CME Understanding the Nasal Airway: Principles and Practice filepercent of specimens.2 Subsequent...

CME

Understanding the Nasal Airway: Principlesand PracticeBrian K. Howard, M. D., and Rod J. Rohrich, M. D.Dallas, Texas

Learning Objectives: After studying this article, the reader should be able to: 1. Describe the soft-tissue, cartilaginous,and bony anatomy of the nose. 2. Describe the anatomy and function of the nasal valves. 3. Discuss the governingphysiologic principles responsible for airflow dynamics. 4. Discuss the various functions of the nose. 5. Demonstrate anappropriate evaluation of the nasal airway. 6. Discuss the differential diagnosis of nasal obstruction. 7. Discuss appropriatemanagement options for nasal airway obstruction.

The nose is a complex, multifunctional organ that re-quires respect and understanding from the rhinoplastysurgeon. The etiologic and pathologic characteristics ofeach patient’s nasal airway problem determine the treat-ment of the nasal airway. Frequently, medical manage-ment is sufficient without operative intervention. Recentadvances have shown that nasal valves in airway patencymay play a more important role than the septum. Therhinoplasty surgeon’s understanding of the anatomy andphysiology of the nasal airway, along with the causes ofobstruction, can pave the way for a proper evaluation andappropriate management of nasal airway problems. Lackof understanding can result in misdiagnosis and misman-agement. This article outlines current concepts of medicaland surgical management of nasal airway problems anddiscusses in detail the key concepts and principles in thepractical management of the nasal airway. (Plast. Recon-str. Surg. 109: 1128, 2002.)

Understanding the anatomy and physiologyof the nasal airway, causes of obstruction,proper evaluation, and appropriate manage-ment is essential for the rhinoplasty surgeon.Lack of such understanding results in misdiag-nosis and mismanagement. Current treatmentfrequently consists of routine submucous resec-tion of the septum and/or inferior turbinatesurgery. Although, occasionally, these are cor-rect management choices, the decision to per-form such procedures should be the result ofappropriate evaluation and diagnosis. The eti-ology of many nasal airway obstruction prob-lems is not structural; rather, it is physiologicand can be treated with medical management

and patience. The ideal rhinoplasty includespreservation or correction of the nasal airway,which involves a systematic evaluation of thepatient. The purpose of this article is to reviewthe key concepts and principles in the practicalmanagement of the nasal airway.

HISTORY

Galen was the first to describe the anatomyand various functions of the nose 2000 yearsago. Nonetheless, very few additional advancestook place until the nineteenth century.

Phylogenetically, the original function of thenose was solely that of an olfactory organ; therole of respiratory function developed muchlater.1 As humans evolved from a quadruped toan upright biped mammal, airflow became re-directed away from the olfactory mucosa alongthe roof of the nasal vault, which diminishedthe olfactory sense. Gradual atrophy of thissensory organ resulted because it was no longeressential to survival. Now, only a few squarecentimeters of specialized mucosa along thecribriform plate remain. Atrophy also resultedin an enlarged nasal vault, through which de-veloped an effective respiratory conduit. Respi-ration is now the primary role of the humannose.

Septal deformities were among the earliestdescribed causes of nasal airway obstruction.MacKenzie studied 2152 skulls in his A.D. 1657treatise, noting septal bony deformities in 75

From the Department of Plastic Surgery, University of Texas Southwestern Medical Center. Received for publication October 1, 1999; revisedJanuary 11, 2001.

1128

percent of specimens.2 Subsequent studies byZuckerkandl,3 Schaeffer,4 and Spector5 are alsoof historical interest, supporting the role of theseptum in symptomatic nasal airway obstruc-tion. Septal deviations have been implicated invarious maladies, such as emphysema andheadaches, as reviewed by Horton.6

Casserius7 first provided a detailed descrip-tion of the turbinates in 1609. Kayser, who firstdescribed the nasal cycle,8 identified enlargedturbinates as a contributing cause for airwayobstruction in 1895. Ten years previously,MacKenzie had noted the similarity betweenthe sinusoidal tissue of the inferior turbinateand the erectile tissue of the penis.9 The mid-twentieth century was the stage for heated de-bates on the management of enlarged turbi-nates. On the one hand, Proetz,10 Thomsonand Negus,2 Dutrow,11 and House12 argued thatalteration of airflow by turbinate resection onlyled to other problems that were often untreat-able. On the other hand, Fry13,14 later endorsedroutine turbinectomy for enlarged turbinates.

Rhinitis as a cause for nasal airway obstruc-tion received little attention until 1950, whenHolmes and associates listed eight commoncauses of nasal vascular engorgement15 (TableI). Multiple stimulants for rhinitis were subse-quently described by Hinderer,16 Stahl,17

Reed,18 Wolfe,19 Jaffe,20 Dolowitz,21 Blue,22 Reesand Wood-Smith,23 and Beekhuis.24 Bridger ini-tially described the importance of the internalnasal valve.25 Much work that has since beendedicated to the management of disorders ofthe nasal valves will be discussed in latersections.

ANATOMY

The nasal anatomy is generally divided intotwo subunits: soft tissue and the osseocartilag-inous framework. For the purpose of emphasis

in this article, we will discuss the nasal valves ina third, separate category. Although the soft-tissue envelope is less commonly involved withnasal airway disorders, the perinasal muscula-ture plays a vital role in maintaining nasal valvecompetence, as is most eloquently demon-strated in patients with facial nerve palsies.

Soft Tissue: Perinasal Musculature

The muscles of the nose are divided into anintrinsic group of seven paired muscles (havingboth origin and insertion within the perinasalarea), and an extrinsic group containing threepaired muscles.26

The intrinsic group includes the procerus,which raises the dorsum and lowers the lateralcartilages. Its distal aponeurosis blends withthe pars transversa of the nasalis muscle to formthe superficial musculoaponeurotic system ofthe nose. The pars transversa provides lateralwall rigidity and can even be a dilatory muscle.By contrast, the pars alaris is the primary dila-tory muscle of the ala and is responsible foralar flaring. The remaining nasal intrinsic mus-cles are of doubtful importance in nasal airwaypatency.

Of the extrinsic muscles, the levator labii su-perioris alaeque nasi is the most important dila-tor. The zygomaticus minor and orbicularis orissecondarily provide lateral wall stability (Fig.1).

The alae consist of fibrofatty areolar tissuedevoid of cartilage and are lined by epitheliuminternally and externally. Collapsing alae canbe a cause of airway obstruction and will bediscussed further.

TABLE ICauses of Nasal Vascular Engorgement

Contact with infectious agentsInhalation of irritant dusts or chemical fumesInhalation of pollen or other substances to which the patient

is sensitiveLife experiences provocative of conflict, resentment, and

frustrationChilling of the body surfaceMenstruation and pregnancySexual excitementStrong odors and bright lights

Adapted from Holmes, T. H., Goodell, H., Wolf, S., and Wolff, H. G. The Nose: AnExperimental Study of Reactions within the Nose in Human Subjects during Varying Life Expe-riences. Springfield, Ill.: Charles C. Thomas, 1950.15 FIG. 1. The anatomy of the relevant perinasal muscles.

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Osseocartilaginous Vault

The septum serves as the central support forthe nose (Fig. 2). The perpendicular plate ofthe ethmoid articulates with the posterior edgeof the quadrangular (septal) cartilage. Bothstructures articulate with the vomer inferiorly.The vomer itself rests on the maxillary andpalatine crest. The tongue-and-groove articula-tion between the quadrangular cartilage andthe maxillary and palatine crest deserves spe-cial mention. The perichondrium of the carti-lage is only partially contiguous with the peri-osteum of the crests. Other fibers pass throughthe articulation to join the contralateral peri-chondrium (Fig. 3). This crossed configurationmakes a contiguous submucoperichondrial dis-section difficult. This same anatomic configu-ration also allows some movement between thecrest and the septum, and it is this instabilitythat explains the frequent posttraumatic find-ing of a displaced quadrilateral septal cartilagefrom the groove of the crest. Caudally, themost projecting part of the premaxilla is theanterior nasal spine.

The lower aspect of the nose is also sup-ported by the upper and lower lateral carti-lages. The junction of the cephalic edge of thelateral crus and the caudal edge of the upperlateral cartilage is called the scroll. Most pa-tients have some overlap of the cartilages,which may enhance support at this level.27 Su-periorly, the perichondrium of the upper lat-eral cartilage is contiguous with the periosteumof the nasal bones, making up the keystonearea. The nasal bones actually overlap the ce-phalic upper lateral border by several millime-ters, thus producing a firm adherence between

the structures. Subsequently, any motion of thebones moves the entire unit as a whole. Theupper lateral cartilages are fused in the mid-vault area and become separated only near thecaudal edge. This requires sharp release of theupper lateral cartilage from the septum whenplacing a spreader graft.

Internally, the anterior head of the inferiorturbinate occupies a significant portion of thenasal passage. It is composed of dense lamellarbone originating from the medial maxillae andis covered with erectile mucosal tissue. Themucosa consists of pseudostratified ciliated co-lumnar epithelium. The submucosa containslarge amounts of seromucinous glands and vas-cular channels containing cavernous sinusoids.These channels are under autonomic controland are the end targets for decongestant med-ications. The sympathetic system regulatesblood flow to the nasal mucosa (resistance ves-sels), whereas the parasympathetic system reg-ulates the blood volume of the nasal mucosa(capacitance vessels). Thus, alpha-adrenergicagents cause vasoconstriction and cholinergicagents result in vasodilatation. The submucosaalso contains large numbers of mast cells, eo-sinophils, plasma cells, lymphocytes, and mac-rophages. Chronic inflammation of the turbi-nates can lead to fibrous deposition andchronic hypertrophy of the turbinate.

Valves

Internal nasal valve. A bottleneck exists atthe level of the anterior head of the inferiorturbinate. This internal nasal valve accounts forapproximately half of the total airway resis-tance.28,29 The boundaries of this valve are bor-

FIG. 2. The septal cartilage articulates with the perpen-dicular plate of the ethmoid superiorly, the vomer posteri-orly, and the maxillary crest inferiorly.

FIG. 3. Note the decussating perichondrial fibers.

1130 PLASTIC AND RECONSTRUCTIVE SURGERY, March 2002

dered medially by the septum, inferiorly by thenasal floor, laterally by the inferior turbinate,and superiorly by the caudal border of the up-per lateral cartilage (Figs. 4 and 5). The junc-tion between the septum and upper lateral car-tilage is normally 10 to 15 degrees.

External nasal valve. The external nasal valveexists at the level of the inner nostril. It isformed by the caudal edge of the lateral crus ofthe lower lateral cartilage, the soft-tissue alae,the membranous septum, and the sill of thenostril (Figs. 4 and 5). This is an occasional siteof obstruction in the compromised nasal airwaypatient, particularly in the secondary rhino-plasty patient with the pinched alae deformity.

PHYSIOLOGY

The seven basic functions of the nose arerespiration, humidification, temperature mod-ification, particle filtration, olfaction, phona-tion, and secondary sex organ. As mentioned,the formerly most important olfactory functionhas diminished significantly, and the nose nowserves primarily as a respiratory organ. Respi-ratory physiology can be described using well-known laws of physics.

Ohm’s Law

According to Ohm’s law, flow is directly pro-portional to the difference in pressure andinversely proportion to the resistance.28

Flow � dP/Resistance (V � IR, I � V/R) (1)

When a pressure difference exists betweenthe external nares and the nasopharynx, air-flow occurs through the nose. As Ohm’s lawshows, increased resistance leads to decreasedflow. Thus, structural limitations caused by hy-pertrophic turbinates, septal deflections, valveincompetence, or intraluminal masses lead todecreased airflow.

Nasal resistance can also be mathematicallydescribed by the following formula:

1/Total Resistance � 1/Left Nostril Resistance

� 1/Right Nostril . . . . (2)

From this equation, it can be seen that aseptal perforation can have a dramatic effecton lowering total nasal airway resistance. Byfollowing the path of least resistance, a perfo-ration allows the airflow from the more resis-tant side to redirect to the other, less resistant,side, thus lowering total resistance. It is alsointeresting to note that despite the short nasalcanal relative to the remaining respiratory tree,approximately half of the total respiratory re-sistance occurs within the nose.28,29

When laminar flow exists, air moves througha straight tube in a predictable manner. Airnear the walls of the tube is nearly still, whereasair in the central lumen flows more rapidly.

FIG. 4. The internal nasal valve angle is normally 10 to 15degrees. The boundaries of both valves are shown.

FIG. 5. The boundaries of the internal and external nasalvalves are shown.


Turbulent airflow exists when laminar flow iscompromised. Airflow follows random paths inturbulent airflow with whorls and eddies. Toovercome turbulence, a greater pressure gradi-ent must be generated. By definition, nasalairflow is never truly laminar, because airflowdoes not follow a straight course through thenasal passage. The inspiratory current is nor-mally described as a parabolic curve through thenasal vault. Air enters at the level of the naresand gently arcs superiorly above the head ofthe inferior turbinate. The main flow of air isthrough the middle meatus. A small amountcourses through the inferior meatus and aneven smaller amount uptoward the cribriformplates (Fig. 6). The airstream flowing throughthe middle meatus is approximately 1 mm inwidth. The choanae, which mark the posteriorboundary of the nasal vault and entry into thenasopharynx, lie slightly inferior to the middlemeatus. Therefore, the curve of the airflowmust arch again slightly inferiorly as it entersthe nasopharynx. This results in a paraboliccourse from nostril to choanae. Because astraight tubular architecture is not present,laminar flow in the true sense does not exist.This is another built-in mechanism of resis-tance to airflow. The less laminar the airflow,the higher the resistance and the less the air-flow. Even so, at low pressures (less than 1 cmof water), airflow approximates laminar flowand becomes increasingly more turbulent withhigher pressures.30 Quiet respiration usuallycreates pressures of less than 1.5 cm of waterand, therefore, is essentially laminar.

Bernoulli’s Principle

Bernoulli’s principle provides that total air-flow at each end of a tube must be equal. If the

diameter between the two ends is different, thevelocity of airflow will vary. In constricted areas,velocity increases and a relatively negative pres-sure is generated.31 Clinically, this is seen in theincompetent internal or external nasal valve.Because these are bottleneck areas, airflow isincreased at the level of the valve, resulting ina lowered negative internal pressure in relationto the outer extranasal pressure. This gener-ates collapsing forces on the valves. Theseforces are exacerbated during heavy inspira-tion or sniffing.

Poiseuille’s Law

Bernoulli’s principle can be mathematicallyevaluated using Poiseuille’s law, which statesthat flow is directly proportional to the differ-ence in pressure multiplied by the radiusraised to the fourth power. Flow is also in-versely proportional to the length of the tube.31

Flow � Constant(K)�dP�r4/Length (3)

It can be seen that a minimal increase in theradius of the tube results in significant in-creases in flow.31

The cross-sectional area varies throughoutthe nose. It is smallest at the internal nasalvalve (30 to 40 mm2), larger at the level of themidturbinates, and largest at the level of theposterior choanae. Thus, the internal valvelevel is a bottleneck to airflow and is reportedby some to be the most frequent area of nasalairway obstruction in Caucasians.32–34Air flowacross the internal nasal valve can reach 125mph during heavy nasal inspiration.35

Humidification

Ninety percent of air humidification occursbefore the air reaches the lungs during inspi-ration. Approximately 1 liter per day of water isused in the humidification process.10

Some animals have developed efficientmechanisms for water conservation. Camelsand some other desert animals, for example,have well-developed and complex turbinatesystems that can extract water during respira-tion, minimizing water loss.36 In humans, con-servation mechanisms are poorly developed.Inhaled air is humidified to 100 percent as itreaches the alveoli. A small amount of thiswater is extracted during exhalation because ofthe slight degree of cooling of the air as weexhale. Because cool air holds less moisturethan warm air, a small amount of water is re-

FIG. 6. The primary inspiratory current is an arched path-way through the middle meatus.


covered during exhalation.36 The net balancefor human respiration is water loss of approx-imately 250 to 500 cc/day.37

Temperature Regulation

Air is heated almost to body temperaturebefore reaching the larynx. Even air at 5°C isheated to between 31°C and 37°C during in-spiration.38 This process requires 70 to 100 cal-ories per day. Some heat is resorbed duringexpiration, although humans lose most of theirexpiratory heat. Rather than use respiration astheir main method of heat release, humanslose most of their heat through their skin. Mostanimals, however, use respiration as their pri-mary mode of thermoregulation by panting.Thick layers of hair prevent effective heat lossthrough their skin.

Filtration

The nasal cavity uses four mechanisms for aircleaning (Table II). Impingement is the phe-nomenon by which particles suspended in agas are deposited on walls downstream from abend or constriction. Two such bands exist inthe nasal cavity—in the internal nasal valve,where the airstream is changed from a columninto a sheet, and at the posterior nasopharynx,where the airstream is sharply deflected inferi-orly. The impingement phenomenon causes85 to 90 percent of particulate matter greaterthan or equal to 5 microns to be deposited atthese two impingement areas. A negative elec-trostatic charge of particulate matter attracts it tothe positively charged mucociliary blanket.The zone of vibrissae just within the nares en-traps larger particles. Finally, the dynamic mu-cociliary blanket sweeps entrapped matter to thenasopharynx at a rate of approximately 1 cm/min.28 The mucous blanket is a thin, sticky,adhesive sheet with a pH slightly more acidicthan serum. It is produced by serous and mu-cous glands, and by the goblet cells of themucosa, at a rate of approximately 250 cc/day.The mucous blanket has two layers: the deeperlayer is thinner and less viscid, and it surroundsthe cilia; the superficial layer is thicker and

more viscid, and it houses the cilia tips.38 Thisorganization allows the cilia to beat (at 1000beats/minute) in a low viscosity layer while thetips of the cilia propel the more viscous outerlayer.

Olfaction

As previously described, olfaction is an al-most vestigial function of the nose. Our senseof taste is clearly enhanced by olfaction. Con-versely, unpleasant odors may serve as warningsignals for potential environmental dangers.There is also a strong association betweenodors and memory. Many causes of olfactorydisturbance are recognized; the most commonis ethmoid sinusitis. Other causes includetrauma, mechanical obstruction, endocrinedisorders, Kallmann’s syndrome (congenitalhypogonadism with anosmia), and variousmedications. Olfaction can be disturbed afternasal surgery, especially septal surgery; fortu-nately, this is most often temporary.

Phonation

The sinonasal vault plays a role in voice pro-duction. It serves as a resonance chamber toaffect pitch and as an escape valve for theproduction of vowels and consonants. Nasalsurgery has not been associated with change inresonance or voice. Septal perforations can,however, result in the production of nasal whis-tling during quiet respiration.

Secondary Sex Organ

A recent surge of interest in the humanvomeronasal organ (Jacobson’s organ, Ruyschtube) has shown the near-universal presence ofpaired bilateral blind ducts in the mucosa ofthe anterior third of the human septum.39–42

These organs contain specialized epithelium ofunknown function but are proposed to play arole in reproductive behavior as possible pher-omone chemosensory receptors. They exist asseparate and anatomically distinct units fromour olfactory system. Careful examination ofthe septal mucosa just posterior to the columel-lar base and 1 mm above the maxillary grooveoccasionally will reveal the presence of the ex-ternal opening of the duct.42 In addition, it isknown that mucosal engorgement occurs dur-ing sexual arousal.43

Nasal Cycle

Approximately 80 percent of the populationexperiences cyclical engorgement and contrac-

TABLE IIFour Filtration Mechanisms

ImpingementElectrostatic chargeVibrissaeMucociliary blanket


tion of the nasal mucosa (the cycle of Minz).While one airway is enlarging, the other isconstricting.8,43 Total airflow and resistance re-main constant throughout the process, whichrequires between 30 minutes to 5 hours percycle.36 The function of the nasal cycle is notknown.

EVALUATION

History

A careful history should always be obtainedof the duration and frequency of symptoms,unilateral versus bilateral disorder, perennialversus seasonal problems, previous trauma,prior nasal surgery, allergy symptoms, andmedications. It should be determined if a geo-graphic pattern exists to the nasal symptoms(e.g., only occurring at work, while outdoors,or during the spring when grass pollens aretypically heavy). This would indicate an atopicdisorder and would merit medical manage-ment and avoidance behavior. It is importantto differentiate obstruction during quietand/or heavy inspiration. Obstruction in bothinstances may indicate a fixed obstruction (i.e.,enlarged turbinate, significant septal deflec-tion, or mass), whereas obstruction that occursonly during heavy inspiration may indicate anincompetent valve.

Physical Examination

The patient is optimally evaluated whileseated in a chair with his or her head at the eyelevel of the examiner. Careful observation mayreveal valuable information. A patient withdark pigmentation in the lower eyelid and in-jected conjunctivae most likely has an allergiccomponent contributing to nasal obstruction.The alae are examined during respiration forcollapse of the external nasal valve. Palpationover the frontal, ethmoid, and maxillary si-nuses is performed to elicit tenderness, whichis a strong indication of sinusitis. The patient isasked to breathe through the nose while oc-cluding one nostril at a time to depict the worstside of the obstruction. The Cottle test is used toconfirm the presence of nasal valve pathology.While the patient breathes quietly, the cheek isretracted laterally to open the nasal valve. Ifbreathing is improved, the Cottle test is posi-tive and suggests an incompetent nasal valve.Alternatively, the valves can be evaluated bygently supporting them with a cotton tip appli-cator during quiet and heavy inspiration. The

seventh cranial nerve should be tested for anyfacial nerve weakness.

The basic instruments needed for adequateevaluation of the anterior nasal airway (anteri-or rhinoscopy) are a light source and nasalspeculum. Most important is a bright lightsource, optimally positioned coaxially to theline of vision of the examiner. Either a head-light or reflective mirror is adequate. The nasalspeculum is held in the dominant hand and isspread in a vertical fashion (Fig. 7), whichallows direct visualization of the anterior thirdof the nasal passage. Posterior rhinoscopy isindicated when the initial examination fails toreveal likely causes of obstruction, or if a dis-order in the posterior area is otherwise sus-pected. Visualization of the posterior passage ismost easily performed using either a 0-degreeor 25-degree nasal endoscope (posterior rhi-noscopy). Alternatively, using a warmed dentalmirror and looking through the oral cavity,while keeping external traction on the tongue,can be an indirect approach to examining theposterior passage. Posterior rhinoscopy re-quires much practice by the examiner becauseit is quite easy to cause significant discomfortor to elicit a gag reflex. One can detect poste-rior nasal masses, adenoid hypertrophy, orchoanal atresia.

Evaluation is performed before and after va-soconstricting the nasal mucosa, using 0.25%phenylephrine or 1% ephedrine sulfate, whichare most effectively applied by using a mistingdelivery system. If these agents are not avail-able, direct topical application using cottonoidpledgets is also useful. Topical cocaine is an-other time-honored agent effective for vaso-constriction and topical anesthesia.

FIG. 7. The proper method of anterior rhinoscopy is tospread the speculum in a vertical direction.


Inferior turbinate size is examined beforeand after vasoconstriction. If subjective nasalairway improvement is accompanied bymarked shrinkage of the turbinates, then stim-ulated erectile mucosa is the likely cause ofobstruction and will most likely respond tomedical management.

As the turbinates shrink from the vasocon-striction, other structural abnormalities maybecome more apparent. Middle and posteriorvault septal deviations or a dislocated caudalseptum may now be visible. One can also nowevaluate the internal nasal valve during quietand dynamic inspiration. A collapsing valve ora valve having less than a 10-degree angle mayrequire surgical intervention.

If, after vasoconstriction, no significant re-duction in size of the turbinates occurs, twopossibilities should be considered. The patientmay be an abuser of over-the-counter nasalsprays, or even cocaine. In these cases, themucosa seems erythematous and fragile, withprofuse watery rhinorrhea. The mucosa buildsa tolerance to decongestants over time. Oneshould carefully inspect for septal perforations,which occur with some frequency in this pop-ulation. Placing a light source into one nostrilwhile looking through the opposite nasal pas-sage often will reveal otherwise obscure septalperforations. More commonly, though, the tur-binates fail to shrink because of hypertrophy ofthe underlying conchal bone or fibrotic hyper-trophy of the conchal mucosa. These patientswill require surgery to improve their symptoms.

Some patients note subjective improvementdespite a lack of visible improvement in thenasal airway after vasoconstriction. Althoughthis may be a solely placebo effect, it morelikely is explained by a slight decrease in mu-cosal thickness, just enough to improve thepatient’s obstructive symptoms. In both cases,medical management is warranted.

The last scenario is that of the patient whodenies subjective improvement after vasocon-striction, despite showing significant objectiveimprovement. Such patients are unlikely to besatisfied regardless of the therapy delivered,and subsequent conservative medical manage-ment is best in such cases rather than surgery.Lack of improvement may be secondary tosome unforeseen secondary gain by the pa-tient. Disturbances in the normal pattern ofairflow can also create the sensation of nasal“stuffiness” by causing focal areas of dry mu-cosa and inspissated overlying mucosa.

One should note the presence of pus, pol-yps, and nasal masses; the color of the turbi-nates; and the presence of ulcerations, perfo-rations, and foreign bodies. Pale-coloredturbinate mucosa may indicate allergy, whereaserythematous mucosa may indicate infec-tion, inflammatory process, or rhinitismedicamentosa.

Rhinomanometry

Nasal resistance can be objectively quantifiedby measuring nasal pressure and airflow. Resis-tance is calculated from two measurements:nasal airflow and transnasal pressure differen-tial. Airflow is measured either with a nozzleseated in the naris or a tightly fitting mask overthe face. Transnasal pressure is measured byrelating pressure at the choanae to the pres-sure at the nares. Choanal pressure is mea-sured transorally. Constantian has contributedsignificantly with his work using rhinomanom-etry.32,44 Rhinomanometry has also been stud-ied extensively by Kern,34 Cottle,45 and McCaf-frey and Kern,46,47 and more extensively in theEuropean literature.48,49 A significant advance-ment in the value of rhinometry is the intro-duction of acoustic rhinometry,49–51 a noninva-sive method, based on acoustic reflections, ofmeasuring cross-sectional areas of the nose at agiven distance from the nostril. Acoustic rhi-nometry has been validated for its accuracy incomputed tomographic scanning52 and mag-netic resonance imaging53 studies from exami-nation of the nasal anatomy. It has been shownthat patients with abnormal preoperative rhi-nomanometry results tend to report better sub-jective improvement after surgery. Althoughthese tests are seemingly superfluous, managedcare is starting to require these preoperativestudies to be submitted before authorization oftreatment.

Nasal Cytology

Microscopic analysis of nasal mucus can beof help in differentiating allergic from infec-tious rhinosinusitis. A mucus sample issmeared on a slide and stained with Wright’sstain. The presence of eosinophils may be in-dicative of allergic rhinitis, whereas a largenumber of polymorphonucleocytes suggests in-fection.54 This test remains of unproved valueto date.


Radiology

Radiology is most commonly used for diag-nosing paranasal sinus disease. A Waters viewplain film may reveal air/fluid levels or sinusopacification, but too frequently it provides nosignificant or useful information. A paranasalsinus computed tomographic scan is the defin-itive standard for evaluating sinus disease. Acomputed tomographic or magnetic reso-nance imaging scan can also reveal obstructivemasses or anatomic abnormalities in the nasalairway.55

TREATMENT

Treatment is directed at the identified caus-e(s) of obstruction. It is important to realizethat there may be more than one cause, andtherefore more than one directed therapyindicated.

Rhinitis

Rhinitis is thought by some to be most com-mon cause of nasal obstruction.32 Rhinitis hasmany pathogeneses, and these will be discussedindividually (Table III).

Infectious rhinitis. The most common type,infectious rhinitis, is nearly always caused by avirus (rhinovirus, or “the common cold”). Al-though viral upper respiratory infections aretypically self-limiting, oral or topical deconges-tants are helpful during the acute phase (TableIV). Topical decongestants are safe, if used ona short-term basis to avoid rhinitis medicamen-tosa. A good rule of thumb is to recommendusing topical decongestants for no more than 3days at a time.56 Antibiotics are rarely indicatedunless the patient also develops secondarysinusitis.

Acute adult sinusitis is of Gram-positive bac-terial origin and is treated with a combinedregimen of saline nasal lavage, mucolyticagents (Table V), decongestants, and a 2- to3-week course of directed antibiotic treatment(Tables VI and VII).57–59 It is important to note

the extended course of antibiotic necessary toadequately treat bacterial sinusitis. Unique fea-tures of the sinus cavities and mucosa liningare responsible for this. Cilia of the mucosalining, responsible for mucus clearance, aredamaged during both viral and bacterial infec-tions and require 2 to 3 weeks for regenera-tion.60,61 Thus, even after initial clearance of aninfection with a short course of antibiotics,secondary mucostasis frequently leads to earlyreinfection, and often with resistant organisms.Mucosa edema is significant during infectionand lasts for several weeks. This can criticallynarrow drainage ostia and can again result inmucostasis and recurrent infection. Finally,poor antibiotic penetration into infected sinusmucosa may make complete bacterial eradica-tion difficult.

Allergic rhinitis. The prevalence of allergicrhinitis in the United States is between 14 and31 percent.62 True allergic rhinitis is an antigen-antibody reaction mediated by immunoglobu-lin E, most commonly occurring in seasonalform from an airborne pollen or fungal spore.Associated symptoms include sneezing, itching,and choryza. Many medication options areavailable for conservative medical manage-ment, each having its own specific indicationsfor use. The most useful classes of medicationsinclude decongestants, second-generation an-tihistamines63 (Table VIII), chromalyn sodiumnasal spray (mast cell stabilizer), nasal topicalsteroids (Table IX), ipratropium bromide nasalspray (anticholinergic), and steroid injection ofthe inferior turbinate.64 Often, these medica-tions are used in various combinations to max-imize the treatment for each patient. Systemic(oral) corticosteroids are infrequently indi-cated because of the variety and severity of po-tential adverse effects.57 Avoidance behavior is

TABLE VMucolytic Agents

GuiafenesinIodinated glycerolHumidification/steamNormal saline sprays

TABLE IIICauses of Rhinitis

InfectiousAllergicVasomotorAtrophicRhinitis medicamentosaPostoperativeHypertrophicOther

TABLE IVCommon Decongestants

Pseudoephedrine (oral)Phenylephrine (oral/topical)Oxymetazoline (topical)Xylometazoline (topical)


important if the particular antigen(s) can beidentified. When these treatment options proveinsufficient, referral to an allergist is warranted.Benninger et al.65 provide further useful elab-oration on medical management.

Bordley et al. first reported the effectivenessof steroids in the allergic patient in 1949.66

Wall and Shure followed in 1952 with a reportof submucosal infection of cortisone in theinferior turbinate.67 Inferior turbinate injec-tion of corticosteroids has been proved effec-tive in the temporary treatment of allergic rhi-nitis, rhinitis medicamentosa, postrhinoplastyrhinitis, vasomotor rhinitis, pregnancy-inducedrhinitis, and acute nasal polyposis.64,68 Ourmethod includes placing a small cotton ballsoaked in 2% aqueous lidocaine on the ante-rior head of the inferior turbinate for 4 min-utes. After removal of the cotton ball, 0.3 to 0.5cc of triamcinolone acetonide (40 mg/kg) isslowly injected intramucosally into the head ofthe inferior turbinate with a 27-gauge needleand a tuberculin syringe, forming a bleb. Min-imal pressure is used, and one will note themucosa blanching on injection. After with-drawing the needle, a small cotton ball soakedin phenylephrine is applied to the injectionsite and left for 5 minutes. The beneficial ef-fects should be noted by day 3, and they usuallylast 3 to 6 weeks. Possible adverse effects in-clude brief facial flushing, scant bleeding, anda rare incidence of temporary or permanentblindness.64,69 Visual loss, thought to be fromeither retrograde embolization of injected ma-

terial into the retinal circulation or retinal va-sospasm,69 is considered to be technique-dependent with an estimated incidence of0.006 percent.64 Mabry reports no visual com-plications in over 13,000 injections in his ownlarge study.68 Our experience has shown thistechnique to be safe and effective in the appro-priate patient.

Vasomotor rhinitis. An imbalance in the sym-pathetic/parasympathetic autonomic systemscan lead to continuous watery rhinorrhea. Nor-mally, the sympathetic system outbalances theparasympathetic drive and maintains mucosalvasoconstriction and decreased mucus produc-tion. The balance favors the parasympatheticsystem in vasomotor rhinitis. Although this con-dition may be related to emotional or endo-crine factors, including pregnancy, most oftenit is idiopathic. Conservative management withoral decongestants is the most common form oftherapy.

A more aggressive treatment option is a trans-nasal vidian neurectomy,70–73 which is an un-common treatment approach to intractablevasomotor rhinitis. The vidian nerve, whichcarries parasympathetic fibers from the greatersuperficial petrosal nerve and sympathetic fi-bers from the deep petrosal nerve en route toinnervation of the sinonasal mucosa, istransected at the level of the sphenopalatineforamen. The results may be transient, and theprocedure can be cumbersome with significantadverse effects. This procedure requiresproper surgical training and expertise in headand neck anatomy to minimize the risk ofcomplications.71–73

Atrophic rhinitis. Atrophic rhinitis has beenassociated with overaggressive turbinectomyprocedures, although this issue remains debat-ed.74,75 This rare condition is characterized by

TABLE VIAcute (Adult) Infectious Rhinosinusitis

TypeFrequency

(%)

Streptococcus pneumoniae 31Unencapsulated Haemophilus influenzae 21Anaerobes 6Staphylococcus aureus 4S. pyogenes 2Moraxella catarrhalis 2

TABLE VIIAcute Adult Infectious Rhinosinusitis-Effective Antibiotics

Amoxicillin/clavulanateCefuroximeCefaclorTrimethoprim/sulfamethoxisoleLoracarbefClarithromycinCefprozilLevofloxacin

TABLE IXNasal Steroid Sprays

Beclomethasone dipropionateDexamethazone sodium phosphateFlunisolideFluticasone propionateTriamcinalone acetonide

TABLE VIIISecond-Generation Antihistamines

ClaritinAllegraZyrtec


progressive, slow atrophy of the nasal mucosawith crusting and foul drainage (ozonae), typi-cally beginning at puberty.28 Several organismshave been grown from patients having thisbothersome condition, but their exact role inthe pathogenesis is unclear.76,77 Treatment con-sists of frequent nasal saline lavage. Althoughthe association of this disease with turbinectomyprocedures is widely questioned, this potentialcomplication may behoove the rhinoplasty sur-geon to consider a more conservative approachto turbinoplasty.

Rhinitis medicamentosa. Rhinitis medicamen-tosa occurs frequently in patients with nasalobstruction, and the appropriate history shouldalways be sought. Prolonged use of sympatho-mimetic nasal drops or sprays (e.g., Afrin,Dristan, Neosynephrine) leads to tachyphylaxis,resulting in a rebound phenomenon with mu-cosal engorgement and profuse rhinorrhea.The patient should be instructed to halt the useof these medications, but complete resolutionoften takes several weeks. A short course of oralsteroids is helpful during the withdrawal phase.

Postrhinoplasty rhinitis. In postrhinoplastyrhinitis, postoperative nasal obstruction symp-toms are common. Almost all patients experi-ence some obstruction from transient mucosaledema and crusting, and appropriate preoper-ative counseling is provided. Patients with pre-operative allergic disorders or vasomotor rhi-nitis may experience a transient postoperativeexacerbation of their condition. Beekhuisfound a 10 percent incidence of postoperativeobstructive symptoms in his rhinoplasty pa-tients.24 Often, no treatment is required exceptreassurance to the patient that the condition isself-limiting. If deemed necessary, oral decon-gestants, topical nasal steroid sprays, or turbi-nate steroid injection can be offered as intervaltreatment.

Hypertrophic rhinitis. Chronic inflammatoryconditions may lead to turbinate hypertrophy.This will be further discussed with turbinatedisorders.

Miscellaneous causes of rhinitis. Systemicpharmaceuticals such as oral contraceptives, be-ta-blocker antihypertensives, and antidepres-sants have been implicated as causes of rhinitis.Infrequent additional causes include Wegen-er’s granulomatosis, lethal midline granuloma(polymorphic reticulosis), cystic fibrosis, syph-ilis, hypothyroidism, and poorly controlleddiabetes.28,54

Turbinate Disorders

The medical management of certain inflam-matory conditions of the inferior turbinateshas already been discussed. Chronic mucosalswelling may result in hyperplastic turbinates.Histologic examination shows mucous glandenlargement, thickening of the basementmembrane, and interstitial fibrosis. Hypertro-phy of the conchal bone is the last stage. Dis-orders of the inferior turbinate, diagnosed byfailure of the mucosa to shrink after vasocon-striction and necessitating surgical manage-ment, include bony and/or chronic mucosahypertrophy, with the goal being reduction ofthe turbinate mass. Hypertrophic rhinitis canonly be managed effectively with surgical inter-vention with turbinoplasty.

Complete turbinectomy has fallen out of fa-vor, because the important physiologic role ofthe inferior turbinate is now better under-stood. This procedure may put the patient atincreased risk for developing atrophic rhinitis,although it is our opinion that the risk hasnot been definitively proved. Nevertheless,we advocate a more limited approach toturbinoplasty.

A limited excision of the anterior third ofthe turbinate may be the best overall surgicalapproach, in our opinion. As described byMabry, a medial mucoperiosteal flap is ele-vated and laid back down over the resectededge of the conchal bone. This approach de-creases the risk of postoperative bleeding fromthe raw bone edge, relieves obstruction at thelevel of the internal nasal valve, and preservesportions of the turbinate that are unlikely tocontribute to airway obstruction.78

Principato described his success using turbi-nate cryosurgery on more than 1400 pa-tients.79,80 This method induces mucosal injuryby intracellular crystal formation and ischemicinfarction and, therefore, is limited to cases ofmucosa hypertrophy. Prolonged crusting is areported complication.

Placement of an electrocautery needle intothe submucosa of the turbinate is an alterna-tive approach. This option is limited to mucosahypertrophy cases and has been associated withprolonged crusting, discomfort, delayed epi-staxis, and recurrence of the hypertrophiedcondition.74

Laser turbinoplasty has gained some popu-larity. Various lasers have been described forthis technique, including the neodymium yttri-


um-argon-garnet laser contact system, CO2 la-ser, potassium-titanyl-phosphate laser, argonlaser, holmium yttrium-argon-garnet laser, andmagnet laser. Lasers allow for a quick and rel-atively bloodless turbinoplasty81– 88 and aremost appropriate when the obstruction is dueto hypertrophy of the turbinate mucosa. It istheorized that after laser application, scar for-mation within the submucosa impairs local al-lergic inflammation and decreases the thick-ness of the mucosa.89

All procedures may be coupled with turbinateoutfracturing. This maneuver physically relocatesthe head of the inferior turbinate more laterally,thus theoretically increasing the cross-sectionalarea at the internal nasal valve. This might pro-vide only temporary benefit, however, becausethe turbinate may gradually return to its originalposition postoperatively.90,91

Guyuron objectively showed the potentialdecrease in nasal airway after various nasal os-teotomies. He recommended simultaneousturbinate reduction if medial transposition ofthe turbinate is noted after completion of theosteotomy. A high-to-low approach may mini-mize this risk.92

Courtiss provided long-term follow-up of re-duction turbinoplasty patients and saw no casesof atrophic rhinitis. He reported a small inci-dence of recurrent turbinate hypertrophy andsynechiae formation.93–95

Many authors have asserted that inferior tur-binate enlargement is the most frequent causeof nasal airway obstruction (Table X). The in-ferior turbinate is not the only turbinate thatcan obstruct airflow, however. The middle tur-binate may become too large because of anenlarged air cell, called a concha bullosa. Endo-scopic resection of the lateral wall of the air cellwill relieve the obstruction.96 Polypoid degen-eration of the middle turbinate results fromsevere atopy. These polyps usually originatefrom the lateral surface of the middle turbinatebut may progress to occlude the entire nasal

passage and sinus cavities (Fig. 8). On occa-sion, these polyps will resolve completely, al-beit temporarily, with a pulse dose of oral cor-ticosteroids. The long-term maintenanceprotocol typically required to control recur-rence of the polyps consists of nasal salinelavage, topical nasal steroid sprays, or intrana-sal inferior turbinate steroid injection, antihis-tamines, and chromalyn sodium. In addition,prolonged immunotherapy by a trained aller-gist may be required. Immunotherapy hasbeen proved effective for managing allergicrhinitis, but the required prolonged durationof therapy makes immunotherapy less popularfor some patients. Some of these patients willeventually require endoscopic sinus surgery be-cause of the recidivistic nature of allergic pol-ypoid sinus disease.97

Internal Nasal Valve

An increasingly important role of the nasalvalves as the cause for nasal airway obstructionhas been elucidated by the studies of Constantianand Clardy,32 Constantian,44 and Sheen.98 It islikely that the valves contribute much more toobstruction than previously realized and that theseptum may play a much smaller overall role.

Internal nasal valve incompetence can beeither primary or secondary. Several primarycauses have been alluded to previously. Second-ary causes deserve further mention. Most impor-tant is understanding the mechanisms causingsecondary incompetence and how to prevent it.

Dorsal hump resection is a common compo-nent of reduction rhinoplasty. Care should betaken to free the medial portion of the upperlateral cartilage and mucosa from the septum ifthe hump resection puts this junction at risk.Not doing so risks injury and destabilization ofthis complex and may result in collapse of theinternal nasal valve. Moreover, scar tissue maydeform the normal 10- to 15-degree angle orcause obstruction by webbing or mass effect.The medial upper lateral cartilages should beanatomically stabilized to the septum beforeclosure.

If the internal nasal valve is acutely angledless than 10 degrees, a spreader graft should besecured between the upper lateral cartilageand septum. If a shortage of vestibular skin iscausing a web, either a skin or mucosal graft isindicated. As noted by Goode,99 one should“replace what is missing with like material.” Ifthe problem is an absence or weakening oflower or upper lateral cartilage, then a carti-

TABLE XCauses of Nasal Airway Obstruction

Inferior turbinateSeptumPolypsConcha bullosaInternal nasal valveExternal nasal valveTumorsCongenital


lage graft is indicated. Lack of both indicates acomposite graft.

Scar tissue causing a valve web should beexcised and replaced with a patterned graft.Common donor sites include the upper eyelidskin, postauricular skin, and buccal/labial mu-cosa. The valve should then either be stentedwith Xeroform gauze or splinted to preventearly recurrence.100

In patients with combined incompetent skinand cartilage, a composite ear graft is com-monly used. Again, a patterned excision andgraft should be performed. As an alternative, atwo-stage procedure can be done with initialskin grafting, followed by a secondary cartilagegraft. Either a stent or splint should beused.100,101

Many techniques have been described forthe management of cases with incompetentcartilage support or narrowed nasal valve an-gle. Perhaps the most significant is thespreader graft popularized by Sheen. A carti-lage graft is placed between the septum andthe upper lateral cartilage (Fig. 9). These graftsare designed to lateralize the upper lateral car-tilage and increase the cross-sectional ar-ea.98,102,103 Stucker and Hoasjoe placed conchalcartilage over the nasal dorsum and securedthe upper lateral cartilages to the graft, thus

increasing the angle.104 Parks described a su-ture technique that spans over the dorsal sep-tum and connects the upper lateral cartilages.Tightening of this flaring suture allows incre-mental adjustment of the valve.105

Septum

Constantian and Cardy illuminated a possi-bly less important role of the septum as a pri-mary cause of nasal airway obstruction.32 Notall deviated septa need correction, as it is com-mon to have an asymptomatic septal devia-

FIG. 8. Advanced sinonasal polyposis, shown by the arrows on the left, obliterating the nasalairway and sinus cavities. Compare this with the images in the right panel, which show a patentsinonasal passage but a deviated septum with compensatory right inferior turbinate hypertrophy.

FIG. 9. The proper placement of a spreader graft isshown.


tion.106 When deviation occurs anteriorly andinferiorly (i.e., in the area of the internal nasalvalve), it is more likely to be a source ofobstruction.

A surgical approach to the septum may beperformed by means of an open or closed rhi-noplasty approach. The most important maxim isto preserve as much cartilage as possible. Autoge-nous septal cartilage is a valuable commoditywith many indicated uses in plastic surgery.Only the obstructive elements should be ex-cised or manipulated. When the septum isshifted from the bony crest, the mucoperi-chondrium is freed on both sides to allow re-location to the crest and/or anterior maxillaryspine.107 After the mucoperichondrium is ele-vated, the anatomic deformity is reassessed.Depending on the type of deformity, four dif-ferent options are available: resection, mor-selization, crosshatching, or swinging doorflaps.108 In all cases, an intact L-strut, 8 to 10mm wide, is maintained for support (Fig. 10).

For septal deflections located more posteriorlyin the zone of the bony septum, Gruber andLesavoy described a closed septal osteotomy.109

External Nasal Valve

The anatomy of the external nasal valve hasbeen previously described. Normal function ofthis valve depends on adequate soft-tissue cov-erage, functional perinasal musculature, andskeletal stability. Violation of the structural in-tegrity of the valve may be a congenital oracquired phenomenon. Some of the potentialcauses include facial nerve palsy, unstablelower lateral cartilages, pinched ala deformity,and vestibular stenosis. Diagnosis can be madeby observation during quiet and forced inspi-ration while supporting the external nasal valvewith a cotton-tipped applicator.44

Treatment varies with the exact nature of theobstruction. Gunter and Friedman described alateral crural strut graft for treating alar rimcollapse, concave lateral crura, and malposi-tioned lateral crura.110 In their technique, au-togenous cartilage is sutured to the deep sur-face of the lateral crura. Teichgraeber treatedsimilar deformities using lateral crural span-ning grafts to support the area of greatest col-lapse.111 Parks used suture techniques to sup-port the upper lateral cartilages, but theseprocedures could be used on the lower lateralcartilages as well.105 McCollough and Fedokreported using the excised cartilage from acephalic trim to treat the pinched aladeformity.112

For external nasal valve deformities involv-ing both cartilage and vestibular skin, Sheenand Sheen113 and Kamer and McQuown114 de-scribed patterned auricular composite grafts.For vestibular stenosis accompanied by alarbase malposition, Constantian115 describedtreatment with an alar base flap. In Constan-tian’s experience, this combined deformity ismost frequently a result of previous rhinoplastyand overresection of the alar base.

CONCLUSIONS

This review demonstrates that the nose is acomplex, multifunctional organ that requiresrespect and understanding from the rhino-plasty surgeon. Treatment of the nasal airwayvaries with the etiologic and pathologic char-acteristics of the problem. Management canfrequently be accomplished using nonsurgicalmethods. For those problems requiring surgi-cal intervention, recent advances in our under-

FIG. 10. Submucoperichondrial flap elevation of cartilag-inous septum, leaving an intact 8- to 10-mm L-strut forsupport.


standing have elucidated a more importantrole of the nasal valves in airway patency, andperhaps a less important role of the septum. Athorough grasp of knowledge of the nasal air-way will allow proper evaluation, diagnosis, andtreatment of nasal airway problems.

Rod J. Rohrich, M.D.Department of Plastic SurgeryUniversity of Texas Southwestern Medical Center5323 Harry Hines Boulevard, E7.210Dallas, Texas [email protected]

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Self-Assessment Examination follows onthe next page.


Self-Assessment Examination

Understanding the Nasal Airway: Principles and Practiceby Brian K. Howard, M.D., and Rod J. Rohrich, M.D.

1. WHICH OF THE FOLLOWING IS NOT CONSIDERED A PRIMARY FUNCTION OF THE NOSE?A) PhonationB) ThermoregulationC) HumidificationD) Mucus productionE) Air filtration

2. OF THE FOLLOWING, WHICH IS THOUGHT TO BE THE MOST FREQUENT CAUSE OF NASAL AIRWAYOBSTRUCTION?A) Post-rhinoplasty rhinitisB) Turbinate disordersC) Rhinitis medicamentosaD) TraumaE) Ozonae

3. THE MOST IMPORTANT EXTRINSIC DILATORY MUSCLE IS:A) Zygomaticus minorB) RisoriusC) Pars transversaD) Zygomaticus majorE) Levator labii superioris alaeque nasi

4. THE FOLLOWING STEPS ARE IMPORTANT PARTS OF A GOOD NASAL AIRWAY EXAMINATION, EXCEPT:A) A careful historyB) Orthostatic turbinate changesC) Anterior rhinoscopyD) Nasal valve evaluationE) Mucosal vasoconstriction

5. SUBJECTIVE IMPROVEMENT OF NASAL OBSTRUCTION FOLLOWING SURGERY IS BEST PREDICTED BY:A) Cottle testB) Presence of normal nasal cycleC) Abnormal preoperative rhinomanometry resultsD) Turbinate hypertrophyE) History of nasal trauma

6. THE MAJORITY OF TOTAL AIRWAY RESISTANCE USUALLY OCCURS AT THE:A) Limen vestibuliB) Olfactory mucosaC) Keystone areaD) Distal alveoliE) Internal nasal valve

7. WHICH OF THE FOLLOWING IS THE BEST TREATMENT FOR POST-RHINOPLASTY RHINITIS?A) Vidian neurectomyB) Saline nasal lavagesC) SeptoplastyD) No treatmentE) Inferior turbinectomy

8. TREATMENT OF AIRWAY OBSTRUCTION AT THE LEVEL OF THE INTERNAL NASAL VALVE INCLUDES:A) Alar base flapB) Lateral osteotomiesC) Resection of the upper lateral cartilagesD) Cephalic trimE) Spreader graft

9. OVERAGGRESSIVE RESECTION OF THE INFERIOR TURBINATES HAS BEEN ASSOCIATED WITH:A) Septal perforationB) Atrophic rhinitisC) Cerebrospinal fluid leakD) Cosmetic deformityE) Diplopia

10. APPROPRIATE MANAGEMENT OF A SYMPTOMATIC DEVIATED SEPTUM INCLUDES ALL EXCEPT:A) Limited submucous resectionB) Closed septal osteotomyC) MorselizationD) Leaving an intact 8- to 10-mm strutE) Total septectomy

To complete the examination for CME credit, turn to page 1218 for instructions and the response form.

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