Enhanced fibrinolysis detection in a natural occurring canine model with intracavitary effusions: Comparison and degree of agreement between thromboelastometry and FDPs, D-dimer and fibrinogen concentrations
Autoři:
Andrea Zoia aff001; Michele Drigo aff002; Christine J. Piek aff003; Helena Calcini aff001; Marco Caldin aff004; Paolo Simioni aff005
Působiště autorů:
Division of Internal Medicine, San Marco Veterinary Clinic, Padua, Italy
aff001; Department of Medicina Animale, Produzione e Salute, Padua University, Legnaro, Italy
aff002; Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands
aff003; Division of Clinical Pathology, Laboratorio d’Analisi Veterinarie San Marco, Padua, Italy
aff004; Department of Cardiologic, Thoracic and Vascular Sciences, University of Padua Medical School, Padua, Italy
aff005
Vyšlo v časopise:
PLoS ONE 14(11)
Kategorie:
Research Article
doi:
https://doi.org/10.1371/journal.pone.0225089
Souhrn
Dogs with intracavitary effusion have coagulative abnormalities indicative of primary fibrinolysis/hyperfibrinolysis. The aim of this case control study was to investigate by rotational thromboelastometry (ROTEM) and standard coagulation tests (fibrin-fibrinogen degradation products, D-dimer and fibrinogen) fibrinolysis in dogs with intracavitary effusions. Thirty-two dogs with intracavitary effusion and 32 control sick dogs without effusion were studied. Frequency of fibrinolysis grade of severity (i.e., hypofibrinolysis/basal fibrinolysis vs increased fibrinolysis vs hyperfibrinolysis) by ROTEM and standard coagulation tests were compared between groups. Pattern of fibrinolysis by ROTEM (i.e., late vs intermediate vs fulminant) and type of fibrinolysis by standard coagulation tests (i.e., hypofibrinolysis/basal fibrinolysis vs primary fibrinolysis vs secondary fibrinolysis vs primary hyperfibrinolysis vs secondary hyperfibrinolysis) were also compared between groups. Dogs with intracavitary effusion had a lesser degree of hypofibrinolysis and basal fibrinolysis and a higher degree of increased fibrinolysis and hyperfibrinolysis compared to controls, both by ROTEM and by standard coagulation tests (P = 0.042 and P = 0.017, respectively). Nevertheless, there was a poor agreement between the two classification schemes (34.4%, K = 0.06, 95% CI = -0.14 ‒ +0.26). Dogs with intracavitary effusion showed, by ROTEM, a lesser degree of hypofibrinolysis and basal fibrinolysis and a higher degree of late, intermediate, and fulminant fibrinolysis compared to controls (P = 0.044). Finally, dogs with intracavitary effusion had, by standard coagulation tests, a higher frequency of primary fibrinolysis and primary hyperfibrinolysis and a lower frequency of secondary fibrinolysis compared to controls. Dogs with intracavitary effusion showed an increased frequency and a different and more severe pattern of fibrinolysis compared to controls.
Klíčová slova:
Blood – Blood plasma – Dogs – Fibrinogen – Fibrinolysis – Plasmins – Veterinary diagnostics
Zdroje
1. Carey M, Cressey DM. Hyperfibrinolysis—is it common? Measurement and treatment including the role of thromboelastography. Clin Risk. 2009; 15: 188–191.
2. Rodgers MG. Acquired coagulation disorders. In: Greer JP, Arber DA, Glader B, List AF, Means RT Jr., Paraskevas F RG, editor. Wintrobe’s Clinical Hematology. 13th ed. Lippincott Williams and Wilkins, WoltersKluwer Health; 2014. p. 1186–1217.
3. Hunt BJ, Segal H. Hyperfibrinolysis. J Clin Pathol. 1996; 49: 958. doi: 10.1136/jcp.49.12.958 9038728
4. Mazzi G, Raineri A, Lacava E, De Roia D, Santarossa L, Orazi BM. Primary hyperfibrinogenolysis in a patient with anaphylactic shock. Haematologica. 1994; 79: 283–285. 7926982
5. Sallah S, Gagnon GA. Reversion of primary hyperfibrinogenolysis in patients with hormone-refractory prostate cancer using docetaxel. Cancer Invest. 2000; 18: 191–196. doi: 10.3109/07357900009031823 10754987
6. Wyseure T, Declerck PJ. Novel or expanding current targets in fibrinolysis. Drug Discov Today. 2014; 19: 1476–1482. doi: 10.1016/j.drudis.2014.05.025 24886765
7. Levi M, Keller TT, van Gorp E, ten Cate H. Infection and inflammation and the coagulation system. Cardiovasc Res. 2003; 60: 26–39. doi: 10.1016/s0008-6363(02)00857-x 14522404
8. Spiel AO, Maayr FB, Firbas C, Quehenberger P, Jilma B. Validation of rotation thrombelastography in a model of systemic activation of fibrinolysis and coagulation in humans. J Thromb Haemost. 2006; 4: 411–416. doi: 10.1111/j.1538-7836.2006.01715.x 16420574
9. Sato N, Takahashi H, Shibata A. Fibrinogen/fibrin degradation products and D-dimer in clinical practice: interpretation of discrepant results. Am J Hematol. 1995; 48: 168–174. doi: 10.1002/ajh.2830480306 7864025
10. Song KS, Kim YA, Kim HK, Park Q. Incidence and possible reasons for discordant results between positive FDP and negative D-dimer latex assays in clinical specimens. Yonsei Med J. 1999; 40: 107–111. doi: 10.3349/ymj.1999.40.2.107 10333712
11. Zoia A, Augusto M, Drigo M, Caldin M. Evaluation of hemostatic and fibrinolytic markers in dogs with ascites attributable to right-sided congestive heart failure. J Am Vet Med Assoc. 2012; 241: 1336–1343. doi: 10.2460/javma.241.10.1336 23113526
12. Zoia A, Drigo M, Simioni P, Caldin M, Piek CJ. Association between ascites and primary hyperfibrinolysis: A cohort study in 210 dogs. Vet J. 2017; 223: 12–20. doi: 10.1016/j.tvjl.2017.03.008 28671065
13. Zoia A, Drigo M, Piek CJ, Simioni P, Caldin M. Hemostatic findings of pleural fluid in dogs and the association between pleural effusions and primary hyperfibrino(geno)lysis: A cohort study of 99 dogs. PLoS One. 2018; 13: 1–19.
14. Agarwal S, Joyner KA, Swaim MW. Ascites fluid as a possible origin for hyperfibrinolysis in advanced liver disease. Am J Gastroenterol. 2000; 95: 3218–3224. doi: 10.1111/j.1572-0241.2000.03299.x 11095345
15. Diab SM, Fathy EM, Soliman HH, Zaghloul SG. Original Article Hyperfibrinolysis in Advanced Liver Disease: Does Ascites Have a Role? Arab J Gastroenterol. 2005; 6: 124–130.
16. Denny GP, Minot GR. The coagulation of blood in the pleural cavity. Am J Physiol. 1916;39:455–458.
17. Widström O, Kockum C, Nilsson BS. Fibrinogen, fibrin(ogen) degradation products and fibrinopeptide A in pleural effusions. High turnover of fibrinogen in pleurisy. Scand J Respir Dis. 1978;59:210–215. 694476
18. Napoli VM, Symbas PJ, Vroon DH, Symbas PN. Autotransfusion from experimental hemothorax: levels of coagulation factors. J Trauma. 1987;27:296–300. 3560271
19. Delgado MA, Monreal L, Armengou L, Ríos J, Segura D. Peritoneal D-dimer concentration for assessing peritoneal fibrinolytic activity in horses with colic. J Vet Intern Med. 2009;23:882–889. doi: 10.1111/j.1939-1676.2009.0344.x 19566853
20. Broadie TA, Glover JL, Bang N, Bendick PJ, Lowe DK, Yaw PB, et al. Clotting competence of intracavitary blood in trauma victims. Ann Emerg Med. 1981;10:127–130. doi: 10.1016/s0196-0644(81)80375-7 7469150
21. Schved JF, Gris JC, Gilly D, Joubert P, Eledjam JJ, D’Athis F. [Fibrinolytic activity in traumatic hemothorax fluids]. Ann Fr Anesth Rèanim. 1991;10:104–107. doi: 10.1016/s0750-7658(05)80449-6 1711800
22. van der Wal JBC, Jeekel J. Biology of the peritoneum in normal homeostasis and after surgical trauma. Colorectal Dis. 2007;9 Suppl 2:9–13.
23. Lévy VG, Opolon P, Pauleau N, Caroli J. Treatment of ascites by reinfusion of concentrated peritoneal fluid—review of 318 procedures in 210 patients. Postgrad Med J. 1975;51:564–566. doi: 10.1136/pgmj.51.598.564 1234342
24. Greig PD, Langer B, Blendis LM, Taylor BR, Glynn MF. Complications after peritoneovenous shunting for ascites. Am J Surg. 1980;139:125–131. doi: 10.1016/0002-9610(80)90241-x 7350836
25. Patrassi GM, Martinelli S, Sturniolo GC, Cappellato MG, Vicariotto M, Girolami A. Fibrinolytic study in plasma and ascitic fluid of cirrhotic patients before and after ascites concentration; reinfusion technique. Eur J Clin Invest. 1985;15:161–165. doi: 10.1111/j.1365-2362.1985.tb00162.x 2412833
26. Schölmerich J, Zimmermann U, Köttgen E, Volk BA, Hasler C, Wilms H, et al. Proteases and antiproteases related to the coagulation system in plasma and ascites. Prediction of coagulation disorder in ascites retransfusion. J Hepatol. 1988;6:359–363. doi: 10.1016/s0168-8278(88)80054-0 2455746
27. Scottcoombes DM, Whawell SA, Vipond MN, Crnojevic L, Thompson JN. Fibrinolytic-Activity of Ascites Caused by Alcoholic Cirrhosis and Peritoneal Malignancy. Gut. 1993;34:1120–1122. doi: 10.1136/gut.34.8.1120 8174965
28. Görlinger K, Iqbal J, Dirkmann D, Tanaka KA. Whole Blood Assay: Thromboelastometry. In: Management of Bleeding Patients. 2016. p. 37–64.
29. Dirkmann D, Görlinger K, Peters J. Assessment of early thromboelastometric variables from extrinsically activated assays with and without aprotinin for rapid detection of fibrinolysis. Anesth Analg. 2014; 119: 533–542. doi: 10.1213/ANE.0000000000000333 24977914
30. Stokol T, Brooks M, Erb H, Mauldin GE. Evaluation of kits for the detection of fibrin(ogen) degradation products in dogs. J Vet Intern Med. 1999; 13: 478–484. doi: 10.1892/0891-6640(1999)013<0478:eokftd>2.3.co;2 10499733
31. Caldin M, Furlanello T, Lubas G. Sensitivity and specificity of citrated plasma FDPs and D-dimer in the diagnosis of disseminated intravascular coagulation (DIC) in dog: Preliminary findings. In: Proceedings of the Annual Meeting of the American College of Veterinary Internal Medicine, San Diego, USA. San Diego; 1998. p. 726.
32. Caldin M, Furlanello T, Lubas G. Validation of an immunoturbidimetric D-dimer assay in canine citrated plasma. Vet Clin Pathol. 2000; 29: 51–54. doi: 10.1111/j.1939-165x.2000.tb00398.x 12070811
33. Schochl H, Frietsch T, Pavelka M, Jambor C. Hyperfibrinolysis after major trauma: differential diagnosis of lysis patterns and prognostic value of thrombelastometry. J Trauma. 2009; 67: 125–131. doi: 10.1097/TA.0b013e31818b2483 19590321
34. Brohi K, Cohen MJ, Ganter MT, Schultz MJ, Levi M, Mackersie RC, et al. Acute Coagulopathy of Trauma: Hypoperfusion Induces Systemic Anticoagulation and Hyperfibrinolysis. J Trauma Inj Infect Crit Care. 2008; 64: 1211–1217.
35. Fletcher DJ, Rozanski EA, Brainard BM, Laforcade AM De, Brooks MB. Assessment of the relationships among coagulopathy, hyperfibrinolysis, plasma lactate, and protein C in dogs with spontaneous hemoperitoneum. J Vet Emerg Crit Care. 2016;26:41–51.
36. Song JG, Jeong SM, Jun IG, Lee HM, Hwang GS. Five-minute parameter of thromboelastometry is sufficient to detect thrombocytopenia and hypofibrinogenaemia in patients undergoing liver transplantation. Br J Anaesth. 2014; 112: 290–297. doi: 10.1093/bja/aet325 24065728
37. Chapman MP, Moore EE, Ramos CR, Harr JN, Chin TL, John R, et al. Fibrinolysis greater than 3% is the critical value for initiation of antifibrinolytic therapy Michael. J Trauma Acute Care Surg. 2014; 75: 961–967.
38. Kashuk JL, Moore EE, Sawyer M, Wohlauer M, Pezold M, Barnett C, et al. Primary fibrinolysis is integral in the pathogenesis of the acute coagulopathy of Trauma. Ann Surg. 2010; 252: 434–442. doi: 10.1097/SLA.0b013e3181f09191 20739843
39. Moore H, Moore E, Gonzalez E, Chapman M, Chin T, Silliman C, et al. Hyperfibrinolysis, physiologic fibrinolysis, and fibrinolysis shutdown: The spectrum of postinjury fibrinolysis and relevance to antifibrinolytic therapy. J Trauma Acute Care Surg. 2015; 77: 811–817.
40. Cap A, Hunt B. Acute traumatic coagulopathy. Curr Opin Crit Care. 2014; 20: 638–645. doi: 10.1097/MCC.0000000000000158 25340382
41. Levrat A, Gros A, Rugeri L, Inaba K, Floccard B, Negrier C, et al. Evaluation of rotation thrombelastography for the diagnosis of hyperfibrinolysis in trauma patients. Br J Anaesth. 2008; 100: 792–797. doi: 10.1093/bja/aen083 18440953
42. Carroll RC, Craft RM, Langdon RJ, Clanton CR, Snider CC, Wellons DD, et al. Early evaluation of acute traumatic coagulopathy by thrombelastography. Transl Res. 2009; 154: 34–39. doi: 10.1016/j.trsl.2009.04.001 19524872
43. Tauber H, Innerhofer P, Breitkopf R, Westermann I, Beer R, El Attal R, et al. Prevalence and impact of abnormal ROTEM® assays in severe blunt trauma: Results of the “Diagnosis and Treatment of Trauma-Induced Coagulopathy (DIA-TRE-TIC) study.” Br J Anaesth. 2011; 107: 378–387. doi: 10.1093/bja/aer158 21705350
44. Ostrowski S, Sørensen A, Larsen C, Johansson P. Thrombelastography and biomarker profiles in acute coagulopathy of trauma: A prospective study. Scand J trauma, resusciataion, Emerg medicne. 2011; 19: 1–10.
45. Peyvandi F, Haertel S, Knaub S, Mannucci PM. Incidence of bleeding symptoms in 100 patients with inherited afibrinogenemia or hypofibrinogenemia. J Thromb Haemost. 2006; 4: 1634–1637. doi: 10.1111/j.1538-7836.2006.02014.x 16839371
46. Cade JF, Robinson TF. Coagulation and Fibrinolysis in the Dog. Can j comp med. 1975; 39: 296–298. 1139411
47. Theusinger OM, Wanner GA, Emmert MY, Billeter A, Eismon J, Seifert B, et al. Hyperfibrinolysis diagnosed by rotational thromboelastometry (ROTEM) is associated with higher mortality in patients with severe trauma. Anesth Analg. 2011; 113: 1003–1012. doi: 10.1213/ANE.0b013e31822e183f 21918164
48. Koami H, Sakamoto Y, Furukawa T, Imahase H, Iwamura T, Inoue S. Utility of rotational thromboelastometry for the diagnosis of asymptomatic hyperfibrinolysis secondary to anaphylaxis. Blood Coagul Fibrinolysis. 2016; 27: 450–453. doi: 10.1097/MBC.0000000000000441 26569513
49. Lombardini C, Helia RE, Boehlen F, Merlani P. “Heparinization” and hyperfibrinogenolysis by wasp sting. Am J Emerg Med. 2009; 27: 1176.e1–1176.e3.
50. Hess JR, Brohi K, Dutton RP, Hauser CJ, Holcomb JB, Kluger Y, et al. The coagulopathy of trauma: A review of mechanisms. J Trauma—Inj Infect Crit Care. 2008; 65: 748–754.
51. Lisman T. Decreased Fibrinolytic Capacity in Cirrhosis and Liver Transplantation Outcomes. Liver Transplant. 2019; 25: 359–361.
52. Kushimoto S, Gando S, Saitoh D, Ogura H, Mayumi T, Koseki K, et al. Clinical course and outcome of disseminated intravascular coagulation diagnosed by Japanese Association for Acute Medicine criteria. Comparison between sepsis and trauma. Thromb Haemost. 2008; 100:1099–1105. 19132236
53. Chandler W. Hyperfibrinolysis. In: Management of Bleeding Patients. 2016. p. 31–36.
54. Raza I, Davenport R, Rourke C, Platton S, Manson J, Spoors C, et al. The incidence and magnitude of fibrinolytic activation in trauma patients. J Thromb Haemost. 2013; 11: 307–314. doi: 10.1111/jth.12078 23176206
55. Kapsch DN, Metzler M, Harrington M, Mitchell FL, Silver D. Fibrinolytic response to trauma. Surgery. 1984; 95: 473–478. 6710342
56. Smith AA, Jacobson LJ, Miller BI, Hathaway WE, Manco-Johnson MJ. A new euglobulin clot lysis assay for global fibrinolysis. Thromb Res. 2003; 112: 329–337. doi: 10.1016/j.thromres.2004.01.001 15041279
57. Gall LS, Brohi K, Davenport RA. Diagnosis and Treatment of Hyperfibrinolysis in Trauma (A European Perspective). Semin Thromb Hemost. 2017; 43: 224–234. doi: 10.1055/s-0036-1598001 28219084
58. Caron P, Bennet A, Camare R, Louvet JP, Boneu B, Sié P. Plasminogen activator inhibitor in plasma is related to testosterone in men. Metabolism. 1989; 38: 1010–1015. doi: 10.1016/0026-0495(89)90014-0 2507874
59. Schöchl H, Maegele M, Solomon C, Görlinger K, Voelckel W. Early and individualized goal-directed therapy for trauma-induced coagulopathy. Scand J Trauma Resusc Emerg Med. 2012; 20: 1–11. doi: 10.1186/1757-7241-20-1
60. Vorweg M, Hartmann B, Knüttgen D, Jahn MC, Doehn M. Management of fulminant fibrinolysis during abdominal aortic surgery. J Cardiothorac Vasc Anesth. 2001; 15: 764–767. doi: 10.1053/jcan.2001.28337 11748531
61. Kozek-Langenecker SA. Perioperative coagulation monitoring. Best Pract Res Clin Anaesthesiol. 2010; 24: 27–40. 20402168
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PLOS One
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