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Platelet count increase as well as platelet survival after transfusion is related to the dose of platelets infused and to the patient's body surface area (BSA). Usually these values are less than what would be expected. Corrected platelet count increment (CCI) = platelet increment at one hr x BSA (m 2) / # platelets infused x 10 11
Higher platelet transfusion thresholds have been used in premature neonates, but this has been based on limited evidence. [19] There is now evidence that using a high platelet count threshold (50 x 10 9 /L) increases the risk of death or bleeding compared to a lower platelet count threshold (25 x 10 9 /L) in premature neonates. [20]
Blood compatibility testing is routinely performed before a blood transfusion.The full compatibility testing process involves ABO and RhD (Rh factor) typing; screening for antibodies against other blood group systems; and crossmatching, which involves testing the recipient's blood plasma against the donor's red blood cells as a final check for incompatibility.
Platelet transfusion alone is normally not recommended except in an emergency and is usually unsuccessful in producing a long-term platelet count increase. This is because the underlying autoimmune mechanism that is destroying the patient's platelets will also destroy donor platelets, and so platelet transfusions are not considered a long-term ...
Platelet transfusion refractoriness is the repeated failure to achieve the desired level of blood platelets in a patient following a platelet transfusion. The cause of refractoriness may be either immune or non-immune. Among immune-related refractoriness, antibodies against HLA antigens are the primary cause.
Exposure of blood to the subendothelial space initiates two processes: changes in platelets, and the exposure of subendothelial platelet tissue factor to coagulation factor VII, which ultimately leads to cross-linked fibrin formation. Platelets immediately form a plug at the site of injury; this is called primary hemostasis.
The prototype for these drugs is aspirin, which inhibits the production of thromboxane. NSAIDs (for example Ibuprofen) inhibit the activation of platelets, and thereby increase the risk of bleeding. The effect of aspirin is irreversible; therefore, the inhibitory effect of aspirin is present until the platelets have been replaced (about ten days).
The covalent bonds increase the stability of the fibrin clot. Thrombin interacts with thrombomodulin. [14] [15] As part of its activity in the coagulation cascade, thrombin also promotes platelet activation and aggregation via activation of protease-activated receptors on the cell membrane of the platelet.