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Imaging Role in Pulmonary TB Diagnosis and Treatment
- 1. PULMONARY TB PRESENTED BY :DR ALMA SWATHI DSOUZA MODERATOR: DR KRISHNA KIRAN
- 2. “ Role of imaging in CTB ▪ Diagnosis ▪ Treatment evaluation- response assessment, residual activity ▪ Detection of disease complications/sequelae. 2
- 3. CXR ▪ initial investigation ▪ evaluate unexplained cough ▪ Apicogram/lordotic view (for lung apices) and lateral view are of limited utility 3
- 4. USG ▪ Pleural effusion detection, characterization, guiding drainage, and follow-up. ▪ Differentiating minimal effusion from residual thickening 4
- 5. CT ▪ Assessing disease activity, and evaluating complications ▪ CECT is IOC for mediastinal LN ▪ HRCT detect miliary and centrilobular nodules 5
- 6. MRI ▪ problem-solving modality ▪ T1 and T2W + DWI & subtracted CE ▪ evaluate mediastinal nodes and assess disease activity 6
- 7. FDG-PET) ▪ work-up of PUO ▪ sensitive in detecting infection, inflammation & malignancy ▪ Active TB shows increased uptake ▪ pose as a cancer mimic 7
- 8. “ Primary MTB Progressive primary MTB Post Primary MTB 8
- 9. Primary Tuberculosis Lymphadenopathy Parenchymal Disease Pleural Effusion Airway Disease 9
- 10. Lymphadenopathy ▪ M/C radiologic manifestation of primary TB ▪ Right paratracheal and hilar lymph nodes ▪ low-attenuation center with peripheral rim enhancement- Rim sign ▪ D/D: Nontuberculous mycobacterial infection Lymphoma Metastatic carcinoma 10
- 11. 11
- 12. 12
- 13. Parenchymal Disease ▪ + Cavitation progressive primary disease ▪ ~ bacterial pneumonia ▪ + lymphadenopathy can be a clue ▪ Slow resolution , 2 years ▪ On CT, the air-space consolidation in primary TB is dense, homogeneous, and well-defined 13
- 14. 14
- 15. “ “Ghon Lesion” ▪ focus is a granuloma ▪ sequela of primary tuberculosis. “Ghon Complex” parenchymal granuloma + hilar LN “Ranke complex” late fibrocalcific lesions of the lung and lymph node evolved from the Ghon complex 15
- 16. “ 16
- 17. Pleural Effusion ▪ 25% of primary TB in adults ▪ Unilateral ▪ L/C in children ▪ L/C in post primary disease ▪ Tuberculous empyemas typically loculated associated with pleural thickening and enhancement, ▪ complicated with bronchopleural fistula or extension into the chest wall (empyema necessitatis) 17
- 18. 18
- 19. 19
- 20. 20
- 21. 21 Cold abscess
- 22. Airway Disease ▪ Bronchial wall involvement seen in primary and postprimary tuberculosis ▪ Bronchial stenosis occurs in 10%–40% of patients with active tuberculosis Main radiographic features: ▪ segmental or lobar atelectasis ▪ lobar hyperinflation ▪ mucoid impaction ▪ postobstructive pneumonia 22
- 23. 23
- 24. 24
- 25. Miliary Tuberculosis ▪ Hematogenous dissemination ▪ Immunocompromised and pediatric patients ▪ Occur in primary or postprimary tuberculosis ▪ Chest radiograph or CT image diffuse 1–3-mm nodules in a random distribution 25
- 26. 26
- 27. “ 27
- 28. Postprimary Tuberculosis ▪ Reactivation of dormant MTB infection ▪ 2nd infection with different strain ▪ Apical and ULZ predominance 28
- 29. “ 1. Liquefaction of caseous necrosis 2. Formation of cavities 3. Progressive fibrosis and lung destruction 4. Bronchogenic spread. 29
- 30. Hallmarks of active PPT ▪ Consolidations ▪ alveolar opacities on CXR ▪ clustered nodules ▪ centrilobular nodules on CT 30
- 31. Consolidation and cavitation ▪ Patchy, poorly marginated consolidation ▪ strong predilection for the apical and posterior segments of UL & superior segments LL ▪ 3%–6% a noncalcified nodule known tuberculoma may be predominant manifestation 31
- 32. Postprimary tuberculosis ▪ Cavitation is a common finding ▪ Several centimeters in largest dimension and develop thick and irregular walls ▪ Seen within areas of consolidation and may be multifocal 32
- 33. 33
- 34. 34
- 35. 35
- 36. 36
- 37. 37
- 38. 38
- 39. 39
- 40. Centrilobular nodules ▪ Endobronchial spread ▪ Caseous necrosis & granulomatous inflammation fill respiratory bronchioles & alveolar ducts ▪ Manifests radiologically as centrilobular nodules & tree-in-bud sign ▪ 95% of cases of active tuberculosis 40
- 41. 41
- 42. Tuberculosis in Immunocompromised Patients ▪ higher risk of developing primary & postprimary TB ▪ severely immunosuppressed patients with PTB, CXR may be normal ▪ immune reconstitution inflammatory syndrome 42
- 43. 43
- 44. 44
- 45. 45
- 46. 46
- 47. 47
- 48. Tuberculoma ▪ persistent nodules or mass-like lesions ▪ seen in both primary TB and PPT ▪ subcentimetric to 5 cm in diameter ▪ solitary or multiple ▪ satellite lesions around main lesion. 48
- 49. Pediatric Tuberculosis ▪ M/C form of active TB in children is primary disease ▪ Hilar & mediastinal lymphadenopathy hallmark of pediatric TB ▪ 0–3 yrs 50% of cases isolated lymphadenopathy ▪ 5–14 yrs 9% . ▪ Extrinsic compression of adjacent bronchi airway compression or postobstructive pneumonia 49
- 50. Latent Tuberculosis ▪ + lab tests in absence of radiographic or clinical E/O active disease ▪ stable fibronodular changes, including scarring & nodular opacities in apical & ULZ ▪ Fibronodular change is associated with higher risk of TB reactivation 50
- 51. 51
- 52. 52
- 53. 53
- 54. ▪ Parenchymal complications ▪ Aspergilloma colonization in tuberculous cavities. ▪ Destructive lung changes ▪ Scar carcinoma ▪ Airway complications ▪ Vascular complications ▪ Pleural complications ▪ Mediastinal complications 54 Complications of CTB
- 55. 55
- 57. 57 Nontuberculous mycobacterial disease ▪ Mycobacterium avium complex & Mycobacterium kansasii ▪ manifests in two major forms: classic (cavitary) and nonclassic (bronchiectatic)
- 58. Classic (cavitary) nontuberculous mycobacterial infection ▪ Classic same as postprimary tuberculosis ▪ upper lobe cavitary lesions and centrilobular and tree-in-bud nodules 58
- 59. 59
- 60. 60
- 61. 61 nonclassic (bronchiectatic) nontuberculous mycobacterial infection ▪ manifests as chronic bronchiectasis and bronchiolitis ▪ mid to lower lung zone predominance
- 62. “ 62
- 63. THANK YOU
Editor's Notes
- CXR – part of the initial investigations performed in adults suspected to have TB. evaluate unexplained cough. It is the primary modality for diagnosis and follow-up, and may be the only imaging required in sputum-positive cases. Apicogram/lordotic view (for lung apices) and lateral view are of limited utility CT is the next investigation in case of equivocal CXR.
- USG - Sonography is very useful for pleural effusion detection, characterization, guiding drainage, and follow-up. Helps in Differentiating minimal effusion from residual thickening also be used to evaluate associated hepatosplenomegaly, ascites, and abdominal lymphadenopathy
- It enables earlier and more accurate diagnosis of pulmonary lesions can be used to differentiate the etiologies of pneumonia. evaluation of bronchiectasis, cavitation, associated fungal balls, and assessment of necrosis in the LNs, identifying pleural/airway/diaphragmatic pathologies and evaluating visualized bones. CECT is the investigation of choice for evaluation of mediastinal LNs and also aids in depicting pleural enhancement in empyema. HRCT detect miliary and centrilobular nodules, ground-glass opacities, and air-trapping.
- MRI - MRI is a problem-solving modality and conventional sequences (T1 and T2W images) should be combined with diffusion-weighted imaging (DWI) and subtracted contrast-enhanced (CE) imaging for optimal evaluation. Presence of diffusion restriction in the LNs and peripheral enhancement suggest active disease. It can be used to better evaluate mediastinal nodes and assess disease activity Since it is free from ionizing radiation, MRI can be employed for follow-up of mediastinal nodal disease in young patients to reduce radiation exposure. MRI has been proven to be superior to non-contrast CT in the evaluation of mediastinal nodes, pleural abnormalities, and presence of caseation.
- fluorodeoxyglucose -positron emission tomography (FDG-PET) plays an important role in the work-up of patients with pyrexia of unknown origin (PUO), high sensitivity in the detection of infection, inflammation, and malignancy. Active TB shows increased uptake with high standardized uptake values (SUVs) and may pose as a cancer mimic.
- Several different patterns of tuberculous infection have been described, These include primary MTB, progressive primary MTB, and post primary MTB. Traditionally, primary TB was considered a disease of childhood, and postprimary tuberculosis was believed to always represent reactivation of latent infection in adults. these notions to be somewhat inaccurate. Because of more-effective therapies and the declining prevalence of tuberculosis in developed countries, 23%–34% of adult tuberculosis cases in developed countries are actually primary tuberculosis With regard to postprimary tuberculosis, evidence suggests that patients in endemic areas are more likely to be infected by a second strain of tuberculosis than to experience reactivation of a previously infected strain
- Primary TB is acquired by inhalation of airborne organisms and occurs in patients not previously exposed to Mycobacterium tuberculosis Primary TB may involve lung parenchyma, LNs, tracheobronchial tree, and pleura. Classically, four entities are described: Gangliopulmonary TB, TB pleuritis, miliary TB, and tracheobronchial TB. Only the gangliopulmonary form is characteristic of primary TB and the rest may be seen in post-primary disease as well. Gangliopulmonary TB is characterized by the presence of mediastinal and/or hilar LN enlargement with associated parenchymal abnormalities
- Mediastinal and hilar lymphadenopathy is the most common radiologic manifestation of primary tuberculosis Lymphadenopathy typically demonstrates a low-attenuation center with peripheral rim enhancement on CECT due to central caseous necrosis with peripheral granulomatous inflammatory tissue The differential diagnosis of necrotic lymphadenopathy includes nontuberculous mycobacterial infection, lymphoma, and metastatic carcinoma Lymphadenopathy is seen more pediatric cases of primary tuberculosis and than adult cases and typically involves the right paratracheal and hilar lymph nodes. Within the pediatric population, mediastinal and hilar lymphadenopathy may be the only radiologic finding. At resolution of lymphadenopathy, calcified normal-sized lymph nodes
- Lymphadenopathy from primary tuberculosis in a 6-month-old male infant. Axial CECT image shows necrotic mediastinal lymphadenopathy (arrow) and a small right-sided pleural effusion.
- gross pathologic specimen shows tuberculous lymphadenitis with central caseous necrosis
- Parenchymal disease most frequently manifests as consolidation depicted as an area of opacity in a segmental or lobar distribution Cavitation occurs in a minority of patients with primary tuberculosis and when cavitation occurs, it is known as progressive primary disease Parenchymal disease often appears similar to bacterial pneumonia, but the presence of lymphadenopathy can be a clue that points toward primary tuberculosis. Resolution of pulmonary consolidation is generally slow, taking as long as 2 years; and in many cases, residual opacities are seen . After resolution, residual parenchymal scarring can be seen at sites of prior consolidation in 15%–18% of patients and is referred to as a Ghon focus, or Ghon tubercle
- Lymphadenopathy and consolidation in a 6-month-old male infant with primary tuberculosis (same patient as shown in Fig 2). Frontal chest radiograph shows thickening of the right paratracheal stripe, consistent with lymphadenopathy (arrow), and consolidation (arrowhead) in the right middle and lower lobes
- A “Ghon Lesion” or focus is a granuloma in the lung from a previous tuberculous infection. It is a sequela of primary tuberculosis. When there is a combination of a parenchymal granuloma and an involved hilar lymph node on the same side, the two together are called a “Ghon Complex”. The combination of late fibrocalcific lesions of the lung and lymph node which evolved from the Ghon complex is referred to as the “Ranke complex
- Pleural effusion is seen in approximately 25% of primary tuberculosis cases in adults, with majority being unilateral is less common in children also less common in post primary disease Tuberculous pleural effusions usually result from hypersensitivity to tuberculous protein, rather than frank pleural infection; and therefore, isolation of M tuberculosis from pleural fluid is uncommon. In PPT, effusion is usually small, loculated, and associated with parenchymal lesions. Since it originates from rupture of a cavity into the pleural space, cultures are usually positive Tuberculous empyemas are typically loculated and associated with pleural thickening and enhancement If not treated early, tuberculous empyemas may be complicated with bronchopleural fistula or extension into the chest wall (empyema necessitatis) An air-fluid level within an empyema in the absence of instrumentation is suggestive of a bronchopleural fistula (20). After treatment and healing, residual pleural thickening with calcification can develop, potentially leading to fibrothorax
- Multiseptated tuberculous empyema. US image shows numerous linear echogenic structures in the pleural cavity representing multiple septa, findings that are typically seen in postprimary tuberculosis.
- Tuberculous empyema Axial CECT image shows a loculated right-sided pleural effusion with thickened, enhancing pleura (arrows) as well as infiltration of the extrapleural fat (arrowhead).
- Empyema necessitatis in a 35-year-old man with chronic empyema related to tuberculosis. Axial nonenhanced chest CT image shows pleural calcifications (arrowheads), a loculated pleural effusion with marked pleural thickening, and extension into the chest wall (arrows).
- Usual clinical feature are painless cystic masses without inflammatory signs on the skin giving the appearance of a cold abscess or a solid tissue mass and can be sometimes mobile. However, it affects the ribs more than the sternum, clavicle and vertebra Chest computed tomography showing anterior chest wall mass B: Chest computed tomography findings showing anterior chest wall abscess with pleural involvement and multilocular form.
- Bronchial wall involvement may be seen in primary and postprimary tuberculosis, although it is more common in the former Bronchial stenosis occurs in 10%–40% of patients with active tuberculosis and is due to direct extension from tuberculous lymphadenitis by means of endobronchial or lymphatic dissemination The main radiographic features of proximal airway involvement are indirect, including segmental or lobar atelectasis, lobar hyperinflation, mucoid impaction, and postobstructive pneumonia. At CT, airway involvement can manifest as long segment narrowing with irregular wall thickening, luminal obstruction, and extrinsic compression Calcified peribronchial LNs can erode into or cause distortion of adjacent bronchus (more common on the right side), producing broncholiths. Presence of calcium near an area of lung collapse may be a subtle indicator of broncholithiasis.
- Airway involvement with tuberculosis in a 41-year-old woman. chest radiograph shows right upper lobe collapse (arrow).
- (b) Coronal CECT image at the level of the central bronchi shows irregular thickening of the right upper lobe bronchus (arrow), as well as right upper lobe volume loss.
- Hematogenous dissemination results in miliary tuberculosis, especially in immunocompromised and pediatric patients. Miliary disease may occur in primary or postprimary tuberculosis. In primary tuberculosis, miliary disease often manifests as an acute, severe illness with high mortality On the chest radiograph or CT image, miliary disease manifests as diffuse 1–3-mm nodules in a random distribution.
- Miliary tuberculosis in a 53-year-old man. Axial chest CT image shows numerous micronodules in a random distribution. Note subpleural (arrowhead) and centrilobular (arrow) nodules.
- Miliary tuberculosis. (a) Radiograph of the left lung shows diffuse 2–3-mm nodules, findings that are typically seen in miliary tuberculosis
- Postprimary tuberculosis is typically thought to result from reactivation of dormant M tuberculosis infection owing to immunosuppression, malnutrition, senility, and debilitation. but may also result from a second infection with a different strain, especially in endemic areas The apical and upper lung zone predominance may be related to the relatively reduced lymphatic drainage and increased oxygen tension in these regions, factors that facilitate bacillary replication
- PPT is characterized by: Liquefaction of caseous necrosis Formation of cavities Progressive fibrosis and lung destruction Bronchogenic spread. Initially, there is liquefaction of regions of caseous necrosis, which then communicate with the tracheobronchial tree to form cavities. Coughing may result in bronchogenic spread to other lung segments
- Imaging in PPT often shows extensive abnormalities in predisposed locations. Features of active endobronchial infection - consolidations, alveolar opacities on CXR, clustered nodules, centrilobular nodules on CT - are hallmarks of active PPT.
- Patchy, poorly marginated consolidation is an early and consistent feature of postprimary tuberculosis Consolidation and cavitation have a strong predilection for the apical and posterior segments of the upper lobes as well as the superior segments of the lower lobes in postprimary tuberculosis
- Cavitation is also characteristic of PPT, radiographically evident in 40% of cases, and walls may be thin and smooth or thick and nodular. Thick-walled cavities and cavities with surrounding consolidation indicate active infection, while thin-walled cavities suggest healed infection. Thin-walled cavities may be difficult to differentiate from bullae, cysts, or pneumatoceles. Air-fluid levels in the cavity occur in 10% of cases and can be due to superimposed bacterial or fungal infection. Fibro-parenchymal lesions causing distortion of lung parenchyma and cicatricial bronchiectasis develop with healing of active infection. Tuberculous cavities can rupture into pleural space, resulting in empyema and even bronchopleural fistula. Erosion into the pulmonary artery branches can lead to massive hemoptysis (Rasmussen pseudoaneurysm). Erosion into systemic vessels or pulmonary veins can lead to hematogenous dissemination and miliary TB. Healing of PPT occurs with fibrosis and calcification.
- Figure 11a. Postprimary tuberculosis in a 50-year-old man. (a)PA chest radiograph shows patchy airspace opacities (arrows) in the right upper lobe, with a cavitary lesion (arrowheads).
- (b) Axial chest CT image shows right upper lobe consolidation (arrows) with associated cavitation (arrowheads).
- Figure 12. Postprimary tuberculosis in a 63-year-old man. Coronal chest CT image shows a thick-walled cavitary lesion (arrow) in the right upper lobe.
- Figure 14a. Tuberculous cavity in a 32-year-old man with hemoptysis. (a)PA chest radiograph shows two left-sided cavitary lesions (arrows), with an air-fluid level in the larger lesion (arrowhead), and scattered reticulonodular opacities.
- (b) Bronchial artery angiographic image shows blush of contrast material around the cavitary lesions (arrow). The patient subsequently underwent bronchial artery embolization.
- (c) Phrenic artery angiographic image shows recruitment of additional vasculature (arrow). Embolization of the superior branch of the phrenic artery was also performed.
- Rasmussen aneurysm in a 42-year-old man with active postprimary tuberculosis and massive hemoptysis . (a) Contrast-enhanced CT scan at the level of the upper lobes shows, in an area of cavitation, a small rounded bilobed enhancing lesion (arrows) that arises from a branch of the pulmonary artery (arrowhead). (b) Conventional angiogram shows contrast material filling two aneurysms (arrowheads) in a segmental branch of the right upper lobe pulmonary artery.
- Centrilobular Nodules.—Active tuberculosis often communicates with the bronchial tree, which results in endobronchial spread (2). Histologically, caseous necrosis and granulomatous inflammation fill respiratory bronchioles and alveolar ducts (Fig 15). This histologic finding manifests radiologically as centrilobular nodules and the tree-in-bud sign (Fig 16). At CT, centrilobular nodules are seen in approximately 95% of cases of active tuberculosis (2). Unlike cavitary lesions and consolidation, centrilobular nodules may be seen in the lower lobes, distant from the cavitary lesions (16). Involvement of the airways and pleura is less common in postprimary than in primary tuberculosis but shows similar imaging features.
- Figure 16. Airway dissemination of tuberculosis in an 86-year-old man with active tuberculosis (different patient from Fig 15). Axial chest CT image shows centrilobular (arrow) and tree-in-bud (arrowhead) nodules, as well as more confluent areas of consolidation.
- Immunocompromised patients are at a higher risk of developing primary and postprimary tuberculosis. For example, HIV-positive patients with latent tuberculosis infection are 20–30 times more likely to develop active tuberculosis, when compared with HIV-negative patients. Although most tuberculosis cases in immunocompromised individuals are related to reactivation of latent tuberculosis, the radiologic and clinical manifestations more closely resemble those of primary tuberculosis (ie, with consolidation and lymphadenopathy) (Fig 17a). In severely immunosuppressed patients with pulmonary tuberculosis, chest radiographs may be normal 10%–40% of the time. Miliary tuberculosis also occurs at a higher rate in patients with severe immunosuppression. Treatment of patients with HIV infection by using highly active antiretroviral therapy in patients infected with tuberculosis may result in a paradoxical worsening of pulmonary disease, an entity known as the immune reconstitution inflammatory syndrome.
- Figure 17a. Primary tuberculosis in a 39-year-old man with AIDS. (a, b) Magnified contrast-enhanced chest CT images from the same CT examination. (a) Coronal reformatted image (soft-tissue window) at the level of the clavicular heads shows necrotic lymphadenopathy (arrow).
- (b) Axial chest CT image (soft-tissue window) at a level just below the carina shows an air collection in the subcarinal region, a finding that represents esophageal perforation with a fistula or sinus tract (arrow) to a necrotic lymph node. (c–e) Sequential magnified axial chest CT images (lung window) at a level just below the carina.
- (c) Three weeks after the onset of administration of highly active antiretroviral therapy, the CT image shows multiple centrilobular nodules (arrows)
- (d) One week later, diffuse consolidation has developed, representing tuberculosis-associated immune reconstitution inflammatory syndrome. A pneumothorax (arrows) is also depicted.
- (e) One month later, after antituberculous treatment, the consolidation has resolved, and the nodules have markedly improved.
- Tuberculoma Tuberculomas are persistent nodules or mass-like lesions which can be seen in both primary TB and PPT. Pulmonary tuberculomas can range in size from being subcentimetric to 5 cm in diameter, and may be solitary or multiple. They are most often the result of healed primary TB and are usually smooth-walled and sharply defined. The majority of these lesions remain stable in size and may calcify. Nodular or diffuse calcification can be seen in 20-30% of tuberculomas. Cavitation is seen in 10-50% of cases. In 80% of cases, small round opacities (satellite lesions) may be observed in the immediate vicinity of the main lesion.
- The manifestation of tuberculosis in pediatric patients differs from that in adult disease. The most common form of active tuberculosis in children is primary disease The likelihood of developing active tuberculosis decreases with age. Older children and adolescents with active tuberculosis are more likely to show an adult pattern of disease, with postprimary tuberculosis being more common than primary tuberculosis Hilar and mediastinal lymphadenopathy is the radiologic hallmark of pediatric tuberculosis and may be transiently seen in asymptomatic patients (Fig 2). Earlier in childhood (ages 0–3 years), nearly 50% of cases can manifest as isolated lymphadenopathy, as compared with only 9% of cases later in childhood (ages 5–14 years) (20). Extrinsic compression of adjacent bronchi may cause symptoms related to airway compression or postobstructive pneumonia
- latent infection refers to positive findings on laboratory screening tests in the absence of radiographic or clinical evidence of active disease Inactive tuberculosis is characterized by stable fibronodular changes, including scarring (peribronchial fibrosis, bronchiectasis, and architectural distortion) and nodular opacities in the apical and upper lung zones Fibronodular change is associated with a considerably higher risk of developing tuberculosis reactivation (55). In contrast, calcified granulomas (Figs 20, 21) and calcified lymph nodes are associated with an extremely low risk of reactivation and are commonly seen in other granulomatous diseases, such as endemic fungal infections and sarcoidosis (55). Healed tuberculous cavities may persist after active disease resolves and can be complicated by hemoptysis, bacterial infection, or mycetoma.
- Figure 19a. Fibronodular scarring at the lung apices in a 46-year-old man with previous (inactive) tuberculosis. (a)PA chest radiograph shows upper lobe fibrosis (arrowhead) and volume loss with a residual cavity (arrow).
- (b) Axial CT image shows peribronchial fibrosis (arrowhead) and architectural distortion in the lung apices, with a residual cavity (arrow)
- Calcified nodules from an old granulomatous infection in a 52-year-old woman with a positive tuberculin skin test before initiation of biological therapy for inflammatory arthritis. PA chest radiograph shows scattered calcified nodules (arrows).
- Parenchymal complications Aspergilloma colonization in pre-existing tuberculous cavities. Destructive lung changes Scar carcinoma Airway complications - tracheobronchial involvement (including broncholithiasis and secondary amyloidosis) Vascular complications (pseudoaneurysms, hypertrophied bronchial arteries, and systemic collaterals), which present with hemoptysis Pleural complications (chronic empyema, fibrothorax, bronchopleural fistula, and pneumothorax) Mediastinal complications: Mediastinal fibrosis, esophageal involvement (in the form of strictures, traction diverticulae, or fistulae), pericarditis, pneumothorax, and spondylodiskitis.
- Imaging findings in tuberculous complications. (A) Axial CT shows thin-walled cavities in both upper lobes and presence of aspergilloma in RT upper lobe cavity. (B) Axial CECT shows contrast-filled pseudoaneurym (arrow) arising from the superior division of RT pulmonary artery (Rasmussen aneurysm) in the background of fibro-cavitary lesions in both upper lobes. (C) Axial CECT shows chronic empyema LT side with volume loss and pleural calcifications. \ (D) Coronal CT depicts abnormal communication of pleural space with bronchial tree suggesting a bronchopleural fistula. (E) Axial CECT shows calcified LN in RT hilum causing post-obstructive atelectasis of RT middle lobe
- chest wall tuberculosis occurs by reactivation of latent foci formed during hematogenous or lymphatic dissemination of primary tuberculosis, while others opine that it occurs by direct extension from contiguous lung/pleura. Rib tuberculosis – patient 8. Frontal radiographs of the ribs (A, B) show an expansile osteolytic lesion with sclerosis involving the posterior end of the left 10th rib (arrows). Lateral skull radiograph (C) of the same patient shows a sharply marginated osteolytic lesion, with marginal sclerosis in the right parietal bone (curved arrow)
- Nontuberculous mycobacterial disease in the lungs is most commonly seen with Mycobacterium avium complex—also referred to as Mycobacterium avium-intracellulare complex—and Mycobacterium kansasii Nontuberculous mycobacterial disease manifests in two major forms: classic (cavitary) and nonclassic (bronchiectatic)
- Classic (cavitary) nontuberculous mycobacterial infection can have an appearance and clinical manifestations indistinguishable from those of postprimary tuberculosis; classic nontuberculous mycobacterial infection is characterized by upper lobe cavitary lesions and centrilobular and tree-in-bud nodules Upper lobe architectural distortion is often also depicted. Classic nontuberculous mycobacterial infection most commonly affects elderly men with chronic lung disease (typically, emphysema). When compared with tuberculosis, classic nontuberculous mycobacterial infection tends to progress more slowly, and cavities tend to be smaller with thinner walls
- Classic nontuberculous mycobacterial infection with M kansasii in a 64-year-old man with emphysema. (a)PA chest radiograph shows patchy consolidation in the right lower lobe and the apices (arrowheads), with possible cavitation. A left-sided basilar pneumothorax (arrow) is incidentally depicted.
- (b) Axial chest CT image shows a cavitary lesion (arrowhead), with surrounding centrilobular nodules (arrow), in the left lung.
- In contrast, nonclassic (bronchiectatic) nontuberculous mycobacterial infection manifests as chronic bronchiectasis and bronchiolitis with a mid to lower lung zone predominance (74). This form of nontuberculous mycobacterial infection is most commonly seen in elderly women without predisposing factors. It is generally not mistaken for tuberculosis, given the mid lung zone distribution and bronchiectasis. However, if there is more bronchiolitis than bronchiectasis, this infection could mimic active postprimary tuberculosis. The lack of upper lung zone predominance should help distinguish these two entities
- Classification of Tuberculosis on the Basis of Clinical and Radiologic Findings