1. Large Airways Obstruction

1.1 Epidemiology

• General Context
  • Airways diseases refer to conditions causing obstruction of the bronchial tree or small airways, including asthma and COPD.
  • More than 5 million people in the UK have asthma, and 900,000 have a formal diagnosis of COPD; COPD is predicted to be the third leading cause of death by 2030.
• Large Airways Disease
  • In contrast to the more prevalent small or medium airways pathologies (asthma, COPD), diseases of the trachea and main bronchi are rare but can be life-threatening.
  • Around 20% of patients with lung cancer develop complications associated with large airways obstruction; other causes of large airway disease are uncommon.

1.2 Aetiology

• Obstructive Lung Pathology: Basic Principles
  • Obstructive lung diseases are characterised by an inability to fully empty the lungs, leading to trapped air.
  • Affected patients have a reduced forced vital capacity (FVC) and an especially reduced forced expiratory volume in the first second (FEV₁), resulting in a low FEV₁:FVC ratio.
  • Total lung capacity (TLC) is often increased due to air trapping.
• Large Airways Obstruction
  • Caused by lesions in the main bronchi, trachea, larynx, or pharynx that narrow or occlude the lumen.
  • The speed of onset varies (Table below) and influences clinical presentation.

1.3 Risk Factors

• Malignancy: Leading cause of subacute large airways obstruction (e.g., lung cancer, lymphoma).
• Infectious Disease: Bacterial (e.g. diphtheria, abscess), mycobacterial (TB).
• Trauma or Iatrogenic Injury: Prolonged intubation, radiotherapy, surgical changes.
• Vasculitis: Granulomatosis with polyangiitis (formerly Wegener’s).
• Endocrine Causes: Goitre (particularly retrosternal) leading to extrinsic compression.

1.4 Symptoms

• Varied Presentation: Depends on both cause and speed of onset.
• Acute Presentation (e.g., sudden stridor) can be life-threatening.
• Chronic Obstruction: Gradually increasing breathlessness and cough, with the possibility of distal bronchiectasis.
  • Often misdiagnosed initially as asthma or COPD.
• Stridor:
  • A harsh, vibrating noise that can vary with posture.
  • Mild obstruction may be silent, but resting breathlessness signals severe disease.
• Additional Malignant Features: Haemoptysis, hoarseness, chest pain, dysphagia (if the oesophagus is compressed).

1.5 Diagnosis

• History and Examination:
  • Stridor is highly specific and warrants urgent investigation.
• Imaging:
  • X-ray (Chest and Neck): May show tracheal deviation, large mass, consolidation, bronchiectasis, or lobar collapse distal to the obstruction.
  • CT Scan (Neck/Chest): Identifies the site, cause, and severity of obstruction.
• Pulmonary Function Tests:
  • Spirometry: Demonstrates obstructive physiology (reduced FEV₁:FVC ratio).
  • Peak Expiratory Flow Rate (PEFR): Usually reduced.
  • Flow Volume Loop: Characteristic shapes help determine if the obstruction is dynamic vs. fixed, and extrathoracic vs. intrathoracic.
  • Empey Index (FEV₁ in mL : PEFR in L/min): A ratio >10 suggests large airways obstruction.
• Bronchoscopy:
  • Most sensitive technique for visualising and confirming the cause, location, and degree of airway compromise.
  • Permits biopsy, though caution is needed in severe obstruction where bleeding or swelling can acutely worsen the obstruction.

1.6 Immediate Management

• Severe or Acute Obstruction:
  • High-flow oxygen or heliox (oxygen–helium mix) to reduce airflow resistance.
  • High-dose corticosteroids to decrease airway oedema.
  • Nebulised bronchodilators and adrenaline (epinephrine) if indicated.
  • Surgery: Possible for rapidly deteriorating airway patency.
• Additional Therapies (Subacute/Chronic Cases):
  • Endobronchial Intervention: Stenting, balloon dilatation, laser ablation.
  • Tracheostomy: Last resort when other measures fail.

1.7 Long-Term Management

• Malignant obstructions carry a poorer prognosis.
• Definitive Therapy:
  • Focus on treating the underlying cause (infection, malignancy, extrinsic compression).
  • Surgical or endobronchial correction if feasible.
• Follow-Up:
  • Monitor symptoms, repeat spirometry, and imaging to detect recurrence or progression.
• Prognosis:
  • Acute stridor is life-threatening and demands immediate treatment.
  • Infective causes have more favourable outcomes.

2. Asthma

2.1 Epidemiology

• Prevalence
  • Asthma is the most common chronic respiratory disease, affecting an estimated 300 million people worldwide.
  • In the UK, 5.4 million individuals have asthma.
  • More frequent in high-income countries but incidence is rising globally, including in low- to middle-income regions.
• Demographics
  • Common in childhood, but can occur at any age.
  • There is a second incidence peak in people older than 60 years.
  • Women are slightly more affected than men in adulthood.
  • Higher prevalence is linked to obesity.

2.2 Aetiology

• Hyper-reactivity and Chronic Inflammation
  • Asthma involves variable airflow obstruction, initially fully reversible, driven by airway hyper-responsiveness and chronic inflammatory processes.
  • If uncontrolled, it can lead to irreversible airway changes over time.
• Mechanism
  • Classically thought to be due to a type I hypersensitivity reaction – however, we now know that type IV, V & VI hypersensitivity reactions can also play a role (see latest EAACI position paper on hypersensitivity reactions published 2023 in references below)
  • Main pathophysiological mechanism in summary – type I & type IV reactions:
    • Sensitised individuals have allergen exposure → activation of Th2 cells → secretion of IL-4, IL-5, IL-10.
    • IL-4 mediates class switching to IgE, IL-5 attracts eosinophils, and IL-10 further encourages Th2 activity
    • Re-exposure triggers IgE-mediated mast cell activation and subsequent release of histamine and leukotrienes (C4, D4, E4) causing bronchoconstriction, oedema, and inflammation.

2.3 Risk Factors

• Genetic Predisposition: Family history of asthma or other atopic conditions (i.e. the atopic march – think eczema, hay fever or food allergy).
• Early-Life Influences:
  • Bronchiolitis in childhood, low birth weight, prematurity.
  • Maternal vitamin D deficiency during pregnancy.
• Environmental and Lifestyle:
  • Exposure to tobacco smoke (especially in childhood).
  • Occupational triggers (paint sprayers, bakers, cleaners, chemical workers, solderers).
  • Allergens (dust mites, pollen, animal dander, moulds).
  • Airborne irritants (pollution, smoke, fumes, cold air).
  • Physical activity and certain foods (e.g. sulphites).

2.4 Symptoms

• Common Presentations
  • Episodic breathlessness and wheeze.
  • Dry cough (often worse early morning or night, and can be triggered by exercise or environmental factors).
• Exacerbations
  • Worsened after viral URTIs, exposure to fumes, or weather changes.
  • Nocturnal episodes causing waking.
• Between Episodes
  • Patients may be asymptomatic if well-controlled.
• Associated Atopy
  • Eczema, hay fever, nasal polyps frequently coexist.
• Severe Attacks
  • Tachycardia, tachypnoea, pulsus paradoxus, hyperexpanded chest, bilateral poor expansion, and a widespread expiratory wheeze.
  • Marked breathlessness at rest indicates a potentially severe exacerbation.

2.5 Diagnosis

• Clinical Assessment:
  • Suspect asthma in individuals with episodic dyspnoea, wheeze, cough, or significant variability of symptoms.
  • A response to bronchodilators or steroids that improves symptoms or lung function is suggestive.
• Spirometry
  • Demonstrates obstructive pattern (↓FEV₁, ↓FEV₁:FVC ratio).
  • ≥15% increase in FEV₁ post-bronchodilator indicates reversibility.
• Peak Expiratory Flow Rate (PEFR)
  • Diurnal variation (often lower in the morning).
  • Improvement with inhaled or oral corticosteroids.
• Chest X-Ray
  • Commonly normal, but can show hyperinflation in severe or poorly controlled disease.
• Allergy and Blood Tests
  • Skin prick tests identify specific allergens (dust mites, pets, mould).
  • Mild eosinophilia or raised IgE levels may be noted.
• Bronchial Challenge
  • Histamine or methacholine challenge used rarely when diagnosis is uncertain.

2.6 Immediate Management

• Non-Pharmacological Measures
  • Address triggers: Weight loss if overweight, smoking cessation, allergen avoidance.
  • Breathing exercises (e.g. Buteyko) for dysfunctional breathing patterns.
• Reliever Inhalers
  • First-line: Long-acting beta agonists (LABA e.g. formoterol) PLUS inhaled corticosteroids (ICS e.g. beclometasone) – example Fostair inhaler, used PRN (as needed) for acute symptom relief
  • Second-line: Short-acting beta agonists (e.g. salbutamol) used PRN (as needed) for acute symptom relief.
• Acute Exacerbations
  • High-dose inhaled bronchodilators (e.g. nebulised salbutamol) – typically given in hospital setting.
  • Systemic corticosteroids (oral prednisolone or IV hydrocortisone).
  • Oxygen supplementation if hypoxic.
  • Monitor for severe features.

2.7 Long-Term Management

• Stepwise Therapy – i.e. start at bottom with as needed therapy, and work your way up until the patient has adequate asthma control:
  1. Low-dose LABA + ICS inhaler PRN
  2. If still uncontrolled then –> Low-dose LABA + ICS inhaler maintenance AND PRN (i.e. MART)
  3. If still uncontrolled then –> Medium-dose LABA + ICS inhaler MART
  4. If still uncontrolled then –> add on LAMA & consider High-dose LABA + ICS MART:
     • Also refer for specialist investigation (i.e. disease endotype)
     • Patient should be considered for specialist biological therapies
• Monitoring
  • Assess symptom control, reliever use, and lung function (PEFR or spirometry).
  • Regular review to adjust therapy up or down.
• Specialist Therapies
  • Specialist biological therapies as per disease endotype:
    • Anti-IgE (omalizumab) – usually for severe allergic asthma with high IgE.
    • Anti-IL5/IL5R
    • Anti-TSLP
    • Anti-IL4R alpha
  • Bronchial thermoplasty in a minority of severe steroid-dependent cases.
• Prognosis
  • Generally good if treated effectively.
  • Mortality (e.g. ~1100 deaths/year in the UK) often reflects inadequate long-term control or suboptimal acute management.

3. Chronic Obstructive Pulmonary Disease (COPD)

3.1 Epidemiology

• Global Disease Burden
  • A major cause of morbidity and mortality worldwide, with about 65 million people having moderate to severe COPD.
  • Predicted to become the third leading cause of death globally by 2030.
• Regional Variations
  • Prevalence ranges from 0.2% (Japan) to 6.3% (USA).
  • In the UK, ~900,000 people have a formal COPD diagnosis, with an additional 2 million likely undiagnosed.
• Demographics
  • Typically presents in middle‐aged to elderly individuals (median diagnosis age ~53 years).
  • Historically more common in men, but prevalence in women is rising where female smoking rates have increased.

3.2 Aetiology

• Definition
  • COPD is an umbrella term for chronic, largely irreversible airflow obstruction caused by prolonged exposure to an environmental irritant, most often tobacco smoke.
  • Pathological changes include chronic bronchitis and emphysema.
• Emphysema:
  • Destruction of alveolar air sacs leading to reduced elastic recoil and airway collapse on exhalation.
  • Types:
    1. Centriacinar (Centrilobular): Typically in upper lobes, damage begins around bronchioles. Strongly associated with smoking.
    2. Panacinar: Uniform destruction of alveoli, commonly in lower lobes. Often linked to alpha‐1 antitrypsin (A1AT) deficiency.
    3. Paraseptal: Distal airway involvement, sometimes forming apical bullae (can predispose to spontaneous pneumothorax).

3.3 Risk Factors

• Smoking
  • Single most common cause in high‐income countries.
  • All forms of tobacco use (cigarettes, cigars, pipes, shisha, cannabis, crack cocaine) increase the risk.
• Indoor Air Pollution
  • Burning solid fuels (e.g. biomass) is a major contributor in low‐ to middle‐income countries.
• Alpha‐1 Antitrypsin (A1AT) Deficiency
  • Genetic condition leading to unopposed proteolysis and alveolar destruction (panacinar emphysema).
  • About 1 in 4000 people in the UK have clinically significant A1AT deficiency.
• Other Factors
  • Childhood exposure to smoke, maternal vitamin D deficiency during pregnancy, low birthweight, poor diet, occupational dust/chemicals.

3.4 Symptoms

• Gradual Development
  • Progressive dyspnoea on exertion, often over years.
  • Chronic cough with sputum production.
  • Frequent “chest infections” or acute bronchitis episodes.
• Exacerbations
  • Characterised by acute worsening of baseline dyspnoea, cough, or sputum beyond normal day‐to‐day variations.
  • Often triggered by viral or bacterial infections, changes in temperature, or pollution.
  • May lead to confusion/drowsiness from type 2 respiratory failure (hypoventilation).
• Emphysema‐Dominant (Pink Puffer)
  • Marked dyspnoea, minimal sputum, pursed‐lip breathing, weight loss, “barrel chest” (hyperinflation), late‐stage hypoxaemia and cor pulmonale.
• Chronic Bronchitis‐Dominant
  • Chronic productive cough, repeated infections, more likely to develop “blue bloater” phenotype with earlier hypoxaemia, hypercapnia, and cor pulmonale.
• General
  • Variation in disease presentation: degrees of reversible vs. permanent obstruction, frequency of infective exacerbations, severity of bullae, and presence of comorbidities.

3.5 Diagnosis

3.5.1 Clinical Assessment

• History: Long‐term progressive breathlessness, chronic cough/sputum, repeated exacerbations.
• Examination: Possibly normal in milder disease, or signs of hyperinflation, wheezing, decreased breath sounds, signs of cor pulmonale.

3.5.2 Investigations

1. Spirometry
   • Confirms largely irreversible obstruction (FEV₁:FVC ratio <0.7 post‐bronchodilator).
   • FEV₁ <80% predicted = probable COPD, provided symptoms are consistent.
2. Lung Volumes
   • ↑Residual Volume, ↑Total Lung Capacity = air trapping/hyperinflation.
   • Emphysema reduces transfer factor (TLCO, KCO).
3. Chest X-Ray
   • May show hyperinflated fields, flattened diaphragms, bullae, or minimal markings in emphysema.
   • Helps exclude pneumonia, pneumothorax, or other pathologies.
4. CT Scan
   • Further delineates emphysematous changes, bullae, or alternative diagnoses (e.g. bronchiectasis).
   • Possibly used for pre‐operative assessment if lung volume reduction surgery is considered.
5. Blood Tests
   • Serum alpha‐1 antitrypsin in younger patients or those with basal emphysema.
   • Screen for polycythaemia in advanced disease or check for comorbidities.
6. ECG and Echocardiogram
   • Identify cor pulmonale or exclude cardiac causes of dyspnoea.
7. Sputum Culture
   • Identifies potential pathogenic bacteria during acute exacerbations.

3.5.3 GOLD Classification

• Persistent airflow limitation: FEV₁:FVC ratio <0.7 post‐bronchodilator.
• GOLD Stages (FEV₁ % predicted):
  • GOLD 1 (mild): ≥80%
  • GOLD 2 (moderate): 50–79%
  • GOLD 3 (severe): 30–49%
  • GOLD 4 (very severe): <30%
• ABE GOLD Groups: Incorporate exacerbation risk and symptom burden to classify patients:
  • Group A: Low risk, fewer symptoms (mMRC <2 or CAT <10; 0–1 exacerbations/year not requiring hospitalisation).
  • Group B: Low risk, more symptoms (mMRC ≥2 or CAT ≥10; 0–1 exacerbations/year not requiring hospitalisation).
  • Group E: High risk, any level of symptoms (≥2 exacerbations/year or ≥1 requiring hospitalisation).

3.6 Immediate Management (Acute Exacerbations)

1. Initial Treatment for all exacerbations:
   • Short‐acting beta‐2 agonist (e.g. nebulised salbutamol) ± short‐acting muscarinic antagonist(ipratropium).
   • Systemic corticosteroid (e.g. prednisolone 30 mg once daily for 5 days).
2. Oxygen Therapy
   • Titrate carefully to achieve saturations of 88–92% to avoid hypercapnic respiratory failure.
   • Use Venturi masks to deliver 24–28% oxygen.
   • Check arterial blood gases (ABGs) after 30–60 minutes and if clinical status changes.
3. Ventilation
   • Non‐Invasive Ventilation (NIV) if, despite optimal medical therapy, the patient has respiratory acidosis (pH <7.35, PaCO2 >6.0 kPa) and no contraindications.
   • Invasive mechanical ventilation only after careful consideration, including escalation policy and ceilings of care.
4. Antibiotics
   • Indicated if increased sputum purulence plus increased volume or dyspnoea, or if mechanical ventilation is required.
   • Choice guided by local guidelines, with a usual duration of 5–7 days.
5. Other Support
   • Monitor fluid balance, treat comorbidities, consider prophylaxis against thromboembolism.
   • Offer nicotine replacement therapy if the patient is a smoker.

3.7 Long‐Term Management

1. Non‐Pharmacological Measures
   • Smoking Cessation: Crucial for slowing disease progression.
   • Pulmonary Rehabilitation: Improves exercise tolerance, reduces symptoms and hospital admissions.
   • Vaccinations (influenza, pneumococcal).
   • Nutritional Support if underweight or wasting is present.
2. Pharmacological Therapy:
   • Short‐Acting Bronchodilators: For intermittent symptoms in all groups.
   • Long‐Acting Bronchodilators (LABAs, LAMAs): Key for symptomatic improvement.
   • Inhaled Corticosteroids (ICS): Add if exacerbations continue, especially if eosinophilic phenotype is suspected.
3. Stepwise Therapy According to GOLD
   • All patients receive a short‐acting bronchodilator for rescue relief.
   • Group A (low risk, fewer symptoms): Start with a short‐ or long‐acting bronchodilator.
   • Group B (low risk, more symptoms): Prefer LABA/LAMA combination or monotherapy if combination unavailable.
   • Group E (high risk, any symptoms): LABA/LAMA combination first‐line.
     • Triple therapy (LABA/LAMA/ICS) may be added if blood eosinophils ≥300 cells/µL or frequent exacerbations.
   • Therapy escalation or de‐escalation is based on follow‐up symptom burden, exacerbation frequency, inhaler adherence and technique.
4. Long‐Term Oxygen Therapy
   • Indicated if Pao2 <7.3 kPa on two stable readings or if specific heart‐ or lung‐related complications exist.
   • Ambulatory oxygen may be offered to improve exercise tolerance in those with exertional desaturation.
5. Surgery
   • Lung volume reduction surgery for emphysema-dominant disease in selected patients.
   • Bullectomy if large bullae compress healthy lung tissue.
   • Transplantation rarely considered in severely symptomatic, younger patients who have failed maximal therapy.

4. Allergic Bronchopulmonary Aspergillosis (ABPA)

4.1 Epidemiology

• Incidence
  • ABPA is an allergic complication occurring in patients with asthma or cystic fibrosis.
  • Prevalence varies according to the frequency of predisposing conditions (moderate/severe asthma, CF).
• Clinical Context
  • A significant cause of poorly controlled asthma or bronchiectasis in at‐risk populations.

4.2 Aetiology

• Definition
  • ABPA represents an allergic reaction to fungal spores of Aspergillus, commonly Aspergillus fumigatus.
  • Inhaled spores trigger a hypersensitivity response in susceptible individuals (those with asthma or CF).
• Pathophysiological Changes
  • Ongoing inflammation in the airways leads to:
    1. Episodes of increased airways obstruction (leading to poorly controlled asthma).
    2. Proximal bronchiectasis.
    3. Tenacious sputum plugging, potentially causing lobar collapse and bronchoceles (fluid‐filled dilated bronchi).

4.3 Risk Factors

• Pre‐existing Asthma:
  • Patients with moderate or severe asthma have a higher risk of ABPA.
• Cystic Fibrosis (CF):
  • Bronchial mucus plugging and recurrent infections predispose CF patients to ABPA.
• Allergic Predisposition:
  • Underlying atopy or hyper‐reactive airways may also contribute.

4.4 Symptoms

• Poorly Controlled Asthma:
  • Episodes of wheeze, dyspnoea, and cough that do not respond well to usual therapies.
• Increased Sputum Production:
  • Sometimes with brownish plugs or casts.
• Potential Lobar Collapse:
  • Resulting from thick sputum obstructing the bronchi.
• Associated Features:
  • Patients often have a long history of asthma or CF. Symptoms may wax and wane with repeated episodes of acute bronchial obstruction.

4.5 Diagnosis

1. Laboratory Tests
   • Very high total serum IgE (often >1000 IU/mL).
   • Sensitisation to Aspergillus: Elevated Aspergillus‐specific IgG, IgE; positive Aspergillus skin prick test.
2. Imaging
   • Chest X‐ray or CT: May show proximal bronchiectasis, lobar collapse (due to sputum plugging), or bronchoceles.
3. Clinical History
   • Asthma or CF background.
   • Recurrent exacerbations not fully explained by usual triggers.

4.6 Immediate Management

• Treat Exacerbations:
  • If presenting as an acute severe asthma exacerbation, manage according to acute asthma guidelines (e.g. high‐dose bronchodilators, corticosteroids, oxygen if needed).

4.7 Long‐Term Management

1. Anti‐inflammatory and Bronchodilator Therapy
   • Managed similarly to chronic asthma: inhaled corticosteroids, bronchodilators.
   • Many patients need oral corticosteroids to achieve adequate control due to the severity of allergic inflammation.
2. Antifungal Agents
   • Itraconazole or other azoles may help reduce the fungal load and dampen allergic responses.
3. Monitoring for Bronchiectasis
   • Ongoing assessment with imaging and lung function tests to detect progressive bronchial dilation or complications like respiratory failure.
4. Prognosis
   • Irreversible airways obstruction (mimicking COPD features) can develop over time if not well controlled.
   • A minority of patients develop progressive bronchiectasis and possible respiratory failure.

5. Other Causes of Irreversible Airways Obstruction and Chronic Bronchitis

5.1 Epidemiology

• Non‐COPD Fixed Airways Obstruction
  • A subset of patients with fixed airway obstruction do not meet the criteria for COPD, or they have never smoked.
  • Such cases often overlap with conditions like chronic asthma, allergic bronchopulmonary aspergillosis (ABPA), bronchiectasis, or cystic fibrosis.

5.2 Aetiology

1. Non‐COPD Irreversible Obstruction
   • Chronic asthma and ABPA: Persistent airway remodelling can leave patients with fixed obstruction.
   • Bronchiectasis and cystic fibrosis: Bronchial dilatation and scarring result in a chronic obstructive pattern.
   • Post‐tuberculosis: Residual scarring and airway deformities.
   • Bronchiolitis Obliterans:
     • Autoimmune: e.g. rheumatoid arthritis, Sjögren’s syndrome.
     • Post‐viral: Usually following childhood infection.
     • Graft‐versus‐host disease: After stem cell or lung transplantation.
     • Medication‐induced: e.g. penicillamine.
     • Chronic microaspiration.
     • Toxic fume exposure.
   • These entities may behave similarly to COPD in terms of fixed airway obstruction, yet have distinct underlying pathologies.
2. Chronic Bronchitis
   • A condition of persistent productive cough lasting ≥3 months per year over ≥2 consecutive years.
   • Strongly associated with smoking, though any chronic irritant may contribute.

5.3 Risk Factors

• Non‐COPD Irreversible Obstruction
  • Underlying diseases: Asthma, CF, prior tuberculosis, autoimmune conditions.
  • Transplant recipients: Subject to graft‐versus‐host processes.
  • Environmental/occupational exposures: Toxic fumes or repeated aspiration events.
• Chronic Bronchitis
  • Smoking: The prime risk factor; also includes second‐hand smoke exposure.
  • Other inhaled irritants (pollutants, dust).

5.4 Symptoms

5.4.1 Other Irreversible Obstruction

• Airflow Limitations not fully reversed by bronchodilators.
• Overlap with Pre‐existing Disease: e.g. bronchiectasis (productive cough), chronic asthma (episodic wheeze) or ABPA features.
• Exacerbations: Repeated infections or inflammatory episodes can worsen baseline breathlessness and cough.

5.4.2 Chronic Bronchitis

• Prolonged Productive Cough
  • Sputum typically excessive due to hypertrophy of mucous glands.
• Cyanosis (“Blue Bloaters”)
  • Mucus plugs → retention of CO₂ (hypercapnia) → hypoxaemia.
• Increased Infection Risk and potential for cor pulmonale.

5.5 Diagnosis

5.5.1 Non‐COPD Irreversible Obstruction

• Clinical Evaluation: Assess background of asthma, CF, or autoimmune disorders.
• Pulmonary Function Tests: Demonstrate an obstructive pattern not reversing significantly with bronchodilators.
• Imaging:
  • CT scans may show bronchiectasis, scarring, or bronchiolitis obliterans.
  • Might be used to exclude alternative diagnoses (e.g. tumour).
• Specific Aetiological Tests:
  • E.g. tuberculin skin test or IGRA for post‐TB scarring, or autoimmune serologies (rheumatoid factor, etc.).

5.5.2 Chronic Bronchitis

• Clinical Definition: Productive cough ≥3 months in ≥2 consecutive years.
• Spirometry: Typically an obstructive pattern with reduced FEV₁:FVC ratio.
• Other: Check for hypoxaemia, hypercapnia, and signs of cor pulmonale if disease is advanced.

5.6 Immediate Management

• Non‐COPD Irreversible Obstruction
  • Symptom relief often parallels COPD management, but typically yields a minimal response to bronchodilators or corticosteroids.
  • Address underlying condition (e.g. treat TB sequelae, immunosuppression for autoimmune processes).
• Chronic Bronchitis (Acute Exacerbations)
  • Short‐acting bronchodilators for prompt relief.
  • Oral steroids if indicated.
  • Antibiotics if bacterial infection is suspected (increased sputum purulence).
  • Oxygen therapy carefully titrated to avoid CO₂ retention.

5.7 Long‐Term Management

• Non‐COPD Irreversible Obstruction
  • Similar supportive measures as in COPD: smoking cessation, vaccinations, pulmonary rehabilitation.
  • Control comorbidities (e.g. rheumatologic diseases), prompt treatment of respiratory infections.
  • If bronchiectasis is present, manage with physiotherapy (airway clearance techniques) and sputum culture‐directed antibiotics.
• Chronic Bronchitis
  • Smoking cessation vital for preventing progression.
  • Inhaled bronchodilators (short‐acting or long‐acting) can reduce dyspnoea.
  • Regular vaccinations (influenza, pneumococcal).
  • Monitor for cor pulmonale and treat accordingly.