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IMAGING IN ABDOMINAL
TUBERCULOSIS
Imágenes en tuberculosis abdominal
Tatiana Suárez1
Vanessa García2
Tamara Estrada3
Federico Acosta3
Nodal tuberculosis
Lymphadenitis is the most frequent manifestation of intra-
abdominal tuberculosis and is present in 9% to 93% of cases (5).
It usually affects periportal lymph nodes, followed by peripan-
creatic, inter-aortocaval and mesenteric nodes (6). This is due
to the fact that the drainage sites of the organs most commonly
affected by tuberculosis are the ileocecal region, right colon,
liver and spleen. It may be the only manifestation of tuberculosis.
The routes of dissemination to the lymph nodes include the
intake of contaminated food, the bloodstream and the lymphatic
system. Lymph node size and appearance vary, with sizes rang-
ing between 1 and 2-4 cm, indicating self-limiting growth. Ad- Figure 1. Contrast abdominal CT in the portal phase in a 32 year-old male showing multiple
mesenteric and retroperitoneal lymphadenopathies with hypointense cores and peripheral
ditionally, they are usually lobulated and clustered. Periportal enhancement (arrows). No other organs were involved.
lymph node involvement manifests as obstructive jaundice,
thrombosis or portal hypertension. Cases of renal vascular hy-
pertension have been described because of compression of the
renal arteries by the lymph node disease.
In patients with HIV infection in AIDS stage, lymphatic
spread is more frequent with involvement of more than one
lymph node chain. These patients also suffer more often from
generalized symptoms such as fever, sweating and weight loss.
From a histopathological point of view, there are several
stages in the disease: lymphoid hyperplasia, caseification necro-
sis, capsular destruction, cold abscess formation, and cure with
fibrosis and calcification. The imaging appearance of the lymph
node disease depends on the pathological phase of the nodes:
On ultrasound, the nodes appear hypoechoic with a more
hypoechoic core due to caseification. In a late phase they ap-
pear calcified.
On computed tomography (CT) they appear hypodense,
mainly at the core, and contrast scans reveal their presence in the
periphery, in the non-caseified area. This enhancement pattern Figure 2. Contrast abdominal CT and coronal reconstruction with maximum intensity view
is the most frequent and characteristic in tuberculosis, although of a 48 year-old male. Nodal disease was found in multiple non-enhancing hypogastric,
inguinal and mesenteric node chains (arrows) with no necrotic cores.
it is not pathognomonic (Figure 1). This same pattern may be
seen in mestastatic disease in the ovaries and testicles, lymphoma
(especially after treatment), Crohn’s disease, sarcoidosis, and
Whipple and Castleman disease. bladder, uterus, cervix, adnexa, prostate, testicles, epididymus
and seminal vesicles. It is a significant, though infrequent form
Other imaging patterns in tuberculous nodal disease include
of tuberculosis.
homogenous enhancement or non-enhancement (Figure 2). Mag-
It is found in 2% to 20% of all patients with pulmonary
netic resonance imaging (MRI) may also suggest tuberculous
tuberculosis. Symptoms are non-specific, leading to late diag-
findings when lymphadenopathies appear in the form of conflu-
nosis and treatment. It is frequently associated with secondary
ent masses with central necrosis, accompanied by edema of the
renal failure and destruction or urogenital organs (8). The most
surrounding soft tissues. The enhancement pattern is similar
important clinical manifestation is the presence of hematuria,
to that seen on CT, with central liquefaction. The nodes may
which only occurs when the infection affects the bladder in very
appear hypointense in T2 due to the presence of free radicals,
advanced stages of the disease (9).
secondary to caseification necrosis.
Genitourinary tuberculosis occurs as a result of the blood-
Genitourinary tuberculosis borne spread of the mycobacterium from the lung to the renal
After lymphadenopathy, the urinary tract is the second sys- capillaries. Later on, the mycobacerium filters through the urine
tem most often compromised in extrapulmonary tuberculosis (7). and colonizes the urothelium. Granulomas are formed inside
All the organs in the system may be involved: kidneys, ureters, the renal parenchyma and the mycobacterium may remain
Renal tuberculosis
Once the mycobacterium reaches the renal capillaries, it
forms small granulomas that give rise to the miliary form of the
disease, which is usually bilateral, and is missed in patients with
adequate immunity. The latency period for this miliary infec-
tion ranges between 1 and 47 years. After the latency period, if
there is any immune alteration, the mycobacterium may infect
the rest of the renal parenchyma in an insidious and destructive
way, which is usually asymmetrical (destruction is bilateral in
up to 30% of cases).
In the acute phase of the infection, the kidney may appear
normal on imaging or enlarged because of the growth and
coalescence of the granulomas, which appear hypoechoic on
ultrasound (US) and hypodense on CT. As the disease advances,
renal function declines, and there is delay in uptake, concentra- Figure 3. Contrast abdominal CT in a 62 year-old male. There is evidence of severe renal
tion and washout of the contrast medium. atrophy and peripheral calcification of the entire renal cortex as a result of chronic type IV
(mixed) tuberculosis. It occurs in 34% of cases. The size of the kidney is variable and it shows
The extension of the disease to the medulla produces papil- lobulated contours. There are hypoechoic areas associated with calcifications (arrow).
lary necrosis, a characteristic but non-specific finding in renal
tuberculosis. On ultrasound, it appears in the form of swollen and In summary, urographic and CT-scan findings of renal
hypoechoic papillae due to cavitation or secondary detachment; tuberculosis include moth-eaten calices, parenchymal mass,
in the urogram and on CT, it is frequent to find papillae with a amputated infundibula, autonephrectomy, thickening of urinary
moth-eaten appearance. In the late phases, residual calcifications tract walls, parenchymal and cavity calcifications, cavities in
are the main presentation (50%) in the form of stones, caseous the renal parenchyma, hydrocalcinosis, hydronephrosis and
debris or replacement of the entire renal parenchyma, giving hydroureter secondary to segmental stenosis (13).
rise to autonephrectomy. Secondary amyloidosis may occur in tuberculosis or any
The collecting cavities and the renal pelvis may show other chronic inflammatory disease associated with high con-
obstruction and tortuousness secondary to areas of stenosis, centrations of acute-phase reactants, such as Type A amyloid
or calcifications in the cavities. At the same time, residual cal- protein. This disease must be suspected in all patients with
cifications and obstructive uropathy lead to total loss of renal tuberculosis beginning with proteinuria, generally within the
function. It is important to bear in mid that a solid mass may be nephrotic range. The diagnosis is confirmed once amyloid
a manifestation of renal tuberculosis; in this case, the differential deposits are documented in the renal biopsy (14). Likewise, it
diagnosis is a neoplastic lesion, and histology is required. is important to take into consideration differential diagnoses
Xuefang Rui et al. assessed 258 patients with renal tuber- for renal tuberculosis, including fungal or drug-related chronic
culosis and proposed a classification of ultrasound finding into pyelonephritis, renal ischemia and lymphoma.
five stages, according to the pathological course (12):
Type I. Nephrectasia. Found in 15% of patients. The capsule Ureteral tuberculosis
is irregular and the renal parenchyma shows multiple, poorly- Continuous renal parenchymal involvement leads to bacil-
defined, hypoechoic areas. It may be associated with complex, luria secondary to the rupture of the renal granulomas into the
thick-walled cysts. collecting cavities. This produces a descending infection that
a b
Figure 5. Abdominal ultrasound (a) and contrast abdominal late-phase CT (b) in a 65 yar-old male. Regular concentric thickening of the bladder mucosa (arrow) with a very reduced
repletion volume. Presence of a bladder catheter (asterisk). Bladder tuberculosis without renal damage.
b c
Figure 6. Contrast abdominal CT with multiplanar axial (a), sagittal (b) and coronal (c) reconstructions in a 25 year-old woman. There is lymph node clustering in the pelvic region
and infiltration of the Fallopian tubes and ovaries. There is no cleavage plane with the uterus (asterisk). The distal third of the ureter is compromised with hydronephrosis (arrow). The
findings are consistent with pelvic peritonitis and secondary bilateral tubo-ovarian abscess due to tuberculosis.
is rare, and it is usually associated with extensive abdominal consists of mesenteric thickening and lymph node caseification
disease (25). Usual associations include immune deficiency, (27) (Figure 8).
cirrhosis, alcoholism, diabetes, a history of peritoneal dialysis CT findings in tuberculous peritonitis include smooth thick-
and intravenous drug abuse. It is believed to spread through the ening and enhancement of the peritoneum, thickened nodular
bloodstream, but it may occur due to gut perforation or extension mesentery, high-density ascites (25-45 HU) and low-density
from the Fallopian tubes or the lymph nodes (26). lymph nodes (28). The differential diagnosis includes perito-
Clinical symptoms may include abdominal pain, bloating neal carcinomatosis, amyloidosis, peritoneal mesothelioma and
lymphoma (1).
and symptoms arising from other organs, including the lungs.
Involvement is divided into three types: wet, fibrous and dry.
These forms are frequently found together. Wet peritonitis is the Hepatic tuberculosis
most common form of tuberculous peritonitis and consists of free Liver involvement is frequent in miliary tuberculosis. It
or septated ascites (Figure 7). The second type is fibrous peri- manifests as liver insufficiency and hepatomegaly. It may be
tonitis, characterized by large omentum and mesenteric masses found on occasions in immunocompetent patients without lung
with fixed intestinal loops. The dry form is less common and disease (29,30). In miliary tuberculosis, spread to the liver is
*
*
Figure 7. Contrast abdominal CT of a 10 year-old boy. (a) Axial view and (b) coronal reconstruction showing free ascitic fluid that appears hyperdense
(asterisk) when compared to urine (arrow), indicating high protein content. It is accompanied by mensenteric lymphadenopathies (arrow head)
and wet tuberculous peritonitis.
b c
Figure 8. Contrast abdominal CT in a 38 year-old woman. (a) Axial section, (b) sagittal reconstruction and (c) coronal section showing thickening of the greater omentum and mesentery
(asterisk) that produces a desmoplastic reaction and tethering of the intestinal loops. The involvement extends to the pelvis (arrow) due to mixed fibrotic dry peritonitis.
through the hepatic artery. In its localized forms, the route of severe abdominal tuberculosis affecting the peritoneum, the
propagation may be the portal vein (31). mesentery and the lymph nodes. On imaging, the appearance
The macronodular form (tuberculoma and abscesses) is in- is non-specific, showing a thick-walled gall bladder or a central
frequent and the diagnosis may be difficult when it occurs. The soft tissue mass. It must be considered as part of the differential
most common symptoms include right upper quadrant pain, fever, diagnosis for gall bladder carcinoma or adenomyomatosis (34).
anorexia and weight loss (32). Elevated transaminases may be
present in two thirds of the cases. It is often accompanied by ane- Splenic tuberculosis
mia and elevated globular sedimentation rate. CT findings include The spleen is the fifth organ most commonly infected in mili-
multiple small hypodense nodules in the miliary form (Figure 9) ary tuberculosis after the lung, the liver, the lymph nodes and
and gross calcification in the chronic stages. The macronodular the bone marrow (35). Splenic tuberculosis occurs mainly in im-
form presents with larger single or multiple hypodense non-en- munosuppressed patients. It manifests in the form of low-density
hancing nodules. These nodules may coalesce to form abscesses. micronodules and splenomegaly on CT. On ultrasound there
Biopsies of these lesions may reveal the presence of granulomas. is a diffuse increase in echogenicity and multiple hypoechoic
Tissue culture provides bacteriological confirmation (33). or echogenic nodules. Calcifications may be identified in the
The gall bladder is rarely infected with tuberculosis because chronic forms (1,5,36).
the normal mucosa and the wall of the gall bladder are resistant The differential diagnosis in the miliary form includes metas-
to the mycobacterium. Involvement is usually associated with tasis, lymphoma, sarcoidosis and fungal infection (37). Another
6 Imaging in abdominal tuberculosis, Suárez T, García V, Estrada T, Acosta F
Review Articles
Adrenal tuberculosis
Adrenal tuberculosis occurs only in 6% of patients with ac-
tive tuberculosis. In most cases it is bilateral but asymmetrical
(40). In the acute and subacute stages of the disease there is
evidence of diffuse and homogenous increase in the size of the
gland, or a hypodense core with peripheral enhancement, sug-
gesting necrosis. It may also appear as a solid mass with non-
specific characteristics; however, a solid mass with preserved
Figure 11. Contrast abdominal CT of an elderly, 73 year-old female patient, with a history
glandular contours is more suggestive of granulomatous disease of pulmonary tuberculosis, previously treated. The left adrenal grand appears enlarged
rather than neoplasia (41). with heterogenous uptake of the contrast medium and incomplete annular calcification
In the later stages, the size of the gland diminishes and is (thick arrow); ascitic (arrow head) and pleural (thin arrow) fluid. Residual left adrenal
tuberculosis.
replaced by gross calcifications (Figure 11). The differential
diagnosis includes metastasis, lymphoma, primary neoplasia and
hemorrhage. Because of progressive destruction of both glands,
Pancreatic tuberculosis may be focal or diffuse. In the focal
the clinical findings suggest Addison’s disease (42).
form, it appears as a poorly-defined mass, whereas in the diffuse
Pancreatic tuberculosis form there is and overall increase in gland size, with or without
Pancreatic tuberculosis is extremely rare and is normally stenosis of the main pancreatic duct.
due to miliary propagation. It is more frequent in AIDS patients. On ultrasound, the lesion appears as a focal hypoechoic mass
The lesion is found in the head or the neck of the pancreas, and, on CT, it appears as a low-attenuation, peripherally-enhanc-
although tail lesions have also been described. Clinical mani- ing mass. An abscess may form on the site of the lesion and
festations include weight loss, low-grade fever, anorexia and later on it may be replaced by residual calcifications. Pancreatic
upper abdominal pain. However, unlike pancreatic carcinoma, involvement due to tuberculosis may be associated frequently
pancreatic tuberculous lesions rarely produce back pain or with peripancreatic lymphadenopathies, making diagnosis much
obstructive jaundice (43). more difficult. On MRI, the lesions appear hypointense in T1 and
hypo or hyperintense in T2. The common biliary duct and the
Ileocecal tuberculosis
The most frequent location is the ileocecal region (90%).
This does not happen by accident and is explained on the basis of
the venolymphatic stasis and the abundance of lymphoid tissue
found in this area. The mycobacterium penetrates the mucosa
Figure 12. High-frequency linear-probe US of the right iliac fossa in a 28 year-old woman.
and remains in the submucosal lymphoid tissue where an inflam- There is diffuse concentric thickening of the walls of the distal ileal loops and the caecum
matory response is triggered, with lymphangitis, endarteritis, (arrow).
granuloma formation, caseous necrosis and mucosal ulceration.
The clinical manifestations are highly non-specific and
include abdominal pain, anorexia, asthenia, fever, nocturnal carcinoma and sarcoidosis. Ileocecal tuberculosis may extend
sweating, weight loss, diarrhea, constipation, rectal bleeding, to the appendix and produce acute or chronic appendicitis (48).
right iliac fossa mass, and ascites. The presence of ascites may Endoscopic findings include ulcers, stenoses, pseudopolyps,
be a useful clue in differentiating this condition from Crohn’s fibrous bands, fistulae and ileocecal valve deformity (49).
diease, where ascites is not a common finding. Esophageal tuberculosis
Radiological signs are non-specific and the differential di- Esophageal tuberculosis is found most frequently in AIDS
agnosis with Crohn’s disease, lymphoma or cecal carcinoma is patients and manifests in the form of dysphagia and painful
difficult. Barium studies during the early stages may show spasm swallowing. It occurs by swallowing of infected sputum and
and reactive hypermotility of the ileocecal valve, longitudinal invasion into the mucosa, usually through a pre-existing mucosal
submucosal ulcers of the small intestine and transverse colonic lesion. It may also occur through the bloodstream, lymphatic
ulcers along the path of the lymphoid follicles, as well as ileoce- drainage or direct invasion from the lymph nodes or the lungs.
cal valve incompetence. In later stages there is thickening of the Non-specific findings include esophagitis, mucosal thicken-
valve lips and a larger gap between the valve and the thickened ing, ulcers, plaques, fistulae and stenoses, these latter two in the
terminal ileum (Fleischner’s sign). late stages of the disease. There is also extrinsic compression
In advanced states, due to fibrosis, there are symmetrical due to adjacent lymphadenopathies, mainly at the carina. In the
annular stenoses (napkin ring) and obstruction associated with late stages there is diverticular formation due to traction result-
tethering and shortening. The terminal ileum is narrow and stiff, ing from chronic fibrotic changes and stenosis. CT is used to
the ileocecal valve expands with a shortened tapered caecum determine mediastinal extension of the disease.
(Stierlin’s sign), representing acute inflammation overimposed on
chronic inflammation of the same segment. Later on there is cecal Gastric tuberculosis
retraction outside the iliac fossa into the hepatic flexure. Deep Gastric involvement in tuberculosis is extremely rare
fissures and fistulae may form in the final stages of the disease. and is due to extension from the lymph nodes or through the
Figure 13. Contrast abdominal CT of a 33 year-old male patient. (a) Axial section and (b) coronal reconstruction showing concentric and irregular thickening
of the distal ileum, the ileocecal valve and the caecum (arrows), as well as pericecal valve striation (arrow head).
bloodstream. The antrum and distal corpus of the stomach are fistulae formation. Ultrasound plays a very limited role due to
the sites most commonly affected. Barium studies reveal two gas interposition, but it may show concentric mural thicken-
patterns: an ulcerative pattern mimicking peptic ulcer disease, ing. In contrast, CT is the most useful method, revealing mural
and a hypertophic pattern mimicking a malignancy. Additionally, thickening, obstruction or subobstruction secondary to stenosis,
adjacent lymphadenopathies may produce extrinsic compres- lymphadenopathies and ascites.
sion. Complications include outflow tube obstruction and fistula
formations. The CT scan reveals regional lymphadenopathies Tuberculosis of the abdominal aorta and
and submucosal masses. its branches
Tuberculosis of the aorta and its branches is extremely rare.
Duodenal tuberculosis Although any segment of the aorta may be involved due to
This form of tuberculosis is found in 2% of all patients bloodstream spread or direct extension from adjacent lymph-
with intestinal tuberculosis. It usually involves the third and adenopathies, more cases have been described in the abdominal
fourth portions of the duodenum. It manifests in the form of portion (51). Likewise, the disease may manifest in the form of
compression secondary to adjacent lymphadenopathies, and arteritis with areas of stenosis or aneurysmal dilations, mainly
may become complicated with fistulae secondary to chronic of the sacular type. Aortal dissections may also occur, although
mucosal inflammation. The CT scan reveals thickening of the
less frequently.
duodenal folds, regional lymphadenopathies and thickening of
Vascular granulomatous infection must be suspected in
the mesenteric root.
patients with a history of disseminated tuberculosis and associ-
Jejunal tuberculosis ated abdominal aneurysm. Characteristically, these aneurysms
The isolated involvement of the jejunum is rare and is almost are not associated with calcifications, unlike those of athero-
always associated with peritonitis. Imaging characteristics are sclerotic origin.
non-specific, with the presence of ulcers, thickened folds and
stenosis.
Conclusion
Although the clinical and imaging manifestations of ab-
Colonic tuberculosis dominal tuberculosis may mimic other pathologies, a high
Isolated colitis with no ileocecal valve involvement is rare. degree of suspicion is required in populations at risk. The
It occurs in 9% of intestinal tuberculosis cases. The clinical prevalence of the disease is still high in our setting. Abdominal
manifestations are non-specific and include diarrhea and weight manifestations of tuberculosis depend on the patient’s immune
loss. It usually affects one colonic segment (ascending, trans- status and they may appear late, with the resulting sequels for
verse or descending). Pancolitis is unusual and it is difficult to the organ involved. The most acute manifestations are usually
differentiate from ulcerative colitis (50). accompanied by pulmonary infection. Imaging recognition
Barium studies show spike formation, spasms and stiff- helps guide the clinician in the search and demonstration of
ness in the early stages. In the late stages there is stenosis and the mycobacterium.
Rev Colomb Radiol. 2010; 21:(4):1-11 9
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Correspondence
Tatiana Suárez
Universidad de Antioquia
Medellín, Colombia
tatisuarez@hotmail.com