The document covers the second edition of the Malaysian clinical practice guidelines (CPG) for chronic obstructive pulmonary disease (COPD), emphasizing its definition, pathophysiology, and systemic effects. It highlights the critical role of smoking as a primary risk factor and outlines the management strategies for stable COPD and exacerbations. Lastly, it covers the importance of early diagnosis through spirometry and the need for effective smoking cessation interventions.

1. CHRONIC OBSTRUCTIVE
PULMONARY DISEASE:
The New Malaysian 2nd Edition CPG – Its Importance
From The Perspective of Emergency Medicine
K S CHEW
School of Medical Sciences
Universiti Sains Malaysia

2. FREE DOWNLOAD at:
Malaysian Thoracic Society Website
http://www.mts.org.my/resources.html

3. DEFINITION

4. DEFINITION OF COPD
• COPD is defined as a preventable and
treatable respiratory disorder largely
caused by smoking, is characterised by
progressive, partially reversible airflow
obstruction and lung hyperinflation with
significant extrapulmonary (systemic)
manifestations and co-morbid conditions
all of which may contribute to the severity
of the disease in individual patients.
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

5. SYSTEMIC EFFECTS OF COPD
• Several recent studies have clearly shown
that COPD is associated not only with an
abnormal inflammatory response of the
lung parenchyma but also with evidence of
systemic inflammation, including systemic
oxidative stress, activation of circulating
inflammatory cells and increased levels of
pro-inflammatory cytokines
Agusti AG. Systemic effects of chronic obstructive pulmonary disease. Proc Am Thorac Soc 2005;
2 (4):367-70; discussion 71-2.

6. Examples of Co-morbidities Associated
With COPD
• Ischaemic heart disease
• Osteopenia, osteoporosis and bone
fractures
• Cachexia and malnutrition
• Normochromic normocytic anaemia
• Skeletal muscle wasting and peripheral
muscle dysfunction

7. SYSTEMIC EFFECTS OF COPD
• Various studies have shown that the lung
inflammatory response is characterised by
• increased numbers of neutrophils, macrophages
and T-lymphocytes with a CD8+ predominance
• augmented concentrations of proinflammatory
cytokines, such as leukotriene B4, interleukin
(IL)-8 and tumour necrosis factor (TNF)-a
• evidence of oxidative stress caused by the
inhalation of oxidants (tobacco smoke) and/or the
activated inflammatory
Agusti AG. Systemic effects of chronic obstructive pulmonary disease. Proc Am Thorac Soc 2005;
2 (4):367-70; discussion 71-2.

8. WHY SYSTEMIC EFFECTS?
Hypothesis
• The tobacco smoke alone causes
oxidative stress
• The pulmonary inflammatory process in
the lung itself is the source of these
systemic inflammation.
• The increased surface expression of
several neutrophil adhesion molecules
may be due to genetic predisposition
Agusti AG. Systemic effects of chronic obstructive pulmonary disease. Proc Am Thorac Soc 2005;
2 (4):367-70; discussion 71-2.

9. DISEASE BURDEN

10. COPD is projected to be the third
biggest cause of mortality by 2020
1990 2020
Ischaemic heart disease 1st Ischaemic heart disease
Cardiovascular disease 2nd Cardiovascular disease
Lower respiratory infection 3rd COPD
Diarrhoeal disease 4th Lower respiratory infection
Perinatal disorders 5th Lung cancer
COPD 6th Road traffic accident
Tuberculosis 7th Tuberculosis
Measles 8th Stomach cancer
Road traffic accident 9th HIV
Lung cancer 10th Suicide
Murray CJ & Lopez AD. Lancet 1997;349:1498–1504.

11. Percent Change in Age-Adjusted Death
Rates, U.S., 1965-1998
Proportion of 1965 Rate
3.0
Coronary Stroke Other CVD COPD All Other
2.5 Heart Causes
Disease
2.0
1.5
1.0
0.5
0
–59% –64% –35% +163% –7%
1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998
Source: NHLBI/NIH/DHHS

12. Model Projections of Moderate-Severe
COPD in Population Aged ≥ 30 Years
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

13. PATHOPHYSIOLOGY

14. INFLAMMATION IN COPD
SMALL AIRWAY PARENCHYMAL
DISEASE DESTRUCTION
Airway Inflammation Loss of alveolar
attachment
Airway Remodeling
Decrease of elastic recoil
AIRFLOW LIMITATION

15. Pathogenesis of
COPD
Host factors
Amplifying mechanisms
Source: Peter J. Barnes, MD

16. Inflammatory Cells Involved in COPD
Source: Peter J. Barnes, MD

17. Oxidative Stress in COPD
Macrophage Neutrophil
Anti-proteases
SLPI α1-AT
Proteolysis
Plasma leak Bronchoconstriction
↑ Mucus secretion
Source: Peter J. Barnes, MD

18. Inflammation plays a central role in the
pathogenesis and pathology of COPD
Cigarette smoke
(and other irritants)
Genetic susceptibility
Lung Inflammation
• Inflammatory cells
• Inflammatory mediators
• Oxidative stress
• Proteases
COPD pathology
Obstructive Mucus Alveolar
bronchiolitis hypersecretion wall destruction
Adapted from Global Initiative for Chronic Obstructive Lung Disease (GOLD) Guidelines, 2009. Available from http://www.goldcopd.com/

19. DIAGNOSIS AND
CLASSIFICATION OF SEVERITY

20. DIAGNOSIS
• Spirometry is essential for the diagnosis of
COPD.
• The diagnosis should be confirmed by
spirometry showing a post-bronchodilator
FEV1/FVC ratio of less than 70%.
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

21. DIAGNOSIS
• A clinical diagnosis of COPD should be
considered in any individual with
symptoms of chronic cough, sputum
production or dyspnoea and a history of
exposure to risk factors for the disease,
especially cigarette smoking.
• But every effort should be made to refer
the patient for spirometry to confirm the
diagnosis.
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

22. CLASSIFICATION
OF COPD
SEVERITY
Spirometry is essential
for the diagnosis of
COPD and is useful for
assessment of the
severity of airflow
obstruction (Grade C)
(Malaysian COPD CPG,
2nd Edition, Nov 2009)

23. The Modified Medical Research Council
(MMRC) Dyspnoea Scale
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

24. Classification of
COPD Severity Based
on Spirometric
Impairment and
Symptoms
(Malaysian COPD CPG,
2nd Edition, Nov 2009)

25. Reversible Irreversible
Source: Peter J. Barnes, MD

26. (Malaysian COPD CPG, 2nd Edition, Nov 2009)

27. RISK FACTORS

28. RISK FACTORS
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

29. RISK FACTORS
• Cigarette smoking is the best known and
most studied risk factor for COPD.
• About 15% of smokers develop COPD.
• However, tobacco smoke is the risk factor
for as much as 90% of the cases of
COPD.
• Non-smokers may also develop the
disease
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

30. TOBACCO SMOKE
• Some studies have suggested that women
are more susceptible to the effects of
tobacco smoke than men
• Quantification of tobacco consumption:
total pack-years = (number of cigarettes
smoked per day ÷ 20) x number of years
of smoking
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

31. TOBACCO SMOKE
• Smoking cessation is the single most
effective - and cost effective - intervention
to reduce the risk of developing COPD and
stop its progression.
• Even a brief (three-minute) period of
counselling to urge a smoker to quit results
in smoking cessation rates of 5-10%.
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

32. PHARMACOTHERAPIES FOR SMOKING
CESSATION
• Nicotine replacement therapy (NRT) in the
form of transdermal patches, gums,
lozenges and nasal sprays
• Varenicline
• a nicotinic acetylcholine receptor partial
agonist
• Bupropion
• Nortriptyline
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

33. 5’A’s FOR SMOKING CESSATION
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

34. VICIOUS CIRCLE HYPOTHESIS:
HOW INFECTION CONTRIBUTE TO THE
PATHOGENESIS AND PROGRESSION
OF COPD
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

35. MANAGEMENT OF STABLE COPD
AND EXACERBATIONS

36. (Malaysian COPD CPG, 2nd
Edition, Nov 2009)

37. MANAGING STABLE COPD
• COPD patients at any stage of disease
severity should be advised to quit smoking
if they still smoke. [Grade A]
• In patients with mild COPD who are
symptomatic, SABA or SAAC or a
combination of both may be prescribed
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

38. MANAGING STABLE COPD
• In patients with moderate to very severe
COPD with persistent symptoms, but
without frequent COPD exacerbations,
either a LAAC or LABA may be initiated.
• If symptoms persist despite this treatment,
an ICS/LABA combination should be
added; and vice versa. [Grade A]
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

39. INDICATIONS FOR HOSPITALISATION
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

40. Algorithm for Managing AECOPD:
Home Management
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

41. Algorithm for Managing AECOPD:
Hospital Management
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

42. INDICATIONS FOR NIV
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

43. CONTRAINDICATIONS FOR NIV
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

44. INDICATIONS FOR MECHANICAL
VENTILATION
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

45. ANTIBIOTICS
• Antibiotics should be given to patients with
AECOPD having at least 2 out of 3
cardinal symptoms (i.e., purulent sputum,
increased sputum volume and/or
increased dyspnoea).
• Antibiotics are beneficial during AECOPD
but have no proven benefit to prevent
exacerbations
(Malaysian COPD CPG, 2nd Edition, Nov 2009)

46. Understanding Potential Long Term
Impacts on Function with Tiotropium
(UPLIFT) TRIAL
• Tiotropium confers symptomatic and
spirometric improvement in patients with
COPD but does not influence the
underlying gradual decline in lung function
as measured by FEV1
– Tashkin DP et al. A 4-year trial of tiotropium in
chronic obstructive pulmonary disease. N Engl
J Med 2008 Oct 9; 359:1543.

47. RECENT TRIALS

48. Towards a Revolution in COPD Health
(TORCH) study
• In this study of COPD patients, inhaled
therapy with fluticasone plus salmeterol
was associated with a 2.6 percentage-
point reduction in mortality that just failed
to reach statistical significance (p=0.052).
– Calverley PMA et al. Salmeterol and fluticasone
propionate and survival in chronic obstructive
pulmonary disease. N Engl J Med 2007 Feb 22;
356:775-89.

49. Towards a Revolution in COPD Health
(TORCH) study
• In several respects, salmeterol
monotherapy appeared superior to
fluticasone monotherapy — an interesting
outcome given the current controversy
about potential harms with long-acting ß-
agonists in asthma.
– Calverley PMA et al. Salmeterol and fluticasone
propionate and survival in chronic obstructive
pulmonary disease. N Engl J Med 2007 Feb 22;
356:775-89.

50. Towards a Revolution in COPD Health
(TORCH) study
• At the current moment, the conclusion
from TORCH study is:
• combination therapy offers several
advantages (but not clear-cut mortality
reduction)
• that steroid monotherapy should not be
advocated
• that salmeterol monotherapy appears to be
safe
• the increased incidence of pneumonia with
fluticasone requires further investigation.

51. OPTIMAL TRIAL
• Addition of fluticasone–salmeterol to
tiotropium therapy did not statistically
influence rates of COPD exacerbation but
did improve lung function, quality of life,
and hospitalization rates in patients with
moderate to severe COPD
• Aaron SD et al. Tiotropium in combination with
placebo, salmeterol, or fluticasone–salmeterol for
treatment of chronic obstructive pulmonary
disease. A randomized trial. Ann Intern Med
2007 Feb 19;

52. Can we give COPD
patients a brighter start
to their day and reduce
their future risk ?

53. The impact of COPD Exacerbations
Increased symptoms Reduced lung function
“I get less air… I panic and
think now I’m going to die” 1
Increased mortality2,3 Reduced quality of life
Lower QoL is a powerful 91% of patients reported an
indicator of hospitalisation & impact on activities of daily living
mortality4 50% of patients stop all activities1
1 Vogelmeier et al, ATS abstract 2004.
2 Donaldson et al, Thorax 2002.
3 Fabbri et al, Thorax 1998
4 Fan et al; Chest; August, 2002

54. Increased frequency of exacerbations
increases the risk of mortality in COPD
1.0 0 exacerbations
1–2 exacerbations
≥ 3 exacerbations
0.8
Survival probability
P < 0.0002
0.6
P < 0.0001
0.4 P = 0.069
0.2
0
0 10 20 30 40 50 60
Time (months)
Soler-Cataluna JJ, et al. Thorax 2005;60:925–931.

55. COPD symptoms are the worst in the morning
Patients (%)
50
46% All COPD patients (N=803)
Severe COPD patients (N=289)
45
40
37%
35 34%
30 28%
27%
25%
25
21%
20
17%
16%
15
11%
10 9% 9%
7%
5 4%
0
Morning Mid-day Afternoon Evening Night No particular Difficult to say
time of day
Results from 803 interviews in seven EU countries and the USA
Partridge MR et al. Current Medical Research and Opinion 2009; 25(8): 2043-2048

56. A slow and difficult morning can impact the rest of the day
• Getting out of bed
• Washing
• Dressing
• Walking up and down stairs
• Making breakfast
Partridge MR et al. Current Medical Research and Opinion 2009; 25(8): 2043-2048

57. COPD patients want faster symptom relief
Faster symptom relief 55%
Longer intervals between flare-ups 40%
Fewer side effects 36%
Better ability to cope with daily chores 27%
Lower costs of treatment 27%
Better doses 23%
0 10 20 30 40 50 60
Patients (%)
Results from 1100 interviews in five EU countries and the USA
Miravitlles M, et al. Respir Med 2007;101:453–460.

58. Fast relief in the morning
is a window of
opportunity for
better symptom control

59. PHARMACOLOGY OF
SYMBICORT

60. Budesonide
• Anti-inflammatory agent
+ Formoterol
• Long-acting bronchodilator
• Fast onset within 3-5
hours • Onset as fast as salbutamol
• Demonstrated dose (1-3 minutes)
response
• Demonstrated dose
response 6 µg to 54 µg/day
• Greater efficacy in
combination with
formoterol vs. higher
doses of budesonide
alone
®
Only Symbicort Turbuhaler can be
prescribed in this manner
Symbicort® Turbuhaler® Product Monograph

61.  Formoterol has a rapid onset with long duration of
action
 Whereas salmeterol, though has an equivalent
bronchodilator effect, has a slower onset of action
 This probably reflects the fact that formoterol is a
full agonist, whereas salmeterol is a partial agonist
1. Barnes PJ. Scientific rationale for using a single inhaler for asthma control. Eur Respir J. 2007 Mar;29
(3):587-95.
2. Bousquet J, Boulet LP, Peters MJ, Magnussen H, Quiralte J, Martinez-Aguilar NE, Carlsheimer A.
Budesonide/formoterol for maintenance and relief in uncontrolled asthma vs. high-dose salmeterol/
fluticasone. Respir Med. 2007 Dec;101(12):2437-46.
3. Kuna P, Peters MJ, Manjra AI, Jorup C, Naya IP, Martinez-Jimenez NE, Buhl R. Effect of budesonide/
formoterol maintenance and reliever therapy on asthma exacerbations. Int J Clin Pract. 2007 May;61(5):
725-36.

62.  Formoterol is a full β2-agonist, whereas salmeterol
is a partial β2-agonist.
 Therefore, increasing the dose of formoterol in the
presence of ICS is associated with increased
protection from exacerbations.
 But higher doses are not recommended with
salmeterol because it has a plateau in its efficacy at
around 100µg/day.
1. Barnes PJ. Scientific rationale for using a single inhaler for asthma control. Eur Respir J. 2007 Mar;29
(3):587-95.
2. Bousquet J, Boulet LP, Peters MJ, Magnussen H, Quiralte J, Martinez-Aguilar NE, Carlsheimer A.
Budesonide/formoterol for maintenance and relief in uncontrolled asthma vs. high-dose salmeterol/
fluticasone. Respir Med. 2007 Dec;101(12):2437-46.
3. Kuna P, Peters MJ, Manjra AI, Jorup C, Naya IP, Martinez-Jimenez NE, Buhl R. Effect of budesonide/
formoterol maintenance and reliever therapy on asthma exacerbations. Int J Clin Pract. 2007 May;61(5):
725-36.

63. ICS upregulates the β2-receptors
LABA increases the nuclear
translocation of glucocorticoid Barnes PJ. Scientific rationale for using a single
inhaler for asthma control. Eur Respir J. 2007 Mar;
receptors 29(3):587-95.

64.  Direct bronchodilator effect
 Non-bronchodilator effects
◦ Reduced plasma exudation
 by relaxes the endothelial cells, thus closes the gap
◦ Mast cell stabilization
◦ Reduced neutrophils
 Thus reduce the releases of reactive oxygen species via
the activated neutrophils
Barnes PJ. Scientific rationale for using a single
inhaler for asthma control. Eur Respir J. 2007 Mar;
29(3):587-95.

65. Barnes PJ. Scientific rationale for using a single
inhaler for asthma control. Eur Respir J. 2007 Mar;
29(3):587-95.

66. How to help COPD patients achieve their
goals in everyday life ?

67. Therapy at each stage of COPD
I: Mild II: Moderate III: Severe IV: Very Severe
• FEV1/FVC < 70%
• FEV1 < 30%
• FEV1/FVC < predicted
• FEV1/FVC < 70% 70% • or FEV1 < 50%
 50% ≤ FEV1 <  30% ≤ FEV1 < predicted plus
• FEV1/FVC < 70% 80% 50% predicted chronic
predicted respiratory failure
• FEV1 ≥ 80%
predicted
Active reduction of risk factor(s); influenza vaccination
Add short-acting bronchodilator (when needed)
Add regular treatment with one or more long-acting
bronchodilators (when needed); Add rehabilitation
Add inhaled glucocorticosteroids if
repeated exacerbations
Add long-term
oxygen if chronic
respiratory failure
Consider surgical
treatments
Global Initiative for Chronic Obstructive Lung Disease
FVC = forced vital capacity (GOLD) Guidelines, 2008. Available from http://www.goldcopd.com/

68. Symbicort® rapidly improves FEV1 within 5 minutes
Symbicort® + TIO+ works faster than TIO+ alone Symbicort works faster than Sal/Flu#
Morning FEV1 (I) FEV1 change from pre-dose (ml)
1.32 120
Symbicort + tiotropium
Symbicort ® 320/9 µg bid
1.28 P < 0.001
100 P < 0.001
1.24 P < 0.001 P < 0.001
80
1.20
1.16 60
Sal/Flu 50/500 µg bid
1.12 40
1.08 tiotropium
20
1.04
1.00 0
-1 0 5 10 15 0 5 10 15
Time (minutes) since drug intake Minutes post-dose
+TIO = tiotropium # Sal/Flu = salmeterol/fluticasone
Adapted from Welte et al. Am J Respir Crit Care Med 2009, 180: 741-750 Partridge MR, et al. Ther Adv Respir Dis 2009

69. Greater control over morning activities with Symbicort®
Symbicort® 320/9µg bid
salmeterol/fluticasone 50/500µg bid
Change in CDLM questionnaire scores from run-in
0.30
+
0.25
≠
+
0.20
0.15
0.10
0.05
0.00
TOTAL Wash Dry Get Eat Walk early Walk late
SCORE yourself yourself dressed breakfast
Bid = twice daily; CDLM = Capacity of Daily Living During the Morning
+p<0.02 vs salmeterol/fluticasone ≠p<0.05 vs salmeterol/fluticasone
Partridge MR et al. Ther Adv Respir Dis 2009

70. Greater control over morning activities with
Symbicort® + tiotropium vs tiotropium alone
Change in CDLM total score from run-in*
0.35
0.30 Symbicort + tiotropium
0.25
p=0.001†
0.20
0.15
p=0.027^
0.10 tiotropium
0.05
0
1 2 3 4 5 6 7 8 9 10 11 12
Weeks
^Treatment comparison from randomisation to first week of treatment
†Treatment comparison from randomisation to last week of treatment
Adapted from Welte et al. Am J Respir Crit Care Med 2009, 180: 741-750

71. Better symptom relief during the day and night
with Symbicort® *
Mean difference in COPD symptom score from run-in to full treatment period
Breathlessness Chest tightness Night time
Cough
awakenings
Better symptom relief
with reduced COPD
-0.142* -0.161* symptom score
-0.142* -0.142* -0.157*
0.1
P<0.001 P<0.001 P<0.001 P<0.001
0.2
* Symbicort + tiotropium vs tiotropium alone
Adapted from Welte et al. Am J Respir Crit Care Med 2009, 180: 741-750

72. Less reliever use with Symbicort® *
Reliever use at run-in and 12 week (last week)
Mean number of inhalations Symbicort + tiotropium
P<0.001 tiotropium
0.165
0.160
0.155
0.150
P<0.001
0.145
0.140
0.135
0.130
Run-in Week 12 Run-in Week 12
Daytime Night-time
* Symbicort + tiotropium vs tiotropium alone
Adapted from Welte et al. Am J Respir Crit Care Med 2009, 180:741-750

73. Greater improvement in health status
with Symbicort® *
Symbicort + tiotropium
Adjusted mean difference in SGRQ-C score tiotropium
6
P = 0.023
5
4 3.8
3
2
1.5
1
0
SGRQ-C total
Comparisons are from randomisation to last visit
* Symbicort®+ tiotropium vs tiotropium alone
Adapted from Welte et al. Am J Respir Crit Care Med 2009, 180:741-750

74. 62% lower rate of severe exacerbations
with Symbicort®*
Exacerbations/patients/3 months
0.4 Ratio: 0.38 (95% CI: 0.25-0.57)
P<0.001
0.3
tiotropium
0.2
Symbicort + tiotropium
0.1
0.0
15 30 45 60 75 90
Days since randomisation
N=660
*Symbicort + tiotropium vs tiotropium alone
Adapted from Welte et al. Am J Respir Crit Care Med 2009, 180: 741-750

75. 65% less Hospitalization/ER treatments
with Symbicort®*
Events/1000 patients/3 months
100
90 Ratio: 0.35 (95% CI: 0.16-0.78)
80
P=0.011
80
70
60
50
40
30 28
20
10
0 tiotropium Symbicort + tiotropium
N=331 N=329
*Symbicort + tiotropium vs. tiotropium alone
Adapted from Welte et al. Am J Respir Crit Care Med 2009, 180: 741-750

76. Budesonide and the risk of pneumonia:
a meta-analysis of individual patient data
• Budesonide, with or without formoterol, is not associated
with an increased risk of pneumonia adverse events (AE) or
serious adverse events (SAEs)
• The two most important risk factors for pneumonia AEs or
SAEs in patients with COPD are increasing age and
reduced lung function
Sin DD et al. Lancet 2009; 374:712–719.

77. Risk of pneumonia as an AE
No significant difference between treatment groups
N=7042 Szafranski et al.1 1.26 (0.64–2.49)
Calverley et al.2 1.54 (0.67–3.53)
Rennard et al.3 0.88 (0.57–1.36)
Tashkin et al.4 1.14 (0.56–2.33)
Bourbeau et al.5 0.79 (0.12–5.17)
Pauwels et al.6 2.08 (0.85–5.10)
Vestbo et al.7 0.56 (0.23–1.34)
Overall8 1.05 (0.81–1.37)
0.1 0.2 0.5 1 2 5 10
1. Szafranski W et al. Eur Respir J 2003; 21:74–81,
Hazard ratio (95% CI) 2. Calverley PM et al. Eur Respir J 2003; 22:912–919,
3. Rennard SI et al. Drugs 2009; 69:549–565,
Control treatment Inhaled budesonide treatment 4. Tashkin DP et al. Drugs 2008; 68:1975–2000,
5. Bourbeau J et al. Am J Respir Crit Care Med 1994; 149(4 Suppl 2):A183,
Data were adjusted for age, sex, smoking status, body mass index and % of 6. Pauwels RA et al. N Engl J Med 1999; 340:1948–1953,
predicted FEV1. 7. Vestbo J et al. Lancet 1999; 353:1819–1823,
AE = adverse event; CI = confidence intervals 8. Sin DD et al. Lancet 2009; 374:712–719.

78. Risk of pneumonia as an SAE
No significant difference between treatment groups
N=7042 Szafranski et al.1 0.82 (0.32–2.07)
Calverley et al.2 1.21 (0.45–3.36)
Rennard et al.3 0.72 (0.37–1.37)
Tashkin et al.4 1.06 (0.40–2.83)
Bourbeau et al.5 0.79 (0.12–5.17)
Pauwels et al.6 5.48 (0.66–45.7)
Overall7 0.92 (0.62–1.35)
0.1 1 10 100
Hazard ratio (95% CI) 1. Szafranski W et al. Eur Respir J 2003; 21:74–81,
2. Calverley PM et al. Eur Respir J 2003; 22:912–919,
Control treatment Inhaled budesonide treatment 3. Rennard SI et al. Drugs 2009; 69:549–565,
4. Tashkin DP et al. Drugs 2008; 68:1975–2000,
Data were adjusted for age, sex, smoking status, body mass index and 5. Bourbeau J et al. Am J Respir Crit Care Med 1994; 149(4 Suppl 2):A183,
FEV1 (% predicted) 6. Pauwels RA et al. N Engl J Med 1999; 340:1948–1953,
CI = confidence intervals; SAE = serious adverse event 7. Sin DD et al. Lancet 2009; 374:712–719.

79. SUMMARY
• COPD is no longer just considered a lung
parenchymal pathology, but one with
significant systemic effects
• Spirometry is required for both diagnosis
and assessment of severity. Every effort
should be made to refer patient for
spirometry.

80. SUMMARY
• Smoking cessation is the single most cost
effective - intervention to reduce the risk of
developing COPD and stop its
progression. Even a brief 3-min of
counselling may result in smoking
cessation rates of 5-10%

81. SUMMARY
• The combination of LABA/ICS has been
shown to improve lung function, quality of
life and reduce exacerbations compared
with placebo in COPD patients with FEV1
< 65% predicted.
• Consider NIV in patients with persistent
hypercapnoeic respiratory failure despite
optimal medical therapy