Bronchiectasis is an irreversible and abnormal dilation in the bronchial tree caused by cycles of bronchial inflammation leading to mucous plugging and progressive airway destruction. Bronchiectasis is classified according to etiology as either cystic fibrosis (CF) bronchiectasis or non-CF bronchiectasis (e.g., secondary to severe or protracted pneumonia, immunodeficiency, or COPD). The characteristic clinical feature is a chronic cough with copious mucopurulent sputum. Other symptoms may include dyspnea, rhinosinusitis, and hemoptysis. Physical examination reveals crackles and rhonchi on auscultation, often accompanied by wheezing. High-resolution computed tomography confirms the diagnosis and usually shows thickened bronchial walls, with so-called “signet-ring” and “tram track” signs. Patients can periodically experience an acute worsening of symptoms, referred to as an acute exacerbation of bronchiectasis, which commonly requires antibiotic treatment. The goal of long-term management of bronchiectasis is to control symptoms and prevent exacerbations, and includes pulmonary physiotherapy and pharmacological therapy. Massive hemoptysis is a rare complication of bronchiectasis and requires surgery or pulmonary artery embolization.
- Bronchiectasis: an irreversible and abnormal dilation of the bronchial tree that produces chronic respiratory symptoms (e.g., chronic productive cough)
- Acute exacerbation of bronchiectasis: a deterioration in the symptoms of bronchiectasis that requires a change in the regular treatment (e.g., adding antibiotics, increasing airway clearance techniques) 
Bronchiectasis requires the combination of two important processes taking place in the bronchi: either local infection or inflammation along with either inadequate clearance of secretions, airway obstruction, or impaired host defenses. These processes result in the permanent dilation of airways.
- Pulmonary infections (i.e., bacterial, viral, fungal), especially severe or chronic infections
- Disorders of secretion clearance or mucous plugging
- Bronchial narrowing or other forms of obstruction
- Immunodeficiency (e.g., , hypogammaglobulinemia, )
- Chronic inflammatory diseases (e.g., , , )
- Chronic productive cough (lasting months to years) with copious mucopurulent sputum ;
- Hemoptysis: usually mild or self-limiting, but severe hemorrhage that requires embolization may occur
- Nonspecific symptoms (i.e., fatigue, weight loss, pallor due to anemia)
- Clubbing of nails (uncommon)
- Exacerbations of bronchiectasis
- Confirm the diagnosis with imaging studies in patients with features suggestive of bronchiectasis.
- Identify the underlying etiology.
In patients with suspected bronchiectasis, diagnosis is confirmed using imaging studies, preferably a HRCT scan. Additional diagnostic studies are useful to identify the underlying cause and possibly provide specific treatment.
- Imaging modalities
Bronchial dilation ; 
- Cylindrical or tubular (most common) : parallel tram track sign and signet ring sign
- Saccular or cystic (most severe form)
- Thickened bronchial walls; , mucus plugging, honeycombing (suggests late-stage bronchiectasis)
- Specific findings suggestive of the underlying etiology
- Focal distribution : localized disease (e.g., tumors, foreign bodies, strictures)
- Diffuse distribution: fibrosing diffuse lung diseases
- Perihilar lymphadenopathies (e.g., sarcoidosis, tuberculosis)
- Situs inversus (seen in primary ciliary dyskinesia)
- Bronchial dilation ; 
Identification of the underlying etiology
Studies to determine the underlying etiology of bronchiectasis are usually requested by a specialist. In many cases, it is not possible to reach a specific diagnosis and the disease may be classified as idiopathic. 
Initial workup 
Laboratory studies 
- CBC: Findings are variable and depend on the underlying etiology.
- Consider ABG (e.g., in patients with ↓ SaO2 on room air): may show hypercapnia
- Quantitative measurement of serum immunoglobulins and electrophoresis (IgA, IgG, IgM, and IgG subclasses): to exclude immunodeficiencies 
- Aspergillus fumigatus IgG and IgE: to exclude ABPA
- Sputum culture and smear: culture induced sputum or bronchoalveolar lavage for all of the following pathogens to detect infection or colonization 
- Spirometry: not needed to establish a diagnosis but useful to monitor disease progression 
Additional diagnostics 
These studies may be considered depending on clinical suspicion if the initial workup was not diagnostic.
- Specific antibodies (e.g., rheumatoid factor, ANAs, anti-CCP antibodies, ANCAs): suspected connective tissue or autoimmune diseases
- Sweat chloride test and/or genetic testing for CFTR mutations: suspected CF
- HIV testing , serum α1-antitrypsin levels , nasal nitric oxide testing for primary ciliary dyskinesia
- Upper GI studies (e.g., upper endoscopy, barium swallow, esophageal manometry): consider for suspected gastroesophageal reflux disease or recurrent pulmonary aspiration
- Colonoscopy with biopsies: if associated inflammatory bowel disease is suspected (e.g., GI bleeding)
If the initial workup does not identify the underlying cause, perform further studies guided by the patient's clinical features and consider referral to a specialist.
This section focuses on the management of non-CF bronchiectasis. See “” for specific recommendations regarding that condition.
Management of acute exacerbations
- Provide supportive treatment and oxygen therapy as needed.
- Optimize mucoactive agents (see “Pharmacotherapy for airway clearance in bronchiectasis”).
- Optimize .
- Obtain a new sputum culture and start empiric antibiotic therapy, based on the most recent sputum culture.
- Tailor antibiotics to the most recent sputum culture once available and preferably complete 14 days of therapy.
Monitoring and disposition 
- Outpatient treatment: for hemodynamically stable patients with mild to moderate symptoms
- Consider inpatient treatment in the following cases:
|Common empiric antibiotic regimens for bronchiectasis exacerbations |
|Outpatient treatment || |
|Inpatient treatment |
Acute exacerbations are defined as acute deterioration or worsening local symptoms and/or additional systemic symptoms such as fever or malaise. Exacerbations are associated with increased inflammation and progressive damage to the lungs. 
Management goals are to stop or delay disease progression, reduce exacerbation frequency (goal ≤ 2 per year), achieve symptom control, and improve the patient's quality of life.
- Educate the patient regarding prognosis and the use of long-term medications.
- Promote lifestyle changes like regular exercise and smoking cessation.
- Educate the patient on airway clearance techniques. 
- Administer vaccinations (i.e., seasonal influenza vaccine, pneumococcal vaccine).
- Consider treatment with mucoactive agents, bronchodilators, or corticosteroids if airway clearance is difficult.
- Provide specific treatment for the underlying cause if identified.
- Follow-up: Perform follow-ups every 6–12 months to identify disease progression.
- Disease progression
- Advanced disease
Perform a careful reassessment of patients who are progressively deteriorating (i.e., patients with increased frequency and/or severity of exacerbations, frequent hospital admissions, worsening symptoms, rapid decline in lung function). Identify the cause of bronchiectasis if still unknown, and exclude any comorbidities or exacerbating conditions such as new pathogen colonization.
Pharmacotherapy for airway clearance in bronchiectasis
Consider in patients with difficulty expectorating or persistent symptoms despite adequate airway clearance techniques; continue use based on clinical benefits. There is a paucity of evidence for the benefit of mucoactive agents in bronchiectasis. 
- Nebulized mucoactive agents: Trial for at least 3 months. 
- Oral mucolytics: Trial for at least 6 months, e.g., N-acetylcysteine .
Consider on a case-by-case basis. Evidence to support the use of bronchodilators in bronchiectasis is limited. 
- Short-term bronchodilators (e.g., SABA): in patients with airway reactivity and bronchospasm or prior to inhaled mucoactive treatment 
- Long-term bronchodilators (e.g., LABA, LAMA): may be used in patients with severe dyspnea
- Regular use of bronchodilators (e.g., for asthma or COPD): Continue as usual.
Corticosteroids are not routinely recommended because of the limited benefit and 
- Inhaled corticosteroids: Continue if already indicated for asthma or COPD.
- Systemic corticosteroids: indicated in patients with 
For patients receiving multiple inhaled treatments and chest physiotherapy, consider the following order of treatment to avoid bronchospasm: bronchodilators, mucoactive agents, respiratory physiotherapy, inhaled antibiotics. 
Long-term antibiotic therapy 
The goal is to suppress bacterial growth and to reduce symptoms and exacerbations as a measure of secondary prevention in patients with ≥ 3 exacerbations per year. Antibiotic therapy should be administered for at least 3 months and may be extended based on clinical response and tolerability.
|Long-term antibiotic therapy for bronchiectasis|
|No colonization with P. aeruginosa|
|Colonization with P. aeruginosa || |
|Isolation of other pathogens|
Chronic macrolide use can increase the growth of macrolide-resistant mycobacterial strains. It is recommended to rule out active nontuberculous mycobacterial infection with a negative culture before starting treatment.
Long-term macrolides can lead to QT-prolongation and fatal arrhythmias. Before starting treatment, perform an ECG and review whether any medications the patient is taking are known to alter the QT interval. 
Invasive procedures 
- Surgical resection of bronchiectatic lung or lobectomy: indicated in pulmonary hemorrhage, inviable bronchus, and poor control of symptoms despite optimal medical therapy in unilateral bronchiectasis with well-localized disease
- Pulmonary artery embolization: indicated in pulmonary hemorrhage
- Lung transplantation: Consider for severe disease or rapid disease progression.