Much has evolved over the past 25 years regarding the coagulopathy of liver disease. Paradoxically, this form of coagulopathy is relatively hypercoagulable despite the common clinical impression of a hemorrhagic tendency. The latter is largely driven by portal-mesenteric venous pressure (i.e. portal hypertension) and has little to do with hemostatic pathways. It cannot be emphasized enough that the INR really does not offer a meaningful measure in this situation and may lead to interventions such as FFP that can actually worsen portal pressure and hence pressure-driven bleeding. With regard to procedure-related bleeding, we point out substantial differences in the definition of high risk procedures and we have proposed a new operational definition dependent on the applicability of local hemostatic measures, although this requires further investigation. The common occurrence of venous thrombosis in these patients requires careful consideration of hemostatic pathways and overall risk and benefit of intervention. The decision regarding anti-coagulation therapy needs to be driven by a global assessment including history of non-portal hypertensive related bleeding, but also by fall risk in patients prone to encephalopathy which can result in head trauma. This is probably best estimated by frailty but has yet to be adequately investigated. In the background of these concerns, several super-imposed and complicated conditions including infections and renal dysfunction should be taken into account. Inherited forms of thrombophilia in the setting of cirrhosis perhaps do not outweigh the thrombophilia inherent to liver disease but warrant further consideration.


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