Indications and Technique for Treating the Narrow Midvault in Closed Rhinoplasty
Shruti C. Tannan
Jeffrey R. Claiborne
Mark B. Constantian
DEFINITION
A narrow middle vault can be defined anatomically or functionally.
Anatomically, a narrow middle vault is defined as any part of the upper cartilaginous vault that is at least 25% narrower than the upper or lower nasal third.
Functionally, a narrow middle vault is defined as inadequate internal nasal valve support.
ANATOMY
The middle vault is composed of the paired upper lateral cartilages (ULCs) and the dorsal nasal septum.
The ULCs extend superiorly beneath the paired nasal bones approximately 5 mm, in a region known as the keystone area.
Laterally, the ULCs attach to the bony piriform aperture via the piriform ligament.
Inferiorly, the ULCs are supported by their attachment to the lower lateral cartilages in a region called the scroll area.
Aesthetically, the middle vault is the location of a smooth transition from the narrower nasal bones superiorly to the wider nasal base inferiorly.
In the midline, the ULCs fuse with the septum to create a T in cross section, an intersection that creates an angle known as the internal nasal valve (FIGS 1 and 2).
FIG 1 • Internal nasal valve.
The internal nasal valve is bounded medially by the septum, laterally by the ULCs, and inferiorly by the inferior turbinate.
The internal nasal valve is the narrowest portion of the nasal airway and therefore the site of highest airflow resistance.
The width and stability of the middle vault, the critical area of the internal nasal valve, is determined by three factors:
Width of the nasal bony vault
Height and width of the middle vault roof
Soft tissue rigidity
PATHOGENESIS AND NATURAL HISTORY
As air enters the region of the narrow internal nasal valve, airflow speed increases according to the Poiseuille law and the Venturi principle: when air goes through a narrow passage, it speeds up and increases the transmural pressure on the nasal sidewall, just as water running through a brook speeds up as it passes between a narrow channel. Additionally, the Bernoulli principle dictates that with increased flow speed, the intraluminal pressure decreases, which places the valve at risk for collapse from the lower pressure.
FIG 2 • Nasal valves.
FIG 3 • Pathogenesis of iatrogenic middle vault collapse.
Poiseuille law states that flow is proportional to the radius to the fourth power. Thus, seemingly diminutive changes in middle vault size have dramatic implications in nasal airflow.
A decrease in middle vault size or weakening of the structural integrity of the nasal valve places the patient at risk for nasal airflow obstruction.
Any resection of the middle vault roof greater than 2 mm during hump reduction destabilizes this most critical area, allowing the upper lateral cartilages to fall medially and produce a characteristic “inverted V” deformity and result in obstruction at the internal valves (FIG 3).
Reducing the dorsum and creating an open middle vault and interval valvular incompetence will decrease the postoperative airway by 50%.
The middle vault and internal nasal valve are at risk in three specific circumstances:
The midvault is congenitally narrow.
The nasal bones are short, therefore leaving a larger proportion of nasal sidewall supported by the ULCs (internal valves) and the lateral crura (external valves).
The surgeon reduces the dorsum by more than 2 mm, which in most patients will open the cartilaginous roof.
The most common motivation for secondary rhinoplasty is an iatrogenic deformity from the previous surgery.1
A narrow middle vault has been shown to be present preoperatively in 38% of primary and 87% of secondary rhinoplasty patients.2
A study of 600 consecutive patients undergoing surgery for airway obstruction between 1991 and 2008 with a mean follow-up of 27 months found the following2:
Septal and valvular surgery corrected the airway obstruction in more than 95% of patients in a single operation, despite the fact that two-thirds of patients were secondary rhinoplasty patients with more severe deformities.
Septoplasty improved airflow ipsilateral to an obstruction but made no impact on total nasal airflow.
Internal valvular reconstruction with dorsal or spreader grafts doubled nasal airflow.
Dorsal and spreader grafts were equally effective at improving nasal airflow.
External valvular reconstruction doubled nasal airflow.
The greatest improvement in nasal airflow was observed after both internal and external valvular reconstruction (a fourfold improvement in airflow).
Septoplasty in addition to valvular surgery did not offer any clinical benefit compared with valvular surgery alone.
In patients with lateralized symptoms, the septum was deviated away from the obstructed side in 45% of cases, thus emphasizing the importance of valvular obstruction in creating airway symptoms.
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.
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.
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.
When the entire 600-patient group was stratified, the greatest improvement was observed in those patients observed for more than 12 months, suggesting that the airway continues to enlarge as postoperative edema resolves.
By measuring airflow during quiet and forced inspiration, sidewall stiffness could be quantified and increased following valvular reconstruction by dorsal, spreader, or alar wall grafts.
Based on this study indicating that reconstruction of the internal nasal valve can double airflow, iatrogenic injury to the internal nasal valve can conversely reduce airflow by 50%, and this assumption has been corroborated by recent studies.3
PATIENT HISTORY AND PHYSICAL FINDINGS
Four anatomic findings place patients at high risk for unfavorable results and should be identified preoperatively.4
Low radix or low dorsum
Inadequate tip projection
Narrow middle vault
Alar cartilage malposition
Of these four, narrow middle vault and alar cartilage malposition (cephalic rotation of the lateral crus) impact the airway because they indicate preoperative threats to the internal and external nasal valves, respectively.
The exam findings of an obstructing septum or turbinate do not often correlate well with patient symptoms.2
Patients frequently breathe better on the apparent “obstructed” side, indicating that septal and turbinate obstruction do not explain the entire airway dysfunction.
Eighty percent of nasal septa in the population are deviated, yet only a small portion have clinical obstruction
Patients with straight septa or prior successful septoplasty and turbinectomy frequently still have persistent symptoms of nasal obstruction.
History
Organized approach to obtaining history: first inquire about the airway and subsequently discuss aesthetic concerns.
Many patients become accustomed to a poor nasal airflow and have forgotten how much better their airway used to be prior to trauma or other surgeries—thus, this part of the history requires that the physician guide the interview with direct questions.
It is important to inquire about a history of prior trauma because unhealed septal fracture lines may extend to the dorsal septal edge and therefore threaten dorsal strut stability.
Recent trauma (within 3 months) is an indication to postpone the rhinoplasty until any fractures have healed and until postoperative edema allows accurate judgment of the aesthetic contours.
Ask about periodic or cyclic airway obstruction including which airway is worse, any nasal trauma history, seasonal allergies, clear rhinitis and suppurative sinusitis, snoring, epistaxis, sinus headache, frequent nose blowing, and what nonsurgical remedies the patient has tried to date.
Often, secondary rhinoplasty patients with poor airways chronically self-medicate with steroid or vasoconstrictive sprays that must be identified and discontinued 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 cocaine use.
Valve examination: Watch your patients breathe!
Sidewall collapse with inspiration is surprisingly common. If this occurs, it is important to determine the etiology (prior surgery, intrinsic weakness, cartilage malposition).
Perform a modified Cottle maneuver and compare airflow between sides. This maneuver is not specific, because even with septal deviation, traction on the sidewall will open the airway. Obstruction must be localized at the valves before valvular surgery is undertaken.
Support 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; thus, you can guarantee that valvular reconstruction will improve the airway similarly.
It is important to assess whether a high septal deviation exists because hump removal will unmask the curvature: in the middle of the operation, the nose can suddenly look newly asymmetrical. When a high septal deviation exists, the surgeon needs to be prepared to place unilateral or asymmetric spreader grafts. The correction is straightforward, but the surgeon must be attentive to new intraoperative deformities.
Turbinates
Obstructing turbinates are relatively low in the hierarchy of causes of nasal obstruction.
Given their function to warm and humidify air, turbinate reductions should be planned conservatively.
Because the majority of turbinate hypertrophy is due to bony (not mucosal) overgrowth, most patients should be treated with turbinate crushing and outfracture.5 If septal and valvular causes of airway obstruction have been corrected, the turbinates will not become enlarged again, unless the patient is atopic.Related posts:
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