TB Intensive Tyler, Texas June 2-4, 2010 Diagnosis of TB: Radiology David Finlay, MD June 3, 2010 2stages stages- Tuberculosis 1. primary infection 2. reactivation, or post primary disease 2 1
Primary Tuberculosis hilar or paratracheal lymphadenopathy with or without a parenchymal infiltrate is characteristic. bilateral lymphadenopathy in up to 15% lymphadenopathy may result in lobar atelectasis due to bronchial compression. 3 2
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Primary Tuberculosis acquired by inhalation of airborne organisms right middle lobe, lower lobes most frequent focal pneumonitis, with caseous necrosis and lymphatic spread to ipsilateral hilar and mediastinal nodes most common radiographic appearance normal. 7 4
Primary tuberculosis immunity results in 90-95% 95% of patients with development of lung and hilar mediastinal granulomas, often calcified, which may or may not be visible on chest x-ray. 10 5
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Primary tuberculosis may have hematogenous spread, which also becomes inactive and calcifies as immunity develops. Ghon lesion calcified nodule with parenchymal scar. Ranke complex Ghon lesion & calcified hilar node. 13 Primary Tuberculosis usually asymptomatic in 5-10% the infection is poorly controlled, resulting in progressive primary tuberculosis. 14 7
Progressive primary tuberculosis extensive cavitation of tuberculous pneumonia with endobronchial spread rupture of necrotic nodes into bronchi results in further endobronchial spread, as well as hematogenous spread pleural effusion (25%) hypersensitivity reaction. 15 8
Reactivation or Post Primary Tuberculosis as hypersensitivity develops, granulomas heal with calcification and fibrosis viable organisms may survive, and enter dormant phase reactivate at later date with immunosuppresion, stress, and/or reexposure 18 9
Reactivation tuberculosis characteristically have apical abnormalities.(up to 90%) usually posterior segment upper lobe. 19 Reactivation tuberculosis Radiographic findings patchy consolidation with streaky opacities (100%) primarily apical posterior upper lobes (90%) cavitation 45% bronchogenic spread of disease with ill-defined nodules (20-25%) fibrosis (30%) pleural effusion (20%) 20 10
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Inactive vs. Active Tuberculosis may be impossible to tell on x-ray active disease suggested by focal consolidation with cavities in upper lobes or superior segment of lower lobes endobronchial spread due to active disease often results in poorly defined nodules between 5-10mm in size, acinar nodules if radiograph changes with treatment, active disease. lack of change on radiographs over 6 months suggests disease inactivity. 23 12
Pleural effusions primary TB (25%) hypersensitivity reaction to TB proteins organisms uncommonly isolated from fluid may be unassociated with obvious parenchymal disease on CXR 26 13
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Pleural effusion post primary TB (20%) caused by rupture of a tuberculous cavity into the pleural space, causing empyema may cause bronchopleural fistula with air fluid levels often results in irreversible pleural thickening and calcification 31 16
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CT / HRCT findings airspace consolidation cavitation ill defined air space nodules (endobronchial spread) small diffuse nodules (miliary) due to hematogenous dissemination 36 18
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CT/ HRCT findings pleural effusion lymph node enlargement with central necrosis interlobular septal thickening bronchovascular distortion and impaction 42 21
Tuberculous cavities usually have thick, irregular walls with treatment, walls thin and cavity shrinks and usually collapse 44 22
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With treatment, increase in bronchovasular distortion, emphysema, fibrosis and bronchiectasis 47 HRCT findings of active disease Rosettes of centrilobular nodules, 2-10mm in diameter branching centrilobular opacities-- tree-inbud 48 24
Tree in bud represents solid caseous material filling or surrounding terminal bronchioles or alveolar ducts. may coalesce, resulting in focal areas of bronchopneumonia usually reversible, resolving within 5-9 months of treatment 49 25
Miliary TB fine nodular or reticulonodular pattern, evenly distributed distinguished from endobronchial spread by uniform size of nodules and even distribution can occur with reactivation of progressive Primary TB 51 26
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Lymphadenopathy more common in primary TB than post primary TB central necrosis particularly high incidence in AIDS, associated with rim enhancement (85%) 57 29
CT / HRCT more sensitive than chest radiography in detection and characterization of parenchymal and mediastinal disease, particularly in primary tuberculosis more accurately defines and characterizes lymphadenopathy 59 Reactivation TB complications pneumothorax due to cavity rapture into pleural space can also occur due to formation of subpleural blebs 60 30
Mycetomas (fungus balls) common in patients with cavitary tuberculosis colonization of cavities by aspergillus best shown by CT 61 Mycetoma intracavitary mass with an air-crescent sign changes position in cavity with prone/ decubitus scans not specific to tuberculous cavities (sarcoid, bulla, etc.) 62 31
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TB and AIDS TB reported in up to 10% of AIDS patients radiographic appearance is more similar to primary TB, although reactivation is the most likely mechanism non cavitary consolidation in upper & lower regions associated with hilar / mediastinal lymphadenopathy 67 34
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TB and AIDS atypical mycobacterial disease also commonly seen AIDS indicator disease in HIV patients with CD4 counts below 200 radiographic findings of TB in HIV/AIDs reflects extent of cellular immune compromise 71 TB and AIDS if CD4 count greater than 200, tuberculosis is indistinguishable from non-hiv patients (upper lobe cavitary infiltrates) if CD4 count less than 200, radiographic findings are similar to primary tuberculosis (80%) Dissemination is also more common in patients with greater degrees of immunocompromise, with miliary and extrapulmonary disease 72 36
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TB and AIDS Normal CXR reported in up to 15% of AIDS / HIV patients with isolated TB CT much more sensitive in these cases 78 39
TB and AIDS 30-60% with tuberculosis have extra pulmonary foci, and only half of these have identifiable concomitant pulmonary infection abscesses of multiple organs including prostate, liver, spleen, chest and abdominal wall, and pancreas 79 Extrapulmonary manifestations of Tuberculosis exposure of superficial mucosal surfaces to infected respiratory secretions contiguous spread lymphohematogenous dissemination (especially in immunocompromised hosts) 80 40
Hematogenous dissemination involves organ systems in proportion to blood flow spleen,liver,lungs, bone marrow, kidneys, adrenals, eyes splenomegaly or hepatomegaly with small abscesses meningitis, choroid plexus, pericarditis 82 41
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Hematogenous dissemination tuberculous meningitis thought to occur via rupture of a subependymal tubercle into the subarachroid space basal meninges most commonly involved Secondarily results in cortical and lacunar brain infarction, and spinal cord infarction 85 43
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Bone involvement Potts disease Tuberculous spondylitis destructive lesions in spine primarily centered in vertebral discs, and secondarily involving vertebral end plates, resulting in kyphosis. May result in paravertebral abscess Cold abscess. Extends under anterior longitudinal ligament, involving multiple vertebra. 110 55
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Bone involvement also involves other joints hip, knee, tarsal joints cartilage destruction with articular defects 114 57
GI involvement increased incidence in AIDS ingestion of tuberculous sputum ileocecal area, ascending colon, most common sites 115 Tuberculous peritonitis complication of GI involvement ascites low density lymphadenopathy adhesions with bowel obstruction 116 58
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Urinary tract hematogenous spread to kidney hematuria, sterile pyuria 75% unilateral 135 Urinary tract tuberculomas form in renal parenchyma calcification Ureteral involvement develops from direct spread, resulting in stricture, and obstruction putty kidney tuberculous pyonephrosis autonephrectomy small, shrunken, calcified, scarred, and nonfunctional 136 68
Bladder involvement direct spread interstitial cystitis with thickened bladder wall ulceration also involves spinal opssicles and epididymus in males 137 69