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Chronic Rhinosinusitis

and Nasal Polyposis


Presenter : Suresh Shanmugam
13012123554

1. Maxillary sinus
2. Ethmoidal bulla
3. Ethmoidal cells
4. Frontal sinus
5. Uncinate process
6. Middle turbinate
7. Inferior turbinate
8. Nasal septum
9. Ostiomeatal complex

Infections induce changes in sinus
mucosa
B
MT
MS
I T
The ostiomeatal complex
Key

B: bulla
ethmoidalis
IT: inferior
turbinate
MT: middle
turbinate
MS: maxillary sinus
Ventilation
and
Drainage
Inflammation
and
Remodeling
Anatomy & physiology
Coronal Axial
Ethmoid sinus
Frontal sinuses
RADIOGRAPHIC ANATOMY OF THE PARANASAL SINUSES
Maxillary sinus
Sphenoid sinus
Anterior ethmoid
Posterior ethmoid
Sphenoid sinus
Anterior Posterior
Anatomy and physiology
MUCOSAL IMMUNITY

Anatomical and mechanical factors: Epithelial barrier
Mucus/mucociliary clearance
Mucosal immune system:
Innate immunity: Antimicrobial peptides: Defensins
Receptors: Toll-like receptors
Cells: Macrophages, neutrophils,
dendritic cells, NK cells, mast cells
Adaptive immunity: Antigen-presenting cells
T-lymphocytes
B-lymphocytes => IgA

Rapid, non-
specific
Specific,
memory
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 and
allergens
Drug induced, rhinitis
medicmentosa
Irritants induced rhinitis
Atrophic rhinitis

After International Consensus Report on the diagnosis and
management of rhinitis. Allergy Suppl 19,49,1994
Anatomy and physiology

COMMON COLD
BACTERIAL SUPERINFECTION
Strep 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
Underlying conditions
Sinusitis and Immunodeficiencies






Sinusitis and cystic fibrosis
Humoral immunodeficencies
frequently associated with sinusitis
Congenital immunodeficencies
Selective IgA deficency, Common variable IgG immunodeficency,
Agammaglobulinemia, specific antibody deficency, (rarely IgG Subclass
deficency)
Acquired immunodeficencies
Immunosupressive agents, HIV
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 obstruction
OR
CT scan abnormality: mucosal changes within ostiomeatal complex or sinus
cavity


EAACI Position Paper on Rhinosinusitis and
Nasal Polyps, Allergy 2005: 60: 583-601
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
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
Microbiology
Normal sinuses: Free of growth
Acute rhinosinusitis:
Viral
Bacterial (Strept. Pneumoniae,H. Influenzae, M. Catharralis)
Chronic rhinosinusitis:
Anaerobes: Propionibacterium, Bacteriodes, Peptococcus
Aerobes: Staphylococcus, Corynebacterium, Pseudomonas
Fungi (Aspergillus fumigatus, Curvularia, Dreschelaria)
Dental sinusitis: Microaerophilic strept. species
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!
Septal
deviation
Dental
sinusitis
Chronic
Sinusitis
Nasal
polyps
The signs and symptoms of acute
sinusitis
(>10 days and < 12 weeks):
Prerequisite symptoms
Persistent upper respiratory
infection (>10 days)
Persistent muco-purulent nasal or
posterior 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
Diagnosis of acute bacterial sinusitis
(ABS)

or
Have not improved after
10 days
Have worsened after 5
to 7 days
A diagnosis of ABS is suggested when
Symptoms of a viral URI
International Rhinosinusitis Advisory Board. ENT J 1997;76(suppl):1;
Lanza and Kennedy. Otolaryngol Head Neck Surg 1997;117:S1.
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 respiratory
tract infections
0.5%2% of cases complicated by acute bacterial infection (>20
million cases)
Brook. Primary Care 1998;25:633; Gwaltney. Clin Infect Dis 1996;23:1209;
Gwaltney et al. N Engl J Med 1994;330:25.
Therapy

Decongestives/pain
Saline washes
Antibiotics (oral, IV)
Corticosteroids (local, oral)
Surgery:
Adenoidectomy (child)
Endoscopic sinus surgery (adult)
chronic
acute
Definitions and classification
CLINICAL 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 obstruction
OR
CT scan abnormality: mucosal changes within ostiomeatal complex or sinus cavity

EAACI Position Paper on Rhinosinusitis and Nasal
Polyps, Allergy 2005: 60: 583-601
The signs and symptoms
of chronic sinusitis
(symptoms persisting >12 weeks):
Prerequisite symptoms
Purulent nasal and posterior
pharyngeal discharge
Plus:
Facial pain/pressure
Persistent nasal obstruction
Cough/post-nasal drip/throat
clearing

Supporting symptoms
Hyposmia, anosmia
Sore throat
Malaise
Fever
Headache, facial pressure,
dental pain
Halitosis
Sleep disturbance
Fatigue
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
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.)

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.
Chronic rhinosinusitis: why?
Chronic inflamed (eosinophilic) mucosa
Possible superimposed infections
Bacteria
Fungi
Superantigens
Biofilms
Osteitis
Chronic rhinosinusitis
with and without nasal polyps

Chronic
Rhinosinusitis
Nasal Polyps
Nasal Polyps
The spectrum of sinus disease
Rhinosinusitis
- Eosinophils +
Chronic rhinosinusitis
with and without nasal polyps
Chronic
Sinusitis
Nasal
Polyposis
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
Chronic sinusitis - without nasal polyps
Prevalence of 14.7% in the
normal population

Th1 type Inflammation with
increased IFN
increased TGF and
remodeling

Pathogenic role of infections
is unclear
Nasal polyps
A polyp is an oedematous mucous membrane which forms a
pedunculating process with a slim or broad stalk or base. Nasal
polyps originate in the upper part of the nose around the
openings to the ethmoidal sinuses.
The polyps extend into the nasal cavity from the middle meatus,
resulting in nasal blockage and restricted airflow to the olfactory
region. The polyp stroma is highly oedematous with a varying
density of inflammatory cells.
Nasal polyposis, consisting of recurrent, multiple polyps, is part
of an inflammatory reaction involving the mucous membrane of
the nose, paranasal sinuses, and often the lower airways
Broadly defined, nasal polyps
are abnormal lesions that
originate from any portion of
the nasal mucosa or paranasal
sinuses.

Polyps are an end result of
varying disease processes in the
nasal cavities.

The most commonly discussed
polyps are benign
semitransparent nasal lesions
that arise from the mucosa of
the nasal cavity or from one or
more of the paranasal sinuses,
often at the outflow tract of the
sinuses.
Nasal
polyps
Pathogenesis &
Pathophysiology
The pathogenesis of nasal polyps explains how the
polyps start and grow.

The pathophysiology of nasal polyps explains the events
and processes taking place in the outgrowth of nasal
polyps.

Several pathogenetic theories on the formation of nasal
polyps have been published during the last 150 years
that have been summarised previously These theories
are based on oedema, an increase in tubulo-alveolar
glands, the presence of the cysts of mucous glands and
on mucous glands of NP.
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 the
nasal mucosa, pushing the epithelium and the original nasal glands outwards.

Hopmann did not find any glands in the NP from his study and interpreted
NP as soft fibromas, protruding towards the nasal mucosa.
Necrotizing Ethmoiditis Theory
This theory supposes that ethmoiditis leads to periostitis and
osteitis of the ethmoid bone and causes bone necrosis.
Hayek argued strongly against this theory, based on the fact
that he could not found bone necrosis in the ethmoid sinus.
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 causes
obstruction of the ducts of basal glands, leading to the formation of
cysts in the nasal mucosa.
The cysts expand and push the nasal mucosa downwards, forming a
polyp.

Mucosal Exudate Theory
Hayek believed that the formation of NP started
via an exudate localised deep in the nasal
mucosa, which pressed outwards caudally.

According to this theory, both layers of the
tubulo-alveolar sero-mucous nasal glands
should be displaced outwards and be found in
the distal part of the polyp.
Theory on Cystic Dilatation
of the Excretory Duct of Nasal
Glands and Vessel Obstruction
According to this theory in chronic inflammation of the nasal
mucosa, excretory ducts of nasal tubulo-alveolar glands are
obstructed, distended and dilated into cystic structures.

The capillaries and veins (which are arranged around the
excretory ducts and the gland mass) become stretched and
obstructed, resulting in increased permeability, transudation and
oedema.

This theory has been used to explain polyp formation in cystic
fibrosis.

Blockade Theory
The theory of Jenkins is based on the premise that
the polyp formation is always preceded by the
same degree of chronic inflammation, either
infectious or allergic.
The polyp itself is an accumulation of intercellular
fluid dammed up in a localised tissue.
The dam is usually caused by an infiltration of
round cells, producing blockade of intercellular
spaces and local lymph oedema.
Peri-Phlebitis and Peri-
Lymphangitis Theory
The theory of Eggston and Wolff is based upon the
recurrent infections that lead to the blocking of
intercellular fluid transport in the mucosa and oedema
of the lamina propria.

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

Glandular Hyperplasia Theory
Krajina found in cases of chronic infection or allergy
localised infiltrates in the nasal mucosa and localised
hyperplasia of nasal glands.

The glands will increase in size and cause bulging of the
mucosa.


Epithelial Rupture Theory
In the initial stage of polyp
formation, an epithelial
rupture or necrosis caused
by inflammation and tissue
pressure from the
oedematous and infiltrated
lamina propria takes place.

Lamina propria protrudes
through the epithelial
defect, and the adjacent
epithelium tends to cover
the defect by migrating
from the surroundings.

If the epithelial defect is
not covered soon
enough or if it is
insufficiently covered,
the prolapsed lamina
propria continues to
grow and the polyp,
with its vascular stalk, is
established.

After epithelialization of
the polyp, the
characteristic new, long
tubulous glands are
formed

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 particular
concentration 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 widely
from those of the nasal glands.

The most striking glands are the long tubular glands, which may be 18 mm of
length.
Some are very simple, narrow tubes other have prominences of small, round,
alveolar bulges on their sides.

Long, simple tubular
glands (a, f).

Long tubular
glands with some branches
(be).

Short, simple tubular
glands (g).

Short, branched
tubular glands (h, i).

Tubular glands with
flask-shaped dilatation
(j, k).

Tubulo-alveolar
glands, which are found
extremely rarely (l)
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 caused
by increased transendothelial migration and increased survival time in
the 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 concentration
has been found in polyps from patients with non-allergic asthma and
acetylsalicylic acid (ASA) intolerance.

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

In the ASA intolerant patients, a lowered
prostaglandin E2 (PGE2) production has been
observed.

PGE2 has a significant anti-inflammatory
activity, including inhibition of eosinophils.

A possible intrinsic defect in PGE2 production
might, therefore, be responsible for a further
increase of eosinophilic accumulation in ASA
intolerant patients.
Role of Staphylococcus aureus
enterotoxins (SAE)

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

It is positive in about 30-50% of the patients
with NP and in about 60-80% of nasal polyp
subjects with asthma

Nasal polyposis: aetiology and pathogenesis

Chemokines
T B
Cytokines

Hyper
IgE
Eosinophils
( apoptosis)
Superantigens
IL-5
ECP
Albumin
Eotaxin
Polyclonal IgE
Epithelial damage (barrier
dysfunction)
chronic microbial trigger
S. Aureus enterotoxins: disease modifiers
Polyps recommended treatment - 2007
Treat underlying sinusitis
High dose nasal CCS
Fluticasone (FP), either nasal drops (EU) or MDI (USA) through nasal
adapter (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