Michael Nabil Khoury1, Symeon Missios1, Natasha Edwin1, Susmita Sakruti1, Gene Barnett1, Glen Stevens1, David M Peereboom1, Alok A Khorana1, Manmeet S Ahluwalia1. 1. Department of Neurooncology, H. Lee Moffitt Cancer Center and Research Institute, 12902 Magnolia Drive, Tampa, Florida (M.N.K.); Department of Oncological Sciences, University of South Florida, Tampa, Florida (M.N.K.); Department of Neurosurgery, Louisiana State University, 1501 Kings Hwy, Shreveport, Louisiana (S.M.); Department of Internal Medicine, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio (N.E.); Department of Hematology/Oncology, University Hospital, 11100 Euclid Avenue, Cleveland, Ohio (S.S.); Department of Neurosurgery,Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio (G.B.); Department of Neurology,Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio (G.S.); Department of Hematology and Oncology,Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio (D.M.P., A.A.K., M.S.A.); Rose Ella Burkhardt Brain Tumor and Neuro-Oncology Center, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio (G.B., G.S., D.M.P., M.S.A.).
Abstract
BACKGROUND: Venous thromboembolism (VTE) is a complication of glioblastoma. Anticoagulating patients with glioblastoma carries a theoretical risk of intracranial hemorrhage (ICH). METHODS: We performed a retrospective cohort study of consecutive glioblastoma patients (2007-2013) diagnosed with VTE. RESULTS: The study population comprised of 523 glioblastoma patients of whom 173 (33%) had VTE events. Seventeen (10%) had ICH: 6 (35%) subdural hematomas and 11 (65%) intratumoral hemorrhages. In total, 4 patients with ICH required neurosurgical intervention. Enhancement in the area of subsequent intratumoral hemorrhage was noted in 9 of 10 with available pre-ICH scans. Multivariable regression did not show associations between ICH and tumor enhancement diameter or use of vascular-endothelial-growth-factor inhibitor. Fifteen (16%) patients receiving anticoagulation had ICH compared with 2 (2.6%) not receiving anticoagulation (P = .005). The method of anticoagulation was not associated with development of ICH. Median survival times from nondistal VTE diagnosis to death were 8.0 and 3.5 months (P = .05) in patients receiving anticoagulation and those not on anticoagulation, respectively. CONCLUSION: Patients with glioblastoma and VTE on anticoagulation have increased incidence of ICH. However, development of ICH was not associated with lower median survival from time of VTE. Intratumoral hemorrhage occurred within the enhancing portion of tumor; however, no relationship was identified between the development of ICH and (i) the median diameter of enhancement or (ii) type of anticoagulant used. However, patients with absence of enhancing tumor did not have intratumoral bleed, suggesting gross total resection may limit this adverse outcome. It is appropriate to initiate anticoagulation in glioblastoma patients with VTEs.
BACKGROUND: Venous thromboembolism (VTE) is a complication of glioblastoma. Anticoagulating patients with glioblastoma carries a theoretical risk of intracranial hemorrhage (ICH). METHODS: We performed a retrospective cohort study of consecutive glioblastoma patients (2007-2013) diagnosed with VTE. RESULTS: The study population comprised of 523 glioblastoma patients of whom 173 (33%) had VTE events. Seventeen (10%) had ICH: 6 (35%) subdural hematomas and 11 (65%) intratumoral hemorrhages. In total, 4 patients with ICH required neurosurgical intervention. Enhancement in the area of subsequent intratumoral hemorrhage was noted in 9 of 10 with available pre-ICH scans. Multivariable regression did not show associations between ICH and tumor enhancement diameter or use of vascular-endothelial-growth-factor inhibitor. Fifteen (16%) patients receiving anticoagulation had ICH compared with 2 (2.6%) not receiving anticoagulation (P = .005). The method of anticoagulation was not associated with development of ICH. Median survival times from nondistal VTE diagnosis to death were 8.0 and 3.5 months (P = .05) in patients receiving anticoagulation and those not on anticoagulation, respectively. CONCLUSION: Patients with glioblastoma and VTE on anticoagulation have increased incidence of ICH. However, development of ICH was not associated with lower median survival from time of VTE. Intratumoral hemorrhage occurred within the enhancing portion of tumor; however, no relationship was identified between the development of ICH and (i) the median diameter of enhancement or (ii) type of anticoagulant used. However, patients with absence of enhancing tumor did not have intratumoral bleed, suggesting gross total resection may limit this adverse outcome. It is appropriate to initiate anticoagulation in glioblastoma patients with VTEs.
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