1

CLINICAL PRACTICE GUIDELINES IN THE DIAGNOSIS AND MANAGEMENT OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) IN THE PHILIPPINES
Report of the Council on COPD & Pulmonary Rehabilitation Philippine College of Chest Physicians Third Update: 2008 Version Editor: Lenora C. Fernandez Assistant Editors: Rommel Tipones Prescillano Zamora PROPONENTS: Chair: Luisito Idolor Members: Deogracias Abe II, MD Ethel Aonuevo, MD Joven S. Araneta, MD Tito A. Atienza, MD, FPCCP Ma. Rowena G. Balcita, MD Daphne D. Bate, MD, FPCCP Agnes Lucy G. Belleza, MD, FPCCP Veyda Christine Bringas, MD Celeste Mae Campomanes, MD, FPCCP Nolasco Capati Jr., MD Ma. Teresa V. Catacutan, MD Chona De Vera, MD Virginia Delos Reyes, MD, FPCCP Oscar Ferdinand L. Feliciano, MD Lenora C. Fernandez, MD, FPCCP Norberto A. Francisco, MD, FPCCP Claudette Gabrillo, MD Elmer Garcia, MD, FPCCP Suset Gargalicana, MD Aileen Guzman-Banzon, MD, FPCCP Renato Herradura, MD, FPCCP

2 Charina N. Hipolito, MD Luisito F. Idolor, MD, FPCCP Manuel Antonio Ko, MD Romeo Labao Jr., MD Josefina Lagunzad, MD Isaias A. Lanzona, MD, FPCCP Caesar Julius Ligo, MD, FPCCP Lai Lee L. Lim, MD Perla Manlapaz, MD, FPCCP John Clifton Martyr, MD Buenaventura Medina, MD, FPCCP Caesar Mendoza, MD, FPCCP Jenny Mendoza, MD, FPCCP Jennifer Ann Mendoza-Wi, MD, FPCCP Jessie F. Orcasitas, MD Rodolfo Pagcatipunan Jr., MD Rolando Perez, MD, FPCCP Mary Alexis Pollentes, MD, FPCCP Percival Punzal, MD, FPCCP Evelyn Ragos, MD Tomas M. Realiza, MD, FPCCP Rhoderick Ian Reyes, MD, FPCCP Joel M. Santiaguel, MD, FPCCP Ma. Bella R. Siasoco, MD, FPCCP Bobbin Sy, MD, FPCCP Sullian Sy-Naval, MD, FPCCP Jose Edzel V. Tamayo, MD, FPCCP Marietta Tan-Tanchoco, MD, FPCCP Dennis Teo, MD, FPCCP Romulo Uy, MD, FPCCP Editor: Lenora C. Fernandez, MD, FPCCP First Update: 2003 Version PROPONENTS: Chair: Lenora C. Fernandez, MD, FPCCP Interim Chair: Tito C. Atienza, MD, FPCCP Co-Chair: Norberto A. Francisco, MD, FPCCP

Members: Jubert Benedicto MD. Celeste Mae Campomanes MD, FPCCP Annette David-Rubio MD Virginia delos Reyes MD Elmer Garcia MD, FPCCP Renato Herradura MD, FPCCP Luisito Idolor MD, FPCCP Isaias Lanzona MD, FPCCP Julius Ligo MD, FPCCP Perla Manlapaz MD, FPCCP Buenaventura Medina Jr., MD Cesar Mendoza MD, FPCCP Jenny Mendoza MD Jennifer Ann Mendoza-Wi, MD, FPCCP Rodolfo Pagcatipunan MD Rolando Perez, MD, FPCCP Percival Punzal MD, FPCCP Tomas Realiza MD, FPCCP Rhoderick Ian Reyes MD Joel Santiaguel MD Ma. Bella Siasoco MD, FPCCP Bobbin Sy, MD, FPCCP Sullian Sy-Naval MD, FPCCP Marietta Tanchoco-Tan MD, FPCCP Dennis Teo MD, FPCCP Romulo Uy MD, FPCCP Advisers: Rodolfo Carungin, MD, FPCCP Teresita de Guia MD, FPCCP Camilo Roa, Jr. MD, FPCCP Daniel Tan MD, FPCCP Charles Yu MD, FPCCP Family Medicine Practitioner Advisers: Erle Castillo MD, FPAFP Leilani Nicodemus MD, FPAFP 1999 (First) Version Proponents:

4 Chair: Percival A. Punzal, MD Members: Norberto A. Francisco, MD. Aileen V. Guzman, MD. Abner T. Koh, MD. Isaias A. Lanzona, MD. Buenaventura Medina Jr., MD. Ma. Bella R. Siasoco, MD. Advisers: Teresita de Guia, MD. Rodolfo Carungin, MD. Camilo Roa Jr., MD. Daniel Tan, MD. Renato Dantes, MD. Member Societies/Groups/Individuals of Multisectoral Consultative Groups: Philippine College of Chest Physicians Philippine Academy of Family Physicians Philippine Society of Rehabilitation Medicine Philippine Association of Pulmonary Care Philippine Association of Thoracic and Cardiovascular Surgery, Inc. Department of Health Philippine Nurses Association Nutritionists Priest

5 TABLE OF CONTENTS: I. Introduction II. What is COPD? III. What are the risk factors for COPD? IV. How do we diagnose COPD? A. Detection of COPD B. Confirmation of COPD C. Additional investigations D. Grading of COPD severity E. How is COPD differentiated from other common causes of obstructive lung diseases in the Philippines, specifically asthma & bronchiectasis? F. Ongoing monitoring and assessment V. How do we manage patients with stable COPD? A. Smoking cessation B. Pharmacologic management 1. General principles of pharmacologic management 2. Pharmacologic agents C. Non-pharmacologic management D. Management continuum for Stable COPD VI. How de we management a COPD patient in Acute exacerbation? A. Definition of COPD in acute exacerbation B. Common causes of acute exacerbation of COPD C. Severity classification of COPD in acute exacerbation D. Home management 1. Bronchodilator therapy 2. Antibiotics 3. Glucocorticosteroids E. Hospital management 1. Initial management of exacerbations of COPD in the emergency department or the hospital 3. The inclusion criteria for admission in the Intensive Care Unit (ICU) 4. Indications for hospital assessment or admission PAGE

6 F. Intensive care unit management 1. Candidates for NIPPV 2. Indications for starting invasive mechanical ventilation G. Hospital discharge and follow-up 1. Discharge criteria 2. Follow-up assessment H. Indications for Specialist Referral I. Ethical issues

I. INTRODUCTION
Chronic Obstructive Pulmonary Disease (COPD) is one of the most important diseases of the 21st century, being a major cause of death and disability. Most epidemiological studies have found that the prevalence of morbidity and mortality due to COPD have increased over time and are greater in men than in women. The impact of COPD is not only confined to its ill effects on the individuals health but also permeates into the social and economic aspects as well. The 1998 World Health Organization Report states that non-communicable diseases, including COPD, is the cause of nearly 40% of all deaths in developing countries and that these areas account for 67% of all COPD deaths worldwide.1 In these developing countries, the indirect cost of COPD from loss of work and productivity may be more important than the cost of medical care. A local study2 done in a rural community in Laguna, Philippines estimated the prevalence of COPD based on spirometric measurements to be 3.7%. In a recent workshop in the Asia Pacific region3, the prevalence of COPD in the Philippines was cited at 6.3% utilizing data from a study of Dans and colleagues.4 In response to the need to help prevent and manage COPD better, the Philippine College of Chest Physicians published the Philippine Consensus Report on COPD in 1999 (see Appendix 1). This is the third update of the Philippine Consensus report and this version takes into account the new studies that have been published on COPD and the latest version of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop Report entitled Global Strategy for the Diagnosis, Management, and Prevention of COPD as well. The Philippine Consensus Report hopes to cater to the specific needs of the Philippines as a developing country and is intended for the use of practicing physicians and other health professionals involved in the care of patients with chronic obstructive pulmonary disease (COPD). The goals of this practice guideline are to: 1. assist primary health care practitioners in identifying and initiating management of patients with COPD. 2. assist hospital-based physicians in providing appropriate and costeffective care for COPD patients. 3. recommend measures for the prevention of further deterioration of lung function and subsequent complications; and in the improvement in the quality of life of COPD patients. 4. assist allied health care workers in the care of COPD patients.

8 5. identify areas for further research in the diagnosis and management of COPD in the Philippines. The process used in updating this practice guideline was by: (a) selection of a Core Group to review the previous guideline and identify topics/areas that needed revision, (b) selection of committee members to handle each identified topic, (c) search for recent data in the literature, (d) grading of available evidence, (e) assessment of locally available resources, (f) formulation, presentation and revision of draft recommendations, and (g) formulation of final statements. Levels of evidence are assigned to the statements, where appropriate, following the system of the US National Heart, Lung, and Blood Institute (NHLBI) which is comparable to the classification used in the 1999 practice guideline: DESCRIPTION OF LEVELS OF EVIDENCE
Evidence Category Sources of Evidence Randomized controlled trials (RCTs). Rich body of data Definition Evidence is from endpoints of welldesigned RCTs that provide a consistent pattern of findings in the population for which the recommendation is made. Category A requires substantial numbers of studies involving substantial numbers of participants. Evidence is from endpoints of intervention studies that include only a limited number of patients, post-hoc or subgroup analysis of RCTs, or meta-analysis of RCTs. In general, Category B pertains when few randomized trials exist, they are small in size, they were undertaken in a population that differs from the target population of the recommendation, or the results are somewhat inconsistent. Evidence is from outcomes of uncontrolled or nonrandomized trials or from observational studies. This category is used only in cases where the provision of some guidance was deemed valuable but the clinical literature addressing the subject was deemed insufficient to justify placement in one of the other categories. The Panel Consensus

Randomized controlled trials (RCTs). Limited body of data

C D

Nonrandomized trials. Observational studies

Panel consensus judgment.

9
is based on clinical experience or knowledge that does not meet the abovelisted criteria.

Discussion on the most appropriate recommendations with the advisers and stakeholders was lengthy and painstaking. The ultimate deciding factor in all the recommendations was what could benefit the typical Filipino COPD patient most. This document is divided into five parts that discusses the (1) definition of COPD, (2) risk factors for developing COPD, (3) diagnosis, classification and monitoring of COPD, (4) management of stable COPD, (5) and management of COPD in acute exacerbation. Recommendations for the aspects of COPD needing further research and references used are placed at the end of each chapter. The sections are written in a brief and concise manner to help the reader imbibe the key points quickly so that the document can be used at bedside or in the clinics. For further elaboration of the guidelines, the proponents will be disseminating the document through focused group discussions on a nationwide basis starting Year 2008.

10

II. WHAT IS COPD? Key Points:

COPD is a preventable and treatable disease characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. Systemic effects of COPD

Definition & Pathophysiology COPD is a preventable and treatable disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. The constant pathologic abnormality in smokers is an inflammatory reaction in the airways and parenchyma consisting of neutrophils and alveolar macrophages. In addition to inflammation, oxidative stress and imbalance of proteinases and antiproteinases in the lung are also implicated in the development of COPD. The ensuing pathologic changes in COPD involve the central and peripheral airways, lung parenchyma and pulmonary vasculature. Mucus gland hypertrophy, goblet cell metaplasia and airway thickening occur in the central airways and these are responsible for the chronic cough and sputum production that are characteristic of COPD. The major site of airways obstruction, however, occurs in the peripheral airways mainly due to airway wall thickening and fibrosis. Destruction of the lung parenchyma leads to the pathology of emphysema or dilatation and destruction of respiratory bronchioles. Subsequent gas exchange abnormalities and eventual pulmonary hypertension and right heart failure (cor pulmonale) result as the disease progresses.

11

III. HOW PREVALENT IS COPD IN THE PHILIPPINES?

Chronic Obstructive Pulmonary Disease is a growing cause of morbidity and mortality worldwide. The WHO Global Burden of Disease Project estimated that COPD was the fifth leading cause of death worldwide in 2001 and will be the third leading cause by 2020. 6,7,8 The 1998 World Health Organization Report states that non-communicable diseases, including COPD, is the cause of nearly 40% of all deaths in developing countries and that these areas accounts for 67% of all COPD deaths worldwide.1 In 1987, a local study done in a rural community in Laguna, Philippines estimated the prevalence of COPD based on spirometric measurements to be 3.7%.2 In a 2002 workshop in the Asia Pacific region,3 the prevalence of COPD in the Philippines was cited at 6.3% utilizing data from a study of Dans and colleagues. 4 In the past, available information about COPD was not obtained by consistent methods, and evidence suggests that rates of disease are generally underestimated. In the recently concluded Burden of Obstructive Lung Disease (BOLD)study, standardised methods for estimating COPD prevalence and for obtaining information about risk factors were developed.5 Data collection using core questionnaires and postbronchodilator spirometry was completed for 12 sites worldwide which included Manila. A total of 918 respondents aged 40 years and older were studied in Manila. The prevalence of COPD in Manila that was GOLD stage I or higher (postbronchodilator FEV1/FVC < 0.7) was reported to be 13.8%. COPD prevalence was noted to be greater in men(19.6%) than in women(8.6%). The prevalence of Stage II or higher COPD was 12.5% overall in Manila compared to a lower 10.1% overall across all 12 sites, 18.7% for men in Manila compared to a lower 11.8% for men across all 12 sites, and 6.8% for women in the Manila site compared to greater 8.5%for women across all 12 sites. These estimates of the overall prevalence and staging of COPD are consistently higher than figures in previous studies, which accord with claims that COPD has generally been underestimated in the past. The Manila site, along with 2 other sites (Capetown,South Africa and Lexington,USA) reported a prevalence of stage II disease that was more than twice that of stage I, ranking 3 rd highest in prevalence of COPD stage II or higher in all 12 sites, suggesting a much higher than usual burden of clinically significant COPD in these populations. Generally, the prevalence of COPD that is GOLD Stage II or higher increased steadily with age for men and women. Unlike most of the other sites in the BOLD study which reported a less than 5% prevalence of COPD GOLD Stage II or higher in individuals aged 40-49 years, the Manila site reported a much higher prevalence of 11.5% for men in this age group. For those aged 70 years and older, the prevalence was 46.6% for men and 20.5% for women in Manila. For men, prevalence increased with increasing pack-years, and the prevalence among male participants who had never smoked tended to be similar to that for those who had ever smoked and who had 0-10 packyears of cigarette smoking exposure. However, for women in Manila, prevalence did not increase with increasing pack-years. Manila also had the highest reported levels of prior tuberculosis for men, the highest number of male respondents with a year or more in a dusty job, and the 3rd highest number of female respondents with a year or more in a dusty job,raising important questions about the role of environmental exposures other than smoking. Future work from the BOLD Initiative will look into the prevalence of COPD in the rural areas of the country. The increasing prevalence of COPD that has been reported demands

12 attention for future health-care planning and for more studies on the effects of prevalent local diseases like tuberculosis and on environmental exposures other than smoking. References: 1. The World Health Report 1998- Life in the 21st century- a vision for all by the World Health Organization. 2. Yu CY, Chavez JC, Blanco JB et al. Prevalence of chronic obstructive pulmonary disease in a rural Philippine community barangay Banca-banca, Victoria, Laguna. Phil J of Chest Diseases 1987; 137-151. 3. Seale JP. The Prevalence of COPD in Asia Pacific. RespirAsia Report Issue 1 January 2002. 4. Dans A, Fernandez L, Fajutrao et al. The economic impact of smoking in the Philippines. Phil J of Int Med Nov-Dec 1999;37(6):261-68. 5. Buist SA, McBurnie MA, Vollmer WM et al. International variation in the prevalence of COPD(The BOLD Study):a population-based prevalence study. Lancet 2007;370:741-50. 6. Lopez AD, Shibuya K, Rao C, Mathers CD, Hansell AL, Held LS, Schmid V, Buist S. Chronic obstructive pulmonary disease:current burden and future projections. Eur Respir J 2006:27:397412. 7. Murray CJL, Lopez AD, editors. The global burden of disease:a comprehensive assessment of moratlity and disability from diseases, injuries and risk factors in 1990 and projected to 2020. Cambridge MA:Harvard University Press; 1996. 8. Murray CJL, Lopez AD. Alternative projections of mortality and disability by cause 19902020:Global Burden of Disease study. Lancet 1997;349:1498-1504.

13

IV. WHAT ARE THE RISK FACTORS FOR COPD? Key Points
Cigarette smoke is the major risk factor for COPD Since cigarette smoking is the most important risk factor for COPD, smoking prevention and cessation should be given the utmost priority. Modifying factors other than smoking have been shown to have a strong association with the development of COPD Disease prevention by avoidance of risk factors is of crucial importance because of the irreversible and progressive nature of COPD.

1. SMOKING Tobacco use is the single most important factor in the pathogenesis of COPD and it causes 80% to 90% of COPD cases.5 As graphically represented in the survival curve of Fletcher and Peto (Figure 3.1)6, only a portion of chronic smokers show a rate of decline of lung function that is typical of patients who present with breathlessness due to COPD. Susceptible smokers have an accelerated rate of decline of lung function (50-90 mL of Forced Expiratory Volume at 1 second (FEV1)/year compared with 20-30 mL of FEV1/year after the age of 30 years in non-smokers). Subjects with COPD who stop smoking have a slower rate of progression of their disease which may approach the expected decline in FEV1 in non-smokers. Despite the often cited and scientifically associated relation between smoking and airway obstruction, only 10-20% of chronic heavy smokers ever develop symptomatic COPD.7 This indicates that there are genetic and/or environmental factors which contribute to the development of COPD.

14

Figure 3.1. Graph of survival from Fletcher C, Peto R, Br Med J, 1:1645-1648, 1977

2. SECONDHAND SMOKE There is a small but significant difference in the prevalence of respiratory symptoms and lung function in adults and children who are regularly exposed to secondhand smoke.8 It is still unclear whether secondhand smoke causes COPD. 3. ALPHA-1 ANTITRYPSIN DEFICIENCY Another well established9 risk factor for the development of COPD is a deficiency in the function and/or quantity of the protective protease inhibitor, alpha-1 antitrypsin (AAT). This accounts for 5% or less of all cases of COPD and these cases are mostly found in the Western hemisphere.10 This is an autosomal recessive (PiZZ genotype) disorder. 4. AIR POLLUTION AND OCCUPATIONAL EXPOSURE Whether atmospheric pollution itself can cause or contribute to the development of COPD or not is still uncertain. Outdoor air pollution may vary in different areas. As with the problem of smoking, there will be individuals who will be more susceptible to the effects of atmospheric pollution than others. An epidemiologic study in the Philippines 11 comparing the effect of outdoor air pollution among jeepney drivers, airconditioned bus drivers and commuters in Metro Manila showed that cumulative exposure levels to air pollutants far exceeded standard levels and

15 was significantly higher among jeepney drivers. The prevalence of COPD among jeepney drivers was 32.5%, 16.4% for air-conditioned bus drivers and 14.8% for commuters. Jeepney drivers had an odds ratio of 2.33 for developing COPD as compared to air-conditioned bus drivers and commuters. The prevalence of smoking, however, among jeepney drivers was 69.4% and this probably affected to a significant degree the increased probability of jeepney drivers to develop COPD. Occupational exposure. Any occupation wherein the immediate environment is polluted increases the risk of developing COPD. In addition, there is evidence that cadmium and silica also increases the risk of development of COPD. Occupations at risk include coal miners, construction workers who handle cement, metal workers, grain handlers, cotton workers and workers in paper mills. However, the effect of smoking far outweighs any influences from the work environment. Indoor air pollution. Numerous sources of airborne contaminants have been identified in indoor environments and include pollutants found in home, office and transportation environments. In the home, the principal combustion sources are tobacco-smoking, gas cooking stoves, unvented kerosene heaters and biomass fuels (Table 3.1). Biomass fuels used by women for cooking account for the high prevalence of COPD among nonsmoking women in parts of the Middle East, Africa, and Asia (references)
Table 3.1
Common Biomass Fuels1 Crop Residues sugar cane bagasse Agricultural waste coconut husk, rice straw, palay shell Firewood Charcoal

5. SOCIOECONOMIC STATUS Studies attempting to identify a relationship between COPD and socioeconomic status often encounter an association between social class and indoor air pollution, with COPD being more prevalent in the lower socioeconomic strata.13 This may be related to poor housing condition,
1

Adapted from Biofuels, ,Air Pollution and Health Smith, East-West Centre, Honolulu, 1987

16 nutritional status and use of fossil fuels without adequate ventilation. Also, there is a higher prevalence of smoking in the lower socioeconomic strata, and they are more likely to be employed in jobs where they may be at risk from occupational exposure. 6. INFECTIONS The role of viral upper and lower respiratory tract infections in the pathogenesis of COPD remains to be clarified. Viral infections in the lung enhance inflammation and predispose to bronchial hyperreactivity. Epidemiologic studies suggest that childhood infections, usually due to adenovirus and respiratory syncitial virus, are independent risk factors for the development of COPD in adulthood.14,15 Furthermore, adenoviral DNA is frequently found in the lungs of heavy smokers.14 Once COPD is established, repeated infectious exacerbations may accelerate the decline in lung function.

PREVENTION OF RISK FACTORS

Disease prevention by avoidance of risk factors is of primary importance because of the irreversible and progressive nature of COPD. Since cigarette smoking is the most important risk factor for COPD, smoking prevention and cessation should be given the utmost priority in decreasing the incidence of the disease. Reduction in total personal exposure to dusts, fumes, and gases in the outdoor, indoor, and occupational setting should also be addressed when considered to be significant. Currently, there is inadequate basis for recommending respiratory protective equipment or air cleaners for use in the workplace or home as means to minimize contact with noxious particles and gases. Avoidance of exposure to these substances is strongly advised.

RESEARCH RECOMMENDATIONS 1. Philippine prevalence studies on COPD

The prevalence of COPD in the rural setting in the Philippines will be studied soon. Risk factors unique to the rural setting such as exposure to indoor air pollution through biomass fuel cooking will be included in these studies.

17 2. Burden of Illness Study

Cost of care for COPD is perceived to be high but there are no local studies documenting the overall impact of this disease on the individual and national level.

3. Studies on the role of secondhand smoke as a cause of COPD (delete already if studies already present) 4. Determine the incidence of AAT Deficiency among Filipino emphysematous patients
AAT was previously thought to be a condition of Caucasions; however, a Japanese study has suggested that a form of this condition may exist as a mutation in Asians.

REFERENCES:
1. The World Health Report 1998- Life in the 21st century- a vision for all by the World Health Organization. 2. Yu CY, Chavez JC, Blanco JB et al. Prevalence of chronic obstructive pulmonary disease in a rural Philippine community barangay Banca-Banca, Victoria, Laguna. Phil J of Chest Diseases 1987; 137-151. 3. Seale JP. The prevalence of COPD in Asia Pacific. RespirAsia Report Issue 1 January 2002. 4. Dans A, Fernandez L, Fajutrao et al. The economic impact of smoking in the Philippines. Phil J of Int Med Nov-Dec 1999; 37(6):261-68. 5. US Surgeon General. The health consequences of smoking: chronic obstructive lung disease. US Department of Health and Human Research, 84-50205, 1984. 6. Fletcher C, Peto R. The natural history of chronic airflow obstruction. BMJ 1977; 1:1645-8. 7. Roth MD, Tashkin DP, Arora A, et al. Airway inflammation in the young and tobacco smokers. Am J Respir Crit Care Med 1998; 157: 928-37. 8. Leuenberger P, Schwartz J, Ackermann-Liebrich U, et al. Passive smoking exposure in adults and chronic respiratory symptoms (SAPALDIA study). Am J Respir Crit Care Med 1994; 150: 12228. 9. Silvermann EK, Chapman HA, Drazen JM, et al. Genetic epidemiology of severe, early-onset chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1998; 157: 1770-1778. 10. Sandford AJ, Weir TD, Pare PD. Genetic risk factors for chronic obstructive pulmonary disease. Eur Respir J 1997; 10: 1380-1391.

18
11. Subida, Torres, Borja, Tanchuco. Epidemiology of chronic respiratory symptoms & illness among jeepney drivers, airconditioned bus drivers and commuters exposed to vehicular emissions in Metro Manila, 1990-91. unpublished. 12. Dennis RJ, Maldonado D, Norman S et al. Woodsmoke exposure and risk for obstructive airways disease among women. Chest 1996; 109: 115-119. 13. Prescott E, Lange P, Vestbo J. Socioeconomic status, lung function, and admission to hospital for COPD: results from the Copenhagen City Heart study. Eur Respir J 1999; 13: 1109-1114. 14. Tager IB, Speizer FE, et al. The relationship between respiratory illness in childhood and chronic airflow obstruction in adults. Am Rev Resp Dis 1983; 127: 508-523. 15. Gold DR, Tager IB, Weiss ST. Acute lower respiratory illness in childhood as predictor of lung obstruction. Am Rev Resp Dis 1984; 129: 412-422. 16. Samet JM, Marbury MC, Spengler JD. Health effects and sources of indoor air pollution. Am Rev Resp Dis 1987; 136: 1486-1503. 17. Matsuse T, Hayashi S, Kuwano K, et al. Latent adenoviral infection in the pathogenesis of chronic airways obstruction. Am Rev Resp Dis 1992; 146: 177-184.

19

V. HOW DO WE DIAGNOSE COPD?

KEY POINTS:
A diagnosis of COPD is considered in any patient who: Is 40 years or older Has cough, sputum production or dyspnea Has a history of exposure to risk factors for the disease The diagnosis is confirmed by a post-bronchodilator FEV1/FVC <70%. Once COPD is diagnosed, the severity of the disease can be classified into mild (Stage I), moderate (Stage II), severe (Stage III) and very severe (Stage IV) based on the patients post-bronchodilator FEV1 value, signs and symptoms. Once COPD is detected and confirmed, ongoing monitoring and assessment should include evaluation of: (1) continued exposure to risk factors, especially tobacco smoke; (2) disease progression and development of complications; (3) pharmacotherapy and other medical treatment; (4) exacerbation history; (5) co-morbidities.

A. DETECTION OF COPD
Age The disease commonly appears in the fifth decade of life. It is rare to encounter COPD in patients younger than 40 years old1. Symptoms COPD patients usually develop cough as the initial symptom 2. Acute chest illnesses characterized by increased cough, purulent sputum, wheezing, dyspnea, and occasionally fever may occur intermittently. Progressive dyspnea worsening over a period of months or years, is a typical feature of COPD.5 In the advanced stage of the disease, cor pulmonale with right heart failure and edema may develop. Cyanosis may also be present especially during acute exacerbations. Risk factors Cigarette smoking is the single most important factor in the pathogenesis of COPD, and accounts for 80-90% of the risk of developing COPD. In addition,

20 attention has focused on bronchial hyperreactivity, secondhand smoke, air pollution, and alpha-1-antitrypsin deficiency. Although alpha-1-antitrypsin deficiency is of comparable importance with tobacco smoking, this only accounts for < 1 % of COPD. Little data is available to identify persons susceptible to develop COPD when exposed to these risk factors. Physical Examination The physical examination is not a sensitive means of detecting airflow obstruction8. Among the physical findings, wheezing during quiet breathing11 and prolonged expiratory time (> 5 seconds) are useful indicators of airflow limitation. These signs, however, are of no value as guides to severity and their absence does not exclude COPD.9

B. CONFIRMATION OF COPD SPIROMETRY

For any individual suspected of COPD, a postbronchodilator FEV1/Forced Vital Capacity (FVC) <70% confirms the diagnosis. The following diagram is suggested in order to arrive at a diagnosis of COPD: Exposure to risk factors Symptoms
Cough Dyspnea Sputum production

COPD Suspect

Spirometry

Post-bronchodilator FEV1/FVC < 70%

Post-Bronchodilator FEV1/FVC > 70%

COPD

Not COPD

21

Figure 4.1. Diagram for the Diagnosis of COPD. Spirometry should measure the maximal volume of air forcibly exhaled from the point of maximal inspiration (forced vital capacity, FVC), the volume of air exhaled during the first second of this maneuver (forced expiratory volume in one second, FEV1), and the ratio of these two measurements (FEV1/FVC) should be calculated 19. Patients with COPD typically show a decrease in both FEV1 and FVC. The degree of abnormality in the FEV1 generally reflects the severity of COPD. Assessment of airflow obstruction before and after giving a short-acting bronchodilator (Bronchodilator Reversibility Testing), at the time of diagnosis, is recommended. This is to obtain the post-bronchodilator FEV1 and FVC values that will confirm the diagnosis of COPD20. The presence of a post-bronchodilator FEV1/FVC<70% confirms the presence of COPD where airflow limitation is not fully reversible11. The Bronchodilator Reversibility Testing is also helpful in distinguishing the asthmatic from the COPD patient 11,21,22. Bronchodilator reversibility can both be seen in asthma and COPD. If FEV1/FVC returns to > 0.70 the predicted normal range after administration of a bronchodilator, the patients airflow limitation is most likely due to asthma. However, the presence of bronchodilator reversibility in COPD does not predict disease progression, deterioration of health status or frequency of exacerbation. Likewise, small changes in FEV1 after administration of a bronchodilator do not reliably predict the patients response to treatment. A protocol for the performance of Bronchodilator Reversibility Testing is listed in Fig. 4.2 11.

22

Figure 4.2. Bronchodilator Reversibility Testing

Preparation 1. The test should be performed when patients are clinically stable and free from infection. 2. Patients should not have taken inhaled short-acting bronchodilators in the previous six hours, long-acting Beta-2 (B2) agonists in the previous twelve hours, or sustained release theophyllines in the previous 24 hours.

Spirometry 1. FEV1 & FVC should be measured before a bronchodilator is given. 2. 3. The bronchodilator should be given by metered dose inhaler or by nebulizer. Suitable dosage protocols for bronchodilators are 400 micrograms of B2-agonists, 80 micrograms of anticholinergic agents, or the two combined. FEV 1 & FVC should be measured again 30-45 minutes after the bronchodilator is given.

Results 1. A postbronchodilator FEV1/FVC < 70% confirms the diagnosis of COPD. 2. An increase in the FEV1 that is both greater than 200 ml and 12% above pre-bronchodilator FEV1 is considered a significant bronchodilator response.

C. ADDITIONAL INVESTIGATIONS
Chest radiograph The standard postero-anterior and lateral chest radiograph is useful in the initial assessment of COPD patients to exclude or identify other conditions such as tuberculosis, lung cancer, pneumothorax, or pneumonia. Chest X-ray findings that may be suggestive of COPD include hyperlucency of the lungs, rapid tapering of the vascular markings, and signs of hyperinflation (flattened hemidiaphragms, and an increase in the volume of the retrosternal space)11. A normal Chest X-ray, however, does not rule out the diagnosis of COPD. Arterial blood gas measurement Measurement of arterial blood gases with the patient breathing room air is recommended in the assessment of patients with moderate to severe COPD18 when signs of right heart failure or respiratory distress are present. As the disease progresses, hypoxemia becomes more severe and hypercapnia supervenes. Peak flow determination The definite correlation between peak expiratory flow rate (PEF) and FEV1 has not yet been proven since PEF may underestimate the degree of airflow

23 obstruction6. Therefore, the use of peak expiratory flow rate determination in confirming the diagnosis of COPD is not recommended. Computed Tomography Computed tomography (CT) scanning is not recommended in the routine assessment of COPD. Its role is limited to the preoperative evaluation of patients with COPD who are about to undergo surgical procedures such as bullectomy or lung volume reduction surgery11,23. Alpha-1 antitrypsin deficiency screening Alpha-1-antitrypsin deficiency screening may be valuable to identify coexisting alpha-1 antitrypsin deficiency in patients who develop COPD at a young age (<45 years) or among those who have a strong family history of the disease 11. However, this test is not available in the local setting.

D. DIAGNOSING COPD IN AREAS WHERE SPIROMETRY IS NOT READILY AVAILABLE

In the Asia Pacific Region, particularly in rural areas, spirometry is not readily available to confirm the diagnosis of COPD. The Asia Pacific COPD Roundtable Group (2005) thus emphasized the importance of history, symptoms and physical signs in suspecting COPD (Reference). The expert panel mentioned that the forced expiratory time (FET) can be a useful bedside maneuver in determining airways obstruction. An FET of more than 6 seconds is a good guide to the presence of an FEV1/ FVC ratio < 50%. FET is defined as the time taken for an individual to complete a forceful exhalation after maximal inspiration (Reference). Airflow is auscultated using the bell of a stethoscope placed over the suprasternal notch. A stopwatch is used to measure the time between the first sound of forced expiratory flow and the point at which airflow is no longer audible. Different investigators have studied the usefulness of history and physical examination in the detection of obstructive airways disease using spirometry as the gold standard. Methodologies are varied and results are wide-ranging to come up with satisfactory recommendations (Reference). Thus, after systematic review of literature, two multinational trials were conducted by the Clinical Assessment of the Reliability of Examination-Chronic Obstructive Airways Disease (CARE-COAD) Group to determine the accuracy of history and physical examination in the diagnosis of obstructive airways disease (OAD).

24 Results of the 2 studies demonstrated several elements in history and physical examination had significant correlation with OAD.using spirometry as gold standard expressed in likelihood ratios. The first study (CARE-COAD1, 2000) mentioned that self-reported history of OAD (LR 7.3), more than 40 pack-year smoking history (LR 8.3) and age more than 45 years (LR 1.3) were among the elements significantly associated with OAD. The second study (CARE-COAD2, 2002) found that self-reported history of COPD (LR 4.4), wheezing on physical examination (LR 2.9) and forced expiratory time (FET) greater than 9 seconds (LR 4.6) correlated with the diagnosis of COPD. The investigators recommend that less emphasis should be placed on the presence of isolated symptoms or signs in the diagnosis of COPD. Clinicians should take into account the combination of the different elements in history and physical signs in order to have substantial basis in diagnosing COPD without spirometry. Further studies are needed to validate this recommendation.

E. GRADING OF COPD SEVERITY

Several practice guidelines have different ways of grading the severity of COPD and apparently depends on the different needs of each country. The most recent classification proposed by the GOLD Workshop Report is a pragmatic approach aimed at practical implementation and should only be regarded as an educational tool, and a very general indication of the approach to management. 11 The spirometric classification in the GOLD document has been shown to predict health status, utilization of healthcare resources, exacerbation occurrence, and mortality among COPD patients 27-29. It is, therefore, also adopted in this document to facilitate the grading of severity of a patients COPD. In the Philippines, however, it is an accepted reality that a significant number of health workers providing care to COPD patients may have limited access to spirometers. In such a situation, clinical features can aid in determining the severity of COPD. In this guideline, the clinical signs and symptoms from the British Thoracic Society guidelines24 were utilized in the severity classification based on the previous clinical experience with Filipino COPD patients 25. The body mass index and dyspnea have also proved useful in predicting outcomes such as survival in COPD and would warrant further validation among Filipino patients26. (elaborate on PHCA study on BODE index). It cannot be overemphasized that the identification of individuals in Stage 0 or those who have or have been exposed to the risk factors for COPD, may or may not have the signs and symptoms of COPD and still have no obstructive defect on spirometry is considered to be very important. This is one of the most crucial

25 period when interventions to reduce or remove these risk factors (e.g. smoking cessation, change in occupation, etc.) will have the greatest impact in preventing the occurrence of COPD. There are four stages of COPD based on spirometry and signs and symptoms. In the 2005 guidelines, the grading of COPD severity included Stage 0 (At Risk) to identify those who have or have been exposed to risk factors for COPD and who have minimal signs and symptoms but with normal spirometry. In this new document, Stage 0 is no longer included because there is insufficient evidence to show that individuals classified in this stage necessarily progress to Stage 1 (Reference). The proposed classification of COPD is shown in Table 4.1 below. Table 4.1. Grading of COPD Severity
Stage I: Mild COPD Spirometry* FEV1/FVC < 70% FEV1 > 80% predicted Signs/Symptoms No abnormal signs With or without symptoms of: - smokers cough - Little or no breathlessness Variable abnormal signs (general reduction in breath sounds, presence of wheezes) With or without symptoms of: - smokers cough - Little or no breathlessness Variable abnormal signs (general reduction in breath sounds, presence of wheezes) Breathlessness on exertion Cough and chronic sputum production Breathlessness on any exertion/at rest Wheeze and cough often prominent Lung overinflation usual; cyanosis; peripheral edema and polycythemia in advanced disease, especially during exacerbation

II: Moderate COPD

FEV1/FVC <70%; FEV1>50% but < 80% predicted

III: Severe COPD

FEV1/FVC <70% FEV1>30% but <50% predicted

IV: Very Severe COPD

FEV1/FVC < 70% FEV1 < 30% predicted or FEV1 < 50% predicted with respiratory failure or clinical signs of right heart failure

26 *All FEV1 values refer to postbronchodilator FEV1. The above mentioned COPD severity grading based on FEV1 values has been widely accepted in different guidelines and is correlated with mortality. , validation in terms of correlation with clinical outcomes such as mortality is still lacking (Reference). COPD has systemic manifestations that may not be accurately reflected by FEV1 alone (Reference). A more accurate way of assessing severity is by using the Body-Mass Index (BMI), Airflow Obstruction, Dyspnea and Exercise Capacity Index in COPD (BODE Index). This multidimensional grading system using a 10-point scale has been prospectively validated in a cohort of 625 patients. The risk of death among COPD patients from any cause or respiratory causes can be predicted from the BMI, obstruction (FEV1 % of predicted), Dyspnea (Modified Medical Research Council dyspnea scale) and exercise capacity (six-minute walk test). The higher the scores using the 10-point scale, the higher is the risk of death. The hazard ratio per one-point increase in the BODE score was 1.34 (95% CI, 1.26 to 1.42; P<0.001) and hazard ratio for death from respiratory causes is 1.62 (95% CI, 1.48 to 1.77; P<0.001).

F. HOW IS COPD DIFFERENTIATED FROM OTHER COMMON CAUSES OF OBSTRUCTIVE LUNG DISEASES IN THE PHILIPPINES, SPECIFICALLY ASTHMA & BRONCHIECTASIS?25
In general, most patients presenting with airways obstruction can be categorized into either COPD or Bronchial asthma based on clinical history, physical examination, radiographic findings, pulmonary function test results and on occasion, a therapeutic trial of medication12,13. Bronchial asthma is also a chronic inflammatory disorder of the airways involving other kinds of inflammatory cells. This inflammatory process causes symptoms that are usually associated with widespread but variable airflow obstruction that is often reversible. This is in contrast to the progressive and irreversible airways obstruction of COPD. It may be difficult to differentiate COPD from asthma especially in the elderly who may present with persistent airflow obstruction due to airway remodeling associated with uncontrolled chronic asthma. Since the two conditions are based on distinct disease processes, one must recognize that both may be present simultaneously. Table 4.2 shows the features that may differentiate Bronchial asthma from COPD14. Table 4.214 - Differences Between Asthma and COPD
Features Asthma COPD

27
Onset at a young age Major symptoms Frequently Usually episodic Wheezing Breathlessness Non-productive cough Chest tightness Aeroallergens Occupational antigens Exogenous irritants Exercise Cold air Aspirin and NSAIDs Reflux esophagitis Infections Occasionally present Often present Rhinitis Pale nasal mucosa Prolonged expiration Wheezing Almost never Usually daily Dyspnea with exertion (progressive over time) Productive cough

Triggers

Daily activities Cold air Infections

Smoking history Allergies Physical findings

Complete blood count Alpha-1 antitrypsin level Spirometry

Eosinophilia Normal Reduced FEV1 Reduced FEV1/FVC May be normal when asymptomatic or with treatment Usually present Spirometry may normalize

Usually present and of significant duration Occasionally present Diminished intensity of breath sounds in advanced disease Pursed lip breathing Signs of right heart failure (distended jugular veins, right ventricular heave, loud pulmonic component of the second heart sound, ascites, pedal edema) Early inspiratory crackles Wheezing Polycythemia in advanced disease Occasionally low Reduced FEV1 Reduced FEV1/FVC Reduced values may improve but usually do not return to normal values even with treatment May be present Values usually do not return to normal values

Significant Bronchodilator response in spirometry Lung volumes

TLC is usually normal RV may be increased Normal or increased

Diffusing capacity for carbon monoxide (DLCO) Chest radiograph

TLC may be normal or increased emphysematous changes RV is increased Reduced with emphysematous changes

with

Chest CT scan

Usually normal Occasionally hyperinflated lung fields during attacks Usually normal

Hyperinflation with emphysematous changes Bullae may be present Emphysematous changes, diminished vascularity Blebs, bullae,

Bronchiectasis is characterized by irreversible dilatation of one or more proximal and medium-sized bronchi as a result of destruction of the muscular and elastic supporting tissues of the bronchial walls15. It is another disease which may present itself as chronic airways obstruction. It is common among Filipinos as it can follow necrotizing pneumonias caused by tubercle bacillus and other

28 microorganisms. A high prevalence of asthma in patients with bronchiectasis among Asians has been reported16. Localized bronchiectasis is often present in patients with COPD. As a rule, however, bronchiectasis is characterized by dilatation of the airways rather than narrowing. Cough and sputum production ,frequently purulent, often more severe on awakening are observed in 90% of all patients with bronchiectasis. Radiographic techniques should be requested to support the diagnosis. Chest radiographs are crucial to document regions of increased markings, cavities and atelectasis. When clinical symptoms and plain chest raiographs suggest bronchiectasis, a high resolution computed tomography (HRCT) is the imaging modality of choice for confirming or ruling out the diagnosis17. In all subjects with symptoms of COPD, a possible concomitant diagnosis of tuberculosis should be also be considered especially in the Philippines which is endemic for tuberculosis.

G. ONGOING MONITORING AND ASSESSMENT11

Once COPD is detected and confirmed, ongoing monitoring and assessment should include evaluation of: (1) continued exposure to risk factors, especially tobacco smoke; (2) disease progression and development of complications; (3) pharmacotherapy and other medical treatment; (4) exacerbation history; (5) comorbidities. Monitor Disease Progression and Development of Complications COPD is usually a progressive disease. Lung function can be expected to worsen over time, even with the best available care. Symptoms and objective measures of airflow limitation should be monitored to determine when to modify therapy and to identify any complications that may develop. As at the initial assessment, follow-up visits should include a physical examination and discussion of symptoms, particularly any new or worsening symptoms. A list of commonly asked questions during follow-up visits of COPD patients is provided in Appendix 2. 11 Pulmonary function. A patients decline in lung function is best tracked by periodic spirometry measurements. Useful information about lung function decline is unlikely from spirometry measurements performed more than once a year. Spirometry should be performed if there is a substantial increase in symptoms or a complication.

29 Arterial blood gas measurement. Measurement of arterial blood gas tensions should be performed in all patients with FEV 1 < 50% predicted or when clinical signs of respiratory failure or right heart failure are present. Respiratory failure is indicated by a PaO 2 < 60 mm Hg with or without PaCO 2 > 45 mm Hg in arterial blood gas measurements made while breathing air at sea level. Screening patients by pulse oximetry and assessing arterial blood gases in those with an oxygen saturation (SaO 2 ) < 92% may be a useful way of selecting patients for arterial blood gas measurement. Diagnosis of right heart failure or cor pulmonale. Elevation of the jugular venous pressure and the presence of pitting ankle edema are often the most useful findings suggestive of cor pulmonale in clinical practice. Firm diagnosis of cor pulmonale can be made through a number of investigations, including radiography, electrocardiography, echocardiography, radionucleotide scintigraphy, and magnetic resonance imaging. However, all of these measures involve inherent inaccuracies of diagnosis. Hematocrit. Polycythemia can develop in the presence of arterial hypoxemia, especially in continuing smokers. Polycythemia can be identified by hematocrit > 55%. Exercise testing. Several types of tests are available to measure exercise capacity, and are indicated for preoperative evaluation and pulmonary rehabilitation. Monitor Pharmacotherapy and Other Medical Treatment In order to adjust therapy appropriately as the disease progresses, each followup visit should include a discussion of the current therapeutic regimen. Dosages of various medications, adherence to the regimen, inhaler technique, effectiveness of the current regime at controlling symptoms, and side effects of treatment should be monitored. Monitor Exacerbation History During periodic assessments, health care workers should question the patient and evaluate any records of exacerbations, both self-treated and those treated by other health care providers. Frequency, severity, and likely causes of exacerbations should be evaluated. Increased sputum volume, acutely worsening dyspnea, and the presence of purulent sputum should be noted. Monitor Comorbidities In treating patients with COPD, it is important to consider the presence of concomitant conditions such as bronchial carcinoma, tuberculosis, sleep apnea, and left heart failure. The appropriate diagnostic tools (chest

30 radiograph, ECG, etc.) should be used whenever symptoms (e.g., hemoptysis) suggest one of these conditions.

Research Recommendations:
1. Develop a prediction model to help diagnose and classify COPD using variables that are readily available to the Filipino clinician (e.g., history and PE findings). Such a model may be more useful and acceptable in a developing country such as ours where resources (i.e., spirometers and trained operators) are lacking.

REFERENCES:
1. 2. 3. American Thoracic Society. Medical section of the American Lung Association. Standards for the Diagnosis and Care of Patients with COPD and Asthma. Am Rev Respir Dis 1987; 136: 225-244. Georgopoulos D, Anthonisen SR. Symptoms and signs of COPD. In: Chermiack NS, ed. Chronic Obstructive Pulmonary Disease. Toronto: WB Saunders; 1991. p.357-63. Medical Research Council. Definition and classification of chronic bronchitis for clinical and epidemiological purposes: a report to the Medical Research Council by their committee on the etiology of Chronic Bronchitis. Lancet 1965; 1: 775-80. Burrows B, Niden AH, Barclay WR, Kasik JE. Chronic obstructive lung disease obstruction. Am Rev Respir Dis 1965 ; 665-78. Vermiere P. Definition of COPD. Chapter 1 pp 1-11. In: van Heraarden CLA, Repine JE, Vermiere P, van Weel C (eds): COPD Diagnosis and Treatment. Amsterdam: Excerpta Medica 1996. Kelly CA, Gibson GJ. Relation between FEV1 and peak expiratory flow in patients with COPD. Thorax 1988; 43:335-6. Meliton A, Ocampo-Chuatico MR, Punzal P, de Guia T, Blanco-Limpin ME, Lingad R. The use of PEFR measurement in obstructive airways diseases. Phil J Chest Dis 1999; 7(1): 21-27. McIvor A, Chapman KR. Diagnosis of COPD and differentiation from asthma. Current Opinion in Pulmonary Medicine 1996; 1(2): 148-154. Bone RC. Bronchiectais. Part G Ch. 6 pp. 1-7. In Bone RC (ed.): Pulmonary and Critical Care Vol 1 Mosby Yearbook, St Louis, 1997 Update.

4. 5. 6. 7. 8. 9.

10. Strauss SE, McAlister FA, Sackett DL, Deeks JJ (for the CARE-COAD1 Group). The accuracy of patient history, wheezing, and larngeal measurements in diagnosing obstructive airway disease. JAMA April 2000; 14: 1853-7. 11. Global Initiative for Chronic Obstructive Lung Disease. April 2001; NIH Publication No. 2701B 12. Scott, JA, Mahler DA. Diagnosis of COPD and differentiation from asthma. Curr Opin in Pulm Med 1995;1(2):144149. 13. American Thoracic Society. Medical section of the American Lung Association. Standards for the diagnosis and care of patients with COPD and asthma. Am Rev Respir Dis 1987; 136: 225-44. 14. Kaliner M, Lemanski, R. Rhinitis and asthma. JAMA 1992;268:2807-2829. 15. Bone RC. Bronchiectasis. Prt G Chap 6 pp 1-7. Bone RC (ed): Pulmonary and Critical Care Vol 1 Mosby Year Book , St. Louis, 1997 Update.

31
16. Ip MS, So SY, Lam, WK, et al. High prevalence of asthma in patients with bronchiectasis in Hongkong. Eur Resp J 1992; 5(4):418023. 17. 18 19. 20. 21. Webb WR. High resolution computed tomography of obstructive lung disease. Radiol Clin North Am 1994:32(4):745-57. Siafakas NM, Vermiere P, Pride NB. Optimal assessment and management of chronic obstructive pulmonary disease: A consensus statement of the European Respiratory Society. Eur Resp Journal 1995; 8: 1398-1420. American Thoracic Society-Lung Function Testing: Selection of reference values and interpretative strategies. Am Rev Respir Dis 1991; 144: 1202-18. Sourk RL, Nugent KM. Bronchodilator testing: confidence intervals derived from placebo inhalations. Am Rev Respir Dis 1983; 128:153-7. Ries AL. Response to bronchodilators. In : Clausen J, ed. Pulmonary Function Testing: guidelines and controversies. New York Academic Press; 1982. p. 215-221.

22. Anthonisen NR, Wright EC. Bronchodilator response in chronic obstructive pulmonary disease. Am Rev Respir Dis 1983; 128:153-7. 23. Klein JS, Gamsu G, Webb WR, Golden JA, Muller ML. High Resolution CT diagnosis of emphysema in symptomatic patients with normal chest radiograph and isolated low diffusion capacity. Radiology 1992; 182: 817-21. British Thoracic Society. BTS guidelines for the management of COPD. Thorax 1997; 250-252. Philippine Consensus Report on COPD (1999):

24.

25. Philippine College of Chest Physicians Council on COPD. Diagnosis and Management.

26. Celli B, Cote C, Marin J, et al. The Body Mass Index, Airflow Obstruction, Dyspnea, and Exercise Capcity Index in COPD. New England Journal of Medicine 2004;350:1005-12. 27. Mannino et al. Thorax 2003;58:388-393. 28. Tsounakidou et al. Respiratory Medicine 2004; 98:178-183. 29. Antonelli-Incalzi et al. European Respiratory Journal 2003; 22(3):444-9.

32

VI. HOW DO WE MANAGE PATIENTS WITH STABLE COPD? KEY POINTS:

COPD is a preventable and treatable disease. A holistic approach is needed to address the goals of management of COPD. Smoking cessation is the single most effective way of reducing the risk of developing COPD and delaying its progression. Pharmacologic therapy for COPD are mainly for symptom control, improvement in quality of life, functional capacity and decreasing exacerbation rates and severity as there are no pharmacologic agents that have been shown to decrease mortality in COPD. Bronchodilator use is very important for symptom control in COPD. Inhaled formulations are preferred over oral medications. Pulmonary rehabilitation is considered an essential component in the holistic treatment of the COPD patient.

Stable COPD refers to the usual daily condition of the COPD patient when he or she is not having a new respiratory event or sudden worsening of his or her symptoms. Effective management, therefore, of a COPD patients stable state entails long-term care and aiming for the following goals: 1. 2. 3. 4. 5. 6. 7. 8. delay progression of the disease relieve symptoms improve exercise capacity improve quality of life prevent and treat complications prevent and treat exacerbations reduce mortality affordable treatment with the least side effects

To address these goals in the management of a COPD patient, a holistic approach is needed. Slowing down of disease progression by avoidance of risk factors is of primary importance (Evidence A)1-2. Since smoking is the major risk factor in the development of COPD, smoking cessation is one of the most important strategies to address this goal in the management of COPD. The other goals in the management of COPD are addressed by pharmacologic and non-pharmacologic interventions. A. SMOKING CESSATION

33 Smoking cessation is the single most effective way of reducing the risk of developing COPD and delaying its progression (Evidence A)1,84-85 . Studies have shown that merely reducing the number of cigarettes smoked does not alter the rate of decline in lung function among COPD patients who smoke (Evidence B)86-88. All smokers, therefore, should be offered the most intensive smoking cessation intervention available. These include counseling from physicians and other health professionals, pharmacotherapy, self-help and group programs. The employment of a brief (3-minute) counseling to urge a smoker to quit is a simple yet fairly effective method that can be done by all physicians (Evidence A; see Appendix 3)89-90. Every smoker should be offered this brief counseling at every visit to a health care provider. Medications to aid in smoking cessation are now available in the Philippines (e.g. nicotine gum and varenicline). B. PHARMACOLOGIC MANAGEMENT The goals in instituting pharmacologic therapy for COPD are mainly for symptom control, improvement in quality of life, functional capacity and decreasing exacerbation rates and severity as there are no pharmacologic agents that have been shown to decrease mortality associated with COPD (Evidence A)1,38 1. General principles of pharmacologic management There should be a stepwise increase in treatment depending on symptoms. Regular treatment can be maintained for long periods of time and adjusted accordingly if & when side effects occur. Patients should be monitored regularly to assess treatment response (Evidence D). Each treatment strategy should be patient-specific and should take into consideration not only the severity of symptoms and airflow limitation but also other factors including the presence of comorbidities, complications, frequency and severity of exacerbations, cost and possible adverse effects of treatment (Evidence D).

2. Pharmacologic agents Described below are the different classes of pharmacologic agents used in managing of stable COPD. Monitoring of clinical and objective measures of response to treatment is encouraged. A complete list of the different medications under these classes that are available in the country is found in Appendix 4. a. Bronchodilators

34

Bronchodilators are the mainstay in symptom management for COPD (Evidence A)3-8. The recommended first-line bronchodilators are beta 2-agonists and/or anticholinergic agents (Evidence A)18-22. The inhaled route is preferred over an oral formulation (Evidence A)6,10. Long-acting inhaled bronchodilators (e.g. tiotropium, salmeterol, formoterol) have been shown to be more effective and convenient than short-acting bronchodilators, however, these agents are more expensive than the short-acting preparations (Evidence A)27-33. Methylxanthine derivatives are recommended as second-line drugs (Evidence A)9-14. Depending on the severity of symptoms, regular treatment with one or more bronchodilators with different mechanisms and durations of action can be given to improve the degree of bronchodilation for equivalent or lesser side effects (Evidence A)15,1718,20. When treatment is given through the inhalational route, COPD patients may have problems with effective coordination, thus it is essential to ensure that inhaler technique is correct and/or spacer devices are utilized (Evidence D)23. Wet nebulizers are not recommended for regular treatment of stable disease (Evidence B)24-25. Beta2-agonists relax airway smooth muscle by stimulating Beta 2-adrenergic receptors which results in functional antagonism of bronchoconstriction. There are short- and long-acting preparations with durations of action ranging from 4 6 hours and 8 12 hours, respectively7-8,22. Oral and inhaled formulations are available, however, the oral preparations have a slower onset and have more systemic side effects than the inhaled form (Evidence A)6,10. The most frequent side effects of eta 2-agonist treatment include resting sinus tachycardia, somatic tremors, hypokalemia, and mild decrease in arterial oxygenation6, 21. Anticholinergic medications block the effect of acetylcholine on muscarinic (M2 and M3) receptors and may also modify transmission at the pre-synaptic junction15. Short-acting (6 8 hours for ipratropium bromide) and long-acting (up to 24 hours for tiotropium bromide) inhaled preparations are currently available. Studies have shown superiority of tiotropium over placebo and regular ipratropium bromide in improving lung function, symptoms, quality of life and decreasing exacerbations in patients with moderate to severe COPD (Evidence A)28-33,114. Lung function improvement was also significantly larger with tiotropium compared to long-acting B2 agonists over 6-12 months (Evidence B Cochrane review by Barr et al 2007). The most frequent side effect with inhaled anticholinergic use is dryness of the mouth. The incidence of urinary retention and acute glaucoma with ipratropium bromide nebulization is similar to placebo drug use34.

35 The mechanisms of action of methylxanthines and xanthine derivatives still remain controversial, with the non-selective inhibition of phosphodiesterases and stimulation of diaphragmatic contractility among its proposed effects 26. Theophyllines have been proven effective in COPD, however, some studies have demonstrated the lack of additional bronchodilation upon adding theophylline to other bronchodilators and more side effects with theophylline compared to beta 2 agonists and/or anticholinergic agents (Evidence B)9-14. Thus, methylxanthine derivatives like theophylline and doxofylline are still considered as second line drugs in COPD. The side effects associated with theophylline use are headache, insomnia, nausea, heartburn and the more severe adverse effects are convulsions, atrial and ventricular arrhythmias that are dose-related. Doxofylline on the other hand has been noted to be better tolerated and to have lesser side effects (Evidence B)96-98. Combination therapy with bronchodilators having different mechanisms and durations of action may increase the degree of bronchodilation for equivalent or lesser side effects. A number of preparations are currently available, and combinations of inhaled 2-agonists and anticholinergic agents have been found to produce greater and more sustained improvements in FEV1 than either drug alone (Evidence B)15-20. A number of studies have also proposed the use of an inhaled 2-agonist and corticosteroid combination for the treatment of stable COPD45,99, however further evidence is being awaited before it can be recommended for routine use. (delete in red) b. Corticosteroids There are only specific situations where steroids have a role in COPD. 1. Oral Corticosteroids With numerous studies documenting lack of benefit and occurrence of adverse effects, long-term treatment with oral corticosteroids is not recommended in COPD (Evidence A) 36-44. 2. Inhaled Corticosteroids Inhaled corticosteroids are recommended for maintenance therapy in any of the following situations: a. The patient has repeated exacerbations (e.g. 3 exacerbations in 3 years) (Evidence A) 36-44

b. The patient has at least a severe form of COPD (FEV1 < 50% of predicted) (Evidence A) 36-44

36

Regular treatment with inhaled steroids have been shown to decrease the number of exacerbations and improve health status in these types of COPD patients (Evidence A) and withdrawal of inhaled glucocorticosteroids can lead to exacerbations in some of these patients37-44. The long-term safety of inhaled corticosteroids in COPD is still not established, however, a recent 3-year trial noted pneumonia to be significantly higher among those given inhaled steroids. The overall frequency of pneumonia in this trial was not clinically significant and it did not lead to more exacerbations, hospitalizations nor deaths among the affected patients. c. Combination Inhaled Corticosteroids-Long acting beta 2-agonists Inhaled corticosteroids combined with long-acting beta 2-agonist are more effective than its individual components (Evidence A) (Reference: TORCH, Cochrane review of 6 ICS-LABA trials) . In a large 3-year randomized trial, the mortality rate among the COPD patients given inhaled salmeterol-fluticasone was not statistically different from its individual components and from placebo. However, the decline in FEV1 and the other therapeutic endpoints (e.g. exacerbations, quality of life, symptoms) were significantly improved with combination inhaled corticosteroid-long acting B2 agonist therapy compared to its individual components and placebo. The incidence of pneumonia was higher among those given an inhaled steroid component in this trial and such a finding warrants further investigation. d. Immunization There is strong data to support the efficacy of influenza vaccination in reducing serious illness and even death in COPD patients (Evidence A)54-58. Vaccine derived from the most recent strains should be given every year once the new set of vaccines for the year is available (Evidence D). Pneumococcal vaccination is recommended for COPD patients 65 years and older and is also adviced for younger COPD patients with FEV1 < 40% predicted (Evidence B)59-60. (references) e. Mucolytics/Anti-oxidants The widespread use of mucolytic agents cannot be recommended on the basis of present evidence (Evidence B)46. In a large randomized trial, long term use of oral N-acetylcysteine did not decrease the frequency of exacerbations save for those not yet maintained on inhaled corticosteroids (Evidence B)47-50 (add Decramer study as reference)

37 f. Immunomodulators Based on the results of a local meta-analysis on the efficacy of immunomodulators in COPD, its use is not recommended as it does not cause a reduction in the frequency of COPD exacerbations (Evidence B)51. Anti-leukotriene drugs currently used for bronchial asthma have not been found to be useful in COPD (Evidence D)100-101. g. Antibiotics The use of antibiotics other than for treating bacterial infectious exacerbations of COPD is not recommended (Evidence A)52. h. Antitussives The regular use of antitussives in COPD patients is not advisable because cough has a significant protective role (Evidence D)53. i. Oxygen Oxygen therapy can be administered in three ways: long-term continuous therapy, during exercise, and to relieve acute dyspnea. The primary goal of oxygen therapy is to increase the baseline PaO2 to at least 60 mmHg and/or to produce arterial oxygen saturation (SaO2) of at least 88-90%. Long-term oxygen therapy (LTOT) has been shown not only to improve survival but also to improve hemodynamics, exercise capacity, lung mechanics, and mental state in patients with COPD and chronic respiratory failure (Evidence A)61-63 Long-term oxygen therapy is generally indicated in patients with: PaO2 < 55 mmHg or SaO2 < 88%, with or without hypercapnia (Evidence A)64-65 PaO2 between 55 mmHg 60 mmHg, or SaO2 > 89% but with evidence of pulmonary hypertension, polycythemia (hematocrit > 55%) or peripheral edema suggesting congestive heart failure (Evidence D). Oxygen therapy should be given during exercise in those patients who already meet the criteria for LTOT and/or to those who develop significant oxygen desaturation during exercise (Evidence C). Oxygen can also be given as for short periods to control episodes of severe dyspnea (Evidence D).

38 C. Non-Pharmacologic Management 1. Patient Education Education is regarded as an essential component of care of COPD patients. Patient education alone has no direct effect on symptoms and does not improve exercise performance or lung function (Evidence B)66-67. It may however play a role in improving adaptive skills, the ability to cope with illness and acute exacerbations, and general health status (Evidence D)68. It is also an effective way to initiate and accomplish smoking cessation, and to initiate discussions and understanding of advance directives and end-of-life issues (Evidence A)69. 2. Pulmonary Rehabilitation70-83 Pulmonary rehabilitation is a multidisciplinary and comprehensive intervention designed for symptomatic patients with chronic respiratory diseases to reduce their symptoms, optimize functional capacity & social participation, and reduce health-care costs through helping stabilize their disease. Comprehensive pulmonary rehabilitation programs include patient assessment, exercise training, education, and psychosocial support. Pulmonary rehabilitation is considered an essential component in the holistic treatment of the COPD patient regardless of the severity of his lung function abnormality (Evidence A). Among the proven benefits of pulmonary rehabilitation in COPD are (Evidence A): Improvement in exercise capacity Reduction in the perceived intensity of breathlessness Improvement in health-related quality of life Reduction in the number of hospitalizations and days in the hospital Reduction in the anxiety and depression associated with COPD Lower extremity exercise training is the necessary component in a pulmonary rehabilitation program (Evidence A). Strength & endurance training of the upper limbs improves arm function (Evidence B). Respiratory muscle training may be beneficial, especially when combined with general exercise training (Evidence C). Psychosocial intervention is also helpful (Evidence C). There is no consensus on the optimal duration of pulmonary rehabilitation this may range from 4 weeks to 12 weeks (Evidence B). The minimum length of an effective rehabilitation program is two months; the longer the program continues, the more effective the results (Evidence B) 115-117. The benefits of pulmonary rehabilitation may extend well beyond the immediate period after training (Evidence B).

39

Pulmonary rehabilitation is currently available in several medical centers (see Appendix 5 ). 3. Nutrition Several studies have noted that a low body weight and muscle wasting are independent risk factors for mortality in COPD patients (Evidence C). Specific nutritional recommendations, however, seem to have no significant effect on long-term outcomes of COPD patients (Evidence B). A balanced diet though is recommended for any COPD patient. 4. Surgery Surgical intervention for COPD may include bullectomy, lung volume reduction surgery or lung transplantation. Bullectomy or the removal of large bullae may improve gas exchange and reduce dyspnea in carefully selected patients (Evidence C)102. Lung volume reduction surgery (LVRS) entails resection of some parts of the lungs to reduce hyperinflation, improve the mechanical efficiency of the diaphragm and other respiratory muscles, and improve the elastic recoil pressure of the lung. LVRS has been shown to improve the lung function, exercise capacity and quality of life in some patients (Evidence C). Lung volume reduction surgery, though, is not advised for patients who have a low FEV1 (< 20%) and, either homogenous emphysema or a very low carbon monoxide diffusing capacity (Evidence A) 102,108. No local studies on LVRS have been published.

40 D. MANAGEMENT CONTINUUM FOR STABLE COPD

The stepwise holistic approach to treatment based on the severity classification for COPD can be summarized in this diagram. As the disease is assessed to be more severe, different pharmacologic and non-pharmacologic interventions are added on or combined to maximize control of the disease with due consideration of the cost entailed by treatment.

When there are limitations to performing spirometry to properly classify the severity of a patients COPD, treatment may still be initiated and the same principle of stepwise increase in treatment should guide the physician.
Table 5.1. Diagram on the stepwise holistic approach to treatment of a stable COPD patient.
Avoidanc e of risk factors & education X Smoking cessation Influenz a& Pneumo coccal vaccinat ion X RECOMMENDED TREATMENT Short-acting Regular use of Inhaled Bronchodilator single or steroid as needed for combined s *** symptoms* Bronchodilators ** X Pulmonary Rehabilitatio n Others:

STAGE

Stage I: Mild COPD Stage II: Moderate COPD Stage III: Severe COPD Stage IV: Very Severe COPD

Consider surgical treatment options Longterm oxygen therapy if with persistent hypoxemia, respiratory failure Consider surgical treatment options

* Short-acting bronchodilators PRN for symptoms: - Inhaled preferred over oral formulation - Short-acting beta-2 agonists or anticholinergic agents are preferred **Regular use of bronchodilators: - Inhaled preferred over oral formulation. - Inhaled long acting bronchodilators are preferred (e.g. tiotropium, salmeterol, formoterol) although regular and frequent administration of short-acting bronchodilators may be used. If symptoms are still not controlled, a combination of bronchodilators with different

41
pharmacologic sites of action or combination with other pharmacologic classes (e.g. inhaled corticosteroids) can be given to maximize symptom control. - Long acting anticholinergic agent preferred as the single long acting bronchodilator for regular daily use. *** Inhaled corticosteroids: Recommended if the patient has: > significant symptoms > repeated exacerbations (e.g. 3 exacerbations in 3 years) > severe to very severe COPD - documented lung function response with regular use - Inhaled corticosteroid-long acting beta 2 agonist combination: its indications are similar to inhaled corticosteroids as a class although it is more effective than its individual components.

42

43

VII. HOW DO WE MANAGE A COPD PATIENT IN ACUTE EXACERBATION?

KEY POINTS: Acute exacerbation is a new respiratory event or complication superimposed upon established COPD. The most common causes of a COPD exacerbation are infection of the tracheobronchial tree and air pollution. Acute exacerbation can be treated at home or in the hospital using step-wise approaches. Increase in bronchodilator therapy, use of systemic glucocorticosteroids as indicated, controlled oxygen therapy and use of antibiotics when indicated, and vigilant monitoring of the COPD patient are the common therapeutic interventions during an acute exacerbation.

A. DEFINITION OF COPD IN ACUTE EXACERBATION It is recognized that an acute exacerbation of COPD is difficult to define and that its pathogenesis is poorly understood.59 The difficulties in obtaining a standard definition for an exacerbation stem from two main issues: fluctuation of symptoms and the role of co-morbid conditions. As a generalization however, most published definitions characterize an acute exacerbation as a new respiratory event or complication superimposed upon established COPD. Acute exacerbation of COPD is presented as the worsening of the previous stable situation.1-5 Most definitions embrace some combination of the following three clinical findings: worsening of dyspnea, increase in sputum purulence, and increase in sputum volume. In COPD exacerbations, there is a sustained worsening of the patients condition from the stable state and beyond normal day- to-day variations, that is acute in onset and necessitates a change in regular medications for COPD.3 Conditions that may mimic an acute exacerbation include pneumonia, congestive heart failure, pneumothorax, pleural effusion, pulmonary embolism, and arrhythmia.2

44

B. COMMON CAUSES OF ACUTE EXACERBATION OF COPD The most common causes of an exacerbation are infection of the tracheobronchial tree and air pollution, but the cause of about one-third of severe exacerbations cannot be identified (Evidence B). 2

Fig. 5.1. Common Causes of Acute Exacerbations of COPD2

Primary Secondary Tracheobronchial infection Air pollution Pneumonia Pneumothorax Pulmonary embolism Right and/or left heart failure or arrhythmias Inappropriate use of sedatives, narcotics, Bblocking agents Rib fractures/chest trauma

45 C. SEVERITY CLASSIFICATION OF COPD IN ACUTE EXACERBATION Unlike the staging systems for stable COPD, there are no standardized and validated grading systems for severity of an acute exacerbation. Assessment of the severity of an acute exacerbation is based on the patients medical history before the exacerbation, symptoms, physical examination, lung function tests, arterial blood gas measurements, and other laboratory tests.2 Fig 5.2. Medical History and Signs of Severity of Acute Exacerbations of COPD 2, 6-12 Signs of Severity Medical History Use of accessory Duration of worsening or respiratory muscles new symptoms Paradoxical chest Number of previous wall movements episodes Worsening or new (exacerbations/hospitalizati onset central ons) cyanosis Present treatment regimen Development of peripheral edema Hemodynamic instability Signs of right heart failure Reduced alertness

46 D. HOME MANAGEMENT Acute exacerbation can be treated at home when patients present with the following clinical conditions: (a) mild to moderate breathlessness, (b) normal level of consciousness, and (c) generally good condition and level of activity (Evidence C)2. The algorithm reported in Fig 5.3 may assist in the management of an acute exacerbation at home; a stepwise therapeutic approach is recommended.2 Fig. 5.3. Algorithm for the Management of an Acute Exacerbation of COPD at Home
Initiate or increase bronchodilator therapy Consider antibiotics Reassess within hours

Resolution or improvement of signs & symptoms

No resolution or improvement

Add oral corticosteroids Continue management Step down when possible

Reassess within hours

Worsening of signs/symptoms Review Long- term management Refer to hospital

47

1. Bronchodilator therapy Home management of COPD exacerbations involves increasing the dose and/or frequency of existing bronchodilator therapy (Evidence A). If not already used, an anticholinergic can be added until symptoms improve.2 2. Antibiotics Antibiotic use is recommended if the patient has evidence of bacterial infection such as fever, increased sputum volume and purulence, leukocytosis, or change in the chest radiograph (Evidence B).22-27 The antibiotic of choice should reflect known local pattern of resistance. 3. Glucocorticosteroids Systemic glucorticosteroids are beneficial in the management of COPD in acute exacerbation. They hasten recovery and restore lung function more quickly (Evidence A).19-21, 28, 29 Short course systemic corticosteroids should be considered in patients with acute exacerbation who are unresponsive to aggressive inhaled bronchodilator therapy or for patients whose baseline FEV1 < 50% predicted. A dose of 40 mg prednisolone per day for 10 days is recommended (Evidence D).2 E. HOSPITAL MANAGEMENT The risk of dying from an acute exacerbation of COPD is closely related to the development of respiratory acidosis, the presence of significant comorbidities, and the need for ventilatory support.13 Patients with these conditions and those with severe underlying COPD often require hospitalization.

48 Figure 5.4. Algorithm for the Management of an Acute Exacerbation of COPD in the Hospital
Patients with COPD in acute exacerbation presenting at the Emergency Room/Hospital

Initial Management Diagnostics:Chest Xray, ABG Therapeutics: Controlled oxygen therapy Bronchodilators Oral or IV glucocorticosteroids Consider Antibiotics

ICU admission indicated? No

Yes

Admit to ICU

With initial indications for Hospital admission? No Worsening or no improvement of symptoms to initial management within 60 mins? No Continue present treatment Reassess after 4 hours

Yes

Admit to wards

Yes

Admit to wards or ICU

Improvement sustained for 4 hours?

Yes

Consider home treatment

No

Admit to wards or ICU

49

1. Initial Management of exacerbations of COPD in the Emergency Department or the Hospital a. Assess severity of symptoms, blood gases, chest x-ray31 b. Administer controlled oxygen therapy if the patient is hypoxemic. Repeat arterial blood gas measurement 30 minutes after to determine adequacy of oxygen therapy (PaO2 > 60 mmHg, or O2 saturation > 90%). Venturi masks are more accurate sources of controlled oxygen than are nasal prongs. c. Bronchodilator therapy:31 Increase doses or frequency of inhaled bronchodilators Combine beta-2 agonists and anticholinergics32,33 Use spacers or nebulizers Consider adding intravenous aminophylline, if needed 34,35 Inhaled short-acting Beta-2 agonists and anticholinergic agents, as bronchodilators, have similar effects on spirometry and a greater effect than all parenterally administered bronchodilators (that is, parenteral methyxanthines and sympathomimetics) (Evidence A). Both inhaled beta-adrenergic agonists and anticholinergic agents can improve airflow during acute exacerbations of COPD.31,60-62 Beta-adrenergic agonists have not been shown to be superior to anticholinergic agents. 31,60-63 Factors such as time to peak effect (which is slightly more rapid with beta-adrenergic agonists) and the frequency of adverse effects (which are generally fewer and milder with ipratropium bromide) may influence the choice of agents for a given patient. A recent meta-analysis61 supports a strategy of initial use of an inhaled anticholinergic agent, with subsequent addition of a betaadrenergic agonist only if it is needed despite the use of maximal doses of the anticholinergic medication (Evidence B). Equivalent bronchodilation appears to be achieved with the use of metered-dose inhalers or nebulizers (Evidence A). In more severe exacerbation, addition of an oral or intravenous methylxanthine to the treatment can be considered. 2, 34, 35, 60, 63-66 (Evidence B). However, close monitoring of serum theophylline is recommended to avoid the side effects of these drugs2.

50

d. Start oral or intravenous glucocorticosteroids19-21, 31 Oral or intravenous glucocorticosteroids are recommended as an addition to bronchodilator therapy in the hospital management of acute exacerbation of COPD (Evidence A). Thirty to 40 mg of oral prednisone daily for 10 to 14 days is a reasonable compromise between efficacy and safety.2 (Evidence D). The optimal duration of corticosteroid therapy for an acute exacerbation of COPD remains uncertain, but recent data support a course of 5-10 days.20, 67,68 Inhaled steroids are not appropriate in the treatment of acute exacerbation if COPD. e. Consider antibiotic therapy Consider starting antibiotics when there are signs of possible bacterial infection. Antibiotics may be given by the oral and, occasionally, intravenous route.18 Antibiotics appear to be most useful in patients with severe exacerbation. f. Consider noninvasive mechanical ventilation.31, 36-44 g. At all times: 2. Monitor fluid balance and nutrition45, 46 Consider subcutaneous heparin Identify and treat associated conditions (e.g. heart failure, arrhythmias) Closely monitor the condition of the patient

The inclusion criteria for admission in the Intensive Care Unit (ICU) are:47 a. Severe dyspnea that responds inadequately to initial emergency therapy b. Confusion, lethargy, coma c. Persistent or worsening hypoxemia (PaO2 < 50 mmHg), and/or severe/worsening hypercapnia (PaCO2 > 70 mmHg), and/or severe/worsening respiratory acidosis (pH < 7.30) despite supplemental oxygen and non-invasive positive pressure ventilation (NIPPV).

51 3. The following are indications for hospital assessment or admission for acute exacerbations of COPD (Evidence D): 6, 10, 13-17 Marked increase in intensity of symptoms (severe breathlessness, poor and deteriorating condition or level of activity, reduced alertness) Severe background of COPD New onset cyanosis and peripheral edema Failure of the patient in exacerbation to respond to initial medical management Significant co-morbidities Newly occurring arrhythmias Diagnostic uncertainty Older age Insufficient home support

F. INTENSIVE CARE UNIT MANAGEMENT In life threatening exacerbations of COPD, patients should be admitted to the ICU immediately for ventilatory support. 1. Candidates for NIPPV* during acute exacerbation37 NIPPV increases pH, reduces PaCO2, reduces the severity of breathlessness in the first 4 hours of treatment, and decreases the length of hospital stay (Evidence A).36-44 A. Selection criteria (at least 2 should be present): 1. Moderate to severe dyspnea with use of accessory muscles and paradoxical abdominal motion 2. Moderate to severe acidosis (pH 7.30-7.35) and hypercapnia (PaCO2 > 45-60 mmHg) 3. Respiratory frequency > 25 breaths per minute B. Exclusion criteria (any may be present): 1. Respiratory arrest 2. Cardiovascular instability (hypotension, arrhythmias, myocardial infarction) 3. Somnolence, impaired mental status, uncooperative patient 4. High aspiration risk, viscous or copious secretions 5. Recent facial or gastroesophageal surgery 6. Craniofacial trauma, fixed nasopharyngeal abnormalities 7. Burns 8. Extreme obesity

52 2. Indications for starting invasive mechanical ventilation during acute exacerbation The indications are:47, 48 a. severe dyspnea with use of accessory muscles and paradoxical abdominal motion b. respiratory frequency > 35 breaths per minute c. life-threatening hypoxemia (PaO2 < 40 mmHg or PaO2/FiO2 < 200) d. severe acidosis (pH < 7.25) and hypercapnia (PaCO2 > 60 mmHg) e. respiratory arrest f. somnolence, impaired mental status g. cardiovascular complications (hypotension, shock, heart failure) h. Other complications (metabolic abnormalities, sepsis, pneumonia, pulmonary embolism, barotraumas, massive pleural effusion) i. NIPPV failure or with exclusion criteria G. HOSPITAL DISCHARGE AND FOLLOW-UP 1. Discharge criteria:17, 49-53 a. inhaled beta 2 agonist therapy is required no more frequently than every 4 hours b. patient, if previously ambulatory, is able to walk across the room. c. patient is able to eat and sleep without frequent awakening by dyspnea d. patient has been clinically stable for 12-24 hours e. arterial blood gases have been stable for 12-24 hours f. patient (or home caregiver) fully understands correct use of medications. g. Follow-up and home care arrangements have been completed (e.g. visiting nurse, oxygen therapy, meal provisions) h. Patient, family, and physician are confident that the patient can manage successfully at home. 2. Follow-up assessment Ideally, the patient should be followed at 4-6 weeks after discharge. The following components are assessed:54

53 a. b. c. d. e. ability to cope in the usual environment measurement of FEV1 reassessment of inhaler technique understanding of recommended treatment regimen need for long-term oxygen therapy (for patients with severe COPD).

H. SPECIALIST REFERRAL The following conditions or events in COPD patient may warrant referral to a pulmonary medicine specialist for further management: REASON There is diagnostic uncertainty Suspected severe COPD The patient requests a opinion Onset of cor pulmonale second PURPOSE Confirm diagnosis and optimize therapy Confirm diagnosis and optimize therapy Confirm diagnosis and optimize therapy Confirm diagnosis and optimize therapy Optimize therapy and measure blood gases Optimize therapy and exclude inappropriate prescriptions Justify need for long-term treatment or supervise withdrawal Identify candidates for surgery Encourage early intervention Identify candidates for pulmonary rehabilitation Identify candidates for surgery

Assessment for oxygen therapy

Assessment for long-term nebuliser therapy Assessment for oral corticosteroid therapy Bullous lung disease A rapid decline in FEV1 Assessment for pulmonary rehabilitation Assessment for lung volume reduction surgery Assessment for lung transplantation Identify candidates for surgery Dysfunctional breathing Confirm diagnosis, optimize pharmacotherapy and access other therapists Aged under 40 years or a family Identify alpha-1 antitrypsin history of alpha-1 antitrypsin deficiency, consider therapy and deficiency screen family Uncertain diagnosis Make a diagnosis Symptoms disproportionate to lung Look for other explanations function deficit

54 Frequent infections Exclude bronchiectasis; optimize therapy and preventive measures Hemoptysis Exclude carcinoma of the bronchus, tuberculosis and other conditions Preoperative clearance & Optimize perioperative perioperative management for management and prevent complicated or extensive surgery perioperative complications I. ETHICAL ISSUES

All patients with COPD developing acute respiratory failure should be considered for intubation and mechanical ventilation. However, in patients who have poor baseline function, marginal nutritional status, severely restricted activity levels and inexorable deterioration of their latestage pulmonary dysfunction, the decision to forego intubation should be referred to a Bioethics Task Force. It is also recommended in our setting that the following be carried out: 1. Creation of a Bioethics Task Force created from the different local medical societies to set guidelines on the withholding and withdrawal of mechanical ventilatory support based on ethical principles. 2. Establishment of an ethics committee in hospitals to help physicians identify, analyze and resolve ethical problems in patient care. 3. Development by medical societies of a consensus on the definition of quality of life to guide clinical management in the institution of life-sustaining therapy. RESEARCH RECOMMENDATIONS: 1. Develop a reproducible, transportable definition of acute exacerbation in order to provide more consistent and transparent inclusion and exclusion criteria for clinical trials studying this entity. 2. Conduct randomized placebo controlled trials of the newer broadspectrum antibiotics. 3. Research on optimal dose and duration of systemic corticosteroids in acute exacerbation. 4. Research on strategies aimed at preventing and aborting exacerbations. 5. Research on the role of environmental factors and infectious agents in exacerbations.

55

REFERENCES:
1. 2. Gerogopoulos D, Anthonisen NR. Symptoms and signs of COPD. In Cherniak NS (ed.) Chronic Obstructive Pulmonary Disease. Philadelphia: Saunders, 1991: 357-363. Global Initiative for Chronic Obstructive Lung Disease. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. NHLBI/WHO Workshop Report. National Institutes of Health. National Heart, Lung, and Blood Institute. Publication Number 2701. March 2001. Rodriguez-Roisin R. Toward a consensus definition for COPD exacerbations. Chest May 2000; 117(5 Suppl 2): 398S-401S. Huchon G. Epidemiological data on chronic bronchitis in France. Presse Medical October 27, 2001; 30(31 Pt 2): 7-10. Fein A, Fein AM. Management of acute exacerbations in chronic obstructive pulmonary disease. Current Opinion in Pulmonary Medicine March 2000; 6(2): 122-126. Almagro P, Calbo E, Ochoa de Echaguen A, Barreiro B, et al. Mortality after hospitalization for COPD. Chest May 2002; 121(5): 1441-1448. Lau AC, Yam LY, Poon E. Hospital readmission in patients with acute exacerbation of chronic obstructive pulmonary disease. Respiratory Medicine November 2001; 95(11): 876884. Garcia-Aymerich J, Monso E, Marrades RM, Escarrabill J, et al. Risk factors for hospitalization for a chronic obstructive pulmonary disease exacerbation EFRAM study. American Journal of Respiratory and Critical Care Medicine September 15, 2001; 164(6): 1002-7. Vitacca M. Exacerbations of COPD: predictive factors, treatment and outcome. Monaldi Archives for Chest Disease April 2001; 56(2): 137-143. Miravitlles M, Guerrero T, Mayordomo C, Sanchez-Agudo L, et al. Factors associated with increased risk of exacerbation and hospital admission in a cohort of ambulatory COPD patients: a mutiple logistic regression analysis. The EOO Study Group. Respiration 2000; 67(5): 495-501. Seemungal TA, Donaldson GC, Bhowmik A, Jeffries DJ, et al. Time course and recovery of exacerbations in patients with chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine May 2000; 161(5): 1608-1613. Dewan NA, Rafique S, Kanwar B, Satpathy H, et al. Acute exacerbation of COPD: factors associated with poor treatment outcome. Chest March 2000; 117(3): 662-671. Connors AF Jr., Dawson NV, Thomas C, Harrell FE Jr., et al. Outcomes following acute exacerbation of severe chronic obstructive lung disease. The SUPPORT investigators (Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments). American Journal of Respiratory and Critical Care Medicine 1996; 154: 959-967. Ojoo JC, Moon T, McGlone S, Martin K, et al. Patients and carers preferences in two models of care for acute exacerbations of COPD: results of a randomized controlled trial. Thorax February 2002; 57(2): 167-169. Roberts CM, Lowe D, Bucknall CE, Ryland I, et al. Clinical audit indicators of outcome following admission to hospital with acute exacerbation of chronic obstructive pulmonary disease. Thorax February 2002; 57(2): 137-141. Pant PK, Owen JL, Elliot MW. Non-invasive ventilation in acute exacerbations of chronic obstructive pulmonary disease: long term survival and predictors of in-hospital outcome. Thorax September 2001; 56(9): 708-712. Kessler R, Faller M, Fourgaut G, Mennecier B, Weitzenblum E. Predictive factors of hospitalization for acute exacerbation in a series of 64 patients with chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine January 1999; 159(1): 158-164. Anthonisen NR, Manfreda J, Warren CP, Hersfield ES, et al. Antibiotic therapy in exacerbations of chronic obstructive pulmonary disease. Annals of Internal Medicine 1987; 106: 196-204.

3. 4. 5. 6. 7. 8.

9. 10.

11. 12. 13.

14. 15. 16. 17.

18.

56
19. Thompson WH, Nielson CP, Carvalho P, Charan NB, Crowley JJ. Controlled trial of oral prednisone in outpatients with acute COPD exacerbation. American Journal of Respiratory and Critical Care Medicine 1996; 154: 407-412. 20. Davies L, Angus RM, Calverley PM. Oral corticosteroids in patients admitted to hospital with exacerbations of chronic obstructive pulmonary disease: a prospective randomized controlled trial. Lancet 1999; 354: 456-460. 21. Niewoehner DE, Erbland ML, Deupree RH, Collins D, et al. Effect of systemic corticosteroids on exacerbations of chronic obstructive pulmonary disease. Department of Veterans Affairs Cooperative Study Group. New England Journal of Medicine 1999; 340: 1941-1947. 22. American College of Physicians Task Force on Adult Immunization. Infectious Disease Society of America. Guide for adult immunization. 2 nd ed. Philadelphia. American College of Physicians, 1990. 23. Shapiro ED, Berg AF, et al. The protective efficacy of polyvalent pneumococcal polysaccharide vaccine. New England Journal of Medicine 1991; 325: 1453-1460. 24. Seretta M, Di Stephano A, et al. Activated T-lymphocytes and macrophages in bronchial mucosa of subjects with chronic bronchitis. American Review of Respiratory Disease 1993; 147: 306-310. 25. Russo R, DAprille M. Role of antimicrobial therapy in acute exacerbation of chronic obstructive pulmonary disease. Annals of Pharmacotherapy May 2001; 35(5): 576-581. 26. Stockley RA, OBrien C, Pye A, Hill SL. Relationship of sputum color to nature and outpatient management of acute exacerbation of COPD. Chest June 2000; 117(6): 1638-1645. 27. Adams SG, Melo J, Luther M, Anzueto A. Antibiotics are associated with lower relapse rates in outpatients with acute exacerbation of COPD. Chest May 2000; 117(5): 1345-1352. 28. Maltais F, Ostinelli J, Bourbeau J, Tonnel AB, et al. Comparison of nebulized budesonide and oral prednisolone with placebo in the treatment of acute exacerbations of chronic obstructive pulmonary disease: a randomized controlled trial. American Journal of Respiratory and Critical Care Medicine March 1, 2002; 165(5): 698-703. 29. Saymer A, Aytemur ZA, Cirit M, Unsal I. Systemic glucocorticoids in severe exacerbations of COPD. Chest March 2001; 119(3): 726-730. 30. Wood-Baker R, Walters EH, Gibson P. Oral corticosteroids for acute exacerbation of chronic obstructive pulmonary disease. [update of Cochrane Database Systematic Reviews. 2000; (2): CD001288; 10796635.], 2001. 31. Bach PB, Brown C, Gelfand SE, McCrory DC. American College of Physicians-American Society of Internal Medicine. American College of Chest Physicians. Management of acute exacerbations of chronic obstructive pulmonary disease. Annals of Internal Medicine April 3, 2001; 134(7): 600-620. 32. Moayyedi P, Congleton J, Page RL, Pearson SB, et al. Comparison of nebulised salbutamol and ipratropium bromide with salbutamol alone in the treatment of chronic obstructive pulmonary disease. Thorax 1995; 50: 834-837. 33. Fernandez A, Munoz J, de la Calle B, Alia I, et al. Comparison of one versus two bronchodilators in ventilated COPD patients. Intensive Care Medicine 1994; 20: 199-202. 34. Barbera JA, Reyes A, Roco J, Montserrat JM, et al. Effect of intravenously administered aminophylline on ventiation/perfusion inequaity during recovery from exacerbations of chronic obstructive pulmonary disease. American Review of Respiratory Disease 1992; 145: 1328-1333. 35. Mahon JL, aupacis A, Hodder RV, McKim DA. Theophyline for irreversible chronic airflow limitation: a randomized study comparing n of 1 trias to standard practice. Chest 1999; 115: 38-48. 36. Meyer TJ, Hill NS. Noninvasive positive pressure ventilation to treat respiratory faiure. Annals of Internal Medicine 1994; 120: 760-770. 37. Clinical indications for noninvasive positive pressure ventilation in chronic respiratory failure due to restrictive lung disease, COPD, and nocturnal hypoventilation- a consensus conference report. Chest 1999; 116: 521-534. 38. Bott J, Carroll MP, Conway JH, Keilty SE, et al. Randomised controlled trial of nasal ventilation in acute ventilatory failure due to chronic obstructive airways disease. Lancet 1993; 341: 1555-1557.

57
39. Plant PK, Owen JL, Eliott MW. Early use of non-invasive ventilation for acute exacerbations of chronic obstructive pulmonary disease on general respiratory wards: a multi-centre randomised controlled trial. Lancet 2000; 355: 1931-1935. 40. Dikensoy O, Ikidag B, Filiz A, Bayram N. Comparison of non-invasive ventilation and standard medical therapy in acute hypercapnic respiratory failure: a randomised controlled study at a tertiary health center in SE Turkey. International Journal of Clinical Practice March 2002; 56(2): 85-88. 41. Rizvi N, Mehmood N, Hussain N. Role of Bi-pap in acute respiratory failure due to exacerbation of COPD. Journal of Pakistan Medical Association December 2001; 51(12): 414-417. 42. Conti G, Costa R, Maviglia R, Conti M, et al. NIV in the treatment of acute exacerbation of COPD and status asthmaticus. Minerva Anestesiologica April 2001; 67(4): 223-227. 43. Vanpee D, Dalaunois L, Gilet JB. Non-invasive positive pressure ventilation for exacerbation of chronic obstructive pulmonary patients in the emergency department. European Journal of Emergency Medicine March 2001; 8(1): 21-25. 44. Keenan SP, Gregor J, Sibbald WJ, Cook D, et al. Noninvasive positive pressure ventilation in the setting of severe, acute exacerbations of chronic obstructive pulmonary disease: more effective and less expensive. Critical Care Medicine June 2000; 28(6): 2094-2102. 45. Vermeeren MA, Schols AM, Wouter EF. Effects of an acute exacerbation on nutritional and metabolic profile of patients with COPD. European Respiratory Journal October 1997; 10(10): 2264-2269. 46. Saudny-Unterberger H, Martin JG, Gray-Donald K. Impact of nutritional support on functional status during an acute exacerbation of chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine September 1997; 156(3 Pt 1): 794-799. 47. Nevins ML, Epstein SK. Predictors of outcome for patients with COPD requiring invasive mechanical ventilation. Chest June 2001; 119(6): 1840-1849. 48. Vitacca M, Clini E, Porta R, Foglio K, et al. Acute exacerbations in patients with COPD: predictors of need for mechanical ventilation. European Respiratory Journal July 1996; 9(7): 1487-1493. 49. Reguero CR, Hamel MB, Davis RB, Desbiens N, et al. A comparison of generalist and pulmonologist care for patients hospitalized with severe chronic obstructive pulmonary disease: resource intensity, hospital costs, and survival. SUPPORT investigators. Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatment. American Journal of Medicine 1998; 105: 366-372. 50. Mushlin AI, Black ER, Connolly CA, Buonaccorso KM, et al. The necessary length of hospital stay for chronic pulmonary disease. Journal of the American Medical Association 1991; 266: 80-83. 51. Sala E, Alegre L, Carrrera M, Ibars M, et al. Supported discharge shortens hospital stay in patients hospitalized because of an exacerbation of COPD. European Respiratory Journal June 2001; 17(6): 1138-1142. 52. Skwarska E, Cohen G, Skwarski KM, Lamb C, et al. Randomized controlled trial of supported discharge in patients with exacerbations of chronic obstructive pulmonary disease. Thorax November 2000; 55(11): 907-912. 53. Cotton MM, Bucknall CE, Dagg KD, Johnson MK, et al. Early discharge for patients with exacerbations of chronic obstructive pulmonary disease: a randomized controlled trial. Thorax November 2000; 902-906. 54. The COPD Guidelines Group of the Standards of Care Committee of the BTS. BTS guidelines for the management of chronic obstructive pulmonary disease. Thorax 1997; 52 Suppl 5: S1-S28. 55. Lynn J, Ely EW, Zhong Z, McNiff KL, et al. Living and dying with chronic obstructive pulmonary disease. Journal of the American Geriatrics Society May 2000: 48( 5 Suppl): S91S100. 56. Claessens MT, Lynn J, Zhong Z, Desbiens NA, et al. Dying with lung cancer or chronic obstructive pulmonary disease: insights from SUPPORT. Journal of the American Geriatrics Society May 2000; 48(5 Suppl): S146-S153.

58
57. McNeely PD, Hebert PC, Dales RE, OConnor AM, et al. Deciding about mechanical ventilation in end-stage chronic obstructive pulmonary disease: how respirologist perceive their role. Canadian Medical Association Journal January 15, 1997; 156(2): 177-183. 58. Siasfakas NM, Vermeire P, Pride NB, Paoletti P, Gibson J, Howard P, et al. Optimal assessment and management of chronic obstructive pulmonary disease (COPD). The European Respiratory Society Task Force. Eur Respir J 1995; 8:1398-420. 59. American Thoracic Society. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1995; 152:S77-121. 60. McCrory DC, Brown C, Selfand SE, Bach PB. Management of exacerbations of COPD: a summary and appraisal of the published evidence. Chest 2001;119:1190-1209. 61. Snow V, Lascher S, Mottur-Pilson C. Evidence base for management of acute exacerbations of chronic obstructive pulmonary disease. Ann Intern Med 2001;134:595-599. 62. Ferguson GT. Recommendations for the management of COPD. Chest 2000;117:Suppl:23S28S. 63. Sherk PA, Grossman RF. The chronic obstructive pulmonary disease exacerbation.. Clin Chest Med 2000;21:705-721. 64. Wrenn K, Slovis CM, Murphy F, Greenberg RS. Aminophylline therapy for acute bronchospastic disease in the emergency rrom. Ann Intern Med 1991;115:241-247. 65. Rice KL, Leatherman JW, Duane PG, et al. Aminophylline for acute exacerbations of chronic obstructive pulmonary disease: a controlled trial. Ann Intern Med 1987;107:305-309. 66. Siedenfeld JJ, Jones WN, Moss RE, Trem,per J. Intravenous aminophylline in the treatment of acute bronchospastic exacerbations of chronic obstructive pulmonary disease. Ann Emerg Med 1984; 13:248-252. 67. Sayiner A, Aytemur ZA, Cirit M, Unsal I. Systemic glucocorticosteroids in severe exacerbations of COPD. Chest 2001;119:726-730. 68. Stanbrook MB, Goldstein RS. Steroids for acute exacerbations of COPD: how long is enough? Chest 2001;119:675-676. 69. National Institute for Clinical Excellence: National Collaborating Centre for Chronic Conditions. Clinical Guideline 12: COPD: Management of COPD in adults in primary and secondary care. February 2004. www.nice.org.uk/CG012NICEguideline.

59 APPENDIX SECTION. APPENDIX 1. SUGGESTED QUESTIONS FOR FOLLOW-UP VISITS OF COPD PATIENTS.

assessment instrument. The validity and reliability of these questions Suggested Questions for Follow-Up Visits* *These questions are examples and do not represent a standardized assessment instrument. The validity and reliability of these questions have not been assessed. Monitor exposure to risk factors: Have you continued to stay off cigarettes? If not, how many cigarettes per day are you smoking? Would you like to quit smoking? Has there been any change in your working environment? Monitor disease progression and development of complications: How much can you do before you get short of breath? (Use an everyday example, such as walking up flights of stairs, up a hill, or on flat ground.) Has your dyspnea worsened, improved, or stayed the same since your last visit? Have you had to reduce your activities because of dyspnea or other symptoms? Have any of your symptoms worsened since your last visit? Have you experienced any new symptoms since your last visit? Has your sleep been disrupted due to dyspnea or other symptoms? Since your last visit, have you missed any work because of your symptoms? Monitor pharmacotherapy and other medical treatment: What medications are you taking? How often do you take each medication? How much do you take each time? Have you missed or stopped taking any regular doses of your medications for any reason? Have you had trouble filling your prescriptions (e.g., for financial reasons, not on formulary)? Please show me how you use your inhaler. Have you tried any other medicines or remedies? Has your medication been effective in controlling your symptoms? Has your medication caused you any problems? Monitor exacerbation history: Since your last visit, have you had any episodes/times when your symptoms were a lot worse than usual? If so, how long did the episode(s) last? What do you think caused the symptoms to get worse? What did you do to control the symptoms?

60

REFERENCE: Global Initiative for Chronic Obstructive Lung Disease. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. NHLBI/WHO Workshop Report. National Institutes of Health. National Heart, Lung, and Blood Institute. Publication Number 2701. March 2001.

61 APPENDIX 2. BRIEF SMOKING CESSATION INTERVENTION FOR PHYSICIANS THE THREE MINUTE STRATEGY FOR SMOKING CESSATION INTERVENTION Tobacco smoking and nicotine addiction is a chronic disease and without appropriate interventions, only 2-3% of smokers become nonsmokers each year. The primary care physician plays an important and unique role in promoting smoking cessation due to the fact that at least 70% of smokers see a physician at least once a year. Moreover, 70% of smokers report that they want to quit and have made at least 1 selfdescribed serious quit attempt and cite a physicians advice as a significant motivator. Finally, 90% of smokers admit that they would very likely or somewhat likely follow their physicians advice. With this background, it is important that clinicians are prepared to intervene with tobacco users who are wiling to quit. The five major steps, or the Five As are tabulated below. It is important for the clinician to Ask each patient if he or she uses tobacco (Strategy A1), Advise him or her to quit (Strategy A2), Assess willingness to make a quit attempt (Strategy A3), Assist him or her in his quit attempt (Strategy A4) and Arrange for follow up to prevent relapse (Strategy A5). Patients unwilling to make a quit attempt may lack information about the harmful effects of tobacco or may have fears or concerns about quitting or may be demoralized because of previous relapse. Such patients may respond to motivational intervention that provides the clinician an opportunity to educate, reassure and motivate (the Five Rs). Motivational interventions are most likely to be successful when the clinician is empathic, promotes patient autonomy, avoids arguments and supports the patients self-efficacy. Relapses should not be a source of discouragement as they are the rule rather than the exception in smoking cessation. In the Transtheoretical Model of Change, patients go through the stages of Precontemplation, Contempation, Action and Maintenance in a cyclical manner. Only 5% will go through without ever relapsing. Eighty five percent of patients will cycle back with most of them competing 3 to 4 cycles before they are able to maintain a totally smoke free state. An algorithm is presented to simplify the suggested steps in smoking cessation intervention.

62

THE 5 AS FOR BRIEF INTERVENTION Strategy A1: ASK ASK about tobacco use Identify and document tobacco use status for every patient at every visit.

Action

Strategies for implementation

Implement an Expand the vital signs to include tobacco use or use an office wide system alternative universal identification system. that ensures that, for EVERY patient at EVERY clinic visit, VITAL SIGNS tobacco use status Blood Pressures: _________ is queried and Pulse: ______ Weight: _________ documented. Temperature: _________ RR: _____
Tobacco use: Current Former Never (circle one)

Alternatives to expanding the vital signs are to place tobacco- use status stickers on all patient charts or to indicate tobacco use status using electronic medical records or computer reminder systems.

63

Strategy A2: ADVISE Advise to quit In a clear, strong and personalized manner urge every tobacco user to quit.

Action

Strategies for implementation

In a clear, strong, Advice should be: and personalized manner, urge every Clear I think it is important for you to quit smoking tobacco user to now and I can help you. Cutting down while you are quit ill is not enough. Strong As your clinician, I need you to know that quitting smoking is the most important thing you can do to protect your health now and in the future. The clinic staff and I will help you. Personalized Tie the tobacco use to current health/illness, and or its social and economic costs, motivation level / readiness to quit, and /or the impact of tobacco use on children and others in the household.

64

Strategy A3: ASSESS Assess willingness to make a quit attempt. Is the tobacco user willing to make quit attempt at this time?

Action

Strategies for implementation

Ask every tobacco user if he or she is willing to make a quit attempt at this time (e.g., within the next 30 days)

Assess patients willingness to quit: If the patient is wiling to make a quit attempt at this time, provide assistance If the patient will participate in an intensive treatment, deliver such a treatment or refer to an intensive intervention If the patients clearly states he or she is unwilling to make a quit attempt at this time, provide a motivational intervention If the patient is member of special population (e.g., adolescent, pregnant smoker, racial / ethnic minority), consider providing additional information

65

Strategy A4: ASSIST Assist in quit attempt. For the patient wiling to make a quit attempt, use counseling and pharmacothera py to help him or her quit

Action

Strategies for implementation

Help the patient with a quit plan

A patients preparation for quitting: Set a quit date ideally, the quit date should be within 2 weeks Tell family, friends, and co workers about quitting and request understanding and support Anticipate challenges to planned quit attempt, particularly during the critical first few weeks. These include nicotine withdrawal symptoms. Remove tobacco products from your environment. Prior to quitting, avoid smoking in places where you spend a lot of time (e.g., work, home, car)

Provide practical

ABSTINENCE Total abstinence is essential. Not even a single puff after the quit date.

66

counseling (problem solving/skills training)

PAST QUIT EXPERIENCE Identify what helped and what hurt in previous quit attempts. ANTICIPATE TRIGGERS OR CHALLENGES IN UPCOMING ATTEMPT Discuss challenges/triggers and how patient will successfully overcome them. ALCOHOL Since alcohol can cause relapse, the patient should consider limiting/abstaining from alcohol while quitting. OTHER SMOKERS IN THE HOUSEHOLD Quitting is more difficult when there is another smoker in the household. Patients should encourage housemates to quit with them or not smoke in their presence.

Provide intratreatment social support Help patient obtain extratreatment social support Recommend the use of approved

Provide supportive clinical environment while encouraging the patient in his or her quit attempt. My office staff and I are available to assist you. Help patient develop social support for his or her quit attempt in his or her environments outside of treatment. Ask your spouse/partner, friends and co-workers to support you in your quit attempt. Recommend the use of pharmacotherapy found to be effective. Explain how these medications increase smoking cessation success and reduce withdrawal symptoms. The first-

67

pharmacothera py

line pharmacotherapy medications include: Bupriopion SR, Nicotine gum, nicotine inhaler, nicotine nasal spray and nicotine patch. SOURCES Non-government organizations, local heath units TYPE Culturally/racially/educationally/age appropriate for patient LOCATION Readily available at every clinicians workstation.

Provide supplementary materials

Strategy A5: ARRANGE Arrange follow up Schedule follow up contact preferably within the first week after the quit date.

Action

Strategies for implementation

Schedule followup contact, either in person or via telephone

Timing Follow up contact should occur soon after the quit date, preferably, during the first week. A second follow up contact is recommended within the first month. Schedule further contacts as indicated. Actions during follow up contact Congratulate success. If tobacco use has occurred, review circumstances and elicit recommitment to total abstinence. Remind patient that a relapse can be used as a learning experience. Identify

68

problems already encountered and anticipate challenges in the immediate future. Assess pharmacotherapy use and problems. Consider use or referral to more intensive treatment

69

The 5 Rs of MOTIVATIONAL INTERVENTION

Action Strategies for implementation
Encourage the patient to indicate why quitting is personally relevant, being as specific as possible. Motivational information has the greatest impact if it is relevant to patients disease status or risk, family or social situation (e.g., having children in the home), health concerns, age, gender, and other important patient characteristics (e.g., prior quitting experience, personal barriers to cessation). The clinician should ask the patient to identify potential negative consequences of tobacco use. The clinician may suggest and highlight those that seem most relevant to the patient. The clinician should emphasize that smoking low tar / low nicotine cigarettes or use of other forms of tobacco (e.g., smokeless tobacco, cigars, and pipes) will not eliminate these risks. Examples risks are: Acute risks: Shortness of breath, exacerbation of asthma, harm to pregnancy, impotence, infertility, increase serum carbon monoxide. Long-term risks: Heart attacks and strokes, lung and other cancers (larynx, oral cavity, pharynx, esophagus, pancreas, bladder, cervix), chronic obstructive pulmonary diseases (chronic bronchitis and emphysema), long term disability and need for extended care. Environmental Risks: Increased risk of lung cancer and heart

Relevance

Risks

70

disease in spouses: higher rate of smoking by children of tobacco users; increased risk for low birth weight, SIDS, asthma, middle ear disease, and respiratory infections in children of smokers The clinician should ask the patient to identify potential benefits of stopping tobacco use. The clinician may suggest and highlight those that seem most relevant to the patient. Examples of rewards follow: Improved health Food will taste better Improved sense of smell Save money Feel better about yourself. Home, car, clothing, breath will smell better Can stop worrying about quitting Set a good example for children Have healthier babies and children Not worry about exposing others to smoke Feel better physically Perform better in physical activities Reduced wrinkling / aging of skin The clinician should ask the patient to identify barriers or impediments to quitting and note elements of treatment ( problem solving, pharmacotherapy ) that could address barriers. Typical barriers might include: Withdrawal symptoms Fear of failure Weight gain

Rewards

Roadblocks

71

Repetition

Lack of support Depression Enjoyment of tobacco The motivational intervention should be repeated every time an unmotivated patient visits the clinic setting. Tobacco users who have failed in previous quit attempts should be told that most people make repeated quit attempts before they are successful.

ALGORITHM ON THE SUGGESTED STEPS IN SMOKING CESSATION INTERVENTION

General Population

Contact With physician

Ask About Smoking

Never Smoker

Current Smoker

Former Smoker

Congratulate and reinforce non-smoking status

Advise to stop smoking

Congratulate and reinforce abstinence

Assess stage of Change

Precontemplation

Preparation / Wiling to Quit Now

Contemplation

Arrange Follow-up when willing to discuss concerns & benefits of quitting

Assist: Set Quit Date, Discuss Treatment Options, Consider Pharmacotherapy

Motivate: Discuss Concerns and Benefits of Quitting

Succeed

Fail (recycle)

Arrange Follow-up

No Psychiatric or Alcohol Problem

Psychiatric or Alcohol Problem

Set Quit Date, use combination therapy with other agents

Succeed Arrange Follow-up

Fail Refer

Reference: Treating Tobacco Use and Dependence. Clinical Practice Guideline. U.S. Department of Health and Human Services. June 2000.

APPENDIX 3. COMMONLY ENCOUNTERED DRUGS FOR COPD IN THE PHILIPPINES BY GENERIC NAMES, FORMULATION AND DOSAGE.
GENERIC NAME FORMULATION QUANTITY PER DOSE PRESCRIBED DOSAGE AND FREQUENCY

A. Bronchodilators 1. Anti-cholinergic agents Ipratropium Br UDV or nebule PMDI Inhaled solution Tiotropium Inhaled caps 2. Beta-2 agonists Salbutamol syrup sulfate tablet Controlled Release tablet Pressurized metered dose inhaler (pMDI) nebule Terbutaline syrup sulfate tablet Extended Release tablet Inhaled solution Inhaler Turbuhaler Fenoterol HBr Metered aerosol Procaterol HCl Tablet hemihydrate Syrup pMDI Formoterol tablet fumarate Inhaled caps Turbuhaler pMDI Rotadisk Bambuterol Tablet Clenbuterol Tablet Syrup Tolubuterol Tablet 3. Methylxanthine derivatives Doxofylline tablet Theophylline tablet Salmeterol

0.5mg/2mL 0.02mg/puff 0.025% 18g/cap 2mg/5mL 2mg 4mg, 8 mg 100g/dose 2.5 mg/2.5mL 1.5mg/5mL 2.5mg 5mg/ 5mg/2mL 0.25mg/dose 500g/dose 0.1mg/dose 25g 5g/mL 10g/puff 40g 12g/cap 4.5g/dose, 9g/dose 25g/puff 50g/blister 10mg/tab 10 ug/tab 5 ug/5ml 1 mg, 2 mg

1 vial 3 - 4 times a day 2 puffs 4 times a day up to 12 puffs/day 2 mL 3-4 times a day 1 cap daily 2mg to 4 mg every 6 to 8 hours 1-2 tablets 3-4 times a day 1 tab 2 times a day 1-2 puffs every 4 hours, may use 2 puffs prn for acute symptoms 2.5 mg-5 mg 3-4 times a day 2 tsp- 1 tbsp every 6 to 8 hours 1 tablet 3-4 times a day 1 tablet 2 times a day 2.5 5 mg every 6 hous 1 2 puffs every 6 hrs 1 4 puffs per day up to 4 mg per day 1-2 puffs per day up to 8 puffs per day 1-2 tabs 2 times a day 10 mL 2 times a day 2 puffs every 4 hours and prn 2 tabs 2 times a day 1-2 caps per day 1-2 puffs per day max of 4-6 per day 2 - 4 puffs 2 times a day 1-2 blister 2 times a day 1 tab 1-2 times a day 1 tab 1-2 times a day 10 ml 1-2 times a day 1-2 tabs 2 times a day 1 tab 2 3 times a day 1 tab 3 - 4 times a day 1 tab every 6 hours 1 tab 3 - 4 times a day 1 tab every 12 hrs 1-2 tabs 2 times aday 1 tab daily 1 tab every 12 hrs 5mg 6mg/kg in 20-30 min slow IV infusion 1-2 puffs per day max 8 puffs 1 2 mL 3 4 times a day 1 vial up to 4 times a day 1 vial 3 4 times a day 200g to 2000g day in divided doses

400mg 130mg 125 mg 150mg SR tab 175 mg, 250 mg 90, 180 400 200, 300 Aminophylline ampule 25mg/mL 4. Combination anticholinergic with beta-2 agonist agent Fenoterol PMDI 50g/20g HBr/ Ipratropium Inhaled solution 0.5mg/0.25mg Br UDV 1.25mg/0.5mg Ipratropium Br/ UDV or nebule 500g/2.5mg Salbutamol B. Corticosteroids Beclomethasone Inhaler 250g/dose

4
50g/dose 100g/cap 200g/blister 100g/cap 100g 400g 2 times a day Fluticasone 50g/dose, 100g 1000g 2 times a day propionate 12g/dose 125g/dose Rotadisk 50g/dose Nebule 500g/2mL 500g 2000g 2 times a day Budesonide inhaler 100g/dose 400g - 2400g per day divided in 2 to 4 doses 200g/dose Turbuhaler 100g/dose 200g/dose Respules 250g/mL 500g/mL Prednisone tablet 2.5 mg, 5 mg, 7.5 20mg 60 mg daily mg, 10 mg 30 mg Prednisolone Syrup 15 mg/5ml 30-60 mg/day Betamethasone Tablet 500 ug 2-3 mg daily Dexamethasone Tablet 500 ug,750 ug, 3 0.5-10 mg daily mg, 4 mg Vial 4mg, 5 mg/ml 0.05-0.2 mg/kg body weight MethylTablet 4 mg, 16 mg 4-48 mg/day prednisolone Vial 125 mg/2ml 10-40 mg every 4-6 hours IV or IM for 48-72 500 mg/7.7 ml hours 1 gm/ 16 ml Hydrocortisone vial 100mg, 250 mg/2 150 mg to 300 mg daily in divided doses mL C. Inhaled corticosteroids-long acting Beta 2 agonist combination FluticasonePMDI, Diskus 125ug/25 ug, 1-2 inhalations 2x a day salmeterol 250ug/25ug, 100ug/50ug, 250ug/50ug, 500ug/50ug BudesonideTurbuhaler 160ug/4.5 ug 1-2 inhalations 1-2x a day, max 4 inhalations formoterol 80ug/4.5ug 2xday D. Expectorants Ambroxol HCl Tablet 30 mg 1 tab 3 times a day ER tablet 75 mg 1 tab daily Syrup 15 mg/5ml 1 tsp 3 times a day Inhalation solution 15 mg/2ml 1-2 inhalations of 2-3 ml solution daily Vial 15 mg/2ml 1-2 amps 2-3times a day IV or IM Acetylcysteine Effervescent tab 600 mg 600 mg daily or 200 mg 3 times a day sachet 100 mg 200 mg granules 100 mg/5ml Inhalation solution 100 mg/mL 1 amp 1 2 times daily Bromhexine Tablet 8 mg, 16 mg 1 tab 3 times a day Syrup 4 mg/5ml 2 tsp 3 times a day Inhalation solution 2 mg/ml 4 ml of solution diluted 1:1 with normal saline inhale every 12 hours Vial 4mg 1 ampule SC, IM, IV every 8-12 hours Carbocisteine capsule 250 mg 500 mg 3 times a day 500 mg Syrup 250 mg/5ml 10 ml 3 times a day Erdosteine Capsule 300mg 1 cap 2 times a day Guiafenesin Syrup 100 mg/5 ml 5-10 ml 3-4 times a day Lagundi leaves Tablet 300mg, 600 mg 300-600 mg 3-4 times a day Mesna Inhalation or 200 mg/ml 1-2 amps inhalation 1-4 x a day Rotacap Rotadisk cyclocaps Inhaler

5
Instillation solution 1-2 ml diluted with equal volume of distilled water or saline hourly into the endotracheal tube or tracheotomy cannula until fluiditication and evacuation of secretions 7 mg 0.5 mL 0.5 mL 1 cap daily for at least ten days Administer IM once a year Administer SC or IM

D. Other medications Lyophilized capsule bacterial extract Influenza vaccine Pre-filled syringe Pneumococcal vial vaccine

APPENDIX 4.
1. 2. 3. 4. 5. 6. 7. 8.

LIST OF AVAILABLE PULMONARY REHABILITATION PROGRAM SERVICES IN THE PHILIPPINES:

Lung Center of the Philippines Perpetual Help Medical Center, Las Pinas Philippine General Hospital Philippine Heart Center for Asia St. Lukes Medical Center The Medical City University of Santo Tomas Hospital Veterans Memorial Medical Center