• Rhinosinusitis is one of the most common conditions seen in primary care and ENT clinics worldwide
• Acute rhinosinusitis (ARS) affects approximately 6–15% of the general population annually
• Chronic rhinosinusitis (CRS) affects approximately 5–12% of the general population in Western countries
• It is a leading reason for antibiotic prescriptions (often inappropriately, as most cases are viral)

• Highest incidence in adults = Age 45–64
• Highest incidence in children = Age 4–7
• ARS is less common in children younger than 2 years old — the sinus ostia are larger relative to the body of the sinus in younger children, making obstruction less likely
• In the very young, viral antecedent infection predisposes more to acute otitis media (AOM) than rhinosinusitis, partly because antibiotics given for AOM may prevent the evolution toward bacterial rhinosinusitis

• In Hong Kong's subtropical climate, year-round viral URTIs are common, sustaining a high incidence of acute rhinosinusitis
• Allergic rhinitis is extremely prevalent in Hong Kong (estimated 25–40% of the population), and this is a major predisposing factor for both acute and chronic rhinosinusitis
• Air pollution (particularly PM2.5 and NO₂ in urban areas) is recognized as a contributor to mucosal inflammation and CRS
• Nasopharyngeal carcinoma (NPC), which is endemic in Southern China/Hong Kong, can present with nasal symptoms and must be considered in the differential diagnosis of unilateral nasal obstruction with blood-stained discharge (see DDx section later)

• Slight female preponderance in CRS
• ARS peaks in autumn and winter (coinciding with viral URTI season), though in Hong Kong there is a secondary peak during spring/summer influenza seasons

Predisposing factors (from CFB lecture slides) ^[1]:

• Anatomical: Deviated septum, Polyp, Tumour — these physically narrow or obstruct the ostiomeatal complex (OMC), preventing sinus drainage
• Dental root infection — the roots of the upper premolars and molars are in intimate proximity to the maxillary sinus floor; periapical infection can directly seed the sinus (odontogenic sinusitis accounts for ~10–12% of maxillary sinusitis cases)
• Foreign body (especially in children)
• Nasal packing (post-surgical)

• Upper respiratory tract infection ^[1] — the single most common predisposing factor for ARS
• Allergic rhinitis — chronic mucosal oedema narrows ostia
• Non-allergic rhinitis (e.g., vasomotor rhinitis)

• Congenital ^[1]:
  • Cystic fibrosis — abnormal CFTR leads to thick, dehydrated mucus with impaired mucociliary clearance; virtually all CF patients develop CRS with nasal polyps
  • Primary ciliary dyskinesia (PCD) / Kartagener syndrome — dynein arm defects cause immotile cilia → impaired clearance → chronic sinusitis, bronchiectasis, situs inversus (in Kartagener's)
  • Immune deficiencies (e.g., common variable immunodeficiency [CVID], selective IgA deficiency)

• Smoking (active and passive) — paralyses cilia, increases mucosal inflammation
• Immunocompromise — HIV, diabetes mellitus, chemotherapy, organ transplant recipients (especially predisposed to fungal sinusitis)
• GERD — reflux of acid can cause posterior pharyngeal and nasal mucosal inflammation
• Pregnancy — hormonal-mediated mucosal oedema
• Medications — overuse of topical nasal decongestants (rhinitis medicamentosa), cocaine use
• Swimming/diving — barotrauma to sinuses, contaminated water exposure
• Mechanical ventilation / nasogastric tubes — disrupt normal sinus drainage in ICU patients (nosocomial sinusitis)

• Air pollution, occupational dust/chemical exposure
• Dry or cold air (disrupts mucosal moisture barrier)
• Altitude changes / barotrauma (scuba diving, air travel)

The ostiomeatal complex is the functional unit of sinus ventilation and drainage. It is located in the lateral nasal wall at the level of the middle meatus and represents the common drainage pathway for the maxillary, anterior ethmoid, and frontal sinuses.

Key components:

• Middle turbinate
• Uncinate process
• Ethmoid infundibulum
• Hiatus semilunaris
• Ethmoid bulla
• Frontal recess

Why is the OMC so important? Because any process that causes mucosal swelling at the OMC (viral URTI, allergic rhinitis, polyps, anatomical variants) will obstruct drainage of all three anterior sinuses simultaneously. This is why sinusitis rarely involves a single sinus in isolation — it's usually a pan-sinusitis or at least multi-sinus involvement.

The normal sinus works as a self-cleaning system with three key components:

1. Patent ostia — allow ventilation and drainage
2. Mucociliary clearance — the pseudostratified ciliated columnar epithelium with goblet cells produces mucus that traps particles; cilia beat in a coordinated wave (~12–15 Hz) to propel mucus toward the natural ostia
3. Normal mucus composition — the two-layer system (watery sol layer for ciliary beating + viscous gel layer for trapping) must be maintained

When ANY of these three components fails, the stage is set for sinusitis.

• Lighten the skull — hollow cavities reduce skull weight
• Vocal resonance — contribute to voice quality
• Humidify and warm inspired air
• Shock absorption — protect the brain from facial trauma
• Nitric oxide production — sinus epithelium produces NO, which has antimicrobial and vasodilatory functions (important for pulmonary function)

Etiology (from CFB lecture slides) ^[1]:

• Bacterial: aerobic & anaerobic — S. pneumoniae, H. influenzae, M. catarrhalis, S. aureus, etc.
• Viral — Coronavirus, rhinovirus, etc.
• Fungal — Immunocompromised

• Defined as ≥4 episodes of ARS per year with interim symptom resolution
• Suggests an underlying predisposing factor (anatomical, allergic, immune)
• Warrants investigation: CT sinuses, allergy testing, immune workup (immunoglobulins, HIV)

The fundamental pathophysiology of sinusitis can be understood as a three-step vicious cycle:

1. Viral inoculation — virus deposits on nasal or conjunctival mucosa via direct contact or droplet/aerosol transmission
2. Viral attachment and entry — virus attaches to receptors on epithelial cells in the nasopharynx (e.g., rhinovirus binds ICAM-1)
3. Innate immune response — infected cells release pro-inflammatory cytokines (IL-1, IL-6, IL-8, TNF-α), which:
   • Attract polymorphonuclear neutrophils (PMNs) → these accumulate in nasal secretions
   • The colour of nasal discharge correlates with PMN content and enzymatic activity ^[3]:
     • White: small amount of PMNs
     • Yellow: increased PMNs
     • Green: increased PMNs with high PMN enzymatic activity (myeloperoxidase)
   • Colour of nasal discharge does NOT correlate with necessity of antibiotic use — coloured discharge is a normal, self-limited phase of an uncomplicated cold ^[3]
4. Increased vascular permeability — release of albumin and bradykinin causes mucosal oedema, rhinorrhoea, and sore throat
5. Viral rhinitis spreads to paranasal sinuses during nose blowing — nose blowing propels contaminated fluid from the nasal cavity into the sinuses (studies using contrast dye confirm this) ^[3]
6. Sinonasal hypersecretion and oedema → the combination of mucosal oedema, copious thickened secretions, and impaired mucociliary clearance results in sinus obstruction and perpetuates the disease process ^[3]
7. Resolution: in most cases, the immune response clears the virus within 7–10 days, mucosal swelling subsides, and normal drainage resumes

ABRS occurs most commonly as a complication of viral infection — it develops when bacteria secondarily infect an already inflamed sinus cavity ^[3].

The mechanism:

1. Viral-induced mucosal oedema obstructs the sinus ostia
2. Trapped secretions create a warm, moist, low-oxygen environment — ideal for bacterial growth
3. Impaired mucociliary clearance prevents bacterial clearance
4. Bacteria (from the normal nasal flora or introduced during nose blowing) proliferate
5. Bacterial infection causes further inflammation, neutrophil infiltration, and purulent exudate (empyema of the sinus)

ABRS can also be associated with conditions that obstruct the nose or impair local or systemic immune function (allergic rhinitis, anatomical abnormalities, immunodeficiency) ^[3].

CRS is not simply a prolonged acute infection. It represents a complex, multifactorial inflammatory disorder where the relative contributions of infection, mucosal immune dysregulation, and biofilm formation are debated.

Key pathophysiological concepts in CRS:

1. Persistent mucosal inflammation — even without active infection, the inflammatory process becomes self-perpetuating due to:

   • Osteitis (bone inflammation)
   • Mucosal remodelling (basement membrane thickening, goblet cell hyperplasia, subepithelial fibrosis)
   • Disrupted epithelial barrier function

2. Biofilm formation — bacteria form organized communities encased in a polysaccharide matrix that:

   • Are resistant to antibiotics (up to 1000× more resistant than planktonic bacteria)
   • Evade host immune responses
   • Periodically shed planktonic bacteria, causing acute exacerbations

3. Superantigen hypothesis (in CRSwNP) — staphylococcal superantigens (from S. aureus colonizing the sinuses) activate T cells polyclonally, driving a Th2-skewed eosinophilic inflammatory response → polyp formation

4. Aspirin-Exacerbated Respiratory Disease (AERD) / Samter's Triad / NERD ^[5]:

   • Asthma + CRSwNP + aspirin sensitivity = Samter's triad ^[5]
   • Pathophysiology: dysregulated arachidonic acid metabolism → overproduction of cysteinyl leukotrienes and underproduction of prostaglandin E₂ → chronic eosinophilic inflammation → nasal polyps and bronchoconstriction
   • Aspirin/NSAIDs inhibit COX-1, further shifting the balance toward leukotrienes → acute exacerbation
   • Breaking down the acronym: NERD = NSAID-Exacerbated Respiratory Disease (newer term); previously known as AERD

5. Fungal hypothesis — some propose that fungi in the sinuses elicit an exaggerated eosinophilic response in susceptible individuals; this is the basis for allergic fungal rhinosinusitis (AFRS)

The following features suggest complications or an alternative serious diagnosis and require urgent investigation:

Understanding referred pain patterns helps localize the affected sinus:

The pain is referred along branches of CN V:

• Maxillary sinus → CN V₂ (maxillary division)
• Frontal sinus → CN V₁ (ophthalmic division, supraorbital nerve)
• Ethmoid sinuses → CN V₁ (nasociliary nerve)
• Sphenoid sinus → CN V₁ and V₂

• Sinuses develop at different rates (maxillary and ethmoid present at birth; frontal and sphenoid develop later) → frontal sinusitis is rare before age 7–8
• Children have an average of 6–8 viral URTIs per year → more opportunities for ARS
• Clinical presentation may be less specific: chronic cough (especially nocturnal/post-nasal drip), irritability, halitosis, periorbital oedema
• Adenoid hypertrophy can obstruct the posterior nasal cavity and OMC, predisposing to sinusitis
• Cystic fibrosis and primary ciliary dyskinesia should be considered in children with recurrent/chronic sinusitis with or without nasal polyps

• Higher risk of invasive fungal sinusitis (Mucormycosis, Aspergillus)
• Atypical organisms more common (Pseudomonas, Gram-negatives, Nocardia)
• Clinical presentation may be muted (lack of fever, poor inflammatory response)
• Low threshold for imaging (CT sinuses) and tissue biopsy
• Aggressive surgical management often needed

• Mucociliary clearance declines with age → increased susceptibility
• Mucosal atrophy → dryness, crusting
• Often on multiple medications (e.g., anticholinergics that dry secretions)
• May present atypically (confusion, anorexia rather than classic symptoms)

NPC deserves special attention because of its endemic prevalence in Hong Kong and its ability to masquerade as chronic rhinosinusitis.

• Inverted papilloma — benign but locally aggressive; unilateral nasal obstruction, epistaxis; endoscopic appearance is papillomatous/cerebriform; risk of malignant transformation (~5–15%)
• Squamous cell carcinoma of the sinuses — rare; unilateral obstruction, pain, bloody discharge, facial swelling, infraorbital nerve (CN V₂) numbness
• Esthesioneuroblastoma (olfactory neuroblastoma) — arises from olfactory epithelium; unilateral obstruction, epistaxis, anosmia
• Lymphoma — nasal NK/T-cell lymphoma is more common in Asian populations; destructive midline lesion, nasal obstruction, epistaxis, facial swelling

Many patients with "sinus headache" actually have a primary headache disorder. Studies show that up to 80–90% of self-diagnosed or physician-diagnosed "sinus headache" is actually migraine ^[6].

Facial pain in DDx of headache: trigeminal neuralgia, herpes zoster, post-herpetic neuralgia, dental/TMJ diseases, sinusitis ^[6]

These are not "differential diagnoses" per se, but rather extensions/complications of sinusitis that change the clinical picture dramatically and must be recognized urgently.

This is arguably the most important clinical distinction because it determines whether antibiotics are indicated ^[2][3][4].

Differentiated from common cold by persistence, increased severity or worsening of symptoms ^[2]

This distinction is critical because orbital cellulitis is an ophthalmic emergency requiring IV antibiotics and often surgical drainage, while preseptal cellulitis is managed with oral antibiotics.

Orbital cellulitis is an ophthalmic emergency. It does NOT involve the globe itself. More common in young children. Most common cause is rhinosinusitis from ethmoid sinus via lamina papyracea. ^[9]

When a patient presents with chronic sinusitis as part of a multi-system pattern, consider these syndromic associations:

This is the standard used in HKUMed teaching and is directly from the CFB lecture slides:

Inflammation of the nose and the paranasal sinuses characterised by ≥2 symptoms, 1 of which should be either nasal blockage/obstruction/congestion or nasal discharge (anterior/posterior nasal drip), ± facial pain/pressure, ± reduction or loss of smell ^[1]

AND either:

• Endoscopic signs of nasal polyps, and/or mucopurulent discharge primarily from middle meatus and/or oedema/mucosal obstruction primarily in middle meatus
• AND/OR CT changes: mucosal changes within the ostiomeatal complex and/or sinuses ^[1]

Acute: < 12 weeks; Chronic: ≥12 weeks ^[1]

Criteria: sudden onset of ≥2 of (with ≥1 nasal symptom) ^[4][5]:

• Nasal blockage/congestion or nasal discharge PLUS
• Facial pain/pressure and/or ↓ or loss of smell ^[4][5]

This symptom-based definition is practical for primary care where endoscopy/CT is unavailable. It identifies ARS broadly (viral + bacterial).

The critical next step is determining whether ARS is viral (self-limiting, no antibiotics needed) or bacterial (may benefit from antibiotics). Three clinical patterns define acute bacterial rhinosinusitis (ABRS) ^[2][3]:

In contrast:

Acute viral rhinosinusitis: symptoms or signs of ARS < 10 days that are not worsening ^[2][3]

Some sources use a "scoring" approach. Criteria for bacterial rhinosinusitis: ≥3 of the following ^[4][5]:

1. Double sickening
2. Discoloured, purulent nasal discharge
3. Severe, localised pain
4. Fever > 38°C or ↑ESR/CRP ^[4][5]

These criteria complement the three clinical patterns above. They are useful for borderline cases where none of the three patterns is clearly met.

Same symptom criteria as ARS but lasting > 12 weeks ^[5], PLUS objective confirmation:

• Endoscopy: polyps, mucopurulent discharge from middle meatus, mucosal oedema
• AND/OR CT sinuses: mucosal thickening, opacification, air-fluid levels within the ostiomeatal complex and/or sinuses ^[1]

Why is objective confirmation required for CRS but not always for ARS? Because many conditions (migraine, tension headache, allergic rhinitis, TMJ dysfunction) cause chronic facial pressure/pain that patients self-diagnose as "sinus problems." Without endoscopic or radiological evidence of sinus disease, the diagnosis of CRS is unreliable. Studies show that up to 80–90% of patients labelled as having "chronic sinusitis" or "sinus headache" actually have migraine.

Anterior rhinoscopy findings:

• Diffuse mucosal oedema — inflammatory vasodilation and extravasation cause swollen, erythematous nasal mucosa
• Narrowing of middle meatus — oedematous uncinate process and middle turbinate encroach on the critical OMC drainage pathway
• Inferior turbinate hypertrophy — reactive mucosal engorgement; contributes to nasal obstruction
• Copious and purulent discharge — watery in viral/allergic; purulent (yellow-green) in bacterial/late viral, though colour alone is unreliable

Also look for:

• Co-existent anatomical risk factors: polyps, septal deviation ^[4][5]
• Crusting, ulceration, masses (→ think GPA, malignancy)
• Pale, boggy mucosa (→ think allergic rhinitis)

More informative than anterior rhinoscopy — the gold standard for visualising the middle meatus, OMC, sphenoethmoidal recess, and nasopharynx.

Key findings:

• Mucopurulent discharge from middle meatus (maxillary/anterior ethmoid/frontal sinuses) or sphenoethmoidal recess (posterior ethmoid/sphenoid)
• Polyps: grey-white, translucent, mobile, insensitive to pain
• Mucosal oedema/obstruction in the middle meatus ^[1]
• Masses: must visualise the nasopharynx (especially in HK — NPC screening)

Endoscopic signs of nasal polyps, and/or mucopurulent discharge primarily from middle meatus and/or oedema/mucosal obstruction primarily in middle meatus — one of the objective criteria in the EPOS 2020 definition ^[1]

Indicated in patients with symptoms of ear pain, fullness or pressure, hearing loss or tinnitus ^[2][3]. This evaluates for:

• Middle ear effusion (serous otitis media) — from Eustachian tube dysfunction secondary to rhinosinusitis
• Tympanic membrane retraction — negative middle ear pressure due to Eustachian tube obstruction
• Acute otitis media — coexisting or alternative diagnosis, especially in children

• Palpation and percussion of sinus areas (frontal, maxillary, ethmoidal) — tenderness supports sinusitis but is not diagnostic in isolation ^[4][5]
• Transillumination — opacification of maxillary/frontal sinus upon transillumination ^[4][5] — largely historical; low sensitivity and specificity
• Periorbital examination — oedema, erythema, proptosis, ophthalmoplegia → complications
• Oral cavity — dental caries, periapical tenderness → odontogenic sinusitis; palatal eschar → mucormycosis
• Neck — lymphadenopathy → NPC, lymphoma

The advent of biologic therapies has revolutionised the management of severe, recurrent CRSwNP refractory to conventional therapy. These are monoclonal antibodies targeting specific components of the Type 2 inflammatory pathway:

These biologics represent a paradigm shift — moving from blunt immunosuppression (oral steroids) to precision targeting of the specific inflammatory pathway. They are expensive and reserved for severe, refractory disease. However, for patients with Samter's triad or severe eosinophilic CRSwNP who have had multiple FESS procedures with polyp recurrence, biologics can dramatically improve quality of life.

Urgent consult ophthalmologist and ENT ^[9]:

In practice, should urgent consult ENT and do imaging first before consulting EYE. Reason: blindness from orbital cellulitis is NOT very common but patient might die from intracranial spread if underlying sinus infection not treated promptly ^[9].

Why vancomycin? Because MRSA is a concern in orbital/intracranial infections, and the consequences of inadequate coverage are devastating. Vancomycin covers MRSA and other resistant Gram-positives. Combined with a 3rd-gen cephalosporin (ceftriaxone) or β-lactam/β-lactamase inhibitor (tazocin/unasyn) for Gram-negative and anaerobic coverage.

Osteomyelitis of sinus bone ^[2][3]:

• Presents with gradual onset of dull pain at involved site with or without movement ^[2][3]
• Local findings such as erythema, swelling, warmth and tenderness may be present ^[2][3]
• Systemic symptoms such as fever, chills and rigors may be present ^[2][3]

Pott's puffy tumour ^[4][5]:

Why is Pott's puffy tumour important? Because its presence implies frontal bone osteomyelitis, which means the infection has already breached bone. In ~60% of cases, there is concurrent intracranial extension (epidural abscess, subdural empyema). Therefore, any patient with a puffy frontal swelling following sinusitis must have a CT with contrast that includes the brain.

The Chandler classification (1970) stages orbital complications in order of increasing severity:

Complicated sinusitis assessment (from CFB lecture slides) ^[1]:

• Present as orbital swelling/cellulitis
• Check colour vision — early sign of optic nerve compromise
• Check eye movement — ophthalmoplegia indicates post-septal disease
• Admission
• CT scan
• Urgent ophthalmologist assessment
• IV antibiotic and drainage

Why do orbital complications develop from sinusitis?

1. Anatomical proximity: The ethmoid sinus shares the lamina papyracea ("papyrus-like plate") with the orbit. This bone is:

   • Extremely thin (< 0.5 mm in places)
   • Perforated by multiple neurovascular foramina (anterior and posterior ethmoidal arteries and nerves)
   • Has natural dehiscences in up to 10% of the population

2. Routes of spread:

   • Direct erosion: infection literally erodes through the thin bone into the orbit
   • Valveless venous spread: the ethmoidal veins drain into the ophthalmic veins, which connect to the orbital venous plexus. These veins have no valves, meaning infected thrombophlebitis can propagate in any direction — anteriorly into the orbit or posteriorly into the cavernous sinus
   • Pre-existing dehiscences: natural gaps in the lamina papyracea provide a path of least resistance

3. Why children are more affected: The lamina papyracea is thinner in children, the ethmoid sinuses are the first to develop and pneumatise, and the pediatric immune system may mount a more exuberant (but initially less effective) inflammatory response.

Visual loss may occur due to optic neuritis or ischaemia due to compressive CRAO (central retinal artery occlusion) or orbital venous thrombophlebitis ^[9].

Mechanism:

• Increasing orbital pressure from abscess/inflammation compresses the optic nerve or its blood supply
• Central retinal artery occlusion → retinal ischaemia → irreversible visual loss within hours
• Optic neuritis → inflammatory demyelination of the optic nerve from direct extension of infection
• Orbital venous congestion → secondary ischaemia

This is why visual acuity, colour vision, pupil assessment (RAPD), and fundoscopy are essential in any patient with orbital complications — and why declining vision is an indication for immediate surgical drainage, even if the patient is on IV antibiotics.

Septic cavernous sinus thrombosis ^{[2][3][4][5][13]}. Presents with cranial nerve palsies and headache ^[2][3].

Structures within the cavernous sinus (and why CST causes specific signs):