CHRONIC BRONCHITIS

CHRONIC BRONCHITIS

DEFINITION OF CHRONIC BRONCHITIS

Chronic bronchitis may be defined as a disease characterised by cough and sputum for at least 3 consecutive months in a year for more than 2 successive years (Medical Research Council).

AETIOLOGY

Smoking: Smoking causes bronchoconstriction, sluggish ciliary movement, increases airway resistance, hypertrophy of the mucous glands, increased number of goblet cells and hypersecretion of mucus Though smoking is said to be the most important cause, yet only 10%-15 % of the smokers develop COPD. Usually a cigarette smoking history of greater than 20 pack years is associated with the disease. (1 pack year is equivalent to smoking 20 cigarettes a day for 1 year.)
Atmospheric pollution: Industrial and domestic smoke as well as sulphur dioxide are main causes of air pollution whieh are responsible for chronic bronchial irritation and increased resistance to the airflow.
Infection: The role of infection is uncertain, but it appears that once it develops chronic irritation is maintained and progresses to emphysema. The main organisms are Haemophilus influenzae and Streptococcus pneumoniae. Mycoplasma pneymonae may also be involved.
Occupation: Coal-miners and industrial workers are often exposed to dust and fumes which may irritate the bronchial tree.
Familial and genetic abnormalities associated with Alpha antiprotease deficiency may also be present.

TYPES OF CHRONIC BRONCHITIS

Simple chronic bronchitis
Here sputum is mucoid.
Chronic recurrent mucopurulent bronchitis
There is mucopurulent sputum present in absence of localized suppurative disease.
Chronic obstructive bronchitis
Airway obstruction is dominant.
Chronic asthmatic bronchitis
There is long continued cough and sputum with late onset of wheeze.

PATHOGENESIS, PATHOLOGY AND FUNCTIONAL ABNORMALITY

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Mucous glands
Due to chronic irritation, mucous glands undergo hypertrophy which is the main pathological finding in chronic bronchitis. The ratio between the thickness of gland and thickness of bronchial wall is called Reid Index. This is normally 0.26 and in chronic bronchitis it becomes 0.59. This index is the diagnostic criterion of chronic bronchitis.
Goblet cells
In the bronchioles Goblet cells proliferate and are overdistended with mucus
Mucus secretion is enormously increased due to hypertrophy of mucous glands and proliferation of Goblet cells. This is the cause of chronic cough and sputum. Secretion of mucous glands mainly contributes to the sputum volume, while that of Goblet cell is responsible for airway obstruction. Thus there are wheeze, rhonchi and breathlessness. This mucus is chemically altered as its fucose and sialic acid concentration is inereased.
Jufection
Increased mucus predisposes to infection by various organisms, e.g., viruses and bacteria. The main bacteria are H. influenza and Strep. pneumoniae. This leads to severe inflammation of the bronchial tree resulting in mucopurulent sputum, further airway obstruction and constitutional reaction. H. influenza may persist in the sputum and may cause fibrosis and scarring of the distant alveoli or at times emphysema.
Airway obstruction
This is the most important functional abnormality and is caused by numbers of factors, e.g. , overproduction of mucus, inflammatory swelling and oedema, spasm of smooth muscle, fibrosis, air trapping at bronchioles and emphysema. In the earlier part of the disease intermittent and later on permanent obstruction develops. With severe airway obstruction PEF and FEV1 are diminished and the FEV /FVC ratio falls below 75 per cent. However, this does not correlate well.
Emphysema
In about 50% cases of chronic bronchitis, emphysema develops. This is due to repeated infection and air trapping. Centriacinar or panacinar emphysema may develop.
Air diffusion
Due to uneven distribution of the inspired air, there may be diminished diffusing capacity. Airway obstruction gives rise to ventilation perfusion inequality-resulting in increased PaCO2 and reduction in PaO2. With severe ventilatory failure there is falling pH together with compensatory decrease in plasma bicarbonate and respiratory acidosis.
Pulmonary hypertension and Chronic cor pulmonale
As a result of low PaO2 pulmonary vasoconstriction takes place leading to pulmonary hypertension. There are also other undetermined factors. It occurs mostly during infection. Ultimately patient develops right ventricular failure.
CLINICAL FEATURES
Onset is indisidious, usually in the fifth or sixth decade of life.
Symptoms

  • (Cough with expectoration: It starts as attacks of “winter cough” and “smoker’s cough” gradually increasing in severity and duration. The expectoration is mucoid or mucopurulent depending on the presence of infection. Sometimes there may be haemoptysis.
  • (Acute respiratory infection from time to time may give rise to fever, aggravation of cough, and sputum with purulent character.
  • Shortness of breath due to airway obstruction, bronchiolar spasm and in long standing cases due to development of emphysema So with the progress of the disease two Symptom patterns may emerge which are referred to as Blue bloaters (ch.. Bronchitis) and Pink puffers (Emphysema) see below. In average cases features of both these are admixtured. All these symptoms may be present for 10 years or more.
    SINGS
    Definite physical signs are lacking in the early stage.
    General survey
    Build-stocky, respiration rate is hurried, central cyanosis may be present. Suffused conjunctivae, raised temperature, dilated superficial veins are present with warm periphery. Accessory muscles of respiration are prominent and patient may prefer to stoop forwards during respiratory distress. If right ventricular failure exists neck veins may be full with pitting pedal oedema.
    Chest may show no sign on examination or there may be prolonged expiration with transient rhonchi and scattered rales clearing with cough. In late stages features of emphysema will develop.
    SPECIAL INVESTIGATIONS
  • Blood count is usually normal or may show leucocytosis in presence of acute infection. Polycythaemia may develop in long standing cases.
  • Radiological-A straight X-ray of chest does not show irregularities of bronchial lumen. Wide ducts of mucous glands are seen in big sized bronchi Sometimes bronchiectatic picture may also develop. Peribronchial and perivascular marking are present. In advanced disease pulmonary artery is enlarged due to pulmonary hypertension. Doppler echocardiogram may be helpful in estimating pulmonary hypertension. Features of emphysema are present only in late stages. CT scan may be helpful but it is expensive.
  • Bacteriological culture of sputum may yield the pathogenic organisms, most common are H. influenzae, pneumococci, staphylococci, Streptococcus pneumoniae, Morexella catarrhalis but other gram negative organisms less commonly seen.
  • (Pulmonary function tests: In the early stages, dysfunction of small airways, e.g., abnormal closing volume, reduced mid expiratory flow rate, later FEV1 and FEV :FVC are reduced. In severe cases FVC is markedly diminished Lung volume measurements show increased total lung capacity (TLC), marked increase in residual volume (RV) and elevation of RV:TLC ratio indicative of air trapping.
  • Measurement of arterial blood gases shows no abnormality early in the course of the disease other than increase A-aDO2.
  • ECG may show evidences of right ventricular hypertrophy. supraventricular and ventricular arrhythmia.
    DIFFERENTIAL DIAGNOSIS
    Chronic bronchitis should be differentiated from emphysema and bronchial asthma. Though frequently in an average case these three may be admixtured, so pure form of chronic bronchitis or emphysema and asthma are rare particularly in long standing cases (see Table below). Chronic bronchitis must also be differentiated from the following
    Pulmonary Tuberculosis
    There may be evening rise of temperature, progressive emaciation, often haemoptysis, sputum shows acid fast bacilli and skiagram of chest shows variable amount of infiltration with or without cavitation.
    Bronchiectasis
    Here the patient will have profuse purulent sputum related to change of posture. Clubbing is present. Clinical signs are basal and usually bilateral. Bronchogram and CT scan usually reveal the dilated bronchi.
    Bronchogenic Carcinoma
    The patient is usually middle aged male having history of heavy smoking and haemoptysis. Clubbing is present, metastasis lymph nodes may be present. Pulmonary signs are variable. Bronchoscopic aspiration may reveal malignant cells. Skiagram of chest CT scan may reveal the disease.
    Mitral Stenosis
    Here the cardiac findings will be obvious and lung findings are secondary.
    COMPLICATIONS
  • Emphysema.
  • Bronchiolar spasm.
  • Bronchiectasis.
  • Fibrosis of lung.
  • Right heart failure (Chronic cor pulmonale).
  • Hernia in different sites.
  • Haemoptysis.
    TREATMENT
  • Smoking should be avoided.
  • Control of air pollution in urban or industrial areas should be done by law.
  • Steam inhalation or hot drink helps to liquefy the sputum which may be coughed out easily.
  • If there is bronchospasm, Ephedrine or aminophylline can be given. Ipratropium bromide aerosol is superior to other sympathomimetic aerosol in causing bronchodilatation. 2-4 inhalations (18 u g each) every 6 hours is suitable.
  • Control of infection should be done very promptly by Ampicillin, Erythromycin, Ciprofloxacin, Oofloxacin, Pfloxacin or newer antibiotics. Culture of sputum and sensitivity of organism to antibiotics can be known. Long term therapy may be done in patients having purulent sputum persistently. O2 therapy may be required in controlled way when PaO2 is less than 55-60 Torr. Use of steroids is controversial.