Chronic Rhinosinusitis (CRS)
1. Definition: inflammation of the nose and paranasal sinuses lasting > 12 weeks, with ≥2 symptoms, one of which must be nasal obstruction or nasal discharge ±
Facial pain/pressure
Reduced smell
, PLUS objective findings on endoscopy or CT.
Two major phenotypes:
- CRSsNP – chronic rhinosinusitis without nasal polyps
- CRSwNP – chronic rhinosinusitis with nasal polyps
Etiopathogenesis
CRS is a complex syndrome, not simply a prolonged infection, driven by a cycle of inflammation, impaired drainage, and microbial involvement.
Key Mechanisms
- 1. Ostial Obstruction and Mucociliary Dysfunction: Similar to ARS, failure of the Ostio-Meatal Complex (OMC) to drain due to structural or mucosal swelling is key. In CRS, the damage to the mucociliary escalator becomes chronic, leading to persistent stasis.
- 2. Biofilm Formation: Bacteria (often S. aureus, P. aeruginosa) can exist in protective biofilms on the sinus mucosa. These biofilms are highly resistant to antibiotics and host defenses, contributing to chronic inflammation.
- 3. Immune and Inflammatory Dysregulation:
- TH2 Endotype (Typical in CRSwNP): Characterized by high levels of TH2 cytokines (IL-4, 5, 13), recruitment of eosinophils, and high IgE levels, leading to polyp formation. Often seen with asthma and AERD.
- TH1/Neutrophilic Endotype (Typical in CRSsNP): Characterized by neutrophilic inflammation and a less prominent allergic/eosinophilic component.
Predisposing Factors
- Allergic Rhinitis
- Asthma (Strong association)
- Aspirin-Exacerbated Respiratory Disease (Samter's Triad: asthma + nasal polyps + aspirin intolerance)
- Immunodeficiencies (eg, CVID, IgA deficiency)
- Cystic Fibrosis (CF)
- Systemic vasculitis (eg, Granulomatosis with Polyangiitis - GPA)
- Anatomical defects (eg, septal deviation, concha bullosa).