Cough and sputum production

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

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.

BTS chronic-cough practice is based on finding and treating traits, then reassessing. A normal chest radiograph does not end investigation when red flags or persistent unexplained symptoms remain. Conversely, repeated CT, antibiotics or corticosteroids without an identified target can cause harm. When common traits have been addressed and imaging is reassuring, chronic refractory cough can reflect heightened cough-reflex sensitivity and merits specialist, non-judgemental management.

Key points

Define duration and pattern: acute cough is commonly viral, while chronic cough lasting more than eight weeks needs structured assessment of triggers, imaging, spirometry and treatable traits.
Ask whether the cough is dry, productive, nocturnal, meal-related, positional or triggered by cold air, voice, fragrance, exercise or occupational exposure; each pattern changes the differential.
Record sputum volume, colour, odour, blood and daily variability. Purulence reflects neutrophilic inflammation but does not by itself prove a bacterial infection needing antibiotics.
Red flags include haemoptysis, weight loss, persistent fever, hoarseness, dysphagia, focal chest signs, recurrent same-site infection, clubbing and smoking-related cancer risk.
For chronic cough obtain a chest radiograph, quality-assured spirometry and blood count; BTS also supports fractional exhaled nitric oxide where available to identify an eosinophilic airway trait.
Review medicines, especially ACE inhibitors, and stop the culprit where clinically safe; improvement may take several weeks, so replacing it for only a few days is not an adequate trial.
Treat reflux with acid suppression only when typical acid reflux symptoms or objective evidence supports it; proton-pump inhibitors do not routinely treat isolated throat symptoms or cough.
Persistent productive cough, recurrent infections or large sputum volume should prompt culture and consideration of bronchiectasis, aspiration, chronic infection or an obstructing lesion.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Airway inflammation

Viral infection, asthma, eosinophilic bronchitis, smoke and rhinitis sensitise cough receptors and may increase mucus production.

Suppurative or structural disease

Bronchiectasis, cystic fibrosis, chronic infection and an obstructing lesion impair clearance and produce persistent purulent or copious sputum.

Reflux and aspiration

Oesophageal reflux, swallowing dysfunction and laryngeal hypersensitivity can trigger cough with or without classic heartburn, but empirical attribution is unreliable.

Medicines and systemic disease

Angiotensin-converting-enzyme inhibitors commonly cause dry cough, while heart failure, interstitial lung disease and cancer provide important non-airway mechanisms.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Receptor activation
Mechanical, chemical or inflammatory stimuli activate vagal sensory endings in larynx, tracheobronchial tree and related structures.
2
Brainstem cough programme
Afferent signals trigger coordinated inspiration, glottic closure and forceful expiratory muscle contraction, while cortical pathways permit partial voluntary control.
3
Mucus mobilisation
High expiratory flow shears secretions from airway walls, supplementing mucociliary transport when mucus burden rises, which helps produce the characteristic physiological impairment.
4
Cough hypersensitivity
Repeated inflammation can lower sensory thresholds so cold air, speech, perfumes or minor reflux provoke disproportionate chronic cough.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Acute self-limiting 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.

Eosinophilic airway 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.

Suppurative airway disease

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.

Malignancy or focal obstructionRed flag

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.

Aspiration and swallowing dysfunction

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.

Cough hypersensitivity

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.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Chest radiographFirst step
Why
Detect pneumonia, mass, collapse, interstitial change, heart failure or another structural cause.
Interpretation and limitations
Review projection, quality and previous films. Normal radiography is reassuring only in the appropriate context; persistent red flags, haemoptysis or focal symptoms may require CT or urgent referral despite a normal image.
02
Spirometry with bronchodilator testing
Why
Identify airflow obstruction and objective variability supporting airway disease.
Interpretation and limitations
Confirm acceptable manoeuvres before using the result. Reversible obstruction supports asthma, fixed obstruction may support COPD, and normal spirometry does not exclude cough-variant asthma or eosinophilic bronchitis.
03
Fractional exhaled nitric oxide and blood eosinophils
Why
Identify a treatable eosinophilic airway trait when locally available.
Interpretation and limitations
Raised values support corticosteroid-responsive inflammation but are influenced by smoking, atopy, current inhaled corticosteroid and infection. A low value reduces but does not abolish the probability of asthma.
04
Sputum microscopy, culture and sensitivity
Why
Identify pathogens in chronic productive cough, recurrent infection or treatment failure.
Interpretation and limitations
Obtain a good-quality lower-respiratory sample before antibiotics when feasible. Interpret colonisation versus infection using symptoms and prior microbiology; request mycobacterial testing when epidemiology or imaging supports it.
05
Full blood count and targeted blood tests
Why
Detect eosinophilia, anaemia or systemic inflammation and direct further testing.
Interpretation and limitations
Eosinophilia supports but does not prove eosinophilic airway disease. Use renal, liver, immunoglobulin or infection tests only when medicines, bronchiectasis, systemic features or exposure justify them.
06
High-resolution or contrast-enhanced chest CT
Why
Define bronchiectasis, interstitial disease, focal obstruction or malignancy when clinically indicated.
Interpretation and limitations
Do not use CT routinely for every normal-radiograph chronic cough. Choose protocol according to the question, review incidental findings and pursue bronchoscopy when a central lesion, foreign body or unexplained bleeding remains possible.
07
Swallow assessment or laryngoscopy
Why
Evaluate aspiration, laryngeal disorder or persistent upper-airway symptoms.
Interpretation and limitations
Speech-and-language assessment, videofluoroscopy or endoscopic swallow study should follow the suspected mechanism. Laryngoscopy may identify structural or functional laryngeal disease but non-specific erythema does not prove reflux.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Asthma or eosinophilic bronchitis

Variable wheeze, airflow change or eosinophilic markers support asthma; eosinophilic bronchitis causes cough without the same variable obstruction.

Upper-airway cough syndrome

Nasal obstruction, discharge and throat clearing with rhinitis or sinus disease suggest an upper-airway contribution, though findings are not individually diagnostic.

Bronchiectasis

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.

Lung cancer or tuberculosis

Haemoptysis, weight loss, persistent fever, epidemiological risk or focal imaging change requires urgent investigation rather than serial empirical treatments.

Medicine-induced cough

A compatible onset after an ACE inhibitor and resolution after supervised withdrawal supports the diagnosis, while other red flags still require assessment.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01AcuteAcute cough without instabilityFirst stepCough of recent onset with stable physiology and no cancer, sepsis or airway red flags.

1Assess observations, chest signs, comorbidity and duration; identify pneumonia, asthma exacerbation, COVID-19 or influenza risk, pulmonary embolism and heart failure rather than assuming uncomplicated bronchitis.
2Give self-care advice and symptom relief appropriate to the person; NICE advises against routine antibiotics for uncomplicated acute cough because benefit is small and adverse effects and resistance are real.
3Use delayed or immediate antibiotics only when the relevant infection guideline and clinical risk support them, documenting allergy, indication, duration and what failure should trigger.
4Safety-net for breathlessness, haemoptysis, confusion, dehydration, persistent fever, chest pain or cough beyond the expected course; arrange reassessment when risk or diagnostic uncertainty remains.

02Chronic first lineFind common treatable traitsFirst lineCough persisting beyond eight weeks without an established explanation.

1Review smoking, ACE inhibitors, occupation, rhinitis, heartburn, asthma features, sputum, aspiration and warning symptoms; examine the chest, upper airway, nodes and for clubbing.
2Obtain chest radiograph, full blood count and quality-assured spirometry; add FeNO, eosinophils and sputum culture according to the dry or productive phenotype.
3Remove supported triggers and use time-limited, outcome-defined treatment trials for eosinophilic airway disease, rhinitis or symptomatic acid reflux rather than treating every pathway simultaneously.
4EscalationReview after the appropriate interval. Confirm adherence and technique, stop ineffective treatment, and escalate persistent productive cough, red flags or abnormal imaging to respiratory assessment.

03ProductivePersistent sputum and recurrent infectionDaily sputum, recurrent lower-respiratory infection, haemoptysis or coarse crackles.

1Send sputum for routine culture and consider mycobacteria according to risk; obtain chest radiograph and assess exacerbation frequency, aspiration, immune history and smoking.
2Request thin-section CT when bronchiectasis or another structural abnormality is suspected, then investigate underlying causes through the specialist bronchiectasis pathway.
3Use airway-clearance physiotherapy and culture-directed exacerbation treatment when bronchiectasis is established; avoid repeated empirical antibiotics without samples and a prevention plan.
4Investigate focal or same-lobe recurrence for obstruction, malignancy or foreign body rather than accepting recurrent 'chest infections' as a final diagnosis.

04RefractoryChronic refractory coughPersistent cough after investigation and adequate treatment of identified traits.

1Recheck imaging, medicine exposure, adherence and whether objective evidence supported previous treatment; avoid indefinite corticosteroid, antibiotic or proton-pump inhibitor use without benefit.
2Refer for specialist cough assessment, considering cough-control therapy delivered by trained speech-and-language or physiotherapy professionals and selected neuromodulatory treatment.
3Measure meaningful outcomes such as frequency, sleep, urinary incontinence, work and quality of life, and agree a review plan for new haemoptysis, weight loss or physiological change.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Tests and treats a common medicine-induced dry cough without adding suppressive therapy.

ACE-inhibitor withdrawal when clinically appropriate

Stop the ACE inhibitor and substitute an appropriate alternative through the prescribing clinician; allow at least four weeks before judging cough response.

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.

Treats an acid-reflux trait that may contribute to cough in selected patients.

Proton-pump inhibitor for documented acid reflux symptoms

Use an adequate guideline-concordant treatment course only when heartburn or other convincing acid-reflux evidence is present, then review and deprescribe if ineffective.

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.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Sleep and activity disruption

Frequent cough fragments sleep, interrupts speech and work, and can cause severe fatigue and social isolation.

Syncope

Forceful coughing raises intrathoracic pressure and transiently reduces cerebral perfusion, causing presyncope, loss of consciousness and injury risk.

Musculoskeletal injury

Repeated high-pressure contraction can cause chest-wall pain, rib fracture or abdominal and pelvic-floor symptoms, particularly when baseline cardiopulmonary reserve is limited.

Aspiration and secretion retention

An ineffective cough from weakness or bulbar disease permits retained secretions, atelectasis and recurrent lower-respiratory infection.

Delayed serious diagnosis

Repeatedly treating cough as infection or reflux can postpone recognition of malignancy, tuberculosis, interstitial disease or heart failure.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Record cough duration, frequency, night disturbance, sputum volume, haemoptysis and functional effect before treatment so response can be judged rather than assumed.
For inhaled treatment check technique, adherence, symptoms, reliever use and objective airway measures; stop or revise a trial that does not meet its predefined endpoint.
For productive cough track exacerbations, antibiotic exposure and organism history, including resistance and repeated Pseudomonas isolation where relevant.
Ensure every abnormal chest radiograph or CT recommendation has a named clinician, expected timeframe and closed-loop result communication.
Reassess promptly if haemoptysis, weight loss, fever, hoarseness, dysphagia or focal signs develop even after an initially reassuring work-up.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Sputum colour is not a prescription

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.

ACE-inhibitor timing is variable

Cough may begin long after treatment starts and may take weeks to resolve after withdrawal. A short interruption neither confirms nor excludes causality.

Reflux is often over-attributed

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.

Productive and dry cough diverge

Persistent sputum prioritises culture, airway clearance and structural imaging; dry trigger-sensitive cough prioritises eosinophilic traits, medicines, upper-airway assessment and cough hypersensitivity.

A normal radiograph has limits

Central endobronchial disease, early interstitial change and bronchiectasis can be occult. Continuing red flags or focal recurrence justifies more definitive imaging or bronchoscopy.

11Common pitfallsFrequent interpretation and management errors.

01
Prescribing antibiotics solely because sputum is coloured.
02
Calling chronic cough asthma without objective testing or a defined treatment response.
03
Continuing acid suppression indefinitely when there was no heartburn and the cough did not improve.
04
Ignoring ACE-inhibitor exposure because the medicine predates cough onset by months.
05
Using a normal chest radiograph to dismiss haemoptysis, weight loss or recurrent focal infection.
06
Treating refractory cough as psychological rather than recognising cough-reflex hypersensitivity and its physical complications.