Chronic Obstructive Pulmonary Disease

( COPD)
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Why COPD is Important ?

COPD is the only chronic disease that is showing progressive upward trend in both mortality and morbidity COPD is the fourth leading cause of death and affects approximately >16 million persons in the USA It is expected to be the third leading cause of death worldwide by 2020
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Definition
Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease state characterised by airflow limitation that is not fully reversible The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking Although COPD affects the lungs, it also produces significant systemic consequences
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Venn diagram of COPD. Chronic obstructive lung disease is a disorder in which subsets of patients may have dominant features of chronic bronchitis, emphysema, or asthma. The result is airflow 4 obstruction that is not fully reversible.

Component of COPD Include:

Emphysema: characterized by destruction and

enlargement of the lung alveoli Chronic bronchitis: with chronic cough and phlegm, with airflow limitation Small airways disease: a condition in which small bronchioles are narrowed
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Chronic bronchitis is defined clinically as the presence of a chronic productive cough for 3 months during each of 2 consecutive years (other causes of cough being excluded).

Emphysema is defined pathologically as an abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis.
Although some patients predominantly display signs of one of these diseases or the other, most fall somewhere in the middle of the spectrum between the 2 conditions.
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Component of COPD Exclude:

Other causes of chronic airflow obstruction:

Pulmonary cystic fibrosis Diffuse panbronchiolitis Bronchiectasis

Risk Factors
Cigarette smoking: a major risk factor for mortality Airway responsiveness Respiratory infections: childhood and adult Occupational exposures: coal mining, gold mining
and cotton textile dust

from COPD

respiratory infections

Ambient air pollution Passive or second hand exposure Genetic considerations: 1 antitrypsin deficiency Gender: More common in men
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Pathophysiology Pathologic changes in chronic obstructive pulmonary disease (COPD) occur in :

the large (central) airways, the small (peripheral) bronchioles, the lung parenchyma.

The pathogenic mechanisms are not clear but are most likely diverse:
Increased numbers of activated polymorphonuclear leukocytes macrophages release elastases in a manner that cannot be counteracted effectively by antiproteases, resulting in lung destruction.

Pathophysiology Persistent reduction in forced expiratory flow rates = typical finding

Airflow Limitation( airflow obs. ) and Air Trapping

The inflammation, fibrosis and luminal exudates in small airways is correlated with the reduction in FEV1 and FEV1/FVC ratio ( spirometry )
The peripheral airway obstruction traps air during expiration, resulting in hyperinflation Emphysema is more associated with gas exchange abnormalities than with reduced FEV1

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Pathophysiology

Gas Exchange Abnormalities

hypoxemia and/or hypercapnia

Mucus Hypersecretion Pulmonary Hypertension

Hypoxic vasoconstriction of small pulmonary arteries eventually result in structural changes that include intimal hyperplasia and later smooth muscle hypertrophy/hyperplasia

The loss of the pulmonary capillary bed in emphysema may also contribute to increased pressure in the pulmonary circulation
Progressive pulmonary hypertension may lead to right ventricular hypertrophy and eventually to right-side cardiac failure (cor pulmonale)
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Anatomo Pathology
Pathological changes characteristic of COPD are found in:

the proximal airways Distal airways lung parenchyma and pulmonary vasculature
These changes include chronic inflammation and structural changes.

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Gross pathology of advanced emphysema. Large bullae are present on the surface of the lung.

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Pathology
Proximal airways ( trachea, bronchi > 2 mm internal diameter)
Goblet cells hiperplasia and enlarged submucosal glands (both leading to mucus hypersecretion) Squamous metaplasia of epithelium Smooth-muscle hyperthropy and bronchial hypereactivity

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Pathology
Peripheral airways ( bronchioles < 2 mm internal diameter)
Goblet cell metaplasia, replacement of surfactant- secreting cells with mucus-secreting and infiltrating cells and smoothmuscle hypertrophy, these abnormalities may cause: airway wall thickening

peribronchial fibrosis luminal inflammatory exudate airway narrowing (obstructive bronchiolitis)

Increased inflammatory response and exudate correlated with disease severity.
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Chronic bronchitis

Mucous gland hyperplasia =the histologic hallmark of chronic bronchitis.

Airway structural changes include :
atrophy, focal squamous metaplasia, ciliary abnormalities, variable amounts of airway smooth muscle hyperplasia, inflammation, bronchial wall thickening.
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Histopathology of chronic bronchitis showing hyperplasia of mucous glands and infiltration of the airway wall with inflammatory cells.
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Emphysema Emphysema is a pathologic diagnosis defined by permanent enlargement of airspaces distal to the terminal bronchioles=> dramatic decline in the alveolar surface area available for gas exchange =>airflow limitation by 2 mechanisms.

First, loss of the alveolar walls results in a decrease in elastic recoil =>airflow limitation. Second, loss of the alveolar supporting structure =>airway narrowing, which further limits airflow.

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Emphysema has 3 morphologic patterns:

Centriacinar Panacinar Distal acinar, or paraseptal

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Pathology

Normal distal lung acinus

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Pathology

Centriacinar(centrilobular) emphysema 21

Pathology

Panacinar emphysema 22

Pathogenesis

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Pathogenesis
Airflow limitation the major physiologic change in COPD, fibrosis is a significant contributor

The pathogenesis :
1. Chronic exposure to cigarette smoke 2. Inflammation and extracellular matrix proteolysis 3. Apoptosis of structural cells of the lung 4. Ineffective repair

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Clinical Manifestation
History of exposure to risk factors
Tobacco smoke Occupational dusts and chemicals Smoke from home cooking and heating fuel Age of onset: after middle age Season: winter

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Clinical Manifestation Most patients with chronic obstructive

pulmonary disease (COPD) seek medical attention late in the course of their disease.
Patients often ignore the symptoms because they start gradually and progress over the course of years.

Patients typically present with a combination of signs and symptoms of chronic bronchitis, emphysema, and reactive 26 airway disease.

Clinical Manifestation Symptoms:

Dyspnea:
gradually progressive dyspnea is the most common presenting character a.Progressive (worsens over time) b.Persistent (present every day) c.Worse on exercise d.Worse during respiratory infections Described by the patient as an increased effort to breathe,heaviness, air hunger or gasping

Chronic cough
Present intermittently or every day often present throughout the day; seldom only nocturnal

Chronic sputum production

Present for many years, worst in winters. Initially mucoid becomes purulent with exacerbation
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Clinical Manifestation

Recurrent respiratory infection Recurrent attacks leading to cor pulmonale heart disease Unexpected weight loss

Decreased food appetite

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Clinical Manifestation
Physical Signs:
Earlier period: minimal/nonspecific signs Advanced Stage: *Inspection: Barrel-shaped chest ( hyperinflation ) Accessory respiratory muscle participate Prolonged expiration during quiet breathing *Palpation: Weakened fremitus vocalis
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Clinical Manifestation
*Percussion : Hyperresonant Depressed diaphragm Dimination of the area of absolute cardiac dullness *Auscultation: Prolonged expiration Reduced breath sounds wheezing during quiet breathing

The heart sounds are best heard over the xiphoid area
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Clinical manifestations

Patients with predominant emphysema : pink puffers ( thin and noncianotic )

Patients with predominant bronchitis : blue bloaters ( heavy and cianotic )

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 Emphysema characteristics include the following: Patients may be very thin with a barrel chest Patients typically have little or no cough or expectoration

Breathing may be assisted by pursed lips and use of accessory respiratory muscles; patients may adopt the tripod sitting position
The chest may be hyperresonant, and wheezing may be heard

Heart sounds are very distant

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Chronic bronchitis characteristics include the following:

Patients may be obese Frequent cough and expectoration are typical Use of accessory muscles of respiration is common

Coarse rhonchi and wheezing may be heard on auscultation

Patients may have signs of right heart failure (ie, cor pulmonale), such as edema and cyanosis

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Laboratory findings
Spirometry
Diagnosis Assessing severity Assessing prognosis Monitoring progression

The hallmark of COPD = airflow

obstruction
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Laboratory findings
Spirometry
FEV1 Forced expired volume in the first second FVC Total volume of air that can be exhaled from maximal inhalation to maximal exhalation FEV1/FVC% - The ratio of FEV1 to FVC, expressed as a percentage

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COPD classification based on spirometry

GOLD Stage Severity Symtomps Postbronch Postbronch odilator odilator FEV1/FVC FEV1 Predicted
>0.7 80%

At risk

Chronic cough, sputum production

I
IIA

Mild
Moderate

With or without chronic cough or 0.7 sputum production

With or without chronic cough or 0.7 sputum production With or without chronic cough or 0.7 sputum production
38 With or without chronic cough or 0.7

80%
50%-80%

III

Severe

30%-50%

IV

Very Severe

<30%

Laboratory findings
Blood examination:
In excerbation or acute infection in airway, leucocytosis may be detected. Elevated hematocrit => cr.hypoxemia , right ventricular hypertrophy

Sputum examination:
Streptococcus pneumonia Haemophilus influenzae Moraxella catarrhalis Klebsiella pneumonia

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Laboratory findings
Blood gas analysis:
- Arterial blood gas analysis may reveal

hypoxemia (advanced disease.) - In patients with severe hypoxemia : low arterial PO2 and high arterial PCO2.

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Chest X-Ray
Chronic bronchitis
Chest Radiograph (XRay) Non apparent abnormality Or thickened and increased of the lung markings are noted

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Chest X-Ray
Emphysema

Chest findings are also varible flattend and low diaphragm Intercostal space becomes widen A horizontal pattern of ribs A long thin heart shadow Decreased markings of lung peripheral vessels

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Chest X-Ray
Emphysema

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Posteroanterior (PA) and lateral chest radiograph in a patient with severe chronic obstructive pulmonary disease (COPD). Hyperinflation, depressed diaphragm, increased retrosternal space, and hypovascularity of lung parenchyma are 44 demonstrated.

Computed Tomography
CT: greater sensitivity and specificity for emphysema than Chest X-Ray, especially for the diagnosis of bronchiectasis and evaluation of bullous disease

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A computed tomography (CT) scan shows hyperlucency due to diffuse hypovascularity and bullae formation, predominantly in the upper lobes.
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Diagnosis of COPD
Clinical manifestation Auxiliary examinations Significant importance of Pulmonary function test
exposure to cigarettes, environmental or occupational pollutants; presence of cough, sputum production or dyspnea
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Spirometry should be obtained in all patients with :

Stage
Exacerbation:
Gradually progressive cough and sputum Dyspnea and gasping Increased purulent sputum followed by recurrent respiratory infection

Stable :
Stable symptoms of cough and sputum Gasping and dispnea are alleviated

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Differential Diagnosis of COPD

COPD: 1. Mid-life onset
2. Slowly progressing symptoms 3. Long history of smoking 4. Dispnea during exercise 5. Largely irreversible airflow limitation

Asthma: 1. Early onset

2. Symptoms vary from day to day 3. Symptoms at the night/early morning 4. A family history 5. Airflow limitation that is largely reversible 6. Largely reversible airflow limitation 7. Allergy, rhinitis, eczema
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Differential Diagnosis of COPD

Pulmonary carcinoma:
Commonly

occurs in patients over 40 years old with cigarette smoking Obvious radiological abnormality

Tuberculosis:

Onset at all ages Tuberculosis toxic syndrome Lung infiltrate on chest radiography Microbiological confirmation

Sputum examination of positive TB bacterium can confirms the diagnosis!!!

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Differential Diagnosis of COPD

Bronchiectasis:
1. Large volume of purulent sputum 2. Commonly associated with bacterial infection 3. Coarse crack/clubbing on auscultation 4. Bronchial dilation and bronchial wall thickening on X-ray /CT

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Complication Chronic respiratory failure Pneumothorax Chronic pulmonary heart disease

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Treatment-Stable COPD
Education and smoking cessation
Smoking cessation has the greatest capacity to influence the natural history of COPD

Control the occupational and environmental pollution

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Treatment-Stable COPD Aims of Drug Therapy Prevent and control symptoms Increase exercise capacity Reduce the frequency and severity of exacerbations Improve health status

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Approaches to management Stage I (mild obstruction):

reduction of risk factors (influenza vaccine);

short-acting bronchodilator

Stage II (moderate obstruction):

reduction of risk factors (influenza vaccine);

short-acting bronchodilator
long-acting bronchodilator(s); cardiopulmonary rehabilitation
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Stage III (severe obstruction):

reduction of risk factors (influenza vaccine); short-acting bronchodilator as needed;

long-acting bronchodilator(s);
cardiopulmonary rehabilitation; + inhaled glucocorticoids if repeated exacerbations

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Stage IV (very severe obstruction or moderate obstruction with evidence of chronic respiratory failure):
reduction of risk factors (influenza vaccine); short-acting bronchodilator as needed; long-acting bronchodilator(s); cardiopulmonary rehabilitation; inhaled glucocorticoids if repeated exacerbation; long-term oxygen therapy (if criteria met); consider surgical options such as LVRS and lung transplantation
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Treatment- Stable COPD Drug Therapy

1.Bronchodilators:
bronchodilators are central to the symptomatic management of COPD improve emptying of the lungs, reduce dynamic hyperinflation and improve exercise performance

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Treatment- Stable COPD Drug Therapy

1.Bronchodilators:
Three major classes of bronchodilators:

2 - agonists: Short acting: Salbutamol & Terbutaline Long acting : Salmeterol & Formoterol Anticholinergic agents: Ipratropium & Tiotropium Theophylline : a weak bronchodilator, which may have some anti-inflammatory properties
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Treatment- Stable COPD Drug Therapy

2.Glucocorticoids:
Regular treatment with inhaled glucocorticoids is appropriate for symptomatic patients with an FEV1<50% pred and repeated exacerbations Chronic treatment with systemic glucocorticoids should be avoided because of an unfavorable benefit-to-risk ratio

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Treatment
3. Combination therapy:
Combination therapy of long acting 2-agonists and inhaled corticosteroids show a significant additional effect on pulmonary function and a reduction in symptoms Mainly in patients with an FEV1<50% pred !!!

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Treatment
4.Others:
Antioxidant agents Immunoregulators Vaccine Alpha-1 antitrypsin augmentation Mucolytic(mucokinetic,mucoregulator) agents Antitussives

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Treatment
Oxygen:
>15 h /d

Long-term oxygen therapy (LTOT) improves survival, exercise, sleep and cognitive performance in patients with respiratory failure. The therapeutic goal is to maintain SaO2 90% and PaO2 60mmHg at sea level and rest

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Treatment
Long-term Oxygen therapy - LTOT -

Indication:
For patients with a PaO255 mmHg or SaO288%,with or without hypercapnia For patients with a PaO2 of 55~70mmHg or SaO289% as well as pulmonary hypertension / heart failure / polycythemia (hematocrit >55%)
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Treatment Manage exacerbation

Identify the cause of exacerbation:

Virus or Bacteria or Other uncertain reasons

Assessment of severity:
The proceeding history and disease must be considered and comparison is very important

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Treatment Manage exacerbation

2. Bronchodilators:

Increase dose and times properly Atomization and inhalation

3. Glucocorticosteroids:

Oral or intravenous glucocorticosteroids are recommended 30 to 40 mg of oral Prednisolone daily for 7-10 days is effective and safe
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Treatment Manage exacerbation

4. Antibiotics:

Respiratory infection is the usual predisposing factor It is advocated to select antibiotics according to culture of sputum and drug-sensitivity test mechanical ventilation

5. Mechanical Ventilation:
Noninvasive Invasive

mechanical ventilation

6. Others:

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Treatment

Pulmonary rehabilitation Nutrition Surgery:

- Bullectomy

- Lung volume reduction surgery

- Lung transplantation

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