DOCUMENT REGARDING CHRONIC RHINOSINUSITIS

New Document on CRS

1. C H R O NIC R H IN O S INU S ITIS Dr FOUSIYA M

2. Definition Diagnostic criteria for rhinosinusitis Symptoms Primary symptoms ( at least 1 to be present, but if both present -- sufficient to make diagnosis ) Nasal blockage/obstruction/ congestion Nasal discharge (anterior/ posterior) Additional symptoms (at least one is needed if only one of the primary symptoms is present) Facial pain/pressure Olfactory dysfunction Hyposmia /anosmia Duration >10 days, <3 months = acute >3 months = chronic Endoscopy ( any of these ) Nasal polyps Mucopurulent discharge Oedema/mucosal obstruction CT scan findings Mucosal changes within the ostiomeatal complex and/or sinuses

3. PATHOGENESIS DEVELOPMENTAL OF SINUSES The PNS  partially present at birth (maxillary and ethmoidal sinuses) but develop in childhood .

4. SINUS PHYSIOLOGY The sinus cavities pseudostratified, ciliated columnar epithelia interspersed with goblet cells. The cilia sweep mucus toward the ostial opening. Obstruction of the ostia Mucous impaction  decrease oxygenation  anaerobic condition  purulent secretions  growth of bacteria Sinonasal biofilms bacteria and fungus  anchor to the mucosal surfaces.

5. 2. NASAL POLYPOSIS CRSwNP CRSsNP CRSwNP  associated with an eosinophil-mediated TH2 (IL-4–, IL-5–, and IL-13–high) cytokine profile. CRSsNP believed as a noneosinophilic disease.

6. Aetiological mechanisms

7. PATHOPHYSIOLOGY IN CRSSNP Two main defensive strategies against the infection come into play. 1. Nonspecific phase • Mucus and its contents: lysozyme and defensins • VEGF: promote nasal epithelial cell growth and inhibit apoptosis. 2. Innate and adaptive immune response • The innate immunity  phagocytosis of the microorganisms by neutrophils, monocytes, and macrophages . The adaptive immunity  reacts on antigen presentation through formation of immune products (Th1&Ab).

8. PATHOPHYSIOLOGY IN CRS P roinflammatory and neutrophil-associated cytokines including IL-1β, TNF-α, and IL-8. increased neutrophil activation MPO. CRSwNP  eosinophil-rich Th2-dominated cytokine pattern with high IL-5 and, low TGF-β concentrations.

9. PATHOPHYSIOLOGY IN CRSWNP The highest concentrations of IL-5  nonallergic asthma and aspirin sensitivity. Eosinophil recruitment  mediated by the chemokines and eotaxins,in cooperation with IL-5.

10. PATHOPHYSIOLOGY IN CRSWNP Role of Staphylococcus aureus Enterotoxins S. aureus form biofilms - serve as a nidus, allow the microbe to survive antibiotic treatment S. aureus enterotoxins have superantigenic activity. modify the functions of T and B cells, eosinophils, and other inflammatory cells. S. aureus enterotoxins Th2-polarized eosinophilic inflammation and impairment of T regulatory function, multiclonal IgE production.

11. EPIDEMIOLOGY Nasal polyps occur more frequently in Asthmatics with aspirin sensitivity Cystic fibrosis. Churg -Strauss syndrome and Kartagener syndrome (situs inversus ). The incidence of nasal polyps  men > women.

12. MIC R O BI O L O G Y IN C R S C h il d ren • A e r o b e s : A lph a - h e m o l y ti c str e pt o c o cc us , H in f lu e nz a e , S pn e u m o ni a e , S e pid e r m idis , S a ur e us . • A na e r o b e s : 8.0% A du l t s • A e r o b e s : Str e pt o c o cc us sp e c i e s , H In f lu e nz a e , P a e ru g in o s a ) , S a ur e us , a nd M c a t a rrh a li s • A na e r o b e s : Pr e v o t e ll a sp e c i e s , Str e pt o c o cc i , Fus o b a c t e riu m sp e c i e s N osoco m ial • G r a m-n eg at i v e e n t e r i c s p ec i es : P ae r ugino s a , K leb s iell a pneu m oniae , En t e r obac t e r s pecie s , P r o t eu s m i r abili s an d S e rr a t i a m a r ce s cens • G r a m-p os i t i v e cocc i : s t r ep t ococci , s t ap h ylococci C R Sw N P • P o l y m i c r o b i a l ae r obic an d anae r obic flo r a

13. CHRONIC RHINOSINUSITIS WITH POLYPS Nasal polyps  edematous semi translucent masses. originating from the mucosal linings of the sinuses and prolapse into the nasal cavities.

14. CHRONIC RHINOSINUSITIS WITH POLYPS H/O recurrent rhinitis with nasal obstruction / discharge . Anosmia . Viral infections initially, with subsequent bacterial infection. Allergic rhinitis Elevated Ig E

15. Samters triad (AERD)

16. CHRONIC RHINOSINUSITIS WITH POLYPS AERD 15 % of CRS w NP Aspirin sensitivity is suspected after a typical respiratory reaction. Acute asthma and/or rhinitis attacks caused by ingestion of aspirin and other NSAIDs.

17. Primary ciliary dyskinesia (PCD)  autosomal recessive disease abnormal or absent beating of cilia hinders normal mucociliary clearance. Recurrent respiratory tract infection, nasal polyposis and/or bronchiectasis. Kartagener’s syndrome  triad of chronic sinusitis, bronchiectasis and situs inversus . Young’s syndrome  obstructive azoospermia, bronchiectasis and sinus disease.

18. EGPA ( Churg Strauss) asthma eosinophilia of >10% in peripheral blood paranasal sinusitis pulmonary infiltrates, sometimes transient histologic evidence of vasculitis with extravascular eosinophils mononeuritis multiplex or polyneuropathy if ≥4 criteria are present, sensitivity is 85%, and specificity is 99.7%.

19. CHRONIC RHINOSINUSITIS WITH POLYPS Fungal disease  four categories: Acute/ fulminant Invasive Chronic/ indolent Fungus ball Non Invasive Allergic fungal sinusitis; AFS, The most common form and is associated with nasal polyps. The fungus ball

20. FUNGAL BALLS It is dense accumulation of extramucosal fungal hyphae, usually within one sinus. Most common  maxillary sinus. Most common organism : Aspergillus commonly seen immunocompetent , middle aged and elderly females, following dental procedure

21. Radiological findings  sinus opacification, with areas of hyperattenuation . Cheesy or clay like debris within the sinus . Accumulation of fungal hyphae without evidence of tissue fungal invasion microscopically. Non specific chronic sinus inflammation.

22. AFRS non invasive fungal sinusitis from an allergic and immunologic response to the presence of fungal hyphae in the sinuses. seen in young immunocompetent adults. Age : 21-33 years Male : Female : : 1.5 : 2.6 to1.

23. Diagnostic criteria: Bent and Kuhn criteria for AFRS Major criteria Minor criteria Evidence of of type 1 IgE mediated hypersensitivity asthma Nasal polyposis u/l predominance Characteristic CT findings Radiographic bone erosion Eosinophilic mucus Fungal culture Positive fungal smear Charcot leyden crystals Serum eosinophilia

24. Elevated IgE levels. In vivo(skin prick) or in vitro (RAST) test- to demonstrate fungal specific IgE as a diagnostic criteria. CT : CT without contrast is the imaging of choice Heterogenous signal intensities with paranasal sinuses filled with allergic mucin (double density sign or rail-track sign) Expansion of PNS and nasal cavity. Bony erosion.

25. MRI with gandolinium  when diagnosis of AFRS is uncertain or when intra cranial / intra orbital complications are suspected. T1 images shows central areas of hypo-intensity with peripheral enhancement. T2 images shows central areas of hypointensity or signal void with peripheral enhancement.

26. CHRONIC RHINOSINUSITIS WITH POLYPS Invasive forms  Aspergillus flavus . fulminant acute  immunocompromised hosts (e.g., AIDS, CD4+ counts < 50 cells/mL, or neutrophil < 1000 cells/ ml Aspergillus fumigatus  lethal, hematogenous dissemination despite high-dose intravenous antifungal treatment.

27. CHRONIC RHINOSINUSITIS WITH POLYPS Cystic fibrosis Sinusitis  detected in CT The incidence  6 % to 48 %. Mucosal changes in CF  affect the paranasal cavities bilaterally, causing facial deformities such as hypertelorism . F rontal and sphenoid sinuses  hypoplastic or absent.

28. CHRONIC RHINOSINUSITIS WITH POLYPS Bulging of the lateral nasal wall and the erosion of the uncinate process is characteristic of CF.

29. PATIENT EVALUATION IN CRSWNP Diagnosis of CRSwNP  by rigid nasal endoscopy. The extent of disease : CT scan with coronal sections mucosal structures and the delicate anatomy of the sinuses CT scan is mandatory before sinus surgery. MRI scan  fungal disease or tumor or if intra-cranial extension of disease is suspected.

30. PATIENT EVALUATION IN CRSWNP Nasal endoscopy. Turbinate hypertrophy, concha bullosa, CRSsNP , adenoid hypertrophy U nilateral obstruction, nose bleeding, or crusting should be intensively investigated. Papillomas , benign or malignant tumors , meningoencephaloceles S ystemic disease. Asthma, aspirin sensitivity, Churg -Strauss syndrome, inhalant allergies, CF, and other lung diseases.

31. TREATMENT SYSTEMIC ANTIBIOTICS The benefit of antibiotic treatment is questionable. To treat acute exacerbations. Eradication of infection depends on sinus aeration and mucociliary clearance . Macrolides  anti-inflammatory and antibacterial effects. A recent studies are against the use of intravenous antibiotics for uncomplicated CRS.

32. SYSTEMIC ATB IN CHILDREN Amoxicillin (45 or 80 mg/kg daily). Amoxicillin-clavulanate  cover B-lactamase organisms, H influenza Alternative choices: quinolones or clindamycin with a 2nd or 3rd generation cephalosporins

33. TOPICAL ANTIBIOTICS IN CRS The role of topical antibiotics is controversal . In the postoperative period the sinus cavities delivery of medication to the sinonasal mucosa. Consider a 3 to 6 weeks course of topical antibiotics for CRS. With or without a nebulizer. Mupirocin, gentamicin or tobramycin irrigations Sensorineural hearing loss was noted in 23% of patients with CF who had used frequent irrigations.

34. Doxycycline (200 mg on the first day followed by 100 mg once daily for 20 days) significant decrease in polyp size beginning at week 2 and persisting for 12 wks Doxycycline showed a significant effect on postnasal discharge.

35. STEROID NASAL SPRAYS CRSwNP and CRSsNP : Use INS (sprays and aerosols ). reduce nasal obstruction, rhinorrhea, and occasionally hyposmia symptoms recur within weeks or months of discontinuation of treatment . Children: Mometasone fuorate 2 yr , Fluticasone propionate 4 yr

36. TOPICAL STEROID SINUS INSTILLATIONS OR DROPS CRSsNP benefit from topical steroid irrigations . effects on nasal and sinus pain symptoms. CRSwNP controversy results decreased need for sinus surgery (from 78% to 52%) also reduce incidence of polyp recurrence after surgery. inadequate for severe bilateral polyps.

37. SYSTEMIC GLUCOCORTICOIDS CRSsNP : short course of oral steroids . CRSwNP : short-term treatment with oral steroids in because it decreases polyp size and alleviates symptoms . medical polypectomy repeated applications of oral corticosteroid bursts may lead to systemic side effects. beginning with 32 mg of prednisolone and stepwise reducing the dose during a 14 to 20 days oral course Children: When intranasal steroids fail to relieve mucosal inflammation or nasal polyps.

38. SALINE IRRIGATION, AH, DECONGESTANTS, LTRA Saline irrigation Adjunctive treatment Improve medication delivery, healing outcomes, and mucociliary clearance. Determination of the optimal composition and pH of the irrigation . Antihistamines Alpha-adrenergic decongestants No beneficial for maintenance treatment Leukotriene modifiers adjunct to topical steroid in CRSwNP . Montelukast modest symptomatic benefit

39. TREATMENT: CRSWNP WITH AERD Avoidance of aspirin and other NSAIDs prevent exacerbations but does not prevent progression of disease . selective COX-2 inhibitors (celecoxib, rofecoxib ) usually are well tolerated . Oral and/or topical glucocorticosteroids effective but they cause side-effects in long-term usage . relapse of risk in case of noncompliance

40. TREATMENT: CRSWNP WITH AFS Antifungals  indicated only for invasive forms of sinus mycosis or in immuno-compromised patients. Both surgical intervention and the use of systemic and long-term topical corticosteroids are beneficial . Total serum IgE can be helpful in the clinical follow-up an increase in total serum IgE was found to have significant predictive value for the need of recurrent surgical intervention.

41. COMPLICATIONS Empyema of the frontal sinus may lead to meningitis, an epidural or subdural brain abscess.  Immediate intervention Osteomyelitis of the frontal bone  surgical intervention and long-term antibiotic treatment. Recurrent episodes of meningitis may arise from bony defects in the frontal skull base or the sphenoid sinus. Fungal disease, if invasive, can penetrate bony structures and the orbit, cheek, and brain. pyomucocele  surgically drained through the nose.

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