com/article/994274-overview
Nasal Polyps
Author: John E McClay, MD; Chief Editor: Glenn C Isaacson, MD, FACS, FAAP
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 the
images below) 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.
right. The polyp is directly in the center and is pale, glistening, and white.
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:
Allergic rhinitis
Chronic rhinosinusitis
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.
Epidemiology
Frequency
United States
The overall incidence of nasal polyps in children is 0.1%; the incidence in children with CF is 648%. Among adults, the incidence is 1-4% overall, with a range of 0.2-28%.
International
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
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.
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 [see the images below] that
obstructs the nasal cavities, nasopharynx, or both) can cause obstructive sleep symptoms and
chronic mouth breathing.
maxillary wall.
Endoscopic view of the left middle
meatus, showing the septum on the left, the middle turbinate in the center
superiorly, and a large maxillary antrostomy with a curved suction on the right. This
is following antral-choanal polyp removal.
Rarely, patients with cystic fibrosis (CF) and patients with allergic fungal sinusitis (AFS) have
massive polyposes. These can alter the craniofacial structure and cause proptosis, hypertelorism,
and diplopia. See the images below.
uncinate process and inferior portion of the polyp. The lateral nasal wall is on the far
right. The polyp is directly in the center and is pale, glistening, and white.
with cystic fibrosis, showing complete opacification of the maxillary and ethmoid
sinuses. Bulging in the medial maxillary walls is observed.
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
Begin physical examination for nasal polyps with an anterior rhinoscopy procedure (see the
image below). For small children, a handheld otoscope and otologic speculum are typically used.
An otoscope placed in the nasal cavity provides views of the inferior turbinate, anterior septum,
and areas in the nasal cavity extending to the anterior edge of the middle turbinate and
midportion of the septum. The middle meatus (ie, the area under the middle turbinate laterally)
can often be seen using anterior rhinoscopy if the child is cooperative and if no significant
mucosal edema or secretions are present in the anterior nasal cavity.
An anterior endoscopic view of the nasal cavity in a 5month-old infant. The vestibule is seen in the periphery of the picture. In the center
of the picture, the septum is visible to the left, and the inferior turbinate is to the
right. These structures are reddish in hue. Some congestion in the nasal cavity is
usually present. These are often structures that can be seen only by anterior
rhinoscopy. If the area is decongested, the area of the middle meatus can
occasionally be seen.
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 the images below) 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 the image below). 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, a
benign massive polyp, a nasolacrimal duct cyst (as shown below), or any congenital lesion or
benign or malignant tumor listed below.
turbinate.
Axial CT scan section through the orbit,
showing the dilated nasal lacrimal ducts in the medial anterior area
compared to the orbits. Scale on the bottom right is in centimeters.
image.
A frontal view of the decompressed nasal
lacrimal ducts following surgical marsupialization. Swelling in the inferior
medial canthal areas prior to surgery is no longer seen.
dermoid.
Frontal view of a 5-month-old infant,
showing hypertelorism and protrusion in the glabellar region secondary to a
Hemangiomas
An
cavernous sinuses.
Rigid endoscopic view of left
nasal cavity, showing a polyp in the center of the picture, with extension of
the rhabdomyosarcoma. The septum is on the left and the middle turbinate is
on the right.
Lymphomas
Neuroblastomas
Sarcomas
Chordomas
Nasopharyngeal carcinomas
Inverting papillomas
Evaluate all children with benign nasal polyposis for CF and asthma
Differentials
Asthma
Cystic Fibrosis
Neuroblastoma
Neurofibromatosis
Rhabdomyosarcoma
Sinusitis
Laboratory Studies
immunotherapy directed at all antigens for which they are allergic, especially
molds;[4] therefore, allergy testing and treatment may be important in treating
allergic fungal sinusitis (AFS).
Perform a sweat chloride test or genetic testing for cystic fibrosis (CF) in any
child with multiple benign nasal polyps.
A nasal smear for eosinophils may differentiate allergic from nonallergic sinus
diseases and indicate whether the child may be responsive to glucocorticoids.
The presence of neutrophils may indicate chronic sinusitis.