Postoperative Nasal Airway Obstruction


Postoperative Nasal Airway Obstruction

Mark B. Constantian and Mark Albert

Secondary rhinoplasty is the surgery of unintended consequences. Uncorrected or, even worse, iatrogenic, airway obstruction is one of the most common complaints of secondary rhinoplasty patients. This surgical problem is particularly ironic, because it is virtually always avoidable if the primary surgeon makes the correct anatomic diagnosis, locates the critical anatomic variants that control or impair the airway, and uses techniques that are effective and proven.

Unfortunately for the surgeon trying to learn rhinoplasty today, too many surgical techniques have uncertain value, and many opportunities to deliver care with proven value are missed. This chapter outline a system of understanding and treating nasal airway obstruction that is based on surgical methods that are logical, anatomic, expeditious, effective, and proven and that have the least chance of creating new deformities.

Nasal Anatomy Relevant to the Airway

The internal nasal valve is formed by the articulation of the caudal and anterior (or dorsal) edges of the upper lateral cartilages with the anterior septal edge; the external nasal valve is composed of the cutaneous and skeletal support of the mobile alar wall (the alar cartilage lateral crura with their associated external and vestibular skin coverings)1 (Fig. 25.1).

Internal Valves

The width and stability of the upper cartilaginous vault (formed by the upper lateral cartilages and the anterior septal edge), the critical area of the internal nasal valves, depends on the width of the bony vault and the height and width of the middle vault roof. Any resection of the middle vault roof greater than 2 mm during hump reduction removes this most critical anterior stabilizing force on the upper lateral cartilages, which fall medially and produce a characteristic inverted-V deformity and obstruction at the internal valves.2,3 Middle vault collapse virtually always occurs when the cartilaginous roof has been resected and whether osteotomy has been performed but may not be visible if the overlying soft tissues are sufficiently thick; when the nasal skin is thin, the deformity can be impressive (Fig. 25.2). Uncorrected, the patient’s airway will decrease by 50%. To prevent middle vault collapse and internal valvular incompetence, the surgeon should plan to reconstruct the normal forces by a substantial dorsal graft or by spreader grafts,3 which provide the same degree of functional mean nasal airflow improvement as documented by a level 2 outcome study (discussed later).1,4

The middle vault and therefore the internal valves are particularly threatened in three circumstances:

1. When the preoperative middle vault is congenitally narrow

2. When the nasal bones are short, therefore creating a larger percentage of sidewall that is only supported by cartilage (Fig. 25.3)

3. When the surgeon reduces the nasal dorsum by more than 2 mm1

Intersection of the Middle and Lower Cartilaginous Vaults

The upper lateral cartilages are supported caudally by their relationship to the cephalic margins of the lateral crura in the region of the so-called “scroll”; radical alar cartilage resection can compromise middle vault support and may leave an external deformity, typified by deepening and lengthening of the alar creases. The surgeon should resect the upper lateral cartilages submucosally only when failure to do so would allow them to prolapse into the airway or when necessary to shorten the nose.

External Valves

The stability of the lower third of the nasal sidewall depends on the thickness of its external and vestibular skin and the position of the alar cartilage lateral crura. In the primary rhinoplasty population, 50% of lateral crura are cephalically rotated (“malpositioned”) and run along axes that angle toward the medial canthus. In this circumstance, even the unoperated cartilaginous support to the alar sidewall is poorly positioned to support the alar rim against inspired airflow speeds of up to 60 km/hr. In two rhinomanometric studies of external valvular function, most patients with alar cartilage malposition had incompetent external valves that collapsed upon inspiration.5,6 Significant resection of orthotopic lateral crura (those that more closely parallel the alar rims and whose long axes run toward the lateral canthi) or even modest resections of malpositioned lateral crura cause varying degrees of external valvular incompetence, alar hollowing, alar wall notches, or retraction of the rims. Most of these secondary cases require alar wall cartilage grafts, and in cases of severe retraction composite skin and cartilage grafts from the conchal floor. Malposition occurs in 80% of the secondary rhinoplasty population (Fig. 25.4).

What Matters in Functional Nasal Anatomy

Although many patients with obstructed nasal airways improve after septoplasty with or without inferior turbinectomy, not all do. Adding to the frustration of patient and surgeon are three other common observations:

1. There is often a poor correlation between a patient’s symptoms and the apparent site of clinical septal or turbinate obstruction.1,3

2. Patients typically breathe better (preoperatively and even postoperatively) on the “narrower” side (ipsilateral to the septal deviation).

3. Many patients who have undergone prior successful septoplasty and turbinectomy or who have straight, unoperated nasal septa still complain of airway obstruction.

These observations cannot be explained by indicting only septal deviation and contralateral inferior turbinate hypertrophy.

Until recently, efforts to correlate nasal airflow with clinical symptoms had yielded equivocal conclusions. There was argument on both clinical and rhinomanometric grounds that septoplasty either did or did not improve nasal airflow. For such a commonly and easily diagnosed clinical problem as septal deviation, one would expect to find more unanimity in clinical series. These observations were clouded further by the fact that approximately 80% of nasal septa in the population at large are “deviated” and by imprecision in distinguishing internal from external valvular incompetence. Nevertheless, mounting clinical evidence indicates that obstruction at either set of valves may profoundly obstruct the airway, even in the absence of septal deviation.715

Airway Outcome Study in 600 Patients

To help resolve some of these conflicting clinical observations and to provide quantitative measurements of the relative increases in nasal airflow after functional septal or valvular surgery, a level 2 study of 600 consecutive patients undergoing surgery for airway obstruction was undertaken between 1991 and 2008.1,4 Patients with septal perforation, atopic patients, and patients requiring turbinectomy were excluded. The diagnosis of septal obstruction or valvular incompetence was made by observation of the nasal airway and nasal sidewall movement with and without a nasal speculum during quiet and forced inspiration. Septoplasty and valvular reconstruction by cartilage or bone grafts were performed as indicated and as described in this chapter. Anterior, active, mask rhinomanometry was performed according to the method of Mertz, McCaffrey, and Kern.16

That study comprised 600 patients: 78% women and 22% men; 36% primary rhinoplasties and 64% secondary rhinoplasties (median follow-up 14.3 months, mean 27 months). The longer-term data of 362 patients observed for a minimum of 12 months (median 29 months) supported the numbers in the entire group. A summary of the results are presented in Box 25.1.1,4

This study did not answer the question of where turbinates fit into the hierarchy of nasal obstructions. In atopic individuals with gross turbinate hypertrophy or polyps, turbinectomy is unquestionably valuable.17 However, the mean nasal airflow improvements listed previously were achieved without turbinectomy, even in a population of patients with secondary deformities, valvular incompetence, prior intranasal scars, webs, or vestibular atresia, confirming that turbinate obstruction in many patients may be largely reactive or secondary.

1. Septal and valvular surgery corrected the airway obstruction in more than 95% of patients in a single operation. These results were possible even though two thirds of the population were secondary rhinoplasties with more severe deformities.

2. Although septoplasty improved airflow ipsilateral to the obstruction, there was no significant improvement in total (geometric mean) nasal airflow after septoplasty alone.

3. Internal valvular reconstruction by dorsal or spreader grafts doubled nasal airflow.

4. Spreader grafts and dorsal grafts were equally effective in supporting the internal nasal valves.

5. External valvular reconstruction doubled mean nasal airflow.

6. The largest postoperative improvement was seen in patients after correction of both internal and external valvular incompetence (more than four times preoperative values).

7. Septoplasty in addition to valvular reconstruction did not significantly improve nasal airflow over the results obtained by valvular reconstruction alone, even in patients observed more than 100 months postoperatively.

8. These results were produced without performing inferior turbinectomy in any of the patients.

9. In those patients with lateralized symptoms, the septum was contralateral to the more obstructed side in 45% of cases.

10. Of the 384 secondary rhinoplasty patients, 94% had previously undergone adequate septoplasties but were still symptomatically obstructed. Within this group, valvular reconstruction alone corrected the airway in 97% after one operative procedure.

11. When primary and secondary rhinoplasty patients were stratified, the improvement in primary patients equaled or exceeded the improvement achieved in secondary rhinoplasty patients in six of the eight obstructed sites examined.

12. Valvular obstruction was 4 times more common than pure septal obstruction in primary rhinoplasty patients and 12 times more common than pure septal obstruction in secondary rhinoplasty patients.

13. When the entire 600-patient group was stratified, the greatest improvement was observed in those patients observed more than 12 months, supporting the view that the airway continues to enlarge as edema resolves.

14. By measuring airflow during quiet and forced inspiration, sidewall stiffness could be quantified and shown to increase following valvular reconstruction by dorsal, spreader, or alar wall grafts.

15. A decrease in nasal airflow was not obligatory, even in patients with preoperative airway obstruction.

Source: Data from Constantian MB, Clardy RB. The relative importance of septal and nasal valvular surgery in correcting airway obstruction in primary and secondary rhinoplasty. Plast Reconstr Surg 1996;98:38 and Constantian MB. Rhinoplasty: Craft and Magic. St Louis: Quality Medical Publishers; 2009:133–186.

Based on this study and the doubling of airflow from reconstructing incompetent internal valves, we speculated that the rhinoplasty surgeon who reduces a nasal dorsum, opening the middle vault and creating internal valvular incompetence where it did not exist preoperatively, will decrease the postoperative airway by 50%. That speculation has been confirmed by a recent study.15 Furthermore, the results of external valvular reconstruction suggested that lateral crural resection significant enough to cause external valvular incompetence will decrease the postoperative airway by another 50%. The inescapable implication of these observations is that a patient whose internal and external valves have been destabilized by dorsal and tip reduction can lose 75% of his or her preoperative airway in only one rhinoplasty, regardless of whether obstructing septal and turbinate factors have been satisfactorily corrected (Fig. 25.5).

Avoiding Unfavorable Results and Complications in Postoperative Nasal Airway Obstruction

Three distinct differences separate primary and secondary rhinoplasty: (1) tissue tolerance, (2) donor site depletion, and (3) patient depletion (i.e., limited physical and emotional tolerance for uncorrected or new problems). The difficulty in any rhinoplasty is therefore not primarily technical or anatomic; it is recognizing the phenomenology present in nasal structure and function and learning to work within it.

Summary Box

Key Points Relevant to Postoperative Airway Obstruction

• The most common patient motivation for secondary rhinoplasty is an iatrogenic deformity from the previous surgery.18 The primary surgeon must therefore use techniques that minimize the chance of creating secondary deformities.

• There is no strategic difference between primary and secondary rhinoplasty except the donor sites. The surgical approach to all noses must respect the skeletal and soft tissue interdependencies and the contributions of both skin and skeleton to the final outcome. These contributions are often more easily assessed through the endonasal approach than through open rhinoplasty because the soft tissues, which determine 50% of the final result, are largely undisturbed. All key planning decisions can be made from the external and airway examinations.

• Secondary rhinoplasty deformities are not limitless. They form one of three patterns:

Pattern 1: Deformities from soft tissue contraction.

Pattern 2: Deformities from skeletal contraction. Airway deformities typically create this pattern.

Pattern 3: Deformities from imbalance.

• Only four common anatomic variants determine the success of any rhinoplasty2 (Table 25.1):

image Low radix or low dorsum.

image Inadequate tip projection, which determines the lateral view and whether the patient has a straight profile.

image Narrow middle vault.

image Alar cartilage malposition, which determines the frontal view and controls the airway. The latter two must be recognized to aid creating new postoperative airway complications.

• These four critical anatomic variants directly explain all three secondary deformity patterns:

image Inadequate tip projection creates supratip deformity and therefore pattern 1.

image Narrow middle vault and alar cartilage malposition allow skeletal collapse and create pattern 2.

image Low radix and low dorsum affect nasal proportion and create pattern 3.

image The interdependencies of anatomy and postoperative deformity emphasize the importance of correct diagnosis and of recognizing anatomic variations.

• Reconstruction of both internal and external valvular incompetence triples or quadruples airflow in most patients, with or without concomitant septoplasty.

• Most functional primary, secondary, and tertiary deformities can be corrected with only one of two operative strategies: spreader or dorsal grafts to reconstruct or stabilize the middle vault or alar wall or composite grafts to stabilize the external valves.

Table 25.1 Three patterns of secondary deformity that can be avoided by proper primary rhinoplasty technique


Dominant physical findings

1. Deformities from soft tissue contraction

Low dorsum, blunt tip, supratip deformity, re tracted columella or alar rims

2. Deformities from skeletal collapse

Inverted-V deformity, knuckled domes, collapsed alar rims

3. Deformities from nasal imbalance

Low dorsum, large base; high dorsum, small base

The surgeon should inquire about the airway first to avoid becoming distracted by the patient’s aesthetic considerations. Patients become accustomed to a poor airway. Many have never breathed normally; others have lost their basis for comparison after trauma or previous surgery and have forgotten how much better their airways used to be. Ask about periodic or cyclic airway obstruction; which airway is worse; any nasal trauma history; seasonal allergies that obstruct the airway; clear rhinitis and suppurative sinusitis; snoring, epistaxis, and sinus headache or frequent nose blowing; and what nonsurgical remedies the patient has previously tried. Secondary rhinoplasty patients with poor airways commonly will chronically self-medicate with steroid or vasoconstrictive sprays that must be eliminated before surgery. Also important are the patient’s work environment and a history of tobacco or alcohol consumption (either of which may cause nasal congestion) and, more common now than in previous years, cocaine use.


Internal Valves

Sidewall collapse with inspiration at one or both of the nasal valves is surprisingly common.1 It is important to determine why valvular incompetence exists (e.g., prior surgery, intrinsic weakness, or alar cartilage malposition). If sidewall collapse occurs, the surgeon should occlude one nostril and ask the patient to compare flow through the unobstructed airway with and without supporting the collapsing area with a cotton-tipped applicator soaked in 1% pontocaine hydrochloride for the patient’s comfort. Patients with valvular incompetence will notice an obvious and gratifying increase in airway size. The surgeon may observe valvular collapse and substantial airway obstruction even in a patient with a straight, unoperated septum and without turbinate hypertrophy. Here, septoplasty may be indicated to harvest grafts but by itself will not open the airway; the surgeon must also place appropriate valvular grafts (Video 25.1). Some surgeons prefer spreader flaps or autospreader grafts,19 redundant or unresected upper lateral cartilages that are turned medially and fixed to the septal edge by sutures. If redundant upper lateral cartilages are long enough and strong enough to support the middle vault, spreader grafts may be effective. At the time of this writing, however, no study has shown that they prevent or correct internal valvular incompetence. One paper has in fact indicated the contrary.20

External Valves

Once the alar wall has been palpated and the patient has been observed during quiet and forced inspiration, the position of the lateral crus and the strength of the alar wall can be estimated. In primary patients, adequate treatment of cephalic rotation of the lateral crura requires resection and replacement of these structures, relocation of the lateral crura to support the external valves, or supporting the areas of external valvular collapse with autogenous grafts. Correction of external valvular incompetence doubles mean nasal airflow in most patients (2.5 times for primary patients; 4.0 times for secondary patients).1,4

However, most secondary rhinoplasty patients have insufficient remaining lateral crura and require cartilaginous support with septal, conchal, or rib cartilage grafts. When alar rim retraction is severe, the lining must also be replaced in the form of composite skin and cartilage grafts from the conchal floor.21


The septum should be palpated for remaining obstructing cartilage and bone and the mucosal cover examined (indicating the sequelae of allergy, injury, perforation, or chronic cocaine use). It is also important to assess whether a “high” (i.e., toward the anterior edge) septal deviation exists; because hump removal can unmask a high septal curvature, the surgeon should be prepared to camouflage or correct the septal deflection with unilateral or asymmetrically thick spreader grafts.1,3,4


Clinical and rhinomanometric data indicate that obstructing turbinates are relatively low in the hierarchy of common airway obstruction causes in primary and secondary patients. Because turbinates warm and humidify inspired air, the surgeon should plan conservative resections even in atopic patients. Furthermore, histologic studies have shown that turbinate hypertrophy secondary to septal deviation is characterized by bony, not mucosal, overgrowth.22 Therefore most patients who have had good septal and valvular reconstruction can be adequately treated by only turbinate crushing and outfracture (or no treatment at all). Hypertrophy will not return postoperatively in most patients if septal and valvular causes have been corrected.1

Technical Details of Surgical Correction

It is important to identify which of the four critical predisposing anatomic variants are present: low radix or low dorsum, narrow middle vault, inadequate tip projection, or alar cartilage malposition. Everything else is a relative detail. If the surgeon recognizes the four anatomic variants in the primary nose and makes their management part of the surgical plan, the most common secondary deformities can be eliminated.

Surgeons must recognize consistent published and presented data that indicates that secondary patients who have undergone open rhinoplasty have significantly more deformities than those treated endonasally, especially deformities of the columella, external valves, alar rims, and nasal tip—areas invaded or manipulated though the open approach.23 Confusing matters further, no published outcome study has yet demonstrated that either surgical technique creates better results and fewer complications for most patients, which deepens the weeds for novices. Surgeons new to rhinoplasty are advised to question what they read and hear and to expect proof that published functional or aesthetic techniques work consistently before adopting them. Because all patients invest money, time, discomfort, and emotion in their rhinoplasties, what the patients fear most, and need least, are additional disappointments.24

Most functional nasal deformities can be corrected with only one of two operative strategies: spreader or dorsal grafts for internal valvular obstruction or alar wall grafts for external valvular obstruction. In primary cases in which the lateral crura are malpositioned or secondary cases in which the patient’s lateral crura are still present, the surgeon can dissect out the lateral crura, cut them free at the lateral genu, trim the cartilages to a size appropriate to support the alar walls, and replace them along the alar rims to support the collapsing areas25 (Fig. 25.6).

Oct 23, 2018 | Posted by in General Surgery | Comments Off on Postoperative Nasal Airway Obstruction
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