PERILESIONAL BLOOD-FLOW AND EDEMA FORMATION IN ACUTE INTRACEREBRAL HEMORRHAGE - A SPECT STUDY

Citation
Sa. Mayer et al., PERILESIONAL BLOOD-FLOW AND EDEMA FORMATION IN ACUTE INTRACEREBRAL HEMORRHAGE - A SPECT STUDY, Stroke, 29(9), 1998, pp. 1791-1798
Citations number
38
Categorie Soggetti
Peripheal Vascular Diseas","Clinical Neurology
Journal title
StrokeACNP
ISSN journal
00392499
Volume
29
Issue
9
Year of publication
1998
Pages
1791 - 1798
Database
ISI
SICI code
0039-2499(1998)29:9<1791:PBAEFI>2.0.ZU;2-8
Abstract
Background and Purpose-Secondary brain injury and edema formation cont ribute significantly to morbidity and mortality after intracerebral he morrhage (ICH). The pathogenesis of this process is poorly understood. We sought to characterize alterations in perilesional blood flow that occur during the acute phase of ICH and to determine whether progress ive enlargement of edema surrounding ICH is related to increased or de creased perfusion. Methods-We performed paired consecutive CT and Tc-9 9m-hexamethylpropylenamine oxime single-photon emission computed tomog raphy (SPECT) scans during the acute (mean, 18 hours) and subacute (me an, 72 hours) phase of ICH in 23 patients. Hematoma and edema volumes were traced and calculated from CT images. SPECT-derived hypothetical flow deficit volumes (FDV) around each hematoma were calculated by mea suring a ''zero-flow'' volume within a large perilesional region of in terest (based on percent tracer count loss compared with the contralat eral side) and subtracting the corresponding ICH volume. Patients with significant midline shift (>5 mm) or global blood flow reduction were excluded from the analysis. Results-ICH volume (18 mt) did not change , mean edema volume increased by 36% (from 19 to 25 mt, P<0.0001), and mean FDV decreased by 55% (from 14 to 6 mt, P=0.0004) between the acu te and subacute phases. Edema volume on the second CT scan correlated positively with FDV on the first SPECT scan (Spearman's rho=0.48, P=0. 02), and with the volume of reperfused perilesional tissue (FDVacute-F DVsubacute) (Spearman's rho=0.41, P=0.05). Perilesional edema on CT al ways corresponded topographically with perfusion deficits on SPECT. In 4 patients, delayed focal hyperemia was identified in more peripheral cortical regions, but these areas appeared normal on CT. Conclusions- Perilesional blood flow normalizes from initially depressed levels as edema forms during the first 72 hours after ICH, and the eventual exte nt of edema correlates with the volume of reperfused tissue. These res ults suggest that the potential for perilesional ischemia is highest i n the earliest hours after ICH onset and implicate reperfusion injury in the pathogenesis of perihematoma edema formation.