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COPD
Version 2 Final
EBM – COPD
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Document control
Version history
Version Date
Comments
2 Final
19 March 2007
Signed off by MSCMT
2f (draft)
17 March 2007
Comments from customer incorporated
2d (draft)
16 January 2007
Formatting
2c (draft)
5 December 2006
External review by Dr J Munro
2b (draft)
26 September 2006
Internal QA by Dr G Buchanan
2a (draft)
12 September 2006
Initial Draft
Changes since last version
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Introduction
Definition
Chronic Obstructive Pulmonary Disease (COPD) is a chronic, progressive disorder
characterised by airflow limitation.
It may be accompanied by airway hyper-reactivity, and may be partly reversible (i.e.
have an additional asthmatic element).
The GOLD (Global Initiative for Chronic Obstructive Lung Disease) definition is:
A disease state characterised by airflow limitation that is not fully reversible. The
airflow limitation is usually both progressive and associated with an abnormal
response of the lungs to noxious particles or gases. [1]
Although the previous definition
chronic bronchitis and emphysema no longer forms
part of this definition of the disease state, these conditions are still associated with
COPD.
Indeed most patients with COPD, who by definition have airflow obstruction, have
features of chronic bronchitis and emphysema. [2]
COPD is disabling because of the reduced exercise tolerance resulting from
impaired exchange of oxygen and carbon dioxide between the atmosphere and the
pulmonary circulation.
Due to the evolution of the definition of COPD and historical diagnostic labels
some people who fulfil the criteria may report themselves as having:
Chronic obstructive airways disease
Chronic airflow limitation
Chronic
bronchitis
Emphysema
Chronic
asthma
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Description
Aetiology
The development of COPD is associated with the inhalation of atmospheric
pollutants.
The condition usually results from an inflammatory response to noxious particles
and gases, causing irreversible increased airflow resistance in the smaller airways.
[1]
The main cause is cigarette smoking. However, not all smokers develop COPD and
some non-smokers develop the disease.
Additional aetiological factors include environmental exposure and genetic
susceptibility.
The inherited deficiency of anti-protease enzyme alpha1-antitrypsin is associated
with development of COPD. The affected gene has been identified and a number of
variants described. 95% of people with severe deficiency have a greatly increased
risk of emphysema especially in smokers. [2]
There is evidence that dusty occupations and air pollution lead to COPD.
Occupational exposure to coal dust, grain, and various airborne chemicals is
associated with COPD. [3]
Prevalence
COPD is one of the greatest causes of death in the world, ranking fourth in the year
2000 global mortality table. [1]
In the UK it is currently ranked sixth. [4]
COPD is an important cause of morbidity and mortality in the United Kingdom
( 30,000 + deaths per annum ). There are an estimated 3 million people in the U.K.
suffering from the disease (of whom 900,000 are diagnosed and 2.1 million
undiagnosed ) and GP consultation rates for COPD are up to four times that for
Ischaemic Heart Disease. [5]
The prevalence of COPD is closely linked to the prevalence of smoking. The habit
of cigarette smoking is becoming generally less common in wealthy countries and
more common in developing countries.
Even within a single country prevalence and mortality from COPD reflect differences
in smoking habits. They are generally higher in the North and West of England than
in the South and East.
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Over recent decades there has been a relative increase in smoking in women
compared to men.
The smoking rate among UK secondary schoolgirls continues to rise, and in some
age groups the figure is higher than that for boys.
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Diagnosis
History
The airflow limitation causes a history of gradually progressive breathlessness,
which may be associated with wheeze, although this may not become apparent until
the later stages of the disease.
The irreversible component of COPD is associated with loss of lung tissue elasticity,
causing bronchioles to “collapse”. The resultant “air trapping” causes hyperinflation
which increases the effort of breathing.
Chronic bronchitis is associated with COPD and is defined by a history of symptoms
of productive cough on most days for at least three months of two successive years
(having excluded other causes of chronic productive cough). In COPD coughing is
usually associated with the production of small quantities of mucoid sputum.
Emphysema is defined histopathologically as the dilatation of the terminal airspaces
of the lung distal to the terminal bronchiole with destruction of their walls, without
obvious fibrosis. Consequently, there are no aspects of the history referable to
emphysema.
Centri-acinar alveolar
Stenotic bronchiole in
Panacinar dilatation in
dilatation in
chronic bronchitis
emphysema
emphysema
The presentation may therefore be of:
1. Cough and sputum.
2. Progressive breathlessness affecting activities of daily living.
3. A combination of the two.
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Observation
Informal observation of the patient’s activities gives a good indication of the stage of
the disease and of its disabling effects.
Early stages of the disease will show little evidence of exercise intolerance, but as
the disease progresses, gasping tachypnoea, mouth breathing, and the use of
accessory muscles of respiration are induced at lower and lower levels of effort
progressing from walking uphill and climbing stairs, to walking on the flat, and then
to dressing and undressing.
When the condition has progressed even further these clinical signs will be
observable at rest.
A sub-group of individuals do not have good ventilatory drive and tend to become
drowsy and cyanosed with right ventricular failure (RVF) and peripheral oedema in
the later stages of the disease, (formerly known as “blue bloaters”). The terms “blue
bloater” and “pink puffer” are now rarely used and have little relevance to diagnosis
or the assessment of disability.
Examination
There may be no abnormalities in the early stages of the disease. Abnormal clinical
findings will become apparent in the later stages.
Respiratory Features.
The clinical features primarily affect the respiratory system.
Inspection: The chest may be “barrel shaped” with increased AP diameter and held
in the position of near full inflation. The shoulders are held in a “shrugged” attitude.
Measurement of expansion: Reduced expansion may be detected with a tape
measure. The normal change in chest circumference between full inspiration and
full expiration is approximately 5 cms in the average male.
Percussion: Resonance may be increased and drum-like as the chest is continually
hyper-inflated .
Auscultation: Breath sounds may be quieter than normal due to reduced airflow and
the expiration phase is prolonged. There may be added wheezy sounds (high
pitched expiratory rhonchi)
Abdominal palpation: The overexpansion of the lungs may make the liver appear
larger by downward displacement.
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Cardiovascular Features.
Central cyanosis from polycythaemia and hypoxia may be present. Progressive
lung damage results in pulmonary hypertension. This may progress to signs of right
ventricular failure with raised jugular venous pressure (J.V.P.), peripheral oedema,
right parasternal pulsation from a hypertrophied right ventricle, increased splitting of
the 2nd. heart sound and true hepatomegaly (cor pulmonale).
Systemic Features.
With severe COPD many patients show evidence of poor nutrition, muscle wasting
and weight loss, though this may be masked by the development of peripheral
oedema.
Special tests
The gold standard for diagnosis is by spirometry with reversibility testing (British
Thoracic Society and GOLD). [1] [6]
Similarly the NICE guidelines for COPD (February 2004) recommend that all health
care professionals managing patients with COPD should have access to spirometry
and be competent in the interpretation of the results.
Chest X-ray findings correlate poorly with physiological findings. CXR can be
CXR
useful to exclude other causes of dyspneoa.
High-resolution computerised tomography can demonstrate the parenchymal
CT
lung destruction of emphysema. (This investigation is rarely performed).
This is measured by spirometry – and is the Forced Expiratory Volume in the first
second of expiration. It is the single best diagnostic test in patients with airflow
FEV1
limitation. FEV1 measured/FEV1 predicted shows some correlation with effort
intolerance.[6]
This measures the Forced Expiratory Vital Capacity in the first 4 seconds of
expiration. The ratio FEV/FVC remains normal in restrictive lung disease but is
FVC
less than 75% in diffuse airflow obstruction. The FEV/FVC ratio is the single
best indicator of airflow limitation.
Peak expiratory flow rate (also known as PFR) measured with a standard peak
flow meter. PEF (measured) /PEF (predicted) correlates fairly well with effort
PEF
intolerance but not as well as FEV1. PEF underestimates the degree of airway
resistance.[7]
The diffusing capacity of carbon monoxide is a special test providing information
DCO
on gas transfer from the alveoli to the pulmonary circulation. Emphysema
causes a reduction in the transfer factor and coefficient (KCO).
PaO2
Arterial oxygenation is reduced in severe disease
The maximum rate of oxygen uptake on exercise testing on a treadmill or bicycle
VO2 max
ergometer is the best measure of effort tolerance.[8]
This is a measure of energy expenditure as a multiple of resting energy
MET
expenditure. For example a 70kg man while sitting may expend 1.2 kcal/min,
when walking at 4 kph he expends 3.6 kcal/min – i.e. 3 METs.
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Table of diagnostic features and terms
Diagnostic
Term Definition criteria
Chronic
Cough and sputum for 3 months in 2 successive
History of
Bronchitis
years
symptoms
Airways
Diffuse peripheral airway narrowing with
FEV1
obstruction
increased resistance to airflow
PEF
Reversible airways obstruction with airway
Bronchodilator and
Asthma
inflammation and hyper-responsiveness
steroid response
Histopathology
Dilatation of the terminal airspaces with
Emphysema
CT scan
destruction of alveoli
KCO
Respiratory
Failure to maintain arterial oxygen and CO2
failure
tensions
P O
↑
a
2 PCO2
Oedema
Chronic lung disease causing pulmonary
JVP
Cor pulmonale
hypertension and leading to right heart
hypertrophy.
ECG
Echocardiography
Measured in
Effort tolerance
Maximum energy expenditure
METs
Vo
2 max
Diagnostic criteria for COPD (under GOLD or NICE guidelines) is post bronchodilator
FEV1 <80% of predicted FEV1
and FEV1/FVC <70% of predicted FEV1/100%FVC.
However, it has to be acknowledged that these definitions of levels of abnormality
have not been supported by the American Thoracic Society (ATS) nor the European
Respiratory Society. [18] [19]
Differential Diagnoses
Other causes of breathlessness and productive cough should be excluded.
The most important differential diagnosis to make is between Asthma and COPD.
The differentiating features are in the history and in the investigations.
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Clinical features differentiating COPD and asthma
FEATURE COPD
Asthma
Smoker or ex-smoker
Nearly all
Possibly
Symptoms under age 35
Rare
Common
Chronic productive cough
Common
Uncommon
Breathlessness Persistent and progressive
Common
Variable
Night time waking with breathlessness and/or wheeze
Uncommon
Common
Significant diurnal or day to day variability of symptoms
Uncommon
Common
Day to day variation in PEF
Minimal
Usual
Response to bronchodilators
Poor
Good
The table in Appendix A gives other, less common, differential diagnoses.
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Treatment
The first line of treatment is to advise patients to stop smoking. They should also be
advised to avoid occupational dusts and chemicals, and indoor and outdoor
atmospheric pollutants. [9]
Smoking cessation is the single most effective intervention to reduce the risk of
further development of COPD.
The table below indicates which interventions are likely to be beneficial and are
currently recommended, and so may be expected to be reported, in different
conditions
Drug Interventions
Treatment Effect
improved exacerbation rate, symptoms, and
Inhaled anticholinergics
FEV1
Improved FEV
Inhaled anticholinergics plus beta
1 compared with either drug
2 agonists
alone
Inhaled corticosteroids plus long acting beta2 improved exacerbation rate, symptoms,
agonists
quality of life, FEV1
Discontinue if no benefit after 4 weeks
Antibiotics
Possibly overprescribed but indicated if there
is purulent sputum and an increase in
respiratory symptoms with systemic upset.
Long term domiciliary oxygen
beneficial in people with severe hypoxaemia
provided the pCO2 does not rise
unacceptably
Non – drug Interventions
Psychosocial plus pharmacological
interventions for smoking cessation
Pulmonary rehabilitation
General physical activity
Inspiratory muscle training
Peripheral muscle training
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Pulmonary Rehabilitation
Definition A multidisciplinary programme of care for patients with chronic respiratory
impairment that is individually tailored and designed to optimise each patient's
physical and social performance and autonomy.
COPD patients with breathlessness often avoid exercise and become unfit and
de-motivated. They become anxious, depressed and socially isolated.
Pulmonary rehabilitation (PR) addresses all these issues.
The general indication is any patient who considers him or herself to be
functionally disabled by COPD (usually modified MRC dyspnoea scale 2 or
greater [Appx. B]) irrespective of lung function.
It is not suitable for patients unable to exercise.
Those who lack motivation need encouragement.
Pulmonary rehabilitation is effective in improving:
quality of life
exercise
capacity
dyspnoea
There is some evidence of reduced bed days and healthcare consumption. There
is strong evidence that it is cost-effective.
Despite its proven benefits, it is estimated that it is only available to a minority of
suitable patients.
The components of Pulmonary rehabilitation are:
Exercise
Individually tailored and increased during the programme
Involves supervised exercises preferably twice weekly, although once
weekly can be effective
upper- and lower-limb exercises
usually in a group with an exercise regime to be followed at home
Education - main topics include:
Relaxation
Breathing
control
Pathophysiology
Drug
treatment
Self-management
Benefits, social services
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Setting
In the past PR was mainly hospital based, but increasingly it is performed in the
community. This has advantages for patients in terms of access, but it is
important that location and the
programme are risk-assessed. Most programmes comprise 2 or 3 sessions per
week and last for 6 – 12 weeks.
Assessment
It is important that formal assessment of health status and exercise capacity is
measured before and after pulmonary rehabilitation.
Widely used are:
The Incremental Shuttle Walking Test [10]
“Guyatt’s” Chronic Respiratory Questionnaire (CRQ) [11]
St. Georges Respiratory Questionnaire (SGRQ) [12]
Clinical COPD Questionnaire (CCQ) [13]
Other useful questionnaires include
London Chest Activity of Daily Living Scale (LCADL)
Hospital anxiety Depression Score (HAD) [14]
Lung Information Needs Questionnaire (LINQ). [Appx. B]
Follow-up
It is important to offer a means of continuing the exercise programme.
Some have regular follow-up sessions, some refer to exercise on prescription
Schemes, and some to the local patient support group, e.g. Breathe Easy. [5]
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Prognosis
The prognosis is profoundly influenced by smoking habit. Continuation of smoking in
COPD leads to a continuous steady decline in lung function.
With the cessation of smoking the decline in lung function reverts to its normal
gradient within a relatively short time.
120
100
Never
smoked
80
60
Smoker
40
stopping at
age 55
20
Smoker not
0
stopping
25
40
55
70
Age
Graph of decline of lung function with age and smoking with COPD.
Pulmonary rehabilitation can lead to significantly improved effort tolerance in COPD
patients, even though lung function tests are not improved. [15] [16]
Severely dyspnoeic patients benefit less from rehabilitation than moderately
dyspnoeic patients. [17]
Main Disabling Effects
The primary disablement from COPD is due to reduced exercise tolerance.
Initially there is minimal disablement, which may only be apparent when running.
As the disease progresses there is limitation in walking quickly and climbing flights
of stairs.
This progresses to limitation in walking at a normal pace and in climbing a flight of
stairs.
Later the effort of mild exertion limits activities, such as dressing and undressing,
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washing, rising from sitting and walking even a few steps.
Eventually even minimal effort is not tolerated and there will be breathlessness at
rest.
The gold standard for diagnosis of COPD is by spirometry. The diagnosis requires a
post-bronchodilator FEV1 of less than 80% of the predicted value accompanied by
an FEV1 / FVC ratio of less than 70%.
However, functional activity limitation (disability) does not directly correlate with
FEV1 measured/FEV1 predicted (impairment) due to other factors such as body mass
index, general level of fitness, and psychological factors.
Cardiopulmonary exercise testing is a better guide of disability although this is rarely
performed except in experimental work. [8]
Clinical examination findings do not correlate well with functional ability and the
assessment of claimants is best made from the evidence of:
1. The History of Activities of Daily Living (Typical Day) taking variation into
account.
2. Informal Observation of the client’s activities at examination.
3. Medication taken and attendance at Chest Clinic.
Some scales of pulmonary disability assessment are detailed in Appendix B.
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Appendix A - Differential Diagnoses
Breathlessness due to respiratory centre stimulation by hypoxia or excess CO
2
Common causes
Uncommon causes
Pulmonary oedema
Acidosis
Pulmonary embolus
Pregnancy
Pneumothorax
Cyanotic congenital heart disease
Pneumonia High
altitude
Lobar collapse
Arteriovenous fistula
Pulmonary fibrosis
Anaemia
Breathlessness associated with an increased work of breathing (Obstructive
ventilatory defects)
Commoner causes
Uncommon causes
Asthma
Upper airways obstruction
Bronchiectasis Byssinosis
Cystic fibrosis
Other Common causes
Other Uncommon causes
Sarcoidosis Large
tumours
Fibrosing alveolitis
Large hiatus hernia
Extrinsic allergic alveolitis
Lymphangitis carcinomatosa
Pneumoconioses
Connective tissue diseases
Large pleural effusion
Aspiration pneumonitis
Extensive lung resection
Infections
Chest wall deformity. Scoliosis etc.
Pulmonary oedema
Left ventricular dysfunction
Conditions associated with decreased neuromuscular power (these are all relatively
uncommon)
More common causes
Uncommon causes
Myasthenia gravis
Poliomyelitis
Polyneuritis
Motor neurone disease
Muscular
dystrophies
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Appendix B - Some scales used in assessment for
other purposes
Scales used as guidance for assessment of pulmonary dysfunction in IISB.
Table A
Symptoms and signs
Lung Function Impairment
(Severity Category)
Not breathless on exercise
Nil
Breathless on prolonged or heavy exertion
Mild
Breathless on walking uphill or climbing stairs or hurrying
Mild
on level ground
Breathless at normal pace for age on level ground
Mild
Breathless on walking 100 metres or climbing one flight of
Moderate
stairs at a normal pace
Breathless on walking 100 metres at a slow pace or
Moderate
climbing one flight of stairs without stopping
Breathlessness prevents walking 100 metres at a slow
pace without stopping or climbing one flight of stairs
Moderate
without stopping
Breathlessness prevents activity outside the home without
Severe
assistance or supervision
Breathlessness limits activities to within the home
Severe
Able to walk only a few steps because of breathlessness
Severe
Bed and chair bound, totally dependent on carers
Total
because of breathlessness
Table B
FEV1 as a percentage of the predicted value (use
Lung Function Impairment
post-bronchodilator value if available)
(Severity Category)
>80 Nil
60-80 Mild
40-59 Moderate
<40 *
Severe
<40 *
Total
Note that there is no exact correlation between FEV1 value at any level
and functional disability. [8]
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Medical Research Council dyspnoea scale for grading the degree of
a patient's breathlessness
1. Not troubled by breathlessness except on strenuous exercise
2. Short of breath when hurrying or walking up a slight hill
3. Walks slower than contemporaries on the level because of breathlessness, or has to
stop for breath when walking at own pace
4. Stops for breath after about 100 m or after a few minutes on the level
5. Too breathless to leave the house, or breathless when dressing or undressing
MRC: 22 April 2006
Note that this scale (used by thoracic surgeons and others) measures reported
breathlessness as a response to standard questions. It is, again, a subjective
assessment.
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Lung Information Needs Questionnaire (LINQ)
LINQ is a self-complete questionnaire that has measures the information needs
of patients with chronic obstructive pulmonary disease (COPD). LINQ can also be
used for patients with some other chronic lung diseases.
It is not suitable for
patients with asthma.
It has been found particularly use to be used before and after pulmonary
rehabilitation to assess effectiveness
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References
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www.goldcopd.com
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http://www.spirxpert.com/controversies/controversy.html
19.
http://www.spirxpert.com/indices5.htm
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