Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Classify cough by duration and phenotype, recognise infection, malignancy and suppurative lung disease, and investigate treatable traits without reflex antibiotics, acid suppression or repeated empirical inhalers.
Cough is a protective reflex and a symptom shared by airway, parenchymal, upper-airway, gastrointestinal, cardiac, medication-related and neurological disorders. Duration narrows but does not diagnose: an acute cough is often viral, yet pulmonary embolism, pneumonia, oedema, foreign body and asthma can begin abruptly; chronic cough may reflect eosinophilic airway disease, upper-airway symptoms, reflux with heartburn, ACE-inhibitor exposure, smoking, bronchiectasis, interstitial disease or cough hypersensitivity. Several traits may coexist.
The consultation should characterise the sound and triggers without overvaluing them. Determine whether sputum is truly produced from the lower airway rather than postnasal secretions or saliva; quantify approximate daily volume and ask about recurrent antibiotic courses and previous cultures. Establish smoking, vaping and occupation; aspiration and swallowing risk; rhinitis and heartburn; asthma variability; infection and tuberculosis exposure; and cancer warning features. Examination should include voice, upper airway, chest, clubbing, lymph nodes, heart failure and neuromuscular signs.
Viral infection, asthma, eosinophilic bronchitis, smoke and rhinitis sensitise cough receptors and may increase mucus production.
Bronchiectasis, cystic fibrosis, chronic infection and an obstructing lesion impair clearance and produce persistent purulent or copious sputum.
Oesophageal reflux, swallowing dysfunction and laryngeal hypersensitivity can trigger cough with or without classic heartburn, but empirical attribution is unreliable.
Angiotensin-converting-enzyme inhibitors commonly cause dry cough, while heart failure, interstitial lung disease and cancer provide important non-airway mechanisms.
Mechanical, chemical or inflammatory stimuli activate vagal sensory endings in larynx, tracheobronchial tree and related structures.
Afferent signals trigger coordinated inspiration, glottic closure and forceful expiratory muscle contraction, while cortical pathways permit partial voluntary control.
High expiratory flow shears secretions from airway walls, supplementing mucociliary transport when mucus burden rises, which helps produce the characteristic physiological impairment.
Repeated inflammation can lower sensory thresholds so cold air, speech, perfumes or minor reflux provoke disproportionate chronic cough.
Coryza, sore throat and cough without focal chest signs, hypoxaemia or systemic instability usually reflects viral upper-respiratory infection or acute bronchitis. Cough often persists beyond other symptoms, and sputum colour alone does not identify bacterial disease.
Variable cough, wheeze, nocturnal symptoms, atopy, triggers, airflow variability or raised eosinophilic markers suggests asthma or eosinophilic bronchitis. Normal baseline spirometry does not exclude asthma, but treatment should be linked to objective evidence and response.
Daily mucopurulent sputum, recurrent lower-respiratory infections, coarse crackles, haemoptysis or clubbing suggests bronchiectasis or chronic infection. Large-volume or positional sputum and repeated isolation of the same organism strengthen the phenotype.
Haemoptysis, weight loss, persistent hoarseness, focal wheeze, lymphadenopathy, clubbing or recurrent pneumonia in one lobe warrants urgent imaging and cancer-pathway assessment, particularly in people aged forty or over with smoking or asbestos exposure.
Cough during meals, wet voice, recurrent dependent-lobe infection, neurological disease, sedative use or regurgitation suggests aspiration. Silent aspiration may present through recurrent infection or weight loss without dramatic choking.
A dry, intrusive cough triggered by talking, perfumes, temperature change or a throat tickle despite treatment of identified traits supports cough-reflex hypersensitivity. This is a positive clinical phenotype, not evidence that symptoms are imagined.
Variable wheeze, airflow change or eosinophilic markers support asthma; eosinophilic bronchitis causes cough without the same variable obstruction.
Nasal obstruction, discharge and throat clearing with rhinitis or sinus disease suggest an upper-airway contribution, though findings are not individually diagnostic.
Daily purulent sputum, recurrent infection, crackles and bronchial dilatation on CT distinguish structural suppurative disease, with targeted examination and testing used to resolve the uncertainty.
Haemoptysis, weight loss, persistent fever, epidemiological risk or focal imaging change requires urgent investigation rather than serial empirical treatments.
A compatible onset after an ACE inhibitor and resolution after supervised withdrawal supports the diagnosis, while other red flags still require assessment.
Frequent cough fragments sleep, interrupts speech and work, and can cause severe fatigue and social isolation.
Forceful coughing raises intrathoracic pressure and transiently reduces cerebral perfusion, causing presyncope, loss of consciousness and injury risk.
Repeated high-pressure contraction can cause chest-wall pain, rib fracture or abdominal and pelvic-floor symptoms, particularly when baseline cardiopulmonary reserve is limited.
An ineffective cough from weakness or bulbar disease permits retained secretions, atelectasis and recurrent lower-respiratory infection.
Repeatedly treating cough as infection or reflux can postpone recognition of malignancy, tuberculosis, interstitial disease or heart failure.
Green or yellow sputum reflects neutrophil enzymes and can occur in viral or chronic inflammatory disease. Use physiological illness, diagnosis and microbiology rather than colour alone to decide antibiotics.
Cough may begin long after treatment starts and may take weeks to resolve after withdrawal. A short interruption neither confirms nor excludes causality.
Non-specific laryngeal redness and throat clearing do not establish acid reflux as the cough driver. BTS advises acid suppression only when typical symptoms or convincing evidence makes benefit plausible.
Persistent sputum prioritises culture, airway clearance and structural imaging; dry trigger-sensitive cough prioritises eosinophilic traits, medicines, upper-airway assessment and cough hypersensitivity.
Central endobronchial disease, early interstitial change and bronchiectasis can be occult. Continuing red flags or focal recurrence justifies more definitive imaging or bronchoscopy.
Prescribing antibiotics solely because sputum is coloured.
Calling chronic cough asthma without objective testing or a defined treatment response.
Continuing acid suppression indefinitely when there was no heartburn and the cough did not improve.
Ignoring ACE-inhibitor exposure because the medicine predates cough onset by months.
Using a normal chest radiograph to dismiss haemoptysis, weight loss or recurrent focal infection.
Treating refractory cough as psychological rather than recognising cough-reflex hypersensitivity and its physical complications.
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A 52-year-old has a dry cough for twelve weeks. They are stable, take no ACE inhibitor and have no haemoptysis or weight loss. Which set best represents the core first-line assessment recommended in UK chronic-cough practice?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Do not stop heart-failure or renal-protective treatment without an alternative plan. Cough may take longer than four weeks to settle, and persistence should restart structured investigation.
Do not prescribe routinely for isolated throat symptoms or unexplained cough. Long-term therapy has adverse-effect and interaction burdens; response does not exclude coexisting causes.