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Chronic bronchitis Bronchiectasis

Chronic bronchitis is a persisting infection and inflammation of the larger airways The term bronchiectasis is used to describe abnormal and permanently dilated
of the lungs - the bronchi. It occurs as part of the disease complex known as airways. Bronchial walls become inflamed, thickened and irreversibly damaged.
COPD which includes emphysema and small airways disease. Chronic bronchitis The mucociliary transport mechanism is impaired and frequent bacterial infections
specifically refers to chronic cough and daily mucus production for at least three ensue. Clinically the disease present with coughing of large amounts of sputum. The
months of two or more consecutive years. Other causes of chronic cough must be enlarged bronchi can be seen on CT
excluded before making the diagnosis.
Cause s Present in both males and females of all ages, most common in middle-aged males. Can be broken down to congenital and acquired
• Cigarette smoke is the most important factor in developing chronic Congenital
Mucociliary clearance defects
bronchitis. 4-10x more common in heavy smokers regardless of age, sex
• Primary ciliary dyskinesia
occupation and dwelling. There is a direct relationship between intensity of
• Cystic fibrosis
smoking and reductions in lung function and mortality from disease. Those
Defects of bronchial wall elements
who smoke 30 cigarettes per day are 20 times more likely to die from
Pulmonary sequestration
chronic bronchitis and COPD than non-smokers.
• Pollution is a factor for non-smokers who live in heavily polluted places.
Acquired
Airways irritated by inhaled toxins and fumes -> chronic bronchitis
Infections
• Family history
• Adenovirus
• Airway infection is not considered responsible for the initiation of chronic
• M. pneumoniae
bronchitis, it is important factor in maintaining disease and causing
• Measles
exacerbations.
• Pneumonia
• Whooping cough
• Tuberculosis
Chemical irritants
• Aspiration pneumonia
• Ammonia inhalation → can lead to airway inflammation and
bronchiectasis.
Immunological deficiency (HIV, hypogammaglobulinemia) or over-response (allergic
bronchopulmonary aspergillosis) are associated with the disease.
Chronic mechanical obstruction of a bronchus by a tumour or foreign body can also
predispose a patient to bronchiectasis.
Lung fibrosis → increase the tension on the bronchi → airway dilatation and
"traction bronchiectasis”
• connective tissue disease,
• idiopathic pulmonary fibrosis
Pathology In all of the above disorders, the ultimate end result i s di lati on of the sma ller
bronchi and b ronchio les. Mucou s remain s stagnant in the smaller airways
and subsequently gets in fected, which leads to more damage to the wall of the
bronchus, thus making it weaker and more dilated, initiating a vicious cycle.
Presenta tion • Chronic bronchitis is defined clinically as cough productive of sputum for • Chronic persistent cough
at least 3 months a year over 2 consecutive years • Fever
• If airway limitation is present → wheezing, chest tightness and • Halitosis (oral malodor)
breathlessness • Breathlessness
• Symptoms may be worsened by cold, foggy weather and atmospheric • Chest pain
pollution • Symptoms of underlying disease (see causes)
• Cyanosis
• Tachypnoea
• Use of accessory muscles.
• Hyper-expansion of the chest, barrel shaped.
• Reduced chest expansion.
• Reduced breath sounds and crackles.
• Signs of heart failure such as peripheral oedema (swelling) may be present
in advanced disease.
• Smoking history is essential
It is difficult to distinguish symptoms of chronic bronchitis from emphysema and
both conditions commonly occur together. Therefore if you have cough and
breathlessness diagnose COPD, rather than chronic bronchitis alone
Diagno si s Patients with ch ronic b ronchit is are classically described as "blue bloaters" due • FBC for signs of infection and immunodeficiency
to cyanosis and oedema. They have reduced levels of ventilation and are no t • Sputum culture to grow infective organism, prescription of effective
breathless. There are low levels of O2 in the blood and high levels of CO2 antibiotics
Patients with predominantly emphy se ma on the other hand are described as "pink • Lung function tests
puffers" as they are ve ry b reathless and hyperventilating (with pursed lips) but • Chest x-ray
have near normal levels of O2 and CO2 in the blood. • In severe cases, an ECG may be performed
• FBC for signs of chronic hypoxia, ↑RBC
• Chest x-ray to show hyper-expansion of the lungs (chronic bronchitis and **A High resolution CT scan is the test of choice to diagnose this condition
COPD), lung fields, enlarged and empty and may flatted out diaphragm
• ECG can detect signs of right heart failure (a complication)
• Spirometry to detect (non reversible) airflow limitation and obstruction.
• Blood gases to check O2 and CO2 levels, progression of disease
• High resolution CT scan, emphysema and bullae (big dilated air spaces)
Treat ment • Chronic bronchitis treated if airway limitation is present. • Regular postural drainage and chest physiotherapy -> clearing of sputum -
• Same principals as COPD. Control and improve symptoms. > symptomatic relief
• Only smoking cessation and oxygen therapy (in those with advanced • Antibiotics prescribed after sputum culture. Possible argument for
disease) actually alter the course of disease, so stop your patients smoking prophylactic antibiotics
• Bronchodilators (such as Ventolin, Seretide and Atrovent via puffer or • Bronchodilators may help in patients with asthma, ABPA or cystic
nebuliser) and corticosteroids for symptom control fibrosis.
• Antibiotics can be used for short-term exacerbations of disease • Inhaled or oral corticosteroids → slowing of disease progression.
• Mucolytics (acetylcysteine) may reduce the frequency of exacerbations Particularly useful for the treatment of ABPA.
• Chest physiotherapy/pulmonary rehab to help remove secretions in the • Surgery to control localised disease causing severe haemoptysis.
airways
• O2 therapy at home, administered via nasal prongs or mask. Treatment has
been shown to prolong life in patients with severe COPD who have
stopped smoking.  Yearly influenza and pneumococcal vaccine
• Diuretics for right heart failure
Outco mes and • Early in chronic bronchitis, Cough productive of significant amounts of • Prognosis varies on causative mechanism
Progre ssion sputum without any significant breathlessness, caused by enlargement of • Effective antibiotic therapy and vaccination greatly improves life
mucous glands and increased numbers of mucus-secreting goblet cells in expectancy
the airways → small airways become inflamed but at this stage the disease • 5 year mortality rate of 13% in people suffering from this condition
is considered largely reversible. Cessation of smoking will resolve the • Poor prognostic factors
airway inflammation. • volume of sputum produced
• As the disease progresses, Progressive abnormal cell growth (called • pseudomonas aeruginosa.
squamous metaplasia) and fibrosis (hardening) of the bronchial walls →
airflow limitation → shortness of breath Symptoms of breathlessness on Symptoms have often been present for a number of years and are often initiated by
exertion. an episode of pneumonia. The bronchial walls become inflamed, thickened and
• Other signs of COPD, cyanosis, emphysema may also be present at this permanently damaged. More mucous accumulates in the dilated airways,
stage, causing more severe shortness of breath and chest tightness. predisposing the lungs to further bacterial infections. Persistent mucous production
and airway obstruction leads to lung collapse and a reduction in the elastic forces
holding the airways taught. 
Co mplicat ions • Secondary polycythaemia, ↑RBC in response to ↓O2 → ↑ viscosity of • Pneumonia
blood → ↑ risk of clotting. • Haemoptysis
• Right heart failure. • Abscesses (which can travel to other parts of the body (e.g. brain)
• Pneumothorax (punctured lung). • Respiratory failure
• Respiratory failure often caused by acute infective exacerbations. • Right heart failure (cor pulmonale)

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