24 European Position Paper on Rhinosinusitis and Nasal Polyps • Rhinosinusitis: Nasal blockage/obstruction/congestion or nasal discharge + at least one of: – Facial pain/pressure – Hyposmia/anosmia In addition, endoscopic and/or CT changes required to confirm symptoms above of acute rhinosinusitis (ARS)/chronic rhinosinusitis (CRS) <12 weeks = acute >12 weeks = chronic Symptom-free intervals (complete resolution) but >12 weeks in total = recurrent acute <10 days = common cold (viral upper respiratory tract infection, i.e., URTI) Increase in Sx after 5 days OR persistence of Sx after 10 days = non-viral ARS 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: ARS: – 8.4% of Dutch population suffer with ≥ 1 episode of ARS/year – Fifth most common reason for ABx prescription in the United States 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) • Bacterial superinfection of virally damaged mucosa: 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 • 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: Bacteria—pathogens or colonizers? – S. aureus (36%) – Coagulase–ve staphylococcus (20%) – Streptococcus pneumoniae (17%) Fungi—colonize only or promoters of allergic/eosinophilic response? • Osteitis—animal studies only—may explain resistance to ABx • Environmental: Smoking Low income Atmospheric pollutants—no convincing evidence • Iatrogenic: Mucoceles associated with previous ESS Recirculation of mucus from natural to surgical ostia • Helicobacter pylori and LPR—DNA detected in 11 to 33% of CRS patients—causal? • 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: 14 to 52% have +ve family history Twin studies do not show that both develop NPs HLA associations, e.g., A74, DR7 Gene polymorphisms Multiple gene expressions for immune modulation Cystic fibrosis • Environmental factors—unclear • 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 • 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 • Neutrophils predominate • Small numbers of eosinophils, mast cells, basophils • Mucosal changes: BM thickening Goblet cell hyperplasia Subepithelial oedema 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) • 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: IL-5 and IgE = CRS with NPs (TH2) 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 • Endoscopy • Endoscopic-guided nasal swabs—87% accurate • CT scan (± MRI where neoplasia suspected) • Lund–Mackay scoring system for CT: 0 to 2 score for each of maxillary, ant. ethmoid, post. ethmoid, sphenoid, frontal Score of 0 or 2 for OMCs 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: LRT = <20 ppb Nose = 400 to 900 ppb 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. • Oral ABx—after 5/7 • Topical corticosteroid • Oral corticosteroid—if severe to reduce pain • Oral antihistamine—if atopic • Decongestant • Oral antibiotics—after 5/7 • Topical corticosteroids • Saline douching • Long-term ABx (>12/52)—low-dose macrolide, e.g., clarithromycin (if IgE not elevated) • Topical steroids • Saline douching (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 • Oral ABx >12/52 for late relapse—consider doxycycline • Topical/oral steroids—as guided by VAS • Nasal douche • Oral antihistamine—if atopic • As for CRSsNPs postop • Oral ABx • Topical steroids • Saline douching • PPI • Consider the role of: Socio-economic status Severity staging with respect to QoL Prognostic Sx in primary care Endotyping and phenotyping—including how to assess this and the impact upon management and outcomes
24.1 Definitions
24.2 Aetiology
24.2.1 Acute Rhinosinusitis
24.2.2 Chronic Rhinosinusitis without Polyps
24.2.3 Chronic Rhinosinusitis with Nasal Polyps
24.3 Children
24.4 Inflammatory Mechanisms
24.4.1 Acute Rhinosinusitis
24.4.2 CRS without NPs
24.4.3 CRS with NPs
24.5 Investigations
24.6 Recommended Treatment Regimes
24.6.1 Adults with ARS
24.6.2 Children with ARS
24.6.3 Adults with CRS without NPs (Fig. 24.1)
24.6.4 Adults with CRS without NPs Postop
24.6.5 Adults with CRS with NPs (Fig. 24.2)
24.6.6 Adults with CRS With NPs Postop
24.6.7 Children with CRS (Fig. 24.3)
24.7 Future Research Needs and Priorities
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European Position Paper on Rhinosinusitis and Nasal Polyps
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