Today’s lecture focused on the coagulopathy of cirrhosis. It is well known that the INR is not a reliable marker of bleeding tendency. After all, it was created as a standardized test for measuring the effect of warfarin. The assay is devoid of important cofactors in the coagulation cascade, particularly the coagulation profile of cirrhotic patients. Therefore, it is a poor predictor of bleeding risk. Remember, along with the low levels of procoagulants associated with hepatic synthetic dysfunction (factors V, VII, X etc.) there are also low levels of anticoagulant factors (protein S, C, ATIII).
A more important marker may be a platelet count < 60, particularly if there is coexistant renal dysfunction. In fact, an andividual’s INR may actually differ from one medical center to the next, which will effect the MELD score! So, think twice about procedures with thrombocytopenia and renal dysfunction.
The crux of the matter may in fact be the platelet. It has three important functions in hemostasis: attachment, aggregation, activation. Cirrhotics with endothelial dysfunction pose problems for platelet attachment as vWF cannot keep up with advancing disease. There are fewer platelets to aggregate (sequestration, low thrombopoietin, high anti-platelet antibodies). The platelets eventually become “exhausted” and have a harder time activating the rest of the cascade.