CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Definition Chronic obstructive pulmonary disease (COPD) is characterised by irreversible

obstruction to the airflow throughout the lungs. It includes two important disorders of the
lungs, which are pathologically distinct but clinically form a spectrum of a single disease.
Frequently, both co-exist in a single patient, where a clinician has to decide which one is
dominant. This is important from the point of view of management.
These disorders are:

1. Chronic bronchitis with air flow obstruction.

2. Emphysema.

Note: Chronic brochitis without chronic airflow obstruction not included in COPD. Similarly
asthma with reversible airflow obstruction is also not included in COPD

CHRONIC BRONCHITIS

Definition

It is due to chronic inflammation of airways leading to increased bronchial secretions and

airways obstruction. Clinically, it is defined as cough with expectoration on most days at least
three consecutive months in a year for more than two consecutive years. Therefore, this
definition has a force when other causes of productive cough have been ruled out, such as
bronchiectasis, lung abscess and bronchial asthma..

Clinically, chronic bronchitis is separated by some physicians into two categories:

1. Chronic bronchitis or bronchitis with obstruction.

2. Chronic asthmatic bronchitis or chronic infective asthma

Aetiological factors

The following factors contribute to the development of chronie bronchitis:

1. Smoke, atmospheric and industrial pollutants
2. Infection

3. Physical factors and atopy

4. Genetic and familial

Pathology

There are three important pathological changes:

1. Hypertrophy and hyperplasia of mucus secreting glands with increase in the number of
goblet cells.

2. Irreversible damage to the wall of bronchi/bronchioles with mucosal oedema leading to

airflow obstruction especially during expiration.

3. Overdistension of alveoli due to hyperinflation.

Clinical features

Chronic bronchitis occurs in middle age and late adult life, more common in smokers as well as
in males than females. The clinical picture of chronic bronchitis and emphysema constitute
clinical picture of COPD, though. they are discussed here as separately.
Symptoms
1. Productive cough.

2. Breathlessness.
3. Wheezing.
५ haemoptysis

. 5. Associated GI symptoms e.g. nausea, vomiting and anorexia.

Signs
The physical signs are less marked. There may be a increase in respiratory rate, inspiratory and
expiratory rhonchi (wheeze) and crepitations (crackles) at the base.

Diagnosis and investigations

It is based on history of long duration of cough for more than two consecutive years, with
symptoms and signs suggestive of bronchitis.

Chest Xray may be normal

Sputum for culture

Complications :
• Type I and II respiratory failure.
• Pulmonary arterial hypertension and cor pulmonale.
Secondary infections (acute exacerbation,pneumonia).

• Secondary polycythaemia

Treatment

It includes:1. To avoid bronchial irritants:

2 Treatment of infection
3. Inhaled Bronchodilators

They are much less effective in chronic bronchitis, but are still commonly used for symptomatic
benefit. Regular treatment with inhaled -adrenoreceptor stimulants (salbutamol 200 meg or
terbutaline 500 meg every 6 hours), is advisable in mild to moderate chronic bronchitis. If
severe degree of airways obstruction is present, then ipratropium bromide (40-80 mcg 6
hourly) or oxytropium bromide (200 pg twice daily) should be added.
Oral theophylline is the fourth-line management in COPD who do not achieve symptom control
with inhaled anticholinergics, beta-2 agonists and corticosteroids.

4. Mucolytic agents and adequate systemie hydration They may be used. They are now-a-days
added to expectorant mixtures. These include bromhexine and carbocystein. They just make
the secretions thin, so that they can be expectorated easily. Steam inhalation is good at night
in patients with nocturnal wheeze. Cough suppression is contraindicated.
5. Cortecosteroids
(prednisolone 30 mg/day for 2 weeks) is indicated to know the reversible element of
obstruction. If there is improvement in FEV, >15%, then oral steroids are to be replaced with
inhaled steroids. Regular use of inhaled steroids reduce the frequency of exacerbations,
hence recommended in patients with frequent excerbations (two or more per year).
6. O, therapy Long-term O, therapy in low concentration (2 L/min) at home (domicialiary) by
nasal cannula is advised to reverse or to delay the development of pulmonary arterial
hypertension and cor pulmonale. It is given. intermittently. It is useful in hypoxaemic patients
(PaO₂ < 55 <55 mm of Hg). However, some patients with chimneys/factory) should be
avoided which may severe disease need hospitalisation and treatment with O, therapy where
it is monitored. Hypoxemic patients with pulmonary hypertension erythrocytosis, and
morning headache are likely to be beneficial with domiciliary O, therapy.

7. Phosphodiesterase 4 inhibitor, e.g. Roflumilast has been shown to reduce excerabation

frequency in moderate to severe COPD.
8. Vaccines

Patients with COPD should receive influenza and pneumococcal vaccines.

9. Pulmonary rehabilitation by graded aerobic physical exercise programs (eg. walking 20
minutes three times a week or bicycling).

Chronic bronchitis (COPD) with acute exacerbation

Patients with chronic bronchitis develop acute symptoms i.e. fever, increasing dyspnoea,
wheeze, leucocytosis and mucopurulent sputum following infection or inhalation of irritants
called acute exacerbation. These patient have acute respiratory distress, tachypnoea and
wheezing. Cyanosis may be present. There may be an evidence of infection. The frequency of
acute exacerbations increases as airflow obstruction increases. The patient. is hospitalised and
treated as follows:

(i) Antiboitic treatment. Oral or IV. amoxycillin 500 mg 6 hourly or cotrimoxazole

(960 mg 12 hourly) orally are effective in most of patients. initially, then
treatment is modified according to sputum culture and sensitivity report. A daily.
azithromycin in patients of COPD with acute exacerbation, reduces its frequency.

(ii) Nebulised salbutamol (5 mg) or terbutaline (10 mg) in combination with

ipratropium bromide (0.5 mg) 6 hourly. In haled not oral steroids reduce the
frequency of exacerbations by 25%.

३ O, therapy (40-60%) through mask. Monitor blood gas measurement.

 (iv) Respiratory stimulant (doxapram hydrochloride - by I.V. infusion 1.5-4 mg/min)
may be useful in patients with severe respiratory acidosis

. (v) Expectorant mixture may be useful in patients with sputum retention leading to rise
frequency (CO, retention).

If chronic cor pulmonale develops (signs of right heart failure), then diuretics (frusemide 40 mg
I.V. or 40-80 mg oral) salt restriction and ACE inhibitor may be added to the above regimen. If
type II respiratory ventilatory support

EMPHYSEMA

The term emphysema means hyperinflation, or overdistention of alveoli with air. Clinically,
emphysema of lung is defined as hyperinflation of the lungs due to obstruction of airways. It
can also occur due to loss: of elasticity of alveoli. This is a pathological entity included in chronic
obstructive pulmonary disease (COPD

Aetiology

In real sense, chronic bronchitis may be a underlying cause or may even co-exist with
emphysema majority of cases, hence, both collectively are include in a single term of COPD. The
incriminating facto for emphysema are similar to chronic bronch In chronic bronchitis, there is
retention of s amount of air in the alveoli with each expiration, and ultimately overinflation of
lungs occur and leads to the emphysema. The causative factors are:
1 Smoke, dust, fumes, industrial or occupation pollutants

2 Oxidant injury in smokers

3 Genetic and hereditary

The rare genetic abnormality of alpha 1-antitrypsin deficiency is associated with emphysema in
young adults. The deficiency leads to loss of balance between proteinases and antiproteinases
defence in the lungs leading to proteinases injury to the alveoli

Pathology
Pathologically, it is divided into two types:
1. Panacinar. There is generalised destruction of the walls of all the alveoli. In severe cases, lung
become a mass of bullae. It is less common and seen in a antitrypsin deficiency.

2. Centrilobular or Centriacinar. In this type chronic bronchitis is associated with emphysema

3. Irregular or patchy emphysema. In old age, emphysema occurs due to loss of elasticity of
alveoli leading to their over-inflation. It is called 'senile emphysema'. Due to overdistension,
the alveoli may rupture and coalesce to form large air spaces called bullae formation, seen
characteristically on chest X-ray in emphysema of long duration.

Clinical features

In majority of patients, chronic bronchitis is associated

with emphysema, hence, two types of clinical syndromes of chronic obstructive pulmonary
disease (COPD)become apparent.

Type A: Predominant emphysema with some degree chronic bronchitis (Pink-puffers type). of
chroni

Type B: Predominant chronic bronchitis with Type emphysema (Blue-bloater type). However, in
some cases, clinical picture is an equal blend of two syndromes, and it becomes difficult to
decide which component is predominant. This is called "mixed type". The common noticeable
differences between these two types are given in Table 5.9.1. The emphysema per se produces
eexertion and dyspnoea which progresses and leads to respiratory difficulty which varies from
patient to patient. In addition, the patient may complain of cough, sputum and tightness of
chest in both types of emphysema.

Physical signs

The clinical signs of emphysema are given in Table 5.2.9. Pursed-lip breathing is typical of
emphysema (see Fig. 4.9.2). The other clinical symptoms and signs, which occur in COPD, are
given in the Box 3.
Diagnosis
1. Chest X-ray (Fig. 5.9.2) This may show the following abnormalities:

a. Increased translucency with large voluminous lungs.

b. Prominent bronchovascular markings at the hilum with sudden pruning/truncation in the
peripheral fields.
c. Bullae formation.

d. Low flat diaphragm. Sometimes, the diaphragm shows undulations bullae. due to irregular
pressure of

e. Heart is tubular and centrally located.

2. Pulmonary function tests

(a) FEV₁, FEV,/VC and PEF - All are reduced.

(b) Lung volumes: Total lung capacity (TLC) and residual volume (RV) are increased.
(c) Transfer factor for CO(Tco) is reduced.

3. Arterial blood gas analysis Either it is normal or it may show hypoxaemia (PaO₂) or
hypercapnia (†PaCO₂) in severe cases.

4. Complete haemogram It may reveal secondary polycythaemia (PCV >50%).

5. Electrocardiogram (EKG) There may be an evidence of low voltage graph due to hyperinflated
lungs. If cor pulmonale develops, there may be an evidence of right ventricular hypertrophy.
At this stage heart is enlarged on X-ray chest.

Complications
1. Pneumothorax due to rupture of bullae into pleura space.
2. Cor pulmonale (right sided heart failure right ventricular hypertrophy secondary to disease).

3. Type II respiratory failure

Treatment

No specific treatment is required for emphysema, which is an irreversible disease, therefore,

treatment is directed to treat associated bronchitis (see treatment. of chronic bronchitis). If
type II respiratory failure or lung develops, treat it appropriately (see chapter 5.11). pulmonale
develops, then the patient is hospitalie and O, therapy intermittently is given with salt
restriction and diuretics. Angiotensin converting enzyme inhibitors may be added into
moderate t severe heart failure. Digoxin should preferably be avoided because of risk of
arrhythmias. Antibiotin are added to treat superinfection.

Physiotherapy may be successful during exacerbations associated with bronchial infections

encourage expectoration. Regular exercises should b encouraged to reduce disability. Surgery
has no role

Alpha 1-antitrypsin replacement Weekly or monthly infusion of a,-antitrypsin in patients

with low levels of this enzyme and with abnormal lung function may be useful but whether this
modifies the long term progression has still to be determined.

Surgery for COPD

Bullectomy (removal of a large single bulla), lung volume reduction surgery or reduction
pneumoplasty are surgical approaches to relieve dyspnoea and improve exercise tolerance in
patients with advanced diffuse emphysema or COPD. Lung transplantation is the last option in
these patients.