I do find the theory that the last few mls of blood are in reality Super Cells more intriguing.)
Scott
 

Clear bags - blood products are not considered a biohazard (I thought - if my memory serves me correctly on this "Friday where have you been?!!)

Thank you BankerGirl- it worked!  What do I owe you? 

Years ago I worked in micro exclusively for 8 plus years.  In my experience, especially with normally sterile fluids (e.g. CSF, blood) it was not unheard of to have a negative smear (NOS) followed by growth (usually rare colonies).  We would review the slide to ensure we had not missed something on the smear.  I always thought it  was ALOT easier to call a "rare gram pos cocci" on a smear AFTER you got the growth on the plates - many times it looks like stain artifact / debris on initial read. You are initiating treatment on patients (many truly negative) calling a positive smear. This was a real problem with AFB smears and cultures with rare to few colonies growing weeks later.  Now on review of the slide, the supervisor "sees" 2 small bacilli amid a lot of sputum debris!  Really!  That's why micro is a specialty - but still not perfect.  Molecular testing has made a big improvement in this arena. 
 

Simple antigen frequencies always seem to include both D+ and D- people so it is sometimes hard to get the frequency of D- units that are pos for C or E. C+ is more common than E+ and I agree that each is < 1% or so.  We allow the ruling out of E and C specificities in the presence of anti-D with a single heterozygous cell partly because it is so unlikely that a D neg unit will be positive--about in the range of the frequency of the Kpa antigen as I recall.

The frequency is low, I believe less than 1%.  Some labs, like mine only require 1 heterozygous C+ and E+ cell to r/o C,E in the presence of Anti-D.  If that is your procedure, and your panel cells r'r and r"r were both negative (usually cell #5 and #6 ORTHO), then you should be fine. 
 
That said, the crossmatches should be repeated through AHG.  Maybe time for some competency refreshers?

Old school thought was that you had to wait for 24 hours. I think that one to two hours is common practice.
I also remembered reading something in a CAP publication that discussed this and actually managed to find that in one of the threads here. There are references associated. Quoted below....................
Q. How long should you wait after a unit of blood has been transfused before drawing a complete blood count, or doing other lab work, to ensure accurate test results?
A. Optimum timing of post-transfusion phlebotomy is critical for ensuring meaningful laboratory testing results, and medical judgment is required in making this determination. Several factors must be considered, including the type and amount of blood product given, purpose of the test (that is, the question it is intended to answer), and clinical setting.
In general, it is best to perform phlebotomy when the patient’s circulatory system is in homeostasis. A patient who is bleeding or undergoing blood product transfusion, or both, is not in a steady state. Whenever possible, samples for laboratory testing should be postponed until bleeding has stopped and transfusion is complete. One obvious exception to this rule, however, would be the setting of massive transfusion, during which monitoring certain laboratory values, such as cell counts and coagulation parameters, is essential to guide ongoing therapy. Variables such as patient blood volume, cardiac output, renal function, and volume of blood products transfused affect how quickly homeostasis is achieved following transfusion.
For the evaluation of post-transfusion increments in hemoglobin, hematocrit, and platelet counts, a practical approach is to draw blood samples within 10 to 60 minutes after completing transfusion, as this time interval is aimed at measuring peak recovery.1 Results determined from blood samples drawn later than 60 minutes post-transfusion are increasingly affected by confounding conditions, such as splenic sequestration, sepsis, and consumption.1,2 If the intent is to determine the extent of such confounding processes on red cell and platelet counts, one should combine a 10-minute post-transfusion sample with sequential samples drawn at one hour and 24 hours post-transfusion.
Alterations in chemistry test results following transfusion are not usually a concern in the low-volume transfusion setting. However, assay results may be affected for varying periods following transfusion of large amounts of blood products, as seen in massive transfusion, red cell, or plasma exchange—particularly if the recipient has impaired hepatic or renal function. Banked storage of red cells results in elevated plasma levels of hemoglobin, potassium, LDH, and iron in the blood unit that may, particularly in the metabolically impaired patient, be reflected in the post-transfusion laboratory values. In addition, citrate anticoagulant present in blood products may result in transient hypocalcemia in the recipient.3 Therefore, following large-volume transfusions or exchanges, waiting 12 to 24 hours before drawing samples for chemistry assays will provide results that are more reflective of the patient’s underlying metabolic state.
References
Choo Y. The HLA system in transfusion medicine. In: McCullough J, ed. Transfusion Medicine. New York, NY: *McGraw–Hill Book Co;1998:401. Legler TJ, Fischer I, Dittman J, et al. Frequency and causes of refractoriness in multiply transfused patients. Ann Hematol. 1997;74:185–189. Brecher ME, ed. Technical Manual. 15th ed. Bethesda, Md.:AABB;2005;649–650.  
Rita A. Reik, MD
Pathology Consultants of South Broward
Medical Director/Transfusion Medicine Services
Memorial Healthcare System
Hollywood, Fla
 
Edited November 30, 2012 by Justina
Added CAP website find
Justina
Posted December 7, 2012 Articles:
Elizalde JI, et al.Early changes in hemoglobin and hematocrit levels after packed red cell transfusion in patients with acute anemia. Transfusion. 1997 Jun;37(6):573-6
Wiesen AR, et al. Equilibration of Hemoglobin Concentration after Transfusion in Medical Inpatients Not Actively Bleeding. Ann Intern Med. 1994;121:278-280
   
   

If doing a test won't change how you will manage the patient, then I think it is seldom worth doing.  Besides, it will make your computer unhappy and you know how difficult they can be when they are unhappy.

If you wind up sticking with paper - it might be faster if you use tagger guns to attach your paperwork..  These are the same type of tagging guns that are used for clothing labeling.  You can get both the guns and the tagger tails from a place like Staples (Monarch SG Tag Attacher).
Hold up and punch through the paper 1st and then go through one of the little holes on the unit (or very carefully, through some of the outside edge on the unit above the interior area) and then press the trigger.  Works fine for us and stays with the unit.
One word of caution; the needles - when new - are extremely sharp.  I always take a new needle outside and dull it down by swiping it back and forth over some concrete walkway first, prevents finger sticks.  Sounds gruesome, I know, but we have no troubles with the needles (after dulling) and have never harmed a unit.

Some years ago I had a crossmatch order on an elderly gentleman with a hip fracture. At that time we did an auto control with every antibody screen (crazy, I know) and his was positive, though his antibody screen was negative. I did an eluate - perfect, strong, beautiful anti-K. I asked about his transfusion history. Both he and his family members were excellent historians and were adamant that he had not received blood recently, had never received blood or blood products and in fact, had never even been hospitalized before in his entire life. He was a very healthy 90+ year old man who was on no prescription meds and who did not take any supplements or over the counter meds except a rare aspirin. I sent it to the reference lab, because I was thinking maybe I messed up somewhere. They eluted anti-K but insisted he had to have been transfused or there was some medication causing the problem.  I was not convinced by their (weak) explanation and I still think that it was auto-anti-K-like specificity. Only example of this I've seen in I won't say how many years of blood banking.

It would be interesting to note if the patient had received a large volume of crystalloid/colloid.  I've seen a non-B pt receive significant volumes of B red cells and survive for a few days (since their anti-B got diluted by fluids).  However massive hemolysis occurred around day 5 culminating in the demise of the patient. 

Thanks to a very generous invitation from the organisers (in particular Phil Hoffman, aka Dr Pepper on this site, and Maddie Josephs, Chair) I will be attending and speaking at the 69th Annual Clinical Laboratory Science Convention - Central New England (ASCLS - CNE) taking place at the Rhode Island Convention Center between May 9th and May 11th 2017.  I will be talking on Wednesday 10th May 2017, giving a lecture entitled, "An In Depth Description of the Kell Blood Group System." and then, after a well-deserved break for the delegates, and for those that can stand it, a second lecture entitled, "King Henry Viii, McLeod Syndrome, Chronic Granulomatous Disease and Kx."
Sorry if this comes across as being "big headed", but I am really excited about coming back over to the USA.    

Ortho actually describes the dual population as "mixed field" in its interpretation guide and shows pictures of equal amounts of cells on the top and bottom of the tube.  I have a hard time training new techs that a little touch of red at the top is not a mixed field, but trapped fibrin.  Ortho's manual also shows negative results as having a little bit of red cells at the top.

We had graduated to doing ABO/Rh and DAT only on babies born to Rh neg moms. Then...........a new Family Medicine doc came to town and became the head of the OB committee and now we are doing ABO/Rh and DAT on babies born to all O moms as well. The new pediatrician head of the pediatric committee is perfectly OK with testing only the babies born to Rh neg moms - all our newborns are scanned for evidence of elevated bili before discharge, so a high bili is not going to be missed. We are hoping he can eventually win the day and we can go back to testing only the Rh neg babes. One category that we don't automatically get cord bloods on is the moms with clinically significant alloantibodies. I would like to see that change. If a pediatrician doesn't order a DAT on those babies, I find a hemo sample and run one - if it's positive, I would take that info to the medical director for followup with the attending.

Hi gagpinks,
As a UK Biomedical Scientist, if it is the last thing I do, it will be to teach you to use the correct nomenclature!
I can assure you that NHSBT Reference Laboratories DO NOT perform titres on samples of anti-c (or anti-D) from pregnant women, but, instead, perform quantification, and they are reported as IU/mL, and only because the computer system we use will not allow us to report them in the correct nomenclature (IUmL-1)!  Okay, rant over!
I would say that, without a doubt, there is an element of IgM in this lady's anti-c (unless, of course, there is another, as yet unidentified IgM antibody against another antigen expressed by the reverse grouping B red cells) as the reverse grouping B red cells have the Rh phenotype rr.  This may mean that the quantification results are falsely high, because the rr red cells used to perform the quantification are enzyme treated with bromelin to decrease the zeta potential and allow the red cells to come into closer proximity with each other, and this would enhance a reaction with an IgM anti-c, just as well as it would an IgG anti-c.
That having been said, there is no guarantee (at this time) that there is not an element of IgG anti-c present, and as this situation cannot be guaranteed, the pregnancy should be treated as if the entire anti-c is IgG, and that the quantification results are accurate; in other words, the case should, at least for now, be treated as if severe HDFN is a possibility.
So, what to do?  Well, one thing that you should do is send a sample of maternal peripheral blood to the IBGRL for foetal genotyping, to determine if the foetus carries the RHc gene (it almost certainly will, as the biological father is unlikely to also be c Negative, as the mother must be - although it is possible - but then, why would the mother have made an anti-c).  Assuming, therefore, that the foetus carries the RHc gene, and will express the c antigen on its red cells, then, again, you have to treat the pregnancy as if severe HDFN is a possibility.
The other thing that should be done at this stage, either by your own laboratory (if you have the reagents and the SOP, with staff competent in the technique - UKAS, you understand!), or by the Reference Laboratory (more likely) is to treat the maternal plasma with dithiothreitol (or a similar reducing agent - but please, not 2ME - unless you have lost your sense of smell!) to denature the IgM anti-c molecules, to see if there is an element of IgG anti-c present.  If there is an element of IgG present, then, once again, the pregnancy should be treated as if severe HDFN is a possibility.  This could be an unusual, but not unique case, of an antibody causing clinically significant HDFN, where the antibody has been formed after 28 weeks of gestation.
Come what may, the maternal antibody should be monitored from now until delivery as a minimum every two weeks, and, of course, the foetus should also be monitored by MCA Doppler (or something similar) until delivery, just to be on the safe side.
Sorry I can't give you a more definitive answer, but this is both a rare and interesting case.
One thing that I would ask, and that is, if the antibody screen was negative at 28 weeks of gestation, why were you sent another sample at 30 weeks of gestation?  Did the lady have a potential sensitising event, such as a fall?
Malcolm

A few comments:  first, I really like what was said above about this being a pubic forum.  You don't want your employees seeing comments like that.  Second:  if you are in charge then YOU are in charge.  Set the ground rules and enforce them.  You will need your Medical Director to back you up.  Blood Bankers are notorious for not letting go, esp the older ones (like me).  If you feel your techs are not able to perform up to their performance programs document, retrain, document - once they see you documenting things they will get the hint.  Don't let them boss you around.  Ask them what the procedure says.  That's why there are manuals.  If you think they are busting your chops, keep a record and then you can "retrain" as indicated but you also have a record for competencies at evaluation time - but you must make the effort to provide retraining.  If they balk, document . . . It's a fine line to walk.  When you have more management experience you will understand.  In many instances we were promoted to management because we were good serologists . . . suddenly we had to learn to handle people - a whole different ball game.
To the person that started this post:  getting calls at all hours is part of being in charge of the BB.  On the off shifts, I have found that a bit of extra time for training goes a long way in reducing the calls.  No matter how simple the procedure seems to you, esp if you are dealing with generalists, and it is something that occurs infrequently.  Don't make it so they don't call when they really should.  If you have a dedicated BB staff it might be a different story.

I'm on call 24/7.  I tell them to consult the policy first.  If you try and can't find it anywhere in a policy, ask your coworkers to show you where to find the answer.  If nobody else on your shift can point you to it, THEN you call me.  Do not guess!
I get a lot more text messages than I do phone calls.  Usually they already know the answer, they are just wanting me to confirm their answer.  We have quite a few generalists on my eve and night shifts that are not very experienced with difficult BB issues, so I have no problem with them calling me.  I would much rather that than a patient gets hurt.  I feel like it's part of my job as BB Manager to support them and have them feel confident in asking for help when they need it.
I think the key to "weaning" them from calling too much is giving them really great policies (written very simply so anyone can follow them, even if they have not done the test for a while) and some good flowsheets (which I am still working on) for antibody workups, RhIg workups, etc.

I love Helmer products.  Used to be you called up and spoke with one of the Helmers . . . that said.  Had an iseries in NH.  After the first year it would crash, for a number of small reasons, every 10-12 months . . . a gasket deteriorates, the inside unit attached to the fan craps out, nothing major but it forces you to move product, increase documentation.  At my current facility iseries:  fan motor dies, compressor dies, - I think there might be exterior pressures on those parts which I have resolved but still  . . .  I just put in a capital request for one of the Panasonics.   Hopeuflly it will perform more efficiently.
Have had no problems with Helmer Refs except to add coolant sporadically.  Have that built into maintenance schedule where I am now (I think so anyway)

I'm the Lead Tech of my department and I have my phone number posted in the department so the techs can call if they have questions. I tell them I'd rather they call me and I solve their problem/question quickly (hopefully) instead of them either spending a lot of time dithering about it  and delaying results/care or doing something incorrectly, especially in the LIS, and it taking me hours later to sort it out and make the corrections. Additionally I live close by and have told techs, especially on evenings/nights that if they have something come in that they are having trouble handling to call me: example trauma/massive with antibodies. Some techs are comfortable calling me so will be more likely to call, others not so much and won't call even when they should have. I am never upset with someone calling even if they wake me from a sound sleep because if they are unsure enough to call me I don't want them to hesitate because they think I might yell at them. If it's something that they should have known how to do or should be able to follow the procedure I take that up with them the next day/shift that they work. But at the time they're calling me it's all about patient care and getting done what needs to get done.  I was a third shift tech for many years so I know what it's like to be having a problem in the middle of the night and needing someone to ask for help. Luckily no one abuses the courtesy of having me available 24/7 so it's never been an issue for me.

I wouldn't suggest that with all non-specific reactions. Just if you get an impression that there might be a kidd, it's better to error on the side of caution. I've certainly called my fair share of unknown/non-specific reactions. I've seen several antibodies who don't react even with all of the homozygous expressions. Honestly, sometimes its not much more than your blood bank "spidey-sense" that leads you to the antibody ID, when you would have been completely correct (per SOPs) to call something unknown.

There is a way of confirming it by genoty[ing, but it would cost the Earth for very little return.
I would like to know how old is the patient and what is the underlying pathology?
You have to remember that the the A, B and H antigens, in common with other carbohydrate-based red cell antigens, are not direct gene products, simply because only proteins can be direct gene products, whilst sugars cannot.  In the case of an AB individual, at least two different transferase enzymes are responsible for conferring either the N acetyl-D-galactoseamine residue, in the A antigen, or the D-galactose residue, in the case of the B antigen.  These two enzymes are in direct competition with one another as to which one "wins the race" to convert the H backbone to either A or B; sometimes the "A transferase" wins, and sometimes the "B transferase" wins.  In this case, it could be that the A-transferase is winning "hands down", and that the B-transferase is "whimping out a bit"!  Sorry, that last bit wasn't written exactly scientifically, but I hope you understand what I mean!

Just wanted to comment that starting 6/27/2016 I will become the interim Blood Bank Manager for the Cottage Hospital system in Santa Barbara, California.  Looking forward to the challenges and opportunities this will bring my way.

I told you I could be talking rubbish!
What I meant was, however, that if you test the same positive and negative cells (whether they be new or old) against the two different kits (new and old) you should see that the results are at least as strong with the new kit as they are with the old, to check no "nasties" have happened during transit from the manufacturer.  This is what we have to do in the UK (and I stress, I do not necessarily agree with it - I think it is COMPLETE over-kill).