Perilesional blood flow and edema formation in acute intracerebral hemorrhage: a SPECT study

Secondary brain injury and edema formation contribute significantly to morbidity and mortality after intracerebral hemorrhage (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 progressive enlargement of edema surrounding ICH is related to increased or decreased perfusion.

We performed paired consecutive CT and 99mTc-hexamethylpropylenamine oxime single-photon emission computed tomography (SPECT) scans during the acute (mean, 18 hours) and subacute (mean, 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 measuring a "zero-flow" volume within a large perilesional region of interest (based on percent tracer count loss compared with the contralateral side) and subtracting the corresponding ICH volume. Patients with significant midline shift (>5 mm) or global blood flow reduction were excluded from the analysis.

ICH volume (18 mL) did not change, mean edema volume increased by 36% (from 19 to 25 mL, P<0.0001), and mean FDV decreased by 55% (from 14 to 6 mL, P=0.0004) between the acute and subacute phases. Edema volume on the second CT scan correlated positively with FDV on the first SPECT scan (Spearman's p=0.48, P=0.02), and with the volume of reperfused perilesional tissue (FDVacute-FDVsubacute) (Spearman's p=0.41, P=0.05). Perilesional edema on CT always 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.

Perilesional blood flow normalizes from initially depressed levels as edema forms during the first 72 hours after ICH, and the eventual extent of edema correlates with the volume of reperfused tissue. These results suggest that the potential for perilesional ischemia is highest in the earliest hours after ICH onset and implicate reperfusion injury in the pathogenesis of perihematoma edema formation.