The differential diagnosis of this poorly marginated, soft tissue attenuation, anterior mediastinal mass includes a thymic neoplasm, lymphoma, and germ cell neoplasm. Lymphoma is typically associated with lymph node enlargement elsewhere, and germ cell neoplasms such as a mature teratoma frequently have evidence of fat attenuation or calcium.
Thymic epithelial neoplasms, most notably thymoma, account for the majority of anterior mediastinal masses in adult patients. Most thymic neoplasms demonstrate well-defined margins on imaging studies. Two notable exceptions are invasive thymoma and thymic carcinoma. Invasive thymoma refers to a thymoma that has invaded its fibrous capsule. Such lesions tend to spread locally, with invasion of adjacent mediastinal structures, chest wall invasion, and contiguous spread along the pleural surface (usually unilaterally). Thymic carcinoma is a rare thymic neoplasm that may be indistinguishable from an invasive thymoma on imaging studies unless distant metastases are present. Unlike invasive thymoma, a thymic carcinoma tends to metastasize hematogenously.
The chest radiograph reveals a subcarinal mass, with associated lateral convex bulging of the azygoesophageal interface. The differential diagnosis of a subcarinal mass includes subcarinal lymph node enlargement, bronchogenic cyst, and left atrial enlargement. The MRI reveals that the mass is not vascular and has intermediate signal intensity similar to that of skeletal muscle. The MR features are thus most suggestive of lymph node enlargement. In this patient, the enlarged nodes were secondary to metastatic disease from a primary renal cell carcinoma.
Enlarged mediastinal lymph nodes may be encountered in a wide variety of neoplastic, infectious, and inflammatory conditions. Neoplastic causes include metastatic disease (from bronchogenic carcinoma or an extrathoracic primary), lymphoma, and leukemia. Infectious causes include tuberculosis (TB), fungal, viral, and bacterial infections. Although lymph node enlargement may be evident on CT images in the latter two entities, it is not usually evident on conventional radiographs. Inflammatory causes include sarcoidosis, Castleman’s disease, and angioimmunoblastic lymphadenopathy.
Silicosis is a fibrotic lung disease related to the inhalation of dust containing either free crystalline silica or silicon dioxide. Occupational settings related to silica exposure include heavy metal mining, sandblasting, foundry work, and stone masonry. Silicosis is usually a slowly progressive chronic lung disease with a latency period of at least 20 years.
Chronic silicosis is classified into simple and complicated forms. Simple silicosis is asymptomatic and typically presents radiographically with multiple small, nodular opacities, ranging in size from 1 to 10 mm in diameter. The nodules usually have an upper lung zone predominance and frequently calcify. Enlarged nodes are often present and may demonstrate a characteristic peripheral eggshell pattern of calcification, as shown in the first figure.
Complicated silicosis is associated with symptoms and reduced pulmonary function. It is characterized by one or more areas in which silicotic nodules have become confluent, measuring more than 1 cm. Such opacities may be observed in the periphery of the upper lung zone or in the middle lung zone. Over time, these opacities migrate toward the hila, with residual emphysema in the remaining portions of the lungs. In both figures, note the large vertically oriented opacities in the upper and middle lung zones, which are typical of the complicated form of silicosis. As progressive massive fibrosis becomes more extensive, the nodularity in the remaining portions of the lungs usually becomes less apparent.
The HRCT images demonstrate a subpleural distribution of irregular linear opacities, ground-glass attenuation, and traction bronchiolectasis. The last term refers to the small, discrete, cystic lucencies in the lung periphery (best demonstrated in the right lower lobe in the first figure [arrows]), which represent dilated bronchioles. A subpleural and basilar predominance of infiltrative lung disease is characteristic of UIP and NSIP.
UIP is characterized histologically by a variegated pattern composed of foci of normal lung, interstitial cellular infiltrates, and intervening zones of active fibrosis and end-stage fibrosis. UIP is associated with a variety of chronic infiltrative lung diseases, including idiopathic pulmonary fibrosis, asbestosis, connective tissue disorders, and drug toxicity. Characteristic HRCT findings in patients with UIP include a subpleural and basilar predominant distribution of irregular linear opacities, ground-glass attenuation, traction bronchiectasis and bronchiolectasis, and honeycombing.
NSIP is characterized by a subpleural and basilar predominant distribution of ground-glass attenuation, irregular linear opacities, and traction bronchiectasis. In contrast to UIP, honeycombing is typically absent in cases of NSIP.
Progressive systemic sclerosis (also referred to as scleroderma), is a connective tissue disorder that is characterized by fibrosis and atrophy of numerous organ systems, including the skin, lungs, gastrointestinal tract, heart, and kidneys. Pulmonary manifestations include interstitial fibrosis, pulmonary vascular disease, and pleural thickening. Other common manifestations include esophageal dilation and dysmotility, enlarged mediastinal lymph nodes, and calcinosis in the skin and subcutaneous tissues.
Parenchymal consolidation and mediastinal and hilar lymph node enlargement are the hallmarks of primary TB. The term Ghon lesion (or Ghon focus) refers to a lung nodule that is a residuum of primary TB. In patients with primary TB and an adequate host immune response, the area of lung consolidation slowly regresses to form a well-circumscribed nodule. Such a nodule may disappear altogether or may remain as a solitary calcified granuloma, referred to as a Ghon lesion. Lymph node enlargement, another sign of primary TB infection, also regresses. Residual calcified lymph nodes may be seen, as demonstrated in the aorticopulmonary window and left hilum in this patient.
The chest radiograph in the second figure demonstrates several typical findings of interstitial edema, including indistinctness of the pulmonary vessels, peribronchial cuffing, and thickened septal (Kerley) lines. The presence of a recent normal baseline radiograph (first figure) confirms that this is an acute process. Significant ancillary findings include interval slight increase in heart size and increased caliber of upper lobe vessels (cephalization).
Cardiogenic pulmonary edema refers to excess extravascular fluid within the lungs secondary to increased pulmonary microvascular pressure, which is usually due to diseases of the left side of the heart such as left ventricular failure. Cardiogenic pulmonary edema usually follows a typical course. It begins in the interstitial compartment and extends into the alveolar compartment as it increases in severity.
The characteristic radiographic findings of pulmonary venous hypertension and congestive heart failure have been shown to correlate with physiologic parameters such as the PVWP. Normally, the PVWP is lower than 12 mm Hg. As PVWP rises to between 13 and 17 mm Hg, you should expect to see vascular redistribution. At PVWP higher than 17 mm Hg, Kerley lines are usually visible. At PVWP values higher than 20 mm Hg, a right-sided pleural effusion is often evident. When PVWP rises above 25 mm Hg, you should expect to see airspace opacities, usually most prominent in the central, perihilar regions of the lungs.
The chest radiographic features may lag behind the clinical status of the patient as pulmonary edema resolves. Radiographic findings of pulmonary edema may persist despite a return to normal wedge pressure measurements.
Bronchiectasis is defined as abnormal, irreversible dilation of the bronchi. Bronchiectasis may arise secondary to a wide variety of congenital and acquired abnormalities. Cystic fibrosis is the most common associated congenital abnormality, and prior infection, especially childhood viral illnesses, is the most common acquired abnormality. Bronchiectasis is a rare complication of Marfan’s syndrome. Note the characteristic elongated thorax of this patient on the lateral radiograph.
Chest radiographs are frequently normal in patients with mild degrees of bronchiectasis but may occasionally reveal parallel thickened bronchial walls, also referred to as a tram-track appearance. With cystic bronchiectasis, radiographs may reveal clusters of air-filled cysts, often with fluid levels. HRCT is highly sensitive and specific for diagnosing bronchiectasis. Findings include a bronchial wall diameter greater than its adjacent artery (resulting in a “signet-ring” sign when the dilated bronchus and accompanying artery are viewed in cross-section), identification of bronchi within the peripheral centimeter of the lung, lack of normal bronchial tapering, bronchial wall thickening, and strings or clusters of cysts. Because bronchial wall thickening may also be seen in other forms or airways disease, it should not be used as a sole criterion for diagnosis bronchiectasis. Complications of bronchiectasis include recurrent infections, hemoptysis, mucoid impaction, and atelectasis (note the left lower lobe atelectasis in the second figure).
An AVM represents an abnormal communication between the pulmonary arteries and veins in which there is absence of the capillary network that normally separates these vascular structures. This process results in a right-to-left shunt. Although many patients are asymptomatic at the time of initial presentation, complications of right-to-left shunting include cyanosis, dyspnea, stroke, and brain abscess.
Pulmonary AVMs have a lower lobe predominance, and they often occur in the medial third of the lung. AVMs are defined as simple when there is a single feeding artery and a single feeding vein; they are complex when there are two or more feeding arteries and two or more draining veins.
Pulmonary arteriography was historically the modality of choice for defining the number, size, and angioarchitecture of these lesions. However, multidetector CT (MDCT) angiography with multiplanar reformation and three-dimensional reconstructions has been shown to be equivalent to pulmonary arteriography for detection of AVMs and characterization of their angioarchitecture. MDCT is now the imaging study of choice for screening for pulmonary AVMs and may also be used to help select appropriate therapy. Pulmonary AVMs larger than 2 cm are usually treated with endovascular coil embolization or balloon occlusion.
Vascular abnormalities, including aneurysms and vascular variants, are an important cause of middle mediastinal masses. You should consider the diagnosis of an aortic aneurysm whenever you detect a mass in close proximity to the aorta, particularly if a border of the mass is indistinguishable from the aortic contour. The diagnosis can be confirmed with either contrast-enhanced CT or MRI.
A thoracic aortic aneurysm is an abnormal dilation of the aorta. Aortic aneurysms can be classified according to shape, integrity of the aortic wall, and location. With regard to shape, aneurysms may be classified as either saccular or fusiform. Saccular aneurysms are characterized by a focal outpouching of the aorta, as demonstrated in the second figure. Such aneurysms are often traumatic or infectious in etiology. Fusiform aneurysms, conversely, are characterized by cylindrical dilation of the entire aortic circumference. This configuration is typical of atherosclerotic aneurysms.
Based on the integrity of the aortic wall, aneurysms may be classified as either true or false. True aneurysms have an intact aortic wall. The most common cause of a true aneurysm is an atherosclerotic aneurysm. In contrast, false aneurysms are associated with a disrupted aortic wall. Examples of false aneurysms include infectious (mycotic) and posttraumatic aneurysms.
Regarding location, aneurysms may be classified as involving primarily the ascending aorta, aortic arch, or descending aorta. Aneurysms that classically involve the ascending aorta include those related to cystic medial necrosis and syphilis. Other causes of aneurysms, including atherosclerotic, mycotic, and posttraumatic etiologies, most often affect the descending thoracic aorta and aortic arch.
Pulmonary infarcts typically appear as wedge-shaped foci of consolidation, with their bases abutting the visceral pleura. Like pulmonary emboli, they are usually multiple, and they typically have a basilar predominance.
Revel and colleagues recently assessed the sensitivity and specificity of four findings (triangular shape, vessel sign, central lucencies, and air bronchograms) for distinguishing pulmonary infarction from other causes of peripheral consolidation. Among these features, central lucencies and a feeding vessel (vessel sign) were more commonly associated with pulmonary infarction, with likelihood ratios of 23 and 2.9, respectively. Thus, when you identify a wedge-shaped peripheral area of consolidation with central lucencies and/or a feeding vessel, you should carefully assess for coexisting pulmonary embolism.
Lymphoma is a common AIDS-related neoplasm, but thoracic involvement is present in only a minority of AIDS patients with non-Hodgkin’s lymphoma. Thoracic lymphoma is usually associated with disseminated disease involving the central nervous system, gastrointestinal tract, and bone marrow. In AIDS patients, thoracic lymphoma is typically extranodal. Thus, abnormalities of the lung parenchyma (nodules, masses, interstitial parenchymal opacities) and pleura (effusions) are encountered more frequently than lymph node enlargement.
The differential diagnosis of multiple nodules or masses includes infections and other neoplasms, especially Kaposi’s sarcoma. In AIDS-related lymphoma, nodules and masses may grow quite rapidly, with doubling times similar to that of infectious nodules. Thus, a rapid doubling time is not a reliable indicator of benignancy in AIDS patients. With regard to Kaposi’s sarcoma, it can be differentiated from lymphoma by its lack of uptake on gallium scans. In contrast, lymphoma is gallium-avid.
Acute thoracic aortic injury is a serious complication of blunt chest trauma, with an associated high mortality rate. The majority of affected patients die before reaching the hospital, and approximately half of those who present to the hospital die within 1 week without appropriate treatment.
MDCT plays an important role in screening trauma patients for evidence of mediastinal hematoma, an important indirect sign of aortic injury. Although mediastinal hemorrhage is sensitive for detecting aortic injury, it is not very specific. For example, mediastinal hematoma may be associated with injuries to other arterial and venous structures as well as with nonvascular injuries, such as sternal and spinal fractures. When hemorrhage is localized to the periaortic region (first figure), it is more specific for aortic injury. When you identify hemorrhage, you should look carefully for direct signs of aortic injury.
Direct signs of aortic injury include deformity of the aortic contour (second figure), intimal flap (arrow in the second figure), intraluminal thrombus, pseudoaneurysm, and frank extravasation of contrast. Multiplanar and three-dimensional reconstructions provide important complementary information to axial CT images including distance of injury from aortic arch branch vessels, length of injury, aortic diameter above and below the site of injury, and coexisting vascular anomalies. Precise characterization of the injury is important for guiding treatment decisions, including surgical repair and stent placement.
A thyroid goiter is the most common cause of a mediastinal mass in the thoracic inlet region in adults. On chest radiographs, a substernal goiter typically presents as a well-defined mass that extends through the thoracic inlet from the neck and is frequently associated with deviation and/or compression of the trachea. On CT imaging, characteristic features include continuity with the cervical thyroid gland, foci of high attenuation on noncontrast images (reflecting the high iodide content of thyroid tissue), focal areas of cysts and calcification, and intense enhancement following intravenous contrast administration.
Although lymphoma may infrequently present as a thoracic inlet mass, calcification is rarely encountered in untreated cases of lymphoma. In contrast, calcification is a common feature of thyroid goiters.
Exogenous lipoid pneumonia is associated with the inadvertent aspiration of oily substances such as mineral oil. On conventional radiographs, lipoid pneumonia typically appears as chronic alveolar consolidation, which is usually most prominent in the lung bases. Lipoid pneumonia infrequently presents as a focal masslike opacity.
On CT examination, the areas of consolidation are characterized by low density, reflecting their fatty composition. The identification of negative CT density numbers in the range of fatty tissue (e.g., –50 to –150 Hounsfield units) within the consolidation is pathognomonic for lipoid pneumonia. Less characteristically, exogenous lipoid pneumonia may manifest on HRCT as geographic ground-glass attenuation with superimposed smooth septal thickening (“crazy paving” pattern) due to intraalveolar and interstitial accumulation of lipid-laden macrophages and hyperplasia of type II pneumocytes along the alveolar lining.
Affected patients are frequently asymptomatic, but a minority of patients present with chronic symptoms of cough and dyspnea. Such symptoms generally resolve once the patient discontinues using the offending substance.
With regard to the differential diagnosis of chronic alveolar consolidation, you may narrow the differential diagnosis by assessing whether the process is focal or diffuse. Focal areas of chronic consolidation may be seen in lipoid pneumonia, BAC) and lymphoma. Diffuse chronic consolidation can be seen in BAC, alveolar proteinosis, alveolar sarcoid, and lipoid pneumonia. Lipoid pneumonia typically has a dependent distribution, which is not typical of other causes of chronic diffuse alveolar consolidation.
Kartagener’s syndrome is a subset of the dyskinetic cilia syndrome, a congenital cause of bronchiectasis that is associated with an autosomal recessive pattern of inheritance. In patients with the dyskinetic cilia syndrome, ciliary function is typically abnormal throughout the body. Thus, affected males are infertile on the basis of immotile sperm.
Patients with Kartagener’s syndrome typically present in childhood with symptoms related to bronchitis, sinusitis, and rhinitis. Bronchiectasis usually develops in childhood and young adulthood, and it is associated with recurrent pneumonias. Bronchiectasis is typically less severe than in cases of cystic fibrosis, another congenital cause of bronchiectasis. Interestingly, in patients with Kartagener’s syndrome, bronchiectasis has a predilection for the anatomic right middle lobe.
On imaging studies, the combination of situs inversus and bronchiectasis suggests the diagnosis. Ancillary findings may include overinflation of the lungs and focal areas of consolidation and atelectasis.
The tumor-node-metastases (TNM) system for staging lung cancer was revised in 2009. According to this classification system, a centrally obstructing neoplasm with associated postobstructive atelectasis or obstructive pneumonitis that extends to the hilar region but does not involve the entire lung is classified as T2. If the entire lung is involved, then the primary tumor is classified as T3.
Squamous cell carcinomas typically occur in main, segmental, or subsegmental bronchi and grow endobronchially. In contrast, small cell carcinoma is characterized by a submucosal, peribronchial growth pattern and a discrete endobronchial tumor is seldom identified. Small cell carcinoma typically occurs as a large central mass that may narrow the bronchial lumen by extrinsic compression. Adeoncarcinomas of the lung are typically peripheral tumors.
Wegener’s granulomatosis is a necrotizing vasculitis that classically involves the upper respiratory tract, lungs, and renal glomeruli. A limited form of the disease is largely confined to the lung and is associated with a better prognosis than the classic form.
The thoracic radiologic manifestations of Wegener’s granulomatosis are varied, but the most characteristic pattern is that of multiple lung nodules or masses. Such nodules and masses are usually round in configuration, with well-defined margins. They range from 1 or 2 mm to 9 cm in diameter, and cavitation is evident in up to one half of cases. On CT scans, the nodules frequently demonstrate angiocentric features, such as the presence of feeding vessels and a peripheral distribution. The second most common pattern is focal or diffuse alveolar consolidation, which corresponds to the presence of pulmonary hemorrhage.
The diagnosis requires consistent pathologic, radiologic, clinical, and laboratory data. The presence of a cytoplasmic pattern of cANCA, as detected by indirect immunofluorescence of serum, is suggestive of the diagnosis. Treatment with a combination of cyclophosphamide and steroids is successful in most cases.
Invasive pulmonary aspergillosis is the most common fungal infection to affect immunosuppressed patients. It usually affects patients with severe neutropenia, including recent bone marrow transplant recipients, patients with hematologic malignancies, and patients receiving high-dose steroids. Because it is a potentially lethal infection, prompt recognition and treatment are critical.
Aspergillus organisms invade blood vessels, resulting in areas of pulmonary infarction. On chest radiographs, you may observe multiple poorly defined nodular opacities and more confluent areas of consolidation. Foci of consolidation are often wedge-shaped and peripheral in location. When imaged with CT scanning early in the course of infection, the nodules typically demonstrate a halo of ground-glass attenuation, which corresponds to the presence of hemorrhage. In the proper clinical setting (e.g., profound neutropenia), the CT halo sign is highly suggestive of Aspergillus infection. However, it is not specific for Aspergillus, because it may also be seen in association with other infections (mucormycosis), vasculitides, and hemorrhagic metastases. Later in the course of infection, the nodules may undergo cavitation (the “air crescent sign”). Such cavitation occurs after granulocyte recovery and usually indicates a good prognosis.
LAM is a rare disease that affects women during their reproductive years. Pathologically, it is characterized by abnormal proliferation of immature smooth muscle cells and the presence of thin-walled lung cysts. Such cysts may rupture, leading to spontaneous pneumothoraces. Lymphatic obstruction may result in chylous pleural effusions.
On conventional radiographs, you may observe a diffuse linear pattern, with preserved or increased lung volumes. Pleural abnormalities, including pneumothorax and pleural effusion, may also be evident. The hallmark of LAM on HRCT is the presence of numerous thin-walled cysts, which are usually regular and uniform in configuration. The intervening lung is typically normal.
The main differential diagnosis is Langerhans cell histiocytosis (LCH). In this disorder, cysts are usually accompanied by small nodules, which may undergo cavitation. Unlike the cysts in LAM, LCH-related cysts have a more variable appearance, with occasional bizarre configurations. Finally, LCH typically spares the costophrenic sulci, whereas LAM has a more diffuse distribution.
Current treatments for LAM include progesterone and, less commonly, oophorectomy. Lung transplantation is a viable option for patients with severe disease. Multicenter trials are under way to assess new molecular-based therapeutic agents.
Boiselle PM, Tocino I, Hooley RJ, et al: Chest radiograph interpretation of Pneumocystis carinii pneumonia, bacterial pneumonia, and pulmonary tuberculosis in HIV-positive patients: accuracy, distinguishing features, and mimics. J Thorac Imaging 12:47-53, 1997.
The chest radiograph plays an important role in the evaluation of pulmonary infections in HIV-positive patients. Despite some overlapping features among various infections, chest radiograph pattern recognition can help to narrow the differential diagnosis of pulmonary infections in HIV-positive patients.
With regard to a pattern of focal or lobar consolidation, bacterial pneumonia is the most likely etiology. Bacterial pneumonias are especially common early in the course of HIV infection (CD4 greater than 200/mm3), and recurrent bacterial pneumonias are now included as an AIDS-defining illness. Commonly encountered bacterial pathogens include Streptococcus, Haemophilus influenzae, Staphylococcus, and gram-negative organisms.
When focal or lobar consolidation is accompanied by mediastinal and hilar lymph node enlargement, TB should be considered. Other causes of focal or lobar consolidation are less common, including PCP (which more typically presents as diffuse, bilateral parenchymal opacities) and Mycobacterium avium-intracellulare infection.
Lymph node enlargement is a characteristic feature of primary TB, particularly in children. Lymph node enlargement may occur alone or in association with parenchymal consolidation. On contrast-enhanced CT scans of patients with mediastinal tuberculous lymphadenitis, enlarged nodes often demonstrate a low-density center and peripheral rim enhancement. Histologically, such nodes have been shown to demonstrate central necrosis and a highly vascular, inflammatory capsular reaction.
Although low-density nodes are characteristic of TB, they are not specific for this entity. Such nodes may also be encountered in atypical mycobacterial and fungal infections. Neoplastic lymph nodes (e.g., metastatic seminoma) may also demonstrate this appearance.
With regard to TB in HIV-positive patients, the radiographic appearance varies depending on the patient’s CD4 count. In patients with CD4 counts above 200/mm3, a post-primary pattern is typically seen. In patients with CD4 counts below 200/mm3, you will usually observe a primary pattern, including low-density lymph nodes and consolidation.
The classic chest radiographic presentation of Pneumocystis pneumonia is a bilateral perihilar or diffuse symmetric interstitial pattern, which may be finely granular, reticular, or ground glass in appearance. Importantly, the chest radiograph may be normal at the time of presentation in a significant minority of cases of Pneumocystis pneumonia. CT, particularly HRCT, is more sensitive than chest radiographs for detecting Pneumocystis pneumonia and thus may be helpful in evaluating symptomatic patients with normal or equivocal radiographic findings.
The classic CT finding in Pneumocystis pneumonia is extensive ground-glass attenuation, which corresponds to the presence of intraalveolar exudate, consisting of fluid, organisms, and debris. It is often distributed in a patchy or geographic fashion, with a predilection for the central, perihilar regions of the lungs. Ground-glass attenuation is occasionally accompanied by thickened septal lines, and foci of consolidation may also be evident in severe cases. In up to a third of cases of Pneumocystis pneumonia, ground-glass opacities are accompanied by cystic lung disease. Such cysts have an upper lobe predominance and demonstrate varying sizes and wall thicknesses.
Calcified lymph nodes are usually benign, and they are often related to granulomatous processes, such as TB, histoplasmosis, or sarcoidosis. Neoplastic causes of calcified lymph nodes are less common. They include metastases from mucinous adenocarcinomas and lymphoma. With regard to lymphoma, calcification is frequently seen following radiation therapy, but it is rarely encountered in untreated cases.
Ossified lymph nodes are a rare manifestation of metastatic osteosarcoma. Such nodes appear similar to calcified lymph nodes. In patients with osteosarcoma, the presence of lymph node metastases portends a poor prognosis. Lymphatic involvement is usually accompanied by metastases within the lung, a common site of metastases. Lung metastases frequently demonstrate ossification.
Septic infarcts most often originate from right-sided tricuspid endocarditis or from infected thrombi within systemic veins. Other sources include septal defects, central venous catheters, and pacemaker wires. On chest radiographs and CT scans of patients with septic infarcts, you may observe poorly defined nodular opacities and areas of wedge-shaped parenchymal opacification. Such opacities are usually peripheral in location, and they have a predilection for the lower lobes. Cavitation is frequently observed, particularly on CT scans. A characteristic finding on CT scans is the identification of feeding vessels leading to the nodules (arrows in the second figure) and wedge-shaped parenchymal opacities. Thus, the CT finding of cavitating nodules with feeding vessels is highly suggestive of septic infarcts.
Bronchopleural fistula is a relatively uncommon but serious complication following pneumonectomy, with a prevalence of up to 5% and a mortality rate of approximately 20%. Major predisposing factors relate to operative causes of bronchial ischemia, such as a long bronchial stump, too proximal a ligation of the bronchial arteries, and disruption of bronchial blood supply from extensive lymph node dissection. Additional risk factors include preoperative radiation therapy, steroid therapy, malnutrition, and resection through tumor or infection.