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SINONASAL DISEASE
DISCUSSION OF BENIGN POLYPOIDAL ETIOLOGIES
Dr Ranjit Singh Lahel
Resident (Radiodiagnosis)
Reference.
1. Scott- Brown otorhinolaryngology
2. Cummings Otolaryngology
3. Nasal polyposis by T. Metin Önerci
Berrylin J. Ferguson
4.Pubmed indexed Journals.
The silent sinus syndrome represents maxillary
sinus atelectasis that results in painless
enophthalmos, hypoglobus and facial
asymmetry .
The term is restricted to patients with no
history of sinusitis, trauma or surgery .
POLYPS are soft tissue pedunculated masses of
oedematous hyperplastic mucosa lining the
upper respiratory tract…..nasal cavity and
sinuses.
These are benign mucosal lesions.
COMMON CONDITIONS
ASSOCIATED WITH NP
Commonest sites in order of frequency
are;
1. Ethmoids
2. Maxillary antra
3. sphenoids
1. ALLERGY?
• It was believed that allergy is a significant cause of nasal
polyposis as most of the polyps are characterized by
tissue eosinophilia.
• Most studies have failed to show a higher occurrence of
positive skin tests to inhaled allergens in patients with
polyps than in the general population.
• According to Keith et al there is no deterioration of nasal
symptoms or eosinophilia during the pollen season in
polyp patients having a positive skin test to pollen.
Thus, it appears that allergy is not a well documented
cause or aggravating factor in nasal polyposis.
2. ASPIRIN EXACERBATED RESPIRATORY DISEASE (AERD), also known as
Samter’s Triad or Aspirin Sensitive Asthma,
is a chronic medical condition that consists of
•asthma,
•recurrent sinus disease with nasal polyps,
•sensitivity to aspirin and other non-steroidal anti-inflammatory drugs
(NSAIDs).
Approximately 10% of all adults with asthma and 40% of patients with
asthma and nasal polyps are sensitive to aspirin and NSAIDs.
Patients with AERD/Samter’s Triad usually have asthma, nasal
congestion, and nasal polyps, and often do not respond to
conventional treatments.
Many have experienced chronic sinus infections and can lose their
sense of smell. The characteristic feature of AERD/Samter’s Triad is
that patients develop reactions triggered by aspirin or other
NSAIDs.
• In the ASA intolerant patients, a lowered prostaglandin E2 (PGE2)
production has been observed.
• PGE2 has a significant anti-inflammatory activity, including inhibition
of eosinophils.
• A possible intrinsic defect in PGE2 production might, therefore, be
responsible for a further increase of eosinophilic accumulation in ASA
intolerant patients.
3. CYSTIC FIBROSIS:
• Cystic fibrosis (CF), also known as mucoviscidosis, is an autosomal
recessive genetic disorder that affects most critically the lungs, and
also the pancreas, liver, and intestine.
• It is characterized by abnormal transport of chloride and sodium
across an epithelium, leading to thick, viscous secretions.
• Nasal endoscopy demonstated polyp in 45% of adults with cystic
fibrosis.
• A sweat chloride test is recommended in any child with nasal
polyps, to rule out cystic fibrosis.
4. KARTAGENER’S SYNDROME:
• Primary ciliary dyskinesia (PCD), also known as
immotile ciliary syndrome.
• Rare, ciliopathic, autosomal recessive genetic disorder.
• It causes a defect in the action of the cilia lining the
respiratory tract (lower and upper, sinuses, Eustachian
tube, middle ear) and fallopian tube, and also of the
flagella of sperm in males.
• Absent mucociliary clearance and recurrent bacterial
infections result in nasal polyposis in about 40 percent
of the patients.
PATHOGENESIS & PATHOPHYSIOLOGY
• The pathogenesis of nasal polyps explains how the
polyps start and grow.
• The pathophysiology of nasal polyps explains the
events and processes taking place in the outgrowth of
nasal polyps.
• Several pathogenetic theories on the formation of nasal
polyps have been published during the last 150 years.
These theories are based on oedema, an increase in tubulo-alveolar
glands, the presence of the cysts of mucous glands and
on mucous glands of NP.
MUCOSAL EXUDATE THEORY
• Hayek believed that the formation of NP started via an exudate
localised deep in the nasal mucosa, which pressed outwards
caudally.
• According to this theory, both layers of the
tubulo-alveolar sero-mucous nasal glands
should be displaced outwards and be found in
the distal part of the polyp.
PERI-PHLEBITIS AND PERI-LYMPHANGITIS THEORY
• The theory of Eggston and Wolff is based upon the
recurrent infections that lead to the blocking of
intercellular fluid transport in the mucosa and oedema
of the lamina propria.
• If the oedema involves major areas, the result is the
prolapse of the mucosa and formation of polyps.
WHAT ACTUALLY HAPPENS
CELLULAR INFILTRATION
• Eosinophilic inflammation is an important feature in the
pathogenesis of chronic Rhinosinusitis (CRS) with nasal polyps.
• The eosinophilic accumulation in the polyp stroma is basically
caused by increased transendothelial migration and increased
survival time in the tissue, where an increased concentration of
interleukine 5 (IL-5) plays a major role.
• The increased amount of IL-5 is predominantly released from T
lymphocytes,independently of atopy, and the highest concentration
has been found in polyps from patients with non-allergic asthma and
acetylsalicylic acid (ASA) intolerance.
• These are the sub-groups of patients also known to exhibit the
greatest accumulation of eosinophils
PRESENTING FEATURES
• Massive polyposis or a single large polyp (eg:antrochoanal polyp) can
cause:
• 1) Obstructive sleep symptoms
• 2) Chronic mouth breathing
• 3) Altered craniofacial structure (Frog face)
• 4) Proptosis
• 5) Hypertelorism
• 6) Diplopia
Views;
Waters,caldwell,lateral,submental vertex
Features
Opacification of nasal cavity and sinuses
WATERS VIEW
CALDWELL VIEW
CT IS THE MODALITY OF CHOICE
CT is of value for determining anatomical landmarks and variants,to
identify erosive changes,e xcellent to determine intraorbital extension
of sinonasal disease
MRI is next step to assess spread to the cavernous sinus and
intracranial extension.
NCCT is performed…value of NCCT is the following;
* if opacified sinus is seen with hyperdense content it is usually a
benign disease.hyperdensities are due to,blood,fungus,inspissated
secretions.
GENERAL FEATURES OF NASAL POLYPS
1. Hypodense polypoidal,rounded masses in the nasal cavity
and paranasal sinuses enlarging sinus ostium
2.Expansion of the sinuse,thining of sinus walls,nasal and ethmoid
septa.
3.Bulging of the lamina papyracea leading to displacement of the
eyeballs and hypertelorism
4.Widening of the infundibulum.
5.On post contrast images show peripheral or occasionally solid
heterogenous enhancement.
6. Erosive changes at anterior skull base.
ANTROCHOANAL POLYPS
Benign antral polyp which widens the sinus ostium and extends
into nasal cavity;5% of all nasal polyps.
Age
Teenagers and young adults
Features
1. Antral clouding
2. Ipsilateral nasal mass
3. Smooth mass enlarging the sinus ostium
4. No sinus expansion
• Antrochoanal polyps are the most common type of choanal polyp.
• Other sites of origin may be sphenoid, ethmoid, rarely septum, and
inferior turbinate.
• Antrochoanal polyps represent 4–6% of all polyps, and in the
pediatric population, up to 33%.
• They have an antral and choanal component. These typically arise
from the posterior wall of maxillary antrum and often have a thin
“neck” that passes through the maxillary sinus ostium (or accessory
ostium).
• They are often unilateral, but may be bilateral on rare occasions.
SPHENOCHOANAL POLYP is a solitary mass of low
attenuation on computed tomographic (CT) scans that arises from the
sphenoid sinus and extends through the sphenoid ostium, across the
sphenoethmoid recess, and into the choana (the boundary between the
nasal cavity and nasopharynx).
Contiguous axial or coronal magnetic resonance and CT images help
clearly differentiate the rare sphenochoanal polyp from
the more common antrochoanal polyp.
The sinus of origin is important to identify, as the
surgical approach depends on the target sinus.
DIFFERENTIALS
SINUSITIS(air fluid levels,total opacification, enhancement
pattern,hyperintense secretion on T1WI,rim enhancement on post
gad)
NEOPLASM (solid central enhancement).
FUNGAL DISEASE focal or diffuse areas of increased attenuation on
ct,signal voids on mri,rim enhancement on mri).
JUVENILE ANGIOFIBROMA(involvement of
pterygopalatine fossa).
MUCOCELE
is end stage of a chronically obstructed sinus…………an obstructed,
airless,mucoid filled expanded
sinus.
Location;
Frontal(60%),ethmoid(30%).maxillary(10%),sphenoid (rare)
CAUSES. The most common causes of mucoceles are chronic
infection, allergic sinonasal disease, trauma and previous surgery.
Soft tissue density mass….having mucoid attenuation.
Sinus cavity expansion
Bone demineralisation + remodeling late stage but No bone
destruction(DDx from neoplasm)
Surrounding zone of bone sclerosis/calcification of edges of
mucocele(ch sinusitis).
Macroscopic calcification in 5%(superimposed fungal infection)
Uniform thin rim enhancement.
Protrusion into orbit displacing medial rectus muscle laterally.
Expansion into subarachnoid space…. Resulting in CSF leaking.
FRONTAL MUCOCELE
X-ray ;will show an expansion of the sinus cavity with loss of the
scalloped margin of the normal sinus.
Sinus is opaque than normal due to secretions but may on occasions
appear more radiolucent if bone destruction is marked.
CT;will show the full extent of expansion and is usually enough to make
the diagnosis.
MRI;may be used to assess the intracranial extent.
ETHMOID MUCOCELE
Clinically more obvious as palpable mass at medial canthus of
eye,proptosis,epiphora..expansion on lacrimal sac.
Majority are found in the anterior ethmoid cells,expansion of the
posterior ethmoid cells are less common and are associated with
sphenoid mucoceles.
SPHENOID MUCOCELE
Rare
Involvement of optic nerve, cavernous sinus and 3rd nerve is common
due to proximity to these structures.
Imaging plays a key role in diagnosis and its important that condition
be recognized by the radiologist at an early stage and dealt surgically
before vision is compromised.
CT and MRI show rounded or partially rounded expansion of the
sphenoid sinus as opposed to the destruction of bone in situ caused by
malignancy.
MRI
Signal intensity varies with state of hydration,protein content,
hemorrhage,air content,calcification,fibrosis.
Hypointense on T1W1+signal void on T2W1
due to inspissated debris+fungus.
Hydrated secretions are hypo on T1W1 and hyperintense on T2W1.
Peripheral enhancement pattern(DDx neoplasm).
DIFFERENTIALS
Paranasal sinus carcinoma
Aspergillus infection
Ch infection
Inverting papilloma
SINONASAL PAPILLOMA
is a benign epithelial neoplasm of sinonasal tract
WHO has divided sinonasal papilloma into 3 distinct types (El-Naggar:
WHO Classification of Head and Neck Tumours, 4th Edition, 2017):
Inverted papilloma
Exophytic papilloma
Oncocytic papilloma
MRI IN INVERTED PAPILLOMAS
MRI often demonstrates a distinctive appearance, referred to as
convoluted cerebriform pattern, seen on both T2 and contrast-
enhanced T1 weighted images.
This represents alternating lines of high and low signal intensity, the
appearance of which has been likened to, albeit loosely, cerebral cortical
gyrations. This sign is seen in 50-100% of cases and is uncommon in
other sinonasal tumours .
Signal characteristics
T1: isointense to muscle
T2
generally hyperintense to muscle
alternating hypointense lines 6
T1 C+ (Gd)
heterogeneous enhancement 2
alternating hypointense lines 6
CCP PATTERN
Although a CCP is a reliable MR imaging feature of sinonasal IPs, it can
also be seen in various malignant sinonasal tumors.
A focal loss of a CCP might be a clue to the diagnosis of IPs concomitant
with malignancy.
Differential diagnosis
General imaging differential considerations include:
Sinonasal carcinoma: unfortunately imaging is unable to confidently
distinguish between inverted papillomas, inverted papilloma with
malignancy and pure malignancy
Antrochoanal polyp: non-enhancing, peripheral mucosal
enhancement may be present
Inflammatory polyp: non-enhancing, peripheral mucosal
enhancement may be present
Juvenile nasopharyngeal angiofibroma (JNA)
Olfactory neuroblastoma
Paranasal sinus mucocoele
TREATMENT
Complete surgical excision through endoscopic surgery or open radical
procedure is the treatment of choice
Aim is to completely remove all diseased mucosa; lateral rhinotomy and
medial maxillectomy may be required for inverted or oncocytic
papilloma
If treated with local excision only, 50 - 70% may recur, particularly for
inverted subtype

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Sinonasal polyps

  • 1. SINONASAL DISEASE DISCUSSION OF BENIGN POLYPOIDAL ETIOLOGIES Dr Ranjit Singh Lahel Resident (Radiodiagnosis)
  • 2. Reference. 1. Scott- Brown otorhinolaryngology 2. Cummings Otolaryngology 3. Nasal polyposis by T. Metin Önerci Berrylin J. Ferguson 4.Pubmed indexed Journals.
  • 3.
  • 4. The silent sinus syndrome represents maxillary sinus atelectasis that results in painless enophthalmos, hypoglobus and facial asymmetry . The term is restricted to patients with no history of sinusitis, trauma or surgery .
  • 5. POLYPS are soft tissue pedunculated masses of oedematous hyperplastic mucosa lining the upper respiratory tract…..nasal cavity and sinuses. These are benign mucosal lesions.
  • 7. Commonest sites in order of frequency are; 1. Ethmoids 2. Maxillary antra 3. sphenoids
  • 8. 1. ALLERGY? • It was believed that allergy is a significant cause of nasal polyposis as most of the polyps are characterized by tissue eosinophilia. • Most studies have failed to show a higher occurrence of positive skin tests to inhaled allergens in patients with polyps than in the general population. • According to Keith et al there is no deterioration of nasal symptoms or eosinophilia during the pollen season in polyp patients having a positive skin test to pollen. Thus, it appears that allergy is not a well documented cause or aggravating factor in nasal polyposis.
  • 9. 2. ASPIRIN EXACERBATED RESPIRATORY DISEASE (AERD), also known as Samter’s Triad or Aspirin Sensitive Asthma, is a chronic medical condition that consists of •asthma, •recurrent sinus disease with nasal polyps, •sensitivity to aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs). Approximately 10% of all adults with asthma and 40% of patients with asthma and nasal polyps are sensitive to aspirin and NSAIDs.
  • 10. Patients with AERD/Samter’s Triad usually have asthma, nasal congestion, and nasal polyps, and often do not respond to conventional treatments. Many have experienced chronic sinus infections and can lose their sense of smell. The characteristic feature of AERD/Samter’s Triad is that patients develop reactions triggered by aspirin or other NSAIDs. • In the ASA intolerant patients, a lowered prostaglandin E2 (PGE2) production has been observed. • PGE2 has a significant anti-inflammatory activity, including inhibition of eosinophils. • A possible intrinsic defect in PGE2 production might, therefore, be responsible for a further increase of eosinophilic accumulation in ASA intolerant patients.
  • 11. 3. CYSTIC FIBROSIS: • Cystic fibrosis (CF), also known as mucoviscidosis, is an autosomal recessive genetic disorder that affects most critically the lungs, and also the pancreas, liver, and intestine. • It is characterized by abnormal transport of chloride and sodium across an epithelium, leading to thick, viscous secretions. • Nasal endoscopy demonstated polyp in 45% of adults with cystic fibrosis. • A sweat chloride test is recommended in any child with nasal polyps, to rule out cystic fibrosis.
  • 12. 4. KARTAGENER’S SYNDROME: • Primary ciliary dyskinesia (PCD), also known as immotile ciliary syndrome. • Rare, ciliopathic, autosomal recessive genetic disorder. • It causes a defect in the action of the cilia lining the respiratory tract (lower and upper, sinuses, Eustachian tube, middle ear) and fallopian tube, and also of the flagella of sperm in males. • Absent mucociliary clearance and recurrent bacterial infections result in nasal polyposis in about 40 percent of the patients.
  • 13. PATHOGENESIS & PATHOPHYSIOLOGY • The pathogenesis of nasal polyps explains how the polyps start and grow. • The pathophysiology of nasal polyps explains the events and processes taking place in the outgrowth of nasal polyps. • Several pathogenetic theories on the formation of nasal polyps have been published during the last 150 years. These theories are based on oedema, an increase in tubulo-alveolar glands, the presence of the cysts of mucous glands and on mucous glands of NP.
  • 14.
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  • 19. MUCOSAL EXUDATE THEORY • Hayek believed that the formation of NP started via an exudate localised deep in the nasal mucosa, which pressed outwards caudally. • According to this theory, both layers of the tubulo-alveolar sero-mucous nasal glands should be displaced outwards and be found in the distal part of the polyp.
  • 20. PERI-PHLEBITIS AND PERI-LYMPHANGITIS THEORY • The theory of Eggston and Wolff is based upon the recurrent infections that lead to the blocking of intercellular fluid transport in the mucosa and oedema of the lamina propria. • If the oedema involves major areas, the result is the prolapse of the mucosa and formation of polyps.
  • 21.
  • 22.
  • 23. WHAT ACTUALLY HAPPENS CELLULAR INFILTRATION • Eosinophilic inflammation is an important feature in the pathogenesis of chronic Rhinosinusitis (CRS) with nasal polyps. • The eosinophilic accumulation in the polyp stroma is basically caused by increased transendothelial migration and increased survival time in the tissue, where an increased concentration of interleukine 5 (IL-5) plays a major role. • The increased amount of IL-5 is predominantly released from T lymphocytes,independently of atopy, and the highest concentration has been found in polyps from patients with non-allergic asthma and acetylsalicylic acid (ASA) intolerance. • These are the sub-groups of patients also known to exhibit the greatest accumulation of eosinophils
  • 24.
  • 25. PRESENTING FEATURES • Massive polyposis or a single large polyp (eg:antrochoanal polyp) can cause: • 1) Obstructive sleep symptoms • 2) Chronic mouth breathing • 3) Altered craniofacial structure (Frog face) • 4) Proptosis • 5) Hypertelorism • 6) Diplopia
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  • 33. CT IS THE MODALITY OF CHOICE CT is of value for determining anatomical landmarks and variants,to identify erosive changes,e xcellent to determine intraorbital extension of sinonasal disease MRI is next step to assess spread to the cavernous sinus and intracranial extension. NCCT is performed…value of NCCT is the following; * if opacified sinus is seen with hyperdense content it is usually a benign disease.hyperdensities are due to,blood,fungus,inspissated secretions.
  • 34. GENERAL FEATURES OF NASAL POLYPS 1. Hypodense polypoidal,rounded masses in the nasal cavity and paranasal sinuses enlarging sinus ostium 2.Expansion of the sinuse,thining of sinus walls,nasal and ethmoid septa. 3.Bulging of the lamina papyracea leading to displacement of the eyeballs and hypertelorism 4.Widening of the infundibulum. 5.On post contrast images show peripheral or occasionally solid heterogenous enhancement. 6. Erosive changes at anterior skull base.
  • 35.
  • 36.
  • 37. ANTROCHOANAL POLYPS Benign antral polyp which widens the sinus ostium and extends into nasal cavity;5% of all nasal polyps. Age Teenagers and young adults Features 1. Antral clouding 2. Ipsilateral nasal mass 3. Smooth mass enlarging the sinus ostium 4. No sinus expansion
  • 38. • Antrochoanal polyps are the most common type of choanal polyp. • Other sites of origin may be sphenoid, ethmoid, rarely septum, and inferior turbinate. • Antrochoanal polyps represent 4–6% of all polyps, and in the pediatric population, up to 33%. • They have an antral and choanal component. These typically arise from the posterior wall of maxillary antrum and often have a thin “neck” that passes through the maxillary sinus ostium (or accessory ostium). • They are often unilateral, but may be bilateral on rare occasions.
  • 39.
  • 40. SPHENOCHOANAL POLYP is a solitary mass of low attenuation on computed tomographic (CT) scans that arises from the sphenoid sinus and extends through the sphenoid ostium, across the sphenoethmoid recess, and into the choana (the boundary between the nasal cavity and nasopharynx). Contiguous axial or coronal magnetic resonance and CT images help clearly differentiate the rare sphenochoanal polyp from the more common antrochoanal polyp.
  • 41. The sinus of origin is important to identify, as the surgical approach depends on the target sinus.
  • 42. DIFFERENTIALS SINUSITIS(air fluid levels,total opacification, enhancement pattern,hyperintense secretion on T1WI,rim enhancement on post gad) NEOPLASM (solid central enhancement). FUNGAL DISEASE focal or diffuse areas of increased attenuation on ct,signal voids on mri,rim enhancement on mri). JUVENILE ANGIOFIBROMA(involvement of pterygopalatine fossa).
  • 43. MUCOCELE is end stage of a chronically obstructed sinus…………an obstructed, airless,mucoid filled expanded sinus. Location; Frontal(60%),ethmoid(30%).maxillary(10%),sphenoid (rare) CAUSES. The most common causes of mucoceles are chronic infection, allergic sinonasal disease, trauma and previous surgery.
  • 44. Soft tissue density mass….having mucoid attenuation. Sinus cavity expansion Bone demineralisation + remodeling late stage but No bone destruction(DDx from neoplasm) Surrounding zone of bone sclerosis/calcification of edges of mucocele(ch sinusitis). Macroscopic calcification in 5%(superimposed fungal infection) Uniform thin rim enhancement. Protrusion into orbit displacing medial rectus muscle laterally. Expansion into subarachnoid space…. Resulting in CSF leaking.
  • 45. FRONTAL MUCOCELE X-ray ;will show an expansion of the sinus cavity with loss of the scalloped margin of the normal sinus. Sinus is opaque than normal due to secretions but may on occasions appear more radiolucent if bone destruction is marked. CT;will show the full extent of expansion and is usually enough to make the diagnosis. MRI;may be used to assess the intracranial extent.
  • 46. ETHMOID MUCOCELE Clinically more obvious as palpable mass at medial canthus of eye,proptosis,epiphora..expansion on lacrimal sac. Majority are found in the anterior ethmoid cells,expansion of the posterior ethmoid cells are less common and are associated with sphenoid mucoceles.
  • 47. SPHENOID MUCOCELE Rare Involvement of optic nerve, cavernous sinus and 3rd nerve is common due to proximity to these structures. Imaging plays a key role in diagnosis and its important that condition be recognized by the radiologist at an early stage and dealt surgically before vision is compromised. CT and MRI show rounded or partially rounded expansion of the sphenoid sinus as opposed to the destruction of bone in situ caused by malignancy.
  • 48.
  • 49. MRI Signal intensity varies with state of hydration,protein content, hemorrhage,air content,calcification,fibrosis. Hypointense on T1W1+signal void on T2W1 due to inspissated debris+fungus. Hydrated secretions are hypo on T1W1 and hyperintense on T2W1. Peripheral enhancement pattern(DDx neoplasm).
  • 50. DIFFERENTIALS Paranasal sinus carcinoma Aspergillus infection Ch infection Inverting papilloma
  • 51. SINONASAL PAPILLOMA is a benign epithelial neoplasm of sinonasal tract WHO has divided sinonasal papilloma into 3 distinct types (El-Naggar: WHO Classification of Head and Neck Tumours, 4th Edition, 2017): Inverted papilloma Exophytic papilloma Oncocytic papilloma
  • 52.
  • 53. MRI IN INVERTED PAPILLOMAS MRI often demonstrates a distinctive appearance, referred to as convoluted cerebriform pattern, seen on both T2 and contrast- enhanced T1 weighted images. This represents alternating lines of high and low signal intensity, the appearance of which has been likened to, albeit loosely, cerebral cortical gyrations. This sign is seen in 50-100% of cases and is uncommon in other sinonasal tumours . Signal characteristics T1: isointense to muscle T2 generally hyperintense to muscle alternating hypointense lines 6 T1 C+ (Gd) heterogeneous enhancement 2 alternating hypointense lines 6
  • 55. Although a CCP is a reliable MR imaging feature of sinonasal IPs, it can also be seen in various malignant sinonasal tumors. A focal loss of a CCP might be a clue to the diagnosis of IPs concomitant with malignancy.
  • 56. Differential diagnosis General imaging differential considerations include: Sinonasal carcinoma: unfortunately imaging is unable to confidently distinguish between inverted papillomas, inverted papilloma with malignancy and pure malignancy Antrochoanal polyp: non-enhancing, peripheral mucosal enhancement may be present Inflammatory polyp: non-enhancing, peripheral mucosal enhancement may be present Juvenile nasopharyngeal angiofibroma (JNA) Olfactory neuroblastoma Paranasal sinus mucocoele
  • 57. TREATMENT Complete surgical excision through endoscopic surgery or open radical procedure is the treatment of choice Aim is to completely remove all diseased mucosa; lateral rhinotomy and medial maxillectomy may be required for inverted or oncocytic papilloma If treated with local excision only, 50 - 70% may recur, particularly for inverted subtype