Inflammation of the nasal cavity and paranasal sinuses, typically presenting with nasal congestion, purulent discharge, facial pain, and reduced sense of smell.

Exam domain	One-glance essentials
Definition / diagnosis	*EPOS 2020: ≥2 symptoms (≥1 must be nasal blockage/obstruction OR nasal discharge), ± facial pain/pressure, ± hyposmia; AND endoscopic signs or CT changes (required for CRS, not ARS)* ^[1]^[2] Acute (<12 wk) vs Chronic (≥12 wk); CRS subdivided into CRSsNP (~2/3, neutrophilic) and CRSwNP (~1/3, eosinophilic) ^[3]^[4] *Nasal polyps = grey-white, mobile, painless* vs swollen turbinate = pink, fixed, tender — key clinical distinction on exam ^[3]
Epidemiology / risks	Vast majority viral; only 0.5–2% of viral URTIs progress to bacterial ARS (S. pneumoniae, H. influenzae, M. catarrhalis) ^[5]^[4] *Predisposing factors: deviated septum, nasal polyps, tumour, dental root infection, URTI, congenital (CF/PCD), immunocompromised* ^[3]^[6] Unilateral nasal symptoms in HK must raise suspicion for NPC (endemic in southern China) and NK/T-cell lymphoma ^[7]^[8]
Core mechanism	Vicious cycle: trigger → mucosal oedema → OMC obstruction → impaired mucociliary clearance → mucus stasis → bacterial colonisation → more inflammation ^[4]^[5] *Coloured nasal discharge ≠ bacterial infection; it reflects PMN content — not an indication for antibiotics alone ^[5]^[4] Double sickening* = initial viral improvement then worsening at day 5–7 → hallmark suggesting bacterial superinfection of ARS ^[9]^[10]
Clinical picture	Nasal blockage, purulent anterior/posterior discharge, facial pain/pressure (worse on bending), hyposmia; ± fever, halitosis, dental pain ^[3]^[2] ABRS criteria: ≥3 of 4 — double sickening, purulent discharge, severe localised pain, fever >38°C or ↑ESR/CRP; OR symptoms persistent ≥10 days / severe onset ≥3–4 days ^[9]^[10] Red flags for complicated sinusitis: proptosis, ophthalmoplegia, ↓vision, periorbital swelling, meningism, frontal (doughy) swelling, altered consciousness ^[11]^[12] Samter's triad: asthma + CRSwNP + aspirin sensitivity — suspect in recurrent CRS with polyps ^[4]^[13]
Investigations	Diagnosis of uncomplicated ARS is clinical — no investigations needed; sinus XR has poor sensitivity/specificity → NOT recommended ^[2]^[4] CT sinuses (without contrast) = preferred imaging for CRS workup/pre-op; findings: air-fluid levels, mucosal thickening, OMC obstruction, bone erosion (red flag) ^[4]^[5] CT with contrast for suspected complications (orbital/intracranial); MRI for soft tissue detail, tumour staging, intracranial extension ^[12]^[14] Do NOT CT during acute URTI — up to 40% incidental mucosal thickening → false positives; endoscopic culture for C/ST only if complications or treatment failure ^[4]^[15]
Management	*Viral ARS: supportive Tx × 7–14 days — regular analgesia, nasal saline irrigation, nasal decongestants (≤5–7 days to avoid rhinitis medicamentosa), ± intranasal steroids* ^[10]^[16] *ABRS: above + oral antibiotics × 5–10 days; first-line = amoxicillin; only ~2% of viral ARS becomes bacterial yet antibiotics prescribed >85% of the time ^[10]^[15] CRS: predominantly anti-inflammatory — intranasal corticosteroids + nasal saline irrigation long-term; FESS after failure of maximal medical therapy × 8–12 weeks* ^[13]^[16] *Complicated sinusitis: admission, CT with contrast, IV antibiotics, urgent ophthalmology/ENT/neurosurgery referral, surgical drainage if abscess* ^[12]^[11]
Complications	*Orbital (most common): Chandler stages I–V — preseptal cellulitis → orbital cellulitis → subperiosteal abscess → orbital abscess → cavernous sinus thrombosis* ^[11]^[17] *Intracranial: meningitis, epidural abscess, subdural empyema, brain abscess, septic cavernous sinus thrombosis* ^[11]^[14] *Pott's puffy tumour: frontal osteomyelitis + subperiosteal abscess in adolescents — doughy forehead swelling; always evaluate for intracranial extension ^[17]^[14] Assess colour vision + eye movement* in all complicated sinusitis; CN VI affected first in cavernous sinus thrombosis; bilateral orbital signs = hallmark of CST ^[12]^[18]
Prevention / follow-up	Antibiotic stewardship: do not prescribe antibiotics for viral ARS; routine antibiotics do NOT prevent development of complications ^[10]^[15] Limit topical nasal decongestants to ≤5–7 days to prevent rhinitis medicamentosa; avoid NSAIDs in AERD/Samter's triad ^[16]^[4] CRS recurrence prevention: long-term intranasal corticosteroids + daily saline irrigation; post-FESS topical therapy to maintain sinus drainage ^[13]^[16]
Exam traps	~90% of self-diagnosed "sinus headache" is actually migraine — migraine can cause nasal congestion via parasympathetic activation but does NOT cause purulent discharge ^[19]^[4] *Unilateral nasal symptoms in HK* ≠ simple rhinosinusitis until NPC, NK/T-cell lymphoma, inverted papilloma, and fungal ball are excluded ^[7]^[8] Preseptal vs orbital cellulitis: ophthalmoplegia is the key discriminator — orbital cellulitis is an ophthalmic emergency requiring urgent CT with contrast and IV antibiotics ^[18]^[12] CT during acute URTI → 40% false-positive mucosal thickening; imaging should be deferred to avoid misdiagnosis of CRS ^[4]^[5]

References

^[1] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf (Rhinosinusitis definition, slide 14) ^[2] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Diagnostic criteria ARS, p.137); MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (Diagnostic criteria ARS, p.113) ^[3] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf (Rhinosinusitis section, slides 14–15) ^[4] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Sinusitis/Rhinosinusitis, p.133–135); MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (Sinusitis/Rhinosinusitis, p.109) ^[5] Senior notes: Ryan Ho Respiratory.pdf (Rhinosinusitis, p.54); Adrian Lui Pediatrics Notes.pdf (p.158–159) ^[6] Senior notes: Maksim Medicine Notes.pdf (Bronchiectasis — PCD, Kartagener's, CF, Young's syndrome, p.301–303); MBBS Final MB (Medicine) (Felix PY Lai).pdf (Bronchiectasis, p.181) ^[7] AOS material: AOS - Pathology.pdf (NK/T-cell lymphoma, p.26); Lecture slides: GC 215. Common nasal conditions and nasopharyngeal carcinoma.pdf (CRS clinical features, p.23) ^[8] Senior notes: Adrian Lui Pediatrics Notes.pdf (URTI spectrum and differential diagnoses, p.154) ^[9] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Diagnostic criteria ARS, p.137–139); MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (Diagnostic criteria ARS, p.113) ^[10] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf (Acute rhinosinusitis treatment, slide 16) ^[11] Lecture slides: GC 215. Common nasal conditions and nasopharyngeal carcinoma.pdf (Acute bacterial rhinosinusitis complications, p.22) ^[12] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf (Complicated sinusitis management, slides 18–19) ^[13] Senior notes: Adrian Lui Pediatrics Notes.pdf (Chronic rhinosinusitis, p.159) ^[14] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Complications of ARS, p.138–140); MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (Complications of ARS, p.114) ^[15] Senior notes: Ryan Ho Respiratory.pdf (Rhinosinusitis, p.54); Adrian Lui Pediatrics Notes.pdf (p.159) ^[16] Senior notes: Ryan Ho Respiratory.pdf (Rhinosinusitis management, p.54); Adrian Lui Pediatrics Notes.pdf (p.159) ^[17] Senior notes: Ryan Ho Respiratory.pdf (Rhinosinusitis complications, p.54); Adrian Lui Pediatrics Notes.pdf (Rhinosinusitis complications, p.158) ^[18] Senior notes: Ryan Ho Opthalmology.pdf (Orbital cellulitis, p.37) ^[19] Senior notes: Ryan Ho Neurology.pdf (Headache differentials, p.58)

Rhinosinusitis

Rhinosinusitis refers to symptomatic inflammation of the nasal cavity and paranasal sinuses. The name itself tells the story: "rhino" (Greek: nose) + "sinus" (Latin: cavity/hollow) + "itis" (Greek: inflammation). The combined term is preferred because isolated sinusitis virtually never occurs — the nasal mucosa and sinus mucosa form a continuous respiratory epithelium, so inflammation in one invariably involves the other ^[1]^[2]^[3].

"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" — EPOS 2020, as cited in GC lecture slides ^[1].

High Yield – EPOS 2020 Definition (from GC/CFB Lecture Slides)

The definition used at HKUMed follows the European Position Paper on Rhinosinusitis and Nasal Polyps (EPOS) 2020 criteria. The in-house exam may ask you to define rhinosinusitis using these exact symptom criteria. Remember: at least 1 of the 2 symptoms must be nasal blockage or nasal discharge ^[1].

2. Epidemiology

Acute rhinosinusitis (ARS) is one of the most common conditions encountered in primary care worldwide, affecting approximately 6–15% of the population annually.
Most cases begin as viral upper respiratory tract infections (URTIs); only 0.5–2% of viral URTIs develop secondary bacterial rhinosinusitis ^[3].
Adults average 2–5 viral URTIs per year; children average 6–8 per year. A proportion of these develop into clinical rhinosinusitis.
Chronic rhinosinusitis (CRS) prevalence: ~5–12% of the general population (self-reported symptoms); prevalence confirmed by endoscopy or CT is lower (~3–6%).

Highest incidence in adults: age 45–64 ^[2].
Highest incidence in children: age 4–7 ^[2].
ARS is less common in children < 2 years and older children because:
- In younger children, sinus ostia are larger relative to the sinus body, so obstruction is less likely ^[2].
- In very young children, viral URTI more commonly causes acute otitis media (AOM) rather than rhinosinusitis, and early antibiotic treatment for AOM may prevent evolution to rhinosinusitis ^[2].

Hong Kong has a subtropical climate with high humidity, high air pollution (particulate matter, NO₂), and dense living conditions — all contributing to a higher burden of both allergic rhinitis and rhinosinusitis.
Allergic rhinitis prevalence in HK is ~25–40% in the general population, representing the most common predisposing factor for rhinosinusitis locally.
Fungal rhinosinusitis is relatively uncommon in immunocompetent individuals in HK, but invasive fungal sinusitis (e.g., mucormycosis, aspergillosis) must be considered in immunocompromised patients (haematological malignancies, uncontrolled diabetes, transplant recipients).
Nasopharyngeal carcinoma (NPC), which is endemic in southern China/HK, can present with nasal obstruction mimicking CRS — always consider NPC in the differential of unilateral nasal symptoms in this population.

3. Risk Factors

Understanding the risk factors requires understanding what disrupts normal sinus physiology (mucociliary clearance, ostial patency, local immunity):

Factor	Mechanism
Deviated nasal septum	Narrows the ostiomeatal complex (OMC), impairing sinus drainage ^[1]
Nasal polyps	Physical obstruction of sinus ostia → mucus retention → secondary infection ^[1]
Nasal/sinus tumours	Obstruct drainage; also NPC in HK context ^[1]
Concha bullosa (pneumatised middle turbinate)	Narrows middle meatus → impaired drainage
Haller cells (infraorbital ethmoid cells)	Narrow the maxillary sinus ostium
Dental root infection	Maxillary sinus floor is closely related to premolar/molar roots → odontogenic sinusitis (up to 10–12% of CRS cases) ^[1]
Foreign body	Unilateral obstruction → secondary infection (especially in children)

Factor	Mechanism
Upper respiratory tract infection (URTI)	Viral-induced mucosal oedema → ostial obstruction → impaired mucociliary clearance → bacterial superinfection ^[1]^[3]
Allergic rhinitis	Chronic mucosal inflammation and oedema → ostial narrowing
Non-allergic rhinitis (e.g., vasomotor)	Chronic mucosal congestion
Primary ciliary dyskinesia (PCD) / Kartagener's syndrome	Defective dynein arms → immotile cilia → impaired mucociliary clearance → chronic sinopulmonary infections ^[4]
Cystic fibrosis (CF)	Thick, dehydrated mucus → impaired clearance; near-universal nasal polyposis
Aspirin-exacerbated respiratory disease (AERD / Samter's triad)	Asthma + CRS with nasal polyps + aspirin sensitivity — due to upregulated leukotriene pathway
Smoking / air pollution	Direct mucosal irritation, impaired ciliary function, mucosal drying
Cocaine use (nasal)	Vasoconstriction → mucosal ischaemia and necrosis; septal perforation

Factor	Mechanism
Immunocompromised state	Reduced ability to clear pathogens; risk of invasive fungal sinusitis ^[1]
Diabetes mellitus (uncontrolled)	Impaired neutrophil function; risk of mucormycosis
HIV/AIDS	Impaired cellular immunity
CVID / other primary immunodeficiencies	Recurrent sinopulmonary infections
Malnutrition	Impaired immune function ^[5]
Congenital conditions (PCD, CF, Young's syndrome)	See above ^[1]

Factor	Mechanism
Nasogastric / nasotracheal tubes	Mechanical obstruction, mucosal irritation, biofilm
Prolonged nasal decongestant use (rhinitis medicamentosa)	Rebound mucosal congestion on withdrawal
Barotrauma (diving, flying)	Pressure changes → mucosal oedema, haemorrhage into sinus
Hospital-acquired (ICU)	Supine position, impaired mucociliary clearance, intubation

Predisposing Factors – from GC/CFB Lecture Slides

The lecture slides specifically list: anatomical (deviated septum, polyp, tumour), dental root infection, upper respiratory tract infection, congenital, immunocompromised (especially for fungal causes) ^[1]. These are high-yield exam points.

4. Anatomy and Function of the Paranasal Sinuses

Understanding sinus anatomy is essential to understanding why rhinosinusitis develops, which sinuses are most commonly affected, and why complications occur.

Sinus	Development	Drainage	Clinical Relevance
Maxillary	Present at birth; pneumatises by age 4	Via hiatus semilunaris into middle meatus	Most commonly affected in adults. Ostium is located superiorly on medial wall → "drainage against gravity" → prone to mucus retention. Floor is close to molar/premolar roots → odontogenic sinusitis
Ethmoid (anterior & posterior)	Present at birth; multiple small cells	Anterior → middle meatus; Posterior → superior meatus (sphenoethmoidal recess)	Most commonly affected in children. Thin-walled (lamina papyracea laterally → orbital complications). Key component of the OMC
Frontal	Develops ~age 5–6; fully pneumatised by adolescence	Via frontonasal duct into middle meatus (via OMC)	Not clinically significant before age ~6. Complications include Pott's puffy tumour (subperiosteal abscess of frontal bone)
Sphenoid	Develops ~age 5; fully pneumatised by adolescence	Into sphenoethmoidal recess (superior meatus)	Rare isolated sinusitis. Proximity to cavernous sinus, optic nerve, internal carotid artery → dangerous complications

The ostiomeatal complex is the key anatomical bottleneck — the common drainage pathway for the maxillary, anterior ethmoid, and frontal sinuses into the middle meatus. It includes:

Uncinate process
Ethmoid infundibulum
Hiatus semilunaris
Ethmoid bulla
Middle meatus

Why is the OMC so important? Because obstruction of the OMC — whether by mucosal oedema (viral/allergic), polyps, or anatomical variants — blocks drainage from three sinuses simultaneously. This is the fundamental pathophysiological event in rhinosinusitis.

The paranasal sinuses are lined by pseudostratified ciliated columnar epithelium (respiratory epithelium) with goblet cells. Normal function depends on three pillars:

Patent ostia — allows ventilation and drainage
Mucociliary clearance — cilia beat in a coordinated metachronal wave (10–15 Hz) to transport the overlying mucus blanket towards the natural ostium and then into the nasal cavity
Mucus quality — a two-layer system (sol layer for ciliary beating + gel layer to trap particles)

Disruption of any of these three pillars leads to mucus stasis → bacterial colonisation → infection → further mucosal inflammation → further obstruction → a vicious cycle.

Structure	Adjacent Sinus	Clinical Significance
Orbit (lamina papyracea)	Ethmoid	Orbital cellulitis, subperiosteal abscess
Anterior cranial fossa	Frontal, ethmoid	Intracranial abscess, meningitis
Middle cranial fossa	Sphenoid	Cavernous sinus thrombosis
Optic nerve	Sphenoid, posterior ethmoid	Visual loss
Internal carotid artery	Sphenoid	Carotid injury (rare, surgical)
Maxillary dental roots	Maxillary	Odontogenic sinusitis

5. Aetiology

5.1 Acute Rhinosinusitis (ARS)

The vast majority of ARS is viral, arising as a complication/extension of the common cold ^[1]^[3].

Most commonly: rhinovirus, influenza virus, parainfluenza virus ^[3]
Also: coronavirus, adenovirus, RSV, enterovirus
These cause direct mucosal inflammation and oedema → ostial obstruction → impaired drainage
Features: generally mimics viral URI with improvement ≤ 10 days ^[3]

S. pneumoniae, H. influenzae, Moraxella catarrhalis — the "Big Three" of community-acquired bacterial rhinosinusitis ^[1]^[3]
Also: S. aureus (especially in nosocomial sinusitis), anaerobes (especially odontogenic sinusitis), Gram-negative rods (nosocomial) ^[1]
Features: purulent discharge (though inaccurate alone), severe localised unilateral pain, classically "double sickening" (deterioration after initial improvement), lasts > 10 days ^[3]

Key Teaching Point – Double Sickening

"Double sickening" is the classic pattern of acute bacterial rhinosinusitis: initial improvement of viral URTI symptoms → then worsening again (new fever, increased facial pain, worsening/change in nasal discharge). This biphasic course suggests bacterial superinfection ^[3].

Immunocompromised patients ^[1]:
- Invasive fungal sinusitis: Mucor (Rhizopus, Mucor spp.) in uncontrolled DM/DKA; Aspergillus in neutropenic patients → tissue invasion, angioinvasion, necrosis
- Rapidly fatal if not treated (surgical debridement + antifungals)
Immunocompetent:
- Fungal ball (mycetoma): usually Aspergillus; non-invasive collection of fungal debris in maxillary sinus; presents like unilateral CRS
- Allergic fungal rhinosinusitis (AFRS): type I + III hypersensitivity to fungal antigens → thick "peanut butter" mucin, eosinophilic mucin with Charcot-Leyden crystals; associated with nasal polyps, unilateral disease, bone erosion

5.2 Chronic Rhinosinusitis (CRS) — Duration > 12 Weeks

CRS is now understood as a predominantly inflammatory condition rather than a persistent bacterial infection ^[6]. The aetiology is multifactorial:

Predominantly Th1/neutrophilic inflammation
Often associated with persistent bacterial infection/biofilm, anatomical factors, odontogenic sources

Predominantly Th2/eosinophilic inflammation (in Caucasians; in East Asian populations, there is a higher proportion of neutrophilic/mixed CRSwNP)
Associated with:
- Allergic rhinitis
- Asthma (especially late-onset)
- AERD / Samter's triad (NERD): asthma + CRSwNP + aspirin sensitivity ^[6] — due to COX-1 inhibition shifting arachidonic acid metabolism towards the 5-lipoxygenase/leukotriene pathway → eosinophilic inflammation
- CF (nearly universal nasal polyps in CF)
- EGPA (eosinophilic granulomatosis with polyangiitis)

East Asian CRS Phenotype

In Hong Kong/East Asian populations, CRSwNP tends to have a higher proportion of neutrophilic (rather than purely eosinophilic) inflammation compared to Western populations. This has implications for treatment response — neutrophilic CRS may respond less well to corticosteroids and biologics targeting Th2 pathways. However, there is increasing eosinophilic CRSwNP in Asia.

Category	Organisms/Causes	Notes
Viral (most common)	Rhinovirus, influenza, parainfluenza, coronavirus	Self-limiting; majority of ARS
Bacterial (0.5–2%)	S. pneumoniae, H. influenzae, M. catarrhalis, S. aureus	Double sickening, > 10 days
Fungal	Mucor, Aspergillus	Immunocompromised → invasive; immunocompetent → fungal ball/AFRS
Odontogenic	Mixed anaerobes + aerobes	10–12% of maxillary CRS; dental source
Nosocomial	S. aureus, Gram-negative rods, Pseudomonas	ICU patients, NG tubes

6. Pathophysiology

The pathophysiology of rhinosinusitis centres on the vicious cycle of ostial obstruction, impaired mucociliary clearance, mucus retention, and secondary infection.

Initiating event — usually a viral URTI:
- Virus deposits on nasal/conjunctival mucosa → attaches to receptors (e.g., ICAM-1 for rhinovirus) on respiratory epithelial cells → enters cells ^[5]
- Infected cells release pro-inflammatory cytokines (IL-1, IL-6, TNF-α, IL-8) → recruit PMNs and other inflammatory cells ^[5]
- This causes: increased vascular permeability → mucosal oedema and rhinorrhoea; release of albumin and bradykinin → sore throat, nasal congestion ^[5]
- Nasal discharge colour correlates with PMN content (not bacterial infection!): white = few PMNs; yellow = more PMNs; green = high PMN + PMN enzymatic activity (myeloperoxidase). Colour alone does NOT indicate bacterial infection and does NOT correlate with need for antibiotics ^[5]
Ostial obstruction:
- Mucosal oedema narrows/blocks the OMC → impaired ventilation and drainage of maxillary, anterior ethmoid, and frontal sinuses
- Mucus accumulates → oxygen tension falls → sinus pH drops → environment favours bacterial growth
Bacterial superinfection (if it occurs):
- Bacteria (S. pneumoniae, H. influenzae, M. catarrhalis) that normally colonise the nasopharynx gain access to and proliferate in the obstructed, poorly-ventilated sinus
- Bacterial products + host inflammatory response → further mucosal damage, oedema, and pus production → worsening obstruction → vicious cycle
- This manifests clinically as "double sickening"
Resolution (majority):
- Innate + adaptive immunity clear the infection
- Mucosal oedema resolves → ostia re-open → drainage resumes
- Most viral ARS resolves within 7–10 days

CRS pathophysiology is more complex and less well understood. It is predominantly an inflammatory disorder rather than a simple persistent infection ^[6]:

Persistent inflammation → epithelial barrier dysfunction → antigen penetration → sustained immune activation
Biofilm formation by bacteria (S. aureus, Pseudomonas) on sinus mucosa → resistance to antibiotics and host defences → chronic smouldering inflammation
Staphylococcal superantigens → polyclonal T-cell activation → intense eosinophilic inflammation (especially in CRSwNP)
Tissue remodelling: prolonged inflammation leads to mucosal thickening, subepithelial fibrosis (CRSsNP) or oedematous polyp formation (CRSwNP)
Osteitis: inflammation extends to sinus bone → bony thickening/sclerosis visible on CT

CRS with Nasal Polyps (CRSwNP) — Specific Pathophysiology

Polyps are grey-white, oedematous protrusions — essentially oedematous, inflamed stroma covered by respiratory epithelium ^[6]
Mobile, insensitive to pain (cf. swollen turbinate, which is vascular, fixed, and tender) ^[6]
Driven by Th2 inflammation: IL-4, IL-5, IL-13 → eosinophil recruitment, IgE production, goblet cell hyperplasia
In AERD/Samter's triad: COX-1 inhibition (aspirin/NSAIDs) → ↓ PGE₂ (which normally inhibits 5-LOX) → ↑ cysteinyl leukotrienes (LTC₄, LTD₄, LTE₄) → bronchoconstriction + nasal polyp growth + eosinophilic inflammation

Infection can spread beyond the paranasal sinuses via several routes:

Direct extension through thin bony walls (especially lamina papyracea of ethmoid → orbit)
Thrombophlebitis of diploic veins (valveless veins connecting sinuses to orbit and intracranial compartment — the Batson venous plexus)
Erosion/defects in bony walls (congenital dehiscences, surgical, or infection-related)

7. Classification

Classification	Duration	Key Features
Acute rhinosinusitis (ARS)	< 4 weeks ^[2] (EPOS 2020 uses < 12 weeks for acute ^[1])	Usually viral, self-limiting
Subacute rhinosinusitis	4–12 weeks ^[2]	Transitional; often partially treated or slow-resolving
Chronic rhinosinusitis (CRS)	≥ 12 weeks ^[1]^[2]^[6]	Inflammatory rather than purely infectious
Recurrent acute rhinosinusitis	≥ 4 episodes per year with interim symptom resolution ^[2]	Investigate for underlying predisposing factors

EPOS 2020 vs Traditional Classification

The EPOS 2020 guideline (cited on GC/CFB lecture slides) classifies acute as < 12 weeks and chronic as ≥ 12 weeks ^[1]. Some older references (and some clinical practice) still use < 4 weeks for acute, 4–12 weeks for subacute, and > 12 weeks for chronic ^[2]. For exam purposes, follow the EPOS 2020 definition on the lecture slides: acute < 12 weeks, chronic ≥ 12 weeks ^[1].

Classification	Definition
Acute viral rhinosinusitis	ARS with viral aetiology ^[2]
Uncomplicated acute bacterial rhinosinusitis	ARS with bacterial aetiology without clinical evidence of extension outside paranasal sinuses and nasal cavity ^[2]
Complicated acute bacterial rhinosinusitis	ARS with bacterial aetiology with clinical evidence of extension outside paranasal sinuses and nasal cavity (orbital, intracranial, facial) ^[2]

Subtype	Abbreviation	Features
CRS without nasal polyps	CRSsNP (~2/3 of CRS)	Predominantly neutrophilic/Th1; mucopurulent discharge, facial pressure
CRS with nasal polyps	CRSwNP (~1/3 of CRS)	Predominantly eosinophilic/Th2; polyps, anosmia, asthma association
Allergic fungal rhinosinusitis (AFRS)	A subset of CRSwNP	Thick eosinophilic mucin, fungal hyphae, unilateral predominance

Form	Features
Odontogenic sinusitis	Maxillary sinusitis due to dental infection; mixed anaerobic/aerobic flora
Nosocomial sinusitis	ICU patients with NG/nasotracheal tubes; Gram-negatives, S. aureus
Invasive fungal sinusitis	Immunocompromised; Mucor or Aspergillus; tissue necrosis; surgical emergency
Fungal ball (mycetoma)	Immunocompetent; non-invasive; usually unilateral maxillary; calcifications on CT

8. Clinical Features

8.1 Symptoms

Symptoms are organised by the affected structure, with the pathophysiological basis explained inline.

Symptom	Pathophysiological Basis
Nasal congestion/blockage/obstruction	Mucosal oedema → narrows nasal passages and sinus ostia. Engorgement of venous sinusoids in turbinates. In CRSwNP, polyps physically obstruct
Nasal discharge (rhinorrhoea) — anterior or posterior nasal drip	Increased mucus production by goblet cells + transudation of serum proteins due to increased vascular permeability. Anterior = out the nose; posterior = dripping down pharynx (post-nasal drip → throat clearing, cough)
Reduction or loss of smell (hyposmia/anosmia)	Mucosal oedema and/or polyps block airflow to the olfactory cleft (located superiorly in nasal cavity). In CRS, prolonged eosinophilic inflammation can damage olfactory neuroepithelium → persistent anosmia even after treatment. Anosmia is more prominent in CRSwNP (as polyps preferentially fill the olfactory cleft)

Nasal Discharge Colour

Coloured (yellow/green) nasal discharge is a normal self-limited phase of an uncomplicated common cold ^[5]. The colour reflects PMN content and enzymatic activity (myeloperoxidase) — NOT bacterial infection. Purulence alone cannot distinguish between a cold and a sinus infection; colour of nasal discharge does NOT correlate with necessity of antibiotic use ^[5]. This is a common exam trap.

Symptom	Pathophysiological Basis
Facial pain/pressure	Distension of inflamed sinus mucosa + mucus/pus under pressure against the bony sinus walls → referred pain via trigeminal nerve (V1 frontal, V2 maxillary). Worsens with bending over (because gravity-dependent shift of fluid increases pressure on the dependent wall) ^[3]
Radiation to teeth (upper)	Maxillary sinus floor overlies the roots of premolars and molars → referred pain via superior alveolar nerves (branches of V2). Conversely, dental infection can cause maxillary sinusitis (odontogenic)
Headache	Similar mechanism to facial pain; frontal headache with frontal sinusitis, vertex headache with sphenoid sinusitis
Ear fullness/pressure	Eustachian tube opening in nasopharynx may be affected by mucosal oedema/inflammatory exudate → secondary eustachian tube dysfunction → aural fullness, conductive hearing loss

Symptom	Pathophysiological Basis
Fever	More common in bacterial rhinosinusitis (fever > 38°C is one of the criteria for bacterial ARS ^[3]). Mediated by pyrogens (IL-1, TNF-α, IL-6, PGE₂) acting on hypothalamic thermoregulatory centre. New onset or recurrence of fever during a URTI suggests secondary bacterial infection ^[5]
Fatigue/malaise	Systemic inflammatory response; sleep disturbance from nasal obstruction

Symptom	Pathophysiological Basis
Cough (especially in children)	Post-nasal drip irritating pharyngeal and laryngeal mucosa → cough reflex (afferent via glossopharyngeal/vagus nerve). Often appears after onset of nasal discharge and obstruction ^[5]. In children, cough may be the predominant presenting complaint
Sore throat	Post-nasal drip → pharyngeal irritation; also direct inflammatory mediators (bradykinin) causing pharyngeal pain ^[5]
Halitosis	Stagnant mucopurulent secretions in nasal cavity and post-nasal space → bacterial breakdown products (volatile sulfur compounds)
Sneezing	Trigeminal nerve irritation in nasal mucosa → sneeze reflex; more prominent in allergic component
Otalgia/ear pulling (children)	Referred pain via auriculotemporal nerve (V3) and tympanic branch of glossopharyngeal nerve; eustachian tube dysfunction
Decreased oral intake/anorexia (children)	Nasal obstruction impairs feeding (infants are obligate nasal breathers); systemic illness

Feature	Viral ARS	Bacterial ARS
Duration	Improves within ≤ 10 days ^[3]	Persists > 10 days without improvement OR "double sickening" ^[3]
Discharge	Clear → yellow/green → clear (normal sequence)	Discoloured, purulent nasal discharge (persistent) ^[3]
Pain	Diffuse, mild	Severe, localised, often unilateral ^[3]
Fever	Low-grade or absent	Fever > 38°C ^[3]
Inflammatory markers	Normal or mildly raised	↑ ESR/CRP ^[3]

8.2 Signs

Sign	Pathophysiological Basis
Erythema/oedema with tenderness over sinus areas	Inflammation of underlying sinus transmits through thin overlying bone and soft tissue. Maxillary tenderness (over cheeks), frontal tenderness (over forehead superomedially). Not diagnostic in isolation ^[3]
Opacification of maxillary/frontal sinus upon transillumination	Pus/thickened mucosa replaces aerated sinus → does not transmit light. Poor sensitivity/specificity; rarely used in modern practice ^[3]
Periorbital oedema	May indicate orbital complication (preseptal or orbital cellulitis) — especially from ethmoid sinusitis
Facial swelling (forehead)	Pott's puffy tumour — subperiosteal abscess of frontal bone (complication)

Sign	Pathophysiological Basis
Mucosal inflammation: oedema, narrowing of meatus, inferior turbinate hypertrophy	Inflammatory oedema of nasal mucosa; venous engorgement of turbinate mucosa ^[3]
Discharge: copious watery or purulent discharge	Watery = viral/allergic (transudative); purulent = bacterial infection (PMN-rich exudate) ^[3]
Mucopurulent discharge primarily from middle meatus	The OMC drains into the middle meatus → discharge from here localises disease to the maxillary/anterior ethmoid/frontal sinuses ^[1]
Co-existent anatomical risk factors: polyps, septal deviation	Pre-existing narrowing of OMC predisposes to recurrent/chronic sinusitis ^[3]
Nasal polyps: grey-white, oedematous protrusions	Oedematous stroma prolapsing into nasal cavity; hallmark of CRSwNP ^[6]
Polyps are mobile, insensitive to pain (cf. swollen turbinate)	Polyps have no vascular erectile tissue (unlike turbinates) and are essentially oedematous connective tissue → not tender; turbinates are vascular and innervated ^[6]

High Yield – Polyp vs Turbinate

Nasal polyps = grey-white, mobile, insensitive to pain ^[6]. Swollen turbinates = pink/red, fixed position, may be tender. If you probe it and the patient flinches → turbinate. If it's mobile and painless → polyp.

These must be actively sought as they indicate extension beyond the sinuses:

Sign	Complication Indicated
Periorbital/lid oedema, erythema, warmth	Preseptal cellulitis (anterior to orbital septum)
Proptosis, ophthalmoplegia, ↓ visual acuity, pain with eye movement	Orbital cellulitis / subperiosteal abscess (posterior to orbital septum → ophthalmological emergency) ^[3]
Frontal swelling ("doughy" forehead swelling)	Pott's puffy tumour (frontal bone subperiosteal abscess) ^[3]
Meningism (neck stiffness, photophobia)	Meningitis ^[3]
Focal neurological signs, altered consciousness	Intracranial abscess (frontal lobe epidural/subdural/intracerebral) ^[3]
CN III, IV, V₁, V₂, VI palsies; bilateral periorbital oedema; proptosis	Septic cavernous sinus thrombosis ^[3] — thrombophlebitis via valveless veins
Black necrotic tissue on turbinate/palate	Invasive fungal sinusitis (mucormycosis) — surgical emergency

Sign	Significance
Allergic S/S: allergic shiners, allergic salute, Dennie-Morgan folds	Co-existent allergic rhinitis (common association) ^[6]
Allergic rhinitis, asthma, conjunctivitis	The "unified airway" concept — inflammation in one part of the respiratory tract co-exists with others ^[6]
Mouth breathing, hyponasal speech	Chronic nasal obstruction
Endoscopic signs: nasal polyps, mucopurulent discharge from middle meatus, oedema/mucosal obstruction in middle meatus ^[1]	EPOS 2020 diagnostic criteria for CRS requires endoscopic AND/OR CT confirmation

Cardinal S/S of CRS: mucopurulent nasal drainage + blocked nose + facial discomfort + ↓/loss of smell ^[6]

Domain	ARS	CRS
Nasal obstruction	++	+++
Nasal discharge	++ (clear → coloured → clear)	+++ (mucopurulent, chronic)
Facial pain/pressure	++ (acute, severe if bacterial)	+ (dull, chronic)
Anosmia/hyposmia	+ (temporary)	+++ (especially CRSwNP, may be permanent)
Fever	+ (viral) / ++ (bacterial)	Rare (suggests acute exacerbation or complication)
Duration	< 12 weeks	≥ 12 weeks

Understanding these associations is clinically important for exam questions:

Association	Explanation
Allergic rhinitis	Most common predisposing factor for CRS; chronic mucosal inflammation → OMC obstruction
Asthma	"Unified airway" — same Th2 inflammation affects upper and lower airways; 20–70% of CRS patients have asthma
Samter's triad / AERD / NERD	Asthma + CRSwNP + aspirin sensitivity ^[6] — aggressive polyp recurrence
Primary ciliary dyskinesia	AR; immotile cilia → chronic sinusitis, bronchiectasis, situs inversus (Kartagener's), male infertility
Cystic fibrosis	Near-universal nasal polyps; thick mucus → sinopulmonary disease
Young's syndrome	Male infertility + rhinosinusitis + bronchiectasis (acquired ciliary dysfunction?)
Yellow nail syndrome	Yellow dystrophic nails + lymphoedema + pleural effusion + sinusitis/bronchiectasis
Immunodeficiency (CVID, HIV)	Recurrent sinopulmonary infections
Granulomatous diseases (GPA, sarcoidosis)	Destructive nasal/sinus inflammation; GPA → saddle nose, nasal crusting; sarcoidosis → nodular mucosa
EGPA	CRSwNP + asthma + peripheral eosinophilia + vasculitis

High Yield Summary

Definition: Rhinosinusitis = inflammation of nasal cavity + paranasal sinuses. EPOS 2020: ≥ 2 symptoms (≥ 1 must be nasal blockage or discharge), ± facial pain, ± hyposmia, AND endoscopic/CT confirmation.

Classification: Acute ( < 12 weeks) vs Chronic (≥ 12 weeks). CRS divided into CRSsNP (~2/3, neutrophilic) and CRSwNP (~1/3, eosinophilic).

Aetiology: Viral (vast majority) → bacterial superinfection (0.5–2%): S. pneumoniae, H. influenzae, M. catarrhalis. Fungal in immunocompromised.

Pathophysiology: Vicious cycle: trigger → mucosal oedema → OMC obstruction → impaired mucociliary clearance → mucus stasis → bacterial colonisation → more inflammation.

Key Clinical Points:

Coloured nasal discharge ≠ bacterial infection; it reflects PMN content.
Double sickening = hallmark of bacterial ARS.
Nasal polyps: grey-white, mobile, painless (vs turbinate: pink, fixed, tender).
Samter's triad: asthma + CRSwNP + aspirin sensitivity.
Red flags: orbital signs (proptosis, ophthalmoplegia, ↓ vision), meningism, frontal swelling, altered consciousness → complicated sinusitis.

Predisposing factors (lecture slides): deviated septum, polyp, tumour, dental root infection, URTI, congenital, immunocompromised.

Active Recall - Rhinosinusitis (Definition, Epidemiology, Anatomy, Aetiology, Clinical Features)

^[1] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf (Rhinosinusitis section, slides 14–15) ^[2] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Sinusitis/Rhinosinusitis, p.133–135); MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (Sinusitis/Rhinosinusitis, p.109) ^[3] Senior notes: Ryan Ho Respiratory.pdf (Rhinosinusitis, p.54); Adrian Lui Pediatrics Notes.pdf (p.159) ^[4] Senior notes: Maksim Medicine Notes.pdf (Bronchiectasis section — PCD, Kartagener's, CF, Young's syndrome, p.301–303) ^[5] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (Common Cold/URTI pathophysiology, p.95) ^[6] Senior notes: Adrian Lui Pediatrics Notes.pdf (Chronic rhinosinusitis, p.159)

Differential Diagnosis of Rhinosinusitis

The differential diagnosis of rhinosinusitis is essentially the differential of a patient presenting with nasal obstruction, nasal discharge, facial pain/pressure, and/or hyposmia/anosmia — with or without systemic symptoms such as fever. The challenge is threefold:

Is this rhinosinusitis at all, or something mimicking it? (e.g., allergic rhinitis, migraine, dental pathology)
If rhinosinusitis, is it viral or bacterial? (because this determines antibiotic use)
If chronic/recurrent/unilateral, is there an underlying sinister cause? (e.g., malignancy, vasculitis, fungal disease)

The approach to differential diagnosis should be symptom-driven — the presentation determines which mimics you must consider.

1. Differential Diagnosis by Presenting Symptom Complex

Differential	Key Distinguishing Features	Why It Mimics Rhinosinusitis
Allergic rhinitis	Bilateral, watery/clear rhinorrhoea, sneezing, itchy nose/eyes/palate, seasonal or perennial pattern, pale/boggy turbinates on exam, allergic shiners, Dennie-Morgan folds. No fever, no facial pain. Personal/family Hx of atopy (eczema, asthma)	Nasal congestion + rhinorrhoea overlap directly. Allergic rhinitis is also the most common predisposing factor for rhinosinusitis, so the two frequently coexist ^[7]
Non-allergic rhinitis (vasomotor rhinitis)	Chronic nasal congestion/rhinorrhoea triggered by temperature changes, irritants, emotions, spicy food. No itch, no sneezing, negative allergy testing. Normal/engorged turbinates	Nasal obstruction + discharge without allergic features
Rhinitis medicamentosa	History of prolonged use of topical nasal decongestants (oxymetazoline, xylometazoline > 5–7 days) → rebound mucosal congestion when drug wears off → patient uses more → vicious cycle	Severe nasal obstruction; key is the drug history
Common cold (acute coryza)	Viral URTI with rhinorrhoea, sneezing, sore throat, mild malaise. Symptoms improve within ≤ 10 days ^[3]. Self-limiting	The most common precursor to ARS. Distinction is by duration and trajectory — common cold improves, bacterial ARS worsens or fails to improve > 10 days ^[7]^[8]
Adenoid hypertrophy (children)	Chronic mouth breathing, snoring, hyponasal speech, recurrent OM. Lateral neck XR or nasoendoscopy shows enlarged adenoids	Chronic nasal obstruction in a child — consider if not responding to rhinosinusitis treatment
Foreign body (children)	Unilateral foul-smelling, purulent, possibly blood-stained nasal discharge. Young child (2–5 years). Often no fever initially	Unilateral purulent discharge is the classic clue; rhinosinusitis is usually bilateral or at least not associated with a foul unilateral discharge in the absence of dental pathology

High Yield – Unilateral Nasal Symptoms: Think Beyond Rhinosinusitis

In the HK exam context, unilateral nasal obstruction ± epistaxis ± discharge should raise a red flag for: (1) nasal foreign body (children), (2) nasal/sinus tumour, (3) nasopharyngeal carcinoma (NPC — endemic in southern China/HK), (4) fungal ball, (5) odontogenic sinusitis. Always investigate unilateral symptoms further.

Differential	Key Distinguishing Features	Why It Mimics Rhinosinusitis
Migraine	Unilateral pulsating headache, moderate-to-severe, debilitating (worsened by movement), 4–72 h duration, N/V, photophobia, phonophobia, ± aura. No nasal discharge or obstruction ^[9]	Migraine can cause referred facial pain, nasal congestion (via parasympathetic activation), and even clear rhinorrhoea — hence "sinus migraine" is a common misdiagnosis. Studies show up to 90% of self-diagnosed "sinus headaches" are actually migraine
Tension-type headache	Bilateral band-like tightness, mild-moderate, 30 min–7 days, no nausea/vomiting, no photophobia ^[9]	Bifrontal pressure may be mistaken for frontal sinusitis
Cluster headache (trigeminal autonomic cephalalgia)	Severe unilateral periorbital deep, piercing pain, 15 min–3 h, rapid onset, ipsilateral autonomic features (lacrimation, nasal congestion, conjunctival injection, Horner's), restlessness, periodicity/clustering, triggered by alcohol ^[9]	Ipsilateral nasal congestion and lacrimation mimic sinusitis; the severe periorbital pain mimics ethmoid/frontal sinusitis
Dental pathology (periapical abscess, dental caries)	Localised toothache, tenderness on percussion of affected tooth, swollen gum, ± periapical radiolucency on dental XR. Upper premolar/molar pathology can cause secondary odontogenic maxillary sinusitis	Referred pain to maxillary region; also, dental root infection is a genuine predisposing factor for maxillary sinusitis ^[1]
Temporomandibular joint (TMJ) dysfunction	Unilateral preauricular/temporal/mandibular pain, worse with chewing, jaw clicking/locking, tender TMJ on palpation	Referred facial pain in the cheek region
Trigeminal neuralgia	Sudden, severe, lancinating ("electric shock") pain in V2/V3 distribution, triggered by light touch (e.g., eating, wind, shaving), lasts seconds	Brief episodes of severe facial pain — but no nasal symptoms

Differential	Key Distinguishing Features	Why It Mimics CRS
Nasopharyngeal carcinoma (NPC)	Endemic in southern China/HK; EBV-associated. Presents with unilateral nasal obstruction, blood-stained post-nasal drip/epistaxis, unilateral serous otitis media (conductive hearing loss), cervical lymphadenopathy, CN palsies (III–VI if cavernous sinus/skull base involvement). EBV serology + nasoendoscopy with biopsy ^[10]	Unilateral nasal obstruction + post-nasal drip mimic CRS. Always consider NPC with unilateral nasal symptoms in HK patients
Sinonasal malignancy (SCC, adenocarcinoma, esthesioneuroblastoma, NK/T-cell lymphoma)	Unilateral obstruction, epistaxis, facial numbness/swelling, proptosis, loose teeth (maxillary involvement). NK/T-cell lymphoma (nasal type) is CD56+, strongly associated with EBV ^[10] — presents with destructive midline lesion, palate destruction	Progressive unilateral nasal symptoms not responding to medical therapy
Inverted papilloma	Benign but locally aggressive sinonasal tumour; unilateral nasal obstruction, epistaxis. Arises from lateral nasal wall, associated with SCC in ~5–15%	Unilateral polypoidal mass mimicking CRSwNP but is unilateral
Granulomatosis with polyangiitis (GPA, formerly Wegener's)	Destructive nasal/sinus disease: bloody nasal crusting, epistaxis, septal perforation, saddle nose deformity. + pulmonary (nodules, haemorrhage) + renal (RPGN). c-ANCA/PR3 positive	Chronic sinusitis that is destructive and unresponsive to antibiotics
Eosinophilic granulomatosis with polyangiitis (EGPA, formerly Churg-Strauss)	Late-onset asthma + CRSwNP + peripheral eosinophilia + vasculitis (mononeuritis multiplex, cardiac, skin). p-ANCA/MPO may be positive	CRSwNP + asthma overlap — but with eosinophilia and multi-system involvement
Sarcoidosis	Non-caseating granulomas; nasal crusting, nodular mucosa, septal perforation. + bilateral hilar lymphadenopathy, erythema nodosum, uveitis, ↑ACE	Chronic nasal obstruction with granulomatous inflammation
Allergic fungal rhinosinusitis (AFRS)	A form of CRSwNP; unilateral predominance, thick "peanut butter" mucin, eosinophilic mucin with Charcot-Leyden crystals and fungal hyphae on histology, bone erosion on CT mimicking malignancy	Often classified as a subtype of CRS, but the bone erosion and unilateral predominance may initially raise concern for tumour
Invasive fungal sinusitis	Immunocompromised patients (uncontrolled DM, neutropenia, transplant). Rapid progression, black necrotic tissue on turbinate/palate, facial pain, fever. Mucor or Aspergillus	Aggressive sinusitis in an immunocompromised host — surgical emergency
Cystic fibrosis	Children/young adults with CRSwNP + chronic sinopulmonary disease + pancreatic insufficiency (steatorrhoea) + male infertility. Sweat chloride test diagnostic ^[4]	Near-universal nasal polyps and chronic sinusitis in CF
Primary ciliary dyskinesia / Kartagener's syndrome	Chronic sinusitis + bronchiectasis + male infertility. Kartagener's = PCD + situs inversus (dextrocardia) ^[4]. Nasal NO is low	Recurrent sinusitis from birth due to immotile cilia

Red Flags for Malignancy in Chronic Nasal Symptoms

The following features in a patient with "chronic sinusitis" should raise suspicion for malignancy and prompt urgent nasoendoscopy ± biopsy:

Unilateral nasal obstruction or discharge (especially blood-stained)
Progressive cranial nerve deficits
Cervical lymphadenopathy
Proptosis or diplopia
Facial numbness or swelling
Palatal destruction
Unilateral serous otitis media (especially in an adult — think NPC in HK)

This is the most practically important differential in day-to-day practice because it determines whether antibiotics are indicated. The distinction is clinical — no routine laboratory or imaging test is needed ^[3]^[7]^[8].

Feature	Acute Viral Rhinosinusitis	Acute Bacterial Rhinosinusitis
Duration	< 10 days, improving ^[8]	≥ 10 days without improvement ^[8]
Course	Monophasic	"Double sickening": initial improvement then worsening after 5–6 days ^[3]^[8]
Discharge	Clear → yellow/green → clear (normal sequence)	Persistent purulent, discoloured discharge ^[3]
Pain	Diffuse, mild	Severe, localised, often unilateral ^[3]
Fever	Low-grade or absent	High fever (> 38°C) for ≥ 3–4 consecutive days ^[8]
Inflammatory markers	Normal or mildly ↑	↑ ESR/CRP ^[3]
Antibiotic indication	No	Yes

Three clinical scenarios that define acute bacterial rhinosinusitis (from AAP/IDSA guidelines, as reflected in senior notes ^[8]):

Persistent — symptoms ≥ 10 days without improvement

Severe onset — high fever (≥ 39°C) + purulent nasal discharge or facial pain for ≥ 3–4 consecutive days from illness onset

"Double sickening" — worsening after initial improvement, with new fever, increased purulent discharge, or facial pain after 5–6 days

The following flowchart provides a systematic approach to a patient presenting with nasal obstruction, nasal discharge, and/or facial pain:

4. Differential Diagnosis in Specific Populations

Condition	Key Features
Common cold	Most frequent cause of nasal symptoms in children; improves within ≤ 10 days ^[7]
Adenoid hypertrophy	Chronic mouth breathing, snoring, hyponasal speech, recurrent OM
Nasal foreign body	Unilateral foul-smelling, purulent, often blood-stained discharge in a child aged 2–5
Allergic rhinitis	Allergic salute, transverse nasal crease, bilateral clear discharge, itching
Pertussis	Paroxysmal cough (not primarily nasal, but URTI-like catarrhal phase) ^[7]
Cystic fibrosis	CRSwNP + sinopulmonary disease + failure to thrive + steatorrhoea ^[4]
Primary ciliary dyskinesia	Neonatal respiratory distress, chronic sinusitis, bronchiectasis, situs inversus ^[4]
Choanal atresia (neonates)	Bilateral → neonatal respiratory distress; unilateral → chronic unilateral discharge discovered later. Associated with CHARGE syndrome

Condition	Key Features
Invasive fungal sinusitis (Mucor, Aspergillus)	Rapid progression, black eschar on palate/turbinate, facial swelling, orbital involvement. Seen in uncontrolled DM/DKA, neutropenia, transplant, high-dose steroids
Atypical bacterial sinusitis	Gram-negatives (Pseudomonas), S. aureus; poor response to standard antibiotics
Recurrent/chronic sinusitis	Should prompt investigation for underlying immunodeficiency (CVID, IgA deficiency, HIV) ^[4]

Condition	Why Relevant in HK
Nasopharyngeal carcinoma	Endemic in southern China/HK; EBV-associated. Up to 20x higher incidence than Western populations. Must be considered in any HK adult with unilateral nasal obstruction, epistaxis, serous OM, or cervical LN ^[10]
Extranodal NK/T-cell lymphoma, nasal type	EBV-associated, CD56+, more common in East Asian populations. Destructive midline nasal/palatal lesion ^[10]
Allergic rhinitis	Very high prevalence (25–40%) in HK due to perennial dust mite exposure, high humidity, air pollution — the most common predisposing factor for CRS
Tuberculous sinusitis	Rare but should be considered in endemic areas; granulomatous sinus disease

Category	Conditions	Key Differentiating Clues
Infectious	Common cold, influenza, bacterial pharyngitis, pertussis	Duration, systemic features, trajectory
Allergic	Allergic rhinitis, AFRS	Itch, sneezing, clear discharge, atopic history, eosinophilic mucin
Non-allergic rhinitis	Vasomotor rhinitis, rhinitis medicamentosa, hormonal rhinitis (pregnancy), gustatory rhinitis	Triggers, drug history, no itch
Anatomical	Deviated septum, concha bullosa, adenoid hypertrophy, choanal atresia	Chronic obstruction, endoscopic/CT findings
Foreign body	Nasal foreign body	Child, unilateral foul discharge
Dental	Periapical abscess, odontogenic sinusitis	Toothache, dental exam, unilateral maxillary sinusitis
Primary headache	Migraine, tension-type, cluster headache	Minimal/no nasal symptoms; headache pattern; autonomic features in cluster
Neuralgic	Trigeminal neuralgia	Lancinating V2/V3 pain, triggered by touch, seconds duration
TMJ	TMJ dysfunction	Preauricular pain, jaw clicking, worse with chewing
Neoplastic	NPC, SCC, adenocarcinoma, NK/T-cell lymphoma, inverted papilloma, esthesioneuroblastoma	Unilateral, progressive, epistaxis, CN palsies, bone destruction, cervical LN
Granulomatous/autoimmune	GPA, EGPA, sarcoidosis	Destructive midline disease, multi-system involvement, autoantibodies
Fungal	Invasive fungal sinusitis, fungal ball, AFRS	Immunocompromised status, calcification on CT (fungal ball), eosinophilic mucin (AFRS)
Congenital/syndromic	CF, PCD/Kartagener's, Young's syndrome, yellow nail syndrome, immunodeficiencies (CVID)	Recurrent from childhood, bronchiectasis, male infertility, other systemic features

Think of four questions when facing a patient with rhinosinusitis-like symptoms:

Is the problem truly rhinosinusitis?
- Are both nasal symptoms (obstruction/discharge) AND sinus symptoms (facial pain/pressure) present?
- If only facial pain without nasal symptoms → consider non-sinogenic causes (migraine, dental, TMJ, neuralgia)
Acute or chronic?
- < 12 weeks → acute: viral vs bacterial vs allergic exacerbation
- ≥ 12 weeks → chronic: CRS (with/without polyps), but also consider tumour, vasculitis, fungal, congenital
Unilateral or bilateral?
- Bilateral → more likely inflammatory (allergic, infectious, CRS)
- Unilateral → red flag for tumour (NPC!), foreign body, fungal ball, odontogenic, inverted papilloma
Any red flags?
- Epistaxis, CN deficits, orbital signs, cervical LN, bone destruction, black necrotic tissue, immunocompromised

High Yield Exam Trap — 'Sinus Headache'

Most patients (and many doctors) who diagnose "sinus headache" actually have migraine. Studies show that ~90% of self-diagnosed sinus headaches meet ICHD criteria for migraine. The key distinguishing features: migraine has nausea/vomiting, photophobia, phonophobia, aura, debilitation — and while it can cause nasal congestion/rhinorrhoea via parasympathetic activation, it does not cause purulent discharge and is not associated with mucosal disease on endoscopy or CT ^[9].

High Yield Summary

Core differential of rhinosinusitis presentations:

Nasal obstruction + discharge: allergic rhinitis (most common mimic), vasomotor rhinitis, rhinitis medicamentosa, adenoid hypertrophy, foreign body (child — unilateral, foul), NPC (unilateral — HK!)
Facial pain without nasal symptoms: migraine ("sinus headache"), tension headache, cluster headache, dental pathology, TMJ dysfunction, trigeminal neuralgia
Chronic/recurrent: CRS (CRSsNP vs CRSwNP), NPC, sinonasal tumour, GPA, EGPA, sarcoidosis, fungal disease, CF, PCD
Unilateral red flags: always think NPC, NK/T-cell lymphoma, inverted papilloma, foreign body, fungal ball, odontogenic sinusitis
Immunocompromised: invasive fungal sinusitis (Mucor/Aspergillus) — surgical emergency
Viral vs bacterial ARS: distinguished by duration ( < 10d improving vs ≥ 10d persistent), double sickening, severity, fever > 38°C

Active Recall - Differential Diagnosis of Rhinosinusitis

References

^[1] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf (Rhinosinusitis section, slides 14–15) ^[3] Senior notes: Ryan Ho Respiratory.pdf (Rhinosinusitis, p.54); Adrian Lui Pediatrics Notes.pdf (p.158–159) ^[4] Senior notes: Maksim Medicine Notes.pdf (Bronchiectasis — PCD, Kartagener's, CF, Young's syndrome, p.301–303); MBBS Final MB (Medicine) (Felix PY Lai).pdf (Bronchiectasis, p.181) ^[7] Senior notes: Adrian Lui Pediatrics Notes.pdf (URTI spectrum and differential diagnoses, p.154) ^[8] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Diagnostic criteria ARS, p.137); MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (Diagnostic criteria ARS, p.113) ^[9] Senior notes: Ryan Ho Neurology.pdf (Headache differentials, p.58) ^[10] AOS material: AOS - Pathology.pdf (NK/T-cell lymphoma, p.26); Lecture slides: GC 215. Common nasal conditions and nasopharyngeal carcinoma.pdf (CRS clinical features, p.23)

Diagnostic Criteria, Algorithm, and Investigations for Rhinosinusitis

The diagnosis of rhinosinusitis is predominantly clinical ^[3]^[8]. This is a critical concept: unlike many surgical or medical conditions, uncomplicated rhinosinusitis does not require laboratory tests, cultures, or imaging to make the diagnosis. The reasons are:

Frequency — rhinosinusitis is extremely common (millions of episodes/year); routine investigation would be impractical and costly.
Self-limiting nature — the vast majority (> 98%) of ARS is viral and resolves spontaneously.
Low yield — sinus XR has poor sensitivity/specificity; CT shows incidental mucosal thickening in up to 40% of asymptomatic individuals during a viral URTI; nasopharyngeal swab cultures do not reliably correlate with sinus pathogens.
Investigations are reserved for — suspected complications, treatment failure, CRS workup, or exclusion of sinister pathology.

The question then becomes: how do we diagnose rhinosinusitis clinically, and how do we distinguish viral from bacterial?

2. Diagnostic Criteria

This is the definition framework taught at HKUMed and the one most likely to appear on in-house exams.

Rhinosinusitis in adults is defined as 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].

Additionally, for a confirmed diagnosis (especially CRS), EPOS 2020 requires objective evidence:

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].

Criterion	Details
Minimum symptoms	≥ 2 symptoms
Mandatory nasal symptom	≥ 1 must be nasal blockage/obstruction/congestion or nasal discharge
Additional symptoms	± Facial pain/pressure, ± ↓ or loss of smell
Objective confirmation	Endoscopic findings and/or CT changes
Acute	< 12 weeks ^[1]
Chronic	≥ 12 weeks ^[1]

High Yield – EPOS 2020 on GC/CFB Slides

The lecture slides specifically state: "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. AND either endoscopic signs... and/or CT changes..." ^[1]. This is the most likely definition to be tested.

2.2 Criteria for Acute Viral vs Acute Bacterial Rhinosinusitis

This distinction is the most clinically important diagnostic question in ARS because it determines antibiotic use.

Symptoms or signs of ARS < 10 days that are not worsening ^[8].

This is essentially a common cold with sinus involvement. The trajectory is monophasic and self-limiting.

Three clinical scenarios define ABRS (AAP/IDSA criteria, reflected in senior notes) ^[8]:

Scenario	Definition	Reasoning
Persistent	Symptoms ≥ 10 days without evidence of clinical improvement ^[8]	Viral URTI should improve within 10 days; failure to improve suggests bacterial superinfection has developed
Severe onset	High fever (≥ 39°C) AND purulent nasal discharge or facial pain for ≥ 3–4 consecutive days at the beginning of illness ^[8]	The severity from onset (high fever + localised purulence/pain) is atypical for viral infection, which tends to be milder
Double sickening	Symptoms of a typical viral URTI that are slowly improving but worsen again with new/more severe symptoms and signs after 5–6 days ^[3]^[8]	Initial improvement = host controlling viral infection; subsequent worsening = bacterial superinfection taking hold in the obstructed, poorly-ventilated sinus

Some sources use a point-based approach ^[3]:

Criteria for bacterial rhinosinusitis: ≥ 3 of the following:

Double sickening

Discoloured, purulent nasal discharge

Severe, localised pain

Fever > 38°C or ↑ ESR/CRP ^[3]

Exam Approach — Which Criteria Set to Use?

Both the AAP/IDSA "three scenarios" approach and the EPOS "≥ 3 of 4" point-based approach are valid. For the HKUMed exam, be prepared to discuss both — but the three-scenario approach (persistent / severe onset / double sickening) is more commonly tested because it is more intuitive and appears in multiple senior notes ^[8]. The EPOS ≥ 3 of 4 criteria appear in Ryan Ho and Adrian Lui notes ^[3].

CRS uses the same symptom criteria as ARS but with two additional requirements:

Duration ≥ 12 weeks — symptoms must persist continuously for ≥ 12 weeks without complete resolution ^[1]^[3]
Objective confirmation required — unlike ARS (which is purely clinical), CRS diagnosis requires either:
- Endoscopic signs (polyps, mucopurulent discharge from middle meatus, mucosal oedema/obstruction in middle meatus) ^[1]
- CT changes (mucosal changes within the ostiomeatal complex and/or sinuses) ^[1]

Why is objective confirmation needed for CRS but not ARS? Because CRS symptoms overlap with many other conditions (allergic rhinitis, migraine, etc.) and treatment decisions (including surgery) require confirmation of actual sinus disease. A patient with 3 months of facial pressure but a normal CT likely does not have CRS.

The following algorithm integrates clinical assessment, the viral–bacterial distinction, and investigation decision-making:

4. Investigations — When, What, and Why

Scenario	Investigations Needed?	Rationale
Uncomplicated acute rhinosinusitis (viral or bacterial)	NO ^[3]^[8]	Clinical diagnosis sufficient; imaging does not change management
Suspected complications of ARS	YES — urgent CT ± MRI, cultures	Need to define extent of disease beyond sinuses (orbital, intracranial)
Treatment failure (fails ≥ 2 antibiotic courses)	YES — CT + endoscopy + cultures	Need to identify anatomical obstruction, resistant organisms, alternative diagnosis
Chronic rhinosinusitis (≥ 12 weeks)	YES — endoscopy ± CT	Required for objective confirmation of CRS
Unilateral symptoms / suspicion of tumour	YES — endoscopy + biopsy ± CT/MRI	Exclude malignancy (NPC, SCC, NK/T lymphoma, inverted papilloma)
Recurrent ARS (≥ 4 episodes/year)	YES — CT + endoscopy + consider immune/allergy workup	Identify predisposing factors (anatomical, immunodeficiency, allergy)

Key Exam Point — Imaging NOT Indicated in Uncomplicated ARS

Imaging is NOT indicated if uncomplicated ^[3]. This is a commonly tested point. Plain sinus XR has poor sensitivity and specificity → NOT recommended ^[3]^[8]. CT is generally reserved for cases where complications are suspected ^[3]^[8]. Ordering a sinus XR for uncomplicated sinusitis is considered inappropriate.

4.2 Physical Examination (The First "Investigation")

Although not a "test," structured physical examination is the most important diagnostic step.

Anterior rhinoscopy is a simple bedside examination using a nasal speculum and head-light. Findings ^[3]^[8]:

Finding	Interpretation
Diffuse mucosal oedema	Inflammatory response (viral, allergic, or bacterial) causing engorgement of nasal mucosa ^[8]
Narrowing of middle meatus	OMC region oedema → confirms sinus outflow obstruction ^[8]
Inferior turbinate hypertrophy	Chronic mucosal inflammation or allergic rhinitis → engorged venous sinusoids in turbinate mucosa ^[8]
Copious purulent discharge	PMN-rich exudate suggesting active infection; but remember, purulence alone ≠ bacterial ^[8]
Co-existent anatomical factors: polyps, septal deviation	Predisposing factors for recurrent/chronic disease ^[3]

More detailed than anterior rhinoscopy; allows visualisation of the middle meatus, OMC, sphenoethmoidal recess, and nasopharynx. This is the gold standard for assessing nasal and sinus pathology ^[1].

Finding	Interpretation
Nasal polyps	Grey-white, mobile, painless oedematous masses → CRSwNP ^[1]
Mucopurulent discharge primarily from middle meatus	Confirms sinusitis affecting maxillary/anterior ethmoid/frontal sinuses (these drain via OMC into middle meatus) ^[1]
Oedema/mucosal obstruction primarily in middle meatus	OMC obstruction — the pathophysiological bottleneck ^[1]
Mass lesion	Biopsy needed → inverted papilloma, SCC, NPC, NK/T lymphoma
Black necrotic mucosa	Invasive fungal sinusitis (mucormycosis) → surgical emergency
Purulent discharge from superior meatus / sphenoethmoidal recess	Posterior ethmoid or sphenoid sinusitis

EPOS 2020 requires endoscopic signs (polyps, mucopurulent discharge from middle meatus, mucosal oedema in middle meatus) AND/OR CT changes to confirm CRS ^[1].

Indicated in patients with symptoms of ear pain, fullness or pressure, hearing loss or tinnitus ^[8]. Why? Because:

Eustachian tube dysfunction from nasopharyngeal inflammation can cause middle ear effusion (serous otitis media)
Unilateral serous OM in an adult in HK → must exclude NPC obstructing the eustachian tube orifice

4.3 Laboratory Investigations

Test	When to Order	Key Findings
CBC	Suspected complications, systemic sepsis, immunocompromised	Leucocytosis with left shift (bacterial infection); eosinophilia (allergic, AFRS, EGPA); neutropenia (risk for invasive fungal)
CRP / ESR	Criteria for bacterial ARS (fever > 38°C or ↑ ESR/CRP) ^[3]	Elevated → supports bacterial infection; normal → more likely viral
Blood culture	Systemic sepsis, high fever with rigors	Identify bacteraemia (may complicate intracranial/orbital spread)

Test	When to Order	Key Findings & Interpretation
Sinus aspirate / endoscopic culture of middle meatus for C/ST	NOT routinely required ^[3]^[8]; only when there is suspicion of serious complications ^[3], treatment failure, immunocompromised, or nosocomial sinusitis	Gold standard for identifying causative organism. Nasopharyngeal swab is NOT a reliable substitute (does not correlate with sinus pathogens). Culture + sensitivity guides targeted antibiotic therapy
Nasal biopsy	Mass lesion on endoscopy, suspected granulomatous disease (GPA, sarcoidosis), suspected malignancy (NPC, NK/T lymphoma)	Histopathology: squamous cell carcinoma, undifferentiated NPC, granulomas (GPA — necrotising granulomatous vasculitis; sarcoidosis — non-caseating granulomas), fungal hyphae (invasive fungal sinusitis)
Fungal stains and culture	Suspected fungal sinusitis (immunocompromised, fungal ball, AFRS)	KOH preparation, GMS/PAS staining, fungal culture. AFRS: eosinophilic mucin with Charcot-Leyden crystals and scattered fungal hyphae

Test	Rationale	Key Findings
Skin prick test (SPT)	Identify allergen triggers in patients with allergic rhinitis contributing to CRS	Positive wheal to common aeroallergens (dust mite is the most common in HK)
Serum specific IgE (RAST)	Alternative to SPT when SPT is contraindicated (e.g., severe eczema, antihistamine use)	Elevated specific IgE to relevant allergens
Total serum IgE	Elevated in allergic disease, AFRS, ABPA	Markedly elevated (> 1000 IU/mL) in AFRS

Test	Rationale
Serum immunoglobulins (IgG, IgA, IgM, IgG subclasses)	Screen for CVID, IgA deficiency, IgG subclass deficiency — common causes of recurrent sinopulmonary infections
HIV testing	Consider in recurrent/unusual infections
Sweat chloride test / CFTR mutation analysis	If CF suspected (children/young adults with nasal polyps + lower airway disease + GI symptoms)
Nasal nitric oxide	Low in PCD (ciliary dyskinesia reduces NO production)
c-ANCA/PR3, p-ANCA/MPO	Suspected GPA or EGPA

Test	Indication	Interpretation
Saccharin test / mucociliary clearance test	Suspected PCD	Prolonged clearance time (normal < 20 min, PCD > 60 min)
Nasal biopsy for electron microscopy	Confirm PCD — look for ultrastructural ciliary defects (absent outer dynein arms)	Diagnostic of PCD
Aspirin challenge test	Suspected AERD/Samter's triad	Provokes bronchoconstriction/nasal symptoms — performed in controlled setting

4.4 Radiological Investigations

Aspect	Details
Views	Waters (occipitomental — best for maxillary), Caldwell (frontal), lateral
Findings	Opacified sinus with air-fluid level ^[3]
Limitations	Poor sensitivity and specificity → NOT recommended ^[3]^[8]. Poor visualisation of ethmoid sinuses leads to high false-negative rates ^[8]
Current role	Essentially obsolete for rhinosinusitis diagnosis in modern practice. CT has replaced it entirely when imaging is needed

"Sinus XR: poor sensitivity and specificity → NOT recommended" ^[3]. This is a commonly examined negative knowledge point — know what NOT to order.

CT is the preferred imaging modality for rhinosinusitis when imaging is indicated ^[8].

Aspect	Details
Indications	(1) Suspected complications of ARS, (2) CRS workup (required for surgical planning), (3) Treatment failure / refractory disease, (4) Unilateral symptoms (exclude tumour, fungal ball), (5) Pre-operative (FESS planning)
Protocol	Thin-section (1–2 mm) coronal and axial cuts. Non-contrast for routine CRS; CT with contrast is required to identify complications and evaluate extent of involvement beyond the sinuses ^[8]

Key CT Findings and Their Interpretation:

CT Finding	Interpretation	Clinical Significance
Air-fluid levels	Acute fluid collection within sinus (pus, blood, or inflammatory exudate) ^[3]^[8]	Hallmark of acute sinusitis; also seen in trauma (haemosinus)
Mucosal oedema and thickening	Inflammatory thickening of sinus lining ^[3]^[8]	Non-specific; can be seen in ARS, CRS, and even asymptomatic individuals with viral URTI (up to 40% incidental finding) — hence CT should not be done during acute URTI
Air bubbles within sinuses	Air trapped within inflammatory exudate ^[3]	Suggests active infection with gas-producing organisms or recent drainage
Complete opacification	Entire sinus filled with soft tissue density material	Severe sinusitis, fungal ball, mucocoele, or tumour — further assessment needed
Ostiomeatal complex obstruction	Mucosal swelling occluding the OMC	The fundamental pathological finding — explains downstream sinus opacification
Bone erosion/destruction	Bone thinning or frank destruction	Red flag: may indicate malignancy (SCC, NPC, NK/T lymphoma), invasive fungal sinusitis, or mucocoele with pressure remodelling. Also AFRS can cause bone erosion
Calcification within opacified sinus	Hyperdense material within sinus	Characteristic of fungal ball (mycetoma) — calcified fungal concretions
Unilateral disease	Disease limited to one side	Think: fungal ball, odontogenic sinusitis, tumour, inverted papilloma, foreign body
Expansion of sinus with intact bony walls	Sinus filled with material pushing walls outward but not destroying them	Mucocoele — chronic mucus-filled obstructed sinus that slowly expands
Lund-Mackay scoring system	Semi-quantitative grading of CT findings (0–2 per sinus region, max 24 total)	Used to grade CRS severity and guide surgical decision-making. Score 0 = normal, ≥ 4 generally correlates with symptomatic CRS

CT Timing Pitfall

Do NOT order CT sinuses during an acute URTI or within 2–4 weeks of an acute episode. Up to 40% of asymptomatic individuals with a current viral URTI will have incidental mucosal thickening on CT → leads to false-positive diagnosis of sinusitis. CT for CRS should be performed after maximal medical therapy (typically 4–6 weeks of intranasal steroids ± antibiotics) to assess residual disease.

Aspect	Details
Indications	Useful to delineate extent of soft tissue involvement in patients who have complications of acute rhinosinusitis ^[8]; tumour staging (NPC, sinonasal malignancy); intracranial complications (abscess, cavernous sinus thrombosis); differentiation of fungal from non-fungal disease
Advantages over CT	Superior soft tissue contrast; no ionising radiation; better at distinguishing tumour from retained secretions, and identifying intracranial/orbital soft tissue extension
Limitations	Poor bony detail (CT is better for bone); slower acquisition; more expensive; motion artefact

Key MRI Features:

MRI Finding	Interpretation
T1 hyperintense signal in sinus	Proteinaceous/inspissated secretions, fungal material, or haemorrhage
T2 hypointense signal ("signal void") in sinus	Desiccated/inspissated fungal material (very dense → low water content → dark on T2). Helps distinguish fungal ball from simple inflammatory secretions (which are T2 bright)
Enhancing soft tissue	Tumour or active inflammation — requires gadolinium contrast
Intracranial extension (enhancing epidural/subdural collection)	Complication of sinusitis — abscess, empyema
Cavernous sinus filling defect	Septic cavernous sinus thrombosis

Clinical Scenario	First-Line Imaging	Rationale
Uncomplicated ARS	NONE	Clinical diagnosis
Suspected orbital/intracranial complication	CT with contrast (urgent) ± MRI	CT for bone + acute assessment; MRI for soft tissue/intracranial detail
CRS workup / pre-operative planning	CT without contrast	Define anatomy, extent, Lund-Mackay scoring, surgical roadmap
Suspected sinonasal malignancy	CT + MRI	CT for bone involvement; MRI for tumour extent, skull base/orbit/brain invasion
Suspected fungal ball	CT without contrast	Calcification within opacified sinus is characteristic
NPC staging	MRI (primary) + CT	MRI for local extent; CT for bone; PET-CT for distant metastases

Scenario	History/Exam	Bloods	Microbiology	Imaging	Other
Uncomplicated ARS (viral)	Clinical Dx sufficient	None	None	None	—
Uncomplicated ABRS	Clinical Dx (3 scenarios)	CRP/ESR if needed to support bacterial Dx	None routinely	None	—
Complicated ABRS	Red flags on exam	CBC, CRP, blood culture	Sinus aspirate/endoscopic C/ST ^[3]	Urgent CT with contrast ± MRI ^[8]	Ophthalmology/Neurosurgery consult
CRS (initial workup)	Nasal endoscopy	Consider allergy testing	Consider endoscopic culture if purulent	CT sinuses (after maximal medical Rx) ^[1]	Allergy testing, consider immunological workup if recurrent
CRS refractory to medical Rx	Repeat endoscopy	Eosinophil count, IgE, ANCA if vasculitis suspected	Endoscopic culture	CT (pre-op) ± MRI if tumour concern	Biopsy if mass, consider CF/PCD workup
Unilateral nasal symptoms	Endoscopy + biopsy of mass	As indicated	As indicated	CT ± MRI	EBV serology if NPC suspected

High Yield Summary

Diagnosis is predominantly clinical — no investigations needed for uncomplicated ARS ^[3]^[8].

EPOS 2020 diagnostic criteria (from GC/CFB lecture slides): ≥ 2 symptoms (≥ 1 nasal blockage or discharge), ± facial pain, ± hyposmia; AND endoscopic signs or CT changes (required for CRS, not ARS) ^[1].

Acute bacterial vs viral ARS — Three clinical scenarios (persistent ≥ 10d / severe onset ≥ 3–4d / double sickening) ^[8]. Alternative: ≥ 3 of 4 criteria (double sickening, purulent discharge, severe localised pain, fever > 38°C or ↑ ESR/CRP) ^[3].

Sinus XR: poor sensitivity and specificity → NOT recommended ^[3]^[8].

CT sinuses = preferred imaging modality when imaging is indicated ^[8]. Key findings: air-fluid levels, mucosal thickening, opacification, OMC obstruction, bone erosion (red flag), calcification (fungal ball).

CT with contrast for complications; CT without contrast for CRS workup/pre-op ^[8].

MRI for soft tissue complications, tumour staging, intracranial extension ^[8].

Sinus aspirate/endoscopic culture for C/ST — only for suspected serious complications, treatment failure, or immunocompromised ^[3]^[8].

Do NOT CT during an acute URTI — up to 40% incidental mucosal thickening → false positives.

Active Recall - Diagnostic Criteria and Investigations for Rhinosinusitis

References

^[1] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf (Rhinosinusitis section, slides 14–15) ^[3] Senior notes: Ryan Ho Respiratory.pdf (Rhinosinusitis, p.54); Adrian Lui Pediatrics Notes.pdf (p.159) ^[8] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Diagnostic criteria ARS, p.137–139); MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (Diagnostic criteria ARS, p.113)

Management of Rhinosinusitis

Before diving into specific treatments, it helps to understand why we treat rhinosinusitis the way we do, based on the underlying pathophysiology:

Pathophysiological Target	Treatment Strategy	Examples
Mucosal oedema → ostial obstruction	Reduce inflammation / decongest	Intranasal corticosteroids, nasal decongestants
Impaired mucociliary clearance / mucus retention	Mechanically flush / thin secretions	Nasal saline irrigation, adequate hydration
Pain and fever	Analgesia and antipyresis	Paracetamol, NSAIDs
Bacterial infection (if confirmed criteria)	Eradicate bacteria	Antibiotics (only for ABRS)
Chronic inflammation (CRS)	Sustained anti-inflammatory therapy	Intranasal corticosteroids (long-term), short-course oral steroids, biologics
Irreversible anatomical obstruction / polyps / complications	Restore sinus drainage surgically	FESS, polypectomy
Underlying predisposing factors	Treat the root cause	Allergy management, dental treatment, immunodeficiency treatment

Two critical overarching principles:

Routine use of antibiotics does NOT prevent development of complications ^[3]. Only ~2% of viral URTIs progress to bacterial sinusitis, yet antibiotics are VERY commonly (> 85%) prescribed for patients presenting with sinusitis symptoms ^[3]. This represents significant antibiotic overuse.

CRS management leans towards anti-inflammatory agents as it is predominantly due to complex inflammatory changes rather than persistent bacterial infection ^[3].

3. Acute Rhinosinusitis — Treatment Modalities

3.1 Supportive / Symptomatic Treatment (For ALL ARS — Viral and Bacterial)

These form the backbone of ARS management. Even in ABRS, supportive measures are used alongside antibiotics.

Nasal saline irrigation is listed as a first-line treatment on the GC/CFB lecture slides ^[1]^[11].

Aspect	Details
Mechanism	Mechanically flushes mucus, crusts, inflammatory mediators, and pathogens from the nasal cavity. Improves mucociliary clearance by hydrating the sol layer of the mucus blanket. Reduces mucosal oedema by osmotic effect (if hypertonic). The word "irrigation" (Latin: irrigare = to water/supply) tells you this is about washing
Formulations	Isotonic (0.9% NaCl) or hypertonic (3% NaCl). Hypertonic may have slightly better decongestant effect but can cause local stinging
Delivery	Squeeze bottle, neti pot, or commercial spray. High-volume low-pressure irrigation is more effective than simple sprays
Evidence	Moderate-quality evidence supporting symptom improvement. Very safe, inexpensive, and well-tolerated. Recommended by EPOS 2020 for both ARS and CRS
Contraindications	None significant. Avoid contaminated water (risk of amoebic infection — use distilled/boiled water)

Nasal decongestant is listed on the GC/CFB lecture slides as a treatment for acute rhinosinusitis ^[11].

Aspect	Details
Mechanism	Topical α-adrenergic agonists (oxymetazoline, xylometazoline) cause vasoconstriction of dilated venous sinusoids in the nasal mucosa → rapid reduction of mucosal oedema → improved nasal airflow and ostial patency. Oral decongestants (pseudoephedrine) act systemically via the same mechanism
Duration of use	Maximum 5–7 days for topical decongestants. Beyond this → rhinitis medicamentosa (rebound congestion). Why? Prolonged vasoconstriction causes tissue hypoxia → reactive vasodilation and mucosal oedema when drug wears off → patient uses more → tachyphylaxis and worsening cycle
Oral decongestants	Pseudoephedrine — no rebound risk but systemic side effects: insomnia, tachycardia, ↑ BP
Contraindications	Topical: > 7 days use, children < 6 years (risk of systemic absorption and toxicity). Oral: uncontrolled hypertension, severe IHD, MAO inhibitor use, angle-closure glaucoma, hyperthyroidism, BPH (urinary retention)

Rhinitis Medicamentosa — Why Max 5–7 Days?

Topical nasal decongestants should never be used for more than 5–7 days. The rebound congestion (rhinitis medicamentosa) occurs because prolonged α-agonist exposure → downregulation of α-receptors + tissue hypoxia → rebound vasodilation. The treatment of rhinitis medicamentosa is stopping the decongestant (can be difficult — gradual weaning or "one nostril at a time") and substituting intranasal corticosteroids.

Regular analgesia is part of supportive treatment ^[3].

Aspect	Details
Agents	Paracetamol (acetaminophen) and/or NSAIDs (ibuprofen)
Mechanism	Paracetamol: central COX inhibition → ↓ PGE₂ in hypothalamus → antipyresis; also central analgesic effect (exact mechanism debated). NSAIDs: peripheral COX-1/COX-2 inhibition → ↓ prostaglandins → ↓ inflammation, pain, and fever
Caution	NSAIDs should be avoided in patients with AERD/Samter's triad (aspirin-exacerbated respiratory disease) — can precipitate severe bronchoconstriction and worsening nasal polyps due to shunting of arachidonic acid to the 5-LOX/leukotriene pathway

± Intranasal steroids: modest benefit, to be used if symptoms persist ^[3].

Aspect	Details
Mechanism	Corticosteroids inhibit multiple inflammatory pathways: suppress NF-κB → ↓ pro-inflammatory cytokines (IL-1, IL-6, TNF-α), ↓ COX-2 expression → ↓ prostaglandins, ↓ phospholipase A₂ → ↓ arachidonic acid release, ↓ eosinophil recruitment, ↓ vascular permeability → reduction of mucosal oedema. Net effect: open ostia → restore drainage
Common agents	Mometasone, fluticasone, budesonide — all have high topical potency and low systemic bioavailability
Evidence in ARS	Modest benefit ^[3] — modest improvement in symptom scores, particularly nasal obstruction. EPOS 2020 recommends INCS as adjunctive therapy in both viral and bacterial ARS
Evidence in CRS	First-line therapy — strong evidence for both CRSsNP and CRSwNP. Reduces polyp size, improves symptoms
Onset	Slow — takes days to weeks for full effect (not a "quick fix" like decongestants)
Contraindications	Untreated nasal infection (rare concern); recurrent epistaxis (relative — use with caution). Generally very safe for long-term use
Technique	Aim spray laterally (towards ear, not septum) to target middle meatus and avoid septal irritation/epistaxis

3.2 Antibiotic Therapy (For ABRS Only)

Oral Antibiotics × 5–10/7 in ABRS ^[11]. Abx (e.g., amoxicillin × 5d) if bacterial sinusitis only ^[3].

High Yield — From GC/CFB Lecture Slides

The lecture slide explicitly states treatment for acute rhinosinusitis includes: nasal saline irrigation, nasal decongestant, oral antibiotics × 5–10/7 in ABRS. Antibiotics are indicated when criteria for ABRS are met: fever ≥ 38°C, double sickening, unilateral disease, severe pain, raised ESR/CRP ^[11].

Indication	Rationale
ABRS criteria met (persistent ≥ 10d / severe onset / double sickening) ^[8]^[11]	Bacterial superinfection unlikely to resolve spontaneously; antibiotics shorten duration and severity
Watchful waiting alternative (mild–moderate ABRS, non-toxic patient)	EPOS 2020 and IDSA guidelines allow a 7-day period of watchful waiting with supportive measures even in mild ABRS. ~70% of ABRS resolves spontaneously. Consider starting antibiotics only if no improvement after 7 days of supportive care, or if symptoms worsen
Immediate antibiotics	Severe ABRS (high fever + purulent discharge + severe pain), immunocompromised, complicated

Routine use of Abx does NOT prevent development of complications ^[3]. This is important — do not give antibiotics to viral ARS "just in case."

Line	Agent	Dose (Adults)	Duration	Rationale
First-line	Amoxicillin	500 mg TDS or 1 g TDS (high-dose if resistant S. pneumoniae suspected)	5–10 days ^[3]^[11]	Covers the Big Three (S. pneumoniae, H. influenzae, M. catarrhalis). Narrow spectrum, well-tolerated, cheap. High-dose amoxicillin overcomes penicillin-resistant S. pneumoniae (altered PBP mechanism — higher drug concentration → still binds PBP)
First-line alternative	Amoxicillin-clavulanate (Augmentin)	625 mg TDS or 1 g BD (high-dose formulation)	5–10 days	Adds β-lactamase inhibitor → covers β-lactamase-producing H. influenzae and M. catarrhalis. Preferred if recent antibiotic exposure (within 4 weeks), treatment failure, or moderate-severe disease
Penicillin allergy (non-anaphylactic)	Doxycycline	100 mg BD	5–10 days	Good activity against respiratory pathogens including atypicals. Not a β-lactam → safe in penicillin allergy. Avoid in children < 8 years (teeth staining) and pregnancy
Penicillin allergy (non-anaphylactic)	Macrolide (clarithromycin/azithromycin)	Clarithromycin 500 mg BD × 7d; Azithromycin 500 mg day 1, then 250 mg OD × 4d	5–7 days	Increasing resistance among S. pneumoniae limits utility. IDSA guidelines do not recommend macrolides as first-line due to resistance
Second-line / treatment failure	Amoxicillin-clavulanate (high-dose)	Amox 2 g / clav 125 mg BD	5–10 days	Escalation for first-line failure
Second-line / severe	Respiratory fluoroquinolone (levofloxacin / moxifloxacin)	Levofloxacin 500 mg OD; Moxifloxacin 400 mg OD	5–7 days	Excellent sinus penetration, broad-spectrum. Reserved for treatment failure or allergy — not first-line because of serious side effects (tendinopathy, QT prolongation, aortic aneurysm risk, C. difficile, dysglycaemia). "Respiratory" fluoroquinolone = enhanced Gram-positive (pneumococcal) activity compared to ciprofloxacin
Severe / complicated (IV)	IV Ceftriaxone ± metronidazole or IV Ampicillin-sulbactam	Standard doses	Until clinical improvement → step-down to oral	For complicated ABRS requiring hospitalisation; ceftriaxone for broad Gram-negative and pneumococcal cover; metronidazole added if anaerobic cover needed (e.g., odontogenic source, intracranial abscess)

Why Amoxicillin First-Line?

Amoxicillin is preferred because: (1) excellent activity against S. pneumoniae (the most important pathogen), (2) good oral bioavailability (~90% — much better than ampicillin ~50%), (3) well-tolerated, (4) narrow spectrum (good antibiotic stewardship), (5) cheap. High-dose amoxicillin (1 g TDS or 90 mg/kg/day in children) is used when penicillin-resistant S. pneumoniae is suspected (resistance is via altered PBP, not β-lactamase, so higher concentrations overcome it).

Guideline	Duration
GC/CFB lecture slides	5–10 days ^[11]
Senior notes (Ryan Ho, Adrian Lui)	5 days (e.g., amoxicillin × 5d) ^[3]
IDSA 2012	5–7 days (adults); 10–14 days (children)
EPOS 2020	5–10 days

Current trend is towards shorter courses (5–7 days) in adults — equally effective as 10–14 day courses with fewer side effects and less antibiotic resistance. In children, longer courses (10–14 days) are often still recommended.

Reassess at 48–72 hours — if no improvement:
- Reconsider diagnosis (is it really bacterial? Consider viral, allergic, or alternative diagnosis)
- Escalate antibiotic (amoxicillin → amoxicillin-clavulanate → respiratory fluoroquinolone)
- Consider imaging (CT) and ENT referral
- Consider sinus aspirate/endoscopic culture for C/ST
If fails ≥ 2 appropriate antibiotic courses → CT sinuses + nasal endoscopy + ENT referral mandatory

Therapy	Evidence / Recommendation	Notes
Antihistamines	NOT routinely recommended for ARS unless co-existent allergic rhinitis	First-generation antihistamines (chlorpheniramine) may thicken secretions and impair clearance; second-generation (cetirizine, loratadine) less drying. Useful only if allergic component contributing
Mucolytics (guaifenesin)	Weak evidence; may thin secretions	Not strongly recommended
Steam inhalation	No proven benefit; risk of burns (especially children)	Not recommended
Zinc / Vitamin C	Minimal evidence for prevention of viral URTI; no role in treatment of ARS
Oral corticosteroids	Short course (e.g., prednisolone 30 mg × 5 days) may be beneficial as adjunct in severe ARS	Rapid reduction of mucosal oedema → opens ostia; more commonly used in CRSwNP (see below)

4. Chronic Rhinosinusitis — Treatment Modalities

CRS management is fundamentally different from ARS because CRS is predominantly an inflammatory disorder rather than a persistent bacterial infection ^[3]. Therefore, the emphasis is on sustained anti-inflammatory therapy rather than antibiotics.

4.1 Maximal Medical Therapy (MMT) — First-Line for All CRS

MMT is the term for the combination of medical treatments that should be tried before considering surgery. A trial of MMT typically lasts 8–12 weeks.

Aspect	Details
Role	First-line therapy for both CRSsNP and CRSwNP ^[3]
Mechanism	As above — broad anti-inflammatory effects reducing mucosal oedema, eosinophilic inflammation, and polyp size
Delivery	Spray (mometasone, fluticasone) for CRSsNP; drops or high-volume rinse (budesonide added to saline irrigation) may be superior for CRSwNP because drops deliver drug to olfactory cleft and polyp surface more effectively (gravity-dependent — "head-down" position)
Duration	Long-term / indefinite maintenance. Unlike topical decongestants, INCS do not cause rebound or tachyphylaxis
Side effects	Epistaxis (most common — instruct patient to aim spray laterally), nasal dryness, crusting. Systemic effects extremely rare with standard doses

Same principles as ARS but used daily as a maintenance strategy. Large-volume irrigation (240 mL squeeze bottle) is more effective than simple sprays for CRS. Helps clear thick mucus and inflammatory debris, and may serve as a vehicle for budesonide delivery.

Aspect	Details
Indication	CRSwNP with significant polyp burden causing obstruction and anosmia; acute exacerbation of CRS; pre-operative "medical polypectomy" to shrink polyps and improve surgical field
Regimen	Prednisolone 0.5–1 mg/kg/day × 5–14 days (typically 25–50 mg/day for 5–7 days, then taper or stop)
Mechanism	Potent systemic anti-inflammatory → rapid reduction of polyp size (reduces oedema) and improvement of anosmia
Limitations	Effect is temporary — polyps regrow after stopping; cannot be used repeatedly due to cumulative steroid side effects (osteoporosis, DM, AVN, adrenal suppression, cataracts, weight gain, immunosuppression). Maximum 2–3 short courses per year

Use	Details
Short course for acute exacerbation	Similar to ABRS — amoxicillin-clavulanate × 5–10 days for bacterial exacerbation superimposed on CRS
Long-term low-dose macrolide (e.g., clarithromycin 250 mg OD or azithromycin 250 mg 3×/week × 12 weeks)	For CRSsNP refractory to INCS. Mechanism is anti-inflammatory (not primarily antimicrobial at low dose): macrolides reduce IL-8, TNF-α, neutrophilic inflammation, mucus hypersecretion, and biofilm formation. Evidence best for CRSsNP with low IgE (non-eosinophilic phenotype). Monitor for QT prolongation, hearing loss, GI upset, hepatotoxicity, antibiotic resistance
Culture-directed antibiotics	For severe or refractory CRS — endoscopic culture guides targeted therapy

Measure	Details
Allergen avoidance	Dust mite covers, dehumidifiers, air purifiers (HK: dust mite is the dominant perennial allergen)
Oral/intranasal antihistamines	Cetirizine, loratadine, fexofenadine (non-sedating); or intranasal azelastine
Allergen immunotherapy (AIT)	Subcutaneous (SCIT) or sublingual (SLIT) for selected patients with confirmed IgE-mediated allergy and inadequate symptom control. Modifies the underlying immune response (↑ Treg, ↑ blocking IgG₄, ↓ Th2). Takes 3–5 years

Therapy	Role
Leukotriene receptor antagonist (montelukast)	Especially useful in AERD/Samter's triad (blocks CysLT₁ receptor → ↓ leukotriene-driven inflammation). Modest benefit as add-on to INCS in CRSwNP
Aspirin desensitisation	For AERD after FESS — daily aspirin (300–650 mg) maintains desensitised state → reduces polyp recurrence. Must be initiated in controlled setting due to risk of severe reaction
Proton pump inhibitor	If GERD contributing to chronic post-nasal drip and laryngopharyngeal symptoms

4.2 Surgical Treatment

Surgery is indicated when maximal medical therapy fails. The goal is not to "cure" CRS but to restore sinus ventilation and drainage so that topical medical therapy can access the sinuses effectively.

Aspect	Details
Principle	"Functional" (Latin: functio = performance) — the surgery aims to restore the normal function of sinus drainage by removing obstructing tissue, widening natural ostia, and clearing diseased mucosa while preserving normal mucosa. Performed endoscopically (trans-nasal, no external incisions)
Indications	(1) CRS (CRSsNP or CRSwNP) refractory to ≥ 8–12 weeks of MMT, (2) Recurrent acute rhinosinusitis (≥ 4 episodes/year), (3) Complications of ARS (orbital abscess, intracranial abscess requiring drainage), (4) Mucocoele, (5) Fungal ball removal, (6) Biopsy of suspicious mass, (7) Facilitate access for topical medications
Procedures	Uncinectomy (remove uncinate process), anterior/posterior ethmoidectomy, maxillary antrostomy (widen natural ostium), frontal sinusotomy (Draf procedure), sphenoidotomy — extent tailored to disease
Complications	Orbital injury (lamina papyracea breach → orbital haematoma, diplopia, visual loss), CSF leak (cribriform plate/skull base breach), haemorrhage (sphenopalatine artery, anterior ethmoid artery), synechia (adhesions), recurrence, anosmia
Post-operative care	Nasal saline irrigation (essential), INCS (continue long-term), regular endoscopic debridement in the weeks after surgery

Procedure	Indication
Balloon sinuplasty	Dilation of sinus ostia with a balloon catheter — less invasive than FESS, limited evidence; mainly for isolated maxillary or frontal sinusitis
Caldwell-Luc (sublabial approach to maxillary sinus)	Rarely used now; occasionally for fungal ball, inverted papilloma, odontogenic sinusitis if endoscopic approach insufficient
External frontal sinus surgery (frontal trephine, osteoplastic flap)	Complicated frontal sinusitis, failed FESS, Pott's puffy tumour
Septoplasty ± turbinate reduction	Adjunctive — corrects deviated septum / reduces hypertrophied turbinates to improve nasal airflow and sinus drainage

For severe, refractory CRSwNP (failed MMT + FESS, or recurrent polyps after surgery), biologic agents targeting the Th2 inflammatory pathway are now available. EPOS 2020 and subsequent updates (EUFOREA 2023) have established criteria for biologic use.

Biologic	Target	Mechanism	Key Points
Dupilumab (Dupixent)	IL-4Rα subunit	Blocks both IL-4 and IL-13 signalling → ↓ Th2 inflammation, ↓ eosinophilic recruitment, ↓ IgE production, ↓ mucus production	First biologic approved for CRSwNP (FDA 2019). Also approved for asthma and atopic dermatitis — useful for the "unified airway" patient with CRSwNP + asthma + eczema. Most robust evidence
Omalizumab (Xolair)	Free IgE	Anti-IgE monoclonal antibody → prevents IgE binding to FcεRI on mast cells → ↓ mast cell degranulation	Useful in CRSwNP with high IgE / allergic component; also approved for severe allergic asthma
Mepolizumab (Nucala)	IL-5	Blocks IL-5 → ↓ eosinophil maturation, survival, and recruitment	For eosinophil-driven CRSwNP; also approved for severe eosinophilic asthma
Benralizumab (Fasenra)	IL-5Rα	Binds IL-5 receptor + ADCC → direct eosinophil depletion	More potent eosinophil depletion than mepolizumab

Indications for biologics (EPOS 2020 / EUFOREA criteria — need ≥ 3 of the following despite adequate surgery + INCS):

Type 2 inflammation (tissue eosinophils ≥ 10/HPF, or blood eosinophils ≥ 250/μL, or total IgE ≥ 100 IU/mL)
Need for systemic steroids (≥ 2 courses/year)
Significantly impaired quality of life (SNOT-22 ≥ 40)
Significant anosmia
Comorbid asthma requiring regular ICS

Complications (orbital, intracranial, facial) require emergency management:

Principle	Details
Admit to hospital	All complicated rhinosinusitis cases
IV broad-spectrum antibiotics	Cover Gram-positives (S. aureus, streptococci), Gram-negatives, anaerobes. E.g., IV ceftriaxone + metronidazole; or IV ampicillin-sulbactam; add vancomycin if MRSA suspected
Urgent CT with contrast ± MRI	Delineate extent of disease
Surgical drainage	Orbital subperiosteal abscess → endoscopic or external drainage. Intracranial abscess → neurosurgical drainage. FESS for sinus drainage
Ophthalmology consult	For orbital complications — serial visual acuity, pupil, eye movement assessment
Neurosurgery consult	For intracranial complications
Anticoagulation	Controversial in septic cavernous sinus thrombosis — some centres use therapeutic anticoagulation, others do not (risk of haemorrhage into infarcted tissue)

Situation	Management Considerations
Pregnancy	Avoid: fluoroquinolones, doxycycline, oral decongestants (pseudoephedrine — vasoconstriction risk). Safe: amoxicillin, nasal saline, INCS (budesonide is pregnancy category B), paracetamol. Short topical decongestant use acceptable if needed
Children	First-line antibiotic: amoxicillin (45–90 mg/kg/day ÷ BD or TDS) × 10–14 days. Avoid fluoroquinolones (cartilage toxicity). Nasal saline very well tolerated. Topical decongestants: avoid in children < 6 years
Odontogenic sinusitis	Must treat the dental source (extraction, root canal) + antibiotics covering anaerobes (amoxicillin-clavulanate or clindamycin)
Invasive fungal sinusitis	Surgical emergency: urgent debridement of necrotic tissue + IV antifungals (liposomal amphotericin B for Mucor; voriconazole for Aspergillus) + treat underlying condition (correct DKA, reduce immunosuppression)
AERD / Samter's triad	Avoid aspirin/NSAIDs until desensitised. FESS + aspirin desensitisation + INCS + leukotriene antagonist. Biologics (dupilumab) particularly effective. Avoid COX-1 inhibitors

Condition	First-Line Treatment	Second-Line / Add-On	Surgical
Acute viral RS	Supportive: saline irrigation, decongestant (max 5–7d), analgesia, ± INCS	—	Not applicable
Acute bacterial RS	Above + amoxicillin × 5–10d	Amox-clav, doxycycline, resp. FQ	Only for complications
CRSsNP	INCS + saline irrigation (8–12 weeks)	Low-dose long-term macrolide, culture-directed Abx	FESS if medical failure
CRSwNP	INCS (drops/rinse) + saline ± short oral steroids	Biologics (dupilumab, omalizumab, mepolizumab), LTRA	FESS ± polypectomy
AERD	INCS + LTRA + aspirin avoidance	FESS + aspirin desensitisation, biologics	FESS (high recurrence)
Complicated ARS	IV Abx + surgical drainage	Culture-directed Abx	Emergency FESS ± orbital/intracranial drainage
Invasive fungal	IV amphotericin B / voriconazole + debridement	Correct underlying condition	Urgent surgical debridement

High Yield Summary

ARS Management:

Viral ARS: supportive treatment × 7–14 days — symptomatic Tx: regular analgesia, nasal saline irrigation, nasal decongestants ^[3]. ± Intranasal steroids: modest benefit, to be used if symptoms persist ^[3].
Bacterial ARS (ABRS): above + oral antibiotics × 5–10 days ^[11]. First-line: amoxicillin ^[3].
Routine use of antibiotics does NOT prevent development of complications ^[3].
Only ~2% of viral URTIs progress to bacterial sinusitis, yet antibiotics are prescribed > 85% of the time ^[3] — classic antibiotic stewardship point.

CRS Management:

Predominantly anti-inflammatory rather than antibacterial ^[3].
First-line: intranasal corticosteroids + nasal saline irrigation (daily, long-term).
CRSwNP: add short oral steroid courses, LTRA, consider biologics (dupilumab) if refractory.
Surgery (FESS): after failure of maximal medical therapy × 8–12 weeks; restores drainage for topical therapy.

Key Contraindications:

Topical nasal decongestants > 5–7 days → rhinitis medicamentosa.
NSAIDs in AERD/Samter's triad.
Fluoroquinolones in children and pregnancy.
Do not give antibiotics for viral ARS.

Active Recall - Management of Rhinosinusitis

References

^[1] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf (Rhinosinusitis definition, slide 14) ^[3] Senior notes: Ryan Ho Respiratory.pdf (Rhinosinusitis management, p.54); Adrian Lui Pediatrics Notes.pdf (p.159) ^[8] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Diagnostic criteria ARS, p.137); MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (p.113) ^[11] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf (Acute rhinosinusitis treatment, slide 16)

Complications of Rhinosinusitis

Complications of rhinosinusitis are uncommon ^[3], but when they occur they can be life-threatening or sight-threatening. Understanding why complications happen requires revisiting the anatomy:

The paranasal sinuses are surrounded by thin bony walls that separate them from critical structures: the orbit (lamina papyracea of the ethmoid, 0.2–0.5 mm thick, often naturally dehiscent), the anterior cranial fossa (roof of ethmoid/frontal sinus = floor of anterior cranial fossa), and the middle cranial fossa (sphenoid sinus roof = floor of middle cranial fossa near the pituitary, cavernous sinus, and optic nerve).
Infection spreads beyond the sinuses via three routes:
1. Direct extension — through thin/dehiscent bone (especially lamina papyracea)
2. Thrombophlebitis of valveless veins — the diploic veins (within bone) and emissary veins connecting the sinuses, orbit, and intracranial venous sinuses have no valves, allowing bidirectional flow of infected material. The superior ophthalmic vein drains into the cavernous sinus without a valve — this is the key route for septic cavernous sinus thrombosis.
3. Erosion of bone by osteomyelitis or by pressure (mucocoele)

The source sinus determines which complications are most likely:

Source Sinus	Most Common Complication Direction	Key Anatomical Reason
Ethmoid	Orbital (most common overall)	Lamina papyracea is paper-thin and frequently dehiscent
Frontal	Facial (Pott's puffy tumour) + intracranial	Posterior wall of frontal sinus = anterior cranial fossa; anterior wall → subperiosteal abscess
Sphenoid	Intracranial (cavernous sinus thrombosis, meningitis)	Lateral wall contains cavernous sinus, ICA, CN III–VI
Maxillary	Orbital (via floor of orbit) or dental	Thin orbital floor; dental root proximity

Complications are classified into three anatomical categories, as consistently listed across all major sources ^[3]^[8]^[12]^[13]:

Complications of acute rhinosinusitis ^[3]^[12]^[13]:

Facial: facial cellulitis, osteomyelitis of sinus bones (Pott's puffy tumour)

Orbit: preseptal cellulitis, orbital cellulitis, subperiosteal abscess

Intracranial: meningitis, intracranial abscess, septic cavernous sinus thrombosis

High Yield — Complications from GC Lecture Slides

The GC lecture slide (GC 215) explicitly lists: orbital cellulitis, abscess; cavernous sinus thrombosis; intracranial infection — meningitis, encephalitis, abscess ^[12]. The CFB lecture slide (CFB WCS29) adds: orbital cellulitis/abscess, meningitis/intracranial abscess and emphasises assessment of colour vision and eye movement as key clinical checks ^[13].

3. Facial Complications

Aspect	Details
Pathophysiology	Direct extension of sinus infection through the anterior bony wall of the maxillary or frontal sinus → infection of overlying soft tissues (skin and subcutaneous tissue of the face)
Clinical features	Localised facial erythema, warmth, oedema, and tenderness overlying the affected sinus. Low-grade fever. The skin is intact (no fluctuance initially). Typically occurs over the cheek (maxillary) or forehead (frontal)
Diagnosis	Clinical. CT with contrast if not improving or worsening
Management	Oral or IV antibiotics (covering S. aureus and streptococci). Treat underlying sinusitis. Rarely requires drainage unless abscess forms

Aspect	Details
Definition	Osteomyelitis (osteo = bone, myel = marrow, itis = inflammation) of the frontal bone with associated subperiosteal abscess presenting as a soft, "doughy" (puffy) swelling over the forehead
Why "Pott's puffy tumour"?	Named after Sir Percivall Pott (1714–1788). "Tumour" in the original sense means "swelling" (Latin: tumor = swelling), not neoplasm
Pathophysiology	Frontal sinusitis → infection spreads through the anterior table of the frontal sinus bone via thrombophlebitis of diploic veins or direct erosion → osteomyelitis of the frontal bone → pus collects beneath the periosteum on the external surface of the frontal bone → subperiosteal abscess → visible forehead swelling. Can also spread posteriorly through the posterior table → epidural abscess or subdural empyema (therefore often a combined facial + intracranial complication)
Clinical features	Gradually enlarging, non-tender or mildly tender, fluctuant/doughy swelling on the forehead. Fever, headache. Gradual onset of dull pain at involved site with or without movement. Local findings such as erythema, swelling, warmth and tenderness may be present. Systemic symptoms such as fever, chills and rigors may be present ^[8]
Epidemiology	Most common in adolescents — the frontal sinus is the last to pneumatise (age 5–6, fully developed by adolescence), and the diploic venous system is most active during this period
Investigation	CT with contrast (shows frontal bone erosion, subperiosteal collection, ± intracranial extension). MRI to assess intracranial complications
Management	IV antibiotics (prolonged course, 4–6 weeks for osteomyelitis) + surgical drainage (subperiosteal abscess evacuation + frontal sinus drainage ± craniectomy of necrotic bone). Always evaluate for intracranial extension

4. Orbital Complications

Orbital complications are the most common complications of rhinosinusitis, accounting for ~60–80% of all complications. They occur most frequently from ethmoid sinusitis (because the lamina papyracea separating the ethmoid from the orbit is paper-thin). More common in children (ethmoid sinusitis is more common in children, and the lamina papyracea is thinner and more porous).

The Chandler classification (1970) provides a systematic staging from least to most severe:

Stage	Name	Location	Key Features	Pathophysiology
I	Preseptal cellulitis	Anterior to orbital septum	Eyelid oedema, erythema, warmth. NO proptosis, NO ophthalmoplegia, NO visual impairment	Infection limited to eyelid tissues anterior to the orbital septum. Orbital septum acts as a barrier preventing posterior spread. Caused by direct spread from sinus or by inflammatory oedema (reactive, without actual infection of orbital contents)
II	Orbital cellulitis	Posterior to orbital septum (within orbit)	Eyelid swelling + ocular pain + pain with eye movement + proptosis + ophthalmoplegia + diplopia ± visual impairment ^[8]^[14]	Infection has breached the orbital septum (or more commonly entered via lamina papyracea) → inflammation of orbital fat and extraocular muscles. The orbit is a closed compartment — swelling within it pushes the globe forward (proptosis) and compresses extraocular muscles (ophthalmoplegia) and the optic nerve (↓ vision)
III	Subperiosteal abscess	Between periorbita and lamina papyracea	As Stage II but with a defined abscess collection medial to the orbit, displacing the globe laterally and inferiorly. CT shows rim-enhancing fluid collection	Pus collects beneath the periosteum along the medial orbital wall, between periorbita and eroded lamina papyracea. Causes mass effect on orbital contents
IV	Orbital abscess	Within orbital fat (intra-conal or extra-conal)	Severe proptosis, complete ophthalmoplegia, severe visual loss, severe orbital pain	Established abscess within the orbital fat — very high risk of permanent visual loss and intracranial extension
V	Septic cavernous sinus thrombosis	Cavernous sinus (intracranial)	See section 5.3 below	Retrograde thrombophlebitis via the valveless superior ophthalmic vein → cavernous sinus

Preseptal vs Orbital Cellulitis — The Critical Distinction

This is one of the most commonly tested distinctions in medical exams. The key differentiating features (from ophthalmology teaching ^[14]):

Feature	Preseptal cellulitis	Orbital cellulitis
Eyelid swelling/erythema	Yes	Yes
Pain with eye movement	No	Yes
Proptosis	No	Yes
Ophthalmoplegia/diplopia	No	Yes (most important feature) ^[14]
Visual impairment/RAPD	No	May be present
Chemosis	Rarely	May be present
Severity	Not an emergency	Ophthalmic emergency ^[14]
Treatment	Oral antibiotics	High-dose IV antibiotics ^[14]

The orbital septum is the key anatomical boundary. Anything anterior = preseptal = manageable. Anything posterior = orbital = emergency.

The GC/CFB lecture slide emphasises assessing colour vision and eye movement in patients with complicated sinusitis ^[13]. Why these two specifically?

Colour vision — the optic nerve is exquisitely sensitive to compression and ischaemia. Loss of colour vision (especially red desaturation) is one of the earliest signs of optic nerve compromise, even before visual acuity drops. Testing with Ishihara plates or a red pin is quick and can detect impending optic neuropathy.

Eye movement — ophthalmoplegia (restriction of eye movements) is the most important feature distinguishing orbital cellulitis from preseptal cellulitis ^[14]. It indicates involvement of orbital contents (extraocular muscles or their nerve supply — CN III, IV, VI).

Stage	Management
I — Preseptal	Oral antibiotics (amoxicillin-clavulanate or cephalosporin). Close follow-up. Admit if child < 1 year, systemically unwell, or not improving on oral Abx
II — Orbital cellulitis	Admission. IV antibiotics (e.g., IV ceftriaxone + metronidazole ± flucloxacillin). Urgent ophthalmology assessment ^[13]. Serial visual acuity, pupil, colour vision, and eye movement checks (every 4–6 hours). CT sinuses with contrast. ENT referral for sinus drainage if not improving
III — Subperiosteal abscess	Admission. IV antibiotics. CT scan. Surgical drainage ^[13] — endoscopic or external drainage of subperiosteal collection + sinus drainage (FESS). Indications for drainage: abscess > 10 mm, no improvement after 24–48h IV Abx, visual deterioration, large abscess in older child/adult
IV — Orbital abscess	Emergency surgical drainage (orbitotomy) + IV antibiotics + sinus drainage. High risk of permanent visual loss
V — Cavernous sinus thrombosis	See below

5. Intracranial Complications

Intracranial complications are the most dangerous complications of rhinosinusitis, with significant morbidity and mortality. They arise most commonly from frontal and ethmoid sinusitis.

Intracranial complications: meningitis, intracranial abscess, septic cavernous sinus thrombosis ^[3]^[12].

Aspect	Details
Pathophysiology	Infection spreads from sinuses (especially ethmoid, frontal, sphenoid) to the meninges via: (1) direct extension through defects in the skull base (cribriform plate, posterior wall of frontal sinus), (2) thrombophlebitis of valveless veins, (3) haematogenous spread
Clinical features	Headache, fever, neck stiffness (meningism), photophobia, altered consciousness, positive Kernig's and Brudzinski's signs. May have concurrent sinusitis symptoms
Microbiology	Typically S. pneumoniae, S. aureus, streptococci, anaerobes (from sinus flora — different from typical community-acquired meningitis pathogens)
Investigation	LP (if no contraindication — must exclude raised ICP with CT first): CSF shows ↑ WCC (neutrophil predominance), ↑ protein, ↓ glucose, positive Gram stain/culture. CT/MRI with contrast shows meningeal enhancement
Management	High-dose IV antibiotics (e.g., IV ceftriaxone + metronidazole ± vancomycin). ± Dexamethasone (reduces inflammatory complications). Treat the sinus source — FESS/surgical drainage once stabilised

This includes epidural abscess, subdural empyema, and intracerebral (brain) abscess.

Type	Location	Pathophysiology	Clinical Features
Epidural abscess	Between inner skull table and dura	Direct extension through posterior wall of frontal sinus or via osteomyelitis/thrombophlebitis	Gradual onset headache, fever, focal neurological signs if large enough to cause mass effect ^[8]. May be occult (contained by dura)
Subdural empyema	Between dura and arachnoid	Spread via valveless veins → thrombophlebitis → infection of subdural space. Rapidly progressive because subdural space has no anatomical barriers → infection spreads freely over cerebral convexity	Severe headache, high fever, rapid deterioration of consciousness, seizures, focal neurological signs (hemiparesis), meningism. Most dangerous intracranial complication — mortality ~10–20% even with treatment
Brain abscess	Within brain parenchyma (usually frontal lobe — adjacent to frontal sinus)	Direct extension or haematogenous seeding → focal cerebritis → encapsulated abscess	Triad: headache (progressive, worst on waking — raised ICP), fever, focal neurological deficit (depends on location — frontal lobe = personality change, contralateral hemiparesis, expressive aphasia if dominant side). ± Seizures. Ring-enhancing lesion on CT/MRI with contrast

Investigation: CT head with contrast (ring-enhancing lesion with surrounding oedema for abscess; lenticular epidural collection; crescent-shaped subdural collection). MRI with DWI is superior (abscess shows restricted diffusion — bright on DWI — which distinguishes it from tumour necrosis). CT sinuses with contrast to identify source.

Management: Neurosurgical drainage (craniotomy/burr hole evacuation) + prolonged IV antibiotics (6–8 weeks, covering Gram-positives, Gram-negatives, and anaerobes — e.g., IV ceftriaxone + metronidazole ± vancomycin). FESS for sinus source control.

Aspect	Details
Pathophysiology	Infection from sinuses (especially ethmoid, sphenoid) or orbit spreads retrogradely via the valveless superior ophthalmic vein into the cavernous sinus → infected thrombus forms within the cavernous sinus. The cavernous sinus contains: CN III (oculomotor), CN IV (trochlear), CN V₁ (ophthalmic division of trigeminal), CN V₂ (maxillary division), CN VI (abducens — runs directly through the sinus, not in the wall, making it most vulnerable), and the internal carotid artery (ICA). Infection affects these structures
Clinical features	Presents with cranial nerve palsies and headache ^[8]. Specifically: (1) Severe headache (worse than expected for sinusitis), (2) High swinging fever + sepsis, (3) Bilateral periorbital oedema + proptosis (initially unilateral then becomes bilateral as infection crosses via intercavernous sinuses — bilateral involvement is the hallmark), (4) CN palsies: CN VI first (abducens → lateral gaze palsy → diplopia), then CN III + IV (complete ophthalmoplegia), CN V₁/V₂ (facial numbness), (5) Papilloedema (venous congestion), (6) Altered consciousness
Investigation	MRI with MR venography (MRV) — shows filling defect/lack of flow in cavernous sinus. CT with contrast may show expansion of cavernous sinus with heterogeneous enhancement. Blood cultures (often positive)
Management	IV broad-spectrum antibiotics (high-dose, prolonged). Surgical drainage of the sinus source. Anticoagulation (therapeutic heparin) — controversial but increasingly used to prevent thrombus propagation; some centres withhold due to haemorrhage risk. Mortality: 20–30% even with treatment; high morbidity (permanent CN palsies, visual loss, pituitary insufficiency)

Why Does CN VI Get Affected First in Cavernous Sinus Thrombosis?

CN VI (abducens nerve) runs through the body of the cavernous sinus, surrounded by venous blood, unlike CN III, IV, V₁, and V₂ which run in the lateral wall of the sinus. This makes CN VI the most vulnerable to compression, ischaemia, or direct involvement by infected thrombus. Loss of lateral rectus function → medial deviation of the eye → inability to look laterally → diplopia on horizontal gaze.

While the acute complications above are dramatic, CRS also causes significant long-term morbidity:

Complication	Pathophysiology
Mucocoele	Complete obstruction of a sinus ostium → trapped mucus secretion → sinus fills and slowly expands → pressure erosion of bony walls → presents as facial/orbital mass. Most common in frontal sinus. Can become infected (mucopyocoele). Treatment: surgical drainage (endoscopic marsupialization)
Permanent anosmia	Chronic eosinophilic inflammation (CRSwNP) damages olfactory neuroepithelium in the olfactory cleft. May persist even after successful surgery. Significant impact on quality of life and safety (cannot smell gas leaks, smoke, spoiled food)
Lower airway disease	"Unified airway" concept — CRS associated with poorly controlled asthma, bronchiectasis. Post-nasal drip of inflammatory mediators and pathogens into lower airways. Treating CRS improves asthma control
Obstructive sleep apnoea	Chronic nasal obstruction → mouth breathing → pharyngeal collapse → OSA
Quality of life impairment	CRS causes fatigue, poor sleep, depression, reduced productivity — SNOT-22 scores in severe CRS are comparable to other chronic diseases (heart failure, COPD)
Recurrent acute exacerbation	CRS with persistent mucosal inflammation → periodic bacterial superinfection → recurrent episodes of acute-on-chronic sinusitis

Category	Complications	Source Sinus	Key Clinical Clue
Facial ^[3]	Facial cellulitis, Pott's puffy tumour (osteomyelitis + subperiosteal abscess of frontal bone)	Maxillary, frontal	Facial swelling, doughy forehead mass
Orbital ^[3]^[12]^[13]	Preseptal cellulitis, orbital cellulitis, subperiosteal abscess, orbital abscess	Ethmoid (most common)	Eyelid swelling → proptosis, ophthalmoplegia, ↓ vision
Intracranial ^[3]^[12]^[13]	Meningitis, epidural abscess, subdural empyema, brain abscess, septic cavernous sinus thrombosis	Frontal, ethmoid, sphenoid	Severe headache, meningism, focal neurology, bilateral orbital signs (CST)

All clinicians managing rhinosinusitis must recognise these red flags that trigger urgent investigation and referral:

Red Flag	Suspected Complication	Action
Periorbital/lid swelling + erythema	Preseptal or orbital cellulitis	Assess eye movement, vision, pupil → if orbital signs present → emergency
Pain with eye movement, proptosis, ophthalmoplegia ^[13]^[14]	Orbital cellulitis / subperiosteal or orbital abscess	Admission, CT with contrast, urgent ophthalmology + ENT ^[13]
↓ Visual acuity, ↓ colour vision, RAPD ^[13]	Optic nerve compression (orbital abscess or cellulitis)	Urgent surgical decompression
Bilateral periorbital swelling + CN palsies	Septic cavernous sinus thrombosis	MRI/MRV, IV Abx, ± anticoagulation, neurosurgical consult
Frontal "doughy" swelling	Pott's puffy tumour	CT with contrast, IV Abx, surgical drainage
Severe headache + meningism + fever	Meningitis or intracranial abscess	CT → LP if safe, MRI, IV Abx, neurosurgical consult
Altered consciousness, seizures, focal neurology	Intracranial abscess / subdural empyema	Emergency CT/MRI, neurosurgery
High swinging fever + sepsis unresponsive to Abx	Undrained abscess (any location)	CT ± MRI to locate abscess → drainage

Management Algorithm for Complicated Sinusitis — from GC/CFB Lecture Slides

The CFB lecture slide explicitly states the approach ^[13]:

Present as orbital swelling/cellulitis
Assess colour vision and eye movement
Admission
CT scan
Urgent ophthalmologist assessment
IV antibiotic and drainage
Surgical drainage: endoscopic drainage ^[13]

High Yield Summary

Complications of rhinosinusitis are uncommon but potentially devastating ^[3]. They are classified into three categories:

Facial: facial cellulitis, Pott's puffy tumour (frontal bone osteomyelitis + subperiosteal abscess) ^[3]
Orbital (most common): Chandler stages I–V — preseptal cellulitis → orbital cellulitis → subperiosteal abscess → orbital abscess → septic cavernous sinus thrombosis ^[3]^[12]^[13]
Intracranial: meningitis, epidural abscess, subdural empyema, brain abscess, septic cavernous sinus thrombosis ^[3]^[12]

Key exam points:

Preseptal vs orbital cellulitis: distinguished by presence of proptosis, ophthalmoplegia (most important feature), and visual impairment → orbital cellulitis is an ophthalmic emergency ^[14]
Assess colour vision + eye movement in all patients with complicated sinusitis ^[13]
CN VI affected first in cavernous sinus thrombosis (runs through body of cavernous sinus, not in the wall)
Bilateral orbital signs = hallmark of cavernous sinus thrombosis
Pott's puffy tumour: adolescents, frontal sinus, doughy forehead swelling — always evaluate for intracranial extension
Management: admission, CT with contrast, IV antibiotics, urgent ophthalmology/ENT/neurosurgery, surgical drainage ^[13]

Active Recall - Complications of Rhinosinusitis

References

^[3] Senior notes: Ryan Ho Respiratory.pdf (Rhinosinusitis complications, p.54); Adrian Lui Pediatrics Notes.pdf (Rhinosinusitis complications, p.158) ^[8] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Complications of ARS, p.138–140); MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (Complications of ARS, p.114) ^[12] Lecture slides: GC 215. Common nasal conditions and nasopharyngeal carcinoma.pdf (Acute bacterial rhinosinusitis complications, p.22) ^[13] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf (Complicated sinusitis management, slides 18–19) ^[14] Senior notes: Ryan Ho Opthalmology.pdf (Orbital cellulitis, p.37)

High Yield Summary

Classification: Acute ( < 12 weeks) vs Chronic (≥ 12 weeks). CRS divided into CRSsNP (~2/3, neutrophilic) and CRSwNP (~1/3, eosinophilic).

Aetiology: Viral (vast majority) → bacterial superinfection (0.5–2%): S. pneumoniae, H. influenzae, M. catarrhalis. Fungal in immunocompromised.

Pathophysiology: Vicious cycle: trigger → mucosal oedema → OMC obstruction → impaired mucociliary clearance → mucus stasis → bacterial colonisation → more inflammation.

Key Clinical Points:

Coloured nasal discharge ≠ bacterial infection; it reflects PMN content.
Double sickening = hallmark of bacterial ARS.
Nasal polyps: grey-white, mobile, painless (vs turbinate: pink, fixed, tender).
Samter's triad: asthma + CRSwNP + aspirin sensitivity.
Red flags: orbital signs (proptosis, ophthalmoplegia, ↓ vision), meningism, frontal swelling, altered consciousness → complicated sinusitis.

Predisposing factors (lecture slides): deviated septum, polyp, tumour, dental root infection, URTI, congenital, immunocompromised.

High Yield Summary

Core differential of rhinosinusitis presentations:

Nasal obstruction + discharge: allergic rhinitis (most common mimic), vasomotor rhinitis, rhinitis medicamentosa, adenoid hypertrophy, foreign body (child — unilateral, foul), NPC (unilateral — HK!)
Facial pain without nasal symptoms: migraine ("sinus headache"), tension headache, cluster headache, dental pathology, TMJ dysfunction, trigeminal neuralgia
Chronic/recurrent: CRS (CRSsNP vs CRSwNP), NPC, sinonasal tumour, GPA, EGPA, sarcoidosis, fungal disease, CF, PCD
Unilateral red flags: always think NPC, NK/T-cell lymphoma, inverted papilloma, foreign body, fungal ball, odontogenic sinusitis
Immunocompromised: invasive fungal sinusitis (Mucor/Aspergillus) — surgical emergency
Viral vs bacterial ARS: distinguished by duration ( < 10d improving vs ≥ 10d persistent), double sickening, severity, fever > 38°C

High Yield Summary

Diagnosis is predominantly clinical — no investigations needed for uncomplicated ARS ^[3]^[8].

Sinus XR: poor sensitivity and specificity → NOT recommended ^[3]^[8].

CT with contrast for complications; CT without contrast for CRS workup/pre-op ^[8].

MRI for soft tissue complications, tumour staging, intracranial extension ^[8].

Sinus aspirate/endoscopic culture for C/ST — only for suspected serious complications, treatment failure, or immunocompromised ^[3]^[8].

Do NOT CT during an acute URTI — up to 40% incidental mucosal thickening → false positives.

High Yield Summary

ARS Management:

Viral ARS: supportive treatment × 7–14 days — symptomatic Tx: regular analgesia, nasal saline irrigation, nasal decongestants ^[3]. ± Intranasal steroids: modest benefit, to be used if symptoms persist ^[3].
Bacterial ARS (ABRS): above + oral antibiotics × 5–10 days ^[11]. First-line: amoxicillin ^[3].
Routine use of antibiotics does NOT prevent development of complications ^[3].
Only ~2% of viral URTIs progress to bacterial sinusitis, yet antibiotics are prescribed > 85% of the time ^[3] — classic antibiotic stewardship point.

CRS Management:

Predominantly anti-inflammatory rather than antibacterial ^[3].
First-line: intranasal corticosteroids + nasal saline irrigation (daily, long-term).
CRSwNP: add short oral steroid courses, LTRA, consider biologics (dupilumab) if refractory.
Surgery (FESS): after failure of maximal medical therapy × 8–12 weeks; restores drainage for topical therapy.

Key Contraindications:

Topical nasal decongestants > 5–7 days → rhinitis medicamentosa.
NSAIDs in AERD/Samter's triad.
Fluoroquinolones in children and pregnancy.
Do not give antibiotics for viral ARS.

High Yield Summary

Complications of rhinosinusitis are uncommon but potentially devastating ^[3]. They are classified into three categories:

Facial: facial cellulitis, Pott's puffy tumour (frontal bone osteomyelitis + subperiosteal abscess) ^[3]
Orbital (most common): Chandler stages I–V — preseptal cellulitis → orbital cellulitis → subperiosteal abscess → orbital abscess → septic cavernous sinus thrombosis ^[3]^[12]^[13]
Intracranial: meningitis, epidural abscess, subdural empyema, brain abscess, septic cavernous sinus thrombosis ^[3]^[12]

Key exam points:

Preseptal vs orbital cellulitis: distinguished by presence of proptosis, ophthalmoplegia (most important feature), and visual impairment → orbital cellulitis is an ophthalmic emergency ^[14]
Assess colour vision + eye movement in all patients with complicated sinusitis ^[13]
CN VI affected first in cavernous sinus thrombosis (runs through body of cavernous sinus, not in the wall)
Bilateral orbital signs = hallmark of cavernous sinus thrombosis
Pott's puffy tumour: adolescents, frontal sinus, doughy forehead swelling — always evaluate for intracranial extension
Management: admission, CT with contrast, IV antibiotics, urgent ophthalmology/ENT/neurosurgery, surgical drainage ^[13]

Rhinosinusitis

1. Definition

2. Epidemiology

2.1 Incidence and Prevalence

2.2 Age Distribution

2.3 Hong Kong Context

3. Risk Factors

3.1 Local/Anatomical Factors

3.2 Mucosal/Functional Factors

3.3 Systemic/Host Factors

3.4 Iatrogenic/Environmental Factors

4. Anatomy and Function of the Paranasal Sinuses

4.1 The Four Paired Paranasal Sinuses

4.2 The Ostiomeatal Complex (OMC)

4.3 Sinus Physiology

4.4 Sinus Relations (Clinically Relevant for Complications)

5. Aetiology

5.1 Acute Rhinosinusitis (ARS)

5.1.1 Viral (Majority)

5.1.2 Bacterial (0.5–2% of viral ARS cases)

5.1.3 Fungal

5.2 Chronic Rhinosinusitis (CRS) — Duration > 12 Weeks

5.2.1 CRS without Nasal Polyps (CRSsNP) — ~2/3 of CRS [6]

5.2.2 CRS with Nasal Polyps (CRSwNP) — ~1/3 of CRS [6]

5.3 Summary Table of Aetiology

6. Pathophysiology

6.1 Acute Rhinosinusitis

6.2 Chronic Rhinosinusitis

6.3 Complications — Pathophysiology of Spread

7. Classification

7.1 By Duration

7.2 By Aetiology and Clinical Manifestation

7.3 Chronic Rhinosinusitis Subtypes

7.4 Special Forms

8. Clinical Features

8.1 Symptoms

8.1.1 Nasal Symptoms (Cardinal)

8.1.2 Facial/Head Symptoms

8.1.3 Systemic Symptoms

8.1.4 Associated Symptoms

8.1.5 Symptoms Distinguishing Bacterial from Viral ARS

8.2 Signs

8.2.1 External Examination

8.2.2 Anterior Rhinoscopy / Nasal Endoscopy

8.2.3 Signs of Complications (Red Flags)

8.2.4 Signs in Chronic Rhinosinusitis

9. Cardinal Symptoms and Signs Summary

10. Conditions Associated with Rhinosinusitis

Active Recall - Rhinosinusitis (Definition, Epidemiology, Anatomy, Aetiology, Clinical Features)

References

1. Differential Diagnosis by Presenting Symptom Complex

1.1 Nasal Obstruction + Nasal Discharge (the core symptoms)

1.2 Facial Pain/Pressure (± Headache)

1.3 Chronic Nasal Symptoms (> 12 Weeks) — Must Exclude Serious Pathology

2. Key Distinction: Viral vs Bacterial Acute Rhinosinusitis

3. Approach to Differential Diagnosis — Clinical Algorithm

4. Differential Diagnosis in Specific Populations

4.1 Children

4.2 Immunocompromised Patients

4.3 Hong Kong-Specific Considerations

5. Summary Table — Comprehensive Differential Diagnosis

6. How to Systematically Narrow the Differential

Active Recall - Differential Diagnosis of Rhinosinusitis

1. Diagnostic Principles — First Principles

2. Diagnostic Criteria

2.1 EPOS 2020 Criteria (GC/CFB Lecture Slides)

2.2 Criteria for Acute Viral vs Acute Bacterial Rhinosinusitis

Acute Viral Rhinosinusitis (AVRS)

Acute Bacterial Rhinosinusitis (ABRS)

EPOS 2020 / Senior Notes Criteria for Bacterial ARS (Alternative Framework)

2.3 Diagnostic Criteria for Chronic Rhinosinusitis (CRS)

3. Diagnostic Algorithm

4. Investigations — When, What, and Why

4.1 Overview: When Are Investigations Indicated?

4.2 Physical Examination (The First "Investigation")

4.2.1 Anterior Rhinoscopy

4.2.2 Nasal Endoscopy (Rigid or Flexible)

4.2.3 Otoscopy

4.3 Laboratory Investigations

4.3.1 Blood Tests