Use of eptifibatide as a bridge antiplatelet agent for intrathecal drug delivery system placement.

Use of antiplatelet agents is becoming increasingly common, and their management may require new strategies if neuroaxial techniques are to be employed in patients who will not tolerate discontinuation of antiplatelet therapy. The patient was a 46-year-old man with a past medical history significant for coronary artery disease and who had undergone 14 stents. He developed stent thrombosis (ST) while on clopidogrel. Following the ST, he was subsequently placed on prasugrel. While on prasugrel, the patient presented for an intrathecal drug delivery system (IDDS) trial and placement due to severe peripheral neuropathy unresponsive to several conservative medical treatments. He had previously undergone an unsuccessful spinal cord stimulator trial and received no pain relief. In consultation with his outside cardiologist, the patient received permission to hold his prasugrel for 7 days prior to his intrathecal pump trial. During the trial period's inpatient hospitalization, the patient developed chest pain. In consultation with the cardiology service in our institution, it was decided antiplatelet therapy should be re-instituted. The patient was bridged to his IDDS placement after the trial with intravenous eptifibatide. The eptifibatide drip was administered 6 hours prior to the IDDS implant. Functional platelet count was checked one hour before the IDDS was placed and the pump was placed without incident. The eptifibatide drip was reinstituted one hour after the IDDS implantation. The patient was observed for 24 hours on the eptifibatide drip, transitioned to his home dose of prasugrel, and discharged home. At outpatient follow-up one week later, the patient demonstrated no neurologic or hemorrhagic complications and was satisfied with the pain control provided by the IDDS. Prasugrel is an irreversible platelet inhibitor, which prevents ADP-induced platelet aggregation by binding the P2Y12 receptor. Patients taking prasugrel will have deficient platelet activity until new platelets have been produced, a span of approximately 7 days. Eptifibatide is an intravenous glycoprotein IIb/IIIa inhibitor with a short half-life of ½ hours. Inhibition of glycoprotein IIb/IIIa prevents platelet activation and aggregation. The drug effect ceases once it is discontinued and restoration of platelet function is not dependent upon new platelet production. Patients requiring antiplatelet therapy in need of neuroaxial pain management procedures present challenging problems to pain management physicians. Current guidelines from the American Society of Regional Anesthesia have not identified any bridging agent suitable for patients who may not tolerate prolonged withdrawal from their antiplatelet therapy. In this case, eptifibatide was successfully utilized to bridge a patient whose comorbid conditions necessitated continuous antiplatelet therapy without the prolonged washout common to irreversible antiplatelet agents.