Nearnradiolngy
Neuroradiology (1985) 27:189-201
© Springer-Vedag 1985
Review article
CT of the paranasal sinuses P. M. Som Mount Sinai School of Medicine of the City University, New York, NY, USA
Summary. CT scanning has allowed the radiologist to image paranasal sinus disease with an accuracy and detail never before attainable. This information has made the imager an important member of the physician team that evaluates the operability and treatment planning of these patients. The protocol of the CT examination is discussed, the normal CT anatomy is reviewed and an approach to evaluating both inflammatory and malignant disease is presented. Key words: CT - paranasal sinuses - sinus anatomy - sinus infections - sinus tumors
CT is recognized today as the method of choice for examining the head and neck [1-61. This article addresses the technique for sinus evaluation, normal sinus anatomy, and the usual CT appearances of common sinus pathology.
Technique The best plane for CT scans of the paranasal sinuses is parallel to the inferior orbitomeatal (IOM) line (Reid's Bale Line on Line of Frankfurt). This scan angle is nearly parallel to the planes of the hard palate, the zygomatic arches, the lateral portions of the orbital floors and much of the orbital roof. In this plane, the maxillary sinuses are seen in cross section without foreshortening or elongation. The frontal sinuses, particularly the anterior and posterior walls of the sinus, are well demonstrated. The ethmoid sinuses and orbital structures are seen along their longest axes, so each image provides maximal information about these areas. The sphenoid sinuses, bases of the middle cranial fossae, and the nasopha-
rynx are similarly well shown. In addition, use of this standard plane permits rapid and simple comparisons between the CT images and atlases of anatomical cross sections. All scans of the paranasal sinuses should begin at the maxillary alveolus just below the hard palate and should end above the frontal sinuses. This approach assures complete coverage of all the paranasal sinuses, as well as the nasopharynx, parapharyngeal spaces, and skull base. Dental lesions which may present as maxillary sinus disease will be seen. Primary lesions of the anterior cranial fossa which present clinically as paranasal sinus disease and secondary intracranial extension from primary disease of the paranasal sinuses will be imaged successfully. By this technique, significant lesions will not be overlooked. In the author's experience, more mistakes are made by failing to observe the pathology than by making an incorrect diagnosis on observed disease. The thickness of each scan slice should be no greater than 5 mm. Thicker slices will average out important anatomy that may be crucial in determining a diagnosis or establishing operability. Scan slices of 1.5-2.0mm thickness are unnecessary in the vast majority of cases. They are better reserved for those instances where vital information cannot be gleaned from the routine scan. These thin slices need only be utilized for a small region and thus only a few such slices are required. The average case requires only 16-18 5-ram thick slices, depending upon the size of the frontal sinuses and how many scans are needed to cover them. The axial CT scans should be reviewed to determine whether direct coronal scans are necessary. In general, coronal scans are necessary to evaluate structures that are parallel to the IOM plane (Frankfurt Plane) i. e., the palate, the orbital floor and roof, and the roofs of the nasal cavity, ethmoid sinus and sphenoid sinus. Thus as a routine, the coronal scans must be obtained when clinical findings or the initial
190
Fig. 1. Axial CT through the frontal sinus as seen at bone window setting reveals the sinus air to abut directly upon the bony sinus walls indicating the presence of normal sinus mucosa. A septum (short arrow) and the intersinus septum (long arrow) are seen. The scalloped sinus margin occurring with well developed frontal sinuses is easily appreciated at the right sinus margin. The curved posterior sinus wall is also well seen Fig. 2. Axial CT through the base of the frontal sinus reveals pneumatization of the left orbital roof by the frontal sinus Fig.3. Coronal CT reveals bilateral supraorbital ethmoid pneumatization of the orbital roof (curved arrow). There is also pneumatization of the crita galli (straight arrow)
191
axial images suggest that the pathology may have invaded or crossed the palate (mouth to nasal cavity or vice versa), spread across the orbital floor (antrum to orbit or vice versal), or crossed intracranially (nasal cavity, orbital roof, ethmoid or sphenoid sinus to anterior cranial fossa or vice versa). As a routine, the coronal sections are 5 mm thick. The precise angle of the "coronal" scan will depend upon several factors: (1) the specific area to be investigated in the coronal plane, (2) how far the patient's head can be extended while either prone or supine, and (3)how much metallic dental work the patient has (since bridges and fillings should be avoided lest they degrade the image). Usually a lateral "scout" scan of the head is taken and a "modified coronal" scan angle is chosen that runs from the most anterior dental fillings inferiorly, to the most posterior area to be studied superiorly. In the average case, this modified coronal plane makes an angle of 50-75 ° with the IOM plane (Plane of Frankfurt) and proves to be an extremely useful adjunct to the routine axial scan. Intravenous contrast material should be used whenever possible. Contrast enhanced scans help to identify vascular lesions such as hemangioma and angiofibroma, and help to differentiate inflammatory lesions from tumors and tumors from obstructed sinuses that are neither infected nor invaded by tumor. It is probably not necessary to obtain initial noncontrast CT scans in all cases. Most of the time, it is sufficient to detect the differential enhancement between adjacent structures on the contrast-enhanced scan. Any contrast present can be deliberately obscured at wide-window settings, giving the viewer a virtual "noncontrast" scan. Thus, noncontract scans should be obtained if time allows, or if the suspected diagnosis or its differential diagnosis may contain small calcifications that could be obscurred at wide windows. The contrast agent is best given as a combination of a bolus injection followed by a drip infusion, be-
cause this technique provides maximal enhancement throughout the scan period. It is essential to scan as soon as possible after the contrast administration, preferrably while the contrast is running intravenously, Delayed scans underestimate the degree of enhancement present in tumors and inflammatory process and decreases the sensitivity of the scan for a specific diagnosis. Analysis of head and neck pathology requires separate images of the soft tissues and the bones. The muscles, vessels, fat planes, and other soft tissues are best displayed at narrow window widths of 160 to 300. The lower this number, the more sensitive the scan is in detecting small degrees of contrast enhancement: however, the grainier will be the scan. The best images of bony structures require wide window widths of 1000 or more. Because areas of bone pathology will be overlooked if the scan is imaged only at soft tissue windows and because subtle softtissue masses, fat plane infiltrations, mild degrees of enhancement, and subtle calcifications will all be obscured at bone window settings, each image should be viewed at both soft tissue and bone windows [7].
Normal anatomy The normal sinus mucosa is too thin to see in any of the paranasal sinuses [8]. The air in each normal sinus cavity appears to abut directly upon the adjacent bone. Thus, whenever sinus mucosa is seen, the mucosa is abnormal, even if it appears as a relatively uniform zone of soft-tissue density lining the sinus walls. The frontal sinuses develop after birth from anterior ethmoid air cells. The left and fight sinuses develop independently [9]. On average, the top of the frontal sinus is at the level of the mid-vertical height of the orbit at age four years, reaches the height Of the superior orbital rim at age eight years, and rises
Fig. 4 a and b. a Axial CT through the mid frontal sinus region as seen at narrow "brain" window settings. The frontal sinus appears small, but normal, b Same scan as a but now seen at wide bone window settings. Soft tissue inflammatory disease (arrow) is now seen in a moderately well developed frontal sinus which extends further to the left side (arrowheads) than apparent on a Fig. 5 a and b. a Axial CT through the mid ethmoid sinuses reveals the narrower anterior portion of the ethmoid complex. The thin lamina papyracea which separates the sinus from the orbit (arrows) appear incomplete or dehiscent in areas. This is symmetric, with no associated soft tissue mass and is a normal appearance. The individual ethmoid cells can be well seen. b Axial CT through the mid ethmoid sinuses reveals thicker, but normal lamina papyracea than seen in Fig. 5A. The sphenoid sinuses (S) are seen to form the most posterior portion of each medial orbital wall. The wedge shape ofth¢ ethmoid complex is well seen Fig. 6. Axial CT through the lower ethmoid sinuses reveals the upper recesses of the maxillary sinuses ceils. The nasal septum (curved arrow) is seen between the ethmoid cells
(arrows) adjacent to the ethmoid
Fig.7. Axial CT at the uppermost ethmoid level reveals the normal soft tissues of the base of the anterior cranial fossa overlying the ethmoid cells. The intracranial position is marked by the crista galli (arrow). Air is seen in the top of the ethmoid cells (arrowheads)
192
Fig. 8. Coronal CT reveals the small, thin cribriform plates (arrowheads). The area of the crista galli (large arrow)which rests on the mid intracranial aspect of the cribriform plates is seen. The nasal septum (large arrowhead) attaches to the mid undersurface of the plates. The attachments (small arrows) of the middle turbinate (X's) mark the lateral margins of the cribriform plates Fig.9. Axial CT through the maxillary sinuses in a 1½ year old child. The maxillary sinuses (white arrows) have developed to lie at the level of the infraorbital canals (arrowheads) Fig. 10. Axial CT through the mid maxillary sinuses reveals the lateral zygomatic recess of the antrum (arrow).The inferior meatus (m) and the inferior turbinate (t) are seen. The fat planes and muscle of the infratemporal fossa are seen behind the posterolateral antral wall (ITF). The pterygoid plates (arrowheads) and nasopharynx (P) are also seen. Curved arrows point to a region of the medial antral wall formed only by mucosa and no bone. This is normal Fig. 11. Coronal CT through the posterior antra reveals the inferior recess
(large arrow)
(small arrow)and the superior recess under the apex of the orbit
193
above the orbit into the vertical plate of the frontal bone by age ten years [10]. Small or hypoplastic frontal sinuses may be very difficult to differentiate from anterior ethmoid cells, especially when the frontal sinuses rise only to the level of the superior orbital rim. Fortunately such distinction is usually only of academic interest and has little clinical significance. In the better developed frontal sinuses, the borders are usually scalloped, creating septa which project into the sinus cavity. The main intersinus septum lies in the midline inferiorly; however, it may angle far to the left or the right of midline as it rises superiorly. The sinus contour septations and the main intersinus septum can all be imaged on axial CT scans (Fig.l). Septal erosion can be an early plain film finding of a mucocele, so the septa must be carefully examined on routine films. However, CT displays the abnormal sinus mucosa and any intrasinus softtissue mass so deafly that specific attention to the septa is less important in CT diagnosis than in plain film diagnosis of sinus pathology. The orbital plate of the frontal bone, or orbital roof, can be pneumatized in two different ways. First the frontal sinus can have an inferior recess which extends posteriorly (Fig.2), and secondly, superior ethmoid cells (supraorbital cells) can extend independently into the orbital roof (Fig. 3). The differentiation between which of these two sinuses has pneumatized the orbital roof is clinically important. If a pathological process is in a supraorbital ethmoid sinus, the surgical approach to it is different than that used if the pathology lies within the frontal sinus proper. The distinction between these sinuses is best accomplished on coronal images where supraorbital cells are seen as laterally arched extensions of the anterior ethmoid cells extending into the orbital plate diploe (Fig. 3). Axial CT scans will give a clear picture of the posterior extent of these recesses. CT is the most accurate method for detecting frontal sinus pathology and is the method of choice for evaluating the posterior table of the frontal sinus. Whereas this curved surface is very difficult to examine by conventional films and pluridirectional tomography, the integrity of the posterior sinus wall is
assessed easily and accurately by axial section CT (Fig. 1). Thus axial CT is particularly useful for distinguishing between a frontal sinus process which has extended posteriorly into the anterior cranial fossa and intracranial disease that has involved the frontal sinus secondarily. There are two CT findings which can be helpful in making this distinction: (1) the location of the epicenter of the process, and (2) the angles that the periphery of the lesion makes with the posterior sinus table. Acute angles suggest that the process arose intracranially, whereas obtuse angles suggest an epidural (frontal sinus) origin. A point of caution must be mentioned. Accurate distinction between a hypoplastic sinus and a completely airless sinus filled with a tumor or inflammatory mass may only be accomplished if the scans through this area are viewed at bone window settings. Narrow windows such as are usually employed for brain imaging can "white out" the airless sinus, so that the viewer assumes that no sinus is present. Even if sinus air is detected on "narrow window" scans, the presence of degree of mucosal disease is usually overlooked (Fig. 4). The ethmoid sinuses are the only paranasal sinuses which are fully developed at birth. There are between 3 and 15 cells in each ethmoid bone. The posterior cells tend to be larger [11]. Considered together, the ethmoid cell complexes have an overall wedge shape on axial CT scans. The anterior margins near the nasal bones are narrower while the posterior margins abutting the sphenoid are wider (Fig. 5). Thus both medial orbital walls lie slightly oblique to the mid-sagittal plane. It is because of this obliquity that plain films with central rays parallel to the mid-sagittal plane (Caudwell, PA, AP views) do not allow accurate imaging of the entire medial orbital wall. What appears to be the entire medial orbital wall on a Caudwell view is, in fact, only the posterior portion of this wall. The entire medial orbital wall is composed of surfaces from three different bones: lacrimal, ethmoid, and sphenoid. Anteriorly, the lacrimal bone forms the lacrimal fossa and overlies some of the most anterior ethmoid cells. Posteriorly, a small segment of
Fig.12. Axial CT through the lowest portions of the maxillary sinuses and the hard palate. The roots of the molar teeth seen projecting into the antra
(arrowheads)are
Fig. 13. Axial CT through the upper antra. The relatively flat anterolateral orbital floors (o) are seen as bone projected into the sinuses. The nasolacrimal ducts (arrowheads)are well seen Fig.14a and b. a Axial CT through the sphenoid sinuses as seen at "brain" window settings. The left sphenoid sinus appears normal (s), however, the right sphenoid sinus looks hypoplastic (x). There are incidental inflammatory changes in the right ethmoid sinuses, b Same scan as in Fig. 14 a but viewed at bone window settings now reveals an osteoma partially surrounded by air (arrows)in a normally developed right sphenoid sinus Fig. 15. Axial CT reveals bilateral sphenoid pneumatization of the floor of the middle cranial fossae
(arrows).m = maxillary sinuses
194
Fig. 16. Coronal CT reveals lateral sphenoid sinus recesses which extend down into the pterygoid plates (arrows). P = pterygoid plates Fig.17. Axial CT reveals bilateral sphenoid sinus pneumatization of the posterior orbital walls (s) Fig. 18. Axial CT reveals thickened mucosa along the walls of the left antrum (arrows). The overall appearance is smooth surfaced and uniform. This is usually seen with infection, however, scarfing and fibrosis also have this appearance. The right antrum is normal Fig. 19. Axial CT reveals a left antral air-fluid level (arrow). Minimal mucosal thickening is also seen on the anterior antral wall Fig.20. Axial CT reveals complete opacification of the left antrum. The sinus bony walls are normal. This could be a large cyst, polyp, developing mucocele, developing antrochoanal polyp or an early tumor Fig. 21. Axial CT on the same patient as in Fig. 20 taken at a more cephalad level reveals small collections of air (arrows)between the top of an apparently smooth surfaced mass and the sinus walls. This suggests the diagnosis of either a large retention cyst or polyp
195
orbital wall is formed by the anterior margin of the sphenoid bone (Fig. 5). It is because of this latter relationship that sphenoid sinus disease can cause orbital apex symptoms. The majority of the medial orbital wall is formed by the lamina papyracea [12]. This bone is often so thin and incompletely ossified, that it appears incomplete on CT scans (Fig. 5). In specific cases, then, bone defects are best assessed by comparing the left and right sides. If an apparent focal erosion is symmetrical, it is probably a normal variant. If the configuration of the medial orbital wall does not bow inward or outward in the area of suspected erosion, the "erosion" probably is a variant. If no soft-tissue mass is present in either the underlying ethmoid cells or the adjacent orbit, the "erosion" is not an area of pathologic destruction. Two areas create potential errors in interpreting CT scans taken through the ethmoid sinuses. (1)At the level of the lowermost ethmoid cells, a round or ovoid air celI lies just lateral to the ethmoid cells near the apex of the orbital floor (Fig. 6). This cell is often mistaken for an ethmoid cell, but is actually the most-cephalic portion (i. e., apex) of the maxillary sinus. Since this cell represents a separate sinus, pathologic changes in it do not necessarily parallel the changes seen in the ethmoid complex. Thus, when clouding of the sinus apex is observed, the CT scans should be carefully followed throughout the entire maxillary sinus (antrum) in order to evaluate the degree and type of antral disease. (2) At the level of the roof of the ethmoid complex, a "soft-tissue mass" is often seen in the midline (Fig. 7). This mass is often misinterpreted as an upper nasal cavity or ethmoid sinus tumor mass, but actually represents the medialmost portions of the frontal lobes, within the anterior cranial fossae. The thin midline bone density of the crista galli identifies that the level of the CT scan is intracranial. CT sections through the ethmoid cells inferior to the mass will not demonstrate any contiguous mass, and no sinus or nasal mass lesion will be detected on coronal scans. The roof of the nasal cavity is formed by the cribriform plates. These can be identified in several ways: First, the crista galli rests directly upon the
upper surface of the cribriform plates in the midline. Second, the nasal septum attaches to the undersurface of the cribriform plates in the midline. Third, the middle turbinates attach to the lateral margins of the cribriform plates (Fig. 8). The ethmoid roof lies more cephalad on either side. These relationships are easily appreciated in coronal section [13]. The maxillary sinuses are very important clinically, since they are involved by infection, tumor, or trauma more often than any of the other paranasal sinuses. The maxillary sinuses are small at birth; each having a volume of only about 100 cubic mm [11]. In the average case, they develop so that they extend under the infraorbital canal by the age of two years and extend into the zygoma by the age of nine (Fig. 9). The portion of the body of the zygoma pneumatized by the sinus creates the lateral (zygomatic) recess. Axial CT sections demonstrate best the anterior, medial, and posterolateral walls of the maxillary sinuses (Fig. 10). Coronal CT scans demonstrate best the inferior (alveolar) recess and the slanting sinus roof (orbital floor) (Fig.11). The roots of the molar and premolar teeth routinely project into the alveolar recess (Fig.12). Because of this relationship, antral disease often presents clinically as tooth pain, and dental infection can cause antral sinusitis. The medial antral wall is formed by small contributions from several adjacent bones. These bones leave a bone defect (bony sinus ostium) which can be quite large. Mucosa covers the bony ostium and reduces the size of the opening to the small effective sinus ostium seen clinically. This means that a variable portion of the medial antral wall will be composed only of mucosa. The normal mucosal portion of wall must not be erroneously interpreted as bone destruction (Fig. 10) [14]. The anterolateral portion of the maxillary sinus roof is relatively flat (Fig. 13). Medial and posterior to this area, the sinus roof slants upward to the apex of the orbit medially. Axial CT scans through this upper recess create the ovoid lucent air cell described in the ethmoid sinus section. The infraorbital and the nasolacrimal canals can be easily identified projecting into the sinus cavity (Fig.13). Sections
Fig.22. Axial CT reveals an expansile non-enhancing fight antral mass bulging the medial antral wall toward the midline nasal septum. Although the fight posterolateral antral bony wall is slightly displaced away from the sinus cavity, it is thickened, suggesting chronic infection. The most likely diagnosis is a mucocele. A thin rim of enhancement can be seen surrounding the low density central portion of the lesion (between arrows). This indicates the diagnosis of a pyocele Fig.23. Axial CT reveals an enhancing left nasal cavity tumor mass which can be seen to be obstructing, but not extending into the left antrum. There is destruction of the left medial antral wall and portions of the bony nasal septum (arrowheads). Inflammatory mucosal thickening is seen in the right antrum and tumor mass may extend into the posterior right nasal cavity. Nasal plasmacytoma Fig.24. Axial CT reveals a mildly enhancing expansile, bilateral nasal cavity mass which has destroyed part of the anterior nasal septum (arrowhead) and is starting to extend into the antrum by destroying the medial antral walls (arrows). Wegner's granulomatosis
196
Fig. 25. Axial CT reveals destruction of the anterior nasal septum (arrow) and mucosal thickening along the anterior lateral nasal cavity walls. This should be a granulomatous disease. This patient was a chronic cocain abuser Fig. 26. Axial CT reveals opacification of the left sphenoid sinus with marked thickening of the sinus walls indicating chronic infection Fig. 27. Axial CT reveals a soft tissue smooth left antral mass
(arrow). Retention cyst or polyp
Fig.28. Axial CT through the upper ethmoid sinuses reveals a non-enhancing expansile left anterior ethmoid sinus process. The lamina papyracea is bowed laterally by the lesion (arrows). Mucocele Fig. 29. Axial CT viewed at bone window settings reveals several areas of pure bone destruction around both orbital margins an area of thickened bone in the right posterior orbital wall (large arrow). Metastatic prostate carcinoma
(arrows) and
Fig. 30. Axial CT reveals a highly destructive tumor of the right maxilla extending into the soft tissues of the right cheek obliterating the normal fat planes (arrows). Carcinoma
197
through the maxillary sinus also demonstrate the pterygoid plates, the pterygopalatine fossa, and the contour of the pharynx. Fat planes situated just behind the posterolateral sinus wall separate the wall from the infratemporal fossa muscles (Fig.10) [15, 16]. Tumors often spread from the sinuses into these regions. Occasionally, tumors arising from these areas involve the sinuses secondarily [17-19]. The sphenoid sinus is divided into two separate left and right cavities by a septum. However, it is best to consider them initially as one sinus. The sphenoid sinus is nearly absent at birth. Later the sinus develops, so that 60% of the time it extends under the sellar floor and 40% of the time it reaches just up to the anterior wall of the sella turcica. Only in isolated cases does this sinus not extend back to the sella in the adult [20]. The growth of the sinus is roughly uniform, so that the left and the right main sinus cavities develop nearly to the same extent posteriorly. A welldeveloped left sinus cavity will not normally occur with an aplastic or hypoplastic right sinus cavity. If a CT scan suggests such asymmetry, one should suspect that the supposedly smaller sinus has been obliterated by a pathologic condition such as complete sinus opacification, osteoma, etc. The CT scan must then be closely examined at the bone window settings (Fig. 14). Such caution will reduce the chance of overlooking significant pathology. In about one half of the cases, lateral recesses develop from the main sinus cavities [21]. These can extend to aerate an anterior clinoid process, the greater wing of the sphenoid bone along the posterior orbital wall, the floor of the middle cranial fossa, and/or the pterygoid fossa (Figs.15, 16, and 17). These lateral recesses are usually not symmetric on the left and the right sides, and they should not be confused with destructive lesions. Familiarity with their appearance is essential for proper analysis of this region.
Inflammatory disease When the sinus mucosa is seen on CT, it is pathologically involved. If the mucosa has a nearly uniform, smooth, thickened appearance involving most or all of the sinus walls, it usually represents either inflammatory thickening or fibrotic scarfing secondary to bacterial, allergic, or granulomatous disease (Fig. 18).
Bacterial sinusitis usually involves each sinus independently and usually extends to adjacent sinuses as a sinus by sinus event. The patterns of disease vary from involvement of a single sinus (usually the antrum) to involvement of adjacent sinuses on one side of the face to pansinusitis. There may also be some swelling of the nasal cavity mucosa and the turbinates, but the primary CT findings are in the sinus cavities. Most often, the mucosal thickening is relatively uniform. However, if the sinus ostium becomes obstructed, a completely airless (opacified) sinus is found. As an intermediate stage, an airfluid level may be observed before the obstructed sinus becomes totally opacified (Fig.19). In fact, the most common cause of an air-fluid level is acute bacterial sinusitis, and this most often involves just the maxillary sinus. Clinically, patients with bacterial sinusitis have pain or the sensation of pressure over the involved sinuses. The treatment of choice is antibiotics, usually combined with an antral saline washing to promote sinus drainage. Since the saline lavage requires 3-4days to empty from the sinus cavity, roentgen studies should not be taken during this period; differentiation between residual saline and an infected sinus with a recurrent air-fluid level will not be possible. Allergic disease is a systemic process and, as a resuit, there is a strong tendency for symmetrical sinus involvement and pansinusitis [22]. Sinus airfluid levels are rare. Most of the secretions are nasal in origin (rhinorrhea) [24]. Nasal polyposis is often seen in association with the sinus disease. Although pansinusitis may be due to either allergic or bacterial disease, pansinusitis associated with nasal polyposis is more commonly found with allergic disease than it is with bacterial infection. Clinically and radiographically, both allergic and bacterial sinusitis should show some improvement after 2-3 weeks of conservative medical therapy. It is important to document such improvement, especially if the involved sinus was completely opacified on the initial study. If the appearance of the sinus does not improve after 2-3 weeks of therapy, then one of several conditions is probably present, all of which require surgical intervention: (1)There could be a large retention cyst or polyp which completely fills
Fig. 31. Axial CT on a patient after a left partial mandibulectomy. No surgery was performed on the left antrum. Carcinoma has destroyed all of the left antral bony walls and extended into the soft tissues of the mandibular bed Fig. 32. Axial CT reveals an expansile nasal cavity mass which has remodelled some of the surrounding bone some destruction (arrowheads). Melanoma Fig. 33. Coronal CT reveals a partly expansile lary sinuses. Histiocytic lymphoma
(arrows) as well as causing
(arrows) and partly destructive nasal cavity mass which has invaded the ethmoid and maxil-
198 the sinus cavity (Fig. 20). In such cases, a small collection of air can often be detected atop the polypoid mass (Fig. 21). (2) The sinus could be completely obstructed and starting to develop a mucocele (Fig. 22). (3) There could be an antrochoanal polyp which fills the antrum and extends into the nasal cavity. Finally, (4) there could be a tumor which fills the sinus cavity or obstructs the sinus ostium (Fig. 23). Conservative medical therapy may cause temporary relief of clinical symptoms despite persisting tumor mass, so these patients should be followed carefully. If the sinus has not shown improvement on plain film examination after 2-3 weeks of conservative therapy, the possibility that a surgical condition may be present must be realized and a CT scan should be obtained. By following this type of an approach, early tumors will be detected more frequently and hopefully this will lead to a better prognosis for these patients. Granulomatous diseases have no specific distinguishing CT features, other than an overall pattern of disease involvement. Virtually all the granulomatous diseases initially present findings in the nasal cavity. The sinuses are involved secondarily. A diagnosis of granulomatous disease should be considered when CT discloses bulky bilateral nasal cavity masses which usually enhance minimally, small granulomas lining the mucosa of the nasal vault, focal destruction of the walls of the nasal vault, frontal processes of the maxilla, and nasal bones (Fig.24), and/or destruction of the cartilage of the nasal septum (Fig. 25). Unfortunately, lymphoma can also present with identical changes [25]. Accurate differential diagnosis is aided by clinical history and biopsy, but even these may not be conclusive in all cases of granulomatous disease. Less often, a single sinus may be filled with a soft-tissue mass and reveal thickening and sclerosis of the sinus walls (Fig.26). The presence of these bone changes makes chronic infection by far the most likely diagnosis. This particular pattern of disease is most often seen with aspergillosis involving either the sphenoid or maxillary sinuses [25]. Retention cysts result from obstruction of a single mucous gland in the sinus mucosa. They characteristically appear on CT as a homogeneous soft-tissue mass which has a smooth convex margin and which is attached to the sinus mucosa, usually by a broad base (Fig. 27). Retention cysts cannot be distinguished from polyps and, clinically, this is of little concern. The presence of a cyst or polyp may have no clinical significance, since they are found as incidental findings in 10% of people [26, 27]. Mucoceles result from obstruction of the sinus ostium or a septated portion of the sinus cavity. The sinus then fills with mucoid secretions and, at this
stage of development, cannot be differentiated from other inflammatory processes. Once the sinus cavity is completely filled, the secretions start to remodel the sinus walls and push them outwards [3, 28-32]. At this point, the CT appearance of a nonenhancing expansile sinus mass that completely fills the sinus cavity permits one to suggest a diagnosis of mucocele (Fig. 28). If the mucocele continues to grow, pressure necrosis eventually causes bone erosion along the sinus wall. At this point, it may prove impossible to differentiate the mucocele from one of the tumors that can cause bone remodeling. Mucoceles are sterile. If a mucocele becomes infected, it is called a pyocele. On CT, pyoceles usually exhibit a rim of enhancement around the lesion (Fig. 22). Statistically, about 60% of paranasal sinus mucoceles occur in the frontal sinuses; about 30% occur in the ethmoid sinuses, and 10% occur in the maxillary sinuses. Sphenoid sinus mucoceles are rare. Tumor Before the radiographic features of tumors are discussed, a brief word about pain is warranted. In the paranasal sinus region, pain should be equated with infection. It is not, in general, caused by either bone destruction or bone remodelling. If a patient has a tumor and pain, in the great majority of these cases, infection coexists. It is for these reasons that the radiologist plays such an important role in evaluating head and neck disease. If a patient with an unknown tumor and an infection is seen by a clinician, the first treatment is directed to the clinically evident inflammatory process. With proper medical therapy, the infection is cured and the pain is relieved. However, the tumor can remain undiagnosed. If the tumor is not detected radiographically, the patient may not seek medical help again until the tumor has grown and another infection (usually secondary to sinus obstruction) has occurred. By this time, the tumor may have become inoperable [4]. Although pain may be due to perineural invasion by tumor in a few instances, the concept of equating pain with infection will prove correct in the vast majority of cases. Followup radiographic examinations should be obtained in all patients with sinus pain to rule out coexistent tumor. In patients with neoplasms, symptoms usually reflect the mass effect of the tumor itself and include: proptosis, facial swelling or deformity, difficulty in breathing through one or both sides of the nose, epistaxis, and change in the quality of the voice.
199
Fig.34. Axial CT reveals a carcinoma that has destroyed some of the left sphenoid sinus wall (large arrow)the posterior left ~intral wall (small arrow) and a portion of the floor of the left middle cranial fossa (curved arrow). It also has extended into the infratemporal fossa (arrowheads). The extensive nature of the tumor was not known before the CT. There is inflammatory disease in the left antrum Fig. 35. Axial CT on a patient after left total maxillectomy. The pterygoid plates remain intact (19).The mucosa of the new cavity is smooth Fig. 36. Axial CT on a patient after rhinotomy and left medial maxillectomy. The mucosa of the nasal cavity and remaining left antrum is smooth. Portions of the remaining nasal septum (arrows) are seen in the nasal cavity Fig.37. Axial CT on a patient after total left maxillectomy. The entire postoperative cavity has a thickened nodular appearance and a nodular mass is also seen along the left side of the nasal septum. Recurrent tumor Fig. 38. Axial CT on a patient after partial maxillectomy and rhinotomy. A focal nodular mass is seen tumor
The CT diagnosis of a tumor requires the presence of a soft-tissue tumor mass [3, 4]. Changes in the adjacent bones are secondary features. Therefore, any area of bone "destruction" which is not associated with an adjacent soft-tissue mass most probably represents a normal variant or the site of previous surgical intervention. Purely osseous metastases rarely occur in the facial bones. When seen, they
(arrow)in the left antrum. Recurrent
most often are the lytic and blastic changes of metastatic prostate carcinoma (Fig. 29). Categorizing the bone destruction seen on CT as either aggressive bone destruction or bone remodelling aids differential diagnosis [30, 33]. In aggressive bone destruction, the bone is rapidly permeated and destroyed (Figs.30 and 31). Such destruction is seen primarily with squamous cell carcinoma which ac-
200 counts for nearly 80% of all paranasal sinus malignancies. Aggressive sarcomas such as angiosarcomas, some melanosarcomas, and rhabdomyosarcomas, also give this appearance. Metastases, primarily from lung, breast, and lower urinary tract primaries, cause aggressive bone destruction less commonly. The type of contrast enhancement seen within this group of tumors varies from marked enhancement in most melanosarcomas and angiosarcomas, through mild enhancement in rhabdomyosarcomas and most metastases, to minimal or no enhancement with squamous cell carcinomas. Bone remodelling reflects the slow geometric growth of the tumor process. As bone is eroded on the inner osseous surface adjacent to the tumor, new bone is laid down on the outer surface. The net effect of this process is that the bone appears to be pushed away from, or bowed around, the tumor (Figs. 32 and 33). In the paranasal sinus region, the tumors that cause bone remodelling include: the minor salivary gland tumors, extramedullary plasmacytomas, esthesioneuroblastomas, inverting papillomas, histiocytic lymphomas, and some low-grade sarcomas such as fibrosarcomas. Many embryonal rhabdomyosarcomas and melanosarcomas can also cause bone remodelling [33]. In the maxillary sinus, odontogenic lesions such as dentigenous cysts and ameloblastomas must also be considered. The important concept to understand is that the sinus cavity is expanded. Whether or not there are associated areas of focal aggressive bone destruction, the mere presence of bone remodelling should bring these tumors to mind. Bone remodelling may also be observed when a mucocele, large polyp, or large retention cyst coexists with squamous cell carcinoma. The possible concurrence of two lesions must be considered when a biopsy-confirmed (electron microscopy) squamous cell carcinoma is seen in conjunction with bone remodelling. Since other tumors including histiocytic lymphoma, embryonal rhabdomyosarcoma, melanosarcoma, plasmacytoma, and esthesioneuroblastoma can be confused with anaplastic carcinoma, histologically, an alternate possibility is that the histologic diagnosis of anaplastic carcinoma is erroneous, and that the bone remodelling results from these other tumors. Electron microscopy and histochemical testing will then establish the correct diagnosis. Metastases from hypernephromas and thyroid primaries also cause some bone remodelling, as well as dramatic enhancement. Unfortunately, one must not assume that the presence of bone remodelling implies a biologically nonaggressive tumor. It is true that the most common expansile processes of the paranasal sinuses (i.e.,
mucoceles) and of the nasal cavity (i. e., nasal polyposis) are benign processes. However, some of the lesions that cause remodelling (adenoid cystic carcinomas, adenocarcinomas, etc.) have worse five-yearsurvival statistics than does squamous cell carcinoma, which is the classical aggressive bone destroying tumor [4, 30, 33]. The enhancement characteristics of a soft-tissue lesion can be very useful in identifying tumor margins, especially when the tumor bulges into a sinus and obstructs sinus drainage rather than invades the sinus (Fig. 23). Most tumors are isodense or at least minimally enhancing masses, whereas mucous secretions usually exhibit low attenuation and are nonenhancing. Careful attention must be paid to all of the true tumor margins, because these will determine: operability and the surgical approach of choice, field size for radiation therapy, and tumor size for accurately measuring response to either radiation or chemotherapy (Fig. 34).
Postoperative state Once surgery has been performed on the sinonasal cavities, the main task of the radiologist is to determine the presence of early recurrent disease. CT is probably the most sensitive tool for determining early soft tissue recurrences, especially within postoperative cavities that are inaccessible or difficult to examine clinically [8]. If possible, the first and easiest approach is to obtain a baseline postoperative scan of the patient 6-8 weeks after surgery. This time interval allows any postoperative hemorrhage, edema, and infection to subside. The baseline scan is essentially the new normal for this patient and all followup scans can be compared to it (Figs. 35 and 36). The basic concepts for determining mucosal recurrences are simple and can be applied to paranasal sinus CT scans, whether or not a baseline scan is available for comparison. All of the normal postoperative sinonasal cavities are smoothly marginated. Infection and radiation fibrosis both cause uniform mucosal thickening (Fig. 18). Tumor causes mucosal irregularity and/or focal nodular thickening (Figs. 37 and 38). A small localized mucosal irregularity can easily be compared to the baseline scan, if one is available, to evaluate whether or not it was present in the immediate postoperative period. The presence of such mucosal irregularities and/or nodular masses indicates recurrent disease, until proven otherwise. The surgeon can be directed to the area for biopsy confirmation.
201
Routine followup CT examinations at 4-6 month intervals helps to detect early mucosal changes which are often clinically occult. The clinician may then be able to treat these recurrences before they are clinically obvious and, it is hoped, improve the length and quality of patient survival [8].
References 1. Parsons C, Hodson N (1979) Computed tomography of paranasal sinus tumors. Radiology 132:641-645 2. Thawley S, Gado M, Fuller T (1978) Computerized tomography in the evaluation of head and neck lesions. Laryngoscope 88: 451-459 3. Mancuso AA, Hanafee WN (1982) Computed tomography of the head and neck. Williams & Wilkins, Baltimore 4. Som PM (1984) The paranasal sinuses. In: Bergeron RT, Osborn AG, Sore PM (eds) Head and neck imaging excluding the brain. Mosby, St. Louis pp 1-142 5. Carter BL (1982) Computed tomography in radiology of the ear, nose and throat. In: Valvassori GE, Potter GD, Hanafee WN, Carter BL, Buckingham RA (eds) Saunders, Philadelphia pp 212-236 6. Bilaniuk LT, Zimmerman RA (1982) Computed tomography in evaluation of the paranasal sinuses. Radiol Clin North Am 20:51-66 7. Carter BL, Bankoff MS, Fisk JD (1983) Computed tomographic detection of sinusitis responsible for intracranial and extracranial infections. Radiology 147:73%742 8. Som P, Shugar JMA, Biller HF (1982) The early detection of antral malignancy in the postmaxillectomy patient. Radiology 143:509-512 9. Van Alyea OE (1942) Nasal sinuses: anatomic and clinical consideration. Williams & Wilkins, Baltimore 10. Caffey J (1978) Pediatric x-ray diagnosis, 7th ed Year Book Medical Publishers, Chicago 11. Ritter FN (1973) The paranasal sinuses, anatomy and surgical technique. Mosby, St. Louis 12. Goss CM (1963) Gray's anatomy, 27th ed Lea and Febiger, Philadelphia 13. Osborn AG, Mclff EB (1982) Computed tomography of the nose. Head Neck Surg 4:182-199 14. Alberti PW (1976) Applied surgical anatomy of the maxillary sinus. Otol Clin North Am 9:3-20 15. Mancuso AA, Bohman LG, Hanafee WN, Maxwell D (1980) Computed tomography of the nasopharynx. Normal and variants of normal. Radiology 137:113-121
16. Larsson SG, Mancuso A, Hanafee W (1982) Computed tomography of the tongue and floor of the mouth. Radiology 143: 493- 500 17. Mancuso AA, Maceri D, Hanafee WN, Ward P (1981) CT of cervical lymph node cancer. AJR 136:381-385 18. Miller EM, Norman D (1979) The role of computed tomography in the evaluation of neck masses. Radiology 133:145-149 19. Batsakis JG (1979) Tumors of the head and neck: clinical and pathological correlations, 2nd ed. Williams & Wilkins, Baltimore 20. Yanagisawa E, Smith HW (1973) Normal radiographic anatomy of the paranasal sinuses. Otol Clin North Am 6: 429-457 21. Etter LE (1955) Atlas of roentgen anatomy of the skull. Thomas, Springfield 22. Stahl RH (1974) Allergic disorders of the nose and paranasal sinuses. Otol Clin North Am 7:703-718 23. Wilder WH, Hamer SG, Banks PM (1983) Lymphoma of the nose and paranasal sinuses. Arch Otolaryngo1109:310-312 24. Dodd GD, Jing BS (1977) Radiology of the nose, paranasal sinuses and nasopharynx. Williams & Wilkins, Baltimore 25. Finn DG, Farmer JC Jr (1982) Chronic mucormycosis. Laryngoscope 92: 761 - 763 26. Farcenelli FW (1969) Maxillary sinus abnormalities. Arch Otol 90:190-194 27. Dolan KD (1982) Paranasal sinus radiology. Part 1A: Introduction and the frontal sinuses. Head Neck Surg 4:301-311 28. Som PM, Shugar JMA (1980) The CT classification of ethmoid mucoceles. J Comput Assist Tomogr 4:199-203 29. Sore PM, Shugar JMA (1980) Antral mucoceles - A new look. J Comput Assist Tomogr 4:484-488 30. Som PM, Shugar JMA (1980) The significance of bone expansion associated with the diagnosis of malignant tumors of the paranasal sinuses. Radiology 136:97-100 31. Perugini S, Pasquini U, Menichelli F (1982) Mucoceles in the paranasal sinuses involving the orbit. CT signs in 43 cases. Neuroradiology 23: 133-139 32. Chui MC, Briant TDR, Gray T, Horsey WJ, Hudson AR, Tucker W (1983) Computed tomography of sphenoid sinus mucoceles. J Otolaryngol 12:263-269 33. Som PM, Shugar JMA (1981) When to question the diagnosis of anaplastic carcinoma. Mt Sinai J Med 40:230-235 Received: 3 July 1984 P.M.Som, M.D. Department of Radiology The Mount Sinai Hospital One Gustave L. Levy Place New York, NY 10029 USA