Nasal Polyps

Updated: Jun 17, 2016
  • Author: John E McClay, MD; Chief Editor: Ravindhra G Elluru, MD, PhD  more...
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Overview

Background

Broadly defined, nasal polyps are abnormal lesions that originate from any portion of the nasal mucosa or paranasal sinuses. Polyps are an end result of varying disease processes in the nasal cavities. The most commonly discussed polyps are benign semitransparent nasal lesions that arise from the mucosa of the nasal cavity or from one or more of the paranasal sinuses, often at the outflow tract of the sinuses.

Multiple polyps can occur in children with chronic sinusitis, allergic rhinitis, cystic fibrosis (CF), or allergic fungal sinusitis (AFS). An individual polyp could be an antral-choanal polyp, a benign massive polyp, or any benign or malignant tumor (eg, encephaloceles, gliomas, hemangiomas, papillomas, juvenile nasopharyngeal angiofibromas, rhabdomyosarcoma, lymphoma, neuroblastoma, sarcoma, chordoma, nasopharyngeal carcinoma, inverting papilloma). Evaluate all children with benign multiple nasal polyposis for CF and asthma. Educating patients about the chronicity of the disease is important to make them aware of the recurrent nature of the problem.

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Pathophysiology

The pathogenesis of nasal polyposis is unknown. Polyp development has been linked to chronic inflammation, autonomic nervous system dysfunction, and genetic predisposition. Most theories consider polyps to be the ultimate manifestation of chronic inflammation; therefore, conditions leading to chronic inflammation in the nasal cavity can lead to nasal polyps.

The following conditions are associated with multiple benign polyps:

  • Bronchial asthma - In 20-50% of patients with polyps
  • CF - Polyps in 6-44% of patients with CF [1]
  • Allergic rhinitis
  • AFS - Polyps in 85% of patients with AFS
  • Chronic rhinosinusitis
  • Primary ciliary dyskinesia
  • Aspirin intolerance - In 8-26% of patients with polyps
  • Alcohol intolerance - In 50% of patients with nasal polyps
  • Churg-Strauss syndrome - Nasal polyps in 50% of patients with Churg-Strauss syndrome
  • Young syndrome (ie, chronic sinusitis, nasal polyposis, azoospermia)
  • Nonallergic rhinitis with eosinophilia syndrome (NARES) - Nasal polyps in 20% of patients with NARES

Most studies suggest that polyps are associated more strongly with nonallergic disease than with allergic disease. Statistically, nasal polyps are more common in patients with nonallergic asthma (13%) than with allergic asthma (5%), and only 0.5% of 3000 atopic individuals have nasal polyps.

Several theories have been postulated to explain the pathogenesis of nasal polyps, although none seems to account fully for all the known facts. Some researchers believe that polyps are an exvagination of the normal nasal or sinus mucosa that fills with edematous stroma; others believe polyps are a distinct entity arising from the mucosa. Based on a review of the literature and several intricate studies of the bioelectric properties of polyps, Bernstein derived a convincing theory on the pathogenesis of nasal polyps, building on other theories and information from Tos. [2, 3]

In Bernstein's theory, inflammatory changes first occur in the lateral nasal wall or sinus mucosa as the result of viral-bacterial host interactions or secondary to turbulent airflow. In most cases, polyps originate from contact areas of the middle meatus, especially the narrow clefts in the anterior ethmoid region that create turbulent airflow, and particularly when narrowed by mucosal inflammation. Ulceration or prolapse of the submucosa can occur, with reepithelialization and new gland formation.

During this process, a polyp can form from the mucosa because the heightened inflammatory process from epithelial cells, vascular endothelial cells, and fibroblasts affects the bioelectric integrity of the sodium channels at the luminal surface of the respiratory epithelial cell in that section of the nasal mucosa. This response increases sodium absorption, leading to water retention and polyp formation.

Other theories involve vasomotor imbalance or epithelial rupture. The vasomotor imbalance theory postulates that increased vascular permeability and impaired vascular regulation cause detoxification of mast-cell products (eg, histamine). The prolonged effects of these products within the polyp stroma result in marked edema (especially in the polyp pedicle) that is worsened by venous drainage obstruction. This theory is based on the cell-poor stroma of the polyps, which is poorly vascularized and lacks vasoconstrictor innervation.

The epithelial rupture theory suggests that rupture of the epithelium of the nasal mucosa is caused by increased tissue turgor in illness (eg, allergies, infections). This rupture leads to prolapse of the lamina propria mucosa, forming polyps. The defects are possibly enlarged by gravitational effects or venous drainage obstruction, causing the polyps. This theory, although similar to Bernstein's, provides a less convincing explanation for polyp enlargement than the sodium flux theory supported by Bernstein's data. Neither theory completely defines the inflammatory trigger.

Patients with CF have a defective small chloride conductance channel, regulated by cyclic adenosine monophosphate (cAMP), which causes abnormal chloride transport across the apical cell membrane of epithelial cells. The pathogenesis of nasal polyposis in patients with CF could be associated with this defect.

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Etiology

As noted (see Pathophysiology), chronic inflammation (from whatever source) apparently has an initial role in the pathogenesis of nasal polyps. Multiple polyps occur in children with chronic sinusitis, allergic rhinitis, CF, and AFS. An isolated polyp could be an antral-choanal polyp, a benign massive polyp, a nasolacrimal duct cyst, or any of the following congenital lesions or benign or malignant tumors:

  • Nasolacrimal duct cysts
  • Encephaloceles
  • Gliomas
  • Dermoid tumors
  • Hemangiomas
  • Papillomas
  • Juvenile nasopharyngeal angiofibromas
  • Rhabdomyosarcoma
  • Lymphomas
  • Neuroblastomas
  • Sarcomas
  • Chordomas
  • Nasopharyngeal carcinomas
  • Inverting papillomas

Evaluate all children with benign nasal polyposis for CF and asthma.

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Epidemiology

In the United States, the overall incidence of nasal polyps in children is 0.1%; the incidence in children with CF is 6-48%. Among adults, the incidence is 1-4% overall, with a range of 0.2-28%. Worldwide incidence is the same as the incidence in the United States.

Benign multiple nasal polyposis usually manifests in patients older than 20 years and is more common in patients older than 40 years. Nasal polyps are rare in children younger than 10 years. Although the male-to-female ratio is 2-4:1 in adults, the ratio in children is unreported. A review of articles reporting on children whose nasal polyposis required surgery showed apparently equal prevalence in boys and girls, although the data are inconclusive. [4] The reported prevalence is equal in patients with asthma. Nasal polyps occur in all races and social classes.

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Prognosis

No significant mortality is associated with nasal polyposis. Morbidity is usually associated with altered quality of life, nasal obstruction, anosmia, chronic sinusitis, headaches, snoring, and postnasal drainage. In certain situations, nasal polyps can alter the craniofacial skeleton because unremoved polyps can extend intracranially and into the orbital vaults.

Polyposis recurrence is common following treatment with medical or surgical therapy if multiple benign polyps are present (see Treatment, Surgical Care). Single large polyps (eg, antral-choanal polyps) are less likely to recur. The literature contains sparse data comparing treatments. Endoscopic sinus surgery appears to improve both olfaction and quality of life in chronic rhinosinusitis patients with nasal polyps. [5, 6]

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