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Chronic Rhinosinusitis

and Nasal Polyposis

Presenter : Suresh Shanmugam

13012123554
http://webm21a9.ntx.net/ent/nose.htm


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1. Maxillary sinus2. Ethmoidal bulla3. Ethmoidal cells4. Frontal sinus5. Uncinate process6. Middle turbinate7. Inferior turbinate8. Nasal septum

9. Ostiomeatal complex


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Infections induce changes in sinus

mucosa

B

MTMS

IT

The ostiomeatal complex

Key

B: bullaethmoidalis

IT: inferiorturbinate

MT:middle

turbinateMS:maxillary sinus

Ventilationand

Drainage

Inflammatioand

Remodeling


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Anatomy & physiology

Coronal Axial

Ethmoid sinus

Frontal sinuses

RADIOGRAPHIC ANATOMY OF THE PARANASAL SINUSES

Maxillary sinus

Sphenoid sinus Anterior ethmoid

Posterior ethmoi

Sphenoid sinus

Anterior Posterior


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Anatomy and physiologyMUCOSAL IMMUNITY

Anatomical and mechanical factors: Epithelial barrier

Mucus/mucociliary clearance

Mucosal immune system:

Innate immunity: Antimicrobial peptides: Defensins

Receptors: Toll-like receptorsCells: Macrophages, neutrophils,

dendritic cells, NK cells, mast cells

Adaptive immunity: Antigen-presenting cells

T-lymphocytesB-lymphocytes => IgA

Rapid, non-specific

Specific,

memory


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Aetiology of rhinosinusitis

Allergy

Seasonal Perennial

Infection

Acute

Chronic: specific e.g. Bacterial, fungal

or nonspecific Possible host defense deficency

Structural

Ostiomeatal complex:

Deviated nasal septum

Hypertrophic turbinates

Others

Dental, periapical abcess Underlying diseases, cystic

fibrosis

Occupational irritants andallergens

Drug induced, rhinitismedicmentosa

Irritants induced rhinitis

Atrophic rhinitis

After International Consensus Report on the diagnosis and

management of rhinitis. Allergy Suppl 19,49,1994


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Anatomy and physiology

COMMON COLD

BACTERIAL SUPERINFECTIONStrep pneu./Haemo inf./Morax catar.

Increasing symptoms after 5 DAYS

No resolution after 10 DAYS

ACUTE rhinosinusitis

MULTIFACTORIAL ETIOLOGY

CHRONIC rhinosinusitis

EAACI Position Paper on Rhinosinusitis and Nasal

Polyps, Allergy 2005: 60: 583-601


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Underlying conditions

Sinusitis and Immunodeficiencies

Sinusitis and cystic fibrosis

Humoral immunodeficenciesfrequently associated with sinusitis

Congenital immunodeficencies

Selective IgA deficency, Common variable IgG immunodeficency,Agammaglobulinemia, specific antibody deficency, (rarely IgG Subclassdeficency)

Acquired immunodeficencies

Immunosupressive agents, HIV


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Classification: chronic rhinosinusitis

with and without nasal polyps

2 OR MORE MAJOR SYMPTOMS nasal blockage anosmia/hyposmia purulent nasal discharge/post-nasal drip facial pain/pressure

AND EITHER endoscopic findings of polyps mucopurulent discharge edema or obstructionOR

CT scan abnormality: mucosal changes within ostiomeatal complex or sinuscavity

EAACI Position Paper on Rhinosinusitis and

Nasal Polyps, Allergy 2005: 60: 583-601


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Classification: chronic rhinosinusitis


DURATION

ACUTE/intermittent < 12 weeks

complete resolution of symptoms

CHRONIC / persistent > 12 weeks

incomplete resolution of symptoms

EAACI Position Paper on Rhinosinusitis and Nasal Polyps, Allergy

2005: 60: 583-601


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Symptoms associated with rhinosinusitis

Major symptoms: Minor symptoms:

Facial pain/pressure Headache

Facial congestion/fullness Fever

Nasal obstruction/blockage Halitosis

Nasal discharge/purulence/postnasal drip Fatigue

Hyposmia/Anosmia Dental pain

Fever Cough

Ear pain/fullness


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Microbiology

Normal sinuses:Free of growth

Acute rhinosinusitis:

Viral

Bacterial (Strept. Pneumoniae,H. Influenzae, M. Catharralis)

Chronic rhinosinusitis:

Anaerobes: Propionibacterium, Bacteriodes, PeptococcusAerobes: Staphylococcus, Corynebacterium, Pseudomonas

Fungi (Aspergillus fumigatus, Curvularia, Dreschelaria)

Dental sinusitis:Microaerophilic strept. species


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Imaging of sinuses

MRI: only recommended in tumor diagnosis

CT sinuses: current standard imaging- Acute rhinosinusitis: only for possible complications

- Chronic sinusitis: only after 4+ weeks of treatment!


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Septal

deviation

Dentalsinusitis

Chronic

Sinusitis

Nasalpolyps

The signs and symptoms of acute


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The signs and symptoms of acute

sinusitis

(>10 days and < 12 weeks): Prerequisite symptoms

Persistent upper respiratoryinfection (>10 days)

Persistent muco-purulent nasal orposterior pharyngeal discharge

Cough

Supporting symptoms Congestion

Facial pain/pressure

Post-nasal drip

Fever

Headache

Anosmia, hyposmia

Facial tenderness

Periorbital edema

Ear pain, pressure

Halitosis

Upper dental pain

Fatigue

Sore throat

Di i f b i l i i i


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Diagnosis of acute bacterial sinusitis

(ABS)

or

Have not improved after10 days

Have worsened after 5

to 7 days

A diagnosis of ABS is suggested whenSymptoms of a viral URI

International Rhinosinusitis Advisory Board. ENT J 1997;76(suppl):1;Lanza and Kennedy. Otolaryngol Head Neck Surg 1997;117:S1.


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Association between viral and bacterial

sinusitis infections

Viral infections Self-limiting

2 to 3 acute viral respiratory infections per year (6-8 in children)

>80% symptoms resolve in 7-8 days

Often inciting event for development of sinusitis and other respiratorytract infections

0.5%2% of cases complicated by acute bacterial infection (>20million cases)

Brook. Primary Care 1998;25:633; Gwaltney. Clin Infect Dis 1996;23:1209;Gwaltney et al. N Engl J Med 1994;330:25.


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Therapy

Decongestives/pain Saline washes

Antibiotics (oral, IV)

Corticosteroids (local, oral)

Surgery:Adenoidectomy (child)

Endoscopic sinus surgery (adult) chronic

acute


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Definitions and classificationCLINICAL DEFINITION OF RHINOSINUSITIS/NASAL POLYPS

2 OR MORE MAJOR SYMPTOMS nasal blockage smell dysfunction nasal discharge/post-nasal drip facial pain/pressure

AND EITHER endoscopic findings of polyps

mucopurulent discharge

edema or obstructionOR

CT scan abnormality: mucosal changes within ostiomeatal complex or sinus cav

EAACI Position Paper on Rhinosinusitis and Nasal

Polyps, Allergy 2005: 60: 583-601

The signs and symptoms


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The signs and symptomsof chronic sinusitis

(symptoms persisting >12 weeks):

Prerequisite symptoms

Purulent nasal and posteriorpharyngeal discharge

Plus:

Facial pain/pressure

Persistent nasal obstruction

Cough/post-nasal drip/throatclearing

Supporting symptoms

Hyposmia, anosmia

Sore throat

Malaise

Fever

Headache, facial pressure,

dental pain

Halitosis

Sleep disturbance Fatigue


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Diagnosis of chronic rhinosinusitis

Symptoms suggestive of chronic rhinosinusitis

Initial evaluation:

Medical history: major, minor symptoms

General examination

Evaluation of underlying disease and co-morbidities

Anterior rhinoscopy,

Nasal endoscopy

CT scan (not in an acute episode)

Special indications (differential diagnosis


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Special indications (differential diagnosis

and underlying disease)

Allergy tests Microbiology (eventually

sinus puncture)

Challenge test for aspirin

sensitivity

Nasal cytology (eosinophils,

neutrophils)

MRI (if tumor or fungus

suspected)

Ciliary function studies Biopsy

Biopsy Blood examinations

(Wegeners, immunodeficencies) Sweat chloride test Electron microscopy of cilia

Genetic analyses Consultations of other

specialities (ophthalmologist,neurologist etc.)


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Differential diagnosis of chronic

rhinosinusitis

Infectious rhinitis: viral upper respiratory tract infection Allergic rhinitis: seasonal, perennial, occupational

Nonallergic rhinitis: Vasomotor rhinitis, NARES,

aspirin- exacerbated respiratory disease

Rhinitis medicamentosa

Rhinitis secondary to pregnancy, hypothyroidism

Anatomical abnormalities: severe septal deviation,

foreign body

Nasal polyps

Inverted papilloma, benign and malignant tumors

Claus Bachert, Allergy: principles and practice.


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Chronic rhinosinusitis: why?

Chronic inflamed (eosinophilic) mucosa Possible superimposed infections

Bacteria

Fungi

Superantigens Biofilms

Osteitis

Ch i hi i i i


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Chronic rhinosinusitis


Chronic

Rhinosinusitis Nasal Polyps

Nasal Polyps

The spectrum of sinus disease

Rhinosinusitis- Eosinophils +

Ch i hi i i i


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Chronic rhinosinusitis


ChronicSinusitis

NasalPolyposis

Facial pain/pressure Yes Sometimes

Facial congestion/fullness Yes Yes

Nasal obstruction/blockage Yes Yes

Nasal discharge/purulence/postnasal drip Yes Yes

Anosmia Sometimes Yes

Blood eosinophils Sometimes Often

Asthma Yes Often

Aspirin exacerbated respiratory disease Rarely 10% of cases

Ch i i i i i h l l


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Chronic sinusitis - without nasal polyps

Prevalence of 14.7% in thenormal population

Th1 type Inflammation with

increased IFN increased TGFand

remodeling

Pathogenic role of infections

is unclear


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Nasal polyps

A polyp is an oedematous mucous membrane which forms apedunculating process with a slim or broad stalk or base. Nasalpolyps originate in the upper part of the nose around theopenings to the ethmoidal sinuses.

The polyps extend into the nasal cavity from the middle meatus,

resulting in nasal blockage and restricted airflow to the olfactoryregion. The polyp stroma is highly oedematous with a varyingdensity of inflammatory cells.

Nasal polyposis, consisting of recurrent, multiple polyps, is partof an inflammatory reaction involving the mucous membrane of

the nose, paranasal sinuses, and often the lower airways

B dl d fi d l l


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Broadly defined, nasal polypsare abnormal lesions thatoriginate from any portion ofthe nasal mucosa or paranasalsinuses.

Polyps are an end result ofvarying disease processes in thenasal cavities.

The most commonly discussed

polyps are benignsemitransparent nasal lesionsthat arise from the mucosa ofthe nasal cavity or from one ormore of the paranasal sinuses,often at the outflow tract of thesinuses.


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Nasal

polyps

Pathogenesis &
http://www.entusa.com/Nasal%20Photos/nasal_polyp.jpg


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Pathogenesis &Pathophysiology

The pathogenesis of nasal polyps explains how thepolyps start and grow.

The pathophysiology of nasal polyps explains the eventsand processes taking place in the outgrowth of nasal

polyps.

Several pathogenetic theories on the formation of nasalpolyps have been published during the last 150 yearsthat have been summarised previously These theories

are based on oedema, an increase in tubulo-alveolarglands, the presence of the cysts of mucous glands andon mucous glands of NP.

Adenoma and fib oma theo


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Adenoma and fibroma theory Billroth found increased number of long tubulous glands in the polyps.

The NP were interpreted as adenomas that began by growing under thenasal mucosa, pushing the epithelium and the original nasal glands outwards.

Hopmann did not find any glands in the NP from his study and interpretedNP as soft fibromas, protruding towards the nasal mucosa.

Necrotizing Ethmoiditis Theory


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Necrotizing Ethmoiditis Theory

This theory supposes that ethmoiditis leads to periostitis andosteitis of the ethmoid bone and causes bone necrosis.

Hayek argued strongly against this theory, based on the factthat he could not found bone necrosis in the ethmoid sinus.

Gl d l C Th


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Glandular-Cyst Theory This theory is based upon the presence of cystic glands and mucus-

filled cysts in NP.

It is hypothesised that oedema of the nasal mucosa causesobstruction of the ducts of basal glands, leading to the formation ofcysts in the nasal mucosa.

The cysts expand and push the nasal mucosa downwards, forming apolyp.

Mucosal Exudate Theory


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Mucosal Exudate Theory

Hayek believed that the formation of NP started

via an exudate localised deep in the nasalmucosa, which pressed outwards caudally.

According to this theory, both layers of thetubulo-alveolar sero-mucous nasal glandsshould be displaced outwards and be found inthe distal part of the polyp.

Theory on Cystic Dilatation


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y yof the Excretory Duct of NasalGlands and Vessel Obstruction

According to this theory in chronic inflammation of the nasalmucosa, excretory ducts of nasal tubulo-alveolar glands areobstructed, distended and dilated into cystic structures.

The capillaries and veins (which are arranged around theexcretory ducts and the gland mass) become stretched andobstructed, resulting in increased permeability, transudation andoedema.

This theory has been used to explain polyp formation in cysticfibrosis.


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Blockade Theory

The theory of Jenkins is based on the premise thatthe polyp formation is always preceded by thesame degree of chronic inflammation, eitherinfectious or allergic.

The polyp itself is an accumulation of intercellularfluid dammed up in a localised tissue.

The dam is usually caused by an infiltration ofround cells, producing blockade of intercellularspaces and local lymph oedema.

Peri-Phlebitis and Peri-


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Peri-Phlebitis and Peri-Lymphangitis Theory

The theory of Eggston and Wolff is based upon therecurrent infections that lead to the blocking ofintercellular fluid transport in the mucosa and oedemaof the lamina propria.

If the oedema involves major areas, the result is theprolapse of the mucosa and formation of polyps.

l d l l i h


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Glandular Hyperplasia Theory Krajina found in cases of chronic infection or allergy

localised infiltrates in the nasal mucosa and localisedhyperplasia of nasal glands.

The glands will increase in size and cause bulging of themucosa.

i h li l h


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Epithelial Rupture Theory

In the initial stage of polypformation, an epithelialrupture or necrosis causedby inflammation and tissuepressure from theoedematous and infiltrated

lamina propria takes place.

Lamina propria protrudesthrough the epithelialdefect, and the adjacent

epithelium tends to coverthe defect by migratingfrom the surroundings.

If the epithelial defect is


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If the epithelial defect isnot covered soonenough or if it isinsufficiently covered,

the prolapsed laminapropria continues togrow and the polyp,with its vascular stalk, isestablished.

After epithelialization ofthe polyp, thecharacteristic new, longtubulous glands areformed

M l d i l l


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Mucous gland in nasal polyp

In most of the pathogenetic theories, the mucous glands have played a role.

The glandular orifices are irregularly distributed, as there is no particularconcentration of glands in the stalk or in the most distal end of the polyp.

The density of glands in NP is considerably lower than in the nasal mucosa.

The polyp glands are tubular, of different shapes and sizes and differ widelyfrom those of the nasal glands.

The most striking glands are the long tubular glands, which may be 18 mm olength.

Some are very simple, narrow tubes other have prominences of small, round,

alveolar bulges on their sides.

Long simple tubular


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Long, simple tubular

glands (a, f).

Long tubular

glands with some branches(be).

Short, simple tubular

glands (g).

Short, branchedtubular glands (h, i).

Tubular glands with

flask-shaped dilatation

(j, k).

Tubulo-alveolar

glands, which are found

extremely rarely (l)

C ll l I filt ti


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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 causedby increased transendothelial migration and increased survival time inthe 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 concentrationhas been found in polyps from patients with non-allergic asthma andacetylsalicylic acid (ASA) intolerance.

These are the sub-groups of patients also known to exhibit thegreatest accumulation of eosinophils


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Role of Staphylococcus aureus


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enterotoxins (SAE)

Multiclonal IgE antibody formation to SAE canbe seen in nasal polyp tissue, but rarely in CRS.

It is positive in about 30-50% of the patientswith NP and in about 60-80% of nasal polypsubjects with asthma

Nasal polyposis: aetiology and pathogenesis


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Nasal polyposis: aetiology and pathogenesis

Chemokines

TB

CytokinesHyper

IgE

Eosinophils

(

apoptosis)

Superantigens

IL-5

EC

Albumin

Eotaxin

Polyclonal IgE

Epithelial damage (barrier

dysfunction)

chronic microbial trigger

S. Aureus enterotoxins: disease modifiers

Pol ps recommended treatment 2007


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Polypsrecommended treatment - 2007

Treat underlying sinusitis

High dose nasal CCS

Fluticasone (FP), either nasal drops (EU) or MDI (USA) through nasaladapter (such as a baby bottle nipple)

Prednisone 20-30 mg

Daily x 3-4 weeks, then QOD, then taper to 0 Budesonide solution (Pulmicort Respules) dissolved in sinus lavage

Wash with the head positioned with ear turned to the knee

Mupiricin ointment topically or dissolved in sinus lavavge

Consider careful surgery if polyps are persistent, resistant or recur

Consider oral or topical anti-fungal treatment

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