Rhinosinusitis

3,256 views 56 slides Jun 21, 2020
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About This Presentation

include acute and chronic rhino sinusitis


Slide Content

Rhinosinusitis Dr M ohammed N ishad N

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

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

CLASSIFICATION OF RHINOSINUSITIS The Rhinosinusitis Task Force (RSTF) in 2007 proposed a clinical classification system: Acute rhinosinusitis (ARS): symptoms lasting or less than 4 weeks with complete resolution 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 CRS with return to baseline after treatment

T ypes 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

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 T reatment –Symptomatic relief - Nasal douching,Decongestants & T opical steroids based on severity Duration > 10 days consider antibiotics

ABRS --0.5-2% S p neumoniae (27%) , H.Influenzae (44%) , M.catarrhalis (14%) , S . p yogenes , S.aureus

BACTERIOLOGY Streptococcus pneumoniae H e m op h il u s influenzae Moraxella catarrhalis Staphylococcus aureus Neisseria Acute sinusitis Chronic sinusitis Staph. Aureus Streptococcus H. influenzae Bacteroides P s eudomonas

Predisposing factors to ARS Anatomical factors (DNS, Haller cell , C oncha bullosa , etc Allergy Smoking Poor mental health

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

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

Chronic Rhinosinusitis Four cardinal symptoms of CRS Anterior or posterior purulent nasal discharge Nasal obstruction Face pain or pressure Hyposmia or anosmia

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

C lassification Types of CRS: CRS with nasal polyps ( CRSwNP ) CRS without nasal polyps ( CRSsNP )

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

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

Aetiological mechanisms --CRS

FACTORS ASSOCIATED 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 : Ciliary function 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 CRS patients have asthma.

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 : May cause a range of diseases, from noninvasive fungus balls to invasive pathologies . Allergy : A contributing factor to CRS; there is increased prevalence of allergic rhinitis in patients with CRS.

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 Haemophilus influenzae , Streptococcus pneumoniae , Pseudomonas aeruginosa , and Moraxella catarrhalis , although P. aeruginosa and S. aureus appear to convey a worse prognosis

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

Systemic condition causing rhinosinusitis / Possible differential diagnosis

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

Location of facial pain in R h inosin u sitis 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

Palpation to elicit paranasal 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

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

Plain X- ray of Paranasal sinuses Plain X- ray of Paranasal sinuses Water’s view ( Occipito -mental)  maxillary sinus Caldwell’s view ( Occipito -frontal) and lateral view  frontal Rhese’s view (lateral oblique) and lateral view  ethmoids Base skull view ( Submento -vertical) and Pierre’s view ( Occipito -mental with mouth open)  sphenoid Air-fluid level seen in acute sinusitis Mucosal thickening seen in chronic sinusitis

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 of Nose and PNS

Plain C.T. scan Nose and PNS: Maxillary and ethmoid sinusitis

C.T. scan: frontal sinusitis

C.T. scan: sphenoid sinusitis

M.R.I. of P.N.S. Indications − To assess the intracranial extension of sinonasal disease, brain abscess due to sinusitis and meningocele or encephalocele − Malignant neoplasms of sinonasal tract − To evaluate the orbital complications of sinusitis

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

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

(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

(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

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

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

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