Turbinate Reduction Rhinoplasty 

Updated: Oct 31, 2018
Author: Elizabeth Whitaker, MD, FACS; Chief Editor: Mark S Granick, MD, FACS 

Overview

History of the Procedure

Inferior turbinate surgery dates to the 1890s when Jones first described it. In 1900, Holmes described the stages of inferior turbinate hypertrophy and his surgical experience with 1500 turbinectomies. Turbinectomy later fell out of favor because of rising concern over complications such as rhinitis sicca, atrophic rhinitis, and ozena. The enlarged nasal cavity resulting from turbinate resection was believed to increase nasal airflow and reduce the humidifying capabilities of the nasal mucosa, resulting in drying, crusting, and mucosal atrophy. However, several studies have reported large series of turbinectomies without these complications. This aspect of turbinate surgery remains controversial.

Problem

Nasal obstruction after rhinoplasty can result from alteration of the nasal valve or nasal vault narrowing as a result of osteotomies. Beekhuis concluded that nasal obstruction postrhinoplasty resulted primarily from inferior turbinate hypertrophy.[1] Changes in nasal airflow as a result of rhinoplasty may unmask inferior turbinate hypertrophy and obstruction that were not clinically significant or evident preoperatively. See the image below.

(A) Endoscopic view of left nares showing caudal s (A) Endoscopic view of left nares showing caudal septal deflection to the left. (B) Endoscopic view of right nares showing compensatory right inferior turbinate hypertrophy.

Etiology

Mink described the nasal valve in 1903. The nasal valve is formed medially by the septum and laterally by the caudal edge of the upper lateral cartilage and it accounts for approximately 50% of total upper airway resistance. The anterior tip of the inferior turbinate is found in the nasal valve region, and hypertrophy of this structure can cause exponential increases in airway resistance.

Inferior turbinate hypertrophy can result from mucosal hypertrophy, bony hypertrophy, or both. Bony hypertrophy causes a fixed structural obstruction and is best treated with surgery. More commonly, the problem is mucosal hypertrophy causing impingement on the nasal valve, increased nasal resistance, and nasal obstruction. This can be managed medically or surgically depending on the degree of hypertrophy and responsiveness to medical management.

Pathophysiology

The nose is a complex and highly specialized organ that plays a role in olfaction, heat exchange, speech production, respiration, humidification, filtration, and antimicrobial defense.

Mucus production is provided by goblet cells and submucosal and seromucous glands. Mucus production is primarily controlled by parasympathetic innervation. The mucous blanket serves to humidify and clean the inspired air and eliminate debris from the nasal airway.

Nasal obstruction may be produced by overactivity of the parasympathetic innervation or underactivity of the sympathetic innervation. Resistance is important in nasal function and turbulence optimizes inspiratory air contact with the mucous membrane. Resistance must remain within certain limits for the perception of normal breathing. If it is too high or too low, a sensation of obstruction may occur. A cyclic alteration of constriction and dilation of the inferior turbinates, known as the nasal cycle, occurs approximately every 2-7 hours.

The nasal valve provides approximately 50% of total airway resistance. The nasal valve is the region of the nasal airway extending from the caudal end of the upper lateral cartilages and including the anterior end of the inferior turbinate. As airflow enters this constricted segment, it accelerates and the pressure drops (per Bernoulli principle), which can result in nasal valve collapse if the upper lateral cartilages are anatomically weak. The erectile tissue of the nasal septum and inferior turbinate can impinge on the nasal valve and increase resistance. Because the cross-sectional area of the nasal valve is small, minor changes in inferior turbinate congestion can have marked effects on resistance. A major determinant of resistance to airflow is the radius of the nasal vault. However, even in the presence of a normal radius, a sensation of obstruction can occur from turbulent airflow.

Presentation

History

Nasal obstruction is a common complaint. Discerning the etiology is important so that appropriate treatment can be initiated. History should address any alteration or unilaterality of the obstruction, which may indicate a dynamic versus structural problem.

Address symptoms of rhinitis. Obstruction, rhinorrhea, and sneezing may occur with allergic and nonallergic rhinitis. Elicit systemic symptoms of allergy such as watery itchy eyes, asthma, and seasonal variation. Initial general examination should note "allergic shiners" or a facial appearance that may indicate signs of chronic nasal obstruction. Vasomotor rhinitis is typically exacerbated by irritants, temperature or humidity changes, or psychological factors. Nonallergic eosinophilic rhinitis is generally perennial without allergen-induced symptoms. Atrophic rhinitis is characterized by nasal dryness and crusting, frequently with a foul odor. Rhinitis can also be associated with pregnancy and with systemic disorders such as hypothyroidism.

Medications can also cause rhinitis and nasal obstruction. Rhinitis medicamentosa results from rebound vasodilation after prolonged use of topical nasal decongestants. Typically the patient begins using the topical agent to treat an underlying disorder causing the nasal obstruction. Other medications causing increased nasal congestion include certain antihypertensives, antidepressants, antipsychotics, and oral contraceptives.

Examination

Physical examination of the external nose is, of course, critical. In addition to assessing nasal aesthetics, note the patency of the nasal valve and any alar collapse since these may need to be addressed to ensure functionality of the nose postrhinoplasty. The Cottle maneuver involves pulling the patient's cheek laterally to open the nasal valve angle. If nasal airflow symptomatically improves, this may indicate nasal valve pathology. A crooked nose may indicate prior trauma and this history should be elicited. A saddle nose deformity may indicate previous trauma, prior surgery, cocaine abuse, or an inflammatory process.

Additionally, the focus of the physical examination is anterior rhinoscopy, which reveals caudal septal deformities or inferior turbinate hypertrophy that may account for the patient's symptoms. If the patient has a significant caudal septal deflection, typically the inferior turbinate on the side opposite the deviation is enlarged. Apply topical decongestant to evaluate the response of the turbinate mucosa. This may assist in delineating mucosal versus bony hypertrophy.

If indicated based on history, symptoms, or signs, a more extensive examination of the nose can be performed via a rigid or flexible endoscope. This examination allows additional assessment of the septum posteriorly, the nasopharynx, and the sinus ostia. Nasal masses or polyps as a cause of obstruction can be evaluated. Purulent drainage may indicate sinusitis. Evidence of a septal perforation may indicate prior surgery, cocaine or topical decongestant abuse, or an inflammatory disease. Significant crusting or abnormality of the mucosal appearance may indicate a systemic disorder.

History or symptoms and signs of other systemic disorders that may affect the nose and turbinates warrant further investigation. Wegener granulomatosis and sarcoid can result in nasal obstruction and crusting. Infectious rhinitis can result from a variety of organism-caused conditions such as rhinoscleroma, tuberculosis, syphilis, rhinosporidiosis, histoplasmosis, and aspergillosis. If suspected, address a history of exposure and travel and perform further appropriate testing. A significant history of epistaxis may raise the concern of an inflammatory or neoplastic process.

Indications

Nasal obstruction may result from mucosal hypertrophy of the inferior turbinate, structural deformity of the nasal airway (septal deviation, bony inferior turbinate hypertrophy), or dynamic airway collapse.

Typically, in the patient with significant nasal septal deviation, unilateral compensatory turbinate hypertrophy may be present on the side opposite the deviation. However, if the septal deviation is S shaped or deflections exist bilaterally, then bilateral inferior turbinate enlargement may be present. If the hypertrophied turbinate is not addressed, nasal airway obstruction may persist despite correction of septal deformities.

Similarly, relative inferior turbinate hypertrophy occurs in patients with a narrow nasal vault either inherently or secondary to rhinoplasty maneuvers. Failure to perform reduction of the inferior turbinates may result in nasal airway obstruction despite correction of any septal deformities.

Relevant Anatomy

Lateral nasal wall

The lateral nasal wall is composed of the nasal, frontal, occipital, lacrimal, ethmoid, maxillary, and palatine bones. The inferior turbinate constitutes a separate bone and articulates with the maxilla, lacrimal, ethmoid, and palatine bones. The superior and middle turbinates project off the ethmoid bone. The lacrimal process of the inferior turbinate forms the medial wall of the nasolacrimal duct, which drains into the inferior meatus.

Nasal valve

The nasal valve is formed laterally by the caudal end of the upper lateral cartilages and medially by the septum. The anterior tip of the inferior turbinate lies in the area of the nasal valve.

Nasal mucosa

The nasal vestibule, constituting the first 1-2 cm of the nasal cavity, is lined with keratinized, stratified squamous epithelium containing hair follicles and sebaceous and sweat glands. At the mucocutaneous junction (limen nasi), the epithelium transitions to pseudostratified ciliated columnar cells. This epithelium lines most of the sinonasal tract with the exception of the olfactory mucosa.

Blood supply

The arterial blood supply to the nose originates from the maxillary and facial branches of the external carotid artery and from the ophthalmic branch of the internal carotid artery. The anterior facial vein, sphenopalatine vein, and ethmoid vein supply venous drainage. The nasal vasculature is composed of arterioles, submucosal capillary beds, and venules. Specifically, the nasal vasculature of the inferior turbinate is a sinusoidal network of large capacitance vessels. These sinusoidal vessels are found primarily in the inferior turbinate and the anterior septum. The result is that the inferior turbinate functions as erectile tissue.

Constriction of postsinusoidal venules results in engorgement of the sinusoids and an enlargement of the nasal turbinates. In addition, multiple direct arteriovenous anastomoses bypass the capillary beds. This allows significant increases in blood flow and heat exchange without a great increase in nasal blood volume, which facilitates the temperature regulatory function of the inferior turbinates. The nasal mucosal vasculature is intimately related to its autonomic innervation.

Innervation

In general, the nose is innervated by the olfactory nerve, branches of the ophthalmic and maxillary divisions of the trigeminal nerve, parasympathetic secretomotor fibers, and sympathetic fibers. The autonomic nerve supply to the nose regulates vascular tone, turbinate congestion, and nasal secretion. Parasympathetic fibers synapse in the sphenopalatine ganglion before innervating nasal mucosa. These fibers travel with the facial nerve, exiting at the geniculate ganglion as the greater superficial petrosal nerve. The vidian nerve is formed by the union of the greater superficial petrosal and deep petrosal nerves and carries the fibers to the sphenopalatine ganglion, where they synapse.

Sympathetic fibers also pass through the sphenopalatine ganglion but do not synapse there. The sympathetic fibers exit the spine and travel in the cervical sympathetic trunk, synapsing in the superior cervical ganglion. Postsynaptic fibers contribute to the sympathetic plexus of the internal carotid artery from which the deep petrosal nerve originates. It then joins with the greater superficial petrosal nerve to form the vidian nerve and its fibers pass through the sphenopalatine ganglion and along branches of the trigeminal nerve and nasal blood vessels. Thus, branches of the sphenopalatine ganglion carry sympathetic, parasympathetic, and trigeminal fibers.

Contraindications

The inferior turbinates are very vascular structures and one of the risks of surgery is hemorrhage. Patients with coagulopathies are clearly at increased risk of complications. Similarly, patients should not be taking any medications or herbs that affect their coagulation cascade.

Take care when resecting turbinate tissue in patients who have preexisting reports of nasal dryness and crusting secondary to the concern about atrophic rhinitis.

 

Workup

Imaging Studies

CT

CT is not indicated in the workup of inferior turbinate hypertrophy alone. However, if a CT scan of the head, facial bones, or sinuses has been obtained for other reasons, it may provide useful information. Axial and particularly coronal images can help assess the amount of bony versus mucosal hypertrophy.

If clinical presentation raises the concern of other obstructive processes such as nasal polyps or masses, perform CT imaging of the nose and sinuses.

Other Tests

Rhinomanometry

Rhinomanometry is a technique for measuring nasal airway resistance. It is limited in that it does not provide a diagnosis or etiology of the obstruction. It provides a measure of nasal resistance at a specific time.

Perform the technique by applying a tight-fitting mask with a central aperture connected to a low-resistance pneumotachograph flow meter. Measure transnasal pressure at the nostril with a catheter with a pressure-tight seal. A second catheter measures air pressure in the mask. The catheters are attached to a differential pressure transducer and the outputs are recorded as a pressure flow diagram.

This technology has been used in a variety of studies to document changes in nasal resistance with nasal surgery. It has also been used to try and differentiate mucosal from bony hypertrophy with variable results. The use of this technique in routine clinical practice has not been demonstrated.

Allergy testing

The microscopic analysis of nasal mucus for eosinophils can be useful in making the diagnosis of allergic rhinitis.

Patients with allergic rhinitis that is not responsive to medications such as topical corticosteroids and antihistamines may benefit from allergy testing and possible immunotherapy.

Diagnostic Procedures

Rigid nasal endoscopy

When indicated by clinical presentation, more extensive examination of the nose can be performed with a rigid or flexible endoscope. This examination allows additional assessment of the septum posteriorly, the nasopharynx, and the sinus ostia. Nasal masses or polyps as a cause of obstruction can be evaluated.

Purulent drainage may indicate sinusitis. Evidence of a septal perforation may indicate prior surgery, cocaine or topical decongestant abuse, or an inflammatory disease. Significant crusting or abnormality of the mucosal appearance may indicate a systemic disorder.

 

Treatment

Medical Therapy

Medical therapy focuses on treatment of conditions causing mucosal hypertrophy, primarily allergic and vasomotor rhinitis. Allergic rhinitis is addressed with topical glucocorticoids, which decrease capillary permeability, produce vasoconstriction, and reduce edema and inflammation in the nasal mucosa. Antihistamines block the uptake of histamine by target cell receptors and may inhibit the release of inflammatory mediators.

Adrenergic drugs (eg, phenylamines, imidazolines) serve to decrease mucosal congestion and edema. Topical adrenergics can result in rebound nasal congestion, causing rhinitis medicamentosa and irreversible mucosal change. Therefore, restrict their use to approximately 3 days only. Oral adrenergics can cause cardiovascular complications in patients prone to this condition and should be used carefully in patients with hypertension, coronary artery disease, or stroke. Topical glucocorticoids, antihistamines, and adrenergics are also useful in the treatment of eosinophilic nonallergic rhinitis.

Vasomotor rhinitis involves overactive parasympathetic stimulation resulting in vasodilation, edema, and mucous hypersecretion. Irritants, extremes of temperature and humidity, and psychological factors can exacerbate these symptoms. The anticholinergic effects of antihistamines may reduce nasal secretions and topical glucocorticoids may reduce inflammatory mediator release. Topical ipratropium bromide is an anticholinergic agent reducing submucosal gland secretion.

Rhinitis medicamentosa results from rebound vasodilation after prolonged use of topical nasal decongestants. Typically the patient begins using the topical agent to treat an underlying disorder causing nasal obstruction. This disorder still needs to be evaluated. Treatment involves stopping the topical nasal decongestants. Topical glucocorticoids and possibly oral glucocorticoid agents can help minimize edema and inflammation and can be of significant benefit in obtaining compliance with cessation of decongestants.

Other medications causing increased nasal congestion include certain antihypertensives, antidepressants, antipsychotics, and oral contraceptives. If these are suspected, try alternative medications. The submucosal injection of corticosteroids has also been used to offer relief from nasal obstruction by reducing turbinate edema. This technique can be used in a variety of clinical settings including allergy, vasomotor rhinitis, rhinitis medicamentosa, and postseptorhinoplasty. The results are rapid in onset with little systemic adverse effects. However, the results are temporary, lasting weeks to months. This technique serves as a temporizing measure, not as a permanent solution.

Surgical Therapy

Surgical therapies can be categorized into those that reposition the turbinate, address mucosal hypertrophy, address bony hypertrophy, or address both mucosal and bony hypertrophy.

Repositioning the turbinate laterally within the nasal valve area is accomplished by lateral outfracture. See the image below.

Lateral outfracture. Lateral outfracture.

This technique does not address either mucosal or bony hypertrophy but rather the spatial relation of the inferior turbinate within the nasal valve.

Mucosal hypertrophy can be addressed by various techniques focusing either on the mucosal surface or intramurally. The mucosa and submucosa can be addressed with surface electrocautery or laser vaporization. Intramural techniques are designed to produce submucosal tissue injury while preserving overlying mucosa. The resultant tissue loss and subsequent scarring lead to a reduction in bulk of the inferior turbinate mucosa and submucosa. This can be accomplished with cautery (monopolar or bipolar), cryotherapy, or radiofrequency ablation.[2] See the image below.

Intramural cautery. Intramural cautery.

Bony hypertrophy is addressed by submucous resection.[3] A periosteal flap is developed and the underlying bone removed. The flap is then replaced, preserving mucosa and submucosa. See the image below.

Submucous resection. Submucous resection.

Finally, mucosal and bony hypertrophies are best dealt with via a partial inferior turbinectomy or inferior turbinoplasty.[4] A total inferior turbinectomy can be performed but concerns over atrophic rhinitis limit the applicability of this technique. See the images below.

Partial inferior turbinectomy. Partial inferior turbinectomy.
Inferior turbinoplasty. Inferior turbinoplasty.
Total inferior turbinectomy. Total inferior turbinectomy.

 

A retrospective study by Karlsson et al indicated that in patients undergoing septoplasty, concomitant performance of inferior turbinate reduction may reduce the need for revision nasal surgery. The study involved 788 patients who were treated with septoplasty alone, along with 1380 patients who underwent septoplasty and concomitant inferior turbinate reduction, with 5.1% of the septoplasty-only patients subsequently undergoing revision, compared with 2.2% of the septoplasty/turbinate reduction patients.[5]

Preoperative Details

Preoperatively, address risks including but not limited to bleeding, dryness, and crusting. If mucosal hypertrophy is believed to be the primary source of obstruction, a variety of techniques can be used. Many of these techniques depend on inducing tissue damage, with subsequent scarring and contracture, rather than direct tissue excision to reduce turbinate bulk. Therefore, the long-term results are not easily predictable. Counsel patients that if less reduction of turbinate bulk is obtained than is ideal for symptomatic improvement, the procedures may need to be repeated. Additionally, counsel patients with allergic, vasomotor, or other forms of rhinitis that medical therapy likely remains necessary to maximally control their obstructive symptoms.

After visual inspection, topically decongest the turbinates with application of a decongestant on nasal pledgets. If the procedure is performed under local anesthesia, also apply topical anesthetic. This allows vasoconstriction of the turbinate vasculature to decrease risk of intraoperative bleeding and facilitate technical performance of the surgery. Decongestion of the turbinates may be necessary in performing adjunctive septoplasty, if indicated, to allow visualization and access to the septum.

Intraoperative Details

Inferior turbinectomy

Place an elevator underneath the turbinate, infracturing it medially. Then place turbinate scissors with one blade beneath the turbinate and the other on top, removing both the bony and soft tissue of the turbinate. Electrocautery can then be applied to the cut edge for hemostasis, followed by nasal packing against the cut surface.

The primary advantage of this procedure is addressing both bony and mucosal hypertrophy of the entire length of the turbinate. Disadvantages are the risk of bleeding and postoperative crusting. Long-term concerns are rhinitis sicca, ozena, and atrophic rhinitis.

Inferior turbinoplasty

Use an elevator to fracture and mobilize the inferior turbinate. Then make an incision along the anterior tip of the turbinate at its lateral insertion. Extend this downward and halfway along the anterior length of the turbinate.[6]

Create a tunnel with a Freer elevator along the medial conchal bone as far posteriorly as possible. Connect this tunnel to the inferior incision using a blade or Knight scissors, creating a wedge of conchal bone with attached inferior and lateral soft tissue.

Excise this wedge along with the posterior nasal tip using a snare. Use suction cautery for hemostasis. Roll the remaining mucoperiosteal flap on itself medial to lateral and then crush it laterally to form the neoturbinate. Packing may then be placed.

An advantage of this procedure is less risk of bleeding and crusting than with other surgical resection techniques. This procedure spares some turbinate mucosa while addressing more posterior turbinate obstruction.

Microdebrider-assisted inferior turbinoplasty

Make an incision along the anterior tip of the turbinate at its lateral insertion. Create a tunnel with a Freer elevator along the medial conchal bone. The turbinate microdebrider blade is inserted into the pocket created and used to excise bone and submucosa of the anterior aspect of the inferior turbinate. The incision site can be cauterized if significant bleeding occurs from the mucosal edge. Packing may then be placed.

An advantage of this procedure is a lower risk of bleeding and crusting than with other surgical resection techniques. This procedure spares the superficial turbinate mucosa while addressing both bony and submucosal hypertrophy.

Submucous resection

Make an incision along the inferior surface of the turbinate and elevate a mucoperiosteal flap superiorly and inferiorly. Then resect the bony concha of the anterior third of the turbinate. A variety of instruments (eg, scissors, Takahashi forceps, rongeurs) can be used for this. Outfracture any posterior remnant. Lay the mucoperiosteal flaps back down; packing can be placed. Removal of the bony concha allows the inferior turbinate to naturally lateralize and scarring of the turbinate stroma may result in some reduction of soft tissue bulk.

Advantages of this procedure are less risk of bleeding and crusting than with other surgical resection techniques and sparing of turbinate mucosa. Disadvantages are the technical difficulty and that the posterior turbinate, if obstructive, is not addressed.

Partial inferior turbinectomy

Place an elevator beneath the turbinate, which is fractured medially. Then place a straight clamp along the anterior inferior surface of the turbinate that is to be removed. This is left in place for at least a minute to provide additional hemostasis and allows assessment of the hypertrophied concha to be included in the resection. Use turbinate scissors to excise the bone and soft tissue along the anterior inferior edge of the turbinate. Electrocautery can then be applied to the cut edge for additional hemostasis.

The advantage of this procedure is direct removal of hypertrophied bone and mucosa but bleeding is the major potential complication. Additionally, crusting, which heals slowly over several weeks, occurs along the raw surface.

Lateral outfracture

Perform this procedure by placing an elevator underneath the turbinate; initially the turbinate bone is fractured upward and medially. Then place the elevator on the medial surface of the turbinate and apply pressure to outfracture and lateralize the turbinate. This sequence can be repeated 2 or 3 times to ensure a complete fracture rather than a greenstick fracture, which may spring back into position. This maneuver reduces turbinate size and volume of the nasal valve occupied by crushing the turbinate and lateralizing its position in the nasal valve.

The advantages of this procedure are decreased risk of complications such as bleeding and lack of postoperative crusting from mucosal preservation. The disadvantage is that neither the mucosal nor bony turbinate hypertrophy is addressed, and only temporary improvement in the nasal airway may result when this procedure is used alone. When used in conjunction with other techniques that reduce mucosal hypertrophy, more effective lateralization of the turbinate and reduction of nasal valve obstruction may be achieved.

Electrocautery

Electrocautery can be performed with either linear mucosal or submucosal contact. For surface cautery, a wire or needle electrode can be used to streak the turbinate mucosal surface. Submucosal cautery can be performed with either a unipolar or bipolar electrode inducing fibrosis and wound contracture with resultant volume reduction. The unipolar approach coagulates tissue circumferentially around the electrode while the bipolar technique produces coagulation necrosis between the needle electrodes. High tissue temperatures (up to 800°C) can be achieved.

In the bipolar technique, insert a bipolar turbinate cautery tip into the anterior inferior turbinate and apply current. Similarly, in the monopolar technique, insert a 22-gauge spinal needle along the anterior inferior turbinate edge and apply current, usually with a Bovie electrocautery unit. Take care to avoid contact with the ala, columella, or septum, which may cause peripheral tissue injury. Avoid direct contact and cauterization of the conchal bone since this can result in bony necrosis and sequestrum formation.

An advantage of this procedure is the low risk of bleeding. However, crusting at the insertion point and turbinate edema are usually observed for at least a week postoperatively.

Radiofrequency ablation

Radiofrequency ablation creates ionic agitation in the tissue, inducing submucosal necrosis. The resultant fibrosis of the submucosa adheres the mucosa to the turbinate periosteum, reducing the blood flow to the turbinate. Resultant wound contraction causes volume reduction of the inferior turbinate without damage to the overlying mucosa. The target temperature can be controlled at 60-90°C to prevent surrounding tissue damage.

Initially apply topical 4% lidocaine with cotton pledgets along the length of the turbinate. Some authors have described application of topical decongestant as well. However, this reduces the target tissue volume, resulting in a more concentrated thermal effect. Then inject the turbinate with plain lidocaine (1% or 2%). Injection of lidocaine with epinephrine (1:100,000) has also been described.

The turbinate probe is a handheld device, 40 mm long, with an exposed active length of 15 mm. Insert the probe tip into the anterior portion of the inferior turbinate. Also insert a few millimeters of the insulated portion of the probe tip to prevent mucosal contact of the exposed active surface of the probe. A second site along the middle of the turbinate can also be selected for treatment.

In the literature, the amount of energy delivered to the inferior turbinates varies. The radiofrequency generator allows control of the target temperature, wattage, delivery time, and total joules administered. Delivery of up to 900 J per turbinate (at 2 separate probe sites in the turbinate) has been reported without mucosal necrosis.

The advantage of this procedure is mucosal preservation, which reduces risks of bleeding and crusting postoperatively.[7] Additionally, this procedure can be performed under local anesthesia in a clinic setting and can be repeated if optimum results are not achieved initially.[7, 8]

Cryosurgery

Cryosurgery results in the formation of intracellular ice crystals, resulting in denaturation of nuclear and cell membrane proteins. This causes cell membrane destruction, blood vessel thrombosis, tissue ischemia, and resultant tissue destruction.

A nitrous oxide cryosurgery unit is used to perform this procedure. Apply a cryoprobe to the surface of the turbinate and lower the temperature, freezing the contacted surface. Temperatures ranging from -40 to -85°C have been used. Take care to protect the ala, columella, and septum from contact with the probe tip to prevent inadvertent damage.

An advantage is that cryosurgery can be performed under local anesthesia in a clinic setting. A disadvantage is prolonged healing as the necrotic tissue at the turbinate edge sloughs over a period of several days and subsequent healing takes place over a 6-week period. Additionally, the duration of symptomatic relief varies.

Laser turbinectomy

Laser turbinectomy has been described using the carbon dioxide, Nd:YAG, and diode lasers. A defocused laser beam or optical fiber delivery can be used. The tissue is vaporized along the anterior inferior aspect of the turbinate for one fourth to one half of its length. Cross-hatching longitudinally along the complete length of the turbinate can be performed to leave islands of healthy nasal mucosa.

An advantage of this procedure is that it can be performed under local anesthesia in a clinic setting. The hemostatic properties of the laser reduce the risk of bleeding and the need for packing. However, significant postoperative crusting may result.

A study by Kisser et al found no significant difference in the degree to which laser surgery and radiofrequency ablation each reduce nasal obstruction in inferior turbinate surgery. However, the study, which included 26 patients, reported that the radiofrequency group experienced significantly greater intraoperative discomfort.[9]

Argon plasma surgery

Recently, argon plasma coagulation has been described. This high-frequency electrocoagulation can be performed without tissue contact; rather, the electrocurrent is conducted via ionized argon gas. The argon plasma coagulator probe has a side hole through which argon gas is delivered forcefully, producing tissue decussation. The endpoint is gauged by the inferior turbinate surface turning white.

A 1-year follow-up study by Fukazawa et al indicated that 63.6% of patients experience improvement in inferior turbinate congestion.[10] Similarly, 75% of patients experience improvement in symptoms of nasal stuffiness at 1 year.

Postoperative Details

If significant bony or mucosal resection is involved, postoperative packing may be placed. Various dissolvable materials that facilitate hemostasis are available. Traditional nonabsorbable sponge packs can also be placed and are usually removed within 24 hours after surgery. Postoperative bleeding can usually be managed with topical decongestants, hemostatic materials such as Surgicel, or nasal packing. Persistent bleeding despite these measures may require a return to the operating room and possibly endoscopy.

Follow-up

Instruct the patient to avoid heavy lifting or strenuous activity for several weeks after surgery (usually 2-3 wk). Similarly, patients should avoid medications or herbs with anticoagulant effects for a similar period. Nasal saline should be used aggressively to minimize nasal dryness and crusting postoperatively. This should be continued until the mucosa has healed completely. Once this has occurred, adjunctive medical treatments such as topical glucocorticoids can be resumed.

Complications

The primary early complication of inferior turbinate surgery is hemorrhage.[11] As noted previously, the turbinates are very vascular structures and postoperative bleeding has been reported with a frequency of 3.4-8.6% in various studies.

Another complication is the formation of adhesions.[11] This is primarily of concern when inferior turbinate surgery is performed in conjunction with septoplasty, creating the possibility of apposed raw surfaces.

Dryness and crusting may also result.[11] In the early phases of healing, crusting along the inferior turbinate can be observed. This is more common in techniques involving direct mucosal trauma and resolves with healing. A more significant complication is long-term dryness and crusting. This may be the result of an increase in nasal airflow or the turbulence of nasal airflow. The extreme or end stage of this process is atrophic rhinitis. Some authors indicate that this is a significant risk of inferior turbinate resection. Other reported series of inferior turbinectomies do not reveal this to be a significant complication. This area of turbinate surgery remains controversial.

Conchal bone necrosis and sequestrum can occur and require removal of the sequestrum. This complication is best prevented by avoiding cautery of bone.

Outcome and Prognosis

Nasal obstruction after rhinoplasty can result from alteration of the nasal valve or nasal vault narrowing as a result of osteotomies. Changes in nasal airflow as a result of rhinoplasty may unmask inferior turbinate hypertrophy and obstruction that was not clinically significant or evident preoperatively. Therefore, preoperative assessment of inferior turbinate hypertrophy and appropriate operative management can significantly affect nasal function postrhinoplasty. Assessing the contribution of bony versus mucosal hypertrophy is important in determining the appropriate surgical technique to maximize long-term benefit and outcome.

Future and Controversies

The primary controversy in inferior turbinate surgery revolves around inferior turbinectomy and the risk of atrophic rhinitis. Several large series of inferior turbinectomy have not demonstrated evidence of rhinitis sicca or atrophic rhinitis as a complication. However, concern over this potential complication, which can be devastating, remains and is used by many as an argument for a more conservative surgical approach.

Continued development of new technologies, such as radiofrequency ablation, have added to the available armamentarium in addressing mucosal turbinate hypertrophy. However, these techniques do not supplant surgical resection when indicated. Additionally, the deviated nasal septum should be addressed surgically when indicated for nasal airway obstruction.