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) — sample collection and testing are arranged through the hospital pathway, not at the initial GP consultation. The risks of untreated CSF rhinorrhoea: ascending bacterial meningitis (pneumococcal meningitis is the most feared complication), and tension pneumocephalus (air entering the intracranial space). Positioning advice (head elevation, not suppressing sneezing) is not sufficient management and must not delay transfer; antibiotic decisions belong to the specialist team.

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: explain rebound congestion, stop the topical decongestant, use regular intranasal corticosteroid and saline, consider a staged withdrawal if abrupt cessation is not tolerated, and review if symptoms persist or the diagnosis is uncertain. The clinical history that identifies RM: patient using nasal decongestant spray more than twice daily for more than 5 consecutive 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 — allergic rhinitis and asthma commonly coexist. 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. Review asthma control alongside rhinitis treatment.

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 TA1134 (2026) recommends dupilumab for severe uncontrolled CRSwNP 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 — NICE NG79 (2017) advises GPs to consider no antibiotic or a 'back-up' prescription for people with symptoms for around 10 days or more without improvement who are not systemically very unwell, with instructions to use the prescription only if symptoms do not improve within 7 days or worsen rapidly or significantly at any time. The rationale: most acute rhinosinusitis episodes are viral and resolve without antibiotics, commonly within 2–3 weeks; immediate antibiotics provide little benefit and cause harms including diarrhoea, thrush and rash. 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, fever, and severe localised unilateral facial or dental pain — discoloured discharge alone is not an indication. Saline nasal irrigation can be offered as self-care if the patient prefers it.

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). Benefits and eligibility depend on the allergen, product, age and local service — do not promise sustained remission or reduced asthma risk. NICE TA1045 recommends 12 SQ-HDM SLIT for selected people aged 12–65 with moderate-to-severe persistent HDM allergic rhinitis, and TA1087 covers 12 SQ-Bet SLIT for selected birch-homologous tree-pollen allergy; products are not interchangeable and initiation is specialist-led. GPs should be aware that sublingual immunotherapy is available and refer appropriate patients (allergen-consistent history, objectively confirmed sensitisation, troublesome symptoms despite appropriate treatment) for specialist 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). Offer nasal irrigation where tolerated and preferred.

The intranasal corticosteroid technique education is one of the most impactful interventions a GP can make for allergic rhinitis management — many patients with allergic rhinitis use 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.

Reviewing a patient whose sinusitis fails to improve or worsens matters for two reasons: (1) the diagnosis, adherence and need for second-choice treatment (co-amoxiclav after deterioration on first choice, NICE NG79) should be reassessed; 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 rapidly or significantly at any time, including despite antibiotics, the patient should seek same-day review; if periorbital swelling, visual changes, severe headache or neck stiffness develop, or they feel very unwell, the patient should attend A&E immediately (999 if confused or drowsy, a seizure, rapidly worsening vision or unable to travel safely). The complications of bacterial sinusitis are rare 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.