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MR imaging evaluates ulcerative colitis cases


Advances in MR technology have improved the quality of abdominal MRI and hence the ability to assess intestinal diseases. Rapid acquisition sequences have reduced the incidence of motion artifacts from intestinal peristalsis, while the use of phased-array coils has increased spatial resolution. Several intestinal contrast agents have undergone extensive trials. Meanwhile, the use of sequences that modulate MRI signal selectively, for example by suppressing fat tissue signal, can improve gadolinium-related enhancement on T1-weighted images, as well as boosting T2 signal in pathologic tissues.

Advances in MR technology have improved the quality of abdominal MRI and hence the ability to assess intestinal diseases. Rapid acquisition sequences have reduced the incidence of motion artifacts from intestinal peristalsis, while the use of phased-array coils has increased spatial resolution. Several intestinal contrast agents have undergone extensive trials. Meanwhile, the use of sequences that modulate MRI signal selectively, for example by suppressing fat tissue signal, can improve gadolinium-related enhancement on T1-weighted images, as well as boosting T2 signal in pathologic tissues.

These improvements-together with the intrinsic capability of multiplanar acquisition, the use of different imaging parameters, inherently high soft-tissue contrast, and the lack of ionizing radiation-make MRI a useful, effective tool for evaluating the normal bowel and detecting intestinal wall changes indicative of neoplastic and inflammatory bowel diseases.1

The term inflammatory bowel disease (IBD) covers both Crohn's disease and ulcerative colitis. These conditions share an unknown etiology and a chronic lifelong relapsing-remitting course. The efficacy of MRI in diagnosing different aspects of Crohn's disease has been investigated extensively over the past few years. Results have been excellent.2-6 The ability of MRI to evaluate ulcerative colitis, however, has undergone far less study. This may be due to certain intrinsic differences between the two conditions.

Crohn's disease can involve any portion of the gastrointestinal tract. It may affect the small bowel, the large bowel, or both. Involvement is typically discontinuous and unpredictable, though in many cases, the terminal ileum will be affected. Ulcerative colitis, on the other hand, has a predictable course. Affected areas will extend continuously from the rectum to the colon, involving first the left, then the transverse, and finally the right colon. The distal ileum is rarely included. Alternative patterns are referred to as ulcerative proctitis, ulcerative sigmoiditis, left-sided colitis, and pancolitis.

Endoscopy will show rectosigmoid localization in up to 95% of patients with ulcerative colitis, whereas this is rarely observed in patients with Crohn's disease. The mucosal inflammation of the terminal ileum, a hallmark of Crohn's, is rarely observed in ulcerative colitis patients. If this does develop, due to pancolitis (the so-called backwash ileitis), differentiation becomes difficult.7 Histopathologic analysis, however, will always reveal intrinsic macroscopic and microscopic differences between the two conditions.8

Ulcerative colitis is characterized microscopically by an inflammatory process involving the intestinal wall, with leukocyte infiltrates limited to the mucosal and submucosal layers. The muscolaris propria layer and the serosal layer are usually exempt from inflammation. Aphthoid ulcers, mucosal edema, cryptic abscesses, and inflammatory pseudopolyps are the most common findings. Typically, extramural lesions or signs of perivisceral inflammation are not observed. Fatty deposition in the submucosal layer, a common finding in long-standing disease, can be identified easily on both CT and MRI. Macroscopic findings of the chronic inflammatory bowel process include moderate wall thickness, loss of haustration, and widening of the presacral space. Severe complications such as massive bleeding, toxic megacolon, tight bowel strictures or perforation, and colorectal cancer occur occasionally. Enteroenteric fistulas and perivisceral abscesses are not usually seen.

Conversely, Crohn's disease is characterized by transmural inflammation. Leukocyte infiltrates can be found in all wall layers, from the mucosa to the muscolaris propria and serosa. They frequently extend outside the wall and involve adjacent structures. Macroscopic findings of Crohn's disease include a marked wall thickening related to the transmural inflammatory process and mesenteric fibrofatty proliferation. Adhesions, perivisceral abscesses, and/or fistulas are also common.


The micro- and macroscopic differences between Crohn's disease and ulcerative colitis explain why CT and MR evaluations of the two inflammatory bowel conditions are not the same. Each disease requires an alternative clinical and diagnostic management strategy. Final diagnosis of Crohn's disease is usually the more difficult of the two. It requires clinical evaluation plus the combined results of several instrumental examinations, including endoscopy, plain-film and cross-sectional imaging, and histopathology. Endoscopy and biopsy specimens are not sufficient for a complete assessment. Small bowel lesions, the transmural extent of inflammation, and complications such as abscesses or fistulas could be underdetected or missed completely.

Clinical evaluation and endoscopy, on the other hand, are usually sufficient to assess the extent and severity of ulcerative colitis. The inflammatory process involves the colon alone, sparing the small bowel.9 Biopsy specimens of the mucosal and submucosal layers, obtained during endoscopy, can usually detect most of the pathologic features of ulcerative colitis. Plain-film radiography and cross-sectional imaging consequently play a greater role in the diagnosis and evaluation of Crohn's disease than in ulcerative colitis.

Although endoscopy is usually the first choice in diagnosing ulcerative colitis, it can be contraindicated, refused, or incomplete in up to 40% of patients. The examination is invasive, uncomfortable, and associated with significant periprocedural morbidity. Endoscopy is also absolutely contraindicated in acute phases of severe colitis due to the very high perforation risk. Yet diagnostic support could be crucial for patients in this condition. Late complications of ulcerative colitis, particularly tight strictures, can prevent the passage of an endoscope either partially or completely. Alternative imaging modalities may add important information in such cases. MRI, for example, may help evaluate the site and extent of ulcerative colitis, as well as the degree of wall inflammation (disease activity).


Colonic wall thickening is usually less extensive in ulcerative colitis than in Crohn's disease. CT studies have shown the mean value of wall thickening to be 7 mm vs. 13 mm, respectively.10-14 The thickening can be visualized easily on either T1- or T2-weighted MR sequences, preferably on axial images.

Marked thickening of the rectal or colonic wall exceeding 10 mm can be observed in ulcerative colitis as well in severe phases of activity. The wall's inner profile can show a waved configuration in both ulcerative colitis1,3 and Crohn's disease. The outer wall profile is sharper and smoother in ulcerative colitis, due to the intramural rather than transmural extent of inflammation (Figures 1 to 5).

The wall stratification typical of ulcerative colitis is detectable on T2-weighted MRI as a bright, wide line within the two dark stripes of the mucosal and muscolaris propria layers. This finding is probably due to the increased presence of fat or edema in the submucosal layer.13-15 We have found that the wall can be characterized further, and fat distinguished from edema, by selectively suppressing the fat signal. This means that any bright signal remaining after fat suppression will likely be related to disease activity. Persistent bright mucosal and submucosal signal on T2-weighted fat-suppressed MRI is highly indicative of wall edema and active disease. Complete suppression of the submucosal signal suggests fat infiltration and quiescent disease (Figure 1).14 Addition of negative intraluminal contrast (air or superparamagnetic iron oxide particles) is mandatory for the assessment of wall T2 signal.

Bowel wall contrast enhancement obtained after intravenous injection of a gadolinium-based agent is another relevant finding of inflammatory bowel diseases. Usually, it is more detectable on T1-weighted fat-suppressed images. This is observed in active Crohn's disease as well as in ulcerative colitis. The degree of enhancement at the level of the inflamed bowel wall is probably related to the degree of inflammatory activity in ulcerative colitis. Such a correlation has already been proven for Crohn's disease (Figures 2, 4, and 5).2-6,15-17 We have found that in severe active ulcerative colitis, wall enhancement is often associated with marked wall thickening. Moderately active disease still shows wall enhancement, but thickening is reduced. Thickening is extremely low or absent in quiescent disease.14 Enhancement and bright T2 signal are common in severe active ulcerative colitis. These signs, particularly the T2 signal, are less evident in moderate disease.

When considering disease extent, MRI can usually distinguish between proctitis, left-sided colitis, and pancolitis with axial and coronal images.13-14 Coronal planes (Figure 3B) are useful to exclude involvement of the terminal ileum and hence to differentiate ulcerative colitis from Crohn's disease. The appearance of the ileocecal valve and terminal ileum is usually better assessed in the coronal plane. MRI can also detect loss of haustration in any affected colonic segments, strictures, and prestenotic dilations. The coronal plane is more useful for assessment of the transverse colon, whereas the sagittal plane can better display rectal disease and the typical widening of the rectosacral space associated with it.

These findings will all help localize the disease within the colon and distinguish normal from abnormal segments. It is undoubtedly easier to assess active cases than quiescent disease, given the assistance that marked wall enhancement and wall thickening can give in localizing and characterizing the disease on MRI.

Complications associated with ulcerative colitis that will require surgery can also be seen on MRI. These include diffuse dilation of the colonic lumen (toxic megacolon), strictures, and rectal cancer.18 Toxic megacolon can be diagnosed on MRI if severe mucosal disease is observed together with marked and diffuse colonic dilation (upper normal limit, 5.5 to 6.5 cm). The ability of MRI to detect intestinal perforation, a common occurrence with toxic megacolon, has not yet been investigated. Its performance will probably be similar or slightly inferior to CT.

MRI assessment of rectal cancer has been investigated extensively. Studies have shown that MRI is slightly superior to CT for staging rectal lesions, owing to the higher intrinsic contrast and better differentiation of wall layers.19 The modality's accuracy for staging colon cancer needs to be investigated further. Multiplanar views make it easy to assess and characterize strictures on MRI. The site, extent, and degree of a colonic stricture can usually be well detected at any level, particularly after lumen distention with air or any contrast agent. MRI can also distinguish a fibrotic lesion from a neoplastic lesion quite easily in most cases.

Severe ulcerative colitis refractory to medical treatment is usually treated with total colectomy associated with rectal resection. To reproduce the rectal function of the reservoir, an ileal pouch is usually created. Postsurgical complications include chronic wall inflammation of the ano-ileal pouch, or so-called pouchitis. MRI can evaluate the degree of wall inflammation and the pouch's morphology, whenever required, by using the same MR parameters adopted for the evaluation of ulcerative colitis or Crohn's disease.


The best technique for MRI colonic evaluation has yet to be established. Results can still be optimized, however, by following a few practical tips.

Studies should be performed on high-field-strength magnets (1T or 1.5T), preferably with a phased-array coil to maximize spatial resolution. No preparation is recommended in patients with diarrhea. Patients in the remission phase should take a mild laxative the day before examination to cleanse the colon. One or two liters of an iso-osmolar solution, for instance, would be suitable.

All patients should receive an oral dose of superparamagnetic contrast (suspension of iron oxide particles) approximately 90 minutes before imaging. Superparamagnetic contrast produces a negative effect on T1- and T2-weighted images throughout the small and large intestine and makes the bowel content homogeneous (Figure 1). This avoids the possible problem of signal from residual stool (Figure 2). The technique is particularly effective when using T2-weighted turbo spin-echo sequences.20-21

Rectal insufflation with room air will increase the effect of the superparamagnetic contrast and distend the colonic lumen further. Air can also be used without contrast after adequate colon cleansing. Water or water solutions, administered by rectal enema, make a satisfactory alternative to iron oxide-based contrast. These solutions produce a positive effect on T2-weighted MRI and a negative effect on T1-weighted MRI, with good colonic distention.

Most MR studies of IBD are based on T1-weighted fast breath-hold sequences, before and after IV injection of gadolinium-based contrast.2-4,17,18 Use of a negative intestinal contrast agent (air, superparamagnetic iron oxide, or water solutions) highlights the bright wall enhancement obtained after intravenous injection of a gadolinium-based agent on T1-weighted images (Figures 4 and 5). A negative lumen effect leads to improved bright wall contrast enhancement obtained with a gadolinium-based contrast agent. Suppression of fat tissue improves evaluation of wall enhancement further after gadolinium injection. Fat suppression may obscure the evidence of mesenteric lymph nodes, however. We recommend the use of T1-weighted sequences without fat suppression before intravenous contrast administration and use of fat suppression with T1-weighted MRI after contrast injection. Fast pre- and postcontrast T1-weighted sequences (TFE, FLASH, FSPGR, etc.) can provide an extraordinary display of the inflamed bowel walls during active phases of ulcerative colitis. These are characterized by increased gadolinium enhancement.

T2-weighted fast sequences offer an excellent display of the entire small and large intestine following adequate bowel preparation. This is particularly true for T2-weighted HASTE sequences. Plain T2-weighted sequences performed without adequate intestinal contrast have poor contrast resolution. Signal from bowel lumen is very inhomogeneous on T2-weighted MRI and ranges from very bright (fluid) through gray to very dark (air).5,13,14,16 This problem can be overcome by oral administration of an intestinal contrast agent (Figure 1). With a negative intestinal contrast, the additional use of fat-suppressed T2-weighted turbo spin-echo imaging (Figure 1A) can highlight inflammation of the bowel wall and perivisceral mesenteric fat.

Although endoscopy is used routinely for the assessment of ulcerative colitis, MRI can play an important role in overall disease management as well. MRI can assess the extent and severity of ulcerative colitis when endoscopy is incomplete or contraindicated, particularly in hyperacute phases. It can detect the presence of toxic megacolon, determine the severity and activity of mucosal lesions, and evaluate the activity of quiescent disease by distinguishing between submucosal edema and fat. MRI can help distinguish Crohn's disease from ulcerative colitis in uncertain cases by checking whether the distal ileum has been spared and assessing the continuity of colonic involvement.

MRI is a noninvasive technique that involves no ionizing radiation. This is crucial given that ulcerative colitis affects young patients and will be present for the duration of their life.

DR. MACCIONI is a radiologist, DR. PARLANTI and DR. SILIQUINI are residents, and DR. MARINI is a department head, all in the department of radiological sciences at University of Rome La Sapienza in Italy.


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2. Low RN, Sebrechts CP, Politoske DA, et al. Crohn's disease with endoscopic correlation: single-shot fast spin-echo and gadolinium-enhanced fat-suppressed spoiled gradient-echo MR imaging. Radiology 2002;222(3):652-660.

3. Koh DM, Miao Y, Chinn RJ, et al. MR imaging evaluation of the activity of Crohn's disease. AJR 2001;117(6):1325-1332.

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5. Maccioni F, Bruni A, Viscido A, et al. MR imaging in patients with Crohn's disease: value of T2- versus T1-weighted gadolinium-enhanced MR sequences with use of an oral superparamagnetic contrast agent. Radiology 2005 (available online from Dec. 10.1148).

6. Sempere GA, Martinez Sanjuan V, Medina Chulia E, et al. MRI evaluation of inflammatory activity in Crohn's Disease. AJR 2005;184(6):1829-1835.

7. Jewell DP. Ulcerative Colitis. In: Sleisenger MH, Foerdtran JS, eds. Gastrointestinal disease, 4th ed. Philadelphia: Saunders, 1993:1305-1330.

8. Riddell RH. Pathology of idiopatic inflammatory bowel disease. In: Kirsner JB, ed. Inflammatory bowel disease, 5th ed. Philadelphia: Saunders, 1998:427-447.

9. Lasner BH. Clinical features, course, laboratory findings, and complications in ulcerative colitis. In: Kirsner JB, ed. Inflammatory bowel disease, 5th ed. Philadelphia: Saunders, 2000:305-314.

10. Gore RM, Balthazar EJ, Ghahremani GG, Miller FH. CT features of ulcerative colitis and Crohn's disease. AJR 1996;167(1):3-15.

11. Gore RM. Cross sectional imaging of the colon. In: Gore RM, Levine MS, Laufer I, eds. Textbook of gastrointestinal radiology. Philadelphia: Saunders, 1994:1052-1063.

12. Gore RM, Ghahremani GG, Miller FH. Inflammatory bowel disease: Radiologic diagnosis. In: Balfe DM, Levie MS, eds. Syllabus of Radiological Society of North America categorical course in gastrointestinal radiology. Oak Brook: RSNA Publications, 1997:95-110.

13. MRI of colitis F. Maccioni. In: Chapmann AH, ed. Radiology and imaging of the colon. Berlin: Springer-Verlag, 2004:201-214.

14. Maccioni F, Colaiacomo MC, Parlanti S. Ulcerative colitis: value of MR imaging. Abdom Imaging 2005;30(5):584-592.

15. Jones B, Fishman EK, Hamilton SR, et al. Submucosal accumulation of fat in inflammatory bowel disease: CT/pathologic correlation J Comput Assist Tomogr 1986;10(5):759-763.

16. Madsen SM, Thomsen HS, Munkholm P, et al. Active Crohn's disease and ulcerative colitis evaluated by low-field magnetic resonance imaging. Scand J Gastroenterol 1998;33(11):1193-1200.

17. Gourtsoyiannis N, Papanikolaou N, Grammatikakis J, et al. MR enteroclysis protocol optimization: comparison between 3D FLASH with fat saturation after intravenous gadolinium injection and true FISP sequences. Europ Radiol 2001;11(6):908-913.

18. Miner PB. Clinical features, course, laboratory findings, and complications in ulcerative colitis. In: Kirsner JB, ed. Inflammatory bowel disease 5th ed. Philadelphia: Saunders, 2000:299-304.

19. Ferri M, Laghi A, Mingazzini P, et al. Pre-operative assessment of extramural invasion and sphincteral involvement in rectal cancer by magnetic resonance imaging with phased-array coil. Colorectal Dis 2005;7(4):387-393.

20. Giovagnoni A, Fabbri A, Maccioni F. Oral contrast agent in MRI of the gastrointestinal tract, Abdom Imaging 2002;27(4):367-375.

21. Hahn PF, Stark DD, Lewis JM, et al. First clinical trial of a new superparamagnetic iron oxide for use as an oral gastrointestinal contrast agent in MR imaging. Radiology 1990;175(3):695-700.

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