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Discussion on a Case of Bronchiectasis

INTRODUCTION

 

This term describes abnormal and permanently dilated airways. Bronchial walls become inflamed, thickened and irreversibly damaged. The mucociliary transport mechanism is impaired and frequent bacterial infections ensue. Clinically, the disease is characterized by productive cough with large amount of discoloured sputum and dilated thickened bronchi detected on CT-scan as seen in my patient. Bronchiectasis is not caused by a single factor, but a complex interplay between repeated interplay of inflammation and detective immune response to inflammation. Many congenital or acquired abnormalities can prevent normal airway defence and repair, resulting in recurrent infection is ineffective, the immune response is increased and prolonged, potentially causing a vicious cycle of bronchial injury and increased inflammation that eventually leads to bronchiectasis.

 

AETIOLOGY

 

Cystic fibrosis is the most common cause in developed countries and recurrent lung infection from reduced immunity and post TB stenosis in developing worlds.

As seen in my patient who has never been immunized and has had TB before, her recurrent cough of 4 yrs must have resulted from initial defective immune response causing repeated interplay of inflammations. This makes her lungs easily prone to infections and this largely predisposing her to finally developing bronchiectasis.

 

Causes of Bronchiectasis

 

Congenital

Deficiency of bronchial wall elements

Pulmonary sequestration

 

 

 

Mechanical bronchial obstruction

Intrinsic:

Foreign body

Inspissated mucus

Post-tuberculosis stenosis

Tumour

Extrinsic:

Lymph node

Tumour

Post-infective bronchial damage

Bacterial and viral pneumonia, including pertussis, measles and aspiration pneumonia

Granuloma

Tuberculosis*, sarcoidosis

 

Diffuse diseases of the lung parenchyma

e.g. idiophatic pulmonary fibrosis

Immunological over-response

Allergic bronchopulmonary aspergillosis

Post-lung transplant

Immune deficiency

Primary:

Panhypogammaglobulinaemia

Selective immuoglobin deficiencies (IgA and IgG2)

Secondary:

HIV and malignancy

Mucociliary clearance defects

Genetic:

Primary ciliary dyskinesia (Kartagneer’s syndrome with dextrocardia and situs inversus)

Cystic fibrosis

 

 

Acquired:

Young’s syndrome – azoospermia, sinusitis

 

 

 

EPIDEMIOLOGY

 

Although the prevalence of pediatric bronchiectasis has generally been declining in the more developing world, numerous regional studies suggest that it remains a significant problem in the developing world.

 

In Australia, there’s an incidence of 15 cases per 1,000 children of age 15 and below. Asians are 2.5 times more likely to have bronchiectasis than whites and 3.9 times more likely than blacks at least partially related to poor nutrition.

 

CLINICAL FEATURES

 

As seen in my patient, localized areas of the lung are particularly affected, when sputum production will depend on position. As the condition worsens, the patient suffers from persistent halitosis, recurrent febrile episodes with malaise, and episodes of pneumonia. Clubbing may be seen but was not seen in my patient, and coarse crackles can be heard over the infected areas, usually the bases of the lungs. As seen in my patient, when the condition is severe, there is continuous production of foul-smelling, thick, khaki coloured sputum. Haemoptysis can occur either as bloodstained sputum or as a massive haemorrhage but this was not present in my patient. Breathlessness also results from airflow limitation.

 

 

INVESTIGATIONS

 

Chest X-ray may be normal or may show dilated bronchi with thickened bronchial walls and sometimes multiple cysts containing fluid.

High resolution CT Scanning: To show bronchial dilatation with loss of airway tapering at the periphery, bronchial wall thickening and larger than adjacent arteries giving a signet ring appearance.

 

Sputum examination with culture and sensitivity of the organisms is essential for adequate treatment.

 

 

All the above were done for my patient. Other investigations that can be done includes:

 

Sinus X-rays: 30% have concomitant rhinosinusitis

 

Serum immunoglobins: 10% of adults with bronchiectasis have antibody deficiency (mainly IgA).

Sweat electrolytes – If cystic fibrosis is suspected.

 

Mucociliary clearance (nasal clearance of saccharin) A 1mm cube of saccharin is placed on the inferior turbinate and the time measured (normally less than 30 minutes).

 

TREATMENT

 

Postural drainage

Patient can be placed and taught by physiotherapist to tip themselves in a position that places the affected lobe at a higher level for easy drainage for about 10-20 mins three times daily. Unfortunately, this was never done for my patient.

 

 

Antibiotics

My patient was placed on 2/52 of antibiotics to help halt progression of sputum production.

 

Bronchodilators

Bronchodilator are useful in patients with demonstrable airflow limitation but was not used in my patient.

 

Anti-inflammatory agents

Inhaled or oral steroids can decrease the rate of progression.

 

Surgery

Unfortunately, it is rare for bronchiectasis to be sufficiently localized for resection to be practical. Lung or heart-lung transplantation is sometimes required in cases of severe corpulmonale.

 

PROGNOSIS

Although during discharge, my patient’s cough and sputum production had reduced marginally, this would have most likely cleared completely if an effective postural drainage was done. Bronchiectasis irreversible but patient can have normal life expectancy with avoidance of polluted air environment with good ventilation, highly nutritious food and healthy lifestyle.

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