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EXCELLENCE EXPERTISE INNOVATION
Diagnosis of TB: RadiologyDavid E. Griffith, MDMarch 13, 2015
TB for PulmonologistMarch 13, 2015Phoenix, AZ
• No conflict of interests
• No relevant financial relationships with any commercial companies pertaining to this educational activity
David E. Griffith, MD has the following disclosures to make:
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Diagnosis of TB: Radiology
David E. Griffith, M.D.Professor of Medicine UTHSCT
Assistant Medical DirectorHeartland National TB Center
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Primary Tuberculosis
usually asymptomatic: most common radiographic appearance – normal
“Ghon” lesion – calcified nodule with parenchymal scar.
“Ranke complex” – Ghon lesion & calcified hilar node.
may have hematogenous spread, which also calcifies as immunity develops.
in 5-10% the infection is poorly controlled, resulting in progressive primary tuberculosis.
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Primary Tuberculosis
Most commonly in children, immune compromised patients (HIV seropositive, TNFα blockers)
Opacities are seen in middle and lower lungs
Most frequently unilateral, right middle lobe, lower lobes
focal pneumonitis, with caseous necrosis and lymphatic spread to ipsilateral hilar and mediastinal nodes
.
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Primary Tuberculosis
Hilar or paratracheal lymphadenopathy with or without a infiltrates is characteristicand may cause bronchial compression .
Bilateral lymphadenopathy in up to 15%
Lymphadenopathy may result in lobar atelectasis due to bronchial compression.
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http://www.oncoline.nl/index.php?pagina=/richtlijn/item/pagina.php&id=22056&richtlijn_id=396
Lymph nodes associated with the lungs
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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%)
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Courtesy: Dr. Santiago R
Where’s the Adenopathy?
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18 M with HIV
Courtesy: Dr. Santiago R
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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.
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Reactivation tuberculosis
characteristically have apical abnormalities.(up to 90%)
usually posterior segment upper lobe.
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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%)
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Post primary or reactivation tuberculosis
Post primary or reactivation tuberculosis
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Post primary or reactivation tuberculosis
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Tuberculous cavities
usually have thick, irregular walls
with treatment, walls thin and cavity shrinks and usually collapse
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Courtesy: Dr. Santiago Re
Consumption
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Pleural effusions
primary TB (25%)
hypersensitivity reaction to TB proteins
organisms uncommonly isolated from fluid
may be unassociated with obvious parenchymal disease on CXR
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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
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Diagnosis?
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Empyema Necessitatis
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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
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“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
Tree in Bud
Courtesy: Dr. Santiago R
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CT/ HRCT findings
pleural effusion
lymph node enlargement with central necrosis
interlobular septal thickening
bronchovascular distortion and impaction
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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
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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
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Millet Seeds
Slender plant, 1-15 feet
Maize like kernels:
~ 2 mm in diameter
1/6 of world grain
1/3 of grain for 3rd world
Africa and India
Producer: India
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Reactivation TB complications
pneumothorax – due to cavity rapture into pleural space
can also occur due to formation of subpleural blebs
Endobronchial stenosis
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Mycetomas (fungus balls)
common in patients with cavitary tuberculosis
colonization of cavities by aspergillus
best shown by CT
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Mycetoma
intracavitary mass with an air-crescent sign
changes position in cavity with prone/ decubitus scans
not specific to tuberculous cavities (sarcoid, bulla, etc.)
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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
TB: Lymphadenopathy in AIDS
Courtesy of Dr. Diane Strollo
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TB: Lymphadenopathy in AIDS
Central necrosisPeripheral
enhancement
Courtesy of Dr. Sandy Rubin
Tuberculosis and HIV
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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
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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
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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
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Extrapulmonary manifestations of Tuberculosis exposure of superficial mucosal surfaces to
infected respiratory secretions
contiguous spread
lymphohematogenous dissemination– (especially in immunocompromised hosts)
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Extrapulmonary Tuberculosis can affect any organ
Cardiac: pericarditis, pericardial effusion, myocarditis CNS: meningitis, tuberculomas, tuberculous abscesses,
cerebritis, and miliary TB Head and neck: lymphadenitis (scrofula), less common
sinonasal, thyroid, skull base Musculoskeletal: spinal column, pelvis, hip, and knee
(spondilytis, osteomyelitis, arthritis) Abdominal: lymphadenopathy, peritonitis, ileocecal
region, hepatosplenic, adrenal Genitourinary: renal, ureters, bladder, genital (fallopian
tubes in women and seminal or prostate gland in men)
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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
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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
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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.
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Bone involvement
also involves other joints – hip, knee, tarsal joints
cartilage destruction with articular defects
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GI involvement
increased incidence in AIDS
ingestion of tuberculous sputum
ileocecal area, ascending colon, most common sites
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Tuberculous peritonitis
complication of GI involvement
ascites
low density lymphadenopathy
adhesions with bowel obstruction
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1 year old child with “pneumonia”
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24 year old mother of child with “pneumonia”
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