- Email: [email protected]
Perioperative management of a neurosurgical patient requiring antiplatelet therapy
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may not bring about sufficient ventricular concentrations to be effective. Therefore, we believe that strong consideration should be given to IVT antibiotics in cases of intraventricular brain abscess. References 1. Lambo A, Nchimi A, Khamis J, et al. Primary intraventricular brain abscess. Neuroradiology 2003;45:908–10. 2. Lee TH, Chang WN, Su TM, et al. Clinical features and predictive factors of intraventricular rupture in patients who have bacterial brain abscesses. J Neurol Neurosurg Psychiatry 2007;78:303–9.
3. Mogilner A, Jallo G, Zagzag D, et al. Nocardia abscess of the choroid plexus: clinical and pathological case report. Neurosurgery 1998;43:949–52. 4. Pfausler B, Spiss H, Beer R, et al. Treatment of staphylococcal ventriculitis associated with external cerebrospinal fluid drains: a prospective randomized trial of intravenous compared with intraventricular vancomycin therapy. J Neurosurg 2003;98:1040–4. 5. Pruthi N, Devi BI, Shivshankar JJ, et al. Abscess – a rare fourth ventricular mass. Acta Neurochir 2007;149:1179–81. 6. Robinson EN. Staphylococcal meningitis can present as an abscess of a single lateral ventricle. Clin Infect Dis 1993;16:435–8. 7. Vajramani GV, Devi BI, Hegde T, et al. Intraventricular tuberculous abscess: a case report. Neurol India 1999;47:327–9.
doi:http://dx.doi.org/10.1016/j.jocn.2011.11.028
Perioperative management of a neurosurgical patient requiring antiplatelet therapy Khoi D. Than a,⇑, Pratik Rohatgi b, Thomas J. Wilson a, B. Gregory Thompson a a b
Department of Neurosurgery, University of Michigan, 1500 E. Medical Center Drive, Room 3552 TC, Ann Arbor, Michigan 48109-5338, USA Department of Neurosurgery, Pennsylvania State University, Hershey, Pennsylvania, USA
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Article history: Received 11 November 2011 Accepted 28 December 2011
Keywords: Antiplatelet therapy Aspirin Clopidogrel Eptifibatide Ibuprofen Neurovascular stent Ventriculoperitoneal shunt
a b s t r a c t In patients who undergo neurovascular stent placement with postoperative dual antiplatelet therapy to prevent in-stent thrombosis, there is no protocol for balancing the risk of acute stent thrombosis and bleeding if urgent neurosurgical procedures are required. We detail perioperative management of dual antiplatelet therapy in a 66-year-old man with a dolichoectatic aneurysm of the basilar artery treated with a Pipeline stent. Postoperatively, the patient was placed on aspirin and clopidogrel to prevent instent thrombosis. One month after the procedure, his neurological status declined secondary to obstructive hydrocephalus. His condition necessitated urgent placement of a ventriculoperitoneal shunt, despite the dual antiplatelet therapy for the flow-diverting Pipeline stent. Aspirin and clopidogrel were discontinued seven days prior to the planned shunt placement. To minimize time off antiplatelet therapy, aspirin was immediately replaced with ibuprofen. Eptifibatide was then started three days prior to surgery. The ibuprofen/eptifibatide bridge was discontinued at midnight prior to surgery. Aspirin was restarted on the first postoperative day and clopidogrel was restarted on the second postoperative day. The patient tolerated shunt placement without excessive bleeding or hemorrhagic complications. During the remainder of his hospital course, no evidence of stent thrombosis or intracranial hemorrhage was noted. We conclude that management of antiplatelet prophylaxis for neurovascular stent thrombosis in patients requiring urgent neurosurgical procedures may be successfully achieved by bridging aspirin and clopidogrel with ibuprofen and eptifibatide in the preoperative period. Ó 2012 Elsevier Ltd. All rights reserved.
1. Introduction Endovascular neurosurgery procedures are used to manage a growing number of pathologies, ranging from aneurysms to cerebral ischemic diseases to arteriovenous malformations.1–3 Many patients who undergo endovascular procedures are treated with neurovascular stents, requiring postoperative dual antiplatelet therapy with aspirin and clopidogrel to prevent in-stent thrombosis. If these patients require additional neurosurgical procedures, neurosurgeons are faced with the clinical challenge of balancing the risk of acute stent thrombosis with the risk of operative and postoperative bleeding. There are no standards on how to manage patients who undergo endovascular procedures with neurovascular stents who then require postoperative dual antiplatelet therapy with aspirin and clopidogrel to prevent in-stent thrombosis. The literature provides little guidance, as neurosurgical reports are sparse and the work
⇑ Corresponding author. Tel.: +1 734 936 5732; fax: +1 734 936 9294. E-mail address: [email protected] (K.D. Than).
from cardiovascular stenting provides few evidence-based recommendations regarding neurosurgical patients. In this review, we provide an illustrative case detailing the antiplatelet management of a patient who had a ventriculoperitoneal shunt (VPS) placed one month after receiving a Pipeline flow-diverting stent (ev3, Irvine, CA, USA) in the basilar artery, utilizing a preoperative ibuprofen and eptifibatide bridge in place of aspirin and clopidogrel. The patient was managed successfully using this protocol. The aim of this report is to provide one option for minimizing time off antiplatelet therapy in patients with a recently placed intracranial stent. 2. Case report A 66-year-old man presented with a six-month history of progressive dysarthria, urinary incontinence, episodes of choking and aspiration, ataxia, lack of coordination, disequilibrium, and headaches. Six months prior to these symptoms, the patient was in good health and worked as a police officer. Neurological examination demonstrated dysarthria, a wide-based ataxic gait, and right-sided appendicular dysmetria with bilateral tremor. A CT angiogram (CTA) and MRI demonstrated a 2.8 cm 3.1 cm 3.8 cm fusiform dolichoectatic aneurysm of the
Case Reports / Journal of Clinical Neuroscience 19 (2012) 1316–1320
basilar artery arising from both the left and right vertebral arteries through the vertebrobasilar junction and into the origin of the left anterior inferior cerebellar artery with compression of the pons and medulla (Fig. 1). He had a prominent ventricular system with enlarged temporal horns, convexity of the third ventricle, and compression of the fourth ventricle by the aneurysm mass (Fig. 2). Transependymal flow of cerebrospinal fluid (CSF) with mild aqueductal compression was also noted. Basilar cisterns were widely patent and there was no evidence of subarachnoid blood. A decision was made to manage his aneurysm with a Pipeline flow-diverting stent.4,5 The patient underwent coil embolization with Pipeline stenting without complication. His neurological status failed to significantly improve after the procedure, and his relative ventriculomegaly persisted. Repeat brain MRI one month after the procedure re-demonstrated obstructive hydrocephalus with mild increase in ventricular size from prior imaging. At that time, the patient’s overall medical status declined secondary to pneumonia and a urinary tract infection. His neurologic status remained poor and this was thought to be secondary to hydroceph-
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alus. Once his general medical issues were stabilized, CSF diversion was deemed necessary, despite the need for dual antiplatelet therapy. The patient was considered to be at high risk for both stent thrombosis and perioperative and postoperative bleeding. To minimize operative complications, it was determined that the patient should not have any platelet function inhibition during the operation. Consequently, to minimize time without antiplatelet therapy and thus minimize the risk for acute stent thrombosis, an antiplatelet bridge protocol was developed (Table 1). Both aspirin and clopidogrel were discontinued seven days prior to surgery. Aspirin was immediately replaced with ibuprofen at 600 mg twice daily. Eptifibatide was started three days prior to surgery by administering a loading bolus of 180 lg/kg followed by a continual infusion at 2 lg/kg per minute according to the manufacturer’s guidelines. Ibuprofen and eptifibatide were discontinued at midnight prior to the operation. VPS placement was completed without complication or excessive blood loss. Intracranial bleeding was not evident on postoperative head CT scan. Consequently,
Fig. 1. Preoperative (A) angiogram of the left vertebral artery showing a fusiform dolichoectatic aneurysm of the basilar artery with distal filling of the left posterior cerebral artery; and (B) axial T1-weighted, post-contrast brain MRI showing an aneurysm measuring 2.8 cm 3.1 cm 3.8 cm. (C) Axial post-stent T1-weighted, post-contrast brain MRI showing the lumen of the stent (arrow).
Fig. 2. Axial non-contrast head CT scans evaluating hydrocephalus: (A) following stent placement showing ventricular enlargement; (B) following ventriculoperitoneal shunt (VPS) placement without evidence of acute hemorrhage; and (C) three months following VPS placement showing decreased ventricular size without signs of intracranial hemorrhage.
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Table 1 Antiplatelet medication bridge protocol used to perioperatively manage the patient requiring antiplatelet therapy to balance the risks of acute neurovascular stent thrombosis and intracranial hemorrhage (ICH) Time of implementation
Intervention
Preoperative day 7
1. Discontinue aspirin 2. Discontinue clopidogrel 3. Start ibuprofen 600 mg PO BID
Preoperative day 3
4. Eptifibatide bolus at 180 lg/kg 5. Eptifibatide infusion at 2 lg/kg per minute
Midnight prior to surgery
6. Discontinue ibuprofen 7. Discontinue eptifibatide infusion
Postoperative day 1
8. Rule out ICH by CT scan 9. Start aspirin 325 mg PO daily
Postoperative day 2
10. Clopidogrel bolus at 300 mg 11. Resume clopidogrel at 75 mg PO daily
PO = by mouth; BID = twice per day.
the patient was restarted on aspirin on the first postoperative day and clopidogrel on the second postoperative day. During the remainder of his hospital course, no evidence of either stent thrombosis or intracranial hemorrhage was noted.
3. Discussion There are no evidence-based guidelines or standards of care for the management of antiplatelet therapy in patients with recently placed neurovascular stents who require intracranial procedures. Patients with neurovascular stents are commonly treated with dual antiplatelet therapy (aspirin and clopidogrel) to prevent stent thrombosis. This practice is based on the cardiology literature, as primary studies on neurovascular stents are sparse.6 Consensus statements agree that there is a high risk of thrombosis for bare metal coronary stents within eight weeks of implantation.7 Re-endothelialization of coronary vessels continues for four to six weeks after bare metal stent deployment and continues longer with drug-eluting stents. Consequently, dual antiplatelet therapy is continued for at least six months to allow the stent to endothelialize.8 Life-long low-dose aspirin therapy is recommended thereafter.9 Neurovascular stent thrombosis prophylaxis protocols based on the cardiac literature have been largely successful.10,11 In a oneyear follow-up study, 10 patients with symptomatic intracranial atherosclerotic arteries (>60% stenosis) treated by stent placement and maintained on clopidogrel for six months and aspirin indefinitely did not demonstrate re-stenosis (>50%) or ischemic events.10 Patients enrolled in the National Institutes of Health Multicenter Wingspan Intracranial Stent Registry were maintained on clopidogrel for at least four weeks following intracranial stent placement and continued on aspirin indefinitely without significant complication.12,13 Stent patency depends on the inhibition of platelet aggregation. Aspirin inhibits platelet aggregation for the lifespan of platelets by irreversibly inhibiting the cyclooxygenase-1 (COX1) enzyme, which catalyzes the conversion of arachidonic acid to prostaglandin H2.14,15 This is the first concomitant step in platelet-dependant thromboxane A2 (TXA2) generation which, in turn, stimulates activation of new platelets and promotes platelet aggregation.16 Platelet function returns roughly to 50% of normal six days after stopping therapy, as platelets nominally turn over by 10% daily.17 Normal hemostasis is achieved when 20% of platelets have normal COX1 function.18 In healthy volunteers, bleeding times after daily aspirin therapy largely normalize 48 hours after the last dose.19 The abrupt discontinuation of aspirin therapy is associated with
a rebound pro-thrombotic state due to a rebound excess of TXA2 production, which decreases fibrinolytic activity.20,21 Non-steroidal anti-inflammatory drugs (NSAID), such as ibuprofen and naproxen, reversibly inhibit COX1 in a dose-dependent manner with less potency than aspirin.18,22,23 A single dose of ibuprofen inhibits platelet aggregation within two hours, but normalizes after 12 hours.24 In a study of healthy volunteers ingesting 700 mg of ibuprofen every eight hours, platelet function normalized 24 hours after the last dose for all participants as assessed by platelet function analysis (PFA-100 assay).25 Clopidogrel decreases the risk of coronary stent thrombosis and recurrent stroke by 30% but, due to its greater antiplatelet effect compared to COX1 inhibitors, it also increases the risk of spontaneous hemorrhage by 38% compared to placebo.26,27 Clopidogrel, a thienopyridine, decreases thrombosis by irreversible non-competitive inhibition of the P2Y12 adenosine diphosphate receptor.14,28 This receptor promotes platelet aggregation by activating the glycoprotein IIb/IIIa (GP IIb/IIIa) receptor and facilitates fibrinogen-mediated platelet cross-linking.17 Clopidogrel produces measurable inhibition of platelets 12 hours after ingestion of a standard 75 mg dose.20 Loading doses of 300 mg and 600 mg reach therapeutic levels after six and two hours, respectively. Maximum inhibition occurs after four to seven days of continuous treatment, which increases bleeding times from 1.5–3 times that of normal.26 Platelet function normalizes seven days after the last dose.17 Additionally, as clopidogrel has no effect on the COX1 system, its antiplatelet effects work in synergy with those of aspirin.28 Abciximab, eptifibatide, and tirofiban are GP IIb/IIIa antagonists that inhibit platelet aggregation and activation more potently than NSAID or thienopyridines.29 GP IIb/IIIa is a platelet integrin that functions as the main receptor for fibrinogen, which cross-links different platelets, binds to vitronectin, and also binds to von Willebrand factor. Thus, the GP IIb/IIIa antagonists block platelet aggregation regardless of the triggering pathway.17 Full hemostasis is restored when half of the integrin receptors can bind to fibrinogen.18 Eptifibatide was selected for the bridging protocol used in the presented case because of its pharmacokinetic profile. After discontinuing eptifibatide, bleeding times normalize within 15 minutes and platelet function recovers to more than 50% after six hours.20 Premature discontinuation of antiplatelet therapy provides the greatest risk for stent thrombosis.21 Cardiac stent thrombosis occurs roughly 10 days after premature discontinuation of aspirin therapy.26 One neurosurgical study demonstrated that the premature discontinuation of clopidogrel increased stent thrombosis by a hazard ratio of 57, which led to an increase in mortality of 45%.30 Stopping clopidogrel for major surgery within the first three weeks after drug-eluting coronary artery stent placement increased mortality by 30% to 86%.31 Patients undergoing non-cardiac surgery during the coronary stent endothelialization window are at five to 10 times greater risk of stent thrombosis leading to myocardial infarction and mortality as compared to matched patients for whom surgery is appropriately delayed and managed under maximal medical therapy.26,32 Such studies highlight the necessity to maintain appropriate antiplatelet therapy, although the commonly used endpoint in the cardiac literature of myocardial infarction and mortality may be a less-sensitive measure of thrombosis than is needed to assess for neurovascular compromise. The increased complexity of the hemostatic environment in the neurovasculature compared to that of the coronary system suggests that translating cardiology studies to neurosurgical patients may not be straightforward.24,33,34 A growing body of evidence supports the theory that biological differences may lead to different clinical outcomes with regard to long-term stent patency. A retrospective study of 67 patients who underwent intracranial stent placement while on a standard
Case Reports / Journal of Clinical Neuroscience 19 (2012) 1316–1320
antiplatelet regimen demonstrated a re-stenosis rate seven times higher than with bare metal stents placed in the coronary arteries.35 In that study, 10% of patients had subacute stent thrombosis after intracranial stenting, despite antiplatelet therapy. Additionally, in-stent re-stenosis secondary to neointimal hyperplasia has been observed in up to 30% of intracranial stents.36 One case study suggests that on angiography, in-stent platelet aggregation can appear identical to re-stenosis, stressing the importance of maintaining antiplatelet agents.37 However, the risks of acute stent thrombosis must be balanced with the complications of antiplatelet therapy for patients requiring urgent surgery, such as for our patient.7 Patients on any level of antiplatelet therapy are at an increased risk for hemorrhage, ranging from 30% to 50%.38 Additionally, dual antiplatelet therapy with aspirin and clopidogrel increases the risk of spontaneous bleeding by 33%.21 Despite the increased blood loss attributed to antiplatelet therapy, morbidity and mortality rates are not increased except during intracranial neurosurgery.39 Aspirin therapy is a major risk factor linked with fatal outcomes in intracranial neurosurgery secondary to intracerebral hematoma.40 Indirect evidence is mixed regarding how significantly the risk of hemorrhage is increased by aspirin. Chronic aspirin use prior to an intracerebral hemorrhage increases the risk of death by 2.5 times, while a similar study reported no difference in clinical outcome for patients on aspirin therapy following aneurysmal subarachnoid hemorrhage.41,42 For patients with recently placed coronary artery stents, several guidelines recommend that intracerebral interventions should be delayed until the stents are endothelialized.43 When neurosurgical procedures cannot be significantly delayed, some guidelines recommend discontinuing aspirin and clopidogrel five to seven days prior to surgery and restarting antiplatelet therapy within 24 hours after operation.16 Other recommendations include discontinuing clopidogrel 7 days prior to surgery while maintaining aspirin and possibly bridging therapy with eptifibatide and heparin.26 In small studies, tirofiban has been successfully substituted for clopidogrel to bridge patients with drug-eluting stents in need of urgent surgery44,45; however, these studies did not include patients with intracranial disease or history of stroke, and aspirin usage was not standardized. 4. Conclusion Management of antiplatelet prophylaxis for neurovascular stent thrombosis in a patient in need of an urgent neurosurgical procedure was successfully achieved by bridging aspirin and clopidogrel with ibuprofen and eptifibatide in the preoperative period. To our knowledge, this novel approach has not yet been described elsewhere. These substitutions were selected on the basis of each the pharmacokinetic profile of each drug, recommendations found in consensus guidelines, and related case reports. Additional experience with this protocol is necessary to definitively conclude that it is appropriate to manage this clinical situation, but it is our hope that this report provides one option for neurosurgeons faced with similar challenges. References 1. Meyers PM, Schumacher HC, Higashida RT, et al. Indications for the performance of intracranial endovascular neurointerventional procedures: a scientific statement from the American Heart Association Council on Cardiovascular Radiology and Intervention, Stroke Council, Council on Cardiovascular Surgery and Anesthesia, Interdisciplinary Council on Peripheral Vascular Disease, and Interdisciplinary Council on Quality of Care and Outcomes Research. Circulation 2009;119:2235–49. 2. Wakhloo AK, Deleo 3rd MJ, Brown MM. Advances in interventional neuroradiology. Stroke 2009;40:e305–12. 3. Walton MT, Gress DR, Higashida RT. Controversies in neurological surgery: neurovascular diseases. New York: Thieme; 2006.
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4. Fiorella D, Lylyk P, Szikora I, et al. Curative cerebrovascular reconstruction with the Pipeline embolization device: the emergence of definitive endovascular therapy for intracranial aneurysms. J Neurointerv Surg 2009;1:56–65. 5. van Rooij WJ, Sluzewski M. Perforator infarction after placement of a pipeline flow-diverting stent for an unruptured A1 aneurysm. AJNR Am J Neuroradiol 2010;31:E43–4. 6. Wojak JC, Dunlap DC, Hargrave KR, et al. Intracranial angioplasty and stenting: long-term results from a single center. AJNR Am J Neuroradiol 2006;27:1882–92. 7. Riddell JW, Chiche L, Plaud B, et al. Coronary stents and noncardiac surgery. Circulation 2007;116:e378–82. 8. Qureshi AI, Luft AR, Sharma M, et al. Prevention and treatment of thromboembolic and ischemic complications associated with endovascular procedures: Part II–Clinical aspects and recommendations. Neurosurgery 2000;46:1360–75 discussion 75–6. 9. Patrono C, Garcia Rodriguez LA, Landolfi R, et al. Low-dose aspirin for the prevention of atherothrombosis. N Engl J Med 2005;353:2373–83. 10. Lee CY, Yim MB. Primary stent therapy for symptomatic intracranial atherosclerotic stenosis: 1-year follow-up angiographic and midterm clinical outcomes. J Neurosurg 2006;105:235–41. 11. Zaidat OO. Periprocedural management of patients with endovascular treatment of intracranial atherosclerotic disease. J Neuroimaging 2009;19(Suppl. 1):35S–8S. 12. Fiorella D, Levy EI, Turk AS, et al. US multicenter experience with the wingspan stent system for the treatment of intracranial atheromatous disease: periprocedural results. Stroke 2007;38:881–7. 13. Nahab F, Lynn MJ, Kasner SE, et al. Risk factors associated with major cerebrovascular complications after intracranial stenting. Neurology 2009;72:2014–9. 14. Lippi G, Favaloro EJ, Salvagno GL, et al. Laboratory assessment and perioperative management of patients on antiplatelet therapy: from the bench to the bedside. Clin Chim Acta 2009;405:8–16. 15. Silber S, Albertsson P, Aviles FF, et al. Guidelines for percutaneous coronary interventions. The Task Force for Percutaneous Coronary Interventions of the European Society of Cardiology. Eur Heart J 2005;26:804–47. 16. Cahill RA, McGreal GT, Crowe BH, et al. Duration of increased bleeding tendency after cessation of aspirin therapy. J Am Coll Surg 2005;200:564–73. 17. Aiyagari V. Counteracting the effects of anticoagulants and antiplatelet agents during neurosurgical emergencies. Neurosurgery 2006;59:E1152. 18. Lecompte T, Hardy JF. Antiplatelet agents and perioperative bleeding. Can J Anaesth 2006;53:S103–112. 19. Sonksen JR, Kong KL, Holder R. Magnitude and time course of impaired primary haemostasis after stopping chronic low and medium dose aspirin in healthy volunteers. Br J Anaesth 1999;82:360–5. 20. Fiehler J, Ries T. Prevention and treatment of thromboembolism during endovascular aneurysm therapy. Klin Neuroradiol 2009;19:73–81. 21. Mollmann H, Nef HM, Hamm CW, et al. How to manage patients with need for antiplatelet therapy in the setting of (un-)planned surgery. Clin Res Cardiol 2009;98:8–15. 22. Catella-Lawson F, Reilly MP, Kapoor SC, et al. Cyclooxygenase inhibitors and the antiplatelet effects of aspirin. N Engl J Med 2001;345:1809–17. 23. Schafer AI. Effects of nonsteroidal anti-inflammatory therapy on platelets. Am J Med 1999;106:25S–36S. 24. Gerlach R, Krause M, Seifert V, et al. Hemostatic and hemorrhagic problems in neurosurgical patients. Acta Neurochir (Wien) 2009;151:873–900 discussion. 25. Goldenberg NA, Jacobson L, Manco-Johnson MJ. Brief communication: duration of platelet dysfunction after a 7-day course of Ibuprofen. Ann Intern Med 2005;142:506–9. 26. Chassot PG, Delabays A, Spahn DR. Perioperative antiplatelet therapy: the case for continuing therapy in patients at risk of myocardial infarction. Br J Anaesth 2007;99:316–28. 27. Yusuf S, Zhao F, Mehta SR, et al. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med 2001;345:494–502. 28. Sharis PJ, Cannon CP, Loscalzo J. The antiplatelet effects of ticlopidine and clopidogrel. Ann Intern Med 1998;129:394–405. 29. Meadows TA, Bhatt DL. Clinical aspects of platelet inhibitors and thrombus formation. Circ Res 2007;100:1261–75. 30. Fiorella D, Hsu D, Woo HH, et al. Very late thrombosis of a pipeline embolization device construct: case report. Neurosurgery 2010;67:onsE 313–314 discussion onsE4. 31. Sharma AK, Ajani AE, Hamwi SM, et al. Major noncardiac surgery following coronary stenting: when is it safe to operate? Catheter Cardiovasc Interv 2004;63:141–5. 32. Luckie M, Khattar RS, Fraser D. Non-cardiac surgery and antiplatelet therapy following coronary artery stenting. Heart 2009;95:1303–8. 33. Qureshi AI. Editorial comment–Thromboembolic events during neuroendovascular procedures. Stroke 2003;34:1728–9. 34. Qureshi AI, Luft AR, Sharma M, et al. Prevention and treatment of thromboembolic and ischemic complications associated with endovascular procedures: Part I–Pathophysiological and pharmacological features. Neurosurgery 2000;46:1344–59. 35. Riedel CH, Tietke M, Alfke K, et al. Subacute stent thrombosis in intracranial stenting. Stroke 2009;40:1310–4. 36. Korinth MC. Low-dose aspirin before intracranial surgery–results of a survey among neurosurgeons in Germany. Acta Neurochir (Wien) 2006;148:1189–96 discussion 96.
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37. Mazighi M, Saint Maurice JP, Bresson D, et al. Platelet aggregation in intracranial stents may mimic in-stent restenosis. AJNR Am J Neuroradiol 2010;31:496–7. 38. Samama CM, Djoudi R, Lecompte T, et al. Perioperative platelet transfusion: recommendations of the Agence Francaise de Securite Sanitaire des Produits de Sante (AFSSaPS) 2003. Can J Anaesth 2005;52:30–7. 39. Burger W, Chemnitius JM, Kneissl GD, et al. Low-dose aspirin for secondary cardiovascular prevention – cardiovascular risks after its perioperative withdrawal versus bleeding risks with its continuation – review and metaanalysis. J Intern Med 2005;257:399–414. 40. Palmer JD, Sparrow OC, Iannotti F. Postoperative hematoma: a 5-year survey and identification of avoidable risk factors. Neurosurgery 1994;35:1061–4 discussion 4–5.
41. Saloheimo P, Ahonen M, Juvela S, et al. Regular aspirin-use preceding the onset of primary intracerebral hemorrhage is an independent predictor for death. Stroke 2006;37:129–33. 42. Toussaint 3rd LG, Friedman JA, Wijdicks EF, et al. Influence of aspirin on outcome following aneurysmal subarachnoid hemorrhage. J Neurosurg 2004;101:921–5. 43. Di Minno MN, Prisco D, Ruocco AL, et al. Perioperative handling of patients on antiplatelet therapy with need for surgery. Intern Emerg Med 2009;4:279–88. 44. Broad L, Lee T, Conroy M, et al. Successful management of patients with a drugeluting coronary stent presenting for elective, non-cardiac surgery. Br J Anaesth 2007;98:19–22. 45. Savonitto S, D’Urbano M, Caracciolo M, et al. Urgent surgery in patients with a recently implanted coronary drug-eluting stent: a phase II study of ‘bridging’ antiplatelet therapy with tirofiban during temporary withdrawal of clopidogrel. Br J Anaesth 2010;104:285–91.
doi:http://dx.doi.org/10.1016/j.jocn.2011.12.018
Tuberculoma of the brain with unknown primary infection in an immunocompetent host Karthik Madhavan a, Gabriel Widi a, Ashish Shah a, Carol Petito b, Bruno V. Gallo c, Ricardo J. Komotar a,⇑ a
Department of Neurological Surgery, University of Miami School of Medicine, 1095 NW 14th Terrace, Room 2-06, Miami, FL 33136, USA Department of Pathology, University of Miami, Miami, FL, USA c Department of Neurology, University of Miami, Miami, FL, USA b
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Article history: Received 25 October 2011 Accepted 17 December 2011
Keywords: Brain Immunocompetent host Tubercular abscess Tuberculoma
a b s t r a c t Isolated cerebral tubercular abscess is uncommon in immunocompetent hosts. Our patient had a tuberculoma with no known primary and an atypical MRI appearance. We present a 67-year-old African– American male with complex partial seizures. A CT scan of the brain revealed a new right frontal mass which was not found on imaging two years prior. In view of the patient’s age and absence of any known primary malignancy, a primary brain tumor was considered to be the likely diagnosis. On MRI, the mass did not display ring enhancement or necrosis. Rather, the mass was lobulated, with near-uniform enhancement of the lesion with a surrounding high fluid-attenuated inversion recovery signal predominantly in the right frontal region, which extended inferiorly to the parietal region. The lesion showed a few punctate foci of low signal intensity on gradient echo MRI sequences, suggestive of hemorrhage. The mode of infection is unknown. However, it is important to include tuberculosis as a differential diagnosis, especially if the lesion appears to be non-primary, if a primary neoplasm or other metastases are not identified on further investigation, and in a patient of African–American ethnicity. To our knowledge, this is the first record of an isolated tubercular abscess of the brain in a developed country. Ó 2012 Elsevier Ltd. All rights reserved.
1. Introduction Tuberculoma is an uncommon manifestation of cerebral tuberculosis (TB), which is often visible on MRI as a ring-enhancing lesion. TB infection in the US is more common in the immigrant population. African–Americans represent the highest incidence group, at 41% within the TB-infected population of Americans born in the US.1 Tubercular abscess is more common in immunocompromized patients, although lately it has been documented more frequently in several immigrant populations from countries endemic to TB.2 Our patient, however, has lived in a developed country throughout his life and did not have any risk factors for TB. Further, his MRI was atypical with a lobulated solid mass rather than a ringenhancing lesion. We report the third patient with isolated tuberculoma with no primary source of infection, and the first from a developed country non-endemic for TB. Although this report is certainly not a direct indication of an increasing incidence of TB, it
⇑ Corresponding author. Tel.: +1 305 243 4058. E-mail address: [email protected] (R.J. Komotar).
highlights the importance of considering TB in atypical presentations of a primary brain mass. 2. Case report Our patient, a 67-year-old African–American male, presented with complex partial seizures involving the right upper extremity commencing three months prior to presentation. A brain CT scan revealed a right frontal mass just anterior to the left motor cortex, adjacent to the hand area (Fig. 1) that was not seen on previous imaging from approximately two years prior. The patient was admitted and commenced on anti-epileptic medication and he underwent investigation for a primary neoplasm or other metastases, which was negative. His past history was significant for diabetes mellitus, coronary artery disease (for which he underwent bypass surgery), hypertension, bronchitis, chronic sinusitis (for which he had an ethmoidectomy), mitral valve repair due to dilated cardiomyopathy with refractory congestive heart failure and pacemaker placement. Due to the pacemaker, MRI was initially unattainable. Importantly, he did not smoke tobacco, has not traveled outside of the US, and did not report any family history suggestive
Case Reports / Journal of Clinical Neuroscience 19 (2012) 1316–1320
may not bring about sufficient ventricular concentrations to be effective. Therefore, we believe that strong consideration should be given to IVT antibiotics in cases of intraventricular brain abscess. References 1. Lambo A, Nchimi A, Khamis J, et al. Primary intraventricular brain abscess. Neuroradiology 2003;45:908–10. 2. Lee TH, Chang WN, Su TM, et al. Clinical features and predictive factors of intraventricular rupture in patients who have bacterial brain abscesses. J Neurol Neurosurg Psychiatry 2007;78:303–9.
3. Mogilner A, Jallo G, Zagzag D, et al. Nocardia abscess of the choroid plexus: clinical and pathological case report. Neurosurgery 1998;43:949–52. 4. Pfausler B, Spiss H, Beer R, et al. Treatment of staphylococcal ventriculitis associated with external cerebrospinal fluid drains: a prospective randomized trial of intravenous compared with intraventricular vancomycin therapy. J Neurosurg 2003;98:1040–4. 5. Pruthi N, Devi BI, Shivshankar JJ, et al. Abscess – a rare fourth ventricular mass. Acta Neurochir 2007;149:1179–81. 6. Robinson EN. Staphylococcal meningitis can present as an abscess of a single lateral ventricle. Clin Infect Dis 1993;16:435–8. 7. Vajramani GV, Devi BI, Hegde T, et al. Intraventricular tuberculous abscess: a case report. Neurol India 1999;47:327–9.
doi:http://dx.doi.org/10.1016/j.jocn.2011.11.028
Perioperative management of a neurosurgical patient requiring antiplatelet therapy Khoi D. Than a,⇑, Pratik Rohatgi b, Thomas J. Wilson a, B. Gregory Thompson a a b
Department of Neurosurgery, University of Michigan, 1500 E. Medical Center Drive, Room 3552 TC, Ann Arbor, Michigan 48109-5338, USA Department of Neurosurgery, Pennsylvania State University, Hershey, Pennsylvania, USA
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Article history: Received 11 November 2011 Accepted 28 December 2011
Keywords: Antiplatelet therapy Aspirin Clopidogrel Eptifibatide Ibuprofen Neurovascular stent Ventriculoperitoneal shunt
a b s t r a c t In patients who undergo neurovascular stent placement with postoperative dual antiplatelet therapy to prevent in-stent thrombosis, there is no protocol for balancing the risk of acute stent thrombosis and bleeding if urgent neurosurgical procedures are required. We detail perioperative management of dual antiplatelet therapy in a 66-year-old man with a dolichoectatic aneurysm of the basilar artery treated with a Pipeline stent. Postoperatively, the patient was placed on aspirin and clopidogrel to prevent instent thrombosis. One month after the procedure, his neurological status declined secondary to obstructive hydrocephalus. His condition necessitated urgent placement of a ventriculoperitoneal shunt, despite the dual antiplatelet therapy for the flow-diverting Pipeline stent. Aspirin and clopidogrel were discontinued seven days prior to the planned shunt placement. To minimize time off antiplatelet therapy, aspirin was immediately replaced with ibuprofen. Eptifibatide was then started three days prior to surgery. The ibuprofen/eptifibatide bridge was discontinued at midnight prior to surgery. Aspirin was restarted on the first postoperative day and clopidogrel was restarted on the second postoperative day. The patient tolerated shunt placement without excessive bleeding or hemorrhagic complications. During the remainder of his hospital course, no evidence of stent thrombosis or intracranial hemorrhage was noted. We conclude that management of antiplatelet prophylaxis for neurovascular stent thrombosis in patients requiring urgent neurosurgical procedures may be successfully achieved by bridging aspirin and clopidogrel with ibuprofen and eptifibatide in the preoperative period. Ó 2012 Elsevier Ltd. All rights reserved.
1. Introduction Endovascular neurosurgery procedures are used to manage a growing number of pathologies, ranging from aneurysms to cerebral ischemic diseases to arteriovenous malformations.1–3 Many patients who undergo endovascular procedures are treated with neurovascular stents, requiring postoperative dual antiplatelet therapy with aspirin and clopidogrel to prevent in-stent thrombosis. If these patients require additional neurosurgical procedures, neurosurgeons are faced with the clinical challenge of balancing the risk of acute stent thrombosis with the risk of operative and postoperative bleeding. There are no standards on how to manage patients who undergo endovascular procedures with neurovascular stents who then require postoperative dual antiplatelet therapy with aspirin and clopidogrel to prevent in-stent thrombosis. The literature provides little guidance, as neurosurgical reports are sparse and the work
⇑ Corresponding author. Tel.: +1 734 936 5732; fax: +1 734 936 9294. E-mail address: [email protected] (K.D. Than).
from cardiovascular stenting provides few evidence-based recommendations regarding neurosurgical patients. In this review, we provide an illustrative case detailing the antiplatelet management of a patient who had a ventriculoperitoneal shunt (VPS) placed one month after receiving a Pipeline flow-diverting stent (ev3, Irvine, CA, USA) in the basilar artery, utilizing a preoperative ibuprofen and eptifibatide bridge in place of aspirin and clopidogrel. The patient was managed successfully using this protocol. The aim of this report is to provide one option for minimizing time off antiplatelet therapy in patients with a recently placed intracranial stent. 2. Case report A 66-year-old man presented with a six-month history of progressive dysarthria, urinary incontinence, episodes of choking and aspiration, ataxia, lack of coordination, disequilibrium, and headaches. Six months prior to these symptoms, the patient was in good health and worked as a police officer. Neurological examination demonstrated dysarthria, a wide-based ataxic gait, and right-sided appendicular dysmetria with bilateral tremor. A CT angiogram (CTA) and MRI demonstrated a 2.8 cm 3.1 cm 3.8 cm fusiform dolichoectatic aneurysm of the
Case Reports / Journal of Clinical Neuroscience 19 (2012) 1316–1320
basilar artery arising from both the left and right vertebral arteries through the vertebrobasilar junction and into the origin of the left anterior inferior cerebellar artery with compression of the pons and medulla (Fig. 1). He had a prominent ventricular system with enlarged temporal horns, convexity of the third ventricle, and compression of the fourth ventricle by the aneurysm mass (Fig. 2). Transependymal flow of cerebrospinal fluid (CSF) with mild aqueductal compression was also noted. Basilar cisterns were widely patent and there was no evidence of subarachnoid blood. A decision was made to manage his aneurysm with a Pipeline flow-diverting stent.4,5 The patient underwent coil embolization with Pipeline stenting without complication. His neurological status failed to significantly improve after the procedure, and his relative ventriculomegaly persisted. Repeat brain MRI one month after the procedure re-demonstrated obstructive hydrocephalus with mild increase in ventricular size from prior imaging. At that time, the patient’s overall medical status declined secondary to pneumonia and a urinary tract infection. His neurologic status remained poor and this was thought to be secondary to hydroceph-
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alus. Once his general medical issues were stabilized, CSF diversion was deemed necessary, despite the need for dual antiplatelet therapy. The patient was considered to be at high risk for both stent thrombosis and perioperative and postoperative bleeding. To minimize operative complications, it was determined that the patient should not have any platelet function inhibition during the operation. Consequently, to minimize time without antiplatelet therapy and thus minimize the risk for acute stent thrombosis, an antiplatelet bridge protocol was developed (Table 1). Both aspirin and clopidogrel were discontinued seven days prior to surgery. Aspirin was immediately replaced with ibuprofen at 600 mg twice daily. Eptifibatide was started three days prior to surgery by administering a loading bolus of 180 lg/kg followed by a continual infusion at 2 lg/kg per minute according to the manufacturer’s guidelines. Ibuprofen and eptifibatide were discontinued at midnight prior to the operation. VPS placement was completed without complication or excessive blood loss. Intracranial bleeding was not evident on postoperative head CT scan. Consequently,
Fig. 1. Preoperative (A) angiogram of the left vertebral artery showing a fusiform dolichoectatic aneurysm of the basilar artery with distal filling of the left posterior cerebral artery; and (B) axial T1-weighted, post-contrast brain MRI showing an aneurysm measuring 2.8 cm 3.1 cm 3.8 cm. (C) Axial post-stent T1-weighted, post-contrast brain MRI showing the lumen of the stent (arrow).
Fig. 2. Axial non-contrast head CT scans evaluating hydrocephalus: (A) following stent placement showing ventricular enlargement; (B) following ventriculoperitoneal shunt (VPS) placement without evidence of acute hemorrhage; and (C) three months following VPS placement showing decreased ventricular size without signs of intracranial hemorrhage.
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Table 1 Antiplatelet medication bridge protocol used to perioperatively manage the patient requiring antiplatelet therapy to balance the risks of acute neurovascular stent thrombosis and intracranial hemorrhage (ICH) Time of implementation
Intervention
Preoperative day 7
1. Discontinue aspirin 2. Discontinue clopidogrel 3. Start ibuprofen 600 mg PO BID
Preoperative day 3
4. Eptifibatide bolus at 180 lg/kg 5. Eptifibatide infusion at 2 lg/kg per minute
Midnight prior to surgery
6. Discontinue ibuprofen 7. Discontinue eptifibatide infusion
Postoperative day 1
8. Rule out ICH by CT scan 9. Start aspirin 325 mg PO daily
Postoperative day 2
10. Clopidogrel bolus at 300 mg 11. Resume clopidogrel at 75 mg PO daily
PO = by mouth; BID = twice per day.
the patient was restarted on aspirin on the first postoperative day and clopidogrel on the second postoperative day. During the remainder of his hospital course, no evidence of either stent thrombosis or intracranial hemorrhage was noted.
3. Discussion There are no evidence-based guidelines or standards of care for the management of antiplatelet therapy in patients with recently placed neurovascular stents who require intracranial procedures. Patients with neurovascular stents are commonly treated with dual antiplatelet therapy (aspirin and clopidogrel) to prevent stent thrombosis. This practice is based on the cardiology literature, as primary studies on neurovascular stents are sparse.6 Consensus statements agree that there is a high risk of thrombosis for bare metal coronary stents within eight weeks of implantation.7 Re-endothelialization of coronary vessels continues for four to six weeks after bare metal stent deployment and continues longer with drug-eluting stents. Consequently, dual antiplatelet therapy is continued for at least six months to allow the stent to endothelialize.8 Life-long low-dose aspirin therapy is recommended thereafter.9 Neurovascular stent thrombosis prophylaxis protocols based on the cardiac literature have been largely successful.10,11 In a oneyear follow-up study, 10 patients with symptomatic intracranial atherosclerotic arteries (>60% stenosis) treated by stent placement and maintained on clopidogrel for six months and aspirin indefinitely did not demonstrate re-stenosis (>50%) or ischemic events.10 Patients enrolled in the National Institutes of Health Multicenter Wingspan Intracranial Stent Registry were maintained on clopidogrel for at least four weeks following intracranial stent placement and continued on aspirin indefinitely without significant complication.12,13 Stent patency depends on the inhibition of platelet aggregation. Aspirin inhibits platelet aggregation for the lifespan of platelets by irreversibly inhibiting the cyclooxygenase-1 (COX1) enzyme, which catalyzes the conversion of arachidonic acid to prostaglandin H2.14,15 This is the first concomitant step in platelet-dependant thromboxane A2 (TXA2) generation which, in turn, stimulates activation of new platelets and promotes platelet aggregation.16 Platelet function returns roughly to 50% of normal six days after stopping therapy, as platelets nominally turn over by 10% daily.17 Normal hemostasis is achieved when 20% of platelets have normal COX1 function.18 In healthy volunteers, bleeding times after daily aspirin therapy largely normalize 48 hours after the last dose.19 The abrupt discontinuation of aspirin therapy is associated with
a rebound pro-thrombotic state due to a rebound excess of TXA2 production, which decreases fibrinolytic activity.20,21 Non-steroidal anti-inflammatory drugs (NSAID), such as ibuprofen and naproxen, reversibly inhibit COX1 in a dose-dependent manner with less potency than aspirin.18,22,23 A single dose of ibuprofen inhibits platelet aggregation within two hours, but normalizes after 12 hours.24 In a study of healthy volunteers ingesting 700 mg of ibuprofen every eight hours, platelet function normalized 24 hours after the last dose for all participants as assessed by platelet function analysis (PFA-100 assay).25 Clopidogrel decreases the risk of coronary stent thrombosis and recurrent stroke by 30% but, due to its greater antiplatelet effect compared to COX1 inhibitors, it also increases the risk of spontaneous hemorrhage by 38% compared to placebo.26,27 Clopidogrel, a thienopyridine, decreases thrombosis by irreversible non-competitive inhibition of the P2Y12 adenosine diphosphate receptor.14,28 This receptor promotes platelet aggregation by activating the glycoprotein IIb/IIIa (GP IIb/IIIa) receptor and facilitates fibrinogen-mediated platelet cross-linking.17 Clopidogrel produces measurable inhibition of platelets 12 hours after ingestion of a standard 75 mg dose.20 Loading doses of 300 mg and 600 mg reach therapeutic levels after six and two hours, respectively. Maximum inhibition occurs after four to seven days of continuous treatment, which increases bleeding times from 1.5–3 times that of normal.26 Platelet function normalizes seven days after the last dose.17 Additionally, as clopidogrel has no effect on the COX1 system, its antiplatelet effects work in synergy with those of aspirin.28 Abciximab, eptifibatide, and tirofiban are GP IIb/IIIa antagonists that inhibit platelet aggregation and activation more potently than NSAID or thienopyridines.29 GP IIb/IIIa is a platelet integrin that functions as the main receptor for fibrinogen, which cross-links different platelets, binds to vitronectin, and also binds to von Willebrand factor. Thus, the GP IIb/IIIa antagonists block platelet aggregation regardless of the triggering pathway.17 Full hemostasis is restored when half of the integrin receptors can bind to fibrinogen.18 Eptifibatide was selected for the bridging protocol used in the presented case because of its pharmacokinetic profile. After discontinuing eptifibatide, bleeding times normalize within 15 minutes and platelet function recovers to more than 50% after six hours.20 Premature discontinuation of antiplatelet therapy provides the greatest risk for stent thrombosis.21 Cardiac stent thrombosis occurs roughly 10 days after premature discontinuation of aspirin therapy.26 One neurosurgical study demonstrated that the premature discontinuation of clopidogrel increased stent thrombosis by a hazard ratio of 57, which led to an increase in mortality of 45%.30 Stopping clopidogrel for major surgery within the first three weeks after drug-eluting coronary artery stent placement increased mortality by 30% to 86%.31 Patients undergoing non-cardiac surgery during the coronary stent endothelialization window are at five to 10 times greater risk of stent thrombosis leading to myocardial infarction and mortality as compared to matched patients for whom surgery is appropriately delayed and managed under maximal medical therapy.26,32 Such studies highlight the necessity to maintain appropriate antiplatelet therapy, although the commonly used endpoint in the cardiac literature of myocardial infarction and mortality may be a less-sensitive measure of thrombosis than is needed to assess for neurovascular compromise. The increased complexity of the hemostatic environment in the neurovasculature compared to that of the coronary system suggests that translating cardiology studies to neurosurgical patients may not be straightforward.24,33,34 A growing body of evidence supports the theory that biological differences may lead to different clinical outcomes with regard to long-term stent patency. A retrospective study of 67 patients who underwent intracranial stent placement while on a standard
Case Reports / Journal of Clinical Neuroscience 19 (2012) 1316–1320
antiplatelet regimen demonstrated a re-stenosis rate seven times higher than with bare metal stents placed in the coronary arteries.35 In that study, 10% of patients had subacute stent thrombosis after intracranial stenting, despite antiplatelet therapy. Additionally, in-stent re-stenosis secondary to neointimal hyperplasia has been observed in up to 30% of intracranial stents.36 One case study suggests that on angiography, in-stent platelet aggregation can appear identical to re-stenosis, stressing the importance of maintaining antiplatelet agents.37 However, the risks of acute stent thrombosis must be balanced with the complications of antiplatelet therapy for patients requiring urgent surgery, such as for our patient.7 Patients on any level of antiplatelet therapy are at an increased risk for hemorrhage, ranging from 30% to 50%.38 Additionally, dual antiplatelet therapy with aspirin and clopidogrel increases the risk of spontaneous bleeding by 33%.21 Despite the increased blood loss attributed to antiplatelet therapy, morbidity and mortality rates are not increased except during intracranial neurosurgery.39 Aspirin therapy is a major risk factor linked with fatal outcomes in intracranial neurosurgery secondary to intracerebral hematoma.40 Indirect evidence is mixed regarding how significantly the risk of hemorrhage is increased by aspirin. Chronic aspirin use prior to an intracerebral hemorrhage increases the risk of death by 2.5 times, while a similar study reported no difference in clinical outcome for patients on aspirin therapy following aneurysmal subarachnoid hemorrhage.41,42 For patients with recently placed coronary artery stents, several guidelines recommend that intracerebral interventions should be delayed until the stents are endothelialized.43 When neurosurgical procedures cannot be significantly delayed, some guidelines recommend discontinuing aspirin and clopidogrel five to seven days prior to surgery and restarting antiplatelet therapy within 24 hours after operation.16 Other recommendations include discontinuing clopidogrel 7 days prior to surgery while maintaining aspirin and possibly bridging therapy with eptifibatide and heparin.26 In small studies, tirofiban has been successfully substituted for clopidogrel to bridge patients with drug-eluting stents in need of urgent surgery44,45; however, these studies did not include patients with intracranial disease or history of stroke, and aspirin usage was not standardized. 4. Conclusion Management of antiplatelet prophylaxis for neurovascular stent thrombosis in a patient in need of an urgent neurosurgical procedure was successfully achieved by bridging aspirin and clopidogrel with ibuprofen and eptifibatide in the preoperative period. To our knowledge, this novel approach has not yet been described elsewhere. These substitutions were selected on the basis of each the pharmacokinetic profile of each drug, recommendations found in consensus guidelines, and related case reports. Additional experience with this protocol is necessary to definitively conclude that it is appropriate to manage this clinical situation, but it is our hope that this report provides one option for neurosurgeons faced with similar challenges. References 1. Meyers PM, Schumacher HC, Higashida RT, et al. Indications for the performance of intracranial endovascular neurointerventional procedures: a scientific statement from the American Heart Association Council on Cardiovascular Radiology and Intervention, Stroke Council, Council on Cardiovascular Surgery and Anesthesia, Interdisciplinary Council on Peripheral Vascular Disease, and Interdisciplinary Council on Quality of Care and Outcomes Research. Circulation 2009;119:2235–49. 2. Wakhloo AK, Deleo 3rd MJ, Brown MM. Advances in interventional neuroradiology. Stroke 2009;40:e305–12. 3. Walton MT, Gress DR, Higashida RT. Controversies in neurological surgery: neurovascular diseases. New York: Thieme; 2006.
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4. Fiorella D, Lylyk P, Szikora I, et al. Curative cerebrovascular reconstruction with the Pipeline embolization device: the emergence of definitive endovascular therapy for intracranial aneurysms. J Neurointerv Surg 2009;1:56–65. 5. van Rooij WJ, Sluzewski M. Perforator infarction after placement of a pipeline flow-diverting stent for an unruptured A1 aneurysm. AJNR Am J Neuroradiol 2010;31:E43–4. 6. Wojak JC, Dunlap DC, Hargrave KR, et al. Intracranial angioplasty and stenting: long-term results from a single center. AJNR Am J Neuroradiol 2006;27:1882–92. 7. Riddell JW, Chiche L, Plaud B, et al. Coronary stents and noncardiac surgery. Circulation 2007;116:e378–82. 8. Qureshi AI, Luft AR, Sharma M, et al. Prevention and treatment of thromboembolic and ischemic complications associated with endovascular procedures: Part II–Clinical aspects and recommendations. Neurosurgery 2000;46:1360–75 discussion 75–6. 9. Patrono C, Garcia Rodriguez LA, Landolfi R, et al. Low-dose aspirin for the prevention of atherothrombosis. N Engl J Med 2005;353:2373–83. 10. Lee CY, Yim MB. Primary stent therapy for symptomatic intracranial atherosclerotic stenosis: 1-year follow-up angiographic and midterm clinical outcomes. J Neurosurg 2006;105:235–41. 11. Zaidat OO. Periprocedural management of patients with endovascular treatment of intracranial atherosclerotic disease. J Neuroimaging 2009;19(Suppl. 1):35S–8S. 12. Fiorella D, Levy EI, Turk AS, et al. US multicenter experience with the wingspan stent system for the treatment of intracranial atheromatous disease: periprocedural results. Stroke 2007;38:881–7. 13. Nahab F, Lynn MJ, Kasner SE, et al. Risk factors associated with major cerebrovascular complications after intracranial stenting. Neurology 2009;72:2014–9. 14. Lippi G, Favaloro EJ, Salvagno GL, et al. Laboratory assessment and perioperative management of patients on antiplatelet therapy: from the bench to the bedside. Clin Chim Acta 2009;405:8–16. 15. Silber S, Albertsson P, Aviles FF, et al. Guidelines for percutaneous coronary interventions. The Task Force for Percutaneous Coronary Interventions of the European Society of Cardiology. Eur Heart J 2005;26:804–47. 16. Cahill RA, McGreal GT, Crowe BH, et al. Duration of increased bleeding tendency after cessation of aspirin therapy. J Am Coll Surg 2005;200:564–73. 17. Aiyagari V. Counteracting the effects of anticoagulants and antiplatelet agents during neurosurgical emergencies. Neurosurgery 2006;59:E1152. 18. Lecompte T, Hardy JF. Antiplatelet agents and perioperative bleeding. Can J Anaesth 2006;53:S103–112. 19. Sonksen JR, Kong KL, Holder R. Magnitude and time course of impaired primary haemostasis after stopping chronic low and medium dose aspirin in healthy volunteers. Br J Anaesth 1999;82:360–5. 20. Fiehler J, Ries T. Prevention and treatment of thromboembolism during endovascular aneurysm therapy. Klin Neuroradiol 2009;19:73–81. 21. Mollmann H, Nef HM, Hamm CW, et al. How to manage patients with need for antiplatelet therapy in the setting of (un-)planned surgery. Clin Res Cardiol 2009;98:8–15. 22. Catella-Lawson F, Reilly MP, Kapoor SC, et al. Cyclooxygenase inhibitors and the antiplatelet effects of aspirin. N Engl J Med 2001;345:1809–17. 23. Schafer AI. Effects of nonsteroidal anti-inflammatory therapy on platelets. Am J Med 1999;106:25S–36S. 24. Gerlach R, Krause M, Seifert V, et al. Hemostatic and hemorrhagic problems in neurosurgical patients. Acta Neurochir (Wien) 2009;151:873–900 discussion. 25. Goldenberg NA, Jacobson L, Manco-Johnson MJ. Brief communication: duration of platelet dysfunction after a 7-day course of Ibuprofen. Ann Intern Med 2005;142:506–9. 26. Chassot PG, Delabays A, Spahn DR. Perioperative antiplatelet therapy: the case for continuing therapy in patients at risk of myocardial infarction. Br J Anaesth 2007;99:316–28. 27. Yusuf S, Zhao F, Mehta SR, et al. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med 2001;345:494–502. 28. Sharis PJ, Cannon CP, Loscalzo J. The antiplatelet effects of ticlopidine and clopidogrel. Ann Intern Med 1998;129:394–405. 29. Meadows TA, Bhatt DL. Clinical aspects of platelet inhibitors and thrombus formation. Circ Res 2007;100:1261–75. 30. Fiorella D, Hsu D, Woo HH, et al. Very late thrombosis of a pipeline embolization device construct: case report. Neurosurgery 2010;67:onsE 313–314 discussion onsE4. 31. Sharma AK, Ajani AE, Hamwi SM, et al. Major noncardiac surgery following coronary stenting: when is it safe to operate? Catheter Cardiovasc Interv 2004;63:141–5. 32. Luckie M, Khattar RS, Fraser D. Non-cardiac surgery and antiplatelet therapy following coronary artery stenting. Heart 2009;95:1303–8. 33. Qureshi AI. Editorial comment–Thromboembolic events during neuroendovascular procedures. Stroke 2003;34:1728–9. 34. Qureshi AI, Luft AR, Sharma M, et al. Prevention and treatment of thromboembolic and ischemic complications associated with endovascular procedures: Part I–Pathophysiological and pharmacological features. Neurosurgery 2000;46:1344–59. 35. Riedel CH, Tietke M, Alfke K, et al. Subacute stent thrombosis in intracranial stenting. Stroke 2009;40:1310–4. 36. Korinth MC. Low-dose aspirin before intracranial surgery–results of a survey among neurosurgeons in Germany. Acta Neurochir (Wien) 2006;148:1189–96 discussion 96.
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37. Mazighi M, Saint Maurice JP, Bresson D, et al. Platelet aggregation in intracranial stents may mimic in-stent restenosis. AJNR Am J Neuroradiol 2010;31:496–7. 38. Samama CM, Djoudi R, Lecompte T, et al. Perioperative platelet transfusion: recommendations of the Agence Francaise de Securite Sanitaire des Produits de Sante (AFSSaPS) 2003. Can J Anaesth 2005;52:30–7. 39. Burger W, Chemnitius JM, Kneissl GD, et al. Low-dose aspirin for secondary cardiovascular prevention – cardiovascular risks after its perioperative withdrawal versus bleeding risks with its continuation – review and metaanalysis. J Intern Med 2005;257:399–414. 40. Palmer JD, Sparrow OC, Iannotti F. Postoperative hematoma: a 5-year survey and identification of avoidable risk factors. Neurosurgery 1994;35:1061–4 discussion 4–5.
41. Saloheimo P, Ahonen M, Juvela S, et al. Regular aspirin-use preceding the onset of primary intracerebral hemorrhage is an independent predictor for death. Stroke 2006;37:129–33. 42. Toussaint 3rd LG, Friedman JA, Wijdicks EF, et al. Influence of aspirin on outcome following aneurysmal subarachnoid hemorrhage. J Neurosurg 2004;101:921–5. 43. Di Minno MN, Prisco D, Ruocco AL, et al. Perioperative handling of patients on antiplatelet therapy with need for surgery. Intern Emerg Med 2009;4:279–88. 44. Broad L, Lee T, Conroy M, et al. Successful management of patients with a drugeluting coronary stent presenting for elective, non-cardiac surgery. Br J Anaesth 2007;98:19–22. 45. Savonitto S, D’Urbano M, Caracciolo M, et al. Urgent surgery in patients with a recently implanted coronary drug-eluting stent: a phase II study of ‘bridging’ antiplatelet therapy with tirofiban during temporary withdrawal of clopidogrel. Br J Anaesth 2010;104:285–91.
doi:http://dx.doi.org/10.1016/j.jocn.2011.12.018
Tuberculoma of the brain with unknown primary infection in an immunocompetent host Karthik Madhavan a, Gabriel Widi a, Ashish Shah a, Carol Petito b, Bruno V. Gallo c, Ricardo J. Komotar a,⇑ a
Department of Neurological Surgery, University of Miami School of Medicine, 1095 NW 14th Terrace, Room 2-06, Miami, FL 33136, USA Department of Pathology, University of Miami, Miami, FL, USA c Department of Neurology, University of Miami, Miami, FL, USA b
a r t i c l e
i n f o
Article history: Received 25 October 2011 Accepted 17 December 2011
Keywords: Brain Immunocompetent host Tubercular abscess Tuberculoma
a b s t r a c t Isolated cerebral tubercular abscess is uncommon in immunocompetent hosts. Our patient had a tuberculoma with no known primary and an atypical MRI appearance. We present a 67-year-old African– American male with complex partial seizures. A CT scan of the brain revealed a new right frontal mass which was not found on imaging two years prior. In view of the patient’s age and absence of any known primary malignancy, a primary brain tumor was considered to be the likely diagnosis. On MRI, the mass did not display ring enhancement or necrosis. Rather, the mass was lobulated, with near-uniform enhancement of the lesion with a surrounding high fluid-attenuated inversion recovery signal predominantly in the right frontal region, which extended inferiorly to the parietal region. The lesion showed a few punctate foci of low signal intensity on gradient echo MRI sequences, suggestive of hemorrhage. The mode of infection is unknown. However, it is important to include tuberculosis as a differential diagnosis, especially if the lesion appears to be non-primary, if a primary neoplasm or other metastases are not identified on further investigation, and in a patient of African–American ethnicity. To our knowledge, this is the first record of an isolated tubercular abscess of the brain in a developed country. Ó 2012 Elsevier Ltd. All rights reserved.
1. Introduction Tuberculoma is an uncommon manifestation of cerebral tuberculosis (TB), which is often visible on MRI as a ring-enhancing lesion. TB infection in the US is more common in the immigrant population. African–Americans represent the highest incidence group, at 41% within the TB-infected population of Americans born in the US.1 Tubercular abscess is more common in immunocompromized patients, although lately it has been documented more frequently in several immigrant populations from countries endemic to TB.2 Our patient, however, has lived in a developed country throughout his life and did not have any risk factors for TB. Further, his MRI was atypical with a lobulated solid mass rather than a ringenhancing lesion. We report the third patient with isolated tuberculoma with no primary source of infection, and the first from a developed country non-endemic for TB. Although this report is certainly not a direct indication of an increasing incidence of TB, it
⇑ Corresponding author. Tel.: +1 305 243 4058. E-mail address: [email protected] (R.J. Komotar).
highlights the importance of considering TB in atypical presentations of a primary brain mass. 2. Case report Our patient, a 67-year-old African–American male, presented with complex partial seizures involving the right upper extremity commencing three months prior to presentation. A brain CT scan revealed a right frontal mass just anterior to the left motor cortex, adjacent to the hand area (Fig. 1) that was not seen on previous imaging from approximately two years prior. The patient was admitted and commenced on anti-epileptic medication and he underwent investigation for a primary neoplasm or other metastases, which was negative. His past history was significant for diabetes mellitus, coronary artery disease (for which he underwent bypass surgery), hypertension, bronchitis, chronic sinusitis (for which he had an ethmoidectomy), mitral valve repair due to dilated cardiomyopathy with refractory congestive heart failure and pacemaker placement. Due to the pacemaker, MRI was initially unattainable. Importantly, he did not smoke tobacco, has not traveled outside of the US, and did not report any family history suggestive