| disease | Nasal Polyp |
Nasal polyps are a common nasal condition and are also associated with certain systemic diseases. They result from tissue edema caused by long-term inflammatory reactions of the nasal mucosa. Nasal polyps often originate from the middle meatus sinus ostium, the nasal meatus complex, and the ethmoid sinus. The highly edematous nasal mucosa protrudes and droops from the middle meatus and sinus ostium into the nasal cavity, forming polyps. Due to the multifactorial nature of the disease and the significant tendency for postoperative recurrence, nasal polyps hold an important position among nasal diseases.
bubble_chart Epidemiology
According to statistical data from the 1950s to 1960s in China, patients with nasal polyps accounted for 1-3% of otolaryngology outpatient visits. Recent foreign statistics show that nasal polyps account for 8.5% of rhinitis patients (Settipane, 1987). This condition is rare in children, with the majority of cases occurring in middle-aged individuals, and the incidence is slightly higher in males than in females.
The cause of this disease remains unclear. It is currently believed that chronic upper respiratory tract infections and allergic reactions are the main causes of nasal polyps.
I. Chronic Infection Woakes (1885) was the first to propose that repeated infections of the ethmoid sinus cause necrotic inflammation of the mucous membrane, ultimately leading to ethmoid sinus polyps. Many still agree with this view today. During infectious inflammation, bacterial toxins and inflammatory mediators released can obstruct lymphatic drainage in the mucous membrane, cause venous stasis, dilate small blood vessels, increase exudation, and lead to mucous membrane edema. Seasonal toxins also damage the nerve endings that control blood vessels, further dilating the vessels and increasing exudation. Long-term edema weakens the barrier function of the mucous membrane, leading to repeated infectious inflammatory reactions, further exacerbating mucous membrane edema, and eventually promoting polyp formation. Stierna (1991) recently confirmed that blocking the maxillary sinus ostium in animals and introducing pathogenic bacteria into the sinus resulted in polyp formation in the sinus mucous membrane. Additionally, in certain congenital respiratory mucous membrane abnormalities (such as cystic fibrosis and immotile cilia syndrome), repeated respiratory infections often lead to nasal polyps. In such nasal polyp tissues, a higher number of neutrophils is observed, but clinical observations show that antibiotic treatment for nasal polyps is minimally effective. Although X-ray images often show thickened mucous membranes in the sinuses of nasal polyp patients, indicating "sinusitis," pus cells and bacteria are rarely found in sinus lavage fluids (Dawes et al., 1989). Therefore, it is believed that infections may promote polyp growth but are not a necessary condition for polyp formation.
II. Allergic Reactions Kern and Schenck (1933) based on clinical statistical data analysis, believed that nasal polyps are the result of allergic reactions. They found a higher incidence of nasal polyps in allergic respiratory diseases such as asthma and hay fever (seasonal rhinitis), but rarely in infectious respiratory diseases (lung abscess, bronchiectasis, and subcutaneous lung nodules). Many subsequent studies support this view, mainly based on: ① Nasal polyp tissues contain high levels of histamine (Bumsted, 1979; Dong Zhen, 1983); ② Nasal polyp tissues have a large number of eosinophil infiltrations and degranulated mast cells (Friedman, 1989; Drake-Lee et al., 1984, 1987); ③ IgE-producing cells are present in nasal polyp tissues, and IgE levels in polyp fluids are higher than in serum (Drake-Lee, 1984); ④ Specific allergens can stimulate nasal polyp tissues to release chemical mediators similar to those in IgE-mediated allergic reactions (Kaliner et al., 1973); ⑤ Compared to nasal mucous membranes, nasal polyp tissues show significantly increased arachidonic acid metabolism, producing large amounts of leukotrienes and inflammatory cell chemotactic factors (Jung, 1987). These facts suggest that IgE-mediated allergic reactions in the nasal mucous membrane release large amounts of histamine, leukotrienes, and inflammatory cell chemotactic factors. These chemical mediators can cause local vasodilation, increased exudation, tissue edema, glandular hyperplasia, and eosinophil infiltration. Eosinophils can also release cytotoxic substances such as major basic protein (MBP), damaging the nerve endings of small blood vessel walls, further facilitating vasodilation and increased exudation. This localized allergic reaction is difficult to detect with conventional allergen skin tests or serological tests because specific IgE is mainly present in polyp cyst fluids (Jones et al., 1987; Frenkiel et al., 1985). Dong Zhen (1983) found that in some nasal polyp patients, the level of IgG immune complexes in serum was positively correlated with the IgG content in polyp fluid, but the IgG content in polyp fluid was relatively low in these patients. Ogawa (1986) and Small (1986) discovered high levels of IgE immune complexes in polyp fluid. Based on this, it was speculated that type III hypersensitivity (immune complex type) might be one of the mechanisms of nasal polyp formation. However, Jankowski (1989) did not find immune complex deposition around small blood vessels and within the epithelium in polyp tissue using immunofluorescence.Some other scholars, based on large-sample clinical data and laboratory analysis, hold different views on the role of allergic reactions in the formation of nasal polyps. Caplin et al. (1971) found that the incidence of nasal polyps was 0.5% among 3000 specific individuals. Settipane et al. (1977) discovered that among 6037 patients with asthma and rhinitis, the incidence of nasal polyps was 5% in those with positive allergen skin tests, while it was 12% in those with negative skin tests. Drake-lee (1984) investigated 200 consecutive nasal polyp patients admitted to Addenbrooke's Hospital in Cambridge over two years and found no correlation between the patients' medical history, allergen skin tests, serum IgE levels, and allergic reactions. Additionally, children prone to allergic diseases rarely develop nasal polyps. Jan-Kowski et al. (1989) used immunohistochemical methods to find a large number of eosinophils infiltrating the polyp tissue but could not confirm any relationship with allergic reactions, as IgE-producing cells were scarce in the polyp tissue. Therefore, he believed that only by clarifying the mechanism of eosinophil infiltration in polyp tissue can we understand the cause of nasal polyp formation.
Zhao Xiujie et al. (1995) used immunohistochemical methods to find a large number of estradiol receptor-positive cells in nasal polyp tissue, which were related to the number and distribution of mast cells but not to gender. It is known that estradiol can enhance the ability of mast cells to release histamine, so the presence of estradiol receptor-positive cells suggests that estradiol may play a role in the formation of polyps.Petruson et al. (1988) found high concentrations of insulin-like growth factor I (IGF-I) in nasal polyp tissue. Based on this, they speculated that in the enclosed sinuses, due to infectious or allergic inflammatory reactions stimulating the sinus mucosa, macrophages in the mucosa release IGF-I, which accumulates in the mucosa and can stimulate mucosal proliferation for a long time. When the proliferating mucosa fills the sinus cavity, it protrudes into the nasal cavity through the sinus opening. This long-standing growth stimulation and local inflammatory reaction are important factors leading to polyp formation.
In summary, nasal polyps are the result of multiple factors. The primary factors may vary depending on conditions, but they all cause local mucosal inflammatory reactions. Eosinophil infiltration, degranulated mast cells, and extreme tissue edema constitute the pathological basis of nasal polyps.
bubble_chart Pathological Changes
Nasal polyps are composed of highly edematous nasal mucosa. The epithelium is pseudostratified ciliated columnar epithelium, with some areas undergoing squamous metaplasia due to long-term external stimulation. Beneath the epithelium lies edematous loose connective tissue infiltrated with inflammatory cells, including plasma cells, neutrophils, eosinophils, and lymphocytes. The infiltration of eosinophils is a distinctive histological feature of nasal polyps. Mygind (1979) classified nasal polyps into eosinophilic and neutrophilic types, with the latter suggesting purulent infection of the nasal mucosa, which may be related to polyp formation. Historically, nasal polyps have been divided into three pathological types based on histological composition: edematous, glandular, and fibrous types. The first two types result primarily from inflammatory cell infiltration, increased vascular exudation, and active glandular secretion, while the latter arises from fibroblast and collagen fiber proliferation. Kakoi et al. (1987) proposed that the first two types represent active manifestations of nasal mucosal tissue response, whereas the fibrous type represents the terminal stage of tissue response. The complete pathological progression involves round cell infiltration into the sinus mucosa, lamina propria edema, leading to localized mucosal protrusions and glandular hyperplasia. As the lamina propria edema worsens, the protruding mucosa can expand into the nasal cavity through the sinus ostium and continue to grow. This represents the active stage, some of which may progress to the fibrous type, the terminal stage.
bubble_chart Clinical Manifestations
Patients often have a long history of nasal diseases when they seek medical attention. Initially, they may feel as if there is mucus in the nose that cannot be blown out, which is caused by the upper part of the nasal cavity being blocked by polyps. At night, significant stuffy nose may occur, leading to mouth breathing, and over time, this can lead to chronic pharyngitis. The stuffy nose is usually persistent, and nasal decongestants have little effect because polyps have few blood vessels. Since polyps also lack nerve distribution, patients rarely sneeze. However, if there is allergic inflammation of the nasal mucosa, symptoms such as sneezing and clear nasal discharge may occur. The secretions in nasal polyp disease are mostly seromucous, and if infection occurs, there may be purulent secretions. Continued growth and enlargement of polyps not only significantly worsen the stuffy nose but can also cause dizziness or headache, possibly due to sinus involvement. Sinus involvement can occur in two ways: one is due to the same pathology as the nasal polyps, and the other is due to secondary sexually transmitted disease changes caused by polyps obstructing sinus drainage. The former involves hyperplastic thickening of the sinus mucosa, known as hyperplastic sinusitis, and nasal polyps complicated by sinusitis mostly fall into this category. Antibiotics are ineffective for this type of sinusitis, while corticosteroids can provide varying degrees of improvement. The latter, secondary infection, can lead to suppurative sinusitis. Patients with nasal polyps often have reduced or absent sense of smell. Large polyps blocking the posterior nasal cavity or even protruding into the nasopharynx can cause hearing loss and other ear symptoms due to compression of the Eustachian tube orifice.
A few large polyps can also cause invasive complications. Rapidly growing, large polyps can mechanically compress and destroy the walls of the sinuses or the roof of the nasal cavity, subsequently invading the orbit, frontal sinus, anterior cranial fossa, sphenoid sinus, and middle cranial fossa. For example, Kaufman et al. (1989) reported a case where a nasal polyp filled the nasal cavity, extended through the sphenoid sinus into the intracranial pituitary fossa and basal cistern, also invaded the orbit, and compressed the cavernous sinus. The patient exhibited ophthalmoplegia, exophthalmos, and visual field loss.
Since the nasal mucosa is part of the entire respiratory mucosa and there is a nasopulmonary reflex between the nose and the airways, nasal mucosal lesions can be associated with other respiratory diseases through certain mechanisms.
1. Bronchial asthma: A large amount of clinical data has found a higher incidence of asthma in patients with nasal polyps. Moleney et al. (1977) summarized the incidence rate as 2.9-72%, while 23-42% of asthma patients have nasal polyps. Recently, Jäntt-Alanko (1989) found that 34 out of 85 nasal polyp patients had asthma (40%). The earliest to notice the relationship between nasal polyps and asthma was Voltolini (1871), and later Vander Veer (1920) reported that nasal polyp surgery could worsen asthma, drawing attention to the relationship between the two, though the exact mechanism remains unclear. Robison (1962) found in his research that compressing the maxillary sinus mucosa with a balloon could induce asthma attacks, suggesting that the nasopulmonary reflex is involved in this mechanism. The histological changes in both are similar, involving mucosal edema and eosinophil infiltration.
2. Aspirin intolerance and Widal's triad.
3. Congenital abnormalities of the respiratory tract membrane These conditions include cystic fibrosis and immotile cilia syndrome. Among these, patients with cystic fibrosis are more likely to develop nasal polyps. The incidence of polyps in pediatric patients ranges from 7% to 28% (Schwachman, 1962; Schramm, 1980), and reports indicate that up to 48% of adult patients may develop polyps (di Sant'agnese et al., 1979). Cystic fibrosis is a genetic disorder predominantly found in Caucasians, with higher prevalence in North America and Europe, and is extremely rare among Asians. The disease primarily affects the mucus-secreting cells of glands, leading to excessive and viscous secretions. Consequently, patients' respiratory tracts are often obstructed by large amounts of thick secretions, resulting in recurrent infections, pneumonia, lung abscesses, or bronchiectasis and pulmonary fibrosis. A characteristic feature in pediatric patients is that the sodium and chloride levels in their sweat are 3 to 4 times higher than normal, while in adults, a deficiency of trypsin in duodenal fluid can be detected. The recurrent infections caused by these congenital abnormalities of the respiratory epithelium may be related to the formation of polyps.
4. Hypertension Granstrom (1990) investigated 224 patients with nasal polyps and found that 78 of them (34.7%) had hypertension. These patients had a history of nasal polyps for more than 10 years. He suggested that, similar to sleep apnea syndrome, long-term obstruction caused by nasal polyps could contribute to the development of hypertension.
If the medical history is long and the polyp is large, it can cause changes in the nasal appearance. The nasal bridge becomes wider and flatter, with bulges on both sides of the nasal dorsum, known as "frog-shaped nose." If the polyp protrudes from the anterior nostril, due to stimulation from air and dust, the surface of the nasal flesh at the anterior nostril appears light red. In the nasal cavity, the polyp can be seen as a round, smooth-surfaced, soft, grayish-white cystic mass, with its stalk located in the middle nasal meatus. Johansen et al. (1993) proposed a scoring method to describe the size of polyps: a small polyp causing only grade I stuffy nose, not reaching the upper edge of the inferior turbinate, is scored 1; a polyp causing more noticeable stuffy nose, with its size between the upper and lower edges of the inferior turbinate, is scored 2; a polyp causing complete nasal obstruction, with its front end reaching below the lower edge of the inferior turbinate, is scored 3.
bubble_chart Treatment Measures
The treatment principle should be to relieve stuffy nose, prevent recurrence, and adopt the following treatment measures based on specific conditions:
I. Medical Therapy Since nasal polyp is the result of long-term inflammatory response of the nasal respiratory mucosa, adrenal corticosteroids can be used for treatment. Corticosteroids not only can reduce the size of the polyp or even make it disappear, but also can delay or prevent the recurrence of the polyp when applied post-surgery. Corticosteroids can be administered systemically or intranasally. If there are no contraindications for corticosteroid use, systemic application is suitable for the following situations: ① The polyp is large, making it inconvenient to introduce instruments into the nasal cavity during surgery; ② Initial diagnosis cases where the patient is willing to undergo medical treatment. The method is to take 30mg of prednisone orally daily for 7 days, then reduce the dose by 5mg daily, with the entire course not exceeding two weeks. This short-term intensive therapy does not cause significant systemic side effects clinically. Generally, the size of the polyp can be significantly reduced with the above treatment. Some patients experience relief from stuffy nose and significant improvement in smell after a few days of oral medication. At this point, surgical removal or switching to intranasal local application can be considered.
The advantage of intranasal local application of corticosteroids is that it avoids systemic side effects of corticosteroids while maintaining effective drug concentration locally. Local application is suitable for: ① Initial diagnosis cases where the polyp is small and does not extend beyond the lower edge of the middle turbinate; ② Patients who respond well to oral prednisone and are willing to continue medical treatment; ③ Post-surgical removal to prevent recurrence. The most common dosage form for intranasal application of adrenal corticosteroids is aerosol, as it is convenient to use and does not require a specific posture. Additionally, there are nasal drops, which require the correct nasal drop posture but have the advantage of simple preparation and low cost. The main corticosteroids for intranasal application are beclomethasone dipropionate, flunisolide, and budesonide. These corticosteroids are characterized by their low absorption into the bloodstream through the nasal mucosa, thus minimizing systemic side effects. Recently, Johansen (1993) compared the efficacy of budesonide aerosol and nasal drops in treating nasal polyps and found that both dosage forms had the same efficacy. The authors (1995) also achieved good results using 0.1% vinegar triamcinolone acetonide nasal drops. The following situations can significantly affect the efficacy of intranasal medication: ① The nasal polyp is too large, preventing the medication from entering the nasal cavity. In this case, surgical treatment should be performed first, followed by intranasal medication to prevent recurrence. ② Concurrent mixed infection of the nose and sinuses, in which case antibiotic treatment or sinus cleaning should be performed. ③ The polyp itself is in an active stage and growing too fast, in which case a systemic corticosteroid intensive therapy can be considered.
II. Surgical Treatment For cases where the nasal cavity is mostly or completely blocked, severely affecting physiological functions, surgical treatment should be performed first. A comprehensive physical examination should be conducted before surgery. If the patient has cardiovascular diseases or is in an asthma attack stage, surgery should be postponed until the condition stabilizes. The main surgical methods are simple nasal polyp removal and intranasal ethmoidectomy.
1. Simple Nasal Polyp Removal Used for cases with clear root stalks and no history of nasal polyp removal. Under local anesthesia, a nasal polyp snare is used to loop around the stalk of the polyp, tightened, and then pulled out rapidly from the nose, removing the polyp along with its root stalk. If any root stalk remains, it should be completely removed with forceps. Pulling out the polyp may sometimes open the ethmoid sinus. If the sinus mucosa has polypoid changes, it should be treated with seasonal epidemic intranasal ethmoidectomy.
2. Intranasal Ethmoidectomy Mainly suitable for cases where the ethmoid sinus mucosa has been replaced by polyp tissue and there is a history of multiple nasal polyp removals. During the surgery, the ethmoid cells are fully opened, and the polyps within the sinus are completely removed. Thorough surgery can significantly reduce the recurrence rate of polyps. In recent years, the development of endoscopic sinus surgery has provided a precise, accurate, and effective method for ethmoidectomy, significantly reducing the recurrence rate of nasal polyps post-surgery. Literature reports that the recurrence rate can be reduced to below 20%.
In summary, the treatment of nasal polyps should follow the principles outlined below:
1. For first-visit patients, if the polyp is large and severely affects nasal function, surgical treatment should be performed first; for those with smaller polyps and mild stuffy nose symptoms, medical treatment can be considered. If the efficacy is poor after one month, surgical treatment should be performed.
2. For patients with sinus infection, anti-infection treatment should be prioritized, or nasal polyp removal should be performed to facilitate sinus drainage.
3. For recurrent nasal polyps, ethmoid sinusectomy should be performed, followed by intranasal application of corticosteroids for 1 to 2 years postoperatively.
Nasal polyps are mostly bilateral. If a unilateral polyp-like mass is found, the following diseases should be considered:
1. Maxillary sinus posterior polyp: Commonly seen in adolescents. Anterior rhinoscopy or nasal fiber endoscopy reveals a grayish-white, smooth pedicle extending from the anterior part of the middle nasal meatus to the posterior nasal aperture. Posterior rhinoscopy shows the polyp located at the posterior nasal aperture, with larger ones potentially protruding into the nasopharynx or even the oropharynx.
2. Nasal septum hemorrhagic polyp: Commonly seen in young adults. The mass usually occurs on the septum, is dark red, solitary, and not large in size, easily bleeding upon touch. Patients often have a history of epistaxis. It is generally believed to be caused by residual hematopoietic cells during embryonic development.
3. Inverted papilloma: Often associated with a history of epistaxis or bloody nasal discharge. The tumor is red or grayish-red with an uneven surface. Small tumors resemble polyps, but polypectomy results in more bleeding. It also bleeds easily upon touch. Final diagnosis requires pathological examination.
4. Intranasal malignant tumor: The mass is dark red, bleeds easily upon touch, has an uneven surface, and is accompanied by a foul odor. Patients are usually middle-aged or older.
5. Intranasal meningoencephalocele: The mass is usually located at the top of the nasal cavity, smooth, and pink. Nasal congestion is not very obvious, with a long history and slow progression. Commonly seen in children.
6. Other rare intracranial tumors protruding into the nasal cavity: Such as chordoma, neuroblastoma, pituitary adenoma, etc.
Additionally, elderly patients with a history of multiple nasal polyp surgeries should be monitored for the possibility of malignant transformation, especially if there is significant bleeding during surgery.
X-rays of nasal polyp patients often show uniform cloudy opacity in the ethmoid sinus. Thickening of the maxillary sinus mucosa and sometimes small semicircular shadows suggest mucosal polyps in the sinus cavity. These X-ray features are indicative of hyperplastic sinusitis. If secondary infection occurs, it manifests as signs of suppurative sinusitis.
