Nonneoplastic Diseases of The Small Intestine: Differential Diagnosis and Crohn Disease

R e s i d e n t s S e c t i o n S t r u c t u r e d R ev i ew
McLaughlin and Maher

Nonneoplastic Diseases of the Small Intestine
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Residents Section
Structured Review
Nonneoplastic Diseases of the

Small Intestine: Differential
Diagnosis and Crohn Disease
Patrick D. McLaughlin1
Michael M. Maher
McLaughlin PD, Maher MM
Keywords: Crohn disease, differential diagnosis,

nonneoplastic disease, small intestine
DOI:10.2214/AJR.12.8495
Received December 23, 2011; accepted after revision
October 11, 2012.
1
Both authors: Departments of Radiology, University
College Cork, and Cork University Hospital, Wilton,
Cork, Ireland. Address correspondence to M. M. Maher
(m.maher@ucc.ie).
WEB
This is a web exclusive article.
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0361803X/13/2012W174
American Roentgen Ray Society
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Key Points
1. In cases of small-intestinal disease the
length of involvement and the location,
symmetry, and degree of small-intestinal
wall thickening allow interpreting radiologists to refine their differential diagnoses.
2. Submucosal accumulation of fluid or blood
results in characteristic stratification of
mural enhancement that produces a target
sign. Causes of this pattern include hypoalbuminemia, angioedema, vasculitis, Crohn
disease, infection, radiation enteritis, ischemia, and intramural hemorrhage.
3. Acute inflammation of the small intestine
in Crohn disease typically results in segmental wall thickening, submucosal edema, and mucosal hyperenhancement. Although many nonneoplastic diseases of
the small intestine produce these findings,
a diagnosis of Crohn disease can be more
specifically inferred when the changes are
asymmetric and distributed in a multisegmental discontinuous pattern referred to
as skip lesions.
4. Perienteric signs in the mesentery and peritoneum often help the radiologist arrive at
a more succinct differential diagnosis, particularly when characteristic mesenteric fibrofatty proliferation and hypervascularity are observed in association with Crohn
disease. Although absence of inflammatory stranding adjacent to an abnormal segment of small intestine does not exclude
Crohn disease and other benign conditions,
it should raise suspicion of intramural hemorrhage (in the appropriate clinical context)
and neoplasms such as lymphoma.
Compared with the upper gastrointestinal
tract and large bowel, the small intestine is
much less amenable to examination with endoscopy. Radiologic investigations therefore
play a pivotal role in the diagnosis of pathologic conditions of the small intestine. We review the manifestations of small-intestinal
disease, focusing on patterns of wall thickening, which is the hallmark of many smallintestinal diseases. We emphasize important
features, such as the length, location, and degree of small-intestinal wall thickening, that
allow interpreting radiologists to refine their
differential diagnoses. Other valuable imaging findings, such as the attenuation pattern
of the small-intestinal wall, caliber of the involved segment, and the presence of accompanying colonic and perienteric abnormalities
in the mesentery and peritoneum are also reviewed because they often contribute to more
accurate differential diagnosis. Also reviewed
are the pathophysiologic and imaging characteristics of Crohn disease. The primary focus
is on imaging changes as visualized at CT, but
patterns of small-intestinal nonneoplastic diseases are often similarly depicted with other
imaging modalities. Other comprehensive articles detail the techniques and findings encountered during MRI [1, 2] and ultrasound
[3] of the small intestine.
Technique
Appropriate choice of imaging and reconstruction technique is vital to the identification and characterization of small-intestinal
abnormalities. In the case of CT, maximizing the spatial and contrast resolution by acquiring isotropic multiplanar datasets and by
administering IV and neutral enteric contrast agents markedly improves sensitivity
to surpass, in certain clinical circumstances, the sensitivity of other diagnostic alternatives, including wireless capsule endoscopy [4, 5]. The use of positive enteric contrast
agents may still be valuable in the care of patients with low volumes of visceral adipose
tissue and for increasing the conspicuity of
subtle disease in the peritoneum, but mucosal disease and mural enhancement patterns
are much better assessed with neutral enteric
contrast agents [68].
AJR:201, September 2013

Ultrasound and MRI are performed without ionizing radiation and therefore are particularly useful for imaging of young patients
with Crohn disease, who often need repetitive
imaging procedures during the variable clinical course of this disease [9]. Ultrasound of
the small intestine requires a high-frequency
(5-17 MHz) linear array probe, use of which
increases the spatial resolution of the intestinal wall [10]. Color and power Doppler imaging and contrast-enhanced ultrasound provide more detailed information on mural and
extraintestinal vascularity, which reflects inflammatory disease activity [11]. The benefits of MRI of the small intestine include
high soft-tissue contrast on both T2-weighted and contrast-enhanced T1-weighted images [12, 13] and the use of steady-state free
precession sequences, which offer sufficiently high temporal resolution to negate motion artifacts and allow dynamic assessment
of intestinal motility [14]. Steady-state free
precession sequences of the small intenstine
may specifically allow radiologists to differentiate between peristalsis and stricture and
when stricture is present allow more accurate
determination of the stricture grade.
Adequate distention of the small bowel is
vital to the diagnostic accuracy of CT, particularly when neutral enteric contrast agents
are used [8]. Peroral enterography and enteroclysis result in substantially greater distention than routine oral preparation techniques.
Comparative studies, however, have shown
that absolute bowel distention is less with peroral enterography, particularly in the jejunum
[1518]. Diagnostic accuracy rates are not significantly different between peroral enterography and enteroclysis, however, and enterography has significantly greater patient tolerance
[1518]. Enteroclysis also has the disadvantage of additional exposure to ionizing radiation as a result of fluoroscopic placement of
the nasojejunal tube. In the management of
Crohn disease, CT and MR enterography have
comparable sensitivities for identifying active
small-intestinal disease, but image quality is
superior with CT enterography [19].
Diagnostic Approach to Abnormal
Small Intestine
In the evaluation of nonneoplastic smallbowel abnormalities, a number of approaches have been proposed to guide image interpretation and aid in the formation of an
accurate and succinct differential diagnosis.
We have found the approach of Macari et al.
[7] to be a valuable guide for review of small-
bowel imaging studies. This approach characterizes small-intestinal diseases (neoplastic and nonneoplastic) on the basis of length,
degree, and symmetry of mural thickening;
the location of the lesion or abnormal segment; and the pattern of mural enhancement.
Length of Involvement
Ulceration, foreign-body perforations (Fig.
1), secondary thickening from appendicitis,
small-intestinal diverticulitis (Fig. 2), and endometriosis can cause focal (< 6 cm) smallintestinal abnormalities [7]. Although not specifically addressed in this article, malignant
disease of the small intestine frequently also
causes focal imaging abnormalities.
Conditions that typically result in segmental (640 cm) involvement of the small intestine include inflammatory bowel disease
(Fig. 3), intestinal trauma (Fig. 4), infectious
enteritis (Fig. 5), radiation enteritis, intramural hemorrhage, and segmental intestinal ischemia related to vasculitis and other
causes [7]. When long-segment (occurring in
a length greater than 40 cm) abnormalities of
the small intestine are found, pathologic processes such as angioedema, graft-versus-host
disease (Fig. 6), hypoalbuminemia, and generalized intestinal ischemia related to vasculitis and other causes should also be considered [7]. Overall there is an accepted degree
of overlap between these varied pathologic conditions; for example, early Crohn disease and early tuberculous enteritis, can both
cause focal as well as segmental abnormalities of the distal ileum. The severity of ischemia, vasculitis, and angioedema influences
the length of involvement, and these conditions may manifest as segmental rather than
long-segment abnormalities.
Degree of Thickening
The degree of bowel wall thickening is
best assessed when the small intestine is sufficiently distended [7]. In cases of small-intestinal ischemia, the degree of bowel wall
thickening may indicate the nature of vascular insufficiency. In acute transmural infarction, the bowel wall is often thinned or only
mildly thickened [20]. Patients with intestinal ischemia related to mesenteric venous
thrombosis, however, typically have thickening of the small-intestinal wall [20]. Malignancy or submucosal hemorrhage should be
considered when marked small-bowel wall
thickening measuring greater than 20 mm
is found [7]. Most other pathologic entities
involving the small bowel cause moderate
thickening. The differential diagnosis therefore cannot be narrowed in this setting.

Symmetry of Thickening
Asymmetric bowel wall thickening is a
hallmark of Crohn disease and typically is
more prominent along the mesenteric border.
Asymmetric thickening is also seen in many
small-intestinal malignancies. Small-intestinal lymphoma [21] and small-intestinal metastasis from scirrhous-type gastric primary carcinoma [22] may result in bowel wall
thickening that is closer to circumferential
and symmetric.
Location of Disease
With regard to benign diseases of the
small intestine, identification of the location
of disease within the bowel wall (i.e., mucosal, submucosal, serosal) is more valuable in
narrowing the differential diagnosis than is
the location of disease along the length of
the small intestine. On CT and MR images
the mucosa of normal small intestine should
be smooth and continuous [7]. Small-intestinal ischemia, Crohn disease, and tuberculosis all cause mucosal disruption [7, 20]. Submucosal accumulation of fluid or hematoma
results in the characteristic stratification of
mural enhancement that produces the target
sign [7]. Causes of this pattern include hypoalbuminemia, angioedema, vasculitis, Crohn
disease, infection, radiation enteritis, ischemia, and intramural hemorrhage [7]. Serosal lesions may be visualized as discrete
masses on CT and MR images, but tethering with spiculation of the mucosal folds is
the classic sign observed at barium examinations. Causes of serosal disease include peritoneal metastasis, carcinoid tumors, endometriosis, and sclerosing mesenteritis [7, 23].
Mural Enhancement and Attenuation
Enhancement of diseased bowel can be
increased or decreased. Increased mural enhancement can be homogeneous or heterogeneous, although much overlap exists. Mural
enhancement may also be stratified, creating
a target pattern, which results from diseases
that cause submucosal edema or hemorrhage
[7]. Homogeneous enhancement has been described in subacute Crohn disease [24], radiation enteritis, intramural hemorrhage, and
some cases of small-intestinal ischemia [7]. Enhancement patterns, however, can overlap because each of the aforementioned conditions
can also cause the stratified enhancement that
produces the target sign. Heterogeneous en-
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hancement may be seen in Crohn disease, endometriosis, and many small-bowel neoplasms
[7]. Diminished or absent enhancement is frequently identified in cases of acute transmural
small-intestinal infarction [20].
Submucosal fat deposition may mimic submucosal edema, but these two entities can be
differentiated in analysis of mural attenuation.
Analysis with region-of-interest tools typically shows attenuation values in the small-intestinal wall in the range of fat (50 to 150 HU)
in the case of submucosal fat deposition. The
presence of submucosal fat is associated with
chronic inflammation, including Crohn disease
[25], celiac disease [26], and radiation enteritis
[27], but can also develop over short time periods [28]. Submucosal fat has also been found
to be a normal variant in approximately 20%
of abdominal CT examinations and is most frequently seen in the terminal ileum [29].
Fold Thickening
Abnormalities of the small-intestinal folds,
such as reversal of the normal jejunoileal fold
pattern in celiac disease, can be identified
with CT and CT enterography [4, 30]. Heavily T2-weighted MR enterographic and highresolution MR images may also display fold
thickening and asymmetry [1, 2], but subtle
changes involving the small-intestinal folds
are best visualized on barium studies because
of the inherently greater spatial resolution
achieved with this technique [31]. The causes
of mucosal fold thickening (> 3 mm) are many
and result from any process that increases the
volume of fluid or cells in the submucosa and
mucosa of the small intestine. Hemorrhage
or edema into these spaces typically results
in regular thickening of small-bowel folds,
whereas irregular thickening of small-bowel
folds occurs in processes that result in cellular infiltrate and deposition in the bowel wall,
such as infection, inflammation, malignancy,
and rarer disorders such as Whipple disease,
eosinophilic enteritis, and amyloidosis [32]
Colonic Findings
The presence or absence of colonic imaging abnormalities, including wall thickening,
mural enhancement, and attenuation, are important and may allow the radiologist to refine
the differential diagnosis in cases of small-intestinal disease. Most nonneoplastic small-intestinal diseases intrinsically involve the large
bowel. These include inflammatory bowel disease, ischemia, vasculitis, infection, graft-versus-host disease, angioedema, and eosinophilic disorders. Celiac disease in rare instances
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causes colonic dilation, and cases of megacolon related to celiac sprue have been documented in the radiology literature [33].
Perienteric Findings
The mesenteric vessels should be completely scrutinized whenever an abnormal
bowel loop is identified. Thrombus may be
found in even small divisions of the mesenteric vessels and when identified should prompt
immediate review for solid organ infarcts and
ascites, which may indicate vasculitis or cardioembolic arterial occlusion. Dilated mesenteric vessels that produce a comb sign as they
pass through hypertrophic mesenteric fat may
be seen in Crohn disease, and chronic mesenteric venous thrombosis is also recognized.
A vessel whorl pattern may indicate malrotation, volvulus, or internal hernia. Patients
with intestinal obstruction displaying this pattern are more than 20 times as likely as those
without a whorl sign to need urgent abdominal surgery [34]. Abnormal lymph nodes and
inflammatory stranding may be seen in association with many small-intestinal abnormalities, but low-attenuation mesenteric lymph
nodes should prompt suspicion of tuberculosis, Whipple disease, and celiac disease. Lymphatic metastasis from a mucinous primary
malignant tumor or treated lymphoma may
also cause low-density mesenteric lymphadenopathy. An absence of inflammatory stranding adjacent to a thickened segment of small
intestine should raise immediate suspicion of
lymphoma and intramural hemorrhage [7].
Crohn Disease
Crohn disease is a chronic relapsing immune-mediated inflammatory disorder that
results from a dysregulated immune response
to luminal antigens, including normal intestinal bacterial flora in genetically susceptible
individuals [35, 36]. A decrease in common
intestinal infections in Westernized countries
has been accompanied by an increase in noninfectious inflammatory bowel diseases, and
the prevalence of Crohn disease in the United States has dramatically increased since the
1980s [37]. There is a bimodal distribution of
patient age at disease onset: A large peak occurs at 20 years and a smaller peak at 50 years
[38, 39]. Crohn disease often manifests as nonspecific symptoms such as diarrhea, weight
loss, and abdominal pain, but specific clinical
evidence of inflammatory bowel disease, including signs of perianal fistulas, tags, or fissures and aphthous ulceration, may be present
in as many as one third of patients [40].
Most patients with Crohn disease have

small-bowel involvement at presentation [37].
Approximately 15% of Crohn disease patients
initially present with features of colitis alone.
Perianal complications develop in 3545% of
patients over the course of disease [37, 39].
Less commonly, Crohn disease patients present with isolated gastroduodenal and jejunal
disease. This pattern is more common among
pediatric Crohn disease patients [14].
Acute inflammation of the small intestine
in Crohn disease typically results in segmental wall thickening, submucosal edema, and
mucosal hyperenhancement (Fig. 7), but this
pattern is not specific for Crohn disease alone
[41]. Multisegmental discontinuous smallintestinal disease, known as skip lesions,
however, is highly suggestive of Crohn disease [24, 42], particularly when it is asymmetric and preferentially involves the mesenteric border (Fig. 8). Advanced ulceration
in Crohn disease results in longitudinal and
transverse mucosal fissures, giving rise to a
cobblestone appearance, and deep ulcers are
evident as linear, high-signal-intensity foci
within the bowel wall on T2-weighted MR
images [2]. Fat-suppressed T2-weighted sequences are required to identify submucosal
edema, and T1-weighted contrast-enhanced
sequences are required to identify mucosal
hyperenhancement at MRI.
Progression of transmural granulomatous inflammation can result in sinus, fistula, phlegmon, and ultimately abscess formation (Fig.
9) not only in the perienteric tissues but also
in the abdominal wall and subcutaneous compartment. Sinuses and fistula tracks may be
identified at CT and may appear as tracks of
high signal intensity on T2-weighted fat-saturated MR images. Both fistulas and sinuses are avidly enhancing after administration
of gadolinium-based contrast material. The
spectrum of perienteric changes that occur in
Crohn disease ranges from hypervascularity,
fat stranding, and mesenteric fibrofatty proliferation caused by an accumulation of mesenteric fat to inflammatory and fibrotic changes
in the mesentery[43] (Figs. 10 and 11). Inflammatory changes in the mesenteric fat that
appear hyperintense on T2-weighted fat-suppressed MR images and as stranding on CT
images correlate well clinically and histologically with active acute inflammation [44, 45].
Imaging markers of chronic fibrostenotic
disease have been evaluated with more variable
results than the findings of acute inflammatory disease [44, 46, 47]. Identifying the difference between acute inflammatory and chron-

ic fibrotic strictures is important because it can
influence the choice between medical and surgical management [2]. Adler et al. [44] correlated imaging signs at CT enterography with
histologic findings in 22 Crohn disease patients
and found that upstream dilatation of bowel appears to be the most reliable CT indicator of tissue fibrosis (Figs. 12 and 13).
Evaluation of all imaging studies of patients with Crohn disease should always include a search for extraintestinal manifestations of Crohn disease, which include renal
calculi, erosive sacroiliitis (Fig. 14), and evidence of sclerosing cholangitis [48]. Complications of Crohn disease related to the
disease process include gastrointestinal adenocarcinomas and carcinoid tumors [49],
but the radiologist should also be aware of
emerging reports of an increased risk of lymphoma in Crohn disease patients receiving
long-term immunosuppressive medications
such as azathioprine and the antitumor necrosis factor agent infliximab [5053].
Conclusion
In imaging of the abnormal small intestine,
differential diagnosis can be refined by evaluating the length, degree, symmetry, and location of the small-intestinal abnormality. Location should be subdivided into position along
the course of the small intestine (proximal or
distal) and the predominant location within the
bowel wall (mucosal, submucosal, or serosal).
The pattern of attenuation and enhancement
of the abnormal small intestine and the presence of associated perienteric abnormalities in
the mesentery and peritoneum are also used to
narrow the list of differential diagnoses, particularly in the case of suspected Crohn disease.
References
1. Sinha R, Rajiah P, Murphy P, Hawker P, Sanders
S. Utility of high-resolution MR imaging in demonstrating transmural pathologic changes in Crohn
disease. RadioGraphics 2009; 29:18471867
2. Sinha R, Verma R, Verma S, Rajesh A. MR enterography of Crohn disease. Part 2. Imaging and
pathologic findings. AJR 2011; 197:8085
3. Maturen KE, Wasnik AP, Kamaya A, et al. Ultrasound imaging of bowel pathology: technique and
keys to diagnosis in the acute abdomen. AJR 2011;
197:[web]W1067W1075
4. Paulsen SR, Huprich JE, Fletcher JG, et al. CT
enterography as a diagnostic tool in evaluating
small bowel disorders: review of clinical experience with over 700 cases. RadioGraphics 2006;
26:641657; discussion, 657662
5. Huprich JE, Fletcher JG, Fidler JL, et al. Prospec-
tive blinded comparison of wireless capsule endoscopy and multiphase CT enterography in obscure gastrointestinal bleeding. Radiology 2011;
260:744751
6. Aiyappan SK, Kalra N, Sandhu MS, Kochhar R,
Wig JD, Khandelwal N. Comparison of neutral
and positive enteral contrast media for MDCT enteroclysis. Eur J Radiol 2012; 81:406410
7. Macari M, Megibow AJ, Balthazar EJ. A pattern
approach to the abnormal small bowel: observations at MDCT and CT enterography. AJR 2007;
188:13441355
8. Megibow AJ, Babb JS, Hecht EM, et al. Evaluation of bowel distention and bowel wall appearance by using neutral oral contrast agent for multidetector row CT. Radiology 2006; 238:8795
9. Desmond AN, ORegan K, Curran C, et al.
Crohns disease: factors associated with exposure
to high levels of diagnostic radiation. Gut 2008;
57:15241529
10. Strobel D, Goertz RS, Bernatik T. Diagnostics in
inflammatory bowel disease: ultrasound. World J
Gastroenterol 2011; 17:31923197
11. Migaleddu V, Quaia E, Scanu D, et al. Inflammatory activity in Crohns disease: CE-US. Abdom
Imaging 2011; 36:142148
12. Maccioni F, Bruni A, Viscido A, et al. MR imaging in patients with Crohn disease: value of T2versus T1-weighted gadolinium-enhanced MR
sequences with use of an oral superparamagnetic
contrast agent. Radiology 2006; 238:517530
13. Leyendecker JR, Bloomfeld RS, DiSantis DJ, Waters GS, Mott R, Bechtold RE. MR enterography
in the management of patients with Crohn disease. RadioGraphics 2009; 29:18271846
14. Sinha R, Verma R, Verma S, Rajesh A. MR enterography of Crohn disease. Part 1. Rationale,
technique, and pitfalls. AJR 2011; 197:7679
15. Minordi LM, Vecchioli A, Mirk P, Bonomo L. CT
enterography with polyethylene glycol solution vs
CT enteroclysis in small bowel disease. Br J Radiol 2011; 84:112119
16. Negaard A, Paulsen V, Sandvik L, et al. A prospective randomized comparison between two
MRI studies of the small bowel in Crohns disease, the oral contrast method and MR enteroclysis. Eur Radiol 2007; 17:22942301
17. Negaard A, Sandvik L, Berstad AE, et al. MRI of
the small bowel with oral contrast or nasojejunal
intubation in Crohns disease: randomized comparison of patient acceptance. Scand J Gastroenterol 2008; 43:4451
18. Lawrance IC, Welman CJ, Shipman P, Murray K.
Small bowel MRI enteroclysis or follow through:
which is optimal? World J Gastroenterol 2009;
15:53005306
19. Siddiki HA, Fidler JL, Fletcher JG, et al. Prospective comparison of state-of-the-art MR enterogra-
phy and CT enterography in small-bowel Crohns

disease. AJR 2009; 193:113121
20. Wiesner W, Khurana B, Ji H, Ros PR. CT of acute
bowel ischemia. Radiology 2003; 226:635650
21. Gore RM, Mehta UK, Berlin JW, Rao V, Newmark GM. Diagnosis and staging of small bowel
tumours. Cancer Imaging 2006; 6:209212
22. Gollub MJ, Schwartz MB, Shia J. Scirrhous metastases to the gastrointestinal tract at CT: the malignant target sign. AJR 2009; 192:936940
23. Scarmato VJ, Levine MS, Herlinger H, Wickstrom M, Furth EE, Tureck RW. Ileal endometriosis: radiographic findings in five cases. Radiology
2000; 214:509512
24. Choi D, Jin Lee S, Ah Cho Y, et al. Bowel wall
thickening in patients with Crohns disease: CT
patterns and correlation with inflammatory activity. Clin Radiol 2003; 58:6874
25. Amitai MM, Arazi-Kleinman T, Avidan B, et al.
Fat halo sign in the bowel wall of patients with
Crohns disease. Clin Radiol 2007; 62:994997
26. Scholz FJ, Behr SC, Scheirey CD. Intramural fat in
the duodenum and proximal small intestine in patients with celiac disease. AJR 2007; 189:786790
27. Chen S, Harisinghani MG, Wittenberg J. Small
bowel CT fat density target sign in chronic radiation enteritis. Australas Radiol 2003; 47:450452

28. Muldowney SM, Balfe DM, Hammerman A,
Wick MR. Acute fat deposition in bowel wall
submucosa: CT appearance. J Comput Assist Tomogr 1995; 19:390393
29. Harisinghani MG, Wittenberg J, Lee W, Chen S,
Gutierrez AL, Mueller PR. Bowel wall fat halo
sign in patients without intestinal disease. AJR
2003; 181:781784
30. Rubesin SE, Herlinger H, Saul SH, Grumbach K,
Laufer I, Levine MS. Adult celiac disease and its
complications. RadioGraphics 1989; 9:10451066
31. Prassopoulos P, Papanikolaou N, Grammatikakis
J, Rousomoustakaki M, Maris T, Gourtsoyiannis
N. MR enteroclysis imaging of Crohn disease.
RadioGraphics 2001; 21(spec no):S161S172
32. Eisenberg RL. Thickening of small bowel folds.
AJR 2009; 193:[web]W1W6
33. Kappelman NB, Burrell M, Toffler R. Megacolon
associated with celiac sprue: report of four cases
and review of the literature. AJR 1977; 128:6568
34. Duda JB, Bhatt S, Dogra VS. Utility of CT whirl
sign in guiding management of small-bowel obstruction. AJR 2008; 191:743747
35. Podolsky DK. Inflammatory bowel disease. N
Engl J Med 2002; 347:417429
36. Shanbhogue AK, Prasad SR, Jagirdar J, et al.
Comprehensive update on select immune-mediated gastroenterocolitis syndromes: implications
for diagnosis and management. RadioGraphics
2010; 30:14651487
37. Loftus EV. Clinical epidemiology of inflammato-

ry bowel disease: incidence, prevalence, and environmental influences. Gastroenterology 2004;
126:15041517
38. Fleischer DE, Grimm IS, Friedman LS. Inflammatory bowel disease in older patients. Med Clin
North Am 1994; 78:13031319
39. Polito JM, Childs B, Mellits ED, Tokayer AZ,
Harris ML, Bayless TM. Crohns disease: influence of age at diagnosis on site and clinical type of
disease. Gastroenterology 1996; 111:580586
40. Lewis RT, Maron DJ. Anorectal Crohns disease.
Surg Clin North Am 2010; 90:8397
41. Ziech ML, Bossuyt PM, Laghi A, Lauenstein TC,
Taylor SA, Stoker J. Grading luminal Crohns disease: which MRI features are considered as important? Eur J Radiol 2012; 81:e467e472
42. Tolan DJ, Greenhalgh R, Zealley IA, Halligan S,
Taylor SA. MR enterographic manifestations of
small bowel Crohn disease. RadioGraphics 2010;
30:367384
43. Bodily KD, Fletcher JG, Solem CA, et al. Crohn
disease: mural attenuation and thickness at con-
trast-enhanced CT enterographycorrelation with

endoscopic and histologic findings of inflammation. Radiology 2006; 238:505516
44. Adler J, Punglia DR, Dillman JR, et al. Computed
tomography enterography findings correlate with
tissue inflammation, not fibrosis in resected small
bowel Crohns disease. Inflamm Bowel Dis 2012;
15:849856
45. Gee MS, Nimkin K, Hsu M, et al. Prospective
evaluation of MR enterography as the primary
imaging modality for pediatric Crohn disease assessment. AJR 2011; 197:224231
46. Herlinger H, Furth EE, Rubesin SE. Fibrofatty
proliferation of the mesentery in Crohn disease.
Abdom Imaging 1998; 23:446448
47. Koh DM, Miao Y, Chinn RJ, et al. MR imaging
evaluation of the activity of Crohns disease. AJR
2001; 177:13251332
48. Pariente B, Cosnes J, Danese S, et al. Development of the Crohns disease digestive damage
score, the Lmann score. Inflamm Bowel Dis
2011; 17:14151422
49. Boltin D, Levi Z, Halpern M, Fraser GM. Concurrent small bowel adenocarcinoma and carcinoid
tumor in Crohns disease: case report and literature review. J Crohns Colitis 2011; 5:461464
50. Kandiel A, Fraser AG, Korelitz BI, Brensinger C,
Lewis JD. Increased risk of lymphoma among inflammatory bowel disease patients treated with
azathioprine and 6-mercaptopurine. Gut 2005;
54:11211125
51. ODonnell S, Murphy S, Anwar MM, et al. Safety
of infliximab in 10 years of clinical practice. Eur
J Gastroenterol Hepatol 2011; 23:603606
52. Parakkal D, Sifuentes H, Semer R, Ehrenpreis
ED. Hepatosplenic T-cell lymphoma in patients
receiving TNF- inhibitor therapy: expanding the
groups at risk. Eur J Gastroenterol Hepatol 2011;
23:11501156
53. Brown SL, Greene MH, Gershon SK, Edwards
ET, Braun MM. Tumor necrosis factor antagonist
therapy and lymphoma development: twenty-six
cases reported to the Food and Drug Administration. Arthritis Rheum 2002; 46:31513158
Fig. 143-year-old man with acute abdominal pain after ingesting needle.
A and B, Axial (A) and sagittal reformatted (B) contrast-enhanced CT images show linear metallic foreign body (arrow) perforating anterior wall of second portion of
duodenum.
W178
Fig. 258-year-old man with jejunal diverticulitis.

A, Axial contrast-enhanced CT image shows numerous contrast-filled jejunal diverticula (arrowheads).
B, Axial contrast-enhanced CT image shows inflammatory changes surrounding single diverticulum (arrow) with more widespread fat stranding in surrounding mesentery.
Fig. 327-year-old man with Crohn disease. Image

from barium small-bowel series shows separation
of jejunal and proximal ileal loops with segmental
narrowing and dilatation of proximal jejunum with
multifocal mucosal ulceration (arrows).
Fig. 419-year-old man with history of blunt abdominal trauma. Axial contrastenhanced CT image shows segmental wall thickening and submucosal edema of
third portion of duodenum (arrowheads) consistent with duodenal contusion.
Fig. 525-year-old immunosuppressed woman with neutropenic enterocolitis.

Axial contrast-enhanced CT image shows segmental moderate-to-severe
thickening of distal ileum and cecum (arrow).
Fig. 649-year-old man with diarrhea and background of treatment of recurrent

lymphoma with bone marrow transplant. Axial CT image shows diffuse submucosal
edema and mucosal hyperenhancement resulting in characteristic target
appearance (arrow) of entire small intestine consistent with graft-versus-host
disease. Thickening and mucosal hyperenhancement of colon also are evident.
Fig. 727-year-old man with acute exacerbation of Crohn disease. Axial

contrast-enhanced CT image shows segmental mucosal hyperenhancement and
submucosal edema of distal ileum creating target sign (arrow).
Fig. 833-year-old woman with Crohn disease. Axial contrast-enhanced CT

image shows asymmetric thickening of segment of distal ileum (arrow). Mural
enhancement is homogeneous, and irregular alteration of intestinal caliber
consistent with pseudosacculation is evident. These changes are more indicative
of chronic than acute inflammation.
Fig. 965-year-old man with Crohn disease and previous right hemicolectomy.
A, Axial contrast-enhanced CT image shows irregular thickening of ileum with extramural extension toward abdominal wall compatible with penetrating disease (arrow).
B, Axial contrast-enhanced CT image obtained at slightly more superior level shows abdominal wall abscess (arrow).
W180
Fig. 1027-year-old man with Crohn disease.

A, Axial contrast-enhanced CT image shows multifocal small-bowel thickening with characteristic fibrofatty proliferation (arrowheads) of small-bowel mesentery.
B, Axial contrast-enhanced CT image shows multifocal small-bowel thickening with characteristic fibrofatty proliferation of mesentary (arrowheads). Mature
enterocolic fistula (arrow) is also evident in left lower quadrant.
Fig. 1143-year-old woman with Crohn disease.

Coronal contrast-enhanced thick-slab averageintensity-projection CT enterographic image shows
submucosal edema and mucosal enhancement
of loop of distal ileum (arrowheads). Dilated and
engorged mesenteric vessels produce comb sign as
they pass through hypertrophic mesenteric fat close
to inflamed loop.
Fig. 1245-year-old woman with Crohn disease and fibrostenotic ileal stricture.
A and B, Coronal (A) and axial (B) contrast-enhanced CT images show tight stricture (arrowheads) in proximal
ileum. Presence of mild upstream dilatation of ileum is reliable indicator of fibrostenotic Crohn stricture.
Fig. 1321-year-old woman with Crohn disease and

inflammatory distal ileal stricture. Coronal contrastenhanced thick-slab average-intensity-projection
CT enterography image shows tight stricture in distal
ileum (arrowheads). Presence of marked mucosal
enhancement and lack of upstream dilatation of
ileum likely indicates presence of acute inflammatory
Crohn stricture. Short nonobstructing stricture is
present in transverse colon (arrow).
W182
Fig. 1451-year-old man with acute bloody diarrhea.

A and B, Axial (A) and coronal (B) contrast-enhanced
CT images shows diffuse colonic thickening
and dilatation consistent with fulminant colitis
(arrowheads). In this case differential diagnosis can
be narrowed by identification of alternating narrowed
and dilated segments of small intestine consistent
with fibrostenotic strictures (arrow, A).
C, Axial CT image shows erosive sacroiliitis
(arrowheads), which is important finding that may
reduce list of differential diagnoses.

Nonneoplastic Diseases of The Small Intestine: Differential Diagnosis and Crohn Disease

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McLaughlin and Maher