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Home  /  FRACS ENT  /  Study notes  /  Rhinosinusitis and rhinitis

Rhinosinusitis and rhinitis

FRACS ENT LO FRACENT_RHINOLOGY_1 2,597 words
Free preview. This study note covers learning objective FRACENT_RHINOLOGY_1 from the FRACS ENT curriculum. Inside Primex you get AI-graded SAQ practice on this topic, voice viva with the AI examiner, MCQs across the full syllabus, and a curriculum tracker that ticks off every learning objective.

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:

And at least one objective confirmatory finding:

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

CRSwNP

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

Examination

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

Allergy and Immunology

Mucociliary Function

Microbiology


Medical Management

Stepwise Framework

Medical therapy is the foundation of CRS management. Surgery is indicated when adequate medical therapy fails.

First-line and maintenance:

  1. 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)
  2. 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
  3. Allergen avoidance and immunotherapy where allergy drives disease

Short-course systemic corticosteroids (CRSwNP):

Antibiotics:

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

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

Preoperative Preparation

Key Surgical Steps and Anatomy

Osteomeatal Complex anatomy (the surgical target):

Standard FESS sequence (anterior-to-posterior, medial-to-lateral):

  1. 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
  2. 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)
  3. 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
  4. 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
  5. 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
  6. 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

Balloon Sinus Dilation


Postoperative Care


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


Causes of FESS Failure

Systematic analysis before revision surgery:

  1. Residual or inadequately addressed disease: retained ethmoid partitions, missed cells (particularly frontal recess cells), incomplete uncinectomy
  2. Inadequate post-operative medical therapy: failure to maintain INCS, saline irrigation, or address allergy
  3. Anatomical failure: synechiae, lateralised middle turbinate, neo-ostium separate from natural ostium (mucociliary recirculation failure)
  4. Refractory underlying disease: severe AERD, uncontrolled asthma, aspirin sensitivity, immunodeficiency, PCD, or fungal disease
  5. Mucosal biofilm: methicillin-resistant S. aureus, Pseudomonas; consider topical antibiotics and culture-directed therapy

Special Populations and Considerations

Asthma and AERD

Immunodeficiency

Fungal Rhinosinusitis

Cystic Fibrosis

Paediatric CRS


Prognostic Factors and Outcome Measurement

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What is the minimum symptom duration required to diagnose chronic rhinosinusitis (CRS)?
  • Symptoms must persist for more than 12 weeks
  • Symptoms include nasal obstruction, anterior or posterior nasal discharge, facial pain/pressure, and reduction or loss of smell
  • Objective confirmation (endoscopy or CT) is required alongside symptoms
How is rhinosinusitis classified by duration?
  • Acute rhinosinusitis (ARS): symptoms lasting less than 4 weeks
  • Subacute rhinosinusitis: 4–12 weeks (not distinguished in all guidelines; managed individually)
  • Chronic rhinosinusitis (CRS): symptoms lasting more than 12 weeks
What are the two main clinical subtypes of CRS and their dominant inflammatory profiles?
  • CRS with nasal polyps (CRSwNP): Th2-biased eosinophilic inflammation
  • CRS without nasal polyps (CRSsNP): Th1-biased neutrophilic/fibrotic inflammation
  • Significant overlap in symptomatology and mucosal changes exists between subtypes
What objective findings on nasal endoscopy support a diagnosis of CRS?
  • Purulent mucus in the middle meatus or anterior ethmoid region
  • Mucosal oedema in the middle meatus or ethmoid region
  • Nasal polyps in the nasal cavity or middle meatus
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