Sinonasal Disease

Anatomic Considerations

Several issues must be addressed when a patient’s CT is evaluated before FESS. Is the uncinate process apposed to the medial orbital wall (an atelectatic infundibulum)? If so, its vigorous removal may result in orbital penetration. Are there areas of dehiscence in the lamina papyracea, or do the orbital contents protrude into the ethmoid sinus (both of which may lead to unintentional orbital entry from the ethmoid sinus)? Defects in the lamina papyracea have been reported in 5% to 10% of autopsy specimens. Because orbital hematomas are the most common orbital complication of FESS, it is important to identify any gaps in the lamina papyracea. CT is the best means for identifying the thin medial bony wall of the orbit.

Are there areas of dehiscence in the cribriform plate and sphenoid sinus walls ( Fig. 12-10 )? Remember that there is an attachment of the middle turbinate to the cribriform plate and that the carotid canal courses along the sphenoid sinus walls. If the surgeon tugs too hard, the cribriform plate will fall and down will come CSF and/or the brain through the new foramen in the skull base. The potential for intraorbital, intracranial, carotid, or optic nerve perforation at the time of surgery depends on these anatomic variants, found in 4% to 15% of patients. Three percent of people have optic nerves that are in contact with the posterior ethmoid wall—most course along (90%) or through (6%) the sphenoid sinus. There have been limited reports of optic nerve transection during sphenoethmoidectomy from an intranasal approach, and dehiscence of the sphenoid wall may be a predisposing factor. An intersinus septum in the sphenoid sinus that attaches to the carotid canal is important to recognize preoperatively and is typically best identified in the axial view ( Fig. 12-11 ). Overvigorous removal of such an intersinus septum during surgery may result in carotid laceration, a real bloody mess.

Appearance on Imaging

In addition to commenting on the normal anatomic variations in the CT report, the radiologist should identify areas of mucosal thickening and sinus passageway opacification. It has come to be accepted that the location of sinusitis is more important in producing a patient’s symptoms than the extent of the sinusitis. Therefore, a subtle area of opacification in the infundibulum of the OMC may cause more pain and discomfort than nearly complete opacification of the maxillary sinus with a mucous retention cyst and/or polyp.

OMC opacification correlates well with the development of sinusitis ( Fig. 12-12 ). The positive predictive value of infundibular opacification for the presence of maxillary sinus inflammatory disease is approximately 80%. When the middle meatus is opacified, the maxillary and ethmoid sinuses show inflammatory change in 84% and 82% of patients, respectively. The specificity of middle meatus opacification for maxillary or ethmoid sinus disease is more than 90%. These findings support the contention that obstruction of the narrow drainage pathways leads to subsequent sinus inflammation.

Some head and neck radiologists categorize recurrent inflammatory sinonasal disease into five patterns: (1) infundibular, (2) ostiomeatal unit, (3) sphenoethmoidal recess, (4) sinonasal polyposis, and (5) sporadic or unclassifiable disease. The infundibular pattern is seen in 26% of patients and refers to isolated obstruction of the inferior infundibulum, just above the maxillary sinus ostium. Limited maxillary sinus disease often coexists with this pattern, whereas the ostiomeatal unit pattern, seen in 25% of cases, often has concomitant frontal and ethmoidal disease. The ostiomeatal unit pattern is designated when middle meatus opacification is present. Sphenoethmoidal recess obstruction occurs in 6% of cases and leads to sphenoid or posterior ethmoid sinus inflammation. When the sinonasal polyposis pattern is present, enlargement of the ostia, thinning of adjacent bone, and opacified sinuses are usually seen in conjunction with nasal polypoid disease.

The presence of air-fluid levels and/or frothy secretions is more typically associated with acute sinusitis than with chronic inflammatory disease, however this finding is by no means specific for acute sinusitis. Fluid levels can often be seen within the paranasal sinuses of intubated patients and are not necessarily infected. Drowning victims or trauma patients can also present with fluid levels in the sinus, but these sinuses are not necessarily infected. However, in cases of clinically suspected acute sinusitis, air-fluid levels and/or complete opacification of a sinus is present in 63% of cases ( Fig. 12-13 ). Of course, acute sinusitis may be superimposed on chronic changes. The findings suggestive of chronic sinusitis include mucosal thickening, bony remodeling, polyposis, mucous retention cysts, and bone thickening secondary to osteitis from adjacent chronic mucosal inflammation ( Fig. 12-14 ).

Hyperdense secretions on CT may be due to four main causes: (1) inspissated secretions, (2) fungal sinusitis, (3) hemorrhage in the sinus, and (4) calcification. The hyperdense sinus may be the only clue to fungal sinusitis and is an important feature to note. However, chronically inflamed sinuses infected with bacteria occasionally show hyperdense contents on CT, particularly in patients who have very long-standing disease, polyposis, or cystic fibrosis. A hyperdense sinus often corresponds to a hypointense sinus on T2WI ( Fig. 12-15 ).

If you measure the Hounsfield units (HU) you can gain some specificity to the “hyperdense sinus.” Those with HUs greater than 2000 have a 93.3% chance of maxillary sinus aspergillosis. The mean CT density of the sinus concretions without aspergillosis is 778 HU. Make sure this hyperdensity is not reflective of hemorrhage secondary to a traumatized sinus.

The following features of the “calcified” sinus mass have been reported. A single discrete hyperdensity is most likely to be an inflammatory mass (aspergilloma, rhinolith), but multiple discrete calcifications could be seen in tumors (enchondromas, inverted papillomas, meningiomas) or inflammatory lesions. If the intrasinus calcification is central, fine, and punctate-like, it is most likely attributable to fungi. If the calcification is peripheral, curvilinear, and eggshell-like, it is probably nonfungal. If the process is diffusely hyperdense with a well-defined margin, think of a fibroosseous lesion but if it is poorly marginated, consider a high-grade sarcoma (chondrosarcoma, osteosarcoma). Although calcification is not unusual in inverted papillomas it is more likely to be residual bone, not calcifications. By contrast, esthesioneuroblastomas have intrinsic calcifications.

A rhinolith (stone in the nose) is often attributable to a foreign body that has become lodged in the nose and has slowly calcified. This may occur in the setting of traumatic or recreational nasal septum injuries.

While you are evaluating coronal CT scans for sinusitis, do not forget to look at four other related areas: the teeth, sella, nasopharynx, and temporomandibular joints. Maxillary periodontal disease can incite sinus inflammation (odontogenic sinusitis), and therefore thinning and/or dehiscence of the maxillary alveolus adjacent to an inflamed carious tooth necessitates reporting. The sinus disease will not resolve until the offending tooth is removed.

Malocclusions or temporomandibular joint degenerative change may indicate a maxillofacial pain syndrome that may simulate pain from sinusitis. Look for narrowing, osteophytes, or sclerosis at the joint.

Beware of the incidental sellar lesions and nasopharyngeal carcinomas that might be appreciable on routine sinus CT. When these tumors extend into paranasal sinuses, they can simulate the appearance of ho-hum sinus opacification—don’t be fooled! On that note, do not forget to evaluate the imaged portions of the brain for intracranial pathology—all kinds of sneaky buggers might be lurking there and will remain undetected unless you look for them.

Screening sinus CT images are often performed before bone marrow transplantation (BMT) in patients with hematologic malignancies. Of those showing severe sinusitis on initial screening CT scans, two thirds experience clinical sinusitis post-BMT. The presence of sinusitis on pre-BMT studies is also associated with a trend toward overall decreased survival.

Trauma often affects the walls of the paranasal sinuses. Remember that the floor of the orbit serves as the roof of the maxillary sinus, so orbital floor fractures cause blood levels in the sinuses. Similarly, the medial wall blowout fracture affects the ethmoid sinus and orbital roof fractures may affect supraorbital ethmoid cells or the frontal sinus. Direct blows to the forehead may cause inward displacement fractures of the frontal sinuses ( Fig. 12-16 ). Skull base fractures may cross the sphenoid sinus. These air-filled spaces are not necessarily the best buttresses against trauma, being very thin and with nothing but air between them and the directed force.

The sensitivity of MR to mucosal thickening accounts for the visualization of the normal nasal cycle. There is cyclical passive congestion and decongestion of each side of the nasal turbinates, nasal septum, and ethmoid air cell mucosa that rotates from side to side over the course of 1 to 8 hours in humans. Thus, 1 to 2 mm of ethmoid sinus mucosal thickening may not be due to inflammatory disease but may reflect the normal intermittent congestion of the nasal cycle. Be aware of the nasal cycle so you do not overread increased mucosal signal from the turbinates and ethmoid sinus as disease on MR. Even if you use 5 mm of thickness of the mucosa or greater as a determinant of pathology on MR, incidental sinus inflammation is present in more than 32% of asymptomatic patients coming to MR scanning.

Sinonasal secretions are often, but not always, bright on T2WI and dark on T1WI. The change in signal intensity of sinonasal secretions is based on protein concentration and mobile water protons. The changes are probably a result of the increased cross-linking of glycoproteins in hyperproteinaceous secretions, leading to fewer available free water protons and more bound protons to glycoproteins. As protein concentration increases, the signal intensity on T1WI of sinus secretions changes from hypointense to hyperintense, to hypointense again. On T2WI, hypoproteinaceous watery secretions are initially bright, but as the protein concentration and viscosity increase, the signal intensity on T2WI decreases. Therefore, you can get four confusing intensity patterns for sinus secretions: (1) hypointense on T1WI and hyperintense on T2WI in the most liquid form, (2) hyperintense on T1WI and hyperintense on T2WI in the mild-to-moderate proteinaceous form, (3) hyperintense on T1WI and hypointense on T2WI in a highly proteinaceous form, and (4) hypointense on T1WI and hypointense on T2WI when the secretions are in a nearly solid form ( Fig. 12-17 ).

Because air and very hyperproteinaceous secretions appear as a signal void, this is a potential pitfall. You may think the sinus is aerated but it is not. Other potential problems in which hypointensity may be encountered on both T1WI and T2WI include osteomas, odontogenic lesions, osteochondromas, fibrosis, and fungal sinusitis mycetomas. The low signal of fungal sinusitis is thought to result from the paramagnetic effects of either iron or manganese metabolized by the fungi ( Box 12-4 ).

Because obstructed sinus secretions may have any combination of signal intensities, it may become difficult to distinguish inflammation from neoplasm solely based on intensity patterns. For this reason, the presence of peripheral rim enhancement is a reassuring finding that suggests inflammation rather than neoplasm (which enhances centrally).

Post-Functional Endoscopic Sinus Surgery Scanning

There is one classification for types of FESS that is worth remembering; see Table 12-2 . Although postoperative studies will show open OMCs in patients with chronic sinusitis and polyposis, the overall extent of sinus opacification before and after FESS is more often than not minimally changed ( Fig. 12-18 ).

CT is the study of choice in the acute setting of orbital complications after FESS, which usually occur within 48 hours after surgery. CT is reliable in diagnosing an orbital hematoma, assessing for optic nerve compression or inadvertent resection, and planning therapy to relieve increased intraorbital pressure. Often, however, if vision is deteriorating rapidly, this complication is treated on the basis of clinical findings. Acute hematomas are usually hyperdense on CT; occasionally, diffuse orbital fat edema may be the most salient finding. Usually, orbital hematomas are due to transection of an ethmoidal artery at FESS. The artery then retracts into the orbit and continues to bleed. The intraorbital pressure rises with the expanding hematoma, leading to compromise of the flow of the retinal artery and ischemia of the optic nerve. Decompressive canthotomies are emergently performed (within hours), or irreversible nerve damage will occur.

Other complications include trauma to the medial wall of the orbit. While removing the middle turbinate, the lateral attachment to the lamina papyracea (the basal lamella) may be yanked off and injure the medial wall of the orbit. Contusion to the medial rectus muscle, fat herniation into the sinus, and orbital hematomas may follow. Orbital emphysema may be seen.

CSF leaks resulting from trauma to the cribriform plate and damage from overvigorous removal of the superior attachment of the middle turbinate at the fovea ethmoidalis are other potential FESS complications. This may lead to postoperative meningitis, epidural abscess, or pneumocephalus. Fortunately, FESS surgeons are getting good at patching their own dural holes with mucosal free grafts or septal flaps.

Osteoplastic frontal sinus grafts are often placed during frontal sinus obliterative procedures when FESS has been unsuccessful in opening the frontal recess. Postoperatively, patients may develop pain that may be secondary to neuromas, mucoceles, or recurrent sinusitis if the sinus is not plugged completely. Most surgeons use fat to obliterate the sinus. MR imaging with fat suppression can evaluate the frontal sinus after obliteration with adipose tissue to look for mucoceles and to differentiate viable adipose tissue from fat necrosis in the form of oil cysts. The amount of fat intensity in the sinus obliteration decreases over time as fibrosis occurs.

Granulomatous Diseases

Sarcoidosis may affect the sinonasal cavity and is one of the sources of nasal septal perforation (along with cocaine abuse, syphilis, leprosy, and granulomatosis with polyangiitis [formerly Wegener granulomatosis]) ( Fig. 12-19 ). The entities of lethal midline granuloma, Stewart syndrome, midline granuloma syndrome, polymorphic reticulosis, lymphomatoid granulomatosis, and pseudolymphoma have recently been reclassified into cases of granulomatosis with polyangiitis and/or non-Hodgkin T-cell lymphoma. The generic term of “midline destructive lesions of the sinonasal tract” has also been applied to these entities ( Box 12-5 ). Both granulomatous disease processes and non-Hodgkin T-cell lymphoma may present with nasal septal perforations, bony/skull base erosions, and soft-tissue masses in the sinonasal cavity.

Granulomatous disease processes show intracranial involvement in up to 5% of cases, usually manifesting with cranial neuropathies. Meningeal inflammation, vasculitis, and hypophysitis may also coexist.

In cases of non-Hodgkin T-cell lymphoma, bony erosion may be seen, particularly involving the medial wall of the maxillary antrum or the hard palate. Relative preservation of the sinus morphology in the setting of a sinus soft-tissue mass can favor lymphoma over carcinoma, which results in frank destruction of the sinus walls.

Foreign body granuloma, polyarteritis nodosa, lupus, and hypersensitivity angiitis may also present with destructive sinonasal masses. Pseudotumor, an idiopathic inflammatory disease characterized by fibroblasts, histiocytes, and inflammatory cells, can simulate an aggressive sinus process. Pseudotumor has been more recently classified under IgG4-related disease, and can be associated with rhinosinusitis with or without bony destruction; patients have high levels of serum IgG4 levels and respond well to glucocorticoid treatment.