Surface relaxation

In the earliest recorded blood transfusion experiment, Blundel showed that the red cells of a donor of another species underwent rapid intravascular lysis²¹. And in 1824, he suggested the need to use a donor of the same specie for blood transfusions. Ponfick in 1875 supported the idea. Ponfick demonstrated haemolysis when red cells of a donor of a specie are mixed, in vitro, with the serum of another specie²¹.

Wiener and Moloney in 1943,²² using differential agglutination method, demonstrated that the transfused red cells survived but there was destruction of recipients red cells when group O blood was transfused to group A recipients.

Gasser made similar observation in 1945²³.

Ebert and Emerson in 1946,²⁴ noted increased osmotic fragility of the recipients red cells with about 1% frank haemolytic reaction in patients of groups AB, A or B who received group O blood. Delmas - Marshalet et al in 1969²⁵ made

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similar observation in haemophiliacs who received group compatible but not group identical blood.

Haemolytic transfusion reaction (HTR) is a serious complication of blood transfusion. It can be defined as the occurrence after transfusion of measurably increased destruction of red cells of donor or recipient, by alloantibodies²⁶. The reaction may be acute (AHTR), occurring within hours of transfusion, or delayed (DHTR) when it occurs 4 – 10 days^, after²⁶. AHTR usually follows the transfusion of ABO group incompatible blood or group compatible blood transfusion in which the donor or the recipient had immune antibodies or haemolysins. It can also be defined as the occurrence of features of accelerated red cell destruction following transfusion of blood or blood component. Either the recipient or donor red cells or plasma could be involved. In most cases, it is the donor red cells that are destroyed by immune antibodies in the recipient and this is the most severe form.

Transfusion of group incompatible blood is usually more commonly due to clerical errors than to immunological reasons²⁷. To reduce the occurrence, meticulous record keeping and foolproof identification system are required. One way to minimize this type of HTR will be to verify the recipient’s ABO blood group at the bedside immediately prior to the transfusion²⁷. Card or slide haemaglutination method may be used for this purpose, but a recently described

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dipstick technique is ideally suited for bedside ABO grouping as well as a variety of other near–patient testing applications²⁷.

Severe haemolysis may also be seen in patients who receive ABO–

incompatible platelet concentrates and some other blood components because of short supply of group specific components²⁸.

Haemolysins are immune antibodies, which on attachment to RBC antigens fix complement to produce lysis of the red cells. They are usually incomplete IgG antibodies and act optimally at 32-37⁰C. The commonest are immune anti–A and anti–B. The immune characteristic of these antibodies was first described by Ervin et al in 1950⁴. They found that these antibodies were difficult to neutralize and had higher indirect antiglobulin titre than the naturally occurring anti-A and anti-B.

Studies have shown that blacks, in particular Nigerians, have very high haemolytic activity of anti–A and anti–B, especially group O persons²⁹. Adewuyi et. al³⁰ had similar finding in a study amongst white and black Zimbabweans.

The prevalence of these haemolysins appears to differ from one part of Nigeria to the other depending on the ethnic groups²⁹. The prevalence in Ilorin was found to be about 23.2% ⁷. In other parts of the country the figures range between 30 and 50% ^29,31,36. Haemolysin titre are usually in the range of 2–32 but a visual titre of 8 has been observed to be potent enough to cause in–vivo haemolysis^31,45. Alpha

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haemolysins occurred less frequently than Beta hemolysins, but the titre is always higher for alpha than for Beta haemolysin^7,32. The frequency and prevalence of haemolysins are not sex and age related^32.33.. These haemolysins are acquired after allogenic stimulation from ABO incompatible transfusion, pregnancy with ABO incompatible fetus, organ transplantation from a non–ABO matched donors^34.35. Other means are heterogenic antigens like A and B substances found in Tetanus toxoid, anti-tetanus serum (horse type) and typhoid A and B vaccines³⁶.

In haemolytic reactions, antibodies are normally, but not invariably demonstrated in vitro at the time of rapid red cell destruction. Antibodies in the recipient serum in an incompatible transfusion bring about destruction of donor red cells, while destruction of recipient’s red cells by antibodies in the donor serum occurs almost invariably with group compatible transfusions. This idea of group compatible transfusions stemmed from group O being regarded as universal donors (because they lack A and B antigens on their red cells).

However some of these group O donors have, apart from the expected naturally occurring anti-A and anti-B, immune ant-A and anti-B in their sera which are readily lytic in vitro. This universal donor concept is no longer applicable especially in the developed world where there is availability of blood of all groups

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in the blood banks. Destruction of recipient red cells by donor antibodies is hardly seen with group identical transfusions.

Although ABO system is the one most commonly involved in haemolytic transfusion reaction, antibodies of other systems are also frequently involved. A severe reaction caused by a Kidd-antibody, anti-Jk^a has been described ^37,38. In a study conducted by Pineda et al, in which 23 cases of delayed reactions were reviewed, anti-Jk^a antibody accounted for 33% of the reactions along with anti-C, D, E, Fy^a and K antibodies which between them accounted for 91% of the cases

39. Anti-Fy^a and anti-Fy^b were shown to be responsible for delayed haemolytic transfusion reaction in a young female negro with sickle cell disease ^40,41. Joshi et al⁴² found anti-I in a patient with intestinal cancer who developed immediate haemolytic transfusion reaction. Other rare antibodies involved are anti-e^43. and anti-At(a)⁴⁴.