| When performing an antibody investigation, which of the following would indicate an inconsistency that needs to be further investigated? (Select all that apply) | View Page |
| Summary This case study presents a scenario in which a patient had an unexpected antibody that disappeared after he was transfused with 2 units of unmatched group O Rh negative RBC. The patient developed a positive DAT with MFA but an antibody identification using the post-transfusion red cell eluate was inconclusive, making the antibody unidentifiable. Fortunately, the patient improved and further transfusion was not required. Ultimately, the patient's antibody was identified as anti-Jka, with a second antibody to a low frequency antigen (Radin) also unexpectedly present.The case illustrates the risks involved in using unmatched blood. | View Page |
| Think about your responses to each of the following questions, then click on the questions. | View Page |
| The antibody screen is positive but the transfusion of the O Rh-negative RBCs is already in progress. What are the transfusion service (TS) laboratory's priorities in this case?Place the following procedures that will be followed by the TS in the appropriate order of priority. | View Page |
| Which of the following statements about mixed-field agglutination (MFA) are true? Select all that are correct. | View Page |
| In this case, which red blood cells (RBCs) do you think are agglutinating in the DAT and why? | View Page |
| Which of the following most likely accounts for the patient's post-transfusion plasma giving negative panel results? | View Page |
| Consulting the patient's physician If the physician had decided to continue transfusing the patient at this stage, the following information should be communicated: Although all donors appear to be compatible in the post-transfusion crossmatch, they are not. The results are false negatives - the patient's antibody has been "mopped up" by adsorbing to the incompatible transfused O Rh-negative RBC. Given that 6 donors were positive using the pretransfusion plasma, the antigen is a higher frequency antigen and most donors would likely be antigen-positive and incompatible. The patient's physician should consult the TS medical director before any decision to transfuse is made. Transfusing RBC before tests are complete requires physicians to sign an emergency release form in which they assume full responsibility. | View Page |
| Immediate HTR - Signs and symptoms The following signs and symptoms are associated with acute HTR due to ABO incompatibility but can be associated with other blood group incompatibilities. ABO incompatibility typically results from patient misidentification.The more serious symptoms result from intravascular hemolysis (IVH) caused by antibodies such as anti-A and anti-B that can bind complement to C9.Signs and symptoms typically appear within minutes of the transfusion but can occur anytime during the transfusion. They may include: 1. Burning sensation along the vein being transfused (IVH due to complement activation to C9)*2. Lower back pain in the area of the kidneys (renal failure with subsequent oliguria/anuria) *3. Unexplained bleeding/oozing from a surgical site (fibrinolysis following DIC)*4. Hypotension leading to hypovolemic shock (release of vasoactive substances caused by C3a and C5a)5. Tightness in substernal area of the chest (bronchial constriction due to release of vasoactive substances caused by C3a and C5a fragments)6. Other symptoms: fever, chills, skin flushing, dyspnea, wheezing, anxiety, malaise, nausea, headache. * If untreated, these complications may lead to patient death. | View Page |
| Cause of Delayed HTR Delayed HTR result from a secondary (anamnestic) immune response causing a weak, undetectable antibody to become stronger.Upon re-stimulation by donor RBC positive for the antigen corresponding to the patient's antibody:* Patient's memory B cells differentiate into antibody-producing plasma cells.* As new IgG antibody is produced, it sensitizes antigen-positive transfused donor red blood cells.* The IgG-sensitized donor red blood cells are then removed by extravascular hemolysis (EVH) mainly in the spleen. | View Page |
| Investigating weak antibodies In this case the patient's antibody has disappeared from the plasma by adsorbing to transfused donor red cells. It is detectable but unidentifiable in the post-transfusion red cell eluate. Several trial and error procedures exist to enhance weak antibodies. Which methods will enhance the reactivity of a given antibody depend on its characteristics. Methods to investigate weak antibodies include: Use a higher plasma to red cell ratio (add more antibody-containing plasma or eluate) Increase incubation time (if consistent with manufacturer instructions, if applicable) Use enzyme-treated panel red cells (enzymes enhance IgG antibodies in Rh and Kidd blood systems but denature some antigens, e.g., Fya, Fyb, S) Try alternative antibody detection methods, e.g., if using LISS routinely, try polyethylene glycol (PEG) or column agglutination methods such as gel, providing they have been validated for use in the TS laboratory. | View Page |
| Variations in antibody strength The antibody in the pretransfusion specimen (prior to the patient being transfused with two units of unmatched group O Rh-negative RBC) reacted 2+ and 3+ with antibody screen and donor cells.If Jk(a+), the transfused donor RBC would have stimulated increased antibody production and the patient's plasma would be expected to react even more strongly with Jk(a+) red cells than in the pretransfusion specimen.However, the expected increase in antibody strength did not happen. Because Jk(a+) donor cells "mop up" (adsorb) the patient's anti-Jka, initially the anti-Jka decreased in strength. Later, once donor red blood cells are no longer present to adsorb the antibody, the anti-Jka would be expected to become stronger.Currently, (2-weeks post-transfusion) the patient's plasma is only reacting 1+ with Jk(a+b-) RBC and w+ with Jk(a+b+) RBC.This effect is called dosage. Learning points When a secondary immune response occurs, antibody first decreases before it increases. The expected increase in antibody strength will vary depending on the amount of excess antibody available in the patient's plasma at the time of testing versus the amount that had adsorbed to donor rbc and been removed by EVH.~ | View Page |
| Antigen phenotyping A standard follow-up to antibody identification is to antigen phenotype: Patient's red cells (expecting them to lack the corresponding antigen) Donor red cells (in this case, those transfused before an antibody was identified, or, more typically, to find suitable antigen-negative donors to crossmatch prior to transfusion).If you had wanted to type the patient for any antigens at this point in the investigation (2-weeks post-transfusion), which specimen would you have used? Think about any antigen typing problems and how to overcome them before proceeding to the next page. | View Page |
| Antigen phenotyping issues There are two potential problems in typing a recently transfused patient who develops a positive DAT: There will be two cell populations, patient and donor red blood cells. If the typing sera reacts by IAT, the positive DAT will cause false positives. In the case presented, the DAT has become negative. This also suggests that most (if not all) transfused donor red cells have been removed from the patient's circulation.Regardless, to be on the safe side, the patient's initial pretransfusion specimen, which was DAT negative and consisted of only the patient's red blood cells, should be used for antigen phenotyping. | View Page |
| Which of the following statements about antigen phenotyping are true? (Select all that apply) | View Page |