Delayed Blood Transfusion Reactions

The most important delayed posttransfusion reactions are shown in Table 33.1. All these reactions are very uncommon. The most common of these reactions is the occurrence of a delayed hemolytic transfusion reaction. Delayed hemolytic transfusion reactions (DHTR) are due to the technical failure to detect an antibody present in the patient's plasma or serum prior to transfusion. This is not to imply that a procedure was performed technically incorrectly, but that all techniques have limitations in sensitivity and occasionally will result in a false-negative, i.e., failure to detect an antibody when one is present. These red cell antibodies arise as a result of transfusions or pregnancies, and the antibody increases in titer after re-exposure to the antigen on the transfused red cell. Although this may occur as early as 24 hours after the transfusion, it more commonly occurs after 2-7 days. DHTR are due, therefore, to very low levels of undetected pre-existing antibodies. The clinical features of delayed hemolytic reactions tend to be similar to, but milder than those which occur in association with acute hemolytic reactions, and rarely require hospitalization. This is because most of the antibodies are IgG and in many instances, such as the Rhesus system antibodies, do not fix complement. Intravascular hemolysis is, therefore, extremely rare. The vast majority of these reactions are silent being clinically evident only in a small proportion (20% or less). These reactions are often discovered on the basis of an unexplained hyperbilirubinemia or decrease in hemoglobin. Alternatively, these reactions are uncovered by the finding of a positive antibody screen or a positive direct antiglobulin test in the serum of a patient several days or weeks after a red cell

Table 33.1. Delayed transfusion reactions

(24 hours-2 weeks)

(a) Delayed hemolytic reaction

(b) Transfusion associated graft versus host disease (Chapter 37)

(c) Posttransfusion purpura

(d) Transfusion transmitted protozoa (Chapter 35)

Table 33.2. Late complications of blood transfusions

(2 weeks-30 years)

(a) Iron overload hemosiderosis

(b) Transfusion transmitted viruses (Chapter 34)

(c) Transfusion transmitted protozoa or helminths (Chapter 35)

(d) Alloimmunization to red cells and HLA antigens transfusion (in the setting where the pretransfusion antibody screen was negative). These reactions are important to investigate since they have implications for future transfusions for that particular recipient.

When clinical symptoms occur they are typically fever, chills, backache, nausea, vomiting, apprehension, etc. In rare instances, for example, with antibodies against the Kidd system, intravascular hemolysis and hemoglobinemia have been reported. DHTR have a frequency of 1:2,000 to 1:5,000. Fatal DHTR reactions are likely to have a frequency of less than 1:500,000. There is no specific treatment and only rarely is energetic clinical management required. As emphasized in Chapter 7, proper identification of blood specimens at the time of collection allows the Blood bank to trace previous records related to a patient in which the historical presence of an antibody is recorded. This will help prevent DHTR.

All other delayed reactions are exceedingly uncommon. Transfusion associated graft versus host disease (TA-GVHD) occurs between 4-20 days after transfusion. It is a devastating event and is discussed in more detail in Chapter 37. Posttransfusion purpura is another very uncommon complication of blood transfusion which occurs about 8-14 days after blood transfusion. In this situation, patients present typically with bruising or other features of thrombocytopenia, such as epistaxis. The platelet count may be extremely low, often less than 5 x 109/L.

The patient's pretransfusion platelet count, when available, is normal. This reaction is typically observed in cardiac surgery and, therefore, the patient presents 5-10 days after discharge. Posttransfusion purpura is due to the development of an antibody which is capable of causing premature removal of autologous (patient's own) platelets. The most common platelet antigen involved is called PlA1 (HPA 1a) and patients who develop this complication lack this antigen on their platelets. The management of this disease is early recognition and treatment with intravenous gammaglobulin since a high mortality has historically been reported. Steroids may be used and plasma exchange (Chapter 40) may also be performed. The platelet count will increase to normal within 48-72 hours. Platelet transfusions should be avoided in these patients. Red cell transfusions may be necessary in patients who have evidence of bleeding and symptomatic anemia. Although red cells from a PLA1 negative donor are preferable, if at all possible, washing and filtration of the cells may be the only logistic option available, particularly in blood centers, which do have a panel of PLA1 negative donors.

Transfusion transmitted protozoa, causing babesiosis or malaria may sometimes produce clinical symptoms in this time period, especially in splenectomized patients. These are discussed in Chapter 35.

Blood Pressure Health

Blood Pressure Health

Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...

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