The evolving knowledge on primary hemostasis in patients with cirrhosis: A comprehensive review

Abstract

Patients with cirrhosis develop complex alterations in primary hemostasis that include both hypocoagulable and hypercoagulable features. This includes thrombocytopenia, multiple alterations of platelet function, and increased plasma levels of von Willebrand factor. Contrary to the historical view that platelet dysfunction in cirrhosis might be responsible for an increased bleeding tendency, the current theory posits a rebalanced hemostasis in patients with cirrhosis. Severe thrombocytopenia is not indicative of the bleeding risk in patients undergoing invasive procedures and does not dictate per se the need for pre-procedural prophylaxis. A more comprehensive and individualized risk assessment should combine hemostatic impairment, the severity of decompensation and systemic inflammation, and the presence of additional factors that may impair platelet function, such as acute kidney injury and bacterial infections. Although there are multiple, complex alterations of platelet function in cirrhosis, their net effect is not yet fully understood. More investigations evaluating the association between alterations of platelet function and bleeding/thrombosis may improve risk stratification in patients with decompensated cirrhosis. Besides hemostasis, the assessment of von Willebrand factor Ag and ADP-induced, whole-blood platelet aggregation normalized by platelet count (VITRO score and PLT ratio) are promising biomarkers to predict the risk of hepatic decompensation and survival in both compensated and decompensated patients. Further investigations into the in vivo interplay between platelets, circulating blood elements, and endothelial cells may help advance our understanding of cirrhotic coagulopathy. Here, we review the complex changes in platelets and primary hemostasis in cirrhosis and their potential clinical implications.

A combination of clot formation abnormalities in thromboelastometry has a high prognostic value in patients with acute-on-chronic liver failure

“…A complete hemostatic evaluation including thrombin generation test with and without thrombomodulin was not performed [38]. Moreover, vWf antigen to PLT ratio (VITRO) or the ratio between platelet aggregation and platelet count (PLT ratio), which are promising platelet dysfunction biomarkers to predict progression of liver disease or survival [39,40] have not been evaluated.…”

Toward a more precise prognostic stratification in acute decompensation of cirrhosis: The Padua model 2.0

“…Predicting the course of AD, and particularly the development of ACLF, is challenging 3 . Given the recent advances in disease‐modifying therapies of decompensated cirrhosis, refinements in risk stratification are increasingly important 23 . Furthermore, since progression to ACLF typically occurs early after AD, 3 early evaluation for liver transplantation may be indicated in selected patients at higher risk of progression.…”

Predicting de‐novo portal vein thrombosis after HCV eradication: A long‐term competing risk analysis in the ongoing PITER cohort

“…37 Patients with more advanced liver disease in whom SVR seems not to be associated with a significant reversal of coagulopathy 13 would remain at risk of thrombosis. However, whether coagulopathy in patients with cirrhosis is implicated in the pathophysiology of PVT independently of the reduced portal vein blood flow is still under investigation, 38,39 and further studies are required to elucidate the effect of SVR on Virchow's triad in HCV cirrhosis. 4,40,41 Our study had several limitations.…”