Volume 58, Issue 5 pp. 1364-1366
Case Report

Subarachnoid Hemorrhage and Carbon Monoxide Exposure: Accidental Association or Fatal Link?

Fabio De-Giorgio M.D., Ph.D.

Corresponding Author

Fabio De-Giorgio M.D., Ph.D.

Institute of Legal Medicine, Catholic University, Medical School, Largo F. Vito 1, 00168 Rome, Italy

Additional information and reprint requests:

Fabio De-Giorgio, M.D., Ph.D.

Institute of Legal Medicine

Catholic University, Medical School

Largo F. Vito, 1

00168 Rome

Italy

E-mail: [email protected]

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Vincenzo M. Grassi M.D.

Vincenzo M. Grassi M.D.

Institute of Legal Medicine, Catholic University, Medical School, Largo F. Vito 1, 00168 Rome, Italy

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Massimo Miscusi M.D., Ph.D.

Massimo Miscusi M.D., Ph.D.

Department of Medico-Surgical Sciences and Biotechnologies, La Sapienza, University of Rome, Corso della Repubblica 79, 04100 Latina, Italy

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Cesare Mancuso M.D., Ph.D.

Cesare Mancuso M.D., Ph.D.

Institute of Pharmacology, Catholic University, Medical School, Largo F. Vito 1, 00168 Rome, Italy

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Ernesto d'Aloja M.D., Ph.D.

Ernesto d'Aloja M.D., Ph.D.

Department of Public Health, Forensic Medicine Section, Cagliari University, Km 4.500 SS. 554 Bivio per Sestu, 09042 Monserrato, Italy

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Vincenzo L. Pascali M.D., Ph.D.

Vincenzo L. Pascali M.D., Ph.D.

Institute of Legal Medicine, Catholic University, Medical School, Largo F. Vito 1, 00168 Rome, Italy

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First published: 17 May 2013
Citations: 2

Abstract

This case study reports a fatal subarachnoid hemorrhage (SAH) with concomitant accidental carbon monoxide (CO) exposure in 32-year-old man. Autopsy results indicated an antemortem aspiration of smoke, and a massive SAH was identified as the cause of death. Intriguingly, the carboxyhemoglobin level was 30%, suggesting that CO could have played a specific role. Intracranial hemorrhages following CO exposure in brain areas and tissues such as the basal ganglia, globus pallidus, or white matter are rare, but well characterized, whereas SAH related to CO exposure has not been previously described. In this case report, the possible role of CO, either as a primary cause or as a facilitating factor, in the pathogenesis of SAH is discussed. In particular, we propose the hypothesis that the excessive vasodilating effects produced by CO on the cerebral endothelium results in consequential loss of microvascular integrity.

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