Surgically induced intracranial contrast enhancement: potential source of diagnostic error in intraoperative MR imaging

Abstract

Background and purpose: Intraoperative MR imaging is being used increasingly during neurosurgical interventions. The aim of this study was to describe and classify different forms of surgically induced intracranial contrast enhancement observed during intraoperative MR examinations.

Methods: A total of 51 intraoperative MR examinations were performed to assess the extent of brain tumor removal. The intraoperative MR results (T1-weighted images, unenhanced and obtained serially after the IV administration of paramagnetic contrast material) were compared with preoperative and early postoperative MR findings. Animal experiments were conducted to obtain further evidence of the mechanism of surgically induced contrast enhancement.

Results: Four different types of surgically induced contrast enhancement were found: meningeal enhancement, increased enhancement of the choroid plexus, delayed enhancement at the resection margins, and immediate intraparenchymal contrast enhancement. The types of surgically induced contrast enhancement differ regarding their location, configuration, and time course. Their potential to be confused with contrast-enhancing, residual tumor also varies. Three of the four types of surgically induced contrast enhancement were reproducible in an animal model.

Conclusion: Surgically induced contrast enhancement is a potential source of error in intraoperative MR imaging. Careful analysis of the location, configuration, and time course of intraoperatively observed intracranial enhancement is critical to avoid confusing surgically induced contrast enhancement with contrast-enhancing, residual tumor.

fig 1.

Surgically induced meningeal enhancement. The preoperative MR image (left) (674/20/2) does not show contrast enhancement of the pial surface in the central sulcus, which clearly enhances on the intraoperative MR examination (middle, arrow) (532/15/3). This enhancement persists on the early postoperative MR examination (right, arrow) (674/20/2).

fig 2.

Surgically induced, increased enhancement of the choroid plexus. Note that the ventricle has been opened. Intraoperative T1-weighted images (left, 5 minutes postcontrast; middle, 20 minutes postcontrast) (532/15/3) show increased enhancement of the left choroid plexus (arrows) that remains constant during the observed time interval. Early postoperative MR image (right) (674/20/2) shows the persistence of this enhancement (arrow).

fig 3.

Surgically induced, delayed (time-dependent) enhancement at the resection margins. Preoperative MR image (top) (674/20/2) shows a left occipital, contrast-enhancing tumor. Intraoperative T1-weighted images (middle [from left to right], unenhanced and 5, 10, and 20 minutes postcontrast) (532/15/3) show linear enhancement at the resection margin, which is more pronounced the more time has elapsed since the administration of the contrast agent (arrows). Also note the diffusion of the contrast agent into the fluid-filled resection cavity, leading to increased signal intensity of the fluid on the delayed images. The probable cause of this type of surgically induced contrast enhancement is leakage of contrast agent out of surgically opened blood vessels. The enhancement is not present on the preoperative (top) or postoperative (bottom) MR images (674/20/2).

fig 4.

Surgically induced immediate intraparenchymal enhancement. Intraoperative T1-weighted images (upper row [from left to right], unenhanced and 5 and 20 minutes postcontrast) (532/15/3) show a solid-appearing, intraparenchymal contrast enhancement that shows almost no time dependence. Early (day 1 after surgery) postoperative T1-weighted images (lower row: left, unenhanced; right, postcontrast) show a intraparenchymal hyperintensity but no contrast enhancement (674/20/2). This type of enhancement probably represents (transient) blood-brain barrier disruption. The hyperintensity on the unenhanced T1-weighted images of the postoperative examination is possibly caused by contrast agent administered intraoperatively, which is “captured” in the tissue after the blood-brain barrier disruption resolves. It is, however, too early to represent methemoglobin.

fig 5.

Animal model of surgically induced immediate intraparenchymal enhancement. In all animals in which a cortical electrocoagulation (non-vessel-opening brain lesion) had been performed, an intraparenchymal and non-time-dependent contrast enhancement (arrows) surrounding a zone of necrosis was observed. Postcontrast T1-weighted images (from left to right, 5 and 15 minutes after administration of the contrast agent) (500/20/4)

fig 6.

Animal model of surgically induced delayed (time-dependent) enhancement at the resection margins. Only in animals in which a vessel-opening brain lesion had been performed (cortical ablation) was this type of surgically induced enhancement seen (arrows). Postcontrast T1-weighted images (from left to right: 5, 10, and 15 minutes after administration of the contrast agent) (500/20/4)

fig 7.

Surgically induced enhancement: problematic case. Preoperative MR (left) (674/20/2) shows a ring-enhancing lesion. Intraoperative T1-weighted images (middle images, 5 and 20 minutes postcontrast) (532/15/3) show enhancement at the resection margin with some time dependence. A confident differential diagnosis of this enhancement (tumor or not?) could not be made, and the surgery was terminated. Early postoperative MR image (right) (674/20/2) shows possible residual tumor (arrowhead)

fig 8.

Surgically induced enhancement: problematic case. This was one of the first patients in whom an intraoperative MR examination was performed. The tumor is above the level of these T1-weighted images. Preoperative MR image (left) (674/20/2) does not show enhancement in the head of the right caudate nucleus. Problems with hemostasis necessitated repeated electrocoagulations in this region. Intraoperative MR images (middle images, 5 and 20 minutes postcontrast) (532/15/3) partially show solid-appearing contrast enhancement of the head of the caudate nucleus with almost no time dependence during the observed time interval. A small biopsy was taken from this region, which did not show residual tumor histologically. Surgery was terminated. Early postoperative MR imaging (674/20/2) did not show persistent enhancement of the head of the caudate nucleus. The intraoperative enhancement probably represented transient blood-brain barrier disruption