This document provides information about rhinosinusitis, including definitions, classifications, signs, symptoms, investigations and treatment. It defines acute and chronic rhinosinusitis based on duration of symptoms. Common causes include viral and bacterial infections. Chronic rhinosinusitis is classified as with or without nasal polyps. Diagnosis involves symptoms and endoscopy or CT scan findings. Treatment aims to reduce inflammation, bacterial load and improve mucociliary clearance using medications, sinus irrigation and surgery.

1. Rhinosinusitis
Dr Mohammed Nishad N

3. DEFINITION
• Acute rhinosinusitis(ARS) and chronicrhinosinusitis(CRS)
are defined as symptomatic inflammation of the nose
and paranasal sinuses with the distinction between the
two based on the durationof the complaints.
• EPOS – Diagnosis made on clinical grounds
based on the presence of characteristic
symptoms , combined with objective evidence
of mucosal inflammation

5. Severity defined by individual responces on Patient
Reported Outcome Measures (prom) such as SNOT 22
- Mild , Moderate ,Severe

6. CLASSIFICATION OF RHINOSINUSITIS
• The Rhinosinusitis Task Force (RSTF) in 2007 proposed a clinical
classification system:
(a)Acute rhinosinusitis (ARS):symptoms lasting or less than 4 weeks with
complete resolution
(b) Subacute RS:duration between 4 and 12 weeks
• (c) Chronic RS(CRS) (with or without nasal polyps): symptoms lasting or
more than 12 weeks without complete resolution of symptoms
• (d) Recurrent ARS:≥ 4 episodes per year, each lasting ≥ 7-10 days with
complete resolution in between episodes
(e)Acute exacerbation of CRS:sudden worsening of baseline CRSwith
return to baseline after treatment

7. Types
• Acute / sub acute / chronic / recurrent
• Open / Closed (depending on its drainage)
• Unilateral / bilateral
• Maxillary / frontal / ethmoidal / sphenoidal
• Anterior / posterior group
• Bacterial /viral/ fungal / allergic / occupational

8. • A/C viral RS – most common ,Last for less than
10 days,complications are very rare, most
cases resolve spontaneously
• Rhinovirus (50%) , influenza & parainfluenza
virus , adeno virus ,RSV & entero virus
• Treatment –Symptomatic relief - Nasal
douching,Decongestants &Topical steroids
based on severity
• Duration > 10 days consider antibiotics

9. • ABRS --0.5-2%
• S pneumoniae(27%) , H.Influenzae(44%) ,
M.catarrhalis(14%) , S . pyogenes ,S.aureus

10. • BACTERIOLOGY
− Streptococcus
pneumoniae
− Hemophilus
influenzae
− Moraxella catarrhalis
− Staphylococcus
aureus
− Neisseria
• Acute sinusitis • Chronicsinusitis
− Staph.Aureus
− Streptococcus
− H. influenzae
− Bacteroides
− Pseudomonas

11. Predisposing factors to ARS
• Anatomical factors (DNS, Haller cell ,Concha
bullosa , etc
• Allergy
• Smoking
• Poor mental health

12. • Pathophysiology relating to viral agents – Cell
invasion of respiratory epithelium –
inflammatory changes including mechanical
changes ,epithelial damage and activation of
humoral and cellular defences
• In ABRS – superinfection following an initial
viral insult –Epithelial disruption has already
occurred & associated decrease in ciliated
cells and increase in goblet cells –sinus osteal
obstruction

13. • The accumulating mucus causes an initial
increase in the intra sinus pressure followed
quickly by negative pressure due to lack of
ventilation . This then set up a vicious cycle of
further congestion ,mucus retention ,
impaired gas exchange and PH balance –
prevents clearance of inflammatory products
& debris ----ideal medium for bacteria to
flourish

16. Chronic Rhinosinusitis
• Four cardinal symptoms of CRS
(a) Anterior or posterior purulent nasal discharge
(b) Nasal obstruction
(c) Face pain or pressure
(d) Hyposmia or anosmia

17. DIAGNOSIS OF CRS
At least two of the cardinal symptoms + one of the following:
(a) Endoscopic evidence of mucosal inflammation: purulent mucus
or edema in middle meatus or ethmoid region
(b) Polyps in nasal cavity or middle meatus
(c) Radiologic evidence of mucosal inflammation

18. Classification
Types of CRS:
(a) CRSwith nasal polyps (CRSwNP)
(b) CRSwithout nasal polyps (CRSsNP)

19. CRS with nasal polyps (CRSwNP)
• Intense edematous stroma in the sinonasal epithelium,
with
• Albumin deposition
• Pseudocyst formation
• Sub epithelial / perivascular inflammatory cell
infiltration
• Th 2 polarization
• High Ig E
• Tissue eosinophilia
• High IL-5 & IL-13
• High ECP
• Low T-reg activity

20. CRS without nasal polyps (CRSsNP)
• Fibrosis
• Basement membrane thickening
• Goblet cell hyperplasia
• Subepithelial edema
• Mononuclear cell infiltration
• Th-1 polarization
• High IFN-gamma
• Low ECP/MPO ratios
• High T- reg activity
• High TGF-B

21. Aetiological mechanisms --CRS

25. FACTORSASSOCIATED WITH CRS
• Anatomic abnormalities: Septal deviation and spur, turbinate
hypertrophy, middle turbinate concha bullosa, prominent agger
nasi cell, Haller cells, prominent ethmoidal bulla, pneumatization
and inversion of uncinate process.
• Ostiomeatal complex compromise: The common drainage pathway for
frontal, anterior ethmoid, and maxillary sinuses; blockage by inflammation
or infection can lead to obstruction of sinus drainage, resulting in sinusitis.
Mucociliary impairment: Ciliaryfunction plays important role in clearance
of sinuses; loss of ciliary function may result from infection, inflammation,
or toxin; Kartagener syndrome (situs inversus, CRS,and bronchiectasis) may
be associated with CRS.
Asthma: Up to 50% o CRSpatients have asthma.

26. • Bacterial infection: Staphylococcus aureus, coagulase-negative
Staphylococcus, Pseudomonas aeruginosa, Klebsiella pneumoniae,
Proteus mirabilis, Enterobacter, Escherichi coli; with chronicity,
anaerobes develop Fusobacterium, Peptostreptococcus, and
Prevotella.
• Fungal infection: Maycause a range of diseases, from noninvasive
fungus balls to invasive pathologies.
• Allergy:Acontributing factor to CRS;there is increased prevalence
of allergic rhinitis in patients with CRS.

27. • Staphylococcal superantigen: Exotoxins secreted by certain S.
aureus strains; they activate cells by linking -cell receptors with
MHC II surface molecule on antigen presenting cells (APCs)-T
cell activation , Ig E ,IL-5 activation-- which produce localized
eosinophilic inflammatory response
• Osteitis: Area of increased bone density and thickening may be a
marker of chronic inflammation.
• Marker of severity
• Occur more often in revision cases
• cases are resistant to standered oral treatment regimens
Biofilms: 3D structures of living bacteria encased in polysaccharide;
have been found on sinus mucosa in CRS patients.
• Multiple other species have been implicated in biofilm production
in CRS patients as well,including Haemophilusinfluenzae,Streptococcus
pneumoniae, Pseudomonasaeruginosa,and Moraxellacatarrhalis,although P.
aeruginosaand S. aureusappear to convey a worse prognosis

28. • Thick granular(eosinophilic ) mucin –
AFRS/AERD
• Less viscous mucus s/o bacterial super
antigen etiology
• ASAor Samter triad: Nasal polyposis, aspirin (ASA)sensitivity,
and asthma; mediated by production of proinflammatory
mediators, mainly leukotrienes.

29. Systemic condition causing rhinosinusitis/
Possible differential diagnosis

30. Signs of Rhinosinusitis
• Congested and edematous nasal mucosa
• Nasal discharge (anterior and posterior
rhinoscopy)
• Tenderness over the paranasal sinuses
• Postnasal drip, granular pharyngitis
• Cheek swelling in maxillary sinusitis
• Lid edema in ethmoid & frontal sinusitis
• and edematous nasal mucosa

31. • Location of
facial pain in
Rhinosinusitis
Maxillary sinusitis
• Cheek, upper jaw,
forehead that
increases on bending
forward
Anterior Ethmoid:
nasal bridge and
peri-orbital, more on
eye movement
Sphenoid : vertex,
occipital, retro-
orbital pain
Frontal sinusitis
• Forehead that increases
during morning and
decreases by late
afternoon (office
headache)
Posterior
Ethmoid: deep
seated retro-
orbital

32. Palpation to elicitparanasal sinus
tenderness
• Maxillary: over the
canine fossa
• Anterior ethmoid: medial
to medial canthus
• Frontal: Floor of sinus
at the superomedial
aspect of the orbit or
tap over its anterior
wall on the forehead

34. GOLD STANDERED investigations for CRS are
Rigid nasal endoscopy & CT scan of PNS.
Microbiology

35. Plain X-rayof Paranasal sinuses
• Plain X-rayofParanasalsinuses• Water’s view (Occipito -mental) 
maxillarysinus
• Caldwell’s view (Occipito -frontal) and
lateralviewfrontal
• Rhese’s view (lateral oblique) and
lateral view 
ethmoids
• Baseskull view (Submento -vertical)
and Pierre’s view (Occipito -mental with
mouth open) sphenoid
− Air-fluid level seen in acute
sinusitis
− Mucosal thickening seen in
chronicsinusitis

36. • Most reliable imaging modality for
• sinusitis at present
• Plain axial, coronal and sagittal cuts of 3 mm
• Contrast for suspected vascular,
• neoplastic, inflammatory lesions
• Helps to delineate the extent of disease,
define anatomical variants and study the relationship of sinuses with
• surrounding structures
• Indications:
• Recurrent acute/chronic sinusitis not responding to medical treatment
• Before endoscopic sinus surgery
• Impending complications of sinusitis
C.T.scan ofNose andPNS

37. Plain C.T.scan NoseandPNS: Maxillaryand
ethmoidsinusitis

38. C.T.scan: frontalsinusitis

39. C.T.scan: sphenoidsinusitis

40. M.R.I.ofP.N.S.
• Indications
• −To assess the intracranial
extension of sinonasal disease,
brain abscess due to sinusitis
and meningocele or
encephalocele
• −Malignant neoplasms of
sinonasaltract
• −To evaluate the orbital
complicationsof sinusitis

45. Aim of the treatment is
• Reduce the inflammation
• Reduce bacterial load
• Optimize ciliary functionby removing mucus

46. Treatment targeting intrinsic mucosal
inflammation
• (1) intra- nasal corticosteroids
excellent safety profile , low
bioavailability(1%)
low incidence of adverse events (nasal
irritation , crusting , epistaxis etc)
No evidence of nasal mucosal atrophy with long
term use ,or growth retardation in paediatric
population
Fluticasone & Mometasone –Commonly used

47. (2) Systemic corticosteroids
short course of oral steroids
(3) Immunomodulatory antibiotics
Macrolide (roxithromycin)
anti inflammatory effect – target markers including
IL-8,IL-4,IFN-Gamma,TNF-Alpha and have
predominant effect on neutrophil mediated
inflammation
Doxycyclin –Reduce levels of MPO,ECP,MMP-9

48. (4) Leukotriene receptor antagonists
Montelukast
(5) Novel immunoregulation
Monoclonal antibodies
Omlizumab -- Anti-Ig E
Mepolizumab– Anti IL-5
(6) Aspirin desensitization
sampters triad pts –immune tolerance –regular
administration of aspirin (orally/intranasally) –
incrementally increasing dosage of oral aspirin
until several hundred mgs /day are tolerated

50. Treatment aimed at reducing microbial load
• Reducing microbial load or eradicating
pathogen from sinuses
• Culture directed short term antibiotics – used
in a/c exacerbation of CRS
• Biofilm –systemic antibiotics are ineffective
topical antibiotics and surfactants are
beneficial

52. Treatment aimed at improvement in mucociliary
clearance
• Saline irrigation – removal of mucus , infected
crusts & pro inflammatory agents
• large volume positive pressure irrigation –
most effective

56. • THANK YOU