Professional Documents
Culture Documents
DRAFT COPY
Print date: 6/24/2001
INTRODUCTION
Development of this Resource
Drs Phillippa Poole, Henry Doerr and John Wellingham have developed the COPD Booklet and accompanying algorithm on behalf of the
Northern Regional COPD Board. Meeting on a regular basis, they have compared and contrasted several seed guidelines, primarily the British
Thoracic Society Guidelines for the Management of Chronic Obstructive Pulmonary Disease and 1, the Thoracic Society of Australia and New
Zealands Guidelines for the management of chronic obstructive pulmonary disease2 and the American Thoracic Societys Standards for the
Diagnosis and Care of Patients with Chronic Obstructive Pulmonary Disease3. The booklet has gone through several drafts and advice has been
sought from many interested medical practitioners and respiratory specialist throughout New Zealand.
OVERVIEW
1)
Key Points
The critical feature in COPD is the inability to fully reverse airflow obstruction.
As a chronic, slowly progressive respiratory disorder, the characteristic airflow obstruction of COPD does not change markedly over
several months. The term COPD encompasses emphysema, COLD, COAD as well as some asthma and chronic bronchitis. (See
Appendix A for the Venn Diagram)
As no medication has thus far been shown to affect the natural history of COPD, drug use is purely palliative and is
only warranted if it can be shown to improve symptoms. Similarly, escalating treatment without concurrent
symptomatic improvement is not justified.
Smoking cessation is the only intervention which alters the natural history at all stages of the disease. (A) 4,5 Long-term oxygen therapy
(LTOT) improves survival in hypoxic patients (A)6,7 and pulmonary rehabilitation improves quality of life and exercise tolerance (A) 8,9.
2)
Background
ROLE OF SMOKING
An accurate smoking history including age of starting, pack years and current smoking pattern is essential.
Cigarette smoking is the single most important cause of COPD (A)10. Smoking accounts for at least 80-90% of COPD 11 (B); the greater
the total exposure, the greater the risk of developing COPD (B)12,13.
In nearly all cases of COPD, smoking is the key variable which dictates the rate of progression of the disease.
1999 COPD Board, Northern Region
While COPD progresses through stages from asymptomatic disease through to respiratory failure, smoking cessation is the single most
important way of affecting the outcome in patients at all stages (A)14. (See Appendix A for the FLETCHER-PETO diagram15 )
Passive smoking may have important implications regarding both the success of an individuals smoking cessation and
population-based smoking cessation strategies.
The role of passive smoking, though potentially a risk factor in COPD, needs further study (C)16.
It is important to find those at greatest risk of developing COPD. Some smokers will lose FEV1 as fast as 100 ml/year or
more though there is a wide range of deterioration rates.
Normal ageing in the non-smoker accounts for an FEV1 loss of approximately 30 ml/year (A)17. On average smokers lose an additional 33
mls/year but their individual rate of loss ranges widely (A).18 Quitters revert back to the same annual FEV1 loss rate as that of non-smokers.
(A)19.
There is a very wide variation of susceptibility to the damaging effects of cigarette smoke:
The costs of morbidity and mortality are high but are likely to have been underestimated; for example they do not allow for re admissions coded as other co -morbidities.
COPD 4th most common cause of hospital admission in NZ
1999 COPD Board, Northern Region
HFA Northern Region office estimates of the regions direct costs for 1997 were $30 million
27.0 - 29.6 % of Northern Region COPD discharges between 1990 and 1996 were readmitted with COPD within 1 year.
third most common cause of death in NZ
steady rise in incidence as cause of death in both Northern region and NZ 23
The following indicators are associated with an increased risk of death from COPD (Taken from Thoracic Society of Australia and New
Zealand Guideline , though unreferenced) 24
FEV1 < 1 litre
FVC < 2.5 litres
pO2 < 60 mm Hg
pCO2>46 mm Hg
ECG/clinical evidence of cor pulmonale
Despite this remember that some patients with very low FEV1 survive for many years
CONSIDER COPD
1.
1.1 Key Symptoms on Presentation
1.2 Screening
Smoking -- All smokers should be considered at risk for COPD.
Screening by spirometry, although appearing logical, is not presently justified by the evidence.
The only measure, which improves the prognosis in COPD, is smoking cessation. Spirometry, if correctly performed and interpreted, is
useful in the detection of symptomatic and asymptomatic COPD. However, there was no significant improvement in rates of smoking
cessation in COPD identified through spirometry (A) 28.
EXCLUDE
2.
Other Diagnoses
2.1 Differential Diagnosis
The following differential diagnoses should be considered and excluded where possible:
CHF
Hyperventilation
Ca lung
Chronic pulmonary emboli
Bronchiectasis
TB
Interstitial lung disease
Past Medical History of these respiratory and cardiovascular problems is an essential part of the history.
Investigations should include CXR, FBC and consideration should be given to ECG.
As the diagnosis of COPD is made on clinical and spirometric grounds, a CXR may support the diagnosis but cannot be
used in isolation. Its main value is in exclusion of other diagnoses.
Consider alpha -1-antitrypsin deficiency only in younger patients (under 40) with a predominantly emphysematous
presentation.
Alpha-1-antitrypsin deficiency accounts for less than 1% of COPD and the median age for onset of dyspnoea with alpha -1-antitrypsin
deficiency:
in smokers = 40 (B)
in non smokers = 53 29 (A)
The current cost of this test in Auckland (1999) is $11.30 + GST30.
10
CONFIRM
3.
11
Whilst the ideal diagnostic measurement is the FEV1/FVC ratio, FVC is more difficult to measure consistently and is
only dependable where it has been subjected to quality monitoring.
FVC is particularly subject to error in COPD patients when the expiratory manoeuvre is not continued for at least six seconds. (B) 36
Other objective measurements are useful for monitoring response to management plans. For example objective
exercise tolerance measurement tests (e.g. 2 -, 6-, or 12- minute walk test) are useful.
Consensus view is that the appropriate frequency of spirometry is annual; however, in a patient who has stopped
smoking and remains asymptomatic, even an annual FEV1 may be unnecessary.
3.2 Interpretation
The NZ consensus is to adopt the following BTS FEV1 values as they are simple and well-justified.
FEV1 measurements provide a reasonable definition of severity:
Greater than 80 % of predicted means the results are within 2 SD which probably excludes the diagnosis of COPD.
Between 60-80% of predicted means a mild abnormality and predicts subsequent morbidity and mortality from COPD.
Between 40-60% of predicted means a moderate abnormality and provides a reasonably correlation with disability.
Below 40% of predicted means a severe abnormality likely. (C) 37
The FEV1/FVC ratio provides an opportunity to for early diagnosis of COPD if its value is less than 70%
If the ratio of FEV1/FVC is normal (>70%) and the test was performed well, the pattern is not obstructive and the diagnosis is not COPD.
(C)38
1999 COPD Board, Northern Region
12
More than 20% variability in the PF is the NZ consensus value for significant reversibility. NZ consensus also
suggests that if the PF level is 150 or less, the variability is meaningless.
More than 20 % variability in the absolute measurements of serial PF may suggest asthma or a degree of reversibility but when PF is
low, the spontaneous variability of the measurement may exceed this. (B)42
13
MANAGEMENT
4.
a. Smoking Cessation
Doctors should routinely offer Nicotine Replacement Therapy , whether by patch, gum or nasal spray and the Northern
Regional COPD Board strongly supports appropriate government subsidies.
Smoking cessation is the single most important management goal. But, as smoking is both a behavioural disorder and chemical
addiction, effective strategies must address both of these aspects. (C)43 The use of nicotine replacement therapy approximately doubles
quit rates, regardless of the method used. (A) 44, 45
14
Both doctors and their patients need to understand that, while medicines has been shown to have only a minimal effect on the natural
history of COPD, patients may derive some important symptomatic benefit from their appropriate use (A) 46
c. Influenza Vaccination
The 1999 NZ Guidelines for annual influenza vaccination, as promulgated by the HFA, now include those with COPD
under the age of 65.
While the benefits of an annual influenza vaccination have been demonstrated for patients over 65 (B)47, specific work on the COPD
subgroup has not been done. Nevertheless an annual flu injection for all those with COPD is recommended by a ll known Guidelines
(C)48
a. Objectives
to establish those with asthma or a significant reversible component to their COPD by detecting a substantially improvable FEV1
(B) 49 50
to establish post-bronchodilator FEV1 as this is the best indicator of long-term prognosis (B)51
15
b. Definition of Reversibility
To be regarded as significant reversibility, the post-bronchodilator FEV1 values should demonstrate a 15% increase (which must be at
least 200 ml) over the pre-test average value(C).52 53 Note however that a negative response to a single test never justifies withholding
bronchodilator therapy where a positive symptomatic effect is clear (C). 54
Options:
Measure FEV1 before and 15 minutes after nebuliser using salbutamol 2.5-5 mcg.
Measure FEV1 before and 30 minutes after ipratropium 0.5
Measure FEV1 before and 30 minutes after both 55
Patients should not have taken any bronchodilator prior to the test which could be expected to still exert effects, e.g. 6 hrs for short
acting inhaled salbutamol. (C) 56
Patients can use either an inhaler +/- a spacer or a nebuliser
4.3 Devices
If a patient cannot demonstrate correct Metered Dose Inhaler (MDI) technique, then a trial with one of the more
expensive devices (whether autohalers, spacers, dry powder devices or nebulisers) is justified.
MDIs provide the cheapest form of delivery but up to 76% of COPD patients made important errors in use(B).57
16
Dry powder devices are also more expensive than MDIs. 10-40% of COPD patients make significant errors with their use(B). 58
4.4 Pharmaceuticals
a. Bronchodilators
The Northern Regional Group believes that there are three rational bronchodilator use options and that patient
preference is valid
use up to maximum dose of short-acting 2 agonists
use up to maximum use of anti -cholinergics
or use of smaller doses of both
17
Although common practice, the addition of ipratropium when maximum treatment with beta-2 agonists is already used (or vice versa)
does not confer any additional physiological benefit (A). 62
ii. Anti-cholinergics
For bronchodilation and for symptom improvement, as many patients prefer ipratropium as beta-2 agonists (A). 66 Most studies show
that ipratropium is as effective as the Beta-2 agonists and that it may be used either in full doses alone or at lower doses combined with
lower doses of a beta-2-agonist(A) 67, 68, 69
18
improvement in quality of life scores has been shown with salmeterol in doses of 50 mcg bd but not in doses of 100mcg bd (A). 72 In NZ
subsidies do not currently apply for their use in this condition.
iv. Theophyllines
Theophyllines are of limited use in routine circumstances. However, some patients with disabling breathlessness may
derive significant benefit from their use.
Theophyllines have a narrow therapeutic index and many patients experience side effects in the therapeutic range (B). 73 The role of
theophyllines is the subject of a current systematic review 74 including the issue of appropriate dosage.
Only about 25% of COPD patients will show a physiological response to either oral or inhaled steroids (A). 75
Conversely, for the approximately 75% of COPD patients who cannot be shown to respond to steroids (inhaled or oral), steroids
should not be continued (C).76
While those with a positive bronchodilator response are more likely to respond to steroids, a negative response to salbutamol
reversibility testing does not preclude a steroid response(A). 77
Furthermore, a response to a trial of one form of steroid does not necessarily imply that there will be a response to the other form
(A). 78
Patients with substantial responses to inhaled (or oral) steroid trial justify treatment according to chronic asthma guidelines (C) 79
19
ii. Protocols
Inhaled Steroid Trial
NZ consensus suggests the duration of the trial should be 6 to 12 weeks. The data emerging from the Euroscop
and Isolde studies may help clarify this issue
As a precondition, the patient must be clinically stable and the inhaled steroid trial should use at least 1000 mcg of BDP or equivalent
for 6/52 (C). 80Alternatively, the TSANZ guidelines suggest considering 3/12 at 800 - 1600 daily with 4- 6/52 spirometry
assessment.. 81
An adequate inhaler technique is presupposed.
Measurement of Response
The measure of response to inhaled steroids should include both an increase in FEV 1 of 15% (> 200 mls) and an
improvement in symptom score.
Note that the Euroscop data suggested in the order of only 50 mls FEV1 improvement.82
20
85
Conclusions
As approximately 75% of patients will not respond to steroids, whether oral or inhaled, the role of steroids is
limited and requires careful assessment.
1999 COPD Board, Northern Region
21
a. Monitoring
Repeat CXRs are not needed routinely but should be performed if new symptoms develop.
Because sputum cultures are of no routine value, General Practitioners should avoid requesting them.
Routine culture of non-purulent sputum samples is not helpful. (B) 87
Doctors should use caution and restraint when considering prescribing antibiotics in patients with COPD.
Antibiotics are useful only when two of the following three features are positive (increase d breathlessness, increased sputum volume and
increased sputum purulence(A).88.
Exercise tests provide one method to measure change but so do symptom scores, e.g. dyspnoea subscale of CRQ. (See
appendix A).
Exercise tests, done according to standard protocols, are a useful marker of progress, particularly in rehabilitation programs(C). 89
If the O 2 by Pulse Oximetry is 92% or less, consider further evaluation. Pulse Oximeters, increasingly available in A +
M clinics, have the potential to provide rele vant clinical information in primary care. However, like spirometry,
accurate oximetry depends on following well-defined protocols.
O2 exceeding 92% may reduce the need for blood gas evaluation. (B)90
See Appendix C
22
91 92
LTOT requires
d. Pulmonary Rehabilitation
Doctors should consider referring all symptomatic patients for Pulmonary Rehabilitation
Pulmonary Rehabilitation attempts:
to restore the individual to their fullest medical, mental, emotional, social and vocational potential
94
to prevent de-conditioning and to allow patient to cope; outcome measures include increased lung function and exercise (B).
Exercise helps to prevent the de-conditioning cycle where increased breathlessness leads to decreased physical activity
and increased de-conditioning.
Pulmonary Rehab must include an element of exercise training (A).
95
23
e. Other Issues:
The role of Pneumovax is unclear at present but probably is cost-effective in selective cases
The value of prophylactic antibiotics is currently under review. 98
24
APPENDIXES
APPENDIX A
25
Persons with chronic bronchitis and/or emphysema without airflow obstruction (subsets 1,2 & 11) are not classified as having COPD. Patients with airway obstruction due to
diseases with known etiology or specific pathology, such as cystic fibrosis or obliterative bronchiolitis (subset 10) are not included in this definition.
26
APPENDIX B
Grade 1
Grade 2
"I get short of breath when hurrying on the level of up a slight hill"
Grade 3
"I walk slower than most people of the same age on the level because of breathlessness or have to stop for
breath when walking at my own pace on the level"
Grade 4
"I stop for breath after walking 100 yards or after a few minutes on the level"
27
APPENDIX C
Note: Appendix C is specific to South Auckland
INDICATIONS FOR HOSPITALIZATION OF PATIENTS WITH COPD
1. Patient has acute exacerbation characterized by increased dysnoea, cough or sputum production, plus one or more of the following:
Inadequate response of symptoms to outpatient management
Inability to walk between rooms (previously mobile)
Inability to eat or sleep due to dysnoea
Conclusion by family and / or physician that patient cannot manage at home with supplementary home care resources not immediately
available
High risk co-morbidity condition, pulmonary (e.g. pneumonia) or non-pulmonary
Prolonged, progressive symptoms before emergency visit
Altered mentation
Worsening hypoxemia
New or worsening hypercarbia
2. Patient has new or worsening cor pulmonale unresponsive to outpatient management
3. Planned invasive surgical or diagnostic procedure requires analgesics or sedatives that may worsen pulmonary condition
4. Co-morbid condition e.g. severe steroid myopathy or acute vertebral compression fractures, has worsened pulmonary function
From ATS Standards for the Diagnosis and Care of Patients with Chronic Obstructive Pulmonary
28
From ATS Standards for the Diagnosis and Care of Patients with Chronic Obstructive Pulmonary Disease
measurement of FEV1
reassessment of inhaler technique and patients understanding of recommended treatment regime
need for LTOT and / or home nebuliser usage in patients with severe COPD
29
ACTION
WORSENING SYMPTOMS
ACTION
More breathless**
Reduced energy for daily activities
Loss of appetite
Change in amount and / or colour of phlegm**
Cough
Fever
Need to use inhalers / nebuliser more often then usual
** There is some evidence that where 2 or more of these occur, antibiotics help
SEVERE SYMPTOMS
ACTION
CONTACT YOUR DOCTOR FOR
AN URGENT APPOINTMENT
DANGER SIGNS
Very short of breath at rest
Chest pains
High fever
A feeling of agitation, fear, drowsiness or confusion
ACTION
(
DIAL 111 FOR AN AMBULANCE
OR CONTACT THE EMERGENCY DOCTOR
30
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Thoracic Society of Australia and New Zealand, Guidelines for the management of chronic obstructive pulmonary disease. Mod Med of Australia 1995; 38:
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24
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81
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