The bony skeleton of the nose is formed by  the nasal bones and the nasal processes of the maxillae. The nasal septum is comprised of the septal cartilage anteriorly, the vomer posteroinferiorly and the perpendicular plate of the ethmoid bone superiorly. The Kiesselbach’s/Little’s area is located in the anterior/inferior septum, and this is where branches of the sphenopalatine, greater palatine, and facial arteries anastomose; it is the most common site of epistaxis.

The piriform aperture is the anterior bony opening of the nasal cavity. The posterior choana is the posterior opening, divided in the midline by the vomer.

The roof of the nasal cavity is formed by the cribriform plate of the ethmoid bone. The floor is formed anteriorly by the palatine processes of the maxilla and posteriorly by the horizontal processes of the palatine bones.

Three meati (spaces) are present along the lateral wall of the nasal cavity lateral to the superior, middle, and inferior turbinates. They contain the sites of drainage of the paranasal sinuses.

There are three or four turbinates, designated as supreme (variable), superior, middle, and inferior. The inferior turbinate is a separate bone, while the other three are parts of the ethmoid bone. The middle turbinate is attached to the lateral nasal wall by the basal lamella, which separates the anterior and posterior ethmoid air cells. The space between the basal lamella and the ethmoid bulla is the sinus lateralis or suprabullar recess (Fig. 9.1).

The lateral nasal wall is comprised of two ostiomeatal units. The anterior ostiomeatal unit consists of the frontal sinus ostium, frontal recess, maxillary sinus ostium, infundibulum, and middle meatus. The posterior ostiomeatal unit is comprised of the sphenoid sinus ostium, sphenoethmoidal recess, and the superior meatus (Fig. 9.1).

The uncinate process is a sickle-shaped sheet of bone arising from the lateral nasal wall and directed superiorly. Lateral to the superior free edge is the infundibulum. The ethmoid bulla is the largest anterior ethmoid air cell. Its medial wall forms the lateral wall of the infundibulum. The infundibulum is the air passage bounded medially by the uncinate process and laterally by the ethmoid bulla; it connects the maxillary sinus ostium to the middle meatus. The hiatus semilunaris is the crescentic gap between the free edge of the uncinate process and the ethmoid bulla (Fig. 9.2).

The frontal recess is the funnel-like drainage pathway of the frontal sinus. The term “frontonasal duct” is now avoided as no discrete ductal structure exists. The frontal recess drains into the anterior part of the middle meatus and may be divided into a superior compartment that lies below the frontal sinus ostium in the floor of the sinus and an inferior compartment which either opens into the infundibulum (if the uncinate process is directed towards the skull base) or continues into the middle meatus (if the uncinate process is attached to the lamina papyracea) (Fig. 9.3).

The fovea ethmoidalis is the roof of the ethmoid cavity. The cribriform plates are the portion of the ethmoid bone that forms the roof of the nasal cavity medial to the fovea ethmoidalis. They are perforated by the foramina of the olfactory nerves. The crista galli is a vertically oriented midline ridge of bone arising from the cribriform plates and attaching to the falx cerebri (Fig. 9.4). The anterior and posterior ethmoid air cells are separated by the basal lamella of the middle turbinate. The lamina papyracea is the gracile medial wall of the orbit. The agger nasi designates the most anterior ethmoid cells that form due to pneumatization into the lacrimal bone and the frontal process of the maxillae. They may be anterior, inferior, or posterolateral to the frontal recess and may encroach upon it (Fig. 9.3).

The sphenoethmoidal recess is the site of drainage of the sphenoid and posterior ethmoid air cells (Fig. 9.1).

A summary of sinus drainage is provided in Box 9.1.

The commoner anatomic variations are listed in Box 9.2.

The nasal septum is deviated in 25–30 % of the population. Marked deviation, especially with an osteocartilaginous spur, may compromise the middle meatus and predispose to recurrent sinonasal inflammation/infection (Fig. 9.5).

The middle turbinate may be completely pneumatized (concha bullosa) or pneumatized only within its vertical portion (lamellar concha or intralamellar air cell). Concha bullosae may become inflamed and rarely transform into a mucocele. In addition to conchae, paradoxically curved middle turbinates may also crowd the middle meatus leading to maxillary sinus obstruction (Fig. 9.6).

The free edge of the uncinate process may attach to the lamina papyracea (atelectatic uncinate) resulting in a chronically obstructed maxillary sinus ostium and hypoplasia of the maxillary sinus with associated descent of the orbital floor (silent sinus syndrome) (Fig. 9.7). If not recognized preoperatively, the plunging roof of the maxillary sinus may be inadvertently breached by the surgeon. The uncinate process may attach superiorly to the fovea ethmoidalis, in which case excessive traction during surgery may result in violation of the anterior cranial fossa and a CSF leak. The uncinate process may also be pneumatized (uncinate bulla), which encroaches upon the infundibulum and impedes frontal and anterior ethmoid sinus drainage (Fig. 9.7).

A giant ethmoid bulla is an unusually large ethmoidal bulla that compromises the infundibulum (Fig. 9.7).

Haller cells are infraorbital ethmoidal air cells. They may narrow the infundibulum and predispose patients to recurrent maxillary sinusitis (Fig. 9.8).

Onodi cells are the most posterior ethmoid air cells and are intimately related to the optic canal; they can completely surround the optic nerve, increasing the risk of optic nerve injury at surgery. Onodi cell mucoceles may compress the optic nerve (Fig. 9.8).

The sphenoid sinus is usually divided by a single sagittal septum, but multiple septa may be present. Sphenoid septa that insert laterally adjacent to the cavernous internal carotid artery may be associated with arterial injury at surgery. Pneumatization of the sphenoid sinus may extend into the anterior clinoid process and the horizontal carotid canals conferring increased risk of surgical injury to the optic nerves and internal carotid arteries, respectively. The lateral sphenoid sinus walls are occasionally dehiscent allowing the optic nerves and internal carotid arteries to pass through the sinus (Fig. 9.9).

The nasal cycle is a normal, cyclical side-to-side alteration in nasal airway resistance. It can be associated with mucosal hypertrophy, which is detectable on CT and MR imaging, especially around the inferior turbinate; this must not be mistaken for pathology (Fig. 9.10).

Acute inflammation of the sinuses may occur due to viral, bacterial, fungal, or allergic causes. A classic radiographic sign of acute sinusitis is a fluid level, but fluid levels may also be seen in a setting of trauma, prolonged nasogastric intubation, barotrauma, or CSF leak (Fig. 9.11). The presence of frothy secretions in a sinus may also indicate acute inflammation. Given the tendency of acute frontal and sphenoid sinusitis to progress to life-threatening complications, it is imperative that the clinician be alerted to fluid levels in these areas. Acute sinusitis may also manifest as thickened mucosa on CT. The signs of early acute fungal sinusitis may be subtle and are discussed below.

Complications of acute sinusitis may involve the orbits or cranial cavity (Box 9.3). The orbits are most likely to be affected by ethmoid sinusitis. The lamina papyracea is a poor barrier to the spread of infection. The absence of valves in the anterior and posterior ethmoid veins also permits free spread of infection into the orbits. An extensive intradiploic anastomotic venous network allows spread of infection between the frontal sinuses and the meninges.

Orbital complications follow a loosely defined sequence of events (Fig. 9.12). Preseptal cellulitis (stage I) is manifested on CT by thickening and enhancement of the eyelid soft tissues; this can, however, be the consequence of simple transudative edema from impaired sinus venous outflow. At this stage, inflammation is restricted from posterior spread by the orbital septum. With orbital (postseptal) cellulitis (stage II), the intra- and extraconal fat demonstrates increased attenuation and stranding. The presence of a lentiform peripherally enhancing collection, applied to the lamina papyracea or orbital plate of the frontal bone and confined by the periorbita, indicates a subperiosteal abscess (stage III). A similar collection within the orbit itself indicates an orbital abscess (stage IV). Left untreated, this progresses to thrombophlebitis of the superior and inferior ophthalmic veins and then of the cavernous sinus itself (stage V). Enlargement and lack of enhancement of these venous structures, a convex contour to the cavernous sinus, and extraocular muscle engorgement are signs of cavernous sinus thrombosis. While unenhanced MRI may show T1 hyperintense thrombus in the cavernous sinus, contrast-enhanced CT or MRI is the best imaging modality to evaluate this entity. MR venography is usually insensitive to cavernous sinus thrombosis as the normal cavernous sinuses themselves are not well seen.