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Chronic obstructive pulmonary disease
Chronic obstructive pulmonary disease (COPD) represents a spectrum

of obstructive airway diseases. It includes two key components which
are chronic bronchitis-small airways disease and emphysema.
Epidemiology
The most common cause has historically been, and unfortunately
continues to be, smoking. It takes many years of smoking to develop
COPD and as such typically patients are older adults. There are however a
number of other less common risk factors/aetiologies, each with their own
demographics. They include:
 cigarette smoking
 industrial exposure (e.g. mining)
 cystic fibrosis
 alpha-1 antitrypsin deficiency
 intravenous drug use
 immune deficiency syndromes
 vasculitides and connective tissue disorders
Clinical presentation
Symptoms of COPD include dyspnoea on exertion, wheezing, productive
cough, pursed-lip breathing, and use of accessory muscles. Patients with
chronic bronchitis are classically "blue bloaters," while those with
emphysema are known as "pink puffers". In advanced cases, muscle
wasting, asterixis, and peripheral oedema may be seen.
Pathology
In contrast to asthma, the histologic changes of COPD are irreversible and
gradually progress over time. In chronic bronchitis, there is diffuse
hyperplasia of mucous glands with associated hypersecretion and
bronchial wall inflammation.
Emphysema involves the destruction of alveolar septa and pulmonary
capillaries, leading to decreased elastic recoil and resultant air trapping.
The morphological subtypes of emphysema include:
 centrilobular (centriacinar): associated with smoking and spreads

peripherally from bronchioles
 panacinar: homozygous AAT deficiency and uniformly destroys
1
alveoli
 paraseptal (distal acinar): involves the distal airways
Pulmonary function testing (PFT) reveals airflow obstruction, as evidenced
by a decreased forced expiratory volume in 1 second to forced vital
capacity (FEV /FVC) ratio. Administration of bronchodilators has no effect,
1
unlike the reversible obstruction seen in asthma.
Severity classification
The global initiative for chronic obstructive lung disease (GOLD) staging
system is a commonly used severity staging system based on airflow
limitation. According to this, there are 4 key stages:
 stage I: mild, FEV > 80% of normal

1
 stage II: moderate, FEV = 50-79% of normal

1
 stage III: severe, FEV = 30-49% of normal

1
 stage IV: very severe, FEV <30% of normal or <50% of normal with

1
presence of chronic respiratory failure present

The FEV :FVC ratio should be <0.70 for all stages.
1
The GOLD staging system may be insensitive in early stages . 12
Clinical phenotypes
Several distinct clinical phenotypes have been described : 4,6,8
 emphysema predominant
 airways predominant
o small airways predominant
o large airways predominant
 mixed
Radiographic features
Plain radiograph
Findings of chronic bronchitis on chest radiography are non-specific and
include increased bronchovascular markings and cardiomegaly.
Emphysema manifests as lung hyperinflation with flattened
hemidiaphragms, a small heart, and possible bullous changes. On the
lateral radiograph, a "barrel chest" with widened anterior-posterior
diameter may be visualized. The "saber-sheath trachea" sign refers to
marked coronal narrowing of the intrathoracic trachea (frontal view) with
concomitant sagittal widening (lateral view).
CT
Findings of COPD may be seen in a variety of CT chest studies, e.g.
contrast-enhanced CT, CT pulmonary angiography, staging CT chest, HRCT
chest, etc.
Chronic bronchitis
In chronic bronchitis, bronchial wall thickening may be seen in addition to
enlarged vessels. Repeated inflammation can lead to scarring with
bronchovascular irregularity and fibrosis.
Emphysema
Emphysema is diagnosed by alveolar septal destruction and airspace
enlargement, which may occur in a variety of distributions. Centrilobular
emphysema is predominantly seen in the upper lobes with panlobular
emphysema predominating in the lower lobes. Paraseptal emphysema
tends to occur near lung fissures and pleura. Formation of
giant bullae may lead to compression of mediastinal structures, while
rupture of pleural blebs may produce
spontaneous pneumothorax/pneumomediastinum.
Treatment and prognosis

Barring whole-lung transplantation, there is currently no cure for COPD,
but it is highly preventable and treatable.
Lifestyle measures
Risk factor reduction via smoking cessation, occupational health, and air
pollution reduction should be instituted. Patients should also have all
available vaccinations.
Pharmacology
Pharacological management is generally first-line. It involves the use of
bronchodilators, corticosteroids, and other medications (e.g.
methylxanthines, leukotriene receptor antagonists, phosphodiesterase
type-4 inhibitors, omalizumab), as well as supplemental oxygen and
pulmonary rehabilitation. Long-acting β2-agonist (LABA) and long-acting
muscarinic antagonist (LAMA) combination therapies are currently
considered the most effective strategy .
15
Acute exacerbations are treated with high-dose corticosteroids, short-

acting bronchodilators, supplemental oxygen, and antibiotics if indicated.
Surgery
Surgical therapy is usually reserved for COPD refractory to
pharmacological management. In addition to the aforementioned whole-
lung lung transplant, other surgical procedures include:
 endobronchial valve or intrabronchial valve

 bullectomy
 lung volume reduction surgery
COPD : Hiperinflasi (jaraknya melebar secara tinggi),
Kerley B Line : edema interstitial
Atelectasis is collapse or incomplete expansion of the lung or part of the

lung. This is one of the most common findings on a chest x-ray. It is most
often caused by an endobronchial lesion, such as mucus plug or tumor. It
can also be caused by extrinsic compression centrally by a mass such as
lymph nodes or peripheral compression by pleural effusion. An unusual
type of atelectasis is cicatricial and is secondary to scarring, TB, or status
post radiation.
Atelectasis is almost always associated with a linear increased density on

chest x-ray. The apex tends to be at the hilum. The density is associated
with volume loss. Some indirect signs of volume loss include vascular
crowding or fissural, tracheal, or mediastinal shift, towards the collapse.
There may be compensatory hyperinflation of adjacent lobes, or hilar
elevation (upper lobe collapse) or depression (lower lobe collapse).
Segmental and subsegmental collapse may show linear, curvilinear, wedge
shaped opacities. This is most often associated with post-op patients and
those with massive hepatosplenomegaly or ascites .
Atelectasis describes loss of lung volume secondary to collapse. It has many causes, the root of
which is bronchial obstruction with absorption of distal gas. Atelectasis may be subsegmental,
segmental, lobar, or involve the entire lung.
Reference article
This is a summary article; read more in our article on lobar collapse.
Summary
 pathophysiology
o caused by:
 bronchial obstruction
 e.g. inflammation, infection, cancer, foreign body
 adjacent compression
 e.g. a lung tumour, vascular cause, large osteophyte
o results in distal gaseous absorption
 partial or complete loss of volume distal to the obstruction
 lung parenchyma collapses down
 associated volume loss
 role of imaging
o confirm lung collapse
 differentiate from air-space opacification
o help tod determine the cause (may need CT)
o assess for complications, e.g. pleural effusion
Radiographic features
Chest x-ray
Atelectasis is another word for lung collapse. The commonest cause is a bronchial obstruction that
results in distal gas resorption and a reduction in the volume of gas in the affected lung, lobe,
segment or subsegment. As the gas is resorbed, the walls of the alveoli collapse in on themselves and
the size of the affected area reduces.
This volume loss is the most important radiographic sign of collapse. If the cause is an obstructing
lesion, this may be seen on a plain film.

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Chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) represents a spectrum

 centrilobular (centriacinar): associated with smoking and spreads

unlike the reversible obstruction seen in asthma.

 stage I: mild, FEV > 80% of normal

 stage II: moderate, FEV = 50-79% of normal

 stage III: severe, FEV = 30-49% of normal

 stage IV: very severe, FEV <30% of normal or <50% of normal with

presence of chronic respiratory failure present

The GOLD staging system may be insensitive in early stages . 12

Treatment and prognosis

Acute exacerbations are treated with high-dose corticosteroids, short-

 endobronchial valve or intrabronchial valve

Atelectasis is collapse or incomplete expansion of the lung or part of the

Atelectasis is almost always associated with a linear increased density on

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