Treatment of bleeding in patients with liver disease

Abstract

Patients with cirrhosis frequently have complex alterations in their hemostatic system. Although routine diagnostic tests of hemostasis in cirrhosis (platelet count, prothrombin time, fibrinogen level) are suggestive of a bleeding tendency, it is now widely accepted that these tests do not reflect hemostatic competence in this population. Rather, patients with cirrhosis appear to have a rebalanced hemostatic system with hypercoagulable elements. Therefore, routine correction of hemostasis laboratory values, for example by fresh frozen plasma or platelet concentrates, with the aim to avoid spontaneous or procedure‐related bleeding is not indicated as is outlined in recent clinical guidance documents. However, little guidance on how to manage patients with cirrhosis that are actively bleeding is available. Here we present three common bleeding scenarios, variceal bleeding, post‐procedural bleeding and bleeding in a critically ill cirrhosis patient, with specific management suggestions. As patients with cirrhosis generally have adequate hemostatic competence and as bleeding complications may be unrelated to hemostatic failure, prohemostatic therapy is not the first line of management in bleeding patients with cirrhosis, even in the presence of markedly abnormal platelet counts and/or prothrombin times. We provide a rationale for the restrictive approach to prohemostatic therapy in bleeding patients with cirrhosis.

Haemostatic alterations and management of haemostasis in patients with cirrhosis

“…It has been proposed that prohaemostatic therapy is not a first-line therapeutic strategy in many common bleeding scenarios in patients with cirrhosis as these bleeds can be better managed by other strategies depending on the circumstances. 17 The haemostatic status of critically ill patients with cirrhosis Historically, cirrhosis was classified as an acquired bleeding disorder. The combination of abnormal conventional laboratory parameters (thrombocytopenia, prolonged INR) and pervasive clinical bleeding fuelled the notion that the haemostatic changes in cirrhosis were responsible for bleeding.…”

“…In patients with continuous oozing in whom local measures fail to stop the bleeding, addressing contributing factors (renal failure, infection or sepsis, and anaemia) may reduce bleeding while correction of haemostatic abnormalities can be considered on a case-by-case basis. 17 Thus, pro-haemostatic therapy is not always a first-line treatment for active bleeding. Best practices for those cases in which pro-haemostatic therapy is deemed necessary are unknown.…”

Consensus Statement on Hemostatic Management, Anticoagulation, and Antiplatelet Therapy in Liver Transplantation

“…(5.1) Whole blood transfusion should aim to maintain hemoglobin around 8 g/dL. Platelets should be maintained at >50 000/µL and serum fibrinogen >1.3 g/L 90 , 91 (Recommendation 1B).…”

Haemostatic alterations in patients with cirrhosis and hepatocellular carcinoma: laboratory evidence and clinical implications

“…Current theory posits that these alterations lead to a rebalanced haemostatic equilibrium that may easily tilt towards either hypercoagulability (increased thrombotic risk) or hypocoagulability (increased bleeding risk) 18,19 …”

“…17 Current theory posits that these alterations lead to a rebalanced haemostatic equilibrium that may easily tilt towards either hypercoagulability (increased thrombotic risk) or hypocoagulability (increased bleeding risk). 18,19 It is not yet fully understood whether and how HCC destabilizes the rebalanced haemostatic state in patients with cirrhosis. 20 However, there is growing evidence that patients with cirrhosis and HCC present a more hypercoagulable phenotype than controls with cirrhosis without HCC.…”