Does anyone have any references for case reports or policies of giving ABO incompatible RBC units when a hospital runs out of O blood?  We have always planned to never run out of group O RBC units but, the more limited availability of O RBCs, the current likelihood of mass casualty incidents, and the remoteness of some of our hospitals, we want to gather information to inform a policy on why we would or would not allow this in extreme emergencies.  We want to discuss it now, not in the middle of a crisis. Even case reports on accidentally giving ABO incompatible blood could inform us.  I can get the fatality data from the annual FDA report, but I have no data on cases that weren't fatal.  I will happily take expert opinion as well as references!

I have experienced ABO mismatch accidents three times in my career.  Twice the recipients were Group O with reduced isoagglutinin titers and received between 2 and 4 units of Group A RBC.  The other was a middle aged male that was A Pos receiving 8 units of Group B RBC during heart surgery.  The Group O patients experienced an immune boost of their anti-A titer and quickly removed the incompatible RBC from circulation.  The A patient who received 8 units of Group B RBC developed DIC intraoperatively but survived.

I have also experienced a situation where the Group O inventory was reduced to less than 5 units during a liver transplant and major trauma.  It seemed that every patient that needed a transfusion was Group O that day and we ended up harvesting blood from the liver donor and processing it to transfuse to the liver recipient to save the remaining units for other patients.  Fortunately, we restored the Group O inventory quickly.  It did not happen in the face of mass casualties or the level of shortages seen during the COVID shutdown. 

1 hour ago, applejw said:

I have experienced ABO mismatch accidents three times in my career.  Twice the recipients were Group O with reduced isoagglutinin titers and received between 2 and 4 units of Group A RBC.  The other was a middle aged male that was A Pos receiving 8 units of Group B RBC during heart surgery.  The Group O patients experienced an immune boost of their anti-A titer and quickly removed the incompatible RBC from circulation.  The A patient who received 8 units of Group B RBC developed DIC intraoperatively but survived.

I have also experienced a situation where the Group O inventory was reduced to less than 5 units during a liver transplant and major trauma.  It seemed that every patient that needed a transfusion was Group O that day and we ended up harvesting blood from the liver donor and processing it to transfuse to the liver recipient to save the remaining units for other patients.  Fortunately, we restored the Group O inventory quickly.  It did not happen in the face of mass casualties or the level of shortages seen during the COVID shutdown. 

These experiences are very useful for anyone considering this as a possible deviation from normal processes in a dire emergency.

As you know a difficult question. The use of group O blood for non-O patients should be limited as soon as the ABO type is known, and ABO type specific given. There are some old admonitions to never transfuse type specific after X numbers of group O red cells or whole blood. This is nonsense, so do not follow this old precept.  Give only ABO type specific as soon as possible.

As for giving non-O blood to O patients when all other options are exhausted, I would only do this if death were imminent due to bleeding, not ever for routine transfusion.  There are case reports of no hemolysis in such situations, including the one below from my original mentors from half a century ago.  Accidental error but no consequences.  But giving non-O blood to O recipients has the potential to cause rapid death in many instances. We don't know why there are such varied responses.

 

Case Reports

 

Transfusion

 

. 1975 Nov-Dec;15(6):577-82.

 doi: 10.1046/j.1537-2995.1975.15676082233.x.

Unusual response to ABO incompatible blood transfusion

D H Buchholz, J R Bove

• PMID: 1198685
•  
• DOI: 10.1046/j.1537-2995.1975.15676082233.x

Abstract

Three units of group A blood were inadvertently administered to a group O recipient during surgery without evidence of hemoglobinemia, hemoglobinuria, hypotension, disseminated intravascular coagulation, acute renal tubular necrosis, or other signs and symptoms of transfusion reaction. The recipient had normal concentrations of IgG, IgA, and IgM as well as complement (C3) prior to transfusion and anti-A agglutinins titered to 64 (titer of 128 by the antiglobulin technic). Seventeen hours following the transfusion, 28 per cent of the circulating red blood cells were group A (equivalent to 475 ml of packed cells); they were eliminated by day 5 without evidence of hemoglobinuria, hemoglobinemia or hyperbilirubinemia. Anti-A titers (antiglobulin) had risen from a posttransfusion low of 4 to 4,096 by day 10. After treatment of serum with 2-mercaptoethanol, however, hemolytic activity which was first noted on day 5 was lost and the antiglobulin titer dropped to 24 which suggested that most of the anti-A produced in response to the transfusion was IgM rather than IgG. The anti-A titer had dropped to essentialyy pretransfusion levels and the majority of anti-A present was IgM by day 91. The recipient suffered no untoward effects from the transfusion and was in good health three months following the transfusion.