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Symptomatic Acute-on-Chronic Subdural Hematoma

A Clinicopathological Study

Castellani, Rudy J. MD*†; Mojica-Sanchez, Gruschenka MD*; Schwartzbauer, Gary MD, PhD; Hersh, David S. MD

The American Journal of Forensic Medicine and Pathology: June 2017 - Volume 38 - Issue 2 - p 126–130
doi: 10.1097/PAF.0000000000000300
Original Articles

The pathophysiology of acute-on-chronic subdural hematoma (ACSDH) is complex and incompletely understood. Evidence to date indicates that the overall process is initiated by rotational force with movement of the brain inside the skull, which exerts tensile strain and rupture of bridging veins, leading in turn to acute hemorrhage in the subdural potential space. This is followed by the proliferation of mesenchymal elements with angiogenesis and inflammation, which in turn becomes a substrate for repeated hemorrhage and expansion of the lesion. Given the prevalence of traumatic subdural processes in the forensic setting and the importance of proper assessment of timing, etiology, risk factors, and clinicopathological correlation, we studied 47 patients presenting to the University of Maryland Shock Trauma Center, all of whom underwent craniotomy with resection of the outer membrane due to symptomatic ACSDH. The surgically resected tissue was examined for histopathologic features in all cases. Our findings highlight that ACSDH is a condition precipitated by trauma that affects middle-aged and older adults, is relatively indolent, is unilateral or asymmetric, and has a low in-hospital mortality rate. Pathological analysis demonstrates a substantial outer membrane in all cases with varying degrees of inflammation and organization that cannot be precisely dated as a function of clinical presentation. The extrapolation of adult ACSDH to mixed acute and chronic subdural hemorrhage in the pediatric setting is problematic due to substantial differences in clinical presentation, severity of underlying brain injury, gross and microscopic findings, and outcome.

From the *Department of Pathology, University of Maryland School of Medicine, Baltimore, MD; †Center for Neuropathology, Western Michigan University Homer Stryker M.D. School of Medicine, Kalamazoo, MI; and ‡Department of Neurosurgery, University of Maryland School of Medicine, Baltimore, MD.

Manuscript received November 28, 2016; accepted January 22, 2017.

The authors report no conflict of interest.

Reprints: Rudy J. Castellani, MD, Center for Neuropathology, Western Michigan University Homer Stryker M.D. School of Medicine, 300 Portage St, Kalamazoo, MI 49007. E-mail:

© 2017 by Lippincott Williams & Wilkins.