Only in the last few years the medical world has changed views on hemoragic and thrombotic risk assessment in patients with liver cirrhosis. A more accurate understanding of the mechanisms disturbance of hemostasis, coagulation and fibrinolysis, leads to a better management of these patients, that is desirable to be reflected as a decrease in bleeding episodes and the prevention of thrombotic events. In this minireview we intend to present an update of knowledge on the pathophysiology of coagulation and fibrinolysis in liver cirrhosis, the ways of exploring them, their prophylactic and therapeutic consequences. We made a review based on publication in PubMed from 1995 up to now. If in the past the main concern of clinicians on the mentioned issues was the avoidance of haemorrhage, today we know that neither the procoagulant status that cirrhotic patients have, should not be underestimated, as they are prone to thrombosis rather than to hemorrhage and the thrombosis risk is increasing if cirrhosis progresses. Primarily responsible for the prothrombotic status are: decreased anticoagulant factors (antithrombin III, protein C, and protein S), increased levels of factor VIII, elevated levels of von Willebrand factor, the possible presence of thrombophilia. To these it is also added the partial resistance to the action of thrombomodulin, observed in vitro. Tests that explore the intrinsic and the extrinsic pathway of coagulation do not provide information on anticoagulant factors activity. Therefore, it is recommended to study the thrombin generation, which provides a more accurate picture of the coagulation balance, taking into account procoagulant and anticoagulant factors. The dosage level of thrombin generation is easy to realize in practice, either from platelet poor plasma or from platelet-rich plasma, and the result are standardized. Reducing thrombin generation could help reduce the thrombotic events and the rate of liver fibrosis progression.