**3.3 Thrombocyte concentrate (TC)**

Thrombocyte concentrates are transfusion products obtained from full blood by centrifugation. A pooled-donor TC is derived from four to six blood donors to give one therapeutic thrombocyte transfusion unit for an adult patient. A single-donor TC is obtained by apheresis using a platelet separator. Both products contain over 200 x 109 platelets in a 250- to 350-ml plasma volume. The TCs are stored in special storage bags allowing gas exchange on a shaking apparatus at 20-24°C for up to 5 days. In TC infusion, the ABO-blood group/Rhesus factor of the patient must be respected. If a TC of the required blood group is not available, thrombocytes suspended in plasma ABO compatible with the recipient's erythrocytes can be administered. Other options include a TC from an O-blood group donor who has a low titre of anti-A and anti-B agglutinins or the use of platelets resuspended in a plasma substitute. An Rh-positive donor can receive a TC from an Rh-negative donor, but not vice versa [41].

In major surgical procedures, it is recommended to maintain the platelet count above 50 x109/l because of a risk for microvascular bleeding. In cardiac surgery with cardiopulmonary bypass, where platelet-related defects are the most frequent cause of haemostatic abnormality, the recommended platelet count is 50-100 x109/l [42]. An increase above this level is justified only in severe platelet dysfunction. Platelet concentrates should not be administered routinely in cardiac surgery because it has been associated with increase in multi-organ failure and death [43, 44]. One therapeutic TC unit in an adult patient increases the platelet count by 10-20 x109/l. The therapeutic efficacy is assessed by clinical signs (decrease of bleeding) or laboratory evidence of increased platelet counts.

An insufficient increase in platelet counts can be due to reasons such as low TC quality or higher requirements for platelet counts in patients with trauma or disseminated intravascular coagulation. However, the most serious cause involves immune destruction of platelets by alloantibodies or autoantibodies, and this is suspected when other causes are excluded.
