David Saikin

i had an AABB inspection years ago. At the summation the inspector said:  "I know I'd have to dig to find something in Dave's lab."  That should have been a warning.  My only deficiency (which was cited by the Area Chair, who determined the deficiencies based on the Inspection report form) was that I did not have my facility ID on my antibody panel sheets.  I immediately called my area chair and told him I wanted to inspect his lab (UT@Knoxville), which of course is not allowed.  I became an AABB inspector/assessor after that fact.

i had an AABB inspection years ago. At the summation the inspector said:  "I know I'd have to dig to find something in Dave's lab."  That should have been a warning.  My only deficiency (which was cited by the Area Chair, who determined the deficiencies based on the Inspection report form) was that I did not have my facility ID on my antibody panel sheets.  I immediately called my area chair and told him I wanted to inspect his lab (UT@Knoxville), which of course is not allowed.  I became an AABB inspector/assessor after that fact.

i had an AABB inspection years ago. At the summation the inspector said:  "I know I'd have to dig to find something in Dave's lab."  That should have been a warning.  My only deficiency (which was cited by the Area Chair, who determined the deficiencies based on the Inspection report form) was that I did not have my facility ID on my antibody panel sheets.  I immediately called my area chair and told him I wanted to inspect his lab (UT@Knoxville), which of course is not allowed.  I became an AABB inspector/assessor after that fact.

i had an AABB inspection years ago. At the summation the inspector said:  "I know I'd have to dig to find something in Dave's lab."  That should have been a warning.  My only deficiency (which was cited by the Area Chair, who determined the deficiencies based on the Inspection report form) was that I did not have my facility ID on my antibody panel sheets.  I immediately called my area chair and told him I wanted to inspect his lab (UT@Knoxville), which of course is not allowed.  I became an AABB inspector/assessor after that fact.

i had an AABB inspection years ago. At the summation the inspector said:  "I know I'd have to dig to find something in Dave's lab."  That should have been a warning.  My only deficiency (which was cited by the Area Chair, who determined the deficiencies based on the Inspection report form) was that I did not have my facility ID on my antibody panel sheets.  I immediately called my area chair and told him I wanted to inspect his lab (UT@Knoxville), which of course is not allowed.  I became an AABB inspector/assessor after that fact.

I have issued 148 units of products to a guy who was cycle vs car massive haemorrhage - he survived. I have issues 120ish units on an obstetric massive haemorrhage (as well as 20 6-packs on the twins) - all 3 survived. I've issued similar on AAA (with eventual bypass) - survival. I think the key is to use TEG to see whether the clotting is screwed - if they are clotting then keep going... In the grand scheme of things blood is cheap

@Neil Blumberg Exactly. We've all had the odd cases that survive when it doesn't seem they should, and I agree that it's certainly case by case and dependent on hemostasis and coagulation like @Auntie-D said above. We use TEG for coagulation eval as well. I think my trauma surgeons are looking for a prompt to make them aware of how many products they've used, so they can evaluate the futility of continuing versus stopping. Anesthesia is the group transfusing these products, and they can easily lose track as well, so we're looking for an estimate of when the blood bank staff might give them a nudge to let them know they've hit a threshold, and to evaluate the entire picture of the patient with that knowledge, rather than being tunnel visioned into fixing the damage only. I have heard 30-50 units of red cells is the sweet spot as well. We consider more than 30 units of red cells to be a super massive transfusion, so that would jive. 
 

There are no data suggesting a particular limit.  Survival is very unusual after 30-50 units of red cells, but everyone has exceptional cases like those mentioned above. We have discussed futility of care many times, and our practitioners are quite amenable and forthcoming.  We have stopped resuscitation in a young man having a liver transplant go badly, when there was no surgical path to hemostasis after about 250 units, but this is unusual too.  Bottom line, a case by case decision as to whether care is futile and/or the patient's needs endanger the well being of other patients needing transfusion.  Those are the key issues in each case to my way of thinking.

I think they're probably thinking down the TACO route - which is highly unlikely in an MHP situation. If TACO happens when the MHP is triggered, then it likely wasn't an MHP...

I have transfused 400u to 2 patients one night (2 traumatic aneurysms with different etiologies).  Another night a patient w an 8000cc bleed in the OR.  I had never seen folks get so much blood and survive.  All 3 walked out, though one guy was missing 2 limbs.

I have transfused 400u to 2 patients one night (2 traumatic aneurysms with different etiologies).  Another night a patient w an 8000cc bleed in the OR.  I had never seen folks get so much blood and survive.  All 3 walked out, though one guy was missing 2 limbs.

I have transfused 400u to 2 patients one night (2 traumatic aneurysms with different etiologies).  Another night a patient w an 8000cc bleed in the OR.  I had never seen folks get so much blood and survive.  All 3 walked out, though one guy was missing 2 limbs.

I have transfused 400u to 2 patients one night (2 traumatic aneurysms with different etiologies).  Another night a patient w an 8000cc bleed in the OR.  I had never seen folks get so much blood and survive.  All 3 walked out, though one guy was missing 2 limbs.

I have transfused 400u to 2 patients one night (2 traumatic aneurysms with different etiologies).  Another night a patient w an 8000cc bleed in the OR.  I had never seen folks get so much blood and survive.  All 3 walked out, though one guy was missing 2 limbs.

If we have a patient w no detectable ABO isoagglutinins our procedure is to perform an ahgxm in addition to the immediate spin.  When I was validating gel we had a few patients w no detectable ABO abs:  they weren't detectable at ahg either.

If we have a patient w no detectable ABO isoagglutinins our procedure is to perform an ahgxm in addition to the immediate spin.  When I was validating gel we had a few patients w no detectable ABO abs:  they weren't detectable at ahg either.

As Joanne mentioned above, no system is fool proof and there are lots of creative, inventive fools to prove it.  Keep your system as simple as possible which should minimize the need for creative people to find ways around it.  Now to your question, does it actually help prevent problems?  Probably a few but certainly not all!  I've seen people become lax in their diligence when they assume they are protected by the system.  They seem to assume that if they make a mistake someone down the line with catch it.  This is something to be avoided if possible.  The only way that I know of to prevent this type of mind set from developing is through education and convincing everyone involved in the process that their step is critical and by keeping it simple they will be more likely to perform their step as instructed.  

The paedipacks supplied by NHSBT, or, rather, the donors are also tested for unusually high levels of potassium ions, as a result of findings a few years back where babies had been affected by fresh, rather than stored blood from such donors (natural hyperkalaemia).

There is reason NOT to use the freshest possible units. They may be more toxic than intermediate stored units. This is something that made sense but was almost certainly wrong.  See below for the reasoning and published data.  We use <21 days as fresh for this reason and avoid <7 days storage for everyone based upon the randomized trial data.
BMJ 2019;366:l4968 doi: 10.1136/bmj.l4968 (Published 5 August 2019) Page 1 of 1
Letters
Trivella and colleagues present some caveats around the subject of duration of red cell storage and clinical outcomes.1 Studies have been widely interpreted as showing that transfusion is not associated with adverse clinical outcomes. I think this is a serious misinterpretation of the data.
In addition to the concerns raised by the authors, another valid hypothesis, which has received little attention, is that very short storage red cells might be more dangerous than medium storage periods (say 7-21 days) and equally dangerous as longer storage red cells (say 28-42 days). An inverted U shaped curve. The evidence for this comes from a meta-analysis finding that “ultra short” storage of red cells was associated with a post-transfusion increase in nosocomial infection.2 Shorter storage red cells have a greater imbalance of oxidation-reduction potential than longer storage red cells in preliminary studies in vitro.3 Red cell storage duration is also a poor predictor of post-transfusion free haemoglobin and heme, putative mediators of toxicity from transfusions.4 5
We need better metrics for predicting red cell transfusion efficacy and toxicity. The simple expedient of fresher red cells is clearly not that metric and might be leading us to transfuse more toxic red cells (very fresh) in the most fragile patients,
such as premature newborns. A new approach is clearly called for by the current data. At our centre we define fresh as <21 days of storage, and we generally never transfuse a red cell that has been stored for much less than 7-10 days, for the above reasons as well as logistics of supply.
Competing interests: None declared.
1 Trivella M, Stanworth SJ, Brunskill S, Dutton P, Altman DG. Can we be certain that storage duration of transfused red blood cells does not affect patient outcomes?BMJ 2019;365:l2320. 10.1136/bmj.l2320 31186250
2 Alexander PE, Barty R, Fei Y, etal . Transfusion of fresher vs older red blood cells in hospitalized patients: a systematic review and meta-analysis. Blood 2016;127:400-10. 10.1182/blood-2015-09-670950 26626995
3 Schmidt A, Gore E, Cholette JM, etal . Oxidation reduction potential (ORP) is predictive of complications following cardiac surgery in pediatric patients[abstract]. Transfusion 2016;56(Supplement S4):20A-1A.
4 Cholette JM, Pietropaoli AP, Henrichs KF, etal . Elevated free hemoglobin and decreased haptoglobin levels are associated with adverse clinical outcomes, unfavorable physiologic measures, and altered inflammatory markers in pediatric cardiac surgery patients. Transfusion 2018;58:1631-9. 10.1111/trf.14601 29603246
5 Pietropaoli AP, Henrichs KF, Cholette JM, etal . Total plasma heme concentration increases after red blood cell transfusion and predicts mortality in critically ill medical patients. Transfusion 2019;59:2007-15. 10.1111/trf.15218 30811035
Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/ permissions
LETTERS

I agree. You do the best you can with what you have. Unless your blood supplier or a large neighbor who can transfer product is close by, you are not going to be able to ship in product in time. It is cost prohibitive for us to stock product routinely for an event that occurs very infrequently (and your blood supplier may not be very enthused about the constant rotation of product). 
We are 150+ beds, have a NICU, and are one of the 'large' hospitals in our rural area, but still transfer our critical neonates/kids to Children's 150 miles away. We only transfuse babies and small children 1 to 3 times over an average year. Our facility sees quite a few Onc patients, so I do stock a small inventory of irradiated products including 2 O neg Irrad on top of our normal O neg stock (if we can get O neg - fun times!). If we have time to crossmatch, we provide the freshest type specific unit (if we know mom's type) on the shelf, irradiated if requested and we have it in stock. If not, we provide the freshest O neg unit on the shelf, irradiated if requested and available. Children's gives LR as CMV neg equivalent, so that's the policy we follow. I don't stock syringes because we would outdate almost all of them and our software is not set up to split/label units. (It would be very rare for us to even have the possibility of pulling blood off that unit a second time, so not worth setting up.) We hand over the entire unit and the pediatrician/nurses pull what they need for transfusion in the 4 hours after issue.

Best suggestion yet!!!!!!!!!!!!!!!!!!!!!!

Malcolm we can do this for ever!!  The antibodies CAUSE the hemolysis by activating the compliment. 
Here's my analogy, without my finger pulling the trigger the gun doesn't go off and I don't get a bird in the bag. When I do pull the trigger did I kill the bird or did the lead shot kill the bird?  Or did the gun kill the bird? To address the hemolysis of autologous cells with the same analogy. Occasionally 2 birds are close together and both are killed with the same shot.  One was intended the other was not but I still pulled the trigger.  
Take one of the factors out of the equation and the end result does not happen or is significantly altered so the answer to all the questions is YES.  I think what we have here is a case of semantics.  Every step could be said to have CAUSED the end result.  
This is fun.  Let's discuss it over a pint some day.

I may be mistaken but I seem to recall being taught that it was the ABO antibodies interaction with incompatible RBCs which caused the activated complement so without the ABO antibodies you don't get the hemolysis.

Sorry, but I disagree.  In most cases of ABO haemolytic transfusion reactions, it is not the ABO antibodies that cause the haemolysis that destroys the incompatible red cells, but activated complement that, in most cases, also causes "innocent bystander haemolysis", whereby the autologous red cells are also haemolysed.

Mismatched donor red cells (ABO antigens) would be hemolyzed by the patient's antibodies (anti-A, anti-B, anti-A,B), causing the dreaded ABO hemolytic reaction. The patient's antibodies are not going to be as dilute as donor antibodies until massively transfused and the patient is going to continue to produce antibodies to continue attacking donor cells. The red cell stroma from the destroyed mismatched donor cells would do the damage. The rationale with mismatched plasma is that the antibody source of the donor plasma is going to be diluted by the patient's blood volume and the amount transfused is going to be limited by the number of units transfused, enough that the impact on the patient's red cell antigens would be greatly minimized. There won't be as much antibody from the donor to react with the patient's red cells vs the patient antibody to react with mismatched donor cells. Maybe a positive DAT from mismatched plasma, hopefully a delayed removal of affected red cells instead of brisk hemolysis. Better than bleeding to death.