eMedicine Specialties > Pediatrics: Surgery > Otolaryngology

Nasal Polyps

Author: John E McClay, MD, Assistant Professor, Department of Otolaryngology, Division of Pediatric Otolaryngology, Children's Medical Center, University of Texas Southwestern Medical School
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Updated: Oct 22, 2008

Introduction

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 (see Media files 1-3) 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.

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 6-48% of patients with CF
• 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.^1,2

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.

Frequency

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%.

International

Worldwide incidence is the same as the incidence in the United States.

Mortality/Morbidity

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.

Race

Nasal polyps occur in all races and social classes.

Sex

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.³ The reported prevalence is equal in patients with asthma.

Age

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.

Clinical

History

The manifestation of nasal polyps depends on the size of the polyp. Small polyps may not produce symptoms and may be identified only during routine examination when they are anterior to the anterior edge of the middle turbinate. Polyps located posterior to the site are not typically seen during routine anterior rhinoscopy examination performed with an otoscope and are missed unless the child is symptomatic. Small polyps in areas where polyps normally arise (ie, the middle meatus) may produce symptoms and block the outflow tract of the sinuses, causing chronic or recurrent acute sinusitis symptoms.

Symptom-producing polyps can cause nasal airway obstruction, postnasal drainage, dull headaches, snoring, and rhinorrhea. Associated hyposmia or anosmia may be a clue that polyps, rather than chronic sinusitis alone, are present. Epistaxis that does not arise from irritation of the anterior nasal septum (ie, Kiesselbach area) usually does not occur with benign multiple polyps and may suggest other, more serious, nasal cavity lesions.

Massive polyposis or a single large polyp (eg, antral-choanal polyp [Media files 4-12] that obstructs the nasal cavities, nasopharynx, or both) can cause obstructive sleep symptoms and chronic mouth breathing. Rarely, patients with cystic fibrosis (CF) and patients with allergic fungal sinusitis (AFS) have massive polyposes (see Media files 1-3 and Media file 41). These can alter the craniofacial structure (Media files 35-36 and Media file 42-44) and cause proptosis, hypertelorism, and diplopia (see Media files 45-46).

In an article submitted for publication, the author has reported 40% of children with AFS presented with craniofacial abnormalities, compared with 10% of adults with AFS. Massive polyposis rarely causes enough extrinsic compression on the optic nerve to decrease visual acuity. Furthermore, because they grow slowly, massive polyposes usually cause no neurological symptoms, even those that extend into the intracranial cavity.

Physical

For benign nasal polyps, the middle meatus is the most common location. If adequately visible, views of the middle meatus can reveal whether sufficient pathology is present to warrant ordering a CT scan of the sinuses, rather than preforming a rigid or flexible endoscopic procedure that may distress a young patient and the parents. However, rigid or flexible endoscopy is the best method to examine the nasal cavity and nasopharynx to fully assess the nasal anatomy (see Media file 14 and Media files 37-39) and to determine the extent and location of nasal polyps.

For small children, a flexible fiberoptic nasopharyngoscope is often used because it is less traumatic for children who may move their heads from anxiety or discomfort. In older cooperative children and adolescents, a rigid endoscopy can be used to assess the middle meatus and the sphenoethmoid recess. Perform adequate decongestion and anesthesia of the nasal cavities before an endoscopic procedure for any child older than 6 months. Video documentation of the procedure decreases the amount of time necessary for the procedure and later enhances patient and parent education.

For children, evaluating the posterior wall of the oral cavity also can indicate the symptomatology of polyposis (eg, postnasal drainage concomitant with chronic sinusitis). Large polyps or lesions of the nasal cavity may also protrude into the posterior oropharynx from the nasopharynx; these may occur as a lesion behind the palate and uvula or may depress the palate inferiorly and anteriorly (see Media file 10). Perform otoscopic examinations because extensive polyposis that causes eustachian tube dysfunction can cause fluid and infection in the middle ear space. Careful examination of the innervated systems of the cranial nerves and of the craniofacial structure helps define a nasal lesion's potential expansion into surrounding vital structures.

Causes

As described in 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 (see Media files 4-12), a benign massive polyp, a nasolacrimal duct cyst (see Media files 23-27), or any congenital lesion or benign or malignant tumor, including the following:

• Encephaloceles (see Media file 15)
• Gliomas (see Media files 16-17)
• Dermoid tumors (see Media files 28-33)
• Hemangiomas
• Papillomas (see Media file 18)
• Juvenile nasopharyngeal angiofibromas
• Rhabdomyosarcoma (see Media files 19-21)
• Lymphomas
• Neuroblastomas
• Sarcomas
• Chordomas
• Nasopharyngeal carcinomas
• Inverting papillomas

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

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