Thrombelastometry
The thromboelastography or Thromb (o) elastometrie is a diagnostic (viscoelastic) method by which coagulation properties ( hemostasis of whole) blood can be examined. In contrast to conventional coagulation analyzes ( Quick , aPTT ), the strength of the blood clot, its dissolution and various special issues can also be recorded.
development
In 1948 Hellmut Hartert in Heidelberg described the principle of thrombelastography. Due to the complex handling and the sensitivity to vibrations of this "classic thromboelastography", it was hardly able to establish itself in everyday clinical practice, but it found a certain distribution in America (TEG®, Haemoscope, USA).
Resonance thrombography was later developed as a further development (RTG 801, 1977, Fresenius-Medizintechnik Bad Homburg and ROM-4 Orbitometer, 1988, Amelung Lemgo.) This method was carried out in some hemostasis centers, but could not establish itself permanently in clinical application.
At the beginning of the 1990s, the principle of rotational elastography (ROTEG) was further developed, which is essentially insensitive to vibrations and therefore point-of-care capable . For legal reasons, the name was later renamed to rotational thrombelastometry. (ROTEM®, Tem Innovations GmbH, Munich).
Procedure
In classic thrombelastography, the blood clot forms on a stamp that protrudes into a sample vessel with the blood sample that swivels in the longitudinal direction. As the coagulation increases, the movement is transferred to the stamp, which can be represented as a curve over time. In rotation thromboelastometry, however, the plunger rotates when the vessel is stationary. The measurement is carried out with citrated blood , the coagulation is started by adding calcium and activators.
Various commercial ROTEM® systems are available that allow various differential diagnostic statements. With INTEM (contact activation) the intrinsic way is tested, with EXTEM (activator: tissue factor ) the extrinsic way of blood coagulation is tested. HEPTEM can identify the effect of heparin (addition of heparinase ). FIBTEM can differentiate the plasmatic part from the thrombocytic part of the coagulation (addition of cytochalasin D ). APTEM can show the presence of strong hyperfibrinolysis (inhibition of this by aprotinin ). A heparinase test (heparin influence) and a kaolin-activated test (intrinsic system) are available for TEG®.
interpretation
The clotting time or coagulation time (CT, ROTEM) or the r-value (TEG) is the latency from the time the activator is added until the clot starts to form. It corresponds to the Quick value (EXTEM) or the aPTT (INTEM). A prolongation of the clotting time can be caused by coagulation disorders, mainly a lack of coagulation factors or heparin (depending on the test used). A heparin effect can be determined by comparing the clotting time of the INTEM test with the clotting time of the HEPTEM test.
The clot formation time (CFT, ROTEM) or k-value is defined as the time from the onset of clot formation until an amplitude of 20 mm is reached. This value provides an indication of the rate at which the clot forms.
The clot firmness is measured by the maximum clot firmness (MCF, ROTEM) or maximum amplitude (TEG). The lysis index (LI) indicates the decrease 60 minutes after clot formation and indicates fibrinolysis . If it is <85%, there is hyperfibrinolysis. In the case of massive hyperfibrinolysis, the coagulation can be completely eliminated, then the APTEM approach can enable the coagulation and differentiate it from a fibrinogen deficiency.
application areas
Areas of application are unclear bleeding during operations or trauma, suspected hyperfibrinolysis, monitoring of fibrinogen substitution and thrombocytopenia. A reduction of the blood treatment costs by the thromboelastometry in cardiac surgery was shown also therapy decisions in the emergency room occur more quickly. TEM is the gold standard for measuring hyperfibrinolysis, for which no equivalent laboratory parameter exists.
Limitations
Thromboelastometry takes place in an artificial system that does not represent an exact image of the physiological coagulation conditions. The flow behavior in the vascular system is largely ignored. Disorders of primary hemostasis ( Von Willebrand syndrome ), pharmacological effects of acetylsalicylic acid (ASA) and ADP antagonists such as clopidogrel are not recorded at all, glycoprotein IIb / IIIa antagonists or Glanzmann's disease are only partially recorded. The EXTEM value correlates poorly with the Quick value. The coagulation inhibitor potential (antithrombin, protein C, protein S) is also poorly recorded. Controlled studies showing a reduction in mortality are not available.
literature
- Th. Lang, M. von Depka: Diagnostic possibilities and limits of thrombelastography / -metry. In: Hemostaseology. 26 (Suppl. 1), 2006, pp. S20-S29. PMID 16953288
Individual evidence
- ↑ H. Hartert: Blood coagulation studies with thrombelastography, a new examination method. In: Clinical weekly. 26, 1948, pp. 577-583. PMID 18101974 .
- ↑ H. Hartert: Results of resonance thrombography, a new differentiating global determination of blood coagulation. In: Verh. Ber. 21st anniversary. German Work Community f. Coagulation research. Essen 1977, p. 346.
- ↑ H. Hartert: Fibrin elasticity and coagulation. In: Biorheology. 24, 1988, p. 137.
- ↑ A. Calatzis, A. Calatzis, M. Kling, A. Stemberger, R. Hipp: Concept for "bedside" - coagulation monitoring using modified Thrombelastography. In: The anesthesiologist. 44 (2), 1995, p. 437.
- ↑ a b c d e Lang, from Depka 2006.
- ↑ a b C. Jámbor, B. Heindl, M. Spannagl, C. Rolfes, GK Dinges, T. Frietsch: Hemostaseological management in multiple trauma - importance of patient-oriented diagnostic methods. In: Anasthesiol Intensivmed Emergency Med Schmerzther. 44 (3), Mar 2009, pp. 200-209. PMID 19266421 .