1

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 Klebsiellaozenae.

• Disease usually resolves spontaneously after 40.

Secondary1. 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 N\S 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 exposureproduce 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 rhinorrhoea2 . Sneezing attacks3 . Nasal obstruction4 . 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 hypertrophicand 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 routesDecrease in IgE and Increase in IgGAvoid in asthma and B-blockers use

Immunotherapy (Hyposensitization)

•AntihistaminesLocal SteroidsSystemic steroidsSodium cromoglycateVasoconstrictors 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’striad: (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

down3. 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

obstruction3. 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.

Sympathomimetic are helpful but tolerance develops

rapidly.

Topical Ipratropium

for rhinorrhea but no effect

on nasal blockage.

Surgicalreduction 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.

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