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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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