Essentials
Liver diseases are associated with profound
hemostatic changes proportional to severity of illness.
Hemostatic changes in
acute-on-chronic liver failure (ACLF) may in part reflect
critical illness.
Hemostatic changes in ACLF partly overlap with those in
sepsis, with rebalanced hemostasis in both. Patients with
sepsis had hyperfibrinogenemia, associated with a thrombogenic clot structure. ABSTRACT: Background Even the sickest patients with chronic
liver disease (CLD), such as those with
acute-on-chronic liver failure (ACLF) remain in
hemostatic balance due to a concomitant decline in pro- and antihemostatic factors. Objectives We aimed to study whether the
hemostatic status in ACLF is merely an exaggeration from the status in patients with compensated and acutely decompensated
cirrhosis, or whether
sepsis-associated
hemostatic changes contribute. Methods We performed extensive
hemostatic profiling in 31 adult patients with ACLF, 20 patients with
sepsis without underlying CLD, and 40 healthy controls. Results We found similarly elevated plasma levels of the platelet adhesive
protein von Willebrand factor (VWF) and decreased levels of the VWF-regulating
protease ADAMTS13 in both groups compared to healthy controls. In vivo markers of activation of coagulation (
thrombin-
antithrombin III,
D-dimer) were similarly elevated in both groups compared to controls, but ex vivo
thrombin-generating capacity was similar between patients and controls, despite a much more profound international normalized ratio elevation in ACLF. Plasma
fibrinogen levels were much higher in septics, which was accompanied by a decreased ex vivo clot permeability and an increase in ex vivo resistance to clot lysis. All
hemostatic parameters were remarkably stable over the first 10 days after admission. Conclusions We have found
hemostatic changes in ACLF to partially overlap with that of patients with
sepsis, and evidence of preserved
hemostatic capacity in both patient groups. The notable difference was a profound hyperfibrinogenemia, associated with a thrombogenic clot structure and a marked ex vivo resistance to fibrinolysis in patients with
sepsis.