cbaldwin

I am the transfusion service coordinator in the lab of a small rural hospital.  I am retiring at the end of the year and my lab manager has posted my position on this site.  I thought I would add some information.
 
Bishop California, population around 5,000, is located on the east side of the Sierra Nevada mountain range near the Nevada border.  We are 200 miles south of Reno, 300 miles northeast of LA.  We are a vacation destination/retirement community.  In the Sierra to the west, and the White Mountains to the east, there is hiking, backpacking, fishing, camping, hunting, skiing, biking, rock climbing, bird watching and more.   In town there’s a golf course and a bowling alley, two excellent bakeries, several coffee shops, numerous restaurants, a really great hamburger joint and several yoga studios. 
 
The hospital is small.  We have 3 orthopedic surgeons, 2 general surgeons, 3 OB/GYN doctors, a few specialists and numerous ED doctors, hospitalists and generalists.  We transfer critical patients to larger health facilities with higher levels of care. 
 
In the transfusion service, our inventory includes 10 units O positive, 6 units A positive, 2 units A negative, 2 units B positive, 8 units O negative and 10 units frozen plasma.  Our blood supplier is Vitalent in Reno. Monday through Friday a courier delivers and returns blood products.  On weekends and outside of courier hours we make other arrangement with the California Highway Patrol or a hospital courier.  (We seldom need to make such arrangements). 
 
We use Ortho MTS gel (manual) and tube.  We perform antibody screens with a 3 cell screening panel.  We send out positive antibody screens (maybe one every one-two months).  We perform 30-45 type and screens a month.  We transfuse monthly 10-40 pRBCs, 0-4 frozen plasmas, and 0-1 platelets.
 
It was odd that I became the coordinator in 2007 because I had little blood banking experience.  But I managed to get into a SBB program and pass the SBB exam.  I also read the Blood Bank Talk site daily. With my SBB and information from BBT the department is compliant with standards and regulations.  Joint Commission surveyors visit us every two years.  Usually they find one or two “observations” but we passed the last survey with no “observations”.
 
In our lab we have 10 lab techs (generalists), 4 lab assistants, 5 phlebotomists.  We are a happy, friendly group.  I enjoy working with our team.  I have an excellent relationship with the nursing staff and meet with the nursing executives monthly to review transfusion documentation of signatures and vital signs and other transfusion issues.
 
If you would like to live in a quiet town with amazing scenery and great recreational opportunities, and if you would like to run a small transfusion service in a lab with great people, this job is for you!

Thank you for this information. 
I just found the handouts from a lecture Sue Johnson gave in March 2016 at an Immucor Users meeting and I have attached them in case anyone is interested.  It's very good.  She discusses the molecular basis of weak D and partial D and the variability of reagents and methodology, also the recent recommendations of the Inter-organizational Work Group on RHD genotyping for managing pregnant women and transfusion recipients who have a serologic weak D phenotype.
  On page 18 she states that there is a new CPT code 81403 for RHD genotyping (Tier 2 molecular pathology procedure, Level 4) and that reimbursement rates for the Tier 2 code are being established.  Also that the ACOG is updating its Practice Bulletin to recommend molecular testing.
I just got a new phone number to call to see if I can get the price that we will be charged if we request this test.  My OBGYN physicians would like to know.
Catherine
Johnson Handouts.pdf

I was incredibly privileged to hear Sue give a similar lecture on the BioRad Course in Cressier in Switzerland in March 2015, when she explained the difference between a Weak D and a Partial D using "Reece's Pieces" (if I have the name correct) of different colours to demonstrate the different RhD epitopes.  Sadly, I managed to eat all my "Reece's Pieces" before Sue got as far as Weak D Type 1!

Prof. Theirry Burnouf, Prof. Axel Seltsam, Sue Johnson and some English guy ay Cressier in 2015.

Just found out...our reference lab charges $305.  Thanks all for your replies...I am learning...have a lot to learn.  Catherine

Thank you for this information. 
I just found the handouts from a lecture Sue Johnson gave in March 2016 at an Immucor Users meeting and I have attached them in case anyone is interested.  It's very good.  She discusses the molecular basis of weak D and partial D and the variability of reagents and methodology, also the recent recommendations of the Inter-organizational Work Group on RHD genotyping for managing pregnant women and transfusion recipients who have a serologic weak D phenotype.
  On page 18 she states that there is a new CPT code 81403 for RHD genotyping (Tier 2 molecular pathology procedure, Level 4) and that reimbursement rates for the Tier 2 code are being established.  Also that the ACOG is updating its Practice Bulletin to recommend molecular testing.
I just got a new phone number to call to see if I can get the price that we will be charged if we request this test.  My OBGYN physicians would like to know.
Catherine
Johnson Handouts.pdf

Thank you! This is good information.  I will call our Immucor rep.  Catherine

Thank you for this information. 
I just found the handouts from a lecture Sue Johnson gave in March 2016 at an Immucor Users meeting and I have attached them in case anyone is interested.  It's very good.  She discusses the molecular basis of weak D and partial D and the variability of reagents and methodology, also the recent recommendations of the Inter-organizational Work Group on RHD genotyping for managing pregnant women and transfusion recipients who have a serologic weak D phenotype.
  On page 18 she states that there is a new CPT code 81403 for RHD genotyping (Tier 2 molecular pathology procedure, Level 4) and that reimbursement rates for the Tier 2 code are being established.  Also that the ACOG is updating its Practice Bulletin to recommend molecular testing.
I just got a new phone number to call to see if I can get the price that we will be charged if we request this test.  My OBGYN physicians would like to know.
Catherine
Johnson Handouts.pdf

Could I suggest the term "molecular Techniques", rather than "genotyping", as the two terms "(pheno)typing" and "(geno)typing" are, sadly, often confused, particularly by the "lay person" at the front of the office taking calls?  It might work/it might not!

Our blood warmers are in the OR, ER and on the floors. The area that keeps them/uses them would be responsible for making sure that they are cleaned between use, just as they would IV pumps. Biomed does an annual check and I get a copy of it for each blood warmer (which includes the actual temps for alarms). However, they wouldn't have done the same checks on the new rapid infusers unless I had told them that the same type of checks were needed - apparently no one in nursing thought that the functionality of the devices was something Biomed needed to know about. We have no control or input over what they purchase. In fact we wouldn't know they are getting something new unless I happen to hear about it at some committee meeting or other. They can deal with Joint Commission, not me. I have been asked for the Biomed annual checks by CAP but nothing else. So far so good.

I have a question about reporting 1+ or 2+ Rh reactions on the Provue as Rh positive.  
 
Page 4 of the 2005 AABB “Guidelines for Prenatal and Perinatal Immunohematology” states:    "Only when prenatal tests for Rh are unequivocal and clearly reactive (=/>2+) should the woman be considered Rh-positive.”
 
Dr. Joe Chaffin, The Blood Bank Guy, also states a similar opinion in his excellent podcast "Weak in the D's".  Here is a link to his podcast:
 
http://www.bbguy.org/podcast/1012/1012podcast.asp
 
The podcast is 41 minutes long, and if you don't have 41 minutes, skip to 34.12 minutes into the podcast.  That's where he starts talking about OB patients.  At 35.30 minutes into the podcast, he says that transfusion services should consider a lower threshold of positivity for calling Rh negatives--some places call a 1+ reaction or lower in tube testing Rh negative and a 2+ reaction or lower in gel testing Rh negative.  The risk here is giving Rh negative blood when Rh positive blood can be given, but calling these weak Rh reactions Rh negative lowers the risk of immunizing the patient.
 
I am interested in this because last week I realized I didn't have a weak D policy, except that we only perform weak D testing on cord bloods if the mom and baby test Rh negative. 
 
Last week we reported an OB patient as Rh negative, using tube testing with Ortho anti-D bioclone.  The patient's physician informed us that the patient was determined to be Rh positive 2 years ago when the patient had her first child.  I called the lab that performed that testing and found it was a 1+ reaction on the Echo Galileo.  The lab reported that the patient was “Rh Positive by Weak-D test (formerly Du).  RhoGam is not indicated for this patient”.  
 
We use the Ortho MTS gel cards for ABO/Rh testing (manual method) as well as tube testing with Ortho reagents, so we repeated the patient's testing using the gel method, and saw a 1+ reaction for the Rh.  When we performed the tube weak D test, we also saw a 1+ reaction. 
 
(An aside--we are a small lab, performing about 100 type and screens per month, about 40 crossmatches per month, 10 cord bloods per month.  I have been trying to phase the MTS ABD Reverse cards out.  The tube method is more versatile, it is faster in emergencies and according to a cost analysis I did, the tube method is ½ the price of the gel ABO/Rh method.  However, the lab is staffed with generalists, and I have been told it’s better for generalists to use the gel method—no chance of forgetting to add the reagent and more consistency.  We perform antibody screens using the gel method because it is more sensitive (although I realize the gel antibody screen method has its pitfalls such as being a LISS method and possibly missing anti-E and anti-K sometimes, etc.)
 
Anyway, I have come to realize that I need to write a weak-D policy, and I am thinking of including these points: 
Perform weak D testing only on cord bloods when mom and baby are Rh negative, on Rh negative moms when the FMH screen suggests the mom may be weak D positive, and when investigating discrepancies such as the OB patient last week. Calling Rh results less than 2+ in gel and less than 1+ in tube, Rh negative. When the Rh results are less than 2+ in gel and less than 1+ in tube, reporting the Rh as negative and including a comment that indicates the Rh type is weak and atypical and if the patient is a blood donor, the patient would be considered Rh positive, but if the patient is an OB patient or a recipient, the patient should be considered Rh negative. There is a CBBS posting about when the AABB changed the weak D regulations in 2002.  Dr. Judd is quoted as saying that, when it was decided in 2002 that weak D testing was no longer needed to be performed on OB patients, all of a sudden, patients that had been D positive, were suddenly D negative, and this was in the same facility.  Dr. Judd is quoted as saying that these patients were informed of their options...that is, where previously they were D positive and did not require RhIG, they were now D negative, and they could opt to receive RhIG or not...they needed to sign a form.......I hope I remember that correctly....
 
I would like opinions!
 
Thank you!
 
Catherine

You can attend the "Last Chance Review" on-line through a live Webinar...that's what I did last year and it worked very well.  That will save you time and money!  Catherine

Where is the regulation stating that the blood can be out of temperature for 30 minutes? 
 
Since coolers can never really be validated (like someone said, cannot control opening/closing and temperature of the room/car will affect the temperature flux ... plus there's no guarantee the units are actually staying inside the cooler the whole time), and since those little temperature check labels are difficult to validate and expensive (and timely to remember to put them on during an emergency), we take the temperature of the unit of blood at the time it is returned.  FDA made it very clear to us that the blood is 'in storage' if it's sent anywhere in a cooler, so the return temperature must be 1-6oC.
 
Currently, we record the start temp and return temp of the coolers using that as the 'return temp' of the unit ... I'm seriously thinking that is not necessary/valid because the bottom line is the actual temperature of the returned unit, not the cooler.  (Igloo, purchased at local stores in the spring/summer ... red and white = 1-6oC, blue and white = 20-24oC storage.)
 
PS Tried those infrared thermometers ... cannot get them to validate.  Tried the Temp-Check machine ... cannot get it to validate.  Etc.  So, we are still using the old fashioned 'fold it over a precooled thermometer' (precooled because it takes to long to go from room temperature to 1-6oC).  If anyone has a better thermometer that will validate, please post the information so we can purchase one!  Thanks!

R1R2,
 
No, our antibody screen on 4/18 showed the Jka reaction was definitely stronger.  
 
Also, I did not mention this before, in order not to distract from my main question, there was an antibody present to the 0.8% screening cell preservative. 
 
When we performed the gel antibody screen with our usual 0.8% cells, all cells were positive at 2+.  The auto and DAT were negative, and when I XM'd all of our (8) units of O negative units, those XM's were compatible at gel IgG.  So I suspected an antibody to the preservative in the 0.8% cells.  As a backup, we have 3% antibody screening cells for tube, and I made 0.8% cells from these cells.  The antibody screen with the 3% cells made into 0.8% cells was negative. 
 
On 4/18 I ran a antibody screen with the 0.8% cells and the 3% cells made into 0.8% cells.  The 0.8% cells showed the Jka antibody and the antibody to the preservative.  The 3% cells made into the 0.8% and tested with gel IgG showed just the Jka.

Thanks Liz for the explanation of the 3 month period.  It makes sense and it will help me explain to physicians why we need to be concerned about more antibodies forming.

Thanks Liz for the explanation of the 3 month period.  It makes sense and it will help me explain to physicians why we need to be concerned about more antibodies forming.

I think Liz0316 has answered your questions perfectly, and there is NO way that I would not have asked for a fresh sample of blood to test.

R1R2,
 
No, our antibody screen on 4/18 showed the Jka reaction was definitely stronger.  
 
Also, I did not mention this before, in order not to distract from my main question, there was an antibody present to the 0.8% screening cell preservative. 
 
When we performed the gel antibody screen with our usual 0.8% cells, all cells were positive at 2+.  The auto and DAT were negative, and when I XM'd all of our (8) units of O negative units, those XM's were compatible at gel IgG.  So I suspected an antibody to the preservative in the 0.8% cells.  As a backup, we have 3% antibody screening cells for tube, and I made 0.8% cells from these cells.  The antibody screen with the 3% cells made into 0.8% cells was negative. 
 
On 4/18 I ran a antibody screen with the 0.8% cells and the 3% cells made into 0.8% cells.  The 0.8% cells showed the Jka antibody and the antibody to the preservative.  The 3% cells made into the 0.8% and tested with gel IgG showed just the Jka.

Let's answer question # 2 first. In any given unit of donated blood, the red cells are of all ages, new and older. So, since the life span of the RBC in the circulation is approximately 90 days, "recently transfused" means that there is a possibility of donor red cells still in circulation in the patient - therefore, foreign antigens are present that could elicit an antibody response up to 90 days (approx.).
Question #1 - I think you were correct in requesting another antibody work up. Especially with the severe drop in Hgb. If a patient has been recently transfused - with in 3 months, the specimen is only good to work with for 4 days - the day it's drawn plus 3.
Assuming you don't do antibody work ups at your hospital, I believe this patient needed an additional work up at the reference lab.
The 3 month rule is because the body can form an antibody to a foreign antigen at any time that foreign (donated) red cells are actively in the patient's circulation.
I hope that helps, and I'm sure my reference lab colleagues will have more to say
Liz

Thanks Whitney for posting this question!  I do not have an answer, but your question is an opportunity for me to learn. 
 
I was wondering how low prevalence antigens from the MN CHO collection would cause steric hindrance.  After reviewing information in The Antigen Fact Book, I am reminded that the MNS antigens are on GPA and GPB which are single-pass membrane sialoglycoproteins.   One of the major functions of sialoglycoproteins is to contribute to the negative charge of the RBC glycocalyx.
 
The antigens in the MN CHO blood Group Collection, which are more frequently found in Blacks, are also on GPA and GPA and have altered sialic acid. 
 
So, if cell #6 of this Ortho panel has one of these low incidence antigens, there is a stronger negative charge and this stronger charge is weakening the anti-M/M antigen reaction?  Is that correct?  Wow--that would never have occurred to me.
 
I hope you get an answer!  A call to Ortho seems to be in order!
 
And, I hope I do not change the course of this thread too much when I ask if others have seen cases where steric hindrance has caused negative reactions when a positive reaction would be reasonable.
 
Catherine Baldwin CLS, MT(ASCP)SBBcm

This review for the SBB exam is fantastic and is scheduled for February 8-9, 2014.  You can attend "on-line" and if you do so there is no problem hearing the speakers or asking questions.
 
Here is a link for information:
 
http://www.giveblood.org/services/education/sbb-last-chance-review
 
 
 
 
 

We're working on one too; here's a few that should help you.
Warfarin Reversal Guideline 2012.pdf
Warfarin Reversal article.pdf
Warfarin_Reversal_Vitamin_K.pdf
Coumadin_Warfarin_Therapy_Reversal_in_Patients_with_Risk_for_or_Actual_Extracranial-Intracranial_Hemorrhage.doc

Never Terri.

Least incompatible.pdf
 
We do not use the term least incompatible anymore; it's kind of like being "a little pregnant".
 
The grading of your reaction does not correlate to what the clinical significance/impact to the patient will be.  If we are unable to rule out alloantibodies for a warm auto, it doesn't matter if the units appear compatible or not, we call them incompatible and have the physician sign.  We prefer they allow us the time to send it to our reference lab but they are usually too impatient.  grrrr....
 
See attachment for discussion about using least incompatible.

There is an article in Transfusion, "How We evaluate Panagglutinating Sera" on page 1540, volume 49, August 2009.  The authors present an algorithm for panagglutinating sera.  Are you familiar with the information in this article and how does it relate to this patient?
 
I am curious about this situation and it completely baffles me, and hope you don't mind answering these questions...
 
Am I correct in thinking that if, in your workup, the patient's serum reacted with 8 of 11 cells, then this is not really a panagglutinin?  The definition of a panagglutinin, as presented in the aforementioned article, is an agglutinin that reacts with all red cells tested. 
 
Also, you mention that in a later workup the sera was nonreactive at 4C and RT, so doesn't this mean that this is not a cold agglutinin?  You mentioned that in an earlier workup it looked as if a cold agglutinin might be developing.
 
What is the explanation for the nonreactivity with enzyme-treated cells?  Is this an antibody to a HFA or a HTLA that is denatured by enzymes?  In the aforementioned article, in the flowchart presented on page 1541, there is a step where the autocontrol is negative or weaker than the reaction with panel cells, there is persistence of panagglutination after auto- and alloadsorption, there is no reactivity after papain treatement, and the flow leads one to think maybe there is an anti-HFA or anti-CH/RG.....
 
Why are the PEG/IgG crossmatches all compatible, and are they incompatible without the PEG?
 
I would like to understand this situation better, and hope you don't mind my questions...
 
Thank you!