Pneumonia in infants and children: Radiological-pathological correlation

Pneumonia in Infants and Children: Radiological-Pathological Correlation Richard I. Markowitz and Eduardo Ruchelli

NFECTIONS OF THE lung in infants and children are common clinical problems encountered daily by pediatricians and primary care providers. Although clinical symptoms and signs are helpful indicators of the presence of disease as well as etiology, radiographic investigation is often used to confirm a clinical diagnosis and to help sort out whether or not antibiotics or more extensive workup is necessary.1 The chest radiograph is a relatively good macroscopic representation of the anatomy and aeration pattern of the lungs and can depict the extent and distribution of the pathological infectious process. Because the chest radiograph is highly sensitive, but not often specific for the cause, determination of the infecting organism should not be based solely on radiographic findings5 -5 Nevertheless, the radiographic pattern of disease is an accurate reflection of a combination of factors including the route of infection, pathophysiological characteristics of the organism, the patient's age and health status, and the ability of the lung to respond to the infectious insult. Epidemiological and immunological considerations are other important factors to consider during radiological interpretation. This review highlights the major radiological patterns of pulmonary infection in infants and children and correlates these findings with the underlying pathology and clinical manifestations of disease.

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COMMON RADIOLOGICAL PATTERNS OF PNEUMONIA

In general, pulmonary infection in infants and children tends to manifest itself on conventional chest radiography in one of several ways: (1) diffuse peribronchial thickening, (2) focal lobar consolidation, or (3) a delicate, patchy interstitial pattern. Other patterns and combinations of patterns also occur, and there is much clinical variation. 6 These patterns correlate with the anatomic and pathological distribution of the disease within the airways and lung parenchyma. A frequent pattern seen in young infants is caused by diffuse viral infection predominantly involving the airways and referred to as bronchiolitis. When there is extension of the infection and inflammatory re-

sponse into adjacent lung tissue, the situation can be termed diffuse viral bronchopneumonia. BRONCHIOLITIS AND BRONCHOPNEUMONIA

Viral infections constitute most acute bronchopulmonary infections in young children and display a broad range of clinical severity. Respiratory syncytial virus is the most common cause, but other common pathogens include various types of parainfluenza and adenovirus. 7 Most of these moderately contagious infections are acquired by inhalation of infectious material via airborne spread and often occur in epidemic cycles. Mucosal disease is predominant and may extend down the airway to involve both large and small bronchi and especially bronchioles. Edema of the mucosal linings and an outpouring of secretions can lead to narrowing of the airway, which often becomes physiologically significant at the level of the smaller airways where marked impedance of airflow can occur. This, in turn, will lead to trapping of air within the lung manifest radiographically as hyperinflation. Uncomplicated bronchiolitis is a self-limited viral illness of infants manifest clinically by fever, tachypnea, and wheezing. As edema narrows the smaller air passages, diffuse air trapping throughout the lungs occurs with an increased residual lung capacity. Radiographic signs consist chiefly of diffuse overinflation as indicated by flattening and downward sloping of the hemidiaphragms, increased convexity of the anterior chest wall, and widening of the intercostal spaces, often with lung bulging between the ribs (Fig 1). Mild peribronchial thickening is variable. Patients typically recover without incident, and there is no need for further radiological examination. In severe cases of diffuse viral infection, necrotizing bronchiolitis with sloughing of the epithelium and extensive exudate can lead to complete occluFrom the Departments of Radiology and Pathology, The Children's Hospital of Philadelphia, and University of Pennsylvania School of Medicine, Philadelphia, PA. Address reprint requests to Richard L Markowitz, MD, Department of Radiology, The Children's Hospital of Philadelphia, 34th St & Civic Center Blvd, Philadelphia, PA 19104. Copyright © 1998 by W.B. Saunders Company 0037-198X/98/3302-000858.00/0

Seminars in Roentgenology, Vol XXXlll, No 2 (April), 1998: pp 151-162

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Fig 1. Viral bronchiolitis in a 1-month-old infant. (A) Frontal and (B) lateral chest radiographs show diffuse hyperinflation with widening of the intercostal spaces, flattening of the hemidiaphragms, and anterior bowing of the chest wall.

sion of the airway (Fig 2). Thus, when mucous secretions become thick and inspissate, complete plugging of the affected bronchus will result in segmental atelectasis. This frequently involves portions of the right upper lobe and left lower lobe in a segmental distribution. When there is sufficient decrease in ventilation, hypercarbia and hypoxemia can develop necessitating ventilatory support.

Fig 2. Respiratory syncytialvirus bronchiolitis. Photomicrograph (H&E, high power) of lung of a former premature, 3-month-old infant who died of RSV pneumonia. The lumen of a bronchiole is filled with cellular debris secondary to extensive necrosis of the bronchiolar epithelial lining. A typical multinucleated cell is present in the center of the field. The cuboidal cells lining the bronchiole represent early epithelial regeneration.

Inflammation may also extend out into the lung tissue beyond the bronchi and bronchiolar walls. This can produce a radiographic pattern of shaggy peribronchial infiltrates radiating out from the central, perihilar regions (Fig 3). Peribronchial cuffing or thickening, indicated by the circular doughnut-like appearance of major bronchi seen in cross section or as parallel linear "tram-track" lines radiating away from the hilus, are frequently seen. Unfortunately, peribronchial thickening alone is

Fig 3. Two-year-old with bronchopneumonia and reactive airways disease. Note bilateral, central, peribronchial, shaggy infiltrates and subsegmental atelectasis in the right upper lobe.

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not a reliable or specific sign of infection and can mimic other conditions, such as perivascular edema caused by cardiac disease. Patients with known reactive airway disease and allergy may also demonstrate signs of peribronchial thickening. A common pitfall in the interpretation of pediatric chest radiographs is misinterpretation of expiratory films. The child's normal pulmonary blood vessels are often prominent and accentuated on an radiograph obtained at the end-expiration phase of the respiratory cycle leading to misdiagnosis of perivascular edema or infection. Under these circumstances, spurious peribronchial thickening can lead to the erroneous diagnosis of viral pneumonia. Although the pattern of central peribronchial thickening and hyperinflation with or without scattered areas of subsegmental atelectasis is typical of viral infections in infants and small children, bacterial and other infections may present with a similar radiological pattern of disease. For example, despite widescale immunization, cases of permssis continue to occur and typically mimic the radiographic pattern of viral bronchopneumonia (Fig 4). 8 Bacterial bronchopneumonia, also called "focal" pneumonia, 9 is characterized by acute inflammation of the centrilobular portion of individual pulmonary lobules (Fig 5). Coalescence of individual lobular lesions is not infrequent, therefore the differentiation of lobar from focal bronchopneumonia is not always clear.

Fig 4, Pertussis bronchopneumonia in a 4-week-old female with markedly elevated white blood cell count and respiratory failure, Bilateral areas of radiating segmental atelectasis and infiltrate progressed rapidly to dense bilateral consolidation,

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Fig 5. Gross pathology specimen of acute bacterial bronchopneumonia. Note small white areas of consolidation centered around bronchioles (small arrows) on the cut surface of the right upper lobe. The inflammatory process is more confluent near the hilar region of the middle lobe (large arrow) where the pattern is similar to that of lobar pneumonia. Marked hilar adenopathy is also present.

As an additional pitfall in diagnosis, patients with bronchopulmonary viral infections can develop secondary bacterial infections, related to altered immunity and exposure to ubiquitous pathogens. Such secondary infections may be difficult to treat and carry a worse prognosis than the original infection alone (Fig 6). In fact, many deaths due to the major influenza epidemics in the past have been attributed to secondary bacterial pneumonia and sepsis. Although most infants and children recover from viral bronchopneumonia uneventfully, some go on to require hospitalization and a small percentage will require intubation and ventilatory support. The long-term consequences on the growing lung are not entirely known, although cases of obliterative

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bronchiolitis and unilateral hyperlucent lung (Swyer-James) syndrome have been attributed to previous viral infection. It is also postulated that many cases of reactive airway disease in older children are based on alterations of airway dynamics and reactivity induced by a previous viral bronchopneumonia in infancy. BACTERIAL LOBAR PNEUMONIA

The second distinctive pattern of pulmonary infection in children is lobar consolidation. Often involving several adjacent segments or one or more lobes, this focal process of airspace obliteration is typically the result of bacterial infection. The route of infection is not entirely understood, but is most likely the result of aspiration of infectious material. 1° Depending on the virulence of the infecting organism and the underlying host resistance, the inflammatory response can vary in severity. The initial inflammatory response consists of an outpouring of serous exudate into the alveolar air spaces filling them with fluid and displacing air. 11 Vascular congestion and rapid proliferation of bacteria ensue. This, in turn, induces enormous numbers of acute inflammatory cells, especially neutrophils and macrophages, causing further dense consolidation.12 Extravasation of erythrocytes causes a beefy red gross appearance and consistency (Fig 7). At this point, the affected lobe has lost all compliance although the total volume may not be greatly reduced. A fibrinous pleuritis is a common

Fig 7. Lobar pneumonia (gross pathology specimen). The cut surface of the consolidated right middle and lower lobes is dark. There are scattered areas (arrows) that appear dry and granular owing to fibrin deposition in the air spaces. The uninvolved upper lobe has a lighter color and remained crepitant to touch.

Fig 6. Necrotizing Pseudomonas pneumonia in a 15-yearold girl who had a preceding viral illness. A supine, frontal chest radiograph shows extensive, bilateral, coarse, nodular foci of consolidation, which coalesce in the lower lobes. A few of the nodules have cavitated (arrows) and there is a moderate right effusion.

associated feature and helps explain the common symptom of chest pain on inspiration. Lymphatic spread within the lobe may result in widespread consolidation, but not all parts of the lung are affected by the same phase of the inflammatory process simultaneously. Resolution is more gradual and depends on many factors, especially the use of appropriate antibiotics. Under usual circumstances, normal lung architecture is eventually restored; however, particularly severe infections can lead to complications of

PNEUMONIA IN INFANTS AND CHILDREN

tissue necrosis and abscess formation, which may result in fibrotic scars. Clinically, these patients commonly demonstrate high fever, malaise, cough, and chest pain on inspiration. A history of a preceding viral upper respiratory infection is not uncommon, but otherwise normal, healthy children can develop the disease. Chronic debilitation, malnutrition, and lower immunity are also predisposing factors. The initial inflammatory edema may produce rales on chest auscultation, but diminished or absent breath sounds are more characteristic of true consolidation. Pleural friction rubs are variably heard. Abdominal pain and vomiting are not uncommon signs of lobar pneumonia in children, especially when the infiltrate involves a basilar segment of the lower lobe. At times, these symptoms may predominate creating the false impression of acute appendicitis. 13 Radiological findings of lobar pneumonia typically consist of air space obliteration confined to a segment or lobe (Fig 8). Air bronchograms, although not always visible, are typical. Because the consolidated lung becomes fluid filled and heavy, there is regional loss of lung compliance. Thus, it is sometimes difficult to distinguish lobar consolidation from primary atelectasis secondary to mucous plugging or other causes. (Indeed, infection distal to an obstructed bronchus is not unusual. When chronic and persistent, postobstruetive pneumonia can lead to chronic bronchiectasis and irreversible

Fig 8. Lobar pneumonia. Consolidation of the lingula due to pneumococcal pneumonia. Note mild elevation of the hemidiaphragm and decreased intercostal spaces on the left related to volume loss secondary to the consolidation and splinting caused by pleuritic chest pain,

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destruction of lung parenchyma.) However, signs of lobar atelectasis include distortion of the fissures, mediastinal shift, and compensatory overinflation of adjacent normal lung. Although consolidation due to infection results in nonaerated, noncompliant lung parenchyma, the signs of true volume loss are usually absent. Because of the pleural irritation and pain that frequently accompany the infection, patients are reluctant to breathe deeply resulting in diminished volume of nonconsolidated lung on the affected side. Bacterial consolidative pneumonia in otherwise normal healthy children is most frequently caused by Streptococcus pneumoniae--the common pneumococcus. Since the advent of widespread immunization against Hemophilus influenza, it is quite unusual to see pulmonary infection secondary to that organism, although rare cases do spring up from time to time. Staphylococcal pneumonia in infants, once a dreaded problem in neonatal nurseries, is less often encountered in the United States. Occasionally, a lobar pneumonic infiltrate assumes a round or spherical shape on frontal radiographs, which can be mistaken for a true mass (Fig 9). Such "round" pneumonias often involve the lower lobes especially the superior segments. Lateral or other projections are helpful in revealing features that confirm the diagnosis of pneumonia. These patients respond no differently to treatment and are predominantly of interest because of their curious radiographic appearance. Complications of pneumococcal pneumonia are relatively uncommon, but there has been a recent increase in the number of cases associated with parapneumonic effusion (Fig 10), empyema, and lung necrosis. 14 The reasons for this apparent increased frequency of complicated pneumonia among otherwise normal children are not clear, although a change in the virulence of certain pathogenic strains and the widespread use of antibiotics are possibilities. These complicated pneumonia cases are characterized by consolidation of one or two lobes and very often involve the lower lobe on either side. Associated pleural effusion may be transudate or exudate and can be large enough to cause mediastinal shift and significant respiratory compromise. Computed tomography (CT) can be very helpful in these cases demonstrating areas of nonperfusion, lung necrosis, abscess formation, and pleural loculation. Chest tube drainage and

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Fig 9. "Round" pneumonia in a 7-year-old presenting with cough and fever. (A) Frontal view shows round, "mass'Mike consolidation in the right mid chest through which a smaller, less regular density is apparent. (B) The lateral view confirms lobar pneumonia of the superior segment of the right lower lobe as well as prominent, adjacent, hilar adenopathy.

thoracoscopic debridement may be indicated in extreme circumstances. Lung abscess is uncommon in children and may suggest an underlying aspiration or necrotizing pneumonia secondary to gram-negative rods or

staphylococcus. 15 Hyper immunoglobulin E syndrome is a rare condition characterized by recurrent staphylococcal abscesses, which can involve the skin, lung, and joints. Multilobar consolidation of the lung with mixed

Fig 10. Pneumonia with pleural effusion in a 5-year-old presenting with fever, tachypnea, and chest pain. (A) Frontal, erect chest radiograph shows lingula and lower lobe consolidation on the left with a large effusion. Scoliosis toward the left and dilated bowel loops below the left hemidiaphragm are also present. (B) Contrast-enhanced CT scan at the level of the heart shows a large effusion as well as hyperemic enhancement of the consolidated lower lobe with air bronchograms. A thin, peripheral rim of pleural enhancement is present.

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flora, especially in debilitated or neuromuscularly impaired patients, can suggest aspiration pneumonia (Fig 11). Abnormal swallowing or silent aspiration secondary to gastroesophageal reflux can result in repeated episodes of tracheobronchial

Fig 11. Bilateral aspiration pneumonia in a neurologically impaired 1-year-old. (A) Supine chest radiograph shows bilateral, segmental areas of consolidation, which radiate from the center into the dependant portions of lung. (B) Lateral cervical esophagram obtained at the time of a modified barium swallow examination shows contrast penetration of the glottis and aspiration into the subglottic trachea.

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aspiration. Significant aspiration of gastric contents can also cause extensive chemical pneumonitis. Follow-up radiographic study of uncomplicated lobar pneumonia is not indicated when the clinical response to antibiotics is rapid and complete. The findings on chest radiographs lag behind the patient's clinical improvement by days or weeks and should not be a cause for alarm. Total clearing of parenchymal infiltrate is expected after 1 to 2 weeks but may take longer in more virulent infections. Visible scarfing as a sequela of uncomplicated lobar pneumonia is uncommon. Children with sickle cell anemia are prone to acute chest syndrome (ACS), which may be impossible to differentiate from simple lobar pneumonia. Indeed, ACS cases in young children are more commonly associated with infection than adult cases. 16Clinical symptoms include fever and cough, but chest pain is less common than in adults. Etiology is multifactorial and has been related to infection and infarction. It has been hypothesized that regional alveolar hypoxemia, perhaps initiated by infection, leads to microvascular occlusion by abnormally adherent or nondeformable sickle erythrocytes. Regional vasoconstriction ensues further slowing regional perfusion and entrapment of cells leading to further hypoxic damage. 17 Restoring adequate oxygenation as well as appropriate antibiotic therapy are the main therapeutic goals. Blood transfusion can improve oxygenation in children with ACS and can be a valuable adjunct to therapy in some cases, lg Chest radiographs may be normal in the early stages of ACS, but often progress to lobar consolidation, which is very dense and extensive (Fig 12). Associated small to moderate pleural effusion is not uncommon. High-resolution, thin-section CT scan has been used to diagnose microvascular occlusion in ACS and to try to distinguish between infection and infarction. 19 Nevertheless, because of the high association with infection in children, withholding antibiotics on the basis of CT scan findings is probably not warranted. Although Streptococcus pneumoniae is the most common organism associated with ACS in the United States, other infectious agents including ChIamydiapneumoniae and Mycoplasma pneumoniae have been reported to occur commonly in local regions. 2° Recurrence of ACS has been reported as high as 80%. Repeated episodes have been implicated as a contributing factor to the development of early pulmonary deterioration especially in young

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intensive. Immunocompromised individuals are especially at risk for overwhelming disease. Radiological signs are nonspecific, but there is usually less extensive and less-dense parenchymal infiltrate. A diffuse reticulonodular interstitial pattern can be seen in less than one third of cases (Fig 13). Pleural effusion is unusual. UNUSUAL PATTERNS OF PNEUMONIA

Fig 12. Acute chest syndrome (sickle cell disease}. Frontal chest radiograph of a 6-year-old girl showing extensive bilateral lower lobe consolidation and cardiomegaly.

adults, 21 Multifocal interstitial scarring on thinsection CT has been correlated with scarring from multiple episodes of ACS in adults. 22 Chest radiographs in children may also demonstrate subtle interstitial changes following a bout of ACS and should not be misinterpreted as evidence of new disease.

Uncommonly, acute pulmonary infection may lead to an overwhelming inflammatory response involving most, if not all, of the lung and frequently leading to severe respiratory compromise and death. Neonates and immunocompromised individuals are especially prone. Causes include beta-hemolytic streptococcus,24 herpes, Pneumocystis carinii, and cytomegalic inclusion virus among a long list of organisms. Rapid and progressive consolidation leads to complete opacification of the lungs (Fig 14). Complications of ventilatory support include interstitial extravasation of air, that is, pulmonary interstitial emphysema, pneumomediastinum, pneumothorax, pneumopericardium, and air embolism. Mortality is high, but if patients survive, recovery is usually long and protracted. In premature neonates, the radiological findings may be indistinguishable from severe primary surfactant deficiency, but the poor response to surfactant administration and

INTERSTITIAL PNEUMONITIS

A third distribution pattern of pulmonary infection consists of a less dense, reticular, or linear area of infiltrate, which can be a single focus or multiple patchy areas in one or both lungs. These "atypical" pneumonias vary widely in severity and time course. M. pneumoniae is the prototypical, but not exclusive cause? 3 This disease is often seen in older children and adolescents and may have a long and protracted, but not very morbid, course. Patients complain of low-grade or intermittent fever and fatigue. Cough is common and may persist for weeks. Pathologically, the nature of the disturbance is variable, and only the most severe cases are available for study. In general, the walls of the alveoli and interstitial septa are predominantly affected with relative sparring of the alveolar air spaces. Lymphocytes, macrophages, plasma cells, and edema are characteristic. With more virulent organisms or secondary bacterial infection, the inflammatory response will be more extensive and

Fig 13. Atypical pneumonia (Nlycoplasma) in a 14-year-old boy presenting with a 1-week history of low-grade fever, dry cough, and wheeze. Note diffuse interstitial pattern without cardiomegaly or effusion.

PNEUMONIA IN INFANTS AND CHILDREN

Fig 14. Overwhelming pulmonary consolidation due to perinatally acquired herpes in a neonate. Although the lungs were clear on the first day of life, there was a rapid and inexorable progression of diffuse pneumonia as shown on the radiograph, despite antiviral therapy, leading to death on the fifth day.

ventilator support helps differentiate pneumonia from respiratory distress syndrome. Another unusual radiological pattern of pulmonary infection in children is widespread nodules that may range in size from very small to greater than 1 cm. CT is more sensitive for detection and can demonstrate early calcification more readily. The infectious causes of this pattern include varicella, measles, histoplasmosis, and miliary tuberculosis. Bilateral consolidation with large, ill-defined nodular densities that can cavitate can be seen in cases of septic embolization and gram-negative sepsis. In children with AIDS, a nodular pattern may be due to lymphocytic interstitial pneumonitis (LIP) (Fig 15), which is a relatively benign, mildly symptomatic condition wherein aggregates of lymphocytes collect within the interstitium of the lung in clumps (Fig 16). When severe, it may interfere with normal lung compliance causing mild to moderate respiratory symptoms. The cause of LIP is still controversial, but it seems clear that it is an overreaction of lymphoid tissue within the lung to some inciting agent, most probably Ebstein-Barr virus, which is ubiquitous among children. It is also interesting that those AIDS patients who develop LIP are less likely to develop more serious lung infections such as P. carinii pneumonia because of their better immunocompetence, The radiographic findings of early P. carinii pneumonia in children are variable, but often appears as a fine, almost

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Fig 15, Lymphocytic interstitial pneumonitis (LIP) in a relatively asymptomatic 2-year-old with AIDS. Note the diffuse reticulonodular interstitial pattern and mild hilar adenopathy.

Fig 16. Pathology of LIP in a child with AIDS. Gross specimen of lung shows distinct white nodules (arrows) representing aggregates of lymphocytes and plasma cells. The consolidated appearance of the lung is due to the diffuse interstitial infiltrate that accompanies the nodule formation. There is marked lymphoid hyperplasia involving hilar nodes.

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emphysema, occur in the more severe cases requiring major ventilatory support. PULMONARY TUBERCULOSIS IN INFANTS AND CHILDREN

Fig 17. Overwhelming P carinfipneumoma in a child with AIDS. Note the widespread air space infiltration sparing only a small portion of the left upper lobe.

granular, interstitial infiltrate in the dependent portions of the lung, which progresses to more diffuse consolidation and opacification of the lung (Fig 17). Alveolar fluid containing the organism confirms the diagnosis, but biopsy reveals extensive interstitial disease as well (Fig 18). Complications of air block, especially pulmonary interstitial

The clinical and radiological presentation of primary tuberculosis infection in children ranges from quite benign and unnoticeable to overwhelming and fatal. 25 Infections are acquired via airborne spread through close and repeated contact with actively infected persons who usually have secondary or reactivation disease. Malnutrition, poor health conditions, overcrowding, and other social maladies are well-known predisposing factors, although affluent and well-cared-for children are not entirely immune. Once thought to be eradicated as a significant public health problem in the United States, tuberculosis has made a small but significant comeback and should not be discounted as a disease of the past. The pathogenesis of primary tuberculous infection is well knownH: aspirated tubercle bacilli implant on alveolar walls often in a subpleural

Fig 18. Pathology of P carinfi pneumonia. Photomicrographs (H & E) at (A) low and (B) high power show alveoli containing characteristic eosinophilic "frothy exudate" in which cysts were demonstrable using special stains. The interstitium is also expanded by a lymphohistiocytic infiltrate.

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location. A predominantly histiocytic response develops leading to the development of a small tubercle. An allergic response leads to lymphatic enlargement of the draining tracheobronchial nodes. Hilar nodes may be quite large in proportion to the original site of infection. In most cases, the primary lesion is walled off by a fibroblastic response eventually leading to the development of a small granuloma. In some cases, especially infants, the primary infection is poorly controlled by the body's defense mechanism, and more extensive inflammation occurs at the primary site leading to more extensive pulmonary consolidation. Hematogenous spread of the disease can produce widespread infection throughout the lungs giving rise to the miliary pattern. Hepatic and meningeal spread can produce devastating results. Bronchogenic spread of disease can give rise to extensive pulmonary infection especially in neonates. Radiological patterns of primary tuberculosis include a small patchy subpleural focus of infiltrate, regional hilar adenopathy usually unilateral, atelectasis secondary to extensive hilar and mediastinal adenopathy (Fig 19), multilobar pneumonia, or a diffuse nodular interstitial pattern. Pleural effusion may also occur but is less common. As a practical matter, one should consider the diagnosis of primary tuberculosis when there is a history of household contact, when small infiltrates persist despite the usual antibiotic therapy, and when unilateral hilar and or paratracheal adenopathy is detected. SUMMARY

The radiographic characteristics of pulmonary infection in children are many and varied. Although typical patterns are helpful in diagnosis, clinical and laboratory evaluation provide important diagnostic information. An understanding of the basic pathophysiology of infection and an appreciation of the anatomy of the child's growing lung help provide clearer, insightful, and more accurate radiological interpretation.

Fig 19. Primary tuberculosis in a 6-year-old child presenting with fever, cough, and wheezing. (A) Detail of the frontal chest radiograph shows right hiiar and infrahilar densities with splaying and narrowing of the main bronchi. (B) Contrastenhanced CT scan just below the tracheal bifurcation shows a large, posterior mediastinal, conglomerate mass of necrotic nodes with adjacent partial collapse of the right lower lobe. Because a neoplasm was initially suspected, surgical biopsy was performed confirming the diagnosis of tuberculosis.

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