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Done by: Rami Abusaleh
2
R.S
acute
bacterial viral fungal
chronic
infective
simple specific
Non-
infective
atrophic hypertrophic
3
• Inflammation of mucous membranes of the nose &
paranasal sinuses that lasts > 3 months.
• As the lining of the nose and paranasal sinuses are
continuous, it is rare for inflammation to affect one without
the other. As such, the description rhinosinusitis is often
more appropriate.
4
5

 This disorder was known since the time of ancient
Egypt, almost 4,000 years ago, and descriptions of it
are found in the historical medical papyri (1700 BC)
 it was prescribed a treatment based on wine and
breast milk to cure this disease. Even the ancient
Greek civilization and the Indian were aware of
atrophic rhinitis.
6
History
7
• Ozena: a disease of the nose in which there is wasting
away of the bony ridges and internal mucous membranes.
• Diffuse atrophy of mucus membranes of nose &
paranasal sinuses.
• Ciliated columnar epithelium of the nasal mucosa is
replaced by stratified squamous epithelium.
8
Normal VS Atrophy
9
1. . Endocrine Imbalance: F>M especially in
adulthood.
2. Nutritional deficiency: Vit A, Vit D or Iron.
3. Heredity factors.
4. Infections:Klebsiella, Diphtheroids, Proteus, E.coli
5. Autoimmune.
6. Racial factors: Whites > Blacks
 Mnemonic (ENHIAR)
10
Primary
• Most commonly in China, Egypt, and India. It is relatively
common is the Middle East and areas with arid climate.
• Microbiology of primary AR is almost uniformly Klebsiella
ozenae.
• Disease usually resolves spontaneously after 40.
Secondary
1. Complication of sinus surgery (89%)
2. Complication of radiation (2.5%)
3. Following nasal trauma (1%)
4. granulomatous diseases (1%)
5. other infectious processes
11
12
Symptoms:
1- Nasal obstruction.
2- Epistaxis.
3- Anosmia.
4- Bad odor.
Signs:
1- Wide nasal cavity.
2- Septal perforation.
3- Extensive nasal crusting.
4- nasal congestion.
5- Saddle nose.
6- Resorption or absence of turbinates.
N.B: Radiographic and clinical features of primary are similar
to secondary AR.

1. Enlargement of the nasal cavities with
erosion and bowing of the lateral nasal
wall.
2. Mucoperiosteal thickening of the paranasal
sinuses.
3. Hypoplasia of the maxillary sinuses.
4. Bony resorption and mucosal atrophy of
the inferior and middle turbinates.
13
Radiography
14
15
Normal VS Atrophy
16
 Klebsiella ozenae
• May be found in almost 100% of primary AR.
• No predominance in secondary AR.
 Staphylococcus aureus.
 Proteus mirabilis.
 E-coli.
 Corynebacterium diphtheriae.
17
1- Clinically.
2- Biopsy shows:
Squamous metaplasia.
Atrophy of mucous glands.
Scarce or absent cilia.
18
Medically Surgically
 Nasal irrigation using NS
and removal of crusts using
alkaline nasal douches.
 Estradiol spray v.c
 Vitamin D2.
 Oral Potassium iodide loosen
and break up mucus. Used in
asthma, chronic bronchitis…
 Local antibiotics
(Chloramphenicol).
 Systemic Streptomycin.
 Anti-drying agents
Mineral Oil & glycerine
 Decrease the size of both
nostrils together
 Close one nostril for one year
then reopen it and close the
other for another year
alternatively.
N.B: The theory behind this
procedure is that the closed nasal
cavity has time to heal.
19
20
21
Hypertrophic
Chronic R.S
Allergic
Non-Allergic
(vasomotor)
* Eosinophilic
* Non-
eosinophilic
22
23
24
1- Diffuse swelling of the mucus membranes of the nose
and paranasal sinuses.
2- Hyperemia due to congestion of blood vessels
• Hormones , Trauma, Drugs (Rhinitis medicamentosa)
as a rebound effect after long term use of sympathomimetics
(xylometazoline).
25
26
• Very common (30% of population), increasing in incidence in
industrialized countries.
• Frequently associated with otitis media, rhinosinusitis and
asthma.
• Mainly affects individuals <45 years.
• May start to appear as early as 2 years old with a peak at age
between 21-30.
Allergens:
1- Inhalant (96%): high molecular weight particles stick in URT :
A- seasonal, e.g. mould spores in autumn, tree and grass pollen
in spring.
B- perennial, e.g. house dust mite and molds.
2- Ingestant (4%).
27
28
IgE mediated hypersensitivity (type I)
Allergen exposure produce  amounts of IgE Abs
 bound to mast cells in nasal mucosa (sensitization)
Further exposure to allergen bind to IgE
degranulation of mast cells: release of histamine,
slow reacting substance and vasoactive peptides
(leukotrienes, kinins)  vasodilatation, increased
capillary permeability causing early-phase symptoms
such as sneezing, rhinorrhea, and congestion.
29
IgE A.BGranules
*histamine
* slow rxting substance
*vasoactive peptides
32
1 . Watery rhinorrhoea
2 . Sneezing attacks
3 . Nasal obstruction
4 . Conjunctival irritation and lacrimation
•Relationship between appearance of symptoms and
allergen exposure
33
Acute stage: nose : hyperemic , wet,
excessive clear mucus, and this usually
contains an increased number of
eosinophils. The turbinates are frequently hypertrophic
and covered with a boggy pale or bluish mucosa.
Chronic stage: dilated and congested veins
(more than arteries) bluish discoloration
of swollen turbinate.
34
Boggy inferior turbinate in an allergic patient
35
• : Lymphocytosis and increased eosinophilsCBC
• Measures allergen-specific IgE
• Can be performed on a blood sample
• Useful in children for whom skin tests are unsuitable
• More specific, not affected by skin reactivity or medications
• No risk of systemic reaction
• Better tolerated, because it is less traumatic
• Less sensitive than skin testing, especially in regard to
molds
RAST (radio-
allergo
sorbent test):
Skin prick test
•IgE level for atopy.
•Nasal challenge test (dangerous)
Others
36
37
• Most important measure
Avoid the causative agents.
•Increasing doses of each reacting allergen for 2-3 seasons given through different
routes
Decrease in IgE and Increase in IgG
Avoid in asthma and B-blockers use
Immunotherapy (Hyposensitization)
•Antihistamines
Local Steroids
Systemic steroids
Sodium cromoglycate
Vasoconstrictors eg: xylometazoline (Otrivin)
Pharmacotherapy
•If gross hypertrophy of nasal mucosa has occured
Surgical treatment
38

39
40
Increased eosinophils in the nasal
secretion, associated with Samter’s
triad: (P.A.S)
1- Formation of nasal polyps
2- Aspirin sensitivity
3- Asthma.
41
 Clinical features:
1. Purulent rhinorrhoea and sneezing.
2. Increased sensitivity to irritants such as perfume and
tobacco smoke.
N.B: Although a blood count may not always show a raised
eosinophil count, such cells will be present in nasal secretions.
 Treatment
1. Topical nasal steroid (e.g. beclomethasone) or systemic
antihistamine, the response is usually good.
2. Topical ipratropium (anticholinergic) may control the
rhinorrhea.
42
 Intro:
less common than eosinophilic and is thought to be due to
autonomic disturbance of vasomotor tone, with excessive
parasympathetic activity.
 ETIOLOGY: (In most cases no specific cause )
1. Drugs: Anti-HTN , Ganglion blockers, OCP, V.D drugs.
2. Hormonal disturbance: pregnancy, menopause,
hypothyroidism.
3. Overload: Congestive heart failure/Anxiety/Smoking
and occupational irritants.
43
 Symptoms:
1. Purulent rhinorrhoea and sneezing.
2. Nasal obstruction: varies from side to side and is worst on lying
down
3. Symptoms precipitated by change in temperature, bright
sunlight, irritants (e.g. tobacco smoke) or alcohol ingestion
 Signs
1. Nasal mucosa dusky and congested
2. Engorgement of the inferior turbinates leading to the nasal
obstruction
3. Excessive secretions in the nose
N.B: Symptoms are more severe than what examination of the
nose suggests
44
Exercise: by
increasing
sympathetic
tone, often
provides relief.
Sympathomime
tic are helpful but
tolerance develops
rapidly.
Topical
Ipratropium
for rhinorrhea
but no effect
on nasal
blockage.
Surgical
reduction of
inferior
turbinates by
diathermy or
cryotherapy.
* Often no treatment is required because the symptoms are
minor and no significant abnormality is found on examination.
Chronic non infective rhinosinusitis

Summary
Introduction
Abnormal lesions that
emanate from portion
of nasal mucosa or
paranasal sinuses
Endoscopic view of
left nasal cavity. Polyp
protruding from
uncinate process

 Etiology :
1. Unknown
2. Chronic inflammation
3. Autonomic nervous system dysfunction
4. Genetic predisposition
5. Allergic VS Non- Allergic
Nasal Polyps
Allergic (4 A’s) Non- Allergic
1. Asthma
2. Allergic rhinitis
3. Aspirin intolerance
4. Alcohol intolerance
5. N.B: Polyps are more in patients
with non-allergic asthma
1. Cystic Fibrosis
2. AFS (Allergic Fungal
Sinusitis ) 85% have polyps
3. Young syndrome
4. Churg-Strauss syndrome
(chronic sinusitis, nasal polyposis,
azoospermia)

Allergic fungal sinusitis

•inflammatory process affects the bioelectric integrity of the
sodium channels, response increases sodium absorption,
leading to water retention and polyp formation.
Bernstein
theory
•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
Vasomotor
theory
•rupture 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
Epithelia
rupture theory
Mechanisms
(Various theories)
 Epidemiology:
1. Adults > Children
2. All races and social classes
3. M>F
4. Increasing incidence with age
 Clinical Features : (Asymptomatic)
 Airway obstruction
 Postnasal drip
 Dull headaches
 Snoring
 Rhinorhoea
 Hyposmia / Anosmia
 Epistaxis (often other lesion)
 Obstructive sleep apnoea
 Craniofacial abnormalities
 Optic nerve compression
Nasal Polyps

All In One
 Intranasal Glioma
 Nasal papilloma arising
from septum
 Rhabdomyosarcoma
(affecting posterior ethomids, orbit,
left middle fossa and skull base of
cavernous sinuses)
 Nasal polyp. Stalk attached
to medial maxillary wall
 Microdebrider entering left
middle meatus
Pictures

 Sweat test
 RAST / skin testing (radioallergosorbent test )
 Nasal smear
1. Microbiology
2. Eosinophils (allergic component)
3. Neutrophils (chronic sinusitis)
 Coronal CT scan
 MRI scan
 Flexible nasendoscopy
 Rigid nasendoscopy
Investigations
 Coronal CT scan through
anterior sinuses.
Opacification of left
maxillary sinus,
opacification of inferior half
of nasal cavity. Due to
antro coanal polyp.
Investigations
 Pseudostratified ciliated
columnar epithelium
 Thickened epithelial
basement membrane
 Oedematous stroma
Histological findings

 Eosinophils in 80-90% of polyps
 Neutrophils in 7% of polyps
 Histamine - level in polyps 10-1000 times higher than
serum levels
Histological findings

58

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Chronic non infective rhinosinusitis

  • 1. 1 Done by: Rami Abusaleh
  • 2. 2 R.S acute bacterial viral fungal chronic infective simple specific Non- infective atrophic hypertrophic
  • 3. 3 • Inflammation of mucous membranes of the nose & paranasal sinuses that lasts > 3 months. • As the lining of the nose and paranasal sinuses are continuous, it is rare for inflammation to affect one without the other. As such, the description rhinosinusitis is often more appropriate.
  • 4. 4
  • 5. 5
  • 6.   This disorder was known since the time of ancient Egypt, almost 4,000 years ago, and descriptions of it are found in the historical medical papyri (1700 BC)  it was prescribed a treatment based on wine and breast milk to cure this disease. Even the ancient Greek civilization and the Indian were aware of atrophic rhinitis. 6 History
  • 7. 7 • Ozena: a disease of the nose in which there is wasting away of the bony ridges and internal mucous membranes. • Diffuse atrophy of mucus membranes of nose & paranasal sinuses. • Ciliated columnar epithelium of the nasal mucosa is replaced by stratified squamous epithelium.
  • 9. 9 1. . Endocrine Imbalance: F>M especially in adulthood. 2. Nutritional deficiency: Vit A, Vit D or Iron. 3. Heredity factors. 4. Infections:Klebsiella, Diphtheroids, Proteus, E.coli 5. Autoimmune. 6. Racial factors: Whites > Blacks  Mnemonic (ENHIAR)
  • 10. 10 Primary • Most commonly in China, Egypt, and India. It is relatively common is the Middle East and areas with arid climate. • Microbiology of primary AR is almost uniformly Klebsiella ozenae. • Disease usually resolves spontaneously after 40. Secondary 1. Complication of sinus surgery (89%) 2. Complication of radiation (2.5%) 3. Following nasal trauma (1%) 4. granulomatous diseases (1%) 5. other infectious processes
  • 11. 11
  • 12. 12 Symptoms: 1- Nasal obstruction. 2- Epistaxis. 3- Anosmia. 4- Bad odor. Signs: 1- Wide nasal cavity. 2- Septal perforation. 3- Extensive nasal crusting. 4- nasal congestion. 5- Saddle nose. 6- Resorption or absence of turbinates. N.B: Radiographic and clinical features of primary are similar to secondary AR.
  • 13.  1. Enlargement of the nasal cavities with erosion and bowing of the lateral nasal wall. 2. Mucoperiosteal thickening of the paranasal sinuses. 3. Hypoplasia of the maxillary sinuses. 4. Bony resorption and mucosal atrophy of the inferior and middle turbinates. 13 Radiography
  • 14. 14
  • 16. 16  Klebsiella ozenae • May be found in almost 100% of primary AR. • No predominance in secondary AR.  Staphylococcus aureus.  Proteus mirabilis.  E-coli.  Corynebacterium diphtheriae.
  • 17. 17 1- Clinically. 2- Biopsy shows: Squamous metaplasia. Atrophy of mucous glands. Scarce or absent cilia.
  • 18. 18 Medically Surgically  Nasal irrigation using NS and removal of crusts using alkaline nasal douches.  Estradiol spray v.c  Vitamin D2.  Oral Potassium iodide loosen and break up mucus. Used in asthma, chronic bronchitis…  Local antibiotics (Chloramphenicol).  Systemic Streptomycin.  Anti-drying agents Mineral Oil & glycerine  Decrease the size of both nostrils together  Close one nostril for one year then reopen it and close the other for another year alternatively. N.B: The theory behind this procedure is that the closed nasal cavity has time to heal.
  • 19. 19
  • 20. 20
  • 22. 22
  • 23. 23
  • 24. 24 1- Diffuse swelling of the mucus membranes of the nose and paranasal sinuses. 2- Hyperemia due to congestion of blood vessels • Hormones , Trauma, Drugs (Rhinitis medicamentosa) as a rebound effect after long term use of sympathomimetics (xylometazoline).
  • 25. 25
  • 26. 26 • Very common (30% of population), increasing in incidence in industrialized countries. • Frequently associated with otitis media, rhinosinusitis and asthma. • Mainly affects individuals <45 years. • May start to appear as early as 2 years old with a peak at age between 21-30. Allergens: 1- Inhalant (96%): high molecular weight particles stick in URT : A- seasonal, e.g. mould spores in autumn, tree and grass pollen in spring. B- perennial, e.g. house dust mite and molds. 2- Ingestant (4%).
  • 27. 27
  • 28. 28 IgE mediated hypersensitivity (type I) Allergen exposure produce  amounts of IgE Abs  bound to mast cells in nasal mucosa (sensitization) Further exposure to allergen bind to IgE degranulation of mast cells: release of histamine, slow reacting substance and vasoactive peptides (leukotrienes, kinins)  vasodilatation, increased capillary permeability causing early-phase symptoms such as sneezing, rhinorrhea, and congestion.
  • 29. 29
  • 31. *histamine * slow rxting substance *vasoactive peptides
  • 32. 32 1 . Watery rhinorrhoea 2 . Sneezing attacks 3 . Nasal obstruction 4 . Conjunctival irritation and lacrimation •Relationship between appearance of symptoms and allergen exposure
  • 33. 33 Acute stage: nose : hyperemic , wet, excessive clear mucus, and this usually contains an increased number of eosinophils. The turbinates are frequently hypertrophic and covered with a boggy pale or bluish mucosa. Chronic stage: dilated and congested veins (more than arteries) bluish discoloration of swollen turbinate.
  • 34. 34 Boggy inferior turbinate in an allergic patient
  • 35. 35 • : Lymphocytosis and increased eosinophilsCBC • Measures allergen-specific IgE • Can be performed on a blood sample • Useful in children for whom skin tests are unsuitable • More specific, not affected by skin reactivity or medications • No risk of systemic reaction • Better tolerated, because it is less traumatic • Less sensitive than skin testing, especially in regard to molds RAST (radio- allergo sorbent test): Skin prick test •IgE level for atopy. •Nasal challenge test (dangerous) Others
  • 36. 36
  • 37. 37 • Most important measure Avoid the causative agents. •Increasing doses of each reacting allergen for 2-3 seasons given through different routes Decrease in IgE and Increase in IgG Avoid in asthma and B-blockers use Immunotherapy (Hyposensitization) •Antihistamines Local Steroids Systemic steroids Sodium cromoglycate Vasoconstrictors eg: xylometazoline (Otrivin) Pharmacotherapy •If gross hypertrophy of nasal mucosa has occured Surgical treatment
  • 38. 38
  • 40. 40 Increased eosinophils in the nasal secretion, associated with Samter’s triad: (P.A.S) 1- Formation of nasal polyps 2- Aspirin sensitivity 3- Asthma.
  • 41. 41  Clinical features: 1. Purulent rhinorrhoea and sneezing. 2. Increased sensitivity to irritants such as perfume and tobacco smoke. N.B: Although a blood count may not always show a raised eosinophil count, such cells will be present in nasal secretions.  Treatment 1. Topical nasal steroid (e.g. beclomethasone) or systemic antihistamine, the response is usually good. 2. Topical ipratropium (anticholinergic) may control the rhinorrhea.
  • 42. 42  Intro: less common than eosinophilic and is thought to be due to autonomic disturbance of vasomotor tone, with excessive parasympathetic activity.  ETIOLOGY: (In most cases no specific cause ) 1. Drugs: Anti-HTN , Ganglion blockers, OCP, V.D drugs. 2. Hormonal disturbance: pregnancy, menopause, hypothyroidism. 3. Overload: Congestive heart failure/Anxiety/Smoking and occupational irritants.
  • 43. 43  Symptoms: 1. Purulent rhinorrhoea and sneezing. 2. Nasal obstruction: varies from side to side and is worst on lying down 3. Symptoms precipitated by change in temperature, bright sunlight, irritants (e.g. tobacco smoke) or alcohol ingestion  Signs 1. Nasal mucosa dusky and congested 2. Engorgement of the inferior turbinates leading to the nasal obstruction 3. Excessive secretions in the nose N.B: Symptoms are more severe than what examination of the nose suggests
  • 44. 44 Exercise: by increasing sympathetic tone, often provides relief. Sympathomime tic are helpful but tolerance develops rapidly. Topical Ipratropium for rhinorrhea but no effect on nasal blockage. Surgical reduction of inferior turbinates by diathermy or cryotherapy. * Often no treatment is required because the symptoms are minor and no significant abnormality is found on examination.
  • 47. Introduction Abnormal lesions that emanate from portion of nasal mucosa or paranasal sinuses Endoscopic view of left nasal cavity. Polyp protruding from uncinate process
  • 48.   Etiology : 1. Unknown 2. Chronic inflammation 3. Autonomic nervous system dysfunction 4. Genetic predisposition 5. Allergic VS Non- Allergic Nasal Polyps Allergic (4 A’s) Non- Allergic 1. Asthma 2. Allergic rhinitis 3. Aspirin intolerance 4. Alcohol intolerance 5. N.B: Polyps are more in patients with non-allergic asthma 1. Cystic Fibrosis 2. AFS (Allergic Fungal Sinusitis ) 85% have polyps 3. Young syndrome 4. Churg-Strauss syndrome (chronic sinusitis, nasal polyposis, azoospermia)
  • 50.  •inflammatory process affects the bioelectric integrity of the sodium channels, response increases sodium absorption, leading to water retention and polyp formation. Bernstein theory •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 Vasomotor theory •rupture 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 Epithelia rupture theory Mechanisms (Various theories)
  • 51.  Epidemiology: 1. Adults > Children 2. All races and social classes 3. M>F 4. Increasing incidence with age  Clinical Features : (Asymptomatic)  Airway obstruction  Postnasal drip  Dull headaches  Snoring  Rhinorhoea  Hyposmia / Anosmia  Epistaxis (often other lesion)  Obstructive sleep apnoea  Craniofacial abnormalities  Optic nerve compression Nasal Polyps
  • 53.  Intranasal Glioma  Nasal papilloma arising from septum  Rhabdomyosarcoma (affecting posterior ethomids, orbit, left middle fossa and skull base of cavernous sinuses)  Nasal polyp. Stalk attached to medial maxillary wall  Microdebrider entering left middle meatus Pictures
  • 54.   Sweat test  RAST / skin testing (radioallergosorbent test )  Nasal smear 1. Microbiology 2. Eosinophils (allergic component) 3. Neutrophils (chronic sinusitis)  Coronal CT scan  MRI scan  Flexible nasendoscopy  Rigid nasendoscopy Investigations
  • 55.  Coronal CT scan through anterior sinuses. Opacification of left maxillary sinus, opacification of inferior half of nasal cavity. Due to antro coanal polyp. Investigations
  • 56.  Pseudostratified ciliated columnar epithelium  Thickened epithelial basement membrane  Oedematous stroma Histological findings
  • 57.   Eosinophils in 80-90% of polyps  Neutrophils in 7% of polyps  Histamine - level in polyps 10-1000 times higher than serum levels Histological findings