Following trauma, a break in the endothelial lining exposes platelets to the subendothelial connective tissue. This leads to a series of reactions which include the following:
1. adherence of platelets to the exposed collagen, a process that is potentiated by circulating von Willebrand factor;
2. release of platelet granules which contain ADP, serotonin, fibrinogen, lysosomal enzymes, and platelet factor 4;
3. stimulation of prostaglandin synthesis leading to the formation of thromboxane A 2 (TXA2).
The released enzymes, ADP, and TXA2 all promote platelet aggregation and the formation of a primary platelet plug (primary phase). Apart from temporarily sealing the breach in the endothelial lining, the platelet plug provides a surface on which procoagulant reactions can take place. Quantitative and qualitative platelet abnormalities are common in the critically ill (Table 1) and are manifest by symptoms of bleeding or bruising. Bleeding times are often used to assess platelet function.
Table 1 Hemostatic abnormalities in critically ill patients
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