Postrhinoplasty Nasal Obstruction Rhinoplasty 

Updated: Oct 25, 2018
Author: Thomas Romo, III, MD, FACS; Chief Editor: Arlen D Meyers, MD, MBA 

Overview

Background

Difficulty breathing through the nose after rhinoplasty is a serious problem. Patient dissatisfaction can be significant, even when cosmetic results are excellent. Long-term impacts on the quality of life and contributions to the pathophysiology of sleep-related breathing disorders have both been documented. This article focuses on the etiology, diagnosis, and treatment of postrhinoplasty nasal obstruction, with particular attention to the nasal valve area.

An image depicting internal nasal valve anatomy can be seen below.

Rhinoplasty, postrhinoplasty nasal obstruction. No Rhinoplasty, postrhinoplasty nasal obstruction. Normal internal nasal valve anatomy. Notice the relationship between the septum, upper lateral cartilage, pyriform aperture, and inferior turbinate.

Problem

The etiology of postrhinoplasty nasal obstruction can be multifactorial but is primarily the result of the interplay between 2 factors. Unrecognized preexisting nasal conditions (eg, deviated nasal septum, turbinate hypertrophy, mucosal disease) in conjunction with the overresection of cartilages and a subsequent decrease in the nasal valve area after rhinoplasty are responsible for most cases of postrhinoplasty nasal obstruction.

Epidemiology

Frequency

Some investigators (ie, Courtiss and Goldwyn, Beekhuis) report that the prevalence of airway impairment after aesthetic rhinoplasty may be as high as 10%.[1, 2]

Etiology

The cause of postrhinoplasty nasal obstruction is often the interplay between a preexisting but unrecognized nasal abnormality and a reduction in nasal valve area secondary to the aesthetic rhinoplasty.[3]

During the evaluation and assessment of patients with postrhinoplasty breathing problems, Courtiss and Goldwyn and Beekhuis found that uncorrected septal pathology and overzealous resection of lower or upper lateral cartilage were significant causes of nasal airway obstruction after rhinoplasty.[1, 2] When preexisting pathologies (eg, nasal septal deviation, inferior turbinate hypertrophy, allergic rhinitis) are not recognized and addressed, a nasal valve area that is borderline-narrowed but asymptomatic preoperatively can become symptomatic postoperatively because of a further decrease in the nasal valve cross-sectional area.

Grymer used acoustic rhinometry to evaluate the internal dimensions of the nasal cavity in 37 patients before reduction rhinoplasty and again 6 months after surgery.[4] He demonstrated that rhinoplasty decreases the cross-sectional area of the nasal valve by 25% and the piriform aperture by 13%. Cole et al also used rhinomanometry to reveal that changes of as small as 1 mm to the nasal valve size can dramatically increase nasal resistance.[5]

Therefore, the nasal valve, as a regulator of nasal airflow and resistance, has been demonstrated to play a critical role in the function of the nose. Disturbance of the nasal valve area can produce limitations to normal nasal breathing. Multiple schemes can be used to classify the types of nasal valvular dysfunction. One convenient method is to group them according to either internal or external nasal obstruction (see Classification of nasal valve dysfunction).

Kern and Wang divide the etiologies of nasal valve dysfunction into mucocutaneous and skeletal/structural disorders.[6] The mucocutaneous component refers to the mucosal swelling (secondary to allergic, vasomotor, or infectious rhinitis) that can significantly decrease the cross-sectional area of the nasal valve and thus reduce nasal airway patency. The skeletal/structural component refers to any abnormalities in the structures that contribute to the nasal valve area. This includes the nasal septum, upper and lower lateral cartilage, fibroareolar lateral tissue, piriform aperture, head of the inferior turbinate, and floor of the nose.

The skeletal component can be further divided into static and dynamic nasal dysfunction. Static dysfunction is secondary to continuous obstruction at the level of the nasal valve due to deformities such as deviated septum, inferior turbinate hypertrophy, or inferomedially displaced upper lateral cartilage. Dynamic dysfunction is obstruction that varies in severity with respiratory effort and is usually related to deficiencies in the structural support of the lateral nasal wall, including the cartilaginous, fibroareolar, and muscular components. The lateral nasal wall caudal to the bony arch is mobile and responds variably to pressure changes.

The degree to which lateral wall movement occurs depends on the intrinsic stability of its skeletal and soft tissue support and on the pressure changes it is subjected to during quiet and forced inspiration. According to the Bernoulli principle, as the flow velocity of inspired or expired air increases, the pressure inside the nasal vault decreases relative to atmospheric pressure. At a threshold flow velocity, the disparity between pressures inside and outside the nasal vault overcomes the stability of the lateral nasal wall, and collapse occurs. This intrinsic stability derives from the rigidity of the unaltered nasal anatomy or from the support provided by the skeletal and soft tissue elements that remain after rhinoplasty.

Because ventilation involves pressure changes, the nasal airways must be stable both at rest and under the negative pressures created during quiet and forced inspiration. The internal and external nasal valves depend on satisfactory skeletal stability of the upper and lower lateral cartilages, respectively. When either the skeletal or the soft tissue component is congenitally deficient or has been compromised by surgery or trauma, the patient experiences a dynamic collapse of the valve during inspiration, with resultant airway obstruction. Normally, the upper lateral cartilages partially collapse at a ventilatory flow rate of 30 L/min. Thus, even normal nasal valves collapse with vigorous respiratory effort; however, a patient with dynamic nasal valve dysfunction may have a lateral nasal wall that is so weakened that it collapses even during normal nasal breathing.

In summary, nasal valve dysfunction can be secondary to either mucocutaneous problems or skeletal deformities (affecting either the internal or the external nasal valve), which can be dynamic or static. However, the cause is rarely so straightforward. In most instances, the mucocutaneous and skeletal components and the static and dynamic components contribute in varying degrees to the overall nasal valvular dysfunction.

Classification of Nasal Valve Dysfunction

Nasal valve dysfunction is classified below.

Mucocutaneous disease

See the list below:

  • Allergic rhinitis

  • Vasomotor rhinitis

  • Infectious rhinitis

  • Rhinitis medicamentosa

  • Sinusitis

Skeletal deformity

Deformities that affect the internal nasal valve area

  • Static deformity

    • Inferomedially displaced upper lateral cartilage

    • Narrowing of pyriform aperture

    • Scarring at intercartilaginous junction

    • Turbinate hypertrophy

    • Deviated nasal septum

  • Dynamic deformity - Collapsed upper lateral cartilage secondary to disruption of support from the nasal bone, septum, and lower lateral cartilage

Deformities that affect the external nasal valve

  • Static deformity

    • Tip ptosis

    • Cicatricial stenosis

  • Dynamic deformity

    • Collapsed lower lateral cartilage secondary to excessive excision

    • Nasal muscle deficiency

Pathophysiology

Internal nasal valve obstruction

Static dysfunction includes (1) inferomedial displacement of the upper lateral cartilage, (2) narrowing of the piriform aperture secondary to osteotomy, (3) scarring at the intercartilaginous junction, (4) turbinate hypertrophy, and (5) deviated nasal septum, described as follows:

  • Inferomedial displacement of the upper lateral cartilage

    • The middle nasal vault is composed of the paired upper lateral cartilages and the dorsal cartilaginous septum. Understanding that the upper lateral cartilages are joined to the dorsal septum as a single cartilaginous unit in the cephalic two thirds of the vault is important.

    • Sheen recognized that resection of the cartilaginous middle vault roof during hump removal disrupts this important connection between the upper lateral cartilage and the dorsal septum.[7] This allows the upper lateral cartilages, which now lack support medially, to fall toward the narrowed dorsal septal edge. This results in internal valve collapse and a characteristic inverted-V deformity. Thus, nasal valve dysfunction is common in patients after excessive and uncompensated narrowing of the middle nasal vault in rhinoplasty.

    • The amount of inferomedial displacement of the upper lateral cartilages also depends on whether the superior support with the nasal bone or its inferior connection with the lower lateral cartilage has been disrupted. Thus, if the caudal trim of the upper lateral cartilage or the cephalic trim of the lower lateral cartilage is aggressive, the scroll area weakens, which results in further medial displacement of the upper and lower lateral cartilages.

  • Narrowing of the piriform aperture secondary to osteotomy

    • Overly aggressive lateral osteotomies and infracturing can lead to medial displacement of the nasal bone with corresponding displacement of the upper lateral cartilage.

    • This dramatically narrows the nasal valve angle and decreases the valve cross-sectional area, contributing significantly to nasal airway obstruction after rhinoplasty.

  • Scarring at the intercartilaginous junction

    • A basic principle of surgery is that incisions placed across a concave surface risk scarring and distortion. The nasal valve is such a concave area and is frequently involved when an intercartilaginous incision is used.

    • Improper placement and poor closure of intercartilaginous incisions may lead to scar formation and contracture at the nasal valve angle. Surgeons who primarily use internal incisions in rhinoplasty may be more likely to injure the scroll while they make standard intercartilaginous incisions.

    • When intercartilaginous incisions are extended anteriorly and joined to columellar full-transfixion incisions, the risk of mucosal scarring and synechiae is increased, which may lead to blunting of the apex of the internal valve. This is especially likely to occur if the incisions are not sutured well and heal poorly.

  • Turbinate hypertrophy

    • The head of the inferior turbinate contributes to the internal nasal valve area. Thus, inferior turbinate hypertrophy of any cause decreases the cross-sectional area of the nasal valve.

    • While rhinoplasty itself does not cause this deformity, failure to recognize and to correct inferior turbinate hypertrophy contributes to the problem of postrhinoplasty nasal obstruction.

  • Deviated nasal septum: Similar to inferior turbinate hypertrophy, a nasal septum deviated at the nasal valve area contributes to postrhinoplasty nasal obstruction if not recognized and corrected during the rhinoplasty.

Dynamic dysfunction includes collapsed upper lateral cartilage secondary to disruption of support to the nasal bone, septum, and lower lateral cartilage.

  • Collapsed upper lateral cartilage secondary to disruption of support to the nasal bone, septum, and lower lateral cartilage

    • The upper lateral cartilage is connected to and derives support from the nasal bone cephalically, dorsal septum medially, and lower lateral cartilage caudally.

    • After resection of the cartilaginous middle vault roof during hump removal and disruption of the scroll area secondary to cephalic trimming of the lower lateral cartilages, the upper lateral cartilages are prone to medial collapse. This collapse is not only static in that it continuously narrows the nasal valve angle, but it is also dynamic.

    • With the static reduction of the nasal valve angle, greater inspiratory force is needed to generate enough airflow through the narrowed nasal passageway. This increased pressure differential across the nasal valve area can cause dynamic collapse of the unsupported and frail upper lateral cartilage and cause a vicious cycle of further narrowing of the nasal valve angle.

External nasal valve obstruction

External nasal valve collapse is due to collapse of the nostril margin at the opening of the nose (alar collapse) with moderate-to-deep inspiration through the nose. This phenomenon is usually observed in patients with narrow slitlike nostrils, a projecting nasal tip, and thin alar sidewalls.

The cause of external valve collapse may be surgical, congenital (eg, hypoplasia, paradoxical lateral crura), or posttraumatic in nature. This article focuses on only postrhinoplasty-related external valvular collapse. Constantian and Clardy reviewed 160 patients treated for external nasal valve incompetence. Surgical reconstruction was performed with septal cartilage or with composite conchal cartilage-skin grafts. Using rhinomanometry, Constantian and Clardy found that correction of external valvular incompetence increased total nasal airflow during quiet ventilation by more than 2-fold over preoperative values. Thus, the external nasal valve may play a crucial role as the cause of nasal airway obstruction in some patients.

Static dysfunction includes tip ptosis and cicatricial stenosis, described as follows:

  • Tip ptosis

    • The etiology of tip ptosis can be divided into either structural deficiencies in the cartilaginous or ligamentous support of the tip or excess soft tissue bulk that creates a mass effect at the tip.

    • Structural ptosis can result from rhinoplasty as a consequence of weakened support from the medial crura or columella. Furthermore, performing rhinoplasty through the delivery approach and dividing the cephalic margin of the lower lateral cartilage from the caudal margin of the upper lateral cartilage disrupts one of the major tip support mechanisms and may cause caudal slippage of the lateral crura, which results in structural ptosis.

    • Ptosis from soft tissue bulk is usually idiopathic in nature and is the consequence of thick redundant skin and subcutaneous tissue in the tip and supratip regions. Ptosis may also be the consequence of conditions such as rhinophyma.

  • Cicatricial stenosis

    • Cicatricial stenosis is a less common cause of significant external nasal valve dysfunction and may be secondary to iatrogenic injury from poorly placed marginal incisions or may be a result of an inhalation injury.

    • Scar tissue may narrow the valve area through the formation of hypertrophic webs; however, more often, wound contracture causes a cicatricial narrowing.

    • Sheen conservatively estimated that 75-85% of postrhinoplasty patients have some reduction of the nasal vestibule.

Dynamic dysfunction includes (1) flaccid collapse of the lower lateral cartilage after the overresection of cartilage during tip-modeling procedures and (2) nasal musculature deficiency, described as follows:

  • Flaccid collapse of lower lateral cartilage after overresection of cartilage during tip-modeling procedures

    • The cutaneous and skeletal supports of the lower lateral cartilages comprise the structural support of the external nasal valves.

    • Overzealous resection of the cephalic margin of the lower lateral cartilages can lead to flaccid collapse of the cartilaginous framework of the lateral nasal wall. Because of this lack of support, the pressure differential across the nasal valve during inspiration can cause the lateral nasal wall to collapse.

  • Nasal musculature deficiency

    • The nasal musculature normally acts to pull the lateral nasal wall outward to prevent medial collapse during inspiration.

    • The importance of functional nasal musculature can be inferred from the nasal obstruction that occurs in patients with facial nerve paralysis.

    • Nasal muscular deficiency can be secondary to aging or can be due to rhinoplasty surgical damage such as devascularization, partial denervation, or fibrosis.

Presentation

History

Begin with an accurate diagnosis before considering the array of medical and surgical treatments. Focus the history on the relationship between the onset of nasal obstruction and the rhinoplastic procedure. Determine the patient's preoperative nasal function in order to evaluate preexisting nasal deformities (eg, deviated nasal septum, turbinate hypertrophy, allergic rhinitis, vasomotor rhinitis, sinusitis). Record the duration, side (ie, unilateral, bilateral, alternating), timing (ie, continuous vs intermittent), severity, and any associated symptoms. Elicit a history regarding prior medical and surgical treatments for nasal obstruction and their effectiveness. An operative report from the previous surgeon who performed the rhinoplasty may be helpful.

Disease-specific quality of life instruments can be useful to systematically assess symptoms before and after treatment. The Nasal Obstruction Symptom Evaluation (NOSE) scale is a validated instrument assessing the following 5 categories:

  • Nasal congestion or stuffiness

  • Nasal blockage or obstruction

  • Trouble breathing through the nose

  • Trouble sleeping

  • Inability to get enough air through nose during exercise or exertion

Physical examination

The typical postsurgical nose with nasal airway obstruction is overresected, with a narrowed but scooped-out dorsum and a narrow pinched tip. These patients commonly have nasal obstruction due to incompetent nasal valves. When examining a patient who reports nasal obstruction, evaluate the internal and external valves and the septum and turbinates.

The standard Cottle maneuver, which is used to assess nasal valve incompetence by judging improvement in nasal breathing with lateral distraction of the ipsilateral cheek, is a test with nonspecific results. Even the narrow airway produced by anterior septal deviation or turbinate hypertrophy is improved by traction on the cheek. Anterior rhinoscopy is also a poor means of accurately evaluating subtle changes in nasal valve anatomy; the dysfunctional nasal valve is frequently missed because of distortion from the nasal speculum.

A more precise diagnosis can be made based on direct inspection of valvular support during quiet and forced inspiration, without the distortion induced by a nasal speculum. Collapse at the internal nasal valve is usually diagnosed based on the identification of medialization of the caudal margin of the upper lateral cartilages due to negative pressure created upon inspiration through the nose. These patients typically have pinching or medial collapse of the supraalar region.

External nasal valve collapse can be diagnosed based on observation of the nostril margin to determine if the alae collapse with moderate-to-deep nasal inspiration. Next, a modified Cottle maneuver can be performed with a cerumen curette placed intranasally to support the internal or external nasal valve to determine specifically if improvement in nasal airflow results. Minimal distraction of a collapsed internal valve or stabilization of the external valve during inspiration can dramatically increase airflow on the affected side and confirm the diagnosis.

The patient can usually appreciate an immediate improvement in airflow when a flaccid or collapsible valve is supported during inspiration.

Because symptoms are commonly inconsistent with appearances, objective criteria are required for an accurate diagnosis, appropriate therapy, and assessment of results. Objective measurement of nasal airway resistance can be obtained with the use of rhinomanometry.

More recently, Hilberg et al introduced acoustic rhinometry as a noninvasive and reliable objective method for determining the cross-sectional area of the nasal cavity.[8] Acoustic rhinomanometry is based on the analysis of sound waves reflected from the nasal cavities. It provides an estimate of the cross-sectional areas of the nose as a function of the distance from the nostril. Thus, the site (anterior, mid, or posterior) and degree of nasal obstruction can be identified. Also, analysis can be done before and after topical decongestants are applied, allowing discrimination of mucocutaneous versus structural blockage. Standards for age, race, ethnicity and sex have been recently published.

Lam et al demonstrated that validated anatomic, physiological, and subjective nasal measures, while internally consistent, may not correlate with one another, suggesting that various measures may assess different aspects of nasal airway obstruction and provide complementary information.[9]

Indications

The treatment of postrhinoplasty nasal obstruction has no absolute indications. The extent of medical and surgical treatment depends on the severity of symptoms and the patient's desire to improve his or her ability to breathe through the nose.

Relevant Anatomy

Mink first coined the term nasal valve in 1903 to refer to the slitlike opening between the caudal end of the upper lateral cartilage and the nasal septum. This angle is normally 10-15° in the leptorrhine nose (typical nose in whites) and is more obtuse in the platyrrhine nose (typical nose in African Americans). The nasal valve is only a portion of the internal nasal valve area, which is bounded superiorly by the nasal valve, medially by the septum, laterally by the caudal end of upper lateral cartilage and the bony piriform aperture and its adjacent fibrofatty tissue, inferiorly by the floor of the nose, and inferolaterally by the head of the inferior turbinate.

The internal nasal valve area is the narrowest portion of the nasal passage and thus functions as the primary regulator of airflow and resistance. The cross-sectional area of the nasal valve area is 55-83 mm2. As described by the Poiseuille law, airflow through the nose is proportional to the radius of the narrowest portion of the nasal passageway, raised to the fourth power. Thus, changes as small as 1 mm in the size of the nasal valve exponentially affect airflow and resistance through the nasal cavity.

The external nasal valve is also described and is formed by the lateral crura of the lower lateral cartilage and its investing soft tissue cover. Many authors do not differentiate between the internal and external nasal valves. Although internal and external valve problems coexist in many cases, the distinction between these 2 types of valvular deformities is worth making because an accurate diagnosis affects optimal treatment results.

Contraindications

Contraindications to surgical correction of postrhinoplasty nasal obstruction are based on the patient's comorbidities and ability to tolerate surgery. Coexisting medical conditions may put the patient at risk during anesthesia. Additionally, patients with unrealistic expectations should probably not undergo surgical correction. Finally, patient refusal is an obvious contraindication.

 

Workup

Imaging Studies

A well-performed history and physical examination obviate the need for imaging studies (ie, CT scan, MRI).

Diagnostic Procedures

Rhinomanometry, conventional or acoustic, provides an objective measurement of nasal airway resistance.

 

Treatment

Medical Therapy

Seek out any mucocutaneous component to the nasal obstruction and treat it aggressively with medication. Roithmann et al have shown that the cross-sectional area of the nasal valve and, thus, nasal airway patency can be significantly increased if mucosal swelling is reversed.[10]

Mucocutaneous diseases include conditions such as allergic rhinitis, infectious rhinitis, vasomotor rhinitis, and rhinitis medicamentosa. Their specific treatments are beyond the scope of this discussion and can be found in other articles (eg, see Allergic Rhinitis and Nonallergic Rhinitis).

Surgical Therapy

Once nasal valvular dysfunction secondary to mucocutaneous abnormalities has been adequately treated, structural defects of the internal and external nasal valves can be considered for surgical repair.[11] The possible sites and types of abnormalities include the septum, upper and lower lateral cartilage, floor of the nose, head of the inferior turbinate, or a combination of these. Postrhinoplasty valve narrowing is best managed by directly dealing with the cause of the pathology. In most instances, functional rehabilitation requires reconstruction of the incompetent nasal valve with a semirigid implant.

Autologous cartilage continues to be the preferred material for nasal augmentation. Because the tissue is autologous, no risks of disease transmission, immunomodulation, rejection, or toxicity are encountered. Nasal septal cartilage is the first choice for use as grafting material; however, prior surgical excision or trauma may preclude the use of septal cartilage. The next choice of autologous graft material is ear conchal cartilage. However, conchal cartilage is often brittle and difficult to sculpt and may be insufficient when significant dorsal augmentation is required. Costal cartilage can provide large amounts of donor cartilage for grafting but is used infrequently because of the attendant chest scar and the risk of pneumothorax.

Although the use of an autologous cartilage graft is preferred in functional nasal reconstructive surgery, it may not always be available or adequate for use. Many alloplastic materials have been advocated for use in nasal reconstruction, although most have subsequently fallen into disfavor because suboptimal late results and complications are observed. Porous high-density polyethylene is a general description of polyethylene materials that have been available since the 1940s. Medpor is one specific type with internal pores that range from 100-250 µm in size. Pores of this size have been shown to promote extensive soft tissue ingrowth and some bony ingrowth. This tissue invasion lends mechanical stability to the implant in its bed.

Romo et al reported the use of Medpor implants as various graft materials in functional nasal reconstruction in 187 patients, with excellent functional results.[12] Medpor is available in a number of shapes. Thin (1.5-mm) or ultrathin (0.85-mm) sheets can be used to sculpt columellar struts or alar battens. Thus, Medpor can be used in nasal reconstruction as a good substitute when autologous cartilage graft is not available. The same conclusion was noted by Turegun et al in a study on Medpor in this setting.

Internal nasal valve obstruction

Static deformity includes (1) inferomedial displacement of the upper lateral cartilage secondary to hump removal, (2) narrowing of the piriform aperture secondary to osteotomy, (3) scarring at the intercartilaginous junction, (4) turbinate hypertrophy, and (5) deviated nasal septum.

  • Inferomedial displacement of the upper lateral cartilage secondary to hump removal can be treated with spreader grafts, flaring sutures, butterfly grafts, or a combination thereof.

    • Methods of correcting internal nasal valve collapse are focused on the reposition of the upper lateral cartilage or the addition of structural grafts to support the lateral wall of the nose. Spreader grafts are often used for the correction of internal nasal valve collapse. These grafts reposition the upper lateral cartilage in a lateralized position and add width to the middle nasal vault. Numerous other structural grafts have been described as providing support to the lateral nasal wall. Most support the weakened upper lateral cartilage and lateralize the caudal margin of the upper lateral cartilage at the nasal valve. The techniques of repair differ among different authors and can be achieved via either the open or endonasal approach.

    • Spreader graft placement is the workhorse repair of the narrowed internal nasal valve.

      • These grafts are designed to lateralize the upper lateral cartilage by the width of the graft, thereby increasing the cross-sectional area of the nasal valve.

      • Septal cartilage can be harvested and shaped into spreader grafts. If the septum is unavailable, conchal cartilage or Medpor may be used.

      • The grafts are placed in a submucosal pocket between the septum and the upper lateral cartilage. These grafts are typically 1-2 mm thick and extend the entire length of the upper lateral cartilage from the cephalic border beneath the nasal bones to the caudal margin. They are anchored in place with one or two 5-0 polydioxanone horizontal mattress sutures that span from one upper lateral cartilage through the ipsilateral spreader graft, the septum, the contralateral spreader graft, the contralateral upper lateral cartilage, and then back again.

      • Take care not to disrupt the nasal mucosa because this could lead to web formation and further valve stenosis. Final trimming may be required to remove any sharp edges that may be visible or palpable.

      • In a series of 29 patients with pure internal valvular incompetence treated with spreader grafts alone, Constantian and Clardy reported a 2-fold increase in postoperative airflow.[13]

      • Andre et al reported significant improvement in nasal airway patency with autologous endonasal spreader grafts.[14] A total of 89 patients, at an average follow-up of 12.2 months, were reviewed for symptomatic improvement of their nasal obstruction after placement of spreader grafts. Most (88%) had favorable results. Their technique involved placement of the graft within a tight-fitting subperichondrial pocket between the nasal septum and the upper lateral cartilages. Fixation of the grafts was provided via suturing, tissue glue, or simply the tension of a tight pocket.

    • Flaring sutures are a simple way to improve the cross-sectional area of the internal nasal valve by directly changing the internal valve angle.[15]

      • Although the spreader graft moves the dorsal border of the upper lateral cartilage in a lateral direction, the angle of the internal valve is minimally affected.

      • A 4-0 polydioxanone horizontal mattress stitch extends from the caudal/lateral area of the upper lateral cartilage and across the dorsum of the nose and is anchored to the contralateral upper lateral cartilage. As the suture is tightened, both upper lateral cartilages are pulled laterally, with the dorsum serving as a fulcrum. This flaring action directly affects the internal valve angle, and its effects can be witnessed as the suture is tightened.

      • When used in conjunction with spreader grafts, the focal point of the flaring suture is moved laterally to a more optimal position. The addition of a flaring suture to conventional spreader graft placement is simple and quick and dependably improves treatment of the dysfunctional internal nasal valve. Both flaring sutures and spreader grafts serve to move the upper lateral cartilage to a lateral and externally rotated position.

    • An alternative to the flaring suture is the placement of a 3-0 Prolene suspension suture.

      • The suture is tunneled under the superficial musculoaponeurotic system (SMAS) through a stab incision 1 cm anterior/inferior to the medial canthus (over the nasal bone). A separate endonasal intercartilaginous incision is made so that the Prolene can be passed around the upper lateral cartilage, then tunneled back to the superior external nasal incision. The upper lateral cartilage lateralizes upon tightening of the threaded Prolene suture.

      • Rizvi and Gauthier published their experience with this technique in 40 patients with internal nasal valve collapse.[16] Over a follow-up period of 2-3 years, all of the patients reported improvement of their nasal obstruction.

    • Butterfly grafts take advantage of the intrinsic curvature of conchal cartilage to improve the nasal airway.

      • The grafts may be placed endonasally or with an open approach. They are placed at the scroll area between the upper lateral cartilage and lower lateral cartilage in an attempt to widen the valve angle. The caudal border of the graft may be placed deep to the cephalic border of the lateral crura to help camouflage the graft.

      • Grafts are anchored in place with 5-0 polydioxanone to prevent migration.

      • Butterfly grafts, more than other valve-plasty maneuvers, can lead to postoperative cosmetic changes, with marked fullness along the supratip area.

  • Narrowing of the piriform aperture secondary to osteotomy can be treated with revision osteotomy with outfracture of the nasal bones to widen the valve angle.

    • Occasionally, severe valve narrowing occurs after rhinoplasty as a result of lateral osteotomy with infracture, which may not improve with any of the aforementioned procedures. These patients can be treated with revision osteotomy with outfracture of the nasal bones to widen the valve angle. The revision lateral osteotomy is made in the same line as the original osteotomy in order to mobilize the bone that was displaced too far medially. The frontal process of the maxilla and the nasal bones are then lateralized (outfractured).

    • Outfracture can adversely affect cosmesis by widening the nasal dorsum. Therefore, attempt more conservative approaches initially; however, revision osteotomy with outfracture may still be an option to correct significant nasal breathing dysfunction due to valve narrowing after rhinoplasty.

    • Pontell et al compared the cross-sectional area between infracture with the outfracture position and noted an increase of more than 200% with outfracture.[17] A change of 1° in valve angle increased the area by approximately 4 mm2.

  • Scarring at the intercartilaginous junction can be treated with scar excision.

    • Scarring at the valve apex or valve angle can be corrected with scar excision followed by reconstruction with the use of a full-thickness skin graft or local mucosal flap. Finding enough adjacent unscarred lining, skin, or mucous membrane to effectively correct a contracture blunting the apex of the valve is usually difficult.

    • Full-thickness skin grafts and composite grafts are reasonable for the reconstruction of small defects. Full-thickness skin grafts are taken from the upper eyelid or postauricular area. Carefully fit these grafts into the defect using 5-0 or 6-0 absorbable sutures.

    • Larger scars or webs require Z-plasty, V- to Y-plasty, or mucosal advancement flaps from the septum or labial mucosa.

  • Turbinate hypertrophy has many different treatments.[18] The literature includes a multitude of surgical procedures to treat inferior turbinate hypertrophy. The authors' preferred technique is, after injection with 1% lidocaine with 1:100,000 epinephrine, to infracture the inferior turbinate, then to excise the anterior inferior lateral aspect of the inferior turbinate with a turbinate scissor and to obtain hemostasis with suction cautery. The turbinate is then outfractured laterally.

  • Deviated nasal septum can be treated with septoplasty.[19]

    • Septal abnormalities probably represent the most frequent cause of nasal valve obstruction. The septal cartilage, bone, or both may be thickened, be deflected off the nasal spine, be twisted, be scarred, have spurs, or be affected by a combination of these.

    • A septal abnormality that occurs at the nasal valve area can produce nasal airflow obstruction, which can be corrected with the performance of a septoplasty.

Dynamic deformity includes dynamic collapse of the upper lateral cartilage.

  • The dynamic collapse of the internal nasal valve during inspiration secondary to an unsupported upper lateral cartilage can be corrected with the placement of a butterfly graft or a batten graft at the scroll area (caudal aspect of the upper lateral cartilage) to give support to this critical area. Alar batten grafts can be used to correct internal or external nasal valve collapse.

    • For internal nasal valve collapse, place the alar batten grafts in a precise pocket at the point of maximal lateral wall collapse. This point is usually near the caudal margin of the upper lateral cartilage and cephalic margin of the lateral crura of the lower lateral cartilage, where previous volume reduction may have been performed.

    • Spreader grafts can be used in combination with alar batten grafts when excessive narrowing of the middle nasal vault is present.

    • The use of alar batten grafts is discussed in further detail in the section regarding the correction of dynamic external nasal valve collapse after rhinoplasty secondary to overresection of lower lateral cartilage (see Dynamic deformity below).

External nasal valve obstruction

External nasal valve deformity may be a significant source of nasal airway obstruction in some patients. Constantian and Clardy demonstrated that reconstruction of the external valve alone can improve total mean airflow by more than twice that of preoperative valves.[13] Interestingly, this degree of airflow improvement is similar to that observed in patients in whom pure internal nasal valve dysfunction was corrected with dorsal or spreader grafts. Moreover, preliminary data for patients in whom both internal and external valve dysfunction were treated (without septal or turbinate surgery) revealed a mean 3-fold airflow increase, which suggests that the effects of internal and external valve reconstruction may be independent but not strictly additive, presumably because of valve interactions.

Static deformity includes tip ptosis and cicatricial stenosis.

  • Tip ptosis, if significant enough, may cause enough narrowing of the vestibule to warrant a tip-lifting maneuver.

    • For structural ptosis, a tip-lifting stitch of 4-0 clear nylon is placed in a horizontal mattress fashion from the dome of the lower lateral cartilage to the periosteum of the nasal bones.

    • For soft tissue ptosis, the thick sebaceous skin at the supratip area along the borders of the nasal subunits can be excised to produce an aesthetically pleasing scar.

    • Tip ptosis is frequently caused by both cartilaginous and soft tissue laxity, as is often observed in the noses of elderly persons (ie, noses affected by aging), and may require a combination of maneuvers.

  • Cicatricial stenosis is another static deformity.

    • Approaches to repair external valve dysfunction secondary to cicatricial stenosis include primary resection, alar interposition, Z-plasty, skin grafts, and composite grafts.

    • Small webs in the external valve area may be divided primarily and then stented. Alar interposition flaps are easily performed but result in increased nasal base width.

Dynamic deformity includes (1) flaccid collapse of lower lateral cartilage after over resection during tip-modeling procedures and (2) nasal musculature deficiency.

  • Flaccid collapse of lower lateral cartilage after over resection during tip-modeling procedures can be corrected with the placement of structural grafts into the alar lobule to provide support and to prevent collapse.

    • Over resection of the caudal upper lateral cartilage and cephalic lower lateral cartilage results in dynamic collapse of the internal nasal valve (upper lateral cartilage) and the external nasal valve (lower lateral cartilage) during inspiration. Dynamic nasal valve collapse (both external and internal) is secondary to a structurally weak or deficient lateral nasal wall.

    • The use of alar batten grafts is an effective method for the correction of internal and external nasal valve collapse secondary to flaccid or absent lateral cartilages. The grafts act to reposition and to provide support to the lateral nasal wall to prevent collapse upon inspiration. They are placed into a precise pocket at the point of maximal lateral wall collapse or supraalar pinching, with the use of either an endonasal or an external rhinoplasty approach.

    • Both septal and conchal cartilages are excellent sources of graft materials. Ensure the graft is of sufficient length to be seated in the soft tissue over the bony piriform aperture. However, it does not need to be particularly long in a caudal/cephalic dimension. After the cartilage is harvested, it is carved into a rectangular shape that spans from the piriform aperture to the junction between the middle and lateral third of the lateral crura. In most cases, these grafts are 10-15 mm long and 4-8 mm wide.

    • To provide maximal structural support, the battens are wider laterally toward the piriform aperture. To minimize cosmetic distortion, battens must be thin with beveled edges, especially along the medial aspect of the graft. Notching the lateral border of the graft helps anchor the batten against the piriform aperture. The size and precise placement of these battens depend on the corrections needed for each individual. Larger grafts are used in patients with severe collapse or thicker skin to provide increased support.

    • The primary purpose of batten grafts is to reinforce areas of the sidewall or the alar lobule that collapse because of the negative force associated with inspiration. Battens are not intended to change the resting position of the valve. Preoperative assessment is critical in the determination of the site of collapse. Once it is identified, a soft tissue pocket is created for placement of the graft. This pocket is usually at the level of the supraalar crease at the junction of the upper lateral cartilage and lower lateral cartilage where previous volume reduction may have been performed. The convex surface of the graft is laterally oriented to provide lateral support for the collapsed region of the lateral nasal wall.

    • In most cases, alar batten grafts create fullness at the site of the graft. This convexity tends to decrease with time as edema resolves and scar contracture compresses the graft and shifts it medially. Andre et al described placement of the graft in a sub-alar position, which has improved cosmetic results but failed to improve symptoms in one-third of patients.[20]

    • The support and stabilization of the lateral nasal wall increases the internal diameter of the nasal airway, thereby increasing dynamic nasal airflow. The increase in size of the internal airway can be appreciated during intranasal examination, with elimination of alar collapse upon moderate-to-deep inspiration. Alar battens are anchored in place with 4-0 chromic gut through-and-through sutures to tack the batten to the nasal mucosa.

    • Positioning of batten grafts may vary from case to case, depending on whether internal or external nasal valve collapse is being treated. When internal nasal valve collapse is treated, battens are typically placed in a pocket at the site of supraalar collapse and are usually near the caudal margin of the upper lateral cartilage or at the point where the lateral crura may have been previously overexerted. When external nasal valve collapse is treated, the grafts are typically placed into a pocket caudal to the cephalically positioned lateral crura.

    • To maximize effect, grafts must be placed into a precise subcutaneous pocket at the point of maximal lateral wall collapse. A tendency is to place the grafts too far cephalically along the upper lateral cartilage, which may result in persistent fullness of the lateral wall of the nose. If the grafts are placed near the alar lobule, they are better camouflaged by the thicker skin. To correct severe nasal valve collapse, the batten grafts can be extended onto the piriform aperture.

    • Toriumi et al reviewed their experience with alar batten grafts in 46 patients and reported that all but one experienced a dramatic improvement in nasal airway obstruction.[21] Postoperative physical examinations revealed a significant increase in the size of the aperture at the internal or external nasal valve. Palpation of the alar sidewalls revealed increased structural support, and examination of the basal view revealed patency of the external nasal valve upon moderate-to-deep inspiration through the nose. Postoperative fullness in the supraalar region in the area where the graft was applied was minimal. With time, this fullness decreased, which left little evidence of the graft and an overall improvement in the aesthetic result.

    • Toriumi et al conclude that alar batten grafts are effective for long-term correction of internal and external nasal valve collapse in patients who do not have intranasal scarring in the region of the nasal valve, loss of vestibular skin, or excessive narrowing at the piriform aperture.[21]

  • With nasal musculature deficiency, severe cases secondary to facial nerve paralysis are treated with dynamic techniques such as nerve grafts, VII-VII crossover, or XII-VII anastomosis.

Preoperative Details

The surgical repair of postrhinoplasty nasal obstruction is generally performed in an outpatient setting. Patients need to be counseled preoperatively about the possible change in external nasal appearance after surgery. Unreasonable expectations with regard to revision surgery must be dispelled. Discuss benefits, risks, and alternatives of the planned surgical procedure with the patient in detail and obtain informed consent. Documentation of preoperative appearance is imperative. Obtain medical clearance and the appropriate preoperative medical workup (eg, laboratory studies, chest radiography, electrocardiography).

Intraoperative Details

Based on an accurate preoperative evaluation of the specific etiology of the nasal obstruction, the best surgical approach can be chosen to correct the defect. The different approaches are discussed in Surgical therapy.

Postoperative Details

Postoperatively, patients are started on oral antibiotics and given pain medication as needed. Patients are instructed to refrain from any strenuous activity and to avoid blowing their nose. If nasal packing was placed intraoperatively, it is removed 1-2 days after surgery. If a nasal cast was placed, remove it in 5-6 days.

Follow-up

Examine patients within 1 week after the operation. Remove the nasal cast at this time and clean and inspect the intranasal region. Instruct the patient to return in 1 month and in 3 months for postoperative photography.

Complications

Perhaps the most common complication after surgery to correct nasal obstruction is failure to relieve the obstruction. Failure can be due to an inaccurate preoperative diagnosis of the cause of nasal obstruction or a faulty intraoperative surgical technique. Other complications include bleeding, infection, or an unwanted change in external nasal appearance.

Outcome and Prognosis

Provided that the cause of nasal obstruction was appropriately diagnosed and corrected with the correct surgical procedure, the patient has a very good chance of resolution of symptoms of nasal obstruction.

Constantian and Clardy studied 160 patients with septal and/or valvular (internal and external) cause of nasal obstruction.[13] Their data showed only a modest and statistically insignificant improvement in mean nasal airflow after septal surgery alone; however, external valve reconstruction alone increased airflow 2.6 times over preoperative values. Internal valve reconstruction alone (with dorsal grafts or spreader grafts) increased nasal airflow 2 times. The largest improvement in postoperative airflow was observed in patients with combined septal plus internal and external valvular incompetence. These patients had an increase in flow 4.9 times that of preoperative values. Patients in whom valvular incompetence alone was corrected experienced as much relative improvement as patients in whom valvular plus septal obstruction was corrected.

Recently, a study performed by Rhee et al evaluated the disease-specific quality of life of 20 patients after nasal valve surgery.[22] This multicenter prospective evaluation used the Nasal Obstruction Symptom Evaluation (NOSE) to assess a difference in preoperative and postoperative symptomatology after surgical intervention. A statistically significant improvement was observed in the responders at 3 months and 6 months after surgery. Hence, nasal valve repair improved disease-specific quality of life.

Future and Controversies

In order to prevent nasal obstruction after aesthetic rhinoplasty, the surgeon must have a good understanding of the anatomy and physiology of the nasal valve and must recognize the consequences of disturbing this important area. Careful preoperative and intraoperative assessment is necessary.

Recognition and correction of preexisting nasal deformities before or during aesthetic rhinoplasty is important. Mucosal conditions (eg, seasonal and perennial allergic rhinitis, vasomotor rhinitis) must be diagnosed and treated appropriately in individuals who are to undergo rhinoplasty.

Surgery at or near the valve area must be performed carefully and with the knowledge that narrowing in this area can cause significant nasal airway obstruction and difficulty breathing. Factors that predispose patients to postrhinoplasty valve problems include a tall thin nose, pliable cartilage, multiple previous surgeries, and advanced age. Other preoperative nasal configurations (eg, short nasal bones, narrow middle third, alar cartilage malposition) also predispose a patient to valvular incompetence, even after conservative reduction procedures, if appropriate precautionary steps are not taken. The surgeon must recognize these anatomic variations preoperatively to avoid the creation of a postoperative obstruction.

Nasal valvular function must be assessed preoperatively in all patients who undergo rhinoplasty. Preoperative functional nasal examination that is limited to only the septum and turbinates is not sufficient. Aesthetic and reconstructive rhinoplasty procedures should routinely include techniques that maintain or improve the nasal airway.