Page 422 - Essential Haematology

408 / Chapter 29 Blood transfusion

red cells or of the blood component required, reticuloendothelial tissue at the rate of 200 – 250 mg/
accompanied by diuretic therapy. unit of red cells. After 50 units in adults, and lesser
Transfusion of bacterially contaminated amounts in children, the liver, myocardium and

blood This is very rare but may be serious. It can endocrine glands are damaged with clinical conse-
present with circulatory collapse. quences. This is a major problem in thalassaemia

Graft - versus - host disease (GVHD) Th is may major and other severe chronic refractory anaemias
occur when live lymphocytes are transfused to an (see Chapter 4 ).
immunocompromised patient. It is prevented by
irradiation of the blood product. It is almost uni- Reduction of b lood p roduct u se
formly fatal.
Hyperhaemolysis syndrome Some patients In the light of transfusion risks, and limited
particularly with sickle cell anaemia, haemolyse resources, appropriate use of blood components is
donor blood even though no alloantibodies to red of increasing importance.

cells can be detected. The haemolysis appears to be Preoperative correction of anaemia (particularly
caused by overactivity of the recipient s macro- iron deficiency) and cessation of antiplatelet

’
phages. It is prevented by infusion of gammaglobu- therapies (e.g. aspirin) where possible, together
lin and corticosteriod therapy. with lower trigger levels for red cell transfusions
Transfusion - related acute lung injury (TRALI) (7 – 8 g/dL in most surgical patients) can all help to
Th is presents within 6 hours of an infusion as reduce blood use.

pulmonary infiltrates with chest symptoms depend- In surgery the use of alternative fl uid replace-
ing on severity. It is caused by positive transfer ment, intraoperative or postoperative cell salvage,
of HLA antibodies in donor plasma causing biological alternatives (e.g. erythropoetin, recom-
endothelial and epithelial injury. Most of the binant clotting factors, recombinant activated clot-

donors are multiparous women. Management is ting factor VII (VIIa) or fibrin glue) all may help.
supportive.
Post - transfusion purpura This is a rare Blood c omponents

problem of severe thrombocytopenia 7 – 10 days
after transfusion of a platelet - containing product, A blood donation is taken by an aseptic technique
usually red cells. It is caused by an antibody in the into plastic bags containing an appropriate amount
recipient (previously transfused or pregnant) anti of anticoagulant – usually citrate, phosphate,
HPA - 1a against a platelet - specific antigen HPA - Ia dextrose (CPD). The citrate anticoagulates the

AI
(PI ). Both transfused and recipient platelets are blood by combining with the blood calcium. Th ree
destroyed by the immune complexes. It is usually components are made by initial centrifugation

self - limiting but immunoglobulin or plasma of whole blood: red cells, buffy coat and plasma
exchange may be needed. (Fig. 29.1 ).
Viral transmission Post - transfusion hepatitis Red cells are stored at 4 – 6 ° C for up to to 35
may be caused by one of the hepatitis viruses, days, depending on the preservative. After the fi rst
+
although CMV and Epstein – Barr virus have also 48 hours there is a slow progressive K loss from the
been implicated. Post - transfusion hepatitis and red cells into the plasma. In cases where infusion of
+
HIV infection is seen rarely now because of routine K could be dangerous, fresh blood should be used
screening of all blood donations. (e.g. for exchange transfusion in haemolytic disease
Other infections Toxoplasmosis, malaria and of the newborn). During red cell storage there is a
syphilis may be transmitted by blood transfusion. fall in 2,3 - diphosphoglycerate (2,3 - DPG) but after
Transfusion - transmitted nvCJD has probably transfusion 2,3 - DPG levels return to normal within
occurred in three cases in the UK. 24 hours. Optimum additive solutions have been
Post - transfusional iron overload Repeated developed to increase the shelf life of plasma -
red cell transfusions over many years, in the absence depleted red cells by maintaining both adenosine
of blood loss, cause deposition of iron initially in triphosphate (ATP) and 2,3 - DPG levels.