JasonS

When I was working in the Reference Laboratory at the NHSBT and, come to that, when I was working for a short time in a Hospital Blood Bank, we would ALWAYS test for the C, c, E and e antigens, together with the K antigen, both for patients and donors, and we would also test for the antithetical antigen, as well as the cognate antigen (in other words, as in your example, the Jk(a) and the Jk(b) antigen.  We ALWAYS did this, except when the grouping reagent was exceedingly rare (e.g. anti-Dib) or the antibody AND the antigen were extremely rare (e.g. anti-Kpc).

The reason we did this, particularly in the NHSBT Reference Laboratory, was because we wanted to identify very rare phenotypes, such as Kp(a+b-), or even rarer (in most cases), null phenotypes, but there was also a paper that showed that people who were transfusion dependent, such as sicklers and thal patients tend, once they have made an initial atypical antibody (particularly anti-C, anti-c, anti-E, anti-e or anti-K) to make all sorts of specificities (I'll try to look up the paper and get back to you on here).  Other papers comparing their findings actually agreed with them.
I say ALWAYS, but then, of course, the Bean Counters, who know nothing about Blood Group Serology, or about Patient Requirements, and care even less, came along, and we were banned from doing this as, apparently, IT COST TOO MUCH MONEY, except in special circumstances, such as patients from the Black populations, where we were privileged to be able to test for both Fya AND Fyb, in case they were Fy(a-b-) - and, of course, most of those who were found to be Fy(a-b-) had the FYB gene, so would very rarely produce an anti-Fy3,  as they were homozygous for the GATA1 gene mutation.
Unfortunately, what these "suits" seem to forget, despite counting beans for a living, is that, if the patient goes on to produce other, clinically significant, atypical alloantibodies, they will occupy a hospital bed for longer while suitable blood is identified, including, sometimes, cryopreserved units, ALL OF WHICH IS FAR MORE EXPENSIVE THAN THE INITIAL TYPING WAS IN THE FIRST PLACE - but what do we professionals know!

RANT OVER!!!!!!!!!!!!!!!!

I just answered this question.

My Score PASS  

I'm going to be blunt.  This is ridiculous!!  You have the potential of causing far more problems by removing the cubes from their protective container.  

I don't think the XN will allow you to run without the WNR reagent. You wouldn't be able to get an automated differential because the basophil count comes from the WNR. Also, the NRBCs come from the WNR channel, so any WBC count from the WDF channel would also include NRBCs.

Our neonatal intensive care transfusions are all irradiated because many severe immunodeficiency states are not evident until weeks to months after birth.  These are rare, and leukoreduced transfusions probably mitigate the risk of GVHD somewhat, but we are erring on the side of caution.  We irradiate just before transfusion so the storage based problems with irradiated red cells are less of a concern. We define fresh as <21 days of storage, because the data suggest very fresh blood is actually more dangerous to patients than blood stored 7-21 days or so.  Seat of the pants, to be sure, but somewhat data driven. No one knows for sure, but very fresh blood (<7 days storage) is totally unnecessary in terms of proven benefit and may actually be more dangerous, for reasons that are largely unknown.

A new tee shirt I gave myself for my birthday.  I should have had a shave and lost about 70lbs first, but hey!

I just answered this question.

My Score PASS  

Congratulations! Much deserved!

Infamous??????????????????????????  

I would not be performing one hour post-transfusion vital signs unless the patient has signs or symptoms that require assessment.  I would not be reacting to one hour post-transfusion data unless they were consonant with a transfusion reaction.  If fever was the only sign or symptom, it's probably not transfusion related in the vast majority of cases.  Routine vital signs in the absence of a clinical rationale are a problem, not a solution.

I just answered this question.

My Score PASS  

Thanks. Finally found a great journal article about this phenomena - just takes googling the right keywords to find something. Here is a link for those interested.
https://onlinelibrary.wiley.com/doi/full/10.1111/vox.12909

I just answered this question.


My Score PASS  

Can't answer that one John.  From the ER. 

I just answered this question.


My Score PASS  

OK, should be working now.  Definitely in the Default theme, may work in others too.

We usually perform an elution whenever Mom has an antibody & the newborn baby is positive for that antigen regardless of the DAT result. In 25% of cases the eluate is positive . It depends on concentration of Mom's antibody coating the baby's red cells. There could be prozone effect as well. 

PLEASE do not worry.  Your midwife is COMPLETELY wrong, and really should not comment about something she patently does NOT understand, and about which she has a pitiful amount of knowledge.  She should never have answered your questions with her lack of knowledge, but should have left it to your Obstetrician.
I note that you are a fellow "Brit"!
Within the British population, the percentage of people who have the R1R1 type (which is a type within the Rh Blood Group System) is 16%.  Also within the British population, the K- type (which is part of the Kell Blood Group System) is 91%.  What that means is that 91% of 16% of the British population is R1R1, K-, or, give or take, a few decimal points, 15% of the British population (about an eighth of the British population).  On Friday, 19th October 2018, the British population was measured as 66,690,116!  Let's call that 16.5 million in round numbers.  This means that, give or take, 9, 975, 000 in Britain are R1R1, K-.  Now, admittedly, your midwife will only be looking after women, but, even then, that means 4, 987, 500 women will have the same Rh type and K type as you!  How your midwife has only come across your "rare" type four other times in her career, is beyond belief (and I genuinely mean BEYOND belief), unless, as I say, her knowledge of blood groups and blood group serology is incredibly poor, and I repeat, she should NEVER have worried you like this.  Just in case you think that I do not know what I am talking about, I have worked in the field of blood transfusion/blood group serology for 43 years, have been an internationally invited lecturer and am the Chief Examiner in Transfusion Science for the Institute of Biomedical Science in the UK, and am a co-author of the British Society of Haematology's Guidelines for Blood Grouping and Antibody Testing in Pregnancy.  I don't write that to "blow my own trumpet", as it were, but to try to reassure you that I actually do know what I am talking about.
I should warn you that "consulting Dr Google" is equally as useless as listening to your midwife.
You should really relax.  YES, it is possible for you to produce red cell antibodies during your first pregnancy, but it is INCREDIBLY RARE.  It is even more rare for such an antibody to cause any problems in a first pregnancy.
I notice that the report from the Blood Bank was that they detected WEAK reactions with 26 of 30 panel cells, but they could not identify a specificity.  They have requested three further samples of blood to send to the Reference Laboratory.  Again, to give you some comfort, I hope, I ran a Reference Laboratory in London for 16 years before I retired in 2016, and we saw, quite literally hundreds of cases like yours.
For a red cell antibody to cause any problems within you pregnancy, it would have to have a titre of 32 or above (this means that it would still be detectable when it has been diluted THIRTY TWO times).  I can assure you that the mere fact that the Blood Bank reports weak reactions means that there is ZERO chance that the titre will be 32 or above.  If a Hospital Blood Bank, however big or famous the hospital may be, cannot identify an antibody, it is almost universal practice that samples will be sent to a Reference Laboratory for further testing - AGAIN, DO NOT WORRY ABOUT THIS.
There are many, many red cell antibodies that are clinically insignificant, both in terms of transfusion reactions and haemolytic disease of the foetus and newborn (which is what your midwife has left you worried about).
I KNOW it is difficult, but PLEASE do not worry.  PLEASE take no notice whatsoever of your midwife on this matter (I am sure she is an excellent midwife, but she is patently no expert in the field of blood groups), but DO talk to your Obstetrician, who, I hope, will have talked to your hospital's Haematology Consultant, who, in turn, will have spoken to the Consultant in Charge of the Reference Laboratory, and I am sure that they will echo my opinion that there is NOTHING to worry about.
Oh, and lastly, I am R1R1, K- myself!!!!!!!!!!!!!

I just answered this question.


My Score PASS  

We must have a current ABO/Rh done on the current visit.

I know some hospitals where it is done in Hematology, though here it is done in Blood Bank. 
I agree with Malcolm on this issue.
Your calculation uses the total #counted and # of fetal cells. This is a ratio and so the calculation shouldn't change(other than you changing it to the correct number of total cells counted)
 
 

I think these bureaucratic methods corrode the trust and collegiality felt by our bedside practice colleagues.  High risk patients require discussion between the medical staff of the transfusion service and the ordering provider, and a note in the medical record documenting the decision making. Signing forms is a another tip of the hat to bureaucracy and legalese that should have no role in the provision of medical care.  A joint responsibility for such decisions and documentation is far more humane and in the interests of good patient care.  Neither the FDA nor regulatory agencies require such divisive practices and we should abandon them for better patient care and documentation of shared decision making. I realize some of you do not have knowledgeable and enthusiastic physician support, but this responsibility needs to be taken by the transfusion service medical director, who is paid to do so, however reluctant and happy to dump this on medical technologists.  Just saying.

Yes, we do that here. 

Here are the references.
Lancet. 2016 Jun 25;387(10038):2605-2613. doi: 10.1016/S0140-6736(16)30392-0. Epub 2016 May 10. Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral haemorrhage associated with antiplatelet therapy (PATCH): a randomised, open-label, phase 3 trial.
Baharoglu MI1, Cordonnier C2, Al-Shahi Salman R3, de Gans K4, Koopman MM5, Brand A5, Majoie CB6, Beenen LF6, Marquering HA7, Vermeulen M1, Nederkoorn PJ1, de Haan RJ8, Roos YB9; PATCH Investigators. Author information
  Abstract
BACKGROUND:
Platelet transfusion after acute spontaneous primary intracerebral haemorrhage in people taking antiplatelet therapy might reduce death or dependence by reducing the extent of the haemorrhage. We aimed to investigate whether platelet transfusionwith standard care, compared with standard care alone, reduced death or dependence after intracerebral haemorrhage associated with antiplatelet therapy use.
METHODS:
We did this multicentre, open-label, masked-endpoint, randomised trial at 60 hospitals in the Netherlands, UK, and France. We enrolled adults within 6 h of supratentorial intracerebral haemorrhage symptom onset if they had used antiplatelet therapy for at least 7 days beforehand and had a Glasgow Coma Scale score of at least 8. With use of a secure web-based system that concealed allocation and used biased coin randomisation, study collaborators randomly assigned participants (1:1; stratified by hospital and type of antiplatelet therapy) to receive either standard care or standard care with platelet transfusion within 90 min of diagnostic brain imaging. Participants and local investigators giving interventions were not masked to treatment allocation, but allocation was concealed from outcome assessors and investigators analysing data. The primary outcome was shift towards death or dependence rated on the modified Rankin Scale (mRS) at 3 months, and analysed by ordinal logistic regression, adjusted for stratification variables and the Intracerebral Haemorrhage Score. The primary analysis was done in the intention-to-treat population and safety analyses were done in the intention-to-treat and as-treated populations. This trial is registered with the Netherlands Trial Register, number NTR1303, and is now closed.
FINDINGS:
Between Feb 4, 2009, and Oct 8, 2015, 41 sites enrolled 190 participants. 97 participants were randomly assigned to platelet transfusion and 93 to standard care. The odds of death or dependence at 3 months were higher in the platelet transfusiongroup than in the standard care group (adjusted common odds ratio 2·05, 95% CI 1·18-3·56; p=0·0114). 40 (42%) participants who received platelet transfusion had a serious adverse event during their hospital stay, as did 28 (29%) who received standard care. 23 (24%) participants assigned to platelet transfusion and 16 (17%) assigned to standard care died during hospital stay.
INTERPRETATION:
Platelet transfusion seems inferior to standard care for people taking antiplatelet therapy before intracerebral haemorrhage. Platelet transfusion cannot be recommended for this indication in clinical practice.
 
N Engl J Med. 2019 Jan 17;380(3):242-251. doi: 10.1056/NEJMoa1807320. Epub 2018 Nov 2. Randomized Trial of Platelet-Transfusion Thresholds in Neonates.
Curley A1, Stanworth SJ1, Willoughby K1, Fustolo-Gunnink SF1, Venkatesh V1, Hudson C1, Deary A1, Hodge R1, Hopkins V1, Lopez Santamaria B1, Mora A1, Llewelyn C1, D'Amore A1, Khan R1, Onland W1, Lopriore E1, Fijnvandraat K1, New H1, Clarke P1, Watts T1; PlaNeT2 MATISSE Collaborators. Collaborators (124)
  Author information
  Abstract
BACKGROUND:
Platelet transfusions are commonly used to prevent bleeding in preterm infants with thrombocytopenia. Data are lacking to provide guidance regarding thresholds for prophylactic platelet transfusions in preterm neonates with severe thrombocytopenia.
METHODS:
In this multicenter trial, we randomly assigned infants born at less than 34 weeks of gestation in whom severe thrombocytopenia developed to receive a platelet transfusion at platelet-count thresholds of 50,000 per cubic millimeter (high-threshold group) or 25,000 per cubic millimeter (low-threshold group). Bleeding was documented prospectively with the use of a validated bleeding-assessment tool. The primary outcome was death or new major bleeding within 28 days after randomization.
RESULTS:
A total of 660 infants (median birth weight, 740 g; and median gestational age, 26.6 weeks) underwent randomization. In the high-threshold group, 90% of the infants (296 of 328 infants) received at least one platelet transfusion, as compared with 53% (177 of 331 infants) in the low-threshold group. A new major bleeding episode or death occurred in 26% of the infants (85 of 324) in the high-threshold group and in 19% (61 of 329) in the low-threshold group (odds ratio, 1.57; 95% confidence interval [CI], 1.06 to 2.32; P=0.02). There was no significant difference between the groups with respect to rates of serious adverse events (25% in the high-threshold group and 22% in the low-threshold group; odds ratio, 1.14; 95% CI, 0.78 to 1.67).
CONCLUSIONS:
Among preterm infants with severe thrombocytopenia, those randomly assigned to receive platelet transfusions at a platelet-count threshold of 50,000 per cubic millimeter had a significantly higher rate of death or major bleeding within 28 days after randomization than those who received platelet transfusions at a platelet-count threshold of 25,000 per cubic millimeter. (Funded by the National Health Service Blood and Transplant Research and Development Committee and others; Current Controlled Trials number, ISRCTN87736839 .).
 
Front Immunol. 2015 Feb 2;6:28. doi: 10.3389/fimmu.2015.00028. eCollection 2015. Platelet transfusion - the new immunology of an old therapy.
Stolla M1, Refaai MA1, Heal JM1, Spinelli SL1, Garraud O2, Phipps RP3, Blumberg N1. Author information
  Abstract
Platelet transfusion has been a vital therapeutic approach in patients with hematologic malignancies for close to half a century. Randomized trials show that prophylactic platelet transfusions mitigate bleeding in patients with acute myeloid leukemia. However, even with prophylactic transfusions, as many as 75% of patients, experience hemorrhage. While platelet transfusion efficacy is modest, questions and concerns have arisen about the risks of platelet transfusion therapy. The acknowledged serious risks of platelet transfusion include viral transmission, bacterial sepsis, and acute lung injury. Less serious adverse effects include allergic and non-hemolytic febrile reactions. Rare hemolytic reactions have occurred due to a common policy of transfusing without regard to ABO type. In the last decade or so, new concerns have arisen; platelet-derived lipids are implicated in transfusion-related acute lung injury after transfusion. With the recognition that platelets are immune cells came the discoveries that supernatant IL-6, IL-27 sCD40L, and OX40L are closely linked to febrile reactions and sCD40L with acute lung injury. Platelet transfusions are pro-inflammatory, and may be pro-thrombotic. Anti-A and anti-B can bind to incompatible recipient or donor platelets and soluble antigens, impair hemostasis and thus increase bleeding. Finally, stored platelet supernatants contain biological mediators such as VEGF and TGF-β1 that may compromise the host versus tumor response. This is particularly of concern in patients receiving many platelet transfusions, as for acute leukemia. New evidence suggests that removing stored supernatant will improve clinical outcomes. This new view of platelets as pro-inflammatory and immunomodulatory agents suggests that innovative approaches to improving platelet storage and pre-transfusion manipulations to reduce toxicity could substantially improve the efficacy and safety of this long-employed therapy.
 

Check with your blood supplier.  During transport (up to 8-12 hours), platelets are not agitated.