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HowtoTreat
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inside
Epidemiology and
pathogenesis
Diagnosis and
management
Acute
exacerbations
Prognosis

The authors

DR ELI DABSCHECK,
respiratory and sleep physician,
allergy immunology and
respiratory medicine, the Alfred
Hospital, Prahran, Victoria.

Chronic obstructive
pulmonary disease

PROFESSOR CHRISTINE
MCDONALD,
director, department of respiratory
and sleep medicine, Austin
Hospital, Heidelberg, Victoria.

Background
CHRONIC obstructive pulmonary
disease is a progressive condition
that can result in significant physical
disability, frequent exacerbations
requiring hospitalisation, and
increased mortality. Under the diagnostic umbrella of COPD are
included chronic bronchitis, emphysema and asthma with irreversible
airflow limitation.
The Global Initiative for Obstructive Lung Disease (GOLD) defines

COPD as airflow limitation that is

not fully reversible. The airflow limitation is usually progressive and
associated with an abnormal
response of the lung to noxious particles or gases (such as cigarette
smoke).
The characteristic finding on spirometric testing is an obstructive pattern of airflow limitation that is not
fully reversible. Early diagnosis and
treatment of COPD may improve

prognosis and quality of life.

In 1679, Theophile Bonet, in the
first known description of emphysema, described 19 cases of voluminous lung. More than a century
later, Charles Badham, in 1814,
recognised the group of symptoms
we know today as chronic bronchitis. The terms chronic bronchitis and
emphysema were formally defined in
the report of the Ciba Guest Symposium in 1959.

Chronic bronchitis referred to

cough with expectoration that is not
attributable to other lung diseases,
while emphysema was defined in
anatomical terms as enlargement of
airspaces distal to the terminal
bronchioles. The descriptor COPD
was coined in 1965 by William
Briscoe and has now overtaken
other terms to describe this group of
conditions.
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6 May 2011 | Australian Doctor |

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HOW TO TREAT Chronic obstructive pulmonary disease

Epidemiology and pathogenesis

tralians experienced COPD, and this
number is expected to double by
2050. Although often thought of as a
disease predominantly affecting men,
in Australia there is a slight female
predominance in COPD prevalence
(56%).2 COPD is estimated to cost
the Australian community about
$8.8 billion annually.2
Smoking is the most common

EPIDEMIOLOGICAL studies from

developed countries have estimated
the prevalence of COPD to be about
10% of adults over 40.1 The recent
Australian arm of the BOLD study
(Burden of Obstructive Lung Disease) found that symptomatic COPD
(GOLD stages II-IV) affects 10.2%
of the Australian population over 40
years. In 2008, 1.2 million Aus-

cause of COPD. About 20% of

smokers will develop clinically significant COPD-related disability.3
Exposure to indoor pollution from
biomass cooking (cooking indoors
with coal or fire without adequate
ventilation) is recognised as an
important cause of COPD in developing countries.
Other important risk factors for

COPD include:
Passive smoking.
Occupational dusts and chemicals.
Asthma.
Genetic susceptibility.
Past respiratory infections, particularly in childhood, including tuberculosis.
Low socioeconomic status.
Poor nutrition.

Diagnosis
Clinical presentation
THE box, right, summarises
the symptoms and signs of
COPD. COPD should be
considered in current and
past smokers over 35. It
should also be considered in
individuals who give a history of childhood respiratory
disease or of significant passive smoking or industrial or
biomass exposure.

Figure 1: Chest X-ray showing hyperinflation.

Signs and symptoms of

COPD

Figure 2: Chest CT showing severe emphysematous change.

History
Breathlessness, initially on
exertion
Cough
Sputum
Wheeze
History of significant
comorbidities, including
lung cancer, coronary artery
disease, anxiety
and depression

Investigations and
assessment
Spirometry is the cornerstone of diagnosis, and preand post-bronchodilator
readings are recommended.
If spirometry is not available
at point of care, spirometry
testing is available through
respiratory laboratories and
a variety of pathology
providers. COPD is defined
by the presence of a postbronchodilator FEV 1/FVC
ratio <0.7, with an appropriate history, especially of
exposure to noxious particles such as tobacco smoke.
The severity of COPD can
be staged according to the
FEV 1 . This is the most
reproducible spirometric
measurement and correlates
significantly with prognosis.
Frequency of exacerbations,
exercise limitation and
degree of disability are also
important determinants of
severity.
Multidimensional scoring
systems have been devised to
provide a more practical
approach to classifying
COPD and assessing its
effects. One such index, the
BODE index (B standing for
BMI, O for degree of
obstruction, D for dyspnoea
score and E for exercise

Examination*
Chest examination:
prolonged expiration
phase
wheeze
barrel-shaped chest

Table 1: Australian COPD-X guidelines on severity

staging*
Severity

FEV1 (%
predicted)

Functional assessment

Mild

60-80%

Dyspnoea on moderate exertion

Moderate

40-59%

Increasing limitation of daily activities

Severe

<40%

Dyspnoea with minimal exertion,

daily activities significantly limited

*Adapted with permission from The COPD-X Plan, Australian Lung

Foundation, 2010.5

capacity as measured by sixminute walk distance [see

later]) has been shown to be
better than FEV 1 alone in
predicting risk of death from
all causes and from respiratory disease.4
Severity grading according
to FEV1 varies depending on
guidelines. However, a recent

study found that the British

Thoracic Society Classification (which is very similar to the classification used
in the Australian COPD-X
guidelines [table 1]) was
closely associated with allcause and respiratory mortality over five years.
Radiology is not required

to make a diagnosis of
COPD. The chest radiograph is not sensitive for
the diagnosis of COPD
although it may demonstrate hyperinflation or
bullae (figure 1). CT is more
sensitive than the chest radiograph and may demonstrate
emphysematous
change (figure 2).
Arterial blood gas analysis
should be performed in all
patients with severe disease.
Severe hypoxaemia (PaO2<
55mmHg or <60mmHg in
the presence of right heart
failure) indicates the need
for domiciliary oxygen therapy, provided the patient is
not a current smoker. Respiratory acidosis (pH <7.35
and
PaCO 2 >50mmHg)
demonstrates that the
patient is acutely unwell,

and may require ventilatory

support.
If the degree of breathlessness is out of keeping with
the spirometry, further lung
function testing including
measurement of carbon
monoxide transfer factor
(also known as diffusing
capacity) should be performed. If right heart failure
is suspected, an echocardiogram should be considered.
Other smoking-related
diseases such as coronary
artery disease, peripheral
vascular disease and cerebrovascular disease should
be considered. A nutritional
assessment should be
undertaken, as COPD is
associated with poor nutrition, and extremes of BMI
are associated with worse
prognosis.

Hoovers sign:
paradoxical indrawing of
lower ribs during
inspiration
Pursed lip breathing
*Examination can be normal

Management
PRIMARY care physicians play a
vital role in managing patients
with all stages of COPD.

Smoking cessation
Early intervention to assist with
smoking cessation is key. Smoking cessation is one of the only
interventions that definitely
reduces mortality as well as slowing disease progression. Pharmacotherapy such as nicotine
replacement therapy (nicotine
patches became available on
authority through the PBS from 1
February 2011) and support
should be offered.

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| Australian Doctor | 6 May 2011

Stepwise increase of inhaler therapy to control symptoms

Patients with breathlessness and exercise limitation
Short acting beta2 agonist (eg, salbutamol) as required
Patients with persisting breathlessness despite beta2 agonist use, or with
exacerbations
Regular long-acting muscarinic antagonist (eg, tiotropium) or long-acting
beta2 agonist
Patients with two or more exacerbations per year and an FEV1 <50%
predicted

Pharmacological management
of stable COPD
The aims of drug treatment are
firstly to relieve symptoms and
secondly to prevent both acute
and chronic deterioration. A volumetric spacer device should be
used when appropriate for
inhaled medication. Inhaler therapy should be increased stepwise
until symptoms are controlled, as
per the box, left.

Continue inhaler medication as above, plus

Add regular long-acting beta2-agonist and inhaled corticosteroid in a
combined inhaler (eg, fluticasonesalmeterol or budesonideeformoterol
[see table 2, page 30, for doses])

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Inhaler use

It is important to check patients

inhaler technique and, if necessary,
demonstrate the correct technique.

Technique should be reviewed at

regular intervals. A 2008 study
demonstrated that only 10% of
Australian patients with airways
disease used their inhalers correctly.6 There is no clinically significant difference in efficacy
between different delivery devices,
provided they are used correctly.
The use of spacers increases drug
deposition in the lungs and allows
medication inhalation during tidal
breathing rather than rapid forceful inspiration. Such devices may
be particularly beneficial in the
elderly.
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Chronic obstructive pulmonary disease

from page 28

in chronically hypoxic
patients (PaO2<55mmHg or
<60mmHg in the presence of
right heart failure) used for
more than 15 hours a day
improves survival. Patients
must not be current smokers, because of the fire risk.
Patients with arterial oxygen
desaturation during exercise
(SpO2 <88%) may benefit
from intermittent oxygen in
the form of a portable cylinder. (For more details, see
How to Treat Oxygen
therapy, 26 February 2010
[see Online resources].)

Other pharmacological
therapy for stable COPD
Vaccines

Influenza vaccination should

be offered routinely to all
patients with COPD and has
been shown to reduce flareups of COPD, especially
those related to the influenza
virus itself. Pneumococcal
vaccine should be offered to
all patients with COPD and
has been shown to reduce
the incidence of communityacquired pneumonia.7
Prophylactic antibiotics

In general, regular or prophylactic antibiotics are

thought not to reduce exacerbation frequency and have
traditionally not been recommended. Of particular concern is the development of
antibiotic-resistant organisms. However, low-dose
macrolides have been
demonstrated to reduce
airway inflammation and
have been used successfully
in cystic fibrosis and
bronchiectasis for several
years.
A recent trial of 250mg
erythromycin administered
twice daily to patients with
COPD over 12 months
showed a significant reduction in exacerbations compared with placebo. 8
Another recent study
demonstrated that a twomonthly five-day course of
oral moxifloxacin modestly
reduced exacerbation rates.9
Theophylline

Theophylline is rarely used

in practice in Australia but
can be considered when
patients remain symptomatic
despite all the above measures. A recent study suggested low-dose slow-release
preparations (100mg twice
daily) reduce exacerbation
rates.10 However, it is to be
noted that in this study few
patients were receiving the
range of drugs commonly
available to patients in Australia, including long-acting
bronchodilators and inhaled
corticosteroids. The role of
theophylline in the current
Australian clinical environment is therefore unclear.
Limitations to its use include
a myriad of adverse effects
and a narrow therapeutic
index.

Emerging COPD
pharmacotherapies
The development of oncedaily drug regimens may be
expected to improve adherence with prescribed therapy. Indacaterol is the first
once-daily long-acting beta2
agonist to be studied in
COPD. In a recent study in
patients with moderate to
severe COPD, indacaterol
was at least as effective a
bronchodilator as tiotropium. Furthermore the benefits in symptom control and
health status were similar
between the two treatments.11 Indacaterol is not

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| Australian Doctor | 6 May 2011

Fitness to fly

Table 2: Combination Inhalers and their doses in COPD

Long-acting beta2agonist / corticosteroid

Device

Strength

Dose

Fluticasonesalmeterol*

Metered-dose inhaler
Accuhaler

250g/25g
250g/50g,
500g/50g

Two puffs 12-hourly

One dose 12-hourly

Budesonideeformoterol

Turbuhaler

200g/6g
400g/12g

Two doses 12-hourly

One dose 12-hourly

*Subsidised on the PBS for COPD

currently registered for use

in Australia.
Mometasone is a oncedaily inhaled corticosteroid
under development for use
in COPD, with an aim to
combine it with indacaterol
in a single inhaler. Trials are
currently underway.
QVA149 is a dual-action
bronchodilator combining
indacaterol and the longacting muscarinic antagonist
glycopyrronium. A recent
trial has compared the use
of this combination with
placebo and indacaterol
alone in patients with moderate to severe COPD. The
study demonstrated rapid
and sustained bronchodilatation with marked improvements in FEV1 for the combination compared with
indacaterol alone and
placebo.12
Phosphodiesterase-4 inhibitors such as roflumilast and
cilomilast comprise a new
class of oral agents that
reduce airway inflammation
and increase airway smooth
muscle relaxation. Roflumilast has been demonstrated
to improve lung function
and reduce exacerbation
rates in patients with COPD.
Cilomilast has also been
shown to improve lung function. These agents are not

Table 3: Recommendations for in-flight oxygen

Arterial oxygen saturation

Recommendation

SpO2>95%

In-flight oxygen not required

SpO2 92-95%

In-flight oxygen may be required

SpO2 <92%

In-flight oxygen will be required

currently registered for use

in Australia.

Non-pharmacological
management of stable
COPD
Exercise and pulmonary
rehabilitation

Regular physical activity

should be strongly encouraged and may improve quality of life and reduce exacerbation rates.
Pulmonary rehabilitation is
an evidence-based, multidisciplinary and comprehensive
intervention that should be
offered to all patients with
moderate to severe COPD.
The goals of pulmonary rehabilitation are to achieve maximum levels of independence
and functional capacity
through reducing symptoms,
improving quality of life and
increasing participation in
everyday activities. Comprehensive pulmonary rehabilitation includes exercise training, behaviour modification

(especially related to anxiety,

such as dealing with panic
attacks and dyspnoea, as well
as energy conservation and
approach to exercise) and
education, and has been
shown to produce better outcomes than exercise training
alone.13 Programs should be
individually tailored and
address the physical, emotional and social problems of
the participants. Patients with
very severe exercise limitation
may still benefit.
Unfortunately
there
remain some barriers to
accessing pulmonary rehabilitation programs from the
GP setting. Information
about local programs can be
obtained through the Australian Lung Foundation (see
Online resources, page 32).
Domiciliary oxygen therapy

Patients with moderate to

severe COPD should have
arterial blood gas analysis.
Long-term oxygen therapy

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Modern aircraft fly with a

cabin altitude of about
2500m. This is equivalent to
breathing 15% oxygen at
sea level (the usual sea-level
oxygen is 21%). The British
Thoracic Society recommends that patients obtain
further assessment if they
have:
Severe airways disease.
A recent inpatient admission.
Past in-flight medical
problems.
Comorbid cardiac or cerebrovascular disease.14
A resting arterial oxygen
saturation is a useful screening test (see table 3).
Patients with arterial
oxygen saturation below
95% may require further
assessment and should be
referred to a respiratory
physician. A hypoxic challenge test can be performed
to simulate in-flight conditions.
Patients already receiving
supplemental oxygen should
increase the flow rate while
flying.
Psychosocial aspects

Screening for depression and

anxiety, particularly panic
attacks, is important. Both
are seen very frequently in
moderate to severe COPD.
Counselling in the form of
cognitive behavioural therapy and simply offering general support lead to
improved quality of life.
Appropriate use of antidepressant and anxiolytic medications may also improve
quality of life.
Lung support groups may
afford patients and carers
with emotional support and
meaningful social interactions. The Australian Lung
Foundation can provide contact details for more than
100 groups throughout Australia.

Management of
comorbidities
Patients with COPD frequently die of complications
of cardiovascular disease.
For this reason, cardiovascular risk factors should be
screened for and aggressively managed. Osteoporosis is highly prevalent in
both men and women with
COPD and should be managed as per Australian
guidelines.5

Multidisciplinary care
Patients with COPD often
have complex care needs,
with a range of psychosocial issues. These issues
may require input from a
variety of medical and allied
health sources. Social workers, palliative care nurses
and physiotherapists may all
be involved in caring for the
patient. The GP is often the
best person to co-ordinate
the patients care. There are
a number of services with
Medicare item numbers,
including Enhanced Primary
Care, Chronic Disease Management and Team Care
Arrangement that may help
facilitate co-ordination of
these complex care needs.

End-of-life care
Patients should be encouraged
to appoint an enduring
power of attorney (medical
treatment). Some patients
may wish to discuss the
advantages and disadvantages
of different aspects of emergency medical care, including
intubation, mechanical ventilation and cardiopulmonary
resuscitation. Patients may be
interested in learning about
the benefits and burdens associated with these emergency
medical treatments. Completion of an advanced care
directive that clearly states
their wishes regarding their
future health care in the event
of their becoming too unwell
to make their own decisions,
should be discussed.
Palliative care is an important aspect in the comprehensive care of the COPD
patient. The goal of palliative care is to improve
patients quality of life and
control symptoms when the
primary cause remains treatment resistant. Palliative care
extends beyond relief of dypnoea and encompasses the
physical, psychological and
spiritual needs of the patient
and their family. The trajectory of patients with severe
COPD is often unpredictable. It can be challenging to recognise the appropriate time point to begin
this phase of care.
GOLD suggests the following three points to
prompt consideration of palliative care:
Would you be surprised if
this patient were to die in
the next 6-12 months?
Has the patient made a
choice for treatment limitations, perhaps comfort
care only, or do they have
a special need for supportive or palliative care?
Are there specific clinical
indicators of severe
COPD?7
In patients with refractory
dyspnoea, oral opioids can
be very useful. Referral to
community-based palliative
care organisations should be
encouraged. This can
improve the patients quality
of life and allow them to be
supported in their own
accommodation.

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Specialist management
THERE are clinical situations in which referral to a
respiratory physician may be
appropriate (see box, right).

Specialist assessment
The initial step in specialist
management of COPD is to
confirm the correct diagnosis
has been made and investigate for other contributing
factors for the patients dyspnoea.
Full lung function tests
may need to be performed.
Assessing gas transfer may
help assess severity and
explore the pathophysiology.
Severely reduced gas transfer with only mild to moderate obstruction on spirometry is a pattern frequently
observed in coexistent pulmonary vascular disease
(including pulmonary hypertension and chronic thromboembolic disease) and concomitant interstitial lung
disease.
Measuring plethysmographic lung volumes is
required to help distinguish
between gas trapping and
true coexistent restrictive
lung disease. Gas trapping is
diagnosed when the residual
volume is increased out of
proportion to the total lung
capacity. On simple spirometry, gas trapping can give the
appearance of a mixed
obstructiverestrictive pattern.
Arterial blood gas analysis is required in all patients
with moderate to severe disease or in any patient with
reduced arterial oxygen saturation. As mentioned in the
section on domiciliary
oxygen therapy, treatment of
hypoxaemia confers a mor-

When to refer to a respiratory physician

Severity of symptoms not in keeping with spirometry results
Suspected dual pathology, eg, COPD and bronchiectasis or
pulmonary fibrosis
Rapidly progressive symptoms
Severe disease that remains difficult to control despite
maximal medical therapy
Frequent exacerbations
Chronic hypoxaemia (arterial oxygen saturations <88%).
End-of-life care

Specialist assessment
Spirometry with measurement of gas transfer
Assessment of plethysmographic lung volumes to help
distinguish between gas trapping and true coexistent
restrictive lung disease
Arterial blood gas analysis to check for hypoxaemia
Transthoracic echocardiogram to consider heart failure and
pulmonary hypertension
High-resolution CT of the chest if other pulmonary
parenchymal pathology is suspected, eg, bronchiectasis or
pulmonary fibrosis
Cardiopulmonary exercise testing if aetiology of dyspnoea
remains unclear
A sleep study may be required if coexistent sleep disordered
breathing is suspected

tality benefit. Furthermore,

the diagnosis of hypercapnic
respiratory failure (associated with hypoventilation)
has implications for prognosis and disease severity.
Heart failure is very
common in COPD. Studies
have suggested that about

30% of patients with COPD

have a degree of coexistent
heart failure.
Pulmonary hypertension
is a well recognised complication of many chronic
lung diseases. If the dyspnoea and exercise capacity
is out of keeping with the
severity of the spirometry,
pulmonary hypertension
should be considered. The
classic signs of pulmonary
hypertension, including a
loud second heart sound
and a right parasternal
heave, can be difficult to
detect in a patient with a
barrel-shaped chest, due to
hyperinflation, and a
transthoracic echocardiogram should be performed.
As mentioned above,
another clue to the possible
presence of pulmonary
hypertension is severely
reduced gas transfer out of
keeping with the severity of
obstruction seen on spirometry. Unfortunately treatment options for pulmonary
hypertension
secondary to COPD are
limited.
Exercise testing in
patients with COPD is
useful for determining exercise capacity, cause for
exercise limitation and
symptoms, and response to
treatment. The six-minute
walk test is a cheap and
easy-to-perform assessment
of a patients exercise
capacity. It assesses the
patients walk distance,
arterial oxygen desaturation, pulse rate and dyspnoea score. The results are
reproducible, and 25-50m
is about the minimum clinically significant difference

between tests, that is, a difference of at least 25-50m

between tests is required for
it to be a clinically significant difference, and not just
due to day-to-day variability.
Cardiopulmonary exercise testing is the gold standard for determining the
aetiology of a patients exercise limitation and defining
the extent of exercise limitation. This test provides a
comprehensive assessment
of the pulmonary and cardiovascular systems during
exercise.
The cardiopulmonary
exercise test is a maximal
incremental exercise tolerance test usually performed
on a stationary bicycle. It is
a non-invasive method of
testing respiratory parameters including gas exchange,
minute ventilation, maximal
oxygen
extraction
(V O 2 max) and anaerobic
threshold. (The anaerobic
threshold is when the Krebs
cycles ability to deal with
lactic acid aerobically is
exceeded, and ventilation
needs to be significantly
increased to blow off the
excess acid produced. It is
a measure of fitness and
conditioning.) In addition,
electrocardiography, blood
pressure and pulse oximetry are monitored.
A cardiopulmonary exercise test may help distinguish between a pulmonary
cause of exercise limitation,
a cardiac cause of exercise
limitation and deconditioning. The classic pattern seen
in a patient with severe
COPD and no cardiac disease is:

An abnormally high ventilatory response to exercise

with maximum ventilation reached.
A reduced anaerobic
threshold and VO2max.
Significant arterial oxygen
desaturation.
The box, left, provides a
summary of specialist
assessment.

Surgical and other

bronchoscopic treatments for emphysema
Patients with moderate to
severe emphysema and a
single large bulla may benefit from surgical bullectomy.
In a highly selected group
of patients with severe
COPD and upper-lobe predominant emphysema, lung
volume reduction surgery
may improve mortality and
exercise capacity.
These surgical procedures
can lead to a reduction in
gas trapping and hyperinflation. This allows for
much more efficient ventilation, especially during exercise or exertion.
In recent times there has
been growing interest in
bronchoscopic lung volume
reduction. A number of
techniques are under investigation. These include
placement of one-way endobronchial valves, insertion
of fibrin-like gel or application of endobronchial steam
to collapse the emphysematous airways and thus
achieve lung volume reduction. These techniques are
still experimental but may
lead to promising therapeutic options in patients with
upper-lobe predominant disease.

Managing acute exacerbations of COPD

ACUTE exacerbations of COPD
can be defined as an increase in
symptoms beyond normal day-today variation that are typically
associated with worsening dyspnoea, cough and sputum production.

Management in the ambulatory

setting
Increased use of short-acting beta2agonists may provide symptomatic
benefit.
A brief course of oral prednisolone (about 10 days) at 3040mg may improve lung function
and reduce the duration of illness.
A history of increased sputum
purulence suggests a course of oral
antibiotics should be prescribed.
The most frequently isolated organisms include Haemophilus influenzae, Streptococcus pneumoniae and
Moraxella catarrhalis. Australian
guidelines recommend amoxycillin
or doxycycline.15 Persisting purulent sputum and failure to improve
should prompt microbiological
examination of a sputum sample.
The box, right, summarises when
to refer a patient for emergency
management.

When to refer a patient for

emergency (inpatient)
management

Assessment and management in the inpatient setting

ECG:
to exclude cardiac arrhythmias or acute coronary syndrome.

Acutely unwell: unstable vital

signs, hypoxaemia (using a
bedside pulse oximeter), impaired
conscious state
Inability to cope at home or
perform activities of daily living

Chest radiograph:
if consolidation is seen on the chest radiograph, IV antibiotics
may be required for treatment of pneumonia
Arterial blood gas analysis and other blood tests:
acidotic respiratory failure (pH <7.35, PaCO2 >45mmHg) will benefit from
non-invasive ventilation

Failure to improve despite

therapies described above

Cautious use of supplemental oxygen:

Suspected concomitant illness

such as pneumonia or heart failure

Treat heart failure if clinically indicated

Management in the inpatient

setting
The box above right summarises typical inpatient management, in addition to the management described
above for the ambulatory setting.
Patients presenting to hospital with
an acute exacerbation of COPD need
to be further assessed with an ECG,
blood tests including arterial blood
gas analysis and a chest radiograph.
A chest radiograph should be performed to exclude other causes of
acute dyspnoea. A chest radiograph
may help to exclude other important
causes of acute dyspnoea, such as:

target arterial oxygen saturation of 88-92%

Acute pulmonary oedema.

Pneumonia.
Spontaneous pneumothorax.
A negative D-dimer assay may
help exclude pulmonary embolism.
A baseline ECG should be performed to exclude cardiac arrhythmias or acute coronary syndrome.
Supplemental oxygen should be
used cautiously. Oxygen flow rates
should be carefully titrated, aiming to
achieve arterial oxygen saturations
of 88-92%. Over-oxygenation can
lead to worsening respiratory depression and worsening hypercapnia. If
patients require high-flow oxygen,
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alternative diagnoses such as acute

pulmonary oedema or pulmonary
embolism should be considered.
An arterial blood gas analysis is
useful to assess the severity of the
exacerbation and check for hypercapnic respiratory failure. The arterial blood gas analysis also serves as a
useful baseline from which any
changes can be measured. If the arterial blood gas demonstrates acidotic
respiratory failure (pH <7.35, PaCO2
>45mmHg) non-invasive positive
pressure ventilation should be considered.
Non-invasive ventilation is the

delivery of mechanically assisted

breaths without placement of an
endotracheal tube. Ventilation is
delivered via a tightly fitting nasal or
facial mask. Non-invasive ventilation
in acute acidotic respiratory failure
in COPD greatly reduces intubation
rates and significantly reduces mortality.
Patients may present with multiple acute problems. Pneumonia and
cardiac failure are often diagnosed
during an acute exacerbation of
COPD. If the chest radiograph
demonstrates pneumonic consolidation, antibiotics covering typical and
atypical pathogens should be prescribed. IV antibiotics may be
required. For moderate communityacquired pneumonia (assuming no
allergies), Therapeutic Guidelines
suggests intravenous benzylpenicillin
and oral doxycycline, and for severe
community acquired pneumonia,
intravenous ceftriaxone and
azithromycin.15
Patients with heart failure may
require diuretic therapy and a subsequent echocardiogram as well as consideration of an ACEI and possibly a
beta blocker.
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HOW TO TREAT Chronic obstructive pulmonary disease

Prognosis

Evidence-based treatments for COPD

THE global BOLD study projects that

COPD will become the third-most
common cause of death worldwide
by 2020. Patients with hypoxic respiratory failure (PaO2 <55mmHg) have
a three-year survival of about 50%.
Acute exacerbations requiring inpatient care often predict a poor prognosis.
A recent meta-analysis of survival
data after admission for an acute exacerbation of COPD reported a 12month mortality rate of 33%.16 Many
never return to their pre-morbid level
of functioning.
The BODE index is a useful predictor of survival in patients with stable
COPD. Those with the most severe
COPD generally have an overall fouryear survival of less than 20%, while
those with the mildest disease have a
four-year survival rate of 80%.

Intervention

Level of evidence

Smoking cessation to reduce mortality

Level I

Smoking cessation to reduce lung

function decline

Level I

Home oxygen reduces mortality

Level I

Short-acting beta2 agonist inhaler for

short term relief of dyspnoea

Level I

Long-acting anticholinergic inhaler, to

improve symptoms and quality of life

Level I

Pulmonary rehabilitation to improve

symptoms, quality of life

Level I

Pneumococcal vaccine to prevent

pneumonia

Level II

Lung volume reduction surgery in

appropriate patients to improve
symptoms (not mortality)

Level II

Opioids reduce dyspnoea

Level I

Summary

References and further

reading

COPD should be considered in current and past

smokers over 35

Available on request from

julian.mcallan@
reedbusiness.com.au

COPD is defined as a post-bronchodilator FEV1/FVC

ratio <0.7 on spirometry with an appropriate history of
exposure
Assistance with smoking cessation is the single most
important intervention
Inhalers may help control symptoms and prevent
exacerbations (see Management section, page 28, for
details)
Pulmonary rehabilitation may improve symptoms and
quality of life

Online resources
Australian Lung
Foundation:
www.lungfoundation.
com.au
How to Treat Oxygen
therapy. Australian
Doctor, 26 February
2010:
www.australiandoctor.com.
au//htt/pdf/AD_029_036_
FEB26_10.pdf

Hypoxaemic patients benefit from supplemental

oxygen

Authors case study

MR ZA is a 67-year-old
former heavy smoker with
moderately severe COPD.
He has a complex medical
history including atrial fibrillation, permanent pacemaker, ischaemic heart disease and depression. He has
been diagnosed with moderate obstructive sleep apnoea
but declines the use of continuous positive airway pressure therapy.
His usual inhalers include
salbutamol as required, daily
tiotropium and twice-daily
budesonide formoterol
200/6g. His other medications include warfarin,
digoxin, ramipril, atorvastatin and sertraline. He is
up-to-date with his influenza
vaccine.
Mr ZA lives at home
alone and manages independently. He can walk
about 25m before develop-

ing dyspnoea. Despite this,

he still enjoys gardening. He
stopped smoking 18 months

ago after several attempts.

Spirometry performed at
the beginning of 2010

Figure 3: Flowvolume curve.

demonstrated
severe
obstruction, with a reduced
FEV1 and a preserved FVC.
There was no significant
bronchodilator response.
The gas transfer (total lung
capacity) was severely
reduced. The flowvolume
curve was markedly scalloped, consistent with airflow obstruction (the
normal predicted curve is in
green) (figure 3).
In April 2010 Mr ZA presented to the ED with one
week of dyspnoea, fatigue,
reduced mobility and brown
sputum. The important
examination findings were
bilateral wheeze and hypoxaemia (arterial oxygen saturation of 87% on room air).
Mr ZA stated that if he were
to become very unwell he
would not want life support.
The chest radiograph

showed no signs of interstitial oedema or consolidation

(figure 4). Arterial blood gas
analysis demonstrated hypoxaemia, with a PaO 2 of
53mmHg (normal range 70100mmHg) and PaCO2 of
45mmHg (NR 35-45mmHg).
Mr ZA was admitted to
hospital and his usual medications were continued. He
received seven days of prednisolone 30mg oral daily
and oral amoxycillin. He
received daily chest physiotherapy. He was discharged
home on day four, with arterial oxygen saturations of
93% on room air.
He has since completed a
pulmonary rehabilitation
program and has remained
well. He continues with his
maintenance exercises at
home. His local doctor has
given him the pneumococcal
vaccination.

Figure 4: Mr ZAs chest X-ray.

Flow
8
Normal predicted
6

L/minute

-2

-4

-6

-1

2
Volume (L)

4
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HOW TO TREAT Chronic obstructive pulmonary disease

GPs contribution

DR SUE PAGE
Lennox Head, NSW

Case study
ALAN, 78, is a retired pharmacist who has smoked 15
cigarettes daily since the
1950s and who remains
unwilling to quit. He has a
long history of mild to moderate asthma for which he
takes ciclesonide (Alvesco)
160g twice daily and salbutamol (Ventolin) as required.
About once a year he
requires oral prednisone for
acute exacerbations.
He is up-to-date with his
vaccinations, including
Fluvax, Pneumovax, and
Boostrix (there are high pertussis rates in his area). His
exercise tolerance has slowly
declined over the 20 years he
has been attending the prac-

tice and he has a peak expiratory flow rate of

214L/minute (predicted
503), FEV1 2.12L and FVC
3.32L (FEV 1 /FVC 63.9%
pre- and 58.8% post-bronchodilator).
He has had diabetes for
nearly 15 years, initially
responding to metformin but
now requiring the addition
of Novomix insulin. He is
not careful with his diet, and
sugars are usually in the 79mmol/L range. His diabetes
is complicated by hypercholesterolaemia and hypertension, for which he takes
hydrochlorothiazideirbesartan (Karvezide), aspirin, simvastatin (Lipex) and prazosin.
Five years ago he had
chest pains at work and was
found to have two-vessel disease, which responded well
to CABG, followed by stent
repair of his asymptomatic
aortic aneurysm. He developed AF and mildly
impaired cardiac function
with mitral regurgitation,
and warfarin, metoprolol

and digoxin were added.

Although of slim build, he
has sleep apnoea, for which
he uses continuous positive
airways pressure.
He presents with a twomonth history of increasing
cough, not responding to
increased use of his usual
inhalers. Last weekend he
noted blood staining of his
sputum, and the chest X-ray
arranged by the hospital
showed a suspicious lesion.
His sputum cytology has
returned clear of malignancy,
but he has acid-fast bacilli
consistent with tuberculosis.

Questions for the author

Many patients in general
practice have comorbidities
for which the guidelines are
in conflict, such as for
asthma, COPD and cardiac
disease. How should these be
managed?
Cardiovascular disease is a
frequent comorbidity in
patients with COPD and
should be managed appropriately, including with selective beta blockers, if

How to Treat Quiz

required. Diabetes control

may be adversely affected if
oral corticosteroids are
needed frequently for exacerbations of asthma or
COPD, but inhaled therapy
should be maximised to try
to reduce such exacerbations.
As the use of steroids can
reactivate tuberculosis, how
should his asthma be treated
in the short and long term
and what should he use for
COPD exacerbations?
The presence of acid-fast
bacilli in his sputum indicates
active pulmonary tuberculosis. This requires urgent
treatment and the patient
should be in respiratory isolation. Once appropriate
tuberculosis treatment has
started, corticosteroids are
not absolutely contraindicated and any exacerbation
of his airways disease should
be treated on its merits.

General questions for the

author
In patients already using
steroids and bronchodila-

tors for asthma, does concurrent COPD tend to be

more or less severe? That is,
does regular medication
influence the incidence and
progression of COPD such
as in smokers who are also
asthmatic?
This is an excellent question. Inhaled medication in
the form of anti-cholinergics, beta agonists and corticosteroids have not been
systematically studied in a
cohort of patients with
asthma who smoke to
determine whether they may
have a protective role.
There is little evidence
that these medications
retard the progression of
COPD. Their main role is
in symptom control and
prevention of exacerbations.
On the other hand, smoking cessation has been
shown to retard decline in
lung function.
Understanding that chest Xrays are not performed routinely for asthma or COPD,
what should the red flag

indicators be for radiological assessment of long-term

patients?
Patients with unexplained
weight loss, haemoptysis or
a significant change in their
level dyspnoea or exercise
capacity may require further
radiological assessment.
Clinical suspicion of pneumonia or heart failure may
also require further imaging.
As nearly one-third of
COPD patients develop cardiac disease, should this be
routinely screened for and,
if so, how often?
Guidelines do not provide
us with any solid evidence
on this topic. Annual
screening for hypertension,
diabetes and dyslipidaemia
may be a sensible approach.
If lung function is stable but
breathlessness is worsening,
or is out of keeping with the
apparent severity of the
lung disease on lung function testing, underlying cardiac disease should be
excluded.

INSTRUCTIONS
Complete this quiz online and fill in the GP evaluation form to earn 2 CPD or PDP points. We no longer accept quizzes
by post or fax.
The mark required to obtain points is 80%. Please note that some questions have more than one correct answer.

Chronic obstructive pulmonary disease

6 May 2011
1. Which TWO statements are correct?
a) COPD includes chronic bronchitis and
emphysema
b) Predisposing factors for COPD include
smoking, asthma and childhood respiratory
infections
c) A normal physical examination excludes a
diagnosis of COPD
d) A prolonged inspiratory phase on
auscultation is characteristic of COPD
2. Which TWO statements are correct?
a) Post-bronchodilator FEV1/FVC ratio <0.6
excludes a diagnosis of COPD
b) FEV1 is a poor indicator of COPD severity
and prognosis
c) Frequency of exacerbations, exercise
limitation and degree of disability are
important determinants of COPD severity
d) FEV1 of 35% of predicted plus dyspnoea
with minimal exertion and significant
limitation of daily activities is consistent with
severe COPD
3. Which THREE statements are correct?
a) Chest X-ray is a sensitive test for the
diagnosis of COPD
b) PaO2<55mmHg is an indication for
domiciliary oxygen therapy
c) A patient with pH <7.35 and PaCO2
>50mmHg may need urgent ventilatory
support
d) Chronic breathlessness out of keeping with

spirometric abnormality may indicate

pulmonary hypertension or interstitial lung
disease in addition to COPD
4. Which TWO statements are correct?
a) Diffusing capacity testing may be useful for
identifying pulmonary hypertension and
interstitial lung disease
b) Reduced BMI is associated with a poorer
COPD prognosis
c) Smoking cessation in COPD results in
symptomatic improvement but no reduction
in mortality
d) Short-acting beta2 agonists should not be
used in the management of COPD
5. Which TWO statements are correct
regarding the management of COPD?
a) A patient with exacerbations despite prn
salbutamol may benefit from regular
tiotropium therapy
b) A patient on regular tiotropium with one
exacerbation a year and FEV1 of 78% should
have regular long-acting beta2 agonist and
corticosteroid in a combined inhaler added to
their treatment
c) Spacers are designed to work best with rapid
forceful inspiration
d) Influenza vaccination reduces the
development of severe respiratory
complications of the influenza virus
6. Which THREE statements are correct

ONLINE ONLY
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regarding the management of COPD?
a) Current best practice supports the use of
regular antibiotics for prevention of
exacerbations
b) Regular physical activity may improve
quality of life and reduce exacerbation rates
c) Comprehensive pulmonary rehabilitation is
recommended for patients with COPD
d) Long-term oxygen therapy in chronically
hypoxic patients used for more than
15 hours a day improves survival
7. Which TWO statements are correct?
a) Patients with arterial oxygen desaturation
during exercise do not benefit from
intermittent (portable) oxygen
b) COPD patients with oxygen saturation
above 95% usually need in-flight oxygen
c) COPD patients with an oxygen
saturation of 90% usually require in-flight
oxygen
d) Osteoporosis is a very common and
treatable comorbidity in COPD patients
8. Which THREE statements are correct?
a) Oral opioids are contraindicated in the
palliation of refractory dyspnoea in COPD
patients
b) Severely reduced gas transfer with mild
obstruction on spirometry raises the
possibility of COPD with pulmonary
comorbidities
c) About 30% of patients with COPD have

coexistent heart failure

d) Pulmonary hypertension secondary to
COPD can be confirmed using an
echocardiogram
9. Which TWO statements are correct?
a) Exercise testing is usually not helpful in
managing patients with COPD
b) The six-minute walk test assesses the
patients walk distance, arterial oxygen
desaturation, pulse rate and dyspnoea
score
c) A difference of 10m between six-minute
walk tests is regarded as clinically
significant
d) Cardiopulmonary exercise testing may
distinguish the contribution of cardiac
causes, pulmonary causes, and the
effect of deconditioning on a patients
exercise limitation
10. Which TWO statements are correct?
a) Bullectomy and upper-lobe lung reduction
surgery do not usually improve ventilatory
function
b) Amoxycillin or doxycycline are first-line
antibiotics for infective exacerbations of
COPD
c) Oral prednisolone is not recommended for
exacerbations of COPD
d) Suspected pneumonia or heart failure in
COPD patients warrants inpatient
management

CPD QUIZ UPDATE

The RACGP requires that a brief GP evaluation form be completed with every quiz to obtain category 2 CPD or PDP points for the 2011-13 triennium. You can
complete this online along with the quiz at www.australiandoctor.com.au. Because this is a requirement, we are no longer able to accept the quiz by post or
fax. However, we have included the quiz questions here for those who like to prepare the answers before completing the quiz online.

HOW TO TREAT Editor: Dr Giovanna Zingarelli

Co-ordinator: Julian McAllan
Quiz: Dr Giovanna Zingarelli

NEXT WEEK Addictions are treatable this is no longer an area of medicine to put aside as a social or legal problem with no effective treatments. The next How to Treat starts a two-part miniseries on this
absorbing topic. The authors are Dr Susan Boyd, specialist in public health and addiction medicine, and director, Practice of Health, St Leonards, NSW; and Dr Simon de Burgh, senior staff specialist, drug
and alcohol, Royal North Shore Hospital, St Leonards, NSW.

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| Australian Doctor | 6 May 2011

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