Читать книгу Anterior Skull Base Tumors - Группа авторов - Страница 79

When the epicenter of the tumor is located in the nasal cavity or the ethmoid, the checklist for assessing the 3D extent should include six “vectors of growth” to be scrutinized and reported.

1. The anterior vector of spread. The infiltration of nasal bones or invasion of the anterior wall of the frontal sinuses are contraindications to a pure TES. These bone structures cannot be properly reached by endoscopes due to the unfavorable angulation. Since a reconstruction could not be performed after resection of the bones, a deformity of the face would result. To properly assess this path of growth, the axial plane should be integrated by at least one sagittal plane (CT or MRI). Primary malignant neoplasms of the frontal sinus are very rare, with a reported incidence less than 2% [28].

2. The posterior vector of spread. A growth along this direction leads the tumor into the sphenoid sinus (above), choana, and nasopharynx (below). Primary malignant neoplasms arising from the sphenoid sinus are infrequently found, with an incidence of approximately 4% [31]. As for the anterior pattern of spread, the acquisition of sagittal planes is suggested.

When the tumor extends toward the sphenoid sinus, the checklist has to report whether the neoplasm simply obstructs the mucus drainage by blocking the sphenoethmoidal recess or if it grows into the sinus cavity. If the cavity is partially or completely occupied by tumor tissue, detailed analysis of the bone walls is mandatory. Tumor spread through the lateral wall eventually implies the invasion of the foramen rotundum, superior orbital fissure (below), Meckel’s cave (more posteriorly), and the cavernous sinus (above; Fig. 2). To properly evaluate this area, the anterior clinoid process (ACP) may be used as a landmark, particularly on high-resolution coronal CT and MR sections. In this plane of section, below and lateral to the ACP the posterior portion of the superior orbital fissure (fat tissue and nerves) is detectable. Medial to the ACP runs the optic nerve (surrounded by CSF) and the anterior genu of the intracavernous ICA. The morphology of the ACP itself needs to be evaluated to identify variants such as pneumatization (in this case, mucus retention is possible) or neoplastic involvement replacing the cancellous signal and eroding its cortical rim. More posteriorly (and below) is Meckel’s cave, filled with CSF.

Overall, the anatomical arrangement in this area is quite unique: it includes CSF-surrounded structures, cortical-cancellous bone boxes, venous-filled containers, and fat tissue-stripes. A combination of high-resolution T2W and postcontrast T1W, preferably volumetric sequences, is recommended. A postcontrast CISS sequence offers the simultaneous depiction of CSF and contrast-enhancing structures such as the venous network of the cavernous sinus (Fig. 3). The analysis should extend to the sphenoid sinus roof (sellar floor) and the posterior wall, where – beyond the cortical rim – a variable amount of cancellous bone is present. The medial wall is the least resistant, and is frequently transgressed. When the floor of the sphenoid sinus is invaded, the tumor accesses the roof of the nasopharynx – a sagittal plane, combined with a coronal one, is very useful to precisely delineate tumor spread.

In nasoethmoidal tumors that extend posteriorly, but mostly below the sphenoid sinus, a lateral spread at the level of the choana assumes great relevance for treatment planning. In fact, lateral to the choanae lies a crucial crossroads, the pterygopalatine fossa (PPF), which contains nerves (and vessels) and is in strict relationship with the inferior and superior orbital fissures. Imaging findings indicating tumor invasion of the PPF include destruction of the pterygoid laminae, with possible involvement of the pterygoid process, and obliteration of the fat tissue within the PPF, replaced by tumor signal. While CT easily shows the erosion of laminae and cortical rims, MRI has a greater sensitivity for bone marrow invasion, the submucosal extent of a tumor into fissures, and perineural spread (PNS) [32, 33] (Fig. 7). Even if CT can reveal cancellous bone sclerosis, its intrinsic contrast resolution is insufficient to detect bone marrow enhancement. A combination of pre- and postcontrast T1W sequences is the proper strategy to demonstrate the replacement of the hyperintense signal of fat (present both in fissures and bone marrow) by the low signal of the tumor (on plain T1W) and its enhancement after contrast administration. A significant thickening of the cancellous framework of the pterygoid process can be frequently observed in adenoid cystic carcinoma and lymphoma. It translates into marked hypointensity on plain T1W sequences [34]. A further lateral extent of the tumor into the infratemporal fossa has to be reported. Such a situation usually requires additional surgical approaches [35]. Indeed, invasion of the superior orbital fissure and apex cannot be approached by TES alone.

Fig. 7. Adenoid cystic carcinoma. a 3D isotropic GE sequence after contrast administration, axial plane. The neoplasm (T) occupies the posterior nasal cavities. Invasion of both sphenopalatine foramina and pterygopalatine fossae (black curved arrows) with bilateral PNS along the vidian canals. On the right side the linear enhancement reaches the petrous apex (possible PNS along the greater petrosal nerve, white arrow). The middle meningeal artery (ma) at the foramen spinosum, foramen ovale, and mandibular nerve (V3) are indicated, as is the horizontal segment of the left internal carotid artery (ica). b In the sagittal plane (TSE T1 after contrast administration) a thickened and enhancing vidian nerve (vn) runs across the vidian canal. Extensive sclerosis of the walls of the canal and of the clivus (black arrows) suggests the presence of permeative bone invasion.

Even if the patient does not show any neurological abnormalities, meticulous imaging is recommended to assess or rule out PNS along nerves, the distribution of which corresponds to the innervation of the sinonasal tract. This is a crucial point, since extracranial segments (and intraforaminal portions) of the maxillary and mandibular nerves and the vidian nerve can be resected by expanded TES. Conversely, intracranial segment involvement is a contraindication both for the difficulty to be reached and for the absence of improved survival of the patient. A key technical strategy to improve PNS detection by imaging consists in selecting technical parameters that maximize both spatial and contrast resolution. On CT and MRI, PNS may appear both as segmental thickening and asymmetric enhancement. Advanced involvement may result in significant nerve enlargement, leading to remodeling/erosion of fissures or foramina. In addition, the enlarged nerve causes obliteration of the fat planes or of the venous “coating” that accompanies the cranial nerves along skull base foramina. High spatial and contrast resolution are strongly recommended. High-resolution 3D gradient echo T1W sequences (VIBE, THRIVE, LAVA) provide an excellent solution. On these sequences, the normal nerve is hypointense, clearly detectable where it is surrounded by the enhanced venous plexus, for example along bony grooves and canals – like the vidian, maxillary, and mandibular nerves through their respective foramina. Muscular denervation is also a sign of PNS. Changes in the acute and late phase include edema and enhancement of the muscle(s) involved, and atrophy and fatty replacement, respectively.

Fig. 8. Adenocarcinoma. MRI in coronal planes obtained with a TSE T2 (a) and TSE T1 (b) sequence after contrast agent administration. The large tumor (T) is centered in the midline and grows toward the ACF floor (white arrows) without contacting the planum sphenoidale, above which are shown the olfactory tracts (ot), surrounded by normal CSF signal. The lesion, with a non-characteristic very low signal intensity on T2, shows exceptional postcontrast enhancement on the TSE T1 plane (b). Enhancement of a short segment of the dura (white arrows) lining the left portion of the planum sphenoidale is demonstrated. The enhancing dura is uniformly thin, without any nodular thickening. The absence of any “interruption” of the planum on the TSE T2 sequence (where the planum appears as a continuous regular black line) and the pattern of enhancement of the dura on the TSE T1 sequence are more consistent with an inflammatory reaction than with neoplastic invasion. The “short enhancing segment” is confined to the planum sphenoidale: its extent, therefore, does not contraindicate a TES approach. aea indicates the anterior ethmoidal artery canal leaving the left orbit.

Fig. 9. Adenocarcinoma. MRI in coronal planes obtained with a TSE T2 (a) and a TSE T1 sequence (b) after contrast agent administration. The neoplasm (T) reaches the sphenoid sinus roof where a segment of the bone is invaded (the black arrows indicate the invaded bone tract). Above the invaded segment the intracranial extent is limited by a thin continuous black line that, after contrast administration, shows a linear enhancement on the TSE T1 plane, indicating a reaction of the dura (a, b). A thin film of fluid, hyperintense on T2, hypointense on T1, corresponds to the CSF (csf, a, b). The overall pattern of signals indicates the intracranial extent without imaging findings of dura invasion.

Fig. 10. Intestinal-type adenocarcinoma. TSE T1 (a, b) in the coronal plane with fat saturation and after contrast agent administration. a The ethmoidal neoplasm (T) blocks the drainage from the maxillary (ms) and frontal (fs) sinuses where a thickened and enhancing mucosa outlines the walls of the sinuses, filled by mucus. The neoplasm invades the left ACF floor (arrows). On a more posterior plane (b), the enhancement of the dura (arrows) extends far over the left orbit roof, well beyond the midline, a contraindication for a TES approach. ss, sphenoid sinus.

3. The cranial vector of spread. Focal contact, infiltration of the ASB floor (cribriform plate or roof of the ethmoid), or of the overlying dural layer are not considered contraindications to TES [5] (Fig. 8, 9). However, if the infiltration of the dura extends over the orbit beyond the mid-orbital line (Fig. 10) or a massive infiltration of the brain is detected, the endoscopic approach must be combined with an open access technique. Therefore, intracranial invasion requires thorough evaluation and to be graded via a proper imaging technique.

The intracranial extradural tumor extent is defined as a tumor growing through the bone but confined to the dural layer, which is raised and enhanced, but without a significant thickening. In fact, in the absence of thickening, dural enhancement alone has high sensitivity (88%) but poor specificity (50%) for transdural invasion [33]. The specificity reaches 100% if changes like nodularity or thickening greater than 5 mm are observed [36]. High-resolution 3D gradient echo T1W sequences (VIBE, THRIVE, LAVA) are indicated. Images reconstructed along planes perpendicular to the ASB floor (coronal, sagittal) are very useful [7]. Pial enhancement, when observed, has a very high predictive value for malignant invasion [33]. Unfortunately, the sensitivity is poor (50%). Therefore, preoperative MRI cannot rule out pial involvement. Further intracranial tumor progression can lead to brain parenchyma compression or invasion. Because brain compression by the tumor can cause edema, only the detection of intraparenchymal enhancement continuous with the tumor is a reliable sign of brain invasion. Hence, a combination of T2W, FLAIR, and postcontrast T1W sequences should be obtained (Fig. 11).

Fig. 11. Two patients, both affected by a nasoethmoidal squamous cell carcinoma with intracranial invasion. a In the sagittal TSE T2 plane, the neoplasm (T) “permeates” the black line of the ACF floor (curved white arrows), growing intracranially displacing the brain (white arrows), which appears mostly separated from the neoplasm by the CSF signal. The tumor invades the frontal sinus: anterior vector of spread (black arrow). b In the second patient, the sagittal TSE T2 plane shows a more extended permeation of the ACF floor (curved white arrows) and a larger intracranial invasion (white arrowheads). Apart from a short area of contact, sited posteriorly (black arrowheads), no CSF interface separates the tumor signal from the brain. An extensive area of brain edema (e) at the interface with the tumor indicates extensive cerebral invasion.

When substantial intracranial intradural neoplastic extent is detected by imaging, its relationships with the proximal branches of the anterior cerebral artery should be reported. CTA and MR angiography are used.

4. The lateral vector of spread. “High-risk” areas in this direction of growth are the medial wall of the orbit and lacrimal pathway. Most ethmoid and nasal neoplasms contact and displace the medial orbital wall, as soon as they reach an intermediate size. Because focal contact or focal infiltration does not contraindicate TES, the challenge for imaging is to grade the degree of orbital involvement, particularly when early invasion is suspected [3, 5, 30]. Bone erosion alone does not equal invasion. It is the periorbita, the fibrous capsule investing the whole orbital content, that is crucial, being more resistant to infiltration. The periorbita is not detectable by CT, but it can be identified by MRI as a thin regular stripe with low intensity on both T2W and T1W sequences (Fig. 12). Linear enhancement of the periorbita can also be observed, on the condition that fat saturation is used (Fig. 13). Focal interruption of the line by tumor indicates the presence of limited invasion. In this setting, MRI has been reported to be more sensitive and specific than CT in grading the tumor-orbit relationship, particularly in predicting early orbital invasion [37]. Special attention has to be paid to the orbital adipose tissue. Advanced orbital invasion should be reported when the tumor tissue replaces the extraconal fat, extends into the fat space between the extraocular muscles, and causes enlargement or abnormal signal intensity of the muscles. Tumor invading the extraocular muscles will require orbital clearance and thus an open approach [38, 39]. When focal or limited invasion involves the medial wall close to the orbital apex, the analysis of the fat planes surrounding the annulus of Zinn becomes more troublesome. High-resolution imaging in axial and coronal planes is recommended.

Fig. 12. Intestinal-type adenocarcinoma. Both the axial CT (a, postcontrast) and TSE T2 MR sequence (b) detect the invasion of the left medial orbital wall (white arrows). The intraorbital nodule is characterized by a regular outline (though lobulated), suggesting that the periorbita may still contain the neoplasm, a finding more clearly shown by a continuous “black line interface” on the MRI sequence. A compression on the medial rectus (mr) is present. acp, anterior clinoid process; sof, superior orbital fissure; oa, ophthalmic artery; im, impacted mucus.

The checklist should include assessment of the lacrimal pathways. Epiphora, or the presence of dilation of the lacrimal sac, requires a meticulous evaluation. The bony walls of the lacrimal canal are well imaged by CT, while the lining mucosa of the lacrimal duct is better analyzed by MRI. Limited involvement of the canal, especially the medial wall, does not contraindicate TES [5, 30]. Lacrimal drainage can be re-established via endoscopic dacryocystorhinostomy. On the contrary, an extensive invasion of the canal and the duct requires open access.

5. The medial vector of spread. Neoplastic invasion through the septum has to be reported, along with a detailed description of the tumor extent into the contralateral nasal cavity and ethmoid labyrinth. Special attention has to be paid to the involvement of the contralateral medial orbital wall.

6. The inferior vector of spread. When the tumor reaches or invades the hard palate, TES is contraindicated, since both the resection and reconstruction of the defect are very difficult to achieve via this approach alone [5].

Fig. 13. Sinonasal neuroendocrine carcinoma. Five MRI sequences in the coronal plane are obtained to analyze the relationship of the neoplasm with the orbital walls: two TSE T2 sequences without (a) and with (b) fat saturation, two TSE T1 sequences before (c) and after (d) contrast agent administration, and one VIBE sequence after contrast administration (e). The right nasoethmoidal neoplasm (T) grows into the maxillary sinus, blocking the drainage. The dehydrated impacted mucus (deh) has a signal lower than CSF on the T2W sequences (a, b) and higher on the T1W sequences (c–e). Non-dehydrated blocked mucus fills the right frontal sinus (white arrow): hyperintense on T2W sequences (a, b), and hypointense on T1W sequences (c–e). A mucocele arises from an anterior ethmoid cell (asterisk) blocked by tumor. The mucocele remodels the medial orbital wall (black curved arrow). Below the mucocele, it is the tumor itself that contacts the orbital wall, which is thickened (white arrows). The interface between the mucocele (above) and the tumor (below) with the displaced orbital wall is better appreciated on fat-saturated sequences (compare a to b). Although the administration of contrast agent improves the differentiation between mucus and tumor (compare c to d) and improves the detection of the mucosa (white dotted arrows in d, e), the association of T1W “coupled” to fat saturation (e) amplifies enhancement of the periorbita (black curved arrows in e). ion, infraorbital nerve.