**3. Mechanisms of haemolytic transfusion reactions**

Red blood cells undergo haemolysis in the intravascular mechanism, in blood or extravascular vessels, that is, organs involving cells of the reticuloendothelial system, primarily spleen and/or liver. Clinically significant differences between the above mechanisms of red blood cells destruction are based on the time of onset of haemolysis and the destruction rate of red blood cells. Intravascular haemolysis is characterised by the destruction of red blood cells at a rate of about 200 ml of transfused cells within 1 h of transfusion. It is manifested by a rapid decrease in haemoglobin, haemoglobinemia and haemoglobinuria and can potentially be life threatening [2]. In contrast, extravascular haemolysis is less dramatic, with a rate of destruction of red blood cells of approximately 0.25 ml/h/1 kg of recipient's body weight. For example, for 70 kg recipient, about 18 ml of transfused red blood cells are destroyed per hour. However, it is worth noting that despite the low intensity of haemolysis, the survival time of red blood cells after transfusion is significantly reduced [2]. In general, intravascular haemolysis is called as an early acute haemolytic transfusion reaction. It can occur during transfusion or up to 24 h after transfusion of red blood cells. In comparison extravascular haemolysis is called delayed haemolytic transfusion reaction and usually occurs 24 h or days after the end of the transfusion. The quoted breakdown of reactions is somewhat artificial, because the symptoms associated with haemolytic reactions sometimes overlap [1].

**93**

**Table 1.**

*Post-Transfusion Haemolytic Reactions DOI: http://dx.doi.org/10.5772/intechopen.91019*

are often non-specific [1, 8].

transfusion reaction [9].

blood cell antigens.

**Blood group system**

and is shown in **Figure 1**.

**3.1 Intravascular haemolysis**

The occurrence and severity of individual clinical symptoms can vary widely and

Red blood cell transfusion can also stimulate the production of alloantibodies without the occurrence of haemolysis. This phenomenon is called delayed serologic transfusion reaction (DSTR) and should be differentiated from delayed haemolytic

Most often intravascular haemolysis is the result of the destruction of red blood cells by the complement system, stimulated by the presence of alloantibodies or autoantibodies. Among alloantibodies, such haemolysis is induced by anti-A and anti-B, rarely anti-Jka, anti-Jkb, anti-Vel, anti-P, anti-Lea and very unique antibodies with other specificities [10, 11]. In all these cases, haemolysis takes place via the classical pathway of complement activation. Its occurrence and severity, in addition to the class of antibodies, is also affected by the number of antigenic determinants with which the antibodies react. The reaction is most severe in the case of antigens

contrast, the presence of antigens from the Rh, Kell, Kidd and Duffy systems on the

Antibodies combined with antigens by triggering the complement cascade lead to cell lysis. This mechanism is called the classic pathway for complement activation

The starting point is the antigen-antibody complex present on the surface of the cell membrane [14, 15]. Antibodies of the IgM and IgG class (outside the IgG4 subclass) bind the C1q protein in the initial stage of activation. The condition for complement activation is the binding of the C1q molecule by two Fc fragments of adjacent IgG antibodies or by one IgM molecule. It should be noted here that the IgM class is more efficient in starting the process of complement activation than the IgG class [2, 15]. The C1qrs complex is created and activates the C2 and C4 components and their distribution into C2a and C2b as well as C4a and C4b. The C4b2a

> A2 2.5 × 105 B 7.5 × 105

C 7–8 × 104 e 1.8–2.4 × 104

**Antigens The number of antigenic determinants on the surface of the cell** 

**membrane**

shows the number of antigenic determinants on the cell surface for selected red

per cell [12, 13]. In

per cell [12]. **Table 1**

–104

A and B, because their number is estimated at about 5 × 105

surface of red blood cells is determined in the range of 103

ABO A1 8.5 × 105

Rh D 1–2 × 105

Kell K 6.1 × 103 Duffy Fya 1.7 × 104 Kidd Jka 1.4 × 105 MNSs S 1.2 × 104

*Number of antigenic determinants on the cell surface of the red blood cell (according to [12, 13]).*
