Canterbury DHB
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This is characterised by the development of severe thrombocytopenia approximately a week after blood transfusion.
Platelet destruction occurs when immune reactions of uncertain type, involving high titre platelet antibodies, somehow destroy transfused platelets and the patient's own platelets. In more than 85% of cases, the patients are negative for the platelet antigen HPA-1a and their serum contains anti-HPA-1a. Passive transfer of platelet-specific antibody from donor to patient with subsequent clinical PTP has been reported.
6-8 days post transfusion, the platelet count (often <10) drops rapidly. The patient develops petechiae and is at risk of spontaneous bleeding.
This will reveal anti-platelet antibodies, usually of a defined specificity such as anti-HPA-1a or anti-HPA-5b.
Treatment includes intravenous immunoglobulin, with or without steroids. Plasma exchange has sometimes been used to reduce the antibody burden. The platelet count usually improves over several weeks. During the acute phase, HPA-1a negative platelets may be used, but are not always successful. For immediate and future transfusions, the patient should receive only compatible blood products and platelets. These must be compatible with the platelet alloantibody and if these are not available, frozen thawed red cells which contain virtually no platelet antigen may be used, but these may still be complicated by the development of PTP.
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Topic Code: 5133
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