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Since the first description by Laennec in 1819, bronchiectasis has continued to be recognized as a considerable cause of respiratory illness worldwide. It is defined by the permanent dilatation of the bronchi1 and is caused by a recurrent process of transmural infection and inflammation. Patients suffer from chronic cough, excessive sputum production, a progressive decline in respiratory function despite prolonged antibiotic treatment, and occasionally life-threatening hemoptysis once the disease is entrenched. The majority of patients with this ailment can be treated medically, but those who fail or become intolerant of medical therapy are eligible for surgical intervention.
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Early attempts at surgical treatment of bronchiectasis were fraught with complications. Postoperative bronchopleural fistula (BPF) and empyema were common, and perioperative mortality rates were high. The introduction of effective antibiotics in the 1950s paired with improvements in surgical technique led to a decline in perioperative morbidity and mortality. Currently, surgical intervention is mainly reserved for patients with focal disease and persistent symptoms despite optimal medical management. The diffuse form of the disease is best treated with bilateral lung transplantation and will not be discussed extensively in this chapter.
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General Principles and Patient Selection
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Bronchiectasis is subdivided into specific types based on the pathologic or radiographic appearance of the airways (Fig. 94-1). Cylindrical or tubular bronchiectasis is defined by dilated, slightly tapered airways and often is seen in patients with tuberculosis infections. Varicose bronchiectasis resembles the chronic venous state of the same name, with areas of dilatation and narrowing. Saccular or cystic bronchiectasis is characterized by progressive dilatation of the airways which end in sac-like cystic structures that resemble a cluster of grapes. This subtype is more common after obstruction or bacterial infection. Regardless of the subtype, thick mucoid secretions often are seen pooled in the dilated airways causing a chronic, transmural inflammatory state involving the wall of the airway. Lung parenchyma distal to the dilated, ectatic airways is often damaged as well, with fibrosis and emphysematous changes present. The accompanying bronchial circulation and lymph nodes may be engorged and hypertrophied. The left lower lobe is most commonly affected (Fig. 94-2), followed by the lingula and right middle lobe (Fig. 94-3). Occasionally, the process may progress to multilobe involvement with cavitation and parenchymal destruction, requiring pneumonectomy (Fig. 94-4).
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