Bronchogenic carcinoma

General characteristics

Bronchogenic carcinoma, a term referring to tumors originating from the bronchial epithelium, is the leading cause of death from cancer in men and women in the industrialized world. Cigarette smoking is the most important causative factor in the development of bronchogenic carcinoma, and there is a direct link between cigarette smoking and development of bronchogenic cancer, with approximately 85% of deaths directly attributable to tobacco use.

Common extrathoracic sites for metatases of bronchogenic carcinoma: - Brain - Liver - Adrenal - Bone

Histologic Classification

In 2004, the World Health Organization updated its classification of lung tumors based on histologic features. Four cell types account for more than 95% of all primary lung neoplasms:

  • adenocarcinoma (of which bronchioloalveolar carcinoma is a subset),
  • squamous cell carcinoma,
  • large cell carcinoma, and
  • small cell carcinoma.

Mixtures of these cell types may occur within the same primary neoplasm, and some tumors are too poorly differentiated to be further classified.

Rapid growth, early metastatic spread, and responsiveness to chemotherapy and radiation therapy distinguish small cell carcinoma from the others, which has led to the classification of small cell and nonsmall cell carcinoma. Features of the four histologic types are outlined in Table:

  • Nonsmall cell carcinoma
    • Adenocarcinoma
      • Most common type
      • Weak association with cigarette smoking
      • Usually peripheral in location
      • Most common type to have air bronchograms
      • Bronchioloalveolar carcinoma is a subtype
    • Squamous cell carcinoma
      • Second most common type
      • Strong association with cigarette smoking
      • Usually central in location
      • Most common type to cavitate
    • Large cell carcinoma
      • Least common type
      • Usually >3 cm in size
      • Usually in lung periphery
  • Small cell carcinoma
    • Strong association with cigarette smoking
    • Usually central in location
    • Often presents with bulky mediastinal adenopathy
    • Worst prognosis of all types

Bronchioloalveolar carcinoma (BAC)

Bronchioloalveolar carcinoma (BAC) is a subtype of adenocarcinoma that has a lepidic pattern of growth, with cuboidal or columnar cells lining the walls of distal airspaces. The pulmonary interstitium serves as scaffolding for tumor growth. Neoplastic cells can detach from the primary tumor and attach to alveolar septa elsewhere in the lung, resulting in multifocal spread of tumor. The cells can produce abundant mucus, giving rise to bronchorrhea, the expectoration of large amounts of mucus. The radiologic patterns of BAC are protean. The most common radiologic manifestation of BAC is a well-circumscribed peripheral solitary nodule or mass. Actual cavitation is uncommon, although pseudocavitation is a well-known feature. Air bronchograms are commonly seen (Figs. 15-6 and 15-7). The lepidic pattern of growth can look like airspace disease on chest radiography, an appearance similar to that of pneumonia (Fig. 15-8). Less common patterns include multiple nodules or extensive alveolar lung disease involving one or more lobes.

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FIG 5. Adenocarcinoma. A: PA chest radiograph of a 48-year-old man shows an irregular mass in the right upper lobe abutting the mediastinum. B: CT shows the mass extending into the mediastinum. The center of the mass is of low attenuation, secondary to tumor necrosis. C: CT at a more inferior level shows tumor along the posterior wall of the right upper lobe bronchus. D: CT with lung windowing shows the spiculated mass and a background of paraseptal and centrilobular emphysema.

Radiologically, peripheral adenocarcinomas produce a spectrum of ground-glass to solid opacities and can have varying degrees of BAC histology (Fig. 15-9). The greater the solid component, the greater the likelihood of an invasive growth component. A common appearance of adenocarcinoma with a BAC component is a nodule with a central solid component and peripheral ground-glass opacity, the so-called “fried egg” sign (Fig. 15-10). Kodama et al (8) have shown that the radiologic ground-glass component correlates with noninvasive growth (BAC) in pathology specimens. The strict definition of BAC requires that the tumor be composed entirely of a lepidic pattern of growth without evidence of interstitial or stromal invasion (5). In one series, small (<3.0-cm) solitary tumors that comprised an entirely lepidic growth pattern had a 5-year survival rate of 100% (9). BAC can be indolent, growing slowly over many months or years, and should always be considered when serial chest radiographs show chronic alveolar lung disease. It can recur in multiple areas of the lung after resection (Figs. 15-9 and 15-11).

Squamous Cell Carcinoma

Squamous cell carcinoma is the second most common type of bronchogenic carcinoma, and it is strongly associated with cigarette smoking. It is the most common type to cavitate and to be associated with hypercalcemia. Microscopically, squamous cell carcinoma is characterized by the presence of intercellular bridges, individual cell keratinization, and formation of keratin pearls. These tumors are most commonly central in location (within the main, lobar, or segmental bronchi), although approximately 25% are peripheral (Figs. 15-12 and 15-13). The typical radiologic manifestations of central squamous cell carcinomas are postobstructive pneumonia and atelectasis because of the total or partial bronchial obstruction produced by these central tumors (Fig. 15-14). The central tumor mass, adjacent to a displaced fissure from obstructive atelectasis, gives rise to the radiographic Golden S sign (see Chapter 2).

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FIG 6. Adenocarcinoma with bronchioloalveolar carcinoma component. A: PA chest radiograph of a 73-year-old woman with chronic cough and symptoms of pneumonia for 3 months shows airspace disease in the left lower lung. B: CT shows numerous air bronchograms within the left lower lobe airspace opacity. The patient was treated with antibiotics for presumed lobar pneumonia before the diagnosis of cancer was made. Adenocarcinoma, particularly bronchioloalveolar carcinoma, should be considered when chest radiographs show chronic airspace disease.

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FIG 7. Bronchioloalveolar carcinoma. A: PA chest radiograph of a 79-year-old woman with a 50 pack-year history of cigarette smoking shows a subtle nodule superimposed on the shadow of the left sixth posterior rib (arrow). B: CT shows an ill-defined nodule (arrow) with air bronchograms in the posterior segment of the left upper lobe.

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FIG 8. Bronchioloalveolar carcinoma. A: PA chest radiograph shows focal airspace disease in the left lower lobe, obscuring the medial left hemidiaphragm. B: Lateral view shows increased opacification over the lower thoracic spine (the so-called spine sign). The appearance is similar to that of left lower lobe pneumonia.

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FIG 9. Bilateral bronchioloalveolar carcinomas. A: CT of a 71-year-old woman with a 30 pack-year history of cigarette smoking and resection of bronchioloalveolar carcinoma in the right upper lobe 4 years earlier shows a ground-glass nodule in the right lower lobe (arrow). B: CT at a more superior level shows a ground-glass nodule in the left upper lobe (arrow). Both nodules were proven to represent bronchioloalveolar cell carcinoma. Ground-glass nodules are very worrisome for bronchioloalveolar carcinoma, especially in a patient with a history of this type of cancer.

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FIG 11. Recurrent bronchioloalveolar carcinoma. A: CT scan of a 59-year-old woman shows a nodule in the left upper lobe (arrow) with a fried egg appearance. The patient underwent lingulectomy to remove a stage IA bronchioloalveolar carcinoma. B: CT image obtained 2 years later shows a ground-glass nodule with an air bronchogram in the medial right lung (arrow). Wedge resection of the right upper lobe and superior segment of the right lower lobe confirmed recurrence of bronchioloalveolar carcinoma.

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FIG 12. Squamous cell carcinoma. A: PA chest radiograph of a 62-year-old woman with left chest pain shows an ill-defined mass with central lucency in the left middle lung. B: Lateral view confirms that this mass is in the superior segment of the left lower lobe (arrows). C: CT shows a subpleural mass in the superior segment of the left lower lobe, lacking the cavitation that was suggested by the chest radiograph. Approximately 25% of squamous cell lung cancers are peripheral in location.

Peripheral squamous cell carcinoma is the most common type of bronchogenic cancer to cause the Pancoast syndrome. In 1924, Henry Pancoast first described a clinical syndrome diagnostic of an apical lung tumor (10). This syndrome is characterized by pain or atrophy of muscles of the ipsilateral upper extremity, caused by involvement of the lower brachial plexus, and Horner syndrome, which results from involvement of the sympathetic chain and the stellate ganglion. Pancoast tumors can manifest as apical masses or asymmetric apical pleural thickening (Fig. 15) and can be associated with bone destruction and soft tissue invasion. Magnetic resonance imaging (MRI) is superior to CT in determining whether there is tumor involvement of the chest wall, brachial plexus, subclavian artery, vertebral bodies, and spinal canal.

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FIG 13. Squamous cell carcinoma. A: PA chest radiograph of an 82-year-old woman with a history of cigarette smoking shows a mass in the right lower lung. B: Lateral view shows that the mass is anterior (arrows) in the right middle lobe. C: CT shows a lobulated mass in the right middle lobe abutting the major fissure posteriorly.

Large Cell Carcinoma

These tumors are the least common type of bronchogenic carcinoma. They grow rapidly, metastasize early, and are strongly associated with cigarette smoking. The histologic diagnosis is one of exclusion, given only to bronchogenic carcinomas that lack features of squamous, glandular, or small cell differentiation. Large cell carcinomas are appropriately named: they are usually bulky tumors greater than 3 cm in diameter. They are typically located in the lung periphery, but central lesions are not uncommon (Fig. 15-16). The typical radiologic appearance of these tumors is a large peripheral lung mass (11).

Small Cell Carcinoma

Small cell carcinoma is a rapidly growing neoplasm characterized by early and widespread metastases and by a strong association with cigarette smoking. Histologically, small cell carcinoma is characterized by small, uniform, oval cells with scant cytoplasm. Extensive crushing artifact is frequently seen in bronchial biopsy specimens, reflecting the tumor's scant tumor stroma and lack of desmoplastic reaction. Small cell carcinoma has been classified as a neuroendocrine neoplasm of the lung, and it is the most common cell type to cause a clinical hormone syndrome by secreting ectopic hormones. The majority of these tumors are located centrally within lobar and mainstem bronchi. They have extensive necrosis and hemorrhage, invade adjacent structures and lymph nodes, and disseminate along lymphatic routes.

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FIG 16. Large cell carcinoma. A: CT of an 80-year-old woman with dyspnea, wheezing, cough, fatigue, 12-pound weight loss, and no history of cigarette smoking shows a mass partially obstructing the left main bronchus (arrow). B: CT at a higher level shows mediastinal lymphadenopathy causing leftward displacement of the trachea (arrow).

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FIG 17. Small cell carcinoma. A: CT scout image of a 73-year-old woman with a 75 pack-year history of cigarette smoking shows a right hilar mass (arrows). B: CT shows tumor infiltrating the mediastinum.

The chest radiograph usually shows a hilar or perihilar mass associated with mediastinal widening; this can be caused by the primary tumor, metastases to hilar/mediastinal lymph nodes, or a combination of both (Fig. 15-17). The primary tumor may not be evident, and nodal enlargement may be the dominant abnormality. Rarely, small cell carcinoma may manifest as a solitary pulmonary nodule or mass (Fig. 15-18). CT usually shows extensive mediastinal lymph node involvement, with soft tissue “infiltration” of the mediastinum similar to that seen with lymphoma (Figs. 15-19 and 15-20). Small cell carcinoma is the most common primary lung cancer to cause superior vena cava obstruction, secondary to extrinsic vascular compression by the tumor, endoluminal thrombosis, or invasion (12). Surgical resection is considered in selected patients with small cell carcinoma only when the tumor manifests as a solitary pulmonary nodule in the absence of metastases. Most patients have disseminated disease at presentation and undergo chemotherapy and radiation therapy. The response to this treatment is usually dramatic, and the mass can disappear in a relatively short period of time, but most patients still die with rapidly recurrent small cell carcinoma (13).

Staging of Bronchogenic Carcinoma

Staging differs between small cell and non–small cell lung cancer. Small cell carcinoma is generally considered inoperable, except in rare cases of small, localized tumors. It is staged as limited or extensive, depending on whether disease is confined to a single radiation port (limited) (Fig. 15-21) or not (extensive) (Fig. 15-22). Patients with limited disease receive radiation therapy and chemotherapy, whereas patients with extensive disease receive only chemotherapy.

The primary goal of staging non–small cell lung cancer is to determine resectability. Revisions to the stage grouping of the TNM (tumor-node-metastases) subsets (Table 15-3) in the International System for Staging Lung Cancer were adopted in 1997 (14). Refinements in the staging system were made to better evaluate treatment strategies for carefully staged groups of patients. Stage grouping involves the concept of combining subsets of patients classified according to TNM descriptors into categories or stages, with each having generally similar treatment options and survival expectations (Table).

Tumor classification is the most complicated component of the TNM system. Tumors that are classified as anything other than T4 are potentially resectable. T4 tumors invade the mediastinum, heart, great vessels, trachea, esophagus, vertebral body, or carina; or they are associated with a malignant pleural or pericardial effusion or satellite tumor nodules within the ipsilateral primary tumor lobe of the lung. Satellite nodules outside the primary tumor lobe are considered M1 disease (Fig. 15-23). Most pleural effusions associated with lung cancer are malignant, but cytologic proof of malignancy cannot always be obtained. In these cases, the effusion should be excluded as a staging element.

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FIG 20. Small cell carcinoma. A: CT of a 57-year-old woman with hoarseness shows tumor infiltrating the aortopulmonary window and invading the left recurrent laryngeal nerve. B: CT at a level inferior to (A) shows encasement of the left pulmonary artery (arrows) by tumor and extension of tumor posterior to the carina, obliterating the fat plane adjacent to the descending aorta (D). C: CT at a level inferior to (B) shows encasement of the left upper lobe bronchus by tumor (arrows).

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FIG 21. Small cell carcinoma, limited stage. A: CT of a 64-year-old woman shows a lobulated mass in the right lower lobe. B: CT with mediastinal windowing shows calcification or contrast enhancement within the mass. Mediastinal lymphadenopathy was present in the right paratracheal area (not shown). CT and positron emission tomography showed no evidence of extrathoracic tumor. The patient received radiation therapy and chemotherapy.

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FIG 22. Small cell carcinoma, extensive. A: PA chest radiograph of a 47-year-old man with abdominal pain and vomiting shows enlargement of the cardiac silhouette, right pleural effusion, and abnormal opacities in the right paratracheal area, right hilum, and both lung bases. B: CT shows bilateral pleural effusions, bulky subcarinal lymphadenopathy, and a large pleural mass anteriorly. C: CT at a more inferior level shows anterior displacement of the left atrium by bulky tumor. D: CT at a level inferior to (C) shows numerous pleural tumor deposits (arrows). E: CT of the upper abdomen shows bulky celiac lymphadenopathy (arrow). The patient received chemotherapy.

TNM descriptor for staging bronchgenic carcinoma

Primary tumor (T)

  • TX Primary tumor cannot be assessed, or tumor proven, by the presence of malignant cells in sputum or bronchial washing but not visualized by imaging or bronchoscopy
  • T0 No evidence of primary tumor
  • Tis Carcinoma in situ
  • T1 Tumor 3 cm in greatest dimension, surrounded by lung or visceral pleura, without bronchoscopic evidence of invasion more proximal than the lobar bronchusa (i.e., not in the main bronchus)
  • T2 Tumor with any of the following features of size or extent:
    • Tumor > 3 cm in greatest dimension
    • Involves main bronchus, 2 cm distal to the carina
    • Invades the visceral pleura
    • Associated with atelectasis or obstructive pneumonitis that extends to the hilar region but does not involve the entire lung
  • T3 Tumor of any size that directly invades any of the following: chest wall (including superior sulcus tumors), diaphragm, mediastinal pleura, parietal pericardium; or tumor in the main bronchus <2 cm distal to the carina, but without involvement of the carina or associated atelectasis or obstructive pneumonitis of the entire lung
  • T4 Tumor of any size that invades any of the following: mediastinum, heart, great vessels, trachea, esophagus, vertebral body, carina; or tumor with a malignant pleural or pericardial effusionb or with satellite tumor nodule(s) within the ipsilateral primary tumor lobe of the lung

Regional lymph nodes (N)

  • NX Regional lymph nodes cannot be assessed
  • N0 No regional lymph node metastasis
  • N1 Metastasis to ipsilateral peribronchial and/or ipsilateral hilar lymph nodes, and intrapulmonary nodes involved by direct extension of the primary tumor
  • N2 Metastasis to ipsilateral mediastinal and/or subcarinal lymph node(s)
  • N3 Metastasis to contralateral mediastinal, contralateral hilar, ipsilateral or contralateral scalene, or supraclavicular lymph node(s)

Distant metastasis (M)

  • MX Presence of distant metastasis cannot be assessed
  • M0 No distant metastasis
  • M1 Distant metastasis presentc

Hilar node involvement is classified as N1. N2 nodes are ipsilateral mediastinal nodes, and N3 nodes are contralateral mediastinal or hilar nodes. N3 nodes also include any ipsilateral or contralateral scalene or supraclavicular lymph nodes. The distant metastases classification is simple. M0 indicates no distant metastases, and M1 is positive distant metastases.

The staging system is complicated and difficult to remember unless one routinely evaluates and stages lung cancer. Patients with T1N0M0 tumors (stage IA) have a significantly better outcome than patients in the other subsets (15,16) (Fig. 15-24). These patients have a tumor that is 3 cm or less in diameter, surrounded by lung or visceral pleura, without bronchoscopic evidence of invasion more proximal than the lobar bronchus, and without nodal involvement or metastases. In other words, these are patients with a solitary pulmonary nodule and no spread of tumor. Stage IB tumors also have no nodal or distal metastases, but the primary tumor is either larger than 3 cm in diameter, involves the main bronchus, invades the visceral pleura, or is associated with atelectasis or obstructive pneumonitis. Sixty-one percent of patients with clinical stage IA disease and 38% of those with clinical stage IB tumors are expected to survive more than 5 years after treatment. IA and IB subsets have no evidence of lymph node or other metastases and therefore have the best prognosis.

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FIG 23. Adenocarcinoma. A: PA chest radiograph of a 65-year-old man with a 100 pack-year history of cigarette smoking shows a nodule in the right medial lung (arrow). B: PA chest radiograph obtained 1 year later shows widespread parenchymal metastases. C: CT shows numerous circumscribed pulmonary metastases involving both lungs. Note a pathologic rib fracture on the right (arrow). Other images showed metastases to both adrenal glands, multiple lytic bone lesions, and extensive mediastinal lymphadenopathy.

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FIG 24. Adenocarcinoma, stage IA. CT of a 66-year-old woman with pulmonary fibrosis shows a small subpleural nodule (arrow) in the left upper lobe, with no evidence of lymphadenopathy or metastatic disease. Nodes removed at surgery were negative.

Stage IIA, IIB, and IIIA tumors are potentially resectable, although the prognosis after treatment is poor, especially with IIIA tumors. Some surgeons opt not to resect IIIA tumors for this reason. IIIB staging involves either T4 tumors or N3 nodes, making such tumors unresectable. IIIB tumors are confined to the lung, however, which is an important consideration for radiotherapy. Stage IV tumors are defined by an M1 classification and are therefore unresectable and not confined to the lung. If treated, systemic therapy is required.

CT is commonly used for staging bronchogenic carcinoma prior to surgical resection. Patients with bulky N3 nodes are clearly not surgical candidates, and those patients without evidence of nodal involvement are considered surgical candidates (in the absence of T4 or M1 disease). CT is not perfect in detecting nodal involvement, however. In general, nodes greater than 1 cm in short-axis diameter are considered positive or suspicious, but many of these cases will turn out to be false-positive findings. In addition, nodes that are smaller than 1 cm or not visibly enlarged on CT can be positive histologically. Nodes can be sampled percutaneously, transbronchially, or via transcervical mediastinoscopy (requiring general anesthesia). The Chamberlain procedure involves an anterior thoracotomy, usually with removal of the second anterior rib to allow sampling of lymph nodes in the anterior mediastinum, the aorticopulmonary window, and the hilum. Other limitations of CT include the inability to determine mediastinal or chest wall invasion with certainty. MRI plays a role in evaluating these cases, as well as in evaluating for the presence of brachial plexus invasion.

Whole-body positron emission tomography (PET) imaging with [18]-fluoro-2-deoxy-D-glucose (FDG) has become an integral part of staging non–small cell lung cancer. PET improves the detection of nodal and distant metastases and frequently alters patient management (17). Integrated CT-PET scanners allow for the acquisition of coregistered, spatially matched functional and morphologic data. PET is sufficiently sensitive that a patient with negative mediastinal PET results may proceed directly to surgical resection of the primary tumor without a staging mediastinoscopy (18).

Postpneumonectomy Complications

In the United States, the most common indication for pneumonectomy is non-small cell carcinoma of the lung. Most pneumonectomies performed for bronchogenic carcinoma follow an interpleural plane of resection (meaning the parietal pleura is left intact). If there is extension of tumor into the pleural space or parietal pleura, or in the case of malignant mesothelioma, an extrapleural pneumonectomy is generally performed. In this case, the plane of resection is between the parietal pleura and the endothoracic fascia (19).

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FIG 25. Postpneumonectomy bronchopleural fistula. A: AP upright chest radiograph of a 52-year-old man after right pneumonectomy shows shift of the mediastinum to the operative side and an air-fluid level within the right pneumonectomy space (arrows). There is postpneumonectomy pulmonary edema of the left lung. B: AP upright chest radiograph obtained 1 day later shows increased air within the right pneumonectomy space and shift of the mediastinum away from the operative side, consistent with a bronchial stump leak and bronchopleural fistula.

After pneumonectomy, pleural fluid accumulates in the pneumonectomy space, replacing the normal immediate postoperative air that is resorbed at a variable rate. It is not uncommon for multiple air–fluid levels to be present within the early pneumonectomy space, representing loculation of fluid, and this finding on chest radiography does not necessarily suggest a complication. Most of the air is resorbed by 2 weeks after pneumonectomy; residual air may persist for months, however, or, in a small population of patients, it may never be completely resorbed. Eventually, the pneumonectomy space will contract, with ipsilateral shift of the mediastinum and elevation of the diaphragm, and the space will fill with fluid and some degree of solid fibrothorax. Shift of the mediastinum away from the operated side indicates a buildup of air or fluid within the pneumonectomy space. Mediastinal displacement away from the operative side suggests one of five diagnoses, depending on the length of time after surgery (Table 15-5). If the air-fluid level has not continued to rise after surgery, the cause of the contralateral mediastinal shift is likely a bronchial stump air leak. If the air-fluid level has continued to rise, the shift can be a result of hemothorax, chylothorax, or empyema, with or without a bronchopleural fistula. A drop in the air-fluid level indicates that fluid is draining through a chest tube, by thoracentesis, through a dehiscence of the incision, through an opening in the bronchial stump (Fig. 15-25), or through a rent in the diaphragm (19). After the postoperative period, shift of the mediastinum away from the operative side is also suspicious for recurrent tumor (Fig. 15-26), which can be recognized on CT as a soft tissue mass at the site of surgical ligation and soft tissue deposits studding the periphery of the pneumonectomy space. Recurrence can also be seen in the remaining lung (Fig. 15-27). PET scanning can be very helpful in evaluating for recurrence.

Postpulmonectomy complication

Early: - Bronchopleural fistula (stump leak) - Empyema - Hemothorax (blood within pneumonectomy space)a - Chylothorax (chylous leak into pneumonectomy space)

Late: - Recurrent neoplasm - Bronchopleural fistula - Empyema - Hemothorax - Chylothorax

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FIG 26. Recurrence of bronchogenic carcinoma after pneumonectomy. A: PA chest radiograph of a 65-year-old man after left pneumonectomy for bronchogenic carcinoma shows an air–fluid level in the left pneumonectomy space (arrows), left skin staples (arrowheads), and shift of the mediastinum toward the operative side. B: PA chest radiograph obtained 8 months later shows abnormal shift of the mediastinum away from the operative side, an appearance that is consistent with hemothorax, chylothorax, or recurrence of tumor with malignant fluid in the pneumonectomy space. Empyema is less of a consideration in the absence of air within the pneumonectomy space. C: CT shows a soft tissue mass (M) between the surgical clips and soft tissue deposits studding the surface of the pneumonectomy space (arrows). There is malignant fluid within the left pneumonectomy space.

The mortality of pneumonectomy is approximately 6%, with the major causes of death being pneumonia, respiratory failure, pulmonary embolism, myocardial infarction, bronchopleural fistula, and empyema (20,21). The incidence of empyema is 2% to 5%, often with associated bronchopleural fistula (22). In the first postoperative week, empyema is caused by intraoperative soilage or preoperative pleural infection. Delayed onset of empyema is often associated with bronchopleural or esophagopleural fistula. New air within the pneumonectomy space, in a previously opacified hemithorax, with contralateral shift of the mediastinum, is suggestive of empyema or bronchopleural fistula and bronchial stump leak (Fig. 15-28).

A rare complication of right pneumonectomy is obstruction of the left main bronchus, a result of extreme rightward shift and counterclockwise rotation of the mediastinum, causing compression of the left bronchus between the aorta and the left pulmonary artery. This complication is termed the right pneumonectomy syndrome, and it can occur between 1 and 37 years after surgery (23). The diagnosis is suggested on chest radiography by marked mediastinal shift to the right and inversion of the left diaphragm, caused by the trapping of air from a narrowing of the left bronchus (19). There can also be recurrent left lower lobe pneumonia resulting from airway obstruction.