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The incidence of intraspinal hematoma is approximately 0.1 per 100,000 patients per year.1 It is more likely to occur in anticoagulated or thrombocytopenic patients, patients with neoplastic disease, or in those with liver disease or alcoholism.2 The incidence of neurologic dysfunction resulting from hemorrhagic complications associated with neuraxial blockade is estimated to be <1 in 150,000 epidural procedures and <1 in 220,000 with spinal anesthetics. The risk of formation of intraspinal hematoma after administration of neuraxial injections is increased in patients who received anticoagulant therapy or have a coagulation disorder, technical difficulties in the performance of the neuraxial procedures due to anatomic abnormalities of the spine, and multiple or bloody punctures. The American Society of Regional Anesthesia and Pain Medicine (ASRA) issued recommended guidelines for the safe performance of neuraxial blocks in patients who are on anticoagulants.3,4 The third edition of the ASRA guidelines was published in 2010.

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Antiplatelet medications inhibit platelet cyclo-oxygenase and prevent the synthesis of thromboxane A2. Thromboxane A2 is a potent vasoconstrictor and facilitates secondary platelet aggregation and release reactions. An adequate, although potentially fragile, clot may form.5 Platelet function in patients receiving antiplatelet medications should be assumed to be decreased for 1 week after treatment with aspirin and 1 to 3 days with nonsteroidal anti-inflammatory drugs (NSAIDs). New platelets are produced every day, and these new platelets partly explain the relative safety of performing neuraxial procedures in these patients.

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Although Vandermeulen et al6 implicated antiplatelet therapy in 3 of the 61 cases of spinal hematoma occurring after spinal or epidural anesthesia, the results of several large studies demonstrated the relative safety of neuraxial blockade in combination with antiplatelet therapy. The Collaborative Low-Dose Aspirin Study in Pregnancy Group7 included 1422 high-risk obstetric patients who were administered 60 mg aspirin daily and underwent epidural anesthesia without any neurologic sequelae. The studies of Horlocker et al,8,9 of approximately 1000 patients in each study, showed no spinal hematomas, although blood was noted during needle or catheter placement in 22% of the patients. A later study in patients who were on NSAIDs and underwent epidural steroid injections did not develop the signs and symptoms of intraspinal hematoma.10 A review of the case reports of intraspinal hematoma in patients on aspirin and NSAIDs showed complicating factors that included concomitant heparin administration, epidural venous angioma, and technical difficulty when performing the procedure.11

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The thienopyridine drugs, ticlopidine and clopidogrel, prevent platelet aggregation by inhibiting adenosine diphosphate (ADP) receptor-mediated platelet activation. Ticlopidine is rarely used because it causes neutropenia, thrombocytopenic purpura, and hypercholesterolemia. Clopidogrel is preferred because of its increased safety profile and proven efficacy. The maximal inhibition of ADP-induced platelet aggregation with clopidogrel occurs 3 to 5 days after the initiation of a standard dose (75 mg), but within 4 to 6 hours after the administration of a large loading dose of 300 to 600 mg.12 There is a case report of spinal hematoma in a patient on ticlopidine13 and a case of quadriplegia in a patient on clopidogrel, diclofenac, and possibly aspirin.14

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Neuraxial ...

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