Standard Kaolin-active Thromboelastography Cannot Detect Platelet Inhibition by Clopidogrel

In the March 2013 issue of Anesthesiology, Dr. Ahn et al.1 present a thorough and informative review of pain-associated respiratory failure. The review is based on a case report describing a 79-yr-old man with bilateral chest trauma, in whom the treating team decided to use epidural analgesia. This is not an uncommon scenario; however in this case, the patient was taking clopidogrel as prophylaxis after the placement of bare-metal coronary artery stents.As stated in the article, there is little in the way of evidence to guide epidural placement in patients taking antiplatelet agents; furthermore, the response to these agents demonstrates intrapatient variability. The treating physicians used standard coagulation parameters and thromboelastography to assess coagulation before insertion of the epidural catheter.It is my contention, supported by published data, that none of the tests performed on this occasion could have adequately assessed the contribution of clopidogrel to coagulopathy in this patient. Standard kaolin-activated thromboelastography in particular will not reflect any platelet inhibition that is caused by clopidogrel, as the thrombin generated in the sample is enough to fully activate platelets even when pathways reliant on adenosine diphosphate or arachidonic acid are blocked. This topic is more fully covered in an excellent review by Gibbs.2The effect of clopidogrel on a blood sample can be assessed with the thromboelastography equipment using Thromboelastography Platelet Mapping™ assay3 or with other proprietary tests.I have no qualms with the use of epidural analgesia in this patient; the possible risk of hematoma was balanced by the predictable benefits of analgesia on respiratory function. I am concerned that treatment decisions may have been made using an incorrect interpretation of the results of thromboelastography and that as a result of this article physicians might repeat this mistake.