Inflammatory Bowel Disease: Current Role of Imaging in Diagnosis and Detection of Complications: Gastrointestinal Imaging

1. Inflammatory bowel
disease imaging
Dr Karam Manzalawi

2. Inflammatory bowel disease (IBD)
 is a chronic idiopathic disease affecting the gastrointestinal (GI) tract.
 Crohn’s disease (CD) and ulcerative colitis (UC).
 ? an exaggerated and inappropriate immune response to gut luminal
microbes.
 peak age of onset between 15-30 years of age .
 up to 20% of people with IBD are diagnosed during childhood.

3. Classification
 Crohn's disease and ulcerative colitis (UC).
 other forms of IBD
 Microscopic colitis subdivided into collagenous colitis and lymphocytic colitis
 Diversion colitis
 Behçet's disease
 Indeterminate colitis

4. IBD clinical manifestations and
treatment strategies
 Symptoms of IBD often wax and wane, defining periods of “flare” and
“remission”, respectively.
 Clinical manifestations of UC include diarrhea, with or without blood,
abdominal pain, tenesmus, and fecal Urgency.
 manifestations of CD are more variable depending on the extent and location
of the GI inflammation. CD with predominantly colonic involvement often
presents in similar fashion to UC
 whereas in small bowel CD, diarrhea and rectal bleeding are seen less
frequently and symptoms such as fever,fatigue and weight loss are common.

5. Extraintestinal manifestations
 Extraintestinal manifestations, such as arthritis/arthralgias, skin and ocular
involvement and hepatobiliary conditions like primary sclerosing cholangitis,
occur in more than 1/3 of IBD patients
 Linear growth attenuation and pubertal delay are common among children
with IBD. Up to 30% of children with CD.
 Laboratory abnormalities such as anemia, hypoalbuminemia and elevation in
erythrocyte sedimentation rate and C-reactive protein (CRP) can be
supportive but are not specific for IBD and are normal in up to 50% of IBD
patients at the time of diagnosis

6.  The diagnosis of IBD =clinical features +findings on endoscopy and
histopathology.
 There is no medical cure for CD or UC, but medical therapy is effective in
many cases, both at reducing symptoms and at reducing intestinal
inflammation.
 The classes of medications most commonly used to treat IBD include
corticosteroids, antibiotics, anti-inflammatory agents (5-aminosalicylates),
immunomodulators (6-mercaptopurine, azathioprine and methotrexate) and
newer biologic therapies.

8. Surgery
 Surgery in IBD is typically reserved for medically refractory cases.
 In UC, total colectomy with ileal pouch-anal anastomosis is often performed
for medically refractory cases or for patients with IBD-associated dysplasia or
colorectal cancer but is associated with complications including pouchitis and
pouch malfunction/dysfunction.
 Intestinal resections in CD are also frequently performed in medically
refractory cases but disease recurrence is common if not nearly universal.

9. treatment
 While treatment goals in practice have traditionally focused on an
improvement in clinical symptoms, this improvement alone may not predict
underlying disease activity. In CD in particular, the discrepancy between
clinical symptoms and active inflammation can potentially lead to
unnecessary treatments for patients whose symptoms are not due to active
inflammation and to asymptomatic progression of disease and disease-related
complications in patients who are without clinical symptoms despite active
inflammation.
 This discordance has led to a search for additional targets that can be used in
combination with clinical symptoms to help guide treatment decisions.

10.  Candidate targets include CRP, fecal calprotectin, intestinal appearance on
cross-sectional imaging modalities like CT enterography (CTE) and MRE, and
mucosal healing based on endoscopic findings, which is becoming a preferred
objective measure of disease activity as it correlates well with improved
clinical outcomes

12. Current role of imaging in IBD
evaluation
 (1) at the time of initial diagnosis to distinguish UC from CD;
 (2) to assess and track progression of extraintestinal IBD manifestations;
 (3) to visualize penetrating complications of disease that extend outside the
bowel wall;
 (4) to assess disease activity in patients with known IBD during symptomatic
recurrence,

14. Crohn disease vs ulcerative colitis

15. bowel involved
 CD: small bowel 70-80%, only 15-20% have only colonic involvement
 UC: rectal involvement 95%, with terminal ileum only involved in pancolitis
(backwash ileitis)

16. Distribution
 CD: skip lesions typical.
 UC: continuous disease from rectum up.

18. Gender
 CD: no gender preference
 UC: male predilection

19. colonic wall
 fat halo sign seen in 61% of chronic UC cases, but only in 8% of CD
 bowel wall is thicker in CD than in UC (when colon involved)
 serosal surface smooth in UC (95%), irregular in CD (80%)

20. perianal involvement
 UC: although rectal involvement is very common, perianal complications are
not as frequently seen
 CD: common, seen in 82% of patients
 stranding of ischiorectal fossa/perirectal fat (73%)
 fistulas/sinus tracts (22%)

21. mesenteric creeping fat
 CD: common in chronic cases.
 UC: not seen, as small bowel not involved.

22. abscess formation
 CD: common, eventually seen in 15-20% of patients
 UC: uncommon

23. extraintestinal complications
 gallstones: seen in 30-50% of CD patients
 primary sclerosing cholangitis: more common in UC
 hepatic abscess: seen in CD
 pancreatitis: more common in CD

27. Crohn disease" regional enteritis"
 Epidemiology
 Clinical presentation

28. Radiographic features
 The characteristic of Crohn disease is the presence of skip lesions and
presence of discrete ulcers

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

31. features on ultrasound:
 non-compressible, rigid, fixed bowel wall
 perienteric fluid
 creeping fat - echogenic area (representing proliferation of adipose tissue
that extends around active inflammation) separating bowel loops
 gut signature - lost or preserved
 strictures - fibrotic (maintains gut signature) or inflammatory (loss of gut
signature)
 abscess
 fistula

33. USimage -stricture in a patient with active
Crohn's disease

34. Advanced Intestinal Mucosal
Manifestations of Crohn’s Disease
 coarsened and granular appearance of the mucosa
 nodular thickening of the valvulae conniventes.
 Aphthous mucosal lesions
 dilution and/or flocculation of the intraluminal contrast column.

35.  Aphthous lesions. 34-year-old woman with
diarrhea.
 Double contrast barium enema demonstrates
diffuse aphthae throughout the colon (
arrowheads ) manifesting as shallow erosions
surrounded by a zone of edema

36. Advanced Intestinal Mucosal
Manifestations of Crohn’s Disease
 the ulcers take on a linear conformation, typically only 1–2 mm wide and
extending up to 15 cm in length. (along the mesenteric margin)
 because it maintains its pliability, the antimesenteric side may appear
sacculated when compared to the contracted and rigid mesenteric side

37.  Crohn’s disease of the duodenum,
with sacculations. 30-year-old
woman with diarrhea.
 Upper GI study demonstrates
 a diffusely diseased duodenum with
areas of focal dilation ( arrows )
consistent with sacculations.
 Additionally, there are several ulcers
( arrowheads ) and discontinuous
segments offocal narrowing

38.  deep longitudinal, oblique, and transverse linear ulcers intersect
 islands of edematous mucosa, commonly referred to as “pseudopolyps,” may
mimic the appearance of nodules protruding beyond the mucosal surface

40.  Pseudopolyps should be distinguished from true inflammatory polyps, which
occur when focal inflammatory cellular infiltrate and edema cause the
involved mucosa to project above the level of the neighboring mucosa.
 On contrast fluoroscopy, inflammatory polyps will appear as multiple small,
rounded luminal filling defects

41.  The coexistence of regional mucosal denudation and pseudopolyps gives rise
to the characteristic “cobblestone” appearance of advanced Crohn’s disease.
 cobblestoning appears as large and irregular regions of mucosal ulceration
with interspersed pseudopolyps of variable size and shape. The involved
segment of bowel may demonstrate reduced pliability and luminal narrowing

42.  Crohn’s ileitis with cobblestone confi
guration.
 23-year-old woman with chronic
diarrhea, malnourishment, and evidence
of enteric blood loss. Small bowel follow-
through shows loop separation due to
severe mural edema as well as
transverse ( arrowhead ) and linear (
arrow ) ulcerations involving the distal
ileum. The coexistence of pseudopolyps
produces the characteristic cobblestone
appearance

43.  Frayed string appearance. 22-year-old
woman with chronic diarrhea diagnosed
with Crohn’s disease.
 Small bowel follow-through shows
contrast traversing a diffusely narrowed
segment of distal ileum, resembling the
appearance of a frayed string ( arrow ).
Note the eccentric involvement of the
bowel wall, with sacculations along the
antimesenteric margin ( arrowheads )

44. Fibroinflammatory Stenosis in Advanced
Crohn’s Disease
 Intestinal pliability may be compromised in advanced Crohn’s disease by any
combination of fibrosis, inflammatory infiltration, and spasm.
 Because inflammatory stenosis and spasm may be amenable to medical
therapy, whereas fibrous stricture generally requires surgical repair, the
radiologist is often called upon to help distinguish between these entities.

45.  On contrast fluoroscopy, both inflammatory stenosis and fibrous stricture will
appear as luminal narrowing; the classic “string sign” describes a thin column
of intraluminal barium within the narrowed segment of bowel that resembles
a frayed string.
 The key to differentiating stricture :monitoring of luminal distensibility
 in fibrous stricture, luminal distensibility is lost ,
 in spasm, dispensability is preserved;
 in inflammatory stenosis,distensibility should remain at least partially intact

47. Mesenteric Involvement and
Perforating Disease
 “creeping fat” may be suspected when bowel loops appear abnormally
separated.
 fibrosis in the mesentery may result in kinking and fixation of the neighboring
small bowel loops.
 fistulae and/or sinus tracts :extension of contrast agent beyond the expected
boundaries of the intestinal Lumen.
 “internal” fistula.
 “external” fistula.
 Sinus tracts

48.  Colovesical internal fistula. 52-year-
old woman with diffuse Crohn’s
disease status post multiple prior
small bowel resections resulting in
short bowel syndrome.
 This image from a single contrast
barium retrograde rectal enema
demonstrates a narrowed and
irregular rectosigmoid colon, with a
fistula communicating from the
inferior aspect of the sigmoid colon to
the bladder ( arrow )

49.  Terminal ileal deep ulcers and abscess
formation.
 This 25-year-old woman with Crohn’s
ileocolitis underwent ileocecal resection 4
years prior to this study.
 The patient presented with a non-resolving
right lower quadrant mass for over a year.
Small bowel followthrough shows active infl
ammation involving the distal ileum just
proximal to the ileocolic anastomosis. There
 are deep ulcers ( arrowheads ) with medial
perforation into an abscess demonstrated by
irregular collections of contrast material (
arrow )

50.  Fistulogram. 20 mL of water-soluble iodinated
contrast was injected through a percutaneous tube
into a fistulous tract. It demonstrates ramifying fi
stulae, communicating with the distal ileum (
arrows ) and the rectosigmoid ( arrowheads )

52. APTHOUS ULCERS
Firstsign of chron’s disease onbarium

53. APHTHOUS ULCER

54. APHTHOUS ULCER

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

56. Fissuring ulceration in Crohn'sdisease
-graphically called `raspberrythorn'
ulcers.

57. COBBLESTONE- LONGITUDNAL & CIRCUMFERENTIAL FISSURES AND ULCERS SEPARATE ISLANDS OF MUCOSA, GIVING IT AN APPEARANCE REMINISCENT OF
COBBLESTONES.

58. A SMALL BOWEL ENEMA SHOWING EXTENSIVE JEJUNAL DISEASE CHARACTERIZED BY LOSS OF
DISTENSIBILITY, (THE CAPABILITY OF BEING STRETCHED OR DISTENDED), THICKENING OF THE SMALL-BOWEL WALL
AND GROSS DISRUPTION OF THE CIRCULAR HAUSTRAL FOLD PATTERN, WHICH IS LARGELY REPLACED BY A MARKED
COBBLESTONE EFFECT. CD OF THE JEJUNUM

59. COBBLESTONE CROHN DISEASE. THIS IS A MAGNIFIED IMAGE FROM THE RIGHT ILIAC FOSSA PERFORMED AS PART OF
A SMALL BOWEL FOLLOW THROUGH. IT SHOWS THE CLASSIC APPEARANCE OF CROHN DISEASE IN THE TERMINAL
ILEUM – SO-CALLED ‘COBBLESTONING’. THIS IS CAUSED BY EXTENSIVE FISSURES AND ULCERATION IN BETWEEN
AREAS OF INTACT BUT OEDEMATOUS MUCOSA, RESEMBLING COBBLESTONES (ARROWS).

60. ROSE THORN THE DEEP, LINEAR ULCERS (ARROWS) THAT HAVE FILLED WITH BARIUM IN THIS STENOSED TERMINAL
ILEUM ARE KNOWN AS ‘ROSE-THORN ULCERS’ AND ARE TYPICAL OF CROHN DISEASE.

61. String sign:spasm/fibrosis
of bowelwall

62. ILEOILEAL FISTULA:long
standing chron’s

63.  spatial and temporal with good luminal distention

64. CT features of active Crohn disease
 mucosal hyperenhancement(most sensitive indicator of active Crohn disease )
 wall thickening (thickness > 3 mm)
 mural stratification with a prominent vasa recta (comb sign)
 mesenteric fat stranding,
 reactive lymphadenopathy
 complications such as fistulas and abscesses

66. stratification
 mural stratification denotes the visualization of bowel wall layers at CT
 At CT enterography, the edematous bowel wall has a trilaminar appearance,
with enhanced outer serosal and inner mucosal layers and an interposed
submucosal layer of lower attenuation

67. Findings in inactive Crohn disease
 submucosal fat deposition
 pseudosacculation
 surrounding fibrofatty proliferation
 fibrotic strictures.

68.  pseudosacculation of the antimesenteric border, Involvement of the
mesenteric border of the affected bowel segment in the inflammatory
process, with associated asymmetric fibrosis.
 Fibrofatty proliferation in the surrounding mesentery is thought to play a
role in sustaining the inflammatory process related to the production of tumor
necrosis factor a .
 bowel strictures occurring as a complication.
 Submucosal fat deposition is commonly associated with longstanding disease

69. Reversible vs irreversible stricture
 Reversible strictures produced by active disease demonstrate
 mucosal hyperenhancement,
 mural stratification,
 fat stranding,
 engorgement of the vasa recta
 lack of enhancement and loss of stratification might be seen in the presence
of transmural fibrosis
 Is It important to differentiate?

71.  Submucosal fat deposition in
longstanding Crohn disease. Axial
CT enterographic section shows
abnormally low attenuation of
the bowel wall (arrow-heads), a
finding consistent with
submucosal fat deposition.
Submucosal fat deposition in
longstanding Crohn disease. Axial
CT enterographic section shows
abnormally low attenuation of
the bowel wall (arrow-heads), a
finding consistent with
submucosal fat deposition.

72. Recurrent Crohn disease after bowel
resection.

73.  Large bowel involvement in Crohn disease.
Axial CT enterographic sections obtained in
three different patients show luminal
narrowing and dilatation in a segment of the
ascending colon (arrow in a), a perianal
abscess (arrow in b), rectosigmoid
involvement (black arrowhead in c), and a
comb sign (white arrowheads in c).

74.  Capsule impaction in bowel stricture due
to Crohn disease. Anteroposterior
radiograph (a) and axial CT enterographic
section (b) demonstrate the impaction of an
endoscopic capsule (black arrow) within the
lumen of a thick-walled diseased ileal
segment (white arrow in b).

75.  Fistula formation in Crohn disease. Coronal
volume-rendered CT enterographic sections
obtained in two patients depict ileo-ileal
fistulas (arrowheads in a) and an ileocolonic
fistula (arrow in b).

76.  Abscess formation in Crohn disease.
Axial (a) and coronal volume-
rendered (b) CT enterographic
sections show a large fluid collection
(arrows) with attenuation similar to
that of enteric contrast material.
Lack of communication between the
collection and the bowel, as well as
the marked difference in caliber
between the two, helps confirm an
extraluminal location of the
collection. Note the evidence of
active Crohn disease (* in a) in the
terminal ileum

77. Fat halo sign in chron’s disease
Transverse CTscan 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.

78. 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.

80. CECTimage, coronalsection,
venous phase -enterocecal
fistula with secondary traction
of the cecum and right psoas
muscleabscess

81. Bowel distention

There are two techniques to acquire distension of the small bowel:
 MR enterography: oral administration of contrast.
 MR enteroclysis: administration of contrast via a nasojejunal tube.
 We routinely perform MR enterography as it suffices in the large majority of
patients while being less burdensome and more time efficient.

82. Oral contrast
 For oral contrast several options are available.
Mannitol in water solution (2%), which provides good contrast between lumen
and bowel wall on both T1 and T2 sequences and is well accepted by patients.
There is one precaution: no colonoscopy with electrocoagulation should be
performed directly after the MRI because of methane resulting from Mannitol
breakdown.

83. MRI sequences
 Balanced FFE (axial and/or coronal) in breath-hold
 T2 with fat sat (axial) in breath-hold
 T1 pre- and post-contrast (axial/coronal) in breath-hold
Optional sequences:
 T2-FSE without fat sat for additional overview and comparison with T2 with
fat sat.
 Diffusion Imaging (DWI).
 Balanced FFE cine-study for motility.

84. MRI signs of Crohn’s disease.

85. Bowel wall thickness
 With adequate distension the normal bowel wall has a
thickness of 1-3 mm.
 A common categorization is 3-5 mm for mild thickening, 5-
7 mm for moderate thickening and > 7 mm for marked
thickening of the bowel wall.
 T1 weighted post-contrast images or non fatsat T2
weighted images (if available) are preferable for
measurement of bowel wall thickness.

86.  The image is a coronal
post-contrast T1 weighted
image showing disease
activity in the transverse
colon with marked wall
thickening of more than 7
mm and deep ulceration
(arrow).

87.  Increased bowel wall thickness is one of the most common signs of
inflammatory activity, but not specific for Crohn's disease.
 Bowel wall thickness correlates well with the severity of the disease activity.
 Measurements are best performed on the sequence with good luminal
distension.
 Black border artifacts on balanced FFE sequences can distort thickness
measurements.

88.  Balanced FFE image shows
marked bowel wall thickening
and luminal narrowing of the
terminal ileum. Measurement on
the balanced FFE sequence can
be less accurate due to the black
border artifact (arrows).dc

89. Enhancement
 Abnormal bowel wall enhancement after administration of gadolinium is the result
of increased vascular permeability and angiogenesis.
 It is seen both in active disease and fibrosis.
 Enhancement can be graded by comparing to the precontrast images, to normal
bowel loops and nearby vascular structures.
 No abnormal enhancement
Equivalent to normal bowel wall
Minor increased enhancement
More than normal bowel wall, but significantly less than nearby vascular structures
 Moderate enhancement
Somewhat less than nearby vascular structures
 Marked enhancement
Equal or more intense than nearby vascular structures

90.  Thickened terminal ileum segment
with marked enhancement on axial
post-contrast T1W image with fatsat.

91.  The latter two enhancement patterns can only be appreciated when the wall
is thickened.
 There is some discussion about the value of the enhancement pattern.

92. Homogeneous enhancement
 Strong homogeneous enhancement is
seen in active inflammation.
 The image shows a terminal ileum
with a homogeneous enhancement
pattern with moderate (green
arrow) and marked (red arrow)
enhancement on an axial post-
contrast T1 image.

93. Mucosal enhancement
 This is seen as bowel wall
thickening with increased
enhancement of the mucosal layer
relative to the outer layers.
 The image is a post-contrast T1
image with a mucosal enhancement
pattern in the terminal ileum
(arrow).
 There is relatively low
enhancement of the middle and
outer layers

94. Layered enhancement pattern
 This pattern suggests severe disease activity or longstanding chronic disease.
 The three-layered appearance is caused by strong enhancement of the
mucosa and the serosa with no enhancement of the middle layer, which is the
submucosa and the muscular layer.
 This middle layer can consist of fat, edema or fibrotic tissue.
 This can be distinguished using a fat sat T2 sequence.

95.  Layered enhancement
pattern of the rectum
with some surrounding
fat stranding on an
axial post-contrast T1
image (arrow).
Continued
inflammation with a
homogeneous
enhancement pattern
can be seen in the
sigmoid colon (green
arrow). Also, a right-
sided adnexal cyst is
present with enhancing
rim (arrowheads).

96. T2 mural signal intensity
 Increased mural signal intensity on fat-saturated T2 images indicates the
presence of mural edema, suggesting active disease.
 Presence of bowel wall thickening with a low mural T2 signal intensity is more
suggestive of fibrotic disease.
 The psoas muscle can be used as a reference when assessing mural T2 signal.
 Fat suppression is routinely used to differentiate between mural fat
depositions and mural edema.
Fat depositions are the result of chronic bowel inflammation and therefore
quite common in Crohn's disease.
 However, its presence does not indicate active disease.
 Perimural edema or fluid can be identified as well and is associated with
active disease .

97. T2 mural signal intensity can be graded as
follows using a T2 sequence with fat sat:
 No increase
normal bowel wall
 Minor increase
bowel wall appears dark gray
 Moderate increase
bowel wall appears light gray
 Marked increase
bowel wall contains areas of white high signal approaching that of luminal
content.

98.  Actively inflamed terminal ileum
with marked thickening and
moderate mural signal intensity
(mural edema) on an axial T2 with
fat sat.

99.  inflamed small bowel showing wall
thickening and mild mural T2 signal
(arrow) on an axial T2 with fat sat.
Prestenotic dilatation can be seen
proximally of the diseased segment.

100.  Fat suppression is routinely used to differentiate between mural fat
depositions and mural edema.
 Fat depositions are a result of chronic bowel inflammation, but not typical of
active disease.
 These fat depositions can be diffuse but can also present as a layered
pattern.
 The CT equivalent for this pattern is the 'fat-halo sign'.

101.  Wall thickening of the terminal ileum in a
67-year-old male with Crohn's disease
since 11 years. Layered enhancement is
seen on an axial post-contrast T1 image
with fat sat (left). T2 with fat sat
(middle) shows the same pattern with a
middle layer of low intensity. T2 without
fat sat shows an increased signal in the
middle layer, suggesting fat depositions.
Endoscopy showed only superficial
disease

102. Ulceration
 Moderate to deep ulceration can be seen on T1 and T2 images, but small
ulcerations can be difficult to distinguish from mucosal folds depending on
the degree of luminal distension.
 Ulcerations are active spots of inflammation and usually there is increased
enhancement on the post-contrast T1 images.

103.  Coronal post-contrast T1 and T2
fat sat images show multiple
small ulcerations in the
terminal ileum.

104. Loss of haustration
 When the colon is involved in Crohn's disease
a decrease of haustral folds can be seen.
 A complete loss of haustration results in a
smooth surface.
 This is also a common finding in ulcerative
colitis and known as 'lead pipe' colon.
 The coronal post-contrast T1 image shows
loss of haustral folds throughout the colon in
a patient with chronic Crohn's disease.

105. Comb sign
 Increased vascularity of the
mesentery is seen in active
inflammation.
 The engorged vessels have
a linear appearance,
resembling the teeth of a
hair comb (comb sign).

106. Creeping fat

Creeping fat, also called fibrofatty proliferation or fat wrapping, are different
names for hypertrophy of the subserosal fat.
 It is a common finding in longstanding Crohn's disease.
 The image shows creeping fat surrounding the descending colon.
It isolates the colon from surrounding bowel loops.

108. Skip lesions
 Skip lesions and patchy inflammation are a typical finding in Crohn's disease,
in contrast to the continuous inflammation, which is seen in ulcerative colitis.
 Skip lesions refers to the interspersed inflammation "skipping" parts of the
bowel, which are left unaffected (green arrows).

109.  The coronal T1 post-
contrast image (left) and
the T2 image (right) show
skip lesions in the
terminal ileum.
The affected lesions
show increased
enhancement with a
layered pattern (yellow
arrows), while another
part is unaffected or
skipped (green arrows).

110. Stenosis
 Stenosis can present as bowel wall thickening combined with lumen
narrowing.
The presence of a prestenotic dilatation increases the likelihood of a stenosis
 Abnormal contrast enhancement of the affected bowel segment is usually
present.
 In the grading system, only severe stenosis is included as a complication,
which is defined as a stenosis with prestenotic dilatation and a moderate-to-
marked increase in mural T2 signal.

111.  Coronal post-contrast T1 image
with a stenosis at the ileocecal
junction (left). No obvious pre-
stenotic dilatation is seen. The
stenosis was non-passable using
endoscopy (right).

112. Infiltrate
 Infiltrate can be seen as creeping fat between bowel loops with replacement
of the fat signal intensity and tethering and kinking of bowel loops.
 Obstructive symptoms due to adhesions, inflammatory narrowing or fibrosis
are common.
 Fistulas and abscesses are often present.
Due to the complex structure, the exact path of a fistula can be difficult to
define.

114. Fistula
 Sinus tracts and fistulas are common complications in patients with Crohn's
disease.
Both show marked enhancement on T1 images after administration of
gadolinium.
A fistulous track can present with a layered 'tram track' configuration or as a
linear enhancing structure.
 It can be seen going from one bowel loop to another bowel loop, to another
hollow organ or to the skin.

117. Abscess
 Abscesses are often seen in patients with severe active Crohn's disease.
 Abscesses are characterized by rim enhancement on post-contrast T1 images
and central high signal intensity on T2 images.
 The abscess is frequently surrounded by fat stranding.

126.  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 DR2relatedgenes.
 More female predilection, age group 30-40 yrs.
 Clinical symtoms- diarrhoea, tenesmus, bleeding per rectum, passage ofmucus,
crampy abdominal pain.
ULCERATIVECOLITIS

127.  MILD DISEASE:fine granularity
 MODERATE:marked erythema, coarse granularity, contactbleeding
and no ulceration.
 SEVERE:spontaneous bleeding,edematous and ulcerated
 Long standing casesepithelialregeneration- pseudopolyps, pre
cancerous condition
 Eventually shortening and narrowing of colon
 FULMINANT DISEASE:toxic colitis/megacolon
PATHOGENESIS

128. Acute UC – descending colon
has irregular outline. No fecal
residue in colon S/O total colitis

129.  Mucosal inflammation-granular appearance to the surface of
the bowel.
 Mucosal ulcers are undermined -button-shapedulcers
 Islands of mucosa remain giving it apseudo-polyp appearance
 In chronic cases the bowel becomes featureless with loss of
normal haustral markings, luminal narrowing and bowel
shortening- lead pipesign
BARIUMENEMA

130. FINE MUCOSAL
GRANULARITY- FIRSTSIGN
NARROWING OFLUMEN

131. COLLAR
BUTTON
ULCERS

133. LEAD PIPECOLON

134. Back wash ileitis :patulous
ICvalve and dilated granular
terminal ileum

135. COLLAR BUTTON ULCERS- CLASSICALLY SEEN IN THE COLON
ASSOCIATED WITH ACTIVE UC. THE COLLAR BUTTON
APPEARANCE IS FORMED BY MUCOSAL ULCERATION WITH
ASSOCIATED UNDERMINING OF THE EDGE BY LATERAL
SUBMUCOSAL EXTENSION.

136. LEAD PIPE COLON DOUBLE CONTRAST BARIUM ENEMA IN LONG STANDING ULCERATIVE
COLITIS CASE SHOWS CLASSIC ‘LEAD PIPE’ SIGN. THE IMAGE DEMONSTRATES DESCENDING COLON AND SIGMOID COLON TO BE
FEATURELESS WITH LACK OF HAUSTRA AND NARROWING.

137. PSEUDOPOLYPS THIS DOUBLE CONTRAST BARIUM ENEMA REVEALS AN IRREGULAR MUCOSA AND
NUMEROUS SMALL FILLED NODULES OR POLYPOIDS THROUGHOUT THE ENTIRE COLON REPRESENTATIVE
OF INFLAMMATORY PSEUDOPOLYPS IN LONG STANDING ULCERATIVE COLITIS.
ALSO VISIBLE ARE SMALL WORM LIKE STRUCTURES THAT ARE SMALL GROUPS OF RESIDUAL
MUCOSA CALLED FILIFORM POLYPS.

138. CTFINDINGS
 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 fathalo sign
 Extramural deposition of fat, leads to thickening of the perirectal
fat, widening of the presacral space
 Marked muscularis mucosa hypertrophy-lead pipe sign.

139. INFLAMMATORYPSEUDOPOLYPS

142.  Wall Thickening- median wall thickeness of colon
ranges from 4.7 to 9.8 mm, more severe the disease
more thicken thewall
 Increased Enhancement- enhancement of themucosa
with no or less enhancement of the submucosa
 Loss of haustralmarkings
MRI

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

144.  thanks