Clauss fibrinogen assay obviously underestimates fibrinogen level not confirmed in thromboelastometry – A case report

T. Lang1, M. Rieke1, M. Bachler2, B. Schenk2, M. Hermann2, M. Tollnick1, D. Fries2 (1Hohne, Germany, 2Innsbruck, Austria)

Laboratory tests
Date: 17.02.2017,
Time: 17:15 - 18:15

Objective: A case report is presented of presumingly false low fibrinogen value obtained with a commercial fibrinogen assay but not confirmed in Thrombelastometry.

Methods: A 44 year old male patient was scheduled for hip endoprothesis (hip-TEP). Because of a preoperative pathological quick value the patient was assigned to our haematological ambulance . Bleeding history was unconspicuous. Routine coagulation test were performed on ACL Top (Werfen) using RecombiPlasTin (Hemosil®, Werfen), SynthASil (Hemosil®) and Fibrinogen C (Hemosil®). One step assays were used for determination of coagulation factor activities (all deficient plasmas were purchased from Werfen (Hemosil®). Activity/antigen of factor XIII was determinated by a chromogenic/antigen assay. For mixing test normal control plasma (Hemosil®) was used and incubated with patient plasma (1:1) at 37O for 1 hour. Citrated whole blood was used for measurement for EXTEM and FIBTEM assays on ROTEM delta. start-tem and ex-tem reagents were used for EXTEM assay and ex-tem and fib-tem for FIBTEM assay.

Results: Quick 70% (75-120 %) and activated partial thromboplastin time 34 sec. (ref. range: 24-35 sec.), were borderline pathological. Fibrinogen according to Clauss 50 mg/dl (150-400 mg/dl) was pathological. Analysis of coagulation factors showed activities of 30 to 70 %, with exception of factor XIII: activity and antigen were clearly in normal range. Inhibiting antibodies were excluded by mixing Test, which increased fibrinogen to 170mg/dl (normal plasma: 334 mg/dl) and normalized Quick. However citrated whole blood of the patient revealed maximum clot firmness (MCF) of 16mm (12-23mm) for FIBTEM and 68mm (50-72mm) for EXTEM. Fibrinogen assay according to Clauss indicated a severe hypofibrinogenemia and reduced activity of coagulation factors. Dysfibrinogenämia may be an explanation for imparired fibrin formationin vitro coagulation tests. Surprisingly this was not confirmed in thrombelastometry.. Considering lack of bleeding in this patient the fibrinogen assay seems to lead an inappropriate diagnosis of hypofibrinogenenemia. Hip-TEP was proceeded without substitution of coagulation factors and perioperative bleeding complications.

Conclusion: Preoperative unexplained pethological results without bleeding history should be verified by repeated analysis or better by an independent method; in this case Thrombelastometry.