Contrast Staining in Noninfarcted Tissue after Endovascular Treatment of Acute Ischemic Stroke.

BACKGROUND AND PURPOSE

Contrast staining is a common finding after endovascular treatment of acute ischemic stroke. It typically occurs in infarcted tissue and is considered an indicator of irreversible brain damage. Contrast staining in noninfarcted tissue has not been systematically investigated. We sought to assess the incidence, risk factors, and clinical significance of contrast staining in noninfarcted tissue after endovascular treatment.

MATERIALS AND METHODS

We conducted a retrospective review of consecutive patients who underwent endovascular treatment for anterior circulation large-vessel occlusion acute ischemic stroke. Contrast staining, defined as new hyperdensity on CT after endovascular treatment, was categorized as either contrast staining in infarcted tissue if the stained region demonstrated restricted diffusion on follow-up MR imaging or contrast staining in noninfarcted tissue if the stained region demonstrated no restricted diffusion. Baseline differences between patients with and without contrast staining in noninfarcted tissue were compared. Logistic regression was used to identify independent associations for contrast staining in noninfarcted tissue after endovascular treatment.

RESULTS

Among 194 patients who underwent endovascular treatment for large-vessel occlusion acute ischemic stroke and met the inclusion criteria, contrast staining in infarcted tissue was noted in 52/194 (26.8%) patients; contrast staining in noninfarcted tissue, in 26 (13.4%) patients. Both contrast staining in infarcted tissue and contrast staining in noninfarcted tissue were noted in 5.6% (11/194). Patients with contrast staining in noninfarcted tissue were found to have a higher likelihood of having an ASPECTS of 8-10, to be associated with contrast staining in infarcted tissue, and to achieve successful reperfusion compared with those without contrast staining in noninfarcted tissue. In contrast staining in noninfarcted tissue regions, the average attenuation was 40 HU, significantly lower than the contrast staining in infarcted tissue regions (53 HU). None of the patients with contrast staining in noninfarcted tissue had clinical worsening during their hospital stay. The median discharge mRS was significantly lower in patients with contrast staining in noninfarcted tissue than in those without (3 versus 4; = .018). No independent predictors of contrast staining in noninfarcted tissue were found.

CONCLUSIONS

Contrast staining can be seen outside the infarcted tissue after endovascular treatment of acute ischemic stroke, likely attributable to the reversible disruption of the BBB in ischemic but not infarcted tissue. While generally benign, understanding its characteristics is important because it may mimic pathologic conditions such as infarcted tissue and cerebral edema.