Pediatric Nasal Polyps

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emedicine.medscape.com
Pediatric Nasal Polyps

Updated: Jun 27, 2023
Author: John E McClay, MD, FAAP; Chief Editor: Ravindhra G Elluru, MD, PhD
Overview
Practice Essentials
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,
encephalocele, glioma, hemangioma, papilloma, juvenile nasopharyngeal angiofibroma, rhabdomyosarcoma,
lymphoma, neuroblastoma, sarcoma, chordoma, nasopharyngeal carcinoma, inverting papilloma). All children with benign
multiple nasal polyposis should be evaluated 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.
Oral and topical nasal steroid administration is the primary medical therapy for nasal polyposis. Surgical intervention is
required for children with multiple benign nasal polyposis or chronic rhinosinusitis in whom maximal medical therapy fails.
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.
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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, though 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 that polyps are a distinct entity arising from the mucosa. On the basis of a review of
the literature and several intricate studies of the bioelectric properties of polyps, Bernstein derived a convincing theory
regarding the pathogenesis of nasal polyps, building on other theories and information from Tos et al.[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, though
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.
Etiology
As noted (see Pathophysiology), chronic inflammation (from whatever source) apparently plays 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
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Inverting papillomas
All children with benign nasal polyposis should be evaluated for CF and asthma.
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, though the data are inconclusive.[4] The reported prevalence is equal in
patients with asthma. Nasal polyps occur in all races and social classes.
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.
Endoscopic sinus surgery appears to improve both olfaction and quality of life in chronic rhinosinusitis patients with nasal
polyps.[5, 6] In a study of 58 pediatric patients (< 18 years) with antrochoanal polyps who were treated with functional
endoscopic sinus surgery (FESS), Pagella et al reported a recurrence rate of 20.5%.[7]
The literature contains sparse data comparing treatments. Galluzzi et al performed a systematic review (N = 285) aimed at
evaluating recurrence rates after different surgical procedures used to treat antrochoanal polyps in children, including FESS,
a combined approach (FESS with a transcanine sinusoscopy or mini Caldwell-Luc procedure), the Caldwell-Luc procedure,
and simple polypectomy.[8] Recurrence rates were as follows:
All types of surgery - 15%

FESS - 17.7%
Combined approach - 0%
Caldwell-Luc procedure - 9.1%
Simple polypectomy - 50%
Presentation
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
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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.
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.
In a retrospective study, McClay et al reported that 42% of children with AFS presented with craniofacial abnormalities,
compared with 10% of adults with AFS.[9] 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 neurologic
symptoms, even those that extend into the intracranial cavity.
Physical Examination
The patient's facial appearance may vary, depending on the underlying condition (see the images below).
A 3-month-old infant with hypertelorism and bulging of the nasal dorsum, secondary to encephalocele.
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Frontal view of a 2-day-old infant with swelling in the inferior medial canthal area on both sides. The right side appears
more prominent on this picture. CT scan showed infected nasal lacrimal duct cysts.
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.
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Lateral view of a preteenaged child showing infected nasal dermoid. Note the protrusion of the dorsum of the nose.
Preteenaged boy with infected nasal dermoid. A pith is visible over the superior portion of the swelling between the eyes.
Nasal pith is commonly seen with the nasal dermoid.
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Frontal view of a 5-month-old infant, showing hypertelorism and protrusion in the glabellar region secondary to a small
nasal dermoid.
Fifteen year-old adolescent boy with allergic fungal sinusitis causing right proptosis, telecanthus, and malar flattening;
position of his eyes is asymmetrical, and his nasal ala on the right is pushed inferiorly compared with the left.
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Nine-year-old girl with allergic fungal sinusitis displaying telecanthus and asymmetrical positioning of her eyes and globes.
Physical examination for nasal polyps should begin with an anterior rhinoscopy procedure (see the images 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 via anterior rhinoscopy if the child is cooperative and if no significant mucosal edema or secretions are present in the
anterior nasal cavity.
Interior view of the nose and nasal cavities. To the right of the patient's left nostril, the right nasal cavity has no obstruction.
On the left of the picture, a reddish polyp is visible. The reddish mass is a nasal glioma.
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A close-up view of the right nasal cavity and polyp #5 in a 5-month-old infant. The obstructing reddish polyp is visible. This
is an intranasal glioma that was arising from the attachment of the inferior turbinate anteriorly; it was transnasally
removed.
An anterior endoscopic view of the nasal cavity in a 5-month-old infant. The vestibule is seen in the periphery of the
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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 computed tomography (CT) of the sinuses, rather than
performing a rigid or flexible endoscopic procedure that may distress a young patient and the parents. However, rigid or
flexible endoscopy is the best method for examining the nasal cavity and nasopharynx to fully assess the nasal anatomy and
to determine the extent and location of nasal polyps. (See the images below.)
Rigid endoscopic view of the left nasal cavity, showing the septum on the left. Polyps with some blood and hemorrhage
are on top of them in the center portion. The rim of white from 1 o'clock to 4 o'clock indicates the lateral nasal wall
vestibule. The polyps cover the inferior turbinate, which is partially visible at 4 and 5 o'clock.
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Endoscopic view of the left nasal cavity, showing a polyp protruding from the uncinate process. The middle turbinate is to
the left. A suction is visible on top of the inferior portion of the 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.
Endoscopic view of the left middle meatus. The septum is on the far left. The middle turbinate is next to the septum on the
left. A large, glistening, translucent polyp is visible in the center of the screen next to the middle turbinate. The lateral nasal
wall is on the right side of the screen. The inferior turbinate nub posteriorly is in the bottom right hand corner.
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Rigid endoscopic view of the left nasal cavity, showing the septum on the left, inferior turbinate on the right, middle
turbinate superiorly, and antral-choanal polyp among the floor of the nose.
Rigid endoscopic view of the left anterior nasal cavity, showing the septum on the left, a suction pushing the inferior
turbinate on the right, and the clear antral-choanal polyp at the center of the endoscopic view.
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Close-up of the middle meatus, showing the stalk of the antral-choanal polyp emanating from the maxillary sinus behind
the uncinate process on the bottom right-hand side of the picture. The left side of the picture shows the septum and the
middle turbinate being pushed over via suction.
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.
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A rigid rhinoscopy photograph of the left anterior nasal cavity of a 6-week-old infant. The middle turbinate is superiorly in
the midline, and the inferior turbinate is to the right. The septum is to the left.
Anterior nasal papilloma arising from the septum. The skin of the nasal vestibule is seen surrounding the papilloma in the
center of the image.
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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.
Endoscopic view of the left nasal cavity posteriorly, showing a polyp emanating from the sphenoid sinus in the center of
the picture and purulence above and below the polyp. On the left is the septum. On the right is the lateral aspect of the
middle turbinate.
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Rigid endoscopic view of the left nasal cavity. The septum is on the left, and the lateral nasal wall is on the right. The
inferior turbinate is in the center of the picture, and the middle turbinates are visible in the superior midsection of the
picture. The nasal lacrimal duct cyst is the yellow dilated lesion underneath the inferior turbinate.
A rigid rhinoscopy photograph of the the nasal cavity of a 6-week-old infant taken all the way back into the choanae of the
left nasal cavity. The photograph shows the septum on the left, the small adenoids on the posterior superior wall of the
nasopharynx in the center, and the eustachian tube orifice on the right.
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A rigid rhinoscopy photograph taken in the midportion of the left nasal cavity of a 6-week-old infant showing the septum on
the left, the inferior turbinate on the right, and the middle turbinate superiorly. The choanae is seen in the dark area in the
center.
A rigid rhinoscopy photograph taken two thirds of the way back along the floor of the nose of the left nasal cavity of a 6-
week-old infant. This photograph shows the septum on the left, the choanae straight ahead, and the posterior portion
inferior turbinate to the right.
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View just inside the nasal vestibule of a fifteen-year-old adolescent boy with allergic fungal sinusitis showing diffused
polyposis extending into the anterior nasal cavity and vestibule; the septum is on the right, and the right lateral vestibular
wall (nasal ala) is on the left. The polyps are all in the center. The polyps almost hang out of the nasal vestibule.
In small children, a flexible fiberoptic nasopharyngoscope is often used because it is less traumatic for young patients who
may move their heads from anxiety or discomfort. In older cooperative children and adolescents, a rigid endoscope can be
used to assess the middle meatus and the sphenoethmoid recess. Adequate decongestion and anesthesia of the nasal
cavities are necessary before an endoscopic procedure in 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).
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Oral cavity and oropharyngeal view of antral-choanal polyp filling the posterior oral pharynx and pushing the soft palate
anterior and inferiorly. The polyp is visible behind the uvula and the soft palate.
Otoscopic examinations are warranted 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.
DDx
Differential Diagnoses
Acute Sinusitis
Asthma
Genetics of Neurofibromatosis Type 1 and Type 2
Neuroblastoma Imaging
Pediatric Rhabdomyosarcoma
Sinonasal Manifestations of Cystic Fibrosis
Workup
Workup
Laboratory Studies
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Laboratory studies should be directed at the pathologic process believed to be responsible for the nasal polyps.
Children with polyposis that is associated with allergic rhinitis should undergo evaluation for their allergies; this may include
a serologic radioallergosorbent test (RAST) or some form of allergic skin testing. Mabry et al showed a decrease in the
recurrence rate of polyps in children treated with immunotherapy directed at all antigens for which they are allergic,
especially molds[10] ; 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.
Imaging Studies
The criterion standard for evaluating nasal lesions, especially nasal polyposis or sinusitis, is a thin-cut (1-3 mm) computed
tomography (CT) scan of the maxillofacial area, the sinuses axially, and the coronal plane. A compatible CT scan should be
performed if an intraoperative image-guided system is used. Plain film radiography has no significant value after polyps are
diagnosed. Magnetic resonance imaging (MRI) is also warranted in patients with possible intracranial involvement or
extension of benign nasal polyps.
CT and MRI findings can help diagnose the polyp or polyps; define the extent of the lesion in the nasal cavities, sinuses, and
beyond; and narrow the differential diagnosis of an unusual polyp or clinical presentation. CF is associated with a
characteristic symmetrical bulging of the lateral nasal walls medially (see the images below).
Coronal section through the ethmoid maxillary sinuses and orbits. This is a 2-year-old child with cystic fibrosis, showing
complete opacification of the maxillary and ethmoid sinuses. Bulging in the medial maxillary walls is observed.
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Coronal section showing soft tissue windows rather than bony windows. It indicates the infection by the thick mucus in the
maxillary and ethmoid cavities by the heterogeneity of the opacification in the sinuses. Note that the nasal cavity is
completely obliterated by polyp disease.
A coronal CT scan section through the orbit to maxillary sinus. The medial maxillary walls bulge medially, which is a typical
CT scan view of cystic fibrosis. The ethmoid sinuses have scattered disease.
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An antral-choanal polyp may show opacified maxillary sinuses with a protruding lesion heading from the maxillary antrum to
the choana (see the images below).
Axial CT scan section through the maxillary sinuses showing opacification of the left maxillary sinus with antral-choanal
polyp in the posterior nasal cavity and choana exiting from beneath the middle turbinate in the area of the ostiomeatal
complex unit. Scale is in centimeters.
Coronal CT scan through the anterior sinuses showing opacification of the left maxillary sinus with opacification of the
inferior half of the nasal cavity on the left, filled by the antral-choanal polyp. The rest of the sinuses are clear.
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Coronal CT scan section through the posterior nasopharynx showing the sphenoid sinus superiorly and the antral-choanal
polyp filling the nasopharynx in the center of the scan.
A tumor, such as a rhabdomyosarcoma, may show extension of the lesion with invasion of surrounding mucosa (see the
images below).
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Axial MRI scan of the orbits, posterior fossa, and nasal cavity. The solid tumor is seen filling the posterior ethmoid
complex, brain stem, cavernous sinuses, and left anterior cranial fossa.
Axial CT scan through the orbits and ethmoid sinuses, showing the rhabdomyosarcoma in the same areas, including the
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posterior ethmoid complex, left middle fossa, and skull base of cavernous sinuses.
A nasolacrimal duct cyst can show dilation of the nasolacrimal duct (see the images below).
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.
Axial CT scan through the inferior nasal cavities, showing the dilated nasal lacrimal duct cysts at the inferior location.
Scale on the bottom right is in centimeters. The dilated cysts are in the center of the image.
An encephalocele can show expansion of the nasofrontal region (ie, foramen caecum) with herniation of brain or dura.
A glioma can show an isolated nasal lesion that may have a fibrous stalk to the central nervous system (CNS).
Patients with AFS exhibit heterogenous areas in the sinuses on CT and MRI; these areas consist of both the nasal polyposis
and the allergic fungal mucin (see the images below). This allergic fungal mucin appears black on MRI and can be confused
with the absence of disease.
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Coronal CT scan showing extensive allergic fungal sinusitis involving the right side with mucocele above the right orbit and
expansion of the sinuses on the right.
Coronal MRI scan showing expansion of the sinuses with allergic mucin and polypoid disease; the hypointense black
areas in the nasal cavities are the actual fungal elements and debris. The density above the right eye is the mucocele. The
fungal elements and allergic mucin in allergic fungal sinusitis always look hypointense on MRI scanning and can be
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mistaken for absence of disease.
Histologic Findings
Histologically, nasal polyps are characterized by a pseudostratified ciliated columnar epithelium, thickening of the epithelial
basement membrane, and few nerve endings. The stroma of nasal polyps is edematous. Vascularization is poor and lacks
innervation, except at the base of the polyp. Authors report either hyperplasia of the seromucous glands or almost absent or
rare glands when comparing the polyps to the inferior or middle turbinate. Hyperplasia of the gland can cause cystically
dilated and degenerated glands containing inspissated mucous.
Eosinophil cells are the most commonly identified inflammatory cell, occurring in 80-90% of polyps. Eosinophils, which are
found in the polyps of patients with bronchial asthma and allergy, contain granules with toxic products (eg, leukotrienes,
eosinophilic cationic protein, major basophilic protein, platelet-activating factor [PAF], eosinophilic peroxidases, other
vasoactive substances and chemotactic factors). These toxic factors are responsible for epithelial lysis, nerve damage, and
ciliostasis. Specific granule protein, leukotriene A4, and PAF apparently are responsible for the mucosal swelling and
hyperresponsiveness.
Eosinophils in the peripheral blood and in normal nasal mucosa usually last 3 days. In a cell culture of nasal polyps,
eosinophils were present at least 12 days. This delayed apoptosis of eosinophils is mediated, in part, by blockage of the Fas
receptors, typically with proteases that help begin the process of cell death.
Delayed apoptosis is also mediated by an increase in interleukin (IL)-5, IL-3, and granulocyte-macrophage colony-
stimulating factor (GM-CSF) secreted by T cells, which help sustain the eosinophil from death. Glucocorticoids seem to help
reduce polyps or polypoid reactions in patients with tissue eosinophilia, possibly, in part, by inhibiting IL-5.
Another inflammatory cell, the neutrophil, occurs in 7% of polyp cases. This type of polyp occurs in association with CF,
primary ciliary dyskinesia syndrome, or Young syndrome. These polyps do not respond well to corticosteroids because they
lack corticosteroid-sensitive eosinophils. Degranulated mast cells are present. Degranulation presumably occurs in a non–
immunoglobulin (Ig) E–mediated fashion. Increased numbers of plasma cells, lymphocytes, and myofibroblasts also occur.
Chemical mediators
The stromata of nasal polyps have numerous mediators, including cytokines, growth factors, adhesion molecules, and
immunoglobulins; polyps also contain vasoactive amines, serotonin, prostaglandins[11] , leukotrienes, norepinephrine,
kinins, esterases, heparin, and histamine. The level of histamine in nasal polyps is 100-1000 times the level found in the
bloodstream.
Cytokines present in polyps include the following:
IL-1 - Found regularly

IL-3 - Varies according to study, from absent to intermittent at low levels to regularly present
IL-4 - Inconsistently detected
IL-5 - Found regularly; IL-5 is essential for proliferation and differentiation of eosinophils. IL-5 is chemotactic to
eosinophils, promotes the migration of eosinophils from the systemic circulation to the polyps, and inhibits eosinophil
cell death.
IL-6 - Same as in controls (no increase)
IL-8 - Varies, based on study, from undetected to regularly detected; may cause sustained recruitment of leukocytes
into nasal polyps and may decrease fibroblastic proliferation
IL-10 - Same as in controls; no increase regulated on activation, normal T cell expressed and secreted (RANTES);
varies, based on study, from same as controls to regularly detected to increased levels interferon gamma; increases
in eosinophils, seromucous glands, and epithelium of nasal polyps
Growth factors found in nasal polyps include the following:
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Tumor necrosis factor (TNF)-α and TNF-β - Varies, depending on the study, from same as controls to regularly
detected; believed to be from eosinophils
GM-CSF - mRNA and protein amount varies, based on study, from never to intermittent to present
Platelet-derived growth factor (PDGF) - Present
Vascular permeable factors (VPFs) - Present
Vascular endothelial growth factors (VEGFs) - Present
Insulinlike growth factor (IGF)-1 - Present
Stem cell factor - Present
Adhesion molecules include the following:
Vascular adhesion molecule (VCAM)-1 - Present

E and P selectin - Present
Immunoglobulins include the following:
IgG - No increase; same levels as in the middle and inferior turbinate mucosa
IgA - More in polyps than in the middle and inferior turbinate mucosa, especially IgA1 over IgA2
IgM - No increase, same as in the middle and inferior turbinate mucosa
IgD - No increase, same as in the middle and inferior turbinate mucosa
IgE - Increased levels compared with the middle and inferior turbinate mucosa; same level in patients without allergy
as in those with allergy
Staging
In 1993, Lund and Mackay proposed the following three-point system for staging nasal polyps according to endoscopic
appearance[12, 13] :
0 - No polyposis
1 - Polyps confined to the middle meatus
2 - Polyps beyond the middle meatus
Subsequently, this system was modified as follows[14, 15] :
0 - No polyps
1 - Polyps restricted to the middle meatus
2 - Polyps extending below the middle turbinate
3 - Massive polyposis, occluding the entire nasal cavity
Treatment
Approach Considerations
Historically, children diagnosed with cystic fibrosis (CF) already had digestive and pulmonary disease and were the children
with the more severe form of disease. These children were often treated with intravenous (IV) antibiotics directed at the most
common pathogens found in the lungs and the sinuses (eg, Pseudomonas aeruginosa,Staphylococcus aureus), both
preoperatively and postoperatively.
Additionally, these children had pulmonary toilet to increase their lung function in the perioperative period, including IV
steroids, percussion therapy, and inhaled bronchodilators. Much of this process can now be performed on an outpatient
basis, depending on the severity of the associated disease.
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For patients with severe asthma and polyposis requiring surgery, postoperative admission for observation of respiratory
compromise or spasm is determined on an individual basis. Outpatient surgery is usually performed for older children
undergoing endoscopic sinus surgery (ESS) for nasal polyposis without coexisting medical conditions.
Guidelines for the medical management of chronic rhinosinusitis with nasal polyposis (CRSwNP) have been published by
the Joint Task Force on Practice Parameters (JTF-PP), with the support of the American Academy of Allergy, Asthma &
Immunology (AAAAI) and the American College of Allergy, Asthma, and Immunology (ACAAI).[16] These recommendations
are formulated for individuals aged 18 years or older; however, they may also be applicable to younger individuals with this
condition.
Medical Care
Corticosteroids
Oral and topical nasal steroid administration is the primary medical therapy for nasal polyposis.[17, 18, 19] Antihistamines,
decongestants, and cromolyn sodium provide little benefit. Immunotherapy may be useful to treat allergic rhinitis but, when
used alone, does not usually resolve existing polyps. Administer antibiotics for bacterial superinfections.
Corticosteroids are the treatment of choice, either topically or systemically. Direct injection into the polyp is not approved by
the US Food and Drug Administration (FDA) because of reports of unilateral vision loss in three patients after intranasal
steroid injection with Kenalog. Safety may depend on specific drug particle size; high-molecular-weight drugs such as
Aristocort are safer and less likely to be transferred to the intracranial area. Avoid direct injection into blood vessels.
Oral steroids are the most effective medical treatment for nasal polyposis. In adults, most authors use prednisone (30-60
mg) for 4-7 days and taper the medicine for 1-3 weeks. Dosage varies for children, but the maximum dosage is usually 1
mg/kg/day for 5-7 days, which is then tapered over 1-3 weeks. Responsiveness to corticosteroids appears to depend on the
presence or absence of eosinophilia; thus, patients with polyps and allergic rhinitis or asthma should respond to this
treatment.
Patients with polyposis not dominated by eosinophilia (eg, patients with cystic fibrosis [CF], primary ciliary dyskinesia
syndrome, or Young syndrome) may not respond to steroids. Long-term use of oral steroids is not recommended because of
the numerous potential adverse effects (eg, growth retardation, diabetes mellitus, hypertension, psychotropic effects,
adverse GI effects, cataracts, glaucoma, osteoporosis, and aseptic necrosis of the femoral head).
Many authors advocate topical nasal steroid administration for nasal polyps, either as the primary treatment or as a continual
secondary treatment immediately after oral steroids or surgery. Most nasal steroids (eg, fluticasone, beclomethasone,
budesonide) effectively relieve subjective symptoms and increase the nasal airflow when measured objectively (primarily in
double-blind placebo-controlled studies).[20]
A systematic review of 19 studies found similar results. The topical steroid preparations fluticasone, mometasone, and
budesonide were shown to improve nasal symptoms in patients with nasal polyposis.[21] Some studies indicate fluticasone
has a faster onset of action and possible mild superiority to beclomethasone.[22]
Topical corticosteroid administration generally causes fewer adverse effects than systemic corticosteroid use because of the
former's limited bioavailability. Long-term use, especially at high dosages or in combination with inhaled corticosteroids,
presents a risk of hypothalamic-pituitary-adrenal axis suppression, cataract formation, growth retardation, nasal bleeding,
and, in rare cases, nasal septal perforation.
As with any long-term therapy, monitor use of topical corticosteroid sprays. However, long-term (>5 years) studies evaluating
the use of beclomethasone have shown no degradation of the normal respiratory epithelium to squamous epithelium seen in
chronic atrophic rhinitis. Additionally, the later generation of intranasal steroids (eg, fluticasone and mometasone) appears to
have less bioavailability than the earlier nasal steroids, such as beclomethasone.
Leukotriene receptor antagonists
10/16/24, 9:09 PM
Leukotrienes are cytokines made from arachidonic acid in the presence of 5-lipoxygenase. When released, leukotrienes bind
to the cysteinyl-leukotriene receptors CysLT1 and CysLT2, located on the surface of target cells. These receptors are
thought to mediate eosinophil recruitment, bronchospasm, vasoconstriction, mucus secretion, and plasma exudation. In
addition, it is believed that leukotrienes may play a role in the inflammatory response in nasal polyposis.[23]
Montelukast competitively blocks leukotriene receptors. Klapan et al, in a study analyzing leukotriene levels in the nasal
mucosa of patients with sinonasal polyps, found statistically higher levels of leukotriene C4 (LTC4) in patients with recurrent
sinonasal polyps after surgery than in healthy control subjects.[24] Higher LTC4 levels were associated with risk of
recurrence of nasal polyps.
Given the role of leukotrienes in the recruitment of eosinophils and association with recurrence of nasal polyposis, it is
reasonable to hypothesize a beneficial effect of the addition of montelukast in the management of nasal polyps.
Biologics
Biologic response modifiers are medications that target specific components of an individual's immune system by modifying
the chemical responses of the immune system that are causing inflammation thought to be responsible for the growth of
nasal polyps. Biologic agents that have been studied include dupilumab (targeting interleukin [IL]-4 and IL-13), benralizumab
(IL-5), mepolizumab (IL-5), reslizumab (IL-5), omalizumab (immunoglobulin E [IgE]), AK001 (Siglec-8), and etokimab (IL-33).
[16] Further study is needed to define appropriate use in children with nasal polyps.
Surgical Care
Surgical intervention is required for children with multiple benign nasal polyposis or chronic rhinosinusitis in whom maximal
medical therapy fails. Simple polypectomy is effective initially to relieve nasal symptoms, especially for isolated polyps or
small numbers of polyps. (See the image below.) In benign multiple nasal polyposis, polypectomy is fraught with a high
recurrence rate.
Scale is in inches. The left side of the lesion was the portion of the polyp in the nasal cavity. The right was a stalk attached
to the medial maxillary wall.
ESS is a better technique that not only removes the polyps but also opens the clefts in the middle meatus, where they most
often form, which helps decrease the recurrence rate. The exact extent of the surgery needed, whether complete extirpation
(ie, Nasalide procedure) or simple aeration of the sinuses, is not entirely known, simply because of the dearth of studies.
Rare comparisons show that complete extirpation procedures are as effective as or superior to aeration of the sinuses;
complication rates are low with experienced surgeons. The use of a surgical microdebrider has made the procedure safer
10/16/24, 9:09 PM
and faster, providing precise tissue cutting and decreased hemostasis with better visualization. (See the images below.)
A surgical microdebrider entering the middle meatus. The septum is on the far left. The middle turbinate is in the left
center. The surgical microdebrider is on the inferior center. Inferior turbinate is seen on the bottom right. Some blood
overlying the ethmoid cavity is noted where polyps were present in the center of the picture.
Endoscopic view of the left middle meatus, showing the septum on the left, the middle turbinate in the center superiorly,
10/16/24, 9:09 PM
and a large maxillary antrostomy with a curved suction on the right. This is following antral-choanal polyp removal.
Surgery is directed at diseased tissue that is apparent on computed tomography (CT) at the time of surgery. Patients with
diseases such as CF, primary ciliary dyskinesia syndrome, or Young syndrome may proceed to surgery without extensive
medical treatment because these diseases usually do not respond well to corticosteroid treatment. Once diseased tissue
has been removed from the nasal cavity and sinuses, the pulmonary systems usually improve.
Use of an image-guided system should be considered for defining the exact location of intranasal, sinus, orbital, and
intracranial structures for massive polyposis or revision surgery because surgical landmarks may be absent or altered.
For specific techniques in pediatric sinus surgery, with and without polyps, see Pediatric Sinusitis, Surgical Treatment.
Nasal polyposis occurs in 6-48% of children with CF. Surgery is performed when children become symptomatic. Recurrence
of polyps in CF is almost universal, necessitating repeat surgery every few years. In fact, recurrence is typical for many
diseases that cause nasal polyps; patients should receive preoperative counseling about this possibility.
For lesions other than benign nasal polyps that result in a nasal polyp, the polyp should be biopsied or removed, depending
on the disease process.
Complications
Massive polyposis or a single large polyp (eg, an antral-choanal polyp) that obstructs the nasal cavities and/or nasopharynx
can cause obstructive sleep symptoms and chronic mouth breathing. Rarely, massive polyposis, observed in CF and in
allergic fungal sinusitis (AFS) can alter the craniofacial structure. This can result in proptosis, hypertelorism, and diplopia.
In a retrospective study, McClay et al reported that 42% of children with AFS (compared with 10% of adults) presented with
craniofacial abnormalities.[9] Massive polyposis rarely causes enough extrinsic compression on the optic nerve to decrease
visual acuity. One study reported that three of 82 patients with AFS had vision changes from compression of the optic nerve
in the sphenoid sinus that resolved over time with removal of disease. However, because these polyps are slow-growing,
they usually cause no neurologic symptoms, even when they extend into the intracranial cavity.
Activity
No activity restrictions are necessary for a child with nasal polyps. The child's activity level may decrease because of
diminished ability to breathe through the nose, decreasing sport or physical activity performance. After sinus surgery,
activities are limited; these limitation recommendations vary from surgeon to surgeon. Most surgeons specifically restrict
nose-blowing because it may increase intranasal pressure and cause potential problems in areas of already thinned bony
dividers in patients with nasal polyposis.
Consultations
A pediatric otolaryngologist should be notified first, especially if medical therapy has failed or if the origin or diagnosis of the
underlying pathology of the nasal polyp is unknown.
Consider consultation with a pulmonary specialist when benign nasal polyps are identified because they could result from
asthma, allergy, or CF. Patients with these diseases often have associated pulmonary problems.
10/16/24, 9:09 PM
Long-Term Monitoring
Children with benign multiple nasal polyps, whatever the cause, should be monitored closely because recurrence is likely,
regardless of whether the polyps were treated medically or surgically. Postoperative follow-up should occur three or
four times in the first month to monitor healing of the sinus cavities; frequency depends on the patient's own geographic
location and symptoms.
A patient with CF can be monitored symptomatically because surgery is not performed until these patients are symptomatic,
even if nasal polyposis is seen on CT or nasal endoscopy. Certainly, each patient is treated on an individual basis.
For polyps associated with AFS, close follow-up by an otolaryngologist is recommended until the patient is deemed free of
disease, which may be several years or more.
Any accumulation of fungus may accelerate the antigenic process, which causes symptoms and disease to recur.
Recurrence is especially common for polyps, which may be controlled more simply and effectively if recognized early.
Small nasal polyps are recognized early on a routine follow-up in patients with benign multiple nasal polyps.
Other diseases may be treated medically or with smaller surgical procedures. For diseases resulting in nasal polyps other
than benign multiple nasal polyps, the need for inpatient or outpatient care is determined by the extent of disease, symptoms
and situation of the patient, and associated medical conditions.
Guidelines
JTF-PP Guidelines for Medical Management of Chronic Rhinosinusitis With

Nasal Polyposis
In February 2023, the Joint Task Force on Practice Parameters (JTF-PP)—with the support of its parent organizations, the
American Academy of Allergy, Asthma & Immunology (AAAAI) and the American College of Allergy, Asthma, and
Immunology (ACAAI)—issued guidelines for the medical management of chronic rhinosinusitis with nasal polyposis
(CRSwNP).[16] The guidelines included the following recommendations:
In people with CRSwNP, intranasal corticosteroids (INCS) are suggested rather than no INCS.
In people with CRSwNP, biologic agents are suggested rather than no biologic agents.
In people with aspirin (nonsteroidal anti-inflammatory drug)–exacerbated respiratory disease (AERD), aspirin therapy
after desensitization (ATAD) is suggested rather than no ATAD.
Medication
Corticosteroids
Class Summary
Corticosteroids have potent anti-inflammatory action and relieve rhinorrhea, sneezing, itching, and congestion.
10/16/24, 9:09 PM
Prednisolone (Prelone, Orapred ODT, Pediapred)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.
Prednisone (Prednisone Intensol)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.
Dexamethasone (Decadron)
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.
Corticosteroids, Intranasal
Class Summary
These agents induce a nonspecific anti-inflammatory response that should theoretically reduce the size of polyps and
prevent regrowth when continuously used. Available nasal steroid sprays appear to be similarly effective and relatively safe
for both short-term and long-term use.
Mometasone, intranasal (Nasonex)

Nasal spray; demonstrated no mineralocorticoid, androgenic, antiandrogenic, or estrogenic activity in preclinical trials.
Studies concerning bioavailability are established; should be considered first-line therapy for pediatric patients. Not
systemically absorbed like other nasal steroids (eg, beclomethasone).
Fluticasone intranasal (Children's Flonase Allergy Relief, ClariSpray, Flonase

Allergy Relief)
Topical nasal steroid. Has extremely potent vasoconstrictive and anti-inflammatory activity. Has a weak hypothalamic-
pituitary-adrenocortical axis inhibitory potency when applied topically. Studies concerning bioavailability are established;
should be considered first line when treating pediatric patients. Not systemically absorbed like other nasal steroids (ie,
beclomethasone).
Nasal drying, epistaxis, and, in long-term use, septal perforation has been reported. Advise patients to administer spray
toward lateral nasal wall, avoiding irritation to septum or having drug run down back of pharynx.
Budesonide intranasal (Rhinocort Allergy)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.
Triamcinolone, intranasal (Nasacort Allergy 24HR)

10/16/24, 9:09 PM
Beclomethasone, intranasal (Beconase AQ, QNASL)

Delivers 42 mcg/actuation.
Leukotriene Receptor Antagonists
Class Summary
These agents prevent or reverse some of the pathologic features associated with the inflammatory process mediated by
leukotrienes.
Montelukast (Singulair)
Potent and selective antagonist of leukotriene D4 (LTD4) at the cysteinyl leukotriene receptor, CysLT1. Prevents or reverses
some of the pathologic features associated with the inflammatory process mediated by leukotrienes C4, D4, and E4. Used
off-label for nasal polyps.
Interleukin Inhibitors
Dupilumab (Dupixent)
Mepolizumab (Nucala)
Monoclonal Antibodies, Anti-asthmatics
Omalizumab (Xolair)
Questions & Answers

Overview
What are nasal polyps?
What is the pathophysiology of nasal polyps?
10/16/24, 9:09 PM
What causes nasal polyps?
What is the US prevalence of nasal polyps?
Which patient groups have the highest prevalence of nasal polyps?
What is the prognosis of nasal polyps?
Presentation
Which clinical history findings are characteristic of nasal polyps?
Which physical exam findings are characteristic of nasal polyps?
What is included in the physical exam to evaluate nasal polyps?
What is the most common location of benign nasal polyps?
How is an exam for nasal polyps conducted in pediatric patients?
DDX
What are the differential diagnoses for Pediatric Nasal Polyps?
Workup
What is the role of lab tests in the workup of pediatric nasal polyps?
What is the role of imaging studies in the workup of pediatric nasal polyps?
Which histologic findings are characteristic of pediatric nasal polyps?
Which chemical mediators are found in pediatric nasal polyps?
How are pediatric nasal polyps staged?
Treatment
How are pediatric nasal polyps treated?
What is the role of corticosteroids in the treatment of pediatric nasal polyps?
What is the role of leukotriene receptor antagonists in the treatment of pediatric nasal polyps?
What is the role of surgery in the treatment of pediatric nasal polyps?
What are the possible complications of pediatric nasal polyps?
Which activity modifications are used in the treatment of pediatric nasal polyps?
Which specialist consultations are beneficial to patients with nasal polyps?
What is included in long-term monitoring of pediatric nasal polyps?
Medications
Which medications in the drug class Leukotriene Receptor Antagonists are used in the treatment of Pediatric Nasal Polyps?
Which medications in the drug class Corticosteroids, Intranasal are used in the treatment of Pediatric Nasal Polyps?
Which medications in the drug class Corticosteroids are used in the treatment of Pediatric Nasal Polyps?
10/16/24, 9:09 PM
Contributor Information and Disclosures
Author
John E McClay, MD, FAAP Associate Professor of Pediatric Otolaryngology, Department of Otolaryngology-Head and Neck
Surgery, Children's Hospital of Dallas, University of Texas Southwestern Medical Center
John E McClay, MD, FAAP is a member of the following medical societies: American Academy of Otolaryngic Allergy,
American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical
Association
Disclosure: Nothing to disclose.
Specialty Editor Board
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-
in-Chief, Medscape Drug Reference
Alan D Murray, MD Pediatric Otolaryngologist, ENT for Children; Full-Time Staff, Medical City Dallas Children's Hospital;
Consulting Staff, Department of Otolaryngology, Children's Medical Center at Dallas, Cook Children's Medical Center; Full-
Time Staff, Texas Pediatric Surgery Center, Cook Children's Pediatric Surgery Center Plano
Alan D Murray, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of
Otolaryngology-Head and Neck Surgery, American Society of Pediatric Otolaryngology, Society for Ear, Nose and Throat
Advances in Children, American Academy of Pediatrics, American College of Surgeons, Texas Medical Association
Chief Editor
Ravindhra G Elluru, MD, PhD Professor, Wright State University, Boonshoft School of Medicine; Pediatric Otolaryngologist,
Department of Otolaryngology, Dayton Children's Hospital Medical Center
Ravindhra G Elluru, MD, PhD is a member of the following medical societies: American Academy of Otolaryngology-Head
and Neck Surgery, American Academy of Pediatrics, American Bronchoesophagological Association, American College of
Surgeons, American Medical Association, Association for Research in Otolaryngology, Society for Ear, Nose and Throat
Advances in Children, Triological Society, American Society for Cell Biology
Acknowledgements
Orval Brown, MD Director of Otolaryngology Clinic, Professor, Department of Otolaryngology-Head and Neck Surgery,
University of Texas Southwestern Medical Center at Dallas
Orval Brown, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck
Surgery, American Academy of Pediatrics, American Bronchoesophagological Association, American College of Surgeons,
American Medical Association, American Society of Pediatric Otolaryngology, Society for Ear, Nose and Throat Advances in
Children, and Society of University Otolaryngologists-Head and Neck Surgeons
References
10/16/24, 9:09 PM
1. Babinski D, Trawinska-Bartnicka M. Rhinosinusitis in cystic fibrosis: not a simple story. Int J Pediatr Otorhinolaryngol. 2008 May.
72 (5):619-24. [QxMD MEDLINE Link].
2. Bernstein JM, Gorfien J, Noble B. Role of allergy in nasal polyposis: a review. Otolaryngol Head Neck Surg. 1995 Dec. 113
(6):724-32. [QxMD MEDLINE Link].
3. Tos M, Sasaki Y, Ohnishi M, Larsen P, Drake-Lee AB. Fireside conference 2. Pathogenesis of nasal polyps. Rhinol Suppl. 1992.
14:181-5. [QxMD MEDLINE Link].
4. Stammberger H. Surgical treatment of nasal polyps: past, present, and future. Allergy. 1999. 54 Suppl 53:7-11. [QxMD MEDLINE
Link].
5. Lind H, Joergensen G, Lange B, Svendstrup F, Kjeldsen AD. Efficacy of ESS in chronic rhinosinusitis with and without nasal
polyposis: a Danish cohort study. Eur Arch Otorhinolaryngol. 2016 Apr. 273 (4):911-9. [QxMD MEDLINE Link].
6. Andrews PJ, Poirrier AL, Lund VJ, Choi D. Outcomes in endoscopic sinus surgery: olfaction, nose scale and quality of life in a
prospective cohort study. Clin Otolaryngol. 2016 Dec. 41 (6):798-803. [QxMD MEDLINE Link].
7. Pagella F, Emanuelli E, Pusateri A, Borsetto D, Cazzador D, Marangoni R, et al. Clinical features and management of
antrochoanal polyps in children: Cues from a clinical series of 58 patients. Int J Pediatr Otorhinolaryngol. 2018 Nov. 114:87-91.
[QxMD MEDLINE Link].
8. Galluzzi F, Pignataro L, Maddalone M, Garavello W. Recurrences of surgery for antrochoanal polyps in children: A systematic
review. Int J Pediatr Otorhinolaryngol. 2018 Mar. 106:26-30. [QxMD MEDLINE Link].
9. McClay JE, Marple B, Kapadia L, Biavati MJ, Nussenbaum B, Newcomer M, et al. Clinical presentation of allergic fungal sinusitis
in children. Laryngoscope. 2002 Mar. 112 (3):565-9. [QxMD MEDLINE Link].
10. Mabry RL, Marple BF, Folker RJ, Mabry CS. Immunotherapy for allergic fungal sinusitis: three years' experience. Otolaryngol
Head Neck Surg. 1998 Dec. 119 (6):648-51. [QxMD MEDLINE Link].
11. Zhu CJ, Fruth K, Schneider A, Mann WJ, Brieger J. Impact of ozone exposure on prostaglandin release in nasal polyps. Eur
Arch Otorhinolaryngol. 2012 Jun. 269 (6):1623-8. [QxMD MEDLINE Link].
12. Lund VJ, Mackay IS. Staging in rhinosinusitus. Rhinology. 1993 Dec. 31 (4):183-4. [QxMD MEDLINE Link].
13. Lund VJ, Kennedy DW. Quantification for staging sinusitis. The Staging and Therapy Group. Ann Otol Rhinol Laryngol Suppl.
1995 Oct. 167:17-21. [QxMD MEDLINE Link].
14. Mackay IS, Lund VJ. Imaging and staging. Mygind N, Lildholdt T, eds. Nasal Polyposis: An Inflammatory Disease and Its
Treatment. Copenhagen: Munksgaard; 1997. 137-44.
15. Malm L. Assessment and staging of nasal polyposis. Acta Otolaryngol. 1997 Jul. 117 (4):465-7. [QxMD MEDLINE Link].
16. [Guideline] Rank MA, Chu DK, Bognanni A, Oykhman P, Bernstein JA, Ellis AK, et al. The Joint Task Force on Practice
Parameters GRADE guidelines for the medical management of chronic rhinosinusitis with nasal polyposis. J Allergy Clin
Immunol. 2023 Feb. 151 (2):386-398. [QxMD MEDLINE Link]. [Full Text].
17. Kirtsreesakul V, Wongsritrang K, Ruttanaphol S. Clinical efficacy of a short course of systemic steroids in nasal polyposis.
Rhinology. 2011 Dec. 49 (5):525-32. [QxMD MEDLINE Link].
18. Naclerio RM, Pinto J, Baroody F. Evidence-based approach to medical and surgical treatment of nasal polyposis. J Allergy Clin
Immunol. 2013 Dec. 132 (6):1461-1462.e3. [QxMD MEDLINE Link]. [Full Text].
19. Bachert C, Zhang L, Gevaert P. Current and future treatment options for adult chronic rhinosinusitis: Focus on nasal polyposis. J
Allergy Clin Immunol. 2015 Dec. 136 (6):1431-40; quiz 1441. [QxMD MEDLINE Link].
20. Holmstrom M. Clinical performance of fluticasone propionate nasal drops. Allergy. 1999. 54 Suppl 53:21-5. [QxMD MEDLINE
Link].
21. Rudmik L, Schlosser RJ, Smith TL, Soler ZM. Impact of topical nasal steroid therapy on symptoms of nasal polyposis: a meta-
analysis. Laryngoscope. 2012 Jul. 122 (7):1431-7. [QxMD MEDLINE Link].
22. Lund VJ, Flood J, Sykes AP, Richards DH. Effect of fluticasone in severe polyposis. Arch Otolaryngol Head Neck Surg. 1998
10/16/24, 9:09 PM
May. 124 (5):513-8. [QxMD MEDLINE Link].
23. Ragab S, Parikh A, Darby YC, Scadding GK. An open audit of montelukast, a leukotriene receptor antagonist, in nasal polyposis
associated with asthma. Clin Exp Allergy. 2001 Sep. 31 (9):1385-91. [QxMD MEDLINE Link]. [Full Text].
24. Klapan I, Culo F, Culig J, Bukovec Z, Simović S, Viseslav C, et al. Arachidonic acid metabolites and sinonasal polyposis. I.
Possible prognostic value. Am J Otolaryngol. 1995 Nov-Dec. 16 (6):396-402. [QxMD MEDLINE Link].

Pediatric Nasal Polyps

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Pediatric Nasal Polyps

The following conditions are associated with multiple benign polyps:

Bronchial asthma - In 20-50% of patients with polyps

Nasolacrimal duct cysts

All types of surgery - 15%

Genetics of Neurofibromatosis Type 1 and Type 2

Sinonasal Manifestations of Cystic Fibrosis

mistaken for absence of disease.

Cytokines present in polyps include the following:

IL-1 - Found regularly

Growth factors found in nasal polyps include the following:

Adhesion molecules include the following:

Vascular adhesion molecule (VCAM)-1 - Present

Immunoglobulins include the following:

Subsequently, this system was modified as follows[14, 15] :

Leukotriene receptor antagonists

JTF-PP Guidelines for Medical Management of Chronic Rhinosinusitis With

Prednisolone (Prelone, Orapred ODT, Pediapred)

Prednisone (Prednisone Intensol)

Mometasone, intranasal (Nasonex)

Fluticasone intranasal (Children's Flonase Allergy Relief, ClariSpray, Flonase

Budesonide intranasal (Rhinocort Allergy)

Triamcinolone, intranasal (Nasacort Allergy 24HR)

Beclomethasone, intranasal (Beconase AQ, QNASL)

Leukotriene Receptor Antagonists

Monoclonal Antibodies, Anti-asthmatics

Questions & Answers

What are nasal polyps?

What is the pathophysiology of nasal polyps?

What causes nasal polyps?

What is the US prevalence of nasal polyps?

Which patient groups have the highest prevalence of nasal polyps?

What is the prognosis of nasal polyps?

Which clinical history findings are characteristic of nasal polyps?

Which physical exam findings are characteristic of nasal polyps?

What is included in the physical exam to evaluate nasal polyps?

What is the most common location of benign nasal polyps?

How is an exam for nasal polyps conducted in pediatric patients?

What are the differential diagnoses for Pediatric Nasal Polyps?

Which histologic findings are characteristic of pediatric nasal polyps?

Which chemical mediators are found in pediatric nasal polyps?

How are pediatric nasal polyps staged?

How are pediatric nasal polyps treated?

What is the role of corticosteroids in the treatment of pediatric nasal polyps?

What is the role of surgery in the treatment of pediatric nasal polyps?

What are the possible complications of pediatric nasal polyps?

Which specialist consultations are beneficial to patients with nasal polyps?

What is included in long-term monitoring of pediatric nasal polyps?

Contributor Information and Disclosures

Disclosure: Nothing to disclose.

Specialty Editor Board

Disclosure: Nothing to disclose.

Disclosure: Nothing to disclose.

Disclosure: Nothing to disclose.

Disclosure: Nothing to disclose.

May. 124 (5):513-8. [QxMD MEDLINE Link].

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