Bronchiectasis

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

Bronchiectasis results from a self-reinforcing interaction between impaired mucus clearance, airway infection, inflammation and structural damage. The CT sign is a bronchus wider than its accompanying artery, visible airways near the pleura, or failure to taper, but age, inspiration and traction from fibrosis can mimic disease. Reported radiological bronchiectasis without symptoms does not automatically require the same programme as recurrent suppurative disease.

The initial assessment should describe distribution and severity while searching for a treatable cause. Localised disease suggests obstruction, foreign body or previous focal infection; diffuse disease raises immune, mucociliary, systemic inflammatory and post-infective causes. History determines which targeted tests supplement the BTS core panel. Calling disease idiopathic before completing this work-up can miss replacement immunoglobulin, ABPA treatment or genetic counselling.

Stable care aims to reduce daily sputum burden and future attacks while protecting function and quality of life. Airway clearance is the platform. Mucoactive treatment, bronchodilation and long-term antimicrobials are trials for selected phenotypes, not universal prescriptions. Acute exacerbation antibiotics and long-term suppression are covered in the dedicated companion chapter.

Key points

Bronchiectasis is a clinical-radiological syndrome: permanent bronchial dilatation on thin-section CT must be interpreted with chronic cough, sputum, infection, haemoptysis or another compatible presentation.
Suspect it with persistent mucopurulent sputum, recurrent lower-respiratory infections or unexplained haemoptysis, especially with rheumatoid disease, inflammatory bowel disease, childhood infection or chronic rhinosinusitis.
A baseline cause panel matters because immune deficiency, allergic bronchopulmonary aspergillosis, cystic fibrosis, primary ciliary dyskinesia and aspiration can change treatment and family advice.
Obtain routine bacterial and mycobacterial sputum cultures while clinically stable; the microbiological history becomes the map for future exacerbation treatment.
Every patient with clinically significant disease should be taught an individual airway-clearance technique by a respiratory physiotherapist and have technique and adherence reviewed.
Do not prescribe inhaled corticosteroids solely for bronchiectasis; use them for a separate indication such as asthma, COPD or active ABPA.
Vaccination, smoking cessation, exercise, nutritional assessment and pulmonary rehabilitation for limiting breathlessness are core management rather than optional extras.
Chronic Pseudomonas, frequent exacerbations, declining lung function, NTM, ABPA, immune deficiency or advanced disease warrants ongoing specialist follow-up.

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

Post-infective damage

Severe childhood or adult pneumonia, tuberculosis and recurrent infection can permanently injure bronchial walls and mucociliary clearance.

Impaired host defence

Antibody deficiency, cystic fibrosis, primary ciliary dyskinesia and immune suppression permit repeated infection and progressive structural airway injury.

Inflammatory or obstructive disease

Allergic bronchopulmonary aspergillosis, autoimmune disease, inflammatory bowel disease and a focal tumour or foreign body can produce characteristic diffuse or local patterns.

Idiopathic disease

No cause is found after a proportionate screen in many adults, but this label follows assessment for treatable or family-relevant mechanisms.

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

1
Clearance failure
Abnormal cilia, thick secretions or damaged airway structure prevents efficient removal of inhaled organisms and mucus.
2
Persistent infection
Retained secretions support bacterial growth, with repeated or chronic infection sustaining neutrophilic airway inflammation, with effects that increase as the pathological process progresses.
3
Bronchial-wall destruction
Proteases and inflammatory mediators damage muscle and elastic tissue, producing irreversibly dilated, thick-walled bronchi, and the downstream physiological effect determines clinical severity.
4
Self-perpetuating cycle
Dilated airways clear mucus even less effectively, leading to further infection, inflammation, haemoptysis and gradual loss of functioning lung.

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

Chronic suppurative phenotype

Daily cough with mucopurulent or purulent sputum, recurrent antibiotic courses, coarse inspiratory crackles and fatigue is typical. Sputum volume varies and some patients present mainly with recurrent infections.

Haemoptysis phenotypeRed flag

Blood-streaking may accompany an exacerbation, but recurrent or substantial bleeding requires assessment for malignancy, tuberculosis, pulmonary embolism and vascular complications rather than automatic attribution to known bronchiectasis.

Underlying-cause clues

Early onset, male infertility, pancreatitis or malabsorption suggests cystic fibrosis; neonatal distress, otitis, sinusitis or situs abnormality suggests ciliary disease; recurrent unusual infection suggests immune deficiency.

Systemic association

Rheumatoid arthritis, Sjogren syndrome, inflammatory bowel disease, HIV, previous transplantation and immunosuppressive treatment can coexist with or contribute to bronchial damage and alter specialist ownership.

Deteriorating disease

Early relapse after antibiotics, more admissions, weight loss, falling spirometry, increasing breathlessness or new resistant, Pseudomonas or mycobacterial isolates should trigger a fresh cause, adherence and complication review.

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
Thin-section chest CTFirst step
Why
Confirm abnormal airway dilatation and map extent, mucus plugging and associated lung disease.
Interpretation and limitations
Look for bronchoarterial disproportion, lack of tapering and peripheral airway visibility. Central bronchiectasis and mucus impaction suggest ABPA; focal change may justify bronchoscopy to exclude obstruction.
02
Stable sputum microbiology
Why
Establish routine bacterial pathogens and screen for non-tuberculous mycobacteria before future suppressive treatment.
Interpretation and limitations
Record repeated isolates rather than using the vague term colonisation. A first or regrown Pseudomonas isolate with clinical deterioration needs specialist eradication discussion.
03
Core aetiology blood panel
Why
Identify immune deficiency and Aspergillus-related disease that changes management.
Interpretation and limitations
BTS recommends FBC, IgG, IgA, IgM, total IgE and Aspergillus fumigatus sensitisation testing for all. Consider pneumococcal antibody responses with immunology advice when specific antibody deficiency is plausible.
04
Phenotype-directed testing
Why
Investigate inherited, inflammatory or aspiration causes when clinical features support them.
Interpretation and limitations
Use NICE cystic-fibrosis testing, a specialist PCD pathway, autoimmune tests linked to symptoms, AAT testing with basal panacinar emphysema and reflux or swallow evaluation only when indicated.
05
Spirometry and oxygen assessment
Why
Set a functional baseline and detect decline or coexisting airflow obstruction.
Interpretation and limitations
Obstruction is common but normal spirometry does not negate CT-confirmed disease. Unexpected fall should prompt infection, adherence, new obstruction, ABPA and comorbidity review.
06
Bronchoscopy in selected cases
Why
Inspect localised disease for tumour, stenosis or foreign body and obtain targeted samples when sputum cannot be produced.
Interpretation and limitations
Bronchoscopy is not routine for every diffuse case. Its yield should justify sedation and procedural risk, and mycobacterial samples must be labelled and handled correctly.

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

Chronic bronchitis

Productive cough with smoking-related obstruction may occur without CT bronchial dilatation, though COPD and bronchiectasis frequently coexist.

Asthma

Variable wheeze and airflow with little daily purulent sputum favours asthma; persistent focal crackles and recurrent bacterial growth suggest bronchiectasis.

Cystic fibrosis

Early-onset disease, malabsorption, infertility, characteristic microbiology or family history warrants formal CF assessment rather than an idiopathic label.

Pulmonary tuberculosis or NTM disease

Constitutional symptoms, cavitation and repeated mycobacterial cultures distinguish active infection from structural bronchiectasis alone, and the distinction changes the subsequent clinical pathway.

Lung cancer or foreign body

Focal bronchiectasis confined to one segment or lobe raises a mechanically obstructing lesion requiring airway imaging or bronchoscopy.

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

01DiagnoseConfirm a clinical-radiological syndromeFirst stepPersistent productive cough, repeated chest infection, unexplained haemoptysis or suggestive imaging.

1Document sputum pattern, prior pneumonia or tuberculosis, childhood and ENT history, aspiration symptoms, inflammatory disease, fertility and family history, then obtain baseline radiography and diagnostic thin-section CT.
2Send stable routine and mycobacterial sputum, perform the BTS core blood panel and add CF, PCD, immune, autoimmune, aspiration or AAT tests only where phenotype and guideline criteria support them.
3Record aetiology, lobar distribution, exacerbation and admission history, lung function, microbiology and comorbidity; use a severity score to support, not replace, clinical judgement.

02StabiliseBuild everyday airway careBronchiectasis is clinically significant and the patient is not in an acute attack.

1Refer to respiratory physiotherapy for an acceptable airway-clearance method, commonly active cycle breathing or an oscillating positive-expiratory-pressure technique, with posture adapted for reflux and haemoptysis risk.
2Optimise hydration, activity, smoking cessation, influenza and pneumococcal vaccination, oral health, nutrition and treatment of asthma, COPD, rhinosinusitis or reflux when those diagnoses are genuinely present.
3Consider a supervised mucoactive trial when sputum remains difficult to expectorate, assessing bronchospasm risk and continuing only if the patient reports a worthwhile objective or functional benefit.

03EscalateReview persistent burden or progressionEscalationSymptoms, attacks, microbiology or lung function worsen despite the agreed baseline plan.

1Check airway-clearance performance, adherence, aspiration, nutrition and whether an original cause has been missed; repeat cultures including mycobacteria and reconsider ABPA or an obstructing lesion.
2Refer limiting breathlessness for pulmonary rehabilitation and optimise bronchodilator treatment only where breathlessness or coexisting obstructive disease supports a monitored trial.
3Move recurrent infective disease to the companion exacerbation and suppression pathway, with specialist review before long-term antibiotics and a clear outcome and toxicity-monitoring plan.

04BleedingRespond to significant haemoptysisBleeding is more than minor streaking, recurs, affects gas exchange or threatens the airway.

1Assess airway, breathing, circulation, anticoagulants and blood loss; establish IV access, crossmatch when appropriate and involve senior respiratory and critical-care clinicians.
2Treat suspected infection using known microbiology while obtaining urgent imaging and multidisciplinary input; position and airway strategy depend on the bleeding side and severity.
3First linePersistent major bleeding generally requires bronchial-artery embolisation first line, with interventional radiology and thoracic surgery coordinating rescue options.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

Hydrates airway secretions before clearance when sputum remains tenacious despite an optimised technique and adequate oral hydration.

Nebulised hypertonic saline as a mucoactive trial

Concentration, volume and frequency should follow the respiratory physiotherapist's local bronchiectasis protocol after an observed airway-reactivity assessment; there is no single universal UK schedule.

Can provoke cough, wheeze or bronchospasm. Demonstrate nebuliser hygiene, consider bronchodilator pre-treatment only when indicated, avoid continuing an ineffective burdensome treatment and never substitute it for taught airway clearance.

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

Recurrent exacerbations

Increased microbial burden and airway inflammation cause episodic worsening of cough, sputum, breathlessness and systemic symptoms.

Chronic respiratory infection

Persistent organisms, including Pseudomonas in some patients, increase sputum burden, treatment complexity and risk of progressive disease.

Haemoptysis

Inflamed hypertrophied bronchial arteries can bleed, ranging from streaking to life-threatening airway-compromising haemorrhage, and increasing the burden of otherwise local respiratory disease.

Respiratory failure

Extensive bilateral disease may cause obstructive or mixed physiological impairment, chronic hypoxaemia, hypercapnia and pulmonary hypertension.

Treatment toxicity and resistance

Repeated or suppressive antimicrobials can cause adverse effects and select resistant organisms, requiring culture-guided stewardship and monitoring.

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

Review at least annually when stable, and more often for severe disease, chronic Pseudomonas, frequent attacks, long-term antibiotics or a declining clinical trajectory.
At planned review record exacerbations, admissions, sputum burden, breathlessness, haemoptysis, weight, oxygen saturation, spirometry and treatment adherence or burden.
Send routine sputum while well at an interval based on severity and whenever microbiology changes management; obtain mycobacterial samples before macrolide suppression.
Ask a physiotherapist to reassess airway-clearance technique after initiation and periodically, particularly after haemoptysis, reflux symptoms, pregnancy or a change in mobility.
Repeat CT only for a clinical question such as unexpected decline, new focal disease or complication; routine serial radiation is not a substitute for functional follow-up.

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

The CT finding needs a patient

Mild airway enlargement can accompany age or traction from fibrosis. A bronchiectasis treatment label should connect morphology to cough, infection, sputum or another relevant syndrome.

Aetiology can change years later

A previously idiopathic case deserves re-evaluation when the patient is young, deteriorates, develops extrapulmonary clues or new genetic and immune information becomes available.

Sputum history is longitudinal

One culture can reflect treatment or sampling; repeated stable and exacerbation results reveal chronic infection, new acquisition and resistance patterns that guide future choices.

Severity scores do not set ceilings

BSI or FACED can organise risk but cannot capture every comorbidity, bleeding risk or patient priority, and must not be used to deny rehabilitation or specialist review.

11Common pitfallsFrequent interpretation and management errors.

01
Diagnosing bronchiectasis from a chest radiograph or symptoms alone without appropriate thin-section CT confirmation.
02
Writing idiopathic after omitting immunoglobulins, Aspergillus sensitisation and stable routine and mycobacterial sputum culture.
03
Prescribing an inhaled corticosteroid simply because CT shows bronchial dilatation, without asthma, COPD or another steroid-responsive indication.
04
Giving a clearance device without physiotherapist teaching, observed technique, cleaning advice or subsequent review.
05
Attributing major haemoptysis to known bronchiectasis and delaying airway protection, urgent imaging and embolisation assessment.