The term bronchiectasis is derived from the Greek bronchus and ektasis, meaning dilatation. In essence, as pointed out by Hodder and colleagues,¹⁸ the term refers to the abnormal permanent dilatation of subsegmental airways. The history of bronchiectasis parallels that of thoracic surgery and has been outlined previously by Lindskog.²³ The techniques of segmental resection were developed in large part because of this entity. Detailed anatomic descriptions of segmental anatomy by Boyden⁷ led to the development of individual ligation of the hilar bronchovascular structures and significantly decreased postoperative complications. With the development of antibiotics in the 1940s, this entity has not been seen as frequently; but with the emergence of drug-resistant microorganisms and increasing frequency of drug-resistant tuberculosis, an increased incidence of postinfectious bronchiectasis is being noted.

An outline of the etiology of bronchiectasis is given in Table 89-2. Etiologic conditions can be divided into congenital and acquired. The most frequent congenital causes are cystic fibrosis, hypogammaglobulinemia, and Kartagener’s syndrome. The most frequent acquired cause is secondary to an infectious process.

Barker⁵ emphasized that the pathophysiology of bronchiectasis requires an infectious process plus impairment of bronchial drainage, airway obstruction, or a defect in host defense. Bronchial obstruction can be caused by foreign body aspiration or enlarged lymph nodes compressing a bronchus, as seen in middle lobe syndrome. Barker⁵ noted that in immunocompromised patients, there may be ciliary dyskinesia, airway immune effector cells, neutrophilic proteases, and inflammatory cytokines. Regardless of the cause, an intense inflammation results in transmural inflammation, mucosal edema, and bronchial neovascularization.

The terms cylindrical, varicose, and saccular have been used to describe the pathology of bronchiectasis. A classification of
bronchiectasis is given in Table 89-3. Saccular bronchiectasis follows a major pulmonary infection or results from a foreign body or bronchial stricture and is the principal type of surgical importance. Cylindrical bronchiectasis consists of bronchi that do not end blindly but communicate with lung parenchyma. This is frequently associated with tuberculosis and immune disorders. Hood²⁰ noted a third type referred to as varicose, a mixture of the former two, distinguished by alternating areas of cylindrical and saccular disease. Pseudobronchiectasis, a term first reported by Blades and Dugan,⁶ is a cylindrical dilatation of a bronchus after an acute pneumonic process that is temporary and disappears in several weeks or months. This type has no surgical implications. In addition, certain genetic syndromes may be associated with some form of bronchiectasis. These include cystic fibrosis, alpha₁-antitrypsin deficiency, and immunoglobulin A (IgA) and IgG deficiency.

The distribution and frequency of bronchiectasis is given in Tables 89-4 and 89-5. The distribution to some extent is characteristic of the etiology. For example, in patients with Kartagener’s syndrome, hypogammaglobulinemia, and cystic fibrosis, the areas of involvement are generally diffuse and bilateral and involve multiple cystic segments of both upper and lower lobes. Tuberculosis is either unilateral or bilateral and generally involves the upper lobes or superior segment of the lower lobes. Middle lobe syndrome is caused by the involvement of lymph nodes and the middle lobe bronchus from a granulomatous process.

Lung abscess has been recognized since the time of Hippocrates; Wiedemann and Rice⁴³ quote Hippocrates:

Before the antibiotic era, it was realized that unless drainage was achieved, death was inevitable. With the development of antibiotics, treatment improved and mortality decreased. With the development of increasing numbers of immunosuppressed individuals and the increased incidence of nosocomial pneumonia, lung abscess continues to be a problem for practicing thoracic surgeons.

Geppert¹⁶ defines a lung abscess as a subacute pulmonary infection in which the chest radiograph shows a cavity within the pulmonary parenchyma. It is a localized collection of pus contained within the cavity formed by the disintegration of the surrounding tissues. An abscess is defined as acute when the duration of symptoms is <6 weeks. In general, the abscess is
solitary, but it may occasionally be multiple, particularly in the immunocompromised individual.

A classification of lung abscess is given in Table 89-8. Contributing factors to the development of a lung abscess are listed in Table 89-9. Anaerobic infections remain the most frequent etiologic agents. Periodontal disease and aspiration are the two most frequent causes. Fewer than 20% of patients with an anaerobic lung abscess do not have a history of one or the other of these aforementioned causes.

The typical patient has a history of an antecedent event or of pulmonary infection or pneumonia. Patients have an intermittent febrile course with weight loss, night sweats, and cough. Later in the course, the production of purulent sputum becomes common. The patient may have foul breath and often appears quite ill.

The most frequent microorganisms associated with lung abscess are listed in Table 89-10. The microorganism is most likely related to the etiologic cause. The most frequent anaerobic cause is Bacteroides and the most frequent aerobic causes are Staphylococcus aureus and Streptococcus pneumoniae.

Diagnostic techniques include a complete history and physical examination with emphasis on a predisposing event such as dental work or possible aspiration. The symptoms of fever and purulent foul-smelling sputum are highly suggestive. Analysis of the sputum is necessary in the attempt to identify the causative microorganism.

Fiberoptic bronchoscopy is indicated for two reasons. It helps in the bacteriologic assessment with the use of a sterile brush and in obtaining bacterial washings for bacterial analysis. It is also important to rule out an endobronchial tumor or obstruction and to determine whether the abscess is draining internally.

Radiographic imaging is generally required to determine the presence of a lung abscess with certainty. Posteroanterior and lateral chest radiography and CT scanning of the chest are the most frequently used modalities (Figs. 89-3 and 89-4). The most frequent sites of involvement are the superior segments of the right and left lower lobes and the lateral part of the posterior segment of the right upper lobe (the axillary subsegment) (Fig. 89-5). Ninety-five percent of all lung abscesses occur in these locations.

The differential diagnosis of cavitary lung lesions revolves around four entities: (a) cavitating carcinoma, generally squamous cell; (b) tuberculous or other fungal diseases; (c) pyogenic lung abscess; and (d) empyema with bronchopleural fistula. The patient’s history is important in separating the differential diagnosis. Hood¹⁹ suggested that the absence of fever, lack of purulent sputum, and a normal white blood cell count should raise strong suspicion of an underlying neoplasm.

Once the diagnosis is established, appropriate therapy must be instituted. Principles of therapy are given in Table 89-11. The etiologic organisms must be identified as quickly as possible through the techniques previously discussed. Appropriate antibiotics should be instituted based on drug sensitivity. If an aerobic microorganism is suspected, the patient is generally started on clindamycin and gentamicin while awaiting sensitivity study results. Antibiotics are continued for a prolonged period, generally 6 to 8 weeks.

Adequate drainage must be achieved by chest physiotherapy, fiberoptic bronchoscopy, or percutaneous catheter drainage. Only when the abscess does not drain internally into the tracheobronchial tree is external drainage indicated. Wiedemann and Rice⁴³ reported that 80% to 90% of aerobic lung abscesses respond to medical therapy.

When the abscess does not drain internally and the patient experiences a septic course, external drainage can be achieved by closed-tube thoracostomy, CT-directed catheter drainage, or pneumonostomy (Fig. 89-6).