NMS. Surgery

15

Chapter 1 ♦ Principles of Surgical Physiology

F. Thromboelastography (TEG): Measures the strength and stability of the clot. G. Activated clotting time (ACT): Rapidly determines effect of high-dose heparin; used in cardiac surgery. H. Anti-factor Xa activity: Used to monitor low-molecular-weight heparin activity. Specific Hypocoagulopathic States I. First, ensure bleeding is not a surgical complication: Do not blame postoperative bleeding on coagulopathy until surgical bleeding is ruled out! II. Liver disease: In severe liver disease, hepatocytes cannot manufacture clotting factors. PT/INR is elevated. Treatment includes replacing factors with fresh frozen plasma (FFP) . Chronically, vitamin K can improve hepatic synthetic function. III. Renal disease: Uremia causes platelet dysfunction. Treatment can be with Desmopressin (DDAVP), which causes release of von Willebrand factor or FFP. IV. Disseminated intravascular coagulopathy (DIC): Microvascular coagulation due to inflammation from sepsis, trauma, and other severe insults leads to a consumption and deficiency of factors, leading to coagulopathy. Treat the underlying cause. Replacement of factors may exacerbate the condition; paradoxically, anticoagulants may be beneficial. V. Consumption/dilution A. Due to severe trauma, sepsis, major surgery, and their attendant fluid resuscitation; treatment involves correcting the underlying cause and replacing factors with FFP. B. Hypofibrinogen states need cryoprecipitate. C. Hypothermia and acidosis inhibit proper clotting mechanisms. VI. Medically induced A. Aspirin: Permanently binds cyclooxygenase (COX), preventing platelet aggregation. B. Clopidogrel: Blocks adenosine diphosphate (ADP)-mediated platelet aggregation. C. Gp IIb/IIIA inhibitors: Inhibit platelet aggregation. D. Warfarin: Blocks vitamin K-dependent liver synthesis of factors II, VII, IX, and X. E. Heparin and heparinoids: Augment antithrombin-III function. F. Low-molecular-weight heparin: Inhibits factor Xa. G. Direct thrombin inhibitors: Argatroban, dabigatran. H. Factor Xa inhibitors: Apixaban. I. Fibrinolytics: Tissue plasminogen activator (tPA), urokinase, etc., mediate fibrinolysis. VII. Hemophilia A. Hemophilia A: Congenital deficiency of factor VIII; treatment is factor replacement. FFP can be used in emergent situations.