Definition and Classification
Chronic rhinosinusitis (CRS) is symptomatic mucosal inflammation of the nose and paranasal sinuses persisting for 12 weeks or longer, confirmed by objective findings on nasal endoscopy or imaging. It is one of the most prevalent chronic conditions managed in otolaryngology practice and a leading cause of antibiotic prescription and quality-of-life impairment.
Diagnostic Criteria
At least two of the following four cardinal symptoms must be present:
- Nasal obstruction or blockage
- Nasal discharge (anterior or posterior, which may be purulent)
- Facial pain, pressure, or fullness
- Reduction or loss of sense of smell (hyposmia or anosmia)
And at least one objective confirmatory finding:
- Endoscopic evidence: purulent mucus in the middle meatus or ethmoid region, mucosal oedema, or nasal polyps
- CT evidence: mucosal thickening, sinus opacification, or bony remodelling
Phenotypic Classification
| Phenotype | Inflammatory Bias | Key Features |
|---|---|---|
| CRS without nasal polyps (CRSsNP) | Th1-predominant | Neutrophilic; less eosinophilia; more commonly associated with anatomical obstruction or infection |
| CRS with nasal polyps (CRSwNP) | Th2-predominant | Eosinophilic; type 2 cytokines (IL-4, IL-5, IL-13); associated with aspirin sensitivity and asthma |
| Aspirin-exacerbated respiratory disease (AERD) | Th2 + arachidonic pathway dysregulation | Samter's triad: CRSwNP + asthma + aspirin/NSAID sensitivity; severe phenotype |
Recurrent Acute vs Chronic
Patients with recurrent acute bacterial rhinosinusitis (RABS; $\geq 4$ episodes/year) are normal between episodes and should be distinguished from CRS patients, who have persistent baseline symptoms and objective sinonasal abnormality.
Pathophysiology
CRSsNP
- Predominantly driven by Th1 lymphocytes and innate immune activation
- Neutrophil-dominant infiltrate with IFN-$\gamma$ and IL-8 upregulation
- Disrupted mucociliary clearance promotes bacterial colonisation and biofilm formation
- Anatomical factors (e.g. septal deviation, concha bullosa, agger nasi hypertrophy) may perpetuate ostial obstruction
CRSwNP
- Type 2 inflammatory cascade driven by TSLP, IL-25, and IL-33 released from damaged sinonasal epithelium (epithelial alarmins)
- IL-5-driven eosinophil recruitment and survival; IgE synthesis via IL-4 and IL-13
- Polyps arise as oedematous prolapsed mucosa with eosinophilic stroma, originating most often in the ethmoid clefts and middle meatus
- Arachidonic acid metabolism dysregulation in AERD leads to leukotriene overproduction and prostaglandin E2 deficiency, causing mast cell activation on NSAID exposure
Final Common Pathway
Regardless of subtype, the osteomeatal complex (OMC) is the central anatomical bottleneck. Obstruction of the OMC impairs drainage of the maxillary, anterior ethmoid, and frontal sinuses, creating a microenvironment permissive to chronic infection and mucosal inflammation. Mucociliary clearance failure, biofilm formation, and microbial dysbiosis perpetuate this cycle.
Clinical Assessment
History
- Duration, severity, and pattern of cardinal symptoms
- Impact on quality of life (validated tools: SNOT-22 is standard)
- Identify comorbidities: asthma (unified airway), allergic rhinitis, AERD, immunodeficiency (recurrent sinusitis in multiple anatomical sites warrants investigation), cystic fibrosis, primary ciliary dyskinesia
- Drug history: aspirin/NSAIDs, topical decongestant overuse (rhinitis medicamentosa)
- Smoking and occupational exposures
- Previous sinus surgery: scarring, synechiae, lateralised middle turbinate
Examination
- Anterior rhinoscopy: mucosal oedema, secretions, septal deviation, polyps visible in anterior nasal cavity
- Nasal endoscopy (0° or 30° rigid endoscope, or flexible scope): essential for confirming diagnosis
- Assess middle meatus for polyps, purulent mucus, mucosal oedema
- Assess olfactory cleft in polyp cases
- Document Lund-Kennedy endoscopy score at baseline and post-treatment
- Systemic examination: chest (wheeze/prolonged expiration), skin (aspirin sensitivity, urticaria)
Endoscopic Staging of Polyps
| Grade | Description |
|---|---|
| 0 | No polyps |
| 1 | Polyps confined to middle meatus |
| 2 | Polyps extending beyond middle meatus but not causing complete obstruction |
| 3 | Polyps completely obstructing nasal cavity |
Investigation
Imaging
- CT paranasal sinuses (non-contrast axial + coronal reconstruction): gold standard for surgical planning
- Assess extent of disease: Lund-Mackay CT scoring system (0-2 per sinus/OMC; maximum 24)
- Identify anatomical variants: Onodi cells (risk to optic nerve), Haller cells (infraorbital ethmoid cells obstructing OMC), dehiscent lamina papyracea or carotid canal, low-lying skull base
- Note: CT is not the positive gold standard as asymptomatic mucosal thickening is common; correlation with clinical findings is mandatory
- MRI: reserved for suspected complications, orbital or intracranial extension, or when differentiating inflammatory from neoplastic disease (soft tissue characterisation)
Allergy and Immunology
- Skin prick testing or specific IgE for inhalant allergens (particularly relevant for CRSwNP with concurrent allergic rhinitis)
- Total IgE and eosinophil count (markers of type 2 disease; relevant to biologic eligibility)
- Immunoglobulin levels (IgG, IgA, IgM) if recurrent/refractory disease suggests humoral immunodeficiency
- Aspirin challenge or NSAID history to identify AERD
Mucociliary Function
- Saccharin transit time (screening for ciliary dysfunction)
- Nasal nitric oxide: markedly reduced in primary ciliary dyskinesia (PCD)
- Electron microscopy or high-speed video analysis of ciliary ultrastructure if PCD suspected
Microbiology
- Endoscopically directed middle meatal swabs are the standard method for non-invasive culture; diagnostic yield is superior to blind nasal swabs
- Sinus aspirate at time of surgery provides most reliable culture
- Common organisms: Staphylococcus aureus (dominant in CRSwNP), Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis; MRSA increasingly isolated
- Pseudomonas aeruginosa in post-surgical, cystic fibrosis, or immunocompromised patients
Medical Management
Stepwise Framework
Medical therapy is the foundation of CRS management. Surgery is indicated when adequate medical therapy fails.
First-line and maintenance:
- Intranasal corticosteroids (INCS): core therapy for all subtypes; reduces mucosal oedema and polyp burden; demonstrated efficacy on obstruction, discharge, and olfaction; multiple delivery methods (spray, drop [head-down-forward position for polyp disease], high-volume irrigation post-surgery)
- Saline nasal irrigation: large-volume isotonic or hypertonic saline (e.g. 240 mL rinse) improves mucociliary clearance, reduces mucosal oedema, and enhances drug delivery; superior to spray for drug penetration post-operatively
- Allergen avoidance and immunotherapy where allergy drives disease
Short-course systemic corticosteroids (CRSwNP):
- Prednisolone oral course (typically 25-50 mg/day, 5-14 days): rapid reduction in polyp bulk; used pre-operatively to improve surgical field, reduce intraoperative bleeding, and confirm steroid responsiveness
- Perioperative systemic steroids (pre- and short post-operative course) reduce intraoperative bleeding and early recurrence
Antibiotics:
- Acute exacerbations: guided by culture where possible; amoxicillin-clavulanate standard empirical choice for ABRS
- Long-term low-dose macrolides (e.g. roxithromycin 150 mg daily for 12 weeks): anti-inflammatory and immunomodulatory properties; evidence in CRSsNP and CRSwNP without marked eosinophilia; benefit in biofilm disruption
- Topical antibiotics (e.g. mupirocin irrigation for MRSA biofilm): evidence emerging
Leukotriene receptor antagonists: adjunct in AERD and CRSwNP with asthma
Biologic Therapies (CRSwNP)
Indicated for severe CRSwNP inadequately controlled despite maximal medical therapy and ESS. Eligibility criteria are defined by national criteria and include bilateral polyp disease, significant symptom burden, and criteria for type 2 inflammation (elevated total IgE, blood or tissue eosinophilia, comorbid asthma/AERD).
| Agent | Target | Mechanism | Notes |
|---|---|---|---|
| Dupilumab | IL-4R$\alpha$ (blocks IL-4 and IL-13 signalling) | Anti-type 2 inflammation | First-line biologic; robust Phase 3 evidence; also approved for asthma and atopic dermatitis; PBS-listed in Australia for severe CRSwNP |
| Mepolizumab | IL-5 | Reduces eosinophil survival | TGA-approved for CRSwNP |
| Benralizumab | IL-5R$\alpha$ | Eosinophil depletion via ADCC | Evidence from Phase 3 trials |
| Omalizumab | IgE | Blocks free IgE | Benefit in high IgE, allergic comorbidity |
Biologics do not replace surgery but can serve as a bridge, alternative, or post-surgical adjunct. Duration of therapy and criteria for cessation are evolving.
Surgical Management: Functional Endoscopic Sinus Surgery (FESS)
Indications
- CRS with objective disease refractory to adequate medical therapy
- Anatomical obstruction not amenable to medical treatment
- CRS with orbital or intracranial complications (semi-urgent/urgent)
- Fungal rhinosinusitis (allergic or invasive)
- Mucocele causing orbital or intracranial pressure
- Sinonasal neoplasm (diagnostic or therapeutic)
No consensus exists on the minimum duration of "adequate" medical therapy, but most guidelines recommend at least 12 weeks of appropriately delivered INCS and saline irrigation before surgery is considered. Evidence suggests earlier surgery in patients with established disease may improve quality-of-life outcomes compared with prolonged deferral.
Goals of FESS
- Remove obstructing tissue around natural sinus ostia to restore ventilation and drainage
- Eliminate irreversibly diseased mucosa and infected bone while preserving functional mucosa
- Create a surgically accessible sinus cavity that allows topical drug delivery and surveillance endoscopy
- FESS is not curative for CRS; it optimises the environment for ongoing medical therapy
Preoperative Preparation
- CT planning: reviewed on the day of surgery; identify high-risk anatomy (low skull base, Onodi cells, dehiscent carotid/optic nerve, asymmetric skull base)
- Optimise medical therapy preoperatively: systemic steroids in CRSwNP to reduce vascularity and improve visualisation
- Counsel on risks, realistic expectations, and the need for lifelong medical maintenance and surveillance
- Consent for: bleeding, infection, orbital injury (diplopia, blindness), skull base violation (CSF leak, meningitis, intracranial injury), anosmia, dental/lacrimal injury, failure and recurrence
Key Surgical Steps and Anatomy
Osteomeatal Complex anatomy (the surgical target):
- The OMC is the functional drainage unit of the anterior sinuses (maxillary, anterior ethmoid, frontal) and is situated in the middle meatus
- Bounded medially by the middle turbinate, laterally by the lamina papyracea, superiorly by the anterior skull base
- Components: uncinate process, infundibulum, hiatus semilunaris, ethmoidal bulla, and natural maxillary ostium
Standard FESS sequence (anterior-to-posterior, medial-to-lateral):
- Uncinectomy: removal of the uncinate process; the key initial step that exposes the infundibulum and natural maxillary ostium; the medial orbital wall (lamina papyracea) is the lateral boundary; risk: entry into orbit if uncinectomy directed too laterally
- Maxillary antrostomy: enlargement of the natural ostium posteroinferiorly into the posterior fontanelle; the nasolacrimal duct is at risk anteriorly; do not create a counter-opening in the posterior fontanelle separate from the natural ostium (failure of mucociliary recirculation)
- Anterior ethmoidectomy: systematic removal of anterior ethmoid air cells; the ground lamella (basal lamella of the middle turbinate) separates anterior from posterior ethmoid; skull base risk: anterior ethmoid artery marks the anterior skull base; dehiscence or variation in skull base height increases perforation risk
- Posterior ethmoidectomy: removal of posterior ethmoid cells posterior to the ground lamella; the sphenoid face is the posterior boundary; optic nerve risk: Onodi cells (sphetoethmoid cells) contain the optic nerve in their lateral wall
- Sphenoidotomy: opening of the sphenoid face inferomedially, enlarging the natural ostium; the optic nerve, internal carotid artery, and cavernous sinus are in the lateral sphenoid wall and are at risk with aggressive lateral dissection
- Frontal sinusotomy (Draf I/IIa/IIb/III): the frontal recess is the most technically demanding region; bounded anteriorly by the agger nasi cell, posteriorly by the ethmoid roof and skull base, medially by the middle turbinate, laterally by the lamina papyracea; Draf III (modified Lothrop) creates a common frontal drainage tract in refractory frontal disease
Powered Instrumentation
- Microdebrider (oscillating shaver): precise soft-tissue removal while preserving mucosa; reduces bleeding
- Image guidance (electromagnetic or CT-based intraoperative navigation): useful in revision surgery, obliterated landmarks, or high-risk anatomy; does not replace anatomical knowledge or eliminate risk
Balloon Sinus Dilation
- Office-based or intraoperative adjunct for CRSsNP without significant polyposis
- Dilates ostia without mucosal removal; preserves mucosa and bone
- Best evidence in frontal, maxillary, and sphenoid ostia in RABS and mild-moderate CRSsNP
- Not appropriate for CRSwNP requiring polyp removal or significant ethmoidectomy
Postoperative Care
- Debridement and surveillance endoscopy: critical for success; weekly for 4-6 weeks post-operatively; removes crusting, fibrin, and early synechiae under local anaesthetic in clinic
- Topical therapy resumption: INCS irrigation (e.g. budesonide 1 mg in 240 mL saline) commenced from week 1-2 post-operatively; high-volume delivery to the post-surgical cavity is significantly more effective than sprays
- Systemic corticosteroids: short post-operative course (5-10 days prednisolone) in CRSwNP reduces early mucosal recurrence and re-polyposis
- Long-term maintenance: INCS and saline irrigation indefinitely; re-institute systemic steroids for acute exacerbation or polyp recurrence; consider macrolides in non-eosinophilic subtype
- Biologic commencement or continuation post-FESS in eligible severe CRSwNP
Complications of FESS
Intraoperative
| Complication | Mechanism | Management |
|---|---|---|
| Orbital fat herniation | Lamina papyracea breach | Cease dissection laterally; do not cauterise fat; monitor for haematoma |
| Orbital haematoma | Anterior ethmoid artery injury or direct orbital entry | Immediate recognition; orbital decompression (lateral canthotomy/cantholysis) if vision compromised; ophthalmology involvement |
| CSF rhinorrhoea | Skull base perforation (cribriform plate/ethmoid roof) | Intraoperative repair with free graft (fat, fascia, mucosa) or pedicled flap; post-operative lumbar drain if high-flow |
| Major bleeding | Internal carotid or anterior ethmoid artery injury | Packing, nasal tamponade; vascular surgery/interventional radiology for carotid injury; mortality risk |
Postoperative
- Synechiae and adhesion formation: between middle turbinate and lateral wall; prevented by careful mucosal preservation and early debridement
- Middle turbinate lateralisation: obstructs surgical cavity; prevention by middle turbinate suture or partial resection
- Frontal recess stenosis: most common cause of frontal sinusitis failure post-FESS; requires revision Draf IIb/III
- Anosmia: injury to olfactory mucosa in the olfactory cleft; a recognized consent item
- Recurrence of polyps: universal in severe phenotypes; managed with escalated medical therapy and revision FESS if indicated
- Empty nose syndrome: rare, following overly aggressive inferior turbinectomy; paradoxical nasal obstruction with patent airway; difficult to treat
Causes of FESS Failure
Systematic analysis before revision surgery:
- Residual or inadequately addressed disease: retained ethmoid partitions, missed cells (particularly frontal recess cells), incomplete uncinectomy
- Inadequate post-operative medical therapy: failure to maintain INCS, saline irrigation, or address allergy
- Anatomical failure: synechiae, lateralised middle turbinate, neo-ostium separate from natural ostium (mucociliary recirculation failure)
- Refractory underlying disease: severe AERD, uncontrolled asthma, aspirin sensitivity, immunodeficiency, PCD, or fungal disease
- Mucosal biofilm: methicillin-resistant S. aureus, Pseudomonas; consider topical antibiotics and culture-directed therapy
Special Populations and Considerations
Asthma and AERD
- Aspirin desensitisation following ESS reduces polyp recurrence rate and systemic asthma events; requires specialist input
- Asthma optimisation pre-operatively is essential; severe asthma is a risk factor for general anaesthesia
Immunodeficiency
- IgG subclass deficiency, common variable immunodeficiency, and specific antibody deficiency cause recurrent sinusitis; immunoglobulin replacement therapy may reduce surgical frequency
- HIV, haematological malignancy, and transplant patients have higher risk of fungal rhinosinusitis
Fungal Rhinosinusitis
- Allergic fungal rhinosinusitis (AFS): type 1 hypersensitivity to fungi; thick "peanut butter" eosinophilic mucin; characteristically unilateral with heterogeneous CT density; elevated total IgE and fungal-specific IgE; surgical clearance plus prolonged INCS; consider immunotherapy
- Invasive fungal sinusitis: life-threatening; immunocompromised host; Aspergillus or mucormycosis; black necrotic mucosa on endoscopy; urgent surgical debridement plus systemic antifungal therapy; high mortality
Cystic Fibrosis
- CRS universal in CF; Pseudomonas and S. aureus colonisation; FESS primarily to reduce lower airway bacterial burden
- Modified surgical approach: address nasal polyps but avoid aggressive turbinate surgery
Paediatric CRS
- Less common than in adults; exclude adenoid hypertrophy (often first-line adenoidectomy)
- CT radiation concerns: limit use; treat medically longer before surgical commitment
- FESS technique modified: conservative uncinectomy and antrostomy; avoid skull base and frontal recess dissection in young children due to immature anatomy
Prognostic Factors and Outcome Measurement
- SNOT-22 (Sino-Nasal Outcome Test): 22-item validated patient-reported outcome; domain scores for nasal, ear/facial, sleep, and psychological; the standard outcome measure for research and clinical audit
- Lund-Kennedy endoscopy score and Lund-Mackay CT score: objective measures for disease severity and surgical planning
- Factors associated with poorer surgical outcome: asthma, AERD, higher pre-operative CT scores, smoking, immunodeficiency, revision surgery, inadequate post-operative care
- ESS provides durable improvement in quality of life in most patients; long-term results require maintained medical therapy and endoscopic surveillance