CT features of abdominal tuberculosis

CT features of abdominal tuberculosis Poster No.: C-0912 Congress: ECR 2015 Type: Educational Exhibit Authors: F. M. D. Moura, M. Veloso Soares...
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CT features of abdominal tuberculosis Poster No.:

C-0912

Congress:

ECR 2015

Type:

Educational Exhibit

Authors:

F. M. D. Moura, M. Veloso Soares, P. M. F. D. S. Silva, W. Diniz de Paula; Brasília/BR

Keywords:

Abdomen, Gastrointestinal tract, CT, Contrast agent-intravenous, Contrast agent-oral, Infection, AIDS, Tropical diseases

DOI:

10.1594/ecr2015/C-0912

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Learning objectives Early diagnosis of abdominal tuberculosis is challenging, as the definitive diagnosis can only be established by culture of M. tuberculosis, positive acid-fast bacillus or a positive polymerase chain reaction. Diagnostic delay may lead to significantly increased morbidity and mortality. The use of computed tomography (CT) enables detection for abdominal tuberculosis and recognition of the pathological findings is essential for early diagnosis. In this educational poster we aim to review and illustrate CT imaging findings of abdominal tuberculosis affecting the abdominal lymph nodes, peritoneum, gastrointestinal tract, solid organs and urinary tract, and depict the main differential diagnosis.

Background Tuberculosis (TB) is considered a reemerging disease, largely due to the AIDS epidemic and drug resistance. According to the World Health Organisation (WHO), in 2013, the incidence of TB was estimated in 126 cases per 100.000 population and approximately 1.5 million infected patients died (73% among HIV-negative patients). The highest incidences are seen in the sub-Saharan Africa and India.

(1)

While TB may compromise any intra-abdominal organ, the most common sites of infection are the ileocecal region, followed by lymph nodes, peritoneum and solid organs. (3,4)

The main routes of infection of the GI tract are (Fig 1): • • • •

Ingestion of non-pasteurized milk or infected sputum (patients with active pulmonary TB). Haematogenous spread from a primary lung focus, miliary tuberculosis or other organs; Lymphatic spread from infected nodes. Direct spread from adjacent organs.

Miliary TB results from massive lympho-haematogeneous spread throughout the body, with foci in many different organs. Classically it is described in the chest as multiple small (11)

(< 2 mm) nodules

.

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Images for this section:

Fig. 1: Main routes of tuberculosis infection of the gastrointestinal tract

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Findings and procedure details 1) Lymph node involvement: Lymph nodes are the most common site of abdominal TB, usually associated with GI involvement (60%), but it may also appear in association with peritoneal or solid organ (7)

involvement . In rare cases, it can also be the only sign of disease. The most frequently affected lymph nodes chains are the mesenteric, omental, peripancreatic, periportal, pericaval and upper para-aortic, due to the lymphatic drainage (5,6,11)

from the main areas of infection: ileocecum, ascending colon, liver and spleen.

Lymphadenopathy in CT images is usually seen as enlarged and/or confluent lymph nodes, with a hypoattenuating center and variable enhancement patterns, being the peripheral enhancement the most common (60%). (Fig 2) This kind of enhancement (7,8,12)

is highly suggestive of TB, although not pathognomonic . The other enhancement patterns are diffusely heterogeneous or homogeneous. Non-enhancement can be also seen, specially in AIDS patients, due to the reduced inflammatory reaction. Lymph node calcifications are sometimes present. Despite the development of masses due to confluent lymphadenopathy, secondary GI, urinary and biliary obstruction is only rarely seen. Differential diagnosis: These enhancement patterns may also be seen in metastatic malignancy from testicular tumors, carcinoma of the ovaries or GI tract, treated lymphoma, or benign diseases (ex: pyogenic infection, sarcoidosis and Whipple's disease). 2) Peritoneal and mesenteric involvement: (8,9)

Tuberculous peritonitis is usually divided into three types: •





Wet-ascitic: the most common type, presents with large amounts of free or loculated ascites, which is usually slightly hyperattenuating (20-45 HU) due to its high cellular content (Fig 3). Fibrotic-fixed: characterized by soft-tissue attenuating nodular thickening and large omental and mesenteric cake-like masses. Occasionally loculated ascites is seen (Fig 4). Dry-plastic: the least common type, described as mesenteric thickening, fibrous adhesions and caseous nodules.

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Differential diagnosis: disseminated nontuberculous peritonitis and lymphoma.

peritoneal

malignancy,

mesothelioma,

3) Gastrointestinal (GI): The most frequent GI site of infection is the ileocecal region, seen in up to 90% of GI TB cases. Other GI segments, for example the colon (9%) and duodenum (2%), are only rarely involved. In the case of the duodenum, the third and fourth parts are most commonly affected.

(6)

CT may show asymmetric wall thickening of the terminal ileum, ileocecal valve and cecum (Fig 5). The cecal appendix can also be involved, which results in acute or chronic appendicitis. While none of those findings are pathognomonic of gastrointestinal TB, CT imaging may help in defining associated lymphadenopathy with a caseous necrotic center, thickened mesenteric root and ascites.

(4,6,10)

Differential diagnosis: Crohn's disease, neoplasm (mainly lymphoma), radiation enteritis and other infectious diseases are the differential diagnosis to be considered. The key of diagnosis often lays on the secondary findings seen in the abdomen. Narrowing and fat proliferation, for example, are seen in Crohn's disease. Bulky lymph nodes with homogeneous enhancement may be seen in lymphoma. Other infectious causes usually have an acute presentation and findings suggestive of diffuse enteritis. (Fig 6) 4) Solid organs: Solid organ TB is frequently seen as part of multifocal or disseminated disease. 4.1) Liver and spleen: Liver and spleen involvement is found in up to 90% of autopsies in patients with disseminated tuberculosis. The most common form of presentation is the micronodular one, specially in miliary TB, and usually is manifested as hepatosplenomegaly, as the small focal lesions can not be seen in CT images. The macronodular form is uncommon and lesions may be seen as a single nodule or multiple hypoattenuating with ill-defined margins and mostly peripheral (13)

enhancement nodules.

(Fig 7, 8, 9 and 10)

Hepatic and splenic tuberculosis tend to calcify in later stages. (Fig 11)

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Differential diagnosis: Metastasis, lymphoma, sarcoidosis, fungal infection and (6,10,13)

pyogenic abscess. 4.2) Pancreas:

Extremely rare and usually secondary to miliary spread. Imaging shows a focal (4)

hypoattenuating mass with peripheral enhancement in the pancreas head or neck. 4.3) Adrenal glands:

These are a rare site of TB disease. When found, it is usually bilateral. Imaging is not specific, revealing enlarged adrenal glands with areas of central necrosis. In later stages the glands are atrophic and may calcify (Fig 12).

(8,10,13)

5) Urinary Tract: 5.1) Renal tuberculosis: The kidneys are involved in up to 15% of extra-pulmonary TB infections, but only 4-8% of infected patients may develop urinary symptoms. Most commonly the infection is unilateral (3/4 of cases) and the most seen CT finding is renal calcification (1/2 of cases). Other CT appearances are related to focal nephritis, which can be identical to the findings of other microorganisms infections, parenchymal scar formation following fibrotic healing and, rarely, nodular mass formation (tuberculoma), which may appear as irregular pools of contrast media in excretory phase.

(3,8,14)

5.2) Ureteric tuberculosis: Thickened ureteric wall and strictures, predominantly on anatomic narrowing points, are the most commonly seen features of ureteric TB infection. It may also appear as hydroureter.

(3,14)

The findings are often indistinct from other ureteric infections.

5.3) Tuberculous cystitis: The most common finding is reduced bladder capacity. Other CT findings are wall thickening, ulceration and luminal filling defects due to granulomatous material. (10,13)

Chronically, a small and irregular bladder with calcifications may be seen (Fig 13).

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Images for this section:

Fig. 1: Main routes of tuberculosis infection of the gastrointestinal tract

Fig. 2: Peripancreatic, periportal, pericaval and upper para-aortic hypoattenuating lymph nodes with peripheral enhancement secondary to caseous necrosis.

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Fig. 3: 31 y/o male with chronic kidney failure treated with peritoneal dialysis developed loculated ascites due to wet-ascitic type of peritoneal tuberculosis.

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Fig. 4: 56 y/o male undergoing immunosuppression therapy due to kidney transplantation. Fibrotic-fixed type of peritoneal tuberculosis involvement, with mesenteric cake-like masses and soft tissue nodular thickening.

Fig. 5: 33 y/o male presenting with acute abdominal pain. CT shows asymmetric ileocecal wall thickening (green arrow) associated with multiple necrotic mesenteric lymph nodes (white arrows).

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Fig. 6: Differential diagnosis of terminal ileitis.

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Fig. 7: 38 y/o male presenting with right flank pain. After CT images a biopsy was performed and macro nodular hepatic form of TB was diagnosed. a) CT shows multiple hypoattenuating hepatic nodules with peripheral enhancement; b) Post-contrast T1 weighted MR image shows hypointense nodules with peripheral enhancement in the liver; c) 2 years after treatment MR demonstrates no liver lesions

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Fig. 8: 20 y/o male with AIDS and disseminated tuberculosis: a) Caseous cervical lymphadenopathy; b) Miliary tuberculosis of the lungs; c) and e) Hepatosplenomegaly with hypoattenuating splenic nodules and multiple necrotic lymph nodes; d) Ascites due to peritoneal involvement

Fig. 9: 37 y/o female with AIDS: a) Necrotic infraclavicular lyphadenopathy (white arrow); b) Multiple splenic hypoattenuating nodules and hillar necrotic lymphadenopathy (green arrow); c) Hepatosplenomegaly

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Fig. 10: 32 y/o male with AIDS: a) Multiple splenic hypoattenuating nodules and hillar necrotic lymphadenopathy (green arrows); b) Ascites with peritoneal nodular thickening; c) Hepatosplenomegaly

Fig. 11: 88 y/o male with subcapsular splenic calcification and right pleural calcification (white arrows) secondary to tuberculosis.

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Fig. 12: Post-TB adrenal calcification. Imaging is not specific, revealing atrophic and calcified glands in later stages.

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Fig. 13: 38 y/o female with tuberculous cystitis. CT image show bladder wall thickening.

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Conclusion The ascending prevalence of tuberculosis worldwide emphasizes the importance of prompt recognition of CT findings of abdominal TB. Radiologists have a pivotal role since this knowledge is essential to avoid equivocal CT interpretation, specially in the setting of unsuspected clinical disease.

Personal information F. M. D. Moura, MD Radiology Resident Department of Radiology, University Hospital of Brasilia - HUB/UnB Brasília, DF, Brazil. P. M. F. D. S. Silva, MD Radiology Resident Department of Radiology, University Hospital of Brasilia - HUB/UnB Brasília, DF, Brazil. M. Veloso Soares, MD Radiologist Department of Radiology, University Hospital of Brasilia - HUB/UnB Imagens Médicas de Brasília - IMEB Brasília, DF, Brazil. W. Diniz de Paula, MD Radiologist Department of Radiology, University Hospital of Brasilia - HUB/UnB

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Imagens Médicas de Brasília - IMEB Brasília, DF, Brazil.

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3.

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