Nasal polyps are non-cancerous growths that develop on the nasal passages or sinuses due to chronic inflammation. They are most commonly caused by asthma, allergies, or recurring sinus infections. Nasal polyps typically appear as soft, teardrop-shaped masses that hang down from the nasal lining. Treatment involves nasal corticosteroids, oral corticosteroids, antibiotics, and surgery to remove polyps. Endoscopic sinus surgery is often required for large or recurring polyps.

1. NASAL
POLYPS

2. Definition
• Nasal polyps are soft, painless, noncancerous
growths on the lining of your nasal passages
or sinuses.
• They hang down like teardrops or grapes.
• They result from chronic inflammation and
are associated with asthma, recurring
infection, allergies, drug sensitivity or certain
immune disorders.
dr. Albaba Khalil

3. • Multiple polyps can occur with chronic
sinusitis ,cystic fibrosis ,allergic rhinitis or
allergic fungal sinusitis (AFS).
• Single polyp could be an antral-choanal
polyp, a benign massive polyp, or any benign
or malignant tumor
• All children with benign multiple nasal
polyposis should be evaluated for CF
and asthma

4. LATERAL VIEW OF MOST COMMON
ORIGIN

5. EPIDEMIOLOGY
• The prevalence of nasal polyps (NP) in the population has
been grossly estimated as 1–4%.
• It increases with age, reaching a peak in those aged 50 years
and older.
• NP before the age of 20 are unusual and should lead to an
investigation of possible CF or primary ciliary dyskinesia (PCD)
• Male: Female = 2:1
• Nasal polyposis occurs with a higher frequency in groups of
patients having specific airway diseases
• Genetic inheritance has been proposed as a possible etiology
of NP.(CF,AR,ASTHMA, non oesinophilic polyp common in
Asian population)

6. Histologic finding:
NPs are characterized by:
• Pseudo stratified ciliated columnar epithelium
• Thickening of epithelial basement membrane
• Stroma of NP is oedematous
• Vascularization is poor and lacks innervation
• Hyperplasia of seromucous gland when comparing
with inferior or middle turbinate.

7. • The underlying stroma of NPs has historically
been divided into three subtypes:
Edematous, oesinophilic
Fibroinfiammatory
glandular

8. edematous, oesinophilic polyp
• are the most common. representing up to 85% of
polyp specimens.
• These consist of scattered :fibroblasts with tissue
edema and a variable infiltrate of mononuclear
cells and other granulocytes such as neutrophils
and mast cells.
• Colonization with Staphylococcus aurous occurs
in up to 80% of patients with NP and may initiate
the inflammatory response via nonspecific
upregulation of T cells mediated through
superantigen production.
dr. Albaba Khalil

9. Association
• This oesinophilic edematous histopathology may
be seen with a wide variety of conditions that
are associated with NP disease including
 aspirin exacerbated respiratory disease (AERD),
AFRS
Churg-Strauss syndrome
Cystic fibrosis :polyps in CF are more likely to
have significant neutrophilia and therefore
labeled "neutrophilic polyps."

10. THEORIES OF ETIOLOGY AND PATHOGENESIS
• The first of these was the fungal hypothesis
o which attributed all CRS cases to an excessive host response to
Alternaria fungi
o Although most investigators have rejected the basic tenets as
originally proposed
• The leukotriene hypothesis
o proposes that defects in the eicosanoid pathway, most closely
associated with aspirin intolerance
o are also key components in the pathogenesis of other eosinophilic
subtypes of CRS(LT-C4)

11. • The immune barrier hypothesis
o proposes that defects in the mechanical barrier
and/or the innate immune response of the
sinonasal epithelium manifests as CRS.
o Increased microbial colonization and accentuated
barrier damage lead to increased stimulation of
the immune system with a compensatory adaptive
immune response.
dr. Albaba Khalil

13. • The staphylococcal superantigen hypothesis
o proposes that exotoxins liberated by staphylococcal
bacteria foster nasal polyposis via effects on multiple cell
types
o Multiclonal IgE antibody formation to SAE can be seen in
nasal polyp tissue, but rarely in CRS.
o It is positive in about 30-50% of the patients with NP and
in about 60-80% of nasal polyp subjects with asthma
• Biofilm theory The biofilm hypothesis can be
considered an offshoot of the staphylococcal
superantigen hypothesis, as this is the organism most
commonly identified in the biofilms of resistant CRS

14. PATHOGENESIS
Nasal mucosa  becomes edematous due to
collection of ECF
polypoidal change
Sessile  pedenculated
(due to gravity and excessive sneezing)

15. PATHOLOGY
Early stage  Nasal polyp (surface covered by
ciliated columnar epithelium)
Transitional & squamous epithelium
Submucosa  large ICS filled with serous fluid
+ infiltration with eosinophils and
round cells
Metaplastic change
in exposure to
atmospheric irritation
dr. Albaba Khalil

16. • Chemical mediators:
Cytokines:
o IL-5 are found regularly oesinophilic (oesinophilic
attractor)
o IL- 8 (neutrophil attractor )
•Immunoglobulin
IgA = Increased
IgE = Increased

17. SITE OF ORIGIN
• Multiple nasal polyps always arise from the lateral
wall of nose, usually from the middle meatus
• Common sites:
 Uncinate process
 Bulla ethmoidalis
 Ostia of sinuses
 Medial surface & edge of middle turbinate
• Oesinophilic nasal polyp almost Never arise from
the septum or the floor of nose

18. SYMPTOMS
1. Nasal stuffiness leading to total
nasal obstruction may be the
presenting symptom.
2. Partial or total loss of sense of
smell.
3. Headache due to associated
sinusitis.
4. Sneezing and watery nasal
discharge due to associated allergy.
5. Mass protruding from the nostril,
in sever cases
dr. Albaba Khalil

19. SIGNS
• On anterior rhinoscopy, polyps appear as
o Smooth, glistening
o Grape-like masses
o Often pale in color
o May be sessile or pedenculated
o Insensitive to probing
o Do not bleed on touch
o Often multiple and bilateral
• Broadening of nose
• Increase intercanthal distance
• May protrude from the nostril and appear pink and vascular,
simulating neoplasm
• Purulent discharge (associated sinusitis)
long standing case

20. Staging & score by Meltzer
• Staging Polyps can be staged as following
according to their size & palce(Meltzer et al):
A. Stage I: Limited to the extent of middle turbinate.
B. Stage II: Extending beyond the limit of middle
turbinate. „
C. Stage III: Approaching to inferior turbinate.
D. Stage IV: Going up to the floor of nose.

21. Meltzer score used to classify nasal polyp grade.
0: no visible NP
1: small amount of polypoid disease confined within the middle meatus
2: multiple polyps occupying the middle meatus
3: polyps extending beyond the middle meatus
4: poly.

22. TREATMENT
CONSERVATIVE
– Nasal corticosteroids.
– Oral corticosteroids
– Antihistamines
– Antibiotics
– Anti-luckatrins
– Immunotherapy
Surgical
• Classic transnasal
• Fess/Ess.
dr. Albaba Kalil

23. Corticosteroid
 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)
 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.
 In children, 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.

24. New arrival in Palestine
 topical nasal steroid (Aqua soluble)
 administration either as the primary
treatment or as a continual secondary
treatment immediately after oral
steroids or surgery.
 Intranasal corticosteroids help in:
o Reducing polyp size
o Increase nasal patency
o Reduction in rhinitis symptoms
o Reduction in loss of sense of smell
o Reduction in recurrence of polyp
o Improve QOL
dr. Albaba Khalil

25. • decrease capillary permeability.
o decrease arachodinic metabolism (  PG,  LT ).
o inhibition of cytokine & chemokins.
o decrease recurmint & production of eosinophils.
o decrease activity of mast cell & basophils.
o decrease migration of APC, T-cells, B-cells.
o promote IL10 production.
• Side effect :
• local burning, crusting, epistaxis, drying, irritation,
perforation, glaucoma, cataract may occur (as rare
complication)

28. Failure to Rx TREATMENT
SURGICAL
• Endoscopic sinus surgery followed with
medical treatment

29. THANK YOU