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COPD BOARD, NORTHERN REGION, GUIDELINE DEVELOPMENT GROUP DRAFT COPY Print date: 6/24/2001

©1999 COPD Board, Northern Region 1

THE COPD BOOKLET

Guidelines to Best Practice for Management of Stable COPD

The COPD Board, Northern Region, Guideline Development Group

Comments on these Draft Guidelines should be directed to:

Mail: Dr J Wellingham, COPD Guideline Subcommittee 24 Sharon Road, Torbay, Auckland 10

Fax: (09) 623 0774 Email: [email protected]



THE COPD BOOKLET Guidelines to Best Practice for management of stable COPD

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 Zealand’s Guidelines for the management of chronic obstructive pulmonary disease2 and the American Thoracic Society’s 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.

Conflict of Interest Statement Dr Phillippa Poole has acted as a consultant to Glaxo Wellcome Foundation for Medical Education and as an investigator in clinical trials for both Glaxo Wellcome and HMR. Dr Henry Doerr, General Practitioner and Senior Lecturer with the Department of General Practice and Primary Care, Auckland School of Medicine, has no conflicts of interest. Dr John Wellingham, previously with the Goodfellow Unit of the Department of General Practice and Primary Care, Auckland School of Medicine is currently employed by First Health and has no conflicts of interest.

Funding and bias The funding for this process came in part through the Northern Regional COPD Board with money made available to it from the South Auckland COPD Project. The COPD Board contracted the Goodfellow Unit in the Department of General Practice and Primary Care at Auckland University to review both relevant international guidelines and current evidence in order to develop appropriate NZ based COPD guidelines. These current guidelines will be then referred back to the COPD Board for review for further refinement and dissemination.



Level of evidence grading The grading system chosen here is the simpler of the two used by the New Zealand Guidelines Group (NZGG). A based on RCT B based on robust observational and experimental studies C based on more limited evidence and expert opinion How to make the best use of this resource Our judgements are in bold type to differentiate them from the available evidence on which they are based These judgements are derived from the Northern Regional COPD Board’s interpretation of the evidence and have been modified to include feedback from the rest of NZ. (Judgements made concerning the use of this information however, can still vary according to regional resources and customary practices.) They are the basis of the accompanying ALGORITHM. So, while this ALGORITHM is a suggested one, it is clearly our intention that these guidelines be modified and adapted locally as appropriate.

Statements in this booklet w hich expand on or have a direct relationship with the ALGORITHM are boxed in the text.



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.



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 individual’s 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: • 15% of smokers will develop clinically significant COPD (A)20 • 50% will develop chronic bronchitis (A)21 • 50% will never develop any symptomatic physiological deficit (A)22 • all smokers have increased risks for vascular diseases and cancer MORBIDITY AND MORTALITY

• 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



• HFA Northern Region office estimates of the region’s 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



1. CONSIDER COPD 1.1 Key Symptoms on Presentation

The value of reviewing symptoms is that they: • are what matter to the patient • create awareness of possible diagnosis in smokers • may be useful to set and review management goals

Note that breathlessness is not specific for respiratory disease and may reflect anxiety, depression, cardiac disease, anaemia or de -conditioning. For symptoms to be useful in measurement of change they must be scored against a validated table. (See Appendix B )

Symptoms, which may suggest the presence of COPD, include: • decreased exercise tolerance • increasing shortness of breath • morning cough or “smokers cough” +/- sputum • wheeze • recurrent respiratory infections.

However: • In patients with mild COPD there are few or no symptoms (B) 25 • symptoms correlate poorly with FEV1.(A)26



1.2 Screening

Smoking -- All smokers should be considered at risk for COPD.

Spirometry -- Earliest possible diagnosis can only occur by using spirometry.

Most COPD patients have a long asymptomatic phase and the majority do not present with symptoms until FEV1 is less than 50% of predicted value (A)27

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.



2. EXCLUDE 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.

• A Full Blood Count must be done at diagnosis or in an unexplained deterioration.

A FBC may detect unsuspected anaemia (and polycythaemia).



• 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 = 5329 (A)

The current cost of this test in Auckland (1999) is $11.30 + GST30.

2.2 Signs suggesting COPD • Because many of the following signs are very late as we ll as non-specific, they are of limited value.

Not infrequently, particularly in mild to moderate disease, the examination may be normal. Cor pulmonale as evidenced by peripheral oedema and pulmonary hypertension (increased JVP, right ventricular heave and a loud pulmonary valve 2nd sound) is the only sign specific for COPD and has prognostic significance. (A)31 Other “key signs” of COPD, including over-inflation, rhonchi +/- forced expiration, weight loss and central cyanosis only suggest the diagnos is but do not necessarily reflect severity. (Consensus Statement) On the other hand, clubbing is a sign of specific respiratory diseases but is not a sign for COPD. (Consensus Statement)



3. CONFIRM Obstructive Pattern by Spirometry

3.1 Spirometry

• In practice, confirmation of the diagnosis requires spirometry.

• NZ consensus suggests that GPs should use FEV1 in three areas

• to assist early diagnosis of COPD

• to assess its severity (including rate of decline)

• to gauge treatment response (particularly to steroids).

• Variations in FEV1 less than 200 mls should be regarded as experimental error, mean little in practice and should not be

used to draw conclusions.

The allowable variability of FEV1 between testing occasions can be up to 170 mls (B)32 so it is essential that well-trained personnel using standard methods with reliable and calibrated equipment record spirometry when the patient is clinically stable (A) 33 The best guide to progression of COPD is the change of FEV1 over time. (B)34 The British Thoracic Society (BTS) guidelines suggest that at least 3 technically satisfactory readings be taken and that at least 2 must lie within 100 mls or 5% of each other. With serial testing, if FEV1 values change by more than 15 % (or at least 200 mls), then it is unlikely that this is due to chance (B).35



• 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.

FEV 1 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 FEV 1/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



3.3 Peak Expiratory Flow (PF or PEF) Readings

• The value of PFs, either as single measurements or as serial measurements over time, is extremely limited but PFs may be better than nothing if good quality spirometry is unavailable.

Low PF measurements cannot differentiate between obstruction and restriction. (C)39 Furthermore, in COPD, the correlation between PF and FEV1 is poor, so one cannot be predicted from the other. (B)40 In fact, PF may underestimate the degree of airways obstruction in COPD. (C)41

• 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



4. MANAGEMENT Of Obstructive Lung Disease

4.1 General Measures

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

b. Doctor and Patient Education

• Both doctors and patients particularly need to remember that:

• COPD is a systemic disease with respiratory, cardiovascular, nutritional, psychological etc manifestations.

• medicines are palliative rather than curative

• the use pharmaceuticals may inadvertently distract from the importance of smoking cessation.

• There is also the potential, as the patient’s condition gradually deteriorates, to reflexly escalate medicines without objective or subjective improvement or benefit. Prescribers must recognise and resist this common tendency.



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

4.2 Reversibility Testing

• While physiological measurements increase management rigour, acceptable justifications for prescribing a bronchodilator include:

• FEV1 reversibility of greater than 15% (which must be at least 200 m ls) or • improvement in symptom score (see appendix B).

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



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

c. Dose Protocol Options to Assess Reversibility

• Choice of medicine and of waiting time is a local option. While the BTS suggests 15 minutes post salbutamol or 30

minutes post ipratropium, note that the majority of the change usually occur sooner than those recommended times.

• 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



• Dry powder devices are also more expensive than MDIs. 10-40% of COPD patients make significant errors with their use(B). 58

• A spacer should usually be tried before a nebuliser in most circumstances.

• Doctors should reserve the use of nebulisers for those unable to use inhaler devices (including spacers) effectively or for those in whom there is a significant symptomatic benefit over that achieved by the other devices. Their continued use and maintenance must be reassessed on a regular basis by a person skilled in that field.

Nebulisers, if optimally used, can achieve similar airways deposition to a spacer (B)59 but are more costly and have the following additional problems:

• significant side effects from inappropriate dosages • enhanced psychological dependency • problems with machine performance and maintenance.(A)60

One NZ study showed that approximately 40% of patients hospitalised with the diagnosis of COPD were using home nebulisers. (B)61 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 ββ 2 agonists • use up to maximum use of anti -cholinergics • or use of smaller doses of both



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

i. Short-acting Beta-2 Agonists

• As noted above, either positive reversibility testing or symptomatic improvement (as measured by symptom score) justifies the use of Beta-2 agonists. Symptom changes should be quantified by objective exercise tests, validated symptom scores indices or quality of life measures. Bronchodilators are better prescribed and used on a prn basis than on a regular basis. The upper range of their dose should not normally exceed the equivalent of 800 mcg salbutamol/day.

Since FEV1 does not correlate with symptoms, patients can have symptom improvement on Β2 agonist without change in FEV1. (A)63 Short-acting bronchodilators are appropriately used on a prn basis for symptomatic relief or before exercise rather than on a regular basis (A)64. Doses higher than 800 mcg of salbutamol (or equivalent) daily are associated with more side effects and a flattening out of the dose response curve. (A)65

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

iii.Long-acting Beta-2 Agonists

• The place for long-acting bronchodilators in COPD remains undetermined.

Research has not yet resolved the issues of long-term safety and tolerance of these agents for COPD (B) 70 ,71.However, an



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.

b. Rational Steroid Usage

i. General Comments

• Frequently COPD patients are either started or continued on steroids without demonstrated benefit. As three-quarters of patients with COPD will not benefit from steroids, doctors should only prescribe them after a successful inhaled steroid trial. Given the costs and side effects of corticosteroids, doctors should consider steroid reduction or cessation in all other patients.

• 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



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 FEV1 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

Oral Steroid Trial

• NZ consensus does not support oral steroid trials due to systemic effect on increasing feelings of wellbeing. If an

oral trial is used, NZ consensus suggests a trial using between 20 - 40 mg for between 2 - 3 weeks.

Meta-analysis suggests that 10% more people on oral steroids will respond positively (20% FEV1 increase) compared to those on placebo (A). 83



Measurement of Oral Steroid Response

• NZ consensus supports the notion that changes in a patient’s symptom score are not sufficient on their own to support continued oral steroid usage, especially given the risk of long -term side effects.

Because oral steroids affect “well-being”, the BTS guidelines suggests that objective improvements in lung function tests remain the SOLE criteria for a positive response. 84

Transfer from oral to inhaled steroids

• NZ consensus supports the logic of moving directly to an inhaled steroid trial and thereby avoiding the

confounding effects of an oral steroid trial.

After transferring from oral to inhaled steroids, a further assessment of efficacy should be done. 85

Long-term Steroid Effects

• As both oral and inhaled steroids have significant side effects and as inhaled steroids are expensive, further

subgroup analysis of the responders in the Isolde, Euroscop and Copenhagen City studies is awaited.

The Isolde, Euroscop and Copenhagen City studies have evaluated the effect of inhaled steroids for three years on patients with COPD. The significance of this largely unpublished data, which suggests a small improvement in FEV1 of about 50 mls in those using steroids, remains unclear. (A) 86

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.



4.5 Additional Aspects of Comprehensive Management

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 O2 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

b. Acute Exacerbation - See Appendix C



c. Long-term Oxygen Therapy (LTOT)

• Consider referral for long term oxygen therapy (LTOT) assessment if there is evidence for secondary polycythaemia (HCT >55%), cor pulmonale or an O2 Saturation of 92% or less. While patients may gain both symptomatic and psychological benefit from intermittent O 2 usage, the prescription of LTOT in NZ currently depends on physiological assessments.

LTOT improves survival in patients with COPD and chronic hypoxemia when used at least 15 hours per day(A). 91, 92 LTOT requires complete smoking cessation for reasons of efficacy(C) 93 and safety.

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 • to prevent de-conditioning and to allow patient to cope; outcome measures include increased lung function and exercise (B).94

• 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

A meta-analysis of pulmonary rehabilitation has shown significant improvement in:

• exercise tolerance • breathlessness scores • “mastery over the disease” (A). 96, 97



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

• Pharmac does not currently fund Mucolytics

Mucolytics reduce exacerbations by 1.2 episodes per year and 4-5 sick days per year and are widely used in some European countries. (A) 99

f. Indications for Specialist Referral

• Depending on expertise and other local issues, indications for referral of COPD patients for specialist opinion

include the following:

• those who need pulmonary lung function testing

• those with sudden deterioration

• those who require long -term oral steroids

• those with new symptoms

• consideration for Pulmonary Rehab or LTOT



APPENDIXES APPENDIX A

VENN Diagram of COPD Figure 1. Schema of chronic obstructive pulmonary disease. This non-proportional Venn diagram shows subsets of patients with chronic bronchitis, emphysema and asthma. The subsets comprising COPD are shaded. Subset areas are not proportional to actual relative subset sizes. Asthma is by definition associated with reversible airflow obstruction, although in variant asthma special manoeuvres may be necessary to make the obstruction evident. Patients with asthma whose airflow obstruction is completely reversible (subset 9) are not considered to have COPD. Because in many cases it is virtually impossible to differentiate patients with asthma whose airflow obstruction does not rem it completely from persons with chronic bronchitis and emphysema who have partially reversible airflow obstruction with airway hyperreactivity, patients with unremitting asthma are classifies as having COPD (subsets 6,7 & 8). Chronic bronchitis and emphysema with airflow obstruction usually occur together (subset 5) and some patients may have asthma associated with these two disorders (subset 8). Individuals with asthma exposed to chronic irritation, as from cigarette smoke, may develop chronic productive cough, a feature of chronic bronchitis (subset 6). Such patients are often referred to in the US as having asthmatic bronchitis or the asthmatic form of COPD.



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.

FLETCHER-PETO Diagram of COPD Figure 2. The risks of developing chronic obstructive lung disease for smokers: the differences between the lines illustrate the effects that smoking, and stopping smoking can have on the FEV1 t = death, the underlying cause of which is irreversible chronic obstructive lung disease, whether the immediate cause of death is respiratory failure, pneumonia, cor pulmonale or aggravation of other heart disease by respiratory insufficiency. This graph shows the rate of loss of FEV1 for one particular susceptible smoker; other susceptible smokers will have different rates of loss, thus reaching ‘disability’ at different ages. Illustration reproduced with permission from Fletcher C, Peto R. The natural history of chronic airflow obstruction. BMJ 1977; 1: 1645-1648.



APPENDIX B - SYMPTOM SCORE SHEET

MRC DYSPNOEA SCALE

Grade 1 "I only get breathless with strenuous exercise" 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" Grade 5 "I am too breathless to leave the house" The MRC dyspnoea scale is a category scale that can be used to complement FEV1 in the classification of COPD severity (Thorax 1999; 54: 581-586)



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



INDICATIONS FOR ICU ADMISSION OF PATIENTS WITH ACUTE COPD EXACERBATION 1. Severe dysnoea that responds inadequately to initial emergency therapy 2. Confusion, lethargy or respiratory muscle fatigue (the last characterized by paradoxical diaphragmatic motion) 3. Persistent or worsening hypoxemia despite supplemental oxygen or severe / worsening respiratory acidosis (pH < 7.30) 4. Assisted mechanical ventilation is required whether by means of endotracheal tube or non-invasive technique From ATS Standards for the Diagnosis and Care of Patients with Chronic Obstructive Pulmonary Disease FOLLOW-UP OF ACUTE EXACERBATIONS For all patients follow-up assessment 4-6 weeks after discharge from hospital should include: • patient’s ability to cope • measurement of FEV1 • reassessment of inhaler technique and patient’s understanding of recommended treatment regime • need for LTOT and / or home nebuliser usage in patients with severe COPD • follow-up thereafter is as for stable COPD From BTS Guidelines for the Management of Chronic Obstructive Pulmonary Disease



ACTION PLAN FOR PEOPLE WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE ACTION PLAN FOR PEOPLE WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE

WHEN YOU ARE WELL - KNOW THE FOLLOWING ACTION

How much can you do each day Have something to look forward to each dayHow your breathing is at rest and during activity Plan ahead - allow enough time to do thingsWhat makes your breathing worse Exercise every day but pace yourselfWhat your appetite is like Eat a balanced diet - drink adequate fluidsHow well you sleep Avoid factors that make you worseHow much phlegm you have, and its colour Never allow medicines to run out

WORSENING SYMPTOMS ACTIONPhone your medical practice and discuss:

More breathless** Changes in symptomsReduced energy for daily activities Temporary assistance for difficult activitiesLoss of appetite MedicationsChange in amount and / or colour of phlegm** Reschedule your day - allow more timeCough Get plenty of rest and use relaxation techniquesFever Use controlled breathing techniquesNeed to use inhalers / nebuliser more often then usual Huff and cough to clear phlegm

Eat small amounts more often** There is some evidence that where 2 or more of these occur, antibiotics help Drink plenty of fluids

SEVERE SYMPTOMS ACTIONYou are not getting better CONTACT YOUR DOCTOR FOROther AN URGENT APPOINTMENT

DANGER SIGNS ACTION

Very short of breath at rest (Chest pains DIAL 111 FOR AN AMBULANCE High fever OR CONTACT THE EMERGENCY DOCTORA feeling of agitation, fear, drowsiness or confusion



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