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From the Departments of Neurology (Drs. Qureshi and Hanley) and Anesthesiology/Critical Care Medicine (Drs. Wilson and Traystman), The Johns Hopkins Medical Institutions, Baltimore, MD.
Address correspondence and reprint requests to Dr. Richard J. Traystman, Department of Anesthesiology/Critical Care Medicine, Blalock 1408, 600 North Wolfe Street, Baltimore, MD 21287.
OBJECTIVES: To determine the effect of massive intracerebral hemorrhage (ICH) on regional cerebral blood flow (rCBF) and metabolism, and to test the hypothesis that there is persistent ischemia in the perihematoma region after ICH.
BACKGROUND: Cerebral ischemia is postulated to be one of the mechanisms of neural injury after ICH. Presumably the hematoma induces ischemia by mechanical compression of the surrounding microvasculature.
METHODS: The authors induced ICH in eight anesthetized mongrel dogs by autologous blood injection (7.5 mL) under arterial pressure in the deep white matter adjacent to the left basal ganglia. They measured serial rCBF using radiolabeled microspheres in regions around and distant to the hematoma, as well as cerebral oxygen extraction, oxygen consumption (CMRO2), glucose utilization, and lactate production by serial sampling of cerebral venous blood from the sagittal sinus. Mean arterial pressure (MAP) and intracranial pressure (ICP) were monitored continuously. All measurements were recorded at 0.5, 1.0, 2.0, 3.5, and 5.0 hours after induction of ICH and compared with prehematoma values. Evans Blue dye was injected at the end of the experiment, and intensity of staining was compared with three control animals.
RESULTS: Compared with prehematoma ICP (12.5 ± 2.0 mm Hg, mean ± standard error), significant elevation in ICP was observed after ICH peaking at 5 hours (34.4 ± 5.2 mm Hg). Compared with prehematoma MAP (125.8 ± 7.0 mm Hg), significant elevation in MAP was observed at 120 minutes after onset of hematoma (139.1 ± 4.6 mm Hg), with return to the prehematoma value by 5 hours. There were no significant changes observed in cerebral oxygen extraction (51.4 ± 4.3% versus 44.8 ± 4.9%) and CMRO2 (1.8 ± 0.3 versus 1.64 ± 0.2 mL O2/100 g/min) at 5 hours posthematoma (or any other posthematoma measurement) compared with prehematoma values. There were no significant differences observed in rCBF in the perihematoma gray (18.2 ± 0.9 mL/100 g/min versus 20.1 ± 1.5 mL/100 g/min) or white matter (15.6 ± 1.4 mL/100 g/min versus 15.3 ± 1.1 mL/100 g/min) at 5 hours posthematoma (or any other posthematoma measurement) compared with prehematoma values. No changes were observed in cerebral glucose utilization, lactate production, and rCBF in other regions after introduction of ICH. Permeability of the blood–brain barrier was more prominent in the ipsilateral hemisphere in animals with ICH compared with control animals.
CONCLUSIONS: Despite a prominent increase in ICP and MAP after ICH, the authors found no evidence to support the presence of an ischemic penumbra in the first 5 hours after ICH. Thus, other mechanisms for acute neural injury and late rCBF changes after ICH must be investigated.
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