Report cold antibodies or cold autoantibodies

[ckcheng]

I have a case with all 3-cell screen positive (2+) in antibody screen. ABO & Rh show discrepancies which requires warm saline-washed red cells for red cell typing and prewarm plasma and A1 and B cells for reversed grouping.  Potent cold antibody(ies) is suspected, so warm saline tube technique is used to repeat the antibody screen, it gave negative result.

Questions are:

(1) Should I report it as cold antibody(ies) or cold autoantibodies?

(2) Do I need to perform cold autoadsorption, cold agglutinin titer, or other tests before I conclude it is a cold autoantibodies?

(3) What is the different between cold antibody(ies) and cold autoantibody(ies) in an antibody workup report?

Thanks.

[SMILLER]

Its a cold antibody, that is for sure, there is no other testing necessary since the warm saline screen showed no other antibodies.

A cold auto (likely anti-I BTW) would be reactive with the autocontrol assuming you ran one with the initial screen.  (An extremely strong one that fixes compliment may require a blood-warmer for RBC infusion.)

Scott

[Malcolm Needs ☆]

3 hours ago, ckcheng said:

(1) Should I report it as cold antibody(ies) or cold autoantibodies?

(2) Do I need to perform cold autoadsorption, cold agglutinin titer, or other tests before I conclude it is a cold autoantibodies?

(3) What is the different between cold antibody(ies) and cold autoantibody(ies) in an antibody workup report?

I totally agree with Scott's answer, but will try to include some details as to why.

(1) I would think that the "cold reacting" antibody is an auto-antibody, as you say that the red cells of the patient's sample require to be washed in warmed saline to obtain reliable results for ABO and Rh, but, like Scott, I would say that the DAT and/or auto result would be required to be absolutely certain.

(2)  According to Immune Hemolytic Anemias.  Lawrie Petz and George Garratty.  2^nd Edition, 2004, Churchill Livingstone. which is regarded as the authority on the subject suggests that the only test required to determine whether or not a "cold" auto-antibody is its thermal amplitude.  They say that, if the antibody is reactive at strictly 30^oC or above, then it is clinically significant.

Autoadsorption will not aid you, as you already know that the antibody is not reactive at 37^oC, and so you can cross-match safely.

Discovering the specificity of the antibody will not aid you as, if the specificity does happen to be auto-anti-I (as Scott correctly says, this is the most likely specificity), you would not be transfusing the patient with either cord red cells or adult ii red cells.  If it is an auto-anti-H, you would not be transfusing the patient with O_h red cells.  If the specificity is auto-a  It is true that nti-i, there is no such blood as i Negative, and so on and so forth.

Titration of the autoantibody is of no use.  It is true to say that most clinically significant "cold" autoantibodies are high titre (some very high titre), but this is not a universal finding.  A clinically significant auto-anti-I, with a particularly low titre was described by Win N, Needs M, Rahman S, Gold P, Ward S.  An unusual case of an acute haemolytic transfusion reaction caused by auto-anti-I.  Immunohematology 2011; 27 (3): 101-103.

(3) In truth, this probably doesn't matter, as, if the antibody is an allo-antibody, it is not going to be clinically significant at that temperature, and if it is an autoantibody, you are not going to get truly compatible blood anyway (see above).

Scott's comment about giving a transfusion through a blood warmer is well-made, but even then, it is likely that the transfused red cells will not last as long as would be expected.  Indeed, transfusion in cases of CHAD is often clinically ineffective, as the transfused donor cells are rapidly haemolysed by active C3b in the plasma, which binds to virgin CR1 sites on transfused red cells.  The autologous cells are relatively resistant to C3b haemolysis, as all CR1 sites are blocked by C3d/g moities.  The transfusion of donor blood causes a significant release of C5b67 complexes, which haemolyse autologous, as well as transfused cells (reactive haemolysis).

[gagpinks]

How do we manage the patient with CHAD especially with very low Hb?

[Malcolm Needs ☆]

23 minutes ago, gagpinks said:

How do we manage the patient with CHAD especially with very low Hb?

From the point-of-view of blood transfusion, you would give ABO compatible, Rh and K-matched units, as you would for any other case of a transfusion-dependent patient, and you give these units as often as the physician requests (but with the suggestion that a blood warmer may be an idea - but the use of same is still the decision of the physician).

As far as treatment is concerned, that is down to the physician, but usually involves steroids to damp down antibody production and, in extreme cases, possibly splenectomy, BUT, the treatment is not really the concern of either those working in the laboratory or the nurse on the ward: the treatment is purely down to the physician (we may give suggestions, as nurses or laboratory workers, but they must always remain as suggestions, as the treatment per se is not down to us).