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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
with and without nasal polyps
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
with and without nasal polyps
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
with and without nasal polyps
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 &
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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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