**4.3 Anti-factor Xa assay**

The anti-Xa assay is a plasma-based test that measures the ability of UFH to catalyze antithrombin's inhibition of factor Xa. Anti-Xa assay differs from ACT and aPTT as it measures the heparin concentration in the patient's blood [24]. Since the anti-Xa assay only measures one specific action of heparin, the value is used as a surrogate to approximate overall function [19]. The anti-Xa value may be affected in patients with elevated plasma-free hemoglobin, hyperbilirubinemia, hypertriglyceridemia, and antithrombin (depending on test reagants). A point of care anti-Xa test is available, but it is currently not widely used. Anti-factor Xa has been shown to have improved correlation to heparin activity as compared to aPTT and ACT [25]. In addition, a retrospective review of 62 pediatric ECMO patients with a mean anti-factor Xa level >0.2 IU/ml was associated with decreased circuit change [26].

Published literature supports the correlation between anti-factor Xa values and UFH dose. Unfortunately, many studies have shown a poor correlation between anti-factor Xa and ACT and/or aPTT. Multiple cardiac studies evaluating patients

**223**

**Figure 2.**

*30 minutes.*

*Anticoagulation in Pediatric Extracorporeal Membrane Oxygenation*

demonstrate poor correlation to anti-factor Xa levels [31–33].

TEG and ROTEM in conjunction with aPTT and/or anti-factor Xa.

*Thromboelastography (TEG). R, reaction time; K, kinetics; MA, maximum amplitude; LY30, amplitude at* 

requiring cardiopulmonary bypass report disparities between ACT values and anti-Xa as compared to UFH doses [27–30]. ECMO adult studies have shown an improved correlation between aPTT and UFH concentrations, but pediatric studies

Viscoelastic testing such as thromboelastography (TEG) and rotational thromboelastometry (ROTEM) are whole blood tests that measure the interaction of clotting factors, fibrinogen, and platelets as well as fibrinolysis (**Figure 2**). By measuring more than clotting factors, viscoelastic tests can give a more global picture of the coagulation system and allow for tailored transfusion management [3, 19]. **Figure 2** shows the standard TEG measurements including reaction time (R), kinetics (K), and maximum amplitude (MA). The R value is the time necessary for the initial clot formation. This value can be affected by the presence of anticoagulants, factor deficiencies, and hypercoagulable states. The K value measures the time for the clot to strengthen and can be affected by platelet count, fibrinogen, and coagulation factors. The maximum amplitude quantifies the final strength of the clot. Overall clot strength can be affected by the amount and function of fibrinogen and platelets [3]. In general, viscoelastic tests can be limited by static flow conditions [19]. While there is limited evidence in trauma, obstetrics, liver transplantation, and hemophilia using viscoelastic testing to help define coagulopathy and decrease overall blood product transfusions, studies are needed to confirm these results in ECMO patients [34]. Furthermore, prospective studies should examine the use of

*DOI: http://dx.doi.org/10.5772/intechopen.85104*

**4.4 Viscoelastic testing**

requiring cardiopulmonary bypass report disparities between ACT values and anti-Xa as compared to UFH doses [27–30]. ECMO adult studies have shown an improved correlation between aPTT and UFH concentrations, but pediatric studies demonstrate poor correlation to anti-factor Xa levels [31–33].
