Chronic Obstructive Pulmonary Disease (COPD)
is a major cause of chronic morbidity
and mortality throughout the world. Many people suffer from this
disease for years and die prematurely from it or its complications. COPD is the fourth leading cause of death in the world, and further
increases in its prevalence and mortality can be predicted in the coming
decades.
Researchers estimate the prevalence
of chronic airflow obstruction in the world as 4-6%.
Chronic
Obstructive Pulmonary Disease (COPD) is a preventable and treatable disease
with some significant extrapulmonary effects that may contribute to the
severity in individual patients. Its pulmonary component is characterized by
airflow limitation that is not fully reversible. The airflow limitation is usually
progressive and associated with an abnormal inflammatory response
of the lung to noxious particles or
gases. The chronic airflow limitation characteristic of COPD is caused by a
mixture of small airway disease (obstructive bronchiolitis) and parenchymal
destruction (emphysema), the relative contributions of which vary from person
to person.
Etiology
·
Tobacco Smoke:
Cigarette smoking is by far the most
commonly encountered risk factor for COPD. Cigarette smokers have a higher
prevalence of respiratory symptoms and lung function abnormalities, a greater
annual rate of decline in FEV1, and a greater COPD mortality rate than
nonsmokers. Pipe and cigar smokers have greater COPD morbidity and mortality
rates than nonsmokers, although their rates are lower than those for cigarette
smokers. Other types of tobacco smoking popular in various countries are also
risk factors for COPD. Although their risk relative to cigarette smoking has
not been reported. The risk for COPD in smokers is dose-related. Age at
starting to smoke, total pack-years smoked, and current smoking status are
predictive of COPD mortality. Not all smokers develop clinically significant
COPD, which suggests that genetic factors must modify each individual’s risk.
·
Occupational Dusts and
Chemicals:
Occupational exposures are an
underappreciated risk factor for COPD. These exposures include organic and
inorganic dusts and chemical agents and fumes.
The most dangerous combination is work in a harmful environment and smoking.
·
An infectious factor is
considered the second, which joins later, when special conditions appear – on a
background of chronic cough with expectoration , favourable to infecting of
bronchial tree.
·
COPD is a polygenic disease
and a classic example of gene-environment interaction. The genetic risk factor
that is best documented is a severe hereditary deficiency of alpha-1
antitrypsin. A significant familial risk of airflow obstruction has been
observed in smoking siblings of patien with severeCOPD, suggesting that genetic
factors could influence this
susceptibility.
Pathogeny
·
chronic inflammation of bronchial tubes, parenchyma
and lungs
·
Oxidative Stress
·
Protease-Antiprotease Imbalance
Pathological
changes characteristic of COPD are found in the proximal airways, peripheral
airways, lung parenchyma,and pulmonary vasculature. The pathological changes
include chronic inflammation, with increased numbers of specific inflammatory
cell types in different parts of the lung, and structural changes resulting
from repeated injury and repair. In general, the inflammatory and structural
changes in the airways increase with disease severity.
CLINICAL PRESENTATION
The characteristic symptoms of
COPD are chronic and progressive dyspnea, cough, and sputum production. Chronic
cough and sputum production may precede the development of airflow limitation
by many years.
Cough. Chronic cough, often the first symptom of COPD, is often discounted by
the patient as an expected consequence of smoking and/or environmental
exposures. Initially, the cough may be intermittent, but later is present
every day, often throughout the day.
The chronic cough in COPD may be unproductive. In some cases, significant
airflow limitation may develop without the presence of a cough..
Sputum production. COPD patients commonly raise small quantities of tenacious sputum
after coughing. Regular production of sputum for 3 or more months in 2
consecutive years (in the absence of
any other conditions that may explain it) is the epidemiological definition of
chronic bronchitis).
Dyspnea. Dyspnea, the hallmark symptom of COPD, is the reason most patients
seek medical attention and is a major cause of disability and anxiety
associated with the disease. Typical COPD patients describe their dyspnea as a
sense of increased effort to breathe, heaviness,air hunger.
DIAGNOSTICS
·
Central cyanosis, or bluish
discoloration of the mucosal membranes, may be present but is difficult to
detect in artificial light and in many racial groups.
·
Common chest wall
abnormalities, which reflect the pulmonary hyperinflation seen in COPD, include
relatively horizontal ribs, “barrel-shaped” chest, and protruding abdomen.
Resting respiratory rate is often increased to more than 20 breaths per minute
and breathing can be relatively shallow. Ankle or lower leg edema can be a sign
of right heart failure.
Palpation and percussion.
• These are often unhelpful in COPD.
• Detection of the heart apex beat
may be difficult due to pulmonary hyperinflation.
• Hyperinflation also leads to
downward displacement of the liver and an increase in the ability to palpate
this organ without it being enlarged.
Auscultation.
• Patients with COPD often have
reduced breath sounds, but this finding is not sufficiently characteristic to
make the diagnosis19.
• The presence of wheezing during
quiet breathing is a useful pointer to airflow limitation. However, wheezing
heard only after forced expiration has not been validated as a diagnostic test
for COPD.
• Inspiratory crackles occur in some
COPD patients but are of little help diagnostically.
• Heart sounds are best heard over
the xiphoid area.
Lung function tests
show evidence of airflow limitation.
The ratio of the FEV1 to the FVC is reduced and the PEFR is low. In
many patients the airflow limitation is reversible to some extent (usually a
change in FEV1 of < 15%), and the distinction between asthma and
COPD can be difficult. Lung volumes may be normal or increased, and the gas
transfer coefficient of carbon monoxide is low when significant emphysema is
present
Chest X-ray
is often normal, even when the
disease is advanced. The classic features are the presence of bullae, severe
overinflation of the lungs with low, flattened diaphragms, and a large
retrosternal air space on the lateral film. There may also be a deficiency of
blood vessels in the periphery of the lung fields compared with relatively
easily visible proximal vessels
Haemoglobin level and PCV
can be elevated as a result of
persistent hypoxaemia (secondary polycythaemia,
Blood gases
are often normal. In the advanced
case there is evidence of hypoxaemia and hypercapnia
Sputum examination
is unnecessary in the ordinary case as Strep. pneumoniae or H.
influenzae are the only common organisms to produce acute exacerbations.
CLASSIFICATION
Stages of COPD
The impact of COPD on an individual
patient depends not just on the degree of airflow limitation, but also on the
severity of symptoms (especially breathlessness and decreased exercise
capacity). There is only an imperfect relationship between the degree of
airflow limitation and the presence of symptoms. Spirometric staging,therefore,
is a pragmatic approach aimed at practical implementation and should only be
regarded as an educational tool and a general indication to the initial
approach to management.
Stage I: Mild COPD - Characterized by
mild airflow limitation (FEV1/FVC < 0.70; FEV1 ≥80% predicted).Symptoms of chronic cough and sputum production may be
present, but not always. At this stage, the individual is usually unaware that
his or her lung function is abnormal.
Stage II: Moderate COPD -
Characterized by worsening airflow limitation (FEV1/FVC < 0.70; 50% ≤FEV1 < 80% predicted), with shortness of breath typically developing
on exertion and cough and sputum production sometimes also present. This is the
stage at which patients typically seek medical attention because of chronic
respiratory symptoms or an exacerbation of their disease.
Stage III: Severe COPD -
Characterized by further worsening of airflow limitation (FEV1/FVC < 0.70;
30% ≤FEV1 < 50% predicted),
greater shortness of breath, reduced exercise capacity, fatigue, and repeated
exacerbations that almost always have an impact on patients’ quality of life.
Stage IV: Very Severe COPD -
Characterized by severe airflow limitation (FEV1/FVC < 0.70; FEV1 < 30%
predicted or FEV1 < 50% predicted plus the presence of chronic respiratory
failure). Respiratory failure is defined as an arterial partial pressure of O2
(PaO2) less than 8.0 kPa (60 mm Hg), with or without arterial partial pressure
of CO2 (PaCO2) greater than 6.7 kPa (50 mm Hg) whilebreathing air at sea level.
Differential
diagnostics
For differential diagnostics of COPD with other bronchopulmonary
diseases use
bronchoscopy , if necessary – biopsy.
Testimonies
to bronchoscopy
:
1)
suspicion on a neoplasty process ;
2)
intrabronchia
foreign body ;
3)
congenital anomalies of the respiratory system, tuberculosis of bronchial tubes and
lymphatic glands ;
4)
bronchiectasis ,
abscess of lungs;
5)
hemoptysis ,
pulmonary bleeding;
6)
bronchial asthma in combination with a bronchitis,
pneumonia;
7)
with the purpose of sanation of bronchial tubes.
Contra-indications :
1)
stenocardia;
2)
acute myocardial
infarction ;
3)
chronic
decompensated pulmonary heart ;
4)
General
severe condition of patient.
Bronchography is used for
diagnostics of multiple
bronchiectasis.
Main reason of late diagnostics of COPD is absence
of possibility of timely research of FVD.
PHARMACOLOGIC TREATMENT
Pharmacologic therapy is used to
·
prevent and control symptoms,
·
reduce the frequency and
severity of exacerbations,
·
improve health status, and
·
improve exercise tolerance.
Drug Category: Bronchodilators
These agents act to decrease muscle tone in both small
and large airways in the lungs, thereby increasing ventilation. Category
includes subcutaneous medications, beta-andrenergics, methylxanthines, and
anticholinergics.
Bronchodilator medications are
central to symptom management in COPD.
Inhaled therapy is preferred. The
choice between _2-agonist,
anticholinergic,
theophylline, or combination therapy
depends on availability and individual response in terms of symptom relief and
side effects. Bronchodilators are prescribed on an as-needed or on a regular
basis to prevent or reduce symptoms. Long-acting inhaled bronchodilators are
more effective and convenient. Combining bronchodilators may improve efficacy
and decrease the risk of side effects compared to increasing the dose of a single
bronchodilator.
Inhaled
bronchodilators
Drugs
|
Dose (mcg)
|
Duration of action
|
short-acting
beta-agonists:
salbutamol
(Ventolinum),
Fenoterol(Berotek).
|
100
100
|
4-6
4-6
|
short-acting cholinergic antagonist:
Ipratropiya
bromide (Ipravent)
|
20, 40
|
6-8
|
Combined
drugs
(short-acting beta-agonists +
short-acting cholinergic antagonist:
Fenoterol +
Ipratropiya bromide (berodual)
salbutamol
+ Ipratropiya bromide (combivent)
|
||
Long-acting
inhaled β2-agonists
Salmeterol (Serevent)
Formoterol (Zafiron)
|
25,
50
4,
12
|
12
12
|
Long-acting
cholinergic antagonist
Tiotropiya
bromide (Spiriva)
|
18
|
24
|
Theophylline
and its various salts are medium-potency bronchodilators with questionable
anti-inflammatory propertie.
For
maintenance therapy, long-acting theophylline compounds are available and are
usually given once or twice daily. Single-dose administration in the evening
reduces nocturnal symptoms and helps keep the patient complaint-free during the
day. They are now considered second-line therapy, and as such they are rarely
used in acute situations and infrequently in chronic ones.
Drug Category: Corticosteroids
A recent meta-analysis of 16
controlled trials in stable COPD found that approximately 10% of patients
respond to these drugs. The responders should be identified carefully. An
increase in FEV1 >20% is used as surrogate marker for steroid
response. In acute exacerbation, steroids improve symptoms and lung functions.
Inhaled steroids have fewer adverse effects compared to oral agents. Although
effective, these agents improve expiratory flows less effectively than oral
preparations, even at high doses. These agents may be beneficial in slowing
rate of progression in a subset of patients with COPD who have rapid decline
Antibiotics
In patients with COPD, chronic
infection or colonization of the lower airways is common from Streptococcus pneumoniae, Haemophilus influenzae,
and Moraxella catarrhalis.
Empiric antimicrobial therapy must be
comprehensive and should cover all likely pathogens in the context of the
clinical setting. The goal of antibiotic therapy in COPD is not to eliminate
organisms but to treat acute exacerbations. Exacerbations are indicated by increased
sputum purulence and volume and the development of dyspnea along with other
features, including fever, leukocytosis, or infiltrate on a chest radiograph.
The
first-line treatment choices include amoxicillin, or cefaclor.
Second-line
antibiotic regimens are the more expensive antibiotics, including
azithromycin, clarithromycin, and fluoroquinolones.
The use of antibiotics in patients with COPD is
supported by the results of a meta-analysis showing that patients who received
oral antibiotic therapy had a small, but clinically significant, improvement in
peak expiratory flow rate and a more rapid resolution of symptoms. Patients who
benefitted most were those whose exacerbations were characterized by at least 2
of the following: increases in dyspnea, sputum production, and sputum
purulence.
Mucolytic agents
These agents reduce sputum viscosity and improve
secretion clearance. Viscous lung secretions in patients with COPD consist of
mucous-derived glycoproteins and leukocyte-derived DNA.
The oral agent N-acetylcysteine has antioxidant and
mucokinetic properties and is used to treat patients with COPD. However, the
efficacy of mucolytic agents in the treatment of COPD is debatable.
Complications
Respiratory failure is a
syndrome in which the respiratory system fails in one or both of its gas
exchange functions: oxygenation and carbon dioxide elimination. In practice,
respiratory failure is defined as a PaO2 value of less than 60 mm Hg
while breathing air or a PaCO2 of more than 50 mm Hg. Furthermore,
respiratory failure may be acute or chronic. While acute respiratory failure is
characterized by life-threatening derangements in arterial blood gases and
acid-base status, the manifestations of chronic respiratory failure are less
dramatic and may not be as readily apparent.
- The cause of respiratory failure often is evident
after a careful history and physical examination.
·
- Cardiogenic pulmonary edema usually develops in
the context of a history of left ventricular dysfunction or valvular
heart disease.
- A history of previous cardiac disease, recent
symptoms of chest pain, paroxysmal nocturnal dyspnea, and orthopnea
suggest cardiogenic pulmonary edema.
- Noncardiogenic edema (eg, acute respiratory
distress syndrome [ARDS]) occurs in typical clinical contexts such as
sepsis, trauma, aspiration, pneumonia, pancreatitis, drug toxicity, and
multiple transfusions.
Classification of
RF is based on clinical features:
RF has three degrees of severity:
- I degree - patient feels appearance of
shortbreathing during the usual physical exercises (the level of such exercises
is individual for every patient and depends on physical development);
-
II degree
-shortbreathing appears during the insignificant physical exercises (for
example, at walking on an plane surface);
-
III degree
-shortbreathing is observed in a state of rest.
- Pulmonary rehabilitation
- Many patients with COPD are unable to enjoy life
to the fullest because of shortness of breath, physical limitations, and
inactivity.
- Pulmonary rehabilitation encompasses an array of
therapeutic modalities designed to improve the patient's quality of life
by decreasing airflow limitation, preventing secondary medical
complications, and alleviating respiratory symptoms.
- The 3 major goals of the comprehensive
management of COPD are the following:
1.
Lessen airflow limitation
2.
Prevent and treat secondary
medical complications (eg, hypoxemia, infection)
3.
Decrease respiratory symptoms
and improve quality of life