Coagulopathy in the Intensive Care Unit

normal situation, platelets circulate freely and do not attach to the smooth endothelial lining of blood vessels (Figure 1). Also, both procoagulants (eg, prothrombin) and anticoagulants (eg, antithrombin) exist in a delicate balance. Within intact blood vessels, the anticoagulants prevail and keep the blood in a fluid state. The anti-coagulants now receive greater atten-tion as it has become clear that their activity is as important to hemosta-tic physiology as is the activity of the more well-known procoagulant factors1 (Table 1). When a blood vessel is injured, the subendothelium is exposed, and platelets are activated (Figure 2). The platelets change their shape from discs to spheres, become sticky, and along with von Willebrand fac-tor and active glycoprotein receptors begin to clump together.2 Granules within the platelets release substances such as thromboxane A2 and adeno-sine diphosphate, which attract more platelets to the site and enhance platelet aggregation. During this pri-mary phase of hemostasis, a platelet plug is formed. This plug alone can stop bleeding from small vessels; when a larger clot is needed, the platelet aggregates provide a frame-work for formation of fibrin clots. Secondary hemostasis is needed to stop the flow of blood from large