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Thromboelastography used to assess coagulation during treatment with molecular adsorbent recirculating system
Author(s) -
Doria Cataldo,
Mandalà Lucio,
Smith Jan D,
Caruana Giuseppe,
Scott Victor L,
Gruttadauria Salvatore,
Mag Mario,
Marino Ignazio R
Publication year - 2004
Publication title -
clinical transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 76
eISSN - 1399-0012
pISSN - 0902-0063
DOI - 10.1111/j.1399-0012.2004.00172.x
Subject(s) - medicine , thromboelastography , antithrombin , gastroenterology , coagulopathy , coagulation , platelet , fibrinogen , von willebrand factor , immunology , surgery , heparin
Coagulopathy is a life‐threatening complication of liver cirrhosis. We describe the effect of molecular adsorbent recirculating system (MARS), a cell‐free dialysis technique, on the blood coagulation of cirrhotic patients. From February 2002 to July 2002, nine patients – five males (55.5%) and four females (44.4%), age 47–70 yr (median 56) – underwent 12 courses (4–7 sessions each) of MARS. Patients were treated for the following indications: six (66.6%) acute‐on‐chronic hepatic failure, three (33.3%) intractable pruritus. Platelet count, prothrombin time (PT), international standardized ratio and thromboelastography were measured before and after each MARS session. Coagulation factors II, V, VII, VIII, IX, X, XI, XII, XIII, von Willebrand, lupus anticoagulant, protein C, protein S, antithrombin III, plasminogen, α 2 antiplasmin, d ‐dimer, fibrin monomers, complement, and C 1 inactivator were measured before and at the end of each MARS treatment. We found a statistically significant difference (p < 0.05) in the platelet count, PT, all the thromboelastograph variables (reaction and constant time, α angle, and maximal amplitude), factor VIII, von Willebrand, and d ‐dimer, when measured before and after MARS. Previous reports have shown amelioration of blood coagulation following MARS treatments. However, we document that MARS induces coagulopathy through a platelet‐mediated mechanism, whereby platelet may be mechanically destroyed during the passage of blood through the filters and lines. An alternative postulated mechanism is an immune‐mediated platelet disruption – coagulopathy.