(WP)NCD/ICP/NCD/001-E
ENGLISH ONLY
REGIONAL WORKING GROUP ON ADULT CHRONIC RESPIRATORY DISEASES
Convened by the
REGIONAL OFFICE FOR THE WESTERN PACIFIC OF THE WORLD HEALTH ORGANIZATION Manila, Philippines 5-8 June 1989
Not for sale Printed and distributed by the Regional Office for the Western Pacific of the World Health Organization Manila, Philippines August 1989
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NOTE
The views expressed in this report are those of the members of the Working Group and do not necessarily reflect the policies of the World Health Organization.
This report has been prepared by the Regional Office for the Western Pacific of the World Health Organization for governments of Member States in the Region and for the members of the Working Group on Adult Chronic Respiratory Diseases, which was held in Manila, Philippines, from 5 to 8 June 1989.
CONTENl'S
1 ..
IN'I'RODUCfION.. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. . .. .. .. .. .. .. . .. .. .. .. .. . .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .... 1
2.
REVIEW OF EPIDEMIOLOGY FR<JoI COUNTRIES IN THE REGION ••••••••••••• 2 2.1 2 .. 3 2 .. 4 2 .. 5 2 .. 6
IN'rRODUcrION .................... ".. .. .. .. .. .. .. .. .. .. . .. .. . .. .. .. .. .. .. .. . .. .. .. .. .. .. .. .. . .. .. .. .... 2 CHRONIC BRONCHITIS (CB) ...... ".............................................................. ASTIlMA.... .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .... BRONCHIECI' ASIS/BRONCHIOUTIS "............................................................ CONC1,USION ...................................... ".......................................................... 3 3 3 3
2.2 CHRONIC OBSTRUCTIVE AIRWAYS DISEASE (COAD) ••••••••••••••••• 2
3.
REVIEW OF TECHNICAL DISCUSSION ••....••.••••••••.•••.........•••. 4 3.1 3.2 3.3 3.4 3.5 GOAD .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .... 4 AS'l'H.MA .................................................. " .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .... 4
ROLE OF POLLUTION IN DEVELOPMENT OF COAD •••••••••.••••••••• 5 mE SK:lICING CCJfP1JN:EN'I' • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •• 5 ACUTE RESPIRATORY INFECTIONS •••.••••••••••••••••••••••••••• 6 KANAGEMEN'I' • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •• 7
4.
CASE
4.1 INTRODucrION • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •• 7 4.2 DEFINITION AND CLASSIFICATION •••••••••••••••••••••••••••••• 7 4.3 TREATMEN'I' • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •• 8 5.
PREVEN'I'ION ••••••••••••••••••••••.•.•.•••••.••••••••••••••••••••• 9 5.1 5.2 COAD •••.••••••.••••••••••••••••••••••••.••••••••••••••••••• 9 ASTIlMA.. • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •• 10
6.
RECOf1loIENDA TIONS • • • • • • • • • . • • . • . . • . . • .. • .. . . • • .. . • • • .. • • .. • . • • . • • • . • .• 11
ANNEX
ANNEXES: 1 ANNEX 2
ANNEX 3 ANNEX 4 ANNEX 5 ANNEX 6
LIST OF MEMBERS AND SECRETARIAT ••••••••••••••••••••• 13 OPENING REMARKS OF REGIONAL DIRECTOR, WHO REGIONAL OFFICE FOR THE WESTERN PACIFIC ••••••••• 17 CHRONIC RESPIRATORY DISEASES - DEFINITIONS •••••••••• 19 CASE MANAGEMENT PROTOCOLS FOR DIAGNOSIS AND TREATMENT AT THE PRIMARY, SECONDARY AND TERTIARY LEVELS ••••••• 21 GUIDELINES FOR INTRODUCING LUNG FUNCTION TESTING AT DIFFERENl' LEVELS OF HEALTH CARE •••••••••• 27 SUGGESTED DRUG LIST FOR DIFFERENT HEALm CARE LEVELS.................................. 29 REFER.ENCFS •••••••••••••••••••••••••••••••••••••••••• 31
ANNEX 7 TABLES: TABLE 1
PREVALENCE OF CHRONIC OBSTRUCTIVE AIRWAYS DISEASE AND ASTIlMA .................................... 35
FIGURES: FIGURE 1
PREDICTION CHARTS FOR PEF (L/M1n) FOR CHINESE AD~TS
AND CHD..DREN ••••••••••••••••••••••••• 37
1.
INTRODUCTION
Chronic respiratory diseases are an important cause of morbidity and mortality worldwide. From available prevalence and mortality figures we know that deaths from chronic respiratory diseases are extremely common in many countries of the Western Pacific Region, with high death rates in the developing countries. Furthermore, mortality trends appear either to have remained unchanged or to have increased in the last decade. Recognizing the importance of the problem, and wishing to encourage further activities in the field of chronic respiratory diseases, a meeting of the Working Group on Adult Chronic Respiratory Diseases was convened in the Regional Office, Manila, from 5 to 8 June 1989. The Working Group was opened by Dr S.T. Han, Director of the Regional Office for the Western Pacific. Dr Han noted a growing awareness in the Region of the problems caused by chronic respiratory diseases and urged members to consider the special problems of prevention, management and diagnosis in developing countries (Annex 2). The WOrking Group was attended by 9 members from 7 countries in the Region, supported by the secretariat. A list of members and secretariat is given in Annex 1. FollOwing the opening address, Dr Zhong Nan-shan (China) was appointed Chairman, Dr Yong Chol Han (Republic of Korea) Vice-Chairman, and Dr Ann Woolcock (Australia) and Dr Tan Wan Cheng (Singapore) Rapporteurs. 1.1 Obj ectives The Objectives of the working group were: (1) (2) to review the epidemiology and prevention of chronic respiratory disease in the Region; to review diagnostic procedures and case management regimens appropriate to the different levels of health care in developing countries; and to recommend regional priorities in the field of chronic respiratory diseases.
(3)
1. 2 Background The chronic respiratory diseases considered by this Working Group include asthma and a group of disorders characterized by chronic airflow limitation, such as chronic bronchitis (with and without
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airflow limitation), emphysema, bronchiolitis, diffuse pan bronchiolitis (in Japan) and bronchiectasis. The most obvious obstacle to a better understanding of chronic respiratory diseases is the confusion over terminology and the lack of diagnostic criteria for the different diseases that cause chroniC airflow limitation. The prevalences of chroniC respiratory diseases in different countries are unknown as there have been few prevalence studies. Where studies have been carried out, the prevalence figures do not always correspond with the reported mortality rates. This is probably because different criteria have been used in population surveys both within and between countries. This lack of agreed diagnostic criteria, together with the confused terminology, has made comparisons of prevalence unreliable. The causes of many chronic respiratory diseases remain unknown. Clinical studies and observations strongly suggest that the relative importance of the various putative causes such as cigarette smoking, atmospheric pollution, healed tuberculosis and childhood acute respiratory infection varies between countries and especially between developed and developing countries in the Region. Future progress in the prevention, diagnosis and treatment of chronic respiratory diseases depends on the correction of these existing deficiencies in our knowledge of the diseases. This report addresses these problems and makes some recommendations about action needed to make progress in this field.
2.
REVIEW OF EPIDEMIOLOGY FROM COUNTRIES IN THE REGION
2.1
Introduction
The definitions of the diseases discussed are given in Annex 3. Relatively little is known about the prevalence of chronic respiratory diseases in countries of the Western Pacific Region. Available data are shown in Table 1 and the sources of the data are given in the references in Annex 7. Some mortality data are available from WHO statistics. Risk factors for these diseases have not been studied in any detail in this Region. 2.2 Chronic obstructive airways disease (COAD) The prevalence of COAD, defined by abnormal expiratory flow rates, is not known for many countries. In general, in developed countries it is more common in males than females. There is good evidence that in Australia(19) and Japan(20,21) COAD is related to cigarette smoking. Data are available for mortality for some countries but there are difficulties with mortality figures because of the international
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classification of disease (ICD) codes. Figures reported by WHO usually group ICD codes 490-493 (WHO tabulation list 313-315) which include asthma, as well as chronic bronchitis and emphysema. However, since 1979, deaths coded as chronic obstructive pulmonary disease (COPO) are coded in 496 (WHO tabulation list 329) which includes a large number of other chronic respiratory diseases. The mortality data shown in Table 1 include 490-3 plus 496 and slightly overestimate the death rates from COAD.
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2.3 Chronic bronchitis (CB) Chronic bronchitis is common in most countries in the Region but since not all people with CB have COAD or asthma, this information may be of relatively little value. If, within populations with CB, a constant proportion develop COAD, then CB figures could be used as an index of the magnitude in different countries. The existing data, summarized in Table 1 suggest that the prevalence is high in northern China and Papua New Guinea and appears to be as common, if not more common in women as in men in these countries. It is suspected that indoor air pollution is important in the high prevalence of CB in nonsmokers but there are no data to support this suspicion. 2.4 Asthma The prevalence of asthma is extremely variable between populations in the Region. Although data using standardized methods are not available, there are some published figures for the prevalence of wheeze, current asthma and asthma ever. Prevalence figures using a standardized protocol(l) in selected populations of children are available for Australia, New Zealand and southern China. Data from Australia, New Zealand and Singapore suggest that the prevalence of asthma is increasing in children (13,16,18). Mortality from asthma is high in developed countries in the Region. However, there appears to be a poor correlation between mortality and prevalence as measured in selected populations and this observation needs to be explored. The causes of asthma in countries in this region are unknown. There is evidence that house dust mites may be important in some populations and occupational agents playa role in some workers. 2.5 Bronchiectasis/bronchiolitis There are no available data about the prevalence of bronchiectasis in any country. It is thought to be a small but persisting problem in most countries. The presence of diffuse panbronchiolitis (DPB) in Japan is well recognized as a disease that may lead to bronchiectasis(22). 2.6 Conclusion The data shown in Table 1 plus other published data(23-26) from the Region show that chronic respiratory disease 1n the Western Pacific region is a large problem. While it appears that COAD may not be increasing in developed countries, asthma appears to be increasing and is becoming an important chronic disease in many countries both in adults and children. Standardized methods for collecting data in this
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Region, similar to those outlined by WHO Europe(27), are needed to facilitate the collection of comparable data.
3.
REVIEW OF TECHNICAL DISCUSSION
3.1 COAD Chronic obstructive airway disease (COAD) is defined as an abnormal forced expiratory flow rate [forced expiratory volume in one second (FEY 1) or peak expiratory flow rate (PEF)] which remains abnormal after bronchodilator treatment. Patients with emphysema, bronchiolitis, bronchiectasis and chronic bronchitis and asthma may all develop COAD. The term chronic airflow limitation (CAL) is being increasingly used because it is known that not all patients with reduced flow rates have obstructed airways. Those patients with emphysema and no disease of the airways may have reduced flow rates. Other terms that have been used but are considered less precise are chronic nonspecific respiratory disease, chronic obstructive lung disease and chronic obstructive pulmonary disease. The pathology of the airways and lungs of patients with COAD has been studied mainly in developed countries. The pathological abnormalities are well described(28). Chronic bronchitis in developed countries is caused mainly by cigarette smoking and is not necessarily associated with any limitation of expiratory flow rates. In developing countries, CB is very common and in China(3) and Nepal(29) more than half of those with CB also have COAD. In most populations the prevalence of COAD is much higher in smokers than in nonsmokers but in developing countries it is obvious that factors, other than cigarette smoking are acting to cause COAD. Among patients over 40 years, those who had recurrent bronchitis in childhood are likely to develop COAD in later life. In order to detect COAD at an early stage, it is essential to monitor FEV! or PEF in those with a chronic cough or wheeze. The natural history of the changes in the lung and why only some smokers develop the disease are unknown. However, continuing to smoke accelerates loss of lung function and cessation of smoking is the first step in treatment. In patients with more advanced disease, long term orally administered theophyllines may be beneficial in relieving dyspnoea. 3.2 Asthma Asthma is a disease of the airways which causes them to narrow too easily and too much in response to a wide range of provoking stimuli. The causes of this abnormality are largely unknown but allergens and occupational sensitizing agents are known to induce the disease in some people. In these people, mediator releaSing cells in the airway walls become activated and release inflammatory mediators which are responsible for the inflammation which in turn makes the airways hyperresponsive, resulting in episodes of narrowing (attacks). In some
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individuals asthma is intermittent but in others it becomes persistent and is then much more difficult to treat. In this Region, reported figures for asthma prevalence reveal huge variations from more than 50% of children in the Caroline Islands(24) to virtually none in village children in Papua New Guinea(12,13). In addition, guidelines for diagnosis and treatment must take into account the wide variation in the facilities for diagnosis and drugs available for treatment between countries. Although the logical approach to management is to prevent the disease, opportunities for this are limited outside the field of occupational asthma. Clearly more attention needs to be given to research directed at possible causes. There is beginning to be evidence that removing house dust mites decreases the severity of asthma but there are no studies that show that removing them prevents the disease. The diagnosis of asthma is made from a combination of symptoms (including wheeze, chest tightness, cough or shortness of breath) and a demonstration of variable expiratory flow rates. This is best carried out with a simple peak flow meter and a bronchodilator aerosol. If less than 15% improvement occurs after the aerosol, recordings of peak flow rates need to be made several times a day for a few days to document variability. Again 15% variability in PEF is needed to confirm a diagnosis of asthma. The aim of the treatment of asthma is to reduce the severity. This means that ideally, the severity should be assessed in all patients (with PEF variability) and then an action plan introduced on the basis of the drugs available. 3.3 Role of pollution in development of COAD Air pollution consists of a series of pollutants such as suspended particles, nitrous oxide (N0 ), carbon monoxide (CO), sulphur dioxide 2 (S02)' formaldehyde, asbestos, volatile organic compounds and biological agents. S02 is the major air pollutant both outdoors and indoors. S02 and suspended particles may have a synergistic effect in increasing mortality from COAD. The combustion of sulphur-containing coal briquettes yields 1.0 - 4.5 ppm of S02' a concentration known to cause bronchoconstriction in more than 90% of asthmatics. Wood fire smoke constitutes an important factor which probably causes the high prevalence of chronic bronchitis in women. Biological pollution covers a series of antigens (mites, cockroaches, moulds, etc) in house dust that can cause attacks (and perhaps induce) bronchial asthma. It has been shown that the concentration of mites (counts/gm of dust) is related to the prevalence of atopy and to asthmatic symptoms in patients in developed countries(30). 3.4 The smoking component The evidence that cigarette smoking is the most important cause of COAD in developed countries comes from a number of retrospective and prospective studies, including an important study of British doctors(31). Evidence of a relationship with emphysema comes from autopsy studies where the severity of emphysema has been quantified.
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Furthermore, some studies have shown improvement in expiratory flow rates on cessation of smoking. It is thought that up to 30% of smokers show some evidence of COAD but only about half this number actually develop symptoms or have early mortality from COAD. It should be mentioned that there is evidence that cigarette smokers who develop lung cancer frequently have evidence of COAD. The reason why only some smokers develop COAD is not known. There is some evidence of interrelationships with air and occupational pollution in some studies in developed countries. In developing countries there is evidence that cigarette smoking is associated with an increased prevalence of chronic bronchitis and some evidence that it is associated with airflow limitation. However, there is also evidence that COAD can occur in people who have never smoked, particularly in women in northern China and in Papua New Guinea. Data linking passive smoking to COAD are not conclusive but in developed countries children living in houses where parents smoke have an increased risk of respiratory infections and (32) in some cases, of developing asthma. The main aims of prevention programmes are to encourage children not to start smoking and adults to quit. 3.5 Acute respiratory infections Acute respiratory infections (ARI), especially pneumonia are among the leading causes of mortality and morbidity in children in many developing countries in the Western Pacific Region. Mortality from ARI accounts for more than one third of infant deaths in countries where infant mortality rates are more than 30 per 1000 live births. Furthermore, these high mortality rates have remained relatively unchanged in many developing countries in contrast to the notable decrease observed in developed countries. In view of this high mortality, the World Health Organization Western Pacific Advisory Committee (WPAC) for Medical Research in 1977 called attention to the need to conduct studies on the etiology and epidemiology of ARI in order to understand its causes and to determine possible intervention measures. An ARI research project was undertaken in Papua New Guinea in 1979. This was followed by studies carried out in China, Malaysia, the Philippines and Viet Nam. Based on the findings of these studies, WHO drew up standard case management protocols for ARI which help health staff to determine the severity of ARI and to give appropriate treatment. National ARI control programmes have been implemented in 11 countries in the Region. In several countries programmes have been closely monitored. Through these programmes, difficulties in implementing case management have been encountered which indicate the importance of supervision to improve the practice of health staff. However, from selected areas, the beneficial impact of the programme on mortality reduction and the rationalization of practice have been reported. Similar programmes are needed for case management of patients with COAD and asthma. The role of ARI in infancy in the subsequent development of chronic respiratory diseases is unknown. In developed countries, there is
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evidence to link early bronchiolitis with the subsequent development of asthma ( 33).
4.
CASE MANAGEMENT
4.1
Introduction
The working group considered that the introduction of protocols for the diagnosis, management and prevention of COAD and asthma at different levels of health care, with emphasis at the primary health level, is an important initiative for WHO in the Western Pacific Region. A flow chart for primary health care workers and tables for secondary and tertiary health centres are given in Annex 4. It was recognized by the Working Group that most people attending for treatment at a primary health level would be doing so because of an acute exacerbation of the GOAD or of asthma. This requires case management protocols that are based largely on symptoms, simple to execute and require no investigation or procedures. It was also recognized that these protocols will have to be introduced as pilot schemes and tested in different countries to determine their usefulness and to develop them further. With time it will be important to introduce acceptable and uniform terms to describe these diseases. In addition, the widespread introduction of peak flow meters that allow the measurement of airflow limitation is essential if these protocols are to become effective. 4.2 Definition and classification Many terms have been used to describe the group of diseases that include chronic bronchitis, emphysema, bronchiolitis of smokers, diffuse panbronchiolitis (in Japan) and bronchiectasis. Chronic airflow limitation is the common feature of all these conditions. Clinically it may not be possible to distinguish these entities. Until this is possible, the preferred term used to describe this group of conditions is chronic obstructive airway disease (GOAD). There are two subcategories for diagnosis: long term (background or chronic) and short term (acute exacerbation of the underlying disease). The proposed minimal criteria for diagnosis and management of patients with COAD and asthma for each level of health care are shown below. (1) Primary Health Level (a) COAD is present if cough and sputum, with or without breathlessness, exist for more than 2 years. Acute exacerbations of COAD are present if there is a recent increase in the amount and/or a change in colour of the sputum, and/or an increase in breathlessness.
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(b)
Asthma is present if the patient has a history of episodic or spontaneous onset of wheeze, chest tightness, cough or bresthlessness which is relieved by bronchodilator treatment. An acute exacerbation or attack is present when there is an audible wheeze and rhonchi and increasing bresthlessness, all of which improve with adequate doses of a bronchodilating drug.
(2) Secondary Health Level (a) COAD. The clinical diagnosis is made by measuring expiratory flow rates before and after a bronchodilator aerosol. Expiratory flow rates can also be used to assess severity. If the PEF (percent predicted) is >65<80 the COAD is defined as mild, if >50<65 it is defined as moderate and if <50 it is defined as severe. (b) Asthma. The clinical definition is the same as at the primary level. In addition, objective measurements of response to bronchodilator therapy should be made. If the PEF change after bronchodilator is >15% or if the variability of PEF readings over a period of two weeks is greater, then asthma can be diagnosed. A variability of greater than 30% in PEF values over two weeks suggests ~evere asthma. The definition of an attack is the same as at the primary level but the effect of treatment should be monitored with PEF measurements and/or spirometry until no further improvement occurs. (3) Tertiary Health Level (a) COAD. In addition to the clinical criteria, chest radiography, pulmonary function testing (e.g. spirometry, lung volumes and diffusing capacity), sputum culture and baseline arterial blood gas tensions are useful in defining the type and severity of the disease. In acute exacerbations, serial blood gas tensions are helpful to monitor progress. (b) Asthma. Assessment of the severity of asthma should include PEF variability over a period of two weeks or an estimation of bronchial hyperresponsiveness (PD20). The establishment of the atopic status helps to plan treatment. 4.3 Trestment (1) Primary Health Level Medications required at this level consist of antibiotics (procaine penicillin, cotrimoxazole or a broad spectrum penicillin), simple bronchodilators and subcutaneous adrenaline. The minimum drug list for each level of health care is given in Annex 6.
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(2) Secondary Health Level Medications available should include aerosols of bronchodilators, systemic corticosteroids and the long term use of aerosol corticosteroids. (3)
Tertiary Health Level The medications for acute treatment use nebulized bronchodilators together with systemic corticosteroids. Prevention modalities include influenza vaccination, pneumococcal vaccination, reduced exposure to occupational and domestic pollutants, desensitization programmes, and the reduction of household allergens.
5.
PREVENTION
5.1 COAD 5.1.1 Cause reasonably well established (a) Cigarette smoking. It is recognized that both active and passive smoking playa role directly and indirectly in causing COAD. Cessation of cigarette smoking is probably the single most important factor in preventing the disease. (b) Indoor air pollution. There appears to be enough evidence to suggest that SO is an important irritant and may even cause COAD. Recommenaations are needed to reduce the sulphur content of heating/cooking fuels and to ventilate rooms in which these fuels and kerosene are used.
(c) Tuberculosis. Patients who have had severe pulmonary TB cured with drugs often have COAD, even when they are nonsmokers. The control and early diagnosis of TB would eliminate this cause of COAD. (d) Byssinosis. This disease affects only a small number of cotton workers where the cotton being processed is not kept dry. However, it is important since it is a preventable cause of COAD. Cause suspected (a) Tobacco smoking other than cigarettes. The role of smoking cigars and pipes and home cured tobacco needs to be investigated.
5.1.2
(b) Pollution. A number of industrial and indoor pollutants may lead to COAD. These include N0 2 , suspended particulate matter
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and ammonia. It is not known if they cause COAD alone or in combination with other factors; more research is needed. 5.2 Asthma 5.2.1 Known causes (a) Occupational sensitizers such as isocyonates, grain and coffee dusts are known causes in some people and workplace conditions need to be controlled. (b) Allergens such as house dust mites and pollens. Methods are becoming available to measure allergen levels in houses and to reduce household allergen levels. This area of asthma prevention is still at the experimental stage but it may become important to develop and introduce allergen avoidance in populations where asthma prevalence is increasing. 5.2.2 Causal agent suspected (a) Domestic allergens such as moulds and cockroaches. (b) Viral infections. (c) It seems likely that ethnic and genetic factors playa role as well as environmental factors. This possibility could be explored by appropriate studies of different races living in similar environmental conditions in this Region.
GENERAL POINTS IN PREVENTION (1) The acute and early stages of these diseases should be recognized and treated. (2) Peak flow meters should be widely introduced to measure the severity of the airflow limitation. This is essential to both early diagnosis and treatment. (3) It is important to make the public and Governments aware that coughs and sputum and mild breathlessness are not a normal part of the ageing process. It is important to educate the public, the medicsl profession and patients that asthma is a serious disease that rarely remits spontaneously and can have many long term consequences including premature death.
(4)
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6. REOOMHENDATIONS
6.1 Data on prevalence, mortality and risk factors for these diseases should be sought both at the country level and regionally. Standardized definitions and protocols for obtaining these data from selected countries should be drawn up. 6.2 Action-oriented research programmes, using standardized methods, should be developed by WHO. The priority research areas include the following: (a) epidemiological studies of prevalence and risk factors;
(b) clinical studies on diagnosis and treatment at primary health care level; (c) (d) the effects of indoor air pollution, especially on women; and the number of mites to be found in domestic dust in different countries in relation to the prevalence of ssthma.
6.3 Protocols for primary health care should be developed. These protocols should include components on diagnOSis, treatment and prevention. The case management protocols, already developed for acute respiratory infections, could serve as a useful model for the primary health care protocols. Training programmes should be planned for health workers using these protocols. 6.4 The wide use of simple, cheap, peak-flow meters in primary health centres should be encouraged in order to diagnose these diseases, to assess their severity and to monitor treatment. Further, at the secondary care level, the working group recommends the introduction of spirometers. 6.5 A list of essential drugs for the management of patients with COAD and asthma should be drawn up for different levels of health care. 6.6 Guidelines for the primary prevention of COAD and asthma should be developed. Activities should include health education and effective plans to reduce pollution levels inside houses. 6.7 The efforts of WHO to create a tobacco free society were strongly supported. Members were encouraged by the WHO activities and urged Member States to implement WHO recommendations on tobacco control and smoking cessation. 6.8 The members welcomed the initiative of WHO in holding this meeting. They urge WHO to continue to lead and coordinate research activities and the development of prevention and control programmes based on standardized protocols.
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ANNEX 1
LIST OF MEMBERS AND SECRETARIAT
1.
MEMBERS
Dr M. Aoki Director Research Institute of Tuberculosis JATA Iiyose-shi Tokyo 204 Japan
Professor Yoshinosuke Fukuchi Associate Professor Department of Geriatrics Universi ty of Tokyo 7-3-1 Hongo Bukyo-ku Tokyo 113 Japan
Dr Yong Chol Han General Director Seoul National University Hospital 28 Yunkun-Dong, Chongro-ku Seoul 110-744 Republic of Korea
Dr N.D. Huong Director National Institute for Tuberculosis and Respiratory Disease Hoang Hoa Tham Road Hanoi Viet Nam
Dr Tan Wan Cheng Associate Professor Department of MediCine National University Hospital Lower Kent Ridge Road Singapore 0511 Republic of Singapore
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Annex 1
Professor Ann Woolcock Professor of Respiratory Medicine Department of Thoracic Medicine Royal Prince Alfred Hospital Camperdown NSW 2050 Australia
Dr Yan Bi-ya Director Beijing TB Research Institute National Tuberculosis Control and Research Centre Tong-lian, Beijing 101149 People's Republic of China
Dr Calixto Zaldivar Director Lung Centre of the Philippines Quezon City Philippines
Dr Zhong Nan-shan Director Guangzhou Institute of Respiratory Diseases 151 Yang Jian Road Guanazhou People's Republic of China
2.
SECRETARIAT
Dr A. Galvez Regional Adviser in Chronic Diseases WHO Regional Office for the Western Pacific Manila Philippines
Dr R.W.I. Gee (Operational Officer) Regional Adviser in Noncommunicable Diseases WHO Regional Office for the Western Pacific Manila Philippines
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Annex 1 Dr A. Shimouchi Medical Officer, Acute Respiratory Infection WHO Regional Office for the Western Pacific Manila Philippines
Mr S. Tamplin Regional Adviser in Environmental Health WHO Regional Office for the Western Pacific Manila Philippines
Dr E. Chigan
Director Division of Noncommunicable Diseases World Health Organization Geneva Switzerland
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ANNEX 2
OPENING REMAR[s OF DR S. T. HAN, REGIONAL DIRECTOR. WHO REGIONAL OFFICE FOR THE WESTERN PACIFIC AT THE WORKING GROUP ON ADULT CHRONIC RESPIRATORY DISEASES, 5 - 8 JUNE 1989
Distinguished Participants, Ladies and Gentlemen, I am very pleased to be able to welcome you to the Regional Working Group on Adult Chronic Respiratory Diseases. This is the first such meeting to be held in the Western Pacific Region and is an indication of growing awareness of the problems caused by chronic respiratory diseases. In many countries in the Region, these diseases cause significant morbidity. Your discussions will help to give a clearer picture of the extent of the problem, and of the population groups who are at highest risk. In developed countries, tobacco seems to be the major preventable cause of chronic respiratory diseases. In developing countries acute respiratory infections and indoor and outdoor pollution from industries, cooking and heating fires may also be of importance. Much remains to be done in defining the risk factors for chronic respiratory disease. I hope that this group will consider how best chronic respiratory diseases should be diagnosed and managed at the different levels of health care in developing countries. Simple diagnostic measures and rational antibiotic and drug therapy will be important in reducing morbidity and in ensuring cost-effective case management. The World Health Organization, jointly with the International Union Against Tuberculosis and Lung Disease, has sponsored several meetings on chronic respiratory disease. These meetings have been concerned mainly with chronic respiratory diseases in developed countries. I hope that this Working Group will consider the special problema of management in developing countries. A very active programme for acute respiratory infection control and prevention has been developed by the World Health Organization. This programme should be considered by the Working Group and may provide a model for chronic respiratory disease control and prevention. As a Working Group, your task is to recommend regional priorities in the field of chronic respiratory diseases. These recommendations may be directed both to the World Health'Organization and to Member States. They should be practical and provide guidance on the development of further activities in this field. I wish you well in your discussions and an enjoyable stay in Manila.
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ANNEX 3
CHRONIC RESPIRATORY DISEASES - DEFINITIONS
1.
EMPHYSEMA 1.1 Pathological Distension of airspaces with destruction of alveolar walls. 1.2 Clinical/Epidemiological Decreased FEV 1 /FVC ratio plus decreased diffusing capacity. Hyperinflatioft of the chest and decreased breath sounds are suggestive but not diagnostic.
2.
CHRONIC BRONCHITIS 1 2.1 Pathological Increased size of the bronchial mucous glands with an increased Reid index. 2.2 Clinical/ Epidemiological Production of sputum each day for at least 3 months of 2 consecutive years
3.
BRONCHIOLITIS 3.1 Pathological Inflammation of the bronchioles including goblet cell metaplasia and infiltration with inflammatory cells. Diffuse panbronchiolitis is characterized by inflammation of all layers of the respiratory bronchioles with lymphocytes 3.2 Clinical/Epidemiological No definition is possible because there are no symptoms when bronchiolititis is mild. When advanced there is breathlessness, cough and reduction in expiratory flow rates.
4.
BRONCHIECl'ASIS 4.1 Pathological Dilatation and chronic inflammation of the bronchi with loss of lung tissue distal to the affected bronchi. 1 Chronic Bronchitis alone does not cause airway obstruction.
- 20 -
, Annel[ 3
,
4.2 Clinical/Epidemiological Chronic cough with purulent sputum or unexplained haemoptysis, or sputum production on posural drainage.
5.
CHRONIC OBSTRUcrIVE AIRWAYS DISEASE (COAD)2 (CHRONIC AIRFLOW LIMITATION)
5.1 Pathological Any disease of the airways/lungs that leads to chronic, irreversible narrowing of the airways or destruction of alveolar walls. Usually the bronchioles are abnormal.
5.2 Clinical/Epidemiological Decrease in expiratory flow rates below 2 standard deviations of the predicted value after adequate bronchodilator treatment. Symptoms of productive cough and breathlessness, mayor may not be present. 6.
AS1ID1A3 6.1 Pathological Widespread inflammation of the airway walls with eosinophils. edema and damage to the epithelium. 6.2 Clinical/Epidemiological Episodic symptoms of wheeze, chest tightness, cough or breathlessness plus evidence of variable expiratory flow rates.
2 COAD is a clinical term used when the underlying pathology is unknown or mixed. The term CAL is also used because emphysema can cause decreased expiratory flow rates in the absence of obstruction to the airways. 3 Asthma if severe commonly causes irreversible narrowing of airways and is thus a cause of COAD.
- 21 -
ANNEX 4
PRIMARY HEALm CARE CASE MANAGEMENT FOR CHRONIC COUGH Chronic cough with sputum* (more than 3 weeks)
breathlessness
Y ES I_ _ ..... _ NO
wheeze YES t asthma
Give bronchodilator
.. Fever YES I
bronchitis exacerbation of COAD
Give antibiotics**
NO Change of color or increase in sputum YES
» exacerbation of COAD
bronchitis
Give antibiotics
NO
•
Simple Chronic cough
Home care
* Sputum smear should be examined according to national TB control programme guidelines. ** If the symptoms do not improve, refer to hospital.
- 22 -
Annex 4
PROTOCOL FOR CASE MANAGEMENT (Primary Health Care - Diagnosis)
Symptoms/Signs
Duration of Symptoms
Diagnosis
1.
Cough and sputum (+/- breathlessness)
>2 years <2 years
COAD Acute bronchitis Exacerbation of COAD
2.
Cough and sputum with days/weeks (a) recent increase (b) changed colour (+/- change in breathlessness) Wheeze, breathlessness, >days cough or chest tightness (a) episodic (b) spontaneous (c) relieved by bronchodilator Wheeze/breathlessness increased (+/- audible wheeze +/- improvement with bronchodilator) hours or days
3.
Asthma
4.
Exacerbation or "attack" of asthma
- 23 -
Annex 4
PROTOCOL FOR CASE MANAGEMENl'
(Primary Health Care - Treatment)
SYMPTOMS (A) Cough and sputum a. Change in colour b. Recent increase in amount (+/-wheeze,+/-breathlessness) 1. Sputum smear for TB 2. Antibiotic - procaine penicillin - synthetic penicillin 3-10 days, stop when sputum clears (B) Fever 1. Sputum smear
2. Antibiotic*
(C) Increase in breathlessness
Bronchodilator** trial -~secondary health care (if no response) 1.Bronchodilator** for 2 weeks 2.---J secondary health care (if no response)
CD) Audible wheeze (rhonchi - asthma attack)
*
Further research needed to determine the most prevalent organism(s). Bronchodilator = salbutamol and/or aminophylline.
- 24 -
Annex 4 PROTOCOL FOR CASE MANAGEMENT Secondary Health Care - (District Hospital) - Diagnosis and Treatment SIGNS AND SYMPTOMS A. B. Cough and sputum, Breathlessness, LUNG FUNCTION PEF after bronchodilator >65<80% - mild >50<65% - moderate <50% - severe DIAGNOSIS CHRONIC OBSTRUCTIVE AIRWAYS DISEASE (COAD) TREATMENT
>2 years <2
Chronic Exacerbation
?None - Antibiotics (as for primary) - Bronchodilator (a) Salbutamol(nebulized) (b) Aminophylline (tablets or intravenous)
years
C.
Wheeze, breathlessness,
PEF,FEV after bronchohilator >15% increase PEF variability >15%
ASTHMA
> days
Chronic
(a) (b)
Theophylline(tablets) - uncontrolled Salbutamol (aerosol or tablets - controlled till recovery
D.
Wheeze, breathlessness, increased +/- rhonchi PEF decreased hours or days
Acute Exacerbation
- Bronchodilator (a) Salbutamol (nebulized) (b) Theophylline (tablets or intravenous) (c) Adrenaline (subcutaneous) (d) Corticosteroids(oral or intravenous)
- 25/26 Annex 4 PROTOCOL FOR CASE MANAGEMENT Tertiary Health Care (Hospital and Ambulatory) - Diagnosis and Treatment CLINICAL DIAGNOSIS (A) CHRONIC OBSTRUcrIVE AIRWAYS DISEASE (COAD) (I)
INVESTIGA nONS Chest X-ray, PEF Spirometry Lung volume/DLCO Sputum culture Baseline arterial blood gas tensions CAT scan (rarely for bronchiectasis and emphysema) Chest X-ray Serial arterial blood gases and PEF to monitor recovery Sputum culture
TREATMENT - Stop smoking Bronchodilator aerosol Theophylline (oral) Influenza vaccination Home supply of antibiotics Rehabilitation
Chronic (rarely admitted)
(II) Acute
Exacerbation
-
Bronchodilator (nebulized) - +/- 0 - +/- a~tibiotics - +/- physiotherapy - +/- mucolytics/expectorants - Corticosteroids by inhalation - Home monitoring PEF - Oral steroid for PEF fall - Bronchodilator aerosol - Desensitization 17 - Bronchodilator (nebulized) - +/- corticosteroids (oral or intravenous) - +/- aminophylline (oral or intravenous) - +/- antibiotic
(B)
ASTHMA (I) Chronic
- Assess severity (PEF variability for 2 weeks) - Determine best PEF - Atopic status - Serial arterial blood gas tensions - Serial PEF - Sputum examination
(II) Attack (acute exacerbation
PEF ~ Peak Expiratory Flow Rate (Variability - range divided by the highest) DLCO - Diffusing capacityof the lung for carbon monoxide)
- 27/28 ANNEX 5
GUIDELINES FOR INI'RODUCING UlNG FUNCTION TESTING AT DIFFERENT LEVELS OF HEALm CARE.
I NI'RODUCTION If the importance of chronic respiratory diseases is to be recognised and case management protocols introduced, it is ESSENTIAL that the importance of lung function testing be recognized and. appropriate equipment introduced into all countries in the Region. 1. Primary Health Care Level 1.1 Peak Flow Meters Cheap meters are now availsb1e from various sources. Instructions for use and normal values for Chinese and other nationalities should be readily available. Values for Chinese, which can be used for other non-Caucasian nationalities, are attached (Figure 1). 2. Secondary Health Care Hospitals 2.1 Peak Flow Meters need to be available for individual use by all patients for diagnosis and for assessing severity. 2.2 Spirometers are needed to diagnose the nature of the airflow limitation and to assess progress during an acute exacerbation of asthma or of COAD. 3. Tertiary Health Care
Facilities should be available to measure spirometric function, lung volumes, and diffusing capacity; to do bronchial challenge testing and to identify atopy. The ability to assess environmental pollutants should be svailable somewhere in developed countries.
- 29/30 ANNEX 6
SUGGFSTED DRUG LIST FOR DIFFERENT HEALTH CARE LEVELS
REOOMMENDED FOR: PRIMARY
SECONDARY
ANTIBIOTICS
Procaine penicillin * (intramuscular) Cotri.oxazoleAmodcillin
Procaine penicillin (intramuscular) Cotr1moxazoleAmodcillin Cephaledn Ampicillin (intravenous)
BRONCHODILATORS
Theophylline (tablets)* Beta 2 agonist (tablets) SYMPATHOMIMETIC
Theophylline (tablets/intravenous) Beta 2 agonist aerosol/nebulized}
Adrenaline (subcutaneous*) Ephedrine CORTICOSTEROIDS
Adrenaline (subcutaneous)
Prednisone (oral)
Prednisone (oral) Hydrocortisone (intravenous/inhaled)
*
**
Essential in drug list at the primary health care level. Sulphamethoxszole + trimethoprim(cotrlmoxazole).
- 31 -
ANNEX 7
REFERENCES
1. 2. 3.
World health statistics annual 1988. Health Organization, 1988.
Geneva: World
Economic Planning Board (Cause of Death Statistics) Republic of lorea, 1988. Zhong N.S. et al. Prevalence of smoking and chronic bronchitis in Cong-Hua County, a suburb of Guangzhou. Nat Med J. China 1986; 66:(5):312. Zhong N.S. et al. Fu W.X. et al. Shi L.J. et al. Bronchial hyperresponsiveness in young students of Southern China - Relation to respiratory symptoms, diagnosed asthma and risk factors. Abstract. First International Congress on Bronchial Asthma, Guangzhou, 1988.p.5. Yan Bi-ya. Epidemiological studies of chronic respiratory diseases in some regions of China. Proceedings of WHO/IUAT-LD Conference in Chronic Airways Disease, Dubrovnik 1988 (to be published in Chest supplement, 1989). Lin S.Y. Liu Z.B. Prevalence of bronchial asthma in a population of 253 860 in the urban and rural areas of Chang-Sha, Hunan Province. Abstract. Chin J Tub Respir Dis 1987 10:(4):248. Yu C.Y. et al. 137-151. Chest Diseases Journal, 1987; 15:(4):
4.
5.
6.
7. 8. 9.
Huong N.D. Personal communication. Teo J. Quah S.H. Low P.S. Wong H.B. Childhood asthma in Singapore - changing trends. Abstract. 22nd Singapore-Malaysia Congress of Medicine, July, 1988. Chong T.M. Pattern of bronchial asthma in Singapore. Singapore Med J. 1972; 13: 154-160. Anderson H.R. Woolcock A.J. Chronic lung disease and asthma. In: Humsn biology in Papua New Guinea: The Small Cosmos. Attenborough R. Alpers M. (eds) Oxford University Press. 1989.
10. 11.
- 32 Annex 7 12. Woolcock A.J. et al. Asthma and chronic airflow limitation in the highlands of Papua New Guinea: low prevalence of asthma in the Asaro Valley. Eur Respir J 1989 (in press). Gregg I. Epidemiology. In: Clark T.J.H. Godfrey S. (eds). Asthma. London: Chapman and Hall, 1977: 242-284. Yan K. et al. Prevalence and nature of bronchial hyperresponsiveness in subjects with chronic obstructive pulmonary disease. Am Rev Respir Dis 1985; 132: 25-29. Peat J.K. et al. Bronchial hyperresponsiveness in two populations of Australian schoolchildren. II. Relative importance of associated factors. Clin Allergy 1987; 17: 283-290. Salome C.M. et al. Bronchial hyperresponsiveness in tvo populations of Australian schoolchildren. I. Relation to respiratory symptoms and diagnosed asthma. Clin Allergy 1987; 17: 271-281. Woolcock A.J. et al. Prevalence of bronchial hyperresponsiveness and asthma in a rural adult population. Thorax 1987;42:361-368. Asher M.I. et al. International comparison of the prevalence of asthma symptoms and bronchial hyperresponsiveness. Am Rev Respir Dis 1988; 138: 745752. Cullen K.J. Stenhouse N.S. et al. Chronic respiratory disease in a rural community. Lancet 1968; 2:237-242. Toyama T. Kugasu J. Prevalence of chronic bronchitis in Japan. In: Proceedings of the World Conference on Asthma, Bronchitis and Child Conditions (1974), Delhi. Viswanutham R. Jaggi B.P. (eds). Asthma and Bronchitis Foundation of India, 1977;5-19. Aoki M. Epidemiology of chronic airways diseases in Japan. Abstract. Proceedings of WHO/IUAT-LD Conference on Chronic airways disease. Dubrovnik 1988 (to be published in Chest supplement, 1989). Homma H. et al Diffuse pan bronchiolitis. A disease of the transitional zone of the lung. Chest;1983:83(1):63-69. Chai R.S. Prevalence of chronic bronchitis and cor pulmonale in China. Abstract. Proceedings of the IVth National Congress on Chronic Bronchitis and Cor Pulmonale, Cheng-Duo 1984:p.1.
13. 14.
15.
16.
17.
18.
19. 20.
21.
22. 23.
- 33/34 Annex 7 24. Brown P. Gadjusek D.C. Acute and chronic pulmonary disease in Pacific Island Micronesians. Am J. Epidemiol 1978; 108:266-273. Ross I. Bronchial asthma in Malaysia. Br J Dis Chest 1984; 78:369-375. Woolcock A.J. Peat J.K. Epidemiology of bronchial hyperresponsiveness. Clin Rev Allergy 1989; 7 (in press). Methods for cohort studies of chronic airflow limitation. WHO Regional Office for Europe, Copenhagen. European Series no. 12, Florey C. Leeder S. (eds). 1982. Snider G.L. Chronic bronchitis and emphysema. In: Textbook of respiratory mediCine. Murray J.F., Nadel J.A. (eds). Philadelphia: W.B. Saunders, 1988:10691106. Pandey M.R. Prevalence of chronic bronchitis in a rural community of the hill region of Nepal. Thorax 1984;39:337-339. Korsgaard J. Mite asthma and residency. A case control study on the impact of exposure to house dust mites in dwellings. Am Rev Respir Dis 1983; 1228:231-5. Doll R. Gray R. Mortality in relation to smoking: 22 years observation on female British doctors. Br Med J 1980;280:967-971. Colley J.R.T. Holland W.W. Carkill R.T. Influence of passive smoking and parental phlegm in early childhood. Lancet 1974;2:1031-1034. Buist A.S. Acute respiratory infection as a risk factor for bronchiolitis. Proceedings of WHO/IUAT-LD Conference on Chronic Airways Disease, Dubrovnik, 1988 (to be published in Chest supplement 1989). Aoki, M. Personal communication.
25. 26.
27.
28.
29.
30.
31.
32.
33.
34.
- 35/36 -
TABLE 1 PREVALENCE COUNTRY COAD PREVALENCE CB PREVALENCE
or
COAD AJlD ASTHMA IN COUlITI\ISS 1M 'o/BSTBIH PACIPIC REGION
IIORTALITY 100,000
•
I/HEEZS
CUIW!IIT
EVEU CHILDREII
ASTIIItAI
CUlIULATIVE ASTHHAlI
IIORTALITY 100,000
••
-----------------------------------------------------------------------------------------------------------------------------C A II II c A T r T r -----------------------------------------------------------------------------------------------------------------------------Japan 11-4.0 P-1. 7(1) 26 14(1) 4.3(.) 2.8(f)(I) 1.7(1) 3.4 5.0
Korea China(Soutb) 1.4(3) 2.7(3) 2-9(5)
10(2) 25-3.1(4) .2-1.0(6) 57 3.7(7) 3-4(8) 47 10( 11) 17(11) 24( 11) (P-30) 54 63 26(1) 35(1) 20(1) 0(12) 1.6(8) 4.4(9) 0.1(12)
Chlna(North) Hong Kong
40(1)
Phillppine8
Viet Ma. Sillaapore Papua New GuiDea
13.7(9,10)
4.1
Australia Mev Zealand
6.1(14) 5.2(14)
24( 15) 46(18)
7(16) 11(18)
6(17)
10(17) 13(18)
5.0 6.0
K-Hale. ,-, ... le. I-total C-Children, A-Adult ·tabulation List (tnclu4es Aatbaa)
()-lefereace In ADnex 7
IP-SPrevaleace
313-315. 323, 324-27. 329 tor 1986 ot 1987
·-Hale and fea-ie deathe
- 37 PIGUllB 1
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... 1-4-+~4-+-H-+-I-~ *~-+-I-4-+-~-+~~ m~-+-I-4-+-H-+-I-4-+
'''H-++4-+-H-+-I-4-+-~ m~-+~~+-~-+~~+-~
-
-H-+-I-4-+-~-+-I-4-+-~~~
I.~~-L~~~~~~~~I-+-~ "tt 1t711.
j\ge(lear)
PEP IH HORMAL SUlIJECTS( 15-80)
. ,. i.. ... ~,
PEF(L!M1n) -" I
PEF(L/Min) ./ /
I
f'
,
, /
/ / /
I
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no
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I' ,~ ~ ~
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PEF(L/Min) in Doya (5--15 1T8 ) Zhong N.S.
PEF(L/Min) in Girls (5-: 15 1T8 ). for
Prediction Charts for PEP (L/Min) Chinese Adults and Children