bts guidelines for the management of chronic obstructive

1997;52;1-28 Thorax

BTS Guidelines for the Management of Chronic Obstructive Pulmonary Disease

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Thorax 1997;52(Suppl 5):S1 S1

Foreword

This project was initiated by the Standards M C P Apps, Mrs G Barnes, Dr D Bellamy∗,of Care Committee of the British Thoracic Ms G Boote, Professor P M A Calverley∗, DrSociety. A core group of individuals produced I A Campbell, Dr M J Connolly, Dr P Edwards,background papers which were collated into a Dr W F Holmes, Dr D Honeybourne∗, Dr R Csingle document. This was discussed over a Lowry, Dr C R McGavin, Dr D MacIntyre,two day period by a larger group which included Professor W MacNee∗, Dr M D L Morgan,respiratory physicians from both teaching and Dr M F Muers, Dr F Nicol, Dr J C Pounsford,district general hospitals across the UK, geri- Professor N B Pride, Dr C M Roberts, Dr Matricians, general practitioners, nurses, and Rudolf∗, Dr M Somerville, Dr C R Swinburn,public health physicians. Advice was also Dr J G B Thurston, Dr J A Wedzicha∗, Dr J Psought from the Breathe Easy section of the Williams∗.British Lung Foundation.

Participants: Dr M G Pearson∗ (Chairman),Professor R Alderslade, Dr S C Allen, Dr ∗Member of core group

Glossary of terms used in this document:Pa2 arterial oxygen tensionFEV1 forced expiratory volume produced

in first second Pa2 arterial carbon dioxide tensionSa2 arterial oxygen saturationFVC forced vital capacity

VC slow vital capacity LTOT long term oxygen treatmentNIPPV non-invasive intermittent positiveFRC functional residual capacity

TLC total lung capacity pressure ventilationT diffusing capacity for carbon

monoxide or gas transfer factor



S2 Summary of guidelines

Summary of guidelinesimprovement is seen in 10–20% of cases using the criteria1 This document was initiated by the Standards of Care Com-

mittee of the British Thoracic Society and summarises the described above for bronchodilators.(e) A chest radiograph excludes other pathologies but cannotviews of many individuals and organisations (page S1). These

views are based on a combination of clinical judgement and positively diagnose COPD. In some patients bullae canbe identified (page S9).a review of the literature conducted by the participants as well

as a critical reappraisal of the recommendations of published (f) More complex investigations are not normally indicatedexcept in difficult cases.international guidelines. These guidelines are intended to

provide a benchmark for current best practice in the care of (g) Estimation of arterial blood gas tensions in severe COPDis necessary to identify patients with persistent hypox-patients with chronic obstructive pulmonary disease and per-

mit the local development of rational cost effective care. aemia with or without hypercapnia (page S9).5 Treatment of stable COPD2 Definitions

(a) Chronic obstructive pulmonary disease (COPD) is a gen- (a) Mild diseaseeral term which covers many previously used clinical

labels that are now recognised as being different aspects • Bronchodilator therapy: short acting b2 agonist orinhaled anticholinergic as required (page S10)of the same problem.

(b) Diagnostic labels encompassed by COPD include: depending upon symptomatic response.(b) Moderate disease• chronic bronchitis

• emphysema • Bronchodilator therapy: as for mild disease but regulartherapy with either drug or a combination of the two• chronic obstructive airways disease

• chronic airflow limitation may be needed.• A corticosteroid trial should be considered in all• some cases of chronic asthma.

(c) COPD is a chronic, slowly progressive disorder char- patients.(c) Severe diseaseacterised by airways obstruction (FEV1 <80% predicted

and FEV1/VC ratio <70%) which does not change • Combination therapy with a regular b2 agonist andanticholinergic; the addition of other agents (see below)markedly over several months. The impairment of lung

function is largely fixed but is partially reversible by should be considered.• Consider a corticosteroid trial.bronchodilator (or other) therapy.

(d) Most cases are caused by tobacco smoking (page S5). • Assess for home nebuliser using the BTS guidelines.(d) Other considerations(e) COPD causes significantly more mortality and morbidity

than do other causes of airflow limitation in adults (page S5). • Inhaler technique should be optimised and anappropriate device selected to ensure efficient delivery.3 Diagnosis of COPD

(a) The diagnosis is usually suggested by symptoms (see • Theophyllines are of limited value in the routinemanagement of COPD.below) but can only be established by objective measure-

ment, preferably using spirometric tests. • At present, evidence on the value of long acting b2

agonists in COPD is limited and they should only be(b) Unlike asthma, airflow limitation in COPD as measuredby the FEV1 can never be returned to normal values. considered if objective evidence of improvement is

available.However, treatment can improve both symptoms andmeasured airflow limitation. • There is no role for other anti-inflammatory drugs in

the management of COPD.(c) The symptoms and signs vary with the severity of thedisease. -

• Smoking cessation is essential at all stages of the diseaseCategory FEV1 Symptoms and signs (page S10).of COPD (% predicted) • Participation in an active smoking cessation programme

leads to a higher sustained quit rate, especially whenMild 60–80 No abnormal signsnicotine replacement therapy is included.Smoker’s cough

Little or no breathlessness • Smoking cessation cannot restore loss of lung functionModerate 40–59 Breathlessness (±wheeze) on moderate exertion but can prevent the accelerated decline seen in many

Cough (±sputum) patients with COPD (fig 2).Variable abnormal signs (general reduction in

• Exercise should be encouraged where possible (pagebreath sounds, presence of wheezes)S12).Severe <40 Breathlessness on any exertion/at rest

Wheeze and cough often prominent • Obesity and poor nutrition both require treatmentLung overinflation usual; cyanosis, peripheral (page S12).oedema and polycythemia in advanced • Vaccination against influenza is recommended,disease, especially during exacerbations.

especially for moderate to severe disease (page S12).6 In more advanced disease

4 Assessment of stable COPD • Dyspnoea can be assessed by a variety of scales (page(a) In general, spirometric testing is preferred to peak S13).

expiratory flow (PEF) recordings. If the latter are used, • Dyspnoea improves with bronchodilators but is hardserial recordings over one week are needed to confirm to suppress with sedative/opiate drugs at safe doses.the absence of variability (pages S8, S22). Bronchodilator • Pulmonary rehabilitation including outpatient-basedreversibility testing is helpful in excluding patients with programmes have been shown to improve exercisechronic asthma, but many patients with COPD show performance and reduced breathlessness. This shouldsome degree of response to bronchodilators. be considered in moderate/severe disease (page S13).

(b) A positive spirometric response to bronchodilators or • Short burst oxygen is often given to reduce breath-corticosteroids is considered to be present when the FEV1 lessness but the evidence for this is lackingincreases by 200 ml and 15% of the baseline value. (page S13).

(c) A substantial bronchodilator response suggests the • In hypoxaemic patients LTOT prolongs life (page S13).possibility of asthma. Bronchodilator tests vary from day • LTOT should only be prescribed if objectivelyto day and are not clearly related to the extent of demonstrated hypoxia (Pa2 <7.3 kPa) or high cylindersubsequent symptomatic benefit when the patient is use (more than two per week) is present (page S14).treated with the drug tested. • Surgery is indicated for recurrent pneumothoraces

(d) A trial of oral corticosteroids is indicated in assessing and isolated bullous disease. Lung volume reductionmoderate to severe disease. This usually comprises spiro- surgery may be useful in selected patients (page S14).metric tests before and after 30 mg of prednisolone taken • Depression should be identified and treated. Assess-as a single dose daily for two weeks. Subjective improvement of the patient’s social circumstances and the supportment is not a satisfactory end point. Objective available is valuable in management (page S14).



Summary of guidelines S3

• Travel is possible by land and sea in virtually all cases • Mild breathlessness?• Good general condition?but air travel may be hazardous if the Pa2 breathing

air is <6.7 kPa. The availability of oxygen on the chosen • Not receiving LTOT?• Good level of activity?flight should be checked (page S14).

7 Factors for consideration by the GP • Good social circumstances?The greater the number of negative answers, the greater is the(a) In general practice the consultation rates relating to

COPD per 10 000 population rise from 417 at age 45–64 likelihood that admission to hospital is needed.11 Home treatment of acute exacerbations (page S16)to 886 at age 65–74 and 1032 at age 75–84, values that

are 2–4 times the equivalent rates for angina. (a) Add or increase bronchodilators (consider if inhaler deviceand technique are appropriate).(b) In managing COPD the GP needs to consider:

• smoking cessation (b) Prescribe an antibiotic if two or more of the following arepresent:• assessment in well man or woman clinics for smokers

aged 40 and over • increased breathlessness;• increased sputum volume;• access to spirometric tests

• hospital referral/follow up. • development of purulent sputum.(c) Oral corticosteroids may be prescribed in some cases.8 Indications for specialist referral (page S15)

A specialist opinion may be helpful at any stage of the disease. These should not be used unless:• the patient is already on oral corticosteroids;The principal reasons are summarised below:• there is a previously documented response to oral

corticosteroids;• airflow obstruction fails to respond to an increase in

Reason Purpose bronchodilator dosage;• this is the first presentation of airflow obstruction.• Suspected severe COPD • To confirm diagnosis and

optimise treatment 12 Follow up of patients treated at home (page S17)• Onset of cor pulmonale • To confirm diagnosis and • If patient deteriorates, reassess and consider need for

optimise treatmenthospital treatment. If not fully improved in two weeks• Assessment for O2 therapy • To measure blood gases

• Assessment in accordance • To exclude inappropriate consider chest radiography and hospital referral.with nebuliser guidelines prescriptions • Measurement of FEV1.• Assessment of oral • To justify the need for long term • Reassessment of inhaler technique and patient’scorticosteroids treatment or to supervise

understanding of recommended treatment regime.withdrawal• Bullous lung disease • To identify and assess candidates • Emphasise potential benefits of lifestyle management

for surgery (smoking, weight, exercise).• <10 pack years smoking • To confirm/exclude diagnosis13 Hospital treatment of an acute exacerbation (page S17)• Rapid decline in FEV1 • To encourage early intervention

• COPD in patient less than • To identify a1-antitrypsin (a) Hospital treatment of an acute exacerbation is as for40 years deficiency, consider therapy and home treatment except:

screen family• Uncertain diagnosis • To make a diagnosis• Symptoms disproportionate • To look for other explanations

to lung function deficit• Frequent infections • To exclude bronchiectasis Drug Criteria Action

Broncho- Moderate Nebulised b2 agonist or ipratropiumdilator exacerbation bromide. If no response, consider iv

aminophylline.Figure 3 summarises the management of stable COPD at each Severe Nebulised ipratropium bromide and b2stage of the disease. exacerbation agonist in combination. If no response,

consider iv aminophylline.Oxygen Moderate/ Given in ambulance or on arrival,

severe 24–28% mask 2 l/min by nasal prongs.exacerbation Check blood gases within 60 minutes of

starting oxygen, modify flow rateaccording to Pa2 and pH.

(b) If pH is <7.26 and Pa2 is rising consider ventilatorysupport (page S19). This may be by intubation andintermittent positive pressure ventilation (IPPV) or non-invasive IPPV, although the latter is probably best initiatedat a higher pH and is only suitable in cooperative patientswithout excessive secretions. An alternative is the use ofintravenous doxapram.

(c) IPPV is likely to be appropriate when (page S19):

100

0

FEV

1 as

% p

red

icte

d

Increasing investigation and treatment

Symptoms

60

40

80

20

Healthy population

Smoker's coughLittle or no dyspnoeaNo abnormal signs

Dyspnoea on exertionCough and sputumSome abnormal signs

Dyspnoea on mild exertionHyperinflation and cyanosisWheeze and cough

Death

Wo

rsen

ing

lun

g f

un

ctio

n

Smoking cessation

Antibiotics for acute infections

Occasional bronchodilator as requiredMore frequent/combination bronchodilatorsSteroid reversibility trial: inhaled steroids if +ve

Influenza vaccinationPulmonary rehabilitation

Assessment for LTOTAmbulatory oxygen

The COPD Escalator

• there is a clear basis for the current deterioration;• it is the first episode of respiratory failure;Figure 3 The COPD escalator. Summary of the principal• there is an acceptable quality of life/habitual level ofcomponents of a management plan for COPD. Note that, as disease

activity;severity increases, symptoms and signs become more obvious whilst the• the patient has not previously had a full medicalnumber of treatments used rises.

assessment;• there are few if any co-morbidities.

9 Presenting features of acute exacerbations of COPD (d) A senior doctor must make the decision not to institute• Worsening of previous stable condition ventilatory support.• Increased wheeze (e) Neither age nor the Pa2 predict survival (page S19).• Increased dyspnoea 14 Follow up of acute exacerbations• Increased sputum volume For all patients follow up assessment 4–6 weeks after discharge• Increased sputum purulence from hospital should include:• Chest tightness • patient’s ability to cope;• Fluid retention • measurement of FEV1;

10 Questions to ask in deciding whether to treat at home • reassessment of inhaler technique and patient’sor in hospital (page S16) understanding of recommended treatment regime;

• Able to cope at home? • need for LTOT and/or home nebuliser usage in patients• Absence of cyanosis? with severe COPD;• Normal level of consciousness? • follow up thereafter is as for stable COPD (page S15).



S4 Thorax 1997;52(Suppl 5):S4–S6

1Definitions

Introduction

TerminologyChronic obstructive pulmonary diseaseChronic obstructive pulmonary disease (COPD)(COPD) is a chronic, slowly progressive dis-is the internationally preferred term that in-order characterised by airflow obstruction (re-cludes all the clinical labels and acronymsduced FEV1 and FEV1/VC ratio) that does notshown below, either alone or in combination.change markedly over several months. Most of

• Emphysema the lung function impairment is fixed, althoughsome reversibility can be produced by broncho-• Chronic bronchitisdilator (or other) therapy.

• Chronic obstructive bronchitis Thus, a diagnosis of COPD in clinical prac-tice requires:• Chronic airflow limitation (CAL)• a history of chronic progressive symptoms• Chronic airflow obstruction (CAO)

(cough and/or wheeze and/or breath-• Chronic airways obstruction (CAO) lessness);

• Non-reversible obstructive airways disease • objective evidence of airways obstruction,(NROAD) ideally by spirometric testing, that does not

return to normal with treatment.• Chronic obstructive airways disease(COAD) Usually a cigarette smoking history of more

than 20 pack-years is obtained, although• Chronic obstructive lung disease (COLD)COPD does occur rarely in non-smokers.

COPD arises from varying combinations of• Some cases of chronic asthmaairway disease and pulmonary emphysema; it

The clinical diagnosis of COPD is suggested is difficult to define the relative importance ofby symptoms, but can only be established firmly each in an individual patient. The presence ofby an objective measurement indicating airflow “chronic cough and sputum production for atobstruction. The critical feature that char- least three months of two consecutive years inacterises COPD is the inability to reverse this the absence of other diseases recognised toairflow limitation fully. Appropriate treatment cause sputum production” was used by thecan, however, lead to some improvement in MRC1 as an epidemiological definition ofboth measured airflow obstruction and/or clin- “chronic bronchitis” but does not necessarilyically important symptoms. signify the presence of airways obstruction or

These guidelines are intended to: a diagnosis of COPD. The mortality and mostof the morbidity associated with COPD relates• help general practitioners, practice nursesto the airways obstruction and not the chronicand district nurses to recognise, characterisemucus hypersecretion.2

and hence treat patients with COPD ap-The differentiation of severe COPD frompropriately, and to suggest when the use of

chronic severe asthma is difficult since somesecondary services can be most helpful; degree of improvement in FEV1 (reversibility)can often be produced by bronchodilator ther-• help hospital physicians (respiratory, generalapy. Moreover, the pathological changes ofmedical and geriatrician), nurses and physio-bronchial asthma in the large airways can co-therapists to recognise and provide a moreexist with those of COPD which predominantlyuniform and logical approach to care at eachaffects small airways.3 Whether such an as-stage of COPD and thus to use resources insociation occurs more frequently than expectedthe most rational way;by chance is not clear. However, some patients

• help purchasers of health care to define the with COPD have pathological evidence of non-quality and quantity of services necessary for asthmatic inflammation within their airwayspatients with COPD (see box 1). that may respond to anti-inflammatory treat-

ment. The presence or absence of cough andWhere there is a lack of evidence in these sputum, wheeze at any time of day or night, a

guidelines we have declared current opinion. partial response to bronchodilators, or a familyhistory of chest disease are unhelpful in differ-entiating between chronic asthma and COPD.4

The term COPD is not conventionallyused to include other specific conditions thatcan cause airways obstruction such as cysticGoals of the COPD guidelinesfibrosis, bronchiectasis, or bronchiolitis ob-Early and accurate diagnosisliterans.Best control of symptoms

Prevention of deteriorationPrevention of complications

Improved quality of life Aetiology and natural historyThe single most important cause of COPD iscigarette smoking.5 The greater the totalBox 1



Introduction S5

the smoker stops smoking, in 90% of cases thesputum production will cease.16

The best guide to the progression of COPDis the change in FEV1 over time (fig 2). FEV1

declines with normal ageing at about 30 ml/year and this increases to an average of 45ml/year in smokers.14 However, the individualsusceptibility to cigarette smoking is very wide,such that approximately 15% of smokers willdevelop clinically significant COPD whilst ap-proximately half will never develop any symp-tomatic physiological deficit.16

The prognosis is inversely related to the ageof the patient and directly to the FEV1,18−20

with the post-bronchodilator FEV1 correlatingbetter with survival than the pre-bronchodilatorvalue.2 Thus, three year survival figures havebeen estimated as21:

• aged <60 and FEV1 >50% predicted=90%

• aged >60 and FEV1 >50% predicted=80%

25

0Mild

Per

cen

tag

e w

ho

will

dev

elo

p a

n a

bn

orm

al F

EV

1

Category of COPD

Non-smoker1–20 pack-years

20

10

5

15

21–40 pack-years41–60 pack-years61+ pack-years

Moderate Severe

• aged >60 and FEV1 40–49% predicted=75%Figure 1 Proportion of individuals who will develop each grade of airways obstructionfor each of five different levels of cigarette consumption. Reproduced from Burrows et al6 A community survey of COPD in Tucson,with permission. Arizona22 showed that the fall in FEV1 in COPD

was 70 ml per year with a 10 year survival ofabout 30%. Patients with atopy had a sig-

tobacco exposure, the greater the risk of de- nificantly better survival than did irreversibleveloping COPD (fig 1).6 Smoking dominates non-atopic patients.all other aetiological factors. A small additional Stopping smoking produces only small im-contribution to the severity of COPD has provements in the FEV1 but the subsequentbeen reported in patients who work in dusty fall in FEV1 slows to the rate of 30 ml/yearenvironments7 8 or those who live in cities.9

found in healthy non-smokers.2 17 There is noHowever, these effects remain contentious. evidence that acute exacerbations of COPDDeficiency of a1-antitrypsin, an antiprotease lead to an increasing rate of decline in FEV1.enzyme, is associated with emphysema in non- The effect of the FEV1 on prognosis is seen insmokers but the risks of this are greatly all grades of severity of COPD.magnified in enzyme-deficient subjects who No drug treatment has been shown to affectsmoke.10 Other currently proposed risk factors the natural history of COPD. The Lung Healthinclude poor nutrition in utero11 and pre- Study17 showed that treatment with ipra-existing bronchial hyperresponsiveness.12 13

tropium had a small but significant beneficialFletcher and colleagues14 15 showed that, effect on FEV1 whilst the treatment was con-

while chronic bronchitis and progressive air- tinued, but that there was no effect on the fiveways obstruction were both related to inhaling year decline in FEV1. Prospective studies ofcigarette smoke, the two conditions were dis- the effect of long term inhaled steroids on thetinct with respect to prognosis. Sputum pro- decline in FEV1 are expected to report over theduction without airways obstruction is not next two years.associated with increased mortality2 14 and, if With severe disease hypoxaemia develops

with an increase in pulmonary artery pressureleading to the development of right ventricularhypertrophy or cor pulmonale. Pulmonaryhypertension in COPD is slowly progressive23

and its presence implies a poor prognosis,24

although it may not have a direct effect onmortality. Long term oxygen therapy is the onlytreatment known to improve the prognosis inpatients with severe COPD and hypoxaemia.25

Disease burdenIn 1992 there were 26 033 deaths in Englandand Wales attributed to COPD, chronic bron-chitis, or emphysema which accounts for 6.4%of all male and 3.9% of all female deaths. In

100

0

FEV

1 (%

of

valu

e at

ag

e 25

)

Age (years)

50

75

25

50 7525

Never smoked or notsusceptible to smoke

Stoppedat 45

Stoppedat 65

Smoked regularlyand susceptible to its effects

Disability

Death

comparison, 1791 died of asthma.26

Figure 2 Model of annual decline in FEV1 with accelerated decline in susceptibleCOPD is a major cause of morbidity withsmokers. On stopping smoking subsequent loss is similar to that in healthy non-smokers.

Modified from Fletcher and Peto.15 frequent use of both GP and hospital services.



S6 Introduction

The estimated annual health service workload Table 1 Annual health service workload due to chronicrespiratory diseases in an average UK health districtdue to chronic respiratory disease in an average

UK health district of 250 000 people greatly Hospital Inpatient General practiceadmissions bed days consultationsexceeds that for asthma (table 1).27

In a survey of all medical admissions to a Chronic bronchitis,emphysema andUK health region 25% of admissions were dueCOPD 680 9600 14 200

to respiratory diseases and over half of these Asthma 410 1800 11 900

were COPD.28 A survey of medical and geriatricadmissions to another UK region found that,for those aged 65–74 years, 7.3% of male and rates for COPD per 10 000 population rise3.2% of female admissions had COPD.29 The from 417 at age 45–64 to 886 at age 65–74use of health services increases steeply with and 1032 at age 75–84, values that are 2–4

times the equivalent rates for angina.30age. In general practice annual consultation



Thorax 1997;52(Suppl 5):S7–S15 S7

2 Diagnosis and management of stableCOPD

The presence of symptoms can be extremely the existing defect. The combination of the twoproblems often causes enough symptoms forvariable in patients with COPD; a firm diag-

nosis can only be made by objective measure- the patient to ask for medical help.ment of airways obstruction with spirometrictests. COPD is a progressive disorder that ne-cessarily passes through mild and moderate Presentationphases before becoming severe. Mild disease In patients with mild COPD there are few ormay be present in completely asymptomatic no symptoms.31 A history of morning cough,individuals. A patient who presents with severe recurrent respiratory infections, or shortness ofdisease has been “missed” by the health services breath on vigorous exertion or manual labourearlier in the disease course. Table 2 sum- should alert the doctor to the possibility ofmarises the main features of each stage; for COPD. Routine screening, especially of smokers,fuller information please refer to the ap- and occupational surveillance schemes canpropriate section. A justification of the spiro- identify airways obstruction at an early stagemetric levels used to define the degrees of before troublesome symptoms develop.severity appears in Appendix 1. Figure 3 sum- Moderate COPD can present with a widemarises the range of therapies available for the range of respiratory symptoms although theretreatment of COPD and the approximate stage are few clinical signs. There is no single typicalin the illness when they may be introduced. pattern but possibilities include combinationsExacerbations of COPD do not represent a of some or all of the following:worsening of the underlying disease processproducing COPD but are caused by the ad- • cough and sputum production, especially if

the sputum becomes discoloured;dition of a second (often infective) process to

100

0

FEV

1 as

% p

red

icte

d

Increasing investigation and treatment

Symptoms

60

40

80

20

Healthy population

Smoker's coughLittle or no dyspnoeaNo abnormal signs

Dyspnoea on exertionCough and sputumSome abnormal signs

Dyspnoea on mild exertionHyperinflation and cyanosisWheeze and cough

Death

Wo

rsen

ing

lun

g f

un

ctio

n

Smoking cessation

Antibiotics for acute infections

Occasional bronchodilator as requiredMore frequent/combination bronchodilatorsSteroid reversibility trial: inhaled steroids if +ve

Influenza vaccinationPulmonary rehabilitation

Assessment for LTOTAmbulatory oxygen

The COPD Escalator

Figure 3 The COPD escalator. Summary of the principal components of a management plan for COPD. Note that, asdisease severity increases, symptoms and signs become more obvious whilst the number of treatments used rises.

Table 2 Classification, diagnosis and management of COPD

Clinical state Results of measurements Use of health care resources

Mild Smoker’s cough, but little or no breathlessness. No FEV1 60–79% predicted, FEV1/VC and other Unknown – presymptomatic withinabnormal signs indices of expiratory flow mildly reduced the community

Moderate Breathlessness (±wheeze) on exertion, cough FEV1 40–59% predicted, often with increased Known to GP with intermittent(±sputum) and some abnormal signs FRC and reduced T. Some patients are complaints

hypoxaemic but not hypercapnic

Severe Breathlessness on any exertion. Wheeze, cough FEV1 <40% predicted with marked Likely to be known to hospital and byprominent. Clinical overinflation usual, plus cyanosis, overinflation. T variable but often low. GP, with frequent problems andperipheral oedema and polycythaemia in some Hypoxaemia usual and hypercapnia in some hospital admissions



S8 Diagnosis and management of stable COPD

• breathlessness (±wheeze) on moderate ex- mal or there may be wheezes (rhonchi) orfeatures of overinflation. The degree of airwaysertion such as physical work or climbing

hills; obstruction cannot be predicted from symp-toms or signs.34

• acute worsening of symptoms associatedIn patients with severe disease the followingwith an infective exacerbation;

physical signs may be present. None is suffi-• routine screening of a patient who was either ciently diagnostic to remove the need for ob-

tolerating the symptoms as part of the normal jective confirmation of the diagnosis.ageing process or as an “expected” con- • signs of chronic overinflation (loss of cardiacsequence of smoking – for example,

dullness, decreased cricosternal distance, in-“smoker’s cough”.crease in the AP diameter of the chest);

Patients with severe COPD are usually • rhonchi, especially on forced expiration;troubled by progressively disabling breath-• loss of weight is common but may also in-lessness or with complications (such as the

dicate occult carcinoma;development of oedema) or with an acute ex-acerbation with or without respiratory failure. • central cyanosis, but its absence does notAlthough usually severely breathless on min- exclude minor degrees of hypoxaemia;imal exertion or at rest, an individual patient’s

• flapping tremor, bounding pulse, drowsinessperception of breathlessness varies consider-(signs of hypercapnia) may occur duringably for the same degree of airflow limitation32

acute exacerbations, but a high Pa2 canand this may be particularly poor in old age.33

occur in patients with stable severe COPDCough and wheeze are almost invariably pres-without these signs;ent but are poor predictors of severity. “Pink

and puffing” and “blue and bloated” are clinical • peripheral oedema may indicate the presencepatterns which indicate, in the former, a patient of cor pulmonale which is of prognostic sig-who maintains relatively normal blood gas ten- nificance;35

sions until a late stage of the disease at the• raised jugular venous pressure, right vent-expense of severe breathlessness and, in the

ricular heave, loud pulmonary second sound,latter, a patient who develops hypoxaemia oftentricuspid regurgitation. These are signs as-with hypercapnia and pulmonary hypertension,sociated with pulmonary hypertension butcor pulmonale, and peripheral oedema. Thesecan be modified or masked by overinflation.terms describe a minority of patients at either

end of the clinical spectrum. The terms do notdifferentiate between the “emphysematous and

Investigationsbronchitic” patient types and most patients lie between these extremes. The diagnosis rests on objective demonstrationof airways obstruction by spirometric testing.AssessmentThis test should be performed on all patientswith suspected COPD, both to confirm theIn all patients assessment should include adiagnosis and to plan appropriate treatment.clinical history and documentation of the smok-Changes in FEV1 occurring naturally or aftering history (see box 2). A specific record oftreatment are distributed in absolute termsexercise tolerance should also be made in orderwhich can make interpretation of percentageto monitor future changes in breathlessness.changes in the bronchodilator response diffi-A past history of childhood wheeze or bron-cult. Further information on the physiology andchitis, pertussis, atopy, pneumonia, and tuber-how to measure FEV1 are given in Appendix 1.culosis can each suggest alternative diagnoses.• An abnormal FEV1 (<80% of predicted)

with an FEV1/VC ratio of <70% and little variability in serial peak expiratory flowClinical examination and non-pulmonary in- (PEF) strongly suggests COPD.vestigations are likely to be normal in patients

• A normal FEV1 effectively excludes the diag-with mild disease. In patients with moderatenosis.disease the respiratory system may appear nor-

• More than 20% variability in the absolutemeasurements of serial PEF may suggestasthma, but when PEF is low the spon-taneous variability of the measurement maySmoking history exceed this.The smoking history should include both the

number smoked, for how long, and an estimate • A normal PEF (>80% predicted) does notof total pack-years of smoking. exclude mild COPD and, in general, PEFOne pack of 20 cigarettes smoked per day for underestimates the severity of COPD (seeone year=one pack-year Appendix 1).Total pack-years=

(No. cigarettes smoked/day)20

× no. years of smoking A chest radiograph is not needed for the diag-

Box 2 nosis of mild COPD and is only indicated if



Diagnosis and management of stable COPD S9

another diagnosis is being considered. It is notpossible to diagnose mild emphysema radio- Corticosteroid reversibility testing

Response to corticosteroidsgraphically.36 However, the incidence of co-Spirometric values should be measured beforeexisting diseases with moderate and severeand at the end of a course of oral prednisoloneCOPD is relatively high so a chest radiograph(e.g. 30 mg per day) taken for two weeks, or aat first presentation can help to identify em-course of inhaled steroid (e.g. beclomethasonephysematous bullae and to exclude serious500 lg twice daily or equivalent) taken for six

underlying diagnoses such as lung cancer which weeks.45 The criteria for an FEV1 response aremay have precipitated the presentation. as for bronchodilators.

Repeat chest radiographs are not needed A less studied alternative is to use the changeroutinely but should be performed if new symp- in mean PEF measured over the first five days

and last five days of the steroid course,toms develop because there is an increasedaccepting a rise of 20% in mean PEF asincidence of lung cancer in these patients.37

significant. Results of reversibility testingshould be clearly documented in the notes andbe easily available for future reference.45

Reversibility tests to bronchodilators (box 3) Interpretationshould be performed at all stages of COPD A positive response to corticosteroids justifies

prescription of regular inhaled steroids. Theresponse to bronchodilators or corticosteroids

Bronchodilator reversibility testing can set a target against which to compareThe objectives of these tests are both diagnostic future therapy.and prognostic• to detect those whose FEV1 increases Box 4

substantially and are thus really asthmatic;• to establish the post-bronchodilator FEV1

which is the best predictor of long termprognosis.2

since even patients with severe airflowTests should be performed when patients areobstruction can demonstrate reversibility.38clinically stable and free from infection.

Patients should not have taken inhaled short Patients who show a bronchodilator responseacting bronchodilators in the previous six are more likely to respond to a trial of oral orhours, long acting b agonists in the previous 12 inhaled corticosteroids.39

hours, or sustained release theophyllines in thepreceding 24 hours.

The preferred outcome measure is the change in FEV1 because its reproducibility isAn oral corticosteroid reversibility study iswell known and is greater than that of the PEFusually not required in patients with mild dis-(see Appendix 1).ease who are using a bronchodilator for relief

Response to bronchodilator of symptoms up to once per day but should beSpirometric values should be measured before performed in patients with mild disease withand after an adequate dose of inhaled greater bronchodilator usage and in all patientsbronchodilator. The dose should be selected to with moderate or severe disease (box 4). Evenbe high on the dose/response curve and is patients with severe airflow obstruction canusually given by nebuliser to be certain it has demonstrate reversibility.42

been inhaled. An alternative less convenientTrials of oral corticosteroids will producetechnique would be to give a similar dose with

a significant spirometric response (defined asmultiple inhalations from a metered doseabove) in 10–20% of patients with clinicallyinhaler and large volume spacer. Astable COPD.43 A response of 200 ml or morerecommended dosage protocol would be:

• before and 15 minutes after 2.5–5 mg in FEV1 after steroids suggests a better prog-nebulised salbutamol or 5–10 mg terbutaline; nosis over five years.44 Some patients will report

• before and 30 minutes after 500 lg nebulised a short term improvement in “well being” but,ipratropium bromide; or unlike the assessment of reversibility to b2 agon-

• before and 30 minutes after both in ists, the trial should not be considered positivecombination.

unless lung function has also improved in viewof possible long term side effects.Interpretation

• An increase in FEV1 that is both greaterthan 200 ml and a 15% increase over thepre-bronchodilator value is significantly greater than the natural variability of the In patients with mild and moderate COPD itFEV1

40 41 and is the most established is unlikely that any further investigations willdefinition of reversibility. be necessary. In those with severe disease the

• The post-bronchodilator FEV1 provides following tests may be useful.information about prognosis and can be usedas a marker against which to assess futuretreatment.

Arterial blood gas tensions• A negative FEV1 response does not precludeHypoxaemia and hypercapnia are common andbenefit from bronchodilators in terms ofmeasurement of arterial blood gas tensionsimproved walking distance or a reduction in

the perception of breathlessness. should be considered in all patients with severedisease. Pulse oximetry may reduce the need

Box 3 for blood gas tension measurements if the Sa2




is more than 92%,46 but should not replace Drug therapydirect arterial blood sampling when the patient

is deteriorating clinically or when complications Bronchodilators are the cornerstone of symp-tomatic treatment for the reversible componentdevelop.of airways obstruction. They probably act byreducing bronchomotor tone and hence airwayresistance in patients with COPD57 58 and by

CT scanning reducing the level of pulmonary overinflation.CT scanning can be used to quantify the extent Inhaled agents given in small doses are asand distribution of emphysema. However, its efficacious as oral preparations, have fewer sideclinical value is currently restricted to the effects and are therefore preferred.assessment of bullous emphysema.47

Single dose reversibility tests in the laborat-ory are useful in diagnosing COPD and forobtaining prognostic information from thepost-bronchodilator FEV1. However, such testsElectrocardiographydo not predict the degree of symptomatic bene-The electrocardiogram provides useful in-fit an individual will obtain from prolongedformation about the presence of ischaemicbronchodilator use.59 The usefulness of a par-heart disease but is an insensitive method ofticular bronchodilator for any individual canassessing right ventricular hypertrophy.48 Elec-only be assessed by a therapeutic trial, acceptingtrocardiographic criteria for right ventriculareither better lung function or subjective symp-hypertrophy are modified by overinflation.tom improvement as end points. Broncho-dilators can improve the FEV1, FVC, orexercise tolerance independently of eachother.60 An increase in FVC does not reliablyExercise tests

These are of no routine diagnostic value but predict an improvement in symptoms.60

may be useful as a marker of progress in struc-tured rehabilitation programmes.

Short acting b2 adrenergic agonistsShort acting b2 agonists have a relatively rapidonset of action and are recommended for use

Haematology “as required” for symptom relief. Used beforeCorrection of unsuspected anaemia (from an- exercise they can increase exercise tolerance inother cause) may improve the symptoms of some patients with COPD.61

COPD. Polycythaemia (haematocrit >47% in Some patients (particularly the elderly) maywomen or >52% in men) may be present and prefer to take regular doses three or four timesshould not be assumed to be secondary without daily. Although concern has been expressedmeasurement of arterial blood gas tensions. about a possible detrimental effect of regularVenesection may be considered if the packed b2 agonist use in COPD,62 the evidence is notcell volume is greater than 50%.31

strong enough to advise against this practice.There is little evidence of tachyphylaxis to b2

agonists in patients with COPD, but there isdisagreement on whether older patients withSputumCOPD are less likely to respond to theseThe routine culture of non-purulent sputumagents.59 63

samples is unhelpful.

Management This is the single most important way of affect-

Stopping smokinging outcome in patients at all stages of• Smoking cessation reduces the acceleratedCOPD.2 5 14

rate of decline of FEV1 (see fig 2).51

Patients with mild or moderate disease • Sudden cessation of smoking may have ashould have the implications of their continued better success rate than gradual reduction ofsmoking explained to them. Those continuing cigarette intake.52

to smoke are certain to lose FEV1 at an ac- • Medical advice and behaviouralintervention53 is effective in those with highcelerated rate that cannot be prevented by drugmotivation.therapy, and worsening disability is highly likely.

• Nicotine chewing gum54 or nicotine skinStopping smoking is just as important inpatches are effective,55 especially if used insevere COPD as at earlier stages of the disease.5

conjunction with a smoking cessation clinic.Although lost function cannot be restored,• Knowing that the patient has really stoppedthose who stop smoking will deteriorate more smoking may be useful especially for

slowly and have a better chance of benefiting reinforcement. Several methods can be usedfrom treatments such as LTOT.49

– for example, monitoring of breath carbonEven brief advice from health professionals monoxide levels, blood carboxyhaemoglobin

can help patients to stop smoking (box 5). The estimation, or by measuring urinary cotininelevels.56reported success rate of different anti-smoking

methods varies from 10% to 30%. RepeatedBox 5advice and encouragement is often needed.




Long acting b2 agonists up to four times daily” treatment should beused. Dosage regimes should be tailored toThere is only limited evidence on the efficacy

of long acting b2 agonists in COPD.64 65 Until individual patient’s needs and to side effects.more data are available their use should belimited to patients with a demonstrablebronchodilator response to b2 agonists and their Theophyllines

Theophyllines are only modest bronchodilatorsuse monitored by assessment of both symptomsand FEV1. in COPD77 78 with a variable effect on exercise

tolerance and symptoms79–83 which is only stat-Evidence is lacking to support the use ofsustained release oral b2 agonists in COPD. istically significant at the upper end of the

therapeutic range. Oral theophyllines have aslow onset of action. Sustained release pre-parations are preferred since they have moreAnticholinergic drugs

Most clinical studies suggest that anti- predictable pharmacokinetics.Non-bronchodilator effects of theophyllinecholinergic drugs such as ipratropium bromide

are as efficacious as b2 agonists in patients with in COPD include improving the strength andeffectiveness of respiratory muscles which mayCOPD,66 67 and some studies suggest a greater

and more prolonged bronchodilator response explain the reported improvement in exercisetolerance in some patients. However, this andthan b2 agonists.67 68 The addition of ipra-

tropium to a b2 agonist may enhance exercise other non-bronchodilator effects – such as im-proved right ventricular performance, aug-tolerance more than can be achieved by either

drug alone.69 mentation of respiratory drive, and anti-inflammatory actions – are of questionable clin-ical significance.

The therapeutic index of theophyllines isDelivery devicesMetered dose inhalers are the cheapest delivery narrow and some patients experience side

effects even within the therapeutic range.84 In-device currently available. However, if thepatient cannot use a metered dose inhaler cor- fection, hypoxia, smoking, and other drugs

affect theophylline clearance and make therectly then a more expensive device is jus-tifiable. A recent study showed that 76% of control of theophylline dosage difficult, neces-

sitating measurement of plasma theophyllinepatients with COPD made important errorswhen using their metered dose inhaler whilst 4–6 hours after dosing.

These problems limit the value of theophyl-10–40% made similar errors with a dry powderinhaler, depending on the device used.70 Inhaler lines in COPD. The risk/benefit ratio has to

be carefully considered in each patient and intechnique must be demonstrated to the patientbefore prescribing inhalers and should be re- most cases a trial of theophyllines is best re-

served for patients in whom other treatmentschecked before changing or modifying inhaledtreatments. have failed to control symptoms adequately.

Which bronchodilator?Home nebuliser therapyThere is controversy over the use of home Beta agonists used “as required” can be tried

first in view of their more rapid relief of symp-nebuliser treatment in patients with COPD.70 71

Most patients can be treated with broncho- toms. If b agonists do not control symptomsadequately or if regular maintenance therapydilators delivered by metered dose inhalers and

spacers or by dry powder devices. A few with is desired, an anticholinergic can be added orsubstituted.severe disease may benefit from high dose

bronchodilator treatment72 which is more con- Combination bronchodilator therapy has thepotential advantage of convenience and im-veniently given by a nebuliser. The results of

clinical trials comparing metered dose inhalers proved patient compliance. However, com-binations of a b2 agonist and an anticholinergicand nebulisers in stable patients with COPD

are inconsistent.73 74 Treatment is expensive and drug should only be used if the single drugshave been tried and have failed to give adequatemay have important side effects.

Nebulisers should only be supplied to symptom relief. Combinations should only becontinued if there is good subjective or ob-patients who have been assessed fully by a

respiratory physician who is able to advise on jective evidence of benefit. Symptom severityand subjective benefit as reported by the patientthe risk/cost benefit. The assessment should

include ensuring that the diagnosis is correct, are better guides to improvement in quality oflife than are short term changes in spirometricthat optimal use has been made of metered

dose and dry powder inhalers, that patients values after bronchodilators.The addition of oral theophylline should onlyrespond to the nebuliser, and that drugs should

be preceded by a home trial with peak ex- be considered if inhaled treatments have failedto provide adequate relief.piratory flow measurements.75 An appropriate

regime is contained in the BTS guidelines for A summary of the use of bronchodilators ateach stage of COPD is given in box 6.nebuliser therapy.76 These guidelines stress the

need for adequate technical support and followup to be available whenever a home nebuliseris prescribed.

The presence of inflammatory changes in theThere is no general agreement as to whetherregular use (four times daily) or “as required airways of patients with COPD provides a




There is no evidence to support the use ofBronchodilator therapy at each stageprophylactic antibiotics given either con-of COPD

At all stages patients must be taught how and tinuously or intermittently in patients withwhen to use their treatments and there should COPD.be a review of treatments being prescribed for There is no role for other anti-inflammatoryother conditions. Beta-blocking agents drugs such as sodium cromoglycate or nedo-(including eyedrop formulations) should be cromil sodium, antihistamines, or mucolyticsavoided.

in COPD. Mucolytic drugs93 94 are used widelyin continental Europe but are not in the Na-Patients with mild diseasetional Formulary in the UK for use in COPD,• Patients with no symptoms – no drugsince trials of their effectiveness have producedtreatment.

• Patients with symptoms – a trial of an variable results.94 95 Further studies are requiredinhaled b agonist or an anticholinergic taken before these drugs can be recommended. Otheras required by an appropriate inhaler device drugs such as the respiratory stimulant al-may be useful.85 If these drugs are ineffective, mitrine (not presently licensed in the UK) arethey should be stopped. of interest96 97 but side effects have precluded

their use.Patients with moderate diseaseIt is unclear whether the mild increase in• Symptomatic patients will benefit from

pulmonary arterial pressure which is slowlyinhaled bronchodilators.progressive in most patients with stable COPD• The level of treatment depends on thehas a causal association with mortality or isdegree of symptoms and their effect on

lifestyle. merely a reflection of the severity of the dis-• Most will be controlled on a single drug, a ease.98 There is no evidence that pulmonary

few will need combination treatment. vasodilators have any role in patients with• Oral bronchodilators are not usually COPD and pulmonary hypertension.98

required.

Patients with severe diseaseOther aspects of management• Most will justify combination of b2 agonistand anticholinergic bronchodilators if theySince patients with mild disease have few symp-derive increased benefit from this

combination. toms, they should be encouraged to continue• Theophyllines can be tried but must be with all their usual activities which will include

monitored for side effects. all but the most strenuous jobs. Exercise is• Some patients will request “stronger” both safe and desirable. In patients with mod-

therapy. The dose-response curve is limited erate and severe COPD exercise should beby the maximum bronchodilation available. encouraged within the limitations of their air-High dose treatment including nebulised

ways obstruction. Breathlessness on exertiondrugs should only be prescribed after amay be distressing to some patients but is notformal assessment.dangerous and many patients can continuetheir activities and interests in spite of theirBox 6impairment.99 Patients with moderate COPDcan often continue in employment as long asrationale for the use of corticosteroids.86 How-

ever, the relationship between these changes, it does not involve heavy manual work.pulmonary function, and the therapeutic re-sponse is not clearly established.87 88 The issueof whether a response to 30 mg of prednisolone

Weight reduction in obese patients will reduceover two weeks predicts a sustained improve-ment on lower maintenance oral doses or in- the energy requirements of exercise and thus

improve the ability of patients to cope withhaled corticosteroids awaits further studies.45

Uncontrolled retrospective studies in COPD their disability. Appropriate dietary advice andsupport should be offered.suggest that long term oral corticosteroids may

slow the decline in FEV189 90 but this treatment Malnutrition is common in patients with

severe COPD and may contribute to mortal-is not recommended in view of significant sideeffects from systemic corticosteroids. Pre- ity.100 101 Although nutritional support for

patients with COPD seems logical, controlledliminary data suggesting an improvement inFEV1 and reduction in the decline in FEV1 trials of its effect on morbidity, quality of life,

hospital admissions, and mortality are not avail-over one year of treatment with inhaled beclo-methasone91 await confirmation in long term able. Selection criteria for patients and a cost-

benefit analysis is needed before this treatmentstudies.On present evidence, inhaled steroids (up can be recommended.

to the equivalent of 1000 lg beclomethasone,800 lg budesonide, or 500 lg fluticasone/day)should be given to patients who show an ob-

Influenza vaccine is recommended for chronicjective response to corticosteroids, either oralor inhaled. Patients with substantial responses respiratory diseases including COPD,102 but

studies to show the relative efficacy of influenzato an oral steroid trial justify treatment ac-cording to the guidelines on the management vaccine in mild, moderate, and severe COPD

are lacking. Patients who are elderly (but notof chronic asthma.92 Those who do not respondshould not continue on steroid therapy. specifically having COPD) have been shown




to have a 70% reduction in mortality from COPD.121 Quality of life assessment is im-portant in assessing the outcome and is mostinfluenza following vaccination.103 This implies

that vaccination in severe COPD is likely to be easily measured by a health profile ques-tionnaire.106 The outcome should also be as-effective. Further studies specific to mild and

moderate COPD are needed.104 Pneumococcal sessed in terms of the longevity of benefit andan analysis of the cost-benefit ratio.122 Patientvaccine is available and the current capsular

polyvalent polysaccharide may be of value,105 compliance with the programme should alsobe addressed.but no studies specific to COPD have been

performed so it cannot yet be formally re- Meta-analysis of studies of respiratorymuscle training alone has provided little evi-commended.dence of a clinically important benefit inCOPD.123

Patients with moderate to severe COPD mayAdditional management primarily for be considered for pulmonary rehabilitationthose with severe COPD programmes. Rehabilitation protocols are currently bring developed and evaluated in theBreathlessness can be assessed clinically from UK and are predominantly hospital based. Al-the patient’s ability to perform specific tasks though some patients undoubtedly benefit from– for example, climbing stairs, shopping, or rehabilitation, facilities are limited and, untilwalking around the house – and can be quan- more UK data are available, firm recom-tified using a visual analogue scale or the mendations as to who should be treated cannotBorg scale.106 These are useful for short term be made.assessments such as the effects of a drug. More Teaching patients about their disease is partdetailed information about the long term effects of all rehabilitation protocols, and all patientsof breathlessness can be obtained using quality may benefit from fuller explanation of the dis-of life scores107–9 or specific breathlessness ques- ease processes, the effects of treatment, howtionnaires such as the baseline and transitional and when to use inhalers, and when to ask fordyspnoea indices.110

help. Many patients with severe COPD areBronchodilators are the most effective treat- dependent on relatives and carers who alsoment for breathlessness and can improve ex- need to know what they can expect from andercise tolerance even in patients without ask of the patient.measurable bronchodilatation.111

Short bursts of oxygen from a cylinder viaa face mask are widely prescribed to relievebreathlessness. There are no data to support or refute this practice, but good data are avail- Two trials of long term oxygen therapyable on the use of long term oxygen therapy (LTOT) in patients with COPD and chronic(see below). hypoxaemia124 125 showed:

Other drugs such as dihydrocodeine,112 113

• improved survival – in the MRC study fivediazepam,114 and nebulised morphine haveyear survival improved from 25% to 41%been studied but with unconvincing or negativewith 15 hours of oxygen therapy per day;results. Such sedatives are potentially unsafe,

are generally poorly tolerated, and are not re- • less secondary polycythemia;commended for routine use. However, somepatients in the terminal stages may benefit from • prevention of progression of pulmonarymanagement similar to that used for malignant hypertension;disease, using sedatives to control intolerable

• an improvement in neuropsychologicalsymptoms. Such decisions require expert opin-health.ion and assessment.

These studies have been used to produceUK recommendations as to which patientsshould be prescribed oxygen concentrators126

Rehabilitation has been defined as “the res- (see box 7). When home oxygen is arranged, thetype of facility (concentrator and/or portabletoration of the individual to the fullest medical,

mental, emotional, social and vocational po- oxygen) and the recommended flow rate shouldbe recorded.tential of which he/she is capable”.115 The ra-

tionale behind pulmonary rehabilitation is to The long term survival in patients withCOPD on LTOT is inversely related to theprevent deconditioning and to allow the patient

to cope with his/her disease.116 It is essential FEV1. A long term follow up of patients onLTOT showed that survival improved to 62%that treatment directed at reversible airflow

limitation is optimised before considering re- at five years, but was only 26% at 10 years.25

The progressive disturbances in the pulmonaryhabilitation. Rehabilitation has been shown tobe effective in prospective randomised clinical circulation were arrested in this cohort but the

accelerated late mortality was still associatedstudies117 118 and in a recent meta-analysis ofthe literature.119 with the severity of the airflow obstruction. For

a very few patients with nasal problems, orOutcomes of rehabilitation programmes in-clude measuring improvement in lung function in those with refractory hypoxaemia or severe

desaturation on exercise, continuous oxygenor exercise tolerance, although benefit maynot always be apparent in these variables.120 can be delivered by the more technically diffi-

cult transtracheal route.127Psychosocial factors contribute to disability in




young with a1-antitrypsin deficiency, lungtransplantation (usually single lung) may bePrescription of LTOT126

• In England and Wales LTOT can be recommended132 but problems with late bron-prescribed by the general practitioner but it chiolitis obliterans after transplantation re-is recommended that all patients considered main.133

for LTOT are assessed by a respiratory Surgical removal or ablation of expanding orphysician. In Scotland LTOT is prescribed very large bullae may be indicated in someonly by respiratory physicians.

patients134 and can lead to prolonged im-• Arterial blood gas measurements should beprovements in FEV1. Recent reports from themade when the patient is clinically stable andUSA have described lung volume reductionon optimal medical treatment, on at leastsurgery (LVRS) in which various forms oftwo occasions three weeks apart. Failure to

do this results in the inappropriate surgical ablation of severely affected areas ofprescription of domiciliary oxygen.128 129 emphysematous lung have been used. In-

• Patients with COPD who have a Pa2 of dications are still evolving but LVRS would<7.3 kPa, with or without hypercapnia, and seem to be most applicable to patients withan FEV1 of <1.5 litres should receive LTOT. severe disease in whom there is a very marked

• If the Pa2 is between 7.3 and 8.0 kPa and increase in FRC and air trapping.135

there is evidence of pulmonary hypertension,peripheral oedema or nocturnal hypoxaemia,LTOT should be considered. Patients Other issuesprescribed LTOT should have stopped smoking because benefit is unlikely in Depression is very common, especially in ad-continuing smokers,5 and because oxygen vanced disease, and contributes to the per-and smoking can be dangerous. ceived symptom intensity and social isolation.• Blood gas tensions should be measured with

It can be treated with antidepressants.136supplemental oxygen to ensure that the setflow is achieving a Pa2 of >8 kPa without anunacceptable rise in Pa2.

• LTOT must be given for at least 15 hours Many patients with severe COPD ask for advicedaily to achieve benefit.124 125 LTOT is best about travel. The doctor should enquire aboutprovided by an oxygen concentrator and the detail of the proposed holiday and thennasal prongs. The oxygen concentrator assess the potential problems of the journeyshould be set at a flow of 2–4 l/min

and whether the patient’s needs can be met.depending on the blood gas assessments.Travel on land or by sea presents few problems• Studies have highlighted problems with theprovided that help is available for transfers atuse of LTOT and emphasise the need for sixstations and ports. Aircraft are pressurised tomonthly follow up and re-assessment which

can be best arranged by a respiratory health the equivalent of 900–2400 metres above seaworker visiting the patient’s home.130 level which reduces the ambient P2 to

15–18 kPa.137 Patients with COPD who areBox 7 hypoxic at rest at sea level will become more

hypoxic during a journey by air, although theclinical significance of this is not known.

Many patients with chest disease do travel successfully and most emergencies in flight areAmbulatory oxygen therapy can improve ex-not respiratory.138 Relative contraindications toercise tolerance and breathlessness and maytravel include hypercapnia or gross hypoxiaallow greater compliance and longer hours ofwhile breathing air (Pa2 <6.7 kPa). A historyusage of LTOT. Improvement with ambulatoryof previous pneumothorax or the presence ofoxygen therapy may be related to the degreeemphysematous bullae suggests a risk of furtherof arterial oxygen desaturation on exercise.131

pneumothorax as the poorly ventilated airPortable cylinders are the only form of am-spaces fail to respond to the changes in pres-bulatory oxygen therapy available in the UKsure, particularly on descent. Most major air-and provide two hours of use at 2 l/min. Liquidlines, but not most charter operators, are ableoxygen is not available at present on pre-to supply supplementary oxygen as well asscription in the UK. There are no firm criteriasupport to get dyspnoeic passengers to andfor selecting patients for ambulatory oxygenfrom the aircraft if warned in advance.therapy. However, it has been suggested that

The doctor should ensure that the patientprescriptions should be based on a documentedhas sufficient medication to last the holiday, andfall in arterial oxygen saturation of more thanmay consider providing an emergency supply of4%, below 90% on a standard walking test,antibiotics in case of an exacerbation. Withinand associated with an improvement in exercisethe UK it is usually possible to make ar-tolerance or breathlessness with ambulatoryrangements with a local chemist for a temporaryoxygen therapy.131 However, good evidence tosupply of oxygen cylinders for patients onsupport this is lacking.LTOT. However, many patients on LTOT cancope without their oxygen for short periodswithout detriment.

Surgical treatments are applicable for a veryHealth care costssmall number of patients with COPD. FullWithin the European Community and a num-specialist physiological assessment is man-ber of other countries costs of health care aredatory and many assessed will be turned down.

In selected patients, particularly those who are met for all residents under reciprocal agree-




ments, but such agreements do not extend toNorth America and most private travel in- Indications for specialist referral

Reason Purposesurance will not cover an existing problem. TheTherapeutic advice:risk of receiving substantial medical bills will

Suspected severe Confirm diagnosis anddeter many patients from such travel.COPD optimise therapy

Onset of cor Confirm diagnosis and pulmonale optimise therapyA specialist opinion may be helpful at any stage Assessment for Optimise therapy and

oxygen therapy measure blood gasesof the disease. Referral may be to establishAssessment for Exclude inappropriatethe diagnosis, to exclude other pathology, to

nebuliser therapy prescriptionsreassure the patient, to reinforce the need toAssessment for oral Justify need for longstop smoking, to optimise treatment, or to

corticosteroids term treatment or toassess the need for the more complex andsupervise withdrawalexpensive therapies appropriate to severe Bullous lung disease Identify candidates for

COPD. The principal reasons are summarised A rapid decline in surgeryin box 8. FEV1 Encourage early

intervention

Diagnostic advice:Follow up of patients with stable COPDAged under 40 years Identify a1-antitrypsin

or a family history deficiency, considerFollow up of patients with mild or moderateof a1-antitrypsin therapy and screenCOPD will usually take place in primary caredeficiency familyand should include: Uncertain diagnosis Make a diagnosis

Symptoms• highlighting in the case record the diagnosisdisproportionate toof COPD and the values of spirometric testslung function Look for otherperformed at diagnosis;deficit explanations

Frequent infections Exclude bronchiectasis• supervision of smoking cessation;

• documenting the effects of each drug treat-Box 8ment as it is tried;

• recording changes in spirometric parameterstreatment, and need monitoring for LTOT.measured opportunistically at intervals.Shared care between the hospital and GP is

A loss of 500 ml over five years will select the usual pattern although there are no data toout those rapidly progressing patients who may show how care should be provided to achieveneed specialist referral and investigation. Rou- the best combination of clinical and cost effect-tine isolated PEF measurements are of little iveness. All of the recommendations for mild/value because of the discordance between PEF moderate disease apply and, in addition, theand FEV1 (see Appendix 1) Royal College of Physicians has suggested that

respiratory health worker posts are created tohelp with the management of patients withchronic respiratory diseases.139 Their duties

Patients with severe COPD are likely to have should include visiting the patient at home toadvise on both psychosocial and respiratoryfrequent exacerbations leading to hospital ad-

missions. They often have complex problems problems and to improve compliance withtreatment.140with co-morbidities, may be on high levels of




3 Management of acute exacerbations ofCOPD

PresentationAcute exacerbations of COPD present as a Deciding whether to treat an acuteworsening of the previous stable situation.141 exacerbation at home or in hospitalImportant symptoms include:

Treat at Treat in• increased sputum purulence home hospital

Ability to cope at Yes No• increased sputum volumehome

Breathlessness Mild Severe• increased dyspnoeaGeneral condition Good Poor –

• increased wheeze deterioratingLevel of activity Good Poor/confined• chest tightness to bedCyanosis No Yes• fluid retention.Worsening peripheral No Yes

The exacerbation is a new respiratory event oedemaLevel of Normal Impairedor complication superimposed upon es-

consciousnesstablished COPD. The new event in COPD isAlready receiving No Yesmost often an infection but can also be the

LTOTdevelopment of peripheral oedema. DifferentialSocial circumstances Good Living alone/diagnoses to be considered in each patient not coping

include: Acute confusion No YesRapid rate of onset No Yes• pneumonia

Also available at hospital• pneumothoraxChanges on the chest No Present

• left ventricular failure/pulmonary oedema radiographArterial pH level [7.35 <7.35• pulmonary embolusArterial Pa2 [7 kPa <7 kPa

• lung cancerThe more of the referral indicators that are

• upper airway obstruction. present, the more likely the need for admissionto hospital.

Box 9Management of an acute exacerbation inthe community

troduced expensive new brands are not usuallyMany patients can be managed at home butappropriate.some require inpatient support and the decision

whether or not to admit is complicated (seebox 9).

A confident diagnosis of an exacerbation ofBeta agonists and/or anticholinergic drugsCOPD in a patient who does not need ad-should be added to the treatment regimen ormission and who responds to treatment doesthe dosage increased if there is evidence ofnot require further acute investigations.worsening airflow obstruction. The inhaledroute is preferable, but the doctor should ensurethat the patient has a device he or she can

use effectively. Nebulisers are usually not re-The principles of managing acute exacerbations quired.143

of COPD in general practice are summarisedin box 10.

Management of the acute exacerbation1 Add or increase bronchodilators (consider ifAntibiotics inhaler device and technique are appropriate)

These are widely used but have been shown to 2 Antibiotic if two or more of:be effective only if the patient has at least two • increased breathlessnessof the three features shown in box 10.142 A • increased sputum volumemaximum of seven days of treatment is suffi- • development of purulent sputum

3 Oral corticosteroids in some cases (see text).cient. The choice of antibiotic should followlocally produced guidelines derived from local

Box 10bacteriological sensitivity data. Recently in-



Management of acute exacerbations of COPD S17

dependent the patient is under normal cir-cumstances and during the exacerbation);Oral corticosteroids should not be used for

acute exacerbations in the community unless: • current treatments, especially the use ofnebulisers and LTOT;• the patient is already on oral corticosteroids;

• time course of the current exacerbation;• there is a previously documented responseto oral corticosteroids; • the patient’s social circumstances and quality

of life, especially whether living alone/alone• the airflow obstruction fails to respond to anwith support/with family plus an indicationincrease in bronchodilator dose;of the suitability of the accommodation;

• this is the first presentation of airflow ob-• number of previous admissions in the paststruction.

five years, including admissions to the intens-Oral corticosteroids are given usually in a ive therapy unit;

dose of 30 mg per day for one week. They• smoking history.should not normally be continued long term.

There is a need for further research into theplace of oral corticosteroids in the context of

Signsan acute exacerbation of COPD.Signs suggesting a significant deteriorationinclude those of infection (pyrexia, franklypurulent sputum), severe airways obstruction

(audible wheeze, tachypnoea, use of accessory

muscles), peripheral oedema, cyanosis and/orA further review after an acute exacerbation isconfusion.merited if the patient fails to respond fully to

treatment when a chest radiograph and possiblyhospital referral may be indicated. The follow

up visit represents an opportunity to help theUrgent out of hours investigations should al-patient to plan for the future and to try toways include measurement of arterial blood gasprevent further exacerbations. Advice on smok-tensions, noting the inspired oxygen con-ing, lifestyle, activity levels and weight, and acentration (Fi2), and a chest radiograph.review of medication should follow the re-

Investigations within the first 24 hourscommendations for the management of stableshould include a full blood count, urea andCOPD described above.electrolytes, and ECG. An initial FEV1 and/orpeak flow should be recorded and a serial peakflow chart started as soon as possible. If the

Management of an acute exacerbation of sputum appears purulent, it should be sent forCOPD in hospital culture and if pneumonia is suspected, blood cultures are recommended. It is probable that pulmonary emboli arePatients may self-refer or be referred by their more common than is usually recognised inGP. The same indicators as in the previous severe COPD144 but the benefit of prophylacticsection (see box 9) apply in deciding whether anticoagulation treatment has not been evalu-the patient should be admitted or discharged ated.home directly. The indicators will have differingimportance for different patients.

If a patient is to be discharged directly from the Accident & Emergency department Oxygen (box 11)the following extra safeguards should be con- The aim of treatment with oxygen is to achievesidered: a Pa2 of at least 6.6 kPa without a fall in pH

to below 7.26 (secondary to a rise in Pa2).• the patient should have adequate support tobe able to cope at home;

• the patient (or carer) should understand thetreatment prescribed and the use of any delivery Oxygen therapydevices; • In patients with a history of COPD aged 50

years or more, do not give an Fi2 of more• sufficient medication should be supplied to than 28% via a Venturi mask or 2 l/min vialast until the next opportunity for consultation nasal cannulae until the arterial gas tensionswith the GP (or specialist). are known.

• Check blood gases within 60 minutes ofThe patient’s GP should be informed of the starting oxygen and within 60 minutes of a

visit to the Accident & Emergency department change in inspired oxygen concentration.within 48 hours. • If the Pa2 is responding and the effect on

pH is modest, increase the inspiredconcentration of oxygen until the Pa2 isabove 7.5 kPa.History

• If the pH falls (secondary to a rise in Pa2),Particular note should be made of:consider alternative strategies.

• the known exercise tolerance (which shouldinclude a careful record both of how in- Box 11



S18 Management of acute exacerbations of COPD

A pH below 7.26 is predictive of a poor out-come.145 There is no evidence that humid- Choosing an antibiotic in acuteification is necessary. exacerbations of COPD

• Common antibiotics will usually bePatients may have been given oxygen in theadequate; the newest brands are rarelyambulance or on arrival in the A & E de-appropriate. Thus, amoxycillin or tetracyclinepartment. For patients aged over 50 years theare first choice unless used with poormaximum initial inspiratory oxygen con-response prior to admission.centration should be 28% via a Venturi mask.146

• For more severe exacerbations, or if there isVenturi masks deliver the most predictable levels lack of response to the above agents, severalof inspired oxygen. Concentrations from nasal second line alternatives can be consideredprongs are less predictable147 but prongs are less including a broad spectrum cephalosporin oreasily dislodged and may be better tolerated.148 one of the newer macrolides.

If the patient is initially acidotic or hyper-capnic measurement of blood gas tensions Box 12should be repeated within 60 minutes. If theinspired oxygen maintains or improves Pa2 given if two or more of the three featureswithout causing a deterioration in pH, then the

described in box 10 are present. In addition,inspiratory concentration can be increased andall patients with acute on chronic respiratorythe blood gas tensions rechecked until the Pa2 failure (pH <7.35) should receive antibiotics.is >7.5 kPa.144 Monitoring by oximetry may be

The three most likely pathogens in order ofsatisfactory if the arterial blood gas tensionimportance are Haemophilus influenzae, Strepto-measurements have shown that the Pa2 andcoccus pneumoniae, and Moraxella catarrhalis.pH are both normal and the patient remainsAtypical pathogens are not usually a problemstable with no fall in Sa2. although evidence is emerging that ChlamydiaMeasurement of arterial blood gas tensionspneumoniae may occasionally be found.154

should be repeated at any time if the clinicalThe choice of antibiotic depends on the localsituation deteriorates.

antibiotic policy and pattern of pathogens inthe local laboratory, as well as on the antibiotic

Bronchodilators treatment prior to admission. Oral rather thanNebulised bronchodilators should be given on intravenous antibiotics should be used unlessarrival and at 4–6 hourly intervals there- there is a contraindication to oral treatmentafter149–151 but may be used more frequently (see box 12 for a possible approach to antibioticif required (see also British Thoracic Society choice).guidelines on nebuliser treatment76). Many In severe exacerbations of COPD sputumhospitals power nebulisers from a wall mounted culture and sensitivity may be of considerableoxygen supply but in patients with COPD the value. If the chest radiograph shows evidencenebuliser should be driven by compressed air of pneumonia the patient should be treatedif the Pa2 is raised and/or there is a respiratory according to the British Thoracic Societyacidosis. Oxygen can continue to be given by guidelines on pneumonia.155

nasal prongs at 1–2 l/min during nebulisation inorder to prevent the fall in oxygen saturation thatsometimes occurs with the use of nebulisers. Corticosteroids

For moderate exacerbations a b agonist (sal- Whether systemic corticosteroids alter thebutamol 2.5–5 mg or terbutaline 5–10 mg) or course of an acute exacerbation in hospitalan anticholinergic drug (ipratropium bromide remains unclear. One study reported benefit0.25–0.5 mg) should be given. For severe ex- with methylprednisolone over 72 hours156 butacerbations or if the response to either treatment it is not known if these data extrapolate toalone is poor, then both may be administered.152 benefits such as earlier discharge or extendA response to nebulised bronchodilators in the to all COPD exacerbations in hospital. It isacute situation does not imply long term benefit. common practice to use a 7–14 day course ofFormal assessment after recovery from the acute systemic corticosteroids (prednisolone 30 mg/episode is still required (see section on nebuliser day or 100 mg hydrocortisone if the oral routetreatment on page S11). is not possible). This approach is certainly

If the patient is not responding intravenous justified if:methylxanthines by continuous infusion

• the patient is already on oral corticosteroids;(aminophylline 0.5 mg/kg per hour) should beconsidered. If given, blood levels of theo- • there is a previously documented responsephylline should be measured on a daily basis. to oral corticosteroids;There is, however, a paucity of evidence on the • the airflow obstruction fails to respond to aneffectiveness of theophylline in this situation.153

increase in bronchodilator dosage;Nebulised bronchodilators should be con-tinued for 24–48 hours or until the patient is • this is the first presentation of airways ob-improving clinically. Bronchodilators can then struction.be given by metered dose aerosol or dry powder Corticosteroids should be discontinued afterinhalers. the acute episode, usually after 7–14 days of

treatment, unless they have been shown to beeffective when the patient is clinically stable orAntibiotics

The indications are the same as for ex- there is a definite indication for long termtreatment. Clinical improvement from an ex-acerbations in general practice and should be




acerbation while on oral corticosteroids doesnot necessarily indicate the need for long term Factors to encourage use of IPPV

• A demonstrable remedial reason for currentinhaled corticosteroids, the requirement fordecline – for example, radiographic evidencewhich should be assessed separately.of pneumonia or drug overdosage.

• The first episode of respiratory failure.• An acceptable quality of life or habitual levelDiuretics

of activity.Diuretics are indicated if there is peripheraloedema and a raised jugular venous pressure. Factors likely to discourage use of

IPPV• Previously documented severe COPD that

has been fully assessed and found to beAnticoagulantsunresponsive to relevant therapy.The only firm recommendation that can be

• A poor quality of life – for example, beingmade is to follow the advice of the Thrombo-housebound, in spite of maximal appropriateembolic Risk Factors Consensus Group whotherapy.recommend prophylactic subcutaneous hep-

• Severe co-morbidities – for example,arin for patients with acute on chronic res- pulmonary oedema or neoplasia.piratory failure.157

N.B. Neither age alone nor the Pa2 are agood guide to the outcome of assisted

Physiotherapy ventilation in hypercapnic respiratory failuredue to COPD. A pH of >7.26 is a betterThere are few data to support or refute the usepredictor of survival during the acute episode.145of chest physiotherapy to ease problems of

sputum retention in acute exacerbations ofBox 13COPD.158 It is not recommended in acute on

chronic respiratory failure.of doxapram may decline as the facilities forNIPPV increase.

Managing respiratory failure and the Misconceptions about the difficulty of wean-need for intermittent positive pressure ing from a ventilator should not preclude in-ventilation (IPPV) tubation and IPPV. The five year outcome ofVentilatory support, either as non-invasive patients with COPD who suffer respiratoryintermittent positive pressure ventilation failure is better than many doctors appreciate(NIPPV) or invasive intermittent positive pres- and does not depend on the acute level ofsure ventilation via an endotracheal tube Pa2.163 The mean survival of patients who(IPPV) should be considered in a patient with were hypercapnic on admission but who latera pH of less than 7.26 and a rising Pa2 who became normocapnic was 2.9 years.163

fails to respond to supportive treatment andcontrolled oxygen therapy.145

The specialist facilities for NIPPV support Monitoring and management as thevia nasal masks are only available in some patient recovershospitals at present. NIPPV has been shown In addition to the routine hospital observations,in randomised controlled trials to reduce the the following should be considered:number of patients requiring IPPV and the

• FEV1 should be recorded before dischargelength of stay in hospital159 160 and to be offrom hospital;most value if used earlier than recommended

above.161 162 Confused patients and those with • peak flow should be recorded twice dailya large volume of secretions are less likely to until clinically stable;respond well to NIPPV. • in patients presenting with hypercapnic res-The decision to institute or to withhold

piratory failure and those with a low Pa2ventilatory support must be made by a senioron admission the arterial blood gas tensionsperson with as much information as possibleshould be checked on air before discharge.about the patient’s premorbid state. Factors toThis gives a guide to the need for later formalbe considered are shown in box 13 and to thesere-assessment for LTOT therapy.should be added the patient’s wishes if known

– for example, as in a living will – and those of As the clinical condition improves (less dys-pnoea, better PEF, improved Sa2) the nebu-close relatives.

Supportive therapy used to try to avoid the lised bronchodilator can be changed to thepatient’s usual inhaler, ideally at least 24–48need for intubation and IPPV includes the

use of intravenous doxapram and non-invasive hours before discharge. Antibiotics usually donot need to be continued for more than sevenrespiratory support. If either is tried, the

patient’s condition needs to be closely mon- days. If oral corticosteroids have been usedthey can usually be stopped abruptly after sevenitored since a significant proportion will still

need intubation and IPPV. days unless there are positive reasons for longterm usage (see page S12).Doxapram, a respiratory stimulant, may

be considered in patients with an acidosis(pH <7.26) and/or hypercapnia and hypo-ventilation.145 It can tide the patient over for Planning for discharge

Patients with severe COPD often have repeated24–36 hours until the underlying cause – forexample, an infection – is controlled. The use hospital admissions. Discharge planning should



S20 Management of acute exacerbations of COPD

Table 3 Financial help available to patients with COPD in the UK

Number of rates at Criteria for being eligible Means Special conditionswhich benefit is paid tested

Patients under 65 years:Disability living allowance 2 Ability to walk No Disabled for more than 3 months and needed– mobility (DLA-M) • lower rate if can walk but need to be for more than 6 months. If terminally ill, benefit

accompanied. can be obtained immediately.• higher rate if unable or virtually unable to

walk.Disability living allowance 3 Ability to self care No As above– personal care (DLA-P) • the highest and middle rates if care needed

day and night.Disability working 1 Earning capacity limited Yes Must be working at least 16 hours per week andallowance (DWA) be receiving other benefits, renewable 6

monthlyInvalid care allowance 1 Severe disability No Benefit to the carer who helps for more than 35(ICA) hours per week. Patient must be receiving DLA

at middle or high rateIndustrial injuries 10 Loss of physical ability (compared with person No Prescribed diseases include occupational asthmadisablement benefit (and supplements of same age and sex) and, in coal miners only, COPD

also available) • due to an accepted industrial injury orprescribed disease.

Incapacity benefit 3 Physical ability but a concurrent depressive No Replaces sickness benefit after 6 months. Allowsillness should not be overlooked. other benefits to be claimed. Severe

cardiorespiratory failure usually exempts personfrom “all work test”.

Severe disablement 1 Incapable of working for more than 196 days No For those not able to receive incapacity benefit,allowance (and an age • due to loss of physical ability (compared who are 80% disabled or receiving DLA at high

supplement) with person of same age and sex) rate or war pension. Disability may need to beassessed by review of medical notes.

War disablement pension Variable Conditions aggravated by service in HM No Contact War Pension hotline, 12 supplementsforces (during or within 7 years) available

Community care grant Variable Necessitates move to new accommodation or No One off benefit from local authorityadaptation of current property

Patients over 65 years:Industrial injury benefit As for under 65 yearsWar pension As for under 65 years

aim to improve the ability of patients to cope guide any person whose exercise tolerance isless than 100 yards might be entitled to awithin their limitations at home and to reduce

the need for future admissions. A multi- benefit. When completing any applicationforms the applicant should always give the timedisciplinary approach is needed to consider the

following medical and social factors. taken to do any task mentioned on the formand also point out any other disability whichmight enhance the likelihood of a benefit beingpaid.Medication

Benefits are divided into those available for• A review of all medication (including non-patients above or below 65 years of age and arespiratory treatments)few that are independent of age such as mobility

• Inhaler technique allowances and the orange badge scheme tohelp with car parking. A number of the benefits• Ensuring that the patient knows how andmentioned below have an additional mobilitywhen to take his/her medicationcomponent which can be claimed including

• For the few patients discharged on a nebu- exemption from vehicle excise duty and con-liser, the specific reasons for continuing cessions on rail fares. Most benefits go to thenebulised treatment should be recorded. patient but a number are available to the carer.

The more important benefits and how theyrelate to severe COPD are outlined in table

Social factors and ability to manage at home 3. Benefits are claimed through the BenefitsAgency whose address and telephone number• Assessment of mobilisation and giving pre-are available in the telephone directory. If aliminary instruction in rehabilitationdoctor receives a request for a report this should

• Assessment of home needs such as shopping, always describe how the patient is disabledcleaning, obtaining medication, and pro- and handicapped by the condition. Basic lungvision of equipment to assist in daily living. function results with measurements of re-

versibility are helpful in confirming a claim for• Financial assessment: patients with COPDdisability. If in doubt, a Medical Advisor ismay be eligible for financial help from aavailable in all the regions of the UK.number of different benefits.

- For those still smoking before admission, adviceIn the UK patients with COPD may be entitled should be repeated and documented.to benefits from the Department of SocialSecurity. The entitlement is related to thedegree of disability of the patient, but the level ( )

A decision to provide LTOT should not beof disability required before a claimant is en-titled to benefit is not clearly defined. As a made on the basis of hypoxia during the acute




episode alone (see management of stable Planned follow up in hospital or bygeneral practitionerCOPD, page S13). Use of assisted ventilation

(NIPPV) on a chronic basis is confined to a few Follow up arrangements are required for allpatients 4–6 weeks after discharge. At the firstspecialist centres and is still being evaluated.follow up visit (either by a respiratory physicianin the hospital outpatient department or by aGP with an interest in COPD) assessmentshould include:

• the patient’s ability to cope;The patient should be fully informed about the

• measurement of FEV1;nature of his/her condition and its treatment.• re-assessment of inhaler technique and ofIt is probably useful for the patient to have a

the patient’s understanding of recommendedwritten record of the treatment, FEV1 and PEFtreatment regime;readings, and the usual level of Pa2 and Pa2.

Where possible, information leaflets such as • in severe COPD the need for long termthose produced by the Breathe Easy Group of oxygen therapy and/or home nebuliser usage;the British Lung Foundation should be pro-

• advice on smoking cessation as necessary.vided. Discussion should include planning howthe patient should respond to future episodes Follow up thereafter is as for stable COPD

described on page S15.and who should be contacted.




Appendix 1: Physiology

Measurement of FEV1 varying degrees of computerised reports. Themost important considerations when buying 1

? and using a spirometer are:The FEV1 is strongly recommended as the • the spirometer will need calibrating (volu-measurement of choice in COPD for the fol-

metric devices weekly and flow based deviceslowing reasons:at least daily) with a three litre syringe;

• It is a reproducible and objective measure- • the spirometer should produce a hard copyment with well defined normal ranges that of the tests which should be large enough forallow for the effects of age, race, and sex. any computer reported values to be checked

from the graphs. A volume/time plot is man-• It can be measured relatively easily anddatory, a flow volume plot is optional. Itquickly and at all stages of the disease.should be possible to superimpose traces to

• The forced expiratory manoeuvre records compare easily the different attempts by annot only FEV1 but also FVC. An FEV1/FVC individual;ratio of less than 70% is diagnostic of airways

• a spirometer is of limited value withoutobstruction. If the ratio is normal (>70%)trained staff who are able to perform the testand the test was performed well, the patternto the published standards.165 Poorly trainedis not obstructive and the diagnosis is notstaff can produce misleading results;COPD. PEF measurements cannot differ-

entiate whether values are low because of • electronic spirometers without a hard copyobstruction or restriction. tracing may lead to underestimation of the

FEV1 and FVC because it is not possible to• The variance of repeated measurements inverify the reliability of the test.the same person is well documented and is

low. In COPD the variability of the FEV1

between testing occasions is of the sameReporting the resultsabsolute order (about 170 ml).41 Hence, ifBefore interpreting the test values the followingvalues change by more than 200 ml it iscriteria should be satisfied:unlikely that the difference is due to chance.

• there are at least three technically satisfactory• Studies of mortality and of disability havereadings;shown that the FEV1 predicts future mor-

tality18–22 and relates best to the severity of • the expiratory volume/time traces arebreathlessness. smooth, convex upwards, and free from ir-

regularities that suggest either variable sub-• The absolute value of the FEV1 is bettermaximal effort or coughing;related to prognosis and disability than is the

FEV1/VC ratio. This may be because the • there are at least two readings of FEV1 thatmeasurement of VC in COPD is subject to are within 100 ml or 5% of the other;error, especially when the expiratory man-

• the recording has been continued longoeuvre is not continued for more than sixenough for a volume plateau to be reachedseconds.40

on the volume-time plot. This can take up• Serial measurements provide evidence of the to 15 seconds in patients with severe COPD.

disease progression. Abbreviated efforts will underestimate FVC.• In COPD the relationship between PEF and The best FEV1 and best FVC values should

FEV1 is poor and it is not possible to predict be reported as the result and compared withFEV1 from the PEF or vice versa.164

the predicted normal value (based on age,height and sex).40

• PEF may underestimate the degree of air-ways obstruction in COPD.

Thus, FEV1 is the measurement of choice. However, PEF may have some value when used Since most general practices do not at presentserially in a single individual, especially in those possess a spirometer and do not have trainedwith an asthmatic component to their COPD, technicians, some clear health service planningand changes in mean PEF (recorded over sev- will be needed. Three options are:eral days) can be useful. 1. To provide open access for general practice

to the lung function laboratory at each districtgeneral hospital in a similar fashion to radio-graphic services. Some additional staffing 1 ?

Obtaining a spirometer would be needed, but the equipment and ex-pertise and quality control are already in placeThere are many competent spirometers avail-

able. Most cost less than an ECG machine in the hospital service.2. To provide spirometry in individual prac-and adhere to US recommended standards.165

Some measure volume directly while others tices. Many practices will be cautious of spend-ing £1000 or more on equipment that willderive volume from the airflow. There are



Appendix 1 S23

not be heavily used and will have difficulty These data, coupled with the clinical ex-perience of the Guidelines Committee, wereobtaining appropriate training for staff. The

cost effectiveness of this will depend upon the considered sufficient to justify adopting theBritish definitions of mild, moderate, andsize of the practice. In small practices adequate

quality control of testing procedures will not severe disease.Thus, the following severity ranges were es-be easy to achieve.

3. To provide a mobile community spirometry tablished:service. The cost effectiveness of this will need • Mild COPD: presymptomatic within theto be compared with either of the options community and usually unknown to the doc-above. tor. This group is defined as having an FEV1

of 60–79% of predicted with an abnormalFEV1/FVC ratio of <70%.

Justification of mild, moderate, and • Moderate COPD: these patients will usuallysevere categorisation of COPD have presented to their GP with intermittentCOPD describes a spectrum of disease pro- chest problems and may be finding workgressing from the earliest symptomless stages difficult. Their FEV1 is 40–59% of predicted.through to respiratory failure. The medical re-

• Severe COPD: these patients are likely toquirement of patients increases with increasinghave significant symptoms and to have in-severity and the group considered that COPDtermittent admissions to hospital. Theircould usefully be divided into three stagesFEV1 is below 40% of predicted.which approximated to their health care re-

quirements. The precise boundaries chosen areinevitably rather arbitrary and were selected for

Other tests of respiratory functionthe following reasons:Static lung volume measurement documents

• Values of FEV1 above 80% are within two the degree of overinflation and may be usefulstandard residuals of the predicted mean40

when assessing patients for surgery (particularlyand, although it is possible for airway ob- thoracic surgery) and for research studies.struction (FEV1/VC ratio <70%) to be pres- Diffusing capacity or gas transfer factor forent if the VC is high, the clinical significance carbon monoxide (T) is said by some to beof this is probably marginal. helpful in distinguishing asthma from em-

physema and is recommended for that purpose• Choice of 40% and 60% levels: the Americanin the European guidelines.166 However, itsThoracic Society, in assessing levels of res-value in planning treatment is less clear. Thepiratory disability, adopted these levels asT did not discriminate between patientsthe indicators of mild, moderate, and severewho did or did not respond to an oral steroidrespiratory disability.99 Clinical studies oftrial.4

patients with COPD recruited from UK hos-Static and dynamic compliance are not easypital outpatient departments have reported

to measure and, although the latter may bemean FEV1 levels of about 35% of predic-abnormal even before there has been a de-ted,4 45 whereas a study of patients withtectable change in FEV1, neither has beenCOPD recruited from general practice hadshown to be of practical clinical value. Theya mean FEV1 of 50% predicted.62

remain research tools.Bronchial hyperreactivity is characteristic of• The European Respiratory Society guide-

lines166 also divide COPD into three cat- asthma. A degree of hyperreactivity is oftenseen in patients with COPD but whether thisegories of severity but have chosen 90%,

70%, and 50% as defining levels of FEV1. reflects the geometric effect of a reduced start-ing FEV1 or is a true increase remains uncertain,In contrast, the American Thoracic Society

document167 has selected 80%, 50%, and as does its clinical role.The above tests, together with others such35% of predicted as their demarcation levels.

They do not cite any further justification. as measurement of the ventilatory response tocarbon dioxide and tests of respiratory muscleThese levels may reflect the different styles

of medical practice in Europe and the United function, may all be useful when assessing thedifficult patient or when evaluating new drugsStates, though precise demarcation remains

arbitrary. or treatments.



S24 Thorax 1997;52(Suppl 5):S24

Appendix 2: Pathology

Patients with COPD exhibit a variety of patho- connective tissue septae and usually leads toblebs on the lung surface which predispose tological changes throughout the bronchial tree

and alveoli, reflecting differences in duration pneumothorax or to giant bullae within thelung substance.of exposure and response to cigarette smoke.168

Changes in mucus gland thickness relate to The presence of inflammatory cells withinthe airway wall and lumen of both large andsputum production but not to loss of respiratory

function. Most airflow limitation is due to a small airways provides a rationale for the useof anti-inflammatory treatment, at least in somecombination of mechanical obstruction in the

small airways and loss of pulmonary elastic cases.87 168 Airway eosinophilia is associatedwith a measurable bronchodilator response torecoil due to emphysema. In addition, re-

duction of the alveolar attachments around the b agonists and relatively less emphysema for anydegree of airflow limitation.87 Whether clinicalwalls of the small airways makes these airways

more likely to collapse during expiration. markers of inflammation can identify suchpatients is still unclear, but past results are notEmphysema is defined as a permanent de-

structive enlargement of the air spaces distal to encouraging.168 Nonetheless, these pathologicaldata confirm that bronchodilator reversibility isthe terminal bronchioles.169 Smokers are prone

to develop centriacinar emphysema where the possible even in the presence of lung pathologythought to be irreversible.respiratory bronchioles, alveolar ducts, and al-

veoli at the centre of the acinus are destroyed. Circulatory changes are confined to ad-vanced disease when persistent arterial hyp-Some subjects also develop panacinar em-

physema where the whole of the acinus is oxaemia has developed.144 Pulmonary vascularremodelling is now thought to accompany me-destroyed.

Centriacinar emphysema is associated with dial thickening of the pulmonary arterial wallsecondary to hypoxia and to explain why thesemore small airways disease and less loss of

elastic recoil for any level of respiratory func- changes do not resolve with long term oxygentherapy.171tion.170 Paraseptal emphysema occurs close to



Thorax 1997;52(Suppl 5):S25 S25

Appendix 3: Health care provision for themanagement of COPD

Smoking cessation policies should be established comparable to the gen-eral practice access to radiographic facilities;Each health district should ensure that the

implementation of anti-smoking strategies and • there will be a need for more practice nursespolicies is a prominent part of its health pro- to cover the substantial unmet needs ofmotion programme. COPD. These nurses will need formal train-

ing;

• “obstructive airway” clinics similar to asthmaDistrict general hospitals should haveclinics may be worthwhile.• a specified respiratory physician with re-

sponsibility for COPD;

Justification for increased resources for• facilities for spirometric tests in all routineCOPDclinics and spirometric testing should also ’ be available to patients from general prac-

titioners; • The patient wants a definite diagnosis and aclear treatment plan that is consistent from• nursing staff on the wards who have receivedall those involved in his/her health care.training in the assessment and management

of patients with COPD; • Many would like help with smoking cessationbut cannot find such help at present.• sufficient high dependency and, preferably,

intensive care facilities to permit the man- • Patients would like to be informed aboutagement of patients with respiratory failure their condition and to be allowed to par-in hospitals accepting patients with acute ticipate in the decisions leading to treatmentexacerbations; choices.

• a specialised respiratory nurse attached to • Patients would like to be cured but, as thiseach district hospital with responsibility for is not possible, they want to maximise theirliaising over the care plans with primary care; quality of life.

• care planning should involve physiotherapy,occupational therapy, respiratory rehabil-

itation staff, and social services;

• resources to develop respiratory rehabilita- • Less smoking of cigarettes will result in lesstion and to provide assessments for long termCOPD in 10–15 years’ time and also in feweroxygen treatment;patients with mild/moderate disease reaching

• a nebuliser service which includes patient the severe stage at which most treatment andassessment and equipment support; social support is needed. There would also

be reductions in the incidence of lung cancer• provision for terminal and respite care forand coronary artery disease.patients with the most severe COPD.

• Better hospital care combined with links withthe community should reduce the number ofreadmissions for patients with severe COPD.In primary care

• if a practice does not have its own spirometer • Appropriate referral and hospital assessmentshould optimise the use of both domiciliaryand the appropriately trained staff to use

this an open access hospital referral service nebuliser and oxygen therapy.




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