Pulmonary tuberculosis is a chronic infectious disease caused by invasion of Mycobacterium tuberculosis hominis or Mycobacterium tuberculosis bovis to the lungs. Accounting for about 90 % of human tuberculosis, pulmonary tuberculosis is the most common type. The Mycobacterium tuberculosis (MTB) at the intrapulmonary lesions can spread along bronchi within the lungs and even pass through the pleura to cause tuberculous pleuritis. Otherwise, MTB disseminates along with blood and lymph flows to cause both intrapulmonary and extrapulmonary tuberculosis.

1 Etiology

MTB is categorized into the genus of Mycobacterium, the family of Mycobacteriaceae and the order of Actinomycetales. It is an obligate aerobe that grows slowly. On solid medium, its generation time is 18–20 h, requiring 8 days to 8 weeks for culture. On most of the culture medium, the bacterial colony is rough. MTB is also known as acid-fast bacillus characterized by acid-fast and acid-fast alcohol decolorization. It has quite strong resistance to both physical and chemical factors. For instances, MTB in sputum can be killed by boiling for 5 min, and the MTB in dry sputum can survive for several weeks in darkness. However, MTB has quite weak resistance to ultraviolet radiation. It can be killed under sunshine for 2–7 h or in 75 % ethanol for 5 min or at a temperature of 60 °C for 10–30 min or at a temperature of above 80 °C for 5 min. The optimal way for sterilizing is to autoclave (120 °C) for 30 min. The M. tuberculosis complex includes various types of Mycobacterium, which share common properties and high genome homology. However, the main pathogenic type to humans is M. tuberculosis, M. bovis, and M. africanum.

2 Epidemiology

2.1 Source of Infection

The main sources of infection are patients with sputum smear positive or sputum culture positive. The patients with sputum smear positive for pulmonary tuberculosis have the strongest infectivity.

2.2 Route of Transmission

MTB spreads via the respiratory tract. When the patients with active pulmonary TB cough, sneeze, or speak aloud, droplet with singular MTB as the core suspends in the air to infect other people. In addition, MTB excreted by coughs dries and adheres to dust to form MTB carrying dust, which can also infect individuals. MTB rarely spreads via the gastrointestinal tract, urogenital system, and skin.

2.3 Susceptible Population

Populations are generally susceptible to pulmonary TB. Diabetes, HIV/AIDS, silicosis, neoplasm, organ transplantation, and long-term use of immunosuppressant or adrenal cortical hormone can be complicated by tuberculosis. The sociological high-risk factors of tuberculosis include poverty, poor living conditions, and malnutrition.

2.4 Epidemiological Features

Recently, due to increasing mobility of populations as well as the increasing incidences of drug-resistant tuberculosis and HIV/AIDS complicated by tuberculosis, the occurrence of tuberculosis has been increasing worldwide. Based on data released by WHO in 2000, 2 billion people have a history of MTB infection, with 8 million new cases of tuberculosis each year and 3 million cases of death. China is one of the 22 countries with serious prevalence of tuberculosis and meanwhile is one of the 27 countries with serious prevalence of multidrug-resistant tuberculosis. Currently, about 1.3 million new cases of tuberculosis are reported each year in China, accounting for 14.3 % of the total new cases in the world and ranking the second worldwide.

3 Pathogenesis and Pathological Changes

3.1 Pathogenesis

3.1.1 Pathogenicity and Virulence of MTB

The virulence of MTB is possibly related to its components. For instances, repeated injection of small doses of lipoid cord factors (6,6 double mycolic acidic trehalose) into the abdominal cavity of mice can cause obvious toxic effects. Other lipoids, like sulfolipid, can strengthen the toxicity of cord factors and suppress the fusion of lysosome with phagosome to promote the growth and proliferation of MTB in macrophages. Phospholipid can stimulate the multiplication of monocytes, epithelioid cellularization, and formation of the Langerhans cells. Waxiness D is the complex of mycolic acid arabinose Yutian galactan and mucopeptide, which contributes to the formation of liquefaction, necrosis, dissolution, and cavities of tubercular caseous lesions. In addition to the above lipid components, coexistence of polysaccharide with other substances shows bioactivities, which is an important component of complete antigen and plays an adjuvant role in inducing chemical taxis response of neutrophils. The bacterial protein of MTB is a complete antigen, stimulating responses to tuberculin.

3.1.2 Biological Process of MTB Infection and Its Onset

Dannenberg et al. divided the process of MTB infection and its onset into initial stage, T-cell response stage, symbiotic stage, and extracellular multiplication and dissemination stage. The MTB invading the respiratory tract is engulfed by alveolar macrophage, where they survive and replicate themselves with the following spread to adjacent nonactivated alveolar macrophage to cause initial lesions of infection. The initial growth of MTB in alveolar macrophage causes tubercular lesions with central solid caseous necrosis to restrict its further multiplication. During the T-cell response stage, The T-cell-mediated immunity (CMI) and delay type hypersensitivity (DTH) are induced, which play a crucial role in the occurrence, development, and prognosis of TB. In only rare cases, primary tuberculosis occurs during the T-cell response stage. In most cases, MTB is symbiotic with its host. Enwrapped by fibers, the core of caseous necrosis is the place where MTB persistently survives, and an environment with low oxygen, low pH value, and inhibitory fatty acid is unfavorable for its multiplication. However, the immunosuppression of the host is favorable for its multiplication, with reactivated MTB to multiply themselves. Finally, a large quantity of MTB is released from the liquefied caseous lesions to disseminate.

3.1.3 Immune Responses of the Human Body to MTB Infection

The immune responses of the human body to MTB infection include two types: CMI and DTH, both of which are mediated by T cells.

3.2 Pathological Changes

3.2.1 Basic Pathological Changes of Tuberculosis

Human immunity and hypersensitivity as well as the quantity and virulence of the invading MTB are closely related to the quality, range, pathological basis, and developing speed of the lesions.

3.2.1.1 Exudative Lesion

The exudative lesions are demonstrated with congestion, edema, and infiltration of leukocytes. In the early exudative lesions, there are neutrophils, which are gradually replaced by macrophages and lymphocytes. The engulfed MTB can be detected inside the macrophages. The exudative lesions are usually observed at the early stage of the inflammation or during deterioration of the lesions. In addition, it can be detected in patients with serous tuberculosis. When the conditions improve, the exudative lesions can be completely absorbed.

3.2.1.2 Proliferative Lesion

After macrophage engulfs and digests the invading MTB, the phospholipid of MTB enlarges the macrophage to a flat shape resembling to epithelial cell, which is known as epithelioid cell. The epithelioid cell is the major component of proliferative lesions, showing certain specificity for the diagnosis of tuberculosis. Infiltration of the epithelioid cells, Langerhans cells, and lymphocytes forms the typical epithelioid granuloma node, which is the characteristic lesion of tuberculosis. The formation of such node is a development process of phagocytosis by macrophages to kill MTB, confine the lesion, and prevent its dissemination. Most invading MTBs are killed during the formation of phagocytosing and killing the M. tuberculosis, which localizes the lesion and prevents the M. tuberculosis from spreading. Most M. tuberculosis is killed in during the formation of the epithelioid granuloma node. Therefore, by acid-fast staining, MTB is commonly not detectable in the node. The pathological changes with predominant proliferative lesions occur mostly in patients with infection of MTB of a small quantity or in patients with strong CMI.

3.2.1.3 Degenerative Lesion (Caseous Necrosis)

Degenerative lesions occur commonly based on exudative or proliferative lesions. In the patients with compromised immunity or strong allergic responses, or in the patients infected by a large quantity of MTB, the MTBs in exudative lesions successfully fight against the macrophages for multiplication in a large quantity. Consequently, the cells are turbid and swollen to show fatty degeneration, with dissolution, fragmentation, and finally necrosis. The apoptotic inflammatory cells release a proteolytic enzyme to dissolve the tissue, inducing coagulative necrosis. Due to a large quantity of adipose, the degenerative lesion is grayish yellow by naked eye observation, with loose and crisp texture resembling to dry cheese, which is therefore known as caseous necrosis. Under a microscope, an area of coagulated red-stained unstructured necrotic tissue can be observed. The caseous necrosis is subject to liquefaction and cavities, which can be disseminated along the bronchus. Most caseous lesions can be cured after calcification.

The above three types of lesions can concurrently exist in the same one pulmonary lesion, with one predominating. For instances, at the center of exudative lesion and multiplicative lesion, a small quantity of caseous necrosis can be found; in the pulmonary lesion with caseous necrosis predominating, different degrees of exudation and epithelioid granuloma node can be observed.

3.2.2 The Prognosis of the Lesions

The prognosis of the lesions of tuberculosis mainly includes absorption, fibrosis, calcification, dissemination, and deterioration. When the immunity is strong and (or) antituberculosis therapy is used, the lesions can be gradually cured. Exudative lesion can be absorbed via phagocytosis of mononuclear phagocytic system, even leaving no scar. The healing of lesions is commonly accompanied by proliferation of fibrous tissue to form stripe- or cord-like scar. Caseous lesion can also be healed after dehydration, contraction, calcium salt deposition, and calcification of the lesions. The deterioration of tuberculosis is manifested as expansion and dissemination of the lesions. After the initial infection of MTB, the bacteria can be engulfed by macrophages, which reach the hilar lymph nodes along with lymph flow. A small quantity of MTB can gain their access into the blood flow to disseminate all over the body, but with no obvious clinical symptoms (asymptomatic septicemia). In the cases with invasion of vascular vessel by necrotic lesion, the MTB can induce systemic miliary tuberculosis along with blood flow, with the lungs, meninges, bone, kidney, and other organs involved. And the bacteria can also spread to other organs along with lymph flow. After pulmonary tubercular caseous necrosis is liquefied, the bacteria can spread along the bronchus to form new lesions in other parts of the lung. After sputum containing a large quantity of MTB is swollen into the gastrointestinal tract, intestinal tuberculosis and peritoneal tuberculosis may occur. In addition, direct dissemination of pulmonary TB into the pleura is possible, with consequent occurrence of tubercular pleuritis.

4 Clinical Symptoms and Signs

According to the Health Industry Standards of P.R. China issued in 2001, tuberculosis is categorized into five types: primary tuberculosis, hematogenous disseminated pulmonary tuberculosis, secondary pulmonary tuberculosis, tubercular pleuritis, and other extrapulmonary tuberculosis.

4.1 Clinical Symptom

4.1.1 Systemic Symptom

The patients with pulmonary tuberculosis often experience some symptoms of tubercular toxic symptom, which is commonly irregular low-grade fever after noons with a body temperature of 37.4–38 °C that persists for several weeks. In the cases of acute hematogenous disseminated pulmonary tuberculosis, caseous pneumonia with cavitation or complicated by pulmonary infection, the patients may experience high fever and night sweats. Other systemic symptoms include fatigue, poor appetite, emaciation, insomnia, menstrual disorder, and even amenorrhea.

4.1.2 Cough

Cough is always the chief complaint by the patients in their first clinic visit. The cases with cough for at least 3 weeks with bloody sputum should be highly suspected as pulmonary tuberculosis. The patients with pulmonary tuberculosis mainly complain of dry cough. In the cases complicated by bronchial tuberculosis, the patients often experience severe irritated cough. In the cases complicated by compressed trachea and bronchus by mediastinal or hilar lymphatic tuberculosis, the patients may experience spasmodic cough.

4.1.3 Expectoration

Expectoration is rare in patients with pulmonary tuberculosis. The sputum is usually white thick. The patients with pulmonary TB complicated by infection or bronchiectasis often expectorate yellowish thick phlegm. In the cases with caseous liquefaction and necrosis, the patients may also expectorate yellowish thick sputum and even expel necrotic tissue.

4.1.4 Chest Pain

Chest pain is not a specific manifestation of pulmonary tuberculosis. The lesion close to the pleura may adhere to the pleura to cause dull pain or stabbing pain, which has insignificant relationship with respiration. Pulmonary tuberculosis complicated by tubercular pleuritis can cause severe chest pain, which is related to respiration.

4.1.5 Dyspnea

Generally, the patients in the early stage of pulmonary TB rarely experience dyspnea. Only in the cases of pulmonary tuberculosis complicated by a large quantity of pleural effusion or pneumothorax, the patients may experience dyspnea. Bronchial tuberculosis causes narrowing of the trachea or large bronchus, with consequent manifestation of dyspnea. Otherwise, mediastinal, hilar, and paratracheal lymphatic tuberculosis may compress the trachea or bronchus to cause dyspnea. In the cases of advanced pulmonary TB, extensive lesions at both lungs can cause respiratory failure or right cardiac insufficiency, which may also induce dyspnea.

4.1.6 Tubercular Allergy

Pulmonary tuberculosis can cause systemic allergy. Its clinical manifestations resemble to rheumatic fever, mainly including erythema nodosum, multiple arthralgia, behcet disease, and follicular keratoconjunctivitis. The allergy is more common in young female patients, which is non-responsive to nonsteroidal anti-infective drugs but can be effectively treated by antituberculosis therapy.

In general, pulmonary tuberculosis commonly has no specific clinical manifestations. Some patients are even asymptomatic, with the diagnosis defined by routine physical examinations. In the cases with accompanying immunosuppression, the clinical manifestations are atypical, with implicit onset and clinical course. Otherwise, the patients experience acute onset with severe clinical symptoms which are unveiled by primary disease and are subject to misdiagnosis.

4.2 Signs

The pulmonary signs are related to the location, quality, range, and severity of the lesions. In the cases with mild conditions, the pulmonary signs are not obvious, with no specificity. In the cases with extensive pulmonary lesions, corresponding physical signs can be detected. In the cases with obvious cavities or complicated by bronchiectasis, fine moist rales can be heard by auscultation. In the cases with large areas of caseous pneumonia, signs of pulmonary consolidation are detectable, such as strengthened vocal fremitus, flatness or dullness by percussion, and bronchial breathing sound by auscultation. In the cases with huge cavity, hyperresonance or tympany can be heard by percussion and amphoric breathing sound by auscultation. In the cases of bronchial tuberculosis, localized wheezing can be heard. In the cases with extensive fibrosis at both lungs, the affected side of the thorax is subject to collapse, with narrowed intercostal space and shift of bronchus. The other parts may be subject to corresponding signs due to compensatory emphysema, such as hyperresonance by percussion or decreased breathing sound by auscultation.

5 Pulmonary Tuberculosis-Related Complications

5.1 Hemoptysis

When necrotic lesion of tuberculosis involves the pulmonary capillary wall, the patients expectorate bloody phlegm. In the cases with the major vessel involved, hemoptysis in different quantities occurs. In the cases with ruptured aneurysm in the cavity or ruptured bronchial artery, massive hemoptysis occurs possibly to cause death. Tubercular bronchiectasis induced by healing and fibrosis of lung tissue can cause repeated and long-term hemoptysis or bloody sputum after pulmonary TB is cured.

5.2 Spontaneous Pneumothorax

Pulmonary TB is a common cause of pneumothorax. A variety of lesions in the cases of pulmonary TB can cause pneumothorax, such as penetration of subpleural lesion or cavity into the thoracic cavity, emphysema, or ruptured lung bullae induced by fibrosis or scarring of tubercular lesions. The lesions of miliary tuberculosis may affect the pulmonary interstitium to cause interstitial emphysemic lung bullae rupture. The penetration of the lesion or cavity into the thoracic cavity often causes increased exudative fluid in the thoracic cavity, inducing pneumoserothorax or pyopneumothorax.

5.3 Bronchiectasis

The lesions of pulmonary TB damage the bronchial wall and tissue surrounding the bronchus to cause bronchiectasis. Otherwise, bronchial tuberculosis itself causes bronchial deformation and dilation, which is known as tubercular bronchiectasis, which may be accompanied by hemoptysis.

5.4 Secondary Lung Infection

Cavities (especially fibrous cavities), pleural thickening, airway obstruction caused by bronchiectasis, atelectasis, and bronchial tuberculosis are the pathological basis for secondary lung infection or other secondary bacterial infections to bronchial tuberculosis. The pathogenic bacteria are mostly Gram-negative bacilli, with infection of mixed pathogenic bacteria being more commonly found.

5.5 Cardiac and Pulmonary Failures

Cardiac and pulmonary failures are serious complications of pulmonary TB. When pulmonary TB is ineffectively treated, the conditions develop into chronic to destroy lung tissue, resulting in emphysema and pulmonary bulla. These conditions further affect the pulmonary functions and lead to chronic respiratory failure. Pneumothorax and complicating infections can cause acute respiratory failure. Long-term hypoxia and traction of the vascular wall by intrapulmonary fibrous tissue induce pulmonary arterial hypertension, which may further develop into cardiopulmonary disease and right heart failure.

6 Diagnostic Examinations

6.1 Laboratory Test

6.1.1 Common Test

The common tests are nonspecific. The peripheral blood WBC count is commonly within normal range, possibly with decreased hemoglobin (HGB). At the acute progressive stage, the WBC count can be detected with an increase. In the cases of severe infection, hemogram resembling to leukemia can be detected, with rapid blood sedimentation rate and elevated CRP.

6.1.2 Etiological Test

6.1.2.1 Smear Test

Various excretions and secretions such as sputum, urine, pleural effusion, and feces as well as suctions of lymph node puncture can be prepared into smear for examination. The finding of acid-fast bacilli facilitates the diagnosis, but with a low positive rate.

6.1.2.2 Isolation of Pathogenic Bacteria

The separation of pathogenic bacteria for culture has a higher detection rate than the smear test. Meanwhile, it can be applied to exclude the possibility of non-tuberculosis mycobacteria infection, which is a standard test for diagnosis. By using rapid radioactive culture, the drug sensitivity and the bacterial serotype identification can be tested, which increases the primary separation rate by 10 % compared to the modified routine Lowenstein-Jensen culture. The time needed for the detection is also shortened. In addition, the BacT/Alert 3D system can be used to detect tuberculosis mycobacteria and drug sensitivity, with even shorter time required. Direct microscopy requires no costly equipment but is simple and rapid with high sensitivity and specificity, which are, respectively, 97.5 % and 94.4 %.

6.1.2.3 Detection of Specific Nucleic Acid

Nucleic acid probe, PCP, and DRA blotting hybridization can be applied to detect DNA of MTB. The gene chip technology is also applied in identifying MTB, testing drug resistance, and analyzing genes of MTB.

6.1.3 Serological Test

Along with the further studies into molecular biology and immunology of Mycobacterium, ELISA, ELI-SPOT stratification assay, indirect immunofluorescence (IIF), and Western blotting have been applied in clinical practice to detect the relevant antibody in serum, sputum, and pleural effusion. Serological test is an auxiliary test for the rapid diagnosis of pulmonary TB but still with poor specificity.

6.1.4 Tuberculin Skin Test

Currently the commonly applied tuberculin skin test in clinical practice is the purified protein derivative (PPD) of BCG. PPD 5 IU is percutaneously injected at the forearm, with the following observation of the callosity after 72 h at the injection site. A callosity with a diameter being 5–9 mm is defined as weak positive, while 10–19 mm is defined as positive, both of which indicate MTB infection. Strong positive finding in adults, namely, callosity with a diameter no less than 20 mm or smaller than 20 mm but with blisters or necrosis, indicates active tuberculosis.

6.1.5 Endoscopic Examination

Endoscopic examinations include fiber bronchoscope and thoracoscopy, and fibro-colonoscopy provide etiological and pathological diagnoses for certain types of tuberculosis.

6.1.6 Biopsy

As for patients with tuberculosis but no bacterial excretion or tuberculosis with no communication with external environment, such as tuberculosis of the lymph node, bone, joint, liver, and spleen, biopsy can be applied for etiological and pathological diagnosis.

6.2 Diagnostic Imaging

Routine chest X-ray is a radiological examination of choice for suspected cases of pulmonary TB. In most cases, in combination to clinical case history and sputum examination, the diagnosis can be defined. CT scanning can be ordered as a supplementary examination. It can demonstrate acute miliary tuberculosis earlier, tuberculosis lesions at hidden positions, mediastinal and hilar lymphadenectasis, and density changes within lesions. Therefore, CT scanning has an important value for differential diagnosis of some types of tuberculosis, such as tuberculoma.

7 Imaging Demonstrations

7.1 Imaging Demonstrations of Pulmonary Tuberculosis

7.1.1 Primary Pulmonary TB

7.1.1.1 Primary Syndrome

Typical primary syndrome is characterized by primary lesions and interconnecting lesions of lymphangitis and enlarged hilar lymphadenitis to form a dumbbell-like appearance. However, such a radiological sign is rarely found. In some patients, the primary lesion is large to cover the lesions of lymphangitis and lymphadenitis. Local pleural thickening has a corresponding radiological sign.

7.1.1.1.1 X-Ray

The primary lesion is mostly singular, with cloudy or round-like shadow with increased density. Otherwise, the primary lesion is demonstrated as flakes or large flakes of shadows with increased density at the pulmonary segment or lobe, with a size of 0.5–2 cm and poorly defined boundary. The lesions are often located at the posterior segment of the upper lung lobe or the dorsal segment of the lower lung lobe near the pleura.

The lesion of lymphangitis can be found from the primary lesion to the enlarged lymph node, characterized by one or several blurry cord-like shadows with increased density.

Hilar and/or mediastinal lymphadenectasis is radiologically demonstrated as mass-like shadow that protrudes out of the normal tissue contour.

7.1.1.1.2 CT Scanning

The primary lesion is demonstrated as lobular shadow and acinar nodular shadow with poorly defined boundary by CT scanning. CT scanning can well define the primary lesion, draining lymphangitis, and swollen hilar lymph node (Figs. 21.1 and 21.2). CT scanning can also well define lobar or segmental atelectasis caused by compression of the bronchus by swollen lymph nodes and the pleural changes in the vicinity of the primary lesion.

Case Study 1

A male patient aged 16 years was diagnosed with primary pulmonary tuberculosis (primary syndrome).

Fig. 21.1
figure 1

Primary syndrome. CT scanning demonstrates a small quantity of spot-like shadows at the lateral segment of the right middle lobe with fusion of some spot-like shadows, enlarged right hilum that is caused by right hilar lymphadenectasis, and unobstructed adjacent bronchus

Cast Study 2

A female patient aged 20 years was diagnosed with primary pulmonary tuberculosis (primary syndrome).

Fig. 21.2
figure 2

Primary syndrome. (a) CT scanning demonstrates irregular nodular shadows at the apical segment of the right upper lobe, surrounding spot- and cord-like shadows, and flakes of shadows near mediastinum that connect to the mediastinum. (b) CT scanning demonstrates uneven density of the nodules at the right upper lobe, low-density area in the parenchyma, lymphadenectasis at the 2R area of the mediastinum, poorly defined surrounding adipose space, and connection of some adipose spaces with intrapulmonary lesions. (c) Contrast scanning demonstrates marginal enhancement of the nodules at the right upper lung, central low-density area with no enhancement, and uneven enhancement of mediastinal lymph nodes

7.1.1.2 Intrathoracic Lymphatic TB

Due to rapid absorption of primary lesion in the lung but relatively slow absorption of hilar and mediastinal lymphatic lesion, primary tuberculosis is only demonstrated as enlarged hilar and/or mediastinal lymph nodes, which is known as intrathoracic lymphatic tuberculosis. Hilar lymphatic tuberculosis can be further divided into the following two types: inflammatory lymphatic tuberculosis, with enlarged lymph node and surrounding inflammatory infiltration, and mass lymphatic tuberculosis, with absorption of inflammatory lesion surrounding the lymph node and well-defined boundary of the lymph node.

7.1.1.2.1 Hilar Lymphatic TB
7.1.1.2.1.1 Mass Lymphatic Tuberculosis

The lesion of mass type is commonly located at the right hilum, specifically superior margin of the right hilum and the angular area of the right hilum around the right inferior pulmonary artery. The lesion at the left hilar area is commonly located at the superior and exterior margin of the left pulmonary arterial arch and around the left inferior pulmonary artery.

The fully exposed lymph node is nodular, round, or oval in shape with well-defined intact boundary. The partially exposed lymph node is half arch in shape protruding towards the lung field due to its partial overlapping with the hilar vascular vessels. The fusion of large lymph nodes is demonstrated like a mass, with its exterior margin lobulated like plum petals. Plain CT scanning demonstrates some adipose spaces between the lymph nodes, based on which the mass can be distinguished to be formed by fused nodules.

The density of the lesion is homogeneous or heterogeneous (caseous necrosis and liquefaction within lymph lodes). Even calcification can be found.

Contrast CT scanning demonstrates less enlarged lymph nodes with slightly even enhancement and most enlarged lymph nodes with ring-shaped enhancement (peripheral granulation of the lymph node is demonstrated as a ring-shaped or marginal enhancement by contrast scanning, and central necrosis and liquefaction is demonstrated with no enhancement). In the cases with fusion of multiple lymph nodes into large mass, separated enhancement is demonstrated. The enhancement degree of enlarged lymph nodes is markedly distinct from that of blood vessels in the adjacent hilar area (Fig. 21.3).

7.1.1.2.1.2 Inflammatory Lymphatic TB

Inflammatory lymphatic TB shares common radiological demonstrations with mass lymphatic TB.

Due to caseous necrosis and capsular rupture of some lymph nodes, these lymph nodes are demonstrated with rough and poorly defined margin. Otherwise, due to the exudative lesion around the lymph node, the marginal density is demonstrated to be lightened and blurry.

The major vascular branches at the hilar area are mostly demonstrated with smooth blood flow, well-defined and smooth vascular lining, and occasional enlarged lymph nodes. In the cases with the adjacent bronchus involved or with concurrent adjacent bronchial TB, the involved bronchial segment is subject to thickened bronchial wall and narrowed bronchial lumen.

7.1.1.2.2 Mediastinal Lymphadenectasis

The lesion is commonly located at the paratracheal area and tracheobronchial region, especially the right lung.

For the cases with well-defined lymph node, pathological examination indicates intact capsule encapsulating the swollen lymph node. X-ray demonstrates the swollen lymph node in a half arch shape protruding towards the lung field, with wavelike mediastinum. Plain CT scanning demonstrates round- or oval-shaped lymph node with surrounding adipose space, especially prevascular space. There are also swollen lymph nodes anterior to the right trachea and posterior to the vena cava, at the left aortic-pulmonary window and in the right azygoesophageal recess. For the cases with unclearly defined lymph node, its surrounding adipose spaces are partially absent and partially present. The pathological examination indicates caseous necrosis of the lymph node and its penetration out of its capsule. For the cases with fusion of multiple lymph nodes into irregular mass, the mass is commonly located between the major vascular vessels in the mediastinum.

By plain CT scanning, the density of most lymph nodes is homogeneous, and the density of rare lymph nodes is uneven due to caseous necrosis and liquefaction. In some cases, the lymph nodes are demonstrated with internal or marginal calcification. Contrast CT scanning demonstrates homogeneous enhancement of the small lymph nodes, peripheral irregular wall enhancement of large lymph nodes, ring-shaped enhancement of the thin wall, and separated enhancement. By pathology, the enhanced area is indicated to be tubercular granulation tissue with abundant blood flow, and the area with no enhancement is indicated to be mostly caseous necrosis. The separated enhancement is pathologically indicated to be the fusion of multiple lymph nodes containing lesions of caseous necrosis (Figs. 21.4 and 21.5).

Case Study 3

A male patient aged 16 years was diagnosed with intrathoracic lymphatic TB.

Fig. 21.3
figure 3

(a, b) Plain CT scanning demonstrates swollen lymph nodes at the right lower lung hilum with nodular shadows and unobstructed right middle bronchus. (c) Contrast CT scanning demonstrates homogeneous enhancement of the hilar major vascular vessels that obviously distinct from its adjacent nodular shadows of lymph nodes. Obstructive pneumonia is demonstrated at the right middle lung lobe

Case Study 4

A male patient aged 21 years was diagnosed with intrathoracic lymphatic TB.

Fig. 21.4
figure 4

Mediastinal lymphatic TB. (a) CT scanning demonstrates paratracheal nodular shadow at the right upper mediastinum, which is in arch shape protruding towards the lung field. (b) The nodules are in bean shape, with marginal or internal spots of calcification

Case Study 5

A female patient aged 23 years was diagnosed with mediastinal lymphatic TB.

Fig. 21.5
figure 5

Mediastinal lymphatic TB. (a, b) Plain CT scanning demonstrates swollen lymph nodes at the 3R and 4R areas of the mediastinum, absent adipose space between some of the lymph nodes and vascular vessels, and uneven density. (c, d) Contrast scanning demonstrates heterogeneous enhancement of the lymph nodes, with ring-shaped or separated enhancement

By plain MR imaging, the mediastinal lymph nodes are demonstrated as equal T1 and equal T2 signals, with internal patches of slightly long T1 slightly and long T2 signals. By contrast MR imaging, the mediastinal lymph nodes are demonstrated as nodular, ring-shaped, separated, or uneven enhancement. The demonstrations of no central enhancement, peripheral enhancement, and ring-shaped enhancement are characteristic, with high diagnostic value.

7.1.2 Hematogenous Pulmonary TB

7.1.2.1 Acute Hematogenous Pulmonary TB

It is caused by invasion of a large quantity of MTB into the blood flow for once or several times within a short period of time. It is more common in children and during the stage of primary pulmonary TB.

7.1.2.1.1 X-Ray

X-ray demonstrates extensively and evenly distributed miliary sized nodular shadows with increased density. It is characterized by even distribution, even size, and even density, which is known as the three-evens sign. Due to a large quantity of lesions with dense distribution, both lungs are demonstrated with ground-glass opacity. The miliary shadows have a diameter of 1–2 mm and a round or oval shape, with well-defined boundary. In the cases with exudative lesions, the miliary shadows are demonstrated with poorly defined boundary. At the early stage, X-ray only demonstrates enhanced lung markings. After about 2 weeks, typical miliary nodules can be demonstrated. In the advanced stage, the miliary increased density shadows tend to fuse together.

7.1.2.1.2 CT Scanning

Pulmonary interstitial miliary nodules are demonstrated with diffusely distributed military shadows at the interstitium of both lungs. The nodules have a diameter of 1–3 mm with even distribution and even density. Most nodules are well defined and rarely with poorly defined boundary. In the cases with no immediate treatment, the nodules may enlarge to a diameter of about 5 mm. The nodules are morphologically irregular and may fuse into focalized consolidation lesion.

Miliary nodules may be complicated by confined ground-glass opacity, with light density and blurry boundary.

Interlobular septal thickening and intralobular reticular shadows are caused by congestion and edema of alveolar septa during the acute stage, which often coexists with ground-glass opacity. Most patients experience their absence after treatment. In some rare patients, they develop into irreversible reticular fibrosis.

Clustering thin wall cyst shadows can be demonstrated at the progressive stage of the conditions in rare patients, which are reversible.

In the patients with acute hematogenous pulmonary TB but receiving delayed or inappropriate therapy, the conditions progress. The caseous substances formed by TB lesions may involve the alveolar cavity and disseminate along the bronchus. The nodular shadows in both lungs can be demonstrated with random and confined distribution of centrilobular branch shadow and the tree bud sign that may be well defined or poorly defined (Figs. 21.6 and 21.7).

Case Study 6

A female patient aged 14 years was diagnosed with acute hematogenous pulmonary TB.

Fig. 21.6
figure 6

Acute hematogenous pulmonary TB. (ac) CT scanning demonstrates diffuse miliary shadows at both lungs, with even size, even density and even distribution

Case Study 7

A female patient aged 25 years was diagnosed with acute miliary pulmonary TB. During the recent 10 days, the patients experience fever and cough after abortion, with difficulty expectorating. The fever occurs commonly after noons, with a body temperature fluctuating around 37.8 °C, and the cough is paroxysmal.

Fig. 21.7
figure 7

Acute miliary pulmonary TB. (a, b) CT scanning demonstrates diffuse miliary nodular shadows at both lungs with even size, even density, and even distribution

7.1.2.2 Subacute and Chronic Hematogenous Pulmonary TB

Due to repeated invasions of a small quantity of MTB into the blood flow during a long period of time, subacute or chronic hematogenous pulmonary TB occurs. The source of their dissemination is commonly infected veins after urogenital TB or osteoarticular TB.

7.1.2.2.1 X-Ray

X-ray demonstrates three-unevens sign. The size of lesions ranges from miliary to 1 cm in diameter. The density of exudative or proliferative lesions is light, while the density of calcification is dense, with blurry or sharp boundary. The lesions are unevenly distributed at the upper and middle lung fields. The old hard nodular calcifications are mostly distributed at the lung apex and subclavicular area, while the new exudative and proliferative lesions are mostly distributed at the lower lungs.

7.1.2.2.2 CT Scanning

CT scanning demonstrates unevenly distributed lesions that are more commonly distributed at the middle and upper lungs, the lesions with different sizes due to fusion of miliary nodules, and the lesions with uneven density due to inner calcification. These findings are known as the three-unevens sign. Compensatory emphysema can be demonstrated between lesions or at the lower lungs (Fig. 21.8).

Case Study 8

A male patient aged 24 years was diagnosed with subacute hematogenous pulmonary TB.

Fig. 21.8
figure 8

Subacute hematogenous pulmonary TB. (ac) CT scanning demonstrates diffuse miliary nodules at both lungs, with different size and density. Some miliary nodules fuse together at the upper lobe of both lungs

7.1.2.3 Secondary Pulmonary TB

Secondary pulmonary TB is a major type of pulmonary TB, and it is the most common type of pulmonary TB.

7.1.2.3.1 Infiltrative Pulmonary TB
7.1.2.3.1.1 CT Scanning

CT scanning sometimes demonstrates traces of primary infection of tuberculosis. The calcification in the intrapulmonary primary lesions is demonstrated in spots of and nodular lesions with high density. Peripheral inflammation can be demonstrated around the old lesions, with central high density and peripheral patches and small flakes of light blurry shadows. Hilar and mediastinal lymph nodes are demonstrated with calcification.

The lesions of secondary infection of MTB are commonly located at the apical posterior segment of the upper lung lobe and dorsal segment of the lower lung lobe. Multiple lesions can be found within one pulmonary segment or lobe or within unilateral or bilateral lung fields. The exudative lesions are demonstrated as cloud-like shadow with patches, small flakes, or flakes of shadows with increased density. The density of lesions is even or uneven with blurry boundary. The patches of shadows may fuse into flakes of shadows. The proliferative lesions are demonstrated as spots, small nodules, and patches of shadows with increased density and well-defined boundary. The proliferative lesions rarely fuse together. Caseous necrosis can be found at the lesions to induce low-density or semitransparent cavity, which is demonstrated as a transparent area with different sizes and shapes. Infiltrative TB at different stages can be demonstrated with no wall cavity, thin wall cavity, caseous thick wall cavity, tension cavity, and purified cavity. Around the cavity, spots of small nodular shadows are demonstrated, which are technically known as satellite lesions. Bronchial lesions are commonly found at the unilateral or bilateral middle and lower lung fields disseminated from cavity. The calcifications are demonstrated as high-density spots of linear or patches of shadows with well-defined boundary but in regular or irregular shape. At the middle and advanced stages of infiltrative TB, calcification is commonly demonstrated in the lesions. The finding of calcifications in the lesion or at the margin of lesion greatly facilitates the qualitative diagnosis. Meanwhile the finding of calcification indicates that the conditions are tending to stabilize or be improved. The fibrous lesions are demonstrated as cords like or stellate-like shadows with high density and rough boundary. Within a short period of time, the progress and absorption of the lesions are slower than those of lobar pneumonia, lobular pneumonia, mycoplasma pneumonia, and common viral pneumonia. Accompanying pleural effusion occurs. In the cases complicated by hematogenous disseminated pulmonary TB, in addition to intrapulmonary infiltrative lesions, there are also demonstrations of acute or subacute and chronic hematogenous disseminated pulmonary TB (Figs. 21.9, 21.10, 21.11, and 21.12).

Infiltrative pulmonary TB is demonstrated with common concurrence of at least two types of lesions among exudates, proliferation, caseous necrosis, cavity, calcification, and fibrosis. Radiologically, it is characterized by multiple lesions, multiple densities, and multiple shapes. The typical radiological sign of infiltrative pulmonary TB is lesions at the apical posterior segment of both upper lung lobes.

Case Study 9

A male patient aged 20 years was diagnosed with secondary pulmonary TB (infiltrative pulmonary TB).

Fig. 21.9
figure 9

Infiltrative pulmonary TB. (a, b) CT scanning demonstrates spots of small nodular and small patches of shadows at the right upper lung lobe and calcification in the lesions at the apical segment of the right upper lung lobe

Case Study 10

A male patient aged 25 years was diagnosed with secondary pulmonary TB (infiltrative pulmonary TB).

Fig. 21.10
figure 10

Infiltrative pulmonary TB. (a, b) CT scanning demonstrates a transparent area at the posterior segment of the right upper lung lobe, double rail-like draining bronchi between the transparent area and the hilum, spot-like satellite lesions around the transparent area, and spots of bronchial lesions at the right lower lung lobe

Case Study 11

A female patient aged 77 years complained of cough for over 4 months, with rare phlegm, fatigue, chest distress, and shortness of breath. By sputum smear, acid-fast bacillus is positive.

Fig. 21.11
figure 11

Infiltrative pulmonary TB. (ac) CT scanning demonstrates flakes and nodular blurry shadows at both lungs, dilation of local bronchial lumen, thickening of local bronchial wall, and calcification of some lymph nodes

Case Study 12

A female patient aged 43 years. By sputum smear, acid-fast bacillus is positive.

Fig. 21.12
figure 12

Infiltrative pulmonary TB and pleural effusion. (a, b). CT scanning demonstrates multiple thick wall cavities in different sizes at both upper lung lobes, uneven thickness of the thick wall cavities, multiple small patches and cotton wool like shadows around the lesions, observable tree bud sign, and scattering multiple nodular or cord-like shadows in both lungs. There are also enlarged mediastinal lymph nodes and bilateral pleural effusion in small quantities

7.1.2.3.1.2 MR Imaging

T2WI demonstrates exudative and caseous lesions with high signal, proliferative lesions with moderate signal, fibrosis lesions with low signal, calcification lesions with lower signal, and gas in the cavity with extremely low signal.

7.1.2.3.2 Tubercular Lobar Pneumonia and Caseous Pneumonia
7.1.2.3.2.1 Tubercular Lobar Pneumonia

Tubercular lobar pneumonia is an uncommon type of secondary pulmonary TB, which is also known as bronchial pneumonia TB.

By CT scanning, the lesions are commonly located at the upper lung lobe, especially the apical posterior segment. The lesions are commonly demonstrated as large flakes of shadows occupying a whole segment, lobe, or even a lung field. The central area is demonstrated with a large area of consolidation, with light and poorly defined boundary. These demonstrations resemble to those of lobar pneumonia. The large flakes of consolidation are demonstrated with inner air bronchus sign. In some cases, the air bronchus is demonstrated with column-like or bead string-like dilation. The cloud-like shadows are demonstrated with spots of and small nodular high-density lesions. The small nodular shadows are demonstrated at the margin of flakes of shadows, with some marginal lesions being blurry and some others well defined. By radiological examinations, a large flake of lesions is surrounded by many small lesions, which scatter unevenly. Such findings facilitate its differential diagnosis from lobar pneumonia. In the large flake of consolidation or at the marginal flake of consolidation, there are slightly low-density semitransparent areas or small transparent areas, indicating the occurrence of small caseous necrosis and dissolution. The disease progresses rapidly, with infiltration of the lesions, occurrence of surrounding inflammation, and fusion of the lesions. At the affected lung field or contralateral lung field, scattering polymorphic spots of small nodular or patches of TB lesions greatly facilitate its diagnosis (Fig. 21.13).

Case Study 13

A male patient aged 36 years was diagnosed with secondary pulmonary TB (tubercular lobar pneumonia).

Fig. 21.13
figure 13

Tubercular lobar pneumonia. (ac) CT scanning demonstrates a large flake of consolidation at the right upper lung lobe with inner air bronchus sign. The margin of lesions is demonstrated to be poorly defined with small patches and spots of shadows. The middle and lower lobes of right lung are demonstrated with small patches and spots of shadows

7.1.2.3.2.2 Caseous Pneumonia

Caseous pneumonia is the acutest and severest type of secondary pulmonary TB. Some cases of caseous pneumonia are developed from caseous necrosis of exudative lesions due to tubercular lobar pneumonia.

  1. 1.

    X-ray and CT scanning

Caseous lobar pneumonia is demonstrated with large flakes of cloud-like shadows, which gradually develop into a large flake of consolidation shadow with moderate density. The lesion is commonly located at the upper lung lobe, occupying a whole segment, lobe, or even lung field, with poorly defined boundary. The lesion has uneven density, with extensive multiple worm-bitten-like low-density semitransparent area or transparent area in different sizes at the large flake of consolidation shadow. The cavities are morphologically varied, with irregular, unsmooth, and poorly defined cavity wall. Such a sign is more clearly demonstrated by HRCT. Without timely and effective treatment to control its development, the conditions continue to deteriorate with further expansion of multiple worm-bitten-like cavities in different sizes and their fusion. Consequently, large area of the lung is destructed by formation of huge cavity (Fig. 21.14). Bronchial lesions caused by dissemination can be demonstrated at the homolateral or contralateral lung field. Caseous lobular pneumonia is demonstrated with multiple scattering small flakes, small nodules, and spots of shadows at the unilateral or bilateral upper and middle parts of the lung. The small flakes of shadows may fuse into a large flake. In the flakes of, small flakes of and nodular lesions, irregular lesions of caseous necrosis and dissolution can be found in different sizes to show low-density semitransparent or transparent area. Such a sign is of great significance for the diagnosis. At the middle and advanced stages, the lung tissue is subject to extensive and severe damage to cause shrinkage of the lung lobe and thickening of the adjacent pleura.

  1. 2.

    MR imaging

The demonstrations of secondary pulmonary TB based on caseous lesions by MR imaging morphologically resemble to those by CT scanning. The lesions of caseous necrosis are demonstrated with moderate or slightly low T1WI signal and heterogeneous high T2WI signal. In the cases with peripheral fiber or granulation tissue, enhancement can be demonstrated, while the caseous necrotic tissue is demonstrated with no enhancement. In the cases with accompanying large calcification, no signaling shadow can be demonstrated.

Case Study 14

A female patient aged 30 years was diagnosed with secondary pulmonary TB (caseous pneumonia).

Fig. 21.14
figure 14

Caseous pneumonia. (a) CT scanning demonstrates large flakes of shadows at the right upper lung lobe with multiple irregular transparent areas in different sizes in the lesions and cord-like shadows at the left upper lung lobe. (b) Spots of calcification are demonstrated in the lesion

7.1.2.3.3 Pulmonary Tuberculoma

Tuberculoma refers to the spherical lesion formed by a caseous lesion of pulmonary TB encapsulated by fibrous tissues.

  1. 1.

    The lesions are commonly located at the apical posterior segment of the upper lung lobe and dorsal segment of the lower lung lobe.

  2. 2.

    The lesion is mostly singular, but in rare cases, the lesions are multiple.

  3. 3.

    The lesions are round or oval in shape, those with a diameter being less than 2 cm are referred to as fibrous caseous lesion, and those with a diameter being larger than 2 cm are referred to as tuberculoma.

  4. 4.

    The contour of lesion is clear and regular, rarely with incisura and lobulation.

  5. 5.

    The density of the lesion may be homogeneous or with inner semitransparent area due to dissolution. The dissolution area is commonly located near the hilum in the spheric shadow. Cavity can also be demonstrated.

  6. 6.

    At the lung field near the spherical shadow, scattering proliferative or fibrous lesions are commonly found in spots of small nodular and cord-like shadows, namely, the satellite lesions.

  7. 7.

    Between the tuberculoma and hilum of the lung, cord-like shadows are demonstrated, which are residual draining bronchi after formation of the tuberculoma derived from the cavity.

  8. 8.

    Calcification can be found within or at the margin of tuberculoma. The typical demonstration is laminar ring-shaped calcification shadow or scattering spots of calcification.

  9. 9.

    Contrast CT scanning demonstrates linear enhancement of the tuberculoma capsule and no or slight central enhancement (Figs. 21.15, 21.16, and 21.17).

Case Study 15

A male patient aged 39 years was diagnosed with secondary pulmonary TB (pulmonary tuberculoma).

Fig. 21.15
figure 15

Pulmonary tuberculoma. (a) CT scanning demonstrates round-like nodular shadow at the apical segment of the right upper lung lobe, with a well-defined and smooth boundary, multiple linear shadows in different lengths radiating from the nodule outwards, and spots of satellite lesion around the lesion. (b) Spots of calcifications can be demonstrated in the lesion

Case Study 16

A female patient aged 43 years experienced cough and hemoptysis for several months. By sputum smear, acid-fast bacillus is positive.

Fig. 21.16
figure 16

Pulmonary tuberculoma, infiltrative pulmonary TB. (a, b) CT scanning demonstrates spherical lesion at the right middle lung lobe, with marginal irregular calcification and well-defined boundary. The lesion is demonstrated with surrounding satellite lesions. And multiple nodules are demonstrated at the right lower lung

Case Study 17

A male patient aged 35 years experienced cough for over 20 days, with no known causes. He coughed up rare sputum that was white and foamy, with no blood and odor. By sputum smear, acid-fast bacillus is positive.

Fig. 21.17
figure 17

Pulmonary tuberculoma and acute hematogenous pulmonary TB. (a, b) CT scanning demonstrates spherical lesion at the right lower lung lobe near pleura with poor defined boundary and surrounding satellite lesions. There are diffuse miliary TB lesions at both lungs and calcified lymph nodes at the mediastinum and left hilum

7.1.2.3.4 Chronic Fibro-Cavity Pulmonary TB

Tuberculosis has a long illness course, with alternated deterioration and alleviation. Local or most of the lung tissue is subject to severe damage, with concurrent extensive proliferation and repair of fiber tissue around the lesion, namely, the occurrence of fibro-cavity.

  1. 1.

    Irregular fibro-cavities are located at the apical posterior segment of the upper lung lobe or the dorsal segment of the lower lung lobe, namely, the supraclavicular or subclavicular region. Extensive cord-like shadows are demonstrated to surround the lesion. Local lung volume shrinks, commonly leading to elevated hilum at the affected lung. The lung markings are demonstrated like willow. And the trachea and mediastinum are demonstrated to shift to the affected lung.

  2. 2.

    Both old and new tuberculosis lesions are commonly found at the unilateral upper and middle lung fields, namely, concurrence of various lesions including exudative lesions, proliferative lesions, caseous lesions, cavities, fibrous lesions, and calcification.

  3. 3.

    Bronchial lesions due to dissemination are commonly found at the middle and lower lung fields of the affected lung as well as at the contralateral lung field.

  4. 4.

    The unaffected lung field is subject to compensatory emphysema. CT scanning demonstrates bullae of the lung, which is demonstrated as thin wall bullae within or at the margin of the lung.

  5. 5.

    The pleura of the affected lung is subject to long-term invasion, thickening, and adhesion to cause narrowing of local intercostal space and collapse of thorax. Meanwhile, due to shrinkage of the upper lung volume as well as traction by pleural thickening and adhesion, the arches of the superior mediastinum and trachea shift towards the affected lung.

  6. 6.

    CT scanning, especially HRCT, is superior to X-ray in detecting secondary bronchiectasis. The demonstrations are commonly multiple thin wall small bubbles with a honeycomb-like sign (Figs. 21.18, 21.19, and 21.20).

Case Study 18

A male patient aged 44 years was diagnosed with secondary pulmonary TB (chronic fibro-cavity pulmonary TB).

Fig. 21.18
figure 18

Chronic fibro-cavity pulmonary TB. CT scanning demonstrates transparent area at the posterior segment of the right upper lung lobe, smooth and regular lining of the cavity, multiple cord-like shadows at the exterior margin of the cavity that radiate from the cavity wall outwards, and connection of most cord-like shadows with adjacent pleura. Around the transparent area, spots of shadows scatter. Spots and patches of shadows are demonstrated at the apical posterior segment of the left upper lung lobe

Case Study 19

A male patient aged 44 years experienced cough. By sputum smear, acid-fast bacillus is positive.

Fig. 21.19
figure 19

Chronic fibro-cavity pulmonary TB. (ad) CT scanning demonstrates multiple thick wall cavities at the upper lobe of both lungs, accompanying bronchial lesions due to dissemination, and pleural thickening

Case Study 20

A male patient aged 59 years. By sputum smear, acid-fast bacillus is positive.

Fig. 21.20
figure 20

Chronic fibro-cavity pulmonary TB. (a, b) CT scanning demonstrates singular thick wall cavity at the right upper lung lobe and surrounding cord-like shadows

7.1.2.4 Tuberculous Pleuritis

Tuberculous pleuritis is a pleural inflammation caused by access of MTB and its metabolites into the pleural cavity. Clinically, it is categorized into dry pleuritic and exudative pleuritis.

7.1.2.4.1 Dry Pleuritis

Due to rare protein exudates, X-ray demonstrates dry pleuritis with no abnormalities. When local pleura develops thickening and adhesion, local decrease of transparency can be demonstrated, with a dome-shaped shadow at the diaphragm. CT scanning is more sensitive to pleural thickening. In addition, CT scanning can demonstrate slight protrusion of the pleura towards the lung field due to a small quantity of areas with liquid density, with poorly defined boundary (Figs. 21.21 and 21.22). MR imaging demonstrates linear moderate or low T1WI signal shadow and slightly high or high T2WI signal shadow.

7.1.2.4.2 Exudative Pleuritis

Based on the quantity, location, and state of pleural effusion, exudative pleuritis can be categorized into free pleural effusion type and localized pleural effusion type.

7.1.2.4.2.1 Free Pleural Effusion

Free pleural effusion refers to pleural effusion that is not confined or restricted within a certain part of the pleural cavity, whose distribution can change along with change of body posture and is consistent to the distribution of liquid gravity. Based on the volume of pleural effusion, it can be further divided into three types: small quantity, moderate quantity, and large quantity.

Concerning the small quantity type, in the cases with pleural effusion exceeding 250–300 ml, X-ray at the standing posture demonstrates blunt and shallow costophrenic angle at the affected side as well as the normal shape and contour of the diaphragm. CT scanning demonstrates arch shape and narrow strip of liquid density shadow at the medial posterior thoracic wall that is parallel to thoracic wall. The shadow has smooth and regular margin (Figs. 21.23 and 21.24).

Concerning the moderate quantity type, the superior borderline of effusion is commonly above the anterior plane of the 4th rib, but below the anterior plane of the 2nd rib. Ultrasound demonstrates a triangular no echo area of the costrophrenic angle or no echo area due to a small quantity of effusion superior to the liver top. X-ray at standing posture demonstrates the superior borderline of effusion as arch shape shadow with higher exterior and lower interior, which has upper light density and lower dense and even density, and completely absent contour of the diaphragm. CT scanning demonstrates crescent liquid density shadow at the medial posterior thoracic wall, with even density and regular margin. The local lung tissue is slightly compressed.

Concerning the large quantity type, the superior borderline of effusion surpasses the anterior plane of the 2nd rib. The affected lung field has dense and even shadow, with widened intercostal space and lowered diaphragm. The mediastinum shifts towards the unaffected side. In some cases, only the transparent lung apex of the affected thoracic cavity can be found. CT scanning demonstrates the thoracic cavity being occupied by liquid density shadow and the lung being compressed with soft tissue shadows at the hilum.

7.1.2.4.2.2 Localized Pleural Effusion

Encapsulated pleural effusion refers to effusion limited in a certain part of the pleural cavity due to adhesions of visceral and parietal pleura. By ultrasound, the no echo area is limited at a certain part of the pleural cavity with semicircular or irregular shape. In most cases, the no echo area is close to the thoracic wall with wide base, and does not change along with change of body posture. By X-ray radiology, the encapsulated pleural effusion is commonly located at the medial posterior thoracic wall at the lower thoracic cavity. X-ray at tangential position demonstrates semicircular or D-shaped liquid density shadow protruding from the thoracic wall to the lung field, with well-defined and smooth boundary. And the angulation of its superior and inferior margins with the thoracic wall is obtuse. By CT scanning, the encapsulated pleural effusion at the lateral thoracic cavity is demonstrated as a convex-shaped liquid density shadow protruding from the thoracic wall to the lung field, which has broad basement and closely adheres to the thoracic wall. Its angulation with the thoracic wall is commonly obtuse, and its margin is smooth. The adjacent pleura is commonly subject to thickening to form a pleural tail sign. Local lung tissue may be subject to compression (Fig. 21.25).

Interlobar effusion refers to effusion confined to the horizontal fissure and oblique fissure. By X-ray, the cases with oblique fissure effusion are demonstrated with effusion confined at the upper or lower oblique fissure. Based on the demonstrations by anterior-posterior X-ray, the diagnosis can be hardly defined, while the demonstrations by lateral X-ray can facilitate to define the diagnosis. Lateral X-ray demonstrates the typical spindle-shaped shadow at the interlobar fissure, with even density and well-defined boundary. After free pleural effusion gains its access into the interlobar fissure, the effusion is commonly confined at the lower part of the oblique fissure, with triangular increased density shadow with the sharp top pointing upwards to the hilum. By CT scanning, the interlobar area with less vascular vessels is demonstrated with flakes or strips of high-density shadow, sometimes with spindle or sphere shape. In the cases with a large quantity of effusion, mass-like shadow is demonstrated, with the thickened interlobar pleura at its both ends. The lesion is located at the interlobar fissure with liquid density, based on which the diagnosis can be defined. By MR imaging, the morphology and signal of effusion can be demonstrated from multiple perspectives.

Infrapulmonary effusion refers to effusion within the pleural cavity between the diaphragm and the base of the lung. It is more commonly found at the right lung. And its radiological demonstrations change along with change of body posture. By X-ray at standing posture, the diaphragmatic surface at the affected lung is demonstrated with elevation, with outward shift of the highest point of the diaphragmatic dome to the exterior 1/3 part of the diaphragm. X-ray at supine posture demonstrates generally increased density of the affected lung field due to perfusion of liquid into the unilateral thoracic cavity and normal position of the diaphragmatic muscle.

Case Study 21

A male patient aged 41 years was diagnosed with tuberculous pleural thickening.

Fig. 21.21
figure 21

Infiltrative pulmonary tuberculosis and dry pleuritis. (a) CT scanning demonstrates spots and patches of shadows at the posterior segment of the right upper lung lobe. (b) CT scanning demonstrates cord-like shadow at the apical posterior segment of the left upper lung lobe. (c) Arc-shaped cord-like shadow with soft tissue density is demonstrated at the posterior inferior part of the left pleura, with well-defined and smooth pleural surface

Case Study 22

A male patient aged 43 years was diagnosed with pleural tuberculoma, pleural thickening, and calcification.

Fig. 21.22
figure 22

Pleural tuberculoma, pleural thickening, and calcification. (a, b) CT scanning demonstrates patches of shadows at the dorsal segment of the left lower lung lobe, with calcification in the lesion. D-shaped shadow with soft tissue density is demonstrated exterior and anterior to the adjacent right pleura, with well-defined and smooth pleural surface and internal spots of calcification

Case Study 23

A male patient aged 22 years was diagnosed with tuberculous pleural effusion.

Fig. 21.23
figure 23

Tuberculous exudative pleuritis (free pleural effusion). (ac) CT scanning demonstrates spots and patches of shadows at the apical posterior segment of the left upper lung lobe and crescent-shaped liquid density shadow at the left thoracic cavity

Case Study 24

A male patient aged 61 years experienced fever and cough. By sputum smear, acid-fast bacillus is positive.

Fig. 21.24
figure 24

Tuberculous exudative pleuritis (free pleural effusion). (a, b) CT scanning demonstrates small quantities of pleural effusion at bilateral thoracic cavity and enlarged mediastinal lymph nodes

Case Study 25

A male patient aged 66 years experienced fever and cough. By sputum smear, acid-fast bacillus is positive.

Fig. 21.25
figure 25

Tuberculous exudative pleuritis (encapsulated pleural effusion), pleural thickening, calcification, and cavity. (ad) CT scanning demonstrates encapsulated pleural effusion, pleural thickening, calcification, and multiple cavities at both lungs

Studies by PET/CT have demonstrated that an abnormal increased of 18F-FDG uptake can be induced by pulmonary TB, tuberculous granuloma, chronic tuberculous lymphadenitis, tuberculous pleuritis (peritonitis), and bone tuberculosis. In addition, the uptake of 18F-FDG varies in different pathological stages. The nodular lesion of pulmonary TB is demonstrated with hypermetabolism, even in the cases with obvious calcification at the lesion, which indicates active TB with chronic inflammation. Pathologically, the chronic inflammations include infiltration of inflammatory cells, proliferation of macrophages, and formation of granuloma. The non-demonstrated lesions by 18F-FDG PET are caseous and old fibrosis and calcification, which are present in the cases with inactive tuberculosis. For such cases, following up observations is necessary. In the cases with hilum and mediastinal lymph nodes involved, hypermetabolism is demonstrated by 18F-FDG, indicating tuberculous lymphadenitis and proliferative lesion (Figs. 21.26, 21.27, 21.28, and 21.29). PET/CT facilitates in assessing the extrapulmonary active tuberculosis, while 18F-FDG PET can also be applied to assess the therapeutic efficacy against TB. Soussan M et al. divided FDG PET/CT examination for tuberculosis into two types, one is for lung TB and the other for lymphatic TB. The relationship between the two types and the immunity of the patients has been studied. They found that the lesions confined within the lungs with slight hypermetabolism can be defined as lung TB, indicating normal immune functions and the effective immune responses. In the patients with compromised immunity, the lesions caused by MTB cannot be confined within the lungs, and the lymph nodes are involved, with or without involvement of the bone, liver, and spleen. An obvious hypermetabolism demonstrated by FDG indicates lymphatic TB.

By 18F-FDG PET examination, attention should be paid to the differential diagnosis of active tuberculous nodule and lung cancer, for both of which exhibit hypermetabolism. The lesion with signs of lobulation, speculation, vacuole sign, air bronchus, or pleural depression sign supports the diagnosis of lung cancer. In combination to 18F-FLT, the differential diagnosis of benign pulmonary nodule and malignancy can be accurately made. However, well-differentiated lung cancers can also be demonstrated as no or low uptake of 18F-FDG.

Case Study 26

A female patient aged 45 years experienced coughing up bloody sputum for 4 months. And the conditions showed no response to anti-infective therapy. By PPD test 2 months ago, strongly positive was indicated, and the patient received anti-TB therapy. The reexamination after treatment for 2 months, the lesions are demonstrated to be thick and dense at the right upper lung lobe by CT scanning. Following PET/CT examination was ordered. Pathological diagnosis after surgery was pulmonary TB.

Fig. 21.26
figure 26

Tuberculoma. (a) PET demonstrates increased radioactive uptake by nodules at the right upper lung lobe, with SUV max 2.9. (b, c) CT scanning demonstrates a nodule in size of 1.7 cm × 1.3 cm at the posterior segment of the right upper lung lobe. The nodule is shallowly lobulated with smooth and regular margin and internal spots of calcification. (d) PET/CT demonstrations of the lesion

Case Study 27

A male patient aged 46 years experienced fever and right abdominal pain for over 1 month. The patient reported fever and right abdominal pain more than 1 month ago with no known causes. The fever occurred after noons with a body temperature of 38–40 °C and night sweating. After receiving anti-infective therapy, he showed no improvement. By PPD test, strongly positive and the conditions were obviously improved after anti-TB treatment. The clinical diagnosis was tuberculosis.

Fig. 21.27
figure 27

Pulmonary TB and abdominal TB. (a) CT scanning demonstrates irregular spots of shadows comprising a nodular lesion at the apical posterior segment of the right upper lung lobe, with lower density at the center. (b) PET/CT demonstrates increased HDG metabolism around the lesion, with SUVmax11.2 and defective metabolism of the central low-density area. (c) It is demonstrated with enlarged hilar lymph nodes at the right lung, with high FDG metabolism and SUVmax12.8. (d) The abdominal cavity is demonstrated with a mass in size of 4.7 × 3.2 cm, which shows irregular ringlike abnormal increase of the radioactive uptake, with SUVmax9.8, which shows an increase to SUVmax12.4 after 1 h. The central low-density area is demonstrated as caseous change with no metabolism

Case Study 28

A male patient aged 64 years experienced cough with bloody sputum for over 1 year. He had a medical history of pulmonary TB 2 years ago and received anti-TB therapy. After oral medication for 14 months, the symptoms showed no improvement. He reported no recent subjective upset.

Fig. 21.28
figure 28

Pulmonary TB. (a) CT scanning demonstrates spots of nodular and cord-like TB lesions at the posterior segment of the right upper lung lobe, with well-defined boundary. (b) The lesion is demonstrated with no significant increase of the radioactive uptake, with SUVmax1.6

Case Study 29

A male patient aged 71 years was detected with lesions by a routine physical examination.

Fig. 21.29
figure 29

Tuberculoma. (a, b) During a routine physical examination 18 months ago, CT scanning demonstrates spots of calcifications at the posterior basilar segment of the left lower lung lobe. PET/CT demonstrates no metabolism at the lesion. (c, d) By a recent reexamination, CT scanning demonstrates that calcification is surrounded by soft tissue density shadows with smooth and regular margin. PET/CT demonstrates increased metabolism of the soft tissue density shadows with SUVmax11.0, which is suspected to be lung cancer. Pathology after surgery indicates tuberculosis

(Note: the cases of 26–29 and the corresponding figures were provided by Xia GL at the Affiliated Tumor Hospital, Nantong University, Nantong, Jiangsu, China)

7.2 Extrapulmonary Tuberculosis

7.2.1 Tuberculous Meningoencephalitis

Tuberculous meningoencephalitis is a disease caused by the invasion of MTB along with blood flow or directly into the subarachnoid space to involve the pia mater and arachnoid membranes and further involvements of the cranial nerves, brain parenchyma, cerebrovascular vessels, and spinal cord.

7.2.1.1 CT Scanning

CT scanning demonstrates increased meninx density, which is commonly found at the suprasellar cistern, ambient cistern, and lateral cerebral fissure. Extensive thickening and increased density are demonstrated at the contours of the cistern and sulcus as well as the meninx. By contrast scanning, obvious enhancement can be demonstrated.

CT scanning also demonstrates miliary lesions at the brain parenchyma. The fine miliary nodular shadows with equal density are extensively distributed at the cerebral cortex or brain tissue. By contrast scanning, enhancement can be demonstrated.

By CT scanning, ring shape, disk like, mass like and spots of shadows are demonstrated, which are characteristic signs of cerebral tuberculoma. Contrast scanning demonstrates ring-shaped enhancement with central low density and peripheral high density. The surrounding edema is comparatively mild, with slight space-occupying effect.

Ventricular dilation and hydrocephalus can also be demonstrated by CT scanning. Due to various degrees of obstruction at different locations of the passage for cerebrospinal fluid flow, the ventricle is subject to different degrees of dilation. In the cases with slight dilation, the anterior horn of the lateral ventricle is blunt. In the cases with moderate dilation, the lateral ventricle undergoes slight dilation. In the cases with severe dilation, the lateral ventricle undergoes obvious expansion, with compression of the adjacent brain parenchyma. Ventricular dilation and effusion are also commonly demonstrated at the 3rd ventricle.

Cerebral edema is another important sign by CT scanning. The flakes of shadows are demonstrated with low density and poorly defined boundary. The lesion is commonly located around the cerebral TB lesions or around the dilated ventricle due to hydrocephalus. By contrast scanning, the area with hydrocephalus is demonstrated with no enhancement.

Cerebral infarction is demonstrated to be singular or multiple and the lesion is in low density. Due to different sizes of the lesions, the shape of the lesions varies, which are commonly located at the area supplied by the middle cerebral artery. By contrast scanning, the lesion of cerebral infarction is demonstrated with no enhancement.

Cord-like or nodular shadows are also demonstrated by CT scanning. Cord-like shadows are demonstration of tuberculous arteritis, with increased density, and can be enhanced by contrast scanning. Nodular shadows are formed by small tuberculous proliferative lesions, with increased density, and can be enhanced by contrast scanning.

Calcification demonstrated by CT scanning is possibly located at the nodules of cerebral tuberculoma, cistern, and meninges.

7.2.1.2 MR Imaging

MR imaging can demonstrate early or small lesions and can demonstrate early tuberculous meningitis with abnormal signal shadows at the basal cistern, cerebral convex meninges, and sylvian cistern, with relative high T1WI signal and high T2WI signal. After the injection of Gd-DTAP, T1WI demonstrates meningeal enhancement at the basal cistern and diffuse meningeal enhancement (Figs. 21.30 and 21.31).

Brain tuberculoma is demonstrated by T1WI with equal signal to the gray matter and by T2WI with mostly uneven low signal or slightly high signal. Edema around brain tuberculoma is mild with high T2WI signal. After the injection of Gd-DTAP, the lesion of brain tuberculoma is demonstrated with nodular enhancement or ring-shaped enhancement (Fig. 21.32).

Case Study 30

A boy aged 13 years was diagnosed with tuberculous meningitis. In June 2012, he experienced repeated severe headache, non-ejective vomiting of gastric content, and intermittent attacks of fever with the highest body temperature of 39 °C. By laboratory tests, examination of the cerebrospinal fluid following lumbar puncture showed positive protein and WBC 300 × l06/L. The clinical diagnosis was tuberculous meningitis, and the patient was given anti-TB treatment. The symptoms such as headache and vomiting then were improved, and the body temperature returned to normal, but still with intermittent dizziness and poor appetite.

Fig. 21.30
figure 30

Tuberculous meningitis. (ae) MR imaging demonstrates multiple nodular abnormal signal shadows at both brain hemispheres, with low T1WI signal and high T2WI signal. The water suppression sequence demonstrates high signal, and DWI slightly low signal. The lesions are poorly defined with obvious surrounding edema. By contrast imaging, the lesions are demonstrated with nodular enhancement

Case Study 31

A female patient aged 23 years was diagnosed with tuberculous meningitis. In February 2011, she experienced sudden nausea, frequent vomiting of gastric content with no known causes. She also developed aversion to cold, fever, and headache, but no chills. Her highest temperature reached 38.3 °C. After oral intake of the analgesic-antipyretic drug with no prescription, her headache did not improve, but gradually worsened. The high body temperature can return to normal, but with repeated occurrence. On March 7, the patient experienced severe and unbearable headache. By lumbar puncture and following examination, the WBC count increases, indicating infection of the central nervous system.

Fig. 21.31
figure 31

Tuberculous meningitis. (ae) MR imaging demonstrates obvious thickening of meninges at the suprasellar cistern and quadrigeminal cistern, with low T1WI signal and high T2WI signal. The water suppression sequence demonstrates high signal, while DWI slightly high signal. Contrast imaging demonstrates nodular enhancement

Case Study 32

A male patient aged 21 years was diagnosed with cerebral tuberculosis.

Fig. 21.32
figure 32

Cerebral tuberculosis. (ac) MR imaging demonstrates slightly long T1 slightly long T2 signal of patches of shadows at the brainstem, cerebellum, and left temporal lobe, with poorly defined boundary. (d, e) Contrast imaging demonstrates multiple military, nodular enhancement of the lesions at the brainstem, cerebellum, and bilateral brain hemispheres and ring-shaped enhancement of some lesions

7.2.2 Hepatic Tuberculosis

7.2.2.1 Ultrasound

Different pathological types of hepatic TB granuloma are demonstrated with different ultrasound findings. The lesions based on liquefaction, necrosis, and sparse pus are demonstrated with no echo but internal fine light spots. The lesions based on caseous necrosis is demonstrated with low echo, with internal even echo and well-defined boundary. The lesions of fibrous proliferation and calcification are demonstrated as an irregular strong echo.

7.2.2.2 CT Scanning

For the cases with miliary hepatic TB, CT scanning demonstrates enlarged liver and multiple miliary lesions with low density in the liver.

For the cases with nodular hepatic TB, CT scanning demonstrates uneven density in the nodular shadow, commonly with fine spots and spots of calcification. By contrast scanning and marginal enhancement can be demonstrated.

7.2.2.3 MR Imaging

MR imaging demonstrates hepatic TB lesion with low T1WI signal and equal or high T2WI signal.

Case Study 33

A female patient aged 46 years was diagnosed with hepatic TB (Fig. 21.33).

Fig. 21.33
figure 33

Hepatic TB. CT scanning demonstrates round-like shadow at the right liver lobe with mixed density, internal low-density shadow, and scattering spots of calcification. The margins of the lesions are mostly well-defined and regular

7.2.3 Splenic Tuberculosis

7.2.3.1 Ultrasound

Nodular splenic TB is demonstrated by ultrasound as weak echo nodule with well-defined boundary and regular shape. The internal echo is uneven, with less blood flow signal. The demonstrations of abscess splenic TB by ultrasound resemble to those of non-tuberculous splenic abscess, with space-occupying effect of cystic consolidation in the spleen. There are commonly fibrous proliferation and calcification, with irregular strong echo.

7.2.3.2 CT Scanning

CT scanning commonly demonstrates splenomegaly. For the cases with nodular splenic TB, CT scanning demonstrates low or equal density nodular shadows with poorly defined boundary. By contrast scanning, the lesions are demonstrated with no enhancement and ring-shaped enhancement of rare lesions. For the cases of abscess splenic TB, CT scanning demonstrates singular or multiple round-like low-density shadows in the spleen. Contrast scanning demonstrates marginal enhancement. The spleen is also demonstrated with spots or small nodular lesions of calcification.

7.2.3.3 MR Imaging

Nodular splenic TB is commonly demonstrated as mostly equal or low T2WI signal. Abscess splenic TB is demonstrated as equal or low T1WI signal and high T2WI signal or centrally irregular high surrounded by low signal by T2WI.

7.2.4 Intestinal Tuberculosis

7.2.4.1 Barium Meal Radiology

Barium meal radiology or barium enema examination is important for the diagnosis of intestinal tuberculosis. For the cases complicated by intestinal obstruction, barium enema examination is appropriate to avoid aggravated intestinal obstruction by barium meal.

7.2.4.1.1 The Ulcerative Type

At the early stage, due to the stimulation by inflammation and ulceration to the involved intestinal segment, obvious irritation sign as barium passes through is demonstrated. The manifestations include accelerated emptying of barium, with no or a small quantity residue of barium, while favorable filling state of proximal and distal lesion, just like a skip of barium over an intestinal segment, which is known as skip sign. The mucosa at the lesion is subject to irregular thickening and derangement, while the intestinal wall is demonstrated with spots and serration-like niche. In the advanced stage of the lesion, due to shrinkage of fibrous tissue, fibrous proliferation, and thickened intestinal wall, the intestinal lumen is subject to stenosis, deformation, as well as dilation and stasis of the proximal part. In addition, ileocecal TB can induce confined peritonitis to cause adhesion of the peritoneum to its surrounding intestine.

7.2.4.1.2 The Proliferative Type

This type is mainly manifested as irregular deformation and stenosis of the intestinal lumen, with accompanying rough and deranged mucosa, multiple small polypoid, or space-occupying filling defect. But niche and irritation sign are rare. In the cases of simplex proliferative TB, the irritation sign is not obvious. But if accompanied by ulceration, the irritation sign may be observable. Due to submucosal and subserosal proliferation of fibrous tissue, the intestinal wall is thickened to cause intestinal stenosis. In severe cases, partial intestinal obstruction occurs, with dilation of the proximal ileum. When the ileocecal valve is invaded, it is subject to proliferation and thickening, with depression at the inner wall of cecum to affect the emptying of small intestines. When the cecum and ascending colon are involved, the intestinal lumen is subject to narrowing and shortening. The mucosal folds are subject to derangement and proliferation, mostly with polypoid filling defect, which should be differentiated from intestinal cancer. In the cases with ileum and ileocecal valve involved, the diagnosis should be suspected as tuberculosis. If accompanied by lumen adhesion, the intestinal lumen is disorderly arranged and accumulated, and the loops can hardly be separated, with tenderness. In the cases with ascites, the flexure intervals are widened with a floating-like appearance. The flexure can also be compressed to the middle abdomen by ascites, commonly with no intestinal flexure in the pelvic cavity.

7.2.4.2 CT Scanning

CT scanning demonstrates the involved intestinal segment with obvious thickening of the intestinal wall. Contrast scanning demonstrates obvious enhancement of the involved intestinal segment with stratification. In the cases complicated by abdominal lymphatic TB, the swollen lymph nodes are demonstrated with ring-shaped enhancement. Intestinal TB can involve surrounding tissues of the intestinal canal to cause tuberculous inflammation or tuberculous granulation tissue and caseous necrosis. By plain scanning, the surrounding adipose is demonstrated to be turbid with increased density. If accompanied by caseous necrosis, the density is uneven, with obvious peripheral enhancement and no or slight enhancement of caseous necrosis. The mesenteric lymph nodes are enlarged and calcified. The ring-shaped enhancement of lesions around the affected intestinal canal and the enlarged and calcified mesenteric lymph nodes are important and characteristic signs for the diagnosis of abdominal TB.

Case Study 34

A male patient aged 30 years was confirmatively diagnosed with HIV infection 2 months ago. After intake of Zongzi (glutinous rice dumpling), he experienced intermittent abdominal pain and accompanying abdominal distention, nausea, and vomiting. He also reported terminated anal discharge of gas and stool. Abdominal plain scanning suggested intestinal obstruction. Pathology after an exploratory laparotomy demonstrated the diagnosis of abdominal lymphatic TB and mesenteric necrosis (Fig. 21.34).

Fig. 21.34
figure 34

Intestinal TB. (a, b) Plain CT scanning demonstrates thickened intestinal wall with edema, multiple enlarged lymph nodes at the mesenteric root and retroperitoneum, and abdominal effusion. (ce) By reexamination after exploratory laparotomy and following treatment for 2 months, CT scanning demonstrates absent ascites, enlarged lymph nodes at the abdominal cavity, and retroperitoneum. By contrast scanning, the lesions are demonstrated with ring-shaped enhancement

7.2.5 Kidney TB

7.2.5.1 Ultrasound

In the cases of kidney TB with cold abscess or caseous necrosis at the renal parenchyma, ultrasound demonstrates the renal parenchyma with low echo area or liquid dark area with poorly defined boundary. In the cases with fibrosis or calcification, ultrasound demonstrates bright light spots, masses, or strips. In the cases with calcification, posterior acoustic shadow can be demonstrated.

7.2.5.2 CT Scanning

At the early stage of kidney TB, CT scanning demonstrates no abnormalities. But at the advanced stage, CT scanning is superior to intravenous urography in demonstrating the lesions, with protrusion of local kidney contour outwards or enlarged kidney. Thinning and atrophy of mainly renal cortex can also be demonstrated due to stenosis of renal arteries induced by fibrosis of renal TB. The renal parenchyma is demonstrated with multiple round or oval liquid-like density shadows with different sizes and poorly defined boundaries. The renal parenchyma is also demonstrated with spots, small nodules, or egg shell-like calcification. The renal pelvis wall is demonstrated to be thickened, partially with linear or arch-like calcification shadow. The ipsilateral urethral wall is demonstrated to be thickened (Fig. 21.35). The renal pelvis and urethral wall of the affected kidney are subject to dilation and effusion. Contrast CT scanning demonstrates no obvious enhancement of the early lesions at the early stage, and based on which it should be differentiated from neoplasms. Meanwhile, the function of the affected kidney can be assessed.

7.2.5.3 Intravenous Pyelography (IVP)

The typical demonstration by IVP is destructed renal calices. The renal calices are subject to irregular worm-bitten-like margin, narrowed cervix with irregular margin, and deformation. The renal parenchyma is subject to cavities with different sizes and shapes. The pelvis margin is destructed and deformed. The pelvis and urethra of the affected kidney are subject to effusion. Meanwhile, based on the rate and degree of imaging, the function of the affected kidney can be assessed.

Case Study 35

A male patient aged 53 years was diagnosed with right kidney TB.

Fig. 21.35
figure 35

Kidney TB. CT scanning demonstrates enlarged right kidney, and wavelike local kidney margin. There are also multiple oval shape liquid density shadows with different sizes and poorly defined boundaries at the right renal parenchyma, with marginal calcification at one shadow

7.2.5.4 MR Imaging

By T1WI, the corticomedullary interface is absent, with low-density lesions of different sizes at the kidney. The renal sinus shifts or is absent. By T2WI, the lesions are demonstrated with high signal.

7.2.6 Spinal TB

7.2.6.1 Ultrasound

By ultrasound, cold abscess is demonstrated as unilateral or bilateral paravertebral even or uneven low echo areas under the anterior longitudinal ligament with different sizes. In the abscess cavity or on the abscess wall, there are spots and patches of strong echoes, which are caused by calcification of abscess or fragments of sequestra.

7.2.6.2 CT Scanning
  1. 1.

    Bone destruction

    In the cases of spinal TB, bone destruction is common at the vertebra but rare destruction of vertebral appendix. The lesions are morphologically irregular, with worm-bitten-like margin. In some bone destruction areas, small fragments of sequestra can be observed.

  2. 2.

    Narrowed intervertebral space

    The bone destruction at the upper or lower margin of the vertebral body leads to flattening of the affected vertebra, which further causes destruction of adjacent intervertebral disks. By 3-dimensional reconstruction, the lesions of adjacent two vertebral TB induce narrowing of the intervertebral space between the two vertebrae.

  3. 3.

    Paravertebral soft tissue mass

    Around the affected vertebra, soft tissue swelling can be observed. In the swollen soft tissue, there are liquid-like low-density areas with poorly defined boundary and commonly accompanying spots and patches of calcification.

  4. 4.

    Involvement of the spinal canal

    After bone destruction of the vertebra and appendix, the caseous lesions, fragments of sequestra, and granulation tissues penetrate into the adjacent spinal canal to cause secondary spinal canal stenosis (Fig. 21.36).

7.2.6.3 MR Imaging

Spinal TB is demonstrated as low T1WI signal and often mixed high T2WI signal. MR imaging can demonstrate the location and range of paravertebral soft tissue abnormality and cold abscess. Paravertebral soft tissue shadow is commonly demonstrated as low T1WI signal and mixed high T2WI signal, and some are demonstrated as homogeneous high signal. MR imaging can demonstrate the degree and range of spinal involvement as well as spinal ischemia and degeneration (Fig. 21.37).

Case Study 36

A female patient aged 46 years was diagnosed with thoracic spinal TB.

Fig. 21.36
figure 36

Thoracic spinal TB. (ac) CT scanning demonstrates bone destruction of adjacent two thoracic vertebrae with worm-bitten-like margin. At the superior vertebra, small sequestra shadow is observable. The intervertebral space between the two affected vertebrae is narrowed. The spine is subject to slight kyphosis with the two vertebrae as the center. In the paravertebral soft tissue, spindle-shaped abscess shadow can be observed

Case Study 37

A female patient aged 25 years experienced repeated pain at the lower back and the back 3 months ago. The symptoms aggravated several weeks later, with slight impaired movement and numbness of the lower limbs. Chest CT scanning demonstrated abnormal density at the lung and bone destruction at the T9 vertebra, with paravertebral abscess. The diagnosis was then suspected to be tuberculosis. PPD skin test was positive.

Fig. 21.37
figure 37

Thoracic spinal TB. (a, b) CT scanning demonstrates obvious bone destruction at the vertebral body, paravertebral abscess, and stenosis of the vertebral canal. (ch) MR imaging demonstrates obvious compression and bone destruction at T9, with decreased T1WI signal of the vertebral body and increased T2WI signal, with wedge shape change. Local angular deformity penetrates into the vertebral canal, with thin spinal cord at the corresponding level. The adjacent intervertebral discs are demonstrated with decreased T2WI signal and thick homogeneous ringlike signals at paravertebral area of T9, with internal long T1 and long T2 signal. Contrast imaging by Gd-DTPA demonstrates ring-shaped enhancement. T8 and L3 are demonstrated with flakes of high T2WI signal, with enhancement by contrast imaging

8 Diagnostic Basis

The diagnosis of pulmonary TB requires comprehensive analysis of epidemiological data, clinical manifestations, laboratory findings, and radiological demonstrations. The diagnoses are mainly based on findings by X-ray, CT scanning, and sputum examination for pathogenic bacteria. Positive finding by sputum smear for acid-fast bacillus or sputum MTB culture, tuberculous granuloma by biopsy of lung tissue, and tubercles or caseous necrosis are the gold criteria for the diagnosis of pulmonary TB.

8.1 Diagnosis of Pulmonary TB

8.1.1 Primary Pulmonary TB

It is more common in children and adolescents.

The patients experience mild TB toxic symptoms, such as erythema nodosum as well as joint swelling and pain.

The respiratory signs are rare. The children patients often experience hepatomegaly, splenomegaly, and rarely cervical superficial lymphadenectasis.

Fibro-bronchoscopy demonstrates bronchial stenosis, chronic inflammation of bronchial mucosa, and lymphobronchial fistula.

PPD skin test is commonly positive.

Sputum smear for acid-fast bacillus is positive, or gastric fluid examination for acid-fast bacillus is significant to define the diagnosis.

Radiological examinations demonstrate bipolar dumbbell sign or hilar lymphadenectasis and hilar inflammatory infiltration.

8.1.2 Hematogenous Disseminated Pulmonary TB

Prior to onset, the patients may experience conditions to compromise immunity, such as acute infectious disease, alcoholism and catching a cold, fatigue, delivery, and use of large doses of immunosuppressants. Otherwise, they are high-risk population before the onset.

The onset is acute and sudden, with high fever, night sweating, weakness, and dyspnea. The patients may also experience hepatosplenomegaly, cerebral meningeal irritation sign, and sometimes choroidal tubercle at the ocular fundus.

By laboratory tests, blood erythrocyte sedimentation rate is accelerated, with change of WBC count. PPD skin test is positive (negative cannot be excluded). Anti-TB antibody is positive. Sputum smear for acid-fast bacillus is positive.

By radiological examinations, typical miliary nodular shadows are demonstrated at both lungs, with three-evens sign or three-unevens sign.

Various biopsies facilitate to define the diagnosis.

8.1.3 Secondary Pulmonary TB

The clinical manifestations include repeated or prolonged cough with sputum, low-grade fever, night sweating, emaciation, and poor appetite for over 2 weeks. Regular anti-infective therapy is ineffective. High-risk population of TB should be attended more carefully.

By physical examination, no obvious positive sign can be found.

By laboratory test, the blood WBC count is commonly normal, possibly with anemia and rapid ESR. CRP obviously increases and PPD skin test is positive. Sputum smear for acid-fast bacillus is positive, and/or sputum MTB culture is positive. Biopsy of lung tissue can define the diagnosis of TB. BALF smear for acid-fast bacillus is positive. The finding of TB lesions by bronchial or lung tissue biopsy can define the diagnosis. DNA detection of MTB, serum anti-TB antibody test, and effective trial anti-TB therapy facilitate the diagnosis of TB.

X-ray and CT scanning demonstrate cloud-like, nodular patches of lesions with mixed existence, especially the accompanying cavities and its satellite lesions. These lesions fail to be absorbed after short-term anti-infective treatment.

8.2 Diagnosis of Extrapulmonary TB

8.2.1 Tuberculous Pleuritis

8.2.1.1 Tuberculous Dry Pleuritis

Based on the case history, the patients with clinical manifestations of low-grade fever or moderate fever, dry cough, severe stabbing chest pain, and local pleural friction can be diagnosed with tuberculous dry pleuritis. X-ray and CT scanning demonstrate pleural thickening with poorly defined boundary. MR imaging demonstrates linear moderate or low T1WI signal shadow and slightly high or high T2WI signal.

8.2.1.2 Tuberculous Exudative Pleuritis

The patients commonly have a past history of TB and clinically experience moderate fever, early chest pain with following alleviation, and dyspnea.

Radiological examinations demonstrate pleural effusion.

By diagnostic thoracic puncture for routine examination of pleural effusion, biochemical examination and bacterial culture are necessary examinations to define the diagnosis. In such ways, about 75 % of cases with pleural effusion can be etiologically diagnosed.

8.2.2 Tuberculous Meningoencephalitis

The patients commonly have a past history of TB and an unobvious onset with TB toxic symptoms, including intracranial hypertension, meningeal irritation sign, cerebral nerve impairment, and consciousness disturbance.

By laboratory tests, the cerebrospinal fluid is demonstrated with abnormalities, including cell count increase that is mainly lymphocytes, increased protein level, decreased glucose and chloride levels, and detected MTB.

CT scanning and MR imaging demonstrate meningeal thickening that is mainly at the cranial base, obvious enhancement of the choroid and/or tuberculoma at the cerebral parenchyma, and tuberculous granuloma.

8.2.3 Hepatic TB

The patients experience hepatic pain and upset, TB toxic symptoms, extrahepatic TB, and a past history of TB.

Laboratory findings support the diagnosis of TB, such as PCR, TB-Ab, and PPD skin test.

Radiological demonstrations are varied. Localized hepatic TB is commonly located at the marginal liver, with singular or multiple low-density lesions and accompanying fine spots or spots of calcification. In the abdominal cavity, calcified swollen lymph nodes are demonstrated, with ring-shaped enhancement of the lesions by contrast radiological examination.

The diagnosis of hepatic TB can be defined based on liver tissue biopsy.

8.2.4 Splenic TB

The patients usually have extrasplenic TB lesion or a past history of TB, with TB toxic symptoms and signs.

By laboratory tests, the findings include anemia, rapid ESR, as well as increased neutrophils and lymphocytes.

By radiological examinations, the spleen is enlarged, with multiple round lesions in the spleen but no enhancement or slight marginal enhancement.

Puncture of lymph node for biopsy, laparoscopy, or spleen puncture for biopsy demonstrates infection of MTB. By serous cavity fluid examination, MTB is detected.

Experimental anti-TB therapy is effective to alleviate the symptoms.

8.2.5 Intestinal TB

The patients are commonly young and middle age adults with extrenteral TB, especially open pulmonary TB with accompanying gastrointestinal symptoms.

The patients experience fever, night sweating, abdominal pain, diarrhea, and constipation. In addition, the patients may also experience right lower abdominal tenderness, mass, and intestinal obstruction with no known causes.

Barium meal radiology demonstrates irritation sign, barium filling defect, intestinal canal stenosis, as well as intestinal canal shortening and deformation.

8.2.6 Kidney TB

The diagnosis of kidney TB is mainly based on detected MTB in urine specimen and the corresponding radiological demonstrations. The commonly applied radiological examinations include urography and CT scanning, which can demonstrate the range, severity, and stage of the lesions. Especially, urography can demonstrate early renal calices lesion. But CT scanning can sensitively detect the lesions with calcification. Both facilitate to define the diagnosis.

8.2.7 Spinal TB

The symptoms of spinal TB are unobvious, with long illness course. It refers to osteolytic destruction of at least two vertebrae with narrowed or absent intervertebral space and spinal kyphosis. Paravertebral abscess and soft tissue calcification are characteristic X-ray demonstrations of spinal TB. CT scanning can define the unobvious bone destruction as well as the position and range of paravertebral abscess. MR imaging can detect early vertebral TB lesions, which fail to be demonstrated by X-ray and CT scanning. It is superior to CT scanning in demonstrating soft tissue changes and invasions into the spinal canal.

8.3 Pulmonary TB-Related Complications

8.3.1 Hemoptysis

The patients commonly have a history of pulmonary TB and recent history of hemoptysis.

CT scanning demonstrates pulmonary tuberculosis and patches of ground-glass shadows. Reexamination of CT scanning demonstrates obvious absorption or complete absorption of the lesions.

8.3.2 Spontaneous Pneumothorax

X-ray and CT scanning demonstrations provide main evidence to define the diagnosis. The typical demonstrations include increased transparency of the lesion, absent lung markings, and fine linear soft tissue density shadow. In combination to the symptoms, signs, and etiological factors, the diagnosis can be defined.

8.3.3 Tuberculous Bronchiectasis

The patients commonly have a history of pulmonary TB. After appropriate anti-TB treatment, the conditions are stable, with the following occurrence of hemoptysis and expectoration. In addition, bubble sound at the fixed location is commonly heard.

X-ray demonstrates cord-like patches and curled hairlike shadows. CT scanning demonstrates larger diameter of bronchus than its accompanying bronchial artery.

9 Differential Diagnosis

9.1 Lobar Pneumonia

Tuberculous lobar pneumonia and caseous pneumonia are radiologically demonstrated as lobar or segmental exudative consolidation shadows at the lungs. Both commonly occur at the upper lung lobe. Tuberculous exudative lesion is commonly concurrent with proliferative lesion and caseous lesion.

Lobar pneumonia is radiologically demonstrated as lobar or segmental exudative consolidation shadows. Its occurrence is commonly at each lung lobe, with basically even density of flakes of shadows. In the cases with the flakes of shadows involving adjacent interlobar fissure, interlobar pleural septum can be sharply demonstrated. With the interlobar pleura as the separation, the affected side is demonstrated with consolidation shadow, while the contralateral side of the interlobar fissure is the unaffected lung.

9.2 Bronchial Pneumonia, Mycoplasma Pneumonia, and Allergic Pneumonia

Exudative lesion of pulmonary TB is radiologically demonstrated as spots and patches of shadows with poorly defined boundary. In the cases of primary pulmonary TB, the primary lesions are commonly small, commonly concurrent with cord-like shadow of lymphangitis between the lesion and the hilum as well as the hilar and mediastinal lymphadenectasis. Infiltrative lesion of pulmonary TB is commonly located at the apical posterior segment of the upper lung lobe and dorsal segment of the lower lung lobe. The lesion is commonly complicated by proliferative lesion, caseous lesion, cavity, calcification, and fibrosis. Radiologically, the demonstrations are characterized by multiple lesions, multiple densities, and multiple shapes. By short-term observation, the lesions show no obvious change.

Bronchial pneumonia commonly occurs at the middle and medial parts of the middle and lower lung fields at both lungs. The lesions are demonstrated as small flakes or patches of shadows distributed along the bronchi. The density of the lesion is almost the same, which is light with poorly defined boundary. The multiple adjacent small lesions may fuse. And by short-term observation, the lesions show rapid change.

Mycoplasma pneumonia commonly occurs at the low lung lobe. The characteristic demonstration is patches and flakes of shadow extending from the hilum to the peripheral lung field. The density of the shadow is almost the same, which is light with poorly defined boundary and internal courses of lung markings. For about 2 weeks, the lesions can be obviously or completely absorbed.

The lesions of allergic pneumonia are commonly multiple, which are distributed at multiple lobes or segments along the bronchus mostly at the middle and lower lung fields. The lesions are demonstrated as patches or flakes of shadow with equal light density, poorly defined boundary, and internal lung markings. The characteristic demonstration is the rapid change of migrating lesions, namely, the primary lesions are absorbed within several days and new lesions are then present at other lung fields.

9.3 Interstitial Pneumonia

Radiologically, acute hematogenous disseminated pulmonary TB and subacute/chronic hematogenous disseminated pulmonary TB share some commonalities. The lesions disseminate from the hilum to the middle and lower lung fields, mostly bilaterally symmetric at both lungs. The densely distributed lesions at both lung fields cover the lung markings to show decreased lung markings. The lesions of acute hematogenous disseminated pulmonary TB are demonstrated as miliary and small spots of shadows with even density, even size, and even distribution. The lesions of subacute/chronic hematogenous disseminated pulmonary TB are demonstrated as spots of small nodular and patches of shadows and cavities at the upper lung field due to the fusion of small lesions, which are morphologically varied. However, the lesions at the middle lung field are mostly demonstrated as miliary and small nodular shadows, with almost even distribution. The lesions at the upper lung field are mostly old, while the lesions at the middle lung field are mostly new.

The lesions of interstitial pneumonia are commonly located at the middle and lower lung fields, rarely involving the apex of the lung. The lesions may be distributed at unilateral lung or bilateral lung fields with strips of and cord-like shadows or grid-like shadow with well-defined boundary. The lesions are mostly distributed along the lung markings. The strips and grid-like shadows are commonly accompanied by miliary and small spots of shadows with well-defined boundary. Sometimes, at the lateral part of the middle lung field, honeycomb-like transparent shadow and ground-glass shadow are demonstrated. The key point for its differentiation from hematogenous disseminated pulmonary TB is the enhanced lung markings at the affected lung field.

9.4 Pulmonary Abscess and Bronchiectasis

Cavities caused by pulmonary TB are commonly located at the apical posterior segment of the upper lung lobe and dorsal segment of the lower lung lobe, with smooth lining and no liquid in them. Calcification can be commonly demonstrated at the wall of cavity, with consolidation shadow at their external wall. The lesions can also be transparent area formed by proliferative lesion and fibrosis with unsmooth and irregular margin. There are cords like high-density shadow radiating from the cavity wall. Cord-like or double rail-like draining bronchi are commonly found between the cavity and hilum. Around the cavity, spots of satellite lesions are demonstrated. At the ipsilateral or contralateral upper lung field, spots and patches of polymorphic TB lesions are mostly found with different densities. At ipsilateral or contralateral middle and lower lung field, spots and patches of bronchial disseminated lesions are commonly found. Cavity induced by TB lesion mostly remains stable for a long period of time.

At the early stage, pulmonary abscess is demonstrated as a large flake of exudative consolidation shadow, which is commonly found at each lung lobe. The shadow may be found at different lobes or segments with poorly defined boundary. At the shadow, a confined central low-density area can be demonstrated with poorly defined boundary. The lesion further develops to show a characteristic sign of acute pulmonary abscess, namely, a large flake of exudative consolidation shadow with deep gas fluid level and poorly defined boundary of the consolidation shadow. In combination to the clinical acute onset with symptoms of high fever, chills, purulent sputum with unpleasant odor or purulent bloody sputum, as well as laboratory findings of increased WBC count and neutrophil count, the diagnosis can be defined. Treatment for a short period of time, the lesions can be demonstrated with improvement and absorption.

The abscess type of bronchiectasis commonly occurs at the lower lung lobe. The lesions are demonstrated as multiple round or oval thin wall transparent areas of different sizes. Most of the abscess wall has even thickness, with clear and smooth inner and outer abscess wall. Gas or gas fluid level is demonstrated within the abscess. The lesions are commonly accompanied by bronchiectasis and other pathological changes such as thickening of the bronchial wall and widened bronchial lumen. When dilated bronchus is filled with mucus, column shape or bead string-like liquid density shadow can be demonstrated to be accompanied by adjacent vascular vessels with a larger diameter than the vascular vessels. In combination to its long illness course and repeated occurrence of respiratory infection, the diagnosis can be defined.

9.5 Peripheral Lung Carcinoma and Lung Hamartoma

Tuberculoma commonly occurs at the apical posterior segment of the upper lung lobe and the dorsal segment of the lower lung lobe. The lesion is commonly singular with round or oval shape and clear regular margin. The density of the lesion is mostly uneven. The finding of spots or egg shell-like calcification at the internal or marginal tuberculoma facilitates the diagnosis. Tuberculoma composed of cavities is demonstrated with transparent area in the nodular shadow. In some cases, cord-like or double rail-like draining bronchus can be demonstrated between the tuberculoma and hilum. Around the lesion of tuberculoma, spots of satellite lesions are commonly demonstrated. At the ipsilateral or contralateral lung field of tuberculoma, spots, patches, and cord-like lesions are demonstrated with various shapes and densities. Contrast CT scanning demonstrates no or slight enhancement of tuberculoma. The lesion of tuberculoma may be stable, with no change for a long period of time.

Peripheral lung carcinoma may occur at any lung lobe, with more common occurrence at the anterior segment of the upper lobe. The lesion is commonly singular with round-, oval-, or potato-like shape, demonstrated as nodular or mass-like shadow. The lesion has soft tissue density, mostly even and sometimes vacuole sign. In most cases, the lesion is well defined, with lobulation sign and spicule sign. In the nodule, calcification rarely occurs, sometimes with vascular bundle sign between mass-like shadow and hilum. Contrast CT scanning demonstrates mostly obvious enhancement of the nodular shadow of lung carcinoma. The nodular shadow of the peripheral lung carcinoma commonly enlarges during 1–3 months. Clinical symptoms include cough up bloody sputum, with no fever.

Lung hamartoma commonly occurs adjacent to the pleura, mostly singular with round or oval shape. In the nodular shadow, calcification can be observed. The characteristic sign of lung hamartoma is popcorn-like calcification, while its typical manifestation is the concurrent soft tissue density, calcification density, and adipose density within one nodular shadow. Its margin is clear and smooth, with no spicule sign or obvious lobulation sign. By long-term observation, lung hamartoma has no obvious change, and most patients experience no clinical symptoms.