nasal polyp medscape

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NASAL POLYP

Autor:John E McClay, MD Associate Professor of Pediatric Otolaryngology,

Department of Otolaryngology-Head and Neck Surgery, Children's Hospital of Dallas,

University of Texas Southwestern Medical School

http://emedicine.medscape.com/article/994274-overviewUpdated: Apr 18, 2012

McClay JE. Nasal polyps. eMed J 2001;2(12).

www.emedecine.com/ped/topic1550.htm

BACKGROUND

Broadly defined, nasal polyps are abnormal lesions that originate from any portion of thenasal mucosa or paranasal sinuses. Polyps are an end result of varying disease

processes in the nasal cavities. The most commonly discussed polyps are benignsemitransparent nasal lesions (see the images below) that arise from the mucosa of thenasal cavity or from one or more of the paranasal sinuses, often at the outflow tract ofthe sinuses.

Rigid endoscopic view of the left nasal cavity, showing the septum onthe left. Polyps with some blood and hemorrhage are on top of them in the center portion. The rim of whitefrom 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. Endoscopic view of the leftnasal cavity, showing a polyp protruding from the uncinate process. The middle turbinate is to the left. Asuction is visible on top of the inferior portion of the uncinate process and inferior portion of the polyp. Thelateral nasal wall is on the far right. The polyp is directly in the center and is pale, glistening, and white.
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Endoscopic view of the left middle meatus. The septum is on the farleft. The middle turbinate is next to the septum on the left. A large, glistening, translucent polyp is visible inthe center of the screen next to the middle turbinate. The lateral nasal wall is on the right side of thescreen. The inferior turbinate nub posteriorly is in the bottom right hand corner. Multiple polyps can occur in children withchronic sinusitis,allergic rhinitis,cystic fibrosis(CF),or allergic fungal sinusitis (AFS). An individual polyp could be an antral-choanalpolyp, 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 benignmultiple nasal polyposis for CF andasthma.

Pathophysiology

The pathogenesis of nasal polyposis is unknown. Polyp development has been linked tochronic inflammation, autonomic nervous system dysfunction, and geneticpredisposition. Most theories consider polyps to be the ultimate manifestation of chronicinflammation; therefore, conditions leading to chronic inflammation in the nasal cavitycan 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 NARESMost studies suggest that polyps are associated more strongly with nonallergic diseasethan with allergic disease. Statistically, nasal polyps are more common in patients withnonallergic asthma (13%) than with allergic asthma (5%), and only 0.5% of 3000 atopicindividuals 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 believethat 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
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properties of polyps, Bernstein derived a convincing theory on the pathogenesis of nasalpolyps, building on other theories and information from Tos.[1, 2]

In Bernstein's theory, inflammatory changes first occur in the lateral nasal wall or sinusmucosa 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 thenarrow clefts in the anterior ethmoid region that create turbulent airflow, and particularlywhen narrowed by mucosal inflammation. Ulceration or prolapse of the submucosa canoccur, with reepithelialization and new gland formation. During this process, a polyp canform from the mucosa because the heightened inflammatory process from epithelialcells, vascular endothelial cells, and fibroblasts affects the bioelectric integrity of thesodium channels at the luminal surface of the respiratory epithelial cell in that section ofthe nasal mucosa. This response increases sodium absorption, leading to waterretention and polyp formation.

Other theories involve vasomotor imbalance or epithelial rupture. The vasomotorimbalance theory postulates that increased vascular permeability and impaired vascular

regulation cause detoxification of mast-cell products (eg, histamine). The prolongedeffects of these products within the polyp stroma result in marked edema (especially inthe polyp pedicle) that is worsened by venous drainage obstruction. This theory is basedon the cell-poor stroma of the polyps, which is poorly vascularized and lacksvasoconstrictor innervation.

The epithelial rupture theory suggests that rupture of the epithelium of the nasal mucosais caused by increased tissue turgor in illness (eg, allergies, infections). This ruptureleads to prolapse of the lamina propria mucosa, forming polyps. The defects are possiblyenlarged 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. Neithertheory completely defines the inflammatory trigger.

Patients with CF have a defective small chloride conductance channel, regulated bycyclic adenosine monophosphate (cAMP), which causes abnormal chloride transportacross the apical cell membrane of epithelial cells. The pathogenesis of nasal polyposisin 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 withCF is 6-48%. Among adults, the incidence is 1-4% overall, with a range of 0.2-28%.

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

Mortality/Morbidity

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

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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. Areview of articles reporting on children whose nasal polyposis required surgery showedapparently equal prevalence in boys and girls, although the data are inconclusive.[3] Thereported prevalence is equal in patients with asthma.

Age

Benign multiple nasal polyposis usually manifests in patients older than 20 years and ismore common in patients older than 40 years. Nasal polyps are rare in children youngerthan 10 years.

CLINICAL PRESENTATION

The manifestation of nasal polyps depends on the size of the polyp. Small polyps maynot produce symptoms and may be identified only during routine examination when theyare anterior to the anterior edge of the middle turbinate. Polyps located posterior to thesite are not typically seen during routine anterior rhinoscopy examination performed withan otoscope and are missed unless the child is symptomatic. Small polyps in areaswhere polyps normally arise (ie, the middle meatus) may produce symptoms and blockthe 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 cluethat polyps, rather than chronic sinusitis alone, are present. Epistaxis that does not arisefrom irritation of the anterior nasal septum (ie, Kiesselbach area) usually does not occurwith 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 imagesbelow] that obstructs the nasal cavities, nasopharynx, or both) can causeobstructivesleep symptomsand chronic mouth breathing.

Rigid endoscopic view of the left nasal cavity, showing the septum onthe left, inferior turbinate on the right, middle turbinate superiorly, and antral-choanal polyp among the floor
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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. Close-up of themiddle meatus, showing the stalk of the antral-choanal polyp emanating from the maxillary sinus behind theuncinate 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. Axial CT scansection through the maxillary sinuses showing opacification of the left maxillary sinus with antral-choanalpolyp 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 scanthrough the anterior sinuses showing opacification of the left maxillary sinus with opacification of the inferiorhalf 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 showingthe sphenoid sinus superiorly and the antral-choanal polyp filling the nasopharynx in the center of the scan.

Oral cavity and oropharyngeal view of antral-choanal polyp filling theposterior oral pharynx and pushing the soft palate anterior and inferiorly. The polyp is visible behind the

uvula and the soft palate. Scale is in inches. The left side of the lesionwas the portion of the polyp in the nasal cavity. The right was a stalk attached to the medial maxillary wall.

Endoscopic view of the left middle meatus, showing the septum on theleft, the middle turbinate in the center superiorly, and a large maxillary antrostomy with a curved suction onthe 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.


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which is partially visible at 4 and 5 o'clock. Endoscopic view of the leftnasal cavity, showing a polyp protruding from the uncinate process. The middle turbinate is to the left. Asuction is visible on top of the inferior portion of the uncinate process and inferior portion of the polyp. Thelateral 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 farleft. The middle turbinate is next to the septum on the left. A large, glistening, translucent polyp is visible inthe center of the screen next to the middle turbinate. The lateral nasal wall is on the right side of thescreen. The inferior turbinate nub posteriorly is in the bottom right hand corner.

View just inside the nasal vestibule of a fifteen-year-old adolescent boywith allergic fungal sinusitis showing diffused polyposis extending into the anterior nasal cavity andvestibule; the septum is on the right, and the right lateral vestibular wall (nasal ala) is on the left. The polyps


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are all in the center. The polyps almost hang out of the nasal vestibule.Coronal section through the ethmoid maxillary sinuses and orbits. This is a 2-year-old child with cysticfibrosis, showing complete opacification of the maxillary and ethmoid sinuses. Bulging in the medial

maxillary walls is observed. Coronal section showing soft tissuewindows rather than bony windows. It indicates the infection by the thick mucus in the maxillary andethmoid cavities by the heterogeneity of the opacification in the sinuses. Note that the nasal cavity is

completely obliterated by polyp disease. Coronal CT scan showingextensive allergic fungal sinusitis involving the right side with mucocele above the right orbit and expansion

of the sinuses on the right. Coronal CT scan showing typical unilateralappearance of allergic sinusitis with hyperintense areas and inhomogeneity of the sinus opacification; the


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hyperintense areas appear whitish in the center of the allergic mucin. CoronalMRI scan showing expansion of the sinuses with allergic mucin and polypoid disease; the hypointenseblack areas in the nasal cavities are the actual fungal elements and debris. The density above the right eyeis the mucocele. The fungal elements and allergic mucin in allergic fungal sinusitis always look hypointense

on MRI scanning and can be mistaken for absence of disease. Fifteenyear-old adolescent boy with allergic fungal sinusitis causing right proptosis, telecanthus, and malarflattening; position of his eyes is asymmetrical, and his nasal ala on the right is pushed inferiorly compared

with the left. Nine-year-old girl with allergic fungal sinusitis displayingtelecanthus and asymmetrical positioning of her eyes and globes.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 todecrease visual acuity. Furthermore, because they grow slowly, massive polyposesusually cause no neurological symptoms, even those that extend into the intracranialcavity

PHYSICAL

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 theyare anterior to the anterior edge of the middle turbinate. Polyps located posterior to the
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site are not typically seen during routine anterior rhinoscopy examination performed withan otoscope and are missed unless the child is symptomatic. Small polyps in areaswhere polyps normally arise (ie, the middle meatus) may produce symptoms and blockthe outflow tract of the sinuses, causing chronic or recurrent acute sinusitis symptoms.

Symptom-producing polyps can cause nasal airway obstruction, postnasal drainage, dullheadaches, snoring, and rhinorrhea. Associated hyposmia or anosmia may be a cluethat polyps, rather than chronic sinusitis alone, are present. Epistaxis that does not arisefrom irritation of the anterior nasal septum (ie, Kiesselbach area) usually does not occurwith 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 imagesbelow] that obstructs the nasal cavities, nasopharynx, or both) can causeobstructivesleep symptomsand chronic mouth breathing.

Rigid endoscopic view of the left nasal cavity, showing the septum onthe 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. Close-up of themiddle meatus, showing the stalk of the antral-choanal polyp emanating from the maxillary sinus behind theuncinate process on the bottom right-hand side of the picture. The left side of the picture shows the septum
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and the middle turbinate being pushed over via suction. Axial CT scansection through the maxillary sinuses showing opacification of the left maxillary sinus with antral-choanalpolyp 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 scanthrough the anterior sinuses showing opacification of the left maxillary sinus with opacification of the inferiorhalf of the nasal cavity on the left, filled by the antral-choanal polyp. The rest of the sinuses are clear.

Coronal CT scan section through the posterior nasopharynx showingthe sphenoid sinus superiorly and the antral-choanal polyp filling the nasopharynx in the center of the scan.

Oral cavity and oropharyngeal view of antral-choanal polyp filling theposterior oral pharynx and pushing the soft palate anterior and inferiorly. The polyp is visible behind the


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uvula and the soft palate. Scale is in inches. The left side of the lesionwas the portion of the polyp in the nasal cavity. The right was a stalk attached to the medial maxillary wall.

Endoscopic view of the left middle meatus, showing the septum on theleft, the middle turbinate in the center superiorly, and a large maxillary antrostomy with a curved suction onthe 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.


which is partially visible at 4 and 5 o'clock. Endoscopic view of the leftnasal cavity, showing a polyp protruding from the uncinate process. The middle turbinate is to the left. Asuction 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.


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Endoscopic view of the left middle meatus. The septum is on the farleft. The middle turbinate is next to the septum on the left. A large, glistening, translucent polyp is visible inthe center of the screen next to the middle turbinate. The lateral nasal wall is on the right side of thescreen. The inferior turbinate nub posteriorly is in the bottom right hand corner.

View just inside the nasal vestibule of a fifteen-year-old adolescent boywith allergic fungal sinusitis showing diffused polyposis extending into the anterior nasal cavity andvestibule; 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.Coronal section through the ethmoid maxillary sinuses and orbits. This is a 2-year-old child with cysticfibrosis, showing complete opacification of the maxillary and ethmoid sinuses. Bulging in the medial

maxillary walls is observed. Coronal section showing soft tissuewindows 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


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completely obliterated by polyp disease. Coronal CT scan showingextensive allergic fungal sinusitis involving the right side with mucocele above the right orbit and expansion

of the sinuses on the right. Coronal CT scan showing typical unilateralappearance of allergic sinusitis with hyperintense areas and inhomogeneity of the sinus opacification; the

hyperintense areas appear whitish in the center of the allergic mucin. CoronalMRI scan showing expansion of the sinuses with allergic mucin and polypoid disease; the hypointenseblack areas in the nasal cavities are the actual fungal elements and debris. The density above the right eyeis the mucocele. The fungal elements and allergic mucin in allergic fungal sinusitis always look hypointense

on MRI scanning and can be mistaken for absence of disease. Fifteenyear-old adolescent boy with allergic fungal sinusitis causing right proptosis, telecanthus, and malarflattening; position of his eyes is asymmetrical, and his nasal ala on the right is pushed inferiorly compared


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with the left. Nine-year-old girl with allergic fungal sinusitis displayingtelecanthus and asymmetrical positioning of her eyes and globes.In an article submitted for publication, the author has reported 40% of children with AFSpresented with craniofacial abnormalities, compared with 10% of adults with AFS.Massive polyposis rarely causes enough extrinsic compression on the optic nerve todecrease visual acuity. Furthermore, because they grow slowly, massive polyposesusually cause no neurological symptoms, even those that extend into the intracranialcavity

CAUSES

As described in Pathophysiology, chronic inflammation (from whatever source)apparently has an initial role in the pathogenesis of nasal polyps. Multiple polyps occurin children with chronic sinusitis, allergic rhinitis, CF, and AFS. An isolated polyp couldbe an antral-choanal polyp, a benign massive polyp, a nasolacrimal duct cyst (as shownbelow), or any congenital lesion or benign or malignant tumor listed below.

Nasolacrimal duct cysts Frontal view of a 2-day-old infant withswelling 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. Rigidendoscopic view of the left nasal cavity. The septum is on the left, and the lateral nasal wall is on theright. The inferior turbinate is in the center of the picture, and the middle turbinates are visible in thesuperior midsection of the picture. The nasal lacrimal duct cyst is the yellow dilated lesion underneath the
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inferior turbinate. Axial CT scan section through the orbit, showing thedilated 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. A frontalview of the decompressed nasal lacrimal ducts following surgical marsupialization. Swelling in the inferiormedial canthal areas prior to surgery is no longer seen.

Encephaloceles (see the image below) A 3-month-old infantwith hypertelorism and bulging of the nasal dorsum, secondary to encephalocele.

Gliomas (see the images below) Interior view of the nose andnasal cavities. To the right of the patient's left nostril, the right nasal cavity has no obstruction. On the leftof 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 theattachment of the inferior turbinate anteriorly; it was transnasally removed.

Dermoid tumors (see the images below) Lateral view of apreteenaged child showing infected nasal dermoid. Note the protrusion of the dorsum of the nose.

Preteenaged boy with infected nasal dermoid. A pith is visible overthe superior portion of the swelling between the eyes. Nasal pith is commonly seen with the nasal

dermoid. Frontal view of a 5-month-old infant, showing hypertelorism


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and protrusion in the glabellar region secondary to a small nasal dermoid.Axial CT scan (bony windows) showing a 5-month-old infant with nasal dermoid anterior to the nasal andmaxillary bones. No bony dehiscence or bony abnormalities are visible.

A coronal MRI scan through the nasal dermoid of a 5-month-oldinfant. The scale on the left is 2 mm per small bar and 1 cm per tall bar. The arrow points to the lesion.

The lesion appears to be approximately 6-7 mm in this dimension. Aninteroperative view of dermoid removal from a 5-month-old infant.

Hemangiomas

Papillomas (see the image below) Anterior nasal papillomaarising from the septum. The skin of the nasal vestibule is seen surrounding the papilloma in the centerof the image.

Juvenile nasopharyngeal angiofibromas


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Rhabdomyosarcoma (see the images below) Axial MRI scan of theorbits, 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 CTscan through the orbits and ethmoid sinuses, showing the rhabdomyosarcoma in the same areas,including the posterior ethmoid complex, left middle fossa, and skull base of cavernous sinuses.

Rigid endoscopic view of left nasal cavity, showing a polyp in thecenter of the picture, with extension of the rhabdomyosarcoma. The septum is on the left and the middleturbinate is on the right.

Lymphomas Neuroblastomas

Sarcomas Chordomas Nasopharyngeal carcinomas Inverting papillomas

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

Differential Diagnoses

Asthma Cystic Fibrosis

Neuroblastoma Neurofibromatosis
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Rhabdomyosarcoma Sinusitis

WORKUP

Laboratory Studies

Direct laboratory studies at the pathological process believed responsible for the nasalpolyps.

Children with polyposis that is associated with allergic rhinitis should have an evaluationfor their allergies; this may include a serological radioallergosorbent test (RAST) or someform of allergic skin testing. Mabry et al showed a decrease in the recurrence rate ofpolyps in children treated with immunotherapy directed at all antigens for which they areallergic, especially molds;[4] therefore, allergy testing and treatment may be important intreating 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 ofneutrophils may indicate chronic sinusitis.

IMANGING STUDIES

The criterion standard to evaluate nasal lesions, especially nasal polyposis or sinusitis,is a thin-cut (1-3 mm) CT scan of the maxillofacial area, the sinuses axially, and thecoronal plane. Perform a compatible CT scan if an intraoperative image-guided system

is used. Plain film radiography has no significant value after polyps are diagnosed. Also perform MRI in patients with possible intracranial involvement or extension of

benign nasal polyps. CT scan findings 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 thedifferential diagnosis of an unusual polyp or clinical presentation.

CF has a characteristic symmetrical bulging of the lateral nasal walls medially (see the

images below). Coronal section through the ethmoid maxillarysinuses and orbits. This is a 2-year-old child with cystic fibrosis, showing complete opacification of themaxillary and ethmoid sinuses. Bulging in the medial maxillary walls is observed.
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Coronal section showing soft tissue windows rather than bonywindows. It indicates the infection by the thick mucus in the maxillary and ethmoid cavities by theheterogeneity 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 tomaxillary sinus. The medial maxillary walls bulge medially, which is a typical CT scan view of cysticfibrosis. The ethmoid sinuses have scattered disease.

An antral-choanal polyp may show opacified maxillary sinuses with a protruding lesionheading from the maxillary antrum to the choana (see the images below).

Axial CT scan section through the maxillary sinuses showingopacification of the left maxillary sinus with antral-choanal polyp in the posterior nasal cavity and choanaexiting from beneath the middle turbinate in the area of the ostiomeatal complex unit. Scale is in

centimeters. Coronal CT scan through the anterior sinuses showingopacification of the left maxillary sinus with opacification of the inferior half of the nasal cavity on the left,


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filled by the antral-choanal polyp. The rest of the sinuses are clear.Coronal CT scan section through the posterior nasopharynx showing the sphenoid sinus superiorly andthe 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). AxialMRI scan of the orbits, posterior fossa, and nasal cavity. The solid tumor is seen filling the posteriorethmoid 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 posterior ethmoid complex, left middle fossa, andskull 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 dilatednasal lacrimal ducts in the medial anterior area compared to the orbits. Scale on the bottom right is in


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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 incentimeters. 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 CNS. Patients with AFS exhibit heterogenous areas in the sinuses on CT and MRI scans;

these areas consist of both the nasal polyposis and the allergic fungal mucin (see theimages below). This allergic fungal mucin appears black on MRI and can be confused

with the absence of disease. Fifteen year-old adolescent boywith allergic fungal sinusitis causing right proptosis, telecanthus, and malar flattening; position of his eyesis asymmetrical, and his nasal ala on the right is pushed inferiorly compared with the left.

Coronal CT scan showing extensive allergic fungal sinusitis involvingthe 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 andpolypoid disease; the hypointense black areas in the nasal cavities are the actual fungal elements anddebris. The density above the right eye is the mucocele. The fungal elements and allergic mucin in


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allergic fungal sinusitis always look hypointense on MRI scanning and can be mistaken for absence ofdisease.

Procedures

See rigid and flexible endoscopy procedures described in Physical.

Histologic Findings

Histologically, nasal polyps are characterized by a pseudostratified ciliated columnarepithelium, 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 seromucousglands or almost absent or rare glands when comparing the polyps to the inferior ormiddle turbinate. Hyperplasia of the gland can cause cystically dilated and degeneratedglands 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 asthmaand allergy, contain granules with toxic products (eg, leukotrienes, eosinophilic cationicprotein, major basophilic protein, platelet-activating factor, eosinophilic peroxidases,other vasoactive substances and chemotactic factors). These toxic factors areresponsible for epithelial lysis, nerve damage, and ciliostasis. Specific granule protein,leukotriene A4, and platelet-activating factor apparently are responsible for the mucosalswelling 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 delayedapoptosis of eosinophils is mediated, in part, by blockage of the Fas receptors, typicallywith proteases that help begin the process of cell death. Delayed apoptosis is alsomediated by an increase in interleukin 5 (IL)-5, IL-3, and granulocyte-macrophagecolony-stimulating factor (GM-CSF) secreted by T lymphocytes, which help sustain theeosinophil from death. Glucocorticoids seem to help reduce polyps or polypoid reactionsin 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 polypoccurs 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 nonimmunoglobulin E

mediated fashion. Increased numbers of plasma cells,lymphocytes, and myofibroblasts also occur.

Chemical mediators

The stroma of nasal polyps have numerous mediators, including cytokines, growthfactors, adhesion molecules, and immunoglobulins; polyps also contain vasoactiveamines, serotonin, prostaglandins[5] ,leukotrienes, norepinephrine, kinins, esterases,heparin, and histamine. The level of histamine in nasal polyps is 100-1000 times thelevel found in the blood stream.

Cytokines present in polypso IL-1 - Found regularly


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o IL-3 - Varies, based on study, from absent to intermittent at low levels to regularlypresent

o IL-4 - Inconsistently detectedo 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.o IL-6 - Same as in controls (no increase)o IL-8 - Varies, based on study, from undetected to regularly detected; may cause

sustained recruitment of leukocytes into nasal polyps and may decrease fibroblasticproliferation

o IL-10 - Same as in controls; no increase regulated on activation, normal T cellexpressed and secreted (RANTES); varies, based on study, from same as controlsto regularly detected to increased levels interferon gamma; increases in eosinophils,seromucous glands, and epithelium of nasal polyps

Growth factors found in nasal polypso Tumor necrosis factor (TNF) alpha and beta - Varies, based on study, from same as

controls to regularly detected; believed to be from eosinophilso GM-CSF - mRNA and protein amount varies, based on study, from never to

intermittent to presento Platelet derived growth factor - Presento Vascular permeable factors (VPFs) - Presento Vascular endothelial growth factors (VEGFs) - Presento Insulinlike growth factor I - Presento Stem cell factor - Present

Adhesion moleculeso Vascular adhesion molecule 1 (VCAM-1) - Presento E and P selectin - Present

Immunoglobulins (Ig)o IgG - No increase; same levels as in the middle and inferior turbinate mucosao IgA - More in polyps than in the middle and inferior turbinate mucosa, especially IgA1

over IgA2o IgM - No increase, same as in the middle and inferior turbinate mucosao IgD - No increase, same as in the middle and inferior turbinate mucosao IgE - Increased levels compared with the middle and inferior turbinate mucosa; same

level in patients without allergy as in those with allergy

Staging

Polyposis has no uniform staging system

TREATMENT

Medical Care

Oral and topical nasal steroid administration is the primary medical therapy for nasalpolyposis.[6]Antihistamines, decongestants, and cromolyn sodium provide little benefit.

Immunotherapy may be useful to treat allergic rhinitis but, when used alone, does notusually resolve existing polyps. Administer antibiotics for bacterial superinfections.


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Corticosteroids are the treatment of choice, either topically or systemically. Directinjection into the polyp is not approved by the US Food and Drug Administration (FDA)because of reports of unilateral vision loss in 3 patients after intranasal steroid injectionwith Kenalog. Safety may depend on specific drug particle size; large molecular weightdrugs 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 1-3weeks. Dosage varies for children, but the maximum dose is usually 1 mg/kg/d for 5-7days, then taper over 1-3 weeks. Responsiveness to corticosteroids appears to dependon the presence or absence of eosinophilia; thus, patients with polyps and allergicrhinitis 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 tosteroids. 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 asepticnecrosis of the femoral head).

Many authors advocate topical nasal steroid administration for nasal polyps, either asthe primary treatment or as a continual secondary treatment immediately following oralsteroids or surgery. Most nasal steroids (eg, fluticasone, beclomethasone, budesonide)effectively relieve subjective symptoms and increase the nasal airflow when measuredobjectively (primarily in double-blind placebo-controlled studies).[7]A systematic review of19 studies found similar results. The topical steroid preparations fluticasone,mometasone, and budesonide were shown to improve nasal symptoms in patients with

nasal polyposis.

[8]

Some studies indicate fluticasone has a faster onset of action andpossible mild superiority to beclomethasone.[9]

Topical corticosteroid administration generally causes fewer adverse effects thansystemic corticosteroid use because of the former's limited bioavailability. Long-termuse, especially at high dosages or in combination with inhaled corticosteroids, presentsa risk of hypothalamic-pituitary-adrenal axis suppression, cataract formation, growthretardation, 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 y) studies evaluating the use of beclomethasone have shown nodegradation of the normal respiratory epithelium to squamous epithelium seen in chronic

atrophic rhinitis. Additionally, the newer generation of systemic steroids (eg, fluticasone,Nasonex) appears to have less bioavailability than older nasal steroids, such asbeclomethasone.

Surgical Care

Surgical intervention is required for children with multiple benign nasal polyposis orchronic rhinosinusitis who fail maximum medical therapy. Simple polypectomy iseffective initially to relieve nasal symptoms, especially for isolated polyps or smallnumbers of polyps. In benign multiple nasal polyposis, polypectomy is fraught with ahigh recurrence rate.

Endoscopic sinus surgery (ESS) is a better technique that not only removes the polypsbut also opens the clefts in the middle meatus, where they most often form, which helps
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decrease the recurrence rate. The exact extent of the surgery needed, whethercomplete extirpation (ie, Nasalide procedure) or simple aeration of the sinuses, is notentirely known, simply because of the dearth of studies. Rare comparisons show thatcomplete extirpation procedures are as effective or superior to aeration of the sinuses;complication rates are low with experienced surgeons. The use of a surgical

microdebrider (see the image below) has made the procedure safer and faster, providingprecise tissue cutting and decreased hemostasis with better visualization.

A surgical microdebrider entering the middle meatus. The septum is onthe 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 wherepolyps were present in the center of the picture.Direct surgery at diseased tissue that is apparent on the CT scan at the time of surgery.Patients with diseases such as CF, primary ciliary dyskinesia syndrome, or Youngsyndrome may proceed to surgery without extensive medical treatment because thesediseases usually do not respond well to corticosteroid treatment. Once diseased tissuehas been removed from the nasal cavity and sinuses, the pulmonary systems usuallyimprove. Consider use of an image-guided system to define the exact location of

intranasal, sinus, orbital, and intracranial structures for massive polyposis or revisionsurgery because surgical landmarks may be absent or altered. For specific techniques inpediatric sinus surgery, with and without polyps, seePediatric Sinusitis, SurgicalTreatment.

Nasal polyposis occurs in 6-48% of children with CF. Surgery is performed whenchildren become symptomatic. Recurrence of polyps in CF is almost universal, requiringrepeated surgeries every few years. In fact, recurrence is typical for many diseases thatcause nasal polyps; patients should receive preoperative counseling about thispossibility.

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.

Consultations

First notify a pediatric otolaryngologist, especially if medical therapy has failed or if theorigin or diagnosis of the underlying pathology of the nasal polyp is unknown.

Consider consultation with a pulmonary specialist when benign nasal polyps areidentified because they could result from asthma, allergy, or CF. Patients with thesediseases often have associated pulmonary problems.

Diet

Treatment of nasal polyps involves no special diet.
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Activity

No activity restrictions are necessary for a child with nasal polyps. The child's activitylevel may decrease because of diminished ability to breath through the nose, decreasingsport or physical activity performance. After sinus surgery, activities are limited; theselimitation recommendations vary from surgeon to surgeon. Most surgeons specificallyrestrict nose blowing because it may increase intranasal pressure and cause potentialproblems in areas of already thinned bony dividers in patients with nasal polyposis.

MEDICATION

Medication Summary

See Medical Care.

Corticosteroids

Class Summary

Corticosteroids have potent anti-inflammatory action and relieve rhinorrhea, sneezing,itching, and congestion.

View full drug information

Prednisolone (Prelone, Orapred, Pediapred)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes andreducing capillary permeability.


Prednisone (Deltasone, Orasone, Meticorten, Sterapred)

May decrease inflammation by reversing increased capillary permeability andsuppressing PMN activity.


Dexamethasone (Decadron)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes andreducing capillary permeability.

Nasal corticosteroids

Class Summary

These agents induce a nonspecific anti-inflammatory response that should theoreticallyreduce the size of polyps and prevent regrowth when continuously used. Available nasalsteroid sprays appear to be similarly effective and relatively safe for both short-term andlong-term use.


Mometasone (Nasonex)

Nasal spray; demonstrated no mineralocorticoid, androgenic, antiandrogenic, or

estrogenic activity in preclinical trials. Studies concerning bioavailability are established;should be considered first-line when treating pediatric patients. Not systemically
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absorbed like other nasal steroids (ie, beclomethasone). Studies concerningbioavailability are established; should be considered first-line when treating pediatricpatients. Not systemically absorbed like other nasal steroids (ie, beclomethasone).


Fluticasone propionate (Flonase)

Topical nasal steroid. Has extremely potent vasoconstrictive and anti-inflammatoryactivity. Has a weak hypothalamic-pituitary-adrenocortical axis inhibitory potency whenapplied topically. Studies concerning bioavailability are established; should beconsidered first line when treating pediatric patients. Not systemically absorbed likeother nasal steroids (ie, beclomethasone).

Should use nasal steroid spray with fluticasone propionate to help buffer the nose andprevent complications from the spray, such as nasal drying, epistaxis, and, in long-termuse, septal perforation.


Budesonide inhaled (Rhinocort Aqua)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes andreversing capillary permeability.


Triamcinolone inhaled (Nasacort AQ)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes andreversing capillary permeability.


Beclomethasone (Beconase AQ)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes andreversing capillary permeability. Delivers 42 mcg/actuation.

FOLLOW UP

Further Inpatient Care

Historically, children diagnosed with cystic fibrosis (CF) already had digestive and

pulmonary disease and were the children with the more severe form of disease. Thesechildren were often treated with intravenous antibiotics directed at the most commonpathogens found in the lungs and the sinuses (eg, Pseudomonasaeruginosa,Staphylococcus aureus), both preoperatively and postoperatively.Additionally, these children had pulmonary toilet to increase their lung function in theperioperative period, including intravenous steroids, percussion therapy, and inhaledbronchodilators. Much of this process can now be performed on an outpatient basis,depending on the severity of the associated disease.

For patients with severe asthma and polyposis requiring surgery, postoperativeadmission for observation of respiratory compromise or spasm is determined on anindividual basis.

Outpatient surgery is usually performed for older children undergoing endoscopic sinussurgery (ESS) for nasal polyposis without coexisting medical conditions.
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Further Outpatient Care

Closely monitor children with benign multiple nasal polyps, whatever the cause, becauserecurrence is likely, whether medically or surgically treated. Postoperative follow-upshould occur 3-4 times the first month to monitor healing of the sinus cavities; frequencydepends on the patient's own geographic location and symptoms.

A patient with CF can be monitored symptomatically because surgery is not performeduntil these patients are symptomatic, even if nasal polyposis is seen on CT scan or nasalendoscopy. Certainly, each patient is treated on an individual basis.

For polyps associated with allergic fungal sinusitis (AFS), close follow-up by anotolaryngologist is recommended until the patient is deemed free of disease, which maybe several years or more.

Any accumulation of fungus may accelerate the antigenic process, which causessymptoms and disease to recur. Recurrence is especially common for polyps, whichmay be controlled more simply and effectively if recognized early.

Small nasal polyps are recognized early on a routine follow-up in patients with benignmultiple nasal polyps.

Other diseases may be treated medically or with smaller surgical procedures. Fordiseases resulting in nasal polyps other than benign multiple nasal polyps, the need forinpatient or outpatient care is determined by the extent of disease, symptoms andsituation of the patient, and associated medical conditions.

Inpatient & Outpatient Medications

See Medical Care and Medication.

Deterrence/Prevention

See Medical Care.

Complications

Massive polyposis or a single large polyp (eg, an antral-choanal polyp) that obstructs thenasal cavities and/or nasopharynx can cause obstructive sleep symptoms and chronicmouth breathing. Rarely, massive polyposis, observed in CF and in AFS can alter thecraniofacial structure. This can result in proptosis, hypertelorism, and diplopia.

In an article submitted for publication, the author reported that 40% of children(compared with 10% of adults) with AFS presented with craniofacial abnormalities.Massive polyposis rarely causes enough extrinsic compression on the optic nerve todecrease visual acuity. One study reported that 3 of 82 patients with AFS had visionchanges from compression of the optic nerve in the sphenoid sinus that resolved overtime with removal of disease. However, because these polyps are slow growing, theyusually cause no neurological symptoms, even when they extend into the intracranial

cavity.Prognosis

Polyposis recurrence is common following treatment with medical or surgical therapy ifmultiple benign polyps are present (see Surgical Care). Single large polyps (eg, antral-choanal polyps) are less likely to recur. The literature contains sparse data comparingtreatments.

Patient Education

Educating patients about the chronicity of the disease is important to make them awareof the recurrent nature of the problem.

nasal polyp medscape

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