Primary Hemostasis in Chronic Liver Disease and Cirrhosis: What Did We Learn over the Past Decade?

Abstract

Changes in primary hemostasis have been described in patients with chronic liver disease (CLD) and cirrhosis and are still subject to ongoing debate. Thrombocytopenia is common and multifactorial. Numerous studies also reported platelet dysfunction. In spite of these changes, primary hemostasis seems to be balanced. Patients with CLD and cirrhosis can suffer from both hemorrhagic and thrombotic complications. Variceal bleeding is the major hemorrhagic complication and is mainly determined by high portal pressure. Non portal hypertension-related bleeding due to hemostatic failure is uncommon. Thrombocytopenia can complicate management of invasive procedures in CLD patients. Recently, oral thrombopoietin agonists have been approved to raise platelets before invasive procedures. In this review we aim to bundle literature, published over the past decade, discussing primary hemostasis in CLD and cirrhosis including (1) platelet count and the role of thrombopoietin (TPO) agonists, (2) platelet function tests and markers of platelet activation, (3) von Willebrand factor and (4) global hemostasis tests.

Assessing the periprocedural magnitude of platelet count change in response to lusutrombopag

“…6,27 As discussed earlier, multiple factors, including potentially reduced thrombin production when platelet counts are <50 × 10 9 /L, 4 contribute to the possibility of increased bleeding risk in CLD patients. [1][2][3] Studies have identified that the risk of procedure-related bleeding is increased when platelet counts fall below approximately 60 to 75 × 10 9 /L, with the highest risk of bleeding occurring when the platelet count is <10 to 20 × 10 9 /L. [28][29][30] In general, CLD patients with platelet counts < − 50 × 10 9 /L are considered to be at high risk for procedurerelated bleeding.…”

“…Patients with thrombocytopaenia associated with chronic liver disease (TCP-CLD) are at risk for both thrombotic and haemorrhagic complications given the complex, altered balance between thrombosis and bleeding in this patient population. [1][2][3] TCP is a reflection of the severity of CLD and contributes to the potential increased risk of bleeding in CLD patients in conjunction with the interplay between multiple elements in the haemostatic system such as platelet dysfunction, anti-platelet antibodies, platelet sequestration and destruction related to hypersplenism, myelosuppression, and alterations in haematopoietic and coagulation factors. [1][2][3] For example, the risk of bleeding in CLD may be affected by decreased thrombin production when platelet counts fall below approximately 50 × 10 9 /L, 4 yet this is countered by an increase in von Willebrand factor.…”

“…[1][2][3] TCP is a reflection of the severity of CLD and contributes to the potential increased risk of bleeding in CLD patients in conjunction with the interplay between multiple elements in the haemostatic system such as platelet dysfunction, anti-platelet antibodies, platelet sequestration and destruction related to hypersplenism, myelosuppression, and alterations in haematopoietic and coagulation factors. [1][2][3] For example, the risk of bleeding in CLD may be affected by decreased thrombin production when platelet counts fall below approximately 50 × 10 9 /L, 4 yet this is countered by an increase in von Willebrand factor. 1,2 Notwithstanding, TCP influences clinical decisions in CLD patients, in particular when weighing the risks vs. benefits of certain diagnostic or therapeutic interventions.…”

“…[1][2][3] For example, the risk of bleeding in CLD may be affected by decreased thrombin production when platelet counts fall below approximately 50 × 10 9 /L, 4 yet this is countered by an increase in von Willebrand factor. 1,2 Notwithstanding, TCP influences clinical decisions in CLD patients, in particular when weighing the risks vs. benefits of certain diagnostic or therapeutic interventions. [1][2][3] Most clinicians and society guidelines recommend that a patient has a platelet count > − 50 × 10 9 /L before an invasive procedure.…”

“…1,2 Notwithstanding, TCP influences clinical decisions in CLD patients, in particular when weighing the risks vs. benefits of certain diagnostic or therapeutic interventions. [1][2][3] Most clinicians and society guidelines recommend that a patient has a platelet count > − 50 × 10 9 /L before an invasive procedure. [5][6][7][8][9][10][11] Platelet transfusion has been the standard of care to reduce the risk of bleeding in patients with TCP-CLD undergoing invasive procedures.…”