All I know is that the last time I tried to Google my name I found BBT. It doesn't work so well for Malcolm as he apparently shares his name with a celebrity.

Yes, the other, much more famous Malcolm Needs is a film director, with fingers in the theatre industry as well, although I must confess that I have never seen any of his work. Mind you, I don't suppose for one minute that he has seen any of mine either!!!!!!!!!!

There is a paper by Oliver C, Blake D, Henry S. In vivo neutralization of anti-A and successful transfusion of A antigen-incompatible red cells in an animal model. Transfusion 2011; 51: 2664-2675 that may shed some light on this subject - at least in the future.

one more thing if you find some patient or donor with bombay try to screen the whole family even if he or she is just a donor chance to find another one

It's been an interesting sidetrack to the original post as to how to track down antibodies to high incidence antigens. For the average blood banker, though, you would have to be lucky enough to have a panel on hand with a U- or k- etc cell or else hand it off to a reference lab. Most labs don't stock antisera for these antigens either, the shining exception being anti-H. We started talking about the Bombay coming in to your ER gushing blood, which doesn't give much time for the reference lab to help or to test the sibs. Does anyone know of any attempts, successful or otherwise, of actually transfusing Oh patients incompatible blood on an emergency basis? There was the article in Transfusion by Davey et al in 1978 where Cr labeled O cells were down to 10% survival or so just a few minutes after infusion, which didn't bode well for the practice.

I'm sure everyone already knows this, but the 22nd cell on the B panel from Ortho is k-. I had a panagglutination except for A/C on a patient on panel A recently, which are all k+, so I pulled all the 22nd B cells that I had (4) and ran them. Only one was negative but it was a start and I was able to confirm it was E, Jka and S.

I certainly don't knoe of any such attempts Phil. All of my posts are based on theory and prayer; mostly the latter - and that coming from a High Church Atheist!!!!!!!!!!!!!!!!

I'm sure everyone already knows this, but the 22nd cell on the B panel from Ortho is k-. I had a panagglutination except for A/C on a patient on panel A recently, which are all k+, so I pulled all the 22nd B cells that I had (4) and ran them. Only one was negative but it was a start and I was able to confirm it was E, Jka and S.

Actually, not using Ortho, I didn't know that. Thanks. I'd just settle for a RzR1 cell on each panel...........Nice cocktail of antibodies, by the way. Those are the ones that you give yourself a well-deserved pat on the back when you get to the bottom of the pile.

Here is another option, if time permits. Perform a 1.5 to a 2 plasma volume exchange using 5% albumin as replacement fluid. Of course the problem is that there will still be residual Ab left, and hemolysis is still likely to occur. I also do not know how long a plasmapheresis procedure takes, but this could be an option for having a better chance at saving a Bombay that is not gushing blood . . . yet, when transfusion of incompatible blood is the only option.

I wonder how fast after that plasma exchange the anti-H titer would come back to normal. At that time the patient would still have a lot of the H+ cells in his circulation. Of course, maybe by then you could have given something to suppress the immune response and have imported some Oh units.

To a certain extent, Mabel, it depends on the proportion of IgG anti-H to IgM anti-H in the patient as to how quickly the anti-H titre will come back to "normal". 90% of the IgM pool will be intravascular, so there is only 10% elsewhere to worry about, but only 40% of the IgG pool will be intravascular, so there is a whopping 60% lurking elsewhere, and this can come back very quickly.

Hemorrhage implies gushing (to me) and if we had a patient gushing, I am quite sure our uncrossmatched emergency issued O negative units would be transfused before we even got as far as discovering the incompatibility. There wouldn't be time to track down a sibling. Hopefully, there would be an OR close at hand and some kind of cell saver device could be used to help the patient keep as much of their own blood as possible.

Foeto-maternal haemorrhage doesn't mean gushing though Dianna?

Foeto-maternal haemorrhage doesn't mean gushing though Dianna?

True, but to quote one of my medical directors, "you have to stop the bleeding!"

True, but to quote one of my medical directors, "you have to stop the bleeding!"

Oh, absolutely true Dianna.

...and hopefully with something more than a finger in the ****. I hate the ones that they take to OR and "fix", then back to OR again and again cause they keep bleeding....

Hemorrhage implies gushing (to me) and if we had a patient gushing, I am quite sure our uncrossmatched emergency issued O negative units would be transfused before we even got as far as discovering the incompatibility. There wouldn't be time to track down a sibling. Hopefully, there would be an OR close at hand and some kind of cell saver device could be used to help the patient keep as much of their own blood as possible.

This is what I was thinking. I would have long since killed them with my emergency release O neg units. Not a good outcome, but that is probably what would happen.

In a situation like that (gushing) what else could you do Elin - hard as it is to accept?

I am so glad to see all of these points brought forward and saved on this site so that, should this ever happen to any of us, we don't have to think of everything ourselves--even if we are just thinking of how to explain a bad outcome on our FDA report of a transfusion fatality or explain the situation to the physician. We have to do the best we can at the time; rarely, the usual best practice is not the right practice for the situation, but this discussion helps us be wiser, I think.

Decided to Google "transfuse Bombay" and found this article with a case study similar to what we started out discussing. http://www.akamaiuniversity.us/PJST10_1_333.pdf

and this:

A 62-year-old woman was referred to our hospital because of chest pain. She was admitted to the coronary care unit (CCU) ward with diagnosis of unstable angina. Angiography showed severe three-vessel coronary artery disease. After performing percutaneous coronary intervention, her hemoglobin level was checked and it was 90 g/L. The physician ordered one unit of packed red blood cells for her. Her blood sample was taken and sent to the hospital blood bank for performing pretransfusion tests. Her blood group was determined as the O blood group, and one unit of group O red blood cells was prepared for her. During transfusion of O red blood cells, she developed nausea, restlessness, back pain, hypotension, fever, and chills. Transfusion was immediately stopped and with a presumption of transfusion reaction, her before-transfusion blood sample was rechecked for blood grouping and cross-matching. During cell typing (forward typing), it did not show any reaction to anti-A and anti-B antibodies just like a normal O blood group. When cross-matching with the blood bag of group O was done, it showed incompatibility. A direct antiglobulin test on the after-transfusion blood sample was positive. Her blood sample was sent to the local blood transfusion center for detecting the cause of mismatching. Standard cell typing, reverse typing with O group control cells, and antibody screening and identification were performed. There was a discrepancy between cell typing and reverse typing. In reverse typing, her serum showed strong agglutination with O group control cells. The results of antibody identification showed the presence of a strong antibody which reacted with all panel cells through a wide thermal range with a negative autocontrol. Her red blood cells tested with anti-H antibody, but there was not any reaction to anti-H. The probability that the patient was carrying the rare Bombay blood group raised and further confirmation of the Bombay blood group was done by a reference serology laboratory of Iranian blood transfusion organization. Since the hemoglobin level of the patient decreased to 68 g/L after reaction, two units of the Bombay blood group were sent to Yazd from the blood bank of rare blood groups which was established by Iranian Blood Transfusion Organization for such patients. These two units were cross-matched using the patient's serum and found to be compatible. After transfusing two units of Bombay blood, the patient's hemoglobin improved to 100 g/L and she was referred to a specialized cardiac surgery center for CAD management. http://www.ajts.org/article.asp?issn=0973-6247;year=2013;volume=7;issue=1;spage=86;epage=87;aulast=Shahshahani This was just published in Feb.

Thanks Mabel. I'd love to know how much blood she actually received before they noticed the reaction symptoms, since we've been asking ourselves "If we have to give them something besides Oh blood will we kill them?". Also it would appear that the unit was transfused on the typing results alone, as the incompatibility seemed to be discovered after the fact, and it looked like the screen was only done at the local transfusion center.