A study of thrombelastography in hypercoagulable clinical states.
Carl M. Edwards

Thrombosis in the post-operative period is a major cause of morbidity and mortality. In the case of renal transplantation the incidence of thrombosis is higher than in other post-operative settings, but the aetiology of this higher rate is unknown. It is thought that the development of a 'hypercoagulable state' is a primary event in the period leading to thrombosis. There are no widely accepted tests for hypercoagulability, with those that are available being unsuitable for use in an acute clinical setting. The Thrombelastograph (TEG) offered an alternative approach to the available plasma based assays of coagulation, in that it used whole blood, produced a result in a time frame suitable for acute testing and had previously been shown to be sensitive to hypercoagulability.

In this study TEG showed good reproducibility and demonstrated the development of a hypercoagulable state after general surgery, confirming other work on this subject.

The TEG showed a hypercoagulable state to exist in end-stage renal failure patients and patients with malignant disease.

The results of the tests on patients with malignancy were also confirmed using ELISA based assay for fibrin degradation products (D-Dimer). D-Dimer was found to be a more accurate estimate of tumour severity than TEG and showed good differentiation between Dukes' stage B and stage C colorectal tumours.

TEG showed in the first 2 weeks renal transplant appeared to ameliorate the pre-transplant hypercoagulability however, after this there was a return to pre-transplant levels of hypercoagulability, which only started to resolve 6 months after transplantation.

The TEG provided some evidence that the thrombotic episodes in renal transplant associated with rejection may be due to pro-coagulant effects of methylprednisolone therapy.

Cyclosporin A (Cy A) treatment had been associated with thrombosis after transplant, this study showed that Cy A has an apparent anticoagulant effect at high doses in both in vivo and in vitro situations. However, the results of a clinical study indicate that high doses of Cy A do increase the rate of thrombosis, possibly mediated by the endothelial toxicity of Cy A.

Back to homepage