Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature.

Current Management of Nasal Polyposis
Jayson Greenberg, M.D.
September 3, 1998

Nasal polyps are the most common benign intranasal tumor. They are fluid filled sacs composed of an edematous tissue with infiltrating cells, including mast cells, eosinophils, lymphocytes and plasma cells surrounded by a ciliated airway epithelium.

The history of nasal polyps dates back over three thousand years to India where a type of currette was described for eradicating nasal polypi, "a frequent and troublesome disease in many parts of Hindustan." Hippoctrates is largely recognized as the father of Rhinology. His sponge method for polyp removal was included in textbooks as late as 19th century. Three strings were tied to a sponge cut to the proper size and shape. The other ends were fastened together and tied to a malleable probe, which was passed through the nose and into the pharynx. The ends of the strings were passed over a forked probe held in the pharynx. By placing traction, the sponge was forcibly dragged through the nose and pharynx, delivering the polyps with the sponge. Fallopius is credited with developing the snare, using a silver tube with an iron wire forming a loop at one end to engage the polyp. In 1571, Aranzi described using long forceps to forcibly grasp and remove polyps. This method remained popular in England until the early 19th century, being documented in lectures by Sir Astley Cooper. In 1882, Christopher Heath stressed environmental factors. He wrote, "The influence of the weather upon polypus nasi should be noted, damp causing them to increase largely in size." In 1922, the triad of nasal polyps, aspirin intolerance, and asthma was initially described by Widal.

Nasal polyps are seen in patients of all ages. They are present in approximately 2% of the population. There is at least a 2:1 male to female predominance. The frequency of nasal polyps increases with age, reaching a peak in individuals 50 years and older. Nasal polyps are not a disease, but a physical finding with a number of causes and associated conditions. Most commonly, 25%-30% of patients have asthma, while approximately 12 % have aspirin intolerance.

Nasal polyps are found in one-third of patients with aspirin intolerance and 7% of patients with asthma, and in 2% of patients with chronic rhinosinusitis. They are seen in 0.1% of children and in 20% of patients with cystic fibrosis. Any child under the age of 16 with nasal polyps should have a sweat chloride test as part of their evaluation. Nasal polyps are seen in 50% of the eosinophilic vasculitis of Churg Strauss Syndrome. The majority of patients with allergic fungal sinusitis have nasal polyps. They are also seen in disorders of ciliary motility like Kartagener's syndrome, as well as other genetic syndromes such as Young's syndrome, which is bronchopulmonary disease and azospermia.

As I mentioned, there is an association of nasal polyps with aspirin intolerance and asthma. These three factors together are know as Samter's syndrome or the aspirin triad. The prevalence is estimated to be 2%-3% in asthmatic patients in general and 20% of severe asthmatics. The typical patient is a middle-aged white individual with vasomotor rhinitis, perennial bronchial asthma, eosinophilia, negative skin tests to atopic allergens and an intolerance to aspirin and related chemicals. This reaction occurs within 15 to 180 minutes of ingestion and is marked by profuse rhinorrhea, often accompanied by macular erythema and/or nausea, vomiting, intestinal cramps, and diarrhea. An acute bronchial asthma attack ensues. Most patients recover from the acute reaction within 2 hours. Of course, not all patients present in this manner, and the syndrome usually develops over time. The asthma and aspirin intolerance generally develop within one year, with polyps forming up to ten years later. However, there is no greater incidence of positive allergy tests, and the male sex predilection disappears in this subset of patients, suggesting this may be a separate disease process.

All of this aside, the exact etiology of polyps remains unknown. Proposed mechanisms implicated in the development of nasal polyps include allergy, infection, autonomic imbalance, mucopolysaccharide abnormality, enzyme abnormality, drug sensitivity, mechanical obstruction, histamine, and proto-oncogene. The two major schools of thought are allergy and infection.

Before briefly entertaining these two theories, I would like to explore the histologic differences between nasal polyps and the normal nasal mucosa. Nasal polyps consist of respiratory epithelium covering a very edematous stroma infiltrated by a large number of inflammatory cells with eosinophils being the predominant cell. Eighty to ninety percent of polyps contain activated eosinophils. There are also increased goblet cells and areas of squamous metaplasia. Epithelial damage, in the form of an ulceration or desquamation, is another frequent finding. In addition the density of glands in nasal polyps is significantly less then normal turbinate mucosa with no true evidence of seromucinous glands. In addition to the increase in eosinophils and mast cells, there appears to be an up regulation of antigen presenting cells and immunocompetent cells such as B cells and lymphocytes.

The mast cells demonstrate ultrastructural signs of degranulation. Recent results have suggested that interleukins from activated CD4 T cells may play a role. There appears to be a continuous release of histamine, which is found in higher concentrations in polyp fluid. Gaps between endothelial cells of blood vessels allow passage of plasma into tissue. There is massive infiltration and activation of eosinophils with release of products that are cytotoxic and neurotoxic. Electron microscopy demonstrates a lack of innervation of surface epithelium, glands and blood vessels. Thus, these immature leaky blood vessels are devoid of normal vasomotor regulation. However, the specific trigger for this cascade of events remains unknown.

Allergy is suspected because of the predominance of eosinophils in nasal polyps. There is also the increased histamine levels and the presence of IgE. There is no significant difference in serum IgE levels, but researchers have shown increased IgE concentrations in polyp tissue. Mucosal mast cells are increased, but their degranulation does not appear to be IgE mediated. In addition, epidemiological data suggests that nasal polyposis occurs more commonly in non-atopic patients than atopic patients. As I mentioned earlier, nasal polyps are seen in 7% of asthmatics. This breaks down even further to 13% of non-atopic asthmatics vs. 5% of atopic asthmatics. Also, there is no increased incidence of allergies in patients who have nasal polyposis. The etiology may or may not be associated with allergy, but when the two conditions co-exist in the same patient, allergies can cause an exacerbation of nasal polyps.

Per Larsen and Mirko Tos published some interesting cadaver studies evaluating the origin of nasal polyps. They examined cadaver nasoethmoid complexes from autopsy specimens noted on anterior rhinoscopy to have polyps. Their goal was to evaluate if nasal polyps originated from either the nasal mucosa or anterior ethmoid air cells. They found that polyps originate from the nasal mucosa and were consistently related to sinus ostia. So, in theory, the osteomeatal part of the nasal mucosa is exposed to pathologic stimuli from the sinuses. This leads to polyp formation and begins a vicious cycle, leading to blockage of sinus ventilation and further polyp formation. This results in stagnant secretions and resultant infection. This infectious mechanism with stagnant secretions can be linked to polyp formation in Kartagener's Syndrome and cystic fibrosis. Additional support for an infectious etiology lies in the fact that intense antibiotic therapy against pseudomonas along with mucolytic therapy in these patients reduces polyp frequency to 2%-5%. In 1993, Norlander et al induced unilateral maxillary sinusitis in rabbits by blocking sinus ostia and injecting 3 different bacteria: pneumococcus, staph aureus, and bacteroides fragilis. Polyps were present in some 20% to 60% of the infected sinuses regardless of inciting pathogen. They were occasionally accompanied by polyp formation in the adjacent nasal mucosa. Histologically, deep mucosal trauma or epithelial desquamation seemed critical for polyp formation. But, as we all know, chronic sinusitis and hypertrophic mucosa are not always associated with nasal polyposis. Opacification of the paranasal sinuses can be seen in the absence of polyps in the nasal cavity.

The most common initial complaint of patients with nasal polyps is nasal obstruction. Other prominent symptoms include allergic complaints like watery rhinorrhea, sneezing, and itchy eyes. They may also complain of headache, asthma, or postnasal drip. Anosmia is another important symptom to ask about. Pain is usually present when an acute infection exists. Some may have middle ear pathology or rhinitis medicamentosa from chronic vasoconstrictor use. Many have had prior nasal surgery.

In severe cases, on physical examination, the nasal bones may be widened with polyps extruding from the nose. In other cases they can be visualized with a nasal speculum or an endoscope. They appear as smooth, gray, glossy lesions hanging from a narrow stalk. They are soft, mobile, and nontender to palpation. They are frequently multiple, bilateral, and vary in size. With the use of topical steroids, polyps may only be identified at the time of surgery with medialization of the middle turbinate. Other nasal abnormalities including septal deviation, condition of the nasal mucosa, and the presence of pathologic secretions should be noted.

CT scan should be used for evaluation of the paranasal sinuses in all cases. Coronal CT with bone windows is the standard x-ray study obtained. Review of the CT scan is done in a systematic approach with particular attention to the nasal septum, middle turbinates and bony sinus walls. There may be bony expansion and erosion. Air fluid levels and completely opacified sinuses should be noted. Attention should also be directed towards the density of the opacifications.

Although nasal polyps are the most common benign intranasal tumor, the differential diagnosis would include meningoceles or meningomyeloceles that may project through the nose via a cribriform plate defect or a dermoid cyst. Other benign possibilities include hemangiomas or angiofibromas. Other tumors including inverted papillomas, squamous cell carcinomas, and sarcomas can present with features similar to nasal polyposis. However, neoplasms are usually unilateral, friable, firm, and bleed spontaneously.

Before discussing medical and surgical treatment options, I want to briefly discuss means of assessing treatment efficacy. Symptom scores and presence of polyps on physical exam are two of the most common methods of measuring responses. Unfortunately, there is no rhinology equivalent of the pure tone audiogram to measure nasal obstruction, although both acoustic rhinometry and rhinomanometry have been used. Rhinomanometry is a technique for measuring nasal airway resistance. However, because more than 80% of the nasal airway resistance is produced in the valve area, and most polyps are behind that area, rhinomanometry is a rather insensitive method. Acoustic rhinometry is a volumetric method used to describe the geometry of the nasal cavity, which is based on the reflection of an acoustic signal entered into the nasal cavity. Other groups have studied the nasality of speech in healthy subjects versus those with nasal polyposis.

Treatment of nasal polyps revolves around medical and surgical management, or a combination of the two. The goals of medical management of nasal polyposis are to eliminate the polyps and rhinitis symptoms, to re-establish nasal breathing and olfaction, and to prevent recurrence without necessarily eliminating sinus pathology. Complete elimination of sinus pathology may be unrealistic, as many patients can be symptom free despite sinus opacification on their CT scan.

The mainstay of medical treatment is nasal steroids. On a cellular level, steroids bind to cytoplasmic glucocorticoid receptors and, within hours, they modify gene transcription inducing a change in cellular protein synthesis. There is evidence that the inflammatory reaction in asthma, allergic rhinitis, and nasal polyposis is in part driven by T lymphocytes and the cytokines products they produce. Cytokine production and activation is highly steroid sensitive. Studies have shown that topical steroids reduce the total number of T lymphocytes in nasal polyp tissue. Topical steroid therapy has not been shown to have any significant effect on the numbers of mast cells, but they do reduce the number of activated eosinophils. Polyps have leaky blood vessels, which result in an edematous stroma. Steroids have no direct effect on these leaky blood vessels, but they do have an indirect effect through inhibition of the formation of mediators and cytokines. As evidence of this anti-exudative effect, studies of nasal secretions following steroid therapy have shown a decreased albumin level. The clinical effects are manifest over several days.

Topically applied steroids have been studied in several controlled trials. Steroid therapy should at least improve nasal breathing. However, a patent airway is not necessarily a normal airway. Pressure from long standing nasal polyps may have widened the nasal cavity. This is a subjective symptom, and studies do support improvement in nasal breathing. More objective parameters like nasal peak flow and acoustic rhinometry have also demonstrated increases in nasal patency.

Topical steroids do reduce rhinitis symptoms by approximately 50%, but one must remember that these patients suffer predominantly from nasal obstruction with little sneezing and rhinorrhea. Studies do show that over 1-year, the anti- rhinitis effect is maintained and that symptoms slowly recur when treatment is discontinued.

Anosmia is a very annoying symptom for most patients. Clinical studies indicate that the response is poor especially when compared with systemic steroids, although controlled studies often pay little attention to this area. One recent study did show an improvement of 70%-80% of patients using a semiquantitative measurement, but also a 45% improvement in the placebo group. This difference was not statistically significant.

Several controlled studies document results ranging from reduction in polyp size to total polyp disappearance. However, polyps may not be completely eliminated from the upper part of the nose that cannot be reached by a nasal aerosol or spray. Reduction in size may make some patients symptom free, but small polyps still present in the upper nose may continue to compromise the osteomeatal complex and sense of smell. Thus, recurrence should be defined as polyps that can be identified by rhinoscopy and that are symptomatic. Studies have also looked at the effect of nasal steroids on the recurrence of polyps following surgical therapy, and this role of combined treatment will be dealt with shortly.

Adverse effects from nasal steroids are few and range from epistaxis to headaches and dizziness. There is minimal systemic absorption, and the dose is well below that required for adrenal suppression.

Lund et al, in May of 1998, performed a double blind randomized placebo controlled study of 34 patients with nasal polyposis scheduled for ESS. They demonstrated improvement in polyp scores and acoustic rhinometry versus placebo. Nasal obstruction scores also improved by almost 50% after 12 weeks of therapy.

Iin summary, recent studies have examined the effects of topical steroids versus placebo for anywhere from 4 to 26 weeks. They all document statistically significant improvements in subjective symptom scores and objective nasal flow rates. Symptoms can be controlled in anywhere from 50% up to 80% of patients. However, they do not abolish the need for surgical intervention. More study is warranted, especially examining in the area of cost effectiveness of medical treatment in delaying or preventing surgical therapy.

The benefit of systemic steroid treatment has been well documented, but routine use is often not recommended. Van Camp and Clement studied 25 patients with severe polyposis with no contraindications to systemic steroid therapy. These patients were treated with 4 days of 60mg of prednisolone followed by a gradual taper. Seventy-two percent showed subjective improvement with reduction in polyp size. Interestingly, only 52% displayed clear improvement radiographically. Those that did improve by CT scan were maintained on topical steroids. The majority recurred in 5 months. Those that did not improve by CT scan underwent endoscopic sinus surgery. They also note that pre-operative steroid therapy facilitated surgery. Contraindications to systemic therapy included glaucoma, diabetes, and prior tuberculosis. More relative contraindications include hypertension and peptic ulcer disease.

Surgery is an option for those patients whose quality of life is disrupted, who have failed an adequate trial of medical therapy, or who have a contraindication to some aspect of medical therapy. But, surgery is elective, and many feel should be considered as a part of a continuum of therapy and not independent of medical treatment. Surgical removal is not always a complete answer to the problem. The decision to intervene surgically may also depend on the presence of asthma, for which increasing steroid doses are required for control.

The spectrum of surgical treatment encompasses a variety of procedures ranging from snare and forcep polypectomy under local anesthesia to intranasal ethmoidectomy, total sphenoethmoidectomy, or functional endoscopic sinus surgery. For clarity, when I mention surgical therapy, I am referring to functional endoscopic surgery versus other more traditional techniques.

To aid in identifying normal landmarks, ESS usually begins with debulking of polyps as atraumatically as possible. This can be done with a snare, grasping forceps, laser, or a microdebrider. Once the polyps have been removed, the infected sinuses are approached and opened endoscopically. On exam the majority of patients have CT evidence of sinusitis in addition to nasal polyps. The extent of the procedure is variable and should be tailored to the patient's disease.

There have been several series that examine follow-up in patients with nasal polyposis after endoscopic sinus surgery. Study sizes vary from 100 to 250 patients with follow-up ranging from 18 months to 4 years. Determining patient satisfaction through relief of symptoms or examining the sinonasal area for the presence of disease usually assesses treatment outcomes. Studies show 80% -90% of patients reported symptom improvement with follow-up anywhere from one year to four years. These numbers are lower if one looks at patients that are completely symptom free. Others have also showed objective evidence of improvement in nasality of speech and unilateral reductions of airflow resistance.

Kennedy reviewed 120 patients undergoing endoscopic sinus surgery, of which 28% had diffuse polyposis and 31% had polyps arising from the middle meatus. He found the most important predictor of symptom improvement was the preoperative extent of disease. This may relate to the severity of underlying conditions like asthma and Samter's triad. Other researchers have noted that these patients tend to do worse. Also, patients with nasal polyposis who are surgical candidates tend to have more extensive disease involvement.

Despite excellent subjective improvement, many patients may have residual evidence of disease on endoscopic exam. Kennedy found the same degree of subjective symptomatic improvement in patients without polypoid disease, those with middle meatal polyposis, and those with diffuse polyposis. However, the endoscopic findings were vastly different. Seventy-seven percent of those patients without pre-operative polypoid disease had normal nasal cavities on follow up endoscopy at 18 months, while of those patients with diffuse polyposis, only 23% had normal nasal cavities on follow-up endoscopy. It is imperative to identify such early asymptomatic recurrence and to treat it medically or with local debridement before it becomes symptomatic.

Of course, ESS is not without complications, which include, among others, bleeding, orbital hematoma, CSF leak, and meningitis. The most common long-term complication of nasal polyp surgery is recurrence. Scahaitkin and May, in their follow-up of 100 patients for 4 years, noted a drop in success rates from 1- to 4-years, largely from patients with recurrent symptomatic polyposis.

Others have noted that nasal polyps are a symptom of systemic disease, the etiology of which is not altered by surgery. Therefore one should expect a higher rate of recurrence, especially with longer follow-up. Patients with recurrent polyposis compromise anywhere from 20%-40% of series of revision ESS. Perhaps control, rather than cure is a more realistic long-term goal.

The significant incidence of persistent disease highlights the need for continued topical steroid therapy. Anti-histamines and decongestants may improve a patient's symptoms, but they do not prevent recurrence. A number of studies have shown that long term post-operative treatment with topical steroids reduces the severity of recurrence. Patients who present for the first time and those with several years in between recurrences do not necessarily require post-operative treatment. A study by Hartwig et al from 1988, showed that in first time surgical patients, there was no significant effect in recurrence vs. placebo. They did confirm the benefit of post-operative topical steroids vs. placebo in those patients with recurrent nasal polyposis. However, those who had prior polypectomies had worse polyp scores with placebo than those maintained on nasal steroids.

There are no studies that clearly define when post-operative steroids should be started. The majority of studies do not specify this. Some comment that nasal steroids were begun in the post-operative period, while others wait until there is complete healing of the nasal cavities. There has been one study in which 20% of patients begun on post-operative topical steroids developed acute gram positive pan sinusitis. These patients started their topical steroid therapy after endoscopic demonstration of total epithelialization and absence of crustations for 10 days. They developed sinusitis approximately two weeks later.

As I mentioned earlier, treatment of nasal polyposis should involve a combination of medical and surgical management. Yet there have been a few studies that have pitted the two modalities against each other. Settipane et al studied 29 patients that underwent 49 surgical polypectomies with a recurrence rate of 1.7 and mean interval between recurrence of 6.3 years. Ten patients underwent 34 medical polypectomies or prednisone bursts with a recurrence rate of 3.4 and an interval of 0.9 years. Both groups were maintained on nasal steroids. Lilholdt et al randomized 53 patients to snare polypectomy versus an intramuscular steroid injection of Diprospan, a 2-cc suspension of betamethasone diproprionate and betamethasone disodium phosphate. Both groups received nasal steroids during the one year of observation. Both groups showed increases in mean nasal expiratory peak flows and olfaction. In general, the results in the two treatment arms were similar. Initial treatment was repeated in four patients in the medical group vs. three patients in the surgical group.

Surgical series consistently reveal poor control of nasal polyposis in patients with asthma, and this is even more pronounced in patients with the aspirin triad. These patients have increased recurrence rates and decreased control of symptoms. Earlier literature reported that polyp surgery would exacerbate asthma. Even Dr. Samter reported in 1958, that 10% of the 182 patients he studied had the onset of asthma within 9 months of polypectomy. However, research since that time does not support those claims. Series show that most patients showed improvement or at least were unchanged in the control of their asthma after surgery. Jankowski et al studied 50 patients who underwent a radical endoscopic ethmoidectomy. Thirty patients had asthma and 12 of those had aspirin intolerance. After 18 months, 91% of patients improved symptomatically. No patients had more than one asthma attack per week and 75% had fewer than four attacks per year. In addition, 25% were dependent on oral or injected steroids pre-operatively vs. only 8% post operatively. There were no cases of asthma in the control group of 20 patients with only nasal polyposis. There is a minimal risk of intra-operative bronchospasm. This incidence is higher during local anesthesia than general anesthesia.

Control of disease in this subset of patients is very challenging. Recent advances in medical therapy have involved the use of leukotriene inhibitors. Leukotrienes are products of arachidonic acid metabolism. Arachidonic acid is released from cell membrane phospholipids via the enzyme phospholipase A2. This substrate can be metabolized through one of two pathways. Aspirin inhibits the cyclo-oxygenase pathway. The other pathway is the 5 lipo-oxygenase pathway, which produces leukotrienes. Evidence for the role of leukotrienes in the pathogenesis of aspirin sensitivity lies in the fact that urinary leukotriene concentrations are increased after aspirin challenge. These patients also have increased target organ sensitivity to leukotrienes. Published studies support the use of leukotriene inhibitors in aspirin sensitive asthma. These drugs are effective in blocking aspirin-induced asthmatic responses. Their effect on nasal polyposis has yet to be studied.

In closing, I offer this quote from Dr. Mark May from the University of Pittsburgh:
"I'm an old doctor now, but I remember when I was a young doctor. We'd look in the nose with a headlight and speculum, or before electricity, with the reflected light of the sun, sometimes the moon. We saw this glistening stuff in the nose, and we had this little snare that somebody before us had designed. We reached in and pulled them out, and if we got a whole bunch of them, we thought we were doing well. We never really looked in the nose to see the position of the middle turbinate. Then steroids came along and made the polyps go away, but made the face round and the back humped up. It wasn't very good, and when you stopped the steroids, the polyps came back. Then CT scans came along, and we realized, 'Gee, these patients have pansinusitis. That's bad.' Based on the marked changes indicating pansinus involvement on CT scan, we began to think these patients were surgical candidates. It is interesting to note that some of these patients had few or no symptoms. Such a patient is not a surgical candidate. A symptomatic patient with massive polyposis who does not respond to intensive medical therapy and has persistent headache, fullness, and pressure, and postnasal discharge and can't sleep at night because of difficulty breathing often get immediate relief after surgery."

Nasal polyps are the most common benign intranasal tumor. They are associated with other disease states, and their exact etiology is unknown. Treatment revolves around a continuum of medicine and surgery with surgery being reserved for those with extensive disease that have failed adequate medical therapy. Treatment should be aimed toward control of the disease process.

Case Presentation

FK is a 79-year-old female with a chronic history of bilateral nasal obstruction for several years. She had undergone one prior "polypectomy" several years ago in her native country. This procedure initially relieved her obstructive symptoms, however, her symptoms have worsened over the last year, despite treatment with nasal steroids. She also complained of anosmia and occasional postnasal drip. She denies any rhinorrhea, headache, asthma, or aspirin sensitivity.

Past medical history was positive for hypertension. Past surgical history as noted above. Her current medications included Flonase, Adalat, Clonidine, and Lorazepam. She had no known drug allergies.

On physical examination her ears and tympanic membranes were clear and intact bilaterally.

Anterior rhinoscopy revealed polyps present in both nares extending into the vestibule. There was mild erythema of the mucous membranes. Inferior turbinates could be visualized bilaterally. There were no purulent secretions noted. Oral cavity and oropharynx were clear. Her true vocal chords were mobile bilaterally. No neck lymphadenopathy or masses were observed.

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