chronic Rhinosinusitis

EPOS 2020

1. Chronic Rhinosinusitis Dr safika zaman Dept of ent & head neck surgery Rkmsp vims

2. Epidemiology in India International Journal of Otorhinolaryngology and Head and Neck Surgery Khan AR et al. Int J Otorhinolaryngol Head Neck Surg. 2020 May;6(5):969-973 http://www.ijorl.com

3. Cont.. Quality of life Sleep quality Productivity Economic burden for the health care system.

4. Introduction Clinical syndrome, rather than a specific disease. Consensus (EPOS 2020) 1) CRS is typically an ante-grade process with the mucosal inflammation triggered by a dysfunctional interaction between exogenous agents inhaled through the nose and the host immune system. 2) specific causal factors likely vary in importance in individual patients leading to different types or patterns of tissue inflammation. 3) the clinical characteristics (phenotypes),natural history and response to treatment will depend on endotype .

5. Definition of CRS( EPOS 2020) Inflammation of the nose and paranasal sinuses, characterised by two or more symptoms, one of which should be either nasal blockage / obstruction / congestion or nasal discharge (anterior / posterior nasal drip). With or without- - facial pain/pressure; -reduction or loss of smell; for ≥12 weeks. • endoscopic signs of: - nasal polyps and/or - mucopurulent discharge primarily from middle meatus and/or - oedema/mucosal obstruction primarily in middle meatus and/or • CT changes: - mucosal changes within the ostio -meatal complex and/or sinuses.

6. CRS in children Chronic rhinosinusitis (with or without nasal polyps) in children is defined as: presence of two or more symptoms one of which should be either nasal blockage / obstruction / congestion or nasal discharge (anterior/posterior nasal drip) +/-facial pain/pressure; +/-cough For more than 12 weeks.

7. Factors associated with CRS

8. Bacteria The newer molecular microbiome data has provide support for the hypothesis that dysbiosis of the community as a whole, as opposed to individual organisms, may trigger mucosal inflammation. Depletion of two genera ( Corynebacterium and Peptonophilus ) was associated with CRS. Pathogens such as Haemophilus influenzae , Streptococcus pneumoniae , Pseudomonas aeruginosa , Moraxella catarrhalis and S. aureus can all form sinonasal biofilms in CRS patients,

9. Viruses virus infection might contribute to development and exacerbations of CRS, via damaged airway barrier. Viruses commonly associated are- rhinovirus, respiratory syncytial virus and influenza virus, corona virus.

10. Fungi Recent work has suggested that an innate immune defect (possibly in TLR4) may account for fungal accumulation in the sino -nasal cavities of AFRS patients. Fungi have intrinsic protease effects that induce Type 2 cytokine signalling leading to the accumulation of eosinophilic mucin. Same protease effects should foster a type 2 response, leading to local and systemic IgE responses to fungal antigen.

11. Other environmental & host factor Ciliary impairment- primary ciliary dyskinesia. Smoking Environmental pollution-cleaning agents, metal dust, animals, moisture/mould/mildew, poisonous gas Obstructive sleep apnoea Metabolic syndrome and obesity Low vit-D3 Alcohol hyper-responsiveness

12. Cont.. Genetic association - biological role: a. immune system related; b. epithelial barrier related; c. difficult to categorize.

13. Inflammatory mechanisms of CRS The inflammatory mechanisms of chronic rhinosinusitis (CRS) are the molecular pathways leading to the establishment of the mucosal inflammation and tissue remodelling that characterizes this broad syndrome . -Multiple inflammatory mechanisms -Interacting dynamically, -variable patterns of tissue inflammation. -Mucosal barrier penetration by environmental agents also involves Type1, 2 and 3 pathways. -CRS response is chronic and polyclonal.

14. -Tissue remodeling is greatest. fibrin mesh formation and barrier damage. Commonly associated with asthma.

15. Fibrin deposition and polyp formation is less. Neutrophil mediated. Less tissue remodelling

16. Aetiology and pathogenesis of CRS

17. Remodeling in CRS Fibrosis Basement membrane thickening Goblet cell hyperplasia, Epithelial barrier abnormalities Polyp formation Osteitis Angiogenesis

18. Classification

19. Classification

20. Approach in a patient with CRS History Physical examination Nasal endoscopy CT scan of PNS Diagnosis Management

21. Olfactory dysfunction Distinct clinical features of CRS related olfactory dysfunction- Fluctuation of the olfactory complaint Gap between ortho -versus retronasal olfactory function. Low threshold and preserved identification scores. Steroid-dependent reversal.

22. Facial pain Moderate to severe pain. There is no correlation between the location of facial pain and abnormalities.

23. Nasal endoscopy Identification of oedema, pus and/or polyps. Assessment of sinus cavities following surgery. Microbiological sampling when needed. Response assessment. Documentation.

24. Objective nasal patency measurement peak nasal inspiratory flowmetry : objective measure of nasal patency. This measure correlates best with subjective nasal patency. Diagnostic. Evaluation of treatment

25. Diagnostic imaging in rhinosinusitis Imaging is used to assess: • Corroboration of clinical symptoms and endoscopic findings • Anatomy and anatomical variants • Pathology • Diagnosis • Extent.

26. CT scan prior to surgery

27. Biopsy To confirm diagnosis, to assist in endotyping of inflammatory disease and for research purposes. To explore the differential diagnosis (inflammation, respiratory epithelial adenomatoid hamartoma (REAH), infection, granuloma / vasculitis, tumour). To confirm severity of inflammation, cellular composition e.g. eosinophils bacterial and fungal elements. To determine nature of relationship e.g. invasive or non-invasive fungus.

28. Biomarkers of type 2 disease Main biomarkers are- Eosinophils IgE levels Periostin

29. Cont..

30. AR, NAR and CRS Significant Overlap. The radiologic sign of an obstructed ostio -meatal complex is a sign of CRS.

31. Indication of surgery patients with sinus disease refractory to a trial of primary medical therapy. As the aim of surgery is to improve the severity of patient’s symptoms, the decision to operate should only be made in patients with symptomatic disease, with the exception of patients with actual or impending complications.(EPOS 2020)

32. FESS IN CRS Creates a sinus cavity that incorporates the natural ostium- • Allows adequate sinus ventilation. • Facilitates mucociliary clearance. • Facilitates instillation of topical therapies.

33. Future challenges in CRS Better understanding of: 1) the aetiologic factors that drive CRS with a goal towards prevention. 2) Pathophysiologic inflammatory mechanisms and relevant endotype biomarkers with a goal toward targeted therapy. 3) Molecular mechanisms of barrier and tissue remodeling that may play a role in persistence and recurrence.

34. Treatment evidence and recommendations for adult CRS Therapy Level of evidence GRADE recommandation Short term antibiotics for CRS 1b- No effect on symptomatology apart from significantly reduced postnasal drip symptom scores at week 2 . Long term antibiotics for CRS 1a- uncertain whether or not the use of long-term antibiotics has an impact on patient outcomes in adults with CRS Topical antibiotics 1b- Topical antibacterial therapy does not seem to be more effective than placebo in improving symptoms..

35. Cont.. Therapy Level of evedance GRADE recommandation Nasal corticosteroids 1a There is high-quality evidence that long term use of nasal corticosteroids is effective and safe for treating patients with CRS. They have impact on nasal symptoms and quality of life improvement,When administered after endoscopic sinus surgery, nasal corticosteroids prevent polyp recurrence. -Well tolerated. -Low side effect.

36. Cont.. Therapy Level of evidence GRADE recommendation Corticosteroid-eluting implants 1a The placement of corticosteroid-eluting sinus implants in the ethmoid of patients with recurrent polyposis after sinus surgery reduces the need for surgery and reduces nasal polyp score Systemic corticosteroids 1a A short course of systemic corticosteroid, with or without local corticosteroid treatment results in a significant reduction in total symptom score and nasal polyp score.

37. Therapy Level of evidence GRADE recommendation Antihistamines 1b There is insufficient evidence to decide on the effect of the regular use of antihistamines in the treatment of patients with CRS. Anti-leukotrienes 1b- does not recommend montelukast use unless in situations where patients do not tolerate nasal corticosteroids. Decongestant 1b In situations where the nose is very blocked, the temporary addition of a nasal decongestant to nasal corticosteroid treatment can be considered

38. Therapy Level of evedance Recomammandation Nasal irrigation with saline 1a The steering group advises the use of nasal saline irrigation with isotonic saline or Ringer’s lactate with or without the addition of xylitol, sodium hyaluronate , Aspirin treatment after desensitization (ATAD) with oral aspirin in N-ERD 1a can be a treatment for N-ERD patients with CRSwNP whenever there is confidence in the patient’s compliance. Low salicylate diet 1b Diets, like low salicylate diet have been shown to improve endoscopic scores and may improve symptoms compared to a normal diet

39. Therapy Level of evidence recommandation Local and systemic antifungal treatments 1a- Local and systemic antifungal treatments do not have a positive effect of QOL, symptoms and signs of disease in patients with CRS Anti- IgE 1b Anti- IgE therapy has been proposed as a promising biologic therapy for CRS Anti-Il-5 1b Mepolizumab that showed a significant reduction in patients’ need for surgery and an improvement in symptoms.

40. Other medical therapy with poor evidence Probiotics Muco -active agents Herbal treatment Acupuncture and traditional Chinese medicine Nasal furosemide Capsaicin PPI Phototherapy Filgastrim Colloidal nasal silver spray

41. Treatment of CRS in children

42. Dupilimab Dupilumab is a fully human monoclonal antibody to the IL-4 receptor a subunit, which inhibits signalling of IL-4 and IL-13 that is given as a subcutaneous injection.

43. Thank you