Abstract
Patients with liver diseases are in a rebalanced state of hemostasis, due to simultaneous
decline in pro- and anticoagulant factors. This balance seems to remain even in the
sickest patients, but is less stable and might destabilize when patients develop disease
complications. Patients with acute decompensation of cirrhosis, acute-on-chronic liver
failure, or acute liver failure often develop complications associated with changes
in the hemostatic system, such as systemic inflammation. Systemic inflammation causes
hemostatic alterations by adhesion and aggregation of platelets, release of von Willebrand
factor (VWF), enhanced expression of tissue factor, inhibition of natural anticoagulant
pathways, and inhibition of fibrinolysis. Laboratory tests of hemostasis in acutely-ill
liver patients may indicate a hypocoagulable state (decreased platelet count, prolongations
in prothrombin time and activated partial thromboplastin time, decreased fibrinogen
levels) due to decreased synthetic liver capacity or consumption, or a hypercoagulable
state (increased VWF levels, hypofibrinolysis in global tests). Whether these changes
are clinically relevant and should be corrected with antithrombotic drugs or blood
products is incompletely understood. Inflammation and activation of coagulation may
cause local ischemia, progression of liver disease, and multiorgan failure. Anti-inflammatory
treatment in acutely-ill liver patients may be of potential interest to prevent thrombotic
or bleeding complications and halt progression of liver disease.
Keywords
hemostasis - coagulation - inflammation - acute-on-chronic liver failure - acute liver
failure
