1. health and fitness
2. disease
3. asthma

Chronic Obstructive Pulmonary Disease
(COPD)
Australian and New Zealand Management
Guidelines and the COPD Handbook
A joint project of
Version 1, November 2002
For further information contact
The Australian Lung Foundation
Phone (07) 3357 6388 Fax (07) 3357 6988
E-mail [email protected]
PO Box 847 LUTWYCHE QLD AUSTRALIA 4030
1
Foreword
Things are changing in COPD.
·
COPD contributes more to the burden of disease in Australia and New Zealand
than any other lung condition. This impact on mortality, morbidity and disability
will only escalate with an ageing population.
·
Now is the time to consider a proactive approach to chronic disease management
of COPD patients.
·
COPD has long been regarded as an incurable condition for which there is very
little therapy available. It has also been confused with asthma. Apathy towards
COPD treatment may be attributed to an overemphasis on FEV1 as a marker of
treatment success or failure. While it is true that little that can done to restore
destroyed lung tissue and disordered pulmonary physiology, much can be done
to improve quality of life, increase exercise capacity and reduce morbidity and
mortality.
·
A global assessment of the patient and a caring, comprehensive approach to
treatment can do much to improve the outlook and wellbeing of COPD patients.
·
There is renewed interest in the development of protocols and guidelines for
COPD management, and many of the recommendations in this handbook are
based on recent international guidelines, with consideration for treatment
practices and regulations (e.g. those applying to domiciliary oxygen therapy) in
Australia and New Zealand.
·
This guide has been written for primary care teams and others closely involved in
the management of COPD patients.
·
It contains a simple plan for patient careÐ the COPD-X Plan
Confirm diagnosis & assess severity
Optimise function
Prevent deterioration
Develop support network and self-management plan
eXacerbations Ð manage appropriately
·
This plan is a combination of evidence based medicine and consensus
management. In some cases, the recommendations await the results of
appropriate clinical trials to confirm usefulness.
This publication is part of ÔSail OnÕ, a National Public Health campaign to help
people with COPD Ôput the wind back into their sailsÕ.
The Australian Lung Foundation is grateful for financial assistance provided
by:
Foundation sponsors Ð Boehringer Ingelheim, GlaxoSmithKline
Supporters Ð Air Liquide Healthcare, BOC Medical
2
INTRODUCTION
COPD in Australia and New Zealand
Chronic obstructive pulmonary disease is a major cause of disability, hospital
admission and premature death.
·
In Australia, only heart disease and stroke contribute more to the overall
burden of disease1 while in New Zealand, COPD is second only to stroke2.
·
Early COPD symptoms are often attributed to ageing or other causes. The
disease is therefore likely to be underrecognised. More than half a million
Australians are estimated to have moderate to severe disease3 . As the
population ages in developed countries, the burden of COPD is likely to
increase.
·
COPD is costing the nation an estimated $818 to $898 million annually4. This
is a conservative estimate because it is based on 1993 to 1994 figures
extrapolated to the Year 2001. The addition of hidden costs could increase
the estimate to more than $1 billion per annum. Hidden costs include carer
burden, loss of productivity due to absenteeism and early retirement.
·
COPD is the fourth most common cause of death in Australian men and the
sixth most common cause in women. In New Zealand, it is the third most
common cause of death in men and the fourth in women1.
·
Smoking is the most important risk factor for COPD. Smoking-related
diseases are increasing substantially in women and COPD death rates in
women are expected to overtake those in men4.
·
Indigenous communities in Australia and New Zealand have experienced
long-term socioeconomic and health disadvantage. COPD death rates in
indigenous Australians are five times that of non-indigenous Australians 2.
Smoking has been identified as the leading cause of healthy years lost in
Maori men and women.
Evidence Based Guidelines for the Management of Chronic Obstructive Pulmonary
Disease (COPD) and the COPD Handbook
The development of these guidelines was a joint project of the Thoracic Society of
Australia and New Zealand and The Australian Lung Foundation, driven by a
multidisciplinary steering committee representing the major stakeholder groups in
COPD management.
The steering committee was convened according to the principles outlined in the
National Health and Medical Research Council Guidelines for Guideline
Development 5 and met for the first time in May 2001. It agreed to use the Global
Strategy for the Diagnosis, Management and Prevention of Chronic Obstructive
Pulmonary Disease (referred to as GOLD) as the evidence base for these guidelines.
The intention was that GOLD could be a resource used by countries around the
world to produce local, tailored guidelines.
GOLD is conducted in collaboration with the US National Heart, Lung and Blood
Institute (NHLBI) and the World Health Organisation (WHO). Its goals are to
increase awareness of COPD and decrease morbidity and mortality from the
disease.
3
In 2001, GOLD published and distributed the GOLD Workshop Report: Global
Strategy for the Diagnosis, Management and Prevention of COPD6, based on the
available evidence for the most appropriate management and prevention strategies.
The document was reviewed extensively by COPD experts and scientific societies
throughout the world. It included the development of a comprehensive database of
COPD literature, and levels of evidence were assigned to recommendations using a
system developed by the NHLBI (see Figure 1).
It is expected that this document will be updated regularly based on compelling new
evidence (e.g. GOLD updates, Cochrane reviews or meta-analyses).
The Guidelines are presented as the COPDX Plan Ð a summary of best practice
management of COPD, with levels of evidence assigned.
The COPDX Guidelines also act as an index for the COPD Handbook. This is the
first of a range of products, tools and strategies being developed to drive the
implementation of these guidelines. The Handbook provides detailed information on
each of the steps in the guideline. The Handbook is primarily aimed at general
practitioners but should also be a valuable resource for all health professionals
involved in the care of patients with COPD.
Associate Professor David McKenzie
Chairman
COPD Guidelines Steering Committee
4
Figure 1: Levels of Evidence
NHLBI
CATEGORY
SOURCES OF
EVIDENCE
DEFINITION
A
Randomised
controlled trials
(RCTs).
Rich body of data.
Evidence is from endpoints of well-designed RCTs
that provide a consistent pattern of findings in the
population for which the recommendation is made.
Category A requires substantial numbers of studies
involving substantial numbers of participants.
B
Randomised
controlled trials
(RCTs). Limited
body of data.
Evidence is from endpoints of intervention studies that
include only a limited number of patients, postop or
sub-group analysis of RCTs, or meta-analysis of
RCTs. In general, Category B pertains when few
randomised trials exist, they are small in size, they
were undertaken in a population that differs from the
target population of the recommendation, or the
results are somewhat inconsistent.
C
Non rðandomised
trials.
Observational
studies.
Evidence is from outcomes of uncontrolled or non
randomised trials or from observational studies.
D
Panel consensus
Judgment.
This category is used only in cases where the
provision of some guidance was deemed valuable but
the clinical literature addressing the subject was
deemed insufficient to justify placement in one of the
other categories. The Panel Consensus is based on
clinical experience or knowledge that does not meet
the above-listed criteria.
NHMRC
LEVEL
I
[A]
II
[B]
III Ð 1 [C]
III Ð 2 [C]
III Ð 3 [C]
IV
[C]
TYPE OF EVIDENCE
Evidence obtained from a systematic review of all relevant randomised
controlled trials
Evidence obtained from at least one properly designed randomised controlled
trial
Evidence obtained from well-designed pseudorandomised controlled trials
(alternate allocation or some other method)
Evidence obtained from comparative studies (including systematic reviews of
such studies) with concurrent controls and allocation not randomised, cohort
studies, case-control studies, or interrupted time series with a control group
Evidence obtained from comparative studies with historical control, two or
more single arm studies, or interrupted time series without a parallel group
Evidence obtained from case series, either post-test or pretest/ post-test
Source: NHMRC 1999
5
Acknowledgements
Editorial
Dr Jonathan Burdon, respiratory physician, Melbourne
Dr Peter Frith, respiratory physician, Adelaide
Associate Professor David McKenzie, respiratory physician, Sydney
Professor Ian Town, respiratory physician, Christchurch, NZ
Members of COPD Guidelines Steering Committee
Associate Professor Michael Abramson, respiratory physician and epidemiologist,
Melbourne
Professor Norbert Berend, respiratory physician, Sydney
Ms Jenny Bergin, Pharmacy Guild of Australia
Associate Professor Stephen Cala, respiratory physician, Gosford
Associate Professor Alan Crockett, respiratory scientist, Adelaide
Dr Peter Frith, respiratory physician, Adelaide
Dr Peter Gibson, respiratory physician, Newcastle
Dr Christine Jenkins, respiratory physician, Sydney
Associate Professor Sue Jenkins, physiotherapist, Perth
Mr Ross Lisle, consumer representative
Dr Christine McDonald, respiratory physician, Melbourne
Associate Professor David McKenzie, respiratory physician, Sydney
Dr Jitendra Parikh, Royal Australian College of General Practitioners
Professor Harold Rea, respiratory physician, Auckland, NZ
Mrs Marilyn Robinson, respiratory nurse, Townsville
Dr Julian Smith, cardiothoracic surgeon, Melbourne
Dr Greg Snell, respiratory physician, Melbourne
Associate Professor Robin Taylor, respiratory physician, Dunedin, NZ
Mr Marcus Weidinger, Pharmaceutical Society of Australia
Contributors & Reviewers
Dr Jenny Alison, physiotherapist, Sydney
Mr Paul Caffarella, psychologist, Adelaide
Associate Professor Donald Campbell, respiratory physician, Melbourne
Dr Karen Detering, respiratory physician, Melbourne
Dr David Hart, respiratory physician, Melbourne
Associate Professor Peter Holmes, respiratory physician, Melbourne
Associate Professor John Kolbe, respiratory physician, Auckland, NZ
Dr Tom Kotsimbos, respiratory physician, Melbourne
Ms Maria Loder, respiratory nurse, Melbourne
Dr James Markos, respiratory physician, Hobart
Ms Vanessa McDonald, respiratory nurse, Newcastle
Dr Ruth McKenzie, general practitioner, Sydney
Dr Lucy Morgan, respiratory physician, Sydney
Dr Matthew Peters, respiratory physician, Sydney
Professor Robert Pierce, respiratory physician, Melbourne
Associate Professor Robyn Richmond, School of Community Medicine, UNSW
Dr Jonathan Rutland, respiratory physician, Sydney
Professor Paul Seale, respiratory physician, Sydney
Dr Brian Smith, respiratory physician, Adelaide
Ms Laura Smith, PhD student, Adelaide
Ms Sheree Smith, respiratory nurse, Brisbane
Mr Pieter Walker, psychologist, Melbourne
Associate Professor Iven Young, respiratory physician, Sydney
6
TABLE OF CONTENTS
Page
FOREWORD
INTRODUCTION
COPD in Australia and New Zealand
Draft Evidence Based Guidelines for the Management of
Chronic Obstructive Pulmonary Disease (COPD) and the
COPD Handbook
Explanation of Levels of Evidence - COPDX
ACKNOWLEDGEMENTS
C - CONFIRM DIAGNOSIS AND ASSESS SEVERITY
INTRODUCTION
What is COPD?
Aetiology and natural history
Prognosis
CONFIRM DIAGNOSIS
Signs and Symptoms
Spirometry
Assess Severity
ASSESS ACUTE RESPONSE TO BRONCHODILATORS
Confirm or exclude asthma
SUPPORT DIAGNOSIS
Flow volume tests
Complex lung function testing
Exercise testing
Sleep studies
Chest radiographs
High resolution CT scanning (HRCT)
Ventilation and perfusion scans
Transcutaneous oxygen saturation
Arterial blood gas measurement
Sputum examination
Haematology and biochemistry
Electrocardiography and echocardiography
COMPLICATIONS AND COMORBIDITIES
Comorbidities
Complications of treatment
Aggravators of COPD
O Ð OPTIMISE FUNCTION
SYMPTOM RELIEF
Bronchodilator Therapy In COPD
Initial Drug Therapy
Long-acting inhaled bronchodilators
Theophyllines
2
3
3
3
5
6
12
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Assessment of Response and Continuation of
Bronchodilator Therapy
Glucocorticoid therapy in COPD
Short-course oral glucocorticoids
Inhaled glucocorticoids
Combination inhaled glucocoricoid/long acting
bronchodilator
Assess Long Term Medication Response
Glucocorticoid Response Trial
Optimise Inhaler Technique
SURGICAL TREATMENTS
Bullectomy
Lung Volume Reduction Surgery
Lung Transplantation
Fitness for Surgery
IDENTIFY AND TREAT AGGRAVATING FACTORS
Sleep Apnoea/Hypoventilation/Hypoxaemia
Physiology of sleep
The overlap syndrome
Gastro-oesophageal Reflux
Aspiration
Oral/Dental Health
Alcohol and Sedatives
IDENTIFY AND TREAT COMPLICATIONS
Pulmonary hypertension and cor pulmonale
Investigations
Treatment
Left Ventricular Failure
Osteoporosis
IMPROVE FUNCTION
Pulmonary Rehabilitation
Exercise training
Patient Education
Psychosocial support
Comprehensive integrated rehabilitation
Chest Physiotherapy in COPD
Weight Management and Nutrition
SEX & COPD
P Ð PREVENT DETERIORATION
INTRODUCTION
SMOKING CESSATION
Identify stage of readiness to quit
Discuss behavioural and cognitive strategies
Discuss pharmacotherapies: nicotine replacement and
bupropion
Nicotine transdermal patch
Nicotine gum
Nicotine inhaler
Nicotine lozenges
Bupropion
Discuss social support
Discuss prevention of relapse
PREVENT INFECTION AND EXACERBATION
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48
8
Influenza vaccination
Pneumococcal vaccination
Antibiotics
Glucocorticoids
Mucolytics in COPD
REGULAR REVIEW
Monitor disease progression and development of
complications
Monitor pharmacotherapy and other medical treatment
Monitor exacerbation history
Monitor comorbidities
HOME OXYGEN THERAPY
Indications
Long-term continuous oxygen therapy
Intermittent oxygen therapy
Nocturnal oxygen therapy
Contraindications
Initiating oxygen therapy
What the patient needs to know
Review
Dangers
Choosing the right method
Cylinders
Oxygen concentrators
Liquid oxygen systems
Which system is the best?
FITNESS TO FLY
Who requires supplemental oxygen during flight?
FITNESS FOR SURGERY
Preoperative assessment and preparation
History
Examination
Lung function tests
ABGs
Integrated cardiopulmonary exercise testing
Smoking cessation
Control of sputum
Effect of nature of surgery
Management of COD patient postoperatively
D Ð DEVELOP SUPPORT NETWORK AND SELFMANAGEMENT PLAN
Impact on patient and carer
Assess & improve individualÕs supports
GPÕs role
Respiratory specialistÕs role
The multidisciplinary team
Nurse/Respiratory Educator
Physiotherapist
Occupational therapist
Social worker
Clinical psychologist
Speech pathologist/therapist
Pharmacist
48
49
49
49
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9
Dietitian
Non-medical care agencies
Develop multidisciplinary care plan/case conference
INCREASE KNOWLEDGE AND REDUCE STRAIN
Educate patients and carers
Refer to a support group
IMPROVE COPING SKILLS AND SELF MANAGEMENT
BEHAVIOUR. DEVELOP POSITIVE ATTITUDES TO SELFMANAGEMENT AND EXERCISE. REDUCE FREQUENCY OF
EXACERBATIONS/ADMISSIONS
Assess cognitive and coping abilities
Treat anxiety and depression
Address carer strain
Enrol in pulmonary rehabilitation
Ensure optimal use of inhalers
Develop a self-management plan
END OF LIFE ISSUES
PALLIATIVE CARE IN COPD
63
63
63
64
64
65
66
X Ð EXACERBATIONS: MANAGE APPROPRIATELY
71
ACUTE EXACERBATIONS OF COPD
Pathophysiological abnormalities
Causes
Complications
In general practice
In hospital
At resolution
EARLY DIAGNOSIS
EARLY ACTION
Initial assessment of severity
History and examination
OPTIMISE TREATMENT
Bronchodilator therapy
Introduction
Initial treatment
Antibiotic therapy
Glucocorticoids
REFER APPROPRIATELY
Indications for specialist referral
Indications for hospitalisation of patients with COPD
Indications for increased respiratory support or ICU
admission
RESPIRATORY SUPPORT
Controlled O2 therapy
Noninvasive positive pressure ventilation (NIPPV)
Clearance of secretions
MONITOR AND REVIEW
Monitor response to initial treatment
Monitoring response to ongoing treatment
Discharge planning
Psychosocial assessment and activities of daily living
Pulmonary rehabilitation
CONVALESCENCE
Outreach support after discharge
Clinical review/follow up
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Assessment for long-term oxygen therapy
Smoking cessation
Vaccination
Nutrition
ABBREVIATIONS
REFERENCES
83
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84
85
FIGURES
Page
Figure 1.
Figure 2.
Figure 3.
Figure 4.
Figure 5.
Figure 6.
Figure 7.
Figure 8.
Figure 9.
Figure 10.
Figure 11.
Figure 12.
Figure 13.
Figure 14.
Figure 15.
Figure 16.
Figure 17.
Figure 18.
Figure 19.
Figure 20.
Figure 21.
Figure 22.
Figure 23.
Levels of Evidence
COPD, Bronchitis, Emphysema and Asthma
Time-Course of COPD
Indications for considering COPD and performing spirometry
MRC Dyspnoea Scale
Volume-Time Plots
Classification of severity
Assessment of acute beta-agonist/bronchodilator response (at
diagnosis)
Excluding other diagnoses
Flow volume curves
Suggested initial treatment with short acting bronchodilators
Assessing long term medication response
Long term bronchodilator responsiveness protocol
Glucocorticoid response trial period protocol
Explanation of inhaler devices
Advantages and disadvantages of pharmacological treatments for
smoking cessation
Risk factors for postoperative respiratory complications
Proportions to be used in calculating the effect of lung resection
Indications for referral to respiratory specialist
Enhanced Primary Care Item Numbers
Suggested COPD patient education topics
Patient support groups
Adjustments for oxygen settings in acute exacerbations of COPD
5
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30
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55
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11
C
CONFIRM DIAGNOSIS AND ASSESS SEVERITY
Consider COPD in all smokers and ex smokers over the age of 357.
Consider COPD in patients with other smoking related diseases15.
Smoking is the most important risk factor in the development of COPD7,8.
Other risk factors include occupational exposures, indoor and outdoor air
pollution, airway hyper-responsiveness and genetic factors (e.g. alpha-1antitrypsin deficiency)9.
The diagnosis rests on the demonstration of airflow limitation which is not
fully reversible20.
If airflow limitation is substantially reversible treat as asthma.
AIMS
Confirm diagnosis
ACTIONS
History
Examination
Functional Assessment
Spirometry
B
A
A
B
B
D
FINDINGS
Smoking >10 pack years*, strong family
history
Cough, sputum, dyspnoea
Overexpansion, quiet breath sounds
Exercise limitation
FEV1<80%Predicted, FEV1/FVC <0.7 (post
bronchodilator)
Support diagnosis
and
Exclude other
conditions
Assess severity
Identify:
Complications
- disease
- treatment
Comorbidities
- lifestyle
- ageing
CXR, high resolution
CT, Complex lung
function
Hyperinflation, emphysema
Airway narrowing, reduced transfer factor
Physician Review
Echocardiogram
Immunological
screening
Bronchial challenge
Spirometry
Consider:
- Diffusing capacity
- O2 sat, ABGs
Relevant Investigations
Cancer, pneumonia, left ventricular failure,
bronchiectasis, interstitial lung disease,
thromboembolic disease, asthma
Mild FEV1 60-80% (post bronchodilator)
Moderate FEV1 40-59%
Severe FEV1 <40%
Hypoxaemia, hypercapnia and weight loss
indicate poor prognosis
Pneumonia, pleurisy, empyema,
pneumothorax, respiratory failure, pulmonary
hypertension, cor pulmonale, polycythaemia,
deconditioning, osteoporosis, cataract.
Ischaemic heart disease, vascular disease,
carcinoma, aspiration, gastro-oesophageal
reflux, sleep disordered breathing, diabetes
mellitus, dementia.
* 1 Pack year = 20/day for 1 year or equivalent number of cigarettes
The above recommendations are either self-evident or represent consensus-based best
practice, except where levels of evidence have been assigned.
12
Introduction
What is COPD?
Chronic obstructive pulmonary disease (COPD) is a group of disorders characterised
by airway inflammation and airflow limitation that is not fully reversible. COPD should
be distinguished from asthma because it is a progressive, disabling disease with
increasingly serious complications and exacerbations that places a major burden on
the health care system. In contrast with asthma, non-drug treatments such as
pulmonary rehabilitation have a major role. Patients with a clinical history compatible
with asthma whose airflow obstruction is substantially reversible are not considered
to have COPD.
Small airway narrowing (with or without chronic bronchitis) and emphysema due to
smoking are the most common conditions resulting in COPD. Breathlessness with
exertion, chest tightness and wheeze are due to airway narrowing and impaired gas
exchange. Chronic bronchitis is daily sputum production for at least three months of
two or more consecutive years, and not all people with these symptoms have airflow
limitation. Emphysema is a pathological diagnosis, consisting of alveolar dilatation
and destruction. The resultant impairment in gas exchange makes it difficult for
people with emphysema to perform activities without breathlessness. The loss of
lung elastic tissue may result in airway wall collapse during expiration, leading to
dynamic hyperinflation and consequent increased work of breathing. Some people
with early emphysema may not have airflow limitation.
The symptoms, signs and physiology of these conditions can overlap with asthma
and differentiation can be difficult, particularly in middle-aged smokers presenting
with breathlessness and cough. This difficulty is compounded by the fact that the
majority of COPD patients exhibit some degree of reversibility with bronchodilators.
Patients with severe chronic asthma, chronic bronchiolitis, bronchiectasis and cystic
fibrosis may also present with a similar clinical pattern and partially reversible airflow
limitation.
Figure 2. COPD, Bronchitis, Emphysema and Asthma
Recurrent respiratory tract infections are typical in patients with COPD but should
also alert the clinician to the possibility of bronchiectasis, local airway obstruction
(e.g. carcinoma, foreign body), recurrent aspiration, immune deficiency syndromes
13
and cystic fibrosis. Haemoptysis, even when minor, should always be considered as
a possible manifestation of lung cancer or bronchiectasis.
Aetiology and natural history
Cigarette smoking is the most important aetiological factor in the development of
COPD 7,8. It is estimated that in Western societies cigarette smoking accounts for
about 85% of the risk of developing COPD,
and there is a close relationship between the
Consider the diagnosis of
amount of tobacco smoked and the rate of
COPD in all smokers and exdecline in FEV1.
smokers over the age of 35.
Around half of all smokers develop some
airflow limitation and 15-20% of smokers will develop clinically significant disability.
Smokers are also at risk of developing lung cancer, ischemic heart disease and other
tobacco related disorders such as peripheral vascular disease.
Other factors which may contribute to the development of COPD include9:
· occupational dust and fume exposure
· alpha-1 antitrypsin deficiency
Cigarette smoking accounts for
· bronchial hyperresponsiveness
about 85% of the risk of
· environmental tobacco smoke
developing COPD.
· indoor and outdoor air pollution
· recurrent respiratory infections in
childhood
· genetic predisposition
Continued cigarette smoking in susceptible people causes a steady decline in lung
function with the loss of FEV1 of 25-100ml/year. Smoking cessation leads to a small
improvement in lung function in some patients. More importantly it will slow the rate
of decline in lung function to that experienced by non-smokers and delay the onset of
disablement. Smoking cessation at any time is important to preserve remaining lung
function7.
Figure 3. Time-Course of COPD
As the disease progresses, impairment increases but may not be recognised
because of the slow pace of the disease. Patients tend to maintain their activity
levels within their own symptomatic limits and adopt strategies to avoid undue
shortness of breath. Ultimately the patient becomes disabled and hypoxaemia
develops. Hypercapnia, pulmonary hypertension and cor pulmonale may develop.
14
Prognosis
The single best predictor of mortality in COPD is FEV17,21. In one study the five year
survival was only about 10% for those with FEV1 < 20% predicted, 30% for those with
FEV1 between 20 and 29% predicted and about 50% for those with FEV1 between 30
and 39% predicted.
Continued smoking and airway hyperesponsiveness are associated with accelerated
loss of lung function10.
The development of hypoxaemic respiratory failure is an independent predictor of
mortality with a three year survival of about 40% 11. Survival is increased by long-term
administration of oxygen to about 50% with nocturnal oxygen and about 60% with
administration for greater than 15 hours per day12 (see also section ÒPÓ, page 50).
Admission to hospital with an infective exacerbation of COPD complicated by
hypercapnic respiratory failure is associated with a poor prognosis. A mortality of
11% during admission and 49% at two years has been reported in patients with a
PaCO2 > 50 mm Hg13. For those with chronic CO2 retention (about 25% of those
admitted with hypercapnic exacerbations) the five year survival was 11% 14. However,
even if substantial airflow limitation is present, cessation of smoking may result in
some improvement in lung function and will slow progression of disease.
Confirm Diagnosis
Signs and symptoms
The main symptoms of COPD are breathlessness, cough and sputum production15-16.
Patients often attribute breathlessness to ageing or lack of fitness. Occasionally
patients will associate the onset of their symptoms, particularly breathlessness, to a
major life event such as a motor vehicle accident, personal crisis/tragedy, surgery or
to severe illness. More detailed history in these cases will indicate that the condition
was of much longer standing.
Spirometric evidence of moderate to severe airflow limitation is common at the time
of presentation. It is therefore important to consider the diagnosis of COPD and
measure spirometry early in the natural history when interventions such as smoking
cessation will have maximal benefit.
A persistent cough, typically worse in the mornings with mucoid sputum, is common
in smokers. It may occur with or without clinical or spirometric evidence of airflow
obstruction. Other symptoms such as chest tightness, wheezing and airway irritability
are common.
Figure 4. Indications for considering COPD and performing spirometry.
Chronic cough
Chronic sputum production
Acute bronchitis
Dyspnoea that is
History of exposure to risk
factors
present intermittently or every day
often present throughout the day; seldom only nocturnal
any pattern of chronic sputum production may indicate COPD
repeated episodes, often in winter
progressive
persistent
worse on exercise
worse during respiratory infections
tobacco smoke
occupational dusts and chemicals
indoor and outdoor pollution
15
Patients with COPD become more breathless as their disease advances.
Breathlessness will initially develop during heavy exertion and gradually exercise
capacity will decrease. Eventually breathlessness may occur at rest.
Breathlessness and functional
limitation can be rated
numerically with the simple
MRC dyspnoea scale
The MRC dyspnoea scale17 is a simple tool that
reliably grades the impact and disablement from
breathlessness associated with COPD and it is
highly recommended for use in standard clinical
practice (see Figure 5).
It is as easy to apply in a clinical consultation as the New York Health Association's
Cardiac Status gradings, and it fits closely with routine questions often asked about
what activities cause a person to become breathless.
Figure 5. MRC Dyspnoea Scale
Grade 1
Grade 2
Grade 3
Grade 4
Grade 5
"I only get breathless with strenuous exercise"
"I get short of breath when hurrying on the level or walking up a slight hill"
"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"
"I stop for breath after walking about 100 yards or after a few minutes on
the level"
"I am too breathless to leave the house" or Ò I am breathless when
dressingÓ
Acute exacerbations, usually infective, occur from time to time and may lead to a
sharp deterioration in coping ability. Fatigue, poor appetite and weight loss become
increasingly common in advanced disease.
Physical findings vary with severity. The sensitivity of physical examination for
detecting mild to moderate COPD is poor18. Wheezing is not an indicator of severity
of disease and is often absent in stable, severe COPD. In more advanced disease,
hyperinflation of the chest, reduced chest expansion, hyperresonance to percussion,
soft breath sounds and a prolonged expiratory phase are commonly found. Right
heart failure may complicate severe disease and will be recognised by elevation of
the jugular venous pressure and peripheral oedema.
During an acute exacerbation, signs of severe airflow limitation such as tachypnoea,
tachycardia, use of accessory muscles, tracheal tug and cyanosis may be seen.
The presence and severity of airflow limitation
is impossible to determine using clinical signs
alone. Objective measurements of airway
calibre such as spirometry are strongly
recommended. Peak expiratory flow (PEF) is
not a sensitive measure of airway function in
COPD patients because it is effort dependent
and there is a wide range of normal values19.
The diagnosis of COPD rests
on spirometry and the
demonstration of airflow
limitation that is not fully
reversible.
Spirometry
Spirometry is the gold standard for diagnosing, assessing and monitoring COPD.
Most spirometers provide predicted values derived from formulae accounting for
height, age, gender and ethnic background. The values for Asians and most black
16
races are 10 Ð 20% lower than those for northern Europeans (Caucasians). This is
due to ethnic variation in the shape of the chest cavity.
Airflow limitation that is not fully reversible is defined as being present when the postbronchodilator values for the ratio of FEV1 to FVC (FEV1/FVC) is <0.7 and the FEV1
is <80% predicted. The FEV1/VC ratio is sensitive in the recognition of mild COPD.
The FEV1 as a percentage of predicted, is useful in terms of severity assessment and
as a prognostic indicator.
Figure 6. Volume-Time Plots
Assess severity
Spirometry is the most reproducible, standardised and objective way of measuring
airflow limitation, and the one most closely associated with prognosis21 . With the
advent of electronic spirometers, flow-volume tests are now being used more
frequently. In some cases more complex lung function tests such as diffusing
capacity and static lung volumes are useful to assist in the investigation and
management of COPD (see page 21).
17
Figure 7. Classification of severity
(Airflow limitation is indicated by FEV1/FVC <0.7)
Mild COPD
Moderate COPD
Severe
COPD
Spirometry
FEV1% predicted
60-80% predicted
40-59% predicted
<40%
predicted
Functional assessment
(Activities of daily living)
Few symptoms
Increasing
dyspnoea
Dyspnoea on
minimal
exertion
No effect on daily
activities
Breathless on the
flat
Breathless on
moderate exertion
Increasing limitation
of daily activities
No
Exclude
complications
Complications
Consider sleep
apnoea if pulmonary
hypertension
Daily activities
severely
curtailed
Severe
hypoxaemia
(PaO2 <60mm
Hg or 8kPa)
Hypercapnia
(PaCO2
>45mm Hg or
6kPa)
Pulmonary
hypertension
Cor pulmonale
Polycythaemia
Assess acute response to bronchodilators
The response to bronchodilators should be performed at the time of diagnosis, when
clinically stable, in order to:
· assign level of severity (post-bronchodilator)
· help confirm or exclude asthma
The longer term response to bronchodilators and glucocorticoids should also be
assessed to guide rational choice of medication and to establish best attainable lung
function (see Optimise function, page 27).
The change in FEV1 after an acute bronchodilator reversibility test indicates the
degree of reversibility of airflow limitation. This is often expressed as a percentage of
the baseline measurement (e.g. 12% increase). However where the FEV1 is small
(e.g. less than 40% predicted), a more useful measure is the absolute increase in
FEV1 (e.g. >200ml increase). An increase of FEV1 of greater than 12% and 200ml is
greater than average day to day variability and is unlikely to occur by chance22. This
degree of reversibility is not diagnostic of asthma and is frequently seen in patients
with COPD.
18
Figure 8. Assessment of acute beta-agonist/bronchodilator response
(at diagnosis)
Preparation
·
·
Spirometry
·
·
·
·
·
Perform tests when patients are clinically stable and free from
respiratory infection
Patients should not have taken inhaled short-acting bronchodilators in
the previous six hours, long-acting beta-agonists in the previous 12
hours, or sustained-release theophyllines in the previous 24 hours.
Measure baseline spirometry (pre-bronchodilator) and look for
indicators of airflow limitation FEV1 < 80% predicted and FEV1/FVC <
0.70
The bronchodilator should be given by metered dose inhaler through a
spacer device or by nebuliser to be certain it has been inhaled.
Give standard beta-agonist, at a dose selected to be high on the doseresponse curve.
Suitable dosage protocols are 200 - 400 mcg salbutamol from MDI and
spacer
Repeat spirometry 15 Ð 30 minutes after bronchodilator is given, look
for indicators of reversibility.
Confirm or exclude asthma
Asthma and COPD are usually easy to differentiate even though they share many
symptoms. Asthma usually runs a more variable course and dates back to a younger
age (even to recurrent wheezy bronchitis in childhood). Atopy is more common in
asthmatics and the smoking history is often relatively light. Airflow limitation in
asthma is substantially, if not completely, reversible either spontaneously or in
response to treatment (short or long term bronchodilators and/or glucocorticoids). By
contrast COPD tends to be progressive with a late onset of symptoms and a
moderately heaving smoking history (usually >15 pack years). The airflow
obstruction, by definition, is not completely reversible.
However, there is some overlap between asthma and COPD. Longstanding or poorly
controlled asthma can lead to chronic, irreversible airway narrowing even in nonsmokers. Such an outcome is more likely in smoking asthmatics. On the other hand
many patients with COPD and no history to suggest asthma may have clinically
significant but incomplete reversibility of airflow limitation with treatment.
Support Diagnosis
The diagnosis of COPD may be confirmed by the use of more complex lung function
tests and a high resolution CT scan of the lungs. Differentiation from chronic asthma,
airway hyperresponsiveness or significant occupational exposures that may cause a
clinically relevant degree of bronchodilator and/or steroid responsiveness is important
and often requires specialised knowledge and investigations.
The long-term management of most people with COPD will usually take place in
primary care. However referral to a respiratory specialist may contribute to
assessment and management of people with moderate or severe disease
(Indications for specialist referral are listed in Section D, page 61).
Normal spirometry in heavy smokers does not necessarily mean that smoking-related
lung damage has not occurred. In these cases more sophisticated lung function tests
are needed to demonstrate respiratory abnormalities. Neither should normal
spirometric results deter the advice to smokers that it is in their best long-term
interests to quit. Smoking cessation will have tangible benefits even in advanced
19
disease. The effects of smoking on other organ systems also need to be discussed
with the patient. Smoking cessation techniques are discussed in Section P.
Figure 9. Excluding Other Diagnoses
Alternative Diagnosis
Suggestive Features
Asthma
Cardiac failure
Onset early in life
Day to day variability
Nocturnal cough and/or wheeze
Atopic features (eczema, hayfever)
Family history
Substantial reversibility with bronchodilator
Non Smoker
History of hypertension, ischaemic heart disease
Elevated JVP, peripheral oedema
Cardiac enlargement
Bronchiectasis
Large volumes of sputum, often daily
Frequent purulent exacerbations
May date back to childhood or severe infection
May show finger clubbing
Coarse crackles and/or wheeze
CXR/HRCT bronchial dilation, thickened airway walls
Interstitial lung disease
Tachypnoea, clubbing
Bibasal fine inspiratory crackles
Basal reticulonodular shadowing on CXR
HRCT: septal thickening, honeycombing
Chronic bronchiolitis
Usually younger
Non-smokers
Predisposing disorders e.g. rheumatoid arthritis
HRCT: hypodense areas and patchy ground glass
shadowing
Cystic fibrosis
Family history
Usually diagnosed in childhood
History of childhood chest disorder, malabsorption
Finger clubbing, failure to thrive
Unexplained breathlessness
Check FBE to exclude anaemia
Check V/Q scan or CTPA, D-dimer to exclude
thromboembolism
Consider hyperventilation syndromes
Check thyroid function to exclude thyrotoxicosis
Flow volume tests
Electronic spirometers allow for the simultaneous measurement of flow and volume
during maximal expiration. Reduced expiratory flows at mid and low lung volumes
are the earliest indicators of airflow limitation in this patient group.
20
Figure 10. Flow-Volume Curves
Complex lung function testing
Measurement of airways resistance, static lung volumes and diffusing capacity
(DLCO) all assist in the assessment of patients with more complex respiratory
symptoms. In the presence of airflow limitation, a reduction in DLCO below 70% is
highly suggestive of the presence of emphysema. Static lung volumes (total lung
capacity [TLC], functional residual capacity [FRC] and residual volume [RV]) are
usually increased in COPD. The diagnosis of COPD is strongly supported by the
finding of an increase in TLC, FRC and RV in the presence of a reduced FEV1/FVC.
Exercise testing
Simple exercise tests (e.g. six-minute walk, incremental or endurance shuttle walking
test) are useful to determine the extent of disability and as an outcome measure
following intervention e.g. pulmonary rehabilitation. Integrated cardiopulmonary
exercise testing is not routine in the diagnosis of COPD. Laboratory based exercise
tests may be useful to identify the cause of exercise limitation and to differentiate
between breathlessness due to cardiac or respiratory disease and exercise limitation
due to other causes (eg peripheral vascular disease).
Sleep studies
Worsening of blood gas abnormalities during sleep or nocturnal desaturation is
frequently observed in patients with COPD. Mechanisms include worsening of gas
exchange and reduced efficiency of respiratory mechanics in the recumbent posture,
and central hypoventilation during sleep, especially REM sleep. Obstructive sleep
apnoea may co-exist with COPD, and may be responsible for cardiac failure that is
poorly responsive to treatment.
21
Specialist referral is recommended for COPD
Consider the possibility of
patients suspected of having a coexistent sleep
COPD
co-existing with a sleep
breathing disorder. Indications for sleep studies
disorder
in patients with COPD include symptoms
suggesting sleep apnoea, such as excessive
daytime sleepiness, hypercapnia, pulmonary hypertension in the absence of daytime
hypoxaemia, right heart failure or polycythaemia. Overnight pulse oximetry may be
indicated in patients receiving long-term domiciliary oxygen therapy to assess its
efficacy.
Chest radiographs
A plain posteroanterior and lateral chest
radiograph (CXR) is a useful part of the initial
assessment of patients with COPD. It serves as
a baseline for future assessments and also helps
to exclude other conditions such as lung cancer.
The CXR is not sensitive in the diagnosis of
COPD and will not exclude a small carcinoma
(<1cm).
FEV1 and CXRs may be normal
in early disease.
A CXR is an important
baseline test to exclude an
obvious lung tumour.
Hyperinflation of the lung fields is a common feature in the CXR of COPD patients,
but is also seen in other conditions such as chronic asthma and even in fit young
adults. Bullae can be seen in some patients with advanced emphysema. Moderate
emphysema is associated with disruption and attenuation of vascular markings
especially in the upper zones.
High Resolution CT Scanning (HRCT)
HRCT scanning gives precise images of the lung parenchyma and mediastinal
structures. The presence of emphysema and the size and number of bullae can be
determined. This is necessary if bullectomy or lung reduction surgery is being
contemplated. A high resolution CT is the appropriate way to detect the presence of
bronchiectasis. Vertical reconstructions can provide a virtual bronchogram.
Spiral CT scans with intravenous contrast should be used in other circumstances
such as the investigation and staging of lung cancer.
CT pulmonary angiograms are useful in investigating possible pulmonary embolism
especially when the chest radiograph is abnormal.
Ventilation and perfusion scans
Ventilation and perfusion (V/Q) scans are not part of the routine workup of the COPD
patient but may be helpful if pulmonary embolism is suspected. In patients with
COPD the V/Q scan may be difficult to interpret as regional lung ventilation may also
be compromised leading to matched defects. If pulmonary emboli are strongly
suspected a CT pulmonary angiogram may be indicated. V/Q scans are helpful in
assessing patients for suitability for lung resection and lung volume reduction
surgery.
Transcutaneous oxygen saturation
Hypoxaemia may develop in patients with moderate and severe COPD. It may also
occur transiently in acute exacerbations during exercise or during sleep.
Transcutaneous haemoglobin oxygen saturation (SpO2 ), measured by pulse
oximetry, is an easy, non-invasive guide to the adequacy of oxygenation. Currently
available oximeters have an accuracy of plus or minus 2%, which is satisfactory for
routine clinical purposes. Oximetry does not provide any information regarding
22
carbon dioxide status and is inaccurate in the presence of poor peripheral circulation
(e.g. cold extremities, cardiac failure).
Arterial blood gas measurement
In general, if the SpO2 is greater than 92%, arterial blood gas analysis is not
necessary. It should however be considered in all patients with severe disease, those
being considered for domiciliary oxygen therapy, and in all patients with
complications or a rapidly deteriorating clinical state e.g. when the FEV1 is <40%
predicted or <1litre, SpO2 <92%, when pulmonary hypertension is present, and in
those with breathlessness out of proportion to their clinical status. Elevation of arterial
carbon dioxide tension PaCO2 >45mm Hg (6kPa) is a sign of inadequate ventilation
due to critically impaired lung function and/or impaired control of breathing.
Respiratory failure is defined as a PaO2 <60mm Hg (8kPa) or a PaCO2 >50 mm Hg
(6.7kPa).
Sputum examination
Sputum culture may identify the infecting
organism causing an exacerbation of COPD.
However, positive bacterial cultures can also be
found in patients who are clinically stable.
Sputum cultures are often negative even when
the sputum is obviously purulent.
Sputum culture is
recommended when the
infection is not responding to
antibiotic therapy or when a
resistant organism is
suspected.
Routine sputum culture in
clinically stable COPD patients
is unhelpful and unnecessary.
The lack of sputum culture results should not
delay the introduction of antibiotics into the
treatment program if clinically indicated. Once
they are available, the results may guide more
appropriate antibiotic therapy.
Haematology and biochemistry
Haemoglobin and haematocrit measurement are part of the assessment of COPD
patients. Polycythaemia should be confirmed as being secondary to COPD by blood
gas measurement confirming the presence of hypoxaemia. The possibility of sleep
apnoea/hypoventilation should be considered if the awake O 2 saturation is normal.
Occasionally unsuspected anaemia may be detected and when treated may improve
symptoms.
Measurement of thyroid function and acid base status are sometimes useful in
patients in whom the cause of breathlessness is obscure. Hyperthyroidism and
acidosis are associated with breathlessness. Hyperventilation states are associated
with respiratory alkalosis. Hypothyroidism aggravates obstructive sleep apnoea.
Electrocardiography and echocardiography
Electrocardiography is useful when coexistent ischaemic heart disease or an
arrhythmia are suspected. Atrial fibrillation commonly develops when pulmonary
artery pressure rises, leading to increased right atrial pressure.
Echocardiography may be useful in the assessment of right heart function e.g. if cor
pulmonale is suspected. It is also useful when breathlessness is out of proportion to
the degree of respiratory impairment and when conditions such as ischaemic heart
disease, pulmonary embolus and left heart failure are suspected.
23
Complications and Comorbidities
Complications of COPD include a range of conditions, which are discussed in detail
in Sections ÒOÓ and ÒXÓ. The most common are infective exacerbations, pneumonia,
pleurisy and empyema and pneumothorax.
Hypoxaemia, hypercapnia, pulmonary hypertension, polycythaemia and cor
pulmonale are usually late manifestations indicating severe impairment of lung
function. Sleep-disordered breathing should be considered if the degree of
pulmonary hypertension seems excessive for the impairment of lung function.
Deconditioning occurs rapidly in patients with advanced COPD contributing to
disability and poor quality of life. A reduction in body mass index (BMI<20%) is an
independent risk factor for mortality in COPD patients23.
Comorbidities
Patients with COPD are prone to other conditions associated with cigarette smoking
including accelerated cardiovascular, cerebrovascular and peripheral vascular
disease; oropharyngeal, laryngeal and lung carcinoma. Conversely, there is a high
prevalence of COPD among patients with ischaemic heart disease, peripheral
vascular disease and cerebrovascular disease. These patients should be screened
for COPD (including spirometry).
Complications of treatment
Other comorbidities are related to treatment, especially the inappropriate use of highdose inhaled and oral glucocorticoids. Problems include easy bruising, weight gain,
myopathy, hyperglycaemia, hypertension, osteoporosis and cataract.
Aggravators of COPD
COPD and its symptoms may be aggravated by a range of conditions including left
ventricular failure, aspiration, gastro-oesophageal reflux, sleep apnoea, anaemia,
hyperthyroidism and renal failure (e.g. metabolic acidosis). Left ventricular function
may be difficult to assess because of hyperinflation affecting echocardiography and
the respiratory limitation of exercise. The radiographic sign of upper lobe diversion
may not be obvious with the vascular attenuation of emphysema. A gated heart pool
scan may be useful.
24
O
OPTIMISE FUNCTION
Pulmonary rehabilitation reduces dyspnoea, anxiety and depression, improves
exercise capacity and quality of life and may reduce hospitalisation90-91.
Inhaled bronchodilators provide symptom relief and may increase exercise capacity 24-
27,63
Inhaled glucocorticoids should be considered in patients with a documented response
or who have severe COPD with frequent exacerbations59-62.
Oral glucocorticoids are contraindicated for maintenance use in most cases53-57.
In selected patients, a surgical approach may be considered for symptom relief 64-70.
AIMS
Symptom
relief
GOALS
Reduce breathlessness
Improve exercise
capacity/quality of life
Bronchodilatation
- Avoid overdosing
- Avoid drug
interactions
- Stop drug if no benefit
Other approaches
Identify & treat
aggravating
factors
Identify &
Treat
complications
Improve
function
Assess
oxygen status
Sleep apnoea
Reflux, aspiration
Avoid excess alcohol &
sedative use
Pulmonary hypertension
CO2 retention
Osteoporosis
Peripheral and
respiratory
muscle dysfunction
Address psychosocial
issues
Increase daily exercise
Improve knowledge &
self management skills
Optimise nutrition
Chronic hypoxaemia
Exercise hypoxaemia
Sleep hypoxaemia
RECOMMENDATIONS / ACTIONS
A
A
B
A
C
LEVEL
Pulmonary Rehabilitation
A
Optimise inhaler technique
Use inhaled b2 agonist or anticholinergic
Combined b2 agonist and anticholinergic may be
more effective and better tolerated
Consider long acting inhaled bronchodilators
Consider trial of inhaled glucocorticoids
MDI with spacer or dry powder inhaler may be as
effective as nebuliser
Consider theophyllines SR (check serum levels)
Consider bullectomy, LVRS or transplantation
C
A/A
A
Overnight saturations, sleep study
History +/- modified Ba swallow if indicated
Ask, advise, assess, assist, arrange
C
C/D
C
Long term oxygen (> 15 hrs/day)
Low flow oxygen (of 0.5-2 lpm), consider NIPPV
Minimise or cease corticosteroids
Measure bone density and treat
Optimise nutrition
Treat hypoxaemia and avoid systemic steroids
Advise daily physical activity (including walking)
Pulmonary rehabilitation achieves all goals
- Diagnose and treat anxiety/depression
- Encourage physical activity, consider
portable O2
- Enrol in respiratory support group
- Educate patients and carers
- Obtain diet history,
- Advise weight gain or reduction as
appropriate
Formal assessment Ð see section P, page 50
A
B
A
C/D
C/D
C/D
C/D
Where two levels of evidence are given (e.g. A/A) this means evidence is given for both
recommendations/actions.
25
A
B
C
B
C
A
C
B
C
A
C
Symptom Relief
Pulmonary Rehabilitation (see under Improve Function, page 39)
Bronchodilator therapy in COPD
Patients with COPD present with breathlessness during and after exertion.
Individuals who have a sedentary lifestyle will generally have a moderate or severe
lung function abnormality at diagnosis. The two classes of inhaled bronchodilators,
selective beta-adrenoceptor agonists and anticholinergics, relax airway smooth
muscle. However, airway smooth muscle contraction is only one contributor to the
physiological and functional deficits in COPD63.
All bronchodilators have been shown to improve exercise capacity to some degree 29. However, changes in simple measurements of airway function (FEV1, FVC) are
not closely associated with symptomatic improvement or changes in measures of
quality of life32-33,63.
31
The dose response relationship for all
bronchodilators is low in COPD24-27 and the
Nebulisers have a limited role
failure to achieve a large therapeutic response
in management of stable
should not necessarily trigger the use of higher
COPD
doses. Wet nebuliser use is not recommended
for routine use in stable disease 3 4 . The
duration of action of short-acting inhaled anticholinergics is greater than that of shortacting beta-agonists. The combination of beta-agonists35 and anticholinergics may be
more effective and better tolerated than higher doses of either agent used alone35-42.
At all levels of lung function abnormality, efforts to maintain or regain physical fitness
should be encouraged as the effect of this is likely to match or exceed the benefits of
bronchodilator use. The role of pulmonary rehabilitation is discussed on page 39.
Use of a short-acting bronchodilator before an exercise session may reduce dynamic
hyperinflation and allow better training effects to be achieved23.
Initial Drug Therapy
Figure 11. Suggested initial treatment with short acting bronchodilators
Severity
FEV1
Suggested treatment
Mild COPD
60-80%
Moderate COPD
40-59%
Severe COPD
<40%
Modified from GOLD, pages 72
Intermittent bronchodilator - use prn before exercise
Salbutamol 200mcg or
Ipratropium bromide 40mcg
Intermittent or regular bronchodilator
Salbutamol 200-400mcg qid or
Ipratropium bromide 40mcg qid
Combination bronchodilators may be considered
Regular combination bronchodilator
Salbutamol 200-400mcg qid and ipratropium bromide 4080mcg qid
43
26
Long-acting inhaled bronchodilators
Long-acting beta-agonists (e.g. salmeterol and eformoterol) provide bronchodilation
for 12 hours44-46 and are widely used for asthma. They are not currently subsidised
for COPD (as opposed to asthma), though they have been shown to improve
exercise endurance, improve health-related quality of life and reduce both
exacerbation and hospitalisations.
·
·
Salmeterol 50mcg bd has a favourable
effect on measures of health-related
quality of life 5 0 . Again the doseresponse relationship is low, so
compared to the standard dose, the
higher dose of 100mcg bd does not
improve quality of life50.
Long-acting bronchodilators
provide sustained relief of
symptoms in moderate to
severe COPD
Eformoterol 12mcg bd improves lung function and symptoms46.
Tiotropium, an anticholinergic, has a greater than 24-hour duration of effect and is
used once daily. Compared with placebo and regular ipratropium it reduces
dyspnoea and exacerbation rate and improves health status47-49.
Various other chemicals acting on other receptors, enzymes, cells and genes with
anti-inflammatory and bronchodilating properties are in development.
Theophyllines
Theophyllines are rarely used because of the narrow therapeutic index and potential
for significant side effects26,36-37. Some patients with disabling breathlessness may
derive benefit from their use. Theophyllines may have an anti-inflammatory effect and
/or reduce muscle fatigue36-38,51-52. Evidence supports only the slow-release
formulation. Dosage should be adjusted according to trough serum levels.
Assessment of response and continuation of bronchodilator therapy
The response to treatment should be assessed over a period of at least four weeks.
Where there is documented improvement in lung function, symptoms and/or
objective measurements of breathlessness (MRC Scale) or exercise capacity, this
therapy should be continued. An unsatisfactory response to a beta-agonist should
lead to a trial of anticholinergic therapy, and vice versa. The combination is more
useful than either alone and effective bronchodilation may be achieved with lower
doses 35-36,38-42,44. Patients can have a symptomatic and functional improvement
without change in FEV1. When there is still no improvement in either lung function or
symptoms, the justification for ongoing treatment with inhaled bronchodilator is
doubtful. If there is no response to treatment, consider the following questions:
·
·
·
Is the patient using the inhaler device
correctly? Check and educate on
Combination therapy is useful
timing, triggering and technique (see
in moderate and severe
page 31).
COPD.
Are a lack of fitness, deconditioning or
psychosocial factors disabling the
patient? Should exercise or formal rehabilitation be pursued further?
Is another condition causing the exercise impairment? Some examples
include coronary artery disease, cardiac failure, peripheral muscle weakness
and anaemia.
27
Glucocorticoid therapy in COPD
There is a substantial component of inflammation in COPD and clinicians are
tempted to use glucocorticoids in treating this disorder. However the inflammatory
component of COPD is much less responsive to glucocorticoids than the
inflammation of asthma. Caution is necessary because of this limited efficacy and a
likely increase in toxicity in the elderly patients who represent the bulk of individuals
with COPD. The long-term use of systemic glucocorticoids in COPD is not
recommended53-57.
Short-course oral glucocorticoids
There are two main uses for oral
glucocorticoids.
One is during acute
Long-term use of oral
exacerbations, and the other is for therapy
glucocorticoids is not
trials. Controlled trials show that when patients
recommended.
are admitted to hospital with an acute
exacerbation of COPD, treatment with oral
glucocorticoids reduces the rate of treatment failure, increases FEV1 within 24 hours
and shortens the hospital stay180-182 (see Section X, page 77). After recovery from an
acute exacerbation, oral glucocorticoids should be withdrawn promptly. An attempt
should be made to cease oral glucocorticoids in all patients, given the inevitable side
effects that occur with chronic use.
A trial of oral glucocorticoids is warranted in stable patients with moderate and
severe GOPD not currently taking inhaled glucocorticoids (see page 30,
Glucocorticoid Response Trial). There is no benefit to continuing such a trial beyond
two weeks. Further, no extra benefits have been shown from an oral steroid trial for
six weeks in patients already on stable inhaled glucocorticoids200.
Inhaled glucocorticoids
Although inhaled glucocorticoids are widely prescribed for patients with COPD, the
evidence to date indicates that they do not influence the rate of decline in FEV1 in
patients without acute reversibility. Smoking cessation remains the only effective
means of reducing the rate of decline in lung function for these patients (see Section
P). On the other hand, patients with significant but not substantial bronchodilator
reversibility (i.e. not regarded as having asthma) may benefit from long-term inhaled
glucocorticoids. Long-term inhaled corticosteroids are also indicated in patients with
COPD who have significant reversibility of airway function following a more
prolonged trial of bronchodilators and /or glucocorticoids59-62 (see page 29).
In one large RCT of patients with severe non-reversible COPD (mean FEV1
approximately 40% predicted), high-dose inhaled glucocorticoid (fluticasone 1000
mcg daily) slowed the rate of decline in quality of life over a three-year period and the
rate of acute exacerbations without affecting overall decline in lung function61. Some
systemic absorption of the inhaled fluticasone may occur so the modest benefits of
inhaled glucocorticoids must be weighed against the potential risks of easy bruising,
cataract formation and possible contribution to
osteoporosis. Similar results may be expected
Inhaled glucocorticoids
from high doses of other inhaled glucocorticoids
should be trialed in moderate
but are yet to be documented in randomised
and severe COPD with
controlled trials. In another large RCT in milder
objective measures of
COPD, medium dose budesonide had no
response e.g. spirometry,
significant impact59.
performance status, quality
of life.
Given these limitations, the role of inhaled
glucocorticoids in COPD management is
28
currently uncertain. They should be trialed for three to six months in patients with
moderate to severe COPD, and continued if there is objective benefit (see page 30).
The response to glucocorticoids should be assessed with spirometry and measures
of performance status and/or quality of life. Performance status may be assessed
subjectively by history e.g. ease of performing activities of daily living or responses to
categorical dyspnoea scales such as the MRC Dsypnoea Scale (see page 16).
Exercise capacity may be measured objectively. Simple tests which can be
performed by a nurse or physiotherapist, or scientist/technician include the six-minute
walk test and the shuttle walk test.
Health-related quality of life can be measured objectively using sensitive validated
questionnaires. These may be general such as the SF36, or disease specific such as
St Georges Respiratory Questionnaire (SGRQ) or the Chronic Respiratory Disease
Questionnaire (CRDQ). These tools may not be useful in the primary care setting but
documentation of patient and carer well being is recommended.
Combination inhaled glucocorticoid/long-acting bronchodilator
There is at present insufficient evidence published in peer-reviewed journals to
determine the role of combination inhaled glucocorticoid and long-acting
bronchodilators in COPD, though the evidence is strong in people with asthma.
Assess long-term medication response
Long-term responsiveness may be assessed by changes in airway function (e.g.
FEV1, FVC) (see Figure 12). Symptomatic and functional benefits can often be
demonstrated in the absence of an increase in FEV1. Other objective measurements
such as an increase in exercise capacity (e.g. six-minute walk distance) or a
decrease in FRC (which indicates increased inspiratory reserve) may be useful
indicators of physiological improvement. In some patients, increases in airway calibre
require prolonged treatment of up to two months.
Subjective measurements such as quality of life, breathlessness and functional
limitation (e.g. MRC Dyspnoea Scale, see page 16) can also be undertaken to
demonstrate the patientÕs perception of benefit.
Figure 12. Assessing long term medication response
At diagnosis
At next visit
·
·
·
·
·
·
·
Measure and record post beta-agonist FEV1 and FVC
Record MRC Breathlessness Scale score
Prescribe trial medications as per dosage protocols below
Re-measure spirometry and MRC Breathlessness Scale score to
determine response to medications
If FEV1 and/or FVC increases > 12% and > 200 mL following a
treatment trial, and/or MRC Score improves > 1 unit, the tested
medication should be included as ongoing treatment
If FEV1 and/or FVC increase > 20% and 300mL with inhaled or
oral glucocorticoids Ð consider asthma
If no significant response to the tested medication it could be ruled
out for ongoing treatment.
29
Figure 13. Long term bronchodilator responsiveness protocol
Response
Drug
Dose
Delivery
Frequency
Duration of
trial
Beta Agonist
Airway function
Exercise capacity
Breathlessness
QOL
salbutamol
200mcg
MDI/spacer
MDI/spacer
6 hourly
6 hourly
terbutaline
500mcg
DPI
12 hourly
salmeterol
50mcg
MDI/DPI
12 hourly
eformoterol
12 mcg
MDI/DPI
12 hourly
4080mcg
MDI/spacer
6 hourly
up to
1-2 months
Anticholinergic
ipratropium
Glucocorticoid Response Trial
· Some COPD patients show a significant response to oral or inhaled
glucocorticoids.
· A negative reversibility test to bronchodilator does not predict a negative
steroid response.
· A response to oral glucocorticoids does not always predict a response to an
inhaled glucorticoid58,61.
· Patients with a negligible response to glucocorticoids should have them
stopped.
· Doses of inhaled glucocorticoids higher than the recommended protocol (see
Figure 14), may be associated with systemic absorption and adverse effects.
· Long-term oral glucocorticoids should be avoided because of a poor adverse
effect profile and a lack of evidence of efficacy beyond acute exacerbations5357
.
Figure 14. Glucocorticoid response trial protocol
Response
Glucocorticoid response
Drug
prednisolone
Dose
20 - 50 mg
Delivery
Duration
of trial
oral
2 weeks
inhaled
3 months
beclomethasone
·
large
particle
1000-2000mcg/day
·
small
particle
400-800 mcg/day
budesonide
800-1600 mcg/day
fluticasone
500-1000 mcg/day
30
Optimise Inhaler Technique
Careful explanation and demonstration of all inhaler devices is necessary in order for
patients to achieve optimal benefit. Different devices require different inspiratory flow
rates for optimal drug delivery. Check regularly that the patient can demonstrate
correct inhaler technique. Elderly and frail patients, especially those with cognitive
deficits, may have difficulty with some devices. Device training should be part of a
pulmonary rehabilitation program. Available delivery systems are listed below.
Delivery
system
Metered
dose inhaler
(MDI)
Figure 15. Explanation of Inhaler Devices
Available Products
Considerations
Qvar (beclomethasone 50 and
100mcg), Flixotide (fluticasone 50,
125 and 250 mcg),
Atrovent (20 mcg) and Atrovent
Forte (40 mcg) (ipratropium
bromide)
Ventolin, Asmol, Airomir, Epaq
(salbutamol 100mcg)
Most commonly used inhaler.
Some people have difficulty
coordinating the release of
medication with inhalation. It is
therefore recommended that MDIs
be used with a spacer device (see
below).
Serevent (salmeterol 25 mcg)
Spacers
Seretide (fluticasone 50, 125 or 250
mcg, with salmeterol 25 mcg)
Aerochamber, Breath-A-Tech,
Fisonair, Nebuhaler and Volumatic
A small volume spacer is preferable
when the vital capacity is less than
1.5 litres.
Spacer chamber acts as a reservoir
for the aerosol released from an
MDI. The patient can then inhale
from this chamber without having to
coordinate the release of the
medication.
Using spacers with inhaled
corticosteroids reduces side effects
of oral candidiasis and hoarseness
as well as optimising medication
delivery.
MDI with spacer are as effective as
a nebuliser if an equivalent dose is
taken. 10 to 15 puffs of 100mcg
salbutamol MDI via a spacer is
therapeutically equivalent to a 5mg
salbutamol nebule.
Spacers are cheap, portable, easily
cleaned and maintained, do not
require electricity and are simple
and quick to use.
Autohaler
Airomir (salbutamol 100 mcg), Qvar
(beclomethasone 50 and 100 mcg),
Atrovent (ipratropium bromide 20
mcg).
Breath-activated MDI containing 200
doses of medication.
Use can improve lung deposition in
patients with poor MDI inhaler
technique. As the patient starts a
slow and deep breath through the
mouthpiece, a flap valve is triggered
and the dose automatically
releases.
31
Dry Powder Inhalers (DPI)
Accuhaler
Serevent (salmeterol 50mcg),
Flixotide (fluticasone 100, 250,
500mcg)
Seretide (salmeterol 50 mcg and
fluticasone 100, 250, 500 mcg)
Aerolizer
Foradile (eformoterol 12mcg)
Turbuhaler
Bricanyl (terbutaline 500mcg),
Pulmicort (budesonide 100, 200,
400mcg), and Oxis (eformoterol
12mcg)
HandiHaler
Spiriva (tiotropium)
Spiriva has recently been approved
by the TGA and is expected to be
available in 2002/2003.
Nebulisers
The majority of nebulisers are
electric, but there are some
ultrasonic nebulisers that are battery
operated. These ultrasonic models
are not heavy duty, but they are
Breath-activated multi-dose DPI
containing 60 individually sealed
doses of drug. The device has a
dose counter that shows the number
of doses remaining. It delivers
accurate and consistent drug
delivery over a range of inspiratory
flow rates (30-120 L/min).
Lactose powder is combined with
the active medication for patients to
taste and reassure them that they
have inhaled a dose.
Breath-activated single-dose powder
inhaler comes with a sheet of 60
capsules in push-out foil sheet. For
each dose, one capsule is loaded
into the inhaler and pierced before
inhaling.
The Aerolizer produces consistent
drug delivery over a range of
inspiratory flow rates.
Breath-activated multi-dose inhaler,
containing 60 (Oxis) or 200
(Pulmicort, Bricanyl) doses, ensures
delivery without the need to
coordinate inspiration with drug
release.
Dose delivery is halved if the patient
cannot produce inspiratory flow
above 30 L/min. Produces very fine
powder so patients often donÕt taste
anything.
Dose indicator shows when the
inhaler has 20 doses remaining, and
then when it is empty. The inhaler
contains a drying agent that can be
heard when the inhaler is shaken.
This can be misinterpreted that there
is still medication available.
Breath activated dry powder inhaler.
Breath-activated dry powder inhaler.
A capsule containing tiotropium is
dropped into the HandiHaler, and
the capsule is pierced by pressing a
button on the device. The patient
then inhales through the mouthpiece
of the device for effective drug
delivery. Patients with a wide range
of disease severity are able to
generate sufficient inspiratory airflow
(as low as 20L/min) to evacuate the
powder from the capsule.
The aerosol should not be allowed
to enter the eyes if aerosolising
glucocorticoid or ipratropium
bromide to avoid the risk of side
effects such as glaucoma or urinary
32
ideal for travelling. There are also
12-volt pumps that plug into a car
cigarette lighter. If used for inhaled
glucocorticoids, a high-flow, heavyduty pump is necessary.
outlet obstruction. Patients should
be advised to wipe their face dry
after using the nebuliser to remove
medication from their skin.
Ipratropium can be combined with
beta-agonist, but not with
glucocorticoid.
Surgical Treatments
Several operations have been proposed to alleviate the symptoms of advanced
COPD. No operation has been shown to provide a survival advantage. In view of the
potential for serious morbidity and mortality, all surgical treatments for COPD require
careful assessment by an experienced thoracic medical and surgical team.
Bullectomy
This operation involves elective resection of large bullae >5cm. The procedure is
most successful where there are very large cysts compressing adjacent apparently
normal lung64,71,72.. Patient selection is based on the chest HRCT and functional
status.
Lung volume reduction surgery
This procedure involves resection of the most severely affected areas of
emphysematous, non-bullous lung73. This allows improvement in lung elastic recoil
on small collapsed airways and improved diaphragmatic function65.
Careful medical assessment is required to pick the best candidates and avoid
excessive morbidity and mortality. The procedure is most successful in patients with
clear-cut target areas of poorly-perfused lung, gross hyperinflation, reasonable
remaining lung tissue, minimal comorbidities and without cor pulmonale. Patient
selection is based on the chest HRCT, nuclear V/Q scan, detailed lung function tests
and electrocardiogram.
Surgery is performed electively following a pulmonary rehabilitation program. Midline
sternotomy and video-assisted thoracoscopy are most commonly utilised to remove
approximately 25% of each lung.
Physiological improvement takes weeks to months to be achieved e.g. a 40%
improvement in FEV1 (from about 25% predicted normal values to 35% predicted)
and six-minute walk (from about 300m to 420m). The duration of the improvement is
between two and four years. These gains should be weighed against risks of
operative and post-operative mortality (around 5 to 15%), morbidity and cost.
However the natural history of patients with COPD of this severity is a progressive
decline in function and early mortality. LVRS is still an experimental palliative surgical
procedure. Several large randomised multicentre studies are underway to investigate
the effectiveness and cost-benefit of LVRS67.
Lung transplantation
In COPD this procedure usually involves replacement of one diseased lung with a
normal lung from an organ donor. Heart-lung transplantation is rarely necessary in
COPD patients.
Detailed medical and psychological assessment and counselling are required to pick
the best candidates and avoid excessive morbidity and mortality. Severe lung
disease, limited life expectancy and poor quality of life are prerequisites. However
33
malnutrition, severe weakness and steroid and ventilator dependence predict a poor
outcome. The procedure is most successful when lung disease is the recipientÕs only
medical problem.
The waiting time for the procedure is variable but typically around nine months.
Surgery is performed through a single or bilateral thoracotomy approach. Thereafter,
a complex regimen of immunosuppressive therapy and close clinical monitoring
continues for life to minimise complications from rejection and infection.
Physiological improvement takes weeks to months to achieve and would typically
translate to a large improvement in FEV1 (from about 20% predicted normal values to
60% predicted for single lung transplant), exercise performance and quality of life 6870,74
.
Fitness for surgery
The assessment of COPD patients for fitness for surgery is complex (see Section P,
page 55).
Identify & Treat Aggravating Factors
Sleep Apnoea/Hypoventilation/Hypoxaemia
For people with COPD, sleep is the time of maximal hypoxaemia and hypercapnia,
the highest risk of cardiac arrhythmias and highest mortality. Episodes of
hypoventilation may be prolonged (1 to 30 minutes) and exaggerate the changes in
ventilation and gas exchange normally induced by sleep. Short-lived and cyclical
episodes may indicate the coexistence of COPD and obstructive sleep apnoea/
hypopnoea syndrome - the overlap syndrome.
Physiology of sleep
Hypoventilation in sleep results from both increased upper airway resistance due to
relaxation of upper airway dilator muscles, and reduced central drive. Both
mechanisms are exaggerated in REM compared with non-REM sleep. In REM sleep
there is a marked reduction in intercostal muscle activity, which may be important in
patients with hyperinflation and increased work of breathing.
Sleep-related hypoxaemia increases pulmonary artery pressure and may also impair
cardiac contractility and rhythm.
The overlap syndrome
Many patients with COPD also have obstructive sleep apnoea (OSA), the
combination being known as the Òoverlap syndromeÓ. Patients with COPD who also
have OSA have a higher prevalence of pulmonary hypertension and congestive heart
failure compared to those without OSA. There is frequently a history of excessive
alcohol intake. Typically the fall in SpO2 is cyclical in this condition (cycles usually
less than one minute). Some patients with overlap syndrome may develop
progressive hypercapnic respiratory failure with increasing drowsiness. While oxygen
administration may diminish the degree of O2 desaturation, it may increase the
frequency of hypopnoeas in the overlap syndrome.
The general principles of weight reduction to ideal weight, alcohol avoidance and
improvement of nasal patency make sound sense in the COPD group as in OSA
patients generally. Nasal Continuous Positive Airway Pressure (CPAP) can unload
the upper airway and may obviate the need for nocturnal oxygen. If nasal CPAP is
not effective then nocturnal bilevel positive airway pressure ventilation should be
considered, although the benefits of this approach in stable patients remain to be
established in randomised controlled trials. The role of other OSA treatments such as
34
mandibular advancement splinting remains to be further evaluated in the overlap
syndrome.
Many patients with COPD complain of insomnia due to sleep fragmentation whilst
others present with daytime hypersomnolence associated with hypoventilation.
COPD has adverse effects on sleep quality resulting in poor sleep efficiency, delayed
sleep onset, multiple wakenings with fragmentation of sleep architecture and high
arousal index. Arousals are caused by hypoxia, hypercapnia, nocturnal cough and
the pharmacologic effects of methylxanthines and beta-adrenergic agents. Intranasal oxygen administration has been shown to improve sleep architecture and
efficiency as well as SpO2 during sleep.
Indications for full diagnostic polysomnography
in COPD include persistent snoring, witnessed
Diagnostic sleep tests should
apnoeas, choking episodes and excessive
be considered if patients with
daytime sleepiness. In subjects with daytime
COPD have pulmonary
hypercapnia, monitoring of nocturnal
hypertension, hypercapnia,
transcutaneous CO2 should be considered to
daytime somnolence or
assess nocturnal hypoventilation. COPD
witnessed apnoeas.
patients with a stable wakeful PaO2 of more
than 55mm Hg (7.3kPa) who have the
complications of pulmonary hypertension, right heart failure or polycythemia should
also be studied. Overnight pulse oximetry is also useful in COPD patients in whom
long-term domiciliary oxygen therapy is indicated (stable PaO2 less than 55mm Hg or
7.3kPa) for the prescribing of an appropriate oxygen flow rate during sleep.
Gastro-oesophageal Reflux
Gastro-oesophageal reflux is common in patients with COPD. Hyperinflation,
coughing and the increased negative intrathoracic pressures of inspiration may
predispose to reflux, especially during recumbency and sleep. Microaspiration of
oesophageal secretions (possibly including refluxed gastric content) is a risk,
especially with co-existent snoring or OSA. Reflux and microaspiration exacerbate
cough, bronchial inflammation and airway narrowing.
Reflux will be suggested by the history but about 50% of patients with reflux
documented by 24-hour ambulatory pH monitoring will deny typical symptoms.
Diagnosis may be confirmed by pH monitoring, modified Barium swallow or
gastroscopy or a therapeutic trial.
A trial of therapy with H2 -receptor antagonists or a proton pump inhibitor may be
warranted. Lifestyle changes such as cessation of smoking, reduction of caffeine
and alcohol consumption, weight loss and exercise will also help. Elevation of the
head of the bed is also recommended.
Aspiration
Aspiration of food and liquid is common in COPD and may be the cause of recurrent
exacerbations and complications such as pneumonia and patchy pulmonary fibrosis.
COPD patients are more prone to aspiration because of impaired swallowing
efficiency. Hyperinflation impairs lower oesophageal sphincter efficiency, increasing
the likelihood of supine gastric reflux. The upper oesophageal sphincter relaxes
during REM sleep resulting in a high risk of aspiration. Following aspiration, COPD
patients are more prone to develop pneumonia and have reduced ventilatory reserve
than those with healthy lungs.
35
Tachypnoea in COPD patients increases the likelihood of aspiration. COPD patients
also have the same characteristics as the ageing population, which predispose them
to aspiration.
Diagnosis is usually easy with an adequate history from the patient and/or their
partner or carer. Dry biscuits and thin fluids cause the most difficulty. Confirmation
rests with assessment by a speech pathologist and a modified Barium swallow.
These patients ideally should be assessed by a dietitian and speech pathologist.
Treatment involves re-training in safe swallowing techniques. This may include:
· Avoiding talking when eating
· Sitting upright
· Taking small mouthfuls
· Chewing adequately
· Drinking with dry foods
· Using a straw
· Thickened fluids may be necessary
Oral / dental health
Aspiration pneumonia is a major cause of morbidity and hospital admission in the
elderly. After controlling for other variables the number of decayed teeth and other
indices of oral health are significant predictors of aspiration pneumonia.
Patients with COPD are more likely to have poor oral hygiene than age matched
controls. Thus, an examination of oral cavity should include assessment of dental
decay. Dental treatment should be advised when appropriate.
Alcohol and sedatives
Patients with COPD have impaired gas exchange and an exaggerated fall in PaO2
with recumbency and sleep onset. Excessive use of alcohol and sedatives
exacerbates this and predisposes to sleep-disordered breathing.
Heavy cigarette smoking is associated with abuse of other substances in many
individuals. Patients should be asked about substance abuse and appropriate advice
given. Nicotine, caffeine and alcohol also predispose to gastro-oesophageal reflux.
Identify and Treat Complications
Pulmonary hypertension and cor pulmonale
Pulmonary hypertension in COPD results mainly from vasoconstriction of pulmonary
arterioles in response to local hypoxia usually due to impaired ventilation and
vasoconstrictor peptides produced by inflammatory cells75-78. The vasoconstriction
minimises blood flow through poorly ventilated lung reducing the mismatch of
ventilation and perfusion. While this compensatory mechanism initially helps to
maintain the blood gases the price is increased pulmonary vascular resistance,
ultimately leading to right ventricular strain and failure (cor pulmonale). The
vascoconstriction is reversible initially but vascular remodeling occurs eventually and
the condition becomes irreversible. In pulmonary emphysema there is also an
anatomical disruption of capillaries in alveolar walls.
36
Right ventricular hypertrophy is seen in about 40% of patients with FEV1 <1.0 L and
70% of those with FEV1 < 0.6 L. The presence of hypercapnia is strongly associated
with cor pulmonale.
When pulmonary hypertension and cor pulmonale seem out of proportion with the
severity of airway narrowing, additional mechanisms should be considered. These
include sleep apnoea (central and obstructive) leading to repetitive hypoxia,
polycythaemia (either primary or secondary), and recurrent pulmonary
thromboembolism, which occurs with increased frequency in COPD.
The development of pulmonary hypertension and peripheral oedema is a poor
prognostic sign in COPD79. If left untreated, the five-year survival rate is about 30%.
Investigations
(i)
Chest radiographs
Enlargement of proximal pulmonary arteries. Right ventricular enlargement
may be difficult to detect due to hyperinflation.
(ii)
Electrocardiograph
Right axis deviation and pulmonale may be difficult to detect because of low
voltage traces (due to hyperinflation). Multifocal atrial tachycardia and atrial
fibrillation are common.
(iii)
Echocardiography
Echocardiography is the best non-invasive assessment of pulmonary
hypertension but image quality is reduced by hyperinflation. Estimation of
pressure relies on the presence of at least some tricuspid regurgitation.
Other findings include midsystolic closure of the pulmonic valve and
increased right ventricular wall thickness.
Treatment
(i)
Treat underlying lung disease
The logical first step in treatment of cor pulmonale is to optimise lung function
and treat all potential aggravating conditions in order to improve oxygenation
(see Section O).
(ii)
Oxygen therapy
Treatment of hypoxaemia with long-term continuous (>15 hours/day) oxygen
prolongs survival of COPD patients presumably by reducing pulmonary
hypertension11-12,81,82. For a detailed description of oxygen therapy in COPD
(see Section P page 50). Oxygen therapy is appropriate when the
hypoxaemia is due to impaired gas exchange rather than hypoventilation.
Treatment of acute hypoxaemia in exacerbations is discussed in X.
(iii)
Ventilatory Support
For COPD patients with sleep apnoea and/or hypoventilation, ventilatory
support with CPAP (Continuous Positive Airway Pressure) or non-invasive
positive pressure ventilation (NIPPV) may be more appropriate than oxygen
(for more details see Section X, page 79). NIPPV has not yet been proven for
long-term treatment83-86.
37
(iv)
Diuretics
Diuretics may reduce right ventricular filling pressure and oedema. However,
maintenance of cardiac output relies on a relatively high filling pressure so
excessive volume depletion must be avoided. Monitor serum creatinine and
urea to assess volume status. Diuretics may cause metabolic alkalosis (due
to increased hydrogen ion excretion) resulting in suppression of ventilatory
drive.
(v)
Digoxin
Digoxin is not indicated in the treatment of cor pulmonale and may increase
the risk of arrhythmia when hypoxaemia is present. It may be used to control
the rate of atrial fibrillation.
(vi)
Vasodilators
Vasodilators87,88 (hydralazine, nitrates, nifedipine, verapamil, diltiazem, ACE
inhibitors) do not produce sustained relief of pulmonary hypertension in
patients with COPD. Some vasodilators (eg selective calcium channel
blockers) have been shown to reduce right ventricular pressure with minimal
side effects and increased well-being, at least short term. Vasodilators can
worsen oxygenation (by increasing blood flow through poorly ventilated lung)
and result in systemic hypotension. However, a cautious trial may be used in
patients with severe or persistent pulmonary hypertension not responsive to
oxygen therapy.
Left ventricular failure
Left ventricular failure occurs in patients with COPD at least as frequently as in age
matched controls and for the same reasons (ischaemia, heart disease, hypertension,
cardiomyopathy, etc). The treatment is no different other than the caution regarding
diuretic therapy mentioned above, and caution should be exercised with beta-blocker
medication.
Osteoporosis
The COPD population has high rates of bone fracture (11-14%) and low bone
mineral density (BMD) as measured by Dual Energy Xray Absorbitometry (DEXA)
scan, with an average 10% decrease in BMD compared to controls. A 10% drop in
BMD equates to a 2.6 fold increase in fracture risk. Greater deficits are seen in
patients with more severe disease89.
Relevant risk factors for low BMD in COPD patients include periods of
immobilisation/hospitalisation, low FEV1, oral or inhaled corticosteroids, decreased
weight bearing activity and smoking. Other risk factors relevant to the general
population such as low calcium intake, low body mass index, alcohol abuse and
hypogonadism also apply.
No Australian guidelines exist for prevention or management of osteoporosis in
patients with COPD. However guidelines from elsewhere suggest that all patients
who receive corticosteroids including those with COPD should be given lifestyle
advice, including recommendation of regular, weight bearing exercise (e.g. walking
and light resistance training). Those who have had long-term steroid therapy at lower
doses and who have other risk factors should be screened.
Intervention should be targeted at men and women who are taking more than
15mg/day of prednisolone or who have several risk factors for osteoporosis and
whose BMD is <1.5 SDs below the young adult mean. Oral bisphosphonates,
38
particularly risedronate, have been shown to be effective in the prevention and
treatment of bone loss in men and women taking corticosteroids. However only a
minority of patients in those studies had respiratory disease. The studies also
demonstrated a reduction in risk of spinal fracture, especially in post-menopausal
women. Other agents that have been used with some success in patients with
respiratory disease include calcium, vitamin D and medroxyprogesterone acetate.
Selecting COPD patients who may be at increased risk of osteoporosis is most
appropriately done on the basis of conventional risk factors. Further refining of
clinical predictors and more evidence on the cost-effectiveness of such programs still
needs to be resolved before recommendations on a screening strategy can be made.
For more information on prevention and treatment of osteoporosis89.
Improve Function
Pulmonary Rehabilitation
Pulmonary rehabilitation refers to structured usually multi-disciplinary programs that
aim to reduce the symptoms, disability and handicap arising from long-term
respiratory disorders and to help patients reach and maintain a good level of
functioning in the community.
The strategies for achieving these aims are:
(i) Improving cardiovascular fitness, muscle function and exercise endurance;
(ii) Enhancing the patient's self-confidence and coping strategies, and improving
medication adherence and use of respiratory treatment devices;
(iii) Improving mood by controlling anxiety and panic, decreasing depression, and
reducing social impediments.
Pulmonary rehabilitation is mostly offered to patients with moderate to severe COPD,
but can be applied to people with any long-term respiratory disorder characterised by
d y s p n o e a 1 0 2 - 1 0 3 . The greatest amount of high quality evidence supports
comprehensive programs that include exercise training, patient education and
psychosocial support103. Patients should be carefully assessed and treatment goals
agreed at the outset. Outcome assessment is also an important component to
reinforce to the patient the gains made and to evaluate the program. Comprehensive
programs are delivered by a multi-disciplinary team of healthcare professionals,
ideally in close collaboration. Exercise programs alone have clear benefits104, while
the benefits of education or psychosocial support without exercise training are less
well documented102,105-108.
Exercise training
Numerous randomised controlled trials in moderate to severe COPD have shown
decreased symptoms (breathlessness and fatigue) and improved cardiovascular
fitness, exercise endurance, health-related quality of life and mood following exercise
conditioning alone. Improvements in muscle strength and self-efficacy have also
been reported90-101.
Exercise training and encouragement of activity are vital components of pulmonary
rehabilitation. Specific benefits can be measured from endurance and strength
training of upper and/or lower limbs and trunk muscles. The evidence for benefit from
high intensity training of the respiratory muscles is less convincing102,104. Breathing
strategies during exertion including pursed lip breathing are recommended for some
patients, based on both scientific evidence and pragmatism102 . For some very
disabled patients, the teaching of task optimisation to reduce unnecessary energy
expenditure for activities of daily living is also beneficial102.
39
An initial assessment of symptoms and usual activities, and of other significant health
conditions (such as angina, cardiac limitation, peripheral arterial disease and
musculoskeletal problems) that may interfere with training programs is important.
Assessment should also include exercise capacity or endurance, and specific patient
requirements. Using this information the therapists and the patient can set
appropriate and realistic goals.
Supervision of the exercise program is recommended initially so that the possibility of
oxygen desaturation can be monitored and supplemental oxygen provided if
necessary, confidence can be built and improved cardiovascular fitness can be
achieved. Goals can more easily be reset when patients are regularly monitored.
Some patients may benefit from portable oxygen (see P, page 50).
Gains in all outcomes decline with time after a fixed-term program, so maintenance
of activities is essential for continuing the benefits from the initial training program.
Home or community based programs should be encouraged109.
Patient education
There is limited evidence that education alone can improve self-management skills,
mood and health-related quality of life in patients with COPD105-108. Provision of
information and tools to enhance self-management is more effective than didactic
teaching105.
Educational input can be provided by a range of health professionals who will often
work together to establish a set of goals with the patient. Topics usually include
information to improve the patientÕs knowledge about lung health, the benefits of
regular exercise, breathing strategies and the various treatments available to control
breathlessness including relaxation techniques. The single most important outcome
is smoking cessation110. Monitoring tobacco abstinence and support to maintain it
will make sustained quitting more likely. Other important issues that might be
emphasised more in individual consultations, include the need to optimise activities
and maintain (or improve) good nutrition, task optimisation for the more severely
disabled patients, access to community resources, assistance to obtain control over
anxiety, panic or depression, instruction on effective use of medications and
therapeutic devices (including oxygen where necessary), relationships, end of life
and continence issues102,106,111.
Psychosocial support
Improved exercise tolerance, mood, self-efficacy and health-related quality of life
have been reported in COPD from cognitive behaviour therapy alone103.
Depression, anxiety and panic are frequent complications of chronic disabling
breathlessness, with dependency and social isolation being common. General
support, specific behavioural training and the use of appropriate antidepressant
medications may enhance quality of life for the patient, and for the spouse or carer.
Comprehensive integrated rehabilitation
This includes all the components discussed above in an integrated program. There is
strong evidence supporting comprehensive pulmonary rehabilitation as a means of
enhancing health-related quality of life and self-efficacy, improving exercise
performance, reducing breathlessness, and reducing health care utilisation. While the
individual components have benefits, the greatest efficacy is derived from a
comprehensive integrated program90-101,104. Most of the benefits have been observed
in hospital based programs, but there is increasing evidence of benefit from
rehabilitation in the community102-103. The Australian Lung Foundation is developing
a template for pulmonary rehabilitation enabling community based groups to provide
better access to quality programs.
40
Pulmonary rehabilitation should be one part of disease management and patient
support, with close liaison among all care providers and the patient. Clear goals
should be developed for each patient, communicated to the medical and informal
care providers, and reviewed regularly.
After pulmonary rehabilitation, patients should be confident to monitor and manage
their lung condition more effectively so that they need to access emergency
treatment less frequently, and their dependency level is reduced. Pulmonary
rehabilitation should enable patients to collaborate in a more informed manner with
their doctor and other health care providers in planning their own care. Their spouse
or carers should also feel more confident.
After pulmonary rehabilitation, patients should be
confident to monitor and manage their lung
Exercise alone or as part of
condition more effectively so that they need to
comprehensive rehabilitation
access emergency treatment less frequently,
program improves symptoms,
and their dependency level is reduced.
self-confidence, endurance
Pulmonary rehabilitation should enable patients
and quality of life.
to collaborate in a more informed manner with
their doctor and other health care providers in
planning their own care. Their spouse or carers should also feel more confident.
Involvement of patients, their partners or carers in patient support groups may help
sustain the gains made in formal rehabilitation courses. Lung support groups may
provide patients and carers with emotional support, social interaction, and other
social outlets, and help them gain new knowledge and coping strategies. More than
70 groups throughout Australia can be contacted via LungNet. Toll free 1800 654 301
and web-address www.lungnet.com.au. In New Zealand, contact the Asthma and
Respiratory Foundation of NZ.
Chest physiotherapy in COPD
Some patients with COPD have difficulty clearing mucus each day. Others notice
increased mucus production during an exacerbation. In each setting chest
physiotherapy may be of value103.
The aims are to assist sputum removal and improve ventilation without increasing the
distress of the patient. Auscultation plus chest x-ray findings help determine the
region(s) of the lung to be treated. Bronchodilator therapy may be given prior to
treatment if the patient is responsive to bronchodilators, as opening the airways will
result in a more effective treatment. If patients are hypoxaemic (SpO2 < 88%)
supplemental oxygen is given during treatment.
Various techniques and devices are available to aid sputum removal. The choice of
technique depends on the volume of sputum, the patient's condition (eg. extent of
airflow limitation, severity of breathlessness), patient preference and the cognitive
status of the patient.
Weight management and nutrition
Weight management is important for COPD patients because both excess and low
weight are associated with increased morbidity.
Excessive weight increases the work of breathing and predisposes to sleep apnoea Ð
both central hypoventilation and upper airway obstruction.
Progressive weight loss is an important prognostic factor for poor survival 23,112-113.
This may be due to a relative catabolic state (related to high energy demands of
41
increased work of breathing) added to disturbance of nutritional intake (related to
breathlessness while eating). Deleterious consequences include specific mineral or
essential vitamin/anti-oxidant deficiencies as well as combined protein - energy
malnutrition.
Patients with COPD should not eat large meals as this can make breathing more
difficult. Several small nutritious (high energy, high protein) meals are better
tolerated. Snacks may provide a useful addition to energy and nutrient intake.
Referral to a dietitian for advice and individual advice may be beneficial particularly if
the patient is underweight or has recently lost weight.
Sex & COPD
People with COPD should be reassured that having a lung problem doesnÕt
necessarily mean they should stop sexual relations. Neither is it specifically a cause
for loss of interest in sex. Those who have a chronic illness need the love and
comfort of a close, intimate relationship perhaps more than ever.
Sex and intimacy are
necessary and rewarding
parts of life. Attitude and
communication are the keys to
resuming and maintaining
good relationships.
There is no reason why most COPD patients
should not be able to enjoy an active sex life
although energy conservation and breathing
control may need addressing. Check for
psychological problems and drugs that might
affect erectile performance. There is no
contraindication to the use of drugs to facilitate
erection.
42
P
PREVENT DETERIORATION
Smoking cessation reduces the rate of decline of lung function7,110.
Medications have not yet been shown to prevent the long-term decline in
lung function59-61,110.
General practitioners and pharmacists can help smokers quit 117-119.
Relapse is common.
Treatment of nicotine dependence is effective and should be offered to
smokers117-120.
Influenza vaccination reduces the risk of exacerbations, hospitalisation and
death126.
Long-term oxygen (>15 hrs/day) prolongs life in hypoxaemic patients (PaO2
<55 mm Hg or 7.3kPa)11-12,134-136.
Optimal nutrition and regular physical activity are important.
AIMS
Smoking
cessation
Prevent
infection and
exacerbation
Regular
review
GOALS
Implement 5A Strategy
- Ask & identify
smokers
- Advise risks &
benefits, review
options
- Assess dependence
and motivation
- Assist cessation
- Arrange follow up
Influenza vaccination
Pneumococcal
vaccination
Consider:
- Long-acting
bronchodilators
- Inhaled
glucocorticoids
- Antibiotics
- Antitussives,
vasodilators,
immunotherapy
- Mucolytics
Monitor:
- Lung function
-
Performance status
-
Psychological status
Smoking status
Detect/treat
complications
RECOMMENDATIONS / ACTIONS
A
C
A
B
B
B
B
LEVEL
Every patient, at every visit, should
have smoking status documented and
be offered intervention
Even brief counselling is effective
Formal quit programs are effective
Consider nicotine replacement
Consider bupropion SR
Check for multi-substance abuse,
psychological disturbance
Monitor during quit attempt
Annual vaccination (except ovalbumin
allergy)
Recommended every five years for
COPD with frequent exacerbations
C
Patient with frequent exacerbations
B
Patients with frequent exacerbations
Not recommended for long term use
Insufficient evidence to recommend for
widespread use
A
A
D
Mucolytics may have a role for selected
patients (e.g. frequent exacerbations,
tenacious sputum)
B
Annual spirometry
Assess exercise/physical capacity
Consider further pulmonary
rehabilitation
Assess quality of life
Address carer status/strain (see D)
Seek confirmation of cessation
Check O2 sat, ABGs, cardiac echo,
sleep oximetry
D
D
D
A
A
A
A
B
D
A
B
D
D
D
D
43
Patient understands
medications
Stop unhelpful
medications
Maintain exercise
program
Consider device training / medication
card / self-management plan / dose
administration aids
Review medications and drug
interactions
Review compliance with exercise
program
D
D
D
44
Introduction
Identification, reduction and control of risk factors are important steps towards
prevention and treatment of any disease. In the case of COPD, these factors include
tobacco smoke, occupational exposures, and indoor and outdoor air pollution and
irritants.
Cigarette smoking is the major risk factor for
COPD worldwide7,8. Smoking prevention and
cessation programs should be implemented
and be made readily available114. Reduction of
exposure to occupational dust, fumes, and
gases and to indoor and outdoor air pollutants
is recommended115.
Smoking cessation is the
single most effective way to
reduce the risk of developing
COPD and slow its
progression.
Smoking Cessation
Smoking cessation has been shown to halt the accelerated decline in lung function
seen with COPD7,110 . People who continue to smoke despite having pulmonary
disease are likely to be highly nicotine dependent and may require treatment with
pharmacological agents to help them quit116. The 5A strategy should be considered
for every smoker.
Most people who quit smoking relapse 24 to
It is never too late to stop
72 hours after the last cigarette when the
smoking.
withdrawal symptoms are at their peak. To
reduce this early relapse may require nicotine
Smoking cessation will slow
replacement
therapy
(NRT),
other
the rate of decline in lung
pharmacological treatments of nicotine
function compared to that of
addiction (e.g. bupropion, clonidine), or
non-smokers.
cognitive-behavioural
management
techniques. NRT is effective in assisting
dependent smokers to quit121 and no form appears more efficacious than another.
NRT costs less per week than the average cost of smoking. Brief lapses, usually
associated with certain situations, environments and stresses, are best handled by
behavioural approaches.
Identify stage of readiness to quit
Cessation of smoking is a process rather than a single event and smokers cycle
through the stages of being not ready, unsure, ready, quitting and relapsing before
achieving long-term success.
ÒHow do you feel about your smoking?Ó is a good question to determine the
smokerÕs stage of readiness.
Not-ready smokers and unmotivated, unsure about quitting smokers are either happy
or ambivalent about their smoking. They may be seriously considering quitting in the
next six months. Ready smokers are planning to quit in the next 30 days. They have
usually made a 24-hour quit attempt in the past year. The aim of initial intervention
should be to help the smoker advance one stage in the cessation cycle. The most
strenuous efforts should be with those smokers ready to quit.
45
Discuss behavioural and cognitive strategies
Strategies to help people quit are suggested in the acronym DEAD (delay, escape,
avoid, distract).
·
·
·
·
Delay lighting the cigarette until any craving passes (use a nicotine
substitute).
Escape e.g. to another room until the urge to smoke subsides, if motivation is
waning when faced with a group of smokers in a social situation.
Avoid or be aware of cues for smoking (alcohol, coffee and some social
situations).
Distract attention from cravings by drinking a glass of water, having a low
calorie snack, chewing gum or going for a brisk walk.
The environment should be prepared by removing cigarettes.
The new ex-smoker will need to reaffirm that they are strong enough to resist
smoking and will need to be reminded of the negative consequences of smoking
again. Try and encourage smokers to think about the negative impact of smoking on
health, fitness, appearance and saving money.
Cessation rates increase with the amount of support and intervention.
Discuss pharmacotherapies: nicotine replacement and bupropion
All forms of NRT appear to be useful in aiding smoking cessation121 . NRT is most
suitable for highly dependent smokers who are motivated to quit. There is little
evidence about its role in smokers of < 10-15/day. The choice of type of NRT
depends upon patient preference, needs and tolerability.
Nicotine transdermal patch
Patch use avoids the peaks and troughs of plasma nicotine that characterises
smoking, and other forms of NRT. A steady nicotine level sufficient to reduce
withdrawal symptoms is maintained. However the patch does not provide the peak
nicotine levels which reinforce the addiction. A self-administered form of nicotine
such as gum or inhaler in addition may further improve abstinence rates121.
The patch is simple to use and produces blood nicotine levels about half those of
smoking. The strength of patch used depends on the number of cigarettes smoked
daily. Three strengths are available in doubling doses, e.g. 7, 14 and 21mg. Both 24
and 16-hour patches are available. The 24-hour patches achieve higher blood
nicotine levels and provide more relief of morning cravings but both patches have
about the same efficacy. Patch use doubles the success rates of quit attempts
compared to placebo. Six to eight weeks of use are generally required with tapering
of the nicotine dose every two weeks122.
The only significant side effect is skin irritation which is generally mild and rarely
leads to cessation of use.
Nicotine gum
Nicotine is rapidly absorbed through the oral mucous membrane. Gum should be
chewed only two to three times per minute to avoid excessive salivation, swallowing
of nicotine and gastrointestinal side effects. The blood levels achieved by nicotine
chewing gum are one-third (2mg gum) and two-thirds (4mg gum) those of smoking.
Patients should taper the dose gradually but dependence on the gum can occur in up
to 20% of users. Most patients should have ceased the gum within three months.
46
Nicotine inhaler
The nicotine inhaler consists of a plastic mouthpiece and cartridge containing 10mg
of nicotine. The inhaler produces nicotine concentrations that are one-third of those
achieved with smoking. The inhaler is useful for those smokers who miss the handto-mouth action of smoking, or who have problems with the gum. The recommended
use is for 16 weeks.
Nicotine Lozenges
Nicotine lozenges are available in 2mg and 4mg doses. No special technique is
required and the lozenge is moved around in the mouth periodically until it dissolves.
As the lozenge is dissolved, it releases about 25% more nicotine than the equivalent
dose of gum. Patients should reduce the number of lozenges they are using over 12
weeks, remaining on the same strength lozenge throughout. Lozenges may be
preferable for denture wearers who wish to use oral NRT.
Bupropion
Bupropion hydrochloride (Zyban sustained release tablets), an aminoketone, is an
atypical antidepressant that has both dopaminergic and adrenergic actions. In
conjunction with counselling and support, it doubles the quit rates achieved by
placebo, with or without NRT as an adjunct123-125 . It is recommended as first line
pharmacotherapy for smoking cessation alongside NRT, but there are currently
insufficient data to recommend its use in preference to NRT or vice versa. It is also
effective in people who have relapsed and are motivated to quit again. The
recommended dose is 150mg orally once daily for three days then 150mg twice daily
(at least eight hours apart) for between seven and nine weeks, in combination with
counselling. A quit date should be set (e.g. day 5-10).The drug works equally well in
smokers with and without a past history of depression, suggesting that its efficacy is
not due to its antidepressant effect. Bupropion should not be used in patients with a
history of seizures. The commonest side effects are insomnia, dry mouth and
nausea. No patient has been reported to have died during clinical trials of bupropion,
but some have died whilst taking bupropion in routine clinical practice. There is no
evidence that bupropion was responsible for these deaths.
Figure 16. Advantages and disadvantages of pharmacological treatments for smoking
cessation
Treatment
Advantage
Disadvantage
Nicotine
patch
Nicotine gum
Easy to use, few compliance
problems. Available over the counter.
Available over the counter; good to
use as a safety valve in times of
stress. Provides oral substitute for
smoking.
Nicotine
inhaler
Nicotine
Lozenges
Mimics hand-to-mouth behaviour of
cigarette smoking.
Easy to use, useful for denture
wearers as alternative to gum. No
special technique.
Non nicotine; can be used with patch.
Reduces urge to smoke and
withdrawal symptoms.
Bupropion
hydrochloride
Half of the users have skin reactions. Some sleep
disturbances with the 24-hour patch.
Need to spend time explaining correct use.
Common adverse effects are mouth soreness,
hiccups, dyspepsia and jaw ache. Effectiveness
limited by under use and excessive chewing.
Dependence on the gum can occur.
Low nicotine levels. Mild throat irritation and
cough.
Hiccups
Contraindicated in patients with history of
seizures, significant head injury, drugs which
lower seizure threshold and alcohol abuse.
Adverse effects are mild insomnia and dry mouth,
headache, rash and tremor. These are generally
transient.
47
Discuss social support
It is advisable for the person to inform family,
Quit lines:
friends or work-mates of the intention to quit
and request understanding and support. Ask
Australia 131 848
them to communicate caring and concern and
be open and patient with any difficulties in
NZ 0800 778 778
maintaining non-smoking. Other smokers in
the household can reduce the resolve to quit
so the patient might consider quitting with another smoker in the household. Suggest
the patient ring the Quit line or other local services.
Discuss prevention of relapse
Quitting is a dynamic and continuing process often involving repeated attempts. Most
successful ex-smokers take an average of four to five serious quit attempts before
finally succeeding. A brief lapse often occurs at times of stress, in social situations
and sometimes accompanied by alcohol. Relapse is a return to regular smoking
usually within the first three months after quitting.
Ex-smokers who attend for follow-up are more likely to be successful in the long
term. Support is most needed in the first few weeks so encourage regular follow-up
visits then and continue over the first three months.
At follow-up visits:
· Regard brief lapses and relapses as
learning experiences and not failures.
Pharmacotherapies double the
· Provide praise and encouragement
success of quit attempts.
· Identify high-risk smoking situations and
avoid them for a limited time. These can
Behavioural techniques
include drinking with friends and
further increase the quit rate.
negative emotional states such as
conflict, anger, frustration and anxiety.
· Identify specific problems that may cause relapse such as weight gain. Advice
should be given on modifying diet to include more fruit and vegetables,
increasing exercise, and trying stress management techniques such as
meditation. A small increase in weight is less of a risk to health than smoking.
· Plan coping strategies in advance. Discuss problem-solving skills to cope with
and anticipate high-risk situations. Discuss how slips were overcome in the
past.
Prevent infection and exacerbation
Influenza Vaccination
Annual influenza vaccination reduces the
development
of
severe
respiratory
Annual influenza vaccination
complications
and
hospitalisation
or
death from
is recommended for all
126-127
.
both
respiratory
disease
and
all
causes
people with COPD
The vaccine does not contain a live virus and
cannot cause an infection. Side effects include a sore arm the following day and
possibly a mild fever and arthralgia at five to eight days due to the immune response.
48
Pneumococcal Vaccination
Pneumococcal vaccination is known to be highly effective in the prevention of
invasive bacteraemic pneumococcal pneumonia but may be less effective in the
elderly or immunosuppressed. There is no direct evidence of its efficacy in preventing
pneumococcal exacerbations of COPD, but prevention of pneumonia in these
patients with already reduced respiratory reserve is a worthy goal in its own right and
pneumococcal vaccination is therefore recommended in this group. It should be
repeated five yearly. There is no evidence or rationale for vaccinating more
frequently in COPD.
Antibiotics
Current evidence does not support long-term antibiotic use to prevent exacerbations
in COPD131-132. However antibiotics should be used in exacerbations with an
increase in cough, dyspnoea, sputum volume or purulence (see Section X).
Glucocorticoids
High-dose inhaled corticosteroids may reduce the rate of acute exacerbations and
slow the rate of decline of quality of life (see Section O page 28 and Section X page
77) in patients with severe COPD and frequent exacerbations. However the risks of
adverse effects versus potential benefits must be carefully considered and regular
review is recommended with cessation of therapy if no benefit is seen (see Section
O, page 30).
Mucolytics in COPD
People with COPD frequently complain of chronic productive cough. For some,
difficulty in expectorating sputum can be distressing and fatiguing. During
exacerbations, infective or otherwise, sputum may increase in volume and become
purulent.
Drugs that modify the physicochemical
Mucolytics may reduce the
properties of sputum to assist expectoration
frequency and duration of
may play a useful role in some patients with
exacerbations.
COPD. Examples of mucolytic agents include
bromhexine, N-acetylcysteine, ambroxol,
potassium iodide and glycerol guaiacolate. Few side effects have been reported and
mucolytic drugs are generally considered safe.
Some patients do respond to mucolytic agents but criteria for predicting such a
response have not been established. A clinical trial in selected patients, documenting
lung function and symptoms, is justified for patients with difficulty expectorating
sputum.
A Cochrane Review133 concluded that in subjects with COPD or chronic bronchitis
and a higher than average rate of exacerbations, treatment with mucolytic agents
was associated with a small reduction in acute exacerbations and total number of
days of disability. However this finding may not apply to all patients with COPD.
49
Regular Review
Monitor disease progression and development of complications
COPD is usually a progressive disease, and a patientÕs lung function can be
expected to worsen over time, even with the best available care. Symptoms and
objective measures of airflow limitation should be monitored for development of
complications that worsen prognosis, and to determine when to adjust therapy.
·
·
·
·
·
·
Follow-up visits should include a discussion of new or worsening symptoms.
Spirometry should be performed if there is a substantial increase in symptoms
or a complication, and annually to determine rate of disease progression.
Measurement of arterial blood gas tensions should be performed in all
patients with an FEV1<40% predicted, or clinical signs of respiratory failure or
right heart failure.
Elevation of the jugular venous pressure and pitting ankle oedema are signs
of right heart failure.
Screen for daytime or nocturnal hypoxaemia if signs of right heart failure.
Check for recent weight loss.
Monitor pharmacotherapy and other medical treatment
In order to adjust therapy appropriately as the disease progresses, each follow-up
visit should include a discussion of the therapeutic regimen to which the patient is
currently adhering. Dosages of various medications, adherence to the regimen,
inhaler technique, effectiveness of the current regimen at controlling symptoms, and
side effects of treatments should be monitored.
Monitor exacerbation history
Frequency, severity, and likely causes of exacerbations should be evaluated.
Increased sputum volume, acutely worsening dyspnoea, and the presence of
purulent sputum should be noted. An exacerbation is suggested by an increased
need for bronchodilator medication or glucocorticoids and by the need for antibiotic
treatment. Hospitalisations should be documented including the facility, duration of
stay, and any use of critical care or intubation.
Monitor comorbidities
In treating patients with COPD, consider the presence of concomitant conditions
such as bronchial carcinoma, tuberculosis, sleep apnoea and left heart failure. The
appropriate diagnostic tools (such as chest radiograph, ECG) should be used
whenever symptoms (e.g. haemoptysis) suggest one of these conditions.
Home Oxygen Therapy
Indications
Home oxygen therapy is one of the principal non-pharmacologic treatments for
patients with severe COPD. Apart from smoking cessation, domiciliary oxygen is the
only therapy shown to reduce mortality in COPD11-12,134-136. Although effective, it is a
potentially expensive therapy that should only be prescribed for those in whom there
is evidence for benefit.
Oxygen therapy can be administered as long-term continuous, intermittent or
nocturnal therapy.
50
Long-term continuous oxygen therapy
Long-term continuous oxygen therapy (at least
15 hours a day) is appropriate for patients who
Long-term oxygen greater
have PaO2 consistently less than or equal to
than 15 hrs/day prolongs life
55mm Hg (7.3kPa) when breathing air, at rest
in hypoxaemic patients
and awake. If oxygen is prescribed when
PaO2<55 mmHg (7.3 kPa).
unstable (e.g. during an exacerbation) then the
requirement for it should be reviewed four to
eight weeks after initiation. At assessment, the patient's condition must be stable and
all potentially reversible factors treated. The assessment should be made at least
one month after the patient has stopped smoking because gas exchange may
improve substantially on cessation.
Polycythaemia (Hb >170gm/L), clinical or ECG evidence of pulmonary hypertension,
as well as episodes of right heart failure, are consistent with the systemic effects of
chronic hypoxaemia and strengthen the case for therapeutic use of oxygen. Patients
with these complications should be prescribed continuous oxygen if their stable PaO 2
is 55-59 mmHg (7.3-7.9kPa). Continuous oxygen therapy is of most benefit for
patients with increased arterial PaCO2 (>45 mm Hg or 6kPa)12.
As well as prolonging life, long-term oxygen therapy may have a beneficial impact on
haemodynamics, haematologic characteristics, exercise capacity, lung mechanics
and mental state136. In order to maximise the number of hours per day of oxygen
usage, portable oxygen may be advisable for long-term oxygen therapy users,
depending on their circumstances.
Government funding is on the basis of an approved prescriber (usually a Respiratory
Physician). Oxygen is usually supplied free in Australia and in New Zealand
topatients meeting the criteria.
Intermittent oxygen therapy
Available evidence does not allow any firm conclusions to be made concerning the
effectiveness of intermittent ambulatory domiciliary oxygen therapy137 in COPD,
however, use of intermittent oxygen may be considered for:
·
people for whom supplementary oxygen improves exercise capacity. The
benefit cannot be predicted by a resting test. Acute benefit may be
established by comparing exercise endurance when breathing oxygen and
when breathing air, using a treadmill, stationary bicycle or six-minute walk
test.
·
Patients living in isolated areas or prone to sudden life-threatening episodes
while they are awaiting medical attention or evacuation by ambulance.
·
Patients undertaking air travel. Flying is generally safe for most patients with
chronic respiratory failure who are on long-term oxygen therapy. However,
patients should be instructed to increase the flow by 1-2 L/min during the
flight. Ideally, patients who fly should be able to maintain an in-flight PaO2 of
at least 50 mm Hg (6.7 kPa). Careful consideration should be given to any
comorbidity that may impair oxygen delivery to tissues, such as cardiac
impairment. Exertion during flight may aggravate hypoxaemia.
51
Nocturnal oxygen therapy
The use of nocturnal oxygen therapy may be
indicated in patients with nocturnal
hypoxaemia (i.e. without daytime hypoxaemia
or obstructive sleep apnoea) whose nocturnal
arterial oxygen saturation repeatedly falls
below 88% [Evidence level D].
Hypoxaemia during sleep
should be distinguished from
sleep apnoea caused by upper
airway obstruction or impaired
drive to breathe, which require
other forms of therapy.
Nocturnal hypoxaemia may be suspected in
patients whose arterial gas tensions are
satisfactory when awake, but who have daytime somnolence, polycythaemia or right
heart failure. Sleep apnoea should be excluded as the appropriate therapy might be
continuous positive airway pressure or nocturnal intermittent positive pressure
ventilation.
Contraindications
Supplementary oxygen is not indicated for:
·
Patients with severe airflow limitation whose main complaint is dyspnoea, but
who maintain a PaO2 greater than 60mm Hg (8kPa) and who show no secondary
effects of chronic hypoxia.
·
Patients who continue to smoke cigarettes, because of the increased fire risk and
the probability that the poorer prognosis conferred by smoking will offset
treatment benefit.
Initiating oxygen therapy
Before introducing oxygen therapy, ensure optimal treatment of the pulmonary
disorder while monitoring improvement with objective tests such as FEV1 and vital
capacity. Treatment may include maximum therapy for airway obstruction, attention
to nutrition and body weight, an exercise rehabilitation program, control of infection
and treatment of cor pulmonale.
In patients selected for oxygen therapy, assess the adequacy of relief of hypoxaemia
(PaO 2 >60mm Hg (8kPa), SpO2 >90%) and/or improvement in exercise capacity or
nocturnal arterial oxygen saturation while using a practical oxygen delivery system.
What the patient needs to know
Patients receiving oxygen therapy in the home, and their carers, should have the
prescription clearly explained in terms of hours of use, flow rate, and the need to vary
flow rates at given times. The equipment, its care, and how to obtain servicing or
replacements requires explanation. The dangers of open flames (especially
cigarettes, gas heaters and cookers) needs to be emphasised.
Flow should be set at the lowest rate needed to maintain a resting PaO2 of 60 mm
Hg (8kPa) or SpO2 >90%. For COPD patients 0.5 Ð 2L/min is usually sufficient. It
should be increased by 1L/min during exercise.
Humidifiers are generally not needed at oxygen flow rates below 4L/min.
Extrasoft nasal prongs are recommended for continuous oxygen use, but may
become uncomfortable at flow rates over 2-3 L/min and in the long term. Facemasks
52
may be preferred for at least some of the time, although there are theoretical dangers
of rebreathing exhaled CO2 at flow rates below 4 L/min.
In selected patients needing 24-hour oxygen therapy, transtracheal delivery systems
may have advantages, though these need to be weighed against the need for
frequent stoma care and secretion control.
Review
Reassess four to eight weeks after starting continuous or nocturnal oxygen therapy,
both clinically and by measurement of PaO2 and PaCO 2 with and without
supplementary oxygen. A decision can then be made as to whether the treatment
has been properly applied and whether it should be continued or abandoned.
Undertake subsequent review at least annually,
or more often according to the clinical situation.
Some patients will show a sustained rise in
PaO2 to >60 mm Hg (8kPa) when breathing air,
but current thinking suggests this should not
necessarily be a rationale for stopping therapy.
One-month review: confirm
low PaO2 (55mm Hg or
7.3kPa)
Periodic assessment is also recommended for patients on intermittent oxygen
therapy. The review can be undertaken by appropriately trained outreach staff using
a pulse oximeter to confirm hypoxaemia (SpO2<88%) at rest or during daily activities.
They should also check compliance with therapy and smoking status.
Dangers
Supplementary oxygen in patients with increased arterial PaCO 2 may theoretically
depress ventilation, increase physiological dead space, and further increase arterial
PaCO2.
However with long-term low flow oxygen therapy, any increase in arterial PaCO 2 is
usually small and well tolerated.
Sedatives (particularly benzodiazepines), narcotics, alcohol and other drugs that
impair the central regulation of breathing should generally be avoided in patients with
hypercapnia receiving oxygen therapy.
Choosing the right method
Domiciliary oxygen therapy can be delivered
via three systems:
·
The prescription should
always include the source of
supplemental oxygen (gas or
liquid), method of delivery,
duration of use, and flow rate
at rest, during exercise and
during sleep.
Cylinders: These contain compressed
pure oxygen gas and deliver 100%
oxygen at the outlet. Several portable
lightweight cylinders are available
which allow the patient to leave home
for several hours. Electronic
conservation devices are available to trigger oxygen supply on demand
resulting in up to a four-fold reduction in oxygen consumption. Reservoir style
conservers provide similar conservation rates and are a cost effective
alternative (no ongoing fixed cost) that likewise promote convenience by
prolonging cylinder duration.
53
·
Oxygen concentrators: These are floor-standing devices that entrain room
air, extract the nitrogen in molecular sieves and deliver oxygen at the outlet.
They run off electricity. Most of these units deliver 90-95% oxygen at the
outlet when operating at a flow rate of 2 L/min. The percentage falls with
increasing flow rate to about 78% oxygen at 5 L/min, depending on the
model. All units currently available in Australia are imported. A back-up
standard D-size oxygen cylinder may be added in case of concentrator
breakdown or power failure, but adds to the cost and is rarely necessary.
·
Liquid oxygen systems: These systems conserve space by storing oxygen
in liquid form. The oxygen is delivered through coils, where it vaporises. Two
tanks are needed: a large storage tank, which is filled by the supplier as
required (e.g. one unit is equivalent to seven E-size cylinders), and a portable
unit filled from the larger tank for ambulatory use. Ê
Which system is the best?
There is no significant difference in the quality of oxygen delivery among the above
methods, however:
· Concentrators are cheaper than cylinders if use is equivalent to or greater than
three E-size cylinders per month, but electricity costs must be considered.
·
Concentrators can be wheeled around the home but are heavy (about 21-26 kg)
and are difficult to move up stairs and in and out of cars.
·
Concentrators cannot be used for nebulisation, as the pressure delivered is too
low (35-63 kPa, compared with 140 kPa for nebuliser pumps).
·
If the anticipated need is for longer than three years, it is cheaper to buy than to
rent a unit. The units usually have a five -year guarantee. However in each state
of Australia there are specific arrangements for the provision of oxygen therapy to
public patients. More detailed information can be obtained through the respiratory
units at large public hospitals.
Fitness to Fly
Commercial aircraft operate at altitudes of up to 12,500m where outside pressure is
less than 25% that at sea level. Cabins are pressurised to 2100-2400m. At this
ÒaltitudeÓ the alveolar PaO2 for healthy individuals reduces from 103mm Hg
(13.7kPa) to 64mm Hg (8.5kPa) and O2 saturation declines from 97% to 93%. Any
pre-existing hypoxaemia will substantially worsen at altitude. Patients with borderline
hypoxemia at sea level will operate on the steep section of the O2 dissociation curve
when at altitude and thus any further fall in PaO2 will be associated with a marked fall
in oxygen saturation/content.
Who requires supplemental oxygen during flight?
Exercise tolerance determined by walking distance correlates poorly with PaO 2 and
this is unsuitable as a predictor. Oximetry is unlikely to be helpful because the
variation in O2 saturation measured by oximetry equates to a very wide range of
PaO2; a variety of factors including PaCO2 and pH cause shifts in the O2 dissociation
curve. As a general rule however if resting O2 is ³ 95%, supplemental oxygen is
unlikely to be required and if O2 saturation £ 88%, supplemental oxygen is likely to be
required.
Before flying patients should ideally be clinically stable. The patient recovering from
an acute exacerbation is particularly at risk. Those already on long-term oxygen
54
therapy need an increase in flow of 1-2 L/min during flight. Careful consideration
should be given to any comorbidity which may impair tissue oxygen delivery eg.
cardiac impairment, anaemia.
The American Thoracic Society currently recommends that PaO2 during air travel
should be maintained at >50mm Hg (6.7kPa). PaO2 measured on the ground at sea
level (PaO2) is the most reliable value for predicting during flight (PaO 2 alt). PaO2 alt
can be estimated from PaO2 using published nomograms developed on the basis of
hypoxic testing (F1 O 2 =15%) at sea level. Based on these nomograms, if PaO2
<70mm Hg (9.3kPa), PaO2 alt for 2300m is <50mm Hg (6.7kPa). The natural
conclusion is that all patients with PaO2 <70mm Hg (9.3kPa) at rest at ground level
should receive supplemental O2.
Many lung function laboratories perform assessments for fitness to fly. These may
include measurement of ABGs or O2 saturation while breathing a mixture of 15%
oxygen and 85% nitrogen.
Fitness for Surgery
Postoperative respiratory complications are a common clinical problem that can
extend hospital stay significantly (see Figure 17). These complications include
pneumonia, respiratory failure with mechanical ventilation, bronchospasm,
atelectasis and exacerbation of any underlying chronic lung disease, including
COPD.
Figure 17. Risk factors for postoperative respiratory complications
Factor
Risk of Respiratory
Action
Complication
Patient-related
COPD
Increases risk for unselected surgery
3.0 fold and for thoracic or abdominal
surgery 4.7 fold.
Smoking
Increases risk 3.4 fold.
Age >70 years
Risk related to comorbidities
General health status
Poor health increases risk 1.7 fold.
Combinations of
bronchodilators,
physiotherapy, antibiotics,
smoking cessation and
glucocorticoids reduce
respiratory complications.
This is notable even in the
absence of COPD. Risk
reduction greatest if
smoking ceased six weeks
preoperatively.
Risk is less if co-existing
disease (particularly
cardiac) is controlled for.
Evaluate using
standardised Goldman or
American Society of
Anaesthesiologists Risk
Indices or simple clinical
exercise testing.
55
Asthma
Not a risk factor if have a stable lung
peak flow measurement, greater than
80% of personal best and currently
free from wheeze or night symptoms.
Obesity
Not a proven risk factor other than a
predictor of comorbidity.
Can use a brief course of
prednisolone
pre-operatively (e.g. four
days of 50mg daily) with no
increase in post-operative
complications.
Check for diabetes, sleep
apnoea, hypertension.
Procedure-related
Surgical incision
Surgery >3hours
Long-acting
neuromuscular
blockers
(pancuronium)
General anaesthesia
Narcotic analgesia
Increased risk up to 10 fold as the
incision approaches the diaphragm.
Increases risk 3 fold.
Increases risk 3 fold.
Probably increases risk slightly over
spinal/epidural anaesthesia.
Hypoventilation
Laparoscopic procedures
preferable if high risk.
Optimise peri- and postoperative respiratory
support.
Optimise peri- and postoperative respiratory
support.
Avoid general anaesthesia
if possible in high-risk
patients.
Epidural infusion
Preoperative assessment and preparation
Respiratory assessment prior to surgery addresses the wisdom of operating in an
individual patient at that time. Exclude from surgery patients who face major risks of
morbidity or mortality in the postoperative period and those patients whose quality of
life would be severely compromised should the operation proceed.
Some practical examples include:
·
A patient with severe emphysema and recurrent diverticulitis needing semielective hemicolectomy. The risk is extended high dependency and
postoperative respiratory failure related to broncho-pulmonary infection.
·
Resectable lung cancer in a patient with very poor lung function. A curative
operation might be performed technically well but the loss of lung function
may lead to an unacceptable quality of life.
The issues related to surgical risk should be identified at the same time as the need
for surgery. Unless the COPD is known to be mild in severity based on symptoms
and lung function, a specialist assessment is recommended.
History
Ask about cough, sputum, breathlessness, smoking, heart or lung disease, problems
after previous surgery or anaesthesia. If history of lung disease, smoking or
unexplained dyspnoea, define and treat lung disease to reduce risks rather than
exclude surgery.
Examination
Heart and lungs in detail.
Lung function tests
The impact of lung function impairment will vary greatly depending on the surgery
planned. This will be influenced by any significant co-morbidity.
56
·
Assessment of the impact of lung function on safety of lung surgery is a
complex task. Surgery may be possible in some patients with very severe
lung function abnormality. No patient should be denied the opportunity for
lung cancer resection without specialist assessment.
·
Lung resection is possible if the predicted post-op FEV1 and DLCO are > 40%
predicted.
·
Limits of operability can be extended if eligible for lung reduction surgery.
·
Predicted post-op. FEV1 = Pre-op. FEV1 X (1 minus proportion of lung to be
resected) (see Figure 18).
Figure 18. Proportions to be used in calculating the effect of lung
resection
Lung or Lobe for
Resection
Whole lung
Upper Lobe
Middle Lobe
Lower Lobe
Right Side
0.53
0.16
0.11
0.26
Left Side
0.47
0.26 (+ Lingula)
0.21
N.B. Can refine the fraction with quantitative radionuclide lung scanning. Fractions do not apply
to LVRS
·
·
No firm guidelines exist for operability before cardiac surgery and upper
abdominal surgery but FEV1 useful. Lower morbidity if FEV1 >1L or >30% of
predicted.
Recommended before other surgery only in selected patients
ABGs
Not needed routinely but indicated if severe COPD (FEV1 < 40% predicted).
Increased morbidity if PaCO2 > 45 mm Hg (6kPa).
Integrated cardiopulmonary exercise testing
Peak oxygen uptake and anaerobic threshold can be measured from this incremental
testing procedure. Operations that are associated with a metabolic stress in excess
of the anaerobic threshold appear to pose undue risk for intra- or post-operative
mortality or prolonged post-operative recovery.
Smoking cessation
All current smokers who are being prepared for elective general anaesthetics must
be counselled about the risks of smoking and benefits of quitting. The greatest
reduction in post-operative respiratory morbidity/mortality is achieved by cessation at
least six weeks prior to surgery. In many cases, surgery is urgent or semi-urgent and
lesser periods of cessation must be accepted. In urgent cases, it may be necessary
to acknowledge the increased risk but proceed with the operation nonetheless.
Control of sputum
Independent of lung function, sputum production is a risk factor for postoperative
respiratory infection. Therapy should be optimised in the preoperative period.
Patients should be taught appropriate sputum clearance techniques and breathing
techniques with the aim of optimising lung function pre-operatively and minimising
post-operative respiratory complications such as atelectasis and sputum retention.
Post-operative complications may also be minimised by using large volume
ventilation and avoiding excessive FiO2 intra-operatively.
57
Effect of nature of surgery
For abdominal procedures, risks are greater with upper versus lower, and horizontal
rather than vertical incisions. Minimally invasive surgery with smaller incisions should
reduce the pain stimulus that limits respiration and cough and therefore improve
outcomes. This is partially balanced by the fact that procedures may be longer and
there is a longer period for development of intraoperative atelectasis. Induced
pneumoperitoneum increases the potential for development of intraoperative
atelectasis.
Management of postoperative COPD patient
During general anaesthesia, ventilation is controlled and oxygen delivery can be
easily maintained. Few patients with COPD will have respiratory difficulties,
irrespective of the severity of their lung disease.
Some patients because of the severity of their lung disease and/or the nature of the
surgical procedure will be electively managed in an intensive care setting. For
patients who return to ward care, this is the critical period. The general principles are:
·
Optimal analgesia - Most major centres use patient controlled analgesia
supervised by an integrated pain control team including an anaesthetist and
specialist nurse. Some patients will benefit from supplementary epidural
analgesia, as this will limit the total systemic narcotic dosing.
·
Clearance of secretions - For patients who regularly expectorate,
physiotherapy emphasising deep respiration and cough cycles is useful.
Percussion chest drainage is of questionable value. Patients lying on their
side may experience further derangement of V/Q relationships and it is good
practice to have patients use oxygen by nasal prongs in this situation.
Incentive spirometers can be used to encourage full inspiration to overcome
atelectasis but their effectiveness has not been well established.
·
Early mobilisation - This should be emphasised and patients should be
advised pre-operatively that they will be mobilised as soon as possible in the
post-operative period. Sitting out of bed is preferred to lying supine in a
hospital bed. All patients with COPD should have appropriate prophylaxis
against DVT according to the local practice.
·
Discharge planning and later care - Many COPD patients do not have a
physically able spouse or carer. For efficient, effective care the discharge
planning process should commence prior to admission. Almost all significant
procedures will be associated with deconditioning that will limit exercise
capacity to a level often much below that prior to surgery. Where this is
significant, rehabilitation should be part of the discharge plan.
58
D
DEVELOP SUPPORT NETWORK AND SELF-MANAGEMENT PLAN
COPD imposes a handicap which affects both patient and carers.
These carers are sometimes under great strain105-108.
Enhancing quality of life and reducing handicap requires a support
team.
The patient and their family/friends /whanau (NZ) should be actively
involved in a therapeutic partnership with a range of professional
disciplines90,105-108.
Patients should be encouraged to take appropriate responsibility for
their own management146-148.
Multidisciplinary* care plans and individual self-management plans may
help to prevent or manage crises149.
B
C
C
C
C
B
AIMS
RECOMMENDATIONS/ACTIONS
LEVEL
Assess individual's resources and
support and provide improved support
network
Provide access to community based
resources
Minimise barriers to accessing
healthcare
Consider multidisciplinary case
conference
Enrol in pulmonary rehabilitation
program
Educate patient and carers as
appropriate
Develop multidisciplinary care plan*
Enrol in respiratory support group
Assess cognitive and coping abilities
Educate patients and carers as
appropriate
Treat anxiety, panic and depression
Enrol in Pulmonary Rehabilitation
Program
Ensure optimal use of inhaler devices
/ oxygen delivery devices
Develop self-management plan for
maintenance therapy
Develop self-management plan for
acute exacerbations
Include crisis medication pack and
appropriate support
D
Increase patient/carer knowledge
base and reduce patient/carer strain
Improve patient coping skills and self
management behaviour and develop
positive patient attitudes to selfmanagement and exercise
Reduce frequency of exacerbations
and hospitalisations
C
D
A
B
D
C
B
B
D
A
B
D
B
C
* may include: general practitioner, respiratory physician, district or outreach nurse,
respiratory educator, physiotherapist, occupational therapist, social worker, clinical
psychologist, speech therapist, pharmacist, dietitian, oxygen service personnel, nonmedical care.
59
Impact on patient and carer
In the early stages of disease, COPD patients will often ignore mild symptoms. As
the disease progresses impairment and disability increase. In addition, common
complications emerge including depression, anxiety, panic disorder, social isolation,
cor pulmonale, polycythaemia, osteoporosis, proximal and ventilatory myopathies,
upper airway obstruction and altered ventilatory control.
Concurrent conditions commonly seen in
patients with COPD include coronary artery
disease, diabetes, cerebrovascular disease,
dementia and degenerative joint disease.
As a health state, severe
COPD has the third highest
perceived ÔseverityÕ rating, on
a par with paraplegia and
first-stage AIDS 1.
People with chronic conditions are usually
cared for by partners or family members. In
non-respiratory populations, there is evidence that the psychological health status of
carers and patients are linked. Levels of loneliness, social isolation and depression
were similar among carers and their patients.
The quality of care received by the patient from
family carers is linked with the health of the
carer, so that carer health status has been
found to be associated with rates of health care
utilisation.
Carers are critical to and
bound up in care of
respiratory patients: this
results in physical and
emotional health problems.
Assess and improve individual’s supports
Enhancing quality of life and reducing handicap requires a support team (which may
include the GP, a respiratory specialist, specialist nurses and a range of other health
professionals, both from hospitals and in the community).
GP’s role
The GP plays a central role in the management of COPD. As the primary health
provider the GP is uniquely placed to identify smokers and help them quit, diagnose
COPD in its early stages and coordinate care as the disease progresses.
(i)
Smoking cessation
A doctorÕs advice is an important motivator for smoking cessation, especially
if from the family physician. The GP can help initiate the cycle of change by
repeated brief interventions. There are several smoking cessation programs
that have been developed for use in general practice. The GP is also the
appropriate health professional to recommend or prescribe nicotine
replacement therapy and/or pharmacological treatment of nicotine addiction
(for a detailed discussion of smoking cessation interventions see Section P,
page 45).
(ii)
Early diagnosis
The GP is in the most favourable position
to make an early diagnosis of COPD.
Most people visit a GP approximately
annually. Simple questions relating to
daily
cough
and
degree
of
breathlessness should lead to lung
function testing, either at the GP practice
or in a nearby lung function laboratory.
A history of chronic or
recurrent bronchitis,
exertional dyspnoea and/or a
significant smoking history
(>15 pack years) should alert
the GP to the need for
spirometry (see Section C,
page 16).
60
(iii)
Coordinate investigation and management
The GP will manage patients with mild and moderate COPD. Referral to a
consultant respiratory physician may be indicated to confirm the diagnosis,
exclude complications and aggravating factors, and to contribute to a selfmanagement plan (see Figure 19 below and page 67 for Self-management
Plans).
(iv)
Coordinate care in advanced disease
The GP plays a crucial role in the overall medical management of patients
with advanced COPD including terminal care and grieving, and helps to
coordinate a range of services provided by a multidisciplinary team of health
professionals and care agencies.
Respiratory specialist’s role
Although the long-term management of most persons with COPD will take place in
primary care, there are advantages associated with review by a respiratory specialist,
particularly for people with moderate to severe disease.
Respiratory specialists may be able to facilitate patient access to pulmonary
rehabilitation, and generally are responsible for decisions regarding long-term oxygen
therapy, lung volume reduction surgery, lung transplantation, investigation of
ventilation during sleep and prescription of non-invasive positive pressure ventilation.
Figure 19. Indications for referral to respiratory specialist
Factors requiring
Role of respiratory specialist
specialist review
Moderate/severe COPD
Uncertain diagnosis
· <10 pack year smoking
or
· <40 years of age
or
· rapid decline in FEV1
-
Confirm diagnosis and optimise therapy
Stop inappropriate/ ineffective therapies
Assess side effects
Determine need for nebulised therapy
-
Assess complications
-
Confirm diagnosis and exclude other diagnoses e.g.
asthma, pulmonary embolism, cancer, heart failure,
pneumothorax, anaemia
Determine other aetiologic factors
Determine if predisposed e.g.alpha-1 antitrypsin
deficiency
Exclude other conditions e.g. bronchiectasis, cystic
fibrosis, immunologic abnormality, aspiration
Exclude complications of COPD or comorbidities e.g.
pulmonary hypertension, cardiac disease
Consider sleep study
Confirm diagnosis and optimise treatment including
assessment for oxygen or other ventilatory support
Confirm chronic hypoxaemia or nocturnal
hypoxaemia
Assess for ambulatory oxygen therapy
Determine suitability for bullectomy or lung volume
reduction surgery
Determine suitability for LVRS or lung transplantation
or home ventilation
Consider referral to palliative care
-
Recurrent infections
Exacerbations
Symptoms/disability out of
proportion to lung function
impairment
Cor pulmonale
-
Suspect chronic hypoxaemia
-
Bullous lung disease/severe
emphysema
Severe disability/respiratory
failure
-
-
61
The multidisciplinary team
In advanced disease the many comorbidities, social isolation and disability mean that
a multidisciplinary approach to coordinated care may be appropriate. Many health
professionals are in an ideal situation to detect patients who smoke, and assist them
in quitting. In addition to the GP and respiratory specialist, the multidisciplinary team
may include:
Nurse/respiratory educator
Specific aspects of care provided by the nurse in COPD may include:
· Respiratory assessment including spirometry and pulse oximetry
· Implementation or referral for interventions such as smoking cessation, sputum
clearance strategies, oxygen therapy
· Skills training with inhalational devices
· Education to promote better self-management, eg medications and response to
worsening of symptoms
· Organisation of multidisciplinary case conferences and participation in care plan
development
· Assessment of home environment
Physiotherapist
Physiotherapists are involved in a broad range of areas including exercise training,
sputum clearance, breathing retraining, mobility, non-invasive positive pressure
ventilation, post-operative respiratory care (e.g. post LVRS), and assessment and
treatment of musculoskeletal disorders commonly associated with COPD.
Occupational therapist
The occupational therapist provides specific skills in task optimisation and
prescription of adaptive equipment and home modifications. Some therapists also
teach energy conservation for activities of daily living and can help in the set-up of
home and portable oxygen.
Social worker
Social workers can provide counselling for patients and their carers, organisation of
support services, respite and long-term care.
Clinical psychologist
Anxiety and depression are common comorbidities in patients with COPD. Panic
disorder is also frequent and disabling out of proportion to the impairment of lung
function. Clinical psychologists can assess and employ techniques such as
counselling and cognitive behavioural therapy to help address anxiety and
depression.
Speech pathologist/therapist
Speech pathologists can be involved in the assessment and management of
recurrent aspiration, swallowing and eating difficulties due to shortness of breath, and
dry mouth associated with some pharmaceuticals, age and mouth breathing.
Pharmacist
Pharmacists, both in the community and in hospitals, are involved in education about
medications and supply of medications. They can help smokers quit by advising
about nicotine replacement and counsel patients requesting over-the-counter
salbutamol. They are well placed to monitor for medication problems and
complications and suggest solutions (eg individual dosing dispensers). There is an
EPC item number for GPs involved in medication review by a pharmacist (Item 900).
Further information is available at www.health.gov.au/epc/dmmr .
62
Dietitian
Significant weight-loss is a common problem for patients with end stage COPD.
Conversely, obesity in patients with COPD is associated with sleep apnoea, CO2
retention and cor pulmonale. Dietitians can educate on nutrition and prescribe diets
and supplements specific to the needs of the individual.
Non-medical care agencies
Many COPD patients have difficulties with activities of daily living (ADLs) and may
require a range of non-medical support services, including governmental and nongovernmental organisations. Availability of services and organisational structure vary
between states and between areas within states (e.g. urban, rural, remote). Some
examples include:
· Financial support and organisation of oxygen, CPAP, nebulisers, etc
· Homecare
· Government supported assistance with ADLs (showering, cleaning, shopping,
etc)
· Home maintenance
· Meals on wheels
· Exercise programs
· Support groups
Develop multidisciplinary care plan/ case conference
A multidisciplinary care plan is a documentation of the various medical, paramedical
and non-medical services required to keep a patient functioning in the community.
Various generic and disease specific proformas are available (see
www.lungnet.com.au/copd.html for examples). Also check with local Division of GPs,
Alliance of Divisions, etc.
The care plan may be initiated in the context of
a multidisciplinary case conference involving the
GP and at least two other health professionals
(one of whom is not a doctor). The remuneration
varies depending on the level of involvement of
the GP and the location of the patient.
EPC item numbers are
available to support GP
involvement in care plan
development.
GP involvement in case conferences is supported by EPC item numbers (see below)
that also vary according to the level of involvement of the GP and the location of the
patient. The GP may participate by telephone. A consultant physician is also entitled
to claim rebates for organising or participating in a case conference (Item numbers
801-815).
Item numbers for GP involvement in care plans and case conferences appear in the
table below. Further information is available at www.health.gov.au/epc .
Figure 20. Enhanced Primary Care Item Numbers
Item 720
Item 722
Item 724
Item 726
Item 728
Multidisciplinary care plan item numbers
Preparation of a multidisciplinary community care plan
Preparation of a multidisciplinary care plan
Review of a community care plan or discharge care plan claimed for under 720 or 722
Contribute to a multidisciplinary community care plan or review a multidisciplinary
community care plan prepared by another provider
Contribute to a multidisciplinary discharge care plan or review a multidisciplinary
discharge care plan prepared by another provider
63
Item 730
Contribute to a multidisciplinary care plan in a residential aged care facility or review a
multidisciplinary care plan in a residential aged care facility
Multidisciplinary case conference item numbers
Residential aged care facility
Task: Organise, coordinate and attend a case conference at a residential aged care facility (not
being a service associated with a service to which item 730 applies)
Item 734
15-30 minutes
Item 736
30-45 minutes
Item 738
>45 minutes
Task: Participate in a case conference at a residential aged care facility (not being a service
associated with a service to which items 720-730 applies)
Item 775
15-30 minutes
Item 778
30-45 minutes
Item 779
> 45 minutes
Community
Task: Organise, coordinate and attend a community case conference (not being a service
associated with a service to which items 720-730 applies)
Item 740
15-30 minutes
Item 742
30-45 minutes
Item 744
> 45 minutes
Task: Participate in a community case conference (not being a service associated with a service
to which items 720-730 applies)
Item 759
15-30 minutes
Item 762
30-45 minutes
Item 765
> 45 minutes
Discharge
Task: Organise, coordinate and attend a discharge case conference (not being a service
associated with a service to which items 720-730 applies)
Item 746
15-30 minutes
Item 749
30-45 minutes
Item 757
> 45 minutes
Task Participate in a discharge case conference (not being a service associated with a service to
which items 720-730 applies)
Item 768
15-30 minutes
Item 771
30-45 minutes
Item 773
> 45 minutes
Increase Knowledge and Reduce Strain
Educate patients and carers
Health education can play a role in improving skills, ability to cope with illness and
health status105-108. Educational messages should be incorporated into all aspects of
COPD care and may take place in many settings.
Education should be:
· tailored to the needs and environment of the individual patient
· interactive
· directed at improving quality of life
· simple to follow
· practical
· appropriate to the intellectual and social skills of the patient and the care
givers.
Health professionals should discuss patientsÕ fears and apprehensions and issues
affecting adherence, focus on educational goals (see figure 21), tailor treatment
64
regimens to each individual patient, anticipate the effects of functional decline and
optimise the patientÕs practical skills.
In COPD, compliance refers not only to pharmacologic treatments but also to
maintaining an exercise program after pulmonary rehabilitation, undertaking and
sustaining smoking cessation, and using devices such as nebulisers, spacers and
oxygen concentrators properly. Education is most effective when it is interactive and
conducted in small workshops110 (see also Section O, pulmonary rehabilitation, page
39).
Figure 21. Suggested COPD patient education topics
Mild to moderate COPD
Severe COPD
Information and advice re: risk factor reduction
Information about nature of COPD
Instructions on how to use inhalers and other
treatments
Recognition and treatment of acute
exacerbations
Strategies for minimising dyspnoea
Strategies to optimise or correct nutrition status
Benefits of exercise
Support groups
Above topics plus:
Information about complications
Information about oxygen treatment
Advance directives and end-of-life decisions
Task optimisation for ADLs
Maintenance of nutrition
Adapted from Global Strategy for the Diagnosis, Management and Prevention of Chronic Obstructive
6
Pulmonary Disease, NHLBI/WHO workshop report .
Refer to a support group
Psychiatric morbidity is high in people with severe COPD and in many instances
requires more than a prescription aimed at symptom relief. Many patients and their
families are left alone to cope with the functional and emotional difficulties caused by
this irreversible and progressive disease which can severely impair their quality of
life.
Patients who receive education and
psycho so cia l su p p o r t sh ow greater
Health professionals should
improvements in more aspects of health-related
encourage patients to join a
quality of life than those who receive education
support group.
with no ongoing support. One way in which this
aim can be achieved is through patient support groups. Support groups aim to
empower patients with COPD to take a more active role in the management of their
health care and thus reduce the psychosocial impact of their condition.
Figure 22. Patient Support Groups
Typical support group
activities
Regular meetings
Expert guest speakers on COPD topics
Telephone calls, hospital and home visits
Receive and distribute lung health education information
Special seminars and patient programs
Social outings
Rehabilitation assistance and maintenance of exercise
Social enjoyment
65
Benefits of support groups
Reinforce and clarify information learnt from health
professionals
Access new information on lung health
Share experiences in a caring environment
Empower patients to be more actively involved in their
health care, through self-management techniques
Participate in social activities and exercise programs
Encourage patients to think more positively about their lung
disease
Help carers understand lung disease
Improve Coping Skills and Self Management Behaviour.
Develop Positive Attitudes to Self-Management and Exercise.
Reduce Frequency of Exacerbations/Admissions.
Assess cognitive and coping abilities90,105-108
Hypoxic COPD patients often have neuropsychological deficits suggestive of cerebral
dysfunction. The deficits are in the areas of verbal and visual short-term memory,
simple motor skills, visuomotor speed and abstract thought processing. COPD
patients can also develop social phobia, the fear and anxiety of being evaluated
negatively by other people, which leads to feelings of inadequacy, embarrassment,
humiliation and depression. Dyspnoea, coughing, heavy breathing, oxygen cylinders
and taking of medication in public can embarrass COPD patients. Cognitive
impairment may be assessed using the Mini Mental State test (available from
www.mhsfopcls.com/downloads/mmse.pdf). Coping abilities may be assessed using
the Jalowiec Coping Scale or the Ways of Coping Questionnnaire (WAYS).
Treat anxiety and depression149
The strong relationship between anxiety and
COPD has long been established. One report
Identification of individuals at
suggested that as many as 67% of patients with
risk for clinical anxiety and
COPD will develop panic disorder, a figure that
effective interventions for
is at least 10 times greater than in the general
treating panic disorder in
population. Anxiety symptoms lead to repeated
COPD should be priorities.
presentations for hospital admission for many
patients, at a significant financial cost. Current models of anxiety disorders would
predict that COPD is likely to be associated with high rates of panic disorders due to
changes in breathing and heart rate being interpreted as threatening and potentially
harmful. Identification of individuals at risk for clinical anxiety and the development of
effective interventions for treating panic disorder in COPD, or ideally, preventing its
development, should be priorities.
There are many outcome trials demonstrating the effectiveness of cognitive
behaviour therapy in treating panic disorder when no respiratory disease is present.
Cognitive behaviour therapy should also be an effective intervention for treating
patients with COPD-related panic disorder.
Depression is common in patients with chronic illness, and COPD is no exception.
Anxiety and mood disturbances can often be precipitated by respiratory drugs (eg
theophylline and steroids respectively). Pharmacological treatment of depression in
COPD may be hampered by poor tolerance of side effects from drugs which may
affect respiratory control and/or aggravate sleep disturbances.
66
In addition to usual clinical assessment, the presence and/or impact of anxiety and
depression may be reliably predicted with several validated questionnaires, eg, the
HAD Scale (Hospital Anxiety Depression Scale). This self report questionnaire has
good psychometric properties and is widely
used in psychological research with medical
Cognitive behavioural
patients150.
techniques are useful for
anxiety and depression.
Referral to psychiatrists, psychologists, social
Pulmonary rehabilitation also
workers and pulmonary rehabilitation programs
helps.
may assist patients dealing with psychological
problems.
Address carer strain
Caring for someone with COPD can be stressful, and it is not surprising that
significant psychological and physical consequences for carers are well documented.
Carers themselves may require some form of intervention. In fact, some researchers
suggest that carer stress can in some instances be as great or greater than that of
the patient. Carer issues should be addressed as part of the medical assessment,
with objective measurement possible using a career strain assessment tool.
Enrol in pulmonary rehabilitation90-101,138-149
The primary goal of pulmonary rehabilitation has been to restore the patient to the
highest possible level of independent functioning. The effects of pulmonary
rehabilitation begin to dissipate 6-12 months after the intervention if there is no
ongoing maintenance program. Benefits are wide ranging and there are minimal risks
(refer to Section O, page 39).
Ensure optimal use of inhalers111
Elderly and frail patients, especially those with cognitive deficits may have difficulty
with some inhalers. It takes time and patience to find the best device. Device training
is usually included in pulmonary rehabilitation programs (refer to Section O), but is
often addressed by the Respiratory Nurse Educator.
Develop a self-management plan
There is evidence that patients with chronic illness who participate in selfmanagement have better outcomes including reduced health care costs than those
who do not. In asthma, patient education with emphasis on self-management
behaviour improves quality of life and reduces exacerbation severity more than
simply providing information and knowledge. It has not been specifically studied in
COPD, but behavioural education alone is effective, though less effective than
integrated pulmonary rehabilitation programs that include an exercise component.
In patients with COPD, most exacerbations evolve over days rather than hours. In
many patients the baseline lung function is so low that even small changes can
exceed the respiratory reserve, precipitating a major deterioration in functional status.
Viral and bacterial infections play a role in exacerbations of COPD but psychosocial
factors such as depression, anxiety, panic or lack of a carer may also be of major
importance.
The traditional approach to exacerbations of moderate to severe COPD has been
admission to hospital. Recent work exploring the concept of hospital-at-home has
demonstrated that many patients can be managed at home by appropriately qualified
staff146-148. Whether such treatment is cost-effective remains uncertain.
67
The concept of self-management plans for COPD is derived from their success in
asthma management indicating doses and medications to take for maintenance
therapy and for exacerbations. Instructions for crises are often included.
In contrast with asthma, pharmacological treatment of COPD is generally less
effective and the condition is by definition non-reversible. However, some of the
interventions have strong support (e.g. use of bronchodilators for symptoms,
systemic glucocorticoids for exacerbations and antibiotics if there is purulent
sputum). They might be more effective if instituted early in an exacerbation, thereby
preventing crises and hospital admission. The primary care team needs to develop
systems to identify those with more severe COPD who might benefit from more
intensive education and training in self-management skills.
The components of a self-management plan include all the elements of a full
rehabilitation and self-help program. Those patients with a history of exacerbations
should be invited to the practice/clinic for an interview with the practice nurse or
educator to discuss implementation of the plan. The doctor should decide if it is
appropriate for the patient to have an antibiotic and a course of prednisone at home
for use in an exacerbation, and the patient and carer trained in how these drugs
should be taken.
A typical self-management plan might include instructions for maintenance therapy,
exacerbations and crises. Symptom control measures may include drug use or
breathing techniques. Examples can be found at www.lungnet.com.au/copd.html.
GP involvement in review of self-management plans (including medications) may be
undertaken in the context of Care Plan Item Numbers or Domiciliary Medication
Management / Review (DMMR) for which an MBS fee is applicable (Item 900). This
requires the involvement of an accredited pharmacist and patient consent.
The plan should be reviewed after any exacerbation to make adjustments as
appropriate. Patients will often tend to delay initiating actions agreed in their plan in
the hope that they may not need additional treatment. Instead, they should be
encouraged to start their prescribed additional treatment at the earliest sign of an
impending exacerbation.
(i)
Maintenance therapy
Detailed discussion of the maintenance therapy for COPD appears in Section
O, page 26. In general, drug management in COPD does not involve backtitration, which is a core principle in asthma management. The exception is
when oral glucocorticoids have been given for an acute exacerbation.
(ii)
Exacerbations
Detailed discussion of the management of exacerbations is found in Section
X. For mild to moderate exacerbations an increase in inhaled bronchodilator
therapy and an increase in, or introduction of, inhaled glucocorticoid therapy
may be beneficial.
For severe exacerbations there is evidence for the use of antibiotics, systemic
glucocorticoids and supplemental oxygen (if hypoxaemic). Selected patients
may benefit from early intervention with these agents according to a
predetermined plan developed by a GP and/or respiratory specialist.
(iii)
Crisis medication pack
To facilitate early intervention in severe exacerbations selected patients may
be instructed to use a supplied crisis medication pack including:
68
·
·
·
Broad spectrum antibiotics (eg, amoxycillin, tetracycline, cephalosporin)
Prednisolone and dosage schedule (eg, 35-50 mg daily for five days, then
25 mg daily for 5-10 days). Tapering the dose is not required for courses
shorter than three weeks.
O x y g e n. For some patients, who are not hypoxaemic when well,
supplemental oxygen may help to avoid hospital admission. However,
there are often organisational and financial impediments to the timely
supply of oxygen in this setting.
Controlled trials are required to document the efficacy of self-management plans (in
addition to pulmonary rehabilitation) in patients with stable COPD. At this point,
drawing on the success of asthma action plans, education of COPD patients in selfmanagement is recommended. Written plans are usually required to complement
such interventions (see examples at www.lungnet.com.au/copd.html).
End of Life Issues
Terminal COPD patients are usually elderly and have already experienced one or
more decades of increasingly frustrating functional restriction. Their course is likely to
have been punctuated by hospital admissions. They often have several comorbidities
and are frequently dependent on the care of others.
Determining prognosis in end-stage COPD is extremely difficult, though guides to
shortened survival include FEV1 <25% predicted, weight loss (BMI below 18),
respiratory failure (PaCO2>50mm Hg or 6.7kPa), and right heart failure.
The major ethical issues are deciding whether to offer invasive or non-invasive
ventilatory support or alternatively to withhold, limit or withdraw such support. These
decisions are often complex but as in other areas of medicine they are ultimately
constrained by the standard ethical principles of respect for patient autonomy,
ensuring that good is achieved without harm. Most patients with end-stage COPD
wish to participate in end of life management decisions. They would prefer to do so in
a non-acute setting.
The treating doctor should ascertain the preferences of the patient with regard to
ventilation and palliation. This conversation is best conducted when the patient is
stable between exacerbations or in the setting of a pulmonary rehabilitation program.
It may take several meetings for a conclusion to evolve and with the permission of
the patient it can be very helpful to involve significant family or carers. Evidence
suggests that family and other surrogate decision-makers are often unaware of the
patientÕs views. The patient should be encouraged to share such views with
important others.
Information should be provided to help patients and carers answer questions such
as:
· What is it like for the patient to be on a ventilator?
· What is it like for the family?
· What are the chances of getting off the ventilator?
· In what state of health would the patient be then?
The patient should also be reassured that in the event that they choose not to be
ventilated, full supportive care including appropriate sedation will be offered to avoid
discomfort. In some states the patientÕs wishes can be given legal force through the
use of an enduring power of attorney or advance health directive.
69
Although difficult for the health professional and potentially distressing for the patient,
a frank discussion about these often unspoken issues can be beneficial.
Palliative Care in COPD
Palliation means providing supportive care that reduces suffering for the patient
through the terminal phases of illness, and for his/her family. Palliative care is now a
widely-accepted approach for the care of people with terminal malignant diseases
after cure has become impossible. The traditional curative approach taken for
conditions like COPD also needs to be tempered in a similar way.
Symptom relief includes bronchodilators, oxygen and assisted ventilation, but
dyspnoea can also be relived by opioids and anxiety can be suppressed by
anxiolytics. The opioids and many anxiolytics depress ventilatory drive and are
contraindicated in most patients with COPD. When palliation is warranted, however
they should be considered. Referral to a palliative care service to support (not to
replace) the continuity of care provided by the GP is logical.
70
X
EXACERBATIONS: MANAGE APPROPRIATELY
Early diagnosis and treatment may prevent admission.
Multidisciplinary care may assist home management.
Controlled oxygen (28% or 0.5-2 L/min) is indicated for hypoxaemia199.
Inhaled bronchodilators134,165-166 and systemic glucocorticoids 180-182 are
effective treatments for acute exacerbations.
Exacerbations with clinical signs of infection (increased volume and
change in colour of sputum and/or fever, leucocytosis) benefit from
antibiotic therapy176-178.
Non-invasive positive pressure ventilation is effective for acute
hypercapnic ventilatory failure86,173,183-197.
Involvement of the general practitioner in a case conference and care plan
development may facilitate early discharge.
AIMS
GOALS
Early Diagnosis
Patient and carer
recognise
symptoms of
declining function
(see handbook C & D)
Early Action
(see handbook C,O &
D)
Optimise
Treatment
(see handbook O & D)
Refer
Appropriately
(see handbook O & P)
Patient is able to
access prompt
assessment and
treatment
Severity is
assessed
accurately and
other diagnoses
are excluded
Appropriate
bronchodilator
therapy is
commenced
Antiinflammatory
therapy is
considered
Antimicrobial
therapy is
considered
Crisis is averted
ACTIONS
C
B
C
A
B
A
C
LEVEL
Education of the patient and the
support team
Patient uses Action/Crisis Plan
Patient contacts GP and/or outreach
nurse
Review Care Plan, Action/Crisis Plan
Check medications
Use Crisis Medication Pack Ð
steroids, antibiotics etc.
Symptoms/signs cor pulmonale
Spirometry may help determine
severity
Chest X-Ray may exclude other
diagnosis
Pulse Oximetry, Arterial Blood Gases
Bronchodilators (Beta-agonist &/or
Anticholinergic)
- Metered Dose Inhalers (Spacers
improve delivery)
- Dry Powder Inhalers
- Nebulisers
Glucocorticoids (oral where possible, for
7-14 days)
Antibiotics (oral where possible), if signs
of bacterial infection
C
Monitor regularly
- cyanosis, arrhythmia, peripheral oedema
Refer to consultant or for hospital
admission
D
C
C
A
A
B
C
71
Respiratory
support
O2 saturation is
maintained at 8892%
Failing ventilation
is detected and
supported
(see handbook O & P)
Monitor and
review
(see handbook P & D)
Convalescence
Iatrogenic
sedation is
avoided
Sputum
clearance is
optimised
Improvement is
documented:
· airway function
· gas exchange
· functional
status
· coping
strategies
· support
Independent
living is achieved
Relapse is
avoided
Follow up is
arranged
(see handbook P & D)
Function &
quality of life are
improved
Controlled O2 therapy
FiO2 28% or 0.5-2.0 L/min nasal prongs
initially
PaCO2>45, pH<7.3, RR>30
Non invasive positive pressure
ventilation
- reverse acute respiratory acidosis
- avoid intubation if possible
Respiratory stimulants have a limited
role.
Avoid narcotic, analgesic and
sedatives
C
Chest physiotherapy in general is of
limited value, however it may be used
where appropriate based on individual
assessment.
Mucolytics are of limited value
C
A
D
D
B
Review regularly (RR/HR/level of
Consciousness).
· Post bronchodilator spirometry (PEF
unreliable)
· Oximetry +/- ABGs
· Walking distance/ADLs
· Review level of support
· Assess carer strain
C
Encourage early mobilisation/ADLs
D
Ensure appropriate ongoing support
Review self-management plan and
inhaler technique
Step-down treatment (define steroid
Schedule)
Review need for O2
Plan graded exercise
Consider referral for pulmonary
rehabilitation
A
72
Acute Exacerbations of COPD
Acute exacerbations of COPD are characterised by an increase in respiratory
symptoms of cough, wheeze, dyspnoea and/or sputum production 176 . Initial
assessment involves clinical examination of the cardiac and respiratory systems,
including inspection of sputum and spirometry. Chest X-ray is indicated in severe
exacerbations or where there is a suspicion of pneumonia or other complications.
Blood gas analyses are indicated in severe exacerbations or where there is suspicion
of hypercapnia. Treatment is directed at the pathophysiological abnormalities, the
causes of the exacerbation and the complications.
The management of acute COPD exacerbations, which is usually the cause of
hospital admission in COPD, is not well studied.
In one study of more than 1000 patients admitted to several hospitals with an acute
exacerbation of severe COPD, about 50% of the patients were admitted with a
respiratory infection, 25% because of congestive cardiac failure and 30% were
admitted with no known cause for the exacerbation. In a study of 173 COPD patients,
an average of 1.3 (range 0-9.6) exacerbations per annum was found .
Pathophysiological abnormalities
An acute exacerbation of COPD may involve an increase in airflow limitation, excess
sputum production, airway inflammation, infection, hypoxia, hypercapnia and
acidosis. Treatment is directed at each of these problems.
·
Bronchodilators: inhaled beta-agonist (e.g. salbutamol) and anticholinergic
(ipratropium) drugs can be delivered by pressurised metered dose inhaler and
spacer (4 puffs of each drug) or via jet nebulisation (salbutamol 2.5-5mg,
ipratropium 500mcg). The dose interval is titrated to the response and can
range from hourly to 4-6 hourly.
·
Glucocorticoids: oral glucocorticoids hasten resolution and reduce relapse.
Prednisolone 30 to 50mg daily for 2 weeks is adequate. Longer courses add
no further benefit and have a higher risk of side effects.
·
Controlled oxygen therapy is indicated in hypoxic patients, with the aim to
improve oxygen saturation to over 90% (PaO2 >50mm Hg or 6.7kPa). Use a
Venturi mask initially at 24% or 28%. Minimise excessive oxygenation which
can worsen hypercapnia.
·
Hypercapnia and acidosis must be carefully monitored. Deterioration in spite
of medical therapy may indicate a need for ventilatory assistance.
Causes
In patients with COPD the normally sterile lower airway is frequently colonized with
bacteria such as Haemophilus influenzae, Streptococcus pneumoniae and Moraxella
catarrhalis155-159. While the number of organisms (as detected by quantitative culture
techniques) may increase during exacerbations, there will often be difficulty
determining whether an infection is present160-163 . Furthermore sputum can be
contaminated by pharyngeal secretions that include the same organisms.
Exacerbations can also be due to viral infection and to non-infectious causes that
increase airflow obstruction such as left ventricular failure, pulmonary embolus and
possibly other factors such as changes in weather or pollution164.
73
Complications
An acute exacerbation of COPD can result in worsening of cor pulmonale, left
ventricular failure, pneumothorax or pulmonary embolus.
In general practice
Treat with inhaled bronchodilators (MDI via spacer is preferred), oral corticosteroids
and antibiotics if indicated. Follow the response to therapy with clinical assessment
and spirometry, if available. Watch for worsening dyspnoea, drowsiness (CO2
retention), cyanosis and heart failure.
In hospital
Treat with inhaled bronchodilators, oral corticosteroids, antibiotics if indicated,
controlled oxygen therapy and assess the need for chest physiotherapy.
Monitor oxygenation and CO2 retention during therapy to guide management. Add
diuretics if there is peripheral oedema. Assess the patient for complications as
described above.
At resolution
Review maintenance treatment with bronchodilators, smoking cessation, vaccination
against influenza and pneumococcus, and the need for exercise rehabilitation and
long-term oxygen therapy. Provide a treatment plan for the patient to use when the
next exacerbation occurs.
Early Diagnosis
Early diagnosis of exacerbations of COPD and prompt, appropriate treatment may
prevent progressive functional deterioration and reduce the necessity for admission
to hospital.
Education of the patient, carers, other support people and family may aid in the early
detection of exacerbations. This may be part of a pulmonary rehabilitation program,
but should be reinforced by the GP and other healthcare workers.
The patient should have a self-management plan developed in conjunction with the
GP and specialist to indicate how to step-up treatment (see examples at
www.lungnet.com.au/copd.html). This plan should also require the patient to contact
their GP and/or community nurse to allow rapid assessment. Isolated or disabled
patients may require additional home care during exacerbations (see section D, page
67).
Early Action
Prompt assessment and treatment may prevent crisis situations. The selfmanagement plan should indicate medications to take, possibly including antibiotics
and oral glucocorticoids. This action can be supported by the availability of a crisis
medication pack.
Initial assessment of severity
The initial assessment of severity of the current episode is critical to acute
management of these patients. An exacerbation typically includes signs suggesting
significant deterioration such as:
·
increased breathlessness
·
Changes in exercise tolerance and ability to complete activities of daily
living (ADLs)
74
·
·
·
·
Changes in sputum volume, colour and viscosity
Audible wheeze
Chest tightness
Overuse of accessory muscles
There may also be evidence of peripheral oedema or confusion.
The severity of the airway obstruction sometimes means that the patient has an
ineffective cough and is incapable of expectoration.
History and examination
A full history should be obtained from all patients and/or carers, but treatment in
urgent cases should not be delayed. Include:
· Pre-hospital treatment, especially the use of steroids, nebulisers and longterm oxygen therapy
· Time course of the current exacerbation
· Frequency of previous admissions e.g. intensive care admissions
· Episodes of mechanical assisted ventilation
· Smoking history
· Exercise tolerance and ADLs under usual circumstances and at present
· Ability to speak i.e. phrases, sentences, words or not at all
· PatientÕs wishes regarding intubation and resuscitation
· Identify any comorbid illnesses.
Physical examination should include:
· Chest auscultation
· Oxygen saturation (SpO2)
· Work of breathing and level of exhaustion
· Cough
· Jugular venous pressure
· Peripheral oedema
· Cyanosis
· Sweating
Optimise Treatment
Bronchodilator therapy 132,134-135,166-171,174-175
Introduction
Relief of airflow limitation is a major goal of treatment of acute exacerbations and
leads to more effective cough and expectoration. In COPD, the immediate effect of
bronchodilators is small, but may provide significant improvement in clinical
symptoms in patients with severe obstruction.
Studies of acute airflow limitation in asthma indicate that beta -agonists are as
effectively delivered via MDI and spacer as via nebuliser. This may be applicable to
patients with COPD. An adequate dose should be used. The dose equivalence to
5mg of salbutamol delivered by nebuliser is 8-10 puffs of 100 mcg salbutamol via an
MDI and spacer. With nebulisers the driving force needs to be of sufficient rate ³6
L/min to achieve an aerosol. Such high flow rates of oxygen may cause CO2
retention so air should be used. High doses of beta-agonists may induce
hypokalaemia and predispose to cardiac arrhythmias.
Few studies have examined the use of ipratropium bromide in acute exacerbations of
COPD 167-168. One study which compared the effectiveness of ipratropium bromide
75
with a beta-agonist demonstrated that each drug produced a small but significant
improvement in pulmonary function. Inhaled ipratropium bromide also demonstrated
a small but significant increase in PaO2 (av. 6 mm Hg or 0.8kPa) within 30 minutes of
its delivery.
In long-term management of stable COPD, three large randomised controlled trials
have found significant and clinically relevant improvements in FEV 1 when both
salbutamol and ipratropium were used compared to either drug administered on its
own. In the acute setting additional benefit has not been proven for COPD.
The use of oral theophylline and IV aminophylline in the management of COPD has
diminished because of toxicity. One study showed no additional benefit when
aminophylline was added to treatment but demonstrated detrimental side effects. A
contrary outcome was found in a later study. The routine use of aminophylline is not
recommended for acute exacerbations172-173.
Initial treatment
Continuously nebulised beta-agonist bronchodilator (e.g. salbutamol) should be given
on arrival for extremely unwell patients and intermittently in other patients. This will
usually be delivered via high flow air. An anticholinergic agent (ipratropium bromide)
may be delivered together with the nebulised beta-agonist in patients with severe
exacerbations (Triage Categories 1 & 2) or when response to beta-agonists alone is
poor. Nebulised medications can also be administered through the assisted
ventilation circuit if required.
The mode for delivery should be changed to a MDI with a spacer device or a DPI,
within 24 hours of the initial dose of nebulised bronchodilator, unless the patient
remains severely ill167,171,174-175.
Antibiotic therapy176-179
Infection and the subsequent inflammatory reaction increase airway obstruction in
COPD. About one third of respiratory infections in these patients are viral155-158,160,178.
Bacterial infection may have either a primary or secondary role in an exacerbation177178
.
The major bacterial organisms that have been associated with exacerbations include
Haemophilus influenzae, Streptococcus pneumoniae and Moraxella catarrhalis.
Mycoplasma pneumoniae and Chlamydia pneumoniae may also be involved. As
lung function deteriorates (FEV1<35%), bacteria like Pseudomonas aeruginosa and
Staphylococcus aureus may infect airways.
A meta-analysis of nine studies examining the use of oral antibiotics in the treatment
of patients with exacerbations of COPD demonstrated a small but significant clinical
and symptomatic benefit. The greatest amount of improvement was seen in those
patients who had been hospitalised rather than ambulatory patients.
Antibiotic Therapeutic Guidelines recommend the use of oral antibiotics such
doxycycline or amoxycillin (alternatively erythromycin or roxithromycin). If patients
not respond, amoxycillin-clavulanate should be prescribed. If pneumonia
suspected, appropriate antibiotics should be used. Similarly, if Pseudomonas
Staphylococcus is suspected, use appropriate antibiotics.
as
do
is
or
The duration of antibiotics depends on the rate of clinical resolution. Typically a
course of treatment will be 7-10 days. Response is usually seen within 3-5 days and
a change of antibiotic should be considered if the response is unsatisfactory.
76
Parenteral antibiotic therapy should only be used in patients who are very ill, febrile,
with copious sputum, unconscious, unable to swallow safely or otherwise unlikely to
absorb oral drugs. If parenteral administration was commenced, oral treatment
should usually start within 72 hours.
Radiologically proven pneumonia in COPD patients, especially when they have been
frequently hospitalised, may not be restricted to the above organisms. A broader
range may be responsible including Gram negatives, Legionella sp and even
anaerobic organisms. Their presence may significantly alter initial empiric antibiotic
therapy.
Glucocorticoids135,166,175,180-182
A recent randomised controlled trial of 271 patients receiving systemic glucocorticoid
for acute exacerbations of COPD demonstrated a moderate improvement in clinical
outcomes. Maximum improvement was gained with two weeks of therapy. Prolonging
the course of treatment beyond two weeks did not result in further benefit. An
important side effect was the development of hyperglycaemia, often of sufficient
severity to warrant treatment. Optimum dosage has not been established. Oral rather
than inhaled glucocorticoids are more effective in patients with mild to moderate
COPD during an exacerbation. In severe exacerbations parenteral glucocorticoids
may be useful initially.
If the response to parenteral glucocorticoids is adequate, change to oral prednisolone
30-50 mg daily within 48 hours. The continued use of inhaled corticosteroids and
administration technique should be reviewed. At discharge, oral prednisolone 2537.5 mg may be continued for a total of 7 to 14 days and then ceased. Tapering of
glucocorticoids is not necessary following short-term administration. However
patients taking glucocorticoids for more than three consecutive weeks may have
adrenal suppression and their glucocorticoids should not be ceased abruptly.
Patients on long-term oral steroid therapy (>7.5 mg prednisolone daily for more than
six months) are at risk of developing osteoporosis. Prevention and treatment of
steroid-induced osteoporosis should be considered. Steroid-induced hyperglycaemia
may develop in patients prescribed high doses of glucocorticoids. Blood sugar levels
should be monitored.
Refer Appropriately
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 lung function testing
· Those with sudden deterioration
· Those who seem to require long-term oral steroids
· Those with new symptoms (e.g. haemoptysis, chest pain)
· Consideration for pulmonary rehabilitation or LTOT
77
Indications for hospitalisation of patients with COPD
(i)
Patient has acute exacerbation characterised by increased dyspnoea, cough
or sputum production, plus one or more of the following:
·
Inadequate response to outpatient management
·
Inability to walk between rooms when previously mobile
·
Inability to eat or sleep due to dyspnoea
·
Patient cannot manage at home (or supplementary home care resources
not immediately available)
·
High risk comorbidity condition - pulmonary (e.g. pneumonia) or nonpulmonary
·
Prolonged, progressive symptoms before emergency visit
·
Altered mental status suggestive of hypercapnia
·
Worsening hypoxaemia
(ii)
Patient has new or worsening cor pulmonale unresponsive to outpatient
management
(iii)
Planned invasive surgical or diagnostic procedure requires analgesics or
sedatives that may worsen pulmonary condition
(iv)
Comorbid condition e.g. severe steroid myopathy or acute vertebral
compression fractures that has worsened pulmonary function
Indications for increased respiratory support or ICU admission
(i)
(ii)
(iii)
(iv)
Severe dyspnoea that responds inadequately to initial emergency therapy
Confusion, lethargy or evidence of hypoventilation
Persistent or worsening hypoxaemia despite supplemental oxygen or severe /
worsening respiratory acidosis (pH < 7.3)
Assisted mechanical ventilation is required
Respiratory Support
Controlled O2 therapy199
Correction of hypoxaemia to achieve a PaO2 of at least 55mm Hg (7.3kPa) and an
oxygen saturation of 88-92% is the immediate priority. Where there is evidence of an
acute rise in PaCO2 together with signs of increasing respiratory fatigue and/or
obtunded conscious state, assisted ventilation should be considered. Early noninvasive positive pressure ventilation (NIPPV) may reduce the need for endotracheal
intubation (see below for more detail).
A minority of patients with longstanding hypercapnia may develop a worsening of
their respiratory acidosis if they breathe high levels of inspired oxygen. This may
occur within 15 minutes and occurs mainly because of hypoventilation.
Administration of oxygen at an inspired oxygen concentration (FIO2) of 24-28% via a
Venturi mask is usually sufficient to improve oxygenation in most patients. Nasal
cannulae, although more comfortable, deliver a variable level of enrichment but a
flow of 0.5-2.0 L/min is usually sufficient. Gas flow provided through Hudson-type
masks is inadequate when patients are tachypnoeic and therefore these should not
be used. Careful monitoring with oximetry and, where hypercapnia is a potential
concern, ABGs are required. There is no benefit in trying to obtain SpO2 levels >92%
in these patients.
78
Patients should be weaned off supplementary oxygen as soon as possible, with none
for 24-48 hours before discharge unless home oxygen is prescribed.
Figure 23. Adjustments for oxygen settings in acute exacerbations of COPD
PaO2 (mm Hg)
PaCO2 (mm Hg)
PH
Adjustment
>>60 (8 kPa)
(SpO2>90%
by oximetry
Normal (<45)
or
High (>45)
Normal (7.357.45)
or
Low (<7.35)
>60 (8 kPa)
(SpO2 >90% by
oximetry)
(i)
(ii)
Normal (<45)
Increased
(i)
(ii)
Normal
Normal
(iii)
Large increase
(iii)
Low
(i)
Normal or low
(i)
Normal
(ii)
Slight increase
(ii)
Normal
(iii)
Large increase
(iii)
Low
<60 (8 kPa)
(SpO2 <90% by
oximetry)
Reduce O2 FIO2 to
maintain PaO2
closer to 50 (SpO2
90-92%) and
monitor blood
gases
(i)
Continue
same FIO2
(ii)
Same FIO2
but monitor
ABG
(iii)
Consider
assisted
ventilation
(i)
Increase
FIO2 but
monitor
ABG
(ii)
Increase
FIO2 but
monitor
ABG
(iii)
Consider
assisted
ventilation
Source: Frith PA. Treating chronic obstructive pulmonary disease. Current Therapeutics May 1998, pp
21 Ð 33
Noninvasive positive pressure ventilation (NIPPV)183-197
Ventilatory support, either NIPPV or invasive positive pressure ventilation (IPPV) via
an endotracheal tube, should be considered in patients who are unable to ventilate
adequately with rising PaCO2.
NIPPV is an effective and safe means of treatment in COPD patients with acute
respiratory failure. Its use allows preservation of cough, physiologic air warming and
humidification, and normal swallowing, feeding and speech. Early intervention with
NIPPV has been suggested when the respiratory rate > 30 min and pH < 7.35. An
improvement should occur in rate and pH within one hour of starting NIPPV.
Conventional therapy in addition to the application of non-invasive ventilation results
in a reduced need for intubation and therefore the associated potential complications.
NIPPV also results in a more rapid improvement in respiratory rate, dyspnoea score
and blood gas abnormalities than conventional therapy alone. Some of these studies
have also shown an improvement in survival and a reduced hospital length of
stay86,183.
NIPPV is contraindicated in patients who are unable to protect their airway, are not
spontaneously breathing or who have severe facial injury. Relative contraindications
(situations where NIPPV may be less effective) include life-threatening refractory
hypoxaemia (PaO2 < 60 mm Hg or 8kPa on 100% inspired oxygen), bronchiectasis
with copious secretions, severe pneumonia and haemodynamic instability. These
patients may require intubation.
79
Randomised controlled trials of NIPPV show that fewer patients require intubation,
and that there are lower complication rates and reduced mortality.
It is important to ascertain the patientÕs wishes, either directly or from family and
carers, regarding intubation and resuscitation - preferably prior to an admission for
management of respiratory failure. Patients who require ventilatory support during
exacerbations of COPD may have impaired control of breathing and/or apnoeas
during sleep, even when well. Therefore consideration should be given to
undertaking a diagnostic sleep study after discharge.
Clearance of secretions
Patients who regularly expectorate or those with tenacious sputum may benefit from
relaxed breathing exercises in combination with forced expiratory techniques. If
patients have >25mL sputum per day, or if mucus plugging with lobar atelectasis is
present, physiotherapy incorporating the use of postural drainage and associated
techniques such as percussion and vibration may be of benefit.
A systematic review of postural drainage in COPD found that the evidence for
supporting its routine use was inconclusive. The efficacy of mucolytics in patients
requiring hospitalisation has not been evaluated.
Monitor & Review
Monitoring response to initial treatment
The initial aim is to relieve hypoxaemia.
(i)
Clinical examination
Response to treatment is assessed by:
·
Improved level of consciousness
·
Reduction in respiratory rate and heart rate
·
Higher oxygen saturation and/or improved ABGs
·
Improvement in the feeling of chest tightness
·
Improvement in pattern of breathing (e.g. less laboured) and less use of
accessory muscles
·
Less wheezing
(ii)
Pulmonary function monitoring
Where feasible monitoring the patientÕs progress with respiratory function tests
(e.g. FEV1). Peak flow monitoring is unreliable.
Monitoring response to ongoing treatment
The continuing aim is to relieve hypoxaemia which should result in improvement in
clinical signs and symptoms.
(i)
Clinical examination
Response to ongoing treatment should result in further reduction in wheeze,
accessory muscle use, respiratory rate and distress.
(ii) Gas exchange
ABGs and /or pulse oximetry levels should be monitored until stable (SpO2
~90%). When the patient is improving, pulse oximetry is sufficient. Patients
whose condition deteriorates and/or fails to respond to treatment (especially if
80
the PaO2 and PaCO2 are not improving) should be assessed for IRCU and/or
ICU.
(iii) Respiratory function testing
FEV1 should be recorded in all patients after recovery from acute exacerbation.
(iv) Discharge Planning
Discharge planning should be commenced within 24 Ð 48 hours of admission
Discharge planning
Discharge planning involves the patient, external lay and professional carers, the
multidisciplinary hospital and community team and the patientÕs regular GP. It should
commence on or before admission and be documented within 24-48 hours.
Appropriate patient education and attention to preventive management are likely to
reduce the frequency of further acute exacerbations. Assessment of social supports
and domestic arrangements are critical in discharge planning.
Suggested criteria for a patientÕs readiness for discharge include:
¥ Clinically stable and no parenteral therapy for 24 hours
¥ Inhaled bronchodilators required less than 4 hourly
¥ Oxygen ceased for 24 hours (unless home oxygen is indicated)
¥ If previously able, ambulating safely and independently and performing ADLs
¥ Able to eat and sleep without significant episodes of dyspnoea
¥ Patient/caregiver understands and is able to administer medications
¥ Completion of follow-up and home care arrangements (e.g. home oxygen
arranged if required, home-care, Meals on Wheels, community nurse, allied
health, GP, specialist.)
A discharge pack which includes general information about COPD, advice on
medication usage, written instructions on use of inhalation and oxygen devices where
appropriate, and a plan for management of worsening symptoms should always be
provided. Dietary advice for patients who are underweight or have recently lost
weight may also be required. The GP and/or Respiratory Outreach Program (if
available) should be notified during the patientÕs admission. A case-conference
involving the multidisciplinary team may assist successful transition to the
community. The MBS Enhanced Primary Care item numbers may be claimed for
Òparticipation in a case conferenceÓ and Òcontribution to a care planÓ (see Section D,
page 63). On discharge, the patient will be contacted at home to review their
progress, within 2 to 7 days, depending on severity of the exacerbation.
Psychosocial assessment and activities of daily living
The patientÕs home environment needs to be assessed early during admission. This
will enable appropriate planning for supports or changes at home or for alternative
short or long-term accommodation. An early referral to occupational therapy, social
work or aged care teams facilitates optimal management. If home-based support
services (e.g. assistance with showering) are required, an in-hospital assessment by
the occupational therapist should be completed and documented beforehand.
The ability to complete basic ADLs should be properly assessed and documented.
Such activities include dressing, showering, toileting, meal preparation and eating
and should be compared with the patientÕs best or usual status. A simple, objective
test of functional status is the distance walked in six minutes (<150m indicates
severe disability).
81
Therapy to reduce anxiety may also be of value to some patients. Assessment which
considers both physiological impairment and functional disability helps to determine
the need for active interventions. Tools such as the Hospital Anxiety and Depression
Scale may be used. Carer strain may also be measured objectively.
Pulmonary Rehabilitation
Prior to discharge, referral to a comprehensive pulmonary rehabilitation program
should be considered. Patients with pre-existing comorbidities such as severe
arthritis, or unstable angina may be unsuitable to partake in the exercise component
of the program but may benefit from the education and anxiety modulation aspects.
Several randomised controlled trials show that pulmonary rehabilitation programs
add to the quality of life in COPD patients. Comprehensive programs, which combine
education, behaviour modulation and general support with exercise training, have
been shown to be effective in improving quality of life and exercise capacity. The
common indications for referral include:
¥ Dyspnoea with activities, especially ADLs
¥ Loss of independence.
¥ High levels of patient anxiety when attempting activity
Convalescence
Outreach support after discharge
Follow-up at home after discharge from hospital may extend the continuum of care
process commenced within the acute environment, although evidence supporting
benefit from this practice is still being evaluated. To undertake this in a cost effective
way, telephone follow-up may be a way of systematically extending support to
patients and increase their coping strategies at home. Several descriptive papers
have addressed the impact on patient care of telephone follow-up after discharge
and found that 30-50% of patients have unresolved medical and social problems that
need to be addressed. Impact on re-admission rates were not addressed by these
studies.
In older patients, many studies have reviewed interventions aimed at reducing
unplanned re-admission to hospital from poor compliance with medication; unwanted
and adverse side effects from medication; inadequate follow-up and early clinical
deterioration.
The results from the introduction of a respiratory outreach service, including COPD,
provided in Sydney found that an average of three home visits per patient were
required. The service provided education on the disease process and the use of
medications and other therapeutic aids. The outcome demonstrated lowered readmission rates.
Clinical review/follow up198
There are no randomised clinical trials that have addressed the best method for
follow-up. It is recommended that the first review after a hospital admission should be
by the GP and within seven days of discharge. A decision about the need for
specialist review should be made at the time of discharge.
Follow-up care allows further discussion of self-management plans and future
monitoring. If a pulmonary rehabilitation program is considered the GP should be
involved before referral to the program.
82
The following factors should be considered at follow-up:
Assessment of the patientÕs coping ability and strategies
Measurement of FEV1
Reassessment of medication adherence and techniques with inhalation devices
Assessment for long-term oxygen therapy (may require reference to specialist
facility)
·
Consideration of referral to pulmonary rehabilitation
·
·
·
·
The risks and prevention of steroid-induced osteoporosis and its management should
also be considered at this time.
Assessment for long-term oxygen therapy
Patients who are discharged home with domiciliary oxygen therapy need to be reassessed at 30-60 days after discharge. They need to be referred to the Department
of Respiratory Medicine for assessment of the continuation of this therapy (see
Section P page 50).
Smoking cessation
All patients with COPD who continue to smoke should be counselled and assisted/
supported to quit. Strategies such as pharmacological treatment (e.g. buproprion,
NRT) and behavioural therapy may be useful (see Section P, page 45).
Vaccination
Evidence for the protection against both hospitalisation and death in patients with
COPD after influenza immunisation is very strong and it is likely that pneumococcal
vaccination has a similar benefit (see Section P, page 48).
Nutrition
Several studies have demonstrated that at least 50% of patients admitted to hospital
with COPD are malnourished. In malnourished patients, attempts should be made to
restore nutrition as this is a highly significant indicator of early re-admission and
death in severe COPD. Weight gain, though, has proven elusive in several renutrition studies. Several smaller meals per day may assist with reducing dyspnoea
whilst eating.
83
Abbreviations
ABGs
ADLs
ATS
DLCO
DXA
FEV1
FiO2
FRC
FVC
HRCT
JVP
LTOT
LVF
MMEFR
NIPPV
CXR
PaCO2
PaO2
PEF
PA
PTX
RV
SaO2
SpO2
TLC
TLCO
V/Q
VE/VCO2
VE/VO2
arterial blood gases
activities of daily living
American Thoracic Society
diffusing capacity
Dexascan
forced expiratory volume in one second
oxygen pressure in inspired air
functional residual capacity
forced vital capacity
high res CT
jugular venous pressure
long term oxygen therapy
left ventricular failure
maximum mid-expiratory flow
Noninvasive intermittent positive pressure ventilation
chest X-ray
arterial partial pressure of CO2
arterial partial pressure of O2
peak expiratory flow
posteroanterior
pneumothorax
residual volume
oxygen saturation
Transcutaneous haemoglobin oxygen saturation
total lung capacity
transfer factor of carbon monoxide
ventilation and perfusion
ventilatory response to progressive hypercapnia
ventilatory response to progressive hypoxia
84
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