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; ≥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