COPD: GOLD guidelines Ijlal Babar, MD Medical Director Pulmonary CCM, Pulmonary Hypertension Center SRHS

Transcription

1 COPD: GOLD guidelines 2017 Ijlal Babar, MD Medical Director Pulmonary CCM, Pulmonary Hypertension Center SRHS

2 Introduction The Global Initiative for Chronic Obstructive Lung Disease (GOLD) program was initiated in Goal: to provide recommendations for COPD management based on the best scientific information available First report was issued in 2001.

3 Introduction 2017 GOLD report stresses importance of individualized treatment of all patients and has focused on two important aspects: 1. Pharmacologic treatment is based on examination of symptoms and future risk of exacerbations 2. assessment and regular evaluation of inhaler technique has been added to improve therapeutic outcome.

4 Introduction GOLD 2017 guidelines differ from previous guidelines because therapeutic decisions are not based on FEV1 any longer. Symptom burden and frequency of exacerbations have been shown to correlate with prognosis and outcomes Different patients with the same FEV1 can have substantially different exercise tolerance and prognosis. FEV1 is important to assess the patient s level of severity, and to assess for non pharmacologic therapies (lung transplantation, volume reduction )

5 Outline Definition and overview Diagnosis and initial assessment Pharmacologic therapy Management of stable COPD Inhaler techniques

6 Definition and Overview

7 COPD Definition Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases

8 COPD: definition Cigarette smoke is the leading environmental exposure Yet < 50% of heavy smokers develop COPD during their lifetime Besides exposures, host factors predispose individuals to develop COPD. These include genetic abnormalities, abnormal lung development and accelerated aging

9 COPD: Definition(cont) COPD may be punctuated by periods of acute worsening of respiratory symptoms, called exacerbations. In most patients, COPD is associated with significant concomitant chronic diseases, which increase its morbidity and mortality

10 Copd: Prevalence Prevalence of COPD Estimated 384 million COPD cases in Estimated global prevalence of 11.7% (95% CI 8.4% 15.0%). Three million deaths annually. With increasing prevalence of smoking in developing countries, and aging populations in highincome countries, the prevalence of COPD is expected to rise over the next 30 years. By 2030 predicted 4.5 million COPD related deaths annually.

11 COPD: economic burden Economic burden of COPD COPD is associated with significant economic burden. COPD exacerbations account for the greatest proportion of the total COPD burden. European Union: Direct costs of respiratory disease ~6% of the total healthcare budget COPD accounting for 56% (38.6 billion Euros) of the cost of respiratory disease. USA: Direct costs of COPD are $32 billion Indirect costs $20.4 billion

12 Diagnosis and initial assessment

13 Diagnosis and initial assessment COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease. Spirometry is required to make the diagnosis; the presence of a postbronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation. The goals of COPD assessment are to determine the level of airflow limitation, the impact of disease on the patient s health status, and the risk of future events (such as exacerbations, hospital admissions, or death), in order to guide therapy.

14 Diagnosis and initial assessment Concomitant chronic diseases occur frequently in COPD patients, including cardiovascular disease, skeletal muscle dysfunction, metabolic syndrome, osteoporosis, depression, anxiety, and lung cancer. These comorbidities should be actively sought and treated appropriately when present as they can influence mortality and hospitalizations independently

15 Diagnosis and initial assessment

16 Diagnosis and initial assessment Be wary of diagnosing COPD in the Non smoker (MUST get a smoking hx in all patient, and document) Although COPD has been described in association with second hand smoke, environmental exposures (burning of wood, coal for cooking and heating, welding) other causes of dyspnea and cough must be ruled out first. Compared to smokers with COPD, non smokers with chronic airflow limitation have fewer symptoms, milder disease lower burden of systemic inflammation.

17 Diagnosis and initial assessment

18 Diagnosis and assessment Spirometry: it is the most reproducible and objective measurement of airflow limitation. The spirometric criterion for airflow obstruction is a post bronchodilator FEV1/FVC (FEV1/SVC may be more reliable) <0.70 The use of the fixed FEV1/FVC ratio to define airflow limitation may result in more frequent diagnosis of COPD in the elderly, and less frequent diagnosis in adults < 45 years, especially in mild disease.

19 Spirometry: While post bronchodilator spirometry is required to evaluate COPD, the degree of reversibility (12% or 200 ml) has not been shown to augment the diagnosis of COPD, differentiate the diagnosis from asthma, or to predict the response to long term treatment with bronchodilators or corticosteroids.

20 Diagnosis and assessment

21 Diagnosis and assessment Assessment of severity

22 Diagnosis and assessment Assessment of symptoms Chronic Respiratory Questionnaire (CCQ ) St George s Respiratory Questionnaire (SGRQ) Chronic Respiratory Questionnaire (CRQ) Modified Medical Research Council (mmrc) questionnaire COPD Assessment Test (CAT TM )

23 Diagnosis and assessment CAT MMRC

24 Diagnosis and assessment Assessment of exacerbation risk COPD exacerbations are defined as an acute worsening of respiratory symptoms that result in additional therapy. Classified as: Mild (treated with SABDs only) Moderate (treated with SABDs plus antibiotics and/or oral corticosteroids) or Severe (patient requires hospitalization or visits the emergency room). Severe exacerbations may also be associated with acute respiratory failure.

25 Diagnosis and assessment ABCD assessment tool

26 Diagnosis and assessment GOLD A: Low risk, less symptoms 0 to 1 exacerbations per year, and no prior hospitalizations for exacerbation CAT score <10 or MMRC grade 0 to1

27 Diagnosis and assessment GOLD B: Low risk, more symptoms 0 to 1 exacerbations per year, and no prior hospitalizations for for exacerbations CAT score > 10, MMRC grade 2

28 Diagnosis and assessment GOLD C: High risk, less symptoms 2 exacerbations per year or 1 hospitalization for exacerbation CAT score < 10 or MMRC grade 0 to 1

29 Diagnosis and assessment GOLD D High risk, more symptoms 2 exacerbations per year and 1 hospitalization for exacerbation CAT score 10 or MMRC 2

30 Diagnosis and assessment ABCD assessment tool Example Consider two patients: Both patients with FEV 1 < 30% of predicted Both with CAT scores of 18 But, one with 0 exacerbations in the past year and the other with 3 exacerbations in the past year. With the new proposed scheme, the subject with 3 exacerbations in the past year would be labelled GOLD grade 4, group D. The other patient, who has had no exacerbations, would be classified as GOLD grade 4, group B.

31 Pharmacologic therapy

32 Pharmacologic therapy Beta agonists: - Relax airway smooth muscle by stimulating beta2 adrenergic receptors - SABA (albuterol, levalbuterol) and LABA (salmeterol, Formoterol) - SABA effect wears off in 4-6 hrs - LABA effect lasts 12 or more hours - SE: tachycardia, tremors.

33 Pharmacologic therapy Antimuscarinic agents: -block the bronchoconstrictor effect of acetylcholine on M3 muscarinic receptors expressed in airway smooth muscle -SAMA (Ipratropium) and LAMA (tiotropium, aclidinium) -clinical trials have shown a greater effect of LAMAs versus LABAs on exacerbation rates - SE: dryness of mouth, bitter metallic taste (ipratropium), occasional urinary symptoms, acute glaucoma (nebulized)

34 Pharmacologic therapy Inhaled Corticosteroids: -COPD associated inflammation has limited responsiveness to corticosteroids -regular treatment with ICS alone does not modify the long term decline in FEV1 nor mortality -ICS do reduce the rate of exacerbations in moderate to severe COPD. -some studies suggest that eosinophil counts in sputum and blood may serve as a biomarker to predict patients in whom exacerbation rates are decreased by ICS -ICS + LABA is more effective then either agent alone in improving lung function and reducing exacerbations.

35 Pharmacologic therapy SE of ICS - Oral candidiasis, hoarse voice, skin bruising - Increased risk of pneumonia: age >55 yrs, BMI <25 kg/m2, increased dyspnea, severe airflow limitation, - Decreased bone density, variable results - Questionable: increased risk/poor control DM, cataracts.

36 Pharmacologic therapy Oral corticosteroids: Have a role in acute management of exacerbations BUT THEY HAVE NO ROLE IN THE CHRONIC DAILY TREATMENT OF COPD BECAUSE OF A LACK OF BENEFIT BALANCED AGAINST A HIGH RATE OF SYSTEMIC COMPLICATIONS

37 Pharmacologic therapy PDE4 Inhibitor (Roflimulast): - Reduce inflammation by inhibiting the breakdown of C AMP - No direct bronchodilator activity - Reduces moderate and severe exacerbations in patients with severe to very severe COPD - SE: Diarrhea, nausea, reduced appetite, abdominal pain, weight loss, sleep disturbance and headache. - Adverse effects occur early in tx, are reversible, diminish over time with continued treatment

38 Pharmacologic therapy Antibiotics: Azithromycin (250 mg/day or 500 mg TIW) in patients prone to exacerbations reduced the risk of exacerbations compared to usual care over one year Azithromycin use was associated with an increased incidence of bacterial resistance and impaired hearing tests No data beyond one year

39 Management of stable COPD

40 Management of stable COPD OVERALL KEY POINTS: The management strategy for stable COPD should be predominantly based on the individualized assessment of symptoms and future risk of exacerbations. All individuals who smoke should be strongly encouraged and supported to quit. The main treatment goals are reduction of symptoms and future risk of exacerbations. Management strategies are not limited to pharmacologic treatments, and should be complemented by appropriate non-pharmacologic interventions.

41 Common inhalers and devices LAMA LABA/ICS LABA/LAMA LAMA/LABA/ICS Spiriva (Tiotropium) : DPI, SMI Advair (Fluticasone/salmeterol): DPI, pmdi Stiolto (Tiotropium/Olodaterol): SMI Trelegy (flutic/umeclidinium/vila nterol): DPI Tudorza (Aclidinium) : DPI Symbicort (budesonide/formoterol): pmdi Anoro (Umeclidinium/vilanterol) : DPI Incruse (Umeclidinium): DPI Breo (fluticasone/vilanterol): DPI Utibron (Indacaterol/Glycopyrroni -um) : DPI Dulera (formoterol/mometasone ): pmdi Bevespi (glycopyrrolate/formoter ol): DPI

42 Pharmacologic treatment algorithm Group A All Group A patients should be offered bronchodilator treatment based on its effect on breathlessness. This can be either a short- or a longacting bronchodilator. This should be continued if symptomatic benefit is documented

43 Pharmacologic treatment algorithm Group B Initial therapy should consist of a long acting bronchodilator. Longacting inhaled bronchodilators are superior to short-acting bronchodilators taken as needed i.e., pro re nata (prn) and are therefore recommended. There is no evidence to recommend one class of long-acting bronchodilators over another for initial relief of symptoms in this group of patients. In the individual patient, the choice should depend on the patient s perception of symptom relief. For patients with persistent breathlessness on monotherapy the use of two bronchodilators is recommended

44 Pharmacologic treatment algorithm Group B (continued) For patients with severe breathlessness initial therapy with two bronchodilators may be considered. If the addition of a second bronchodilator does not improve symptoms, we suggest the treatment could be stepped down again to a single bronchodilator. Group B patients are likely to have comorbidities that may add to their symptomatology and impact their prognosis, and these possibilities should be investigated

45 Pharmacologic treatment algorithm Group C Initial therapy should consist of a single long acting bronchodilator. In two head-to head comparisons the tested LAMA was superior to the LABA regarding exacerbation prevention, therefore we recommend starting therapy with a LAMA in this group. Patients with persistent exacerbations may benefit from adding a second long acting bronchodilator (LABA/LAMA) or using a combination of a long acting beta 2 -agonist and an inhaled corticosteroid (LABA/ICS). As ICS increases the risk for developing pneumonia in some patients, our primary choice is LABA/LAMA

46 Pharmacologic treatment algorithm Group D We recommend starting therapy with a LABA/LAMA combination because: In studies with patient reported outcomes as the primary endpoint LABA/LAMA combinations showed superior results compared to the single substances. If a single bronchodilator is chosen as initial treatment, a LAMA is preferred for exacerbation prevention based on comparison to LABAs (for details see GOLD 2017 Chapter 3). A LABA/LAMA combination was superior to a LABA/ICS combination in preventing exacerbations and other patient reported outcomes in Group D patients. Group D patients are at higher risk of developing pneumonia when receiving treatment with ICS

47 Pharmacologic treatment algorithm Group D (continued) In some patients initial therapy with LABA/ICS may be the first choice. These patients may have a history and/or findings suggestive of asthma-copd overlap. High blood eosinophil counts may also be considered as a parameter to support the use of ICS, although this is still under debate (for details see Chapter 2 and Appendix). In patients who develop further exacerbations on LABA/LAMA therapy we suggest two alternative pathways: Escalation to LABA/LAMA/ICS. Studies are underway comparing the effects of LABA/LAMA vs. LABA/LAMA/ICS for exacerbation prevention. Switch to LABA/ICS. However, there is no evidence that switching from LABA/LAMA to LABA/ICS results in better exacerbation prevention. If LABA/ICS therapy does not positively impact exacerbations/symptoms, a LAMA can be added

48 Pharmacologic treatment algorithm Group D (continued) If patients treated with LABA/LAMA/ICS still have exacerbations the following options may be considered: Add roflumilast. This may be considered in patients with an FEV1 < 50% predicted and chronic bronchitis,13 particularly if they have experienced at least one hospitalization for an exacerbation in the previous year. Add a macrolide. The best available evidence exists for the use of azithromycin. Consideration to the development of resistant organisms should be factored into decision making. Stopping ICS. A reported lack of efficacy, an elevated risk of adverse effects (including pneumonia) and evidence showing no significant harm from withdrawal supports this recommendation.

49 Inhaler techniques

50 Inhaler techniques A rigorous, prospective observational study of COPD patients discharged from the hospital confirmed appropriate adherence to use of a DPI in only 23% of patients Sulaiman et al: Am J Respir Crit Care Med, 2017

51 Figure 3. Inhaler technique errors. The most common technique error in this cohort of patients with chronic obstructive pulmonary disease was low peak inspiratory flow followed by multiple inhalations (i.e., poor breath hold) and multiple errors (i.e., more than one error in an audio file). PIFR = peak inspiratory flow rate. Am J Respir Crit Care Med,

52 Different types of inhalers pmdi: Meter dose inhaler: pmdi +spacer:

53 Different types of inhalers DPI: dry powder inhaler

54 Different types of inhalers SMI: Soft mist inhaler

55 Different types of inhalation devices Nebulizer

56 Common inhalers and devices LAMA LABA/ICS LABA/LAMA LAMA/LABA/ICS Spiriva (Tiotropium) : DPI, SMI Advair (Fluticasone/salmeterol): DPI, pmdi Stiolto (Tiotropium/Olodaterol): SMI Trelegy (flutic/umeclidinium/vila nterol): DPI Tudorza (Aclidinium) : DPI Symbicort (budesonide/formoterol): pmdi Anoro (Umeclidinium/vilanterol) : DPI Incruse (Umeclidinium): DPI Breo (fluticasone/vilanterol): DPI Utibron (Indacaterol/Glycopyrroni -um) : DPI Dulera (formoterol/mometasone ): pmdi Bevespi (glycopyrrolate/formoter ol): DPI

57 Advantages and disadvantages of different inhalation devices pmdi -ADVANTAGES -High reproducibility -independent of inspiratory flow rate - Option for spacer add-on to optimize delivery - DISADVANTAGES - Requires coordination of actuation and inhalation - Many patients cannot use it correctly - High oropharyngeal deposition

58 Advantages and disadvantages of different inhalation devices pmdi + spacer ADVANTAGES -easier to coordinate -Less oropharyngeal deposition -Higher lung deposition then pmdi DISADVANTAGES -subject to static charge -more expensive then pmdi alone -less portable then pmdi alone

59 Advantages and disadvantages of different inhalation devices DPI ADVANTAGES -does not contain propellant -no coordination needed -quicker time to achieve mastery in technique DISADVANTAGES -requires minimum inspiratory flow -many patients cannot use it correctly -most types are moisture sensitive

60 Advantages and disadvantages of different inhalation devices SMI ADVANTAGES - Multidose device - High lung deposition - Does not contain propellant DISADVANTAGES -may require complex assembly -requires some coordination of actuation and inhalation -relatively expensive

61 Advantages and disadvantages of different inhalation devices Nebulizer ADVANTAGES -may be used at any age -no specific inhalation technique required -may dispense drugs not available with pmdis and DPIS DISADVANTAGES -treatment times can be long -performance varies among nebulizers -risk of bacterial contamination

62 Common breath related technique errors with pmdis and DPIs pmdi Correct technique Most common error Breathe out before actuating No exhalation before actuation Actuate while breathing in deeply and slowly and continue until total lung capacity Forceful inhalation Hold breath No, or short, breath-holding after inhalation

63 Common breath related technique errors with pmdis and DPIs DPI Correct technique Most common error Inhale quickly and deeply Forceful and deep inhalation Stop inhaling prematurely (not inhaling to total lung capacity) Slow and not forceful inhalation Hold breath No breath holding after inhalation

64 Assessing the patient to assist in device selection Conscious inhalation Peak inspiratory inhalation Hand strength Physical ability to load, prime and actuate Manual dexterity to ensure hand-inhalation coordination Cognitive competency

65 Inspiratory flow capabilities The ability to generate sufficient peak inspiratory flow (PIF) for effective DPI use may be compromised in the elderly, especially in those with certain phenotypic characteristics such as short stature, female gender, and lower lung volumes

66 In-Check device to measure peak inspiratory flow

67 Final thoughts The choice of inhaler device has to be individually tailored and will depend on access, cost, and patient s ability and preference It is essential to provide instructions and to demonstrate the proper inhalation technique when prescribing a device, to ensure that inhaler technique is adequate and recheck at each visit that correct use is continuing. Inhaler technique (and adherence to therapy) should be assessed before concluding that current therapy is insufficient.