Patients with liver cirrhosis often have low platelets (splenic sequestration) and elevated INRs due to decreased synthesis of factor VII, among other clotting factors; however, remember that they also have reduced synthesis of anticoagulant proteins like proteins C/S and antithrombin. The quantitative/qualitative platelet defects are offset to some degree by increased platelet activation by endothelium-derived factor VIII and von Willebrand factor (vWF). Furthermore, decreased production of ADAMTS13 means less vWF is cleaved, thereby promoting coagulation.
Remember that in compensated cirrhosis, bleeding episodes are more likely related to sequelae of portal hypertension rather than frank coagulation factor imbalance. On the other hand, in decompensated cirrhosis (e.g., recurrent ascites), multiple organ systems are affected by systemic inflammation. This response wreaks havoc on coagulation and fibrinolysis, making the management of bleeding much more complicated than spontaneous etiologies or provoked after an invasive procedure.
Ultimately, we need to focus on anticoagulating patients with cirrhosis (mainly compensated) more aggressively as they are prone to VTE/PE like any other patient, if not more so. I tend to stick with enoxaparin/UFH in the ICU.
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