5.2.2\ Resection Cavities

5.2.2.1\ Discussion

The space that remains after a tumor is surgically removed is known as the resection cavity. The resection cavity is often lined or packed with hemostatic agents (refer to Chap. 4) and contains variable amounts of cerebrospinal fluid and blood products, especially during the early postoperative period (Fig. 5.11). Oftentimes, resection cavities eventually shrink and collapse, becoming nearly imperceptible (Fig. 5.12), although some cavities stay the same size, particularly if they communicate with the ventricular system.

Variable amounts of tumor may remain adjacent to the cavity depending on whether gross total, near-total, or subtotal resection was performed. The extent of tumor resection depends

a

on several factors, including the location and type of tumor. Tumors that involve eloquent parts of the brain, that are in technically difficult areas to reach, or that involve critical structures, such as cranial nerves or major arteries, can limit the extent of tumor resection. Similarly, it is more difficult to achieve complete resection of infiltrative tumors than well-defined tumors. Ultimately, there is often a trade-off between removing as much tumor as possible versus preserving as much normal tissue and avoiding complications. Comparison with preoperative imaging should be performed when possible to help identify residual tumor.

Surgically induced parenchymal injury, postoperative hemorrhage, and enhancing conditions related to brain tumor surgery and adjunctive treatments are discussed in the following sections.

b

Fig. 5.11  Early surgical cavity with blood products. Axial FLAIR (a), T1-weighted (b), post-contrast T1-weighted (c), and GRE (d) MR images show subacute

blood products within a right temporal resection cavity (arrows). There is no significant mass effect or enhancement

Surgically Induced Parenchymal Injury

Local areas of devitalized brain tissue surrounding the resection cavity are encountered on early postoperative MRI in up to 70% of cases of high-­ grade glioma resection as well as many other tumor resections. This phenomenon manifests as focal areas of restricted diffusion (Fig. 5.13). Enhancement of the devitalized tissue occurs in over 40% of cases between 1 week and several months. Furthermore, this phenomenon can lead to overestimation of residual non-enhancing tumor volume due to the presence of swelling and high signal on T2-weighted sequences during the early postoperative period. Visible encephalomalacia eventually forms around the surgical cavity in over 90% of cases of resection site infarcts. Larger, territorial infarcts are uncommon complications of tumor resection, but are predisposed by proximity to or encasement of major arterial branches and occasionally venous occlusion.

Vasogenic edema can result from forceful intraoperative retraction, which is sometimes performed in order to access large or deep tumors. The edema may be related to hyperemia of the brain surface after the release of retraction. On imaging obtained during the early postoperative period, retraction-induced vasogenic edema appears as swelling along the path of the retractors (Fig. 5.14). Unlike acute infarction, the vasogenic edema demonstrates elevated diffusivity rather than restricted diffusion.

A peculiar complication related to posterior fossa tumor resections is hypertrophic olivary degeneration, which results from disruption of the dentato-rubro-olivary pathway (Guillain-­ Mollaret triangle). This phenomenon can occur after surgical resection of cerebellar tumors. If the resection site involves the central tegmental tract, the ipsilateral olivary nucleus is affected, while if the superior cerebellar peduncle is involved, the contralateral olivary nucleus is affected. Thus, bilateral hypertrophic olivary degeneration results from disruption of the central tegmental tract and superior cerebellar peduncle. Tongue fasciculations are characteristic of hypertrophic olivary degeneration. On MRI, hypertrophic olivary degeneration manifests as T2 hyperintensity with or without enlargement of the anterolateral medulla (Fig. 5.15). The differential diagnosis includes ischemia, demyelination, tumor spread, and infection. The lack of enhancement with hypertrophic olivary degeneration may help differentiate this entity from the other possibilities, such as some neoplasms. In addition, most cases demonstrate associated atrophy of the contralateral dentate nucleus or cerebellar cortex. Signal changes on MRI develop approximately 1 month after surgery and can persist for many years. Hypertrophy of the olivary nucleus tends to develop after several months and can resolve after 2–3 years.

Fig. 5.13  Peri-resection infarction. The patient underwent recent resection of a right posterior temporal lobe glioblastoma. Axial FLAIR (a), DWI (b), and ADC (c)

maps show an area of restricted diffusion posterior to the resection cavity (arrows)

Fig. 5.14  Retraction-induced vasogenic edema. The patient has a history of fourth ventricular medulloblastoma. Preoperative axial FLAIR image (a) shows a large fourth ventricular mass, but no surrounding vasogenic edema. Postoperative FLAIR image (b) shows new areas

of hyperintensity in the bilateral medial cerebellar hemispheres. The diffusion-weighted image (c) and ADC map (d) show corresponding mildly elevated diffusivity (arrows). Small areas of ischemia are also present medially

Fig. 5.15  Hypertrophic olivary degeneration. The patient presented with tongue fasciculations after resection of a right pontine cavernous malformation. Axial T2 MRI (a)

shows the resection site (encircled). Axial FLAIR MRI (b) shows high signal within an enlarged left olivary nucleus (arrow)

Postoperative Hemorrhagic Lesions

Hemorrhage is a relatively common occurrence with tumor resection and usually occurs at the craniotomy site. CT or MRI can readily depict these hemorrhages. The lack of contrast enhancement­

and susceptibility effects help distinguish hematomas from residual tumor (Fig. 5.16). Hemorrhage that results from incomplete­ tumor resection is sometimes termed “wounded tumor syndrome” and is more commonly encountered with vascular tumors, such as melanoma, renal cell carcinoma, and glioblastoma (Fig. 5.17). Other risk factors for postoperative hemorrhage include inadequate hemostasis, underlying coagulopathies, and hypertension.

Chronic hemorrhage after surgery can result in superficial siderosis and mainly occurs when there is a cystic cavity that contains friable vessels or residual/recurrent tumor (Fig. 5.18). Hemosiderin deposits can coat remote leptomeningeal surfaces, particularly the cerebellum and brainstem. On CT, superficial siderosis can appear as a mildly hyperattenuating coating of these structures, which may also become atrophic as a result. MRI is more sensitive for depicting hemosiderin deposits, which appear as very low signal intensity on all sequences. Blooming artifact on T2* GRE or SWI sequences accentuates the lesions. The significance of superficial siderosis is that it may cause symptoms such as ataxia and deafness.

Fig. 5.16  Operative bed hemorrhage. The study was obtained to evaluate for residual tumor following recent meningioma resection. Copious oozing of blood was noted during surgery. Axial T1-weighted (a) and post-­ contrast T1-weighted (b), T2-weighted (c), and GRE (d)

images show an intrinsically T1 hyperintense and T2 hypointense extradural collection (*) with blooming and mass effect upon the underlying brain. There is also a small amount of hemorrhage within the surgical cavity associated with hemostatic material (arrows)

Fig. 5.17  Wounded tumor. The patient underwent subtotal resection of glioblastoma. Preoperative axial T1-weighted (a) and susceptibility-weighted imaging (b) show a large mass (*) in the left frontal lobe with only a few foci of microhemorrhage­ . Postoperative axial T1-weighted (c)

and susceptibility-­weighted imaging (d) show interval appearance of high T1 signal hemorrhage and extensive susceptibility effect within and adjacent to the residual tumor (arrows)

Fig. 5.18  Superficial siderosis. Axial T2-weighted MRI (a) and corresponding SWI (b) show a cystic left frontal lobe resection cavity with layering of blood products (arrows). In addition, there is blooming effect along the

margins of the cavity and along the cerebral sulci. SWI at a more inferior level (c) shows extensive susceptibility effect in a leptomeningeal distribution in the brainstem and cerebellum

Enhancing Lesions in the Surgical Bed Region and Beyond

Many types of enhancing lesions can be encountered on imaging after surgery, as listed in Table 5.1 and depicted in Figs. 5.19, 5.20, 5.21, 5.22, and 5.23. Indeed, several of these conditions can coexist and make interpretation of the imaging a challenge. Differentiation of these conditions from recurrent enhancing tumor is based on morphology as well as timing. Advanced imaging­ techniques,

such as perfusion MRI and MR spectroscopy, are often helpful for problem solving. Nevertheless, in some cases, biopsy or serial imaging can help elucidate ambiguous cases. It is also important to systematically evaluate the areas beyond the surgical bed on imaging exams, particularly with aggressive neoplasms, such as glioblastoma, which can undergo spread to remote parts of the brain, seed the scalp and face soft tissues, and undergo cerebrospinal fluid dissemination.

Fig. 5.20  Perioperative infarct. Pre- (a) and post-­contrast (b) T1-weighted MR images obtained 1 month after surgery in the same case as in Fig. 5.13 show that the infarcted

tissues enhance (arrow). Furthermore, the CBV map (c) shows corresponding hypoperfusion in the area (arrow)

Fig. 5.21  Tumor progression. The patient underwent gross total resection of an oligoastrocytoma (WHO grade II/IV) in the right frontal lobe. Axial FLAIR (a) and post-­ contrast T1-weighted (b) MR images obtained approximately 10 years after resection show a right frontal resection cavity surrounded by non-enhancing FLAIR signal abnormality. Axial FLAIR (c) and post-contrast T1-weighted (d) MR images obtained approximately

1 year later show a new focus of enhancement adjacent to the resection cavity (arrow), but no obvious change in the FLAIR signal abnormality. Axial FLAIR (e), post-con- trast T1-weighted (f), subtraction image (g), and CBV map (h) obtained approximately 6 months later demonstrate marked interval increase in volume of the FLAIR signal abnormality and enhancing adjacent to the resection cavity and associated elevated CBC (arrows)

Fig. 5.23  Metastatic glioblastoma in the spinal canal. The patient presented with back and low extremity pain after gross total resection of a left frontal glioblastoma resection with recurrence. Sagittal post-contrast T1-weighted MRI (a) shows irregular enhancement

involving the bilateral frontal lobes, extending to the meningeal surface. Sagittal post-contrast T1-weighted MRI (b) shows an intradural, extramedullary mass with irregular enhancement in the upper lumbar spinal canal (arrow)

Fig. 5.22  Radiation necrosis. The patient has a history of left frontal lobe glioblastoma that was resected and radiated­ approximately 1 year before. Axial (a) post-­ contrast T1-weighted MRI shows small areas of enhancement in the treatment­ bed region (arrows). There is no

corresponding hypermetabolism on the blood volume map (b). MRI spectroscopy (c) over the abnormality shows a lactate peak, mildly reduced NAA peak, and a Cho peak that is not particularly elevated with respect to Cr