European Position Paper on Rhinosinusitis and Nasal Polyps

24 European Position Paper on Rhinosinusitis and Nasal Polyps


24.1 Definitions


• Rhinosinusitis:


figure Nasal blockage/obstruction/congestion or nasal discharge + at least one of:


– Facial pain/pressure


– Hyposmia/anosmia


figure In addition, endoscopic and/or CT changes required to confirm symptoms above of acute rhinosinusitis (ARS)/chronic rhinosinusitis (CRS)


figure <12 weeks = acute


figure >12 weeks = chronic


figure Symptom-free intervals (complete resolution) but >12 weeks in total = recurrent acute


figure <10 days = common cold (viral upper respiratory tract infection, i.e., URTI)


figure Increase in Sx after 5 days OR persistence of Sx after 10 days = non-viral ARS


figure Severity defined by VAS (0–10)—“How troublesome are your Sx of ARS/CRS?”:


– Mild = 0 to 3


– Moderate = >3 to 7


– Severe = >7 to 10


• Epidemiology:


figure ARS:


– 8.4% of Dutch population suffer with ≥ 1 episode of ARS/year


– Fifth most common reason for ABx prescription in the United States


figure CRS:


– 11% of population suffer with CRS (prevalence)


– ≥15% of outpatient consultations in ENT


– 10,000 sinus procedures per year in the United Kingdom (1999–2010)


– Cost of $500 per year to patients with CRS in the United States


– Increasing incidence of CRS with increasing age—mean age of 53


– Slight male preponderance


– AFRS accounts for ~10% of CRS with nasal polyps (CRSwNPs)


24.2 Aetiology


24.2.1 Acute Rhinosinusitis


• Bacterial superinfection of virally damaged mucosa:


figure Bacteria


Streptococcus pneumoniae


Haemophilus influenzae


Moraxella catarrhalis (esp. children)


• Ciliary impairment—impaired by viral infection


• Allergy—may be a factor but evidence limited


Helicobacter pylori and laryngopharyngeal reflux (LPR)—little evidence


• Presence of NG tube


24.2.2 Chronic Rhinosinusitis without Polyps


• Ciliary impairment—secondary ciliary dyskinesia


• Allergy—may be present in 50 to 90% of patients


• Asthma—many asthmatics will show abnormal mucosal CT findings (approximately 88%)


• Immunocompromised state—low IgA, IgG, IgM; HIV


• Genetics—CF (mutations of CFTR gene) and primary ciliary dyskinesia


• Pregnancy—11 to 32% of women suffer pregnancy rhinitis


• Local host factors—conflicting evidence for DNS, conchae bullosae, etc. Beware of dental infections


• Micro-organisms:


figure Bacteria—pathogens or colonizers?


S. aureus (36%)


– Coagulase–ve staphylococcus (20%)


Streptococcus pneumoniae (17%)


figure Fungi—colonize only or promoters of allergic/eosinophilic response?


• Osteitis—animal studies only—may explain resistance to ABx


• Environmental:


figure Smoking


figure Low income


figure Atmospheric pollutants—no convincing evidence


• Iatrogenic:


figure Mucoceles associated with previous ESS


figure Recirculation of mucus from natural to surgical ostia


Helicobacter pylori and LPR—DNA detected in 11 to 33% of CRS patients—causal?


24.2.3 Chronic Rhinosinusitis with Nasal Polyps


• Polyps present in 0.5 to 4.3% of the population; only two-third seek medical advice


• Allergy—varying reports between 10 and 81%


• Asthma—31 to 42% of patients with NPs (7% of asthmatics have NPs)


• Aspirin sensitivity—36 to 96% have CRS with NPs


• Genetics:


figure 14 to 52% have +ve family history


figure Twin studies do not show that both develop NPs


figure HLA associations, e.g., A74, DR7


figure Gene polymorphisms


figure Multiple gene expressions for immune modulation


figure Cystic fibrosis


• Environmental factors—unclear


24.3 Children


• Day care


• Nasal obstruction


• Passive smoking


• Bottle-feeding


• Urban atmospheric pollution


• Tonsillitis (immunological deficiency)


• OME (immunological deficiency)


• Ciliary dyskinesia, e.g., CF, primary ciliary dyskinesia


24.4 Inflammatory Mechanisms


24.4.1 Acute Rhinosinusitis


• Elevation of IL-1, IL-6, IL-8


• Neutrophils—source of IL-8 and TNF-α


• Expression of intracellular adhesion molecule 1 (ICAM-1)


• T lymphocytes—stimulated by IL-1 and 6, TNF-α


24.4.2 CRS without NPs


• Neutrophils predominate


• Small numbers of eosinophils, mast cells, basophils


• Mucosal changes:


figure BM thickening


figure Goblet cell hyperplasia


figure Subepithelial oedema


figure Mononuclear cell infiltration


• CD4+ TH cells—initiate and regulate inflammation


• Macrophages (CD68+ cells) increase


• Mast cell numbers raised


• Cytokine mediators: IL-1, 3, 6 and 8; tumour necrosis factor-α (TNF-α), GM-CSF, ICAM-1, MPO, and eosinophil cationic protein (ECP)—the latter is the main difference from ARS


• IFN-γ and TGF-β = TH 1 pathway; TGF-β expression higher than CRS with NPs


• Chemokines, e.g., CCR4+


• Eicosanoids—COX-2 mRNA and PGE2 higher than CRS with NPs


• Metalloproteinases—low MMP-9 activity


• Nasal nitric oxide (nNO) shows increase the correlates with subjective and objective measures of improvement


• Neuropeptides such as VIP may play a role


• Mucins—MUC5AC and MUC5B increased in CRS


• Increased vascular endothelial growth factor (VEGF)


• Biofilms—structured specialized communities of adherent micro-organisms encased in a complex extracellular polymeric substance (EPS)


24.4.3 CRS with NPs


• Eosinophils present in 80% = marker of inflammation in CRSwNPs


• Increased numbers of T cells and plasma cells


S. aureus superantigens interact with T cells in 35%


• Macrophages increased with an increase in macrophage mannose receptors in polyps


• Mast cells—more often IgE+


• Increased neutrophils


• Overexpression of MUC8 mRNA and downregulation of MUC5AC mRNA expression—alters mucus composition


• Cytokines and chemokines—differences from CRSsNPs:


figure IL-5 and IgE = CRS with NPs (TH2)


figure Exaggerated humoral and cellular response to airborne fungi


• Adhesion molecules—ICAM-1 among others expressed on polyp surface


• Leukotrienes and their receptors unregulated in NP tissue


S. aureus enterotoxins induce a more severe eosinophilic inflammation and cause multiclonal IgE synthesis


• In CF—very prominent neutrophilic inflammation


• Aspirin sensitivity—inhibition of cyclooxygenase-1 causing release of lipid and non-lipid mediators


• IgE+ cell numbers raised in patients with allergic, fungal, and eosinophilic CRS


• Fungal-specific IgG and IgA higher in CRS with eosinophilic mucus


24.5 Investigations


• Endoscopy


• Endoscopic-guided nasal swabs—87% accurate


• CT scan (± MRI where neoplasia suspected)


• Lund–Mackay scoring system for CT:


figure 0 to 2 score for each of maxillary, ant. ethmoid, post. ethmoid, sphenoid, frontal


figure Score of 0 or 2 for OMCs


figure Max. score = 24 (12 each side)


• Saccharin test for mucociliary clearance—useful if normal (<35 minutes)


• Ciliary beat frequency (>8 Hz for IT = normal) and electron microscopy for PCD


• Nitric oxide:


figure LRT = <20 ppb


figure Nose = 400 to 900 ppb


figure Sinuses = 20 to 25 ppm


• Nasal airway—PIFR/acoustic rhinometry/rhinomanometry/nasal spirometry


• Olfactory testing—see Chapter 34


• Aspirin challenge


• QoL questionnaires—SF-36, RSOM, SNOT-22, RSDI, RQLQ, et al.


24.6 Recommended Treatment Regimes


24.6.1 Adults with ARS


• Oral ABx—after 5/7


• Topical corticosteroid


• Oral corticosteroid—if severe to reduce pain


• Oral antihistamine—if atopic


• Decongestant


24.6.2 Children with ARS


• Oral antibiotics—after 5/7


• Topical corticosteroids


• Saline douching


24.6.3 Adults with CRS without NPs (Fig. 24.1)


• Long-term ABx (>12/52)—low-dose macrolide, e.g., clarithromycin (if IgE not elevated)


• Topical steroids


• Saline douching


24.6.4 Adults with CRS without NPs Postop


(There is a paucity of data to support postoperative management)


• Oral antibiotics for 1 to 2 weeks if pus seen, but long-term ABx also recommended


• Topical steroids


• Short-term oral steroids


• Nasal douching


24.6.5 Adults with CRS with NPs (Fig. 24.2)


• Oral ABx >12/52 for late relapse—consider doxycycline


• Topical/oral steroids—as guided by VAS


• Nasal douche


• Oral antihistamine—if atopic


24.6.6 Adults with CRS With NPs Postop


• As for CRSsNPs postop


24.6.7 Children with CRS (Fig. 24.3)


• Oral ABx


• Topical steroids


• Saline douching


• PPI


24.7 Future Research Needs and Priorities


• Consider the role of:


figure Socio-economic status


figure Severity staging with respect to QoL


figure Prognostic Sx in primary care


figure Endotyping and phenotyping—including how to assess this and the impact upon management and outcomes


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Jul 4, 2016 | Posted by in OTOLARYNGOLOGY | Comments Off on European Position Paper on Rhinosinusitis and Nasal Polyps

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