Nasal Congestion, Runny Nose
Nasal congestion and runny nose (rhinorrhea) are symptoms resulting from inflammation and increased mucus production of the nasal mucosa, commonly caused by infections, allergies, or irritants.
Nasal Congestion and Runny Nose (Rhinorrhoea)
Let's start by breaking down the terms:
-
Nasal congestion (from Latin con- = together, gerere = to carry → "crowding together") refers to the subjective sensation of reduced nasal airflow or a feeling of fullness/blockage in the nasal passages. It results from engorgement of the nasal venous sinusoids and mucosal oedema, reducing the cross-sectional area of the nasal airway.
-
Rhinorrhoea (from Greek rhis/rhino- = nose, -rhoea = flow) literally means "nose flow" — the discharge of fluid from the nasal cavity. It may be anterior (dripping from the nostrils) or posterior (post-nasal drip down the pharynx).
These two symptoms almost always coexist and are among the most frequent presenting complaints in primary care, ENT, and paediatric settings. They are not diagnoses in themselves but rather symptom manifestations of an underlying process affecting the nasal cavity and/or paranasal sinuses.
Key Conceptual Point
Nasal congestion ≠ a structural blockage in all cases. It is most often a physiological response — vasodilatation of the rich submucosal venous plexus (Kiesselbach's plexus anteriorly, the inferior turbinate cavernous tissue) under autonomic control. Think of the nose as an "erectile organ" — the turbinates swell and shrink under parasympathetic and sympathetic tone, respectively.
2. Epidemiology
- Nasal congestion and rhinorrhoea are the most common symptoms in medicine, period. The common cold alone accounts for >200 million days of school absence and >100 million physician visits annually in the US.
- Acute coryza (common cold, viral URI) is the most common type of URTI [1]. Over 200 viral subtypes can cause it.
- Allergic rhinitis (AR) affects 10–30% of the global population; in Hong Kong, AR prevalence in schoolchildren is approximately 40–50% (among the highest worldwide, likely due to subtropical climate, high population density, and indoor allergen exposure — house dust mite Dermatophagoides pteronyssinus is the dominant allergen in HK).
- Chronic rhinosinusitis (CRS) affects ~5–12% of the general population globally.
- GERD-related nasal symptoms are increasingly recognised, as reflux of gastric acid into the nasopharynx can cause chronic rhinitis symptoms [2].
| Feature | Allergic Rhinitis | Viral URTI | CRS with Polyps | CRS without Polyps |
|---|---|---|---|---|
| Age | Children/young adults | Any age | Adults (30–60y) | Adults |
| Sex | M = F | M = F | M > F | M ≈ F |
| Atopy | Strong association | None | 40–60% | Variable |
| HK prevalence | Very high | Universal | ~4% | ~8% |
3. Risk Factors
Understanding risk factors requires understanding what makes the nose swell and run:
- Atopy — genetic predisposition to mount IgE responses to environmental allergens (house dust mite, cockroach, cat dander, fungi). Strongly linked to allergic rhinitis, which is part of the "atopic march" (eczema → AR → asthma) [3].
- Genetic factors — HLA associations, polymorphisms in IL-4, IL-13, and filaggrin genes affect mucosal barrier integrity and immune polarisation.
- Age — children have smaller nasal passages and immature immune systems (more frequent viral URIs: 6–8/year in children vs 2–4/year in adults). Elderly patients may develop senile rhinitis (gustatory rhinitis) from autonomic dysregulation.
- Anatomical variants — deviated nasal septum, concha bullosa (pneumatised middle turbinate), adenoid hypertrophy (children) → impaired drainage → recurrent infection.
- Hypothyroidism — listed as a masquerade [4]. Hypothyroidism causes mucosal oedema throughout the body (myxoedema) including the nasal mucosa, leading to chronic nasal congestion and rhinorrhoea. Always check TFTs in unexplained chronic nasal symptoms.
- Pregnancy — "rhinitis of pregnancy" due to oestrogen-mediated vasodilatation and ↑blood volume → turbinate engorgement.
- Immunodeficiency — IgA deficiency, common variable immunodeficiency (CVID), HIV → recurrent/chronic sinusitis.
- Viral exposure — crowding, daycare attendance, poor hand hygiene. Hand contact is the most important mode of transmission; hand-washing is the most effective method in prevention [1].
- Allergen exposure — indoor allergens (house dust mite faecal pellets, pet dander, cockroach), outdoor allergens (Alternaria fungi, pollens) [5].
- Cigarette smoking — both active and passive smoking damages cilia (ciliotoxic), increases mucus production, and promotes chronic inflammation. A risk factor for URIs and chronic rhinosinusitis [1].
- Air pollution — particulate matter (PM2.5, PM10) and nitrogen dioxide are major contributors in Hong Kong, directly damaging nasal epithelium and enhancing allergen sensitisation.
- Occupational irritants — dusts, fumes, chemicals (wood dust → especially associated with sinonasal adenocarcinoma in furniture workers).
- Drugs — topical OTC sympathomimetics → rhinitis medicamentosa; narcotics [4]. Also: oral contraceptives, antihypertensives (reserpine, methyldopa, ACE inhibitors, β-blockers), aspirin/NSAIDs (Samter's triad), cocaine.
- Cold air/wind — triggers vasomotor rhinitis via trigeminal-mediated parasympathetic reflex.
Masquerades Checklist for Nasal Symptoms
Drugs (topical OTC → rhinitis medicamentosa; narcotics) and Hypothyroidism are listed explicitly in the masquerades checklist [4]. Always ask about:
- Over-the-counter nasal decongestant spray use (oxymetazoline, xylometazoline)
- Thyroid symptoms (fatigue, cold intolerance, weight gain, constipation)
4. Anatomy and Function of the Nose and Paranasal Sinuses
Understanding nasal congestion and rhinorrhoea requires a solid grasp of nasal anatomy. Let me walk you through it systematically:
- Bony framework (nasal bones, frontal process of maxilla) superiorly; cartilaginous framework (upper lateral cartilages, lower lateral/alar cartilages, septal cartilage) inferiorly.
- The nasal valve (the narrowest point of the nasal airway, at the junction of upper and lower lateral cartilages) is critical — even small amounts of mucosal swelling here can produce disproportionate obstruction (Poiseuille's law: resistance ∝ 1/r⁴, so halving the radius increases resistance 16-fold).
- Extends from the vestibule (skin-lined anteriorly) to the choana (posterior nasal aperture opening into nasopharynx).
- Nasal septum (midline): composed of septal cartilage, vomer, and perpendicular plate of ethmoid. Deviation is extremely common (~80% of people have some degree of deviation) and may contribute to unilateral obstruction.
- Lateral wall — the key functional area, containing three turbinates (conchae):
- Inferior turbinate — largest, most important for airflow regulation. Contains cavernous erectile tissue (venous sinusoids) that can swell dramatically under parasympathetic stimulation, causing nasal congestion.
- Middle turbinate — overlies the ostiomeatal complex (OMC), the critical drainage pathway for the maxillary, anterior ethmoid, and frontal sinuses. Obstruction of the OMC is the central event in sinusitis pathophysiology.
- Superior turbinate — small, overlies the sphenoethmoidal recess (drainage of sphenoid and posterior ethmoid sinuses).
The nasal mucosa is a pseudostratified ciliated columnar epithelium (respiratory epithelium) with goblet cells, except in the vestibule (keratinised squamous) and olfactory region (olfactory neuroepithelium).
Key functional components:
- Goblet cells — secrete mucus (~1 litre/day normally). Mucus forms a bilayer: a thin sol (periciliary) layer and a thicker gel layer that traps particles.
- Cilia — beat in coordinated waves (~10–15 Hz) to propel the mucus blanket posteriorly toward the nasopharynx (mucociliary clearance). This is the nose's primary defence mechanism.
- Submucosal glands — serous and seromucous glands secrete additional fluid, especially under parasympathetic (cholinergic) stimulation.
- Venous sinusoids — the capacitance vessels of the inferior turbinate. Richly innervated:
- Sympathetic fibres (from superior cervical ganglion, via vidian nerve) → release noradrenaline → α-adrenoreceptor-mediated vasoconstriction → decongestion
- Parasympathetic fibres (from superior salivatory nucleus → CN VII → greater petrosal nerve → vidian nerve → pterygopalatine ganglion) → release acetylcholine → vasodilatation + glandular secretion → congestion + rhinorrhoea
- A normal physiological phenomenon: alternating congestion and decongestion of each nasal cavity every 2–6 hours, controlled by the autonomic nervous system (hypothalamus).
- Most people are unaware of it. Patients become aware when mucosal inflammation (e.g., viral URI, AR) amplifies the cycle, causing noticeable unilateral or alternating blockage.
Four paired sinuses, all drain into the nasal cavity:
| Sinus | Drainage Site | Clinical Significance |
|---|---|---|
| Maxillary | Middle meatus (via OMC) | Most commonly infected (ostium is high on medial wall → poor gravity drainage) |
| Frontal | Middle meatus (via frontal recess) | Frontal headache; intracranial complications (frontal osteomyelitis = Pott's puffy tumour) [1] |
| Anterior Ethmoid | Middle meatus (via OMC) | Orbital complications (lamina papyracea = paper-thin medial orbital wall) |
| Posterior Ethmoid | Superior meatus | Adjacent to optic nerve |
| Sphenoid | Sphenoethmoidal recess | Adjacent to cavernous sinus, internal carotid, optic nerve |
The nose is not just a passive tube — it is a sophisticated organ:
- Airway conditioning — warms (to 37°C), humidifies (to 100% relative humidity), and filters inspired air before it reaches the lower airways. The turbinates create turbulent airflow that maximises air-mucosal contact.
- Defence — mucociliary clearance traps and removes particles (> 10μm filtered by vibrissae; 2–10μm deposited on mucus blanket). IgA, lysozyme, lactoferrin in nasal secretions provide innate immunity.
- Olfaction — olfactory epithelium in the roof of the nasal cavity (cribriform plate region). Congestion impairs olfaction by preventing odorant molecules from reaching this region (conductive hyposmia). Patients with nasal congestion have hyponasal voice due to inadequate air escape through the nose [6].
- Resonance — contributes to voice quality. Nasal congestion causes a hyponasal voice [6].
- Nitric oxide production — paranasal sinus epithelium produces NO, which is a potent vasodilator and has antimicrobial properties. This is why nasal breathing is physiologically superior to mouth breathing.
5. Aetiology (with Focus on Hong Kong)
Here I'll organise the causes systematically. Think of the nose as having only a few ways it can go wrong: infection, allergy, structural problems, vasomotor dysfunction, or systemic disease.
| Duration | Category | Common Causes |
|---|---|---|
| Acute ( < 4 weeks) | Infectious | Viral URTI (common cold), acute bacterial rhinosinusitis |
| Allergic | Acute allergic rhinitis (seasonal or perennial) | |
| Other | Foreign body (children), nasal trauma, drug-induced | |
| Chronic ( > 12 weeks) | Inflammatory | Chronic rhinosinusitis ± nasal polyps, allergic rhinitis |
| Structural | Deviated septum, turbinate hypertrophy, adenoid hypertrophy | |
| Vasomotor | Non-allergic rhinitis (vasomotor rhinitis) | |
| Drug-induced | Rhinitis medicamentosa, drug side effects | |
| Systemic | Hypothyroidism, granulomatous diseases, pregnancy | |
| Neoplastic | Benign (inverted papilloma) or malignant (SCC, adenocarcinoma, NPC) |
5.2 Infectious Causes
The most common type of URTI [1].
- Virology: > 200 subtypes including rhinovirus (30–50%), coronavirus (10–15%), influenza (5–15%), RSV (5%), parainfluenza virus (5%), adenovirus, enterovirus [1].
- Transmission: by 3 main mechanisms — hand contact (most important), droplet transmission, and aerosol transmission (for selected viruses). Most contagious at onset of symptoms and when febrile [1].
- Risk factors: underlying chronic diseases, psychological stresses, minimal exercise, immunodeficiency, malnutrition, cigarette smoking [1].
Pathophysiology:
- Virus enters nasal epithelium (rhinovirus binds ICAM-1 on epithelial cells; coronavirus binds ACE2).
- Viral replication triggers innate immune response → release of pro-inflammatory cytokines (IL-1, IL-6, IL-8, TNF-α, bradykinin).
- Bradykinin and histamine → vasodilatation of submucosal venous sinusoids → nasal congestion.
- Cholinergic reflex stimulation of submucosal glands → watery rhinorrhoea.
- Cytokine-mediated increased vascular permeability → plasma exudation → adds to secretions.
- Ciliary dysfunction from viral cytopathic effect → impaired mucociliary clearance → mucus retention → mucoid then secondary purulent discharge (colour change reflects neutrophil influx, NOT necessarily bacterial superinfection).
Why does the discharge change from clear to yellow/green? Because neutrophils recruited to the site contain myeloperoxidase (a green pigment). Yellow-green discharge does NOT automatically mean bacterial infection.
Acute rhinosinusitis: symptomatic inflammation of nasal cavity and paranasal sinuses lasting < 4 weeks [1].
- Aetiology: viral URTI → direct spread to paranasal sinuses or ↓sinus drainage with secondary bacterial infection [1].
Pathophysiology:
- Viral infection of nasal mucosa → mucosal oedema → obstruction of the ostiomeatal complex (OMC).
- Sinus ostia are blocked → impaired mucociliary drainage → mucus stasis within the sinus.
- Reduced oxygen tension in the sealed sinus → lowered pH → ideal environment for bacterial growth.
- Bacterial superinfection (if it occurs) → purulent sinusitis with neutrophil infiltration.
- Pain: Why does bending forward worsen sinus pain? Because bending forward increases venous pressure in the head and causes further engorgement of already inflamed sinus mucosa, plus gravitational shift of trapped fluid/pus within the sinus pressing on sensitised nerve endings.
Complications: spread beyond paranasal sinuses [1]:
- Important to distinguish from common cold (higher fever, myalgia, prostration, cough more prominent; rhinorrhoea less prominent than with rhinovirus).
- Relevant in HK: seasonal peaks in winter (Jan–Mar) and summer (Jul–Aug). H3N2 and H1N1 are the predominant circulating subtypes.
- Vaccination is the primary prevention strategy — recommended annually in HK for high-risk groups.
- SARS-CoV-2 (Omicron and later variants) commonly presents with nasal congestion, rhinorrhoea, and sore throat (more "cold-like" than earlier variants).
- Important in the HK context given recurrent waves.
A. Allergic Rhinitis (AR)
The single most common cause of chronic nasal congestion and rhinorrhoea in Hong Kong.
Classification (ARIA 2020):
| Intermittent | Persistent | |
|---|---|---|
| Definition | Symptoms < 4 days/week OR < 4 consecutive weeks | Symptoms ≥ 4 days/week AND ≥ 4 consecutive weeks |
| Severity — Mild | None of the below impairments | |
| Severity — Moderate-Severe | ≥1 of: sleep disturbance, impairment of daily activities/school/work, troublesome symptoms |
Pathophysiology — the Type I Hypersensitivity Reaction:
-
Sensitisation phase (first exposure):
- Allergen (e.g., house dust mite Der p 1 protease) penetrates nasal mucosa → captured by dendritic cells → presented to naïve T cells → Th2 differentiation → IL-4 release → B cell class switching to IgE → allergen-specific IgE binds to FcεRI receptors on mast cells in nasal mucosa.
-
Early phase (within minutes of re-exposure):
- Allergen cross-links IgE on mast cells → mast cell degranulation → release of preformed mediators:
- Histamine → binds H1 receptors → vasodilatation (congestion), increased vascular permeability (oedema, rhinorrhoea), stimulation of sensory nerve endings (itch, sneeze reflex)
- Tryptase → activates complement, cleaves fibrinogen
- Leukotrienes (LTC4, D4, E4) → potent vasodilatation and mucus hypersecretion (leukotrienes are 1000× more potent than histamine as bronchoconstrictors)
- Prostaglandin D2 → vasodilatation, eosinophil chemotaxis
- Allergen cross-links IgE on mast cells → mast cell degranulation → release of preformed mediators:
-
Late phase (4–8 hours later):
- Newly synthesised mediators (leukotrienes, cytokines) recruit eosinophils, basophils, Th2 lymphocytes to nasal mucosa.
- Eosinophils release major basic protein (MBP) and eosinophilic cationic protein (ECP) → epithelial damage → further mucosal hyperreactivity.
- This late-phase inflammation is why patients with AR have persistent nasal congestion even hours after allergen exposure has ceased and why nasal steroids (which target the inflammatory cascade) are more effective than antihistamines (which only block histamine) for congestion.
-
Priming (with chronic exposure):
- Repeated allergen exposure progressively lowers the threshold for mast cell degranulation → progressively smaller amounts of allergen trigger symptoms → explains why AR worsens over the allergy season.
Allergens in Hong Kong:
- Perennial (dominant in HK subtropical climate): house dust mite (Dermatophagoides pteronyssinus, D. farinae), cockroach, cat/dog dander, mould (Aspergillus, Alternaria)
- Seasonal (less prominent in HK than temperate regions): tree/grass pollens (spring), ragweed (autumn) — less relevant in HK
Allergic conjunctivitis often occurs in association with allergic rhinitis [7]. In fact, up to 60–70% of AR patients have concomitant allergic conjunctivitis — think of it as allergic rhinoconjunctivitis.
This is the second most common cause of chronic rhinitis after allergic rhinitis. The nose is "overreacting" to non-specific stimuli without an IgE-mediated mechanism.
Pathophysiology:
- Autonomic imbalance: parasympathetic dominance over sympathetic tone in nasal mucosa → excessive vasodilatation and glandular secretion in response to non-specific triggers.
- Triggers: cold air, strong odours, spicy food (gustatory rhinitis), emotional stress, humidity changes, exercise, cigarette smoke.
- No allergen-specific IgE; skin prick tests and specific IgE are negative.
- Often overlaps with allergic rhinitis ("mixed rhinitis" in ~50% of chronic rhinitis patients).
Rhinitis medicamentosa — caused by chronic use of topical OTC sympathomimetic nasal decongestants (oxymetazoline, xylometazoline) [4].
Pathophysiology:
- Topical α-adrenergic agonists (e.g., oxymetazoline) cause vasoconstriction of nasal venous sinusoids → rapid decongestion.
- With prolonged use (> 5–7 days), tachyphylaxis develops: downregulation of α-adrenoreceptors on vascular smooth muscle.
- On withdrawal of the drug → rebound vasodilatation (the sinusoids, deprived of their normal α-adrenergic tone, dilate excessively).
- Patient uses more spray → worsening cycle → chronic, severe nasal congestion.
- Chronic use also causes direct mucosal damage with loss of cilia and epithelial metaplasia.
Rhinitis Medicamentosa – A Trap!
This is a classic exam trap and a real clinical pitfall. Any patient with chronic nasal congestion MUST be asked about OTC nasal spray use. The history is often volunteered reluctantly. Treatment is to STOP the offending spray (cold turkey or gradual taper with concurrent intranasal corticosteroids to manage rebound congestion).
Other drug-induced causes:
- Narcotics (opioids) → histamine release from mast cells → nasal congestion [4]
- Antihypertensives (reserpine, methyldopa, guanethidine — deplete noradrenaline → sympathetic deficit → nasal vasodilatation)
- β-blockers — reduce sympathetic-mediated vasoconstriction
- ACE inhibitors — increase bradykinin levels → vasodilatation + mucus secretion
- Oral contraceptives / HRT — oestrogen causes mucosal vasodilatation
- Aspirin / NSAIDs — in aspirin-exacerbated respiratory disease (AERD / Samter's triad: asthma + nasal polyps + aspirin sensitivity) — COX-1 inhibition diverts arachidonic acid metabolism to the lipoxygenase pathway → excess cysteinyl leukotrienes → severe nasal congestion, polyps, and bronchoconstriction
- Cocaine — chronic intranasal use → vasoconstriction → ischaemic necrosis of nasal septum → septal perforation and paradoxical congestion
| Cause | Mechanism | Key Features |
|---|---|---|
| Deviated nasal septum | Mechanical narrowing of nasal passage on one side | Unilateral congestion, may be alternating if combined with nasal cycle |
| Turbinate hypertrophy | Chronic mucosal inflammation → irreversible submucosal fibrosis and bony hypertrophy | Bilateral congestion, often in chronic AR |
| Nasal polyps | Oedematous outgrowths of ethmoid sinus mucosa (NOT turbinate mucosa), typically bilateral, arising from middle meatus | Bilateral progressive congestion, anosmia. If unilateral → must exclude neoplasm |
| Adenoid hypertrophy | Enlarged pharyngeal tonsil obstructing posterior choanae | Children: mouth breathing, snoring, nasal speech, recurrent otitis media |
| Foreign body | Physical obstruction of nasal passage | Children: unilateral, foul-smelling, purulent, possibly bloody nasal discharge — pathognomonic presentation |
| Choanal atresia | Congenital bony or membranous obstruction of posterior choanae | Neonates: cyclical cyanosis relieved by crying (because neonates are obligate nose breathers). CHARGE syndrome association |
Defined as rhinosinusitis symptoms persisting > 12 weeks. Two main phenotypes:
A. CRS without Nasal Polyps (CRSsNP):
- Predominantly neutrophilic inflammation, Th1/Th17 driven
- Often a/w anatomical factors (OMC obstruction, septal deviation) and biofilm formation
- More common in Asian populations (including HK)
B. CRS with Nasal Polyps (CRSwNP):
- Predominantly eosinophilic inflammation, Th2 driven (Type 2 inflammation)
- Strong association with asthma (esp. late-onset eosinophilic asthma) and AERD/Samter's triad
- Polyps are pedunculated, pale grey, translucent, insensitive masses (unlike the vascular, pink, sensitive turbinates)
- High recurrence rate after surgery
Pathophysiology of CRS:
- Initial trigger (infection, allergy, or irritant) → persistent mucosal inflammation at the OMC.
- Mucosal oedema → sinus ostial obstruction → impaired mucociliary clearance → mucus stasis.
- Hypoxic, stagnant environment → bacterial colonisation and biofilm formation (Staphylococcus aureus is a key player, producing superantigens).
- Chronic inflammatory infiltrate:
- CRSsNP: neutrophils, Th1 cytokines (IFN-γ), TGF-β → fibrosis and mucosal remodelling
- CRSwNP: eosinophils, Th2 cytokines (IL-4, IL-5, IL-13), IgE → oedematous polypoid degeneration
- Epithelial barrier defect → further antigen penetration → self-perpetuating cycle.
| Cause | Mechanism | Key Features |
|---|---|---|
| Hypothyroidism [4] | Generalised myxoedema → mucopolysaccharide deposition in nasal submucosa → mucosal oedema | Chronic bilateral congestion, hyponasal voice, associated thyroid symptoms |
| Granulomatosis with polyangiitis (GPA, formerly Wegener's) | Granulomatous vasculitis of small vessels → necrotising granulomata in nasal mucosa | Bloody nasal discharge, crusting, septal perforation, saddle nose deformity. c-ANCA/PR3 positive |
| Sarcoidosis | Non-caseating granulomata in nasal mucosa | Nasal obstruction, crusting. Lupus pernio (violaceous nodules on nose) |
| Relapsing polychondritis | Autoimmune destruction of cartilage | Nasal bridge collapse (saddle nose), auricular chondritis |
| Cystic fibrosis | Defective CFTR → thick, tenacious mucus → chronic sinusitis with polyps | Virtually all CF patients have CRS. Nasal polyps in a child = consider CF |
| CSF rhinorrhoea | Clear discharge following direct facial or head injury may represent CSF leakage from a skull fracture [4] | Unilateral, clear, watery. ↑glucose on testing (unlike nasal mucus). Ring sign on filter paper. Post-trauma or post-surgery |
| Nasopharyngeal carcinoma (NPC) | Highly relevant in HK/Southern Chinese (EBV-associated endemic type) | Unilateral nasal obstruction, blood-stained discharge, conductive hearing loss (Eustachian tube obstruction), cervical lymphadenopathy |
| Pregnancy rhinitis | Oestrogen → vasodilatation; ↑circulating blood volume | Onset in 2nd/3rd trimester, resolves within 2 weeks of delivery |
| Atrophic rhinitis (ozaena) | Chronic atrophy of nasal mucosa and turbinate bones → paradoxically wide nasal cavity but crusting blocks airflow | Foul-smelling nasal crusts (ozaena), sensation of blockage despite wide nasal cavity. Historically associated with Klebsiella ozaenae |
Unilateral Nasal Symptoms — Always Think Sinister!
Beware of persistent blood-stained discharge especially if unilateral and obstruction [4]. This should raise suspicion for:
- Nasopharyngeal carcinoma (very high yield in HK)
- Sinonasal malignancy (SCC, adenocarcinoma, olfactory neuroblastoma)
- Inverted papilloma (benign but locally aggressive with malignant potential)
- Foreign body (children)
- Granulomatous disease (GPA)
- Unilateral choanal atresia (neonate)
A practical clinical classification:
Classification of Rhinosinusitis by Duration
| Type | Duration | Subtype |
|---|---|---|
| Acute | < 4 weeks | Viral vs. Bacterial |
| Subacute | 4–12 weeks | — |
| Chronic | > 12 weeks | CRS with polyps (CRSwNP) vs. CRS without polyps (CRSsNP) |
| Recurrent acute | ≥ 4 episodes/year, each lasting < 4 weeks, with complete resolution between episodes | — |
7. Clinical Features
Now, let's put it all together. When a patient presents with nasal congestion and/or rhinorrhoea, what do you look for?
Elicit nature of discharge: watery, mucoid, bloody, ?offensive and volume. Is it acute or chronic, intermittent or continuous? Associations: respiratory symptoms, nasal blockage, post-nasal drip, headache, local pain. Check for possible influence of physical factors: wind, cold, irritants, smoke. Also check for presence of allergic rhinitis or sinusitis. Ask if there is a possible history of head trauma, nose problems or nasal surgery. Also take a drug history, including OTC medications especially sympathomimetics, illicit drugs, prescribed drugs. [4]
7.2 Symptoms with Pathophysiological Basis
| Feature | Pathophysiological Basis |
|---|---|
| Bilateral congestion, alternating sides | Normal nasal cycle amplified by mucosal inflammation (AR, vasomotor rhinitis) |
| Bilateral progressive congestion | Nasal polyps (bilateral middle meatal masses), adenoid hypertrophy (children) |
| Unilateral fixed congestion | Deviated septum, foreign body, unilateral polyp (exclude malignancy!), unilateral choanal atresia |
| Worse lying down | Gravity-dependent venous pooling in turbinates; also loss of sympathetic tone during sleep |
| Worse in specific environments | Allergic rhinitis (house dust mite — worse in bedroom; pet dander — worse at friend's house) |
| Rebound congestion after nasal spray | Rhinitis medicamentosa — α-receptor downregulation |
| Congestion with anosmia | Nasal polyps (mechanical obstruction of olfactory cleft), or viral damage to olfactory neuroepithelium |
Why does nasal congestion worsen at night?
- Recumbent position → loss of gravitational drainage → pooling of blood in nasal venous sinusoids.
- Sleep → reduced sympathetic tone → less α-adrenergic vasoconstriction → turbinate swelling.
- GERD worsens when supine → acid reflux to nasopharynx → mucosal inflammation.
The character of discharge is a critical diagnostic clue:
| Discharge Type | Mechanism | Suggests |
|---|---|---|
| Watery, clear | Parasympathetic-mediated glandular secretion + plasma transudation | Allergic rhinitis (early phase), vasomotor rhinitis, viral URTI (early), CSF leak |
| Mucoid, thick | Goblet cell hypersecretion with ↑mucin production | Chronic rhinitis, CRS |
| Purulent (yellow-green) | Neutrophil recruitment → myeloperoxidase (green pigment) | Bacterial sinusitis (if persistent > 10 days), late viral URI (does NOT always = bacteria) |
| Blood-stained | Mucosal ulceration, vascular erosion, granulomatous inflammation, neoplasm | Persistent blood-stained discharge especially if unilateral = suspect malignancy (NPC, sinonasal tumour), GPA, foreign body [4] |
| Foul-smelling, unilateral | Anaerobic bacterial superinfection of obstructed cavity | Foreign body (children), dental infection with oroantral fistula, atrophic rhinitis |
| Clear, watery, unilateral, profuse | CSF leakage from cribriform plate fracture or erosion | CSF rhinorrhoea after head trauma [4] — test for β2-transferrin or glucose |
Post-nasal drip (PND):
- Mucus dripping from the posterior nasal cavity into the pharynx.
- Causes chronic cough, throat clearing, sensation of a lump in the throat (globus sensation), and morning sore throat.
- The pathophysiology: excessive or abnormally thick posterior nasal secretions that the swallowing mechanism cannot clear efficiently → contact with pharyngeal mucosa → triggers cough reflex via vagal afferents.
- PND is a leading cause of chronic cough (along with asthma and GERD).
- A trigeminal-mediated reflex initiated by irritation of nasal sensory nerve endings (CN V1, V2).
- Histamine (in allergic rhinitis) directly stimulates H1 receptors on sensory nerves → triggers the sneeze reflex.
- Pattern is helpful: paroxysms of sneezing (5–10 in a row, especially in the morning) is classic for allergic rhinitis. A few sneezes is non-specific.
- Histamine-mediated stimulation of sensory nerve endings in nasal mucosa (C fibres).
- Classic for allergic rhinitis. Patients often perform the "allergic salute" (rubbing nose upward with palm) and may develop a transverse nasal crease.
- Itchiness of the nose, eyes, palate, and ears simultaneously = highly suggestive of atopy (because IgE-sensitised mast cells are present in all these mucosal surfaces).
- Conductive (most common): mucosal oedema or polyps physically block odorant molecules from reaching the olfactory epithelium in the roof of the nose. Reversible with decongestion.
- Sensorineural: viral damage to olfactory neuroepithelium (post-viral anosmia — a major feature of COVID-19), neurodegenerative diseases (Parkinson's, Alzheimer's), or olfactory groove pathology.
- URTI is the most common cause of anosmia [8]. Nasal congestion → hyponasal voice [6].
- Associated with sinusitis: mucosal inflammation and trapped secretions in a closed sinus → positive pressure → stimulation of pain-sensitive mucosal nerve endings.
- Location corresponds to affected sinus:
- Maxillary → cheek / upper teeth
- Frontal → forehead / supraorbital
- Ethmoid → between/behind the eyes, nasal bridge
- Sphenoid → vertex, occipital, retro-orbital (often described as "deep" headache)
- Facial pain or pressure (worse with bending over) [1].
- Ear fullness / hearing loss: Eustachian tube dysfunction from nasopharyngeal mucosal oedema → negative middle ear pressure → serous otitis media (middle ear effusion). Especially important in children.
- Otalgia: referred pain from pharynx/nose via CN V, IX, X.
- Fever, malaise, myalgia → suggest infectious aetiology (viral or bacterial).
- General: malaise, low-grade fever (uncommon but can occur in children) [1].
7.3 Signs with Pathophysiological Basis
Key examination: Look for cause. Inspect nose and nasal cavity with a Thudicum speculum or large auriscope. Note the position of the septum, nature of nasal mucosa and look for polyps or other tumours. [4]
| Sign | Pathophysiology | Clinical Significance |
|---|---|---|
| Allergic shiners (dark circles under eyes) | Venous congestion due to impaired drainage from nasal venous plexus → backpressure in periorbital veins | Chronic allergic rhinitis |
| Allergic salute / transverse nasal crease | Habitual upward rubbing of itchy nose | Allergic rhinitis (especially children) |
| Mouth breathing | Nasal obstruction so severe that oral breathing is necessary | Adenoid hypertrophy (children), nasal polyps, severe AR |
| Adenoid facies | Chronic mouth breathing → altered craniofacial development: elongated face, high-arched palate, dental malocclusion | Chronic adenoid hypertrophy in children |
| Saddle nose deformity | Destruction of nasal septum cartilage | GPA, relapsing polychondritis, cocaine use, congenital syphilis, post-surgical |
| Nasal flaring | Accessory respiratory muscle use to overcome nasal obstruction or respiratory distress | Respiratory distress (any cause), significant nasal obstruction |
| Epistaxis | Mucosal dryness, inflammation, or erosion of Kiesselbach's plexus | Dry rhinitis, digital trauma, hypertension, coagulopathy, HHT |
| Sign | Pathophysiology | Clinical Significance |
|---|---|---|
| Pale, boggy, bluish-grey mucosa | Chronic oedema with eosinophilic infiltration; reduced vascularity from chronic oedema | Classic for allergic rhinitis |
| Erythematous, swollen mucosa | Acute vascular engorgement and inflammatory cell infiltration | Viral URTI, acute sinusitis, vasomotor rhinitis |
| Inferior turbinate hypertrophy | Chronic mucosal oedema → submucosal fibrosis → irreversible enlargement | Chronic rhinitis (any cause) |
| Mucosal inflammation: oedema, narrowing of meatus, inferior turbinate hypertrophy [1] | Inflammatory cascade narrowing the airway | Rhinosinusitis |
| Discharge: copious watery or purulent discharge [1] | Glandular hypersecretion vs. neutrophilic exudation | Acute rhinosinusitis |
| Nasal polyps (pale, grey, translucent, insensitive, pedunculated masses) | Oedematous outgrowth of ethmoid sinus mucosa due to chronic Th2 inflammation | CRSwNP — bilateral = inflammatory; unilateral = must exclude neoplasm (inverted papilloma, SCC) |
| Deviated nasal septum | Developmental or traumatic; mechanical narrowing of one side | Unilateral obstruction. May impair OMC drainage → predispose to sinusitis |
| Co-existent anatomical RFs, eg. polyps, septal deviation [1] | Structural factors predisposing to impaired drainage | Chronic/recurrent rhinosinusitis |
| Foreign body | Physical obstruction with secondary infection | Children: unilateral foul-smelling purulent/bloody discharge |
| Crusting, granulation tissue, septal perforation | Granulomatous destruction or ischaemic necrosis | GPA, cocaine, sarcoidosis, post-surgical |
Signs of sinusitis: not diagnostic in isolation [1]:
- Erythema/oedema with tenderness over sinus areas [1]
- Opacification of maxillary/frontal sinus upon transillumination [1]
Sinus tenderness:
- Maxillary: press over cheek below infraorbital ridge
- Frontal: press upward under supraorbital ridge (NOT downward on the forehead)
- Ethmoid: press on lateral side of nose at inner canthus
- Assess for post-nasal drip (mucopurulent secretions coating posterior pharyngeal wall — "cobblestoning" of pharyngeal mucosa from chronic lymphoid hyperplasia).
- Assess for adenoid hypertrophy (children) — obstructs posterior choanae.
- Exclude nasopharyngeal carcinoma — critical in HK patients with unilateral symptoms, especially with conductive hearing loss or cervical lymphadenopathy.
- Middle ear effusion (amber/grey tympanic membrane, reduced mobility, fluid level/air bubbles) — secondary to Eustachian tube dysfunction from nasal/nasopharyngeal pathology.
- Acute otitis media (especially in children) due to Eustachian tube dysfunction and bacterial translocation from upper respiratory tract [1].
| Sign | Suggests |
|---|---|
| Periorbital oedema / chemosis (no erythema) | Allergic rhinoconjunctivitis |
| Periorbital erythema, warmth, proptosis, ophthalmoplegia | Orbital cellulitis (complication of sinusitis — EMERGENCY) |
| Peau d'orange swelling of forehead | Pott's puffy tumour (frontal osteomyelitis) |
| Cervical lymphadenopathy | Infection or malignancy (NPC) |
| Lower airway wheeze | Asthma (coexisting with AR — "united airway disease") |
| Eczematous skin lesions | Atopic dermatitis (part of atopic triad) [3] |
Respiratory compromise in the context of nasal congestion can include: dyspnoea, wheezes, bronchospasm, stridor, nasal congestion, hoarseness — as seen in anaphylaxis [9].
Key investigations: Usually none required [4]. Consider: micro/culture of discharge, X-ray sinuses, CT scan, allergy testing [4].
| Investigation | When to Consider | What It Shows |
|---|---|---|
| Micro/culture of discharge [4] | Suspected bacterial sinusitis not responding to empirical Rx | Identify organism and sensitivity |
| Sinus X-ray [4] | Historical; largely superseded | Poor sensitivity and specificity → NOT recommended [1] |
| CT scan [4] | Generally reserved for cases where complications are suspected [1], pre-operative planning for FESS | Air-fluid levels, mucosal oedema, air bubbles [1] |
| Allergy testing [4] | Suspected allergic rhinitis | Skin prick test (first-line), serum-specific IgE (RAST) |
| Nasal endoscopy (flexible) | Any chronic or suspicious nasal symptoms | Direct visualisation of nasal cavity, OMC, nasopharynx |
| Nasal cytology | Research / specialist setting | Eosinophils (allergic), neutrophils (infectious) |
| β2-transferrin | Suspected CSF rhinorrhoea | Confirms CSF (highly specific) |
| Biopsy | Suspicious mass/lesion | Exclude malignancy or granulomatous disease |
| TFTs | Hypothyroidism on masquerade checklist [4] | TSH ↑, free T4 ↓ |
| c-ANCA/PR3, p-ANCA/MPO | Suspected vasculitis | GPA, EGPA |
Imaging: NOT indicated if uncomplicated rhinosinusitis [1].
9. Special Populations
- More frequent viral URIs (6–8/year is normal).
- Foreign body — always consider in a child with unilateral foul-smelling discharge.
- Adenoid hypertrophy — peaks at 3–7 years, causes nasal obstruction, snoring, otitis media with effusion.
- Nasal polyps in children — consider cystic fibrosis (up to 50% of CF children develop polyps).
- Choanal atresia — neonatal emergency (cyclical cyanosis relieved by crying; unilateral may present later).
- "Rhinitis of pregnancy" affects ~20–30% of pregnant women, typically in 2nd–3rd trimester.
- Safe treatments: nasal saline irrigation, exercise, nasal strips. Intranasal corticosteroids (budesonide preferred — Category B) if needed.
- Avoid: oral decongestants (pseudoephedrine — Category C, risk of gastroschisis in 1st trimester), first-generation antihistamines (sedation risk to fetus).
- Senile rhinitis / gustatory rhinitis — watery rhinorrhoea triggered by eating, due to parasympathetic hyperactivity. Treated with ipratropium bromide nasal spray.
- Atrophic rhinitis (ozaena) — crusting, foul smell. Nasal saline irrigation, topical antibiotics.
- Consider medication-related causes (many elderly are on antihypertensives, opioids).
Diagnostic Tips from Lecture Slides
Beware of persistent blood-stained discharge especially if unilateral and obstruction [4].
Clear discharge following direct facial or head injury may represent CSF leakage from a skull fracture [4].
Consider masquerade diagnoses: Drugs (topical OTC → rhinitis medicamentosa; narcotics) and Hypothyroidism [4].
High Yield Summary
Nasal Congestion & Rhinorrhoea — Core Concepts:
-
Anatomy is key: the inferior turbinate has erectile tissue (venous sinusoids) regulated by sympathetic (vasoconstriction = decongestion) and parasympathetic (vasodilatation + secretion = congestion + rhinorrhoea) tone.
-
Most common cause acutely: viral URTI (common cold), > 200 subtypes, rhinovirus most common. Self-limiting, > 90% resolve in 10 days [1].
-
Most common cause chronically in HK: allergic rhinitis (house dust mite is the dominant allergen). Type I hypersensitivity: sensitisation → early phase (mast cell degranulation, histamine) → late phase (eosinophilic infiltration).
-
Rhinitis medicamentosa: topical OTC nasal decongestants used > 5–7 days → α-receptor downregulation → rebound congestion [4]. Always ask about OTC spray use.
-
Masquerades: Drugs and Hypothyroidism [4].
-
Red flags for sinister pathology: persistent blood-stained unilateral discharge → exclude NPC, sinonasal malignancy, GPA. Clear unilateral discharge post-trauma → CSF leak [4].
-
Acute rhinosinusitis: viral → direct sinus spread or ↓sinus drainage with secondary bacterial infection. Bacterial (0.5–2%): S. pneumoniae, H. influenzae, M. catarrhalis. Complications: orbital cellulitis, intracranial infection, Pott's puffy tumour [1].
-
Nasal polyps: bilateral = inflammatory (CRSwNP), consider AERD (Samter's triad) and CF (in children). Unilateral = exclude neoplasm.
-
History clues: character of discharge, laterality, duration, triggers, drug history (OTC sprays!), trauma history, associated features (itch, sneezing, anosmia, ear symptoms).
-
Exam: anterior rhinoscopy → pale boggy mucosa (allergic), erythematous mucosa (infectious), polyps, septal deviation, discharge character.
Active Recall - Nasal Congestion and Runny Nose
[1] Senior notes: Ryan Ho Respiratory.pdf (Sections 3.1.1.1 Acute Coryza, 3.1.1.4 Rhinosinusitis) [2] Senior notes: Ryan Ho GI.pdf (Section 2.2.1 GERD — laryngopharyngeal reflux) [3] Senior notes: Ryan Ho Rheumatology.pdf (Section 4.2.2.1 Atopic Dermatitis — atopic triad) [4] Lecture slides: murtagh merge.pdf (p68 — Nasal drip/rhinorrhoea: masquerades checklist, key history, key examination, key investigations, diagnostic tips) [5] Senior notes: Ryan Ho Respiratory.pdf (Section 3.2.1 Asthma — allergens and environmental factors) [6] Senior notes: felixlai.md (Section IV. Pathophysiology — Functions of larynx: hyponasal voice with nasal congestion) [7] Senior notes: Ryan Ho Opthalmology.pdf (Section 2.2.2 Conjunctivitis — allergic conjunctivitis with allergic rhinitis) [8] Senior notes: Ryan Ho Neurology.pdf (Section B. Cranial Nerve Examination — CN I, causes of anosmia including URTI) [9] Senior notes: Ryan Ho Critical Care.pdf (Section 1.3.6 Anaphylactic Shock — nasal congestion as respiratory feature)
Differential Diagnosis of Nasal Congestion and Runny Nose
When a patient walks in with a blocked, runny nose, the temptation is to dismiss it as "just a cold." But the differential diagnosis is surprisingly broad, and missing a sinister cause — particularly in the Hong Kong population — can have devastating consequences. The structured approach below follows Murtagh's Diagnostic Strategy framework, which is an excellent way to organise differentials for any symptom [4].
The key principle: think systematically along anatomical site (where is the problem?), pathological process (what is the process — infection, allergy, vasomotor, structural, neoplastic, systemic?), and temporal pattern (acute vs. chronic).
1. Murtagh's Diagnostic Strategy for Nasal Drip / Rhinorrhoea
This is directly from the lecture slides and forms the backbone of the differential [4]:
These account for the vast majority of presentations:
| Diagnosis | Why It Causes Nasal Congestion/Rhinorrhoea |
|---|---|
| Upper respiratory tract infection especially common cold [4] | Viral infection of nasal mucosa → cytokine release (bradykinin, IL-8) → vasodilatation of turbinate venous sinusoids (congestion) + parasympathetic reflex glandular secretion (watery rhinorrhoea) + increased vascular permeability (plasma exudation). Most common type of URTI, > 200 subtypes including rhinovirus (30–50%) [1] |
| Rhinitis: acute infective, allergic, vasomotor [4] | Acute infective: same mechanism as above. Allergic: Type I hypersensitivity — mast cell degranulation releases histamine → H1-mediated vasodilatation, oedema, glandular secretion, and sensory nerve stimulation (itch, sneeze). Vasomotor: parasympathetic dominance → glandular hypersecretion and vasodilatation without an allergic trigger |
| Vasomotor stimulation e.g. cold wind, smoke, irritants [4] | Non-specific trigeminal sensory nerve stimulation → parasympathetic reflex via pterygopalatine ganglion → acetylcholine release at submucosal glands and venous sinusoids → rhinorrhoea and congestion. No IgE involvement — this is a neural reflex, not an immune response |
| Sinusitis → post-nasal drip [4] | Mucosal inflammation and ostial obstruction → mucus stasis within sinuses → mucopurulent secretions drain posteriorly into the nasopharynx → post-nasal drip sensation, throat clearing, chronic cough. Symptoms include nasal congestion, blockage, discharge, loss of smell + facial pain or pressure (worse with bending over) [1] |
| Senile rhinorrhoea [4] | Age-related autonomic dysregulation → parasympathetic hyperactivity → excessive watery nasal secretion, classically triggered by eating (gustatory rhinitis). Also: nasal mucosal atrophy → impaired mucociliary clearance |
The 'Big Five' Common Causes
If you're in a primary care or ED setting and a patient has nasal congestion/rhinorrhoea, statistically > 90% of the time it will be one of: (1) common cold, (2) allergic rhinitis, (3) vasomotor rhinitis, (4) acute sinusitis, or (5) senile rhinitis in the elderly. But you MUST screen for the serious causes below.
These are uncommon but carry high morbidity/mortality if undiagnosed:
| Diagnosis | Why It Causes Nasal Symptoms | Key Distinguishing Features |
|---|---|---|
| Cluster headache [4] | Ipsilateral autonomic features including lacrimation, nasal congestion, conjunctival injection, Horner's syndrome (~30–50%) [10][11]. The trigeminal-autonomic reflex is activated during attacks: trigeminal nerve pain afferents cross-activate the superior salivatory nucleus → parasympathetic outflow via CN VII → pterygopalatine ganglion → ipsilateral nasal mucosal vasodilatation and glandular secretion | Severe unilateral periorbital pain for 15–180 min, strikingly periodic (same hour daily), patient highly agitated (cf migraine — debilitating). Precipitated by alcohol, GTN [10][11] |
| Chronic infective granulomas e.g. TB [4] | Granulomatous inflammation of nasal mucosa → chronic mucosal thickening, crusting, and destruction. Mycobacterium tuberculosis can cause nasal TB (rare) with caseous granulomata. Also consider leprosy, syphilis, rhinoscleroma (Klebsiella rhinoscleromatis) | Chronic unilateral nasal obstruction, crusting, septal perforation, non-healing ulcers. Low index in HK (TB is still endemic) |
| Malignancy: nasal fossa, sinus, nasopharynx [4] | Tumour mass directly obstructs nasal airway; mucosal invasion causes bleeding and secondary infection. NPC (nasopharyngeal carcinoma) is particularly important in HK/Southern Chinese — EBV-driven, arises in fossa of Rosenmüller, obstructs Eustachian tube and posterior choanae | Persistent blood-stained discharge especially if unilateral and obstruction [4]. NPC: triad of unilateral nasal obstruction + conductive hearing loss + cervical lymphadenopathy. Sinonasal SCC/adenocarcinoma: progressive unilateral obstruction, epistaxis, facial numbness (CN V2 involvement) |
| CSF rhinorrhoea — post head injury [4] | Fracture of the cribriform plate (the thinnest bone of the anterior skull base) disrupts the meninges → CSF leaks through into the nasal cavity via the olfactory fila pathways. Can also occur spontaneously (raised ICP, skull base erosion) or post-surgically (pituitary surgery, FESS) | Clear discharge following direct facial or head injury may represent CSF leakage from a skull fracture [4]. Unilateral, watery, increases with Valsalva or bending forward. Positive for β2-transferrin. Halo sign on filter paper |
| Wegener's granulomatosis (now granulomatosis with polyangiitis, GPA) [4] | c-ANCA/PR3-associated necrotising granulomatous vasculitis → destruction of nasal cartilage and mucosa. Vessels in nasal submucosa undergo fibrinoid necrosis → mucosal ischaemia → crusting, ulceration, septal perforation | Bloody nasal crusts, septal perforation, saddle nose deformity. Systemic features: pulmonary nodules/cavities, rapidly progressive glomerulonephritis. c-ANCA/PR3 positive |
NPC in Hong Kong — Do NOT Miss
Nasopharyngeal carcinoma has an incidence of ~20–30/100,000 in Southern Chinese males — one of the highest worldwide. It is EBV-associated and has a bimodal peak (15–25y and 50–60y). Any patient in HK with unilateral nasal symptoms, blood-stained discharge, conductive hearing loss (serous otitis media from Eustachian tube obstruction), or cervical lymphadenopathy MUST have a nasopharyngeal examination. An EBV VCA IgA and EBV DNA titre can be used as screening tools.
These are diagnoses that are frequently overlooked, leading to delayed treatment:
| Diagnosis | Why It Causes Nasal Symptoms | Why It Gets Missed |
|---|---|---|
| Nasal foreign body e.g. in toddlers [4] | Physical obstruction of nasal passage → secondary bacterial infection of stagnant secretions (often anaerobes) → foul-smelling purulent/bloody unilateral discharge | Parents and clinicians may not consider a foreign body in a child who simply has a "runny nose." The key is unilateral foul-smelling discharge — this is virtually pathognomonic |
| Trauma ± blood [4] | Direct mucosal injury → bleeding, oedema, haematoma. Septal haematoma is a particular danger — the blood collection strips the perichondrium from the cartilage → avascular necrosis → septal abscess → saddle nose deformity | Nasal trauma may be dismissed as minor. Always examine for septal haematoma (red/purple bulging of the septum — this is an ENT emergency requiring immediate drainage) |
| Adenoid hypertrophy [4] | Enlarged pharyngeal tonsil obstructs posterior choanae → chronic nasal obstruction, mouth breathing, post-nasal drip. Also obstructs Eustachian tubes → otitis media with effusion | Presents as chronic mouth breathing, snoring, nasal voice in children. Cannot be seen on anterior rhinoscopy — requires lateral neck X-ray or nasopharyngoscopy to diagnose |
| Illicit drugs e.g. cocaine, opioids especially heroin [4] | Cocaine: potent vasoconstrictor → repeated use causes mucosal ischaemia → necrosis → septal perforation → paradoxical congestion and crusting. Opioids/heroin: narcotics cause histamine release from mast cells → nasal congestion [4][9] | Patients may not volunteer illicit drug use. Always ask sensitively in the social history, especially with unexplained septal perforation or chronic nasal symptoms in young adults |
| Inhaled irritant gases or vapour [4] | Chemical irritation of nasal mucosa → acute inflammation, chemical rhinitis. Occupational: chlorine, ammonia, formaldehyde, wood dust. Consider also e-cigarette/vaping aerosols | Occupational history is often forgotten. Always ask "What do you do for work?" and "Are you exposed to any dusts, fumes, or chemicals?" |
| Choanal atresia (rarity) [4] | Congenital bony or membranous obstruction of the posterior choanae. Bilateral = neonatal emergency (obligate nose breathers → cyclical cyanosis relieved by crying). Unilateral = may present later with chronic unilateral nasal obstruction | Rare, but bilateral form is life-threatening in neonates. Associated with CHARGE syndrome (Coloboma, Heart defects, Atresia choanae, Retardation of growth, Genital hypoplasia, Ear anomalies) |
The masquerades checklist for nasal symptoms includes [4]:
| Masquerade | Mechanism | Key to Not Missing It |
|---|---|---|
| Drugs: topical OTC → rhinitis medicamentosa; narcotics [4] | OTC decongestant sprays: α-receptor downregulation → rebound vasodilatation. Narcotics: mast cell degranulation → histamine release → vasodilatation and glandular secretion | Always ask about OTC nasal spray use and duration. Always ask about opioid use (prescribed and illicit) |
| Hypothyroidism [4] | Mucopolysaccharide (hyaluronic acid, chondroitin sulphate) deposition in nasal submucosa → non-pitting mucosal oedema (myxoedema). Also: reduced metabolic activity → impaired mucociliary clearance | Check for associated hypothyroid features (fatigue, weight gain, cold intolerance, constipation, dry skin, bradycardia). Check TFTs in unexplained chronic nasal congestion |
Building on Murtagh's framework, here is a comprehensive differential organised by mechanism, which is how you should think through the problem at the bedside:
3. Differentiating by Key Clinical Features
This is the practical "at the bedside" approach — certain clinical features point you strongly toward specific diagnoses:
| Character | Think of... | Why? |
|---|---|---|
| Watery, clear, profuse | Allergic rhinitis, vasomotor rhinitis, early viral URTI, CSF leak | Histamine/parasympathetic-mediated glandular secretion (allergic/vasomotor). CSF leak if unilateral and post-trauma |
| Mucoid, thick | Chronic rhinosinusitis, late-stage viral URTI | Goblet cell hyperplasia with increased mucin production from chronic inflammation |
| Purulent (yellow-green) | Bacterial rhinosinusitis (if > 10 days or double sickening), late viral URTI | Neutrophil recruitment → myeloperoxidase gives green colour. Remember: colour alone does NOT confirm bacterial infection |
| Blood-stained | Malignancy (NPC, sinonasal tumour), GPA, foreign body, trauma, coagulopathy, epistaxis | Tumour neovascularisation is friable and bleeds easily. GPA causes mucosal necrosis. Foreign body → traumatic mucosal erosion |
| Foul-smelling, unilateral | Foreign body (children), atrophic rhinitis, dental origin sinusitis | Anaerobic bacterial infection of stagnant secretions (FB), or mucosal atrophy with crusting (ozaena) |
| Clear, watery, unilateral, post-trauma | CSF rhinorrhoea [4] | Cribriform plate fracture → CSF drains through olfactory pathways |
| Pattern | Differential | Rationale |
|---|---|---|
| Unilateral | Foreign body, deviated septum, unilateral polyp (→ exclude malignancy), NPC, sinonasal malignancy, CSF leak, GPA, unilateral choanal atresia, dental sinusitis, cluster headache (ipsilateral) | Unilateral pathology suggests a focal/structural/neoplastic process rather than a systemic or bilateral mucosal disease |
| Bilateral | Viral URTI, allergic rhinitis, vasomotor rhinitis, CRS ± polyps, drug-induced, systemic disease | Bilateral involvement suggests a diffuse mucosal process (infection, allergy, inflammation, systemic) |
| Alternating | Nasal cycle amplified by mucosal inflammation (AR, vasomotor) | Normal nasal cycle becomes symptomatic when mucosal oedema is superimposed — the side in the congestion phase of the cycle becomes completely blocked |
| Duration | Differential |
|---|---|
| Acute ( < 4 weeks) | Viral URTI (by far commonest), acute bacterial rhinosinusitis, acute allergic rhinitis, anaphylaxis, trauma, foreign body |
| Chronic ( > 12 weeks) | Allergic rhinitis, CRS ± polyps, vasomotor rhinitis, rhinitis medicamentosa, structural (septum, turbinate, adenoid), drug-induced, systemic (hypothyroidism, GPA, sarcoidosis), neoplasm |
| Recurrent episodic | Allergic rhinitis (with allergen exposure cycles), vasomotor rhinitis (with trigger exposure), recurrent acute sinusitis |
| Associated Feature | Points Toward | Why |
|---|---|---|
| Sneezing, nasal/palatal itch, watery eyes | Allergic rhinitis | Histamine stimulation of sensory nerves (H1-mediated itch and sneeze reflex). Usually associated with other atopic features: sneezing, rhinorrhoea, eczema [7][12] |
| Facial pain/pressure, worse bending forward | Sinusitis [4][1] | Trapped mucopurulent secretions in a closed sinus → positive pressure on inflamed, sensitised nerve endings. Bending forward increases venous congestion and gravitational shift of fluid |
| Lacrimation, conjunctival injection, periorbital pain, agitation | Cluster headache [4][10][11] | Trigeminal-autonomic reflex: trigeminal pain → parasympathetic activation → ipsilateral nasal congestion, lacrimation. Strikingly periodic, same hour daily [10] |
| Unilateral hearing loss, cervical LN | NPC | Tumour in fossa of Rosenmüller → Eustachian tube obstruction (conductive hearing loss via serous otitis media) + lymphatic spread to deep cervical nodes |
| Saddle nose, crusting, haemoptysis, renal symptoms | GPA | Granulomatous vasculitis destroys nasal cartilage (saddle nose), pulmonary capillaries (haemoptysis), and glomeruli (RPGN) |
| Anosmia, bilateral polyps, asthma, aspirin sensitivity | AERD / Samter's triad | COX-1 inhibition by aspirin → shunting of arachidonic acid to lipoxygenase pathway → excessive cysteinyl leukotrienes → nasal polyps (eosinophilic), bronchoconstriction, nasal congestion |
| Asthma, eczema | Atopic disease (AR as part of atopic triad) | Shared Th2 immune polarisation and IgE dysregulation across mucosal surfaces. Atopic eczema associated with FHx of atopic disease (70%), personal Hx of atopy (allergic rhinitis, asthma, food allergy) [3] |
| Mouth breathing, snoring, recurrent otitis media (child) | Adenoid hypertrophy [4] | Enlarged pharyngeal tonsil obstructs posterior choanae and Eustachian tube orifices |
| Rebound worsening after stopping nasal spray | Rhinitis medicamentosa [4] | α-receptor downregulation from chronic topical decongestant use → rebound vasodilatation |
| Weight gain, cold intolerance, fatigue | Hypothyroidism [4] | Myxoedematous infiltration of nasal submucosa |
| Post head trauma/surgery, clear unilateral discharge | CSF rhinorrhoea [4] | Cribriform plate or skull base fracture/erosion |
4. Differentials Unique to Specific Populations
| Diagnosis | Key Clue |
|---|---|
| Foreign body [4] | Unilateral foul-smelling purulent/bloody discharge. Peak age 2–5 years |
| Adenoid hypertrophy [4] | Chronic mouth breathing, snoring, nasal voice, recurrent AOM/OME |
| Choanal atresia [4] | Neonate: cyclical cyanosis relieved by crying (obligate nose breathers). Unable to pass catheter through nostril |
| Nasal polyps | Must exclude cystic fibrosis in any child with bilateral nasal polyps (up to 50% of CF children develop polyps vs. polyps being very rare in non-CF children) |
| Frequent viral URIs | Normal: 6–8/year in children — reassure parents if no red flags |
| Diagnosis | Key Clue |
|---|---|
| Senile rhinorrhoea / gustatory rhinitis [4] | Watery rhinorrhoea triggered by eating (parasympathetic hyperactivity). Responds to ipratropium bromide nasal spray |
| Atrophic rhinitis (ozaena) | Paradoxical congestion despite wide nasal cavity, foul-smelling crusts |
| Medication-related | Many elderly patients are on ACE inhibitors, β-blockers, opioids — all can cause nasal symptoms |
| NPC (second peak) | Second incidence peak at 50–60y in Southern Chinese |
| Diagnosis | Key Clue |
|---|---|
| Invasive fungal sinusitis (Aspergillus, Mucor) | Rapidly progressive sinusitis with tissue necrosis in immunocompromised patients (poorly controlled DM, haematological malignancy, post-transplant). Black eschar on nasal mucosa or palate = mucormycosis. Life-threatening emergency |
| Recurrent/chronic bacterial sinusitis | IgA deficiency, CVID, HIV |
Adapted from senior notes [1]:
| Condition | Suggestive Features |
|---|---|
| Common cold | Nasal symptoms (rhinorrhoea), cough, hoarseness, conjunctivitis [1] |
| Bacterial pharyngitis | Previous close exposure to strep throat, sudden onset sore throat with little viral symptoms (rhinorrhoea, cough, hoarseness), exudative tonsillitis, tender anterior cervical LNs, fever, ± headache and abdominal pain [1] |
| Rhinosinusitis | Prolonged ( > 10–14d) URI symptoms + ≥2 of facial/sinus pain (especially if aggravated by postural changes or Valsalva's manoeuvre), purulent nasal discharge, fever [1] |
| Influenza | Viral URI symptoms + systemic features (fever up to 40°C, myalgia, arthralgia, malaise) ± other system involvement (pneumonia, GE, CNS infections) [1] |
| Non-infectious rhinitis | Pruritus of eyes, nose, palates, ears; watery rhinorrhoea; sneezing; nasal congestion; post-nasal drip [1] |
| Acute bronchitis | Preceding viral URI symptoms with prominent cough and wheezes but not associated with features of pneumonia (e.g. fever, tachypnoea, crepitations, lung consolidation) [1] |
This deserves special mention because it appears under serious disorders not to be missed [4] and may seem surprising for a "nasal" symptom presentation.
The reason: Cluster headache presents with prominent ipsilateral autonomic features: lacrimation, nasal congestion, conjunctival injection [10][11]. A patient may present to a GP or ED complaining primarily of "one-sided blocked nose and watery eye" during an attack. If the clinician focuses on the nasal symptoms and misses the periorbital pain and periodicity, the diagnosis is missed, and the patient suffers unnecessarily from one of the most painful conditions known to medicine.
Key distinguishing features [10][11]:
- Extreme unilateral periorbital piercing/throbbing pain
- Duration 15–180 min, 1–8 episodes/day
- Strikingly periodic: identical headache beginning at the same hour each day
- Clustering: runs of attacks over 6–12 weeks followed by months of remission
- Patient is agitated/restless (cf migraine — patient lies still)
- Precipitated by alcohol, glyceryl trinitrate
- Horner's syndrome in ~30–50% [10]
Teaching point: If someone presents with "recurrent unilateral runny nose and tearing eye" that occurs like clockwork at the same time each day, always ask about accompanying headache. The autonomic features of cluster headache can overshadow the pain in the patient's narrative.
Here's how to narrow the differential at the bedside:
High Yield Summary — Differential Diagnosis
Murtagh's Framework for Nasal Congestion/Rhinorrhoea [4]:
-
Probability diagnosis: Common cold (viral URTI), rhinitis (infective, allergic, vasomotor), vasomotor stimulation (cold, smoke, irritants), sinusitis → post-nasal drip, senile rhinorrhoea.
-
Serious disorders not to be missed: Cluster headache (autonomic nasal symptoms), chronic infective granulomas (TB), malignancy (NPC — extremely important in HK), CSF rhinorrhoea (post head injury), GPA (Wegener's).
-
Pitfalls: Nasal foreign body (toddlers — unilateral foul-smelling discharge), trauma ± septal haematoma, adenoid hypertrophy, illicit drugs (cocaine, heroin), inhaled irritants, choanal atresia.
-
Masquerades: Drugs (topical OTC → rhinitis medicamentosa; narcotics) and Hypothyroidism.
Key differentiating features:
- Unilateral + blood-stained → malignancy / GPA / foreign body until proven otherwise
- Bilateral + itch + sneeze + watery eyes → allergic rhinitis
- Rebound after nasal spray → rhinitis medicamentosa
- Periodic unilateral with periorbital pain + lacrimation → cluster headache
- Clear + unilateral + post-trauma → CSF rhinorrhoea
Active Recall - Differential Diagnosis of Nasal Congestion and Runny Nose
References
[1] Senior notes: Ryan Ho Respiratory.pdf (Sections 3.1.1 URTI overview, 3.1.1.1 Acute Coryza, 3.1.1.4 Rhinosinusitis) [3] Senior notes: Ryan Ho Rheumatology.pdf (Section 4.2.2.1 Atopic Dermatitis) [4] Lecture slides: murtagh merge.pdf (p67–68 — Nasal drip/rhinorrhoea: probability diagnosis, serious disorders, pitfalls, masquerades checklist, key history, diagnostic tips) [7] Senior notes: Ryan Ho Opthalmology.pdf (Section 2.2.2 Conjunctivitis — allergic conjunctivitis with allergic rhinitis) [9] Senior notes: Ryan Ho Critical Care.pdf (Section 1.3.6 Anaphylactic Shock — nasal congestion as respiratory feature) [10] Senior notes: Ryan Ho Neurology.pdf (Section 2.2.3 Cluster Headache and TACs; headache differential tables pp.57–60) [11] Senior notes: Ryan Ho Fundamentals.pdf (Sections pp.312–315 — Headache approach, cluster headache features, sinusitis as headache cause) [12] Senior notes: Ryan Ho Opthalmology.pdf (Section 2.2.2 — allergic conjunctivitis associated with sneezing, rhinorrhoea, eczema)
Diagnostic Criteria, Algorithm, and Investigation Modalities
The diagnosis of the cause of nasal congestion and rhinorrhoea is, in most cases, primarily clinical. The principle to grasp here is that the nose can only respond in a limited number of ways — swell, secrete, bleed, or obstruct — so the history and examination do the heavy lifting, and investigations are reserved for (a) confirming a suspected diagnosis, (b) excluding serious pathology, or (c) guiding management (particularly surgical planning).
Key investigations: Usually none required. Consider: micro/culture of discharge, X-ray sinuses, CT scan, allergy testing [4].
Let that sink in — most patients need NO investigations. The decision to investigate depends on the clinical picture, duration, red flags, and treatment response.
1. Diagnostic Criteria for Specific Conditions
This is the most commonly tested diagnostic framework for nasal symptoms in exams.
Diagnosis: predominantly clinical [1].
A. Acute Rhinosinusitis (ARS) — Clinical Criteria:
Criteria: sudden onset of ≥2 of (with ≥1 nasal symptom) [1]:
- Nasal blockage/congestion OR nasal discharge PLUS
- Facial pain/pressure AND/OR ↓ or loss of smell [1]
Why these specific criteria? Because they capture the two essential components of rhinosinusitis:
- Nasal component (blockage or discharge) — reflects mucosal oedema and glandular hypersecretion
- Sinus component (facial pain/pressure or hyposmia) — reflects sinus ostial obstruction with trapped secretions pressing on sensory nerves, or oedema of the olfactory cleft blocking odorant access
B. Distinguishing Viral from Bacterial ARS:
This is the critical clinical decision because it determines whether antibiotics are warranted.
Criteria for bacterial rhinosinusitis: ≥3 of [1]:
- Double sickening (initial improvement then deterioration — reflects initial viral clearance followed by bacterial superinfection)
- Discoloured, purulent nasal discharge (neutrophil-rich exudate from bacterial proliferation in stagnant sinus — though this alone is insufficient)
- Severe, localised pain (especially unilateral — bacterial sinusitis is often more focal than viral which is diffuse)
- Fever > 38°C or ↑ESR/CRP [1] (systemic inflammatory response to bacterial infection)
Three alternative clinical patterns also suggest bacterial ARS (AAO-HNS / IDSA 2012 guidelines):
| Pattern | Rationale |
|---|---|
| Persistent symptoms > 10 days without improvement | Viral URI should show improvement by day 10; persistence suggests bacterial superinfection |
| Severe onset: fever ≥ 39°C + purulent discharge for ≥ 3–4 consecutive days | The severity and persistence of both fever and purulence suggests bacterial aetiology from the outset |
| Double sickening | New onset of fever, headache, or increase in nasal discharge after initial improvement of a viral URI |
Viral vs. Bacterial ARS — The 10-Day Rule
The most practical bedside tool: if nasal symptoms are improving by day 10, it is almost certainly viral. If symptoms persist unchanged or worsen after day 10, consider bacterial superinfection. This is because the median duration of a viral URI is 7–10 days, and > 90% resolve within 10 days [1]. Bacterial ARS complicates only 0.5–2% of viral URIs [1].
Duration: symptoms for ≥ 12 consecutive weeks without complete resolution.
Clinical criteria (same symptom domains as ARS):
- ≥2 symptoms, with ≥1 being nasal blockage/obstruction/congestion OR nasal discharge (anterior/posterior)
- PLUS facial pain/pressure AND/OR reduction or loss of smell
PLUS objective evidence of at least one of:
- Nasal polyps and/or mucopurulent discharge from middle meatus on nasal endoscopy
- Mucosal changes within the ostiomeatal complex and/or sinuses on CT scan
Why is objective evidence required for CRS but not ARS? Because chronic symptoms lasting > 12 weeks could have many non-sinusitis causes (vasomotor rhinitis, allergic rhinitis, rhinitis medicamentosa). Requiring endoscopic or radiological confirmation ensures diagnostic specificity and avoids unnecessary surgery.
CRS is then subtyped:
- CRSwNP (with nasal polyps): polyps visible at nasal endoscopy
- CRSsNP (without nasal polyps): mucosal inflammation/mucopurulent discharge without polyps
Clinical diagnosis based on:
- Characteristic symptoms: sneezing, rhinorrhoea (watery), nasal congestion, nasal itch — often with palatal/eye itch
- Temporal correlation with allergen exposure
- Confirmed by allergy testing: skin prick test (SPT) or serum-specific IgE showing sensitisation to a clinically relevant allergen
Classification (ARIA):
| Intermittent | Persistent | |
|---|---|---|
| Duration | < 4 days/week OR < 4 consecutive weeks | ≥ 4 days/week AND ≥ 4 consecutive weeks |
| Mild | None of the below | |
| Moderate-Severe | ≥1 of: sleep disturbance, impairment of daily activities/school/work, troublesome symptoms |
Why the 4-day/4-week cut-offs? The older "seasonal vs. perennial" classification was geographically biased (HK has year-round house dust mite exposure, making "seasonal" less relevant). ARIA uses symptom burden regardless of allergen type, which better reflects clinical impact and guides treatment intensity.
This is a diagnosis of exclusion:
- Chronic nasal symptoms (predominantly congestion and rhinorrhoea) for > 12 weeks
- Negative allergy testing (SPT and/or specific IgE)
- No evidence of infection, structural abnormality, or systemic disease
- Often triggered by non-specific stimuli (cold air, strong odours, spicy food, emotional stress)
Diagnostic criteria (clinical):
- History of regular use of topical nasal decongestant (α-agonist) for > 5–7 days [4]
- Rebound nasal congestion upon withdrawal
- Anterior rhinoscopy: erythematous, oedematous ("beefy red") nasal mucosa — distinct from the pale, boggy mucosa of allergic rhinitis
Suspected when: clear discharge following direct facial or head injury [4], or post-surgical, or spontaneous in the setting of raised ICP/skull base erosion.
Confirmatory tests:
- β2-transferrin assay (gold standard): β2-transferrin is a protein found almost exclusively in CSF, perilymph, and aqueous humor — its presence in nasal fluid is essentially diagnostic (sensitivity ~94%, specificity ~100%)
- Glucose testing: CSF glucose is typically > 1.7 mmol/L (> 30 mg/dL) whereas normal nasal mucus has minimal glucose. Glucose oxidase strips (Dextrostix) can be used as a bedside screening test, but false positives occur with blood contamination
- Halo sign (ring sign): when nasal fluid drips onto filter paper, CSF separates from blood forming a clear outer ring around a central blood spot — a useful bedside test but not definitive
This algorithm integrates the history, examination, and investigations into a step-by-step approach:
3. Investigation Modalities — Detailed
Let me walk through each investigation systematically: when to order it, what it shows, and how to interpret the results.
3.1 Bedside / Clinical Investigations
Look for cause. Inspect nose and nasal cavity with a Thudicum speculum or large auriscope. Note the position of the septum, nature of nasal mucosa and look for polyps or other tumours [4].
| Finding | Interpretation | Why |
|---|---|---|
| Pale, boggy, bluish-grey mucosa | Allergic rhinitis | Chronic eosinophilic infiltration causes oedema with reduced vascularity — the mucosa looks pale because the tissue is waterlogged rather than inflamed |
| Erythematous, swollen mucosa | Infectious rhinitis / acute sinusitis | Active vasodilatation and neutrophilic infiltration — the red colour reflects hyperaemia from the inflammatory response |
| "Beefy red," granular mucosa | Rhinitis medicamentosa | Chronic rebound vasodilatation + loss of normal mucosal architecture from prolonged decongestant damage |
| Mucosal inflammation: oedema, narrowing of meatus, inferior turbinate hypertrophy [1] | Rhinosinusitis (any cause) | Mucosal swelling narrows the middle meatus → impairs sinus drainage |
| Discharge: copious watery or purulent discharge [1] | Watery = allergic/vasomotor/viral; Purulent = bacterial or late viral | Character reflects the predominant secretory mechanism |
| Nasal polyps (pale, grey, translucent, insensitive, mobile, pedunculated) | CRSwNP (bilateral), exclude neoplasm (unilateral) | Polyps arise from oedematous ethmoid sinus mucosa due to chronic Type 2 inflammation. They are INSENSITIVE to touch (unlike turbinates, which are vascular and sensitive) — this is a key clinical test |
| Co-existent anatomical RFs, eg. polyps, septal deviation [1] | Predisposing factors for chronic sinusitis | Structural narrowing of OMC → impaired drainage |
| Deviated septum | Unilateral obstruction; predisposes to sinusitis | Mechanical narrowing of nasal passage |
| Septal perforation, crusting, granulation | GPA, cocaine use, sarcoidosis | Granulomatous/ischaemic destruction of septal cartilage and mucosa |
| Foreign body | Direct visualisation (especially in children) | Physical obstruction with surrounding inflammation and mucopurulent secretions |
- Gold standard for direct visualisation of the entire nasal cavity, ostiomeatal complex, and nasopharynx.
- Done with a flexible fibreoptic endoscope passed through the nostril after topical anaesthesia and decongestant.
| Key Findings | Clinical Significance |
|---|---|
| Mucopurulent drainage from middle meatus | Confirms sinusitis (maxillary, anterior ethmoid, or frontal source) |
| Mucopurulent drainage from sphenoethmoidal recess | Sphenoid or posterior ethmoid sinusitis |
| Nasal polyps — number, size, location | CRSwNP staging; unilateral polyp needs biopsy to exclude neoplasm |
| Nasopharyngeal mass | NPC — critical examination in HK patients with unilateral symptoms, conductive hearing loss, or cervical lymphadenopathy |
| Eustachian tube orifice status | Serous otitis media from tubal obstruction |
| Adenoid size (children) | Adenoid hypertrophy grading |
| Post-nasal drip (mucopurulent coating of posterior pharyngeal wall) | Confirms posterior drainage contributing to cough/throat symptoms |
When to Do Nasal Endoscopy
Nasal endoscopy is indicated when: (1) symptoms are chronic ( > 12 weeks), (2) symptoms are unilateral (to exclude neoplasm), (3) response to empirical treatment is poor, (4) complications are suspected, (5) pre-operative assessment for sinus surgery (FESS), (6) follow-up after sinus surgery. It is NOT routinely needed for a simple acute viral URTI.
- Should be performed in every patient with nasal symptoms, especially children.
- Why? Because nasal and nasopharyngeal pathology frequently causes Eustachian tube dysfunction → middle ear effusion.
| Finding | Interpretation |
|---|---|
| Amber/grey tympanic membrane, reduced mobility, fluid level or air bubbles | Serous otitis media (middle ear effusion) secondary to Eustachian tube dysfunction |
| Erythematous, bulging TM | Acute otitis media — complication of URTI, especially in children |
| Test | Technique | Interpretation |
|---|---|---|
| Halo (ring) sign | Allow nasal fluid to drip onto white filter paper or gauze | CSF separates from blood → clear ring around central blood spot. Screening only — not definitive |
| Glucose testing | Glucose oxidase strip (Dextrostix) applied to nasal fluid | CSF glucose > 1.7 mmol/L (positive). Nasal mucus has little glucose. False positives if blood contamination |
3.2 Laboratory Investigations
Allergy testing is listed as a key investigation [4]. Two main approaches:
1. Skin Prick Test (SPT) — first-line:
- Technique: drops of standardised allergen extracts placed on forearm skin → pricked through with a lancet → read at 15–20 minutes.
- Positive result: wheal ≥ 3 mm larger than negative control.
- Mechanism: if allergen-specific IgE is bound to cutaneous mast cells, allergen cross-links IgE → mast cell degranulation → local histamine release → wheal-and-flare response.
- Advantages: rapid (20 min), inexpensive, high sensitivity, tests multiple allergens simultaneously.
- Limitations: must stop antihistamines ≥ 3–7 days prior (suppress mast cell response → false negatives); cannot be done if extensive eczema or dermatographism; risk of anaphylaxis (extremely rare).
Common allergen panel in HK:
- House dust mite (D. pteronyssinus, D. farinae) — the dominant allergen
- Cockroach mix
- Cat and dog epithelium
- Mould (Aspergillus, Alternaria, Cladosporium)
- Grass/tree pollens (less important in HK subtropical climate)
2. Serum-Specific IgE (formerly RAST):
- Technique: blood test measuring circulating IgE antibodies specific to individual allergens.
- When to use: when SPT cannot be performed (extensive eczema, dermatographism, cannot stop antihistamines, young children who will not tolerate pricks).
- Limitations: more expensive, less sensitive than SPT, results take days.
3. Total serum IgE:
- Elevated in atopic individuals but NOT diagnostic alone (non-specific — also elevated in parasitic infections, hyper-IgE syndrome, etc.).
- Useful as supportive evidence of atopy when combined with history and specific IgE.
4. Nasal cytology (smear):
- Swab of nasal secretions examined microscopically.
- Eosinophil-predominant: allergic rhinitis or NARES (Non-Allergic Rhinitis with Eosinophilia Syndrome).
- Neutrophil-predominant: infectious rhinitis.
- Rarely done in routine practice but useful in research and specialist settings.
SPT vs. Specific IgE — What's the Difference?
Both detect allergen-specific IgE, but SPT tests the functional response (mast cell degranulation in skin), while specific IgE measures circulating antibody levels. A positive SPT is more clinically relevant because it demonstrates that the patient's mast cells actually degranulate in response to that allergen. A positive specific IgE only shows sensitisation — the patient may be sensitised but not clinically reactive (asymptomatic sensitisation). Always correlate test results with clinical history.
Micro/culture of discharge [4].
| When | What | Why |
|---|---|---|
| Refractory bacterial sinusitis not responding to empirical antibiotics | Endoscopy-directed middle meatus swab (gold standard) or sinus aspirate | Identifies the causative organism and antibiotic sensitivities. Anterior nasal swabs are unreliable (contaminated by normal nasal flora) |
| Suspected invasive fungal sinusitis | Culture + histopathology of biopsy material | Identify Aspergillus, Mucor — guides antifungal therapy |
| Suspected TB/granulomatous disease | Culture for AFB, fungal culture | Confirm mycobacterial or fungal aetiology |
| Test | Indication | Interpretation |
|---|---|---|
| CBC with differential | Suspected infection, allergy, eosinophilic disease | Eosinophilia ( > 0.5 × 10⁹/L) supports allergic/eosinophilic aetiology; leucocytosis with neutrophilia supports bacterial infection |
| ESR / CRP | Criteria for bacterial ARS: fever > 38°C or ↑ESR/CRP [1] | Elevated in bacterial infection, vasculitis (GPA), malignancy. Normal in allergic rhinitis and viral URTI |
| TFTs (TSH, free T4) | Hypothyroidism — masquerade [4] | ↑TSH + ↓free T4 = primary hypothyroidism causing myxoedematous nasal congestion |
| c-ANCA/PR3, p-ANCA/MPO | Suspected GPA or EGPA | c-ANCA/PR3 positive in ~90% of active generalised GPA. p-ANCA/MPO positive in EGPA |
| EBV serology (VCA IgA, EA IgA) and plasma EBV DNA | Suspected NPC (HK population) | Elevated EBV VCA IgA and EBV DNA titres are used as screening/monitoring tools for NPC in endemic populations |
| ACE level | Suspected sarcoidosis | Elevated in ~60% of active sarcoidosis (produced by granuloma macrophages). Non-specific |
| Total IgE | Supporting evidence of atopy | Elevated in atopic disease but not diagnostic in isolation |
| Sweat chloride test | Suspected CF (child with nasal polyps) | Chloride > 60 mmol/L = diagnostic of CF. The defective CFTR chloride channel fails to reabsorb chloride in sweat ducts |
| β2-transferrin | Suspected CSF leak | Positive = CSF confirmed (unique to CSF, perilymph, and aqueous humor) |
| Test | Indication | Interpretation |
|---|---|---|
| Rapid antigen test (influenza, COVID-19, RSV) | Acute febrile respiratory illness | Rapid POC result; moderate sensitivity, high specificity |
| PCR (multiplex respiratory panel) | Severe or atypical presentation, immunocompromised, surveillance | High sensitivity and specificity; identifies specific viral pathogen |
3.3 Imaging
Sinus XR: opacified sinus with air-fluid level [1]. Poor sensitivity and specificity → NOT recommended [1].
- Why is it poor? Because mucosal thickening > 6 mm and air-fluid levels can occur in asymptomatic individuals, and a normal X-ray does not reliably exclude sinusitis (poor sensitivity for ethmoid and sphenoid disease due to overlapping bony structures).
- Historical use: previously ordered as first-line but now largely supplanted by CT.
- Still occasionally used: in resource-limited settings or as a quick screen.
| View | Best Visualises |
|---|---|
| Waters' (occipitomental) | Maxillary sinuses |
| Caldwell (occipitofrontal) | Frontal and ethmoid sinuses |
| Lateral | Sphenoid sinus, adenoid size |
CT scan is listed as a key investigation [4]. Sinus CT: air-fluid levels, mucosal oedema, air bubbles [1]. Generally reserved for cases where complications are suspected [1].
Indications:
- Chronic rhinosinusitis not responding to medical therapy
- Suspected complications of ARS (orbital, intracranial)
- Pre-operative planning for functional endoscopic sinus surgery (FESS) — provides the surgical roadmap
- Recurrent ARS (≥ 4 episodes/year) to identify predisposing anatomical factors
- Unilateral symptoms suspicious for neoplasm (with MRI)
Key findings and interpretation:
| Finding | Interpretation |
|---|---|
| Air-fluid level within a sinus | Acute sinusitis — trapped fluid (mucus, pus, or blood) behind an obstructed ostium |
| Mucosal thickening ( > 4–6 mm) | Mucosal inflammation — seen in ARS, CRS, allergic fungal sinusitis. Non-specific — also found incidentally in ~40% of asymptomatic individuals |
| Complete sinus opacification | Severe sinusitis, mucocoele, or fungal ball |
| Ostiomeatal complex (OMC) obstruction | Central event in sinusitis pathophysiology — mucosal oedema or anatomical variant blocking the drainage pathway of maxillary/anterior ethmoid/frontal sinuses |
| Bone erosion / destruction | Malignancy (sinonasal SCC, adenocarcinoma), invasive fungal sinusitis, Pott's puffy tumour (frontal osteomyelitis). Urgent concern |
| Heterogeneous opacification with calcification | Fungal sinusitis (allergic fungal rhinosinusitis shows characteristic "double density" sign; fungal ball shows central calcification) |
| Anatomical variants | Concha bullosa (pneumatised middle turbinate), Haller cells (infraorbital ethmoid cells), septal deviation, paradoxical middle turbinate — predisposing factors for CRS |
| Orbital fat stranding / subperiosteal abscess | Orbital complication of sinusitis — emergency |
| Intracranial air, subdural/epidural empyema | Intracranial complication — emergency |
Lund-Mackay scoring system:
- Standardised CT scoring for CRS severity: each sinus (anterior ethmoid, posterior ethmoid, maxillary, frontal, sphenoid) scored 0–2 per side + OMC (0 or 2 per side).
- Total score: 0–24. Score ≥ 4 generally considered abnormal.
- Used in research and pre-operative assessment; helps quantify disease burden.
CT Timing Pitfall
Do NOT order a CT sinuses during or immediately after an acute URTI. Viral mucosal inflammation causes transient sinus opacification in up to 87% of patients with a cold — this will give you a false-positive "sinusitis" on CT. Wait at least 4–6 weeks after the acute episode resolves before scanning for chronic disease assessment.
| Indication | Advantage Over CT |
|---|---|
| Suspected sinonasal / nasopharyngeal malignancy | Superior soft tissue contrast — differentiates tumour from retained secretions/mucosal thickening (both appear opacified on CT). Tumour enhances with gadolinium; retained secretions do not |
| Suspected intracranial complication (abscess, CVST) | Better visualisation of brain parenchyma and venous sinuses |
| Suspected invasive fungal sinusitis with intracranial/orbital extension | Delineates extent of soft tissue invasion |
| Allergic fungal rhinosinusitis | Shows characteristic T1-hypointense, T2-hypointense signal of fungal mucin (due to paramagnetic metals in fungal elements) — "signal void" that mimics an aerated sinus |
Key principle: CT is best for bone and anatomy (surgical planning). MRI is best for soft tissue (tumour staging, intracranial complications). They are complementary, not interchangeable.
| Modality | Indication | Key Finding |
|---|---|---|
| CT cisternography / MRI cisternography | Localising site of CSF leak | Intrathecal contrast or heavily T2-weighted MRI identifies the exact defect in the skull base |
| Lateral neck X-ray | Adenoid hypertrophy (children) | Enlarged adenoid shadow narrowing the nasopharyngeal airway |
| PET-CT | Staging confirmed sinonasal / NPC malignancy | Metabolically active primary tumour and metastases |
| Indication | Technique | What It Shows |
|---|---|---|
| Unilateral nasal mass | Endoscopic biopsy | Histology: inverted papilloma (endophytic growth of squamous epithelium), SCC, adenocarcinoma, olfactory neuroblastoma, lymphoma |
| Nasopharyngeal mass (suspected NPC) | Nasopharyngoscopy-guided biopsy | WHO Type I (keratinising SCC), Type II (non-keratinising, differentiated), Type III (non-keratinising, undifferentiated — most common in HK, strongly EBV-associated) |
| Suspected GPA | Biopsy of affected nasal mucosa | Necrotising granulomatous inflammation with vasculitis |
| Suspected sarcoidosis | Biopsy | Non-caseating granulomata |
3.5 Special Tests
| Test | Purpose |
|---|---|
| Peak nasal inspiratory flow (PNIF) | Objective measure of nasal airway patency. Simple, portable, reproducible. Useful for monitoring treatment response in AR and CRS |
| Rhinomanometry | Measures nasal airway resistance during breathing. More precise than PNIF. Used in research and pre-operative assessment |
| Acoustic rhinometry | Measures cross-sectional area of nasal cavity using sound waves. Identifies the site and degree of nasal obstruction |
- Paranasal sinuses produce high levels of NO. In CRS (especially with polyps), sinus ostia are blocked → reduced nNO.
- Extremely low nNO ( < 77 nL/min) is highly suggestive of primary ciliary dyskinesia (PCD) — a rare but important cause of chronic rhinosinusitis, bronchiectasis, and situs inversus (Kartagener syndrome).
- A saccharin particle is placed on the anterior inferior turbinate. The patient reports when they taste sweetness (indicating the particle has been transported to the nasopharynx by mucociliary action).
- Normal: < 20 minutes. Abnormal ( > 30 min): impaired mucociliary clearance — think PCD, CF, or chronic mucosal damage (smoking, rhinitis medicamentosa).
- UPSIT (University of Pennsylvania Smell Identification Test) or Sniffin' Sticks: standardised psychophysical tests of olfactory function.
- Indicated when anosmia/hyposmia is a prominent complaint.
- Helps distinguish conductive (nasal obstruction → reversible) from sensorineural (viral damage, neurodegeneration → often irreversible) hyposmia.
| Scenario | Key Investigation(s) | Rationale |
|---|---|---|
| Acute nasal symptoms < 10 days, no red flags | None — clinical diagnosis of viral URTI | Self-limiting; investigations add cost without changing management |
| Acute symptoms > 10 days or double sickening | None (clinical diagnosis of bacterial ARS) or ESR/CRP if uncertain | Antibiotics may be warranted; no imaging needed unless complications suspected |
| Suspected orbital/intracranial complication | Urgent CT sinuses with contrast ± MRI brain | Delineate abscess, cellulitis, intracranial extension → generally reserved for cases where complications are suspected [1] |
| Chronic bilateral nasal symptoms with itch/sneeze | Allergy testing (SPT or specific IgE) | Confirm allergic rhinitis and identify specific allergens for avoidance/immunotherapy |
| Chronic bilateral symptoms, no allergic features | Nasal endoscopy + consider CT if endoscopy abnormal | Exclude CRS, polyps, structural abnormalities; CT for surgical planning |
| Chronic symptoms with OTC decongestant use | Clinical diagnosis (rhinitis medicamentosa) — no Ix needed | History is diagnostic; stop the spray |
| Chronic symptoms + thyroid features | TFTs | Exclude hypothyroidism as a masquerade [4] |
| Unilateral bloody discharge | Urgent nasal endoscopy ± nasopharyngoscopy + CT/MRI + biopsy | Beware of persistent blood-stained discharge especially if unilateral and obstruction [4] — exclude malignancy |
| Clear unilateral discharge post-trauma | β2-transferrin ± CT cisternography | CSF leakage from a skull fracture [4] |
| Child with bilateral nasal polyps | Sweat chloride test | Exclude CF (polyps very rare in non-CF children) |
| Crusty nose + septal perforation + systemic symptoms | c-ANCA/PR3, biopsy, urinalysis | Exclude GPA |
Imaging: NOT indicated if uncomplicated [1].
High Yield Summary — Diagnosis
Core Principle: Diagnosis of nasal congestion/rhinorrhoea is predominantly clinical [1]. Usually no investigations required [4].
Acute rhinosinusitis criteria [1]: ≥2 symptoms (with ≥1 nasal: blockage/congestion OR discharge) PLUS facial pain/pressure and/or hyposmia.
Bacterial ARS criteria [1]: ≥3 of double sickening, purulent discharge, severe localised pain, fever > 38°C/↑ESR/CRP. OR: persistent > 10 days, severe onset, or double sickening pattern.
Allergic rhinitis: clinical features (itch, sneeze, watery rhinorrhoea, congestion) + positive allergy testing (SPT preferred over specific IgE).
CRS ( > 12 weeks): clinical criteria PLUS objective evidence on nasal endoscopy or CT.
Key investigations to consider [4]: micro/culture, sinus X-ray (NOT recommended — poor Se/Sp), CT scan (for complications/surgical planning), allergy testing.
Imaging NOT indicated if uncomplicated [1]. CT reserved for suspected complications [1].
Red flag investigations: unilateral bloody discharge → urgent endoscopy + biopsy; clear post-trauma discharge → β2-transferrin; child with polyps → sweat chloride.
Active Recall - Diagnostic Criteria and Investigations for Nasal Congestion/Rhinorrhoea
References
[1] Senior notes: Ryan Ho Respiratory.pdf (Sections 3.1.1 URTI overview, 3.1.1.1 Acute Coryza, 3.1.1.4 Rhinosinusitis) [4] Lecture slides: murtagh merge.pdf (p67–68 — Nasal drip/rhinorrhoea: key investigations, key examination, diagnostic tips, masquerades checklist) [10] Senior notes: Ryan Ho Neurology.pdf (Headache differential tables — sinusitis, cluster headache) [11] Senior notes: Ryan Ho Fundamentals.pdf (Headache approach — sinusitis associated features and further investigations)
Management of Nasal Congestion and Runny Nose
Management follows a simple principle: treat the underlying cause, not just the symptom. A runny, blocked nose is a final common pathway for dozens of conditions, so the management algorithm branches based on the diagnosis reached in the preceding diagnostic steps. I'll walk through the overall algorithm first, then drill into each treatment modality from first principles.
Before discussing specific drugs, let's establish the framework:
- Education and reassurance — the vast majority of nasal congestion/rhinorrhoea is self-limiting or easily controlled. Patients with viral URTI need to understand that antibiotics will not help and that symptoms naturally take 7–10 days to resolve [1].
- Infection control — hand-washing is the most effective method in prevention of transmission [1]. This cannot be overstated.
- Nasal saline irrigation — the foundation of therapy for virtually ALL nasal conditions. Isotonic or hypertonic saline physically washes away mucus, allergens, and inflammatory mediators; reduces mucosal oedema (hypertonic); and improves mucociliary clearance. Cheap, safe, effective, and evidence-based.
- Treat the cause, not the symptom — decongestants provide temporary relief but never address the underlying process. The exception is when symptom relief IS the treatment (e.g., viral URTI where there is no specific antiviral).
3. Management by Condition
3.1 Viral URTI (Common Cold)
Management: ↓stress + rest + infectious control (especially wash hands) ± symptomatic treatment [1].
There is no cure for the common cold. All treatment is symptomatic. Let me explain each modality:
| Drug | Mechanism | Evidence / Notes |
|---|---|---|
| Paracetamol | Inhibits central COX-3 (and possibly COX-2 in CNS) → ↓prostaglandin E2 in hypothalamus → ↓fever setpoint; also has central analgesic effect | Proven to be effective and safe [1]. Does NOT shorten duration of URTI [1]. First-line for fever and sore throat pain |
| NSAIDs (e.g., ibuprofen) | Inhibits peripheral COX-1/2 → ↓prostaglandin synthesis → ↓inflammation, pain, and fever | More effective [than paracetamol for pain] but ↑side effects [1]. Avoided if: (1) not eating well (GI side effects), (2) aspirin-sensitive asthma, (3) renal dysfunction, (4) children due to risk of Reye syndrome [aspirin specifically] [1] |
These directly address nasal congestion by counteracting the vasodilatation of turbinate venous sinusoids.
| Route | Drug | Mechanism | Key Points |
|---|---|---|---|
| Oral | Pseudoephedrine, phenylephrine | Sympathomimetic α-adrenergic agonists → vasoconstriction of nasal submucosal venous sinusoids → ↓turbinate engorgement → ↓congestion | Oral: transient relief of nasal congestion, but side effects common (10–20% children), caution if HTN [1]. Also avoid in: ischaemic heart disease, hyperthyroidism, BPH (urinary retention), MAOI use, closed-angle glaucoma |
| Topical | Intranasal oxymetazoline (Afrin), xylometazoline | Same α-agonist mechanism but applied directly to mucosa → faster onset, more potent local effect | Topical: must be limited to 2–3 days as rebound rhinitis medicamentosa occurs after 72h of use [1]. This is the drug that causes rhinitis medicamentosa when used as topical OTC [4] |
Why is topical more risky than oral? Because topical application delivers a high local concentration directly to the mucosal α-receptors, causing rapid and profound vasoconstriction. This high local exposure accelerates receptor downregulation (tachyphylaxis) far more quickly than the lower mucosal concentrations achieved via oral systemic delivery. Hence the strict 3-day limit for topical use.
The 3-Day Rule for Topical Decongestants
Topical decongestants must be limited to 2–3 days [1]. After 72 hours of continuous use, α-adrenoreceptor downregulation begins, and stopping the spray causes rebound vasodilatation that is worse than the original congestion. This is rhinitis medicamentosa [4]. Counsel every patient who receives a topical decongestant prescription.
| Generation | Examples | Mechanism | Evidence in URTI |
|---|---|---|---|
| First-generation (sedating) | Chlorpheniramine (Piriton), promethazine (Phenergan), diphenhydramine (Benadryl) | Block H1 receptors (reversible competitive antagonism) + significant muscarinic (anticholinergic) activity → ↓glandular secretion, ↓rhinorrhoea, ↓sneezing. Also cross the BBB → sedation | Sedating: reduces sneezing and rhinorrhoea, also promotes rest, but associated with risk of ↑↑sedation and dry mouth/mucous membranes [1]. The anticholinergic "drying" effect is actually why they work in colds — they're functioning more as anticholinergics than antihistamines |
| Second-generation (non-sedating) | Loratadine (Clarityn), cetirizine, fexofenadine | Selective H1 antagonism with minimal anticholinergic activity and minimal BBB penetration | Non-sedating: much less effective [in URTI] due to lack of anticholinergic activity [1]. Reserved for allergic rhinitis where histamine is the primary mediator |
Why do first-gen antihistamines work better in colds than second-gen? Because the runny nose of a cold is largely driven by parasympathetic (cholinergic) glandular secretion, not histamine. First-gen antihistamines are "dirty drugs" — they block muscarinic receptors as well as H1 receptors, and it's the anticholinergic effect that dries up secretions. Second-gen antihistamines are cleaner (selective H1), so they lack this drying effect and are therefore less effective for cold-related rhinorrhoea.
Ipratropium nasal spray: proven to be more effective than placebo and normal saline, but not effective if significant nasal congestion. Use often limited by cost and need for supervision [1].
- Mechanism: Anticholinergic (muscarinic M3 antagonist) → blocks parasympathetic-mediated glandular secretion → ↓rhinorrhoea.
- Why doesn't it help congestion? Because congestion is caused by venous sinusoidal engorgement, which is regulated by sympathetic tone (α-adrenergic), not cholinergic tone. Ipratropium only addresses the glandular secretory component.
- Indication: Watery rhinorrhoea in viral URTI, vasomotor rhinitis, or senile/gustatory rhinitis where runny nose is the predominant complaint.
| Agent | Mechanism | Evidence |
|---|---|---|
| Cromolyn sodium nasal spray | Mast cell stabiliser → prevents degranulation → ↓mediator release | Associated with faster resolution of symptoms with ↓↓side effects [1]. Very safe but needs frequent dosing (QID) which limits adherence |
| Vitamin C (high dose 1–3g) | Antioxidant; may modulate immune function | NOT evidence-based. NO benefit if taken at onset of illness. May shorten illness only in 14% adults, 8% children during prophylaxis [1] |
| Zinc (taken ≤2 days of onset) | May inhibit viral replication (blocks viral attachment to nasal epithelium) and modulate immune response | Inconsistent evidence. May shorten illness by 1–3 days. Up to 20% with side effects (nausea, vomiting, diarrhoea). Cannot prevent illness [1] |
| Category | Examples | Mechanism | Evidence |
|---|---|---|---|
| Expectorants | Ammonium chloride (NH4Cl), guaifenesin, ipecacuanha | Stimulate bronchial secretion or reduce mucus viscosity → easier expectoration | NOT proven to be effective by RCT except some evidence on guaifenesin. High doses may cause nausea and vomiting [1] |
| Cough suppressants (antitussives) | Dextromethorphan (DXM), codeine, pholcodine | Central suppression of cough reflex at medullary level (DXM: NMDA antagonist; codeine: μ-opioid agonist) | Uncertain effectiveness in URTI and C/I in COPD, caution in asthma and children as it causes sputum retention and respiratory depression [1] |
| Mucolytics | Bromhexine, acetylcysteine | Break disulphide bonds in mucus glycoproteins → reduce mucus viscosity | NOT evidence-based, may be useful for chronic lung disease with sputum production (e.g. COPD) [1] |
Common cough mixture formulations in HK [1]:
- Benadryl Expectorant (BE): diphenhydramine + NH4Cl + sodium citrate
- Phensedyl compound linctus: promethazine + DXM + ephedrine
- Cocillana: herbal extract only
- MES (馬尿): ammonium bicarbonate + ipecacuanha
Antibiotics for Viral URTI — Just Say No
Antibiotics have NO role in uncomplicated viral URTI. > 90% of URIs resolve in 10 days [1]. Prescribing antibiotics for colds drives antimicrobial resistance, exposes patients to unnecessary side effects (diarrhoea, allergy, C. difficile), and does not shorten illness duration. Educate patients firmly but empathetically.
3.2 Allergic Rhinitis
This is the condition where pharmacotherapy has the most robust evidence base. The stepwise approach follows ARIA 2020 guidelines.
| Measure | Mechanism | Evidence |
|---|---|---|
| House dust mite (HDM) avoidance: mattress/pillow encasements, wash bedding at ≥ 60°C weekly, reduce carpet/soft furnishings, maintain humidity < 50% | Reduces allergen load → less mast cell activation | Mixed evidence for individual measures; combined multifaceted approach more effective. Important in HK where HDM is dominant |
| Pet avoidance: remove animal from home or at least from bedroom | Reduces dander allergen exposure | Most effective strategy but often impractical (patients are attached to pets) |
| Nasal saline irrigation (isotonic or hypertonic) | Physically removes allergens and inflammatory mediators from nasal mucosa; hypertonic draws fluid out of oedematous mucosa by osmosis | Moderate evidence of benefit; very safe; recommended as adjunct to all pharmacotherapy |
A. Intranasal Corticosteroids (INCS) — THE Cornerstone
| Drug Examples | Mechanism | Why First-Line |
|---|---|---|
| Fluticasone propionate, mometasone furoate, budesonide, beclomethasone, triamcinolone, ciclesonide | Binds intracellular glucocorticoid receptor → translocates to nucleus → suppresses transcription of pro-inflammatory genes (IL-1, IL-4, IL-5, IL-13, TNF-α, COX-2) and upregulates anti-inflammatory genes. Net effect: ↓eosinophil recruitment, ↓mast cell mediator release, ↓glandular secretion, ↓vascular permeability, ↓oedema | Most effective single agent for ALL symptoms of AR — congestion, rhinorrhoea, sneezing, itch, and even ocular symptoms (via naso-ocular reflex). Addresses both early and late phase inflammation. Onset: hours to days, peak effect at 1–2 weeks |
Practical points:
- Technique matters: point spray laterally (toward ipsilateral ear), away from septum, to avoid septal irritation/epistaxis. Sniff gently, don't snort.
- Onset is NOT immediate — counsel patients that it takes days to weeks for full effect. Compliance is the biggest barrier.
- Side effects: epistaxis (most common — from direct spray contact with septum), nasal dryness, rarely septal perforation with long-term incorrect use. Systemic absorption is minimal with modern agents (fluticasone furoate, mometasone — < 1% bioavailability).
- Safe in long-term use — unlike oral corticosteroids, INCS at recommended doses do not cause HPA axis suppression, growth retardation, or osteoporosis.
- Preferred in pregnancy: budesonide (Category B — most safety data in pregnancy).
B. Oral Antihistamines (Second-Generation)
| Drug Examples | Mechanism | Role |
|---|---|---|
| Cetirizine, loratadine, fexofenadine, bilastine, desloratadine, levocetirizine | Selective H1 receptor antagonism → blocks histamine-mediated itch, sneeze, rhinorrhoea | Effective for itch, sneeze, rhinorrhoea but less effective for nasal congestion (because congestion is driven by late-phase eosinophilic inflammation and leukotrienes more than histamine alone). Used as monotherapy for mild intermittent AR or as add-on to INCS |
Contraindications/cautions:
- Cetirizine: mild sedation in some patients (technically "less sedating" rather than "non-sedating")
- Loratadine: least sedating; preferred in pilots/drivers
- Fexofenadine: no sedation; avoid with grapefruit juice (alters absorption)
C. Combination INCS + Intranasal Antihistamine
| Drug | Mechanism | When to Use |
|---|---|---|
| Azelastine/fluticasone combination spray (Dymista) | Dual mechanism: corticosteroid anti-inflammatory + local H1 blockade (azelastine also has mast cell stabilising properties). Onset faster than INCS alone (15 min vs. hours–days) | Moderate-severe AR not adequately controlled with INCS alone. More effective than either component alone |
A. Leukotriene Receptor Antagonists (LTRA)
| Drug | Mechanism | Role | Cautions |
|---|---|---|---|
| Montelukast (from "monte" = mountain, originally designed for asthma at higher altitudes metaphorically; "lukast" = leukotriene antagonist) | Blocks cysteinyl leukotriene receptor 1 (CysLT1) → ↓leukotriene-mediated nasal congestion, mucus secretion, and eosinophil recruitment | Add-on to INCS when congestion persists. Particularly useful in patients with concomitant asthma (addresses both conditions). Also useful in AERD/Samter's triad | FDA boxed warning (2020): neuropsychiatric side effects (agitation, depression, suicidal ideation) — counsel patients. Less effective than INCS as monotherapy |
B. Intranasal Anticholinergic (Ipratropium)
- Add-on when watery rhinorrhoea is the predominant residual symptom despite INCS + antihistamine.
- Blocks M3 muscarinic receptors on submucosal glands → ↓parasympathetic-mediated secretion.
- Does NOT address congestion or itch.
C. Oral / Intranasal Decongestant (Short-Term)
- Oral pseudoephedrine or short-course ( ≤ 3 days) topical oxymetazoline for acute exacerbations.
- Never as maintenance therapy.
A. Allergen Immunotherapy (AIT)
| Route | Technique | Mechanism | Indications |
|---|---|---|---|
| Subcutaneous immunotherapy (SCIT) | Increasing doses of allergen extract injected SC over 3–5 years | Induces immune tolerance: shifts from Th2 → Th1/Treg response, generates blocking IgG4 antibodies, reduces allergen-specific IgE over time | Moderate-severe AR not controlled by pharmacotherapy; mono- or oligosensitised patients (1–2 dominant allergens); patient preference to reduce long-term medication |
| Sublingual immunotherapy (SLIT) | Allergen tablet or drops placed under tongue daily for 3–5 years | Same mechanism as SCIT but via oral mucosal tolerance | Same indications; more convenient (home administration); lower risk of anaphylaxis vs. SCIT; particularly well-established for HDM (important for HK) and grass pollen |
Key points:
- Disease-modifying: the only treatment that alters the natural history of allergic rhinitis. Can prevent progression to asthma and new sensitisations.
- Duration: 3–5 years for sustained benefit.
- Contraindications: uncontrolled asthma (risk of severe bronchospasm), immunodeficiency, malignancy, pregnancy (do not initiate, but can continue if already established).
B. Biologics (for severe uncontrolled AR, often with comorbid asthma/CRSwNP)
| Drug | Mechanism | Role |
|---|---|---|
| Omalizumab ("o-" prefix = humanised monoclonal; "-mab" = monoclonal antibody) | Anti-IgE monoclonal antibody → binds free IgE → prevents IgE binding to FcεRI on mast cells → ↓sensitisation, ↓mast cell degranulation | Severe allergic rhinitis with elevated IgE, comorbid allergic asthma. Also facilitates safer AIT |
| Dupilumab ("du-" = dual; "-lumab" = interleukin monoclonal antibody) | Anti-IL-4Rα monoclonal antibody → blocks both IL-4 and IL-13 signalling → suppresses Type 2 inflammation | CRSwNP with comorbid AR and asthma (addresses the unified airway) |
3.3 Acute Bacterial Rhinosinusitis
Features of viral ARS: generally mimics viral URI with improvement ≤10d [1].
- Most cases of ARS are viral and resolve without antibiotics.
- If symptoms are mild-moderate and do not meet bacterial criteria, watchful waiting for 7 days with symptomatic treatment is appropriate.
- Symptomatic Rx: INCS (reduce mucosal oedema → promote sinus drainage), nasal saline irrigation, analgesics.
Bacterial ARS (0.5–2%): S. pneumoniae, H. influenzae, Moraxella catarrhalis [1].
Antibiotics are indicated when bacterial ARS criteria are met (see Diagnostic Criteria section):
| Line | Drug | Dose | Duration | Rationale |
|---|---|---|---|---|
| First-line | Amoxicillin | 500 mg TDS (adults) or high-dose 1g TDS if risk of resistance | 5–7 days | Covers S. pneumoniae and most H. influenzae. Narrow-spectrum, well-tolerated, cheap. High-dose overcomes intermediate penicillin resistance in pneumococcus |
| First-line alternative (penicillin allergy) | Doxycycline | 100 mg BD | 5–7 days | Covers all 3 common pathogens. Avoid in children < 8y and pregnancy (dental discolouration, bone growth) |
| Second-line (failure after 48–72h) | Amoxicillin-clavulanate | 875/125 mg BD or high-dose 2g/125 mg BD | 7–10 days | Clavulanate inhibits β-lactamases produced by H. influenzae and M. catarrhalis → broadens amoxicillin spectrum |
| Second-line alternative | Respiratory fluoroquinolone (levofloxacin, moxifloxacin) | Levo 500 mg OD; Moxi 400 mg OD | 5–7 days | Reserve for true β-lactam allergy or treatment failure. Broad gram-positive and gram-negative coverage including resistant pneumococcus. Not first-line due to resistance concerns and serious side effects (tendinopathy, QT prolongation, aortic aneurysm risk) |
Contraindications and cautions:
- Amoxicillin: true penicillin anaphylaxis → use doxycycline or respiratory FQ
- Fluoroquinolones: avoid in children/adolescents (cartilage damage in animal models), pregnancy, patients on QT-prolonging drugs, history of tendinopathy
- Macrolides (azithromycin, clarithromycin): NOT recommended first-line for bacterial ARS due to high S. pneumoniae resistance rates (>30% in many regions including HK)
| Therapy | Mechanism | Evidence |
|---|---|---|
| INCS | Reduces mucosal oedema → opens sinus ostia → promotes drainage | Recommended as adjunct to antibiotics; also effective as monotherapy for mild bacterial ARS |
| Nasal saline irrigation | Physical clearance of mucus and inflammatory debris | Recommended as adjunct; improves symptom resolution |
| Oral decongestant (pseudoephedrine) | α-agonist → opens ostia | Short-term symptom relief; no evidence it hastens resolution. Avoid in HTN |
| Topical decongestant | Same but more potent locally | Must be limited to 2–3 days [1] |
| Oral corticosteroids | Short burst (prednisolone 30–40 mg × 3–5 days) can be considered for severe facial pain/swelling | ↓mucosal oedema rapidly; reserved for severe cases |
3.4 Chronic Rhinosinusitis (CRS)
The management of CRS is a long game — think months of medical therapy before considering surgery.
| Step | Treatment | Mechanism / Rationale |
|---|---|---|
| 1 | Nasal saline irrigation (large volume, e.g. 240 mL via squeeze bottle) | Physically clears mucus, crusts, and inflammatory mediators. Improves mucociliary clearance. Foundation of CRS management |
| 2 | INCS (fluticasone, mometasone, budesonide) for ≥ 8–12 weeks | Reduces chronic mucosal inflammation → ↓oedema → promotes OMC patency and sinus drainage |
| 3 | Long-term low-dose macrolide (clarithromycin 250 mg OD × 3 months) — if ↓eosinophils | Anti-inflammatory (not antibiotic) effect at sub-antimicrobial doses: modulates neutrophilic inflammation, reduces IL-8, improves mucociliary clearance. Most evidence in CRSsNP with normal IgE and low tissue eosinophils |
| 4 | Culture-directed antibiotics for acute exacerbations | Based on endoscopy-directed middle meatus swab culture |
| 5 | Functional Endoscopic Sinus Surgery (FESS) if ≥ 8–12 weeks of optimal medical therapy fails | Surgically widens sinus ostia → restores ventilation and mucociliary drainage. Does NOT cure the underlying mucosal disease — medical therapy must continue post-operatively |
| Step | Treatment | Mechanism / Rationale |
|---|---|---|
| 1 | Nasal saline irrigation + INCS (topical budesonide rinses are particularly effective as they reach beyond the nasal cavity into the sinuses) | Same as CRSsNP but need higher drug delivery due to polyp bulk |
| 2 | Short course oral corticosteroids (prednisolone 0.5 mg/kg/day × 1–2 weeks) | Rapidly shrinks polyps by suppressing eosinophilic inflammation. Provides temporary relief and allows topical INCS to penetrate more effectively. Limit to 2–3 courses/year due to systemic steroid side effects |
| 3 | FESS (polypectomy + sinus opening) if medical therapy fails | Debulks polyps and opens sinuses. High recurrence rate (~40–70% over 5 years) because surgery does not address the underlying Type 2 inflammation |
| 4 | Biologics (for recurrent polyps or severe Type 2 CRSwNP) | Target the specific cytokine pathways driving polyp formation: |
Biologics for CRSwNP (EPOS 2020 / currently approved):
| Drug | Target | Effect | Indication |
|---|---|---|---|
| Dupilumab | IL-4Rα → blocks IL-4 and IL-13 | ↓Type 2 inflammation, ↓eosinophil recruitment, ↓polyp size, ↓need for surgery and oral steroids | CRSwNP inadequately controlled after surgery + INCS; comorbid asthma and/or AERD |
| Omalizumab | Free IgE | ↓mast cell sensitisation, ↓eosinophil activation | CRSwNP with elevated IgE and comorbid allergic asthma |
| Mepolizumab | IL-5 | ↓eosinophil production and survival | CRSwNP with peripheral eosinophilia |
| Benralizumab | IL-5Rα | Direct eosinophil depletion via ADCC | Similar to mepolizumab |
- Avoid all COX-1 inhibitors (aspirin, NSAIDs).
- INCS + LTRA (montelukast) + FESS for polyps.
- Aspirin desensitisation: gradual dose escalation of aspirin under medical supervision → induces tolerance → allows daily aspirin maintenance (reduces polyp recurrence and improves asthma). Mechanism: chronic COX-1 inhibition downregulates CysLT1 receptors and reduces leukotriene overproduction over time.
- Biologics (dupilumab) for refractory cases.
| Treatment | Mechanism | Notes |
|---|---|---|
| Trigger avoidance (cold air, strong odours, spicy food, smoke) | Reduces non-specific trigeminal stimulation | Often impractical but should be attempted |
| INCS | Reduces non-specific mucosal hyperreactivity and inflammation | First-line pharmacotherapy; less effective than in AR |
| Ipratropium bromide nasal spray | Muscarinic M3 antagonist → blocks parasympathetic glandular secretion | Proven to be more effective than placebo and normal saline [1]. Particularly effective for the rhinorrhoea-predominant subtype and gustatory/senile rhinitis |
| Azelastine nasal spray | Intranasal antihistamine with additional anti-inflammatory and mast-cell stabilising properties | Effective even in non-allergic rhinitis (mechanism may be via anti-inflammatory action independent of H1 blockade) |
| Capsaicin nasal spray | Desensitises TRPV1 receptors on trigeminal C-fibres → reduces neurogenic inflammation and parasympathetic reflex | Emerging therapy with growing evidence; causes initial burning sensation |
Drugs: topical OTC → rhinitis medicamentosa [4].
| Step | Action | Rationale |
|---|---|---|
| 1 | Stop the offending topical decongestant | Remove the cause of α-receptor downregulation. Can be done cold turkey or by gradual taper (e.g., one nostril at a time) |
| 2 | Start INCS (fluticasone or mometasone) | Reduces mucosal inflammation and oedema from the rebound phase → makes withdrawal tolerable |
| 3 | Short course oral corticosteroids if severe (prednisolone 30 mg × 5–7 days) | Bridges the withdrawal period by systemically suppressing mucosal inflammation |
| 4 | Nasal saline irrigation | Soothes inflamed mucosa and improves clearance |
| 5 | Patient education | Explain the mechanism of rhinitis medicamentosa so the patient understands why they must stop the spray permanently |
| Causative Drug | Action |
|---|---|
| Opioids / narcotics [4] | Reduce dose or switch to non-histamine-releasing opioid if possible; add INCS for symptom control |
| ACE inhibitors | Switch to ARB (which does not increase bradykinin) |
| β-blockers | Switch to alternative antihypertensive if appropriate |
| OCP / HRT | Consider dose reduction or alternative contraception |
| Condition | Procedure | Principle |
|---|---|---|
| Deviated nasal septum | Septoplasty | Realign/trim deviated cartilage and bone to widen the obstructed airway. Indicated when symptomatic obstruction does not respond to medical therapy |
| Turbinate hypertrophy | Inferior turbinate reduction (submucosal diathermy, radiofrequency ablation, partial turbinectomy, microdebrider-assisted) | Reduces bulk of hypertrophied turbinate while preserving mucosal function. Avoid total turbinectomy (causes atrophic rhinitis — the "empty nose syndrome") |
| Adenoid hypertrophy | Adenoidectomy | Remove obstructing adenoid tissue. Indicated when causing significant nasal obstruction, sleep-disordered breathing, or recurrent otitis media |
| Nasal polyps | FESS / polypectomy | See CRSwNP section above |
| Foreign body | Removal under direct vision (anterior rhinoscopy ± endoscopy) | Ensure complete removal; consider GA in uncooperative children. Prescribe short-course antibiotics if secondary infection present |
| Choanal atresia | Surgical repair (transnasal or transpalatal) | Restore choanal patency. Bilateral cases require urgent intervention in neonates (obligate nose breathers). Unilateral can be deferred to later childhood |
| Condition | Management Principle |
|---|---|
| Malignancy (NPC, sinonasal tumour) [4] | Refer to head & neck oncology. NPC: concurrent chemoradiotherapy (cisplatin-based). Sinonasal SCC/adenocarcinoma: surgical resection ± adjuvant radiotherapy |
| GPA (Wegener's) [4] | Refer to rheumatology. Remission induction: cyclophosphamide + glucocorticoids (or rituximab). Maintenance: azathioprine or methotrexate. Nasal saline irrigation for local symptom control |
| CSF rhinorrhoea [4] | Refer to neurosurgery. Conservative trial first (bed rest, head elevation, stool softeners to avoid straining). If persistent: endoscopic surgical repair of skull base defect (often using tissue grafts and tissue sealant). Prophylactic antibiotics controversial |
| Orbital complication of sinusitis | Urgent: IV antibiotics (amoxicillin-clavulanate or ceftriaxone + metronidazole) ± surgical drainage [1]. Complications: orbital cellulitis, subperiosteal abscess requiring emergency ENT + ophthalmology input |
| Intracranial complication of sinusitis | Urgent: IV antibiotics + neurosurgical consultation [1]. Meningitis, intracranial abscess, septic cavernous sinus thrombosis — high mortality without prompt intervention |
4. Special Population Considerations
- Avoid oral decongestants in children < 6 years — risk of adverse effects (agitation, insomnia, tachycardia) outweighs benefit; FDA advisory.
- Avoid codeine in children < 12 years — CYP2D6 ultra-rapid metabolisers → excessive morphine conversion → respiratory depression and death.
- Cough suppressants: uncertain effectiveness in URTI and contraindicated in COPD, caution in asthma and children as it causes sputum retention and respiratory depression [1].
- Intranasal corticosteroids: safe in children ≥ 2 years for AR. Mometasone and fluticasone furoate have the least systemic absorption.
- Antihistamines: cetirizine or loratadine in age-appropriate doses. Avoid first-gen in young children (paradoxical excitation, sedation risk).
| Drug | Safety | Notes |
|---|---|---|
| Nasal saline irrigation | Safe | First-line for all nasal symptoms in pregnancy |
| Budesonide INCS | Category B (preferred) | Most safety data in pregnancy of all INCS |
| Chlorpheniramine (first-gen AH) | Category B | Acceptable if needed; sedation may be problematic |
| Cetirizine/loratadine (second-gen AH) | Category B | Preferred if antihistamine needed |
| Oral decongestants (pseudoephedrine) | Category C — avoid in 1st trimester | Associated with gastroschisis; vasoconstriction may reduce uteroplacental blood flow |
| Topical oxymetazoline | Limited short-term use acceptable | Minimal systemic absorption |
| Montelukast | Category B | Can continue if already established; do not initiate in pregnancy |
| Immunotherapy | Do not initiate; may continue if established | Risk of anaphylaxis to mother and fetus |
- Anticholinergic burden: first-gen antihistamines (chlorpheniramine, diphenhydramine) cause confusion, urinary retention, falls, and constipation in elderly. Prefer second-gen.
- Oral decongestants: avoid in elderly with HTN, IHD, BPH, or glaucoma.
- Senile rhinorrhoea [4]: ipratropium nasal spray is first-line.
- Intranasal corticosteroids: safe and effective; first-line for chronic rhinitis in elderly.
| Approach | Evidence | Mechanism |
|---|---|---|
| Nasal saline irrigation (NeilMed/Neti pot) | Strong evidence in AR, CRS, and post-FESS | Physical clearance + osmotic decongestant (hypertonic) |
| Steam inhalation | Weak evidence; may provide transient subjective relief | Warm moist air may ↓mucus viscosity and promote vasodilation → temporary decongestion. Risk of scalding (especially children) |
| Nasal breathing strips (Breathe Right) | Mild evidence for snoring/nasal valve collapse | Mechanical widening of the nasal valve (the narrowest point) |
| Acupuncture | Some evidence for AR (ARIA 2020: conditional recommendation) | Mechanism unclear; may modulate autonomic tone and cytokine balance |
| Probiotics | Emerging evidence for AR prevention in children | May modulate gut-associated lymphoid tissue → systemic Th1/Th2 balance |
| Butterbur extract (Petasites hybridus) | Comparable to cetirizine in some RCTs for AR | Anti-leukotriene and antihistamine effects. Caution: hepatotoxicity with unpurified preparations |
High Yield Summary — Management
Viral URTI: Supportive care (rest, hand hygiene, fluids) ± symptomatic treatment [1]. NO antibiotics. Topical decongestants limited to 2–3 days [1]. Sedating antihistamines more effective than non-sedating for cold rhinorrhoea (due to anticholinergic activity) [1].
Allergic Rhinitis: Stepwise — (1) allergen avoidance + saline, (2) INCS ± oral 2nd-gen antihistamine, (3) add LTRA or combination spray, (4) immunotherapy or biologics. INCS is the single most effective agent.
Bacterial ARS: First-line antibiotic = amoxicillin 5–7 days. Escalate to amoxicillin-clavulanate if no response in 48–72h. Adjuncts: INCS, saline irrigation.
CRS: Prolonged medical therapy (INCS + saline ≥ 8–12 weeks) before surgery. CRSwNP: short course oral steroid to shrink polyps; FESS for refractory cases; biologics (dupilumab) for severe Type 2 disease.
Rhinitis medicamentosa: STOP the topical decongestant [4] + bridge with INCS ± short oral steroid.
Structural causes: surgical correction (septoplasty, turbinate reduction, adenoidectomy) when medical therapy fails.
Red flag conditions: urgent specialist referral (oncology for malignancy, neurosurgery for CSF leak, rheumatology for GPA).
Active Recall - Management of Nasal Congestion and Rhinorrhoea
References
[1] Senior notes: Ryan Ho Respiratory.pdf (Sections 3.1.1.1 Acute Coryza — management table, symptomatic treatment; 3.1.1.4 Rhinosinusitis — aetiology, bacterial criteria, complications, imaging) [4] Lecture slides: murtagh merge.pdf (p67–68 — masquerades checklist: drugs/topical OTC → rhinitis medicamentosa, narcotics; diagnostic tips)
Complications of Nasal Congestion and Runny Nose
Nasal congestion and rhinorrhoea are, for most patients, self-limiting nuisances. But they can serve as the entry point for a cascade of complications that range from bothersome (post-nasal drip cough) to life-threatening (intracranial abscess). The key insight is that the nose is not an isolated organ — it communicates directly with the paranasal sinuses, the middle ear, the orbit, the lower airways, and the intracranial cavity. Infection, inflammation, or obstruction in the nose can therefore propagate through these anatomical connections.
I'll organise complications by the primary condition causing the nasal symptoms, then by anatomical direction of spread.
1. Complications of Acute Viral URTI (Common Cold)
Complications of viral URTI [1]:
These arise because viral infection of the nasal mucosa impairs the local defence mechanisms (mucociliary clearance, epithelial barrier, local immunity), creating opportunities for secondary bacterial infection and downstream effects.
Acute rhinosinusitis due to ↓mucociliary clearance with viral infection of mucosa [1].
- Pathophysiology: Viral cytopathic effect on ciliated epithelium → ciliary dysfunction → impaired mucociliary transport → mucus stasis within sinuses. Simultaneously, mucosal oedema obstructs the ostiomeatal complex → trapped secretions in a poorly ventilated sinus → reduced oxygen tension and lowered pH → ideal environment for bacterial proliferation.
- Frequency: Radiographic evidence of sinus involvement is present in up to 87% of common colds, but only 0.5–2% progress to bacterial rhinosinusitis [1].
- Clinical significance: Most viral sinusitis resolves spontaneously. Bacterial superinfection (S. pneumoniae, H. influenzae, M. catarrhalis) is suggested by double sickening, symptoms > 10 days, or severe onset [1].
Acute otitis media (especially in children) due to Eustachian tube dysfunction and bacterial translocation from upper respiratory tract [1].
- Pathophysiology: The Eustachian tube (ET) connects the nasopharynx to the middle ear. Viral-induced nasopharyngeal mucosal oedema → ET obstruction → negative pressure in the middle ear → fluid transudation into the middle ear space (serous otitis media). Bacteria from the nasopharynx can ascend through the dysfunctional ET → secondary bacterial infection of the effusion → acute otitis media.
- Why children are more susceptible: The paediatric ET is shorter, more horizontal, and more flaccid than the adult ET → less effective drainage and more susceptible to obstruction. Also, adenoid hypertrophy (common in children) physically blocks the ET orifice.
- Clinical features: Otalgia (ear tugging in infants), fever, irritability, red bulging tympanic membrane, conductive hearing loss.
Lower respiratory involvement due to RSV, parainfluenza, influenza involvement of lungs [1].
- Pathophysiology: Certain respiratory viruses are not confined to the upper airways. RSV and parainfluenza virus have particular tropism for lower airway epithelium → bronchiolitis (infants), bronchitis, or viral pneumonia. Influenza can cause primary viral pneumonia or predispose to secondary bacterial pneumonia (classically S. aureus, S. pneumoniae).
- Clinical features: Worsening cough, dyspnoea, wheezing (bronchiolitis/bronchitis), or crepitations with consolidation (pneumonia).
Asthma exacerbation ?due to ↑airway hyperreactivity with local inflammation [1].
- Pathophysiology: Viral infection of airway epithelium → release of pro-inflammatory cytokines and chemokines → recruitment of eosinophils and neutrophils → airway inflammation → exaggeration of pre-existing airway hyperreactivity in asthmatics. Also, viral damage to epithelium exposes subepithelial nerve endings → heightened bronchoconstrictor reflex. Rhinovirus is the single most common trigger of asthma exacerbations in both children and adults.
- The "united airway" concept: The nasal and bronchial mucosa are continuous and share the same pseudostratified ciliated epithelium. Inflammation in one compartment frequently affects the other. This is why allergic rhinitis and asthma so commonly coexist, and why treating nasal disease improves asthma control.
Post-viral cough: commonly persists past the time nasal and throat symptoms resolve [1].
- Pathophysiology: Viral infection strips the protective epithelial layer from the airways → exposed sensory nerve endings (C-fibres) become hypersensitive to normally innocuous stimuli (cold air, talking, laughing) → heightened cough reflex. Post-nasal drip also contributes by trickling mucus onto the pharyngeal and laryngeal mucosa, triggering the cough reflex via vagal afferents.
- Duration: Can persist for 3–8 weeks after the initial infection. This is the single most common cause of subacute cough (3–8 weeks) and is frequently misdiagnosed as bronchitis or "needing antibiotics."
2. Complications of Acute Rhinosinusitis
Complications: uncommon, due to spread beyond paranasal sinuses [1].
These are the high-yield, exam-critical complications. They are uncommon ( < 3% of bacterial ARS) but potentially devastating. The sinuses are surrounded by the orbit (laterally/superiorly) and the cranial cavity (superiorly/posteriorly), separated only by thin bony walls. Infection breaches these barriers by three mechanisms:
- Direct extension through thin bone (e.g., lamina papyracea, posterior wall of frontal sinus)
- Thrombophlebitis of valveless diploic veins (Breschet veins) that communicate between sinus mucosa and intracranial/orbital venous systems
- Osteomyelitis with bony destruction
Facial: facial cellulitis, osteomyelitis of sinus bones (Pott's puffy tumour) [1].
| Complication | Pathophysiology | Clinical Features | Management |
|---|---|---|---|
| Facial cellulitis | Direct spread of infection from sinus mucosa through bone to overlying soft tissues | Erythema, warmth, swelling, tenderness overlying the affected sinus (usually maxillary or frontal) | IV antibiotics (amoxicillin-clavulanate or ceftriaxone) |
| Pott's puffy tumour | Osteomyelitis of the frontal bone → subperiosteal abscess of the forehead. Despite the name, it is NOT a tumour — "puffy" describes the soft, doughy swelling. Named after Sir Percivall Pott (18th century surgeon) | Tender, fluctuant forehead swelling ("peau d'orange" overlying skin), fever, frontal headache. Most common in adolescents (frontal sinus is actively developing/pneumatising, with rich diploic blood supply) | IV antibiotics + surgical drainage of subperiosteal abscess + often frontal sinus drainage (Draf procedure or trephine) |
Why is Pott's puffy tumour more common in adolescents? Because the frontal sinus completes pneumatisation during adolescence, and the developing diploic bone has a particularly rich blood supply that facilitates haematogenous spread of infection from the sinus mucoperiosteum to the outer table of the frontal bone.
Orbit: preseptal cellulitis, orbital cellulitis, subperiosteal abscess [1][13].
The orbit is separated from the ethmoid sinus by the lamina papyracea ("papyrus-like plate") — a paper-thin bone that is often dehiscent (has natural perforations for neurovascular passage). This is why ethmoid sinusitis is the most common source of orbital complications.
The Chandler Classification grades orbital complications by severity:
| Stage | Name | Pathophysiology | Clinical Features | Key Distinction |
|---|---|---|---|---|
| I | Preseptal (periorbital) cellulitis | Infection of eyelid tissues anterior to the orbital septum. The orbital septum is a fibrous barrier between the eyelid and the orbit | Eyelid swelling, erythema, warmth. Normal eye movements, normal vision, no proptosis | Not an emergency [13] — because the infection is confined to the eyelid and does not threaten the eye or brain |
| II | Orbital cellulitis | Infection has spread posterior to the orbital septum into the orbital fat/tissues. Diffuse inflammation of orbital contents | Proptosis, ophthalmoplegia ± diplopia (most important feature), pain with eye movement, ± visual impairment ± RAPD, chemosis, fever [13] | Ophthalmic emergency [13] — can progress to abscess, visual loss, or intracranial spread |
| III | Subperiosteal abscess | Pus collects between the periorbita and the lamina papyracea (between the orbital wall bone and the orbital periosteum) | As above but often with displacement of the globe (laterally and inferiorly if medial wall abscess from ethmoid source), more severe proptosis | Requires urgent surgical drainage in addition to IV antibiotics [13] |
| IV | Orbital abscess | Discrete abscess within the orbital fat, posterior to the septum | Severe proptosis, complete ophthalmoplegia, marked visual loss, severe constitutional symptoms | Urgent surgical drainage + IV antibiotics |
| V | Cavernous sinus thrombosis | Infection spreads via valveless superior ophthalmic vein to cavernous sinus → septic thrombosis | Bilateral eye signs (because the cavernous sinuses communicate via intercavernous sinuses), CN III/IV/V1/V2/VI palsies, altered consciousness, high fever, rapid deterioration | Life-threatening emergency. IV antibiotics + anticoagulation (controversial) + possibly surgical drainage |
Orbital cellulitis is an ophthalmic emergency [13]. The complications of orbital cellulitis include:
- Subperiosteal abscess (15–59%) [13]
- Orbital abscess (24%) [13]
- Intracranial extension: cavernous sinus thrombosis/CVST, brain abscess, epidural/subdural empyema [13]
- Visual loss due to optic neuritis or ischaemia due to compressive CRAO or orbital venous thrombophlebitis [13]
Why does orbital cellulitis cause visual loss? Two mechanisms:
- Compressive optic neuropathy: swollen orbital contents compress the optic nerve directly → ischaemia → optic neuropathy (RAPD on examination).
- Central retinal artery occlusion (CRAO): raised intraorbital pressure exceeds retinal arterial perfusion pressure → retinal ischaemia → sudden painless visual loss.
Preseptal vs. Orbital Cellulitis — The Exam Classic
The most critical distinction in the exam: preseptal cellulitis has NORMAL eye movements and NORMAL vision — it is a mild condition treated with oral antibiotics. Orbital cellulitis has ophthalmoplegia, proptosis, and threatens vision — it is an emergency requiring IV antibiotics and often surgical drainage. The key question at the bedside: "Can the patient move their eye in all directions? Is the vision affected?" [13]
Intracranial: meningitis, intracranial abscess, septic cavernous sinus thrombosis [1].
These are the most feared complications of rhinosinusitis. They occur when infection breaches the posterior wall of the frontal sinus, the roof of the ethmoid sinus (fovea ethmoidalis), or spreads via valveless veins.
| Complication | Source Sinus | Pathophysiology | Clinical Features | Key Investigations |
|---|---|---|---|---|
| Bacterial meningitis | Any, esp. sphenoid, ethmoid | Direct extension through skull base or haematogenous spread → infection of meninges | Headache, neck stiffness, photophobia, fever, altered consciousness. Complications of meningitis: basal meningeal adhesions → hydrocephalus, CN palsies (III, IV, VI commonest); arteritis/thrombophlebitis → cerebral infarction; parenchymal damage → seizures, intellectual impairment [14] | LP (after CT if focal signs), blood cultures, CT sinuses |
| Epidural abscess | Frontal (most common) | Infection penetrates posterior table of frontal sinus → pus collects between dura and inner skull table | Fever, headache, focal neurological signs (depending on location). May be clinically silent initially | CT/MRI with contrast → rim-enhancing collection |
| Subdural empyema | Frontal, ethmoid | Pus between dura and arachnoid mater. Rapidly progressive and extremely dangerous | Rapid deterioration: high fever, severe headache, seizures, hemiparesis, raised ICP signs. Look for severe headache, protracted vomiting, CN palsies and mental status changes [13] | MRI with contrast (superior to CT) → crescentic collection. Mortality ~10–20% even with treatment |
| Brain abscess | Frontal, ethmoid, sphenoid | Direct extension or haematogenous seeding → focal collection of pus within brain parenchyma, usually frontal lobe (from frontal sinusitis) | Headache, fever (may be absent), focal neurological deficits, seizures, raised ICP | CT/MRI with contrast → ring-enhancing lesion with surrounding oedema. Intracranial tumour, chronic subdural haematoma show similar imaging findings [11] |
| Septic cavernous sinus thrombosis (CST) | Sphenoid (direct adjacency), ethmoid, or via ophthalmic veins | Infection spreads to cavernous sinus → septic thrombosis → obstruction of venous drainage from orbits and cranial nerves within the sinus | Bilateral proptosis, bilateral ophthalmoplegia (CN III, IV, VI traverse the cavernous sinus), CN V1/V2 sensory loss, high fever, altered consciousness, rapid deterioration | MRI/MRV or CT venography → non-enhancing/filling defect in cavernous sinus. Blood cultures. Mortality 20–30% |
Why do intracranial complications of sinusitis spread via veins rather than arteries? Because the diploic veins (within the skull bones) and the emissary veins connecting the sinuses to the intracranial venous sinuses are valveless. This means blood (and therefore bacteria/infected thrombi) can flow in either direction — from sinus mucosa directly into the dural venous sinuses. There is no one-way valve to prevent retrograde spread. This is a fundamental anatomical concept.
When to Suspect Intracranial Complications of Sinusitis
Red flags during treatment of acute sinusitis that should trigger urgent CT/MRI and neurosurgical consultation:
- High spiking fever not responding to appropriate antibiotics
- Severe or worsening headache out of proportion to sinus symptoms
- Altered mental status (drowsiness, confusion, agitation)
- Focal neurological deficits (hemiparesis, aphasia)
- Seizures
- Signs of raised ICP (vomiting, papilloedema, CN VI palsy)
- Bilateral orbital signs (suggesting cavernous sinus involvement)
3. Complications of Chronic Rhinosinusitis
- Pathophysiology: Complete obstruction of a sinus ostium → entrapped mucous secretion → progressive expansion of the sinus as the mucocoele slowly expands under the pressure of accumulating mucus → erosion of surrounding bone (pressure necrosis) → extension into orbit (proptosis, diplopia) or intracranial cavity.
- Most common site: Frontal sinus (60–65%), then ethmoid.
- Clinical features: Slowly progressive unilateral proptosis (downward and lateral globe displacement if frontal mucocoele), periorbital fullness, frontal headache. If secondarily infected → mucopyocoele (acute presentation with pain, fever).
- Imaging: CT shows expanded, opacified sinus with thinning/erosion of bony walls. MRI differentiates from tumour.
- Management: Surgical drainage/marsupialisation via endoscopic approach.
- Pathophysiology: Persistent inflammation → mucosal remodelling → goblet cell hyperplasia, submucosal fibrosis, and oedematous polypoid degeneration (in Type 2 CRS). This creates a self-perpetuating cycle: polyps obstruct drainage → more stasis → more inflammation → more polyps.
- Clinical impact: Progressive bilateral nasal obstruction, anosmia (polyps block olfactory cleft), recurrent infections, reduced quality of life.
- Conductive anosmia: Nasal polyps or severe mucosal oedema physically block odorant molecules from reaching the olfactory neuroepithelium in the roof of the nose. This is reversible with effective medical or surgical treatment.
- Sensorineural anosmia: Chronic inflammation may damage the olfactory neuroepithelium itself over time, or post-viral olfactory nerve damage (especially with COVID-19, influenza). This is less reversible.
- Impact: Often underestimated — anosmia affects taste (flavour perception depends ~80% on olfaction), food safety (cannot smell gas leaks, smoke, spoiled food), and quality of life (depression, social isolation).
4. Complications of Allergic Rhinitis
Atopic march: atopic dermatitis/food allergy (0–3y) → asthma (4–9y) → rhinoconjunctivitis (10+ y) [3].
- Pathophysiology: Allergic rhinitis is part of a systemic Th2-polarised immune dysregulation. The same genetic and immunological predisposition that drives nasal mucosal IgE sensitisation also affects bronchial mucosa (asthma), skin (eczema), and gut (food allergy). Early-onset atopic dermatitis is associated with ↑risk of progression into other forms of atopic conditions [3].
- Clinical significance: Treating AR aggressively (especially with allergen immunotherapy) may modulate the atopic march — there is evidence that AIT reduces the risk of developing asthma in children with AR.
- The "united airway" hypothesis: allergic rhinitis and asthma represent inflammation of the same continuous airway mucosa. Up to 40% of AR patients have asthma, and > 80% of asthmatics have AR.
- Uncontrolled AR worsens asthma control. Treating AR (especially with INCS) improves asthma outcomes.
- Pathophysiology: Chronic allergic nasopharyngeal mucosal oedema → Eustachian tube dysfunction → negative middle ear pressure → serous fluid accumulation in the middle ear.
- Clinical impact: Conductive hearing loss → speech and language delay in young children if untreated. Managed with treating the underlying AR; myringotomy ± grommets if persistent.
- Up to 60–70% of AR patients have concurrent allergic conjunctivitis (allergic rhinoconjunctivitis). Driven by the same IgE-mediated mast cell degranulation in the conjunctival mucosa.
- Usually associated with other atopic features: sneezing, rhinorrhoea, eczema [7].
- Chronic nasal congestion (especially at night — worse when supine due to gravity-dependent venous pooling) disrupts sleep architecture → daytime fatigue, impaired concentration, reduced school/work performance.
- Children with chronic AR have impaired cognitive function and school performance comparable to that seen with chronic illness.
- Chronic mouth breathing from nasal obstruction → altered craniofacial development:
- Adenoid facies: elongated face, high-arched palate, dental malocclusion, open-mouth posture
- Dental caries: mouth breathing dries the oral mucosa → reduced salivary buffering → ↑caries risk
Drugs: topical OTC → rhinitis medicamentosa [4].
| Complication | Pathophysiology |
|---|---|
| Rebound congestion (the defining feature) | α-receptor downregulation → withdrawal vasodilatation → worse congestion than the original disease |
| Mucosal atrophy and metaplasia | Chronic vasoconstriction → ischaemic damage to nasal mucosa → loss of cilia, squamous metaplasia, submucosal fibrosis |
| Psychological dependence | Patients become psychologically dependent on the spray because any attempt to stop causes intolerable congestion. This is a real and significant barrier to treatment |
| Epistaxis | Atrophic, fragile mucosa bleeds easily with minor trauma (nose blowing, digital manipulation) |
Trauma ± blood [4].
| Complication | Pathophysiology | Why It Matters |
|---|---|---|
| Septal haematoma | Blunt nasal trauma → bleeding between the perichondrium and septal cartilage. The haematoma strips perichondrium from cartilage → loss of blood supply to avascular cartilage → avascular necrosis | An ENT emergency. If not drained within 24–72 hours → abscess formation → septal perforation → saddle nose deformity. Always examine the septum after any nasal trauma |
| CSF rhinorrhoea | Fracture of the cribriform plate (anterior skull base) → meningeal tear → CSF leaks into nasal cavity. Clear discharge following direct facial or head injury may represent CSF leakage from a skull fracture [4] | Risk of ascending meningitis if not treated. Confirm with β2-transferrin. Neurosurgical repair if persistent |
| Nasal fracture with cosmetic deformity | Displacement of nasal bones → visible deviation, dorsal hump, or depression | Closed reduction within 10–14 days (before bone healing); open septorhinoplasty if late presentation |
Nasal foreign body e.g. in toddlers [4].
| Complication | Pathophysiology |
|---|---|
| Secondary infection | Foreign body obstructs mucociliary clearance → stagnant mucus → bacterial overgrowth (often anaerobes) → unilateral foul-smelling purulent/bloody discharge |
| Mucosal ulceration and granulation tissue | Chronic mechanical irritation of the nasal mucosa by the foreign body → ulceration → granulation tissue formation that may obscure the foreign body on examination |
| Button battery necrosis | Button batteries are particularly dangerous — they generate an electrical current when in contact with moist mucosa → liquefactive necrosis within 2–4 hours → rapid septal perforation, turbinate destruction. This is a true emergency requiring immediate removal |
| Aspiration | Failed or poorly planned removal attempts may push the foreign body posteriorly → aspiration into the tracheobronchial tree |
| Rhinolith formation | If a foreign body remains in situ for months-years, mineral salts (calcium, magnesium) deposit around it → forms a rhinolith (nasal stone) → chronic unilateral obstruction and infection |
Button Battery in the Nose — Time is Tissue!
A button battery lodged in the nose is a surgical emergency. Liquefactive necrosis begins within hours and can cause septal perforation within 4 hours. Do NOT wait for specialist review — remove immediately if at all possible. This also applies to button batteries in the oesophagus (oesophageal perforation risk).
These are the "downstream effects" of prolonged nasal breathing impairment, regardless of the underlying aetiology:
| Complication | Pathophysiology |
|---|---|
| Obstructive sleep apnoea (OSA) | Chronic nasal obstruction increases upper airway resistance → contributes to pharyngeal collapse during sleep → apnoeas/hypopnoeas → intermittent hypoxia → daytime somnolence, cardiovascular risk |
| Eustachian tube dysfunction / OME | Nasopharyngeal obstruction (polyps, adenoids, tumour) → impaired ET opening → negative middle ear pressure → effusion |
| Oral breathing complications | Chronic mouth breathing → dry mouth (xerostomia) → ↑dental caries, halitosis, gingivitis. In children → adenoid facies, dental malocclusion |
| Lower airway disease | Loss of nasal air conditioning (warming, humidifying, filtering) → cold, dry, unfiltered air reaches lower airways → bronchial hyperreactivity, ↑infection risk, asthma worsening |
| Chronic cough (post-nasal drip syndrome / upper airway cough syndrome) | Mucus dripping from posterior nose onto pharyngeal and laryngeal mucosa → stimulates cough receptors (vagal afferents) → chronic cough. One of the three most common causes of chronic cough (alongside asthma and GERD) |
This is the most systematic way to think about complications in an exam:
| Direction | Source → Destination | Complications |
|---|---|---|
| Local | Nasal cavity itself | Rhinitis medicamentosa, mucosal atrophy, anosmia, epistaxis, polyp formation, mucocoele |
| Lateral | Sinuses → orbit (via lamina papyracea) | Preseptal cellulitis, orbital cellulitis, subperiosteal abscess, orbital abscess [1][13] |
| Superior | Sinuses → intracranial cavity (via skull base) | Meningitis, epidural abscess, subdural empyema, brain abscess [1][14] |
| Posterior | Sinuses → cavernous sinus (via valveless veins) | Septic cavernous sinus thrombosis [1] |
| Anterior | Sinuses → overlying facial soft tissues/bone | Facial cellulitis, Pott's puffy tumour [1] |
| Inferior | Nose → nasopharynx → Eustachian tube → middle ear | Acute otitis media, otitis media with effusion [1] |
| Inferior (airway) | Nose → lower airways | Lower respiratory infection, asthma exacerbation, post-nasal drip cough [1] |
| Systemic | Allergic rhinitis → systemic atopy | Asthma, eczema, food allergy (atopic march) [3] |
High Yield Summary — Complications
Viral URTI complications [1]: acute rhinosinusitis (↓mucociliary clearance), acute otitis media (Eustachian tube dysfunction, especially in children), lower respiratory involvement (RSV, parainfluenza, influenza), asthma exacerbation, post-viral cough.
Rhinosinusitis complications [1]: Organised by spread direction —
- Facial: facial cellulitis, Pott's puffy tumour (frontal osteomyelitis)
- Orbital: preseptal cellulitis, orbital cellulitis, subperiosteal abscess, orbital abscess, cavernous sinus thrombosis
- Intracranial: meningitis, intracranial abscess, septic cavernous sinus thrombosis
Orbital cellulitis [13]: Ophthalmic emergency. Key distinction from preseptal cellulitis: ophthalmoplegia, proptosis, visual impairment present in orbital cellulitis but absent in preseptal cellulitis. Most commonly from ethmoid sinusitis via lamina papyracea. Complications include visual loss from CRAO or optic neuritis, intracranial extension [13].
Intracranial complications spread via valveless diploic/emissary veins — bacteria travel bidirectionally from sinus mucosa to dural venous sinuses.
Allergic rhinitis complications: atopic march [3], asthma (united airway), OME, sleep disturbance, craniofacial maldevelopment in children.
Nasal foreign body: secondary infection, button battery → liquefactive necrosis within hours (emergency).
Rhinitis medicamentosa [4]: rebound congestion, mucosal atrophy, psychological dependence.
Active Recall - Complications of Nasal Congestion and Rhinorrhoea
References
[1] Senior notes: Ryan Ho Respiratory.pdf (Sections 3.1.1.1 Acute Coryza — complications; 3.1.1.4 Rhinosinusitis — complications) [3] Senior notes: Ryan Ho Rheumatology.pdf (Section 4.2.2.1 Atopic Dermatitis — atopic march, comorbidities) [4] Lecture slides: murtagh merge.pdf (p67–68 — Pitfalls: nasal foreign body, trauma; Masquerades: rhinitis medicamentosa; Diagnostic tips: CSF rhinorrhoea) [7] Senior notes: Ryan Ho Opthalmology.pdf (Section 2.2.2 Conjunctivitis — allergic conjunctivitis with atopic features) [11] Senior notes: Ryan Ho Fundamentals.pdf (p315 — Headache causes: sinusitis, intracranial tumour, infection, subdural haematoma) [13] Senior notes: Ryan Ho Opthalmology.pdf (Section 2.6.4 Orbital Cellulitis — pathogenesis, preseptal vs orbital cellulitis, complications) [14] Senior notes: Ryan Ho Neurology.pdf (Sections p144–145 — Meningitis complications: basal adhesions, hydrocephalus, CN palsies, arteritis, parenchymal damage)
High Yield Summary
Nasal Congestion & Rhinorrhoea — Core Concepts:
-
Anatomy is key: the inferior turbinate has erectile tissue (venous sinusoids) regulated by sympathetic (vasoconstriction = decongestion) and parasympathetic (vasodilatation + secretion = congestion + rhinorrhoea) tone.
-
Most common cause acutely: viral URTI (common cold), > 200 subtypes, rhinovirus most common. Self-limiting, > 90% resolve in 10 days [1].
-
Most common cause chronically in HK: allergic rhinitis (house dust mite is the dominant allergen). Type I hypersensitivity: sensitisation → early phase (mast cell degranulation, histamine) → late phase (eosinophilic infiltration).
-
Rhinitis medicamentosa: topical OTC nasal decongestants used > 5–7 days → α-receptor downregulation → rebound congestion [4]. Always ask about OTC spray use.
-
Masquerades: Drugs and Hypothyroidism [4].
-
Red flags for sinister pathology: persistent blood-stained unilateral discharge → exclude NPC, sinonasal malignancy, GPA. Clear unilateral discharge post-trauma → CSF leak [4].
-
Acute rhinosinusitis: viral → direct sinus spread or ↓sinus drainage with secondary bacterial infection. Bacterial (0.5–2%): S. pneumoniae, H. influenzae, M. catarrhalis. Complications: orbital cellulitis, intracranial infection, Pott's puffy tumour [1].
-
Nasal polyps: bilateral = inflammatory (CRSwNP), consider AERD (Samter's triad) and CF (in children). Unilateral = exclude neoplasm.
-
History clues: character of discharge, laterality, duration, triggers, drug history (OTC sprays!), trauma history, associated features (itch, sneezing, anosmia, ear symptoms).
-
Exam: anterior rhinoscopy → pale boggy mucosa (allergic), erythematous mucosa (infectious), polyps, septal deviation, discharge character.
High Yield Summary — Differential Diagnosis
Murtagh's Framework for Nasal Congestion/Rhinorrhoea [4]:
-
Probability diagnosis: Common cold (viral URTI), rhinitis (infective, allergic, vasomotor), vasomotor stimulation (cold, smoke, irritants), sinusitis → post-nasal drip, senile rhinorrhoea.
-
Serious disorders not to be missed: Cluster headache (autonomic nasal symptoms), chronic infective granulomas (TB), malignancy (NPC — extremely important in HK), CSF rhinorrhoea (post head injury), GPA (Wegener's).
-
Pitfalls: Nasal foreign body (toddlers — unilateral foul-smelling discharge), trauma ± septal haematoma, adenoid hypertrophy, illicit drugs (cocaine, heroin), inhaled irritants, choanal atresia.
-
Masquerades: Drugs (topical OTC → rhinitis medicamentosa; narcotics) and Hypothyroidism.
Key differentiating features:
- Unilateral + blood-stained → malignancy / GPA / foreign body until proven otherwise
- Bilateral + itch + sneeze + watery eyes → allergic rhinitis
- Rebound after nasal spray → rhinitis medicamentosa
- Periodic unilateral with periorbital pain + lacrimation → cluster headache
- Clear + unilateral + post-trauma → CSF rhinorrhoea
High Yield Summary — Diagnosis
Core Principle: Diagnosis of nasal congestion/rhinorrhoea is predominantly clinical [1]. Usually no investigations required [4].
Acute rhinosinusitis criteria [1]: ≥2 symptoms (with ≥1 nasal: blockage/congestion OR discharge) PLUS facial pain/pressure and/or hyposmia.
Bacterial ARS criteria [1]: ≥3 of double sickening, purulent discharge, severe localised pain, fever > 38°C/↑ESR/CRP. OR: persistent > 10 days, severe onset, or double sickening pattern.
Allergic rhinitis: clinical features (itch, sneeze, watery rhinorrhoea, congestion) + positive allergy testing (SPT preferred over specific IgE).
CRS ( > 12 weeks): clinical criteria PLUS objective evidence on nasal endoscopy or CT.
Key investigations to consider [4]: micro/culture, sinus X-ray (NOT recommended — poor Se/Sp), CT scan (for complications/surgical planning), allergy testing.
Imaging NOT indicated if uncomplicated [1]. CT reserved for suspected complications [1].
Red flag investigations: unilateral bloody discharge → urgent endoscopy + biopsy; clear post-trauma discharge → β2-transferrin; child with polyps → sweat chloride.
High Yield Summary — Management
Viral URTI: Supportive care (rest, hand hygiene, fluids) ± symptomatic treatment [1]. NO antibiotics. Topical decongestants limited to 2–3 days [1]. Sedating antihistamines more effective than non-sedating for cold rhinorrhoea (due to anticholinergic activity) [1].
Allergic Rhinitis: Stepwise — (1) allergen avoidance + saline, (2) INCS ± oral 2nd-gen antihistamine, (3) add LTRA or combination spray, (4) immunotherapy or biologics. INCS is the single most effective agent.
Bacterial ARS: First-line antibiotic = amoxicillin 5–7 days. Escalate to amoxicillin-clavulanate if no response in 48–72h. Adjuncts: INCS, saline irrigation.
CRS: Prolonged medical therapy (INCS + saline ≥ 8–12 weeks) before surgery. CRSwNP: short course oral steroid to shrink polyps; FESS for refractory cases; biologics (dupilumab) for severe Type 2 disease.
Rhinitis medicamentosa: STOP the topical decongestant [4] + bridge with INCS ± short oral steroid.
Structural causes: surgical correction (septoplasty, turbinate reduction, adenoidectomy) when medical therapy fails.
Red flag conditions: urgent specialist referral (oncology for malignancy, neurosurgery for CSF leak, rheumatology for GPA).
High Yield Summary — Complications
Viral URTI complications [1]: acute rhinosinusitis (↓mucociliary clearance), acute otitis media (Eustachian tube dysfunction, especially in children), lower respiratory involvement (RSV, parainfluenza, influenza), asthma exacerbation, post-viral cough.
Rhinosinusitis complications [1]: Organised by spread direction —
- Facial: facial cellulitis, Pott's puffy tumour (frontal osteomyelitis)
- Orbital: preseptal cellulitis, orbital cellulitis, subperiosteal abscess, orbital abscess, cavernous sinus thrombosis
- Intracranial: meningitis, intracranial abscess, septic cavernous sinus thrombosis
Orbital cellulitis [13]: Ophthalmic emergency. Key distinction from preseptal cellulitis: ophthalmoplegia, proptosis, visual impairment present in orbital cellulitis but absent in preseptal cellulitis. Most commonly from ethmoid sinusitis via lamina papyracea. Complications include visual loss from CRAO or optic neuritis, intracranial extension [13].
Intracranial complications spread via valveless diploic/emissary veins — bacteria travel bidirectionally from sinus mucosa to dural venous sinuses.
Allergic rhinitis complications: atopic march [3], asthma (united airway), OME, sleep disturbance, craniofacial maldevelopment in children.
Nasal foreign body: secondary infection, button battery → liquefactive necrosis within hours (emergency).
Rhinitis medicamentosa [4]: rebound congestion, mucosal atrophy, psychological dependence.
Menstrual/vaginal Complaints
Menstrual and vaginal complaints encompass a range of gynecological conditions including abnormal uterine bleeding, dysmenorrhea, amenorrhea, vaginal discharge, and vulvovaginal irritation that may indicate infectious, hormonal, structural, or systemic disorders.
Nausea, Vomiting
Nausea is the unpleasant sensation of an urge to vomit, while vomiting is the forceful expulsion of gastric contents through the mouth, both mediated by the brainstem vomiting center in response to various peripheral and central stimuli.