Obstructive airways disease

1. Obstructive airways disease COPD Asthma Gordon Christie Consultant Respiratory Physician ARI

2. Objectives • Diagnosis & assessment of severity • Appropriate investigation • When to refer • Empirical treatment • Chronic disease • Acute exacerbations

3. Asthma COPD What is it? • No truly satisfactory definition • Reversible airflow limitation • Bronchial hyperreactivity • Eosinophilic airflow inflammation • Better defined • Irreversible airflow obstruction • Gradually progressive • Inflammation • Usually smoking associated

4. Emphysema (Pathology) Chronic Bronchitis (Symptoms) COPD (Fixed airflow obstruction) Asthma (Reversible Airflow obstruction)

5. Epidemiology • Asthma • Point prevalence ~8-10% in children, 5% in adults • Severe disease much less common • Complex genetic-environmental interaction • COPD • Point prevalence 1.5-2% • Much undiagnosed symptomatic disease • Much asymptomatic airflow limitation (?5-8% of adult population)

6. COPD: Causation • In the UK • Overwhelmingly cigarette smoking • Dose response relationship to smoking exposure • Rare under 20 pack years • Occupational dust exposure of minor (& declining) importance • Some individuals at high genetic risk • Alpha 1 antitrypsin deficiency • Rare familial susceptibility • Passive smoking of minor importance

7. Impact on NHS Grampian • Catchment population 560,000 (~1% of UK) • Relatively low deprivation

8. Making a diagnosis • Asthma • Common at all ages • Usually mild • Usually variable symptoms • Characterised by exacerbations • May well be undiagnosed • Usually frequent “chest infections” or “bronchitis” • Smokers get pure asthma too ! • But may not respond to inhaled steroid nearly as well

9. COPD • Predominantly a disease of older adults • Rare under 40 • Uncommon under 50 • Strong dose response relationship to smoking exposure • Uncommon under 20 pack years

10. Assessing the breathless patient • Is there an existing diagnosis? • Is it right?? • How breathless? • MRC1:Breathless on significant exertion • MRC2:Breathless on moderate exertion • MRC3: Breathless walking with own age • MRC4: Breathless on minimal exertion • MRC5: Breathless at rest

11. History • Duration of breathlessness • COPD long history, gradually progressive; may require careful history taking to elicit • Asthma classically symptom variability • Often associated with triggers • Nocturnal symptoms • Exacerbations: markers of severity/ instability • Childhood symptoms/ school absence • Often recurrent “bronchitis” or “pneumonia”

12. Investigations • Oximetry...hypoxaemia is bad • Spirometry • Fundamental • If normal suspect asthma • Peak flow • Need to seek variability over time (at least 2 weeks) • More detailed pulmonary function • Gas transfer • 6 minute walk • Chest X ray • Primarily to exclude other diagnoses (LVF, ILD etc)

13. Severe airflow obstruction Normal (young, tall, male) Spirometry

14. Peak flow variability

15. Peak flow • Test for asthma • Need 2 weeks or more recorded • First 3-4 days can usually be discarded (practice effect) • Look for 20% variability • Some variability is physiological • Look for morning dips & dips with symptomatic periods • Useful with trial of treatment • But remember timescale of treatment effect

16. Pulmonary function testing • Main test of discriminant value is gas transfer • Measure of lung parenchymal function • Reduced (usually significantly <50% predicted) in significant COPD • Correlates with disease severity • Normal or supranormal in asthma • Functional tests: primarily assess severity • 6 minute walk • Desaturation is ominous • Shuttle walk • Formal cardiopulmonary exercise testing • Limited availability

17. Other tests • CXR: Primarily to exclude obvious LVF, ILD etc. • NOT a diagnostic test for airway disease! • ECG: Primarily to exclude IHD but remember RV changes • Echocardiography • Remember PA pressure/ RV hypertrophy & dilatation • HRCT • Can be helpful assessing structural emphysema (normally unnecessary as diagnosis already made) • Invaluable in assessment of interstitial lung disease

18. Making a diagnosis:COPD • Symptoms • Exacerbations • Smoking history • Signs of hyperinflation clinically if severe • Spirometry confirms obstruction & correlates with severity • Significant function limitation <50% predicted • Often housebound <1 litre absolute FEV1 • Gas transfer may help if uncertain • Beware pulmonary hypertension if advanced disease • May merit echo, 6 minute walk • HRCT rarely necessary

19. Making a diagnosis: Asthma • Variable exertional breathlessness • Childhood & family history common • History of precipitants (exercise, cats, cold, pollen, paint, perfume) • Associated atopy (hayfever, eczema) • Peripheral blood eosinophilia, raised total & specific IgE • Persistent symptoms (cough, sputum, wheeze) imply poor control • Usually no signs on examination & normal spirometry • Peak flow variability common, trial of treatment useful • Sometimes chronic airflow limitation indistinguishable from COPD but exercise tolerance better than expected from spirometry & gas transfer preserved

20. When to refer • Early! (..the drugs take time to work) • Concurrent with trial of empirical treatment • Concurrent with requests for additional straightforward tests (pulmonary function, echo primarily) • If real diagnostic doubt • Poorly controlled disease (persistent symptoms, frequent exacerbations) • Advanced disease • COPD with low absolute FEV1, evidence of right heart failure • Asthma with significant fixed airflow limitation

21. When to treat empirically • Majority of situations • If convincing history & evidence of airflow obstruction • Response to treatment often helpful in secondary assessment • With monitoring of outcomes (peak flow chart, review with repeat spirometry), usually after 6-8 weeks treatment

22. Empirical treatment • Should be designed to achieve rapid results in context of preassessment • Drugs are (generally) safe in short term at high doses • Mainstay is inhaled corticosteroid (beclometasone, budesonide, fluticasone) • Usually combined with long acting beta2 agonist (salmeterol, formoterol) • Bronchodilator for symptom relief • Salbutamol, terbutaline

23. Inhalers made eas(ier).. • Traditional pressurised MDIs... • Deliver 10-15% dose to the lungs • Delivered dose doubled by spacers • Are difficult to use-require coordination & timing • Doses changing with CFC free inhalers • Deposition patterns may change with CFC inhalers (smaller inhaled particles) • Breath actuated devices (easibreathe etc.) • Much liked by health economists extrapolating from RCTs, less favoured by patients & their doctors

24. Dry powder inhalers • Better drug deposition (up to 30-35% delivered dose) • Simpler to use (no requirement for timing) • Effective even at low peak inspiratory flow • Often preferred by patients • Better range of combination inhaled steroid/ LABA products available

25. Practical empirical treatment • Start reliever bronchodilator (usually salbutamol 200mcg as required) • Start combined ICS/LABA • Seretide (50-100-125-250-500 mcg fluticasone; 50mcg salmeterol) • Symbicort (100-200-400 mcg budesonide; 6-12 mcg formoterol) • Monitor outcomes • Peak flow (if asthma) • Clinical review with repeat spirometry in 6-8 weeks

26. Treatment: COPD • COPD • Recent trials • TORCH (COPD, FEV1<60% predicted; RCT, n=6000, placebo vs fluticasone 500 mcg bd alone vs salmeterol 50 mcg bd vs combined fluticasone 500mcg-salmeterol 50mcg bd over 3 years) • Exacerbations, lung function & quality of life all improved with all active teatment • Lung function improved with combination, salmeterol alone • Effects of combination treatment additive compared to single drugs alone • Borderline effect on mortality (p=0.052!) • Combination probably represents current standard of care • Some concern about increased incidence of pneumonia over 3 year followup

27. COPD: Drug choices • INSPIRE: ICS/LABA vs Tiotropium (long acting anticholinergic bronchodilator) • Both improved quality of life, lung function, reduced exacerbations • Combination superior to tiotropium • Cochrane review suggests combination treatment does not have mortality benefit • Clear benefits in exacerbation frequency (down 30-40%), quality of life & lung function (although latter are modest) • UPLIFT: Tiotropium vs placebo • Reduction in exacerbation frequency & improved quality of life • No mortality benefit (P=0.09) • Increased rate of vascular death reported in US meta analysis of anticholinergic treatment in COPD (but not UPLIFT) • No trials of combination ICS/LABA/long acting anticholinergic

28. Other drugs • Mucolytics • 2 good trials (BRONCUS, PEACE) suggesting reduced exacerbation frequency in inhaled steroid naive only • Much cheaper & relevant in resource poor settings, less so in UK • Theophylline • Few good trials but extensively used • Probably safer than was believed used at low doses; no need to chase “therapeutic” drug levels • Narrow therapeutic index • “Boutique” theophyllines (rofilumilast, cilomilast on horizon)-unclear if additional benefit justifies expense • Nebulisers • Inefficient-delivered drug dose usually ~5% • Useful acutely • Not for maintenance treatment

29. Pulmonary rehabilitation • Usually physiotherapist led • 10 week course, twice weekly sessions • Variety of programmes but usually • Exercise (circuits, upper body) • Breathing control, pacing • Education/ anticipatory care • Smoking cessation • Impressive effects • Significant improvement in exercise function • Improvement in quality of life (greater than drug effects) • Shorter readmissions (though not necessarily fewer) • Developing interest in “acute” pulmonary rehabilitation around acute exacerbations

30. ..so what do I do? • ENCOURAGE SMOKING CESSATION! • Brief advice • Refer to local service • Bronchodilator for symptom relief • Combined inhaled steroid/ long acting bronchodilator • Currently Seretide 500 bd via dry powder device (accuhaler) for simplicity & concordance • Probably a class effect • Tiotropium • Low dose theophylline (200mg bd) as next step • Refer for pulmonary rehabilitation (where available)

31. Treatment: Asthma • Empirical treatment: • Step 1: Bronchodilator only • Step 2: Bronchodilator & regular inhaled steroid • Step 3: Add LABA (in practice combination inhalers, as in COPD) or theophylline or leukotriene receptor antagonist • Step 4: Maximise inhaled steroid • Step 5: Add regular oral steroid

32. Empirical treatment • Depends on previous treatment step & current symptoms • Aiming for good perioperative control • Increase to BTS 3-4 if concerned • Will usually take 2-4 weeks to see effect of additional drug & 6-8 weeks to see effect of increased inhaled steroid • GOAL study suggests that benefit of increasing ICS continues to increase over up to 12 months

33. Asthma: Other issues • Treat nasal symptoms aggressively if present (“one airway”) in addition to lower airway • Nasal steroid • Leukotriene receptor antagonists • Antihistamines • Gastro oesophageal reflux also worth treating vigorously

34. Acute exacerbations • Asthma • Oxygen • Nebulised bronchodilators, add ipratropium if severe • IV then Oral steroid (~0.5mg/kg; usually 30-40mg/ day) • Consider magnesium, possibly repeat if severe • Consider IV aminophylline • Antibiotics rarely indicated, some evidence of macrolides

35. Acute exacerbations • COPD • Oxygen (controlled!) • Nebulised bronchodilators • Reasonable evidence for oral steroid • Appropriate antibiotics • Consider aminophylline • NIV....

36. NIV • Good evidence for mortality benefit in acute exacerbations with hypercarbia • Widely available; can be used in ward setting • Preferable to intubation in many circumstances • Provides ventilatory support while other treatment works • Not (routinely) for hypoxic respiratory failure in most circumstances

37. Summary • Diagnosis & assessment of severity • Appropriate investigation • Empirical treatment • Chronic disease • Acute exacerbations • When to refer