2. Pictorial review: CT in abdominal tuberculosis
Received 18 March 1998 and in revised form 8 June 1998,
accepted 26 August 1998.
(Figure la) with hypodense centres and peripheral
hyperdense enhancing rims [2, 3]. Other CT patterns of
lymph node morphology include
(i) conglomerate mixed density nodal masses, most
likely representing multiple confluent nodes due to
perinodal spread of inflammation (Figure lb);
(ii) enlarged nodes of homogeneous density, most
often associated with low density nodes at other
sites; and (iii) increased number (>3 in one CT sec-
tion) of normal sized or mildly enlarged mesenteric
nodes of homogeneous density, usually located
along the mesenteric vessels or adjacent to the
bowel loops (Figure lc). On CT, these diferent
morphological features could signify evolving
pathological stages of the disease, with early non-
caseating granulomas and subsequent caseation
necrosis [2].
Lymph nodes with low density centres, although
characteristic of a tuberculous aetiology and representing
caseous necrosis, are not pathognomonic and can be seen in
metastasis from testicular tumour, Whipple's disease and
rarely in lymphoma following radiotherapy [2, 3]. Nodal
metastases from testicular tumours initially drain into the
"sentinel nodes'' located in the renal perihilar regions and
subsequently spread to paralumbar nodes and nodes at the
aortic bifurcation [4]. On the other hand, tuberculosis
generally involves the mesenteric and peripancreatic lymph
nodes. Associated intestinal and peritoneal changes help in
diferentiating tuberculosis from Whipple's disease.
The involved lymph nodes occasionally show cal-
ciication; although this inding is not pathognomo-nic of
tuberculosis and may rarely be seen in metastases from
teratomatous testicular tumours and non-Hodgkins
lymphoma after treatment [5]. However, nodal calcification
in patients from endemic areas in the absence of a known
primary tumour suggests a tuberculous aetiology,
especially if supported by characteristic distribution and
appearance of nodes.
Tuberculous peritonitis
Peritoneal involvement in tuberculosis occurs primarily
by haematogeneous spread but may be secondary to
ruptured lymph nodes, a perforated gastrointestinal lesion,
or fallopian tube involvement [6, 7]. Peritoneal tuberculosis
is traditionally divided into three types [2, 7]: (i) "wet" with
free or loculated ascites; (ii) "dry plastic" with mesenteric
thickening, caseous lymph nodes and fibrous adhesions;
and (iii) "fibrotic fixed", with mass formation of omentum
and matting of bowel loops. In our experience, there is
considerable overlap between the three types on CT.
Peritoneal tuberculosis is mainly manifested on CT by
varying degrees of mesenteric and/or omental infiltration
with (wet type) or without (dry type) associated ascites
(Figures 2 and 3). It has been suggested that high density
(25—45 HU) ascites may be characteristic of tuberculosis
[2], which could be explained by the high protein and
cellular contents in a tuberculous exudate. However,
tuberculous ascites may also be of near water density
(Figure 2a), perhaps reflecting an earlier transudative stage
of immune reaction [8]. Peritoneal enhancement (Figures
2b and c) is usually associated with smooth uniform
thickening of the peritoneum [6, 7]. Nodular implants with
irregular thickening are extremely uncommon and should
suggest a diagnosis of peritoneal carcinomatosis [7].
All the three described patterns of omental involvement,
i.e. smudged, omental cake and nodular (Figure 3) are
encountered with almost equal frequency and do not help
in differentiating from peritoneal carcinomatosis [6, 7].
Mesenteric infiltration (Figure 3) can range from mild
involvement in the form of linear soft tissue strands,
thickened and crowded vascular bundles, a "stellate"
appearance, and/or subtle increase in mesenteric fat den-
sity, to more extensive involvement resulting in difuse
iniltration with soft tissue density masses involving the
leaves of the mesentery surrounding the adjacent small
bowel loops. Ascitic fluid may occasionally extend into the
mesenteric leaves (Figure 2c). Mesenteric abscess (Figure
3e) probably results from extensive caseation oflarge nodal
masses.
Intestinal tuberculosis
The most common CT inding is mural thickening
afecting the ileocaecal region (Figures 4a-e), either limited
to the terminal ileum or caecum or, more commonly,
simultaneously involving both regions. This mural
thickening is usually concentric, but is occasionally
eccentric and predominantly afects the medial caecal wall
[2, 9]. In some patients, low density areas (Figure 4d) most
likely to represent necrosis, may be noted within the
thickened wall. Ileocaecal involvement is usually
associated with enlarged hypo-dense nodes in the adjacent
mesentery (Figure
4b).
Skip areas of concentric mural thickening may be seen
elsewhere in the small bowel (Figure 4e), usually afecting
the ileal loops. These segments may also show luminal
narrowing, with or without proximal dilatation. The
presence of such lesions in combination with ileocaecal
involvement should strongly suggest the diagnosis of
tuberculosis.
Hepatosplenic tuberculosis
Tuberculosis of the liver and spleen usually occurs in
miliary form with nodules ranging in size from 0.5 to 2
mm, which cannot be detected on CT [2, 6]. Macronodular
involvement is uncommon and is manifested by single or
multiple focal low density, non-enhancing lesions with or
without peripheral rim enhancement (Figures 5a-d).
However, these lesions cannot be diferentiated from
lymphoma, fungal infection or metastasis unless associated
with characteristic lymph node or intestinal involvement
[2, 3, 6]. Image guided ine needle aspiration biopsy has
been helpful in patients with such unusual presentation.
Pancreatic tuberculosis
Pancreatic tuberculosis is unusual and solitary
involvement is rare [2, 3, 6,10]. The pancreas can be
involved in tuberculosis by either the haematogeneous
route in miliary tuberculosis or by direct spread from
contiguous lymph nodes. CT may show an enlarged
The British Journal of Radiology, January 1999 2
3. S Suri, S Gupta and R Suri
pancreas with focal hypodense lesions, usually in the head
region (Figure 6). However, these indings are non-speciic
and may be seen in focal pancreatitis or pancreatic
carcinoma. A tubercular aetiology can be suggested only by
the presence of associated findings such as
characteristichypodense lymph nodes, ascites or mural
thickening in the ileocaecal region [10].
Abdominal tuberculosis in AIDS
Tuberculosis occurs with increased frequency in AIDS
patients as the CD4 count drops below 400 cells per
Whereas extrapulmonary manifestations are seen in only
10-15% of non-HIV infected patients, the incidence is
much higher (about 50%) in patients with AIDS [11].
Mycobacterium tuberculosis infection in AIDS patients
tends to be disseminated and may involve mesenteric
lymph nodes, the peritoneum, solid visceral organs
including the liver, spleen and pancreas and virtually any
portion of the gastrointestinal tract,
The British Journal of Radiology, January 19993
4. particularly the ileum and colon. The imaging findings are
usually indistinguishable from those seen in non-AIDS
patients. Fistulas are, however, more commonly
encountered in AIDS and may occur from any segment of
bowel. Necrotic low attenuation mesenteric
lymphadenopathy is typically seen, although soft tissue
attenuation adenopathy may also be encountered [12].
Infection with atypical mycobacteria (Mycobacterium
avium and Mycobacterium intracellulare, MAC), although
rarely encountered in non-immunocompromised patients, is
one of the most frequent infections in AIDS patients. CT
may show bowel wall thickening, hepato-splenomegaly
with focal lesions and bulky mesenteric and retroperitoneal
lymphadenopathy. Adenopathy shows soft tissue
attenuation in the majority of the patients as granulomas are
rarely formed [12].
(
c
)
5. S Suri, S Gupta and R Suri
Figure 2. Peritoneal involvement. (a) Free ascites with
omental thickening (arrow), (b) ascites with uniform
peritoneal thickening (arrows) and (c) loculated fluid in the
peritoneal cavity (small arrows) as well as in the
mesenteric leaves (arrowhead) along with peritoneal
enhancement. Note ileocaecal thickening (large arrow).
Figure 3. Peritoneal involvement, (a) "Smudged"
appearance (arrows) of the omentum. Note soft tissue
mesenteric infiltration (i) involving the small bowel loops.
(b) Omental "cake" formation (arrows) and ascites. (c)
Omental thickening (arrow), loculated ascites (open arrow)
and soft tissue mesenteric infiltration (asterix). (d) Irregular
thickening of the mesenteric leaves (short arrows). Note
enlarged retroperitoneal nodes (long arrow) and caecal wall
thickening (arrowhead). (e) Large mesenteric abscess
(arrows).
The British Journal of Radiology, January 19995
(
c
)
(
b
)
(
e
)
(
d
)
6. (
d
)
Pictorial review: CT in abdominal tuberculosis
Figure 4. Ileocaecal involvement. (a) Thickened ileo-
caecal valve, along with mural thickening of the caecum
and terminal ileum (arrowhead). (b) Concentric uniform
mural thickening of the caecum (arrows) along with an
enlarged hypodense pericaecal node (open arrow). (c)
Mural thickening involving the terminal ileum (arrow)
only. (d) Gross irregular mixed density mural thickening of
the ileocaecal region (arrows) with polypoidal projections
into the caecal lumen. Note hypodense as well as soft tissue
density nodes in the mesentery. (e) Ileocaecal mural
thickening (white arrow) along with focal mural thickening
associated with luminal narrowing (black arrows) affecting
one of the distal ileal loops.
The British Journal of Radiology, January 1999 6
7. S Suri, S Gupta and R Suri
Figure 6. CT scan showing an irregular hypodense lesion
(arrow) in the pancreatic head.
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