- 1 Congenital and Developmental
- 2 Trauma
- 3 Inflammation and Infection
- 4 Benign and Tumour-Like Lesions
- 5 Malignant Tumours
Congenital and Developmental
Congenital Piriform Aperture Stenosis
Width <11mm, abnormal dentition, midline bony inferior palatal ridge.
Infant with respiratory distress. Posterior choanal obstruction is membranous (15%) or bony (85%). Associated with congenital CNS or other anomalies in 50%. Thickening of the vomer. Stenosis is posterior choanal width <5mm (neonates) or <10mm (adults). May be unilateral and only detected in adulthood.
Anterior Neuropore Abnormalities
Incomplete regression of embryonal dermal connection to invaginating neural plate (dura of brain contacts nasal dermis).
- Nasal ‘glioma’ – Fibrous connection only, extranasal more common than intranasal. Soft tissue has brain characterisitcs. No connection to brain or CSF.
- Dermoid cyst – More common than dermal tracts, which may have intracranial connection in 25% (risk of meningitis, osteomyelitis, intracranial abscess). Overlying nasal dimple or sinus tract.
- Meningoencephalocele – CSF connection.
Standard views include Caldwell, shallow Waters, cross-table lateral and submental vertex. CT for complex fractures or complications (entrapment, optic nerve impingement).
Zygomatic arch fracture – Isolated or part of zygomaticomaxillary complex. Common comminution and depression. Best seen on submentovertex. Deformity may reflect acute or old injury.
Zygomatiomaxillary complex (ZMC) fracture – Usually from blow to face. Tripod, quadripod or trimalar. Variable invovement of arch, zygomaticofrontal suture, infraorbital rim, orbital floor, lateral wall maxillary antrum, lateral wall of orbit. Injury to infraorbital nerve is common. Diastasis of zygomaticofrontal suture may lead to injury of the lateral canthal ligament or suspensory ligament of globe. May cause posteromedial displacement of zygoma causing difficulty in jaw movement, usually associated with lateral (+/- anterior and posterior) wall of maxillary sinus fracture (quadripod).
Maxillary and Sinus Fractures
- Maxillary alveolus fracture (most common) – From blow to chin driving teeth superiorly.
- Palatine process of maxilla and horizontal plate of palatine bone fractures – Usually in sagittal plane near midline.
- Anterolateral wall of maxillary antrum – Most common sinus fracture.
- Frontal sinus fracture may be linear or comminuted and depressed. Open fracture – involvement of both anterior and posterior walls, may -> CSF rhinorrhoea and recurent meningitis or intracerebral abscess, pneumocephalus.
- Sphenoid sinus fracture – Associated with orbital roof, nasoethmoidal complex, midface or temporal bone fractures. Angiography if injury to cavernous ICA is suspected.
LeFort fractures are classically bilateral, all involve the pterygoid plates (anchor facial bones to the skull) and usually nasal region. Rarely seen in their pure forms. Hemi-Leforts are unilateral, may have differing LeFort types on each side.
- LeFort I (transmaxillary, floating palate) – Horizontal through nasal septum, all walls of maxillary sinuses, inferior pterygoid plates. May be associated with mid-palatal or maxillary split fracture, unilateral zygomaticomaxillary complex fracture. Maxilla usually displaced posteriorly.
- LeFort II (pyramidal) – Pyramidal through bridge of nose, nasal septum, frontal process of maxilla, medial wall orbit, inferior orbital rim, superior lateral and posterior walls of maxillary antrum, mid pterygoid plates. Zygomatic arch and lateral orbital walls intact. Usually associated with posterior displacement of facial bones (causing dish-face deformity and malocclusion). Injury to infraorbital nerve is common. Separates nose and maxilla from rest of face with ‘sat-on’ appearance.
- LeFort III (craniofacial dysjunction/separation) – Horizontal near nasofrontal suture, nasal septum, medial and lateral orbital walls, zygomatic arch, base (superior) pterygoid plates. Associated with dish-face deformity and malocclusion. Infraorbital nerve injury less comon than LeFort II. Uncommon, more severe trauma.
Depressed fracture of one or both of the paired nasal bones. Longitudinal (DDx nasomaxillary suture or nasociliary groove) or transverse (more common). May be associated with ethmoidal injury, nasal septum fracture, frontal process maxilla, anterior nasal spine of maxilla. Cartilagenous injury cannot be diagnosed radiographically. Septal haematoma between perichondrium and cartilage may cause cartilage necrosis, breathing difficulty, septal abscess.
Nasoethmoidal complex fracture (orbitoethmoid fracture, nasoethmoid-orbital fracture, facial smash) – Blow to midface between eyes. Variable fracture to lamina papyracea, inferior medial and supraorbital rims, frontal and ethmoid sinuses, orbital roofs, nasal bone, frontal process of maxilla, sphenoid, +/- skull base, clivus. Common orbital injuries including optic nerve, globe. Posterior displacement of the midface, nasion. May cause CSF leak (floor of anterior cranial fossa fracture), olfactory nerve injury (cribriform plate fracture). May cause telecanthus (widening of interorbital distance) from ruptured medial canthal ligaments. May disrput nasolacrimal system causing epiphora (overflow of tears onto face), lacrimal mucocele or CSF rhinorrea.
Highly associated with maxillary alveolar or palatal fractures. Simple fractures do not communicate externally or with the mouth, most commonly ramus and condyle. Compound fractures communicate via tooth socket or laceration; almost all body fractures are compound. Frequently multiple/bilateral. ‘Cortical ring’ sign – well-corticated density above condylar neck on lateral from horizontal orientated fragment of condylar fracture/dislocation. Common association between condyle and contralateral mandibular angle fractures. Ramus and coronoid processes fractures rare. Symphysis/parasymphysis fractures common, but difficult to see due to obliquity of fracture plane. Airway obstruction may be caused by posterior displacement of the tongue (bilateral fractures of body or comminuted fractures) or free mandibular fragment.
Inflammation and Infection
- Infectious rhinitis (common cold) – Mostly viruses (esp adenovirus, echovirus, rhinovirus). Thickened, oedematous, erythematous nasal mucosa with narrowed nasal cavities and enlarged turbinates. May extend to cause pharyngotonsillitis, or have bacterial superinfection.
- Allergic rhinitis (hayfever) – IgE mediated type I hypersensitivity to plant pollens, fungi, animal allergins, dust mites. Marked mucosal oedema, erythema.
- Chronic rhinitis – Repetitive attacks of acute rhinitis, with bacterial superinfection. May have superficial ulceration. May lead to polyposis.
Mucosal thickening <3mm common even in asymptomatic patients esp maxillary and ethmoids, normal mucosal congestion. It is redundant and easily congested in childhood with 60% of asymptomatic infants complete or near-complete opacification. Normal cyclical congestion and decongestion of mucosal over nasal turbinates, nasal septum and ethmoid sinuses from side to side every 1-8hrs.
Acute sinusitis is usually preceded by acute/chronic rhinitis, uncommonly Kartagener syndrome. There is mucosal congestion, apposition of surfaces and obstruction of normal mucus flow, retention of secretions allowing bacterial superinfection. Most commonly ethmoids. Bacteria include Strep.pneumonieae, H.influenze, beta-haemolytic strep, Moraxella catarrhalis. Chronic phase organisms include Staphylococcus, Streptococcus, cornebacteria, Bacteroides, fusobacteria, other anaerobes. Fungi include aspergillus, mucormycosis (severe, esp chronic in diabetics and immunocompromised), bipolaris, drechslera, curvularia, candida. Air-fluid levels, complete opacification or foamy secretions suggest acute sinusitis. Chronic sinusitis causes mucosal thickening, bony remodelling, polyposis, mucous retention cysts, osteitis/hyperostosis (bony thickening). As protein in secretions increases, cross-linking of gyloproteins reduces free water protons; reducing T2 signal, increasing T1 signal before reducing with near solid inspissated protein, mimicing aerated sinus. Infected mucosa enhances peripherally (cf tumours solid or central). Hyperdense (low T2) secretions from inspissated secretions, fungal infection (HU>2000 highly likely aspergillosis), haemorrhage, polyps, mucocoele or calcification. Fungal calcification is fine punctate centrally; nonfungal curvilinear eggshell peripheral.
Patterns of sinonasal disease:
- Infundibular (26%) – Isolated obstruction of inferior infundibulum, just above the maxillary ostium causing limited maxillary sinus disease.
- Ostiomeatal unit/complex (OMU/OMC, 25%) – Middle meatus (hiatus semilunarus) opacification causing ipsilateral maxillary, frontal and anterior 2/3 ethmoidal disease.
- Sphenoethmoidal recess (SER, 6%) – Sphenoid or posterior 1/3 ethmoid disease.
- Sinonasal polyposis – Enlargement of ostia, bone thinning, opacified sinuses.
Lund Mackay staging grades each block on each side (frontal, anterior ethmoid, posterior ethmoid, sphenoid, maxillary, OMU); grade 0 (clear), 1 (partial opacification) or 2 (complete opacification).
Complications from sinusitus include:
- Inflammatory polyps
- Mucous retention cyst – Obstructed mucous glands, common in asymptomatic patients. Up to several cm, round, most common in maxillary antra. Smooth-domed, homogeneous. Usually indistinguishable from a polyp.
- Mucocele – Entire sinus obstructed with expansion of sinus, bony wall thinning and remodeling. From tumours, fibro-osseous bone lesions, trauma, postoperative scarring or haematomas. Most commonly frontal sinus, then ethmoid, maxillary and sphenoid sinuses. Contents usually hyperdense. Mucopyocoele if infected, with peripheral enhancement. May encroach into orbit, brain etc.
- Sinus atelectasis (silent sinus syndrome) – Maxillary ostial obstruction from chronic sinusitis -> chronic negative pressure and hypoventilation -> reduction in sinus volume with orbital floor depression and enophthalmos, maxillary walls retract centripetally, retromaxillary fat fills the space. DDx hypoplastic maxillary antrum.
- Subdural or epidural emphyema
- Intracranial abscess
- Perineural or perivascular spread of infection
- Cavernous sinus thrombosis/thrombophlebitis (esp sphenoid sinus). DDx Carotid-cavernous fistula, Tolosa-Hunt.
- Periorbital/orbital cellulitis, subperiosteal abscess
Direct coronal CT used for planning of functional endoscopic sinus surgery (FESS). Best to scan 4-6/52 post-treatment for acute infection to eliminate effects of reversible congestion, can also use nasal spray decongestants or antihistamines. Anatomical considerations include:
- Uncinate process apposed to medial orbital wall (atelectatic infundibulum) – May cause orbital penetration.
- Dehiscence of lamina papyracea (in 5-10%) – Orbital contents may protrude into ethmoids.
- Dehiscence of cribriform plate and sphenoid sinus walls – May cause intraorbital, intracranial, carotid or optic nerve perforation.
- Optic nerve contacting posterior ethmoid wall (3%), along or through sphenoid sinus. Bony dehiscence over optic nerve.
- Intersinus septum in sphenoid sinus attaching to carotid canal.
- [[Extracranial_Head_and_Neck#Paranasal Sinuses|Normal variants]]
FESS procedures include uncinectomy, ethmoidectomy (agger nasi cells, bulla, anterior +/- posterior cells, frontal sinus opening), sphenoidectomy, maxillary sinus antrostomy. Post FESS fibrosis is similar to inflammation on CT and MR, both enhancing. OMU obstruction will usually resolve, but there is usually ongoing sinus opacification. Frontal sinus may be packed with osteoplastic graft or fat if opening is unsuccessful; may cause mucocele, neuroma or recurrent sinusitis if not plugged completely. Complications post-FESS include:
- Orbital haematoma, increasing intraorbital pressure – Usually from transection of ethmoidal artery which retracts into the orbit. Decompression (canthotomy) required within hours before infarction of the optic nerve.
- Compression or resection of optic nerve.
- Trauma to lamina papyracea (basal lamella attachment) – Causes medial rectus contusion, fat herniation, orbital haematoma, orbital emphysema.
- CSF leak from trauma to cribriform plate (superior attachment of middle turbinate at fovea ethmoidalis) and dural tear – May lead to meningitis, epidural abscess, pneumocephalus. Rhinorrhea, may occur up to 18months after surgery. Nuclear medicine study with intrathecal indium-DTPA accurate even with slow flow. CT with intrathecal contrast more useful due to anatomical detail, best done prone. Intrathecal fluorescein with direct endoscopic visualisation may be the most reliable.
Nonneoplastic hyperplasia or inflamed mucous membranes, may be from allergic rhinosinusitis or nonallergic. Chronic inflammation causes mucosal hyperplasia, mucosal redundancy and polyp formation. May be associated with aspirin intolerance, CF, Kartegener syndrome (immotile cilia syndrome), asthma, allergic rhinitis, nickel exposure. Most blend with mucoperiosteal thickening. Enlarged sinus ostia, rounded intranasal mass, hyperdense sinus contents, thinned bony trabeculae, erosive bony changes at anterior skull base. Most bilateral. Truncation of the middle turbinate (bulbous part missing) present in >50%. Usually peripheral enhancement, but may fold repetitively on itself and have solid enhancement similar to neoplasm. Tx intranasal or oral steroids. Will recur if snared without regard for stalk.
- Antrochoanal/Killian polyp – Antral polyp expanding, prolapsing through ostium (usually accessory) into nasal cavity or nasopharyngeal airway via posterior choana. Stage I (early development) if not yet in nasopharynx; II (fully mature) if accessory maxillary ostium occluded; III (regressive) if accessory ostium only partially occluded.
- Sphenochoanal polyp – Between nasal septum and middle turbinate, extending through sphenoethmoidal recess.
(Mucoviscidosis). AR, viscous secretions with chronic sinusitis, polyposis. Retarded sinonasal development. Frontal sinus hypoplasia, medial bulging of lateral nasal wall (polyposis), ethmoid opacification is highly suggestive.
- Aspergillus – May cause polypoid lesions or fungal balls (rounded, may be lamellated) which are hyperdense, high T1, low T2.
- Allergic fungal sinusitis (AFS) – Hyperdense sinuses, commonly bilateral with complete opacification and expansion, bony erosion/remodelling/thinning, low T2.
- Aggressive invasive fungal infections (mucormycosis, aspergillosis) – May invade orbit, cavernous sinus, neurovasculature. Diabetics and immunocompromised. May cause thrombosis or cerebral infarcts. May spread intracranially (esp mucormycosis) along elastic membrane of vessels, with hyphae penetrating lumen causing thrombosis. Periantral soft tissue infiltration into adjacent fat. Tx excision, antifungal drugs, hyperbaric therapy. Poor prognosis.
Nasal septal perforation (midline destructive lesion of the sinonasal tract) from sarcoidosis, Wegener granulomatosis, cocaine, foreign body reaction, lymphoma (esp T-cell/NK-cell lymphoma), TB, syphilis. May have associated soft tissue mass.
Benign and Tumour-Like Lesions
- Single discrete – Inflammatory eg aspergilloma, rhinolith (often foreign body which has calcified).
- Multiple discrete calcifications – Tumours (enchondromas, inverted papillomas, meningiomas) or inflammatory.
- Diffuse hyperdensity, well-defined – Fibro-osseous lesion.
- Diffuse hypderdensity, ill-defined – High grade sarcoma (chondrosarcoma, osteosarcoma).
Usually frontal sinus. May cause recurrent HA, recurrent sinusitis, mucocele, pneumocephaus (if posterior wall of frontal sinus is breached). Typical history severe sinus pain with takeoffs from flights as osteoma narrows sinus opening. Dense sclerotic bony mass protruding into the sinus. May be associated with Gardner syndrome, Ollier disease.
Common, mono-ostotic or poly-ostotic. Esp walls of sphenoid sinus, central skull base, interstices of ethmoids and maxilla, may involve middle turbinate. Ground-glass density, variable enhancement. Rarely large vascular flow voids. Bony expansion may obstruct ostia.
Adolescent, almost exclusively males with epistaxis, nasal obstruction, facial deformity. Benign from fibrovascular stroma of posterolateral wall of nasal cavity and sphenopalatine foramen, extending into the pterygopalatine fossa, infratemporal fossa, vidian canal; may spread intracranially, sphenoid sinus, cavernous sinus, paranasal sinuses, occasionally parapharygneal space, pterygoid muscles. Isodense, marked enhancement, abundant flow voids with salt-and-pepper appearance (on T2 or post-T1). Recruites vessels including ascending pharyngeal, internal maxillary, petrous and cavernous ICA branches often bilaterally. Adjacent bony erosion and foraminal enlargement. Can become large, may require preoperative embolisation. Recurrence in up to 60%. Staging:
- IA – Limited to posterior nares or nasopharyngeal vault.
- IB – Into paranasal sinus(es).
- IIA – Minimal extension into medial pterygomaxillary fossa.
- IIB – Fully occupies the pterygomaxillary fossa, displaces the posterior wall maxillary antrum forward, superior extension eroding the orbit.
- IIC – Extension into cheek, temporal fossa.
- III – Intracranial extension.
(Schneiderian papilloma). Benign neoplasm of sinonasal mucosa (squamous or columnar epithelium), ?from HPV 6/11, not associated with allergy or chronic infection. Classified into exophytic (most common), inverted (most important) or cylindrical. Inverted papillomas grow into the underlying mucosa, aggressive. Associated with SCC in 15%. Almost always unilateral, typically lateral nasal wall centred on hiatus semilunaris or maxillary sinus. Iso T1, iso/hypo T2, enhances (solid or crenated/convoluted cerbriform), calcification (stippled) in 20%. May have aggressive bone destruction, cross cribriform plate into anterior cranial fossa. Stage I limited to nasal cavity; II ethmoids and superomedial maxillary sinuses; III lateral/inferior maxillary or frontal/sphenoid sinuses; IV outside nose and sinuses. Tx resection with wide mucosal margins, high rate of recurrence which has earlier and greater enhancement than granulation tissue.
Rare in sinonasal cavity, favours nasal septum. Popcorn calcification.
1% of meningiomas are outside the CNS from embryologic arachnoid rests, most in sinonasal cavity esp upper nasal cavity, ethmoids, frontal sinuses. Slightly hyperdense, intermediate on MR, avid enhancement. May or may not have dural attachment.
Bony remodelling of the cranium is uncommon, lesions (benign or malignant) tend to erode with a permeative pattern. Malignant intracranial extension usually has a broad flat base of erosion; benign lesions tend to have rounded polypoid extension. Sphenoid and posterior ethmoid cancers drain to retropharyngeal and high jugular nodes; maxillary to submandibular nodes. Criteria for nonresectability includes distant metastases, optic chiasm invasion, extensive cerebral involvement, bilateral carotid infiltration, poor general health.
Maxillary cancer staging:
- T1 – Limited to mucosa.
- T2 – Erosion of hard palate or middle meatus.
- T3 – Erosion of posterior wall, floor or medial wall of orbit, extension into SC tissues, pterygoid fossa, ethmoids.
- T4a – Invasion into anterior orbit, skin of cheek, pterygoid plates, infratemporal fossa, cribriform plate, sphenoid/frontal sinuses.
- T4b – Invasion into orbital apex, dura, brain, middle cranial fossa, cranial nerves (except V2), nasopharynx, clivus.
Ethmoid cancer staging:
- T1 – Limited to 1 subsite.
- T2 – 2 subsites in single region or nasoethmoidal complex.
- T3 – Invasion of medial wall or floor of orbit, maxillary sinus, palate, cribriform plate.
- T4a – Invasion of anterior orbit, skin of nose/cheek, minimal anterior cranial fossa, pterygoid plates, sphenoid/frontal sinuses.
- T4b – Invasion of orbital apex, dura, brain, middle cranial fossa, cranial nerve3s (except V2), nasopharynx, clivus.
Squamous Cell Carcinoma (80-90%)
Most >50yo, M>F, increased risk with exposure to nickel, chrome pigment, Bantu snuff, cigarettes. Sinus SCC often silent until advanced, causing obstructive sinusitis. Relatively low T2 (cf inflammation), heterogeneous, solid enhancement. Bony destruction in 80%. My have epidural or meningeal invasion (best seen on enhanced coronal FS); discontinuous dural enhancement, nodular enhancement >5mm thick favours neoplastic infiltration over reactive fibrovascular change.
Sinonasal Undifferentiated Carcinoma (SNUC)
Very aggressive, poor prognosis. Most common ethmoids. Early bone destruction, involving nose, skin, orbit, calvarium. Necrosis common, heterogeneous enhancement. High mitotic rate, tumour necrosis, prominent vascularity. High rate of dural metastases.
Minor Salivary Gland Tumours
Minor salivary glands are dispersed throughout the upper aerodigestive tract, most concentrated in the palate. Most are malignant (cf most parotid gland tumours benign).
- Adenoid cystic carcinoma (most common) – High/low T2 with cystic spaces, necrosis. Perineural spread in 60% best seen on contrast enhanced scans along CNV in pterygopalatine fossa, foramen rotundum, foramen ovale, orbital fissures; greater and lesser palatine foramina in hard palate.
- Adenocarcinoma – Esp ethmoids. More comon in wood-workers. Low T2, occasionally high T2.
- Mucoepidermoid carcinoma
- Undifferentiated carcinoma
Metastases to paranasal sinuses are very rare, most commonly RCC. Myeloma and plasmacytomas may have lytic lesions in sinus walls with associated soft tissue mass. High rate of sinonasal involvement by nasopharyngeal carcinoma.
NHL is homogeneous with no necrosis. Common septal perforations. Most nasal and ethmoid lymphoma is T-cell; nasopharyngeal and maxillary B-cell.
NK lymphoma from EBV (previously lethal midline granuloma, polymorphic reticulosis) – Poor prognosis with uncontrolled growth, intracranial extension. Necrosis associated with secondary bacterial infection with sepsis.
Esp nasal cavity nasal, nasal septum then turbinates. May be associated with melanosis with diffuse deposition of melanin along mucosal surfaces of sinonasal cavity. Menanotic melanomas are paramagnetic with high T1, low T2; amelanotic melanomas may be low T1, high T2. Commonly haemorrhage. Common perineural spread, haematogenous metastases.
(Olfactory neuroblastoma). From neurosensory receptor cells (small round cells) of olfactory nerve and mucosa, arising from cribriform plate to turbinates. Uncommon, bimodal peak in males 10-20yo and 50s, with nasal obstruction, epistaxis, reduced olfactory function. May be very destructive at time of diagnosis, commonly extends into anterior cranial fossa via cribriform plate. Relatively low T2. Associated intracranial cysts virtually pathognomonic. Common lymphatic and haematogenous metastases. Recurrence in >50%. Prognosis 40-90% 5-yr.