Reduced Clot Stability by Thromboelastography as a Potential Indicator of Procedure-Related Bleeding in Decompensated Cirrhosis

Abstract

In patients with decompensated cirrhosis, procedure-related bleeding is a potentially lethal complication. Routine coagulation tests such as international normalized ratio and platelet count do not predict bleeding risk. We investigated whether thromboelastography (TEG) can identify patients with cirrhosis who are at risk of procedure-related bleeding. As a part of a prospective study on hemostasis in decompensated cirrhosis, patients had TEG performed on admission and were followed prospectively during hospitalization for the development of procedure-related bleeding. Eighty patients with cirrhosis were included. Among the 72 who had procedures performed, 7 had procedure-related bleeding, which was major in three cases (two following paracentesis and one following thoracentesis). Conventional coagulation tests were comparable between bleeding and nonbleeding patients, whereas TEG parameters of k-time (4.5 minutes vs. 2.2 minutes; P = 0.02), α-angle (34° vs. 59°; P = 0.003), and maximum amplitude (37 mm vs. 50 mm; P = 0.004) were significantly different (all indicative of hypocoagulability). TEG maximum amplitude (MA), a marker of overall clot stability, accurately discriminated between patients who had major, life-threatening bleeding (all with MA < 30 mm) and those who had mild or no bleeding (all with MA > 30 mm), whereas a platelet count < 50 × 10⁹/L could not discriminate between bleeding (minor or major) and nonbleeding patients. Conclusion: In a prospective cohort of hospitalized patients with decompensated cirrhosis, TEG parameters associated with hypocoagulability appeared to predict procedure-related bleeding, particularly a TEG MA < 30 mm. If results are validated in a larger cohort, this could be a threshold to identify patients with decompensated cirrhosis at higher risk for procedure-related bleeding, in whom to consider preprocedural prophylaxis.

FIG. 1

Thromboelastography. (A) TEG measures the properties of clot formation using a small cup that holds the blood sample and slowly oscillates. A pin held by a thin torsion wire is suspended in the blood; as clot forms, it binds the cup and pin together. The torsion on the pin is measured and converted to an electrical signal. Clot strength is directly proportional to torsion on the pin. (B) Graphical presentation of the TEG hemostasis profile for clot formation and lysis, with MA reflecting overall clot stability.

FIG. 2

Flow chart of the study. None of the patients received platelet transfusion before baseline sample collection. Five patients received fresh frozen plasma (3 days before enrollment in 3 patients and 5 days before enrollment in 2 patients). Abbreviations: CKD, chronic kidney disease; ICU, intensive care unit; PVT, portal vein thrombosis; RRT, renal replacement therapy; VH, variceal hemorrhage; VTE, venous thromboembolism.

FIG. 3

TEG maximum amplitude accurately discriminates between patients who had major, life‐threatening bleeding and those who had minor or no bleeding. Overall clot stability, as assessed by TEG maximum amplitude, is significantly diminished (greater bleeding tendency) in patients with cirrhosis who had major bleeding (all with MA < 30 mm) compared to patients with cirrhosis with minor bleeding, patients with cirrhosis with no bleeding, and healthy controls (all with MA > 30). On the other hand, a platelet count < 50 × 10⁹/L (in red) could not discriminate between patients who had a procedure‐related bleeding (minor or major) and those who did not.