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Fatal Subarachnoid Hemorrhage Due to Ruptured Vertebrobasilar Aneurysm Associated With Giant Cell Arteritis in a Child

Corliss, Robert F. MD; Zydowicz, Sara DO; Salamat, M. Shahriar MD, PhD

The American Journal of Forensic Medicine and Pathology: September 2011 - Volume 32 - Issue 3 - p 255-259
doi: 10.1097/PAF.0b013e3181d03ea6
Case Reports

A 3 ½-year-old previously healthy female experienced an episode of sudden unresponsiveness witnessed by her mother. Upon arrival to the local hospital, imaging studies of the still unresponsive child revealed severe bilateral "flash" pulmonary edema and diffuse anoxic brain injury. Aggressive resuscitative efforts were unsuccessful, and she was pronounced dead. External examination at autopsy was essentially unremarkable. Internal examination of the head revealed diffuse basilar subarachnoid blood originating from a collapsed, 2 cm irregular aneurysm arising from the junction of the vertebral and basilar arteries. Additionally, multiple calcified subpleural, parenchymal, and hilar nodal pulmonary granulomas were identified. The remaining internal examination, including that of the aorta and its major branches, was unremarkable. Histologic examination of the aneurysm revealed alternating mural attenuation and thickening, the latter resulting from prominent intimal proliferation with active fibroplasia. Most notably, numerous isolated and clustered multinucleated giant cells were seen, most prominently in areas of more intense inflammation. Specific immunolabeling and silver staining of the pulmonary granulomas revealed evidence of histoplasmosis, but both were negative for fungal elements in the aneurysm, as was ultrastructural examination. The cause of death is fatal subarachnoid hemorrhage due to rupture of a vertebrobasilar artery aneurysm caused by isolated intracranial giant cell arteritis.

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From the Department of Pathology and Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI.

Manuscript received April 13, 2009; accepted September 18, 2009.

Gomori-Methenamine Silver (GMS) staining, combined elastin/trichrome staining, and Hematoxylin & Eosin (H&E) staining were done in the UW/VA Surgical Pathology Laboratory, Madison, WI. Histoplasma capsulatum specific immunolabeling was carried out by ProPath Diagnostic Laboratory, Dallas, TX.

The authors report no conflicts of interest.

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Reprints: Robert F. Corliss, MD, Department of Pathology and Laboratory Medicine, DB1-216 VA, 600 Highland Ave, Madison, WI 53792-3224. E-mail:

© 2011 by Lippincott Williams & Wilkins.