Nasal obstruction is known to be associated with a major decrease in disease-specific quality of life, and nasal valve dysfunction can play a considerable role in nasal airflow obstruction. Diagnosis and treatment of nasal valve dysfunction requires a thorough understanding of normal anatomy and function as well as pathophysiology of common abnormalities to properly treat the exact source of dysfunction. As the pathophysiology of the nasal valves has become better understood, surgery designed to treat its dysfunction has evolved. Here, we explore the progress we have made in treating the nasal valves, and the deficiencies we still face.
Nasal obstruction is known to be associated with a major decrease in disease-specific quality of life, and nasal valve dysfunction can play a considerable role in nasal airflow obstruction. Diagnosis and treatment of nasal valve dysfunction requires a thorough understanding of normal anatomy and function and pathophysiology of common abnormalities to properly treat the exact source of dysfunction.
Anatomy
First described by Mink in 1903, the term “nasal valve” has been used to describe the main site of nasal resistance, which he initially described as a “slit-like opening” placed at the junction between the upper lateral cartilages (ULC) and the lower lateral cartilages (LLC). Historically, the internal valve has been defined as the area between the caudal end of the ULC and the cartilaginous septum. This angle is typically 10 to 15 degrees in the Caucasian nose, and more obtuse in the African American or Asian nose. A more contemporary, three-dimensional description includes the ULC superiorly, cartilaginous septum medially, head of the inferior turbinate posteriorly, nasal floor inferiorly, and nasal alar and bony pyriform aperture laterally in the nasal valve area. Today, the nasal valve is further divided into an internal and external component. The external nasal valve is described as the cross-sectional area caudal to the internal valve under the alar lobule, bounded superolaterally by the caudal edge of the ULC, laterally by the nasal alar and ligamentous attachment of the lateral crus, medially by the caudal septum and columella, and inferiorly by the nasal sill. The primary muscles responsible for maintaining the patency of the external nasal valve include the nasalis and dilator naris muscles.
A contemporary classification system of the internal nasal valve has been described by Miman and colleagues, using endoscopic evaluation to describe various valve characteristics, including convex, concave, sharp angle, blunt angle, twisted caudal border, and angle occupied by the septal body. They found that the internal nasal-valve angle occupied by the septal body was found to have increased nasal resistances compared with the sharp-angled internal nasal-valve type. The authors designated classification groups according to either the upper cartilage’s caudal border status (convex, concave, or twisted), or the angle status (blunt, sharp, or occupied by the septal body).
Physiology
The cross-sectional area of the nasal valve is between 55 to 83 mm 2 and is the main site of greatest nasal resistance. It functions as the primary regulator of airflow and resistance, providing the sensation of normal airway patency. As described by Poiseuille’s law, nasal resistance is inversely proportional to the radius of the nasal passages raised to the fourth power (resistance = [viscosity ∗ length]/radius 4 ). Small changes in the cross-sectional area of the nasal valve produce exponential effects on airflow and resistance.
The nasal valve functions as a Starling resistor, which consists of a semirigid tube with a collapsible segment anteriorly, and collapses with forceful inspiration to limit airflow. As described by the Bernoulli principle, the degree of lateral sidewall collapse depends on the intrinsic stability of the valve and on the transmural pressure changes during normal and forceful inspiration. As flow increases through a fixed space or volume, pressure in that fixed space decreases. As airflow velocity increases, the pressure inside the nasal valve decreases relative to atmospheric pressure, thus increasing the transmural pressure difference. As this transmural difference increases, the likelihood of nasal valve collapse increases. This may be a protective mechanism to prevent large volumes of unheated and unhumidified air from reaching the lower respiratory tract. In individuals with either acquired or congenital valve collapse, this mechanism functions at a transmural pressure that is too low and can lead to premature collapse and difficulty with nasal breathing. Partial collapse of the ULC normally occurs at a respiratory flow rate of 30 L/min, preventing further increases in intranasal pressure from increasing flow.
Nasal valve obstruction can be further divided into static and dynamic dysfunction. Static dysfunction is caused by continuous obstruction at the level of the nasal valve because of structural and skeletal deformities, such as inferior turbinate hypertrophy, deviated nasal septum, cicatricle stenosis, or medially displaced ULC. Static dysfunction requires more intranasal pressure to generate a given amount of nasal airflow. Dynamic dysfunction, in contrast, is caused by collapsible or deficient structural support of the nasal sidewall, including the cartilaginous, fibrofatty, and muscular components, resulting in collapse of the nasal valve at low transmural pressures.
Physiology
The cross-sectional area of the nasal valve is between 55 to 83 mm 2 and is the main site of greatest nasal resistance. It functions as the primary regulator of airflow and resistance, providing the sensation of normal airway patency. As described by Poiseuille’s law, nasal resistance is inversely proportional to the radius of the nasal passages raised to the fourth power (resistance = [viscosity ∗ length]/radius 4 ). Small changes in the cross-sectional area of the nasal valve produce exponential effects on airflow and resistance.
The nasal valve functions as a Starling resistor, which consists of a semirigid tube with a collapsible segment anteriorly, and collapses with forceful inspiration to limit airflow. As described by the Bernoulli principle, the degree of lateral sidewall collapse depends on the intrinsic stability of the valve and on the transmural pressure changes during normal and forceful inspiration. As flow increases through a fixed space or volume, pressure in that fixed space decreases. As airflow velocity increases, the pressure inside the nasal valve decreases relative to atmospheric pressure, thus increasing the transmural pressure difference. As this transmural difference increases, the likelihood of nasal valve collapse increases. This may be a protective mechanism to prevent large volumes of unheated and unhumidified air from reaching the lower respiratory tract. In individuals with either acquired or congenital valve collapse, this mechanism functions at a transmural pressure that is too low and can lead to premature collapse and difficulty with nasal breathing. Partial collapse of the ULC normally occurs at a respiratory flow rate of 30 L/min, preventing further increases in intranasal pressure from increasing flow.
Nasal valve obstruction can be further divided into static and dynamic dysfunction. Static dysfunction is caused by continuous obstruction at the level of the nasal valve because of structural and skeletal deformities, such as inferior turbinate hypertrophy, deviated nasal septum, cicatricle stenosis, or medially displaced ULC. Static dysfunction requires more intranasal pressure to generate a given amount of nasal airflow. Dynamic dysfunction, in contrast, is caused by collapsible or deficient structural support of the nasal sidewall, including the cartilaginous, fibrofatty, and muscular components, resulting in collapse of the nasal valve at low transmural pressures.
Etiologies
As described by Kern and Wang, the etiologies of nasal valve dysfunction can be classified as mucocutaneous or structural/skeletal abnormalities. Conditions that can cause mucosal inflammation and edema, contributing to nasal valve obstruction, include sinusitis, nasal polyposis, and all forms of rhinitis ranging from allergic to vasomotor to infectious. Structural or skeletal causes of nasal valve obstruction include any deformities of individual components of the nasal valve complex. These may include the nasal septum, upper and lower lateral cartilages, fibrofatty sidewall tissue, pyriform aperture, and floor of nose.
Static structural deformities of the internal nasal valve can be caused by inferomedially displaced ULC, narrowed pyriform aperture, scarring at the intercartilaginous junction, deviated nasal septum, and inferior turbinate hypertrophy. Dynamic deformities are often secondary to destabilization of the septum and LLC, resulting in ULC collapse. Static abnormalities of the external nasal valve can be caused by tip ptosis, cicatricle stenosis, or caudal septal deviations, whereas dynamic deformities include musculature deficiencies and either primary or postoperative LLC weaknesses.
Previous nasal surgeries, namely reduction rhinoplasties, can contribute significantly to nasal valve obstruction. Grymer showed that the cross-sectional area at the nasal valve decreased by 25% and the pyriform aperture by 11% to 13% using acoustic rhinometry after reduction rhinoplasty. A recent retrospective review of 53 subjects by Khosh and colleagues showed that previous rhinoplasty was the cause of nasal valve obstruction in 79% of subjects, followed by nasal trauma (15%) and congenital anomaly (6%).
Several rhinoplasty techniques can contribute to postrhinoplasty nasal valve dysfunction. Overaggressive dorsal hump reductions that destabilize the ULC, and surgical over-resections of the LLC, may lead to collapse of the nasal sidewall. Scroll release with knuckling may also occur with overaggressive cephalic trims of the LLC and caudal trims of the ULC. Bossa formation at the nasal tip can occur with scroll release, tip-graft migration, or excessive postoperative scarring, especially in patients with preexisting bifidity or stiff LLC, all of which can lead to nasal valve obstruction postrhinoplasty.
Sheen described that with resection of the middle vault roof, the flaccid ULC, once disarticulated from the nasal septum, tends to fall inferomedially toward the nasal septum. This results in a narrowed middle vault characteristically described as the inverted-V deformity. This may lead to dynamic and static collapse of the ULC caused by their disarticulation from the septum medially, decreasing nasal valve areas, and more readily allowing dynamic collapse with inspiration. Traumatic displacement of the nasal bones, ULC, LLC, or nasal septum is a leading cause of acquired nasal valve dysfunction. When nasal fractures are being repaired, mobilizing and correcting the nasal bones and the attached cephalic border of the ULCs should be accomplished before correction of the internal nasal valve.
Other causes of nasal valve dysfunction include tip ptosis, cicatricial stenosis, facial paralysis, and paradoxical lateral crura. Tip ptosis can be from excess soft-tissue bulk causing narrowing of the nasal vestibule or structural ptosis secondary to saddle nose deformity or weakened LLC medial crura postrhinoplasty. Cicatricial stenosis is an uncommon cause of external nasal valve obstruction and is usually iatrogenic. Facial paralysis can result in collapse of the nasal sidewall caused by loss of muscular tone of the dilator naris and nasalis muscles. Paradoxical lateral crura describes a rare phenomenon where the LLC lack normal external convexity in the lateral crura. These abnormal cartilages may project into the nasal vestibule causing static obstruction and dynamic obstruction with decreased resistance to collapse during inspiration.
Evaluation of the patient
When evaluating a patient for nasal obstruction, a thorough history and systematic physical examination is taken to determine appropriate management. Once the source of nasal obstruction is determined and is amenable to surgery, there are three areas of the nose that are typically involved that require evaluation: the medial nasal wall, the lateral wall, and the nasal valves. Constantinides, Galli, and Miller describe a simple, systematic method of patient evaluation examining these three areas so that surgical treatment can be modified to address the specific anatomic deformity. Preoperative evaluation includes a detailed intranasal examination with a nasal speculum and nasal endoscopy. The Cottle maneuver has been well described in the evaluation of nasal obstruction, where the cheek and lateral nostril are displaced laterally to assess for improved nasal airflow. A modified Cottle maneuver using a small ear curette that examines two separate areas of nasal support, lower lateral cartilage and upper lateral cartilage, can be performed to assess specific deficiencies.
First, the patient is asked to rate their breathing on a 0- to 10-scale, with 0 indicating complete nasal obstruction, and 10 indicating clear inspiration. Each side is rated independently, with the side that is not being rated gently occluded. Then, the ear curette is used to elevate the LLC and then the ULC, just enough to mimic the support that is expected with surgical grafting. At each level of support, the patient is asked again to rate the breathing on the same 0- to 10-scale. Improved nasal airflow with LLC support suggests that the external nasal valve needs grafting. Improved nasal patency with ULC support suggests a need for internal nasal valve correction. This maneuver should be done before and after decongestant therapy. These examination findings help guide the proper management of nasal valve dysfunction.
Nonsurgical treatments of nasal valve obstruction
Nonsurgical and medical interventions for the treatment of nasal valve dysfunction are appropriate for many patients with mild or mucosal etiologies for their dysfunction. Patients with mild-structural dysfunction or those that are poor surgical candidates may find relief with commercial nasal valve dilators, such as Breathe-Right strips (CNS Inc., Minneapolis, Minnesota). A newer nonsurgical technique described by Nyte for correcting nasal valve collapse is a spreader graft like injection with calcium hydroxylapatite (Radiesse, BioForm Medical, Franksville, Wisconsin) into the submucoperichondrial or submucosal plane at points on the ULC and at the junction between the dorsal septum and ULC. This may lateralize the ULC, making it less likely to collapse with inspiration. The author notes successful spreader graft injection in 23 subjects to date, with minimal adverse effects with follow-up ranging from 3 to 10 months, although percentages are not provided. All patients reported subjective improvement in nasal patency or alleviation of snoring.
Patients with symptoms that improve significantly with nasal-decongestant therapy or those associated with inflammatory or infectious processes, should be treated medically, at least initially, but may require surgical intervention for refractory cases. A recent retrospective review by Inanli examining 45 subjects who underwent concurrent functional endoscopic sinus surgery and rhinoplasty demonstrated that combined surgery may be done safely without major complication, may be more cost-effective, and yield pleasing aesthetic and functional outcomes.
Surgical treatments of nasal valve dysfunction
If a patient has exhausted medical management and the site of obstruction is identified, a surgical treatment plan specific to the dysfunctional element is determined. Nasal septal deviations and inferior turbinate hypertrophy can significantly contribute to obstruction of the nasal valve complex and should be addressed at the time of surgery, either alone or in conjunction with additional nasal surgery. Many authors will agree that septoplasty for anterior septal deviation is beneficial. Hypertrophic inferior turbinates can be reduced in multiple ways, including submucous resection, KTP laser, coblation, and radiofrequency ablation, with or without outfracturing.
Internal nasal-valve abnormalities can be corrected with a number of surgical techniques. One may choose to perform these maneuvers with an open or endonasal approach, depending on surgeon preference. The mainstay of treatment has included spreader grafts, harvested from septal, or less favorably, conchal cartilage, which are placed in a submucosal pocket between the septum and the ULC. These grafts are typically 1- to 2- mm thick and extend the full length of the ULC. They are fixed in place with horizontal-mattress sutures that span the ULC, spreader graft or grafts, and dorsal septum. Trimming or tapering of the graft may be necessary to remove excess cartilage that may be visible or palpable ( Fig. 1 ).
