The nose, a prominent facial feature in defining facial beauty, is responsible for the fundamental physiologic functions of heating, humidifying, and filtering inspired air. When the normal balance of laminar and turbulent airflow become disturbed due to anatomic abnormalities, nasal obstruction may result. To successfully restore these basic physiologic functions, the surgeon must have a detailed understanding of the nasal anatomy and be able to successfully identify the specific cause of the nasal obstruction. This article discusses the fundamental surgical anatomy and the various diagnostic techniques and instruments at the surgeon’s disposal.
Key points
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Successful correction of nasal obstruction requires identification of the precise anatomic cause and a comprehensive understanding of the relationships between surface aesthetics, underlying structural anatomy, and functional components of the nose.
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Subjective evaluation of a patient with nasal obstruction should include systematic examination of the nasal-facial aesthetics with external evaluation, including visual inspection, palpation, and photodocumentation, as well as intranasal examination, including an assessment of nasal valve function.
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Patient-specific quality of life instruments, such as the Nasal Obstruction Symptom Evaluation and visual analog scale, are useful tools to help quantify the degree of nasal obstruction both before and after surgery.
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Several tools have been developed for the objective assessment of nasal obstruction; however, most have not gained widespread use outside of the research setting.
Introduction
The primary responsibilities of the nose include heating, humidifying, and filtering inspired air before reaching the larynx, trachea, and lungs. This is accomplished via a balance of laminar and turbulent airflow. The laminar flow is responsible for the transmission of air toward the lungs and the turbulent flow, which is related directly to airway resistance, is responsible for the inspired air contacting the nasal mucosa and exchanging molecules to warm and humidify it. When this normally unconscious action is compromised, nasal breathing may become a source of significant distress and decreased quality of life. Nasal obstruction, which may have many different causes, is a common problem and results from a complex interaction of static and dynamic forces on the nasal mucosa and bony-cartilaginous structure of the nose. Before surgically correcting nasal obstruction, the precise anatomic cause must be identified. The surgeon must have a comprehensive understanding of the surface aesthetics, underlying structural anatomy, and functional components of the nose and how they are all linked. The purpose of this article is to highlight the key anatomic structures involved in nasal obstruction and functional rhinoplasty, as well as discuss the diagnostic techniques at the surgeon’s disposal to ensure the proper diagnosis is made.
Introduction
The primary responsibilities of the nose include heating, humidifying, and filtering inspired air before reaching the larynx, trachea, and lungs. This is accomplished via a balance of laminar and turbulent airflow. The laminar flow is responsible for the transmission of air toward the lungs and the turbulent flow, which is related directly to airway resistance, is responsible for the inspired air contacting the nasal mucosa and exchanging molecules to warm and humidify it. When this normally unconscious action is compromised, nasal breathing may become a source of significant distress and decreased quality of life. Nasal obstruction, which may have many different causes, is a common problem and results from a complex interaction of static and dynamic forces on the nasal mucosa and bony-cartilaginous structure of the nose. Before surgically correcting nasal obstruction, the precise anatomic cause must be identified. The surgeon must have a comprehensive understanding of the surface aesthetics, underlying structural anatomy, and functional components of the nose and how they are all linked. The purpose of this article is to highlight the key anatomic structures involved in nasal obstruction and functional rhinoplasty, as well as discuss the diagnostic techniques at the surgeon’s disposal to ensure the proper diagnosis is made.
Functional anatomy
Bony Pyramid
The bony framework of the nose is pyramidal in shape. It is made up of paired nasal bones that articulate with the frontal bone cephalically and the paired upper lateral cartilages (ULCs) caudally. The confluence of nasal bones, ULCs, and the bony (perpendicular plate of the ethmoid bone) and cartilaginous nasal septum, appropriately known as the keystone area, is critical for midvault support and stability of the nose. The nasal bones articulate with the frontal process of the maxilla laterally, and fuse at the midline. They are approximately 25 mm in length, on average, and progressively thin as they approach their inferior confluence with the ULCs. The bony external opening of nasal cavity, the pyriform aperture, is made up of the nasal and frontal bones superiorly and laterally and the maxilla inferiorly. The maxillary crest articulates with the quadrangular cartilage anteriorly and the vomer posteriorly. The perpendicular plate of the ethmoid bone attaches to the cribriform plate cranially and the vomer caudally ( Fig. 1 ).
Cartilaginous Pyramid
The cartilaginous nasal pyramid is made up of the cartilaginous nasal septum (or quadrangular cartilage) and the ULCs. They form a T-shape, with the angle formed between the septum and ULCs increasing with cephalad progression from approximately 15° at the internal nasal valve (INV) to 80° at the keystone area. The cartilaginous septum connects caudally with the anterior nasal spine, maxillary crest, and vomer, and freely connects with the columella. The connection with the anterior nasal spine involves collagenous decussating fibers. If these are disrupted during septoplasty, reconstruction is essential to prevent destabilization of the septum. Cranially, the cartilaginous septum connects with the ULCs and its dorsal attachment is the perpendicular plate of the ethmoid bone. The cartilaginous septum ranges from 2 to 4 mm in thickness, and is thicker anteriorly, posteriorly, and at its junction with the ULCs and maxillary crest.
The ULCs are connected cranially with the nasal bones, underlapping them by 1 to 2 mm, and the cartilaginous septum medially along their cephalic two-thirds. As they extend inferiorly, they flare away from the septum. The ULCs are free of skeletal support laterally but are connected dorsally and laterally with soft tissue. They connect caudally with the cranial margin of the lower lateral cartilages (LLCs) at the scroll region, which is vital in providing nasal tip support ( Fig. 2 ). Several small, sesamoid cartilages are found throughout the connective tissue between the ULCs and LLCs ( Figs. 3 and 4 ).
Lower Lateral Cartilages
The LLCs (or alar cartilages) are paired cartilages that form the structural component of the nostrils and are the major component of the nasal tip. Each is composed of a medial, intermediate (middle), and lateral crus. The medial crus has a footplate, which attaches to the septal cartilage and is a major source of tip support, and a columellar portion. The medial crus curves and transitions to the intermediate crus at the columellar break point. The intermediate crus is made up of a lobular segment, which is camouflaged by soft tissue and a domal segment, which is responsible for the tip-defining points. The paired intermediate crura are attached to each other via the interdomal ligament. The LLC curves superiorly and forms the lateral crus, which is responsible for determining alar shape. It varies in size (16–30 mm long and 6–16 mm high) and shape (convex, concave, or a combination). The lateral crus is where the caudal LLC and cranial ULC overlap and articulate, forming the scroll area. The posterior border here is attached to the frontal process of the maxilla by dense fibrous tissue and several minor cartilages. Because the lateral crus of the cartilage is angled 45° cephalically, the LLCs only provide support to the medial half of the nasal ala ( Fig. 5 ).
Lobule
The lobule is composed of the 2 LLCs, connective and fatty tissue, and muscles. It is covered with thick skin and sebaceous glands. The surface anatomy of the lobule is complex and is divided into 5 subunits: the tip, alae, columella, nostril, and vestibule. The tip comprises the supratip, the tip-defining points, and the infratip lobule. The alae are the lateral nasal walls, and are structurally composed of skin, muscles, and the lateral crura of the LLC.
Specific mention should be made regarding the mechanisms of nasal tip support, which are traditionally divided into major and minor ( Box 1 ). When performing rhinoplasty, manipulation of any of these mechanisms should be considered carefully to prevent postoperative tip ptosis and resulting nasal obstruction. The tripod theory of nasal tip support, proposed by Anderson in 1968, has become widely accepted by most rhinoplasty surgeons. In this model, the lateral crus of each LLC is described as 2 legs joining the combined medial crura to form a tripod, with the base attached to the frontal plane of the face ( Fig. 6 ). Although simplistic, it helps the surgeon visualize how altering either the length or the position of the legs of the tripod will affect tip position. A modification in the tripod theory is the cantilever model proposed by Westreich and Lawson. This model takes into account the elastic potential energy stored in the nasal tip cartilages, as well as the forces from the bony support structures of the face and nose that balance this energy. The surgeon must understand how these forces act on each other to effectively manipulate the nasal tip.
Major
- 1.
Size, shape, and resilience of the medial and lateral crura
- 2.
Medial crural footplate attachment to the caudal border of the quadrangular cartilage
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Attachment of the upper lateral cartilages (caudal border) to the alar cartilages (cephalic border)
Minor
- 1.
The ligamentous sling spanning the paired domes of the alar cartilages (interdomal ligament)
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The cartilaginous dorsal septum
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The sesamoid complex supporting the connection of the lateral crura to the piriform aperture
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The attachment of the alar cartilage to the overlying skin and musculature (skin and soft-tissue envelope)
- 5.
The nasal spine
- 6.
The membranous septum
The Nasal Valves
The nose itself is an active resistor to nasal airflow. As one inspires, negative pressure forces air through the nasal cavity. The 2 areas responsible for most upper airway resistance are the external and INVs, with the INV being the major flow-limiting segment. When either of these areas is statically narrow, whether the cause is idiopathic, traumatic, or iatrogenic, nasal obstruction results. As air flows through these narrower areas, dynamic valve collapse may also occur. As Poiseuille’s law states, resistance is inversely proportional to radius to the fourth power. As air flows through these narrow portions of the nasal passage, the velocity increases and intraluminal pressure decreases, consistent with Bernoulli’s principle. This drop in pressure can cause collapse, resulting in a cessation of airflow. Properly functioning nasal valves are a chief determinant of a successful functional rhinoplasty.
External Nasal Valve
The external nasal valve (ENV) is delineated by the alar crease of the nostril superiorly and laterally, by the medial crus of the LLC medially, and the nasal spine and soft tissues overlying the nasal floor inferiorly. ENV obstruction can be static from tip ptosis, vestibular scarring, or stenosis. It may also be dynamic, due to weak nasal musculature or a weak or malpositioned lateral crus of the LLC. There is also a considerable amount of structural support of the ENV derived from the alar musculature, which forms a sphincter along the nasal inlet (see later discussion).
Internal Nasal Valve
The INV represents the area bordered by the nasal septum medially, the caudal edge of the ULC superolaterally, the head of the inferior turbinate inferolaterally, and the nasal floor inferiorly ( Fig. 7 ). The INV is the main source of airflow resistance in the upper airway. The angle between the septum and the ULC should measure 10° to 15° in the nose of a person of white ethnicity. This angle is typically more obtuse in non-whites, resulting in less INV collapse. There are 4 functional components of the INV, as described by Cole, and abnormalities in any can result in nasal obstruction ( Table 1 ). Static INV dysfunction can result from medialized ULCs, whether idiopathic or due to failure to stabilize the ULC following reduction rhinoplasty. Similarly, an hourglass deformity can result if the ULCs fall into the nasal cavity following hump reduction. Patients with short nasal bones, thin skin, and an overprojected and narrow middle vault, known as the narrow nose syndrome, are also prone to INV narrowing and nasal obstruction. A caudal septal deformity or hypertrophic inferior turbinates (see later discussion) can also decrease the INV area.
Segment | Description |
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I | INV angle |
II | Bony piriform aperture |
III | Head of the inferior turbinate |
IV | Erectile body of the septum |
Inferior Turbinates
The inferior turbinate is made up a long, thin, curled bone that attaches to the lateral nasal wall and extends medial into the nasal cavity. It is covered by a mucosal layer made up of pseudostratified columnar ciliated respiratory epithelium. Well-developed erectile tissue is located along the inferior turbinate, which is composed of venous sinusoids that drain the capillary system of the nasal mucosa. The inferior turbinate has a large surface area and is largely responsible for the warming, humidifying, and filtering of inspired air, as well as directing it toward the nasopharynx. The head of the inferior turbinate is the inferolateral border of the INV. When it becomes congested it can decrease the cross-sectional area of the valve, resulting in obstructed breathing. Selective submucous resection and lateralization can help to alleviate nasal obstruction; however, this should be done judiciously because over-resection can lead to atrophic rhinitis.
Skin and Soft Tissue Envelope
The soft tissue covering of the osseocartilaginous structure of the nose is made up of skin, subcutaneous tissues, and muscle, and serves as a source of minor nasal tip support. The nasal skin varies in thickness by location on the nose. It is generally thicker over the nasofrontal angle, thins as it approaches the rhinion, where it is thinnest, and then thickens again as it approaches the supratip, tip, and nasal ala, where it is thickest. The skin thins again along the alar margin and columella. The thicker skin is in part due to a higher density of sebaceous glands, particularly at the nasal tip. Non-white patients typically have thicker skin with increased sebaceous glands, which can hide small surgical imperfections but has a higher incidence of postoperative fibrosis and supratip deformities. Conversely, thinner skin is less forgiving and great care must be taken when manipulating the underlying skeleton to ensure aesthetically pleasing results.
The soft tissue envelope of the nose is composed of 4 distinct layers. The superficial fatty layer is tightly adherent to the overlying dermis. Deep to this is the fibromuscular layer, or superficial musculoaponeurotic system (SMAS), which contains the nasal musculature. The next deepest layer is the deep fatty layer, which overlies the perichondrial-periosteal layer that is tightly adherent to the osseocartilaginous components. The avascular plane of dissection used to deglove the nose during open rhinoplasty lies between the fibromuscular and perichondrial-periosteal layers so as to avoid disrupting the SMAS and neurovascular structures.
Muscles
The nasal musculature is ensheathed in the SMAS layer, whose function is to distribute the tensile forces of the nasal musculature and to provide a sling for the mimetic muscles to counteract against. Originally described by Mitz and Peyronie, the nasal SMAS layer covers the external nose from the glabella to the caudal margin of the nostrils and is continuous with the facial SMAS, the platysma, and the galea aponeurosis. Failure to respect the SMAS layer when degloving the nose can lead to retraction of the layer if transected, which can result in scarring of the dermis to the underlying osseocartilaginous components. The nasal musculature that is ensheathed within the SMAS layer is broken down into 4 groups by Griesman : the elevators, the depressors, the minor dilator, and the compressors, as seen in Fig. 8 and Table 2 . These muscles have implications on both the aesthetic and functional aspects of rhinoplasty. For example, overactivity of the depressors can cause tip ptosis, and weak or poorly developed dilators can lead to external valve collapse, both of which result in nasal obstruction.
Muscles | Action | |
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Elevators | Procerus Levator labii superioris alaeque nasi Anomalous nasi | Shorten nose Dilate nostrils |
Depressors | Alar portion of nasalis (dilator naris posterior) Depressor septi | Lengthen nose Dilate nostrils |
Minor dilator | Dilator naris anterior | Dilate nostrils |
Compressors | Transverse portion of Nasalis Compressor narium minor | Lengthen nose Narrow nostrils |
Blood Supply
Most of the nasal vasculature and lymphatics are found within or slightly superficial to the nasal SMAS layer. The arterial supply of the external nose comes from the external carotid artery, via the facial and infraorbital branches, and the internal carotid artery, via the anterior ethmoid branch of the ophthalmic artery ( Fig. 9 ). The vascular supply of the internal nose is supplied by the anterior and posterior ethmoid arteries, the septal branch of the superior labial artery, and the sphenopalatine branch of the internal maxillary artery, which converge in Kiesselbach plexus ( Figs. 10 and 11 ). Venous drainage of the nose is via similarly named veins that accompany the arteries, which drain via the facial vein to the pterygoid plexus and the ophthalmic veins to the cavernous sinus. Notably, the veins are without valves, and infections of the nose can spread intracranially if left untreated.