The life span of platelets ranges from 7 to 10 days. Drugs that interfere with platelet function include aspirin, clopidogrel, prasugrel, dipyridamole, and the glycoprotein IIb/IIIa (GP IIb/IIIa) inhibitors. Approximately 5 to 7 days should pass from the time the drug is stopped until an elective procedure is performed.
Laboratory evidence of trauma-induced coagulopathy is found in up to one-third of severely injured patients at admission. It is distinct from disseminated intravascular coagulopathy and iatrogenic causes of coagulopathy such as hemodilution. Several non–mutually exclusive mechanisms have been proposed. However, the relationship between laboratory coagulation abnormalities and clinically evident coagulopathic bleeding is unclear.
Direct oral anticoagulants have no readily available method for monitoring anticoagulation. A new monoclonal antibody has been approved to reverse coagulopathy due to dabigatran, and agents are currently in clinical trials for the reversal of direct factor Xa oral anticoagulants.
When determining the need for bridging of therapeutic anticoagulation in the preoperative and postoperative setting, the patient’s risk of bleeding should be carefully considered against the risk of thromboembolism and used to guide the need for reversal of anticoagulation therapy preoperatively and the timing of its reinstatement postoperatively.
Damage control resuscitation has three basic components: permissive hypotension, minimizing crystalloid-based resuscitation, and the administration of balanced ratios of blood products.
The need for massive transfusion should be anticipated, and guidelines should be in place to provide early and balanced amounts of red blood cells, plasma, and platelets.
Hemostasis is a complex process whose function is to limit blood loss from an injured vessel. Four major physiologic events participate in the hemostatic process: vascular constriction, platelet plug formation, fibrin formation, and fibrinolysis. Although each tends to be activated in order, the four processes are interrelated so that there is a continuum and multiple reinforcements. The process is shown schematically in Fig. 4-1.
Biology of hemostasis. The four physiologic processes that interrelate to limit blood loss from an injured vessel are illustrated and include vascular constriction, platelet plug formation, fibrin clot formation, and fibrinolysis.
Vascular constriction is the initial response to vessel injury. It is more pronounced in vessels with medial smooth muscles and is dependent on local contraction of smooth muscle. Vasoconstriction is subsequently linked to platelet plug formation. Thromboxane A2 (TXA2) is produced locally at the site if injury via the release of arachidonic acid from platelet membranes and is a potent constrictor of smooth muscle. Similarly, endothelin synthesized by injured endothelium and serotonin (5-hydroxytryptamine [5-HT]) released during platelet aggregation are potent vasoconstrictors. Lastly, bradykinin and fibrinopeptides, which are involved in the coagulation schema, are also capable of contracting vascular smooth muscle.
The extent of vasoconstriction varies with the degree of vessel injury. A small ...