Radiology of small bowel lesions

1. IMAGING OF SMALL BOWEL LESIONS
DR. D. SUNIL KUMAR

2. • The mesenteric small
bowel gradually tapers in
diameter from the
duodenojejunal junction
to the terminal ileum, so
that it normally has a
larger caliber in the
jejunum (up to 3 cm in
luminal diameter) than in
the ileum (up to 2 cm) on
SBFT studies.
ANATOMY

3. • Closely spaced
circumferential folds
(also known as the
valvulae conniventes or
plicae circulares) are
also thicker and
numerous in the
jejunum (normal
thickness of 2–3 mm)
than in the ileum
(normal thickness of 1–
2 mmon SBFT studies.

4. • The folds are composed of mucosa and
submucosa, whereas individual villi lining the
folds are composed only of mucosa and
lamina propria.

5. APPROACH TO DIFFUSE
AND SEGMENTAL SMALL
BOWEL DISEASE
If a disease diffusely or segmentally affects the small
bowel, changes often occur within the wall of the bowel
and alter the normal fold pattern.
Analysis of, first, the fold pattern and, second, the
diffuse or segmental involvement of the small bowel can
be helpful for understanding the underlying pathologic
condition and for developing a reasonable differential
diagnosis

7. TYPE I FOLDS: THIN (<3 MM),
STRAIGHT FOLDS WITH A DILATED
LUMEN

8. CAUSES
• 1. Mechanical obstruction
• 2. Paralytic ileus
• 3. Scleroderma
• 4. Sprue

9. MECHANICAL SMALL
BOWEL OBSTRUCTION
• The common causes of mechanical
obstruction of the small bowel are adhesions
(from a prior abdominal surgical procedure or
severe intraperitoneal infl ammation) or
hernias. Other, less frequent causes include an
obstructing neoplasm, intussusception,
stricture (from Crohn disease, prior ischemia,
or idiopathic), or volvulus.

10. • It usually manifests clinically with nausea,
vomiting, cramping abdominal pain, and
distention.

11. IMAGING FEATURES
• Abdominal radiographs are only 50-60% sensitive
for small bowel obstruction. In most cases, the
abdominal radiograph will have the following
features:
– dilated loops of small bowel proximal to the
obstruction
– predominantly central dilated loops
– three instances of dilatation over 3 cm
– valvulae conniventes are visible
– fluid levels if the study is erect (non-standard
technique)

12. • a Gasless abdomen:
– Repeated episodes of vomiting
– NG tube placement causing decompression
– Higher level of obstruction.

13. a. Dilated small bowel
b. The location is central
within the abdomen
c. Large bowel at the
periphery is collapsed
d. The valvulae conniventes
can be identified across the
full width with thin straight
folds (Type I) of the dilated
loops confirming it to be
small ( not large ) bowel.

14. Dilation of the small bowel
without opacification of the
large bowel.
Perforation is a late
complication of small bowel
obstruction; in this
case gastrografin was the
preferred contrast agent
over barium because of the
risk of barium peritonitis.

15. Small bowel follow-through. The proximal small bowel is
dilated and abruptly narrows from a smooth rounded defect
that eccentrically compresses the lumen and causes partial
obstruction. Notice the straight thin folds in the dilated loop
(arrowhead).

17. • Dilated small bowel loops
with multiple air-fluid
levels consistent with
obstruction. A lamelated
ovoid calcified density is
projected over the lower
abdomen in combination
with branching air seen in
the expected location of
the biliary tree
(pneumobilia). This
combination of findings
constitutes the Rigler's
triad of gallstone ileus.

18. CT
• CT is more sensitive than radiographs and will
demonstrate the cause in ~80% of cases. There
are variable criteria for maximal small bowel
obstruction, but 3.5 cm is a conservative estimate
of dilated bowel.
• Positive oral contrast is not usually necessary for
the diagnosis of small bowel obstruction:
– it usually becomes dilute in the setting of SBO and
does not usually reach the transition point before the
scan occurs
– it may obscure the evaluation of the small bowel wall,
limiting evaluation ofbowel ischemia.

19. • Schematic approach is advised to rapidly and
efficiently identify the transition point. This
approach should begin in a retrograde fashion
by starting at the rectum and proceeding
proximally toward the cecum, ileum, and
jejunum. If the transition point is located
proximally (jejunum or duodenum), the
position should be confirmed by using an
antegrade approach from stomach

20. • Detection of a
transition point is
important for bowel
obstruction
interpretation i.e. the
site of obstruction and
possible
cause. Adhesions are
the presumed
mechanism in many
cases (following
previous surgery)
especially small bowel
obstruction but rarely
is the exact point of
ahesive obstruction
seen on CT as a focal
kink and narrowing of
the lumen by extrinsic
compression.
Dilated fluid-filled small bowel loops with abrupt transition to collpsed small
bowel associated with a focal kink and narrowing of the lumen.

21. Axial CT scan shows dilated small bowel loops (S). There is an abrupt change in caliber
(arrow) between the proximal dilated bowel loops and collapsed distal bowel loops (C). The
change in caliber was due to adhesions.

22. SBO secondary to adenocarcinoma. Axial CT scan shows asymmetric and
irregular mural thickening of an ileal loop (arrow), which causes dilatation of
the proximal small bowel (S).

23. SCLERODERMA
• Gastrointestinal manifestations of
scleroderma can occur in up to 90% of patients
with scleroderma with the commonest site of GI
involvement being the oesophagus.
• Smooth muscle atrophy and fibrosis is thought to
be the chief underlying mechanism.
• The small bowel is affected in more than 60% of
scleroderma patients, the duodenum most
frequently.

24. RADIOGRAPHIC FEATURES
• luminal dilatation (can be massive)
• reduced peristalsis / delayed contrast transit
• mucosal folds appear relatively normal despite
dilatation.
• hidebound bowel sign (crowding of valvulae
conniventes): thought to be pathognomonic of
scleroderma
• sacculation (antimesenteric border, focal
dilatations, pseudo-diverticula due to asymmetric
bowel wall fibrosis, especially in the jejunum)

26. Hidebound bowel sign
• The sign describes the narrow separation
between the valvulae conniventes which are of
normal thickness despite dilatation of the bowel
lumen.
• The cause of hidebound appearance in
scleroderma is thought to be asymmetric smooth
muscle atrophy of the inner circular muscularis
layer relative to the outer longitudinal layer.
Contraction of the longitudinal layer results in
foreshortening of the bowel and close packing of
the valvulae conniventes.

27. Stack of coins is an alternate descriptive term

28. Multiple dilated small
bowel loops are
present. The valvulae
conniventes are thin
and straight (type I
folds) and closely
stacked together.

29. COELIAC DISEASE
• Coeliac disease (also sometimes termed
as non tropical sprue ) is a condition of
gastrointestinal malabsorption (sprue) that
results from the small intestine's response to
dietary gluten.

30. • Small bowel mucosa is primarily affected
(submucosa, muscularis and serosa remain
normal), resulting in progressive degrees of villous
inflammation and destruction (which starts in
duodenum and extends into ilium) with resulting
of induction crypt hyperplasia. Loss of villi, which
absorbs fluid, and hypertophy of crypts, which
produce fluid , result in fluid excess in the small
bowel lumen.

31. RADIOGRAPHIC FEATURES
• Features of small bowel barium studies are not
sensitive enough for confident diagnosis, but
some changes may be seen:
– small intestinal dilatation due to excess fluid
– dilution of contrast
– non-obstructing intussusception
– ileojejunal fold pattern reversal (including
jejunalisation of the ileum)
– moulage sign( dilated loop of bowel with effaced
folds.
– Flocculation(separation of barium into tiny pieces as a
result of dilution).

32. Moulage (within oval),
which is a featureless
bald appearance of the
jejunum caused by
atrophy of folds and wall
edema.

33. The jejunum is devoid of most of its normal mucosal
markings.

34. This case shows flocculation
as a result of dilution.

35. Image shows
flocculation (within
oval at upper right),
dilution (single
arrow), and
dilatation (double
arrow).

36. JEJUNALISATION OF THE ILEUM
• Barium studies reveal dilated small bowel, and
enteroclysis reveals a decreased number of jejunal
folds (one to three folds per inch in celiac disease vs
four to seven folds per inch in control subjects) due to
loss of mucosal surface area. Conversely, the ileum may
have an increased number of folds as a compensatory
adaptation to increase the absorptive capability of the
small bowel. This phenomenon results in reversal of
the normal fold pattern with an increased number of
folds in the ileum relative to the jejunum
(“jejunization” of the ileum), also known as a flip-flop
pattern

38. reversal of the fold
pattern (within oval),
with more prominent
folds in the ileum
than in the jejunum.

39. Mild dilatation of bowel
loops with increased
number of thin, straight
(type I)folds in the ileum.
Reversal of the normal
jejunal and ileal fold
patterns is seen in this case

40. Dilution. CT image shows varying degrees of luminal opacification, from
white to gray to fluid attenuation. This appearance is produced when
opaque oral contrast material is progressively diluted as it passes into fluid-
filled small bowel loops.

41. Flocculation. CT image show irregular dots of barium (arrow) in
fluid-filled bowel loops.

42. Laminar flow appearance in CT
• Small bowel lumen contains both intrinsic
physiologic fluid and administered enteric
contrast material. Peristaltic waves sweeping
periodically through the bowel result in
variable laminar flow of these different fluid
components within the flaccid bowel lumen in
a recognizable pattern.

44. Telescoping and Intussusception
• The small bowel becomes progressively more
flaccid and dilated. The result is telescoping of
bowel loops and ultimately intussusception ,
in which the mesenteric fat and vessels of one
bowel loop are seen within the lumen of an
adjacent bowel loop.

45. Telescoping. CT image shows concentric rings (arrow) in
multiple bowel loops. The concentric rings represent bunching
of folds in cross sections of flaccid loops. Although the folds
collapse and crowd together, mesenteric fat and vessels are
not seen in the lumen, as occurs with intussusception.

46. Intussusception. CT image shows a crescent of mesenteric fat
(arrow) containing vessels within a bowel loop, a finding typical
of true small bowel intussusception.

48. TYPE II FOLDS: THICK (>3
MM), STRAIGHT FOLDS,
CAUSED BY INTRAMURAL
EDEMA OR HEMORRHAGE

49. • Segmental
• 1. Ischemia
• 2. Radiation enteritis
• 3. Intramural hemorrhage
• 4. Adjacent inflammatory process
• Diffuse
• 1. Venous congestion
• 2. Hypoproteinemia
• 3. Cirrhosis

50. INTESTINAL ISCHAEMIA
• Intestinal ischaemia refers to vascular
compromise of the bowel which in the acute
setting has a very high mortality if not treated
immediately.
• Impairment of normal vascular supply can result
from a number of insults including:
– general hypotension/hypoxia especially in the setting
of arterial insufficiency due to stenosis
– arterial occlusion
– bowel obstruction
– venous outflow obstruction

51. • In other words anything which result in a
deficiency in the normal supply of blood and
metabolites to the bowel can result in ischaemia.
• Bowel ischaemia severity ranges from mild
(generally transient superficial changes of
intestinal mucosa) to more dangerous and
potentially life-threatening transmural bowel wall
necrosis

52. • If ischemia is severe enough, and is not relieved
quickly, then a predictable sequence of events
will usually be observed:
– necrosis of the bowel wall
– bacteria proliferation in the bowel wall, releasing gas
in the wall itself (pneumatosis intestinalis)
– gas goes through mesenteric vessels into portal vein
(pneumatosis portalis)
– sepsis and/or intestinal perforation
– death

53. IMAGING FEATURES
• Radiologic findings depend on the timing of
the examination in relation to the vascular
insult. Many abdominal radiographs (up to
half) may be normal or have findings of only
adynamic ileus.
• Suggestive findings include an isolated, rigid,
often dilated, and unchanging small bowel
loop with thickened mucosal folds.

54. Two small bowel loops in the
left upper abdomen are dilated
and contain straight, thickened
(≥3 mm) folds (arrows),
characteristic of a segmental
type II fold pattern

55. Frontal spot image
from SBFT in patient
with ischemia shows
straight-segmental
thickening of folds
(arrows) in loop of
ileum due to
localized submucosal
edema and
hemorrhage

56. USG
• Doppler US could represent a useful modality
for
– the evaluation of severe stenosis in the
mesenteric arteries
– for the evaluation of characteristic intestinal wall
changes; in fact relationship between bowel wall
changes and the severity of ischemia has been
suggested

57. CT
• CT is now the investigation of choice for
patients with suspected intestinal ischaemia.
• In general CT of the abdomen and pelvis
should be performed with intravenous
contrast and a neutral luminal contrast (e.g.
water) so that bowel wall enhancement and
thickness can be adequately assessed.

58. • Multiple contrast phases are typically
obtained:
– non-contrast
– arterial phase (e.g. triggered when abdominal
aorta reaches >100HU)
– portal venous phase, e.g. 30 seconds after arterial
phase finishes

59. Acute arterial mesenteric ischemia
• Early phase: the CT shows the presence of emboli
or thrombi as filling defect in the lumen of the
artery. If they are small and peripherally localized,
the identification can be difficult. The loops of
injured small bowel are contracted in
consequence of spastic reflex ileus and intestinal
wall shows lacking of/poor enhancement.The
mesentery is bloodless, due to reduction in
caliber of the vessels and apparently in number
PATHOGENESIS

60. • Intermediate phase: blood and fluids are
drained by the venous system, not affected by
occlusion. The bowel wall become thin, with a
typical “paper thin” aspect , the loops loose
the tone, and now are only gas filled so spastic
reflex ileus evolves into hypotonic ileus,
peritoneal free fluid can be detected too.

61. • Late phase: If the causative factor is not removed,
the ischemia rapidly evolves into infarction. In the
injured loops mount the liquid stasis, air-fluid
levels appear and a progression from hypotonic
reflex ileus to paralytic ileus can be appreciated.
The wall necrosis lead to parietal, mesenteric,
and even portal pneumatosis or perforation with
pneumo-peritoneum, retropneumoperitoneum
and free fluid in the abdominal cavity due to
increased hydrostatic pressure inside the
intestinal loops that allows extravasation of
plasma and to the peritoneal reaction to the
ischemic injury.

62. Contrast-enhanced
MDCT 2D
reconstruction on
sagittal plane shows
thrombosis with
impairment in the
blood flow in the
superior mesenteric
artery (SMA).

63. Large amount of
poorly enhancing
mildly dilated small
bowel ( jejenum and
proximal ileum ).

64. there is good enhancement of the
jejunum (green area), but lack of
enhancement in the ileum

66. large filling defect is noted in
proximal SMA for lenght of
3.5cm on contrast study s/o
SMA thombosis.

67. Extensive Portal venous
gas due to ischaemic bowel.
Note the extensive
peripheral liver and
mesenteric intravascular gas.

68. USG
• Doppler US can show stenosis, emboli, and
thrombosis in the near visible parts of the
celiac trunk, the SMA and the IMA.
• Systolic velocities of more than 250–300 cm/s
are sensitive indicators of severe mesenteric
arterial stenosis.

69. • In the early phase of bowel ischemia US
examinations may show SMA occlusion, and
bowel spasm.
• In intemediate phase US is not very informative
because of an increased amount of gas in the
intestinal loops causing large acoustic barrier.
• In late phase US may show a fluid-filled lumen,
bowel wall thinning, evidence of extraluminal
fluid and decreased or absent peristalsis.

70. • The location of the venous thrombus relative to the whole
mesenteric circulation, its extension, and the presence or
absence of an adequate collateral circulation are important
factors in predicting the occurrence of subsequent bowel
ischemia with infarction.
• The location of the thrombus is often determined by the
underlying cause. Thrombosis due to intraabdominal
disease (eg, pancreatitis) is usually initiated in larger veins
at the site of compression, and then progresses
peripherally to involve smaller vessels. In contrast,
thrombosis due to hematologic disorders first affects the
smaller venous branches and then progresses to larger
trunks.
Superior mesenteric venous
thrombosis

71. • In cases of superior mesenteric venous thrombosis,
thrombus may be seen in the SMV at the enhanced CT. When
the venous occlusion persists, there is an increase of
intramural blood volume and, consequently, of intravascular
hydrostatic pressure with development of interstitial edema,
so the imaging findings at this stage of disease are related to
mural thickening, intramural hemorrhage, and submucosal
edema.
STAGE OF EVENTS

72. At CT, can be detected a target appearance of the ischemic bowel with an
inner hyperdense ring due to mucosal hypervascularity, hemorrhage, and
ulceration; a middle hypodense edematous submucosa; and a normal or
slightly thickened muscularis propria

73. • . If the vascular impairment persists, there is a
progression to intestinal infarction: the bowel
becomes necrotic and peritonitis develop so
the CT findings in this phase are represented
by mural thickening of the involved segments,
peritoneal fluid, and mesenteric engorgement.

74. Multiple loops of mid and
distal ilium are markedly
oedematous and show
reduced contrast
enhancement within their
walls. The adjacent
mesentery is also markedly
oedematous. Free fluid of
moderate extent in pelvis
and also surrounding liver
and spleen.
The superior mesenteric
vein is occluded by thrombus

75. Some loops of distal ileum have hyperdense walls (yellow dotted line), which would
represent enhancement or, more likely in this setting, submucosal red cell
extravasation. This is why a non-contrast initial scan is useful.

76. CT scans shows acute superior mesenteric vein thrombosis
(black arrow) with bowel wall thickening (white arrowhead),
mesenteric edema (black arrowhead) and ascites.

77. contrast material–enhanced multidetector CT images demonstrate diffuse
circumferential bowel wall thickening (white arrowheads) with abnormal
wall enhancement: Some bowel loops show decreased enhancement (black
arrowheads), consistent with bowel infarction; others show increased
enhancement possibly due to submucosal hemorrhage(arrow ).

78. The “halo sign” (black arrowhead ) is also present. A hypoattenuating venous filling defect
with vein enlargement is seen in the portal vein and SMV (straight arrows in b), consistent
with a thrombosis. There is venous engorgement in the small veins of the mesenteric root
(curved arrow in b). Mesenteric fat edema (f) and ascites (* in b) are also noted.

79. • In late stage venous thrombosis, absence of
mural enhancement, and the presence of fluid
and gas may be evident in the mesenteric and
portal veins, bowel wall, and sub-peritoneal or
peritoneal space.

80. USG
• Ultrasound may show a homogeneously hypoechoic
intestinal wall as a result of edema that occurs earlier in the
course of disease when compared with SMA compromise.
In initial phase US may reveal thrombus at the SMV origin
and mural thickening with hyperechoic mucosal layers and
hypoechoic submucosa attributable to edema of the
affected bowel.
• In intermediate phase US examination may reveal
increased intraluminal secretions and decreased peristalsis.
• In late stage US reveals mural thickening of the involved
segment, intramural or intraperitoneal gas, and peritoneal
fluid.

81. Doppler US image shows absence of flow in the superior
mesenteric vein (SMV). SMA - superior mesenteric artery.

82. Acute venous mesenteric ischemia Sonographic features show mural thickening with
hyperechoic mucosal layers and hypoechoic submucosa attributable to edema of the
affected bowel . In intermediate phase US examination may reveal increased
intraluminal secretions and decreased peristalsis

83. Radiation enteritis
• Radiation enteritis is a bowel pathology
resulting from toxic effects of radiotherapy on
the bowel wall and vasculature.
• Radiation enteropathy occurs in patients who
receive more than 40 Gy (4,000 rad)to the
pelvis for cervical or prostatic carcinoma.

84. • In the acute phase, radiation affects bowel
mucosa causing cell death with ulceration. It
also causes inflammation with mucosal and
submucosal oedema. In the subacute and
chronic phases healing and fibrosis occurs.
• Additionally radiation induces endarteritis
obliterans, which results in a state of chronic
mesenteric ischaemia leading to bowel
strictures.

85. • Fluoroscopic enteroclysis
• acute radiation enteritis
– bowel loops appear spastic with luminal narrowing
and oedma of mucosal folds
• chronic radiation enteritis
– thickening of bowel wall and folds due to oedema or
fibrosis
– “stack of coins appearance” enlarged smooth, parallel
mucosal folds
– single or multiple bowel stenoses
– ulcers

86. Acute radiation enteritis with
regular fold thickening

87. Several loops of small bowel in the
mid abdomen have straight,
thickened folds with separation of
the loops, consistent with a
segmental type II fold pattern. A
case of Acute radiation enteritis

88. SBFT in patient with prior
radiation therapy to
pelvis shows straight-
segmental thickening of
folds (white arrows) in pelvic
loops of ileum with
narrowing, angulation (black
arrows), and lowgrade
obstruction due to radiation
serositis.A case of chronic
radiation enteritis

89. INTRAMURAL
HEMORRHAGE
• The small bowel is the most common site for
intramural hemorrhage, which can be caused by
anticoagulation, bleeding, diathesis, or trauma.
• Spontaneous bleeds such as this one often result
in thick, straight folds with a stack-of-coins
appearance.
• Ischemic bowel or reactive small bowel edema
due to an adjacent inflammatory process also
could result in similar findings on a barium small
bowel examination.

90. A loop of abnormal small bowel is seen in the pelvis. The lumen is slightly
narrowed with thick, straight folds (segmental type II pattern). This patient was
receiving anticoagulant therapy and had a spontaneous intramural hemorrhage

91. Frontal spot image from SBFT
in patient taking warfarin
sodium shows straight
segmental thickening of folds
(arrows) due to localized
submucosal hemorrhage from
anticoagulation. Small-bowel
ischemia may produce similar
findings

92. NECT coronal reformatted image of the abdomen shows segmental hyperdense wall
thickening of duodenum (short arrow) and proximal jejunal loop (long arrow). The
attenuation value of the thickened wall ranged from 50 to 70 HU.

93. Axial NECT scan of the pelvis shows ascites with layering of fluid in the pelvis. High
density fluid is seen in the dependent part suggestive of hemoperitoneum (arrow).

94. CECT coronal reformatted MIP (Maximum intensity projection) image shows normally
enhancing thickened small bowel wall with crowding of jejunal folds (white arrows).

95. CECT coronal reformatted MIP
image shows normal superior
mesenteric artery, vein and
their branches (white arrows)
supplying the thickened small
bowel.
The CT features of segmental
hyperdense wall thickening of
duodenum and jejunum with
normal mesentric vessels in a
patient on oral anticoagulant
with elevated INR suggested
the diagnosis of spontaneous
intramural hematoma of
small bowel with minimal
hemoperitoneum.

96. TYPE III FOLDS: THICK, NODULAR
FOLDS, CAUSED BY INFILTRATIVE
DISEASE OF THE BOWEL WALL

97. • Segmental
• 1. Crohn disease
• 2. Infection
• 3. Lymphoma
• 4. Metastases
Diffuse
1. Whipple disease
2. Intestinal lymphangiectasia
3. Nodular lymphoid
hyperplasia
4. Polyposis syndromes
5. Eosinophilic gastroenteritis
6. Amyloidosis
7. Mastocytosis
8. Lymphoma
9. Metastases

98. GIARDIASIS
• Giardiasis is a disease caused by infection with
the protozoan Giardia lamblia.
• Symptoms are caused by Giardia organisms
infecting the cells of the duodenum and jejunum
of the small intestineand blocking nutrient
absorption.
• Symptoms loss of appetite, diarrhea, loose or
watery stools, stomach cramps, upset stomach,
projectile vomiting (uncommon), bloating and
excessive gas.

99. RADIOGRAPHIC FEATURES
• The radiographic alterations of giardiasis may
occasionally involve most of the small bowel but are
usually limited to the duodenum and jejunum with
varying degrees of spasm, irritability, and lumen
narrowing. Hypermotility and hypersecretion are often
described. The mucosal folds are thickened and
blurred. There is dilution and coarse flocculation of the
barium column due to increased secretions. Tiny
nodular lesions are frequent and result from
hypertrophied lymphoid follicles. A sprue like pattern
may occur in the distal jejunum and ileum, with
reversal of the normal fold pattern. These changes
revert to normal aft er treatment.

100. • The segmentation of the barium column along with
apparent thickening of the proximal small-bowel folds,
seen only on the later films of the small-bowel study,
represents a new subtle radiographic finding in
intestinal giardiasis. This is a manifestation of the
interaction between the barium and the altered
intestinal contents in the proximal small bowel. It is
possible that barium in the trailing part of the column
is in contact with these secretions for a longer period
of time, as proximal intestinal motility decreases when
the distal small bowel is distended.
• It is also possible that the amount of intestinal
secretions increases during the course of the study.

101. Nodular pattern of jejunal mucosa in giardiasis

102. Early film from small-bowel series appears normal. B, Delayed film from same
study demonstrates proximal dilution of barium and apparent fold thickening
in jejunum.

103. Initial film from small-bowel series demonstrates minimal dilution of barium
in jejunum with normal fold pattern. B, 30 mm later, barium column is
segmented, there is coarse flocculation in proximal small bowel, and jejunal
folds appear thickened.

104. WHIPPLE DISEASE
• Whipple disease is caused by the bacillus
Tropheryma whipplei . It is characterized
clinically by malabsorption, arthritis or
arthralgias, lymphadenopathy, abdominal
tenderness, and increased skin pigmentation.

105. PATHOLOGY
• Extensive infiltration of lamina propria with
large macrophages infected by intracellular
tropheryma whipplei causes marked swelling
of intestinal villi and thickened irregular
mucosal folds primarily in duodenum and
proximal jejunum; when they become large
enough to be macroscopically visible , they
may appear as innumerable small filling
defects superimposed on irregularly thickened
folds (sand-like nodules).

106. IMAGING FINDINGS
• Barium studies may reveal thickened, irregular
folds and tiny nodules in the jejunum and, to a
lesser degree, the ileum due to accumulation
of the Whipple bacilli and periodic acid–
Schiff–positive macrophages in the
submucosa and lamina propria.
• Hypersecretion,dilatation, and diff use small
bowel involvement are usually absent, which
helps to diff erentiate this disease from sprue

107. Frontal overhead radiograph
from SBFT in patient with
Whipple disease shows
thickened irregular folds in
jejunum and proximal ileum
.

108. nodular,
thickened folds (type III)
are present throughout
the
proximal small bowel.

109. Irregular thickening of small
bowel folds in Whipple
disease

110. Affected patients may also have mesenteric and retroperitoneal
adenopathy with fat-attenuation nodes on CT scans that are due to
lymphatic obstruction and intranodal deposition of lipids

111. EOSINOPHILIC
GASTROENTERITIS
• Eosinophilic gastroenteritis is a disease of unknown
origin, in which the patient presents with abdominal
pain, diarrhea, vomiting, and occasionally
malabsorption.
• Usually eosinophilia is present on the peripheral blood
smear.
• The stomach is the organ most commonly affected,
followed by the small intestine and the colon.
• Often the clinical course is benign and self-limited,
responding to corticosteroid treatments.
• Some patients have a history of allergy.

112. • The radiographic findings are similar to those
of any other infiltrative small bowel disease.
Marked bowel wall infiltration can result in
luminal narrowing and rigidity of the affected
segment(s). Any portion of the alimentary
tract may be affected.

113. Nodular fold
thickening
is present diffusely
throughout the
visualized dilated
loops of small
bowel. There is also
nodular deformity
of the distal
stomach.

114. NODULAR LYMPHOID HYPERPLASIA
• Enlarged lymphoid follicles may develop in
the terminal ileum as a normal finding in
young adults or as an immunologic response
to enteric infections.
• Barium studies typically reveal multiple,
uniform, round, 1–3-mm nodules separated
by normal mucosa in the terminal ileum.

115. • When these nodules are unusually numerous
or prominent, however, they indicative of
hypogammaglobulinaemia.
Peyer´s glands (lymphoid
nodules) in the ileum (arrows).
NODULAR LYMPHOID HYPERPLASIA

116. double-contrast barium
enema examination (with
reflux into terminal ileum)
shows enlarged lymphoid
follicles(reactive) as small
round nodules (arrows)
separated by normal mucosa
in terminal ileum.

117. • Nodular lymphoid hyperplasia usually is
associated with an immunologic disorder,
primarily an indication of
hypogammaglobulinemia. Occasionally, this
disease may be present without an immunologic
disorder. Malabsorption and an intestinal
infection ( Giardia lamblia , Strongyloides , or
Monilia ) are often associated conditions.
• The main differential consideration is lymphoma;
however, lymphomatous nodules are large, vary
in size, and may ulcerate

118. Multiple tiny nodular filling defects are present throughout the
small bowel (diffuse type III pattern). All the nodules are
uniform in size and shape.

119. • .
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