CHRONIC OBSTRUCTIVE PULMONARY

DISEASE
(1999)

PHILIPPINE COLLEGE OF CHEST PHYSICIANS

Philippine College of Chest Physicians
84-A Malakas St., Brgy. Piñahan, Quezon City
Tel. No.: 924-9204 Fax No.: 924-0144

Executive Board

President Jennifer Ann R. Mendoza-Wi, M.D.

Vice President Ma. Consuelo Mison-Obillo, N.D.
Secretary Josephine B. Blanco-Ramos, M.D.
Treasurer Renato B. Dantes, M.D.

Board Members Tomas M. Realiza, M.D.

Rodolfo Roman T. Bigornia, M.D.
Ricardo C. Zotomayor, M.D.
Marilyn Ong-Mateo, M.D.
Daniel T. Tan, M.D.

Immediate Past President Myrna N. Bañares, M.D.

Council on COPD

Chairman Percival A. Punzal, M.D.

Members Norberto A. Francisco, M.D.

Aileen V. Guzman, M.D.
Abner T. Koh, M.D.
Isaias A. Lanzona, M.D.
Buenaventura Medina, Jr., M.D.
Ma. Bella R. Siasoco, M.D.

Advisers Teresita S. de Guia, M.D.

Rodolfo M. Carungin, M.D.
Camilo C. Roa, M.D.
Daniel T. Tan, M.D.
Renato B. Dantes, M.D.

Member Societies/Groups/Individuals of Philippine College of Chest Physicians

Multisectoral Consultative Group
Philippine Academy of Family Physicians
Philippine Society of Rehabilitation Medicine
Philippine Association of Pulmonary Care
Philippine Association of Thoracic and
Cardiovascular Surgery
Department of Health
Philippine Nurses Association
Nutritionists
Priest

55
CHRONIC OBSTRUCTIVE PULMONARY DISEASE cpm 4TH eDITION

Algorithm of Practical Recommended Steps in

Out-Patient and Hospital Management of COPD Patients
Developing Exacerbations
1
COPD
developing
exacerbations

2


Out-patient Management of Mild

Exacerbation
• increase use of inhaled bronhodilator
• more aggressive chest physiotherapy
• oxygen supplement if there is hypox-
emia
• antibiotics if with infection
• avoid sedatives and tranquilizers

4 5
3 6


Improvement Y Continue same Consider

Reassess  of signs &  management or  long-term
symptoms? reduce intensity management

7 N


Worsening
of signs &
symptoms

8


Add oral

9


Reassess
within
48 hrs

10 11
12


Continue
Improvement Y or reduce Long-term
of signs &  management  management
symptoms? intensity

N
13 14


Worsening Refer to
of signs &  hospital
symptoms

FIGURE 1 - Out-patient Management

56
CPM 4TH EDITION CHRONIC OBSTRUCTIVE PULMONARY DISEASE

1
COPD
developing
exacerbations


Hospital Management
Diagnostics: Chest x-ray
ABG
CBC, electrolytes
Sputum G/S, C/S
Management: Nebulized bronchodilators
IV aminophylline
IV corticosteroids
Low flow oxygen
IV / oral antibiotics if with infection
Check fluid balance and nutrition
Treat other medical conditions

4 5
3 6


• Continue Consider
Reassess Improvement Y present treatment
within 60  of signs &  • Reassess after  long-term
minutes symptoms? management
4 hrs

7 N


Worsening
of signs &
symptoms

8


Abnormal
chest x-ray

9


• Treat new abnormal findings

e.g. pneumonia - antibiotics
pneumothorax - chest tube
• Increase O2 supplement guided
by ABG or oximetry to reach O2
sat. > or = 90%
10


11
Improvement Y Continue
of signs &  treatment
symptoms?

N
12 13


Worsening Transfer to
of signs &  ICU
symptoms

FIGURE 2 - Hospital Management

57
CHRONIC OBSTRUCTIVE PULMONARY DISEASE cpm 4TH eDITION

1
COPD
developing
exacerbations

2 

ICU Management
Non-invasive management
• Continue same medications
• IPPB/CPAP (non-invasive)

3


Reassess

4 5 6


Y Continue Long-term
Improvement?  management  management

7 N


No improvement
or deteriorates
within 72 hrs
8


Invasive
mechanical
ventilation
9 10 11


Improvement Y
Wean from Long-term
Reassess   management
mechanical
9 ventilation?
N
12


No
improvement

13 14 15


Continue Improvement Y
Wean from Long-term
invasive   management
management mechanical
ventilation?
16 N 17


Continue
No
 invasive
improvement
management

FIGURE 3 - ICU Management

58
CPM 4TH EDITION CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Philippine Consensus Report on Chronic Obstructive
Pulmonary Disease (COPD): Diagnosis & Management
I. INTRODUCTION
Disease Burden of Chronic Obstructive Pulmonary
Disease (COPD)
Chronic obstructive pulmonary disease (COPD) is
one of the most important diseases of the 20th century
being a major cause of disability and death. The 1998
World Health Organization Report has stated that non-
communicable diseases (including COPD) now cause
nearly 40% of all deaths in developing countries and
that developing countries account for 67% of all COPD
deaths worldwide.1
In 1990, chronic obstructive pulmonary disease was
ranked number 12 in the list of leading causes of disease
burden in developing countries measured in terms of
daily-adjusted life year (DALY) (or the loss of year's
health life). In WHO's projection for year 2020, chronic
obstructive pulmonary disease will be ranked number
4 just behind mental depression, road-traffic accidents,
and ischemic heart disease.2
The reasons for the expected rise in the disease burden
of COPD are:
(a) Demographic transition wherein the proportion of
adult population is increasing sharply so that the
proportion of the total disease burden in the popula-
tion will also rise.
(b) The rapid increase in tobacco use in developing
countries will predictably lead to a massive rise in
smoking-related disease burdens in the coming 25
years.
3
Although the American Thoracic Society (ATS) , Eu-
4
ropean Respiratory Society (ERS) , British Thoracic
5
Society (BTS) and Thoracic Society of Australia and
6
New Zealand (TRANZ) have issued guidelines which
generally concur on the diagnosis and management
of patients with COPD, these guidelines differ in ap-
proaches and arrive at different recommendations at
some points. Given the differences in socio-cultural and
economic setting in the Philippines and the realization
that in the next several years COPD cases will increase
in developing countries like the Philippines due to
trend of aging population and the unchecked problems
of smoking and air pollution, the COPD Council of the
Philippine College of Chest Physicians (PCCP) initiated
the development of a local practice guideline in the diag-
nosis and management of COPD among Filipinos.
The guidelines are intended for use by practicing phy-
sicians and other health professionals involved in the
care of patients with COPD. The goals of these practice
guidelines are:
1. To assist primary health care physicians identify
and initiate management of patients suffering from
COPD.
2. To assist hospital-based physicians in providing ap-
propriate cost-effective care for COPD patients.
3. To recommend measures for the prevention of lung
function deterioration, subsequent complications
and improvement in the quality of life of COPD
patients.
4. To make allied health workers adept in the care of
these patients.
5. To identify reasearch gaps in the diagnosis and man-
agement of COPD in the Philippines.
Methodology in the Development of the Practice
Guideline
Cinical Practice Guidelines (CPG) are formulated to
improve health care delivery by providing practitioners
with scientifically valid indications for diagnostic and
therapeutic interventions used in managing specific
health problems. Creation of these practice guidelines
should rest on conclusions derived from scientifically
sound clinical and basic science investigations when-
ever possible or on expert consensus in the absence of
high grade investigative data. Central to the develop-
ment of these guidelines is the effort in constructing
pragmatically sound statements that can be effectively
applied by practicing physicians. This practical ap-
proach to guideline development intends to ensure the
rapid dissemination and prompt application of recom-
mendations, with goals of promoting health of patients
at risk for specified health conditions.
The COPD Practice Guideline development for the
Philippines was organized under the sponsorship of the
COPD Council of the Philippine College of Chest Phy-
sicians (PCCP). The Council followed the enumerated
steps in the creation of the Clinical Practice Guidelines
for COPD in the Philippines: (a) selection of Core Group
and advisers, (b) identification for participation of mul-
tisectoral groups (medical and non-medical) who had a
stake in the proper management of COPD, (c) topic se-
lection, (d) committee member selection for each topic,
(e) determination of the questions/issues to address per
topic, (f) searching the literature for the evidence, (g)
grading the evidence, (h) formulation of draft recom-
mendations, (i) getting feedback from advisers/stake-
holders, and (j) formulation of final statements.
Subsequently, dissemination of the guidelines will
be done through "academic detailing" and interactive
59
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
small group presentations/discussions with concerned
physicians nationwide using specific and real patient
examples. Also evaluation of physicians' compliance
and impact of practice guidelines on health outcome of
Filipino COPD patients will be carried out.
The Council, whenever possible, assigned a letter grade
designating the overall strength of the scientific evidence
for each recommendation based on the level evidence
(Annex 1). Ratings reflect both the quality of the studies,
including study design and methods used.
Definition of COPD
COPD is defined as a disease characterized by the pres-
ence of airflow obstruction due to chronic bronchitis
or emphysema; the airflow obstruction is generally
progressive, may be accompanied by airway hyperre-
activity, and may be partially reversible.7 This definition
excludes other causes of chronic airflow obstruction
such as upper airway obstruction, bronchiectasis, asthma
8 ratio of mortality from COPD in 1992 was 1.8 to 1.
and cystic fibrosis.
The European Respiratory Society (ERS) has defined
airflow obstruction in COPD as a reduced expiratory
flow and slow forced emptying of the lungs; features
4
which do not change markedly over several months.
Such chronic airways obstruction is caused by changes
9 some Asian countries.
in the airways and/or lung parenchyma.
Chronic bronchitis is defined as the presence of chronic
cough for 3 months in each of two successive years in
a patient in whom other causes of chronic cough have
10,11,12
been excluded.
Emphysema is defined as an abnormal permanent
enlargement of the airspaces distal to the terminal bron-
chioles, accompanied by the destruction of their walls
and without obvious fibrosis. Destruction is defined as
lack of uniformity in patterns of airspace enlargement;
the orderly appearance of the acinus and its component
13
is disturbed and may be lost. It is manifested predomi-
14
nantly as dyspnea.
II. How big a problem is COPD in the
Philippines?
Although there is no large population-based preva-
lence survey available on the problem of COPD in
the country, the current picture of smoking habits
of Filipinos will bring about a massive rise in COPD
cases in the next several years as predicted by WHO
for developing countries.
Summary of Evidence
There are currently no available data on the burden
of COPD problem in the Philippines based on a large
60
cpm 4TH eDITION
surveillance study. A single study on the prevalence of
COPD in our country was done in 1986 in a rural town
101
called Banca-Banca in Laguna. From a total of 1033
eligible subjects from 246 households, 726 subjects were
interviewed. Based on clinical criteria for suspected
COPD together with spirometric findings of obstructive
airflow pattern using 95% confidence interval around
a normal mean, the prevalence was 3.7%. The male to
female ratio was 3.5 to 1 with a mean age of 51 years.
According to the Philippine Health Statistics, in 1992,
COPD and allied conditions ranked 7th among the
ten leading causes of mortality with a rate of 14.4 per
100,000. Since the data were gathered from reported
certificates of death, the diagnosis of COPD per se may
still be questionable. Also this may be an overestimation
as this figure included allied conditions like asthma and
bronchiectasis. Nevertheless the total death rate from
COPD increased from a previous 5-year average rate
of 2.4% (7,521 cases or 12.5/100,000) to 2.9% in 1992
(9,391 cases or 14.4/100,000). The male to female
A comparison of the death rates from COPD in some
Asian countries is shown in Table 1. (It must be noted,
however, that the diagnostic criteria test used and the
102,103,104
age population surveyed differed).
Table 1. Reported studies on COPD mortality in
Country Mortality rate
(per 100,000 population)
Philippines (1992)
COPD + allied conditions 14.4
Japan (1993)
Mortality rate attribute to COPD
for age more than 65 years old 27
Taiwan (1992)
Mortality rate of COPD and
asthma 10.09
Thailand (1987-1991)
Mortality rate of chronic airflow
obstruction 2.3
A National Prevalence Survey on Smoking carried out
in 1989 showed the following results:44 (a) 46% of the
surveyed Filipino population smoked and majority of
these were males; (b) there was no difference in the
number of smokers in the urban and rural population;
(c) the modal age for male and female smokers in both
urban and rural population was 21-25 and 26-30 years
old, respectively; (d) adults nonsmokers had higher
educational attainment than the smokers; (e) the modal
age at which the adults smokers started smoking was
13-18 years; (f) peer group pressure was the predomi-
nant reason for starting smoking in over 50% of adult
CPM 4TH EDITION CHRONIC OBSTRUCTIVE PULMONARY DISEASE
and urban smokers.
An unpublished article entitled "Smoking: a compara-
tive study among urban and rural high school students"
done in 1992 showed that out of 878 students, 138 (16%)
105
were smokers. The study further revealed that urban
adolescents were more likely to be smokers than rural
adolescents. Also, a similar study of the prevalence of
drug and substance abuse among Filipino high school
students conducted from 1989-1990 revealed that
cigarette smoking, with a rate of 21%, ranked second
106
to alcohol use.
As can be garnered from these studies, smoking prac-
tice is quite prevalent in the country, especially among
the young population. Twenty to thirty years down the
road, COPD is likely to be a major health problem of
the country.
III. How should COPD be diagnosed?
Detection Strategies
Suspect COPD in patients with the following:
>50 years old (Grade A) smoker for many years
(Grade A) and with symptoms of progressive and
increasing shortness of breath on exertion and/or
chronic productive cough.
Summary of Evidence
HISTORY
Age
It is rare to encounter COPD patients under the age of 40
years. The disease commonly appears in the fifth decade
of life with productive cough and dyspnea on effort.7
Risk Factors
Cigarette smoking is the single most important factor
in the genesis of COPD, and accounts for 80 to 90% of
the risk of developing COPD.
15
In addition, attention has focused on bronchial hyper-
activity, passive smoking, air pollution, and α-1-antit-
rypsin deficiency. Although α-1-antitrypsin deficiency
is of comparable importance with tobacco smoking, this
only accounts for <1% of COPD. Little is known about
the factors that identify persons susceptible to develop
COPD when exposed to these risk factors. The most
important risk factors for COPD are listed in Table 1:
Table 1. Risk factors for COPD
Degree of Environmental Congenital
certainty factors factors
Certain Cigarette smoking Alpha-1-
Occupational antitrypsin
exposure (cadmium deficiency
and silica)
Likely Environmental pol- Low birth
(burden of lution (especially SO2) weight
proof good) High IgE
Low socio-economic Airway
status hyperres-
Alcohol ponsiveness
Passive smoking in Positive
childhood family
history
Possible Adenovirus infection Genetic pre-
Vitamin C deficiency disposition
blood group A
and IgA non-
secretor)
From Epidemiology of COPD by D.S. Postma: COPD: Diagnosis and
Treatment, 1996
Symptoms
A history of productive cough in the early morning
is more typically elicited from patients with COPD
16
especially those with chronic bronchitis. Acute chest
illnesses characterized by increased cough, purulent
sputum, wheezing, dyspnea and occasionally fever may
occur intermittently.
Progressive dyspnea worsening over a period of months
9
or years, is a typical feature of COPD. Wheezing ap-
preciated at rest may indicate a reversible component
of the airway obstruction.
In the advanced stage of the disease, COPD patients
may complain of morning headache suggestive of
hypercapnia. Cor pulmonale with right heart failure
and edema may also develop. Cyanosis may be present
during acute exacerbations.
PHYSICAL EXAMINATION
The physical examination is a crude and intensive means
17
of detecting airflow obstruction. Furthermore, physical
examination is not useful in separating patients with ob-
structive lung diseases into the conventional diagnostic
findings (as those with chronic bronchitis, emphysema
18
or asthma). This can be partially explained by a study of
19
Stubbing et.al. In this particular study they mentioned
that physical examination findings in patients with air-
flow obstruction may be entirely normal until the forced
61
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
expiratory volume in one second (FEV1) is reduced to
less than 50% of the predicted value.
Among the physical findings, wheezing during tidal
breathing and prolonged expiratory time (>5 seconds)
are useful indicators of airflow limitation. These signs,
however, are of no value as guides to severity and their
20
absence does not exclude COPD.
Chest Radiography
The standard postero-anterior and lateral chest radiog-
raphy is an insensitive means of detecting airflow ob-
20
struction. It is, however, useful in the initial assessment
4
of COPD patients. At presentation, this can exclude
other conditions such as lung cancer, pneumothorax,
or pneumonia.
In emphysema, findings of hyperinflation (depression
and flattening of the diaphragm on the PA film and
increased width of the retrosternal of the lung fields
21
(absence of vasculature) are considered specific. The
presence of thickened bronchial walls and prominent
lung markings (dirty lung pattern) is more suggestive
22
of chronic bronchitis.
Sputum Examination
In exacerbations, the sputum becomes purulent with an
influx of neutrophils and the gram stain showing numer-
7 of 15% in the predicted normal FEV1 is recommended
ous mixtures of organisms. Most frequent pathogens
cultured from sputum are Streptococcus pneumonia,
Hemophilus influenzae and Moraxella catarrhalis. In
the outpatient setting, however, cultures or even Gram
stains are rarely necessary before instituting antimicro-
23
bial therapy.
Complete Blood Count
22
Laboratory tests are nonspecific. Elevated hemoglobin
and hematocrit are frequently seen in advanced disease
as a result of hypoxemia.
Electrocardiogram
Electrocardiogram abnormalities occur in patients
with COPD who develop pulmonary hypertension and
right ventricular hypertrophy. These include right axis
deviation greater than 100 degrees without right bundle
branch block; R wave greater than S wave in V1 or V2;
24
and R wave less than S wave in V6. However, such
electrocardiographic findings tend to occur late in the
disease process.
Confirmation Strategies
Spirometry should be done on all patients suspected
of having COPD. Diagnosis of COPD is established
if FEV1/FVC ratio is <70% of the predicted value
62
cpm 4TH eDITION
(Grade A). A postbronchodilator response of less
than 15% in predicted normal FEV1 is in favor of
the diagnosis of COPD rather than asthma.
Summary of Evidence
Spirometry
Airways obstruction is the sine qua non condition
25
to the defintion of COPD. The presence of airways
obstruction as measured by spirometry is recognized
as a reduction in FEV1 to vital capacity (VC) or forced
vital capacity (FVC).21 In moderate to severe disease,
the severity of airway obstruction is best assessed by
26
FEV1 in relation to reference values.
Spirometry should be performed in all patients in
27,18
whom the diagnosis of COPD is being considered.
It may identify those with early disease when symptoms
are mild.
Response to Bronchodilators
Assessment of the reversibility of airflow obstruction
after bronchodilator therapy is considered a routine pro-
cedure in specialist practice. This is performed in order
to distinguish the reversible asthmatic from the irrevers-
28
ible COPD patient. Expression of the bronchodilator
response as a percentage of the predicted normal FEV1
4,28
can be considered as the most useful method. A change
as a criterion of reversibility.28 A post-bronchodilator
response, therefore, of <15% in the predicted normal
FEV1 (irreversibility) is in favor of a diagnosis of
COPD rather than asthma. However, there are caveats
which have to be remembered in interpreting the test:
a) symptomatic improvement may occur without a sig-
29,30
nificant increase in FEV1; and b) an acute response
in FEV1 is neither sufficiently sensitive nor specific to
19
differentiate asthma from COPD.
Other Lung Function Tests (Lung volumes, DLco,
ABG)
Functional residual capacity (FRC), residual volume
(RV) and the ratio of RV to total lung capacity (TLC) are
characteristically increased in COPD. In severe COPD,
the TLC is increased. In a study by Kesten and Rebuck,
the best parameter for distinguishing COPD from asthma
was the residual volume-total lung capacity ratio which
was increased more in COPD than in asthma.
31
Diffusion capacity (DLco) is perhaps the most informa-
32
tive additional parameter of lung function in COPD. It
is helpful in separating emphysema and chronic bron-
chitis. In emphysema, the DLco is reduced as a result
of destruction of lung parenchyma, whereas in chronic
bronchitis the DLco is usually normal.
CPM 4TH EDITION CHRONIC OBSTRUCTIVE PULMONARY DISEASE

associated increase in airway responsiveness to a variety

Measurement of arterial blood tensions with the patient
breathing room air is recommended in the assessment
4
of patients with moderate or severe stable COPD. As
the disease progresses, hypoxemia becomes more severe
and hypercapnia supervenes. Sequential measurements
of the blood gas tensions are, therefore, essential in the
33
follow-up of those with severe airflow obstruction.
Computed Tomography
High resolution CT scanning is sufficiently sensitive
to diagnose emphysema in patients with normal chest
34
radiographs. Despite this, CT scanning is not recom-
mended for routine assessment. Its role in patients with
COPD is limited to evaluation of bullae and investiga-
35
of stimuli.
It is difficult to differentiate COPD from asthma espe-
cially in the elderly with persistent airflow obstruction of
4
chronic asthma. Since the two conditions are based on
distinct disease processes, one may accept that both can
be present simultaneously. Thus, in some patients the
characteristics of each process need to be identified in
9
order to determine which of the two is dominant.
In general, most patients can be categorized into of
these two diagnoses based on clinical history, physical
examination, radiographic findings, pulmonary func-
tion test results and on occasion, a therapeutic trial of
22 36

tion of coexisting bronchiectasis.

4
medication. See Table 3

The following laboratory examinations are therefore Table 3. Features that differentiate asthma and COPD
recommended in the routine screening for COPD:
FEV1, VC or FVC and chest radiograph. For the special Features Asthma COPD
indications for the diagnosis and initial assessment of
4 Onset at a Frequently Almost Never
COPD, the following investigations are recommended
young age
(Table 2):
Major Usually episodic Usually daily
Table 2. Indications for special tests for COPD Symptoms • Wheezing • Dyspnea with
• Breathlessness exertion
SPECIAL INDICATION TEST (progressive over
• Non-productive time) or
Moderate or severe COPD Lung volumes cough productive cough
SaO2 &/or blood • Chest tightness
gasses
EKG Triggers Aeroallergens Daily activities
Hemoglobin Occupational Cold air
Persistent purulent sputum Sputum culture and antigens Infections
sensitivity Exogenous
Emphysema in younger patients α-1-antitryp­sin irritants
level Exercise
Assessment of bullae CT-scan Cold air
Disproportionate breathlessness Exercise test Aspirin and
Maximum expi­ NSAIDs
ratory pressures Reflux esophagitis
Suspected obstructive sleep apnea Nocturnal sleep Infections
study
Smoking Occasionally Usually present
History present

IV. How is COPD differentiated from Allergies Often positive Occasionally

other common causes of obstruc- positive
tive lung diseases in the Philip-
pines, specifically, asthma & bron- Physical Rhinitis Diminished inten-
chiectasis? findings Pale nasal mucosa sity of breath
Prolonged expira- sounds (advanced
Asthma is a chronic inflammatory disorder of the air- tion disease)
ways in which many cells play a role, including mast Wheezing Pursed lip breathing
Right heart failure
cells, eosinophils, T-lymphocytes and neutrophils.
(distended jugular
In susceptible individuals, this inflammation causes veins, right
symptoms which are usually associated with widespread ventricular heave,
but variable airflow obstruction that is often reversible loud P2, ascites,
either spontaneously or with treatment, and causes an
63
CHRONIC OBSTRUCTIVE PULMONARY DISEASE cpm 4TH eDITION

pedal edema)
Early inspiratory Bronchiectasis is characterized by irreversible dilata-
crackles tion of one or more proximal and medium-sized bronchi
Wheezing as a result of destruction of the muscular and elastic
20,37
supporting tissues of the bronchial walls. It is another
Complete Eosinophilia Polycythemia
blood count
disease which may present itself as chronic airways
obstruction. It is common among Filipinos as it can
α-antitrypsin Normal Occasionally low follow necrotizing pneumonias caused by tubercle
bacillus and other microorganisms. A high prevalence
Spirometry Reduced FEV1 Reduced FEV1 of asthma in patients with bronchiectasis among Asians
38
Reduced FEV1/ Reduced FEV1/ have been reported.
FVC FVC
May be normal May improve (but Localized bronchiectasis is often present in patients with
when asymp- not to normal COPD. As a rule, however, bronchiectasis is character-
tomatic or with with treatment)
ized by dilation of airways rather than narrowing.
treatment

Broncho- Usually present Improvement Cough and sputum production (frequently purulent),
dilator (200 mL and often seen but often more severe on awakening are observed in 90%
Response 15% increase in spirometry does of all patients with bronchiectasis. Radiographic tech-
FEV1 with not normalize niques should be requested to support the diagnosis.
inhaled broncho- Chest radiographs are crucial to document regions of
dilators) increased markings, cavities and atelectasis.
Spirometry may
normalize When clinical symptoms and plain chest radiographs
suggest bronchiectasis, a high resolution computed
Lung Total lung capacity Total lung capacity
volumes usually normal normal (chronic
tomography (HRCT) is the imaging modality of choice
39

bronchitis) or for confirming or ruling out the diagnosis.

increased (em-
physema) V. How is the severity of COPD grad-
Residual volume Residual volume ed?
may be increased increased
Severity of COPD is graded as follows (Table 4):
Diffusing Normal or Reduced in
capacity for increased emphysema Table 4. Grading of Severity of COPD
carbon Normal in chronic
monoxide bronchitis Category of FEV1 Signs/
(corrected for COPD (% of Pred) Symptoms
Hgb)
Mild 60-79 No abnormal signs
Chest Usually normal Hyperinflation Smoker's cough
radiography Occasionally (flattened dia- Little or no breath-
hyperinflated phragm and lessness
lung fields during increased retro-
attacks sternal airspace) Moderate 40-59 Breathlessness (+ or -
Bullae often present wheeze on moderate
(lower lobe pre- exertion)
dominance Cough (+ or - sputum)
suggests panaci- Variable abnormal signs
nar (general reduction in
disease as with breath sounds, pre-
α-1-antitrypsin sence of wheezes)
disease)
Severe <40 Breathlessness on any
Computed Usually normal Emphysema
exertion / at rest
tomography Blebs and bullae
Wheeze and cough
scan of the common
often prominent
chest Diminished
Lung overinflation
vascularity
usual; cyanosis;
Adapted from Kaliner and Lemansky36 peripheral edema and
64
CPM 4TH EDITION
polycythemia in
advanced disease;
especially during
exacerbation
Grade C
Summary of Evidence
It seems that the grading for severity in COPD depends
on the different needs of each country. In the USA as
adopted by the ATS, the allocation of resources and
the directives to formulate healthcare models are given
high priority. The ATS divided patients into stage I, II,
and III (FEV1 > or = 50, 35-49 and < or = 34% of the
predicted value, respectively). The reason behind the
narrower banding for patients with more severe dis-
ease in the ATS was the stages II and III usually have
significant disease and they use a greater proportion of
health care resources. It was in this group of patients
that an improvement in COPD management would be
40
most beneficial.
The ERS divided patients into mild, moderate, and
severe (FEV1 > or = 70%, 50-69%, and < or = 50%
of the predicted value, respectively). The narrowest
band was for patients with mild to moderate COPD.
It emphasized that the vast majority of COPD patients
do not have severe diseases. As a result, the group of
patients with milder disease is a major user of resources
and, to that end, improvements in the management of
this group of patients may be beneficial in reducing
40
health expenditure.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
was markedly increased among the 10 to 15 percent
of sesceptible cigarette smokers. Clinical disability
did not occur until late in the course of the disease,
when the FEV1 had declined by about 70%. Typically,
disability developed at approximately 65 years of age,
when smoking cessation prolonged life only slightly.
It was also observed that the improve longevity and
quality of life, smoking cessation must occur at an
early age. This underscores the importance of under-
taking periodic evaluation of patients who smoke and
vigorous attempts at breaking the smoking habit before
disability occurs.
The study of Fletcher was confirmed by the COPD
43
Early Intervention Trial or Lung Health Study. This
study was a randomized controlled trial comparing the
rate of change and cumulative change in FEV1 over
a 5-year period among patients assigned either to (a)
smoking intervetnion plus bronchodilator, (b) smoking
intervention plus placebo or (c) no intervention. The
study concluded that an aggressive smoking intervention
program significantly reduces the age-related decline
in FEV1 in middle-aged smokers with mild airways
obstruction.
VII. What are the elements of a suc-
cessful smoking cessation pro-
gram?
Smoking cessation can be achieved by initiation,
early follow-up, continuing reinforcement, and re-
view of failure recividism.

The British Thoracic Society guidelines also divide
COPD into mild, moderate, and severe with correspond-
ing clinical features and FEV1 values.41 These data
coupled with clinical experience with Filipino COPD
patients favored the adoption of the British definitions
of mild, moderate, and severe COPD by the COPD
Council.
VI. What advise should be given to
COPD patients regarding smoking
cessation?
Smoking cessation is the single most important way
of affecting favorably the outcome of patients at all
stages of COPD (Grade A). It must be done at an
early age before disability becomes evident.
Summary of Evidence
Fletcher and colleagues studied nearly 800 male trans-
port workers in London, both smokers and non-smokers,
42
over an 8-year period with serial recordings of FEV1.
The investigators observed that the rate of decline in
FEV1, which normally begins at about age 25 years,
1. Initiation - physician or health care worker would
initiate quitting, explaining risks of cigarette smoking
for the individual and offering strong admonition to
quit. Establishment of a quit date is encouraged and
referral for self-help or group program is offered.
2. Early follow-up - telephone patient within three days
after quit date. Review progress and counsel regarding
recruitment of support person. Call again one to two
weeks after quit date. Repeat as needed.
3. Continuing reinforcement - further follow-up should
be arranged by physician or health care worker. Next
regular visit should be less than 2 months after initiat-
ing cessation program. If abstinent, review and reward
success and reinforce prior warning. May follow up by
phone monthly until next visit; follow up at increasing
interval for 12 months after quit date.
4. Failure or recividism - if patient is able to achieve
abstinence or does so but relapses, physician or
health care worker should review program with
patient emphasizing element of success and identify-
ing circumstances and explore alternatives. Nicotine
replacement maybe offered to control withdrawal
symptoms. Hypnosis may be considered.
65
CHRONIC OBSTRUCTIVE PULMONARY DISEASE cpm 4TH eDITION

Well implemented programs in a specialist setting result hours

in a 20 to 30% success rate in 1 year and in an improve-
45
ment in FEV1.
VIII. How do you manage patients with
stable COPD?
STEP CARE OF COPD
• With Mild Symptoms
1. Smoking cessation (Grade A)
2. Protection from or reduction of environmental expo-
sure
3. Annual influenza vaccination (Grade A)
4. For those with variable symptoms:
- selective ß2 agonist metered dose inhaler (MDI),
1-2 puffs every 2-6 hours as needed (not to exceed
8-12 puffs/24 hours) (Grade A)
For those with continuing symptoms
- anticholinergic MDI aerosol, 2-6 puffs every 6-8
hours (not to be used more frequently) (Grade A)
plus selective ß2-agonist MDI 1-4 puffs as required
(for rapid relief when needed)
5. Theophylline (long acting) / long acting ß-agonist
6. Trial of steroids
7. Pulmonary rehabilitation
8. Assessment for long term oxygen therapy (Grade A)
If inhaled bronchodilators are not available, oral ß2-
agonist preparations can be used as regular alternative
medications.
Table 5 shows the relationship of spirometric values and
symptoms of patients. Included are the corresponding
recommendations for each degree of severity.
Table 5. COPD escalator - Relationship of symptoms
with PFT values and recommended treat-
ment
FEV1 as Signs & Treatment
% of pred Symptoms
80-100% Healthy (a) smoking cessation
population

If inhaled bronchodilator is not available or non-acces- 60-79% Smoker's cough (a) plus
sible or affordable, use oral short short-acting ß2 agonist (mild) No abnormal (b) Influenza vaccina-
e.g. terbutaline, clenbuterol, salbutamol, as needed; signs tion
however, the high incidence of side effects with these Little or no (c) inhaled short-
oral preparations must be recognized. dyspnea acting β2-agonist
(with mild MDI 1-2 puffs q
• With Moderate Symptoms variable symp- 2-6 h prn not to
As above, numbers 1 to 3 recommendations toms) exceed 8-12 puffs
per 24 h
4. Inhaled combined anticholinergic plus ß2-agonist at
(for continuing (d) regular inhaled
2-4 puffs every 4-6 hours (Grade A)
mild symptoms) anticholinergics
5. If response to step 4 is unsatisfactory, add theophylline MDI 2-6 puffs q 6-
(long acting), 200-300 mg twice daily or 400 mg once 8 h plus prn
a day at bedtime for nocturnal bronchospasm (Grade inhaled β2-agonist
A) and/or long acting inhaled ß2-agonist (Grade A)
6. Consider use of a mucokinetic agent (Grade C) 40-59% Dyspnea on (a), (b), plus
7. If response to step 5 is unsatisfactory, consider a (moderate) exertion (e) regular inhaled
corticosteroid trial of Prednisone 30 mg per day for Cough, + or - combined
2 weeks (Grade B) sputum (mode- anticholinergic &
rate persistent β2-agonist
- if improvement occurs, taper down to daily or
symptoms) (f) if response to (e)
alternate dosing at 5 mg/day
is unsatisfactory
- if no improvement occurs, stop immediately add SR
- if steroid appears to help, consider possible use theophylline
of aerosol MDI e.g. budesonide, fluticasone or 200-300 mg twice
beclomethasone, for 6 weeks (Grade C) daily or 400 mg OD
8. Pulmonary rehabilitation (Grade A) at bedtime or long
acting β2-agonist
If inhaled bronchodilators are not available, oral ß2- (g) consider mucoki-
agonist preparations (e.g. bambuterol), can be used as netic agent
(h) steroid reversibility
regular alternative medications.
trial w/ prednisone;
• With Severe Symptoms
if (+) taper down to
Numbers 1 to 3 recommendations daily or alternate
4. Increase inhaled combined ipratropium + ß2-agonist dosing at 5 mg/day;
dosage to 2-4 puffs every 3-4 hours or inhalant solu- consider also in-
tion of combined ipratropium + ß2-agonist every 4-8 haled steroids
66
CPM 4TH EDITION
(i) Pulmonary rehabi-
litation
<40% Dyspnea on mild (a), (b), plus
(severe) exertion (e) increased inhaled
Hyperinflation combined
and cyanosis bronchodilator
Wheeze and (anticholinergic &
cough β2-agonist) plus
(f), (g), (h), (i)
(j) assessment for Long
Term Oxygen
Therapy (LTOT)
Summary of Evidence
Patients with COPD have been shown to demonstrate
significant bronchodilator response to ß-agonists. Onset
of action with these drugs are rapid but duration of action
46
is generally short. The side effects of ß-agonists which
stem from activation of ß1-receptors include tachycar-
dia, dysrhythmias, tremor and insomnia. These drugs are
best taken by COPD patients on an "as needed" basis.
There is little evidence of tachyphylaxis to ß2-agonist
in patients with COPD, but there is disagreement on
whether older patients with COPD are less likely to
respond to these agents.
47,48
Quaternary ammonium atropine derivatives like iprat-
ropium bromide have less mucous absorption and fewer
side effects. The inhaled anticholinergic bronchodilator
has a relatively slow onset but it has a longer duration
of action than do most ß-adrenergic agonists. The in-
cidence of side effects is low and the side effects are
generally minor. Hence, it is more suitable for use on
regular basis. Submaximal bronchodilatation has been
demonstrated using two puffs four times daily; conse-
quently the number of inhalations may be doubled or
99
tripled, without notable side effects. Some studies have
reported that ipratropium bromide produced greater
bronchodilation in chronic bronchitis than do conven-
49,99
tional doses of ß- agonists. A recent large multicenter
double blind clinical trial compared the efficacy of ß-
agonist albuterol with that of ipratropium bromide and
a combination of the two agents in 534 patients with
50
severe COPD. The combination of the drugs resulted
in greater change in FEV1 from baseline than did either
drug alone; the benefit persisted over the 85 days of the
study. The additive effects may derive from the agents'
disparate mechanisms and sites of action, as well as
their difference in time courses for bronchodilation. No
tachyphylaxis has been reported, even when ipratropium
bromide was used for as long as 5 years. Extended use
of the agent, however, does not appear to influence
43
long-term decline in FEV1.
Theophylline relaxes bronchial smooth muscle and
increases diaphragmatic contraction and endurance.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Oral theophylline or intravenous aminophylline have
comparable or less bronchodilating effects than ß2-ago-
107,108
nist and anticholinergic agents. Also it has narrow
therapeutic window. Theophylline's unique multisystem
effects, additive actions with other bronchodilators,
and availability in sustained release oral formulations
provide a role for the agent in maintenance regimens for
100
patients with COPD. Nevertheless, the potential for
serious side effects requires that serum levels be care-
fully monitored, particularly in elderly patients.
Long acting ß-agonists may have a role in COPD but
their specific role still needs to be determined with
prospective clinical trials.
IX. What is the role of antibiotics
in the acute exacerbations of
COPD?
Antibiotic is recommended if patient has evidence of
infection such as fever, leukocytosis, or change in the
chest radiograph (Grade A). The antibiotic of choice
should reflect local pattern of resistance.
Summary of Evidence
Antibiotics are not of proven value in the prevention
or treatment of COPD exacerbation unless there is
evidence of infection such as fever, leukocytosis or a
54,55,56
change in the chest radiograph.
X. What are the roles of influenza
and pneumococcal vaccinations
as secondary preventive measures
in COPD?
Influenza vaccine can reduce the number of ex-
acerbations in COPD (Grade A). Pneumococcal
vaccination is likely to be effective (Grade C) but
there is insufficient informations for its general
recommendation.
Summary of Evidence
Vaccination has been used with the dual aim of reducing
the number of exacerbations and their consequences.
Studies show that influenza vaccine can reduce the
number of purulent exacerbations in COPD. Pneumo-
coccal vaccination is likely to be effective but there is
insufficient information for its general recommenda-
tion.
54,55
XI. What is the role of cortico­
steroids in the management of
COPD?
Short courses of systemic corticosteroids should
be considered in patients with acute exacerbations
67
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
who are unresponsive to aggressive inhaled bron­cho­
dilator therapy (Grade C). Patients with docu­mented
physiologic improvement following steroid trial can
be considered for long term therapy and the aim is to
use the lowest possible dose (Grade C).
Summary of Evidence
Inflammatory changes in the airways of patients with
COPD provides a rationale for the use of corticoster-
56
oids. However, the relationship between these changes,
pulmonary function and therapeutic response is not
57,58
clearly established. Oral or intravenous corticoster-
oids produce a favorable response during acute COPD
exacerbations, improving symptoms and reducing the
59
length of hospitalization. Corticosteroids also reduce
the rate of relapse in COPD patients with acute and
109
frequent exacerbations. Thus, short courses or bursts
of corticosteroids should be considered in patients with
acute exacerbations who are unresponsive to aggressive
inhaled bronchodilator therapy.
Long term use of steroids should be considered
ONLY in patients who have continued symptoms or
severe airflow limitation despite maximal therapy
with other agents. Only 20% to 30% of patients show
objective benefits from long-term corticosteroid
administration.
Long term indiscriminate use often leads to adverse
effects without any benefits. To date, no predictors of
long term response to corticosteroids in COPD patients
have been found. Response to corticosteroid therapy
during an acute COPD exacerbation does not necessarily
indicate that a patient will benefit from long term use. A
closely monitored clinical trial is needed to determine
which patients will benefut from this type of therapy.
Only those patients with documented physiologic im-
provement following steroid trial should be considered
for long term therapy and the goal is to achieve the
lowest possible dose. Spirometric values should be
measured before and at the end of the corticosteroid
trial. An increase in FEV1 that is greater than 200 mL
or a 15% increase over pre-treatment value is consid-
ered a positive response to corticosteroids and justifies
prescription of regular inhaled steroids.
Regular long term use of low-dose corticosteroids has
been suggested to retard the rate of decline in FEV1 in
COPD patients. Preliminary reports suggest that inhaled
corticosteroids do not alter disease progression. Ongo-
ing studies are evaluating the early, regular use of oral
and inhaled corticosteroids as a means of retarding
disease progression. The use of corticosteroids solely
to retard the progression of COPD cannot be recom-
mended until further data are available.
68
cpm 4TH eDITION
XII. Is there a role for mucolytics in
the management of COPD?
Mucolytics are of questionable benefit in the manage-
ment of COPD (Grade C). The value of water, includ-
ing aerosolized water, has not been demonstrated to
benefit with COPD.
Summary of Evidence
In one large multicenter randomized placebo-controlled
clinical trial, it was shown that iodinated glycerol im-
proves subjective measures - such as cough frequency,
cough severity, chest discomfort, ease of expectora-
tion and overall health status. However, there was
insufficient evidence of benefit in terms of objective
parameters.
60
Other agents, like aerosolized water and acetylcysteine,
have not been demonstrated to benefit patients with
COPD.61
XIII. What is the role of Pulmonary Re-
habilitation in the management
of COPD?
Pulmonary Rehabilitation Programs for patients
with chronic pulmonary diseases are means of
enhancing standard medical therapy in order to
alleviate symptoms and optimize the patients'
functional capacity. The primary goal of the
program is to restore the patients to the high-
est level of independent function. This goal is
accomplished by helping patients become more
knowledgeable about their disease and more in-
dependent in performing daily care activities.
Summary of Evidence
Table 6 shows a summary of recommendations and
evidence grades for the components of pulmonary
rehabilitaion for patients with COPD as reported by
the Joint ACCP/AACVPR Pulmonary Rehabilitation
62
Guideline Panel is as follows.
Table 6. Summary of the Joint ACCP/ACCVPR Pul-
monary Rehabilitation Guidelines
Component/ Recommendations Grade**
Outcome
Lower extre- Lower extremity training A
mity training improves exercise tolerance
and is recommended as part
of pulmonary rehabilitation
Upper extre- Strength and endurance B
mity training training improves arm func-
CPM 4TH EDITION
tion; arm exercises should be
included in pulmonary reha-
bilitation
Ventilatory Scientific evidence does not B
muscle support the routine use of
training VMT in pulmonary rehabi-
litation; it may be considered
in selected patients with
decreased respiratory muscle
strength and breathlessness
Psychosocial, Evidence does not support the C
behavioural benefits of short-term psycho-
and educatio- social interventions as single
nal compo- therapeutic modalities; longer-
nents and term interventions may be
outcomes beneficial; expert opinion sup-
ports inclusion of educational
and psychosocial intervention
components in pulmonary
rehabilitation
Dyspnea Pulmonary rehabilitation A
improves the symptom of
dyspnea
Quality of Pulmonary rehabilitation B
life improves health-related QOL
Health care Pulmonary rehabilitation B
utilization has reduced the number of
hospitalizations and days
of hospitalization
Survival Pulmonary rehabilitation C
may improve survival
Grade A = scientific evidence provided well-designed, well
conducted controlled trials (randomized and non-randomized)
with statistically significant results that consistently support the
guideline recommendation; B = scientific evidence provided
by observational studies or by controlled trials with less con-
sistent results to support the guideline recommendation; C =
expert opinion.
Locally, long term benefits have been achieved in a
group of Filipino COPD patients followed up for more
than a year.63 In Metro Manila, there are 4 medical
centers actively involved in pulmonary rehabilitation,
namely, Philippine General Hospital, Lung Center of
the Philippines, Philippine Heart Center and National
Kidney Institute.
XIV. Is there a place for nutritional
supplemen­tation as an adjunctive
treatment of COPD patients?
Patients should maintain an optimum weight by eat-
ing a nutritious diet (Grade C). Several small meals
per day may be recommended to maintain adequate
caloric requirements and at the same time avoid
undue fatigue and shortness of breath.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Summary of Evidence
The association of increasing weight loss, severity of
65,66
airflow obstruction and mortality is known. Driver
showed that in patients with COPD who developed
episodes of respiratory failure, the degree of malnutri-
67
tion is much higher than those who did not. About
25 percent of patients with COPD suffer from under-
nutrition (body weight less than 90 percent of ideal).
64
Malnutrition affects the integrity of both the diaphragm
and extremities. Arora noted that nutritionally depleted
patients had significant reductions in respiratory muscle
strength as assessed by maximal inspiratory and expira-
tory pressure.
68
Even when receiving nutritional supplementation, many
patients are unable to gain weight perhaps because of
an underestimation of caloric needs or an inability to
maintain adequate caloric intake. Dyspnea may play a
role in limiting intake. Recent studies have shown that
the increased carbohydrate intake does not necessarily
lead to excess production of carbon dioxide. Chronic
hypercapnia can occur when the total caloric intake
markedly exceeds caloric needs. Thus, hypercapnic pa-
tients do not need to avoid carbohydrates, but maintain
a normal nutritious diet and optimum weight.
XV. Is long term oxygen therapy ef-
fective in prolonging survival of
COPD patients?
Long term oxygen therapy (LTOT) improves sur-
vival of patients with COPD and chronic respiratory
failure (Grade A).
Indications for the long-term supplemental oxygen
include a resting PaO2 of < or = 55 mmHg or evi-
dence of tissue hypoxia and organ damage, such as
cor pulmonale, secondary polycythemia (hematocrit
> 55%), edema from right heart failure, or impaired
mental status. In patients who are normoxemic at
rest but desaturate during exercise and sleep (PaO2
< 55 mmHg), exercise capacity and endurance may
be improved with oxygen supplementation.
Summary of Evidence
The value of long-term supplemental oxygen therapy
for hypoxemic patients with severe COPD has been
demonstrated in 2 major clinical trials, namely: the
National Heart, Lung, and Blood Institute's Nocturnal
69
Oxygen Therapy Trial and the British Medical Re-
search Council study.
70
The Nocturnal Oxygen Therapy Trial involved 6 centers
in the United States and 203 patients with hypoxemic
chronic obstructive lung diseases who were randomly
allocated to either continous (O2) therapy or 12-hour
nocturnal O2 therapy and followed for at least 12 months.
The results showed that the overall mortality in the
69
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
nocturnal O2 therapy was 1.94 times more than that in
the continuous O2 therapy group.
The British Medical Research Council study involved
3 centers in the United Kingdom and 87 patients who
chronic bronchitis or emphysema with irreversible
airways obstruction, severe arterial hypoxemia, carbon
dioxide retention and a history of congestive heart
faiulre. The patients were randomized to oxygen therapy
or no oxygen. Oxygen was given by nasal prongs for
at least 15 hours daily, usually at 2 L/min. The results
showed that 19 of the 42 oxygen treated patients died
in five years of survival follow-up campared with 30
out of 45 control patients.
XVI. What is COPD in acute exacerba-
tion?
Acute exacerbation is a new respiratory event or com-
plication superimposed upon established COPD. Acute
exacerbation of COPD is presented as the worsening
71
of the previous stable situation. Symptoms include
the following: (a) increased sputum production, (b)
change in sputum volume and color, (c) increased
dyspnea, (d) increased wheezes, (e) chest tightness, (f)
fluid retention.
The differential diagnoses to be considered in each pa-
tient include: pneumonia, pneumothorax, left ventricular
failure, pulmonary edema, pulmonary embolism, lung
cancer and upper airway obstruction.
XVII. When can acute exacerbation be
treated at home?
Acute exacerbation can be treated at home when
patients present the following clinical conditions: (a)
mild to moderate breathlessness, (b) normal level of
consciousness, and (c) generally good condition and
level of activity (Grade C).
XVIII. When is hospital confinement
necessary in acute exacerba-
tion?
Hospital confinement is necessary in acute exacerbation
when patients present the following clinical conditions:
(a) severe breathlessness, (b) poor and deteriorating
level of condition and activity, (c) presence of peripheral
cyanosis and impaired consciousness, (d) rapid and
progressive symptoms, (e) worsening hypoxemia and
hypercarbia (Grade C).
XIX. How is acute exacerbation man-
aged at home?
Management of acute exacerbation at home consists
of the following:
70
cpm 4TH eDITION
1. Increase dose and frequency of combination bron-
chodilator
2. Antibiotics if needed
3. Oral corticosteroids may be prescribed in some
cases
4. Oxygen therapy as deemed necessary
5. Chest physiotherapy as needed
6. If symptoms worsen, contact physician or emergency
room
XX. How is acute exacerbation man-
aged at the hospital?
Management of acute exacerbation at the hospital:
1. Assessment of condition: physical examination, chest
x-ray, arterial blood gas, ECG
2. ß2-agonist + anticholinergic by nebulization every
2 hours. Re-assess; if there is improvement, reduce
frequency of nebulization
3. Intravenous aminophylline
4. Intravenous methylprednisolone 50-100 mg or hy-
drocortisone 100 mg initially then every 6-8 hours;
taper as soon as possible
5. Antibiotics if indicated
6. Assess for signs of acute respiratory failure
7. Endotracheal intubation for mechanical ventilatory
support if deemed necessary
8. Wean from mechanical ventilatory support
9. Follow-up care upon discharge
XXI. How is peri-operative care insti-
tuted in COPD patients?
For patients with mild disease, operative risks are
similar to the general population and thus, these
patients would be handled similarly. Patients with
moderate to severe disease should be admitted to the
hospital at least 24 hours before the procedure and
should be treated aggressively.
COPD patients may have several diseases that will re-
quire surgery. The risk factors are identified by history,
physical examination, chest x-ray, arterial blood gas
analysis, spirometric studies, exercise tests and other
cardiovascular screening examinations. The incidence
of post-operative complications varies. However,
careful attention to peri-operative respiratory manage-
ment of this group of patients can improve outcome. In
patients with mild disease, operative risks are similar to
72
the general population. For patients with moderate to
severe disease, it is prudent to exercise greater degree
of care and caution. This may mean, in certain cases, a
longer stay at the surgical intensive unit, if indicated.
A multidisciplinary team composed of the primary at-
tending physician, pulmonologist, respiratory therapist
and anesthesiologist are gathered to lend their expertise
to the case.
CPM 4TH EDITION CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Patients with moderate to severe disease should be
admitted in the hospital at least 24 hours before the
73
procedure and should be treated aggressively. Maneu-
vers such as breathing exercises, coughing techniques,
lung inflation procedures such as incentive spirometry,
nebulization and intermittent positive pressure breathing
(IPPB) may be very useful in this group of patients.
74
XXII. Does lung volume reduction sur-
gery improve survival of COPD
patients?
Early results of lung volume reduction on small
number of patients followed for a mean of 6.4 months
have shown improvement in airflow, relief of dyspnea,
improved exercise tolerance and improved quality
of life. However, the current status of lung volume
reduction surgery for emphysema remains to be elu-
cidated; long term effects are unknown. Prospective
studies performed in carefully selected centers are
necessary. (Grade C)
Summary of Evidence
Bilateral pneumectomy or lung volume reduction sur-
gery consists of removal of 20 to 30 percent of each
lung through median sternotomy. Early results from 20
patients followed for a mean of 6.4 months have shown
a reduction in measured lung volumes, improvement in
airflow, relief of dyspnea, improved exercise tolerance,
and improved quality of life.
75
Laser resection of emphysematous bullae via thoracos-
76
copy has been described. Unfortunately, prolonged
postoperative air leaks complicate the procedure,
and patient improvement following surgery has been
limited.
XXIII. Does lung transplantation
improve the survival of COPD
patients?
Lung transplantation has shown improvement
in the survival of COPD patients undergoing the
procedure.
Summary of Evidence
Actuarial survival curves following single lung trans-
plantation for emphysema demonstrate a 2-year survival
77
of 77 percent and a 3-year survival of 75 percent. The
survival rate following transplantation for emphysema
is significantly higher than for interstitial fibrosis or
primary pulmonary hypertension. However, cost of the
procedure and lack of an adequate supply of donor lungs
remain problematic (Grade C).
XXIV. What are the indications for
referring COPD patient to a pul-
monary specialist?
Although no studies were found to assess when re-
ferrals to specialists led to better patient outcome, a
specialist opinion may be helpful at any stage. Based
on experts' opinion (Grade C), reasons for referral
can include the following: establish the diagnosis, ex-
clude other pathology, reassure the patient, reinforce
the need for smoking cessation, optimize treatment,
or assess the need for more complex and expensive
5
therapies appropriate to severe COPD.
Specific indications for specialist referral can be the
following:
• Diagnostic
1. Symptoms disproportionate to lung function abnor-
mality
2. Frequent infections
3. Uncertain diagnosis
• Therapeutic
1. Rapid decline in FEV1
2. Bullous lung disease
3. Assessment for corticosteroids, nebulizer therapy and
oxygen therapy
4. Cor pulmonale
5. Suspected severe COPD
6. Recurrent hospital confinement
Summary of Evidence
It is often general thinking that specialists (including
pulmonologists), due to their advanced education and
training, possess in-depth expert understanding of a
limited number of diseases within their respective do-
mains and are qualified to perform many diagnostic and
therapeutic procedures not in the repertoire of general
practitioners. Although there is evidence for superior
knowledge and practices of specialists in selective dis-
eases like myocardial infarction and congestive heart
failure, there are other disease areas where generalists
either outperform or do equally well as the specialists
(e.g. back pain).
For chronic obstructive lung disease, small and less
well-designed studies have shown no differences be-
78
tween generalists and specialists in their management.
A small retrospective analysis showed that in 2 commu-
nity hospitals, pulmonologists disagreed with one third
79
of general internists' spirometry interpretations.
Indirectly, in the management of other obstructive pul-
monary disease like asthma, much larger studies have
shown that pulmonologists and allergists use more ap-
propriate pharmacotherapy for individuals with asthma
than do generalists. Generalists tended to undersue
inhaled corticosteroids and overuse long-term oral cor-
ticosteroids, while undersuing high-dose corticosteroids
80,81
for acute exacerbations.
71
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
More effective specialty care may be the product of
more time, labor, and financially intensive management
by the specialist and his/her ancillary staff. For instance,
intensive multidisciplinary specialty interventions in
individuals with severe asthma have been shown to
lead to improved pharmacotherapy, fewer emergency
department visits, reduced admission rates, lenghts of
82,83,84,85,86
hospital stay, and overall costs.
In addition to more rational use of antiasthmatic agents
by specialists, these studies showed that spending more
time to educate patients along with improving provider
and ancillary staff availability during minor exacerba-
tions, resulted in better disease control.
Studies need to be done to assess patient outcomes when
comparing the generalists and specialists care of varying
severity of COPD.
XXV. How is disability evaluated in
patients with COPD?
Evaluating a patient for impairment and disability
entails an accurate diagnosis of the condition and
assessment of its severity. Impairment from respira-
tory disease adversely affects the patient's physical
functioning. Spirometric parameters are widely used
to evaluate disability. In Table 7, the American Tho-
racic Society utilizes the following parameters: FVC,
88
FEV1/FVC, DLco. Among the different disability
evaluations, the ATS recommendation for this pur-
pose is deemed to be most applicanle (Grade C).
Table 7. Rating of Impairment
Impairment FVC FEV1 FEV1/ DLco
FVC
Normal > or = > or = > or = > or =
80% 80% 75% 80%
Mild 60-79% 60-79% 60-74% 60-79%
Moderate 51-59% 41-59% 41-59% 41-59%
Severe 50% 40% 40% 40%
or < or < or < or <
Mildly impaired individuals usually do not have dimin-
ished ability to perform most jobs. Moderate impairment
indicates diminished ability to meet the physical require-
ments of many jobs and severe impairment indicates
inability to meet the physical demands of most jobs.
88
Although the primary responsibility of physicians is to
evaluate claimants for impairments, at times they may
be involved in disability determination.
72
cpm 4TH eDITION
XXVI. Among patients with COPD who
develop acute respiratory fail-
ure and require mechanical
ventilation, when is it ethical
to withold or withdraw me-
chanical ventilation?
All patients with COPD developing acute respira-
tory failure should be considered for intubation and
mechanical ventilation. However, patients who have
poor baseline function, marginal nutritional status,
severely restricted activity levels and inexorable de-
terioration of their late-stage-pulmonary dysfuntion,
may elect to forego intubation when, in their physi-
cian's judgement, it will only temporarily interrupt
the terminal phases of the disease.
It is also recommended in our setting that the following
be carried out:
a. Creation of Bioethics Task Force created from the
different local medical societies to set guidelines on
the withholding and withdrawal of mechanical venti-
latory support based on Filipino values and Christian
ethical principles.
b. Establishment of ethics committee in hospitals to
help physicians identify, analyze and resolve ethical
problems in patient care.
c. Development by medical societies of a consensus on
the definition of quality of life to guide clinical man-
agement in the institution of life-sustaining therapy.
Summary of Evidence
The primary ethical concern in COPD focuses on the
institution and withdrawal of mechanical ventilation
particularly in the hospital setting. Majority of COPD
patients with acute repiratory failure can be managed
with conservative therapy but approximately 35% of
89
these patients will require mechanical ventilation.
Institution of ventilatory support is a highly expensive
medical alternative in our setting but it appears to be
the only therapeutic tool available to avoid an imminent
90, 91
fatal outcome.
The long-term prognosis of COPD patients surviving
mechanical ventilation is similar to that of patients with
the same degree of underlying respiratory impairment
who have not required mechanical ventilation. In gen-
eral, therefore, it appears that patient with COPD whose
course is complicated by acute respiratory failure requir-
ing life-support measures do not have that devastating
overall prognosis. Consequently, no fundamental ethical
dilemma exists in considering all patients with COPD
for intubation and mechanical ventilation. However,
patients who have poor baseline function, marginal
nutritional status, severely restricted activity levels and
inexorable deterioration of their late-stage pulmonary
CPM 4TH EDITION CHRONIC OBSTRUCTIVE PULMONARY DISEASE
dysfunction may elect to forego intubation when, in their
physician's judgment, it will only temporarily interrupt
the terminal phases of the disease.
The withholding and withdrawing of life support are
processes by which various medical intervention either
are not given to or are taken away from patients with
92, 93
the expectation that they will die as a result. This
concept is entirely compatible with the ethical principles
of beneficience (being of benefit to the patient), nonma-
leficience (doing no harm to the patient) and autonomy
94
(self determination). Recommendations and guidelines
95
have been published by the Stanford Ethics Committee,
96
the American College of Chest Physicians, and the
97
American Thoracic Society. These guidelines although
discussed philosophically rather than morally, can be
98
applied to our patients.
The severity of the patient's underlying COPD and
the presence of co-morbid conditions do correlate to a
degree with clinical outcome and allow physicians to
assist patients with advance directives when the patients
are well and competent. Respect for autonomy direct
physicians to honor request of patients to forego life
support measures even when that decision will cause
the patient's death. If the request, however, seemed
inappropriate in the clinical circumstance (mechanical
ventilation is not futile), the duty of the physician to
preserve life takes precedence. The ethical principle of
stewardship may be applied to the patient. Lastly, it is
morally right for the patient or the surrogate decision
maker to withhold, withdraw or limit any futile medical
intervention.
Because survival after respiratory failure is most closely
linked to baseline function and co-morbid conditions, as
previously stated, decisions regarding limitations of care
are best made during stable periods before respiratory
failure or other life-threatening conditions occur.
RESEARCH RECOMMENDATIONS
1. Continuing nationwide surveilance study on the
prevalance of COPD to monitor improvement or
worsening of the situation related to specific interven-
tions/exposures.
2. Development and validation of practical diagnostic
tools for COPD (e.g. match stick test) that can be used
in areas where spirometry is not available.
3. Finding better diagnostic modalities to differentiate
asthma and COPD.
4. Searching for cost effective interventions that will
improve the detection and diagnosis of COPD, espe-
cially among general practitioners.
5. Determine the outcome of management of patients
handled by generalists and specialists.
6. Determine the most effective feasible approach for
smoking cessation in local condition.
7. Search the effective and practical means of prevention
of smoking initiation among Filipino school children
and adolescents.
8. Assessment of impact of therapeutic interventions on
"quality of life" of Filipino COPD patients.
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ANNEX 1
For therapeutic or interventional studies:
Levels Grades of
of Evidence Recommendations
I. Randomized trials with low false A
positive (alpha errors) and low
false negative (beta errors)
II. Randomized trials with high false B
positive (alpha errors) and high
false negative (beta errors)
III. Nonrandomized concurrent controls C
IV. Nonrandomized historical controls C
V. Case series C
Levels of evidence for rating studies on the accuracy
of diagnostic tests:
Level 1 All 5 of the following criteria are satisfied:
(a) There was an independent interpretation of the
result of the diagnostic test (without knowl-
edge of the result of the gold standard).
(b) There was an independent interpretation of the
result of the gold standard (without knowledge
of the result of the diagnostic test).
(c) The study patients consisted of patients sus-
pected (but not known) to have the disorder
of interest.
(d) The diagnostic test and gold standard are
both described in sufficient detail to allow
reproducibility.
(e) The study population consists of at least 50
patients with and 50 patients without the
disorder of interest.
Level 2 4 of the 5 criteria are met
Level 3 3 of the 5 criteria are met
Level 4 2 of the 5 criteria are met
Level 5 1 of the 5 criteria are met
Level 6 None of the 5 criteria are met
Grading system for recommendations:
Grade A The recommendation is based on one or
more studies at level 1.
Grade B The best evidence available is at level 2.
75
CHRONIC OBSTRUCTIVE PULMONARY DISEASE cpm 4TH eDITION

Grade C The best evidence available is at level 3 or Cough (+ or - sputum)

lower and includes expert's opinion.
Summary of Guidelines
Definitions
Chronic Obstructive Pulmonary Disease (COPD) is
defined as a disease characterized by the presence of
airflow obstruction due to chronic bronchitis or emphy-
sema. The airflow obstruction is generally progressive,
may be accompanied by airway hyperreactivity and may
be partially reversible.
Chronic bronchitis is characterized by the presence of
chronic cough for three months in each of two succes-
sive years in a patient in whom other causes of cough
have been excluded.
Emphysema is defined as an abnormal permanent
enlargement of the airspaces distal to the terminal bron-
chioles, accompanied by the destruction of their walls.
This disease is manifested predominantly by dyspnea.
Diagnosis of COPD
Detection Strategies
Suspect COPD in patients with the following: are greater
than 50 years old, smoker for many years and with symp-
toms of progressive and increasing shortness of breath
on exertion and/or chronic cough. Physical examination,
chest x-ray, sputum examination, electrocardiogram,
and complete blood count are non specific diagnostic
tests for COPD.
Confirmation Strategies
Spirometry should be done on all patients suspected
of having COPD. Diagnosis of COPD is established if
FEV1/FVC ratio is < 70% of the predicted value. A post
bronchodilator response of less than 15% in predicted
normal FEV1 is in favor of the diagnosis of COPD rather
than asthma. Other lung function tests (e.g. diffusing
capacity, arterial blood gas), CT scan and other ancillary
procedures are indicated for specific conditions.
Grading of Severity of COPD
Category of FEV1 Signs/
COPD (% of Pred) Symptoms
Mild 60-79 No abnormal signs
Smoker's cough
Little or no breath-
lessness
Moderate 40-59 Breathlessness (+ or -
wheeze on moderate
exertion)
76
Variable abnormal signs
(general reduction in
breath sounds, pre-
sence of wheezes)
Severe <40 Breathlessness on any
exertion / at rest
Wheeze and cough
often prominent
Lung overinflation
usual; cyanosis;
peripheral edema and
polycythemia in
advanced disease;
especially during
exacerbation
STEP CARE OF COPD
With Mild Symptoms
1. Smoking cessation
2. Protection from or reduction of environmental expo-
sure
3. Annual influenza vaccination
4. For those with variable symptoms:
• selective β2-agonist metered dose inhaler (MDI),
1-2 puffs every 2-6 hours as needed (not to exceed
8-12 puffs/24 hours)
For those with continuing symptoms
• anticholinergic MDI aerosol, 2-6 puffs every 6-8
hours (not to be used more frequently) plus selec-
tive β2-agonist MDI 1-4 puffs as required (for rapid
relief when needed)
If inhaled bronchodilator is not available or non-ac-
cessible or affordable, use oral short-acting β2-agonist
e.g. terbutaline, clenbuterol, salbutamol, as needed;
however, the high incidence of side effects with these
oral preparations must be recognized.
With Moderate Symptoms
As above, numbers 1 to 3 recommendations
4. Inhaled combined anticholinergic plus β2-agonist at
2-4 puffs every 4-6 hours
5. If response to step 4 is unsatisfactory, add theophylline
(long acting), 200-300 mg twice daily or 400 mg once
a day at bedtime for nocturnal bronchospasm and/or
long acting inhaled β2-agonist
6. Consider use of mucokinetic agent
7. If response to step 5 is unsatisfactory, consider a
corticosteroid trial of Prednisone 30 mg per day for
2 weeks
• if improvement occurs, taper down to daily or
alternate dosing at 5 mg/day
• if no improvement occurs, stop immediately
• if steroid appears to help, consider possible use
of aerosol MDI e.g. budesonide, fluticasone or
beclomethasone, for 6 weeks
CPM 4TH EDITION CHRONIC OBSTRUCTIVE PULMONARY DISEASE
8. Pulmonary rehabilitation 6. If symptoms worsen, contact physician or emergency
room.
If inhaled bronchodilators are not available, oral β2- At the hospital:
agonist preparations (e.g. bambuterol), can be used as 1. Assessment of condition: physical examination, chest
regular alternative medications. x-ray, arterial blood gas, ECG
2. β2-agonist + anticholinergic by nebulization every
With Severe Symptoms 2 hours. Re-assess; if there is improvement, reduce
Numbers 1 to 3 recommendations frequency of nebulization
4. Increase inhaled combined ipratropium + β2-agonist 3. Intravenous aminophylline
dosage to 2-4 puffs every 3-4 hours or inhalant solu- 4. Intravenous methylprednisolone 50-100 mg or hy-
tion of combined ipratropium + β2-agonist every 4-8 drocortisone 100 mg initially then every 6-8 hours;
hours taper as soon as possible
5. Theophylline (long acting)/long acting β-agonist 5. Antibiotics if indicated
6. Trial of steroids 6. Assess for signs of acute respiratory failure
7. Pulmonary rehabilitation 7. Endotracheal intubation for mechanical ventilatory
8. Assessment for long term oxygen therapy support if deemed necessary
8. Wean from mechanical ventilatory support
If inhaled bronchodilators are not available, oral β2- 9. Follow-up care upon discharge
agonist preparations can be used as regular alternative
medications.
ACKNOWLEDGEMENTS
NON-PHARMACOLOGIC MANAGEMENT OF
STABLE COPD Ma. Cecilia Abad
Raquel Are
1. Smoking cessation is essential at all stages of the Mary Ann Baliva
disease. Success can be achieved by initiation, early Fr. Ramon Bernal
follow-up, continuing reinforcement and review of Dr. Lenny Canizares-Fernandez
Meredith Castro
failure.
Bernadette Conception
2. Pulmonary rehabilitation is recommended for patients
Jean de la Cruz-de Leon
with moderate to severe COPD. It has been shown Dr. Rey Desales
to reduce shortness of breath and improve exercise Loreta Evangelista
performance. Dr. Jose Alvin Mojica
3. Indications for Long Term Oxygen Therapy (LTOT) Dr. Nerissa Narciso
include: resting PaO2 less than or equal to 55 mmHg Ma. Flordeliza Sanchez
or evidence of tissue hypoxia and organ damage, Dr. Renato Torres
edema from right heart failure, or impaired mental Rosalind Vianzon
status. In patients who are normoxemic at rest but
desaturate during exercise or sleep, exercise capacity
or endurance may be improved with oxygen supple-
mentation. LTOT improves survival of patients with
COPD.
4. Patients should maintain an optimum weight by eating
a nutritious diet. Several small meals per day may be
recommended to maintain adequate caloric require-
ments and at the same time avoid undue fatigue and
shortness of breath.

MANAGEMENT OF ACUTE EXACERBATION

At Home:
1. Increase dose and frequency of combination bron-
chodilator
2. Antibiotics if needed
3. Oral corticosteroids may be prescribed in some
cases
4. Oxygen therapy as deemed necessary
5. Chest physiotherapy as needed
77
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Drugs Mentioned in the Treatment Guideline
This index lists drugs/drug classifications mentioned in the treatment guideline. Prescribing Information of these
drugs can be found in the Philippine Pharmaceutical Directory (PPD) 8th edition. Opposite the brand name is its
page number in the PPD 8th edition.
Anticholinergics
Ipratropium Br
Atrovent S262
Berodual* S262
Combivent* S262
β-Adrenergic Agonists
Aminophylline
Weimer
Aminophylline Inj S274
Bambuterol HCl
Bambec S268
Clenbuterol
Spiropent S271
Salbutamol
Activent S266
Asbumox S266
Asbunyl S266
Asbunyl Plus* S266
Asfrenon S266
Asfrenon GF
Expectorant* S266
Asmacaire S266
Asmafort S266
Asmalin S266
Asmalin Broncho* S266
Asmalin Metered Dose
Inhaler S268
Biogenerics Salbutamol S268
Broncaire Expectorant
Syrup* S254, S268
Broncaire Tab S268
Butovent Spray S268
Clarituss Plus S254
Combivent* S262
Drugmakers Salbutamol S268
Drugmakers Salbutamol
+ Guaifenesin* S270
Emplusal S270
Europharma Salbutamol S270
Librentin/Librentin Clenil/Clenil Forte Spray S264
Bronchoneb S270
Pharmachemie-
Salbutamol Cyclocaps S270
Pharmacia Salbutamol S270
Resdil S271
Resovent S271
Respolin S271
Salbumed S271
Salvex S271
78
cpm 4TH eDITION
Sedalin S271 Fluticasone
Socamol S271 Flixotide S264
Solmux Broncho Flixotide Nebule S264
(Reformulated)* S260
Vamsler Salbutamol S272
Ventolin S272
Ventolin Expectorant* S261
Ventolin Volmax S272
Terbutaline
Alloxygen S266
Asbutel S266
Bricanyl O217, S268
Bricanyl Expectorant* S268
Myrex Terbutaline
Sulfate Syrup S270
Terbulin S271
Terbusol S271
VCP Terbutaline Sulfate S272
Theophylline
Aerophil S272
Asbral* S272
Asmasolon S272
Brondil (Reformulated) S272
Europharma
Theophylline* S272
Hallex* S272
Marax* S272
Nuelin S273
Phenedrine S273
Tedral S273
Theodur S273
Uni-Dur S274
Mucokinetic Agents
Acetylcysteine
Fluimucil S256
Systemic Corticosteroids
Beclomethasone dipropionate
Becotide/Becloforte S262
Pharmachemie-
Beclomethasone
Dipropionate S264
Budesonide
Budecort S264
Pharmachemie-
Budesonide
Cyclocaps S264
Primavent S264