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TB
This document discusses the various radiological manifestations of tuberculosis (TB) in the chest and other body systems. It covers pulmonary TB including primary and post-primary TB pneumonia, cavitary TB, tuberculomas, and miliary TB. It also discusses mediastinal TB, airway TB such as endobronchial TB and bronchiectasis. Extrapulmonary manifestations including pleural TB, lymphadenopathy, skeletal TB, and special forms are described. For each topic, the pathogenesis, location, and characteristic radiological findings are summarized. Differential diagnoses are also provided for some conditions.
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TB
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- 4. TB or notTB that is the question Chest Doctor
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- 8. Radiological manifestations ofTB TB Parenchymal TB Mediastinal TB Airway TB Vascular TB Pleural TB Chest wall TB
- 9. Parenchymal TB • TBpneumonia. • Cavitary TB. • Tuberculoma. • Miliary TB.
- 10. Parenchymal TB TB pneumonia CavitaryTB Tuberculoma Miliary TB 1ry Post-1ry Post-1ry 1ry Post-1ry 1ry Post-1ry
- 11. Complications of parenchymal TB FibrosisCavitation Endo-bronchial spread Aspergilloma Bronchogenic carcinoma
- 12. Tuberculoma Pathogenesis: • Localized parenchymalTB with alternating activation and healing. • it may occur in the setting of 1ry and post-1ry TB. Location: Right upper lobe (but can occur in any other lobe). Radiological manifestations: • Rounded nodule with well defined margins. • 0.5 - 4cm in diameter • Usually single but may be multiple. • +/- calcification. • +/- cavitation. • +/- satellite nodules.
- 13. nodule nodule nodule DD: Nodule 1. Tuberculoma 2.Hamartoma 3. Metastases 4. Hydatid Tuberculoma
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- 15. 1ry TB pneumoniaPost-1ry TB pneumonia Children Adult Segmental or lobar consolidation. Patchy & nodular opacities which may be bilateral Involve any part of the lung. apico-posterior segment of UL. Superior segment of LL. Associated with lymphadenopathy. Not associated with lymphadenopathy. Healing is complete without any sequelae. Healing by fibrosis. Caviatation. Or both.
- 16. 1ry TB pneumoniawith lympadenopathy
- 17. Miliary TB Etiology: • Itresults from hematogenous dissemination of infection from pulmonary nidus. • It can be 1ry or post-1ry TB. Location: Randomly distributed with mild basilar predominance. Radiology: CXR: miliary shadows (nodules < 2mm). CT: sharply defined miliary shadows (nodules < 2mm). Association: TB chronic lesions Consolidation, cavitation or calcified LN.
- 18. Millet seeds (الدخن)بذور The term miliary is derived from the radiographic picture of diffuse discrete nodular shadows about the size of millet seeds = 2mm.
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- 28. Airway lesions ofTB • Endobronchial tuberculosis. • Bronchiectasis. • Broncho-stenosis. • Broncholithiasis.
- 29. Endobronchial TB Pathogenesis: • Cavitation& communication with bronchial tree Location: • Lower dependent lung zones, distant from the original cavity. Radiological manifestations: • X-ray: • Micro-nodules with lobar or segmental distribution. • CT: • Tree in bud opacities. Association: • Cavitation.
- 30. Tree in budopacities
- 32. Bronchiectasis • Irreversible dilatationof the cartilage containing airways. Pathogenesis: • Cicatricial bronchiectasis: Due to endobronchial TB & subsequent fibrosis. • Traction bronchiectasis: Due to pulmonary TB & subsequent fibrosis. Location: • Unilateral apical bronchiectasis is highly suspicious of TB. Radiological manifestations: • Dilated bronchi. • Bronchocele (dilated bronchi filled with mucus with branching tubular opacities giving finger in glove appearance).
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- 34. Broncho-stenosis Pathogenesis:: • Endobronchial TB. •Extrinsic pressure from enlarged peribronchial TB. Location: • Central air ways. CT: • Active stage: Irregular luminal narrowing with wall thickening, enhancement & enlarged adjacent lymph nodes. • Fibrotic stage: Concentric narrowing, uniform thickening with involvement of a long segment.
- 35. • Lymphadenopathy withpartial obstruction of the left main bronchus resulting in obstructive emphysema of the left lung. Bronchoscopy and biopsy revealed T.B.
- 36. DD of broncho-stenosis EndobronchialTB Bronchogenic carcinoma Double obstructive lesions Low density mass at the obstructive site. Multiple bronchial wall calcifications Sever distortion of the bronchi
- 37. Broncholithiasis • Presence ofcalcified or ossified material within the lumen of the tracheo-bronchial tree. Pathogenesis: • Erosion of bronchial wall by calcified peribronchial lymph node. CT: • Calcified lymph node with findings of bronchial obstruction.
- 39. Vascular TB • Hypertrophyof bronchial vessels. • Rasmussen aneurysm.
- 40. Hypertrophy of bronchialarteries Pathogenesis: • Due to vasculitis. C.P: • Hemoptysis. Location: • Peribronchial. CT: • Peribronchial rounded & tubular densities similar to enlarged lymph nodes. • It may protrude into the lumen of the ectatic bronchi.
- 42. Rasmussen aneurysm Pathogenesis: • Vasculitisof a pulmonary artery within a tuberculous cavity. Location: • Within a tuberculous cavity. CT: • Rounded enhancing lesions within a tuberculous cavity. • It may cause life threatening hemoptysis.
- 44. Medically treated aneurysms Rasmussenaneurysm Pulmonary pseudoaneurysm in Behcet syndrome Anti-tuberculous therapy Corticosteroid therapy
- 45. Mediastinal TB • TBLymphadenopathy. • TB pericarditis. • Esophageal TB. • Fibrosing mediastinitis.
- 46. TB lymphadenopathy • Isthe hall mark of primary T.B. • Its incidence decreases with age. Pathogenesis: • Formation of tuberculous caseating granulomas in the lymph nodes. Location: • Right paratracheal and hilar lymph nodes. CT: • Central low attenuation. • Peripheral rim enhancement. • Obliteration of the perinodal fat. • Usually nodal size doesn’t exceed 2 cm. Association: Parenchymal involvement.
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- 48. Sequelae of TB lympadenopathy HealingComplications Fibrosis Calcification Compression of adjacent bronchus Extranodal extension
- 49. DD of lymphadenopathy •1- Metastases • 2- Lymphoma • 3- other infections e.g. histoplasmosis & varicella. • 4- Sarcoidosis
- 51. Esophageal TB Pathogenesis: • Extensionfrom adjacent lymph nodes. Location: • subcarinal region (due to anatomic proximity of the esophagus to lymph nodes). Radiological manifestations: • Traction diverticula (triangular in shape). • Esophago-mediastinal or esophago-bronchial fistula, manifested as (pneumomediastinum). • Esophagobronchopleural fistula:
- 52. Esophageal traction diverticulum •Triangular or tent shaped. • Wide neck. • It empties when the esophagus is collapsed as it contains all layers. • Calcified mediastinal LN adjacent to the diverticulum.
- 53. Esophageal diverticulum Traction diverticulumPulsion diverticulum
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- 56. Pericardial tuberculosis Pathogenesis: • Extensionfrom adjacent lymph nodes due to close anatomic proximity of the lymph nodes & posterior pericardial sac. Location: Radiological manifestsions: • Pericardial effusion: • Constrictive pericarditis – Pericardial thickening > 4 mm. – Pericardial calcification. Association: • Lymphadenopathy.
- 58. Fibrosing mediastinitis • N.B:the most common cause of mediastinitis is histoplasmosis. Pathogenesis: • TB lymphadenitis with reactive fibrous changes. Radiological manifestations: Plain x-ray: • Mediastinal widening or localized mass. CT: • Mediastinal or hilar mass with or without calcification. • Diffuse obliteration of mediastinal fat. • Tracheo-bronchial narrowing. • Vascular encasement.
- 60. Pleural manifestations ofTB • Pleural effusion. • Chronic TB empyema. • Fibrothorax. • Broncho-pleural fistula. • Pneumothorax. • Malignancy associated with chronic empyema. Pleural TB
- 61. TB empyema • Persistentpurulent pleural fluid containing TB bacilli. Pathogenesis: • Rupture of subpleural cavity. • Hematogeneous dissemination. • Direct extension from infected lymph nodes. Location: • almost always unilateral. Radiological manifestations: • Plain x-ray: • CT: • L oculated fluid collection. • Pleural thickening. • Pleural calcification. • Extrapleural fat proliferation. • Milk of calcium with calcium / fluid level. • Pseudochylous effusion with fat / fluid level. • Associated pulmonary TB (subpleural cavitation)
- 62. TB empyema Proliferation ofextra-pleural fat
- 63. TB empyema withsubpleural cavity
- 64. TB empyema withmilk of calcium Ca / fluid level
- 65. TB empyema withpseudochylus effusion Fat / fluid level
- 66. DD of pleuralcalcification • TB (usually unilateral). • Old hemothorax (usually unilateral). • Asbestosis (usually bilateral).
- 67. Pleural manifestations ofTB • Empyema necessitans. • Pott’s disease of the dorsal verebrae. • Sternum • Rib. • Sternoclavicular joint. Chest wall TB
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- 70. Skeletal TB • TBspondylitis. • TB arthritis. • TB osteomyelitis.
- 71. TB spondylitis TBarthritis TB osteomyelitis 50% of skeletal TB 34% of skeletal TB 16% of skeletal TB Any age Middle age & elderly Children < 5 y (rare in adults) Thoraco-lumbar region Large weight bearing joints Any bone can be affected. Paradiscal type. Central type. Anterior type. Appendicial type. Mono-articular. Metaphyseal.
- 72. TB spondylitis TBarthritis TB osteomyelitis Hematogeneous spread (Batson venous plexus). Trans- cartilagenous spread into disc material. Subligamentous spread (beneath anterior longitudinal ligament) Hematogeneous spread Transphyseal spread to the epiphysis (on the contrary to pyogenic osteomyelitis).
- 73. Tuberculous spondylitis Pyogenic spondylitis Early preservation ofthe disc space. Early & sever narrowing of the disc space. Absent reactive sclerosis Reactive sclerosis. Marginal calcification of psoas abscess. No calcification Skip lesions No skip lesions
- 74. Tuberculous arthritis Pyogenicarthritis Gradual narrowing of the joint space. Early & sever narrowing of the joint space. Peripheral bone erosions. Central bone erosions. Fibrous ankylosis Bony ankylosis. Kissing sequestra
- 75. Phemister triad • Periarticular osteopenia. •Marginal bone erosions. • Gradual narrowing of the joint space. DD: Rheumatid arthritis. (polyarticular).
- 76. Tuberculous osteomyelitis Pyogenic osteomyelitis Transphyseal spread. Notransphyseal spread. Little or no periosteal reaction. Periosteal reaction. Little or no surrounding sclerosis Surrounding sclerosis.
- 77. Special forms ofTB osteomyelitis • TB dactylitis. • Cystic TB.
- 78. TB dactylitis Spina ventosa •Spina = sail. • Ventosa = expanded with air Ventosas
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- 80. TB spondylitis 1. MaginalParadiscal (commonest). 2. Central. 3. Anterior (subperisteal). 4. Posterior (appendiceal).
- 81. Marginal (paradiscal) TBspondylitis Plain x ray: • Disc space narrowing: • Due to involvement of the disc material. MRI: • Abnormal bone marrow signal along adjacent vertebral end plates. • Disc space narrowing.
- 83. Anterior (subperiosteal) lesion Plainx-ray: • Anterior scalloping (gouge effect): • Due to stripping of the periosteum and ALL ischemia & pressure necrosis of the anterior vertebral body. MRI: • Subligamentous abscess. • Preservation of the discs. • Abnormal signal involving multiple vertebral segments.
- 85. Gouge • Is aspecial type of chisel
- 86. Central lesion • Centeredon the vertebral body. • Disc is not involved. • Spread of infection through Baston’s venous plexus. Plain x-ray: • Central rarefaction. • +/- Vertebral collapse (vertebra plana). MRI: • abnormal signal along the vertebral body with preservation of the disc material. • DD with metastasis, lymphoma & eosinophilic granuloma.
- 88. Posterior (appendicial) type •Isolated infection of the pedicles, lamina, transverse processes & spinous process. • Erosive lesions with paravertebral abscess.
- 90. Skip lesions • Involvementof non contiguous vertebrae.
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- 92. • Located ata some distance below the original lesion due to gravitation along the fascial planes. • Calcifications are pathognomonic.
- 93. Angular kyphotic deformity gibbusdeformity
- 94. CNS TB meningitis: • Leptomeningealthickening & enhancement along the basal cisterns. Parenchymal tuberculoma: • Multiple ring enhancing lesions.
- 105. Gastrointestinal TB • Mostcommon location is ileocecal junction. • Hypertrophy of ileocecal valve (Flischner sign). • Cone shaped cecum (normally the cecum is purse shaped). • Pulled up cecum (fibrosis). • DD: Crohn’s disease.
- 106. Ileocecal TB • Pulledcecum. • Narrowed terminal ileum
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- 109. DD of Conedcecum • Crohn's - TI involved more than cecum • TB - colon involvement greater than TI; usually have pulmonary TB; no reflux from cecum to TI • Amebiasis - cecum involved in 90% of chronic amebiasis; TI normal; ileocecal valve fixed in open position • UC - backwash ileitis occurs 10% of time through gaping ileocecal valve • Actinomycosis - uncommon may simulate appendicitis, palpable abdominal masses and draining fistulas • Typhlitis - necrotizing process of multifactorial origin involving predominantly the right colon; most common in children with leukemia; typically begins 1-2 weeks following chemotherapy - may also occur in adults with hematologic malignancy - there is bowel wall thickening, mucosal ulceration, intramural hemorrhage and necrosis
- 110. TB peritonitis Pathology: • Directhaematogenous spread, • Rupture of a tuberculous intra-abdominal lymph node. Types: • Wet type (commonest). • Dry type. • Fibrotic type.
- 111. Wet TB peritonitis •Exudative high attenuation ascites. • May be free or loculated. • Measurement of ascitic fluid adenosine deaminase level is diagnostic.
- 114. Dry type • Mattedsmall bowel loops.
- 115. Fibrotic type • Omental& mesenteric caking
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- 117. Cervical TB lymphadenopathy scrofula US: •Nodal matting. • Surrounding soft tissue edema is less marked than would be expected given the size of the collections. Duplex: • Prominent hilar vascularity (on the contrary of malignant LN which show prominent peripheral vascularity). US guided FNAC: • Has 92% sensitivity & 97% specificity.
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- 122. Renal size • Diffuselyenlarged (T.B pyonephrosis from ureteric stricture). • Focally enlarged with displacement of adjacent calyces (tuberculoma). • Shrunken kidney small scarred non functioning kidney with dystrophic calcification (putty kidney). • May be normal size.
- 123. Renal papillae • Papillaryirregularity (moth eaten calyces) earliest sign. • Irregular papillary surface due erosions. • Papillary necrosis (blunted dilated calyces). • Parenchymal cavities communicating with collecting system.
- 124. Parenchymal calcifications • Amorphous. •Punctate. • Confluent calcifications. • Cumulus cloud opacity: • Due to calcification in caseous material in caverno-caseous type. • Complete cast of calcification (putty kidney) end stage renal TB (autonephrectomized kidney).
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- 126. Collecting system Uneven caliectasis: unequaldilatation of renal calyces due to varying degree of stenoses. Hydrocalicosis: • dilated calyx due to infundibular stenosis. Phantom calyx: • non opacified calyx due to infundibular stenosis.
- 127. Renal pelvis • Reducedcapacity. • Sharp kinking (Kerr kink). • Mural thickening.
- 128. Ureter • Spread: • Directspread from renal involvement: • Early: • Multiple filling defects (mucosal granulomas) • Saw tooth ureter: • Dilated ureter with irregular contour & mucosal ulcerations.
- 129. Late (fiborsis): • Beadedureter: alternating strictures & dilatations. • Cork screw ureter: alternating strictures & dilatations with tortuousity. • Pipe stem ureter: rigid, thick straight ureter.
- 130. Bladder • Thickened contractedlow capacity urinary bladder (thimble bladder).