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Published bySharon Hubbard Modified over 6 years ago
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Ipsilateral Cerebral Venous Outflow Obstruction Is Associated with Fatal Edema of MCA Infarction
Wengui Yu, Joanna Rives, Babu Welch, Jonathan White, and Duke Samson UT Southwestern Medical Center, Dallas, TX
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Introduction MCA infarction accounts for 10 % of ischemic stroke
Approximately 40% of patients with large MCA infarction develop fatal edema. Mortality rate of malignant MCA infarction was reported to be 88% with medical therapy.
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Hemicraniectomy improves outcome of malignant MCA stroke
2007;6(3):215-22 Hemicraniectomy improves outcome of malignant MCA stroke 3 clinical trials: DECIMAL, HAMLET, and DESTINY. 93 patients randomized to surgical or medical therapy. Patients ≤60 years of age. The timing of surgery <48 hrs after stroke onset. Outcome with mRS at 1 yr.
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Questions Not every MCA stroke patient develops fatal edema.
Hemicraniectomy could be associated with complications, such as intracranial hemorrhage, infection, and CSF leakage. How to predict which patient will need surgery?
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Prediction of the Development of Fatal Edema
Early predictors of fatal edema include infarct size, young age, female gender, NIH Stroke Scale score > 20 on admission, elevated white blood cell counts, hypertension, heart failure, ipsilateral abnormal circle of Willis, and carotid occlusion. Infarct size is the major determinant, but its predictive value is only moderate.
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Aim of Our Study To investigate the relevance of the ipsilateral cerebral venous sinuses in the development of fatal edema.
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Methods A retrospective study
All consecutive patients with large MCA infarction admitted to our Neurointensive Care Unit from January 2007 to October 2008 were included. Medical records, laboratory data, and imaging studies were analyzed. Patients with malignant MCA infarction were compared with those with non-malignant MCA infarction.
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Results
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Table 1. Demographics and Clinical Features
Pt Age Sex Infarction Etiology Maximal midline shift (mm) Ipsilateral transverse Sinuses (TS) internal jugular vein (IJ) mRS at discharge 1 67 m R-MCA Embolic 2 dominant 3 81 f 3.4 NA 4 69 L-MCA ICA occlusion 16.1 hypoplastic 6 60 4.6 5 38 6.4 37 Vasculitis NP 7 64 ICA dissection 16.8 occluded 8 46 1.9 9 70 R-MCA/ACA 24.3 atresic 10 54 7.2 11 9.8 12 48 12.7 hypoplasia 13 ICA stenosis 16.6 14 47 6.3 Note: NA, normal appearance.
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Table 2. Clinical features of malignant and non-malignant MCA infarction
# of patients 9 5 Age (y) 54.4 ± 14.9 58.8 ± 10 (p=0.422) Female, n (%) 2 (22.2%) 2 (40%) R MCA, n (%) 6 (66.7%) 4 (80%) Infarction volume 196 ± 70 327 ± 36 (p<0.001) Maximal midline shift 4.7 ± 3.1 17.3 ± 4.9 (p<0.001) Ipilateral TS or IJ Atresia or occlusion Hypoplasia 2 (40% Mortality rate (%) 0% 80%
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Malignant MCA infarction
Day Ipsilateral atresia of TS Day Ipsilateral hypoplasia of TS and IJ Non-malignant MCA infarction Day Bilateral TS and IJ
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Conclusions Our preliminary findings suggest that occlusive disease of the ipsilateral cerebral venous sinuses is associated with early fatal edema of MCA infarction. Anomaly of the ipsilateral cerebral venous sinuses in patients with large MCA stroke may be an indication for early hemicraniectomy.
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