This document discusses the imaging modalities used to diagnose abdominal tuberculosis. It begins with an introduction stating that abdominal tuberculosis accounts for 11% of extra-pulmonary tuberculosis cases. It then covers the various routes of infection and clinical presentations. The key imaging investigations discussed are ultrasound, CT and barium studies. Specific findings are highlighted for different types of abdominal tuberculosis including tubercular peritonitis, lymphadenopathy, and involvement of the gastrointestinal tract and viscera. Differential diagnoses such as Crohn's disease and carcinomatosis are also mentioned.

1. By-Dr.Sahil Chaudhry
Moderator-Dr.Chidananda Murthy
DEPARTMENT OF RADIODIAGNOSIS
AJIMS MANGALORE

2. • INTRODUCTION
• DEFINITIONS
• IMAGING MODALITIES
• DIFFERENCE BETWEEN CROHN’S
AND UC
• DIFFERENTIAL DIAGNOSIS

3. • Group of chronic disorders that cause inflammation and
ulceration in small and large bowel.
• Mainly two most common diseases are –chrohn’s disease and
ulcerative colitis
• AUTOIMMUNE
• Atypical-
• Diversion Colitis
• Behcet’s
• Microscopic colitis
• Indeterminate colitis
INTRODUCTION

6. • Idiopathic, chronic, transmural inflammatory
process of bowel - affect whole GI system starting
from mouth to anus also known as RGIONAL
ENTERITIS with frequent systemic involvement
• Most commonly involved- terminal ileum, ileocaecal
valve and caecum with regional enteritis.
• SKIP LESIONS ARE PATHOGNOMIC
• Diagnosed typically between 15-25 years of age
group.
• No gender predilection, runs in families.
• Smokers - more affected.
CROHN’S DISEASE

7. • Crohn’s disease can be –Stricturing,Penetrating,Inflammatory
• Etiology – idiopathic, genetic(DR5 DQ1 alleles), immunologic,
microbial, psychosocial
• Clinical presentation- diarrhoea, abdominal pain, weight loss
• Intermittent attacks of active disease followed by periods of
remission.
• Disease re-activation by triggers like stress, dietary factors,
smoking.
• Risk of colonic adenocarcinoma is increased in long standing
cases.

8. • on X-ray- plain radiograph of abdomen is usually helpful in
cases of obstruction secondary to crohn’s or extraintestinal
manifestations

9. • MUCOSAL ULCERS
– APTHOUS ULCERS initially
– deeper transmural ulcers typically either longitudinal or
circumferential in orientation
– when severe leads to COBBLESTONE APPEARANCE
– may lead to sinus tracts and fistulae
• thickened folds due to oedema
• pseudodiverticula formation: due to contraction at the site
of ulcer with ballooning of the opposite site
• STRING SIGN: tubular narrowing due to spasm or stricture
depending on chronicity partial obstruction
Barium small bowel follow-through

10. APTHOUS ULCERS
• Pathologically these represent shallow mucosal
erosions on the surface of hyperplastic lymphoid
follicles in the lamina propria surrounded by a small
halo of edema.
• In appropriate clinical setting this finding is considered
highly specific for Crohn’s disease. As the disease
progresses, aphthous ulcers enlarge to form satellite,
serpiginous or linear areas of ulceration.

11. APTHOUS ULCERS
First sign of chron’s
disease on barium

12. Cobblestone
appearance: due
to deep fissuring
ulcers around
inflammed
mucosa

13. Fissuring ulceration in Crohn's disease -
graphically called `raspberry thorn'
ulcers.

14. String sign: spasm/fibrosis of
bowel wall

15. ILEOILEAL
FISTULA: long
standing
crohn’s

17. ULTRASOUND
• limited role, it has been evaluated as an initial screening tool
• Typically examination is limited to the small bowel and wall
thickness assessed:
Bowel wall thickness should be <3 mm, normally
• thickness < 3 mm helps exclude the disease in a low risk patient.
• thickness > 4 mm helps establish the diagnosis in a high risk
patient.
• Ultrasound in the assessment of extraintestinal manifestations.

19. US image - stricture in a patient with active Crohn's disease

20. • FAT HALO SIGN
• COMB SIGN
• Bowel wall enhancement
• Bowel wall thickening (1-2 cm) -terminal ileum
• strictures and fistulae
• mesenteric/intra-abdominal abscess or
phlegmon formation
CT FINDINGS

21. Fat halo sign in crohn’s disease
CT scan shows the central fatty submucosal layer of low attenuation
(*) surrounded by higher-attenuation inner (long arrow) and
outer(short arrow) layers grossly corresponding to the mucosa and
muscularis propria and serosa of the descending colon, respectively.

23. COMB SIGN:Hypervascular appearance of the mesentery in active
Crohn's disease. Fibrofatty proliferation and perivascular inflammatory
infiltration outline the distended intestinal arcades. This forms linear
densities on the mesenteric side of the affected segments of small
bowel, which give the appearance of the teeth of a comb.

25. CECT image,
coronal section,
venous phase -
enterocecal
fistula with
secondary
traction of the
cecum and right
psoas muscle
abscess

26. CT AND MR ENTEROGRAPHY
• Useful for both mural and extramural spread
of disease.
• Inflammed bowel loops show thickening and
contrast enhancement.
• Extramural spread: fibrofatty proliferation-
thickening of extramural fat:vascular
engorgement(comb sign)
• Stenosis and strictures

27. • Introduction of the 12 to 14-F enteroclysis tube
(under fluoroscopy or through duodenoscope).
• Contrast is administered either on the fluoroscopy
table or after transferring the the patient to the CT
unit for commencement of the CT scan (usually 1.5-
2L of oral contrast).
• In the CT unit, the position of the enteroclysis tube is
checked in the topogram.
• In case negative oral contrast will be used,
intravenous contrast injection will be given
(approximately 100-150ml).
CT ENTEROCLYSIS

28. • MRI enteroclysis - placement of a nasojejunal
catheter through which 1.5-2 L of contrast
solution (e.g. water with polyethylene glycol
and electrolytes) are injected.
• When disease is transmural, with cobblestone
appearance, the abnormalities are evident as
high T2 signal linear regions.
CT AND MR ENTEROCLYSIS

31. Perirectal phlegmon on axial T2 Single Shot TSE (left) and T1 contrast
enhanced (right) sequences. Rectal wall thickening with avid contrast
uptake due to active disease. Perirectal phlegmon surrounded by a
hyperenhancing perirectal fascia, displaces the rectum anteriorly.

32. • For extraintestinal disease:
• Perianal fistula/abscess
• Hepatobiliary manifestations
• Sacroiliac joints
ROUTINE MRI

33. • It is an autoimmune ,intermittent, inflammatory
disease predominantly affecting the colon involving
the mucosa and submucosa with extraintestinal
manifestations and surgical resectability.
• Causes superficial ulceration of colon and rectum.
• It starts from rectum and retrogradely involves whole colon continuously.
• In total colitis- back wash ileitis.
• More common in DR2 related genes.
• More MALE predilection.
• Clinical symtoms- diarrhoea, tenesmus, bleeding per rectum, passage of
mucus, crampy abdominal pain.
ULCERATIVE COLITIS

34. • MILD DISEASE: fine granularity
• MODERATE: marked erythema, coarse granularity, contact bleeding
and no ulceration.
• SEVERE: spontaneous bleeding,edematous and ulcerated
• Long standing cases epithelial regeneration- pseudopolyps, pre
cancerous condition
• Eventually shortening and narrowing of colon
• FULMINANT DISEASE: toxic colitis/megacolon
PATHOGENESIS

36. • Mucosal inflammation-granular appearance to the surface of
the bowel.
• Mucosal ulcers are undermined –BUTTON SHAPED ULCERS
• Islands of mucosa remain giving it a PSEUDO
POLYP appearance
• In chronic cases the bowel becomes featureless with loss of
normal haustral markings, luminal narrowing and bowel
shortening- LEAD PIPE SIGN
BARIUM ENEMA

37. FINE MUCOSAL GRANULARITY-
FIRST SIGN
NARROWING OF LUMEN

38. COLLAR
BUTTON
ULCERS

40. LEAD PIPE COLON

41. Back wash ileitis : patulous IC
valve and dilated granular
terminal ileum
‘SPILL OVER
PHENOMENON”

42. CT FINDINGS
• INFLAMMATORY PSEUDOPOLYPS
• Inflamed and thickened bowel - target appearance, due
concentric rings of varying attenuation- MURAL STRATIFICATION
• In chronic cases, submucosal fat deposition is seen particularly in
the rectum FAT HALO SIGN
• Extramural deposition of fat, leads to thickening of the perirectal
fat, widening of presacral space
• Marked muscularis mucosa hypertrophy-lead pipe sign

43. INFLAMMATORY PSEUDOPOLYPS

46. 3d virtual
colonoscopy

47. • Wall Thickening- median wall thickeness of colon
ranges from 4.7 to 9.8 mm, more severe the
disease more thicken the wall
• Increased Enhancement- enhancement of the
mucosa with no or less enhancement of the
submucosa
• Loss of haustral markings
MRI

48. Mri image reveals thickening
of colon with loss of haustral
markings

49. Submucosal fat deposition with
WIDENED PRESACRAL SPACE
Perianal abscess

50. Extraintestinal manifestations
•Eyes: Uveitis, Episcleritis, Conjuctivitis
•Joints: Peripheral arthropathy, arthralgia, ankylosing
spondylits, inflammatory Back pain
•Skin: Erythema nodosum, pyoderma gangrenosum
•Liver and Biliary tree: Sclerosing cholangitis [UC]
•Nephrolithiasis [Oxalate Stone in pt with small bowel disease
or after resection] (CD)
•Oral apthous lesions (CD)
•Gall stone(CD)
•Venous thrombosis

51. DIFFERENCES-
ROLE OF HISTORY TAKING

52. INVESTIGATIONS
CD UC
Blood Test
•CP with morphology: Normocytic
normocromic anemia of chronic disease
•Serum B12 level may be low.
•Raised ESR, CRP and raised WBC count.
•Hypo albuminaemia.
•Blood culture in septicaemia.
•Fe deficiency anemia
•Raised white cell and platelet count
•Raised ESR, CRP
•Hypo albuminaemia
Serological Test
•Saccharamyces cerevisiae antibody is
usually present
•P-ANCA negative
•P-ANCA may be positive
Stool culture
•Should always be performed in both to rule out infective cause

53. DIFFERENCES
CROHN’S DISEASE
• 70-80%Small bowel
involvement
• Skip lesions
• Fat halo IN SMALL BOWEL
• APTHOUS ulcers are seen
• Irregular serosal surface
• Perianal fistula/sinus/abscess
more common
• Creeping fat and abscess are
very common in chronic
cases
ULCERATIVE COLITIS
• 95% cases rectal involvement
• Continuous spread from rectum
upwards
• Fat halo sign is seen
• Collar button ulcers are seen.
• Smooth serosal surface
• Perianal disease rare
• Mesenteric creeping fat and
abscess are uncommon.
• Carcinoma is more common in
long standing cases.

54. DIFFERENCES
• CROHN’S DISEASE
• ENDOSCOPY
Deep geographic and serpiginous
(snake-like) ulcers
• GRANULOMAS ON BIOPSY
May have non-necrotizing non peri-
intestinal crypt granulomas
HEPATIC ABSCESSES
PANCREATITIS
CHOLELITHIASIS
NEPHROLITHIASIS
PSEUDO DIVERTICULOSIS AT
ANTIMESENTERIC BORDER
• ULCERATIVE COLITIS
• ENDOSCOPY
Continuous ulcer
CRYTPIC ABSCESSES
• TOXIC MEGACOLON
• PRIMARY SCLEROSING CHOLANGITIS

55. Greenstein AJ, Janowitz HD, Sachar DB . "The extra-intestinal complications of Crohn's disease
and ulcerative colitis: a study of 700 patients". Medicine (Baltimore) 55 (5): 401–12.

56. • Ileocaecal tuberculosis
• Ischaemic colitis
• Pseudomembranous colitis
• Ischaemic and chemical colitis
DIFFERENTIAL DIAGNOSIS

57. Ischemic colitis
• On CT:
• segmental region of abnormality
• submucosal oedema may produce low-density ring
bordering lumen (target sign)
• intramural or portal venous gas
• mesenteric oedema WITH NON ENHANCING BOWEL
WALL
• superior mesenteric artery or vein
thrombus/occlusion may be demonstrated

60. Ischemic colitis(thumb printing ): edematous
thickened bowel wall will cause indentations
into the air-filled colonic lumen

61. Pseudomembranous colitis
• Pseudomembranous colitis-caused by the
bacterium Clostridium difficile due to bacterial
overgrowth of the colon in patients who are
treated with broad-spectrum antibiotics.
• ascites and hyper enhancement of the bowel
wall with submucosal edema and edema in
the mesocolon.

62. Ct findings:
• Circumferential
and diffuse mural
thickening with
submucosal
edema.
• Prominent
haustrae.
• Eccentric polypoid
wall thickening.
• Shaggy luminal
contour.

63. Accordion sign
• The sign is described as alternating
edematous haustral folds separated by
mucosal ridges filled with oral contrast
material

65. DIAGNOSIS OF ABDOMINAL
TUBERCULOSIS : ROLE OF
IMAGING

66. INTRODUCTION
• Tuberculosis has been declared a global
emergency by the WHO.
• The prevalence of extra-pulmonary tuberculosis
seems to be rising, due to increasing prevalence
AIDS.
• In patients with extrapulmonary tuberculosis,
abdomen is involved in 11% of patients being
sixth most common after lymph nodes,Gut,Bone
and joint,miliary and meninges
• Causative organsim is M.TB hominis(more
common) ,M.bovis,Atypical Mycobacteria

67. Routes of infection
• Ingestion of milk
• Swallowing of sputum in active PTB
• Hematogenous spread from active pulmonary
lesion, miliary tuberculosis to submucosal
lymph nodes
• Contiguous spread from infected foci like
fallopian tubes, mesenteric lymph node
• Very rarely as a consequence of peritoneal
dialysis

68. RADIOLOGICAL INVESTIGATIONS
• Evidence of tuberculosis in a chest
radiograph supports the diagnosis, but
a normal chest radiograph does not
rule it out.

70. INVESTIGATIONS
• anaemia, hypoalbuminaemia and an elevated ESR.
• Mantoux Test may be positive but is of not much value.
• Serological tests like (SAFA) &(ELISA) are not sensitive and
are non-specific.
• Adenosine deaminase (ADA) is increased in tuberculous
ascitic fluid. In coinfection with HIV, the ADA values can be
normal or low.
• High interferon levels in tubercular ascitis have been found
to be useful.Combining both ADA and interferon may
increase the sensitivity and the specificity.

71. Clinical spectrum
• Disease of young
• Slight female preponderance
• Children : more gastrointestinal disease
• Adults : adhesive peritoneal and lymph nodal
disease
• Can present as acute, chronic, acute on
chronic
• Most patients have constitutional symptoms

72. ABDOMINALTUBERCULOSIS
GIT
PERITONEUM AND
ITS REFLECTIONS
ABDOMINAL
LYMPHATIC SYSTEM
VISCERA

73. 1. Tubercular peritonitis
• Originate primarily as result of reactivation of latent
TB foci in the peritoneum or secondary to a
ruptured lymph node or due to tubercular salpingitis
TB
PERITONITIS
WET ASCITIC
FIBROTIC
FIXED
DRY OR
PLASTIC TYPE

74. Wet ascitic type
• Most common type ( 90%)
• Large amounts of free or loculated ascitic fluid
• USG: fine, multiple ,complete or incomplete,
mobile strands of fibrin and debris in ascitis

75. Wet ascitic type
• CT : usually slightly
hyperattenuating
(20–45 HU) relative
to water due to its
high protein and
cellular content
• Ascites (arrows)
that is
hyperattenuating
relative to urine
within the bladder
(arrowheads).

76. Fibrotic fixed type
• Large
omental and
mesenteric
cake like
masses with
matting of
bowel loops.
• Occasionally
ascitis may
be present

77. Dry/ Plastic type
• Mesenteric
thickening, fibrous
adhesions, and
caseous nodules.
• The omentum
appears smudged,
caked, or
thickened (arrow
heads)
• Peritoneal
thickening with
associated
enhancement
occurs

78. Omentum
TB :
• thin omental line (
fibrous wall covering
the infiltrated omentum
)
• SMUDGING
• Peritoneal
carcinomatosis :
Irregularly thickened
outer contour of the
infiltrated peritoneum
• CAKING,NODULES

79. Small bowel mesentry
• Mesentric nodular lesions ( solid or cystic
nodules , lymph node or abscess )
• Mesentric thickening ( > 15mm )
• Loss of normal mesentric configuration

80. USG
STELLATE SIGN
• Fixed loops of bowel
and mesentry standing
out as spokes radiating
out from the mesentric
root
CLUB SANDWICH SIGN
• Due to localised or focal
ascites radially oriented
bowel loops due to local
exudation from
inflamed bowel or
ruptured lymph nodes

81. CT
Large volume of high density ascitic fluid (*). It is also visible pronounced peritoneal and
mesenteric thickening and enhancement (arrows).

82. •CA 125 ELEVATION CAN
BE MISLEADING!

83. Mesenteric thickening, with loss of normal mesenteric architecture and increased
vascularity (arrows). Thickened mesentery also shows contrast enhancement.
Small volume of ascites in the left parietocolic gutter is also visible in this section (*).

84. Sclerosing encapsulating peritonitis
( Abdominal cocoon)
• Small bowel
loops
congregated
to the centre
of abdomen
encased by a
soft tissue
density
mantle

88. 2. Tubercular lymphadenitis
• Abdominal lymphadenopathy is the most
common manifestation of abdominal
tuberculosis.
• Involvement of periportal, anterior
pararenal,upper paraaortic and lesser omental
lymph nodes.
• The characteristic pattern is mesenteric and
peripancreatic lymph node group enlargement,
with multiple groups affected simultaneously .

89. Isolated retroperitoneal LN
involvement highly
uncommon !
Dorfman et al Radiology,1991 (29)

90. • APPROACH TO TUBERCULAR
LYMPH NODE ASSESEMENT

91. • Normal sized to massive conglomerates with matting,latter
resulting from adhesions due to periadenitis
• Usg patterns-
• Central hypoechogenicity with mixed heterogenous echotexture
• Heterogeneity of echopattern in nodes of single anatomic
subgroup prior to treatment is strongly suggestive of Tb,rather
than lymphoma
• Caseation and calcification : highly suggestive of TB , uncommon
in lymphoma

92. USG

95. MATTED TB LYMPH NODES

96. Power Doppler sonogram of a hypoechoic tuberculous
lymph node which appears apparently avascular.

97. Power Doppler sonogram showing a tuberculous node with extensive intranodal
cystic necrosis (arrows), which displaces the vascularity towards the peripheral of
the node (arrowheads).

99. Rarely
• Biliary obstruction due to direct ductal
compression by infected nodes
• PV thrombosis and portal hypertension due to
involvement of hepatic hilar LN
• Renovascular hypertension due to vascular
compression by nodes
Caroli et al. j clin Gastroenterol 1997;25:541-43

100. Patterns of nodal enhancement on
CECT
• The CECT have been described as –
peripheral rim enhancement,
non-homogenous enhancement,
homogenous enhancement and
homogenous non-enhancement, in that order of
frequency.
• Different patterns are seen same nodal group,
possibly related to the different stages of the
pathological process.

101. 1. Peripheral rim
enhancement with
low attenuation
centre
• D/D : metastasis
from testicular
tumors, head and
neck squamous
cell
cancers,lymphoma
, whipples disease,
Crohns ds.

102. Multiple mesenteric lymphadenopathy forming a conglomerate mass (arrows)
Most enlarged nodes have central hypoenhancing areas due to necrosis.

103. 2. Homogeneous
enhancement
Seen in
patients with
MAIC infection
and HIV
positive
patients

104. Role of MRI in TB Lymphadenopathy
Differentiate enlarged nodes that are
abutting the pancreas from a cystic
neoplasm of the pancreas

105. 3. Gastrointestinal tuberculosis
• Can involve any segment of bowel
• However, it almost always involves the
ileocecal region (90% of cases), usually both
the terminal ileum and the cecum

106. PATHOLOGICAL SPECTRUM
• The intestinal lesions produced by
tuberculosis are of three types -
ulcerative
hypertrophic
stricturous.
• A combination of the three morphological
forms of lesions i.e., ulcero-constrictive or
ulcerohypertrophic may occur.

107. Esophageal TB
• Usually secondary to advanced pulmonary or
mediastinal disease
• MC involves the tracheal bifurcation
• C/F : dysphagia , odynophagia, chest pain or
cough

108. (A and B) Esophagograms showing a long
Stricture in the middle third of the esophagus with multiple diverticula

109. Gastric tuberculosis
• Rare ( 0.36-2.3% of patients with pulmonary
TB)
• Occurs due to spread from adjacent lymph
nodes or hematogeneous spread
• Usually affects antrum and distal body

110. Marked narrowing of the body of
stomach due to TB

111. Duodenal tuberculosis
• 2 % of intestinal tb cases
• Lymph nodes causing extrinsic compression
on C loop of duodenum
• Ulcer /stricture
• Hyperplastic growth
• Incompetence of sphincter of oddi
• Perforation / fistula

112. Widening of the C loop of duodenum

113. Long stricture of duodenum due to TB

114. Tubercular enteritis
Stage 1
• Accelerated intestinal transit
• Disturbances in tone and peristaltic
contractions : hypersegmentation of barium
column (chicken intestine )
• Flocculation / dilution of barium
• Irregular , crenated intestinal contours
• Softened , thickened folds

115. Stage 2
• Ulcerations
Fig : marked
spiculations in
the asc
colon,caecum
and terminal
ileum

116. Stage 3
• Hour glass stenosis of bowel
• Multiple strictures with segmental dilatation
• Fixity/ matting of loops

117. Ileocaecal tuberculosis
MC affected in small bowel TB because of
• Physiological stasis
• Abundant lymphoid tissue
• Increased rate of absorption in the region and
closer contact of bacilli with the mucosa of the
region

118. Ileocecal involvement is
seen in 80%–90% of
patients with abdominal
tuberculosis.

119. CLINICAL SPECTRUM
• Chronic diarrhoea and malabsorption -
Ulcerative type
• Rarely rectal bleeding - colonic tuberculosis.
• Subacute intestinal obstruction - Stricturous
type in the form of obstipation, vomiting,
abdominal distension, and colicky abdominal
pain.

120. Barium studies
• MOC for evaluating mucosal changes in
ileocecal TB.
• 70-100 % sensitivity.
• Earliest finding: accelerated transit time due
to spasm and hypermotility of the bowel.

121. Fleischner sign
• Thickening of the
ileocaecal valve
lips and/or wide
gaping of the
valve, with
narrowing of the
terminal ileum
• Inverted
umbrella sign

122. Pulled up caecum
• Caecum
becomes
conical,
shrunken,
retracted out
of the illiac
fossa due to
contraction
of the
mesocolon

123. Goose neck deformity
• Loss of normal
ileocaecal angle
and dilated
terminal ileum
appears as
suspended and
hanging from a
retracted ,
shortened
caecum

124. Stierlin’s sign
• Conical and shrunken
cecum, widely open
ileocecal valves,
narrowing terminal
ileum, rapid emptying
of diseased segment
• Represents acute
inflammation
superimposed on a
chronically involved
segment of the ileum,
caecum or ascending
colon

125. String sign
• Persistent
narrow
stream of
barium in
the distal
ileum

126. Both stierlin’s sign and string sign
are noted in Crohns disease and
should not be considered specific for
tuberculosis !

128. Group1: Highly s/o intestinal TB if one or more of the following
features are present
a. Deformed ileocaecal valve with dilatation of
terminal ileum
b. Contracted caecum with an abnormal
ileocaecal valve and/or terminal ileum
c. Stricture of the ascending colon with
shortening of and involvement of ileocaecal
region

129. Group 2 : suggestive if any of the following
features are present
a. Contracted caecum
b. Ulceration or narrowing of the terminal ileum
c. Stricture of the ascending colon
d. Multiple areas of dilatation, narrowing and
matting of small bowel loops

130. USG shows thlckened, echogenic mesentery containing multiple enlarged hypoechoic,
discrete, and conglomerate lymph nodes. Small amount of ascites is seen (arrows).
Dilated, fluid-filled, thick-walled bowel loops at periphery.

131. Pseudo kidney sign
• Ileocaecal
region is pulled
upto
subhepatic
region

132. CT
Preferential thickening of the medial
caecal wall with an exophytic mass
engulfing the terminal ileum associated
with massive lymphadenopathy is
characteristic of tuberculosis !

133. Regular and concentric thickening of the ascending colon (arrow
in a) and cecum (arrow in b)

134. Differential Diagnosis
MASS
• Appendicular mass
• Actinomycosis
• Crohns disease
• Caecal carcinoma
• Lymphoma

135. TB CROHN’S
Involvement of
terminal ileum
shorter longer
Features Narrowed, thickened,
rigid terminal ileum
with pulled up
ceacum
Asymmetry and
cobblestoning
Longitudinal
Ulceration
absent present
CXR + -
Omental and
peritoneal thickening
+ +
Creeping Fat - +
TUBERCULOSIS VS CROHN’S

136. The ulceration in TB is
circumferential while that in
Crohn’s disease is along the
mesentric border

137. Anorectal TB
• Fistula, stricture, chronic ischiorectal abscess
• Anal canal : ulcer fissures, fistulae, abscess,
warty growths

138. 4. Visceral tuberculosis
• Hepatic Tb
• Splenic Tb
• Pancreatic Tb

139. Hepatosplenic Tuberculosis
• Common in patients with disseminated disease and
is either micronodular- miliary or macronodular
• Miliary hepatic involvement is seen in patients with
miliary pulmonary tuberculosis
• Macronodular hepatic tuberculosis is uncommon
and occurs due to spread via portal vein or hepatic
artery from the para aortic or portal nodes.

140. In a patient with PUO, marked elevation
of serum alkaline phosphatase(3 to 6
times) with mild elevation of
S.transaminases, normal PT, S.albumin
and a slight increase in bilirubin hepatic
tuberculosis should be suspected !

141. Multiple hepatic and splenic abscesses (arrows) appearing as
hypoenhancing, nodular, well defined lesions. They have a slightly rim
enhancement.

142. Hepatic tuberculomas eventually tend to calcify, and the presence of calcified
granulomas at CT in patients with known risk factors and in the absence of a known
primary tumor should raise suspicion for tuberculosis.
• CT shows multiple
calcified granulomas
within the liver,
spleen, periportal
and peripancreatic
lymph nodes.

143. D/D
• Tuberculous microabscesses : metastases,
fungal infections (histoplasmosis), sarcoidosis
and lymphoma.
• Macronodular form : metastases, abscess and
primary malignancy.

144. Pancreatic tuberculosis
• Often associated with miliary tuberculosis and
occurs more often in immunocompromised
• May present as acute or chronic pancreatitis
• May mimic malignancy
• FNAC and biopsy are helpful

145. CECT : focal attenuated mass with peripheral
enhancement
USG : hypoechoic lesion
MRCP : pancreatic head mass compressing on CBD

147. One approach that may increase the diagnostic accuracy
of PET for tuberculosis includes the combined use of F-18
FDG and C-11 acetate, as the la er accumulates in tumors
but not in inflammatory lesion. Thus, C-11 acetate may
help differentiate inflammation from neoplasms.
In the future, labeling antituberculous drugs like isoniazid
and rifampicin with positron emitting isotopes may
culminate in the development of TB-specific PET
radiopharmaceuticals.