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Correspondence  |   October 2013
Standard Thromboelastography Should Not Be Used to Assess Candidacy for Neuraxial Procedures in Patients Taking P2Y12 Inhibitors
Author Affiliations & Notes
  • Adam B. Lerner, M.D.
    Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts. alerner@bidmc.harvard.edu
  • (Accepted for publication July 1, 2013.)
    (Accepted for publication July 1, 2013.)×
Article Information
Correspondence
Correspondence   |   October 2013
Standard Thromboelastography Should Not Be Used to Assess Candidacy for Neuraxial Procedures in Patients Taking P2Y12 Inhibitors
Anesthesiology 10 2013, Vol.119, 993. doi:10.1097/ALN.0b013e3182a44648
Anesthesiology 10 2013, Vol.119, 993. doi:10.1097/ALN.0b013e3182a44648
To the Editor:
We read with interest and concern the case scenario by Ahn et al.1  describing the use of the thromboelastograph to guide thoracic epidural placement in an elderly patient with chest trauma taking clopidogrel and aspirin. Despite presumed platelet inhibition, this patient’s thromboelastograph demonstrated a slightly hypercoagulable state with an increased maximum amplitude of 76.1 mm. We agree that trauma-induced inflammation and acute-phase reaction are possible causes of the reported thromboelastograph findings in this patient. However, we are concerned about the authors’ use of standard, kaolin-activated thromboelastography as a method to assess platelet function in the setting of a P2Y12 antagonist as well as aspirin.
Thrombin is, by far and away, the most potent activator of platelets.2  This activation is accomplished through thrombin-mediated cleavage of the protease-activated receptors. Adenosine diphosphate, in contrast, is a relatively weak activator of platelets.3  Adenosine diphosphate agonism of the P2Y12 receptor serves to amplify the platelet in response to thrombin and to stabilize platelet aggregates. This results in a critical issue that practitioners using the thromboelastograph to guide interventions need to understand; kaolin-activated coagulation generates thrombin in quantities that are sufficient to overcome the effects of P2Y12 antagonists on platelet function as assessed by thromboelastography.4  In a similar manner, platelet inhibition by aspirin is also masked in kaolin-activated thromboelastography.
Platelet inhibition can be assessed by a modified thromboelastograph assay known as TEG Platelet Mapping® (Haemonetics, Niles, IL). The details related to this assay can be found elsewhere. Despite the fact that authors’ discussion correctly identifies the need for this modified thromboelastograph assay to assess platelet inhibition from clopidogrel and aspirin, the assay was not used in the presented case. Instead, a supranormal maximum amplitude result from a standard thromboelastograph assay was incorrectly interpreted as representing a safe environment for neuraxial intervention.
Fortunately, the patient described in this scenario did not appear to suffer any consequence. As the authors themselves note, several studies have found the risk of epidural hematoma to be extraordinarily low even in patients taking clopidogrel on the day of placement. Despite this, we strongly discourage the use of results from standard, kaolin-activated thromboelastography as evidence of a safe hemostatic milieu for neuraxial anesthesia or analgesia in a patient receiving any P2Y12 antagonist. Instead, we recommend using TEG Platelet Mapping® or another assay capable of assessing platelet inhibition from these medications.
John McNeil, M.D., Adam B. Lerner, M.D.* *Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts. alerner@bidmc.harvard.edu
References
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