copd indian guidelines

8/9/2019 COPD Indian guidelines

1/64

SPECIAL ISSUE ISSN 0377-9343 VOL. 56, 2014


2/64

ATTENTION SUBSCRIBERS

Subscription Rates

Individual Institutes/Hospitals/Colleges, etc.India Overseas (Airmail) India Overseas (Airmail)(in R ) (in US $) (in R ) (in US $)

Single Issue 400.00 60.00 500.00 100.00Per Volume(4 issues) 1300.00 200.00 1800.00 350.00____________________________________________________________________________________________

1. Overseas subscription rates include airmail postal charges.

2. Subscription Agencies are eligible for a 10% discount on annual rates for institutional subscriptiononly. Agencies must provide complete address of the institution for which subscription is sent intheir subscription order.

3. Payments should be made only by Banker’s Cheque/Demand Draft; drawn in favour of TheDirector, V.P. Chest Institute, Delhi.

4. Subscription rates are not subject to any Tax Deduction at Source .

5. Subscribers are advised to get their copies by “Registered Post” by making an advance payment of R 400/- per year in addition to Subscription rates, if subscription is made for one year (in case of asingle copy, R 100/- to be added).

6. The rates are subject to revision at any time by announcement in the Journal.

7. Subscription can be enrolled only on receipt of full payment in advance. Copies will not be sent if part payment is received.

8. Our responsibility ceases once we hand over the copies to the Post/Courier Office. We are notresponsible for any delay/loss/damage in transit. We hold the receipt from the Post/Courier Officeas proof. The Journal Office is not liable to replace copies lost in transit.

9. Requests for missing issues will be considered if made within one month of the publication of aparticular issue (i.e. for January-March issue ➔ upto April, for April-June issue ➔ upto July, for July-September issue ➔ upto October and for October-December issue ➔ upto January) . Supply ofreplacement copy will be subject to availability.

Director/Editor-in-Chief


3/64

SPECIAL ISSUE

Guidelines forDiagnosis and Management

ofChronic Obstructive Pulmonary Disease

Joint Recommendations ofIndian Chest Society

andNational College of Chest Physicians (India)


4/64


5/64

Founded byProfessor R. Viswanathan

Founder-Director,Vallabhbhai Patel Chest Institute

Editor-in-ChiefRajendra Prasad, Delhi

EditorsS.K. Jindal, ChandigarhAshok Shah, DelhiS.K. Sharma, New DelhiAlladi Mohan, TirupatiS.K. Chhabra, Delhi

Associate EditorsDheeraj Gupta, Chandigarh J.M. Joshi, Mumbai J.C. Suri,New Delhi

Journal CoordinatorsR.K. Gupta, DelhiD.K. Sahu, Delhi

THE INDIAN JOURNAL OF

CHEST DISEASESANDALLIED SCIENCES

THE INDIAN JOURNAL OF CHEST DISEASES AND ALLIED SCIENCES(ISSN 0377-9343) is published quarterly, by the Vallabhbhai Patel Chest Institute,University of Delhi, Delhi in association with the National College of ChestPhysicians (India). The Journal covers the Clinical and Experimental work dealing with all aspects of Chest Diseases and Allied Sciences. It publishesOriginal Articles, Review Articles, Radiology Forum, Case Reports, Short

Communications, Book Reviews.Copyright © with Vallabhbhai Patel Chest Institute, University of Delhi, Delhi.All rights reserved; no part of this publication should be reproduced and/orstored in a retrieved system or transmitted in any form or by any means,electronic, mechanical, photocopying, recording or otherwise, without the priorpermission from the Publishers in India and/or in the USA by the CopyrightClearance Center , 222, Rosewood Drive, Danvers, MA 01923.

The statements and opinions contained in this Journal are solely those of theauthors/advertisers. The Publishers and Editor-in-Chief, its Editorial BoardMembers, and employees disown all responsibility for any injury to persons orproperty resulting from any ideas or products referred to in the articles oradvertisements contained in this Journal.

The Journal has a wide International and National Circulation/ Exchange and isabstracted and indexed in Index Medicus, Medline, IndMed, INSEAR, and Ulrich'sDirectory.

2014;Vol.56 The Indian Journal of Chest Diseases & Allied Sciences 3

Editorial Board

R. Agarwal, ChandigarhA.N. Aggarwal, ChandigarhG. Ahluwalia, Ludhiana J.N. Banavaliker, DelhiR.S. Bedi,PatialaD. Behera, New DelhiKazi S. Bennoor, BangladeshArati Bhatia, DelhiNarendra Bhatta, NepalMridula Bose, DelhiDhruva Chaudhry, RohtakP.N. Chhajed, MumbaiAnuradha Chowdhary, DelhiD.J. Christopher, Vellore

Brian H. Davies, UK R.K. Dewan, New DelhiS.N. Gaur, DelhiR. Guleria, New DelhiK. Guntupalli, USAK.B. Gupta, RohtakV.K. Jain, BikanerA.K. Janmeja, ChandigarhT. Kadhiravan, PuducherryS. Kashyap, ShimlaG.C. Khilnani, New Delhi Jai Kishan, PatialaRaj Kumar, DelhiDushantha Madegedara, Sri Lanka

T. Mohan Kumar, CoimbatoreA.A. Mahashur, MumbaiAtul C. Mehta, USAB.K. Menon, DelhiB.N. Panda, BhubneshwarM. Rahman, DelhiG.K. Rath, New Delhi J.K. Samaria, VaranasiR. Sarin, New DelhiRaj B. Singh,ChennaiVirendra Singh, JaipurR.N. Solanki, AhmedabadZ.F. Udwadia, Mumbai


6/64

4 The Indian Journal of Chest Diseases & Allied Sciences 2014;Vol.56

NATIONAL COLLEGE OF CHEST PHYSICIANS (INDIA)

GOVERNING COUNCIL[w.e.f.: 1st April 2014]

President (2014-2015) Vice-President (2014-2016)Dr S.K. Luhadia Dr Vikram Kumar JainUdaipur Jaipur

President-Elect (2015-2016) Immediate Past President (2013-2014)Dr Narayan Mishra Dr J.C. SuriOdisha New Delhi

Secretary (2013-2016) Joint Secretary (2014-2015)Dr S.N. Gaur Dr Rajesh N. SolankiDelhi Ahmedabad

Treasurer (2012-2015)Dr V.K. SinghDelhi

Councillors (2013-2015)

Dr Rajendra Prasad Dr V.K. Jain Dr Surya KantDelhi Jaipur Lucknow

Councillors (2014-2016)

Dr K.B. Gupta Dr Bharat Gopal Dr K. Bhupendra MeghwalRohtak New Delhi Jaipur

Zonal Chairmen

North South Central East West Dr J.C. Suri Dr P. Ravindran Dr S.K. Katiyar Dr Narayan Mishra Dr N.K. JainNew Delhi Trivandrum Kanpur Ganjam, Odisha Jaipur

Co-opted Members (NAPCON-2014)

Dr Rakesh Bhargava Dr Santosh KumarAligarh Agra


7/64

Note: These guidelines are being published simultaneously in Lung India and The Indian Journal of Chest Diseases and AlliedSciences (Official periodicals of ICS and V.P. Chest Institute and NCCP (India), respectively).Correspondence and reprint requests: Dr Dheeraj Gupta, Professor, Department of Pulmonary Medicine, PostgraduateInstitute of Medical Education and Research (PGIMER), Chandigarh - 160 012, India; Phone: 91-172-2756823; Fax: 91-172-2748215;E-mail: [email protected]

Guidelines for Diagnosis and Management of ChronicObstructive Pulmonary Disease: Joint Recommendations ofIndian Chest Society and National College of Chest Physicians (India)

Dheeraj Gupta 1, Ritesh Agarwal 1, Ashutosh Nath Aggarwal 1, V.N. Maturu 1, Sahajal Dhooria 1,K.T. Prasad 1, Inderpaul S. Sehgal 1, Lakshmikant B. Yenge 1, Aditya Jindal 1, Navneet Singh 2,A.G. Ghoshal 2, G.C. Khilnani 3, J.K. Samaria 2, S.N. Gaur 3, D. Behera 1 and S.K. Jindal 1 for the

COPD Guidelines Working Group

Department of Pulmonary Medicine, Postgraduate Institute of Medical Education and Research (PGIMER) 1 ,Chandigarh; Indian Chest Society 2 and National College of Chest Physicians (India) 3

COPD Guidelines Working Group (In alphabetical order)

Narayan Mishra, BehrampurSabir Mohammed, BikanerDharmesh Patel, VadodraRajendra Prasad, Delhi

Pallab Ray, ChandigarhSundeep Salvi, PuneP. Sarat, ChandigarhHoney Sawhney, ChandigarhNusrat Shafiq, ChandigarhNavneet Sharma, ChandigarhU.P.S. Sidhu, LudhianaVirendra Singh, Jaipur J.C. Suri, New Delhi J.S. Thakur, Chandigarh

Pranab Baruwa, GuwahatiR.S. Bedi, PatialaAshish Bhalla, ChandigarhDhruva Chaudhry, Rohtak

Rajesh Chawla, New DelhiS.K. Chhabra, DelhiVishal Chopra, PatialaD.J. Christopher, VelloreGeorge D’Souza, BengaluruD. Dadhwal, ChandigarhMandeep Garg, ChandigarhVikas Gautam, ChandigarhBharat Gopal, DelhiAbhishek Goyal, Chandigarh

Randeep Guleria, New Delhi

K.B. Gupta, Rohtak

Indranil Haldar, Kalyani

Ajay Handa, New Delhi

Jai Kishan, Chandigarh

Nirmal K. Jain, Jaipur

Sanjay Jain, Chandigarh

A.K. Janmeja, Chandigarh

Surya Kant, Lucknow

Surender Kashyap, Karnal

Parvaiz Koul, Kashmir

Raj Kumar, Delhi

Samir Malhotra, Chandigarh

[Indian J Chest Dis Allied Sci 2014;56:5-54]


8/64

COPD Guidelines : Joint Recommendations of ICS/NCCP (I)6

7. Exposure to biomass fuel smoke is a strong risk factor for COPD. (1A)

8. There is limited data on the association of ambient air pollution and COPD, and its

causative role in COPD needs further evaluation.9. There is insufficient evidence to attribute an

aetiological role of pulmonary tuberculosis incausing COPD.

10. A subgroup of chronic asthma may clinically behave like COPD; whether it is true COPDremains to be established. (UPP)

When to Suspect COPD?

1. A diagnosis of COPD should be considered inpersons having chronic symptoms of cough,sputum production, shortness of breath, and/orwheezing, especially among those withprolonged exposure to risk factors for thedisease. (1A)

2. A diagnosis of COPD should not be excluded inthe absence of physical signs. (2A)

3. Forced expiratory time (FET) of more than sixseconds is suggestive of airflow obstruction.(2B)

SYNOPSIS OF RECOMMENDATIONS

Chronic obstructive pulmonary disease (COPD) is acommon, preventable lung disorder characterised by

progressive, poorly reversible airflow limitation oftenwith systemic manifestations, in response to tobaccosmoke and/or other harmful inhalational exposures.As of now valid spirometry-based nationwideprevalence data for COPD in India are not available.In most of the critical analyses, validatedquestionnaire-based data has been accepted asreasonable for the assessment of prevalence of COPDdespite its limitations. COPD poses enormous burdenin terms of morbidity and mortality globally and inIndia. COPD poses a huge economic burden in termsof direct and indirect costs.

The Indian Chest Society and the National College

of Chest Physicians (India) have joined hands tocome out with these evidence-based guidelines tohelp the physicians at all levels of healthcare todiagnose and manage COPD in a scientific manner.

The modified grade system was used forclassifying the quality of evidence as 1, 2, 3 or usualpractice point (UPP) (Table 1). The strength of recommendation was graded as A or B dependingupon the level of evidence (Table 1).

Table 1. Classification of level of evidence and grading of recommendation based on the quality of evidence supporting the recommendation

Classification of Level of Evidence

Level l High-qual ity evidence backed by consistent resul ts from well-performed randomised controlled tr ia ls , or

overwhelming evidence from well-executed observational studies with strong effectsLevel 2 Moderate-quality evidence from randomised trials (that suffer from flaws in conduct, inconsistency, indirectness,

imprecise estimates, reporting bias, or other limitations)

Level 3 Low-quality evidence from observational evidence or from controlled trials with several serious limitations

Useful Practice Not backed by sufficient evidence; however, a consensus reached by working group, based on clinical experiencePoint and expertiseGrading of Recommendation: Based on the Quality of Evidence

Grade A Strong recommendations to do (or not to do) where the benefits clearly outweigh the risk (or vice versa) for most, if not all patients

Grade B Weaker recommendations where benefits and risk are more closely balanced or are more certain

What Are the Risk Factors for COPD?

1. Tobacco smoking is the most well established risk factor for COPD. (1A)2. Both smokeless and smoking forms of tobacco are

associated with serious health hazards, althoughonly smoking tobacco is primarily responsible forCOPD. (1A)

3. Bidi and other indigenous forms of tobaccosmoking are at least as (or even more) harmfulthan cigarette smoking. (1A)

4. Low tar or filtered cigarettes are not “lessharmful”. (2B)

5. There is no minimum number of cigarettes/ bidi perday below which the risk for COPD decreases. (1A)

6. Exposure to environmental tobacco smoke is adefinitive risk factor for COPD. (1A)

What is the Role of Spirometry in the Diagnosis ofCOPD? Whether Fixed Ratio or Lower Limit ofNormal Should be Used for Diagnosis?

1. Spirometry should be performed in all patientssuspected of having COPD. (1A)

2. In the absence of availability of spirometry,patients suspected of having COPD should bereferred for spirometric evaluation to a centrewith the facility. (UPP)

3. A post-bronchodilator forced expiratory volumein the first second/forced vital capacity (FEV 1/FVC) below the lower limit of normal (LLN, lowerfifth percentile of values from a referencepopulation) should be preferably used as thecriterion for diagnosis of airflow obstruction. (1A)


9/64


4. However, in the absence of reference equationsfor LLN, FEV1/FVC


10/64


7. Long-term SABA monotherapy on regular basisis not recommended. (2A)

8. Long-acting beta-agonist (LABA) monotherapycan relieve symptoms and decrease the

exacerbation rate in patients with stable COPD(FEV1


11/64


Figure. Algorithm for deciding place of management afterhospitalisation.B=BUN >24mg/dL; A=Altered mental status; P=Pulse rate>110/minute; 65-age >65 years; BAP-65 scores= 0- age 65 years, 2- one risk factor, 3- two riskfactors, 4- three risk factors; ICU=Intensive care unit.

How to decide the site of management of apatient with COPD exacerbation?

The decision to admit the patient can be made on

the level of severity as shown in table 4 while BAP-65score may help in deciding patients who needmanagement in an intensive care unit (Figure).

2. Inhaled SABAs should be used as the first-lineagent because of the quicker onset of action. (3A)SAMAs are, however, in no way inferior to SABAs.

3. Nebulised salbutamol at a dose of 2.5 mg every20 minutes (or salbutamol pressurised metereddose inhaler [pMDI] 100 µg 2-4 puffs every 20minutes) for one hour can be given initially. (3A)Further dosing would depend on the clinicalresponse, generally every 4-6 hours. (3A)

4. If additional bronchodilatation is desired, acombination of ipratropium (500 µg nebulised or20 µg 2-4 puffs with pMDI) and salbutamol(2.5 mg nebulised or salbutamol pMDI 100 µg 2-4puffs) every 4-6 hourly can be used. (3A).

5. Nebuliser or pMDIs with spacer are equallyeffective. (2A)

6. Nebulisation should not be driven by oxygen;patients should receive oxygen separatelythrough nasal cannula, with monitoring of oxygen saturation. (2A)

7. Intravenous methyl xanthines should not beroutinely used. (1A)

8. The use of intravenous or subcutaneous route of administering bronchodilators should bereserved in the most seriously ill mechanicallyventilated patients demonstrating inadequateresponse to inhaled therapy. (3B)

What is the role of glucocorticoids in AECOPD?1. Systemic steroids shorten recovery time, improve

lung function, oxygenation, reduce length of hospital stay, and are associated with fewertreatment failures. (1A)

2. A short course of oral prednisolone (or equivalent)at a dose of 30-40 mg per day is recommended formanaging acute exacerbations. (2A)

3. The duration of systemic steroid therapy should be 5-10 days. (2A)

4. Intravenous steroids should be given in patientswho are being mechanically ventilated or cannottolerate oral medication. (UPP)

5. ICS are not routinely recommended in themanagement of AECOPD. (1A)

Should antibiotics be used in patients with AECOPD?1. Antibiotics should be prescribed for all

exacerbations of COPD. (2A)2. The choice of antibiotics should be guided by

local flora and sensitivity pattern. (2A)3. Fluoroquinolones should not be used routinely

in treating AECOPD. (1A)4. Patients with AECOPD being managed in the

outpatient setting may be treated with first-lineantibiotics. (2A)

5. Hospitalised patients or those requiringmechanical ventilation (non-invasive/invasive)should be treated with second-line drugs. (2A)

6. The duration of therapy should be 5-7 days. (2A)

Table 4. Severity assessment (indications for hospitalisation)of exacerbation of COPD*Symptoms

Marked reduction in activity of daily living due to dyspnoeaAltered sensoriumNew onset cyanosis

Signs

Use of accessory respiratory musclesParadoxical chest wall movements

Central cyanosisSystolic blood pressure 30/minuteHeart rate >110/minuteAsterixisAltered mental status

Others

Presence of severe comorbid conditionsLack of social support

Pulse oximetry

SpO 2


12/64


What is the role of procalcitonin in deciding forantibiotic therapy?

1. Biomarkers do not have any role in the

management of AECOPD. (2A)2. Procalcitonin should not be used routinely inguiding antibiotic usage in COPD. (2A)

When should oxygen be prescribed, and at what dose?

1. Oxygen should be prescribed to hypoxaemicpatients with a target SpO 2 between 88%-92%. (1A)

2. Oxygen should be delivered preferably by aVenturi mask, and by nasal cannula uponrecovery. (2A)

3. Arterial blood gas (ABG) monitoring isrecommended in patients receiving oxygentherapy, wherever available. (2A)

What is the indication of non-invasiveventilation (NIV) during AECOPD?

1. NIV should be used early in the management of respiratory failure due to AECOPD. (1A)

2. NIV can be used even in settings where ABGmonitoring is not routinely available. (UPP)

Should Smoking Cessation be Advised? Whatare the Methods of Smoking Cessation?

1. A smoking history, including pack years or

smoking index (number of bidis/cigarettessmoked per day multiplied by number of yearssmoked; mild, moderate and heavy smokersare defined as having a smoking index of 300 respectively) should bedocumented for all patients with COPD. (UPP)

2. All COPD patients, regardless of age, should beencouraged to stop smoking, and offered help todo so, at every opportunity. (1A)

3. Nicotine replacement therapies, varenicline or bupropion, combined with an appropriatesupport programme should be offered to peoplewho are planning to stop smoking. (1A)

What is the Role of Health Education in COPD?1. Health education is an integral component of a

COPD management programme. Specialimportance should be given to inhaler technique,which should be demonstrated to the patientand accompanying attendants and reinforced atevery visit. This is particularly true for elderlypatients. (UPP)

2. For COPD patients who are not active smokers,potential aetiological exposures (environmentaltobacco smoke, biomass fuel smoke, and others)should be asked for and avoided. (UPP)

What is the Role of Pulmonary Rehabilitation?1. Structured pulmonary rehabilitation programmes

should be set up where feasible. (1A)2. In the absence of structured programmes, patients

should be advised regarding unsupervised dailyphysical activity. (3A)

3. All patients should be assessed for nutritionalstatus (at least by Body Mass Index [BMI]) at theinitial visit and followed up by serial BMIestimation at every visit. Any patient found to bemalnourished should be referred for nutritionaladvice to a specialist. (UPP)

What are the Indications for Oxygen Therapy inStable COPD?1. Long term supplemental oxygen therapy is

indicated for those with severe daytime restinghypoxaemia (1A) defined as:(a) PaO 2 of


13/64


What are the Surgical Treatments that can beOffered for the Treatment of COPD atAppropriate Centers?

1. Bullectomy in properly selected patients. (3A)2. Lung volume reduction surgery may be offered toproperly selected patients. (1A)

3. Lung transplantation may be offered to properlyselected patients. (1A)

Are Influenza and Pneumococcal VaccinationsUseful in Patients of COPD?1. Influenza vaccination is likely to be beneficial in

patients with severe COPD and/or frequentexacerbations. (UPP)

2. Pneumococcal vaccination is likely to be beneficial in patients with severe COPD and/orfrequent exacerbations. (UPP)

What is the Role of Prophylactic Antibiotics inCOPD?

Antibiotics should not be prescribed as a routine forthe prevention of exacerbations of COPD. (2A)

What Should be the Advice for Patients of COPDRegarding Air Travel?

Patients with severe COPD and those on long-termoxygen therapy should be assessed before air travel bya specialist. (UPP)


14/64


THE INDIAN JOURNAL OF CHEST DISEASES AND ALLIED SCIENCESVallabhbhai Patel Chest Institute, University of Delhi, Delhi-110 007

Director and Editor-in-Chief : Prof. Rajendra PrasadPlace of Publication : Vallabhbhai Patel Chest Institute, University of Delhi, DelhiWeb Address : http://www.vpci.org.inISSN No. : 0377-9343Language : EnglishPeriodicity : Quarterly (Published in the months of January, April, July and October)Method of Printing : Offset ProcessOverall Size : 27.5 cm x 20.5 cmPrint Area : 24.0 cm x 17.0 cm (Advertisement materials required in Print Area size only)

Spectrum of Readership : The readership comprises faculty members of medical colleges/researchinstitutions, chest physicians, cardiologists, medical practitioners,postgraduate students, research scholars, biomedical scientists and librariesof medical colleges/hospitals; including 800 fellows/members of theNational College of Chest Physicians (India)

Countries where it isCirculated : India, USA, Canada, South American countries, USSR, UK, The Netherlands,

Germany, Italy, African countries, Middle East, Japan, China, Australia andNew Zealand

International Standing : Abstracted and indexed in the globally reputed abstracting periodicals such

as Index Medicus, Medline, IndMed, INSEAR, and Ulrich’s Directory, etc

ADVERTISEMENT RATES* (w.e.f. 1st January 2011)

Per Issue Per Volume (4 issues)

Ordinary Full Page R 8,000.00 R 25,000.00Back Cover R 15,000.00 R 55,000.00Inside Cover R 12,000.00 R 45,000.00Facing Contents R 15,000.00 R 55,000.00

Colour Ads 50% extra on above rates

*Note: 1. The above rates are not subject to any Tax Deduction at Source .2. Advertisement materials (four positives in case of colour ads) are to be provided by

the advertiser in a CD with a print out (hard copy) of the advertisement.3. A discount of 10% will be offered to Advertising Agencies only.4. Advertisement Payments (along with the space order and advertisement material)

should be made inadvance through Banker’s Cheque / Bank Drafts only andshould be drawn in favour of the DIRECTOR, V. P. CHEST INSTITUTE, DELHI.

E-mail: [email protected] and [email protected]; Fax: 91-11-27666549; Phone: 91-11-27667102,

27667667, 27667441 Extn 135


15/64


ABSTRACTChronic obstructive pulmonary disease (COPD) is amajor public health problem in India. Althoughseveral International guidelines for diagnosis andmanagement of COPD are available, yet there are lotof gaps in recognition and management of COPD inIndia due to vast differences in availability andaffordability of healthcare facilities across thecountry. The Indian Chest Society and the NationalCollege of Chest Physicians (India) have joinedhands to come out with these evidence-basedguidelines to help the physicians at all levels of healthcare to diagnose and manage COPD in ascientific manner. Besides the Internationalliterature, the Indian studies were specificallyanalysed to arrive at simple and practicalrecommendations. The evidence is presented underthese five headings:(a) definition, epidemiology and disease burden,(b) disease assessment and diagnosis,(c) pharmacologic management of stable COPD,(d) management of acute exacerbations; and(e) non-pharmacologic and preventive measures.

Key words: Chronic obstructive pulmonary disease, Chronic bronchitis, Asthma, Emphysema.

INTRODUCTION

COPD is a common, preventable lung disordercharacterised by progressive, poorly reversibleairflow limitation often with systemic mani-festations, in response to tobacco smoke and/orother harmful inhalational exposures. As of nowvalid spirometry- based nation-wide prevalencedata for COPD in India are not available. In most of the critical analyses, validated questionnaire-baseddata has been accepted as reasonable for theassessment of prevalence of COPD despite itslimitations. COPD poses enormous burden in termsof morbidity and mortality globally and in India.COPD poses a huge economic burden in terms of direct and indirect costs.

METHODOLOGY

The process of development of guidelines fordiagnosis and management of patients of chronicobstructive pulmonary disease (COPD) in India wasundertaken as a joint exercise of the two National

Pulmonary Associations (Indian Chest Society andNational College of Chest Physicians), by theDepartment of Pulmonary Medicine, PostgraduateInstitute of Medical Education and Research,Chandigarh. The committee constituted for thispurpose included representation of the twoassociations, and experts from other institutes andmedical colleges including those from disciplines of Internal Medicine, Microbiology, Pharmacology,Radiodiagnosis, and Community Medicine.

For the development of guidelines, an extensivedesk-review was followed by a joint workshop. Thereview of literature was performed by searchingelectronic sources (PubMed, EmBase). The majorinternational guidelines available from the GlobalInitiative for Chronic Obstructive Lung Diseases(GOLD), American Thoracic Society (ATS) andNational Institute of Clinical Excellence (NICE) werealso reviewed.

The search was conducted under five subgroups:(a) definitions, epidemiology and disease burden,(b) disease assessment and diagnosis,(c) pharmacologic management of stable COPD,(d) management of acute exacerbations, and (e) non-

pharmacologic and preventive measures. Importantquestions were framed on the basis of discussions onissues with reference to the Indian context. Literaturereview and discussions in each area were coordinated by Group Chairs and recorded by rapporteurs. Theavailable evidence as well as the questions werecirculated to all the group members before the jointworkshop. Discussions for grading of evidence andrecommendations were held independently in fiveparallel group sessions, and thereafter together in the joint meeting of all the groups. Final decisions in the joint group were based on a consensus approach onthe majority voting.

The modified grade system was used forclassifying the quality of evidence as 1, 2, 3 or usualpractice point (UPP) (Table 1). 1 The strength of recommendations was graded as A or B dependingupon the level of evidence (Table 1). Grade Arecommendations in the guidelines should beinterpreted as “recommended” and the grade Brecommendations as “suggested”. While making arecommendation, the issues of practicality, costs, andfeasibility in the country at different levels of healthcare was also taken into consideration. 2

The final document was reviewed by all thecommittee members, as well as by other externalexperts.

Guidelines for Diagnosis and Management of ChronicObstructive Pulmonary Disease: Joint Recommendations of

Indian Chest Society and National College of Chest Physicians (India)


16/64


DEFINITION, EPIDEMIOLOGY ANDRISK FACTORS OF CHRONIC

OBSTRUCTIVE PULMONARY DISEASE

What is the Definition of Chronic ObstructivePulmonary Disease (COPD)?Obstructive airway diseases, emphysema and chronic bronchitis as separate disease enti ties were fi rstdefined in Ciba Guest Symposium in 1958. 3 Latervarious organisations came with their owndefinitions in their respective guidelines.Modifications have been made over the years withsubsequent updates of guidelines. Till date there is nosingle satisfactory definition of this common disease.Different definitions given by various organisationshave focused on common features of COPD. 4-7 The

definition endorsed by Global Initiative for ChronicObstructive Lung Diseases (GOLD), in its latestedition is comprehensive and elaborate, but complex. 8Retaining the key components of various definitionsand using simple terms, we recommend thefollowing definition of COPD:

“Chronic obstructive pulmonary disease is acommon, preventable lung disorder characterised by progressive, poorly revers ible airflow limitationoften with systemic manifestations, in response totobacco smoke and/or other harmful inhalationalexposures.”

What is the Prevalence of COPD?COPD affects more than 400 million people worldwide.The reported prevalence of COPD is highly variableranging from 0.2% in Japan to 37% in the UnitedStates. According to the 12-site BOLD (Burden of Obstructive Lung Disease) study, the averageprevalence of COPD is 10.1%, with wide variations. 9Prevalence estimates based on spirometry are reportedto be higher than those based on questionnaire-basedstudies. 10, 11 Before the turn of 20 th Century, there werefew studies from India, which reported the prevalenceof COPD. Most of them were limited by small samplesize and were based on un-validated questionnaire-interviews making them unreliable for any nationalassessment. 12-14 Nevertheless, the prevalence of COPDreported in these studies varied from 2%-22% in malesand from 1.2%-19% in females. There were threeattempts to systematically review and analyseavailable data until the results of the INSEARCH(Indian Study on Epidemiology of Asthma, RespiratorySymptoms and Chronic Bronchitis in Adults) phase IIwas published. 13-15All the reviews concluded that datawas insufficient to derive national representativefigures for prevalence of COPD. After publication of the results of INSEARCH II, some nation-wideprevalence data are available. Together, the INSEARCH

I and II involve 16 centres across the country, included

121,776 individuals of more than 35 years of age, andwas based on a well validated questionnaire. 16 Thestudy population had rural and urban representationof both genders. 17,18The prevalence of COPD in Indiaaccording to these studies was 3.7% (4.5% and 2.9%among males and females, respectively). The estimated burden of COPD in India is about 15 mil lion cases(males and females contributing to 9.1 and 5.8 million,respectively). These figures may, however,underestimate the true burden since questionnaire- based prevalence rates tend to underestimate the truespirometry-based prevalence of COPD.

As of now, valid spirometry based nation-wide prevalence data for COPD in India are not available. Inmost of the critical analyses, validated questionnaire-based data has been accepted as reasonable for theassessment of prevalence of COPD despite its

limitations.What are the Implications of COPD onMorbidity and Mortality?

Globally, COPD is the ninth leading cause of loss of Disability Adjusted Life Years (DALYs) according tothe baseline projections made in the Global Burden of Disease Study (GBDS).19 In India, chronic respiratorydiseases (CRDs) account for 3% of DALYs, and COPDis the major cause among CRDs. 20 COPD alsoaccounts for more than 3 million deaths per yearglobally making it the third leading cause of death

worldwide.21

It accounts for 2.3%-8.4% of all deaths.This proportion is more among males than females,and more among the elderly as compared to theyoung. 11,22 In India, COPD causes about 500,000deaths per year. 23 A review of data from multiplesources suggested that COPD causes more deathsthan tuberculosis and pneumonia. 24 Recently, theState Health Systems Resource Centre reported thatCOPD is the leading cause of death in Maharashtrastate, surpassing coronary artery disease,cerebrovascular accident and diabetes combinedtogether. 25 According to the preliminary report of the“Million Death Study”, CRDs were the second

common cause of death among Indian adults. Theseare second and the third common causes of death inrural and urban population, respectively. 26

COPD poses enormous burden in terms of morbidityand mortality globally and in India.

What is the Economic Impact of COPD?

The estimated economic loss in India due to COPD isabout R 35,000 crores for the year 2011 and ispredicted to exceed R 48,000 crores for the year 2016.20These economic losses are more than the annual budget of the Ministry of Health and Family Welfare

(MHFW) for the year 2010-2011, which was R 25,124


17/64


crores. 23 In a study 27 that assessed the costs of treatment amongst 423 COPD patients in India, it wasfound that patients spent 15% of their annual incomeon smoking products and 30% on disease

management. It has been calculated that properprogramme-based or guideline-based management of COPD can reduce these costs by approximately 70%. 20

COPD poses a huge economic burden in terms of direct and indirect costs.

What are the Risk Factors for COPD?

There are numerous factors that are thought toaffect lung function at various stages of development and ageing of lung (Table 5). Some of them have strong evidence to qualify as beingcausative for COPD; however there are others for

which such causative associations are yet to beestablished. Exposure to multiple risk factors tendsto have an additive effect.

Tobacco Smoking

Non-communicable diseases (NCDs) account forapproximately 36 million deaths per year across theglobe; among them tobacco alone causesapproximately 6 million deaths and is the leadingmodifiable risk factor for NCDs. 28,29

Tobacco is abused in two main forms, mainlysmoking and smokeless tobacco. Globally, the rate of current smokers is estimated to be about 1 billion. 29 Inthe INSEARCH study, the prevalence of tobacco usewas 28.5% and 2.1%, respectively among adult malesand females. 18 According to the Global Adult TobaccoSurvey (2009-2010) conducted in India, theprevalence of tobacco use in any form was 34.6%(47.9% and 20.3% among males and femalesrespectively). Of them, 14% (24.3% males and 2.9%females) smoked tobacco. The rise in COPD incidencehas paralleled the rise in tobacco smokingthroughout the world. 30, 31 There is a strong dose-response relationship (for amount and duration)

between tobacco smoking and COPD. 16,32 InINSEARCH II study, the adjusted odds ratio (OR) fordeveloping COPD among smokers as compared tonon-smokers was 4.08. In addition, smoking tobacco

has additive effect with most of the other risk factorsfor COPD.29Tobacco is consumed in both smoked and

smokeless forms. It is well known that tobacco smokecontains more than 4000 harmful chemicals, of whichover 50 are known carcinogens. Smokeless tobacco(chewing, sniffing and others) is associated withcancer, hypertension and heart disease. Noassociation has been reported with COPD. Indeveloping countries including India, indigenousforms of smoking tobacco are more prevalent thancigarette smoking. 32, 33 It was thought that, having lowtobacco content, bidi smoking would be less harmful

than cigarette smoking. However, contrary to this belief, COPD is more common among bidi and hookahsmokers as compared to cigarette smokers. 17, 18, 32-34Chutta, chillum and hookah are other traditionalmethods of smoking prevalent in India, and these areassociated with even greater risk for developingCOPD than cigarette smoking. 32,33,35 Low tar cigarettesare filtered to prevent tar from being inhaled.However, the adverse effects of tobacco smoking arenot limited to the amount of tar. Shifting to low-tarcigarettes in an attempt to decrease the risk of lungcancer was not effective. 36Another review 37 suggestedthat the effect of low-tar cigarettes on COPD areinconsistent.

The risk of COPD increases with increase in thenumber of cigarettes/ bidis as well as with theduration of smoking. Any amount of smoking isharmful, although the risks are lower at low dose. 38 Inone study, 32 the prevalence of CRDs among smokerswith 2.5 and >13.5 pack years was found to beapproximately 13% and 60%, respectively. Similarlyanother study 16 reported that prevalence of COPD insmokers with less than 20 pack years was 9.6%,which increased to 18% in subjects who smoked morethan 20 pack years.

Table 5. Risk factors for chronic obstructive pulmonary disease

Established Probable

Tobacco smoking Outdoor air pollutionEnvironmental tobacco smoke Pulmonary tuberculosis

Exposure to biomass fuel smoke Poorly treated asthma

Occupational exposure Intrauterine growth retardation

Alpha-1-antitrypsin deficiency Poor nourishment

Repeated lower respiratory infections during childhood

Others

Age

Male gender

Low socio-economic status


18/64


Environmental Tobacco Smoke (ETS)

About 25%-45% of patients with COPD are neversmokers. Recent evidence suggests that factors otherthan smoking are strongly associated with COPD. 39, 40In INSEARCH-II study, approximately 60% patientswith chronic bronchitis were non-smokers. 18 ETSexposure among non-smokers, especially women andchildren is common in many Asian countries. TheINSEARCH study established the association of ETSexposure with COPD. The adjusted OR for COPDamong those with ETS exposure was reported to be1.99 (95% confidence intervals [CI], 1.69-2.34).18 Theodds for combined childhood and adult exposure washigher than that with ETS exposure during eitherchildhood or adulthood alone, suggesting acumulative effect.

Burning of Biomass Fuel

The combustion of biomass fuel, such as dried dung,wood and crop residue is associated with generationof several toxic gases and particles which areresponsible for various health hazards, includingrespiratory problems. 41, 42 Globally about 3 billionpeople are exposed to biomass fuel smoke, comparedwith 1.01 billion people who smoke tobacco. 39, 43According to the third National Family HealthSurvey, about 75% of households in India stillcontinue to use biomass fuel for cooking. Respiratorysymptoms were reported in 13% of 3608 non-smokingwomen involved in domestic cooking. 44 One study 45found the prevalence of airflow limitation to bealmost double in residents of households using biomass fuel compared to households using liquefiedpetroleum gas (LPG) (8.1% versus 3.6%). Contrary toprevious studies, this study displayed similarpatterns for males as well as females. Two recentmeta-analyses suggest that exposure to biomass fuelcombustion is an important risk factor for COPD. 46, 47In fact, it has been argued that in India, where morethan 70% people use biomass fuel for cookingpurposes compared to 25% who smoke, exposure to biomass fuel may be a bigger risk factor for COPD inIndia. 40

Occupational Exposures

A systematic review of epidemiological data by theAmerican Thoracic Society suggests that about 15% of COPD cases might be related to exposure atworkplace. 48 In subsequent studies, the proportion of patients with COPD attributable to occupation wasabout 19% overall and 31% in never smokers. 49 Thelist of occupations associated with increased risk of COPD include rubber, plastic and leathermanufacturing, textile mill product manufacturingand food product manufacturing. 50

Alpha-1 Anti trypsin Deficiency and Other Genetic Factors

Alpha-1 antitrypsin (AAT) deficiency is the only well-

known genetic risk factor for emphysema.51

While theprevalence of AAT deficiency is significant in Europeand North America, it is not very commonly reportedfrom the Asian continent including India. Two studiesfrom India 52, 53 suggest that some interleukin genotypes,and mutation in glutathione s-transferase 1, have someassociation with COPD.

Outdoor Air Pollution

Ambient air pollution in metropolitan cities has beenfrequently implicated as a causative agent for variousrespiratory diseases including COPD, especially inAsian countries where urban air pollution is high. 54

In one study, 55 respiratory symptoms were found to bemore common in the higher pollution zones among4171 randomly selected residents. Also, theemergency room visits for COPD increased by 24.9%when the levels of pollutants in ambient air exceededthe acceptable limits. 55

Pulmonary Tuberculosis

The association of pulmonary tuberculosis (PTB)with COPD has occasionally been described. Theprevalence of airflow obstruction varies from 28% to68% of patients with treated PTB. 56 In a nation-wide

survey of 13,826 adults in South Africa, a history of PTB was associated with COPD with odds of 4.9 formales and 6.6 for females. 57 Whether this finding of obstructive functional defect in post-tubercular sequel behaves as COPD, or is di fferent, remains to beestablished in long-term prospective cohort studies.

Asthma

Patients with active asthma were found to have10-fold increased risk of chronic bronchitis and17-fold increased risk of emphysema as compared tothose without asthma, even after adjustment forconfounding factors. 58A subsequent review 59 alsosuggests that a subset of patients with asthma mayhave COPD phenotype.

Miscellaneous Factors

An increased association of COPD is reported withdemographic and socio-economic factors, such asadvancing age, low socio-economic status and urbanresidence with lower socio-economic status. Thisassociation may perhaps be attributed to the greaterprevalence of smoking and cumulative effects of smoking and other exposures with age. Low socio-economic status and infections have been listed asadditional risks.


19/64


Recommendations

1. Tobacco smoking is the most well established risk factor for COPD. (1A)

2. Both smokeless and smoking forms of tobacco areassociated with serious health hazards, althoughonly smoking tobacco is primarily responsible for COPD. (1A)

3. Bidi and other indigenous forms of tobacco smoking are at least as (or even more) harmful than cigarettesmoking. (1A)

4 . Low-tar or filtered cigarettes are not “less harmful”. (2B) 5 . There is no minimum number of cigarettes/bidis per

day below which the risk for COPD decreases. (1A) 6 . Exposure to ETS is a definite risk factor for COPD. (1A) 7 . Exposure to biomass fuel smoke is a strong risk

factor for COPD. (1A) 8. There are limited data on the association of ambient

air pollution and COPD, and its causative role inCOPD needs further evaluation.

9. There is insufficient aevidence to attribute anaetiological role of PTB in causing COPD.

10. A subgroup of chronic asthma may clinically behavelike COPD; however whether it is true COPD remainsto be established. (UP P)

DIAGNOSIS AND ASSESSMENT OFCOPD

When to Suspect COPD?COPD is one of the important differential diagnosis inpatients presenting with symptoms of chronic cough,sputum production, breathlessness and/orwheezing. 60-62 This is especially true when patientshave a history of prolonged exposure to risk factors.There is no definite duration of exposure to the risk factors that can result in COPD. However, in general, aprolonged exposure to risk factors is required for thedevelopment of the disease. Some patients presentingwith differently from the afore-mentioned symptoms(as detailed under the next subheading) might also bedetected to have COPD on further evaluation.

Recommendation A diagnosis of COPD should be considered in personshaving chronic symptoms of cough, sputum production, shortness of breath, and/or wheezing,especially among those with prolonged exposure torisk factors for the disease. (1A)

What are the Symptoms of COPD?COPD patients may present to a healthcare facility infour typical ways:1. With one or more of the characteristic respiratory

symptoms of chronic progressive breathlessness,cough, sputum production, wheezing and/or

chest tightness. Recent studies reveal thatpresence of one or more of these symptomsincreases the odds for the diagnosis of COPD. 60-62

2. Without respiratory symptoms, like breath-

lessness, because patients might have reducedtheir physical activity unknowingly to very lowlevels. They might just complain of fatigue.

3. With symptoms attributed to complications of thedisease, like weight loss (COPD related cachexia)or leg swelling (due to cor-pulmonale).

4. With an exacerbation (as discussed in the sectionon exacerbation).

BreathlessnessPatients may variously describe their breathlessnessas: “my breathing requires effort”, “I cannot getenough air in”, “I feel out of breath” or “I feel hungerfor more air”. 63 There may be individual and culturalvariations in the description of breathlessness. 64Breathlessness is usually present on exertion untillate in the course of the disease. Orthopnoea occursearly and more commonly in heart failure, which isan important differential diagnosis, while it isreported infrequently and late (if ever) in patientswith COPD. The severity of breathlessness may begraded on various scales. A simple and widely usedscale is the modified Medical Research Council(mMRC) questionnaire 65 (illustrated in Table 6).Table 6. Modified Medical Research Council grading of

breathlessnessGrade Patient’s Description of Breathlessness

Grade 0 I only get breathless with strenuous exercise

Grade 1 I get short of breath when hurrying on the level orwalking up a slight hill

Grade 2 I walk slower than people of the same age onthe level because of breathlessness or have tostop for breath when walking at my own paceon the level

Grade 3 I stop for breath after walking about 100 yards orafter a few minutes on the level

Grade 4 I am too breathless to leave the house or I am breathless when dressing

Cough and Sputum ProductionCough may be the only presenting symptom. On theother hand, a smoker might consider his cough to be anatural consequence of smoking, and might neglect itas a symptom. An increasing intensity or change inthe nature of cough may be reported. It may be moreprominent in the morning. Cough may beaccompanied by mucoid or purulent sputumproduction that may vary greatly in amount. 66 Again,patients may find it a normal phenomenon associatedwith smoking and might even feel that smoking helpsin easing out the passage of sputum. Immediatelyfollowing smoking cessation, cough and sputum may


20/64


Table 7. Useful physical signs for the diagnosis of thechronic obstructive pulmonary disease

Inspection

Pursed-lip breathing

Use of accessory muscles of respiration Jugular venous distension during expirationRetraction of suprasternal, supraclavicular and intercostalspaces during inspirationShort tracheaPulsus paradoxusIncreased antero-posterior diameter of the chest (barrel-shaped chest)Reduced chest movementsPeripheral oedemaDyspnoea-relieving postureMuscle wasting

Palpation

Restricted chest expansionSubxiphoid shift of maximum impulse of the heart

Percussion

Chest hyper-resonanceObliteration of cardiac dullnessLower level of liver dullnessLower diaphragmatic levels

Auscultation

Diminished breath soundsEarly inspiratory cracklesLoud pulmonic component of second heart sound

Special Maneuver

Forced expiratory timeSnider’s match test

become more bothersome, but generally improve withcontinued abstinence. 67 The epidemiological definitionof chronic bronchitis (regular production of sputum forthree or more months for two consecutive years) is

arbitrary and might not apply to a given patient.However, it might identify an “at risk” individual.

Wheezing Patients may complain of wheezing, variouslydescribed as noisy breathing or a whistling sound.Wheezing may have diagnostic value when seen inthe light of other clinical features. 60-62

Chest TightnessPatients may complain of chest tightness, “chestcongestion” or an “obstructed chest”.

Chest Pain and HaemoptysisThese are not the usual symptoms of COPD. Theirpresence is often a pointer to an alternative diagnosis(e.g., lung malignancy, PTB etc.).

What are the Signs of COPD?COPD patients may demonstrate various physicalsigns that may either be due to the primary disease oran associated complication (Table 7). 68 Diminished breath sounds and wheezing on auscultation have been shown to increase the odds for a diagnosis of COPD.60 An important clinical sign is the forcedexpiratory time (FET). 69 An FET of more than sixseconds suggests airway obstruction.

Importantly, COPD patients, especially thosepresenting early, might lack any of the above-mentionedsigns. A diagnosis of COPD cannot be rejected due tothe mere presence of a normal physical examination.

Recommendations1 . A diagnosis of COPD should not be excluded

in the absence of physical signs. (2A) 2 . Forced expiratory time of more than six seconds

is suggestive of airflow obstruction. (2B)

What Medical History should be Obtainedfrom Patients Suspected of having COPD?

A patient suspected to have COPD should be askedabout the exposure to risk factors, especially tobaccosmoking and exposure to smoke from biomass fuelcombustion. A history of allergic disorders, asthmaand other respiratory diseases, presence of comorbidities, family history of allergic andrespiratory disorders, history of previousexacerbations and hospitalisations, and impact of disease on patient’s life (including limitations of activities of daily living and the associatedpsychosocial morbidity) should also be documented.

What is the Role of Spirometry in the Diagnosis ofCOPD? Whether Fixed Ratio or Lower Limit ofNormal should be Used for Diagnosis?Demonstration of airflow obstruction is essential tomake a definitive clinical diagnosis of COPD.Spirometry is a simple and accurate tool to assessairflow obstruction. Spirometry should be performedas per standard guidelines. 70, 71 Table 8 summarisessome of the important points elaborated in theseguidelines regarding the equipment and performanceof spirometry. 70, 71 Both forced expiratory volume in firstsecond (FEV1) and forced vital capacity (FVC) should be assessed, and the FEV 1/FVC ratio calculated.

The criterion for defining airflow obstruction has been a subject of much debate in recent years. 72, 73 TheGOLD committee suggests use of a post- bronchodilator FEV 1/FVC less than an arbitrarilyfixed value of 0.7 (FR0.7) as the criterion for thediagnosis of COPD. 8 However, guidelines onspirometry recommend the use of statistically derivedlower limit of normal (LLN) FEV 1/FVC as the cut-off to define airflow obstruction. 70 The LLN is defined asthe lower fifth percentile of values in the reference


21/64


population. The age and gender adjusted referenceequations for this purpose are generated fromspirometric data from a cohort of normal healthy non-smoking individuals sampled from the particularpopulation in a geographical area. LLN is thencomputed as the difference between the predictedvalue and 1.645 times the standard error of estimateof the reference equation.

A systematic review 74 analysed the findings of 18studies that compared these two spirometricdefinitions. Most of these studies reported that use of FR0.7 leads to a much higher proportion of subjects being diagnosed as having airflow obstruction thanuse of LLN.75-86 FR0.7 misclassifies more than 20% of subjects as having airflow obstruction whencompared to LLN. 87 Further discordance between thetwo methods in classifying obstruction increases inthe elderly as LLN values decrease with advancingage.88 Thus, elderly individuals having a FEV 1/FVCvalue which might be within a statistically normalrange for their age and gender, face the risk of beingdiagnosed as having COPD by using FR 0.7.

Two studies 80, 89 analysing longitudinal datahave concluded that subjects having FEV 1/FVCabove the LLN but below FR 0.7 (the so called“discordant” group) had an increased risk of mortality than those having FEV 1/FVC >0.7. But thecomparison of mortality was between the“discordant” group and a group of healthyindividuals without respiratory symptoms, thus, itdoes not hold valid for those who consult the

physician for respiratory symptoms. 90 Also, as therelationship between lung function and the risk of death is a continuum, it follows that any arbitrarycut-off would potentially have a difference inmortality among subjects falling on either sidewithout representing true disease. 91 A recentstudy 90 has shown that rate of decline of lungfunction in the discordant group is half the valueobserved in those with FEV 1/FVC below LLN, whileit is similar to those with FEV 1/FVC above bothLLN and FR 0.7 cut-off. Thus, the LLN has betterdiscriminatory value for identifying patients with ahigher rate of lung function decline. An analysis of the afore-mentioned studies suggests that usingFR0.7 criterion leads to over-diagnosis of the diseaseas compared to a more statistically sound LLNcriterion. Moreover, studies have also shown thatFR0.7 also potentially ‘under-diagnoses’ youngerpatients with airflow obstruction. 92 Young patients,especially below the age of 40 years might have aFEV1/FVC below the LLN for their age, but mightget misclassified as normal as the ratio may begreater than the fixed cut-off of 0.7. 88

Going by the current evidence, the LLN is a morerobust criterion for diagnosis of airflow obstructionthan the FR 0.7. Several reference equations derivedfrom healthy individuals from various regions of India are available for this purpose. 93-98 However,there are still concerns among the experts regardingthe validity of these equations for populations fromall parts of the country. It is imperative that

Table 8. Equipment and performance of spirometry

Equipment

It is the responsibility of the manufacturers to manufacture pulmonary function testing systems that satisfy the latest acceptedpublished guidelines. It is also the duty of the user that the system being used complies with the latest recommendations and givesaccurate measurements during the course of its running.

The equipment should meet the recommended requirements for volume, flow, resistance and time of flow.Calibration checks for volume, leak, volume and flow linearity should be performed regularly.

Performance

Each test performed should meet certain within-maneuver and between-maneuver criteria. Individual spirograms are acceptable if they are free from artifacts (cough during first second of exhalation, glottis closure, early termination, sub-maximal effort orobstructed mouthpiece), have good starts with extra-polated volume 6 seconds or a plateau in the volume-time curve).Acceptable spirograms should meet the between-maneuver criteria. Out of three acceptable spirograms, the two largest values of FVCshould be within 0.15L of each other, the two largest values of FEV 1 should also be within 0.15L of each other. If these criteria are notmet, testing should be continued until the above criteria are met with additional acceptable spirograms or a total of eight maneuvershave been performed.

Bronchodilator Administration and Post-Bronchodilator Testing

Four separate doses of salbutamol 100µg and/or ipratropium bromide 40µg are delivered through a valved spacer device at 30seconds intervals.Spirometry should be performed after 10-15 minutes later for salbutamol and after 30 minutes for ipratropium bromide.

Evaluation

A post-bronchodilator FEV 1/FVC less than the lower limit of normal signifies obstruction. Further severity classification is doneaccording to the FEV 1 value.

Appropriate reference equations should be used for determining the lower limit of normal.FVC=Forced vital capacity; FEV 1=Forced expiratory volume in the first second.


22/64


spirometry reference equations should be generatedfor various population subsets in India. Meanwhile,the criterion of FR 0.7 might be used only in the absenceof a valid reference equation for FEV 1/FVC in a

particular region of the country.Recommendations

1. Spirometry should be conducted in all patientssuspected of having COPD. (1A)

2. In the absence of availability of spirometry, patientssuspected of having COPD should be referred for aspirometric evaluation to a centre with the facility.(UPP)

3. A post-bronchodilator FEV 1 /FVC below the lower limit of normal (LLN, lower fifth percentile of values from areference population) should be used as the criterion for diagnosis of airflow obstruction. (1A)

4. In the absence of reference equations for LLN, FEV 1 / FVC


23/64


Recommendation

Peak expiratory flow should not be routinely used for screening, diagnosis or monitoring in COPD. (1A)

How Should the Severity of COPD be Classified?

Severity staging of COPD is important for diseaseprognostication as well as for treatment. GOLDguidelines classify COPD into mild (FEV 1 >80%predicted), moderate (50%


24/64


other respiratory disorders in patients with symptomssuggestive of COPD. In one such study, 146 among 516patients with a PFT suggestive of obstruction, HRCTwas helpful in establishing an aetiology other than

COPD in 12.7% patients. Total lung capacity (TLC) is increased in COPDdue to air trapping and emphysema. DLCO isdecreased in emphysema due to reduction in the areaof the alveolar capillary membrane. The reduction inDLCO correlates well with pathological emphysemaand emphysematous changes in HRCT. 147-149Adecreased DLCO may also help in predictingmortality in patients with COPD. There is no clearthreshold value. 150,151 DLCO is typically withinnormal limits in COPD with a primarily chronic bronchitis phenotype.

Detailed cardiopulmonary exercise testing (CPET)

is useful to assess functional status to establishexercise restrictions and to assess the impact of therapeutic interventions. 152-155 CPET has also beenshown to be useful in patients with exertionaldyspnoea, out of proportion to their lung functionabnormality, to assess additional contributing factorslike myocardial ischaemia. 156-158 Six-minute walk test(6MWT), a simpler surrogate for formal CPET, hasalso been found to be useful in assessment of functional status, effectiveness of therapy, andprognosis in COPD. 159-163

Alpha-1 Antitrypsin Deficiency

Data on the prevalence of AAT in Indian patientswith COPD is sparse. 164 Western data suggest thatapproximately 3% of patients with COPD might haveAAT. 165 In the absence of an effective therapy forAAT, it would be prudent to restrict AAT testing foratypical cases of COPD with a high probability of AAT deficiency (such as a young patient with lowerlobe emphysema).

Recommendations

1. All new COPD suspects with cough of more than twoweeks’ duration should undergo sputum smear examination for acid-fast bacilli to rule out pulmonarytuberculosis as per the standard practice of Revised National Tuberculosis Control Programme (RNTCP).(UPP)

2. Pulse oximetry should be used to screen for hypoxaemiain stable disease with FEV 1


25/64


What Drugs are Available for the Management ofPatients with Stable COPD, and What are TheirRecommended Doses?

The three main groups of drugs available for themanagement of stable COPD include inhaledanticholinergics, inhaled beta-2-agonists, and ICS.The currently available drugs and their commonlyprescribed doses are summarised in table 11. Otherdrugs which can also be used include the oral drugs, beta-agonists, methylxanthines, and selectivephosphodiesterase-4 (PDE4) inhibitors.

Table 9. Differential diagnoses of chronic obstructivepulmonary disease

Asthma

Early age of onset

Episodic symptoms with asymptomatic periods in-betweenWide variation of symptoms day to daySymptoms worse at night/early morningChronic productive cough is uncommonHistory of atopy may be presentFamily history of asthma may be presentReversibility of airway obstructionIncreased diffusing capacity for carbon monoxide

Congestive Heart Failure

Cardiomegaly/pulmonary oedema in chest radiographPulmonary function test suggestive of restrictive abnormality

Bronchiectasis

Copious purulent sputumClubbing, coarse cracklesHigh resolution computerised tomography (HRCT) shows bronchial dilatation and bronchial wall thickening

Tuberculosis

Fever, anorexia, weight lossChest x-ray opacity, fibrocavitary diseaseMicrobiological diagnosis

Constrictive Bronchiolitis

Non-smoker, young ageHistory of rheumatoid arthritis, fume exposure, lung/bonemarrow transplantationHRCT shows mosaic attenuation

Diffuse Panbronchiolitis

Non-smokerAssociation with chronic sinusitisHRCT shows centrilobular nodules, hyperinflation and air-trapping

Table 10. Treatment goals in a patient with stable chronicobstructive pulmonary diseaseReduction in Current Symptoms

Relief in breathlessness and other symptomsImprovement in exercise toleranceImprovement in overall health-related quality of life

Reduction of Future Risk

Prevention (or slowing down) of disease progression

Prevention of disease exacerbationsReduction in disease-related mortalityMinimising Adverse Effects from Treatment

Adapted from GOLD guidelines8

The goals should be individualised, and assessedand monitored objectively. For instance, breathlessness can be easi ly evaluated using themMRC grading. Similarly, exercise tolerance can beassessed through the 6MWT, and the QoLevaluated by using any one of the several validatedquestionnaires (such as, SGRQ). Diseaseprogression is measured by calculating the rate of decline in FEV1.

Table 11. Commonly used drugs and dosages for pharmaco-therapy of stable diseaseDrug Category Recommended Dose

Inhaled Agents * AnticholinergicsShort actingIpratropium bromide 20-40 µg as needed

Long actingTiotropium 18 µg once daily

Beta-agonistsShort actingSalbutamol 100-200 µg as neededLevosalbutamol 45-90 µg as neededTerbutaline 250-500 µg as needed

Long-actingSalmeterol 25-50 µg twice dailyFormoterol 6-12 µg twice dailyIndacaterol 150-300 µg once daily

CorticosteroidsFluticasone 25-500 µg twice dailyBudesonide 100-400 µg twice dailyBeclomethasone 100-400 µg twice dailyCiclesonide 80-160 µg twice dailyMometasone 25-500 µg twice daily

Oral AgentsBeta-agonistsSalbutamol 2-4 mg twice/thrice dailyBambuterol 10-20 mg once dailyTerbutaline 2.5-5 mg thrice daily

MethylxanthinesSustained release theophylline 100-400 mg once dailyDoxophylline 400 mg twice/thrice daily

Selective PDE4 InhibitorsRoflumilast 0.5 mg once daily* Recommended doses are those for a pressurised metereddose inhaler. These drugs are also available as dry powderinhalers and for nebuliser use, for which doses may vary.

What is the Ideal Route and Method of DrugDelivery?

Inhaled therapy is now established as the mainstay of the treatment for patients with stable COPD. It allowslow doses of bronchodilators or corticosteroids to bedelivered rapidly and directly into airways, therebyachieving high local concentrations at the site of action, while significantly reducing systemic adverse


26/64


effects as compared to oral or parenteral therapy.Several patients continue to receive oral agents, because of patient preferences, ignorance, financialconstraints, and/or lack of availability or acceptance

of inhaled drugs.Three kinds of aerosol devices are available for thetreatment in COPD, namely pressurised metered doseinhalers (pMDIs), dry powder inhalers (DPIs), andnebulisers. The pMDIs are commonly used, but manypatients (especially elderly) find it difficult to use themcorrectly, often because of problems in actuation-inhalation coordination. The pMDIs used with a valvedspacer further improves drug delivery to airways andreduces oropharyngeal deposition. Breath-actuatedpMDIs may also obviate some of these issues. A widearray of DPIs are available that vary significantly ingenerated particle size and airway delivery. The DPIs

are breath-actuated, so coordination issues are muchless. Even then, many patients are unable to use thesedevices correctly as relatively higher airflows arerequired to generate good aerosol. In an observationalstudy 173 of 3811 patients with COPD or asthma, criticalerrors in technique, that potentially affected drug

delivery, were observed in 28% of pMDI users and,depending on the specific device, 11%-32% of DPI users.Another review 174 found that 43%, 55% and 59%patients, respectively could correctly use pMDI, pMDI

with spacer, and DPI, and teaching substantiallyimproved technique. It is important to educate patientsregarding correct inhaler technique, with regularmonitoring of technique at follow-up visits. The correcttechnique of pMDI use is summarised in table 12.Nebulisers use oxygen, compressed air, or ultrasonicpower to generate fine aerosol from drug solutions orsuspensions that is passively delivered to airways viamask or mouth-piece. However, these are bulky, muchmore expensive, require electrical power for operation,and need regular maintenance. Their overall dosedelivery is largely comparable to pMDIs with spacer, orgood quality DPIs.

Two large systematic reviews174, 175

have concludedthat the type of aerosol device has no effect on clinicaloutcomes in patients with COPD. The AmericanCollege of Chest Physicians and the American Collegeof Asthma, Allergy and Immunology have alsorecently concluded that when patients use these

Table 12. Correct technique for using pressurised metered dose inhalerSteps for Using Pressurised Metered Dose Inhaler1. Sit up straight, and remove inhaler cap2. Hold inhaler upright by placing index finger on top of the canister while providing support on the bottom of the device with the

thumb, and shake well3. Take a few deep breaths and breathe out gently away from the device4. Put mouth-piece between teeth without biting and close lips to form good seal, keeping the tongue relaxed and not blocking the

mouth-piece5. Start breathing in slowly through mouth, and simultaneously press down firmly on canister with the index finger, once only, to

release one puff of medicine6. Continue to breathe in slowly, evenly and deeply over 5-7 seconds, till the lungs seem completely filled7. Hold breath for about 10 seconds, or as long as comfortable8. While holding breath, remove inhaler from mouth9. Breathe out slowly away from the device, and then inhale normally10. If an extra dose is needed, wait 30 seconds to a minute, and then repeat steps 2 to 911. Replace inhaler capSteps for Using Pressurised Metered Dose Inhaler with a Spacer Device1. Sit up straight, and assemble spacer device2 . Remove inhaler cap3. Hold inhaler upright by placing index finger on top of the canister while providing support on the bottom of the device with the

thumb, and shake well4. Insert inhaler upright into spacer5. Put mouth-piece between teeth without biting and close lips to form good seal, keeping the tongue relaxed and not blocking the

mouth-piece6. Take a few deep breaths and breathe out gently away from the device7. Hold spacer horizontally at level of mouth, and press down firmly on canister with the index finger, once only, to release one puff

of medicine8. Breathe in slowly, evenly and deeply, till the lungs seem completely filled, and then hold breath for about 10 seconds or as long

as comfortable OR breathe in and out normally for four breaths9. Remove spacer from mouth10. Breathe out gently away from the device, and then inhale normally11. Remove inhaler from spacer12. If an extra dose is needed, wait 30 seconds to a minute, and then repeat steps 3 to 11

13. Replace inhaler cap and disassemble spacer device


27/64


inhalation devices as prescribed, all of them work equally well. 175 In real-life clinical practice, selectionof a delivery device ideal for a particular patientdepends on several factors, such as clinician and

patient preference, availability, cost, patient age anddexterity, patient motivation and understanding,relative ease of device use, and others.

What is the Role of Long-acting AntimuscarinicAgents (LAMA) in the Management of StableCOPD?The most widely used inhaled LAMA for themanagement of stable COPD is tiotropium bromide.It has pharmacodynamic specificity for M1 and M3receptors and has a half-life of more than 24 hours,resulting in a convenient once daily dosing. Thelargest study till date on the use of tiotropiummonotherapy in stable COPD is the UPLIFT(Understanding Potential Long-term Impacts onFunction with Tiotropium) trial. 176 There was nodifference in the primary end point (rate of decline of lung function) between the two groups althoughpatients receiving tiotropium had better FEV 1 andFVC values at all-time points during the studyperiod. Importantly, there was a significant decreasein the exacerbation rates and mortality with the useof tiotropium. Also, there was improvement in theQoL scores and lesser cardiac and respiratoryadverse events in this group. A subgroup analysis of the UPLIFT trial focusing on the patients withmoderate COPD (FEV 1 50%-70%) confirmed the benefi ts of tiotropium monotherapy in decreasingexacerbations and improving QoL and lungfunction, although there was no reduction inmortality. 123 Other subgroup analyses have alsoshown that the beneficial effects of tiotropium areobserved in all patients with COPD, irrespective of their gender, ethnicity or smoking status. 177-179 Arecent Cochrane review of 22 randomised controlledtrials comparing tiotropium monotherapy withplacebo also confirmed the beneficial effects of tiotropium. 180 In this meta-analysis, tiotropium usein stable COPD was associated with significantimprovement in QoL and reduction in exacerbations(with a number needed to treat of 16 to prevent oneexacerbation). A subgroup analysis based on FEV 1(FEV1 >50% and FEV1


28/64


mortality. 196, 197 Ipratropium use has also beenassociated with higher risk of arrhythmias and strokein large retrospective observational studies. 198, 199

In a meta-analysis of 17 studies, Singh et al

concluded that inhaled anticholinergics increase risk of cardiovascular death, myocardial infarction andstroke. 200 This meta-analysis 200 clubbed trials of tiotropium and ipratropium, and also combinedplacebo-controlled and active-controlled trials.Further, the healthy survivor effect was not taken intoconsideration. Three other meta-analyses, and aCochrane review that included only placebocontrolled trials of tiotropium, all concluded thatuse of tiotropium is not associated with anincreased cardiovascular morbidity or mortality. 180, 194, 201, 202After the results of the UPLIFT study and a pooledanalysis of 29 trials, the United States-Food and Drug

Administration (US-FDA) also concluded that the useof tiotropium was not associated with an increasedrisk of stroke, cardiovascular events or death. 203However, it is also important to note that the twolargest trials evaluating tiotropium-monotherapy (theUPLIFT trial and the POET-COPD (Prevention of Exacerbations with Tiotropium in COPD) trialexcluded patients with unstable coronary artery ordecompensated cardiac diseases. 176, 204 Hence, inhaledanticholinergics should be judiciously prescribed topatients with unstable cardiac diseases.

In contrast to tiotropium use by dry powderinhaler, the use of tiotropium by soft mist inhaler

(Respimat device, currently not available in India) has been consistently shown to increase the risk of mortality. 205 Though the exact reason is not clear, it ispostulated that this increase in adverse events could be due to higher drug deposition seen with soft mistinhalers.

Recommendations

1. Short-acting antimuscarinic agent (SAMA) can beused as rescue medication to relieve patient symptoms. (1A)

2. Long-term SAMA monotherapy on regular basisis not recommended. (1A)

3. Long-acting antimuscarinic agents (LAMA) areuseful in patients with stable COPD (FEV 1


29/64


30/64


confounders. Similarly, another prospectiveobservational study 234 of 460 patients of COPD withpneumonia showed that use of ICS did not lead to anincrease in mortality. It appears that although ICS use

increases risk of developing pneumonia, this does nottranslate to worse clinical outcomes.A meta-analysis that exclusively focused on the

risk of fractures with ICS use 235 showed a modest butstatistically significant increase in the risk of fractures(number-needed-to-harm, 83). This modest risk doesnot outweigh the beneficial effects of ICS indecreasing COPD exacerbations.

Recommendations1. Inhaled corticosteroids have a beneficial effect in

subgroup of COPD patients with FEV 1 2 exacerbations per year). (1A)

3. The risk-benefit profile favours the use of ICS in patients with severe COPD. (1A)

Which is Better for the Management of COPD:Tiotropium or LABA?The largest study 204 comparing tiotropium with LABA(salmeterol) is the POET-COPD trial that randomised7376 patients of COPD (FEV1


31/64


What are the Benefits of ICS Plus LABACombination Therapy Over LABA Monotherapy?

The first landmark trial which assessed the ICS-

LABA combination therapy was the TRISTAN (TRialof Inhaled Steroids and long-acting beta-2 agonists)study. 242 This study randomised 1465 patients andfollowed them for one year. The combination therapyled to better symptom scores, QoL scores and lungfunction, as compared to LABA monotherapy.However, there was no decrease in the exacerbationrates. The largest study on this issue till date is theTORCH study 207 , which randomised and followed up6112 patients for three years. The ICS-LABAcombination decreased exacerbation rates andimproved lung function and QoL when compared toLABA monotherapy. However, there was an increase

in pneumonia rates. Also the ICS-LABA combinationdecreased the risk of cardiovascular adverse events,though the exact mechanism remains unexplained. 223

A Cochrane review 243 analysing 14 studies (11794patients) compared ICS-LABA combination therapyto LABA monotherapy, and concluded thatcombination therapy decreased exacerbation ratesand improved symptom scores, lung function andQoL, without affecting mortality rates. There was anincrease in the incidence of pneumonia withthe use of combination therapy. Two separatemeta-analyses also have also shown mortality benefit with use of ICS-LABA combination therapy. 208, 244

What are the Benefits of ICS Plus LABACombination Over LAMA (tiotropium)Monotherapy?

The only large study 245 comparing ICS-LABAcombination therapy with tiotropium monotherapyis the Investigating New Standards for Prophylaxisin Reduction of Exacerbations (INSPIRE) study thatrandomised and followed 1323 patients for twoyears. Though the dropout rates were more in thetiotropium arm (34.5% versus 41.7%), thecombination therapy was better than tiotropium in

decreasing mortality and improving QoL. There wasno difference in the exacerbations in this study. ACochrane review 246 also addressed this issue but didnot draw any conclusions due to lack of goodquality randomised trials and a very high dropoutrate in the INSPIRE study.

What are the Benefits of Triple Therapy(ICS Plus LABA Plus LAMA)?

A total of seven randomised trials 220, 247-252 and twoobservational studies 253, 254 (one retrospective and oneprospective) have assessed the benefits of triple therapy.All seven randomised trials consistently showimproved lung function and QoL scores with the

use of triple therapy. 220, 247-252 Two of these studies 249, 250have also shown a beneficial effect of triple therapyin decreasing exacerbations. One retrospectiveobservational study 253 of 3333 patients also showed a

33% decrease in risk of exacerbations. Another smallprospective observational study 254 on 46 patientsshowed that triple therapy improved lung function andQoL scores. A meta-analysis 255 of four randomised trialsof triple therapy concluded that such therapy improvedthe lung function, dyspnoea and QoL scores; howeverthe effect on decreasing exacerbations was not clear.

Recommendations1. LAMA plus LABA may be used in patients who

continue to have symptoms on monotherapy,except for those with frequent exacerbations. (1A)

2. LABA plus ICS should be preferred over LABA

alone in patients with FEV 1


32/64


Theophylline induced HDAC activation occurs atplasma concentration


33/64


analysis 275 of 30 studies on patients with chronic bronchitis or COPD concluded that mucolytic therapymay result in minor reduction in acute exacerbationrates, but has negligible impact on lung function or

overall QoL. Quality of several included studies waspoor with a high degree of heterogeneity.

RecommendationRoutine use of mucolytic agents is not recommended in patients with COPD. (2A)

What is the Indian Strategy for the Managementof Stable COPD?When a patient initially presents to a physician witha diagnosis of COPD, he should be categorised intoone of the three severity categories as per stagingcriteria described earlier (Table 2). As initial therapy,physicians can prescribe a preferred treatmentschedule, or an alternative schedule if the patientcannot take (or does not want to take) the preferredschedule for some reason (Table 3). If a patientcontinues to be symptomatic despite such treatment,other drugs can be given as add-on therapy. Duringfollow-up, if a patient shifts from one severity categoryto another, therapy should be modified accordingly.For example, if a patient of mild COPD developsworsening symptoms, he would be labelled asmoderate COPD and the treatment should be changedaccordingly. Similarly, if a patient with mild ormoderate COPD develops frequent exacerbations orFEV1 falls below 50%, he would be categorised assevere COPD and the treatment changed accordingly.

ACUTE ECUTE EXACERBATIONS OF COPD

What is the Definition of Acute Exacerbation ofCOPD (AECOPD)?An exacerbation of COPD is an acute eventcharacterised by a sustained worsening of any of thepatient’s respiratory symptoms (cough, sputumquantity and/or character, dyspnoea) that is beyond

the normal day-to-day variation and leads to a changein medication, and where other causes of acute breathlessness have been clinically excluded. 276-278

What is the Impact of Exacerbation on Patients?COPD is a progressive disease with a gradual declinein lung function. However, the course of COPD ispunctuated by exacerbations, some of which may besevere enough to cause hospitalisation; this may notonly lead to increase in mortality but is alsoassociated with increased cost of treatment. 279-282Exacerbations are associated with a greater andirreversible decline in lung function. 282,283 Theoccurrence of a severe exacerbation requiring

hospitalisation increases the risk of furtherexacerbation. Patients have 25 times higher risk of re-admission to hospital after the tenth hospitalisation,as compared to the first hospitalisation. 282 In fact,

there is five-fold increase in the risk of death aftertenth hospitalisation. 282 Exacerbations are associatedwith progression of emphysema measured on serialCT scans.284 Moreover, exacerbations are associatedwith significant decline in QoL, 285, 286 and add to thecumulative economic burden. 287 The mortality is 40%at one year in those requiring mechanical ventilation(MV), and all-cause mortality may be as high as 49%at three years after hospitalisation. 287, 288

What are the Precipitating Factors forExacerbation?Several precipitating factors, both infectious andnon-infectious, have been implicated in AECOPD(Table 13).289, 290 Infections are the most frequent causeof exacerbations, and both bacterial and viralinfections have been detected during exacerbations. 291-294 Acquisition of a new strain of Hemophilusinfluenzae, Moraxella catarrhalis, Streptococcus pneumoniae,or Pseudomonas aeruginosais stronglyassociated with the occurrence of an exacerbation. 295A pooled analysis of studies utilising bronchoscopicsampling with the use of a protected specimen brushrevealed that bacteria were present in clinicallysignificant concentrations in the airways of 4% of healthy adults, 29% of adults with stable COPD, and54% of adults with COPD exacerbation. 295-298

The non-infectious precipitants of AECOPDinclude non-adherence to medication, or inhalation of irritants, like tobacco smoke or particles. Air pollutionhas been implicated in causing AECOPD. The effectsof diesel particulates, sulphur dioxide (SO 2), andothers have been studied and potential mechanisms by which airway inflammation is enhanced (increasein bronchial neutrophils and methyl histamine) have been proposed. 299,300 The role of air pollution incausing exacerbation is primarily based uponepidemiological studies implicating increased air

levels of SO2 , nitric dioxide (NO 2), and black smokeparticulate matter. 301,302Conditions like heart failure, pulmonary embolism,

cardiac arrhythmias, pneumothorax, pleural effusion,and pneumonia can cause acute worsening of symptoms in patients with COPD and are consideredCOPD exacerbation mimics. 121,276,290,303,304

What is the Differential Diagnosis of AECOPD?The differential diagnosis of AECOPD includes the6Ps; pneumonia, pulmonary embolism, pneumo-thorax, pleural effusion, pulmonary oedema [heartfailure] and paroxysmal atrial tachycardia[arrhythmias], and these need to be excluded in


34/64


35/64


6. Sputum cultures: Hemophilus influenzae, Streptococcus pneumoniae,and Moraxella catarrhalisare are the mostcommon bacterial pathogens involved in an exacerbation.In severe exacerbations requiring invasive ventilation,

Pseudomonas aeruginosais an important consideration,121, 309

and sputum cultures may help in identifying the correctpathogen.

Recommendations1. No investigations apart from pulse oximetry are

routinely required in patients with acuteexacerbations managed in an outpatient setting.(2A)

2. In those hospitalised with AECOPD, serumelectrolytes, liver and renal function tests, completeblood count, chest radiograph, electrocardiogramand arterial blood gas analysis (if available) should

be performed. (1A) 3. If an infectious exacerbation does not respond to theinitial antibiotic treatment, a sputum culture and anantibiotic sensitivity test should be performed. (2A)

How to Decide the Site of Management of aPatient with COPD Exacerbation?More than 80% of exacerbations can be managed onan outpatient basis. 122, 176, 310The decision to hospitalisea patient is based on overall assessment (Table 15).The presence of any one of the listed features may

warrant hospitalisation. Old age, poor nutritionalstatus, presence of comorbidities, acidaemia, alteredmental status and hypotension are associated withpoor outcomes in patients hospitalised with COPD. 311

A prospective study312

evaluating CURB-65 scores inAECOPD reported 30-day mortality rates of 2.0%,6.7% and 21.3%, respectively, in low risk (scores 0-1),moderate risk (score 2) and high risk (scores 3-5)groups. It was concluded that CURB-65 score could be used for predicting early mortality in patients withAECOPD.312 In another study, 88,704 patients withAECOPD were assessed for the purpose of stratifyingin-hospital mortality. Three variables had highdiscrimination score of outcomes (blood urea nitrogen>24 mg/dL, acute mental status change and heartrate >110/minute). The investigators used these threeparameters along with age, and proposed a new

score, i.e. BAP-65. In those with all three factors, themortality rates were 13.1% and 14.6% in thederivation and validation cohorts, respectively,compared to 0.3% in both cohorts without any of thethree factors and age 5 mL/kg), respiratory rate (


36/64


the management of AECOPD. There were nosignificant differences in FEV 1 change in patientstreated with beta-agonists or ipratropium bromide,and no additive benefit of adding ipratropium to

beta-agonist.320

Also, the optimal dosing andfrequency of bronchodilators in AECOPD is notestablished. There was no difference in clinicaloutcomes in patients treated every four hours witheither 2.5 mg or 5 mg of nebulised salbutamol. 321 Therewas also no significant difference in improvement inFEV1 between hourly and 20-minute dosing of salbutamol. 322 However, post-hoc analysis revealedsignificantly better improvement with the 20-minuteprotocol in th

copd indian guidelines

Documents