All individuals have turbinate dysfunction at some point in their lives. Symptoms of turbinate dysfunction range from total nasal obstruction to mild congestion and/or rhinorrhea. Causes of turbinate dysfunction include upper respiratory infection (URI), allergic rhinitis, and vasomotor rhinitis. Drugs or hormones may also induce turbinate dysfunction. This article discusses the common and less common causes of this problem and its focused management. See the images below.
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Mucosal hypertrophy of the right inferior turbinate with total airway obstruction.
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Normal-sized right inferior turbinate with a moderate inferior septal deflection.
Nasal congestion is the most common symptom associated with turbinate dysfunction. Symptoms may be mild, or the congestion may be so great that the only relief is to overuse (abuse) topical decongestants such as oxymetazoline or phenylephrine. Many patients have tried over-the-counter (OTC) oral decongestants with limited success. The key to successful management is to identify the underlying cause of the turbinate hypertrophy and either correct or treat the cause. Infectious and inflammatory causes are the most common etiologies.
Turbinate dysfunction is universal. Every person experiences some degree of turbinate dysfunction at some point in his/her lifetime. Persistent dysfunction is not uncommon and involves approximately 50% of the population.
A study by Clark et al of 1906 patients from different US regions with sinonasal complaints found the prevalences of nasal valve collapse, septal deviation, and inferior turbinate hypertrophy were 67%, 76%, and 72%, respectively. Of the 1211 patients with the most severe/extreme Nasal Obstruction Symptom Evaluation (NOSE) scale scores (55 or above), the prevalences were 73%, 80%, and 77%, respectively. Thus, these three sources of nasal obstruction occurred at comparable rates in both groups.[1]
The etiology of turbinate dysfunction is multifactorial. Because the turbinates have a very rich blood supply and are governed by the parasympathetic nervous system, anything that affects either of these 2 systems affects the turbinates and, hence, the nose.[2]
Allergic rhinitis is the most common cause of turbinate dysfunction. Allergic rhinitis is due to environmental allergens that come in contact with the nasal membranes, causing an inflammatory reaction and resultant congestion and increased drainage. This category is so large that any nonallergic cause of turbinate dysfunction is known as vasomotor rhinitis. Vasomotor is a term that indicates the neurovascular control of the nasal membranes. Causes of vasomotor rhinitis include, but are not limited to, the use of cardiovascular and antihypertensive drugs, female hormones, changes in temperature, and rhinitis of disuse.
Any medication a patient takes that stimulates the parasympathetic nervous system can also affect the turbinate mucosa and cause congestion. Female hormones, specifically progesterone, may have a similar effect; therefore, congestion can frequently be experienced during the premenstrual phase of the menstrual cycle and the third trimester of pregnancy. Some female hormone replacement therapy and oral contraceptives that have a higher concentration of progesterone may have similar effects, although a 2006 small clinical study did not demonstrate that effect.[3]
Condensation rhinitis is well known to snow skiers and is due to the reaction of the nasal membranes to the colder outside environment. An equivalent example is that of taking a cold beverage can outside on a hot day and finding condensation developing on the outside of the can.
Rhinitis of disuse occurs in patients who no longer use their noses for airflow (eg, patients who have undergone laryngectomy) or those who abuse topical nasal decongestants (rhinitis medicamentosum). In the first case, the underlying pathophysiology is rebound inflammation due to a lack of feedback from the normal nasal airflow. In the second case, a rebound vasodilation of the turbinates occurs as a response to the topical sympathomimetics.
Similar to the rest of the upper respiratory tract (URT), the membranes of the turbinates are composed of ciliated, pseudostratified, glandular, columnar epithelium. The cilia beat in unison to propel the mucus from the nasal cavity toward the nasopharynx, where the mucus can then be swallowed. Mucociliary transport relies on mucus production and ciliary function. Normally, the nose and paranasal sinuses produce approximately 1 quart of mucus in a 24-hour period. When inflamed, that amount can more than double. Mucus contains immunoglobulin A (IgA), immunoglobulin E (IgE), and muramidase.
Both the blood supply and the autonomic nervous system control the secretions and level of congestion of the turbinates. The autonomic nervous system provides the general innervation to the nose, with the parasympathetic nerves supplying the resting tone and controlling secretions. The nerve supply originates from the facial nerve at the inferior salivatory nucleus and follows along the distribution of the facial nerve through the sphenopalatine ganglion. The blood supply to the nose comes from branches of both the internal and external carotid artery systems. The terminal branches of the internal maxillary artery supply most of the mucosal surfaces of the nasal cavity.
Patients with turbinate dysfunction report nasal congestion, postnasal drainage, and occasionally, midfacial headaches or facial pain and discomfort. Anterior rhinorrhea is less common but may be noted. These symptoms can occur irrespective of etiology. If marked swelling of the turbinates results in contact with the septum or lateral nasal wall, then nasal headaches may occur. Patients report pressure and headaches in the central forehead and medial canthal regions. Symptoms of congestion in some cases may be so bad that the patient develops an addiction to OTC nasal sprays containing either oxymetazoline or phenylephrine. This condition is known as rhinitis medicamentosum. See the image below.
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Mucosal hypertrophy of the left inferior turbinate with impingement of the septum and narrowed nasal airway.
Intermittent blockage of 1 nasal passage followed by switching of the congestion to the other nasal passage is a common report and is known as the nasal cycle. Patients may describe positional congestion, such as when lying on 1 side while sleeping. The nose is thought to shut down 1 nasal passage every 2-4 hours in order to prevent desiccation and irritation from inhaled air. The extent of this shutdown can range from complete obstruction to a slight degree of congestion that is hardly noticed. Treatment is not required unless the symptoms are exaggerated because this shutdown is part of normal nasal physiology.
If a middle turbinate is paradoxically bent (curved or angled laterally) or if it contains a sinus (concha bullosa), the ostiomeatal complex may be compromised more easily and lead to acute or recurrent acute rhinosinusitis. This anatomic deformity may require surgical correction after failure of medical management. Concha bullosa occurs in approximately 30% of the population and is usually an incidental finding on imaging modalities.
Indications for the management of turbinate dysfunction include a clinical history of bothersome nasal congestion and postnasal drainage with or without paranasal sinus disease or a significant septal deformity.
Because the ability to breathe out of one's nose is a quality of life issue, many patients take it for granted, and when the nasal airway is diminished, people often tolerate it. Many treatments are available for this disorder, and isolating the etiology is hallmark for successful therapy. Identifying whether symptoms are due to allergies or other causes is the first step. A careful history and allergy testing, if indicated, are most useful. Offending medications may be substituted or at least identified. If the patient continues to have symptomatic turbinate dysfunction, then initiate medical therapy. Surgical therapy is reserved for those patients that do not respond to appropriate medical therapy and clinically remain symptomatic.
A study by Sharhan et al found that the inferior turbinate in patients with allergic rhinitis did not demonstrate greater hypertrophy than that in patients with nonallergic rhinitis. Consequently, the investigators suggested that when septoplasty is performed on patients with symptoms of nasal obstruction, surgical reduction of inferior turbinate hypertrophy be considered even in the absence of allergic rhinitis.[4]
The 3 paired turbinates are located on the lateral nasal wall. The superior and middle turbinates are part of the ethmoid bone, whereas the inferior turbinates form a separate and unique bone. Covered by both respiratory and olfactory epithelium, the superior turbinate is located high in the nasal vault and usually arises from the cribriform plate of the ethmoid bone. The middle turbinate has a wide variation in origination. This bony extension of the ethmoid can be observed arising from the cribriform plate, the lamina papyracea, or the uncinate process in some cases.[5]
For more information, please see the Medscape Reference articles Nasal Anatomy; Nasal Cavity Anatomy, Physiology, and Anomalies on CT Scan; and CT Scan of the Paranasal Sinuses. The inferior turbinate bone arises on the inferior portion of the lateral nasal walls. The bone itself is penetrated heavily by vascular channels, which supply the overlying respiratory epithelium. The lacrimal duct exits into the nose below the inferior-anterior portion of this structure.
Surgical therapy is reserved for symptomatic patients with persistent hypertrophy of the turbinates who are not responding to medical management or in whom medical management is contraindicated. See Surgical therapy.
Sinus CT scanning is useful for delineating the extent of disease in patients who have underlying chronic rhinosinusitis or acute recurrent rhinosinusitis. Anatomic relationships between the middle turbinate, the septum, and lateral nasal wall may also be useful in the evaluation of nasal headaches. Preferred scans are those in a coronal plane with 2- to 3-mm thickness and bony windows. Contrast is not helpful. See Nasal Cavity Anatomy, Physiology, and Anomalies on CT Scan.
Rhinomanometric testing is useful as a research tool to evaluate certain parameters of nasal airflow. Rhinomanometry is most useful for comparing nasal airflow from side to side and also in the preoperative evaluation of nasal airflow as compared with the postoperative situation. See the Medscape Reference article Nasal Physiology.
Eosinophilic infiltration of the mucosal membranes leads to suspicion of allergic causes for turbinate inflammation. Infiltration by other inflammatory cells is also observed but is less diagnostic.
Medical therapy is the first-line approach to the treatment of turbinate dysfunction; however, the appropriate choice of therapy relies on the appropriate diagnosis. Several categories of medications are available that have an effect on the turbinate mucosa and affect patients' symptoms. Nasal decongestants, in both topical and oral forms, are some of the most effective drugs available for reducing congestion of the turbinate mucosa. Topical sprays, oxymetazoline and phenylephrine, are extremely powerful alpha-agonists, and prolonged use can cause a rebound effect. Rebound develops within 4-5 days and if prolonged is known as rhinitis medicamentosum.
Oral decongestants are also very effective for reducing congestion and do not cause rebound swelling of the mucosa with prolonged use. Pseudoephedrine and phenylephrine are 2 common forms of oral decongestants. Main concerns regarding their use include elevation of blood pressure in hypertensive patients and urinary retention in patients with benign prostatic hypertrophy. Prolonged use of oral decongestants may lead to tolerance and ineffectiveness. Phenylpropanolamine was voluntarily withdrawn by the Food and Drug Administration (FDA) because of cases of hemorrhagic stroke occurring in women. This drug is presently unavailable for use as an oral decongestant.
Antihistamines are agents that affect the turbinates by blocking the effects of histamine at H1 receptor sites. Many antihistamines are available OTC and by prescription. These medications are only indicated in patients with allergic rhinitis. Used in conjunction with oral decongestants, antihistamines can relieve congestion and drainage symptoms. Adverse effects are drug specific and range from sedation and memory effects (with the earlier generation antihistamines that cross the blood-brain barrier) to excessive dryness. Antihistamines are contraindicated in patients with glaucoma.
Intranasal steroid sprays are useful for turbinate dysfunction. These medications are labeled for the management of allergic rhinitis but, like all steroids, also have nonspecific anti-inflammatory effects. The newest sprays in this class are extremely safe and have no significant suppression of the hypothalamus-pituitary axis (HPA).
Intranasal steroids are administered every day and require continued daily use for any significant benefits. Proper direction of the spray nozzle to the lateral nasal wall prevents the most common adverse effects of nasal dryness, which include epistaxis and septal perforation (rare). Tolerance should not occur with prolonged use. The latest controversy concerning the use of nasal steroids in children is growth suppression. The latest studies investigating the use of oral steroid inhalers, which have a higher level of absorption, do not support this concern in at least 2 of the available steroid sprays.
The leukotriene receptor antagonist montelukast is also approved for use in cases of seasonal and perennial allergic rhinitis. Improvement in daytime symptom scores of nasal congestion, rhinorrhea, and sneezing were evident in clinical studies. Adverse effects are similar to those of a placebo.
Intraturbinate injections of steroids are also used to treat inflammatory mucosal hypertrophy. Care must be taken because cases of blindness have been reported with this technique. A preliminary report of intraturbinate injection of botulinum toxin A for vasomotor rhinitis showed symptom improvement compared with placebo in a small cohort study.[6]
Surgical therapy is reserved for symptomatic patients with persistent hypertrophy of the turbinates who are not responding to medical management or in whom medical management is contraindicated. Because the function of the turbinates is important, care must be taken to avoid excessive resection and the resultant dry nose syndrome (ozena).
The most important decision-making factor in the surgical management of the symptomatic patient with enlarged turbinates is whether the hypertrophy is bony, mucosal, or a combination of both. If bony hypertrophy is present, then some form of resection is necessary, either by way of an actual trimming of the bone and mucosa or submucosal resection of the turbinate bone.[7] Submucosal resection of the inferior turbinate preserves most of the mucosa and allows for preservation of function. This technique is less likely to cause atrophic rhinitis when performed properly. Turbinate trim allows for resection of the turbinate through both the bone and mucosa. If excessive mucosa is resected, prolonged healing and mild-to-moderate nasal dryness may occur postoperatively.
More options are available for the care of the patient with turbinate dysfunction that is due entirely to mucosal hypertrophy. Every physical treatment imaginable has been tried on the turbinate mucosa at one time or another. Because no single superior technique is clearly available, the experience of the surgeon and the intraoperative findings play the greatest role in the choice of techniques.
Physical injury to the mucosa consists of cryosurgery (cold), thermal ablation (heat), or radiofrequency ablation. Both cryosurgery and radiofrequency ablation require special and costly equipment. Superficial thermal ablation can be performed with a laser or cautery unit. Intramural ablation can be preformed with a cautery unit or with a radiofrequency device.[8] Phenol application to the turbinate mucosa has been used in the past but is no longer used because of toxicity issues. Trimming the excessive mucosa is also very effective for the management of turbinate hypertrophy. Care must be taken to not be overly aggressive in the amount of mucosa removed for the previously stated reasons.
A newer technique using a very small (2 mm) microdebrider blade through a small stab incision shows great promise in reducing the size of the inferior turbinates without requiring external physical injury to the mucosal membranes. This technique also shows excellent long-term results compared with diathermy and radiofrequency ablation.[9] See the video below.
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A stab incision is made at the anterior head of the inferior turbinate. Blunt dissection beneath the mucoperiosteum elevates tissue for subsequent microdebridement. The microdebrider is turned in all directions, but mucosa is entirely preserved. Video courtesy of Vijay R Ramakrishnan, MD.
A randomized, double-blind study by Barham et al found that medial flap turbinoplasty had better outcomes in inferior turbinate reduction than did submucosal electrocautery and submucosal powered turbinate reduction. At 5-year follow-up, decongestants were being used only occasionally or not at all in 90.2% of the turbinoplasty nasal cavities, compared with 15.8% and 37.8% of the cavities that underwent electrocautery and submucosal powered turbinate procedures, respectively. Moreover, just 12% of the turbinoplasty cavities required a revision procedure, versus 54% and 40% of the electrocautery and submucosal powered turbinate procedure cavities, respectively.[10]
Preoperative evaluation is important in determining whether the turbinate hypertrophy is bony, mucosal, or a combination of both. Determining whether or not a significant septal deformity is contributing to the patient's symptoms is critical. If septal deformity is present, correction of the septum at the time of the turbinate surgery provides the appropriate management and ensures a successful outcome.
Maximally decongesting the nose with any of the topical decongestants in the office affords a relatively easy way to determine the extent of bony and mucosal hypertrophy. This allows the surgeon to plan the appropriate procedure and discuss the risks and benefits of those procedures with the patient preoperatively. Decongesting the nose also provides a better view of the septum posteriorly.
In cases in which middle turbinate surgery is considered in the management of nasal headaches, a trial of maximum decongestion preoperatively may relieve the headache symptoms temporarily and help confirm the presumptive diagnosis. The author uses a strict regimen of a topical decongestant bid or tid for 4 days in combination with an oral decongestant. The patient is instructed to record whether this improves or resolves the headache while on this regimen. The patient is told that this is only a diagnostic test and cannot be used indefinitely because of rebound effects. Bony hypertrophy impacting the septum or lateral nasal wall is not expected to respond to this medication trial. Steroids are not used because effects are nonspecific and may be misleading. Preoperative airflow studies are not routinely performed but can be useful in comparison of the preoperative and postoperative states.
Careful examination of the state of the turbinate mucosa is made before and after vasoconstriction to allow for the right treatment plan. The turbinates are decongested and, if surgical therapy is anticipated, injected with a vasoconstrictive agent usually in a vehicle of lidocaine. This helps minimize bleeding during the procedure. If excessive bleeding is noted, elevated blood pressure may be the culprit; ask the anesthesiologist to assist in this matter. Topical decongestants and/or packs may be applied for further control of bleeding.
Following completion of the procedure, removable or absorbable nasal packs are placed. Septal splints are applied as appropriate. If general anesthesia is used, the patient is gently extubated to avoid undue elevations of blood pressure and increased risk of bleeding. See the image below.
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Bony hypertrophy of the right inferior turbinate following topical vasoconstriction.
Because nasal packs are present in the immediate postoperative period, humidified air is provided for patient comfort. Pain control is used, but care is taken to avoid respiratory depressants. Antiemetics and other routine medications are also available as necessary. Packs are removed when appropriate, usually on the first or second postoperative day. Absorbable packing materials are becoming more commonplace and reduce the discomfort of packing removal while trading for a longer period of congestion postoperatively. Postoperative antibiotics are usually continued until the packing has been removed.
The patient is instructed to keep the nose well moisturized postoperatively to aid in healing and comfort levels. The patient is provided or instructed to obtain a lubricating spray of the physician's preference, usually saline. Nose blowing is discouraged for several weeks, and sneezing is aided by an opened-mouth technique. Avoidance of heavy lifting and straining is recommended for the first few weeks following surgery.
The patient usually returns to the surgeon's office for a postoperative visit within the first week. Packs are removed, if present, and the postoperative instructions are again reviewed. Follow-up appointments are scheduled based on the procedure performed and patient healing.
Depending on the procedure performed, the most common complications of turbinate surgery are bleeding and prolonged nasal dryness with crusting. Bleeding is minimized by careful surgical techniques and the use of packing. Antihypertensive medications are started immediately following surgery. Postoperative trauma can lead to bleeding and so the patient is instructed to keep the nose well moisturized with the use of a nonmedicated nasal spray. Avoidance of nose blowing and opening of the mouth with sneezing are very helpful. No heavy lifting or straining is permitted for the first 2-3 weeks.
Doing all of the above and staying well hydrated can minimize crusting. Vaseline can be applied to the anterior nares for symptomatic relief at bedtime and throughout the day as needed. Atrophic rhinitis (ozena) can develop in a patient with over-resected inferior turbinates. Increased nasal hygiene is necessary in those circumstances.
When performed for the appropriate reasons, turbinate reduction surgery is very successful in reducing symptoms of congestion. Because no surgical procedure cures the underlying condition, further medical therapy may be necessary, especially in patients with allergic rhinitis; however, even these patients experience a significant improvement in both nasal airway and drainage symptoms.[11]
A prospective study by Vijay Kumar et al comparing radiofrequency ablation with the microdebrider technique in the treatment of inferior turbinate hypertrophy found that, while both modalities were effective in relieving nasal obstruction, preoperative symptoms recurred in a small portion of the radiofrequency group. The study included 60 patients with chronic nasal obstruction caused by inferior turbinate hypertrophy that had been unresponsive to medical treatment. The patients were divided evenly between the two treatments and were followed up postoperatively at 1 week and at 1, 3, and 6 months. Although significant improvement occurred in all preoperative symptoms in both groups over the course of the follow-up period, symptoms recurred in three of the patients treated with radiofrequency ablation. No recurrence was seen in the microdebrider group.[12]
A study by Nilsen et al suggested that for patients with nasal obstruction, treatment with a combination of septoplasty and radiofrequency therapy of the inferior turbinates (RFIT) may be more effective than RFIT alone. Using the visual analogue scale to assess symptoms, the investigators found that patients who underwent septoplasty/RFIT had a postoperative nasal obstruction score of 27.5, compared with 37.2 for patients treated only with RFIT.[13]
As with any medical condition, advances in the understanding of both allergic and vasomotor rhinitis will lead to better medical therapies. Surgical therapy will continue to be reserved for patients whose conditions are refractory to medical therapy. The relationship between turbinate hypertrophy and sleep-disordered breathing problems is also currently under investigation.
The major controversies surrounding turbinate surgery continue to be centered on the best techniques for management. Avoidance of overly aggressive therapies and control of the underlying disease states are paramount to disease management. The toughest issue to reconcile is that turbinate dysfunction is a quality of life issue. Management of this problem is not mandatory but very helpful for patients' quality of life.
What is turbinate dysfunction?What is the role of nasal congestion in turbinate dysfunction?What is the prevalence of turbinate dysfunction?What causes turbinate dysfunction?What is the pathophysiology of turbinate dysfunction?Which clinical history findings are characteristic of turbinate dysfunction?Which anatomic abnormality may cause turbinate dysfunction?When is treatment of turbinate dysfunction indicated?Which nasal anatomy is relevant to turbinate dysfunction?What are the contraindications to surgery for turbinate dysfunction?What is the role of imaging studies in the workup of turbinate dysfunction?What is the role of rhinomanometry in the workup of turbinate dysfunction?Which histologic findings are characteristic of turbinate dysfunction?What are the initial treatments for turbinate dysfunction?What is the role of surgery in the treatment of turbinate dysfunction?What is included in the preoperative evaluation for turbinate dysfunction surgery?How is bleeding minimized during turbinate dysfunction surgery?What steps are taken immediately following completion of turbinate dysfunction surgery?What is included in postoperative care following turbinate dysfunction surgery?What is included in long-term monitoring following turbinate dysfunction surgery?How are the possible complications of turbinate dysfunction surgery prevented?What is the prognosis of turbinate dysfunction following treatment?What are the controversies related to turbinate dysfunction treatment?
Sanford M Archer, MD, Professor, Department of Surgery and Pediatrics, Department of Otolaryngology-Head and Neck Surgery, University of Kentucky Medical Center
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Dominique Dorion, MD, MSc, FRCSC, FACS, Dean, Professor of Surgery, Division of Otolaryngology-Head and Neck Surgery, Faculty of Medicine, Université de Sherbrooke, Canada
Disclosure: Nothing to disclose.
Chief Editor
Arlen D Meyers, MD, MBA, Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;Cliexa;The Physicians Edge;Sync-n-Scale;mCharts<br/>Received income in an amount equal to or greater than $250 from: The Physicians Edge, Cliexa<br/> Received stock from RxRevu; Received ownership interest from Cerescan for consulting; .
Acknowledgements
Gregory Branham, MD Vice-Chair, Director, Associate Professor, Department of Otolaryngology-Head and Neck Surgery, Division of Facial Plastic and Reconstructive Surgery, St Louis University School of Medicine
Gregory Branham, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American College of Physician Executives, and Missouri State Medical Association
Disclosure: Nothing to disclose.
Acknowledgments
Medscape Drugs and Diseases thanks Vijay R Ramakrishnan, MD, Assistant Professor, Department of Otolaryngology, University of Colorado School of Medicine, for assistance with the video contribution to this article.
Mucosal hypertrophy of the right inferior turbinate with total airway obstruction.
Normal-sized right inferior turbinate with a moderate inferior septal deflection.
Mucosal hypertrophy of the left inferior turbinate with impingement of the septum and narrowed nasal airway.
A stab incision is made at the anterior head of the inferior turbinate. Blunt dissection beneath the mucoperiosteum elevates tissue for subsequent microdebridement. The microdebrider is turned in all directions, but mucosa is entirely preserved. Video courtesy of Vijay R Ramakrishnan, MD.
Bony hypertrophy of the right inferior turbinate following topical vasoconstriction.
Normal-sized right inferior turbinate with a moderate inferior septal deflection.
Bony hypertrophy of the right inferior turbinate following topical vasoconstriction.
Mucosal hypertrophy of the right inferior turbinate with total airway obstruction.
Mucosal hypertrophy of the left inferior turbinate with impingement of the septum and narrowed nasal airway.
A stab incision is made at the anterior head of the inferior turbinate. Blunt dissection beneath the mucoperiosteum elevates tissue for subsequent microdebridement. The microdebrider is turned in all directions, but mucosa is entirely preserved. Video courtesy of Vijay R Ramakrishnan, MD.
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