CSF rhinorrhoea is a diagnosis that must not be missed — a traumatic or spontaneous dural tear allows cerebrospinal fluid to drain through the cribriform plate into the nasal cavity. The distinguishing features: watery, clear, unilateral discharge that worsens on bending forward or performing a Valsalva manoeuvre; salty taste; often associated with anosmia (if cribriform plate involved). The halo test (placing a drop of the discharge on filter paper — CSF will form a clear halo around a central bloody spot) has limited sensitivity. The gold standard test: beta-2 transferrin assay (a CSF-specific protein absent from blood, tears, and nasal secretions) — any positive beta-2 transferrin in nasal discharge confirms CSF. The risks of untreated CSF rhinorrhoea: ascending bacterial meningitis (pneumococcal meningitis is the most feared complication — 80% fatal without antibiotics), and tension pneumocephalus (air entering the intracranial space). Patients should be told not to suppress sneezing (increased intracranial pressure can worsen the leak) and to keep the head elevated. Prophylactic antibiotics are controversial but many centres give penicillin or amoxicillin.

Rhinitis medicamentosa (RM) is one of the most common and most easily preventable causes of chronic nasal obstruction seen in primary care — it is caused by the rebound vasodilation (tachyphylaxis) that follows prolonged use of topical alpha-adrenergic decongestants (oxymetazoline, xylometazoline, naphazoline). These preparations work by vasoconstricting the nasal turbinate vessels within 2-5 minutes; the problem is that repeated use causes progressively shorter duration of action and paradoxically worsening nasal congestion as the drug effect wears off, driving the patient to use the spray more and more frequently. The pharmacological mechanism: down-regulation of alpha-adrenergic receptors + rebound vasodilation mediated by reduced nitric oxide synthesis. The GP management: stop the decongestant spray immediately (cold turkey approach) + start intranasal corticosteroid (mometasone or fluticasone — allows withdrawal without unbearable rebound congestion). The clinical history that identifies RM: patient using nasal decongestant spray more than twice daily for more than 3 days, without relief lasting more than 2-3 hours, and having started the spray for a common cold that resolved weeks ago.

The united airway disease concept is clinically important for GP management of allergic rhinitis — approximately 50% of allergic rhinitis patients have coexisting asthma, and approximately 80% of asthmatic patients have rhinitis symptoms. The reason: the upper and lower respiratory tract are anatomically and immunologically continuous — the same type I hypersensitivity response (mast cell degranulation, IgE-mediated) occurs in both nasal mucosa and bronchial mucosa in response to the same allergens (house dust mite, pet dander, pollen). The clinical implication: inadequately treated rhinitis worsens asthma control (post-nasal drip triggers bronchospasm; mouth breathing in nasal obstruction bypasses upper airway humidification and filtering; nasal nitric oxide production — which is bronchodilatory — is impaired). Every asthmatic patient should have their rhinitis formally assessed and treated. Conversely, treating allergic rhinitis with intranasal corticosteroids reduces asthma exacerbation rates by approximately 25-30% — an underutilised strategy in primary care asthma management.

The type 2 inflammation pathway is the unifying mechanism behind the triad of eosinophilic CRS with nasal polyps, atopic asthma, and atopic eczema — all three conditions are driven by Th2 lymphocyte activation, IL-4, IL-5, and IL-13 signalling, which drives eosinophil recruitment and IgE production. This shared pathway explains why dupilumab (a biologic that blocks IL-4Rα, the shared receptor subunit for both IL-4 and IL-13 signalling) simultaneously improves nasal polyps, asthma, and eczema when all three coexist. NICE approved dupilumab for severe uncontrolled CRSwNP (TA new in 2023) and for severe atopic eczema (TA534) and for severe asthma (TA751). In a patient with all three conditions, dupilumab can potentially be prescribed for one indication while also benefiting the other two — this requires specialist coordination between ENT, respiratory, and dermatology. GPs should identify patients with this triple burden (CRSwNP + asthma + eczema) and refer to the appropriate specialist for biologic consideration.

The delayed antibiotic prescription for acute rhinosinusitis is an important antimicrobial stewardship strategy — the NICE guidance and SIGN guidelines both recommend that GPs offer a 'delayed' or 'back-pocket' prescription for acute bacterial rhinosinusitis to patients who are not severely unwell, with instructions to fill the prescription only if symptoms do not improve after 5-7 days or worsen. The rationale: the majority of acute rhinosinusitis episodes (approximately 80%) are viral and resolve without antibiotics within 2-4 weeks; immediate antibiotics provide minimal benefit (NNT approximately 8 for symptom relief, with antibiotic-related harms including diarrhoea, thrush, rash in approximately 1 in 10). The features that increase the probability of bacterial sinusitis requiring antibiotics: symptoms worsening after initial improvement (the 'double-sickening' pattern), symptoms persisting beyond 10 days without improvement, high fever above 38.5°C, and unilateral facial pain/tenderness. Saline nasal irrigation (nasal douche with isotonic saline) is a highly evidence-based treatment for acute rhinosinusitis that significantly reduces symptom duration and reduces antibiotic use — it should be first-line recommended for all patients with rhinosinusitis symptoms.

Allergen immunotherapy (AIT) is the only disease-modifying treatment for allergic rhinitis — all other treatments (antihistamines, intranasal steroids, decongestants) are purely symptomatic. AIT works by inducing immune tolerance to the specific allergen through repeated low-dose exposure: subcutaneous injections (SCIT — monthly after updosing) or sublingual tablets/drops (SLIT — daily self-administered at home). The evidence base: multiple meta-analyses confirm that AIT reduces allergic rhinitis symptoms by approximately 30-40% relative to placebo, reduces asthma exacerbations, and reduces the development of new allergies (preventing the 'allergic march'). The SLIT preparations licensed in UK (Grazax for grass pollen — Merck, and Acarizax/Actair for house dust mite) are GP-initiatable in some formulary areas after allergy testing. GPs should be aware that sublingual immunotherapy is available and refer appropriate patients (moderate-severe allergic rhinitis not controlled by step 3 medications) for allergen testing and AIT consideration.

The nasal saline irrigation evidence for rhinosinusitis and CRS is stronger than many GPs appreciate — a Cochrane review (Chong 2016) found that nasal saline irrigation significantly reduces nasal symptoms, improves quality of life, and reduces medication use in CRS and acute rhinosinusitis, with minimal side effects. The mechanism: physical removal of thick mucus, allergens, and inflammatory mediators from the nasal mucosa; improvement in mucociliary clearance; reduction of nasal mucosal oedema. The standard preparation: 240 ml (8 oz) isotonic saline (0.9% NaCl) delivered at positive pressure via a neti pot or squeeze bottle into one nostril, allowing it to drain from the other. Hypertonic saline (2-3% NaCl) provides additional benefit for CRS. Commercial preparations (Sterimar, NeilMed, etc.) are convenient but expensive — patients can make their own saline at home (1/4 tsp non-iodised salt + 1/4 tsp bicarbonate of soda in 240 ml previously boiled and cooled water). GPs should recommend nasal irrigation as first-line treatment for all patients with rhinosinusitis before prescribing antibiotics.

The intranasal corticosteroid technique education is one of the most impactful interventions a GP can make for allergic rhinitis management — a study of over 1,000 patients with allergic rhinitis found that approximately 80% were using their nasal spray incorrectly (tilting the head back rather than forward, aiming toward the septum, sniffing forcefully after spraying). Incorrect technique delivers drug to the posterior pharynx (causing throat irritation and systemic absorption) rather than the nasal mucosa, dramatically reducing efficacy and potentially causing septal bleeding. A 1-minute demonstration of correct technique (head tilted forward, aim away from septum, gentle sniff, breathe out through mouth) significantly improves outcomes. The NHS has a 'how to use your nasal spray' educational video available on the NHS website — GPs should signpost to this at the first INCS prescription.

The post-treatment review at 1 week for antibiotic-treated acute bacterial rhinosinusitis is important for two reasons: (1) treatment failure is relatively common (approximately 15-20% of patients do not improve on first-line amoxicillin, due to beta-lactamase-producing organisms — these patients need co-amoxiclav 625 mg TDS); and (2) complications of bacterial sinusitis (orbital cellulitis, meningitis, brain abscess) require immediate identification. Safety-netting for bacterial sinusitis must be explicit: if symptoms worsen rather than improve after 48 hours of antibiotics, or if periorbital swelling, visual changes, severe headache, or neck stiffness develop, the patient should attend A&E immediately. The complications of bacterial sinusitis are rare (estimated 1 in 10,000 episodes) but can be life-threatening, and the GP who has given antibiotics needs to ensure the patient understands the red flag symptoms requiring emergency care.