CHAPTER I

INTRODUCTION

Chronic obstructive pulmonary disease (COPD) is one of a group of non-

communicable diseases that has become a health problem public in Indonesia. This is
caused by increased life expectancy and higher exposure to risk factors, such as host
factors that are suspected to be associated with COPD events, the increasing number
of smokers, especially in the younger age group, and air pollution indoors and
outdoors and in the workplace.
In 2007 in the United States, COPD was the leading cause of third death. In
Indonesia there is no accurate data on the frequency of COPD. In 1992 showed that
death rates due to asthma, chronic bronchitis and emphysema were ranked 6th out of
10 most common causes of death in Indonesia.
Therefore proper and early management of COPD is needed. Management of
COPD generally aims to prevent the progression of the disease, reduce symptoms,
increase tolerance for activity, improve health status, prevent and manage
complications, prevent and treat exacerbations, and reduce mortality.
To be able to provide management as early as possible,also needed accurate
diagnosis is. The diagnosis of COPD is made onbasis of theclinical features and
investigations this is because the symptoms and signs of COPD are very varied,
ranging from asymptomatic, mild to severe symptoms. So that in some cases of
physical examination found no obvious abnormalities and signs of pulmonary
inflation. In this situation the supporting examination of COPD is very helpful, one of
them is plain radiographic examination.

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 CHAPTER 2
LITERATURE REVIEW

2.1. COPD
Chronic obstructive pulmonary disease (COPD) is a chronic lung diseaseby
characterized non-airway obstruction in the airway reversible or partially reversible,
and a pulmonary inflammatory response to harmful particles or gases (GOLD, 2009).

2.2. Epidemiology
Most COPD patients are male. This is due to more smokers found in men than
in women. The Survey (Susenas 2001 National Socioeconomic) shows that 62.2% of
the male population is smokers and only 1.3% of women smoke. As many as 92.0% of
smokers stated their habit of smoking inside the house, when with other household
members, thus most of the household members were passive smokers.

2.3. Risk
Factors COPD risk factors are things that are related and or that cause COPD
to a particular person or group. These risk factors include host factors, smoking
behavior factors, and factors environmental. Host factors include genetic, hyper-
responsive airway and lung growth. The main genetic factor is the lack of alpha 1
antitrypsin, which is a serine protease inhibitor. Hyperresponsive airway can also
occur due to exposure to cigarette smoke or pollution. Lung growth is associated with
pregnancy, birth weight and exposure during childhood. Decreased lung function due
to impaired lung growth is thought to be related to the risk of getting COPD
(Helmersen, 2002).
Smoking is the most important risk factor for COPD. The prevalence highest
of respiratory disorders and decreased lung function is in smokers. Age of starting
smoking, the number of packs per year and active smokers are related to mortality.
Not all smokers will suffer from COPD, this might also be related to genetic factors.
Passive smokers and smoking during pregnancy are also risk factors for COPD.

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Passive smokers found a significant decrease in annual VEP1 in young people who
were not smokers (Helmersen, 2002).
The relationship between smoking and COPD shows a relationship dose
response, meaning that more cigarettes are smoked every day and the longer the
smoking habit is, the greater the risk of the disease. The relationship dose response can
be seen in the Brigman Index, namely the number of cigarettes consumed per day
multiplied by the number of days of smoking (years), for example 10 packs of
bronchitis, meaning that if someone smokes a day a pack, then someone will suffer
from chronic bronchitis at least after 10 years of smoking ( Suradi, 2009).
Air pollution consists of indoor pollution(indoor)such as cigarette smoke,
smoke stoves, wood smoke, and others, pollution outside(outdoor), such as flue gas
industry, motor vehicle exhaust, road dust, and other - other, and pollution in the
workplace, such as chemicals, dust / irritants, toxic gases, and others. Continuous
exposure to air pollution isrisk factor for another COPD.

2.4. Pathogenesis
Airway and lungs function for the process of respiration, namely the uptake of
oxygen for metabolic purposes and the removal of carbon dioxide and water as a result
of metabolism. This process consists of three stages, namely ventilation, diffusion and
perfusion. Ventilation is the process of entry and exit of air from the lungs. Diffusion
is the event of gas exchange between alveoli and blood vessels, whereas perfusion is
the distribution of oxygenated blood.disorders Ventilation consist of restriction
disorders, which are impaired lung development and obstruction disorders in the form
of slowing air flow in the airways. The parameters that are often used to look at
restriction disturbances are vital capacity (KV), whereas for obstruction disorders used
theforced expiratory volume parameter first second(VEP1), and the ratio of the first
second forced expiratory volume to forced vital capacity (VEP1 / KVP) (Sherwood,
2001 ).

2.5. Diagnosis

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 Diagnosis of COPD starts from history, physical examination, and
investigation. Diagnosis based on history, physical examination and chest X-ray can
determine Clinical COPD. If continued with spirometry examination will be able to
determine the diagnosis of COPD according to the degree of disease.

2.5.1. History
a. There are risk factors risk
Importantfactors are age (usually middle age), and a history of exposure,
whether in the form of cigarette smoke, air pollution, orpollution workplace. Smoking
is the singlecausal cause most important, far more important than other causative
factors.
b. Clinical
Symptoms of COPD are mainly related to respiration. Complaints of
respiration must be examined carefully because it is often regarded as a symptom that
usually occurs in the aging process. Chronic cough is a cough that goes away for 3
months that does not go away with the treatment given. Sometimes the patient states
only continuous sputum without coughing. In addition, shortness of breath is a
symptom that is often complained of patients, especially when doing activities. Often
patients have adapted to shortness of slow progressive breath so that the tightness is
not complained.

2.5.2. Physical Examination

Examination findings starting from inspection can be in the form of a chest like
a barrel (barrel chest), there is a way of breathing purse lips breathing (like a person
blowing), visible use and hypertrophy of the aids of breathing muscles, widening of
the rib cage, and if it has failed right heart visible jugular venous distension and leg
edema. In percussion, a hypersonor is usually found. Examination of auscultation can
be found weakening fremitus,vesicular breath sounds weak or normal, prolonged
expiration, crackling, and wheezing (PDPI, 2003).

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2.5.3. Supporting Examination
a. Spirometry (VEP1, predicted VEP1, KVP, VEP1 / KVP)
b. Radiology (chest radiograph)
Radiological examination results can be found pulmonary abnormalities in the
form of hyperinflation or hyperlucent, horizontal diaphragm,bronchovascular pattern
increased, pendulum heart, and dilated retrosternal space. Although sometimes the
results of radiological examination are still normal in mild COPD, this radiological
examination also serves to rule out the diagnosis ofdiseases other lungor rule out a
differential diagnosis of patient complaints (GOLD, 2009).
c. Routine blood laboratory
d. Blood gas analysis
e. Sputum microbiology (PDPI, 2003)

2.5.4. Different Diagnosis

COPD is easier to distinguish from bronchiectasis or post-syndrome
pulmonary TB, but it is often difficult to distinguish from bronchial asthma orheart
failure chronic.

2.6. COPD Acute exacerbation Acute

Exacerbation in COPD means worsening compared to the previous condition.
The definition of acute exacerbation in COPD is an event acute in the natural course of
the disease characterized by changes in basal breathlessness, coughing, and / or
sputum that are outside normal limits in day-to-day variations (GOLD, 2009).
The cause of acute exacerbation can be primary, namely tracheobronchial
infection (usually due to a virus), or secondary to pneumonia, heart failure,
arrhythmia,
pulmonary embolism, spontaneous pneumothorax, inappropriate use of oxygen, use of
drugs (inappropriate antidepressant drugs, diuretics), Metabolic diseases (diabetes
mellitus, electrolyte disruption), poor nutrition, bad environment or air pollution,
repeated aspirations, as well as in the later stages of disease respiratory (respiratory

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muscle fatigue) (PDPI, 2003).
The main symptoms of exacerbation include increased tightness, increased
sputum production, and a change in sputum consistency or color. According to
Anthonisen et al.(1987), acute exacerbations can be divided into three types, namely
type I (exacerbations severe) if they have 3 main symptoms, type II (moderate
exacerbations) if they only have 2 main symptoms, and type III (mild exacerbations) if
they have 1 symptom the main plus the presence of upper respiratory tract infections
for more than 5 days, fever without other causes, increased coughing, increased
wheezing or increased frequency respiratory> 20% baseline, or pulse frequency> 20%
baseline (Vestbo, 2006).

2.7. Management of acute COPD Exacerbations

The principle of management of acute COPD exacerbations is to deal with
theimmediately exacerbationand prevent death. The risk of death from exacerbations
is closely related to the occurrence of respiratory acidosis, the presence of
comorbidities, and the need for ventilation equipment (GOLD, 2009). Treatment of
acute exacerbations can be done at home (for mild exacerbations) or in hospitals (for
moderate and severe exacerbations). Management of exacerbations acute in hospitals
can be done on an out patient or in patient basis and is done in an out patient clinic, in
patient room, emergency room, or room ICU (PDPI, 2003).

2.7.1. Bronchodilators The

Preferred bronchodilators for COPD exacerbation therapy are short-acting
inhaled B2-agonists. If an immediate response from this drug has not been reached, it
is
recommended to add anticholinergics, although scientific evidence of the effectiveness
of this combination is controversial. Despite its extensive clinical use, the role of
methylxanthine in exacerbation therapy is still controversial. Now methylxanthines
(theophylline, aminophylline) are considered second-line therapy, when there is no
adequate response from the use of short-acting inhaled B2-agonists. There are no

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clinical studies evaluating the use of long-acting inhaled B2- agonists with / without
inhalation of glucocorticosteroids during exacerbations (GOLD, 2009).
If outpatient B2-agonists and anticholinergics must be given with increasing
doses. Inhalers are still quite effective when used in theway right, nebulizer can be
used in order to be more effective bronchodilators. Be careful with the use of a
nebulizer that uses oxygen as a compressor, because the use of 8-10 liters of oxygen to
produce steam can causeretention CO2. The xanthine group can be given together with
other bronchodilators because it has the effect of strengthening the diaphragm muscle.
In hospital treatment , bronchodilators are given intravenously and nebulizers,
withadministration more frequentneed to monitor closely the emergence of
palpitations as a side effect of bronchodilators (PDPI, 2003).

2.7.2. Corticosteroids
Oral / intravenous corticosteroids are recommended as additional therapy in the
management of COPD exacerbations. The exact recommended dose is unknown, but
high doses are associated with significant risk of side effects. An oral prednisolone
dose of 30-40 mg / day for 7-10 days is effective and safe (GOLD, 2009). According
to PDPI (2003), corticosteroids are not always given depending on the severity of
exacerbations. At moderate exacerbations a prednisone of 30 mg / day can be
administered for 1-2 weeks, at a severe degree given intravenously. Giving more than
two weeks does not provide better benefits, but more side effects.

2.7.3. Antibiotics
Based on current evidence, antibiotics should be given to (GOLD, 2009):
a. Exacerbation patients who have three cardinal symptoms, namely an increase in
sputum volume, sputum becomes increasingly purulent, and increased shortness of
breath
b. Exacerbation patients who have two cardinal symptoms, if an increase in
purulence is one of the two symptoms
c. Exacerbation patients who need mechanical ventilation.

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 The choice of antibiotics is adjusted to the pattern of local germs and the
composition of the latest antibiotic combination. The administration of antibiotics in
hospital should be by drip or intravenous, while for outpatient care when
exacerbations moderate should be given in combination with macrolides, and if mild
can be given single. Antibiotics that can be given at the health center are line I:
Ampicillin, Kotrimoksasol, Erythromycin, and line II: Ampicillin combination
Chloramphenicol, Erythromycin, combination of Chloramphenicol with
Kotrimaksasol plus Erythromycin as Macrolide (PDPI, 2003).

2.7.4. Oxygen Therapy

In acute exacerbations of oxygen therapy is first and foremost, aimed at
improving hypoxemia and preventing - life threatening conditions, it can be done in
the emergency room, ward or in the ICU. An adequate level of oxygenation (PaO2>
8.0 kPa, 60 mmHg or SaO2> 90%) is easily achieved in COPD patients without
complications, but CO2 retention can occur slowly with slight changes in symptoms
so
a strict evaluation of hypercapnia is needed. Use a lid with a predetermined level
(ventury mask) 24%, 28% or 32%. Note whetherhoods rebreathing or non-
rebreathing, depending on levels of PaCO2 and PaO2. If therapy oxygen cannot
achieve adequate oxygenation conditions,ventilation must be used mechanical(PDPI,
2003).

2.7.5. Mechanical ventilation

The main purpose of using mechanical ventilation in severe exacerbation of
COPD is to reduce mortality and morbidity, and improve symptoms.ventilation
Mechanical consisting of intermittent non-invasive ventilation (NIV), both of which
use
a positive or a negative pressure (NIPPV) and invasive mechanical ventilation by oro-
tracheal tube or tracheostomy. First the use of NIPPV, if you fail to think about the
use of mechanical ventilation with intubation. The use of NIV has been studied in

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several Randomized Controlled Trials in cases ofrespiratory acutefailure, which
consistently show positive results with a success rate of 80-85%. These results show
evidence that NIV improveacidosis respiratory lower respiratory rate, severity of
spasms, and duration of hospitalization (GOLD, 2009).

2.8. Complications
Complications that can occur in COPD are chronic respiratory failure, acute
respiratory failure in chronic respiratory failure, recurrent infections, and cor
pulmonale. Chronic respiratory failure shown by the results of blood gas analysis in
the form of PaO2 <60 mmHg and PaCO2> 50 mmHg, and the pH can be normal.
Acute respiratory failure in respiratory chronic failure is characterized by shortness of
breath with or without cyanosis, sputum volume increased and purulence, fever, and
decreased consciousness. In COPD patients , excessive production of sputum causes
the formation of germ colonies, this facilitates recurring infections. In addition, in this
chronic condition the immunity body's becomes lower, marked by decreased blood
lymphocyte levels. The presence of cor pulmonale is characterized by P pulmonary on
the ECG, hematocrit > 50%, and can be accompanied by right heart failure (PDPI,
2003).

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 CHAPTER 3
CONCLUSION

The characteristics of COPD can be seen by the presence in of non-reversible

or partial reversible airway obstruction the airway, and the presence of pulmonary
inflammatory responses to harmful particles or gases. For this reason, the diagnosis of
COPD starts from history, physical examination, and supporting examination in the
form of chest X-ray can determine Clinical COPD.
Anamnesis aspect needed for diagnosis is the presence of risk factors and
clinical symptoms experienced by the patient. COPD symptoms are mainly related to
respiration. Clinical symptoms can include chronic coughing and shortness of breath
when doing activities. On the physical examination aspect, it is usually found shape
chest like a barrel (barrel chest), there is a way of breathing purse lips breathing (like
a
person blowing), visible use and hypertrophy of the aids of the breathing muscles,
widening of the ribs, and if there has been a right heart failure there is distension
jugular veins and limb edema. In percussion, a hypersonor is usually found.
Examination of auscultation can be found weakening fremitus, vesicular breath
sounds weak or normal, long expiratory, crackling, and wheezing. In addition, the
findings of the history and physical examination should be in tune with the results of a
chest X-ray examination, where the results examination found pulmonary
abnormalities in the form of hyperinflation or hyperlucent, horizontal diaphragm,
increased bronchovascular pattern, pendulum heart, and dilated retrosternal space.
Although sometimes the results of the examination are still normal in mild COPD,
chest X-ray examination also serves to rule out the diagnosis of other lung diseases or
rule out a diagnosis differential of patient complaints.

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