Malcolm Needs

You are quite correct in asking, "what if the original titre was performed incorrectly?", but you have to draw the line somewhere. If you are performing the titre of an anti-Jka, you would (I hope) use a red cell sample that types as Jk(a+b+)? From the text books, you would assume that the red cells express 7, 000 Jka antigens per red cell (given that there are, on average 14, 000 Kidd antigen sites per red cell), but, this is an estimation in itself, and is also the average of the various experiments performed to find out the number of Kidd antigens per red cell. It follows that, unless you use exactly the same source of red cells each time you are performing the anti-Jka titration, you cannot guarantee that the titre of the QC will be within one dilution of the previous result. The same applies for, for example, ABO titres, where the number of antigen sites differs from one individual to another, but also from the age of the various individuals. The adult A1 red cell has between 810 000 and 1 170 000 antigen sites per red cell. The red cells of a new-born will only carry between 250 000 and 370 000 copies of the A1 antigen. Now, I am not suggesting for a single minute that you would use the red cells of a new-born, but there is still quite a difference between an adult with just over 800, 000 A1 sites per red cell, and almost 1, 200, 000 sites per red cell. As long as such a situation is an unusual occurrence, and not a regular occurrence, I wouldn't worry.

Yes John, I was definitely talking about a mass casualty situation.

Welcome alialameen.

True Scott, but these people don't exclusively make anti-D; they could make virtually any specificity, even if D Negative blood had been given. For example, if they had made an anti-c, they would be in equally in the deep and nasty, if they have another emergent situation in the future, and are given rr units!

Roughly speaking, it is 15% hyper-responders, 70% normal responders and 15% non-responders (but those figures are rough). I tend to agree with your last sentence John. I was thinking more in terms of a single unit in an average sized adult.

Welcome BBKaren.

Welcome Krissy8733.

Welcome Debbie Mantel.

Before I attempt to answer your query, I must explain that I am NOT a doctor. I am what is called in the UK, a Biomedical Scientist and, as such, am not qualified to make a diagnosis, but I am the Chief Examiner in Transfusion Science for the Institute of Biomedical Science, and used to by the Reference Laboratory Manager in the Red Cell Reference Laboratory in the National Health Service Blood and Transplant Centre in Tooting, London, so I can claim some expertise. Although a warm auto-antibody in a person's plasma is by no means common, it is something we use to see on a daily basis at Tooting. To put it at its most basic, it results from your immune system producing an antibody directed against a red cell antigen expressed upon your own red cells, which could, under certain circumstances, lead to you becoming (usually mildly) anaemic. The "autologous adsorption" bit means that the laboratory, either at your hospital, or at a Reference Centre has been able to remove the antibody from the plasma in your blood sample by using your own red cells (thus proving beyond doubt that the antibody is indeed an auto-antibody). They have then tested this adsorbed plasma in tests to see if there are any unusual antibodies in your plasma that are directed against antigens expressed on the red cells of other individuals; so called allo-antibodies. They include in their report the caveat that concerning the "common blood group antigens" because it is all but impossible to test for antibodies against all the known antigens, of which there are well over 600, some of which are incredibly rare. Most auto-antibodies have a specificity within the Rh Blood Group System, which, at present, contains 55 different antigens (but other antigens are being found on a regular basis). Most of these auto-antibodies are directed against either the Rh antigen known as Rh17, or against that known as Rh18 (I realise these names will mean nothing to you - but bear with me). Almost everybody in the world expresses both of these antigens on there red cells, and the actual specificity of the auto-antibody is not really of any consequence. It is highly unusual, to say the least, for a maternal auto-antibody to cause any problems with a condition known as haemolytic disease of the foetus and new-born (or HDFN), particularly at an early stage of pregnancy. To me, this suggests that your early miscarriages and your auto-antibody status are coincidental, rather than the auto-antibody being the cause of your early miscarriages. Red cells are not really produced in early foetal life (indeed, there is not much in the way of blood in a foetus until about 12 weeks of gestation), so there are very few foetal red cells available to be affected by your auto-antibody. Having said all of that, I would reiterate that I am NOT a doctor, and even if I were, it would be impossible (and stupid in the extreme) to even attempt to make a diagnosis without FULL knowledge of your case. As such, I would suggest that you do discuss your case with your own physician (or your obstetrician) and be guided by what he or she suggests in terms of further testing. I hope that helps a little bit, and that I have not "blinded you with science" (which was not my intention), and I apologise for me English spelling!

Welcome aow85.

As a NON-CLINICIAN, as I understand it, in the case of a female of child-bearing potential (in the UK, 0 to 50), once the patient has settled, the first thing that would be attempted would be an exchange transfusion (probably a double exchange, if sufficient D Negative units can be located), and then an estimation would be made of the volume of the residual D Positive red cells, and then the anti-D immunoglobulin (almost certainly the IV type) would be estimated and given. This would be followed-up after 72 hours, and more given as necessary, and then followed up again, and at 6 months. If there was insufficient D Negative units after the patient has settled, we may try massive doses of anti-D immunoglobulin, but almost certainly not, as this will have the effect of clearing the D Positive red cells, but there would be nothing with which to replace them. In such a situation, I think we would explain the situation to the patient (or their relatives if they were either too young to understand, were mentally incapable of understanding or were unconscious, and sit back and be thankful that we still have a live patient. If the patient was either a male or a female of greater than 50 years of age, we wouldn't bother.

Welcome NICEMERENCIANA.

Welcome AshleyK.

Yes, I lived all my life in England, in or around London. The bombs were the Chelsea Barracks bomb in 1981, the Hyde Park Corner bomb in 1982 and the Harrod's bomb in 1983.

Particularly if the massive transfusion event is a major incident, and during a time when there is only a minimum number of people working, we used to have a list of telephone numbers for, primarily, people who work in blood transfusion, but also those who work in blood transfusion as a sort of secondary discipline, and we give this to the microbiologist to contact the required number of staff (on the grounds that the microbiologist, brilliant in their own discipline as they may be, are less likely to be of use in the Blood Bank when units are required urgently, than are the staff who are already running around like headless chickens). I was lucky enough (????????) to be involved with three IRA bombs and two train crashes in my time - and the system did work.