• Joseph D Burns, Jeffrey T Jacob, Patrick H Luetmer, and Eelco F M Wijdicks.
• Department of Neurology, Boston University School of Medicine, Collamore Building, C-3, 72 East Concord St, Boston, MA 02118, USA. joseph.burns@bmc.org
• Neurocrit Care. 2010 Apr 1;12(2):261-4.

BackgroundCardiac arrest and aneurysmal subarachnoid hemorrhage both cause sudden, severe cerebral hypoperfusion at ictus. Animal studies indicate that the resultant microvascular dysfunction and cerebral perfusion abnormalities are important determinants of the associated cerebral injury in both conditions. Although this suggests that perfusion imaging might be a useful tool for prognostication in patients with these conditions, this hypothesis has not been thoroughly investigated in humans.MethodsCase report.ResultsA 49-year-old man developed cardiac arrest upon rupture of an intracranial aneurysm. When he arrived at our institution 10 h later, he was comatose, had neurogenic hyperventilation, absent corneal reflexes, and continuous multifocal myoclonus. Despite normal intracranial pressure, normal cerebral perfusion pressure, normal flow in the proximal cerebral arteries on CT angiography, and a lack of diffuse cerebral edema, CT perfusion imaging performed 12 h after ictus showed severe, diffuse hypoperfusion. After the development of refractory intracranial hypertension, physiologic support was withdrawn and the patient died.ConclusionsEarly global cerebral hypoperfusion can be demonstrated by CT perfusion imaging after cardiac arrest associated with high-grade aneurysmal subarachnoid hemorrhage and may be indicative of poor neurologic outcome. CT perfusion should be investigated as a prognostic tool in these conditions.

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