Pulmonary tuberculous diseases are contagious infections caused by bacterial organisms or bacilli of the Mycobacterium family (Mycobacteriaceae). The most common species is tuberculosis but other types produce similar pathologic changes. The disease is spread by the aerolization of respiratory secretions, and infection occurs by inhalation of the tubercle bacilli (TB). Not everyone infected with TB will become sick immediately. Most patients are asymptomatic because of the host’s immune-cell-mediated defense mechanisms, which entrap and wall off the bacilli, thereby containing the infection. The isolated bacilli may form granulomas which may lie dormant for years. Others will experience a short illness associated with malaise, low-grade fever, cough, and weight loss. If the body’s immunity becomes compromised, a full-blown infection may ensue. Most frequently, these patients will develop extensive pulmonary infiltrates with a febrile illness and dyspnea associated with the concomitant pneumonia. If the walled-off granulomas break down, cavities form and accumulate secretions causing a productive cough. Infection of the pleural lining (pleurisy) may result in chest wall pain or pleural effusions with shortness of breath. Spontaneous pneumothorax may occur as a consequence of excessive coughing and will present with acute dyspnea. Long-standing infections may result in parenchymal destruction, bronchiectasis with erosion into adjacent pulmonary arteries (Rasmussen’s aneurysm)¹, and massive hemoptysis.² These large cavities may lead to secondary fungal infection with Aspergillus (see Chapter 102). In some patients, extensive lung destruction can produce chronic lung collapse and contraction.

The World Health Organization estimates that one-third of the world’s population is currently infected with TB bacillus and 5% to 10% of those infected become infectious or sick at some stage during their lifetime. Individuals with HIV/AIDS are most at risk for developing the full-blown infection. The largest number of new cases of TB in 2010 occurred in southeast Asia (35%); however, the incidence of new cases in sub-Saharan Africa is nearly twice that of southeast Asia with 350 cases per 100,000 people. In 2009, over 1.7 million individuals died from TB. Although the incidence of TB appears to be stable or falling, adjusted for population growth, the number of new cases is rising annually (Table 105-1).³

The US Food and Drug Administration currently approves 10 drugs for the treatment of TB. Of these, the core first-line treatment for active TB includes isoniazid, rifampin, ethambutol, and pyrazinamide. Regimens have an initial treatment phase of 2 months, followed by a continuation phase of 4 to 7 months. Treatment completion is determined by the number of doses ingested over a given period of time. Modifications to this basic regimen are made under special circumstances including HIV infection, drug resistance, pregnancy, and in pediatric patients.⁴

The surgical treatment of TB is reserved mainly for treating the complications of the disease arising from previous surgical treatment or progression of the underlying disease and secondary complications of chronic infection. Occasionally, the diagnosis of TB is an incidental pathologic finding after resection of a pulmonary nodule or mediastinal lymphadenopathy. The surgical treatment of chronic constrictive pericarditis or pleural effusions with or without lung entrapment also may reveal unexpected TB. Strains of multidrug-resistant (MDR) TB have been documented with resistance to all first-line drugs and multiple second-line drugs for which adjuvant surgery may be considered.⁵ The remainder of this chapter focuses on surgical treatment specific to the complications of previous operations or secondary complications of chronic infection that necessitate surgical intervention.

Thoracoplasty

Toward the end of the nineteenth century, it was thought that healing of tuberculous cavities would be facilitated by collapse of the lung and thoracoplasty. It was hoped that this operation would promote scar retraction of the tuberculous cavities and subsequent healing. Schede thoracoplasty was widely practiced up to the late 1930s. The thoracoplasty operation is covered in Chapter 106.

The operation, as originally described, became obsolete with the advent of pulmonary resections and drug therapy in the 1940s. In this operation, the infection is controlled by tube thoracostomy drainage or a Clagett window as an initial procedure. Subsequently, the residual space is obliterated by filling the cavity with antibiotics and closing the window or leaving the patient with a permanent window.

In recent years, closure of a residual space or bronchopleural fistula, if present, is accomplished by the interposition of various types of muscle flaps or an omentoplasty.⁶ Still, there are some surgeons who continue to perform a limited thoracoplasty with intrathoracic muscle transposition.^7,8 Other investigators have performed a cavernostomy combined with a muscle flap transposition as a single-stage procedure.⁹ The overall success rate for the control of infection and obliteration of space issues is about 75% for TB.¹⁰

Plombage Therapy and its Late Complications

In 1926, Tuffier described a procedure called apicolysis whereby a space was created using an extrapleural or extrafascial dissection and the space was filled with the patient’s own fatty tissue. This operation formed the basis of extrapleural plombage collapse therapy, whereby the space was filled with heated paraffin or Lucite balls. Plombage therapy fell out of favor because of long-term complications. These have included infections, migration of these balls with erosion through the chest wall possibly into adjacent lung parenchyma, vascular structures or organs like the esophagus, and compression of the brachial plexus. Plombage therapy has been completely abandoned as a treatment of residual pleural spaces and removal of the foreign material is recommended whenever such patients are identified, as long as the operative risk is acceptable.^11,12 Subsequently, the space is handled by transposition of muscle flaps with or without a limited thoracoplasty.

Lung Destruction, Extensive Bronchiectasis, Residual Disease

Unilateral partial or complete lung destruction is a well-recognized complication of chronic tuberculous lung infection. It is rarely seen in the developed world today but may still be encountered in patients from less developed countries. Usually, it is a consequence of failure of diagnosis, poor compliance, or inadequate medical therapy for primary tuberculosis. It is characterized by extensive scarring with fibrosis and contraction of the underlying lung. The underlying parenchyma is destroyed with multiple cavitations and extensive bronchiectasis. These patients present with general debilitation, productive cough, shortness of breath, and may have massive hemoptysis. The left side is more frequently involved.

Lobectomy or pneumonectomy should be considered when the underlying lung is destroyed, but these are high-risk operations and patients need to be started on adequate antituberculous therapy prior to undertaking surgical resection. Adequate preoperative preparation including nutritional support also must be provided. Careful intraoperative planning and technical expertise is essential. These patients are at high risk for developing a bronchopleural fistula, and satisfactory coverage of the bronchial stump with a muscle flap is imperative. A space issue following resection may necessitate the use of rotational muscle flaps with or without a limited thoracoplasty. Occasionally, the obliteration of the pleural space with extensive scarring and contraction will render an anatomic lobectomy or intrapleural pneumonectomy technically very challenging and high risk. In such circumstances, an extrapleural pneumonectomy should be considered.¹³

A retrospective review of 172 cases of destroyed lung was analyzed by Bai et al.¹⁴ The ages ranged from 7 to 72 years with a median of 38.4 years. The male-to-female ratio was roughly equal. Forty-nine patients had sputum positive for Mycobacterium tuberculosis preoperatively yielding a positive TB rate of 28.5%. Of the group, 116 cases had destroyed left and 56 had destroyed right lungs. In all, 110 patients underwent a complete pneumonectomy, 37 an extrapleural pneumonectomy, and 11 lobectomy. Eleven patients developed bronchopleural fistulae and four had subsequent thoracoplasties because of persistent infection or empyema. The overall perioperative mortality rate was 2.9% with an 18.6% complication rate. The sputum negative conversion rate was 87.8% and clinical cure 91.9%.¹⁴