Hematological issues in liver disease

Abstract

Patients with liver disease have long been considered at risk for bleeding complications. Although bleeding in patients with cirrhosis occurs frequently on the basis of portal hypertension, evidence accumulated over the last 10 years suggests that the underlying state of hemostasis in patients with cirrhosis and acute liver failure appears to be "re-balanced," such that redundant mechanisms exist to compensate for deficient pro-coagulant, liver-derived factors. Recent clinical and in vitro research has demonstrated that stable patients with acute and chronic liver failure actually exist in a relative hypercoagulable state, which may propagate the progression of liver disease itself as well as cause systemic thrombotic complications. Surely, treating such patients with blood and blood products has the potential to exacerbate the hypercoagulable state and cause harm. The following will summarize much of the background to the new concept of re-balanced hemostasis in patients with cirrhosis and acute liver failure, and suggest therapeutic options other than repleting blood products to achieve a "goal," the often unattainable normalization of standard coagulation laboratories.