Published online May 7, 2020. doi: 10.3748/wjg.v26.i17.2097
Peer-review started: February 11, 2020
First decision: February 27, 2020
Revised: March 26, 2020
Accepted: April 24, 2020
Article in press: April 24, 2020
Published online: May 7, 2020
Hemostasis of patients suffering from liver cirrhosis is challenging due to both, pro- and anticoagulatory disorders leading to hemostatic alterations with distinct abnormalities of coagulation. Pathological changes in conventional coagulation analysis and platelet count are common manifestations of decreased liver synthesis of coagulation factors and reduced platelet count in these patients. However, conventional coagulation analysis and platelet count do not reflect in-vivo coagulation status or platelet function. The purpose of this present observational study was therefore to assess the haemostatic profile including plasmatic coagulation using thrombelastometry and impedance aggregometry for platelet function in patients suffering from liver cirrhosis.
To assess the hemostatic profile of cirrhotic patients according to model for end-stage liver disease (MELD) score.
Our study included both in- and outpatients suffering from liver cirrhosis attending the out- and inpatient care of the department of hepatology. Demographic and biochemical data as well as medical history including cause of liver cirrhosis, end stage kidney failure and medication with anticoagulants were recorded. To assess the hemostatic profile, platelet function was analyzed by multiple electrode aggregometry (MEA) using Multiplate® (ADP-, ASPI- and TRAP-test) and thrombelastometry using ROTEM® (EXTEM, INTEM, FIBTEM). Data were compared using Mann-Whitney U- or χ2-test. Spearman correlation was performed to analyze the association between MELD Score and results of thrombelastometry and MEA.
A total of 68 patients attending the out- and inpatient care suffering from liver cirrhosis were screened. Of these, 50 patients were included and assigned to groups according to MELD score 6 to 11 (n = 25) or ≥ 17 (n = 25). Baseline patient characteristics revealed significant differences for MELD score (8 vs 22, P < 0.0001) and underlying laboratory parameters (international normalized ratio, bilirubine, creatinine) as well as fibrinogen level (275 mg/dL vs 209 mg/dL, P = 0.006) and aPTT (30 s vs 35 s, P = 0.047). MEA showed a moderately impaired platelet function (medians: AUCADP = 43U, AUCASPI = 71U, AUCTRAP = 92U) but no significant differences between both groups. Thrombelastometry using ROTEM® (EXTEM, INTEM, FIBTEM) revealed values within normal range in both groups. No significant correlation was observed between MELD score and results of MEA/thrombelastometry.
Our data demonstrate a partially impaired hemostatic profile in liver cirrhosis patients unrelated to MELD score. An individual assessment of a potential coagulopathy should therefore be considered.
Core tip: The results of our study show a moderately decreased platelet aggregation but no substantial impairment of the maximum clot firmness considering thrombelastometric results. Correlation analysis indicated that impedance aggregometric and thrombelastometric results did not correlate with model for end-stage liver disease score. Our data indicate that a potential coagulopathy in advanced liver cirrhosis may not be reflected by thrombelastometry or multiple electrode aggregometry as the underlying mechanisms may be beyond the platelet function of hemostasis. Rather, an individual assessment of a potential coagulopathy in patients with advanced disease is reasonable.