The septum constitutes the main central support for the nose, which is composed of the perpendicular plate, the quadrangular cartilage and the vomer bone (see Figure 1.17 in Chapter 1). The perpendicular plate of the ethmoid is in continuity with the posterior edge of the quadrangular cartilage and both structures are aligned caudally with the vomer. The most anterocaudal portion of the septal cartilage also rests on the maxillary crest in a tongue-and-groove relationship. This point of articulation is unique in that the perichondrium of the cartilage is only partially contiguous with the periosteum of the crest, allowing a decussation of fibers that joins the contralateral perichondrium.¹ This configuration can make a submucoperichondrial dissection tedious. Starting the dissection from the posterior caudal septum and continuing it in the anterior direction may overcome the difficulty. This relationship between the cartilage and the bone renders this portion of the septum susceptible to post-traumatic displacement of the cartilage from the groove of the crest, correction of which is paramount for the successful straightening of the septum and consequently the external nose.

The area of overlap at the junction between the cephalic upper lateral cartilages and the nasal bones, which makes up the keystone area, is characterized by a firm adherence between these structures. Trauma to the nasal bones can shift this entire unit. A longstanding shift of the midline structures cannot be simply corrected with an osteotomy and forceful repositioning. It requires component separation and realignment of all the structures individually, including the nasal bones, the septum, and the upper lateral cartilages.

Adjustment of the size of the turbinates plays a cardinal role in the restoration of nasal function following correction of nasal deviation. The inferior turbinate occupies a large portion of the nasal airway and can account for up to two-thirds of the total airway resistance.² The turbinates are covered with an erectile mucosal tissue composed of pseudostratified ciliated columnar epithelium. The submucosa contains many seromucinous glands and vascular channels containing cavernous sinusoids. These channels are under the influence of the autonomic nervous system and thus serve as the end target for decongestant medication. The sympathetic system regulates the resistance vessels (and therefore blood flow) and the parasympathetic system regulates the capacitance vessels (and therefore blood volume) of the nasal mucosa. The submucosa also contains large numbers of mast cells, eosinophils, plasma cells, lymphocytes, and macrophages. Thus, chronic inflammation secondary to stimulation of these abundant proinflammatory cellular constituents can lead to fibrous deposition and chronic hypertrophy of the turbinate.¹ Long standing deviation of the septum, especially if it occurs at an early age, results in enlargement of the inferior and/or middle turbinate facing the concave side of the septum (Figure 17.1).

Figure 17.1 Longstanding deviation of the septum to the patient’s right has resulted in enlargement of the left turbinate.

The internal nasal valve accounts for approximately 50% of the total airway resistance and is the narrowest segment of the nasal airway.^3,⁴ It is formed by the angle between the junction of the nasal septum and the caudal margin of the upper lateral cartilage and is typically 10–15°, as mentioned in earlier chapters⁵ (see Figure 1.13 in Chapter 1).

The importance of the nasal valves in nasal airflow cannot be overstated and has been studied extensively.⁶^–⁹ The internal nasal valve is a crucial regulator of nasal airflow dynamics and should be preserved and/or reconstructed during rhinoplasty. Injury and destabilization of this complex, by either surgery or trauma, may result in collapse and subsequent nasal airway obstruction. The external nasal valve, which serves as the entrance to the nose, is formed by the caudal edge of the lateral crus of the lower lateral cartilage, the soft tissue alae, the membranous septum, and the sill of the nostril (see Figure 1.13 in Chapter 1). This is an occasional site of obstruction secondary to extrinsic factors, such as foreign bodies, or intrinsic factors, such as weak or collapsed lower lateral cartilages, a loss of vestibular skin, or cicatricial narrowing.⁵ Normal function of this valve depends on the structural integrity of the lower lateral cartilages, the perinasal musculature, and adequate soft tissue coverage. Functional compromise can occur with encroachment of the nasal spine, and especially the footplates, into the nostril opening. Architecturally weak lateral crura further compound the effects of a widened columella.¹⁰ Other causes for external valve collapse include facial nerve palsy, pinched alar deformity, and postsurgical vestibular stenosis secondary to synechiae and over-resection of the lower lateral cartilages.

The septum and the nasal bones control the direction of the nose. Thus, deviation of the nose can result from misalignment of one or the other, or a combination of both. Often, the nasal bones follow the direction of the deviated septum. However, these structures may move independently. Midvault deviation consistently accompanies at least anterior and commonly mid- and posterior septal deviation. Deviation of the lower nose may involve the caudal septum, anterior nasal spine, and lower lateral cartilages. Previous studies by the author’s team and others have detailed and categorized the types of septal deviation.^5,¹¹^–¹⁴

There are six classes of septal deviation.¹¹ The most common type is a septal tilt, in which the septum itself has no significant underlying curvature but is tilted to one side because the caudal septum is dislodged to one side of the vomer bone (Figure 17.2). In most cases of septal tilt, the internal dislodgement of the septum is to the left and the external deviation of the nose is to the right. This is usually accompanied by an enlargement of the inferior turbinate ipsilateral to the external deviation.