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Please let me know if you would like me to do more "mock-up cases" with RHCE variants. I can look for some good ones. I think it is fun to interact with case studies here. (I mean it is quite fun to pick Malcolm's brain and learn from him... cough cough).

Mabel, helicopter (and ambulance) use is the ideal place for LTOWB. The main reason we are even considering its use is to cut down on wastage. Without trauma center and other hospitals becoming a rotation site, LTOWB wastage can easily exceed 30%. Like you, the cost is the reason we have not moved forward.

Does anyone know of a remote community hospital (~250 beds) that is using WB for traumas that is not a satellite hospital for a level 1 trauma center? I just can't figure out the logistics for making the cost benefit ratio work here. We are 3.5 hours' drive from our supplier, transfuse an average of one "real" massive transfusion patient a month (one that uses over 6 units of RBCs) and cover a land area the size of the Netherlands (as I recall). The price for LTOWB is about 3X that of a RBC unit. Would it do any good if our helicopter carried 2 units of whole blood even if we didn't keep it at any of our hospitals? Also, can anyone share their QC process for packing the WB to packed cells once it is too old to use as WB? You have to prove you get the right Hct at least a percentage of the time, correct? Does the packing process require FDA registration? It didn't use to.

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.

They should have, or create a policy to replace/reattach the armband. Get your pathologist and QA involved.

My main concern would be the cold ambient temp in the OR.

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

Haha. I copied that info right out the demographic sheet and typed "not pregnant or transfused" not thinking much about his gender. opps! I am surprised by this positive eluate as well. I was just "shooting in the dark" and performed the eluate blindly when I saw these reactions with e+ cells (since I saw way too much warm autoantibodies with relative anti-e specificity). Further serology results are- this antibody is weakly reactive w+ with 1 of 3 hrB- cells tested (all of them are C-e+) it is weakly reactive with 1 of 2 hrS- cells tested (both of them are C-e+) Genomic sequencing results in RHD gene (sequenced 1-10 exons) the following heterozygote changes were observed- c.410C>T, c.455A>C, c602C>G, c667T>G and 819G>A - predicted to be RHD*DIIIa or RHD*DAR3.01 A normal D gene was also observed. So the prediction was a normal D gene in Trans position to RHD*DIIIa heterozygote. Since RHD gene was associated with altered RHCE gene, RHCE sequencing was reflexed (sequenced 1-10 exons and some intronic flanking regions) variants - c.48G>C, c.676G>C, c733C>G, c.1006G>T - predicted to be RHCE*ceVS.03 in trans with RHCE*cE (because serologic phenotype is D+C-E+c+e+) So when I looked up RHCE*ceVS.03, I found it to be associated to V-VS+hrB-. So your suspicion is right on the spot! It is most likely anti-hrB!! At this point anti-C was not excluded but the transfusion recommendation was R2R2 blood, so we are ok here. In terms of eluate, it most likely is warm auto antibody with relative anti-D specificity due to the presence of normal D gene in hetrozygote expression. I am still puzzled by a negative auto-control. However since the antibody was eluated out of his untransfused red cells, so I can accept that it is most likely an autoantibody. Please let me know what your thoughts are and any further results that you may need. Hope this is a good case study!

Okay, so let's have a think. My first reaction is that I am glad this "31 year old African American male" has not been pregnant!!!!!! On the face of it, the patient has an anti-C (or, more likely anti-Ce), but has almost certainly also got an anti-hrB (rather than an anti-hrS), as anti-hrB mimics an anti-C+e, reacting more strongly with the C antigen, than the e antigen, whereas anti-hrS mimics an anti-ce (anti-f). To resolve this once and for all, the plasma should be tested against known hrB Negative and hrS Negative red cells. However, many such red cells have been mis-typed (even those used by reputable Reference Laboratories, as the antibodies made by individuals with a partial e antigen are a heterologous lot in terms of actual specificity, and so, these days the RHCE gene should be sequenced to ensure it is known what partial e is actually present (and, come to that, the C and c antigens are also often partial in nature). Obviously, the patient's own RHCE gene should also be sequenced. Like my friend yan xia, I was a little flummoxed by the auto-control being negative, but the eluate reacting weakly with D Negative red cells, but quite strongly with D Positive red cells. I mean, if the gentleman has never been transfused (and has not been pregnant!), one wonders why an elution was performed in the first place, but then I thought, if his Hb and hct are low (information not given), it could be that he has a WAIHA that has a negative DAT (see Sachs UJH, Röder L, Santoso S, Bein G. Does a negative direct antiglobulin test exclude warm autoimmune haemolytic anaemia? A prospective study of 504 cases. British Journal of Haematology 2006; 132: 651-661). Like yan xia, I think this could be an auto-anti-LW (it is highly unlikely to be an allo-anti-LW) (see, for example, Giles CM, Lundsgaard A. A complex serological investigation involving LW. Vox Sanguinis 1967; 13: 406-416). This can be "proved" by reacting the eluate with group O, D Negative cord red cells, as D Negative cord red cells express the LW antigen strongly. However, I then remembered that all three of the LW antigens are sensitive to DTT, and so, as you corrected the original to say that the antibody in the eluate reacted with DTT-treated red cells, it cannot be an auto or an allo-anti-LW. I am, therefore, stumped at present, as to the specificity of the antibody/antibodies in the eluate.

Agree - also, what blood type is the mother? From an operational stand-point you have a couple of options: Call the blood type "indeterminate" or "unable to determine" or call the baby AB. Either way, we would suggest repeat testing at 4-6 months and include A1 lectin typing if discrepancy still exists. In the meantime we would give group O red cells and AB plasma/platelets until resolved.