In a massive transfusion setting, the patient’s forward and reverse type will reflect the use of group O RBCs and the patient may even fully type as group O, depending on the number of units transfused.  Group O RBCs are very precious and in short supply so we need to switch the patient back to his/her own type as soon as feasible.  RBCs in additive solution (e.g. SAGM) have only minimal residual plasma so the load of anti-A,B from the O cells is minimal.  In my organization, we did not titer ABO hemolysins in blood donors.

Here is my approach:

1. Use fresh specimen to perform forward and reverse type
2. Check the reverse type:  does it show either anti-A and/or anti-B from the group O massive transfusion?
   1. If anti-A detected, do not give group A RBCs.
   2. If anti-B detected, do not give group B RBCs.
   3. If both anti-A and anti-B detected, continue using only group O RBCs.

Some people would recommend performing a full AHG crossmatch using the patient’s current plasma and RBCs of the original ABO type:

1. If compatible, return to the original ABO type.
2. Otherwise, continue using group O RBCs.

I did NOT do the full AHG crossmatch and had no hemolytic transfusion reactions if the RBCs were compatible with the current reverse type plasma.

This is an updated version of a lecture I gave in 2010 to a Saudi Ministry of Health blood bank meeting on this topic. It may still be useful as a teaching document.

This is an update of a presentation I gave while working as Head of Transfusion Medicine for Saudi Arabian National Guard Affairs, King Abdulaziz Medical City at Riyadh. I used this strategy there and later at HMC Doha.

Fortunately we had access to rare antisera such as anti-Tja (anti-PP1Pk) which we could purchase from Diamed AG and its successor Biorad. I emphasize that we only sparingly used these rare antisera AFTER ruling out more common high-incidence antibodies.

This is an updated version of a previous post.

Whenever I had a “nonspecific” antibody, I had to first rule out issues with the reagents themselves. The following example shows weak to 2+ reactions in the panel cells and autocontrol.

The variability in the reactions made me initially uncomfortable about called this WAIHA. I then checked the panel details: the testing was done only six days before the panel outdate.

I told my staff to repeat the workup with the new panel expiring five weeks later. The difference is astounding!!

Remember:  if you work in the Middle East, the environmental conditions can be extreme in summer (>50C).  Do you know how your reagents were handling during transport?

My advice: if you are concerned there is a clinically significant antibody but cannot confirm it, consider repeating the workup using fresh reagents and a fresh specimen. Repeating the workup after a few days may make the detection clearer.

Original Panel with Near Expiry Reagents:

Test performed 7/2/06, reagents expire 13/2/06:

Same Patient with New Reagents and New Sample:

Test Performed 14/2/06, reagents expire 20/306:

This is a repost of this rare antibody with a few new additional comments.

This is a rare anti-Jka antibody that only reacts with polyspecific AHG and only in homozygous Jka+ cell.  In the past three decades, I have only seen three of these.

Almost all anti-Jka and anti-Jkb antibodies can be detected using heavy-chain gamma specific AHG.  I prefer to use this reagent since it minimizes interference from cold antibodies.

Whenever you have a nonspecific antibody, never discount the possibility of a Kidd antibody.  Consider doing extended phenotyping and include Jka and Jkb typing and always check for dosage effect.  I have a specific post on my approach to nonspecific antibodies.

Select antibody screening cells including homozygous Jka+ and homozygous Jkb+.  This usually requires a three-cell screen.

Never forget that a negative result only means not-detected.  If there is other evidence for hemolysis, consider performing additional studies.