The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Daniel E Singer - One of the best experts on this subject based on the ideXlab platform.
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comparison of frequency and outcome of major gastrointestinal Hemorrhage in patients with atrial fibrillation on versus not receiving warfarin therapy from the atria and atria cvrn cohorts
American Journal of Cardiology, 2015Co-Authors: Margaret C Fang, Yuchiao Chang, Jeffrey M Ashburner, Kristi Reynolds, Lisa Fredman, Katie M Applebaum, Daniel E SingerAbstract:To date, there have been few studies evaluating outcomes of patients with atrial fibrillation (AF) who have experienced gastrointestinal (GI) Hemorrhages. We examined short- and long-term mortality of major GI Hemorrhage in patients with AF on and off warfarin in recent clinical care. We evaluated this association in the large Anticoagulation and Risk Factors in Atrial fibrillation (ATRIA) and ATRIA-Cardiovascular Research Network (CVRN) California community-based cohorts of patients with AF (study years 1996 to 2003 and 2006 to 2009, respectively), where all events were clinician adjudicated. We used proportional hazards regression with propensity score adjustment to estimate the short- (30 days) and long-term (>30 days for 1 year) mortality rate ratio for patients using warfarin compared with those who were not using warfarin at the time of GI Hemorrhage. In the 414 ATRIA participants with major GI Hemorrhage, 54% were taking warfarin at the time of the Hemorrhage; in the 361 ATRIA-CVRN participants with major GI Hemorrhage, 58% were taking warfarin. Warfarin use at the time of GI Hemorrhage was not associated with 30-day mortality in the ATRIA cohort but was associated with significantly reduced 30-day mortality in the ATRIA-CVRN cohort (adjusted mortality rate ratio [95% confidence interval], ATRIA 0.97 [0.54 to 1.74]; ATRIA-CVRN 0.38 [0.17 to 0.83]). There was a modest suggestion of lower mortality on warfarin after 30 days in both cohorts. In conclusion, our study demonstrates that GI Hemorrhages on warfarin are certainly no worse and may be less life threatening than those occurring off warfarin. These findings are in stark contrast to the deleterious effect of warfarin on mortality from intracranial Hemorrhage and add another factor favoring anticoagulation in clinical decision making for patients with AF.
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death and disability from warfarin associated intracranial and extracranial Hemorrhages
The American Journal of Medicine, 2007Co-Authors: Margaret C Fang, Elaine M Hylek, Lori E Henault, Nancy G Jensvold, Yuchiao Chang, Alan S Go, Daniel E SingerAbstract:OBJECTIVES: Little is known about the outcomes of patients who have hemorrhagic complications while receiving warfarin therapy. We examined the rates of death and disability resulting from warfarin-associated intracranial and extracranial Hemorrhages in a large cohort of patients with atrial fibrillation. METHODS: We assembled a cohort of 13,559 adults with nonvalvular atrial fibrillation and identified patients hospitalized for warfarin-associated intracranial and major extracranial Hemorrhage. Data on functional disability at discharge and 30-day mortality were obtained from a review of medical charts and state death certificates. The relative odds of 30-day mortality by Hemorrhage type were calculated using multivariable logistic regression. RESULTS: We identified 72 intracranial and 98 major extracranial Hemorrhages occurring in more than 15,300 person-years of warfarin exposure. At hospital discharge, 76% of patients with intracranial Hemorrhage had severe disability or died, compared with only 3% of those with major extracranial Hemorrhage. Of the 40 deaths from warfarin-associated Hemorrhage that occurred within 30 days, 35 (88%) were from intracranial Hemorrhage. Compared with extracranial Hemorrhages, intracranial events were strongly associated with 30-day mortality (odds ratio 20.8 [95% confidence interval, 6.0-72]) even after adjusting for age, sex, anticoagulation intensity on admission, and other coexisting illnesses. CONCLUSIONS: Among anticoagulated patients with atrial fibrillation, intracranial Hemorrhages caused approximately 90% of the deaths from warfarin-associated Hemorrhage and the majority of disability among survivors. When considering anticoagulation, patients and clinicians need to weigh the risk of intracranial Hemorrhage far more than the risk of all major Hemorrhages.
Jeffrey I Zwicker - One of the best experts on this subject based on the ideXlab platform.
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intracranial Hemorrhage in patients with brain metastases treated with therapeutic enoxaparin a matched cohort study
Blood, 2015Co-Authors: Jessica Donato, Federico Campigotto, Erika Coletti, Griffin M Weber, Donna Neuberg, Erik J Uhlmann, Jeffrey I ZwickerAbstract:Venous thromboembolism occurs frequently in patients with cancer who have brain metastases, but there is limited evidence supporting the safety of therapeutic anticoagulation. To assess the risk for intracranial Hemorrhage associated with the administration of therapeutic doses of low-molecular-weight heparin, we performed a matched, retrospective cohort study of 293 patients with cancer with brain metastases (104 with therapeutic enoxaparin and 189 controls). A blinded review of radiographic imaging was performed, and intracranial Hemorrhages were categorized as trace, measurable, and significant. There were no differences observed in the cumulative incidence of intracranial Hemorrhage at 1 year in the enoxaparin and control cohorts for measurable (19% vs 21%; Gray test, P = .97; hazard ratio, 1.02; 90% confidence interval [CI], 0.66-1.59), significant (21% vs 22%; P = .87), and total (44% vs 37%; P = .13) intracranial Hemorrhages. The risk for intracranial Hemorrhage was fourfold higher (adjusted hazard ratio, 3.98; 90% CI, 2.41-6.57; P P = .65). We conclude that intracranial Hemorrhage is frequently observed in patients with brain metastases, but that therapeutic anticoagulation does not increase the risk for intracranial Hemorrhage.
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intracranial Hemorrhage in patients with brain metastases treated with therapeutic enoxaparin a matched cohort study
Blood, 2015Co-Authors: Jessica Donato, Federico Campigotto, Erika Coletti, Griffin M Weber, Donna Neuberg, Erik J Uhlmann, Jeffrey I ZwickerAbstract:Venous thromboembolism occurs frequently in patients with cancer who have brain metastases, but there is limited evidence supporting the safety of therapeutic anticoagulation. To assess the risk for intracranial Hemorrhage associated with the administration of therapeutic doses of low-molecular-weight heparin, we performed a matched, retrospective cohort study of 293 patients with cancer with brain metastases (104 with therapeutic enoxaparin and 189 controls). A blinded review of radiographic imaging was performed, and intracranial Hemorrhages were categorized as trace, measurable, and significant. There were no differences observed in the cumulative incidence of intracranial Hemorrhage at 1 year in the enoxaparin and control cohorts for measurable (19% vs 21%; Gray test, P = .97; hazard ratio, 1.02; 90% confidence interval [CI], 0.66-1.59), significant (21% vs 22%; P = .87), and total (44% vs 37%; P = .13) intracranial Hemorrhages. The risk for intracranial Hemorrhage was fourfold higher (adjusted hazard ratio, 3.98; 90% CI, 2.41-6.57; P < .001) in patients with melanoma or renal cell carcinoma (N = 60) than lung cancer (N = 153), but the risk was not influenced by the administration of enoxaparin. Overall survival was similar for the enoxaparin and control cohorts (8.4 vs 9.7 months; Log-rank, P = .65). We conclude that intracranial Hemorrhage is frequently observed in patients with brain metastases, but that therapeutic anticoagulation does not increase the risk for intracranial Hemorrhage.
Wink S Fisher - One of the best experts on this subject based on the ideXlab platform.
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screening for ocular Hemorrhages in patients with ruptured cerebral aneurysms a prospective study of 99 patients
Neurosurgery, 1997Co-Authors: Tyler R Frizzell, Robert Morris, Cammie Quinn, Ferenc Kuhn, Wink S FisherAbstract:BACKGROUND: Terson's syndrome (vitreous Hemorrhage) and other ocular Hemorrhages (retinal Hemorrhages) have been reported to occur in up to 40% of patients with ruptured cerebral aneurysms. Because microsurgical vitrectomy can safely restore vision in patients with visual loss secondary to Terson's syndrome, we hypothesized that prospectively screening a selected group of patients with aneurysms would result in a higher rate of vitrectomy in patients with more extensive subarachnoid Hemorrhage. METHODS: Ninety-nine patients with ruptured cerebral aneurysms were prospectively screened for Terson's syndrome and other forms of ocular Hemorrhage by an ophthalmologist. Follow-up data were obtained for seven of eight cases of Terson's syndrome, and vitrectomy was performed for visual restoration when indicated. RESULTS: Ocular Hemorrhages were present in 17% of patients with ruptured cerebral aneurysms, and Terson's syndrome was present in 8% of patients. Screening of patients with histories of transient or prolonged comas sensitively identified patients with ocular Hemorrhages in 100% of the patients with Terson's syndrome and 89% of the patients with other ocular Hemorrhages. Fifty-five percent of the patients in the overall series had histories of transient or prolonged comas, and 53% (specificity) of those patients had ocular Hemorrhages. Two of the eight patients with Terson's syndrome underwent vitrectomy, with dramatic improvement in vision. No other ocular Hemorrhages required surgery. CONCLUSIONS: Ophthalmological screening of patients with histories of transient or prolonged comas after ruptured cerebral aneurysms very sensitively identifies patients with ocular Hemorrhages, which are relatively common in patients with subarachnoid Hemorrhage treated in an academic neurosurgical practice. The present study underestimates the true incidence of Terson's syndrome in that patients who died shortly after their subarachnoid Hemorrhage were not included. Vitrectomy for patients who do not exhibit spontaneous improvement in vision results in a dramatic reversal of blindness.
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screening for ocular Hemorrhages in patients with ruptured cerebral aneurysms a prospective study of 99 patients
Neurosurgery, 1997Co-Authors: Tyler R Frizzell, Robert Morris, Cammie Quinn, Ferenc Kuhn, Wink S FisherAbstract:BACKGROUND: Terson's syndrome (vitreous Hemorrhage) and other ocular Hemorrhages (retinal Hemorrhages) have been reported to occur in up to 40% of patients with ruptured cerebral aneurysms. Because microsurgical vitrectomy can safely restore vision in patients with visual loss secondary to Terson's syndrome, we hypothesized that prospectively screening a selected group of patients with aneurysms would result in a higher rate of vitrectomy in patients with more extensive subarachnoid Hemorrhage. METHODS: Ninety-nine patients with ruptured cerebral aneurysms were prospectively screened for Terson's syndrome and other forms of ocular Hemorrhage by an ophthalmologist. Follow-up data were obtained for seven of eight cases of Terson's syndrome, and vitrectomy was performed for visual restoration when indicated. RESULTS: Ocular Hemorrhages were present in 17% of patients with ruptured cerebral aneurysms, and Terson's syndrome was present in 8% of patients. Screening of patients with histories of transient or prolonged comas sensitively identified patients with ocular Hemorrhages in 100% of the patients with Terson's syndrome and 89% of the patients with other ocular Hemorrhages. Fifty-five percent of the patients in the overall series had histories of transient or prolonged comas, and 53% (specificity) of those patients had ocular Hemorrhages. Two of the eight patients with Terson's syndrome underwent vitrectomy, with dramatic improvement in vision. No other ocular Hemorrhages required surgery. CONCLUSIONS: Ophthalmological screening of patients with histories of transient or prolonged comas after ruptured cerebral aneurysms very sensitively identifies patients with ocular Hemorrhages, which are relatively common in patients with subarachnoid Hemorrhage treated in an academic neurosurgical practice. The present study underestimates the true incidence of Terson's syndrome in that patients who died shortly after their subarachnoid Hemorrhage were not included. Vitrectomy for patients who do not exhibit spontaneous improvement in vision results in a dramatic reversal of blindness.
Steven Brem - One of the best experts on this subject based on the ideXlab platform.
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terson s syndrome a reversible cause of blindness following subarachnoid Hemorrhage
Journal of Neurosurgery, 1992Co-Authors: Andrew M Garfinkle, Irena R Danys, David A Nicolle, Austin R T Colohan, Steven BremAbstract:✓ Terson's syndrome refers to the occurrence of vitreous Hemorrhage with subarachnoid Hemorrhage (SAH), usually due to a ruptured cerebral aneurysm. Although it is a well-described entity in the ophthalmological literature, it has been only rarely commented upon in the neurosurgical discussion of SAH. Fundus findings are reported in a prospective study of 22 consecutive patients with a computerized tomography- or lumbar puncture-proven diagnosis of SAH. Six of these patients had intraocular Hemorrhage on initial examination. In four patients vitreous Hemorrhage was evident on presentation (six of eight eyes). In the subsequent 12 days, vitreous Hemorrhage developed in the additional two patients (three of four eyes) due to breakthrough bleeding from the original subhyaloid Hemorrhages. The initial amount of intraocular Hemorrhage did not correlate with the severity of SAH. Two of the six patients with intraocular Hemorrhage died, whereas five of the 16 remaining SAH patients without intraocular Hemorrhage...
Hideharu Funatsu - One of the best experts on this subject based on the ideXlab platform.
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retinal vasculitis and vitreous Hemorrhage associated with mixed connective tissue disease retinal vasculitis in mctd
International Ophthalmology, 2007Co-Authors: Tatsuya Mimura, Tomohiko Usui, Shiro Amano, Satoru Yamagami, Kyoko Ono, Hidetaka Noma, Hideharu FunatsuAbstract:Background Retinal vasculitis associated with mixed connective tissue disease (MCTD) has rarely been reported in the literature. We describe a rare case of a patient with serious retinal vasculopathy and vitreous Hemorrhages associated with MCTD. Case A 53-year-old woman with MCTD who has had recurrent retinal vasculitis and vitreous Hemorrhage in the right eye since 2000 presented with blurred vision in the right eye in April 2003. The best-corrected visual acuity was counting finger in the right eye. The patient was clinically diagnosed as having retinal and vitreous Hemorrhages and retinal infarction. Prednisolone was administered orally in a daily dose of 20 mg. Results The retinal and vitreous Hemorrhage improved in 7 days. The best-corrected visual acuity improved to more than 20/20 on prednisolone alone. Conclusion MCTD can be associated with retinal vasculitis and vitreous Hemorrhage which in our case responded well to systematic low doses of corticosteroid therapy.
