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  Vol. 66 No. 1, January 2009 TABLE OF CONTENTS
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Association of Subdural Hematoma With Increased Mortality in Lobar Intracerebral Hemorrhage

Pratik V. Patel, MD; Emilie FitzMaurice, AB; R. N. Kaveer Nandigam, MD; Pavan Auluck, MD, PhD; Anand Viswanathan, MD, PhD; Joshua N. Goldstein, MD, PhD; Jonathan Rosand, MD, MS; Steven M. Greenberg, MD, PhD; Eric E. Smith, MD, MPH, FRCPC

Arch Neurol. 2009;66(1):79-84.

Objective  To determine the prevalence of subdural hematoma (SDH) in patients presenting with primary nontraumatic lobar intracerebral hemorrhage (ICH) and characteristics associated with the presence of SDH.

Design  Retrospective analysis of data collected in a prospective cohort study.

Setting  Hospital.

Patients  Consecutive sample of 200 patients with primary lobar ICH and 75 patients with deep hemispheric ICH.

Main Outcome Measures  Presence of SDH and mortality.

Results  Subdural hematoma was present in 40 of 200 patients (20%) with primary lobar ICH. By contrast, SDH was not present in any of 75 consecutive patients with deep hemispheric ICH (P < .001 for comparison with lobar ICH). Intracerebral hemorrhage volume higher than 60 cm3 was the only independent predictor of SDH (odds ratio [OR], 2.69; 95% confidence interval [CI], 1.14-6.34; P = .02). Subdural hematoma thickness more than 5 mm was an independent predictor of increased 30-day mortality (OR, 7.60; 95% CI, 1.86-30.99; P = .005) after controlling for other factors including ICH volume. Further analysis showed that the effect of SDH on mortality depended on ICH volume, with larger odds for mortality in those with low ICH volume (OR, 12.85; 95% CI, 2.42-68.23; P = .003 for those with ICH volume <30 cm3). Cerebral amyloid angiopathy was present in 8 of 9 patients with pathological specimens.

Conclusions  Nontraumatic SDH frequently accompanies primary lobar ICH and is associated with higher 30-day mortality, particularly when the ICH volume is relatively low. Rupture of an amyloid-laden leptomeningeal vessel, with extravasation into the brain parenchyma and subdural space, may be the pathogenic mechanism.


Author Affiliations: Hemorrhagic Stroke Research Program, Department of Neurology (Drs Patel, Nandigam, Viswanathan, Rosand, Greenberg, and Smith and Ms FitzMaurice), Neuropathology Service, Department of Pathology (Dr Auluck), Department of Emergency Medicine (Dr Goldstein), and Center for Human Genetics Research (Dr Rosand), Massachusetts General Hospital, Boston.



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