Crohn’s Disease of the Small Bowel

Clinical Considerations

Crohn’s disease is an idiopathic inflammatory disease that can affect any part of the gastrointestinal (GI) tract from the mouth to the anus. Patients with this disease have a genetic predilection to an abnormal immunologic response to environmental factors, including food, and gut flora leading to a chronic inflammatory response. The small bowel is the major site of involvement. With the exception of malignant neoplasms, Crohn’s disease can be the most devastating disease to involve the GI tract. Its prevalence has increased, mostly in younger age groups, with a peak age between 15 and 25 years. It has a worldwide distribution but is most common in northern Europe, North America, and Japan. Four studies have shown a bimodal distribution, with the first peak in the second or third decade of life and the second, smaller peak in the sixth or seventh decade. However, four other studies have shown a unimodal distribution, peaking in the second or third decade, and decreasing thereafter. The colonic predominance in older adults has led some to speculate that the second peak incidence in this cohort is caused by ischemia or diverticulitis. Both genders are equally affected, although some studies have shown a slight female predominance. A familial tendency has frequently been described.

The small bowel is commonly involved by Crohn’s disease, with the terminal ileum being the most common location. In a review combining multiple population-based studies on the natural history of adult Crohn’s disease, approximately one-third of patients had ileitis, one-third had colitis, and one-third had ileocolitis. Isolated perianal disease occurs in 2% to 3%, but perianal or rectal fistulae are common in colonic or rectal disease (10% to 37%). Upper GI tract involvement is being recognized with increasing frequency but almost invariably occurs with small bowel or colonic disease.

Although the focus of this chapter is on Crohn’s disease of the small bowel, there are differences in presentation from colonic disease. Patients with colonic Crohn’s disease are more likely to present with blood loss, perianal disease, toxic colitis, and extraintestinal complications. Crohn’s disease in the small bowel has a slightly better prognosis, although there are more likely to be complications such as abscesses, fistulae, and obstruction. Abdominal pain, mild diarrhea, weight loss, and pyrexia are common clinical findings. Other patients may present with a right lower quadrant mass, representing the diseased ileum or cecum. Delays of 3 to 4 years have been reported between the onset of often subtle symptoms and the diagnosis of Crohn’s disease in the small bowel.

Many factors contribute to the development of diarrhea in patients with Crohn’s disease. An inflamed bowel mucosa causes increased secretion of fluid and electrolytes. Extensive terminal ileal disease or resection impairs bile salt reabsorption, leading to the malabsorption of fat and fat-soluble vitamins. Bacterial overgrowth secondary to strictures, fistulae to the colon, adhesions, aneurysmal dilation, or bypassed loops can also cause diarrhea. The combination of decreased food absorption and intermittent obstruction may lead to significant weight loss in these patients. ^,

Classification and Therapy

Over the years, attempts have been made to classify Crohn’s disease anatomically, clinically, and operatively. This has evolved from the International Working Party in 1991 to the Vienna classification in 1998, and finally to the Montreal revision of the Vienna classification in 2005. ^,

The Montreal revision classifies the disease into age of diagnosis, location, and disease behavior. Disease behavior is classified into nonstricturing, nonpenetrating (uncomplicated, active inflammatory alone), stricturing, and penetrating, with the addition of perianal disease as a modifier. It is the behavior subcategory that is of interest in regard to the radiographic manifestations. As a result of these morphologic subtypes, radiologists and even gastroenterologists have concluded that they are separate entities. The problem with this discrete approach is that the complex relationship between active inflammatory and stricturing disease and stricturing and penetrating disease has been forgotten or avoided. Crohn’s disease is a progressive process, starting with acute inflammation. It may be stopped or retarded with therapy; there may be mucosal healing. However, when it progresses, it often progresses to the fibrostenotic phase, with stricture formation. Active inflammation commonly coexists in the presence of stricture formation. ^, There is also strong pathologic and clinical evidence that fistulae form in the face of fibrostenosis. Two pathologic series have shown that fistula formation without stricturing disease is uncommon to rare (4% to 7% of the time). ^, Thus, if there is no stricture, penetrating disease (sinus tracts, fistulae, abscess, or free perforation) will be very unlikely. Because of the potential progression of disease from acute inflammation to fibrostenosis and then fistulization, it is important for the radiologist to think more broadly than using the Montreal and Vienna classifications, especially with computed tomography (CT) and magnetic resonance (MR) enterography. We are thus beginning to use the following terms— active inflammatory disease, mixed active inflammatory and fibrostenotic disease, fibrostenotic disease, and inactive or quiescent disease with the addition of penetrating disease (generally in the presence of mixed disease) based on radiographic findings (see later, “Nomenclature for Computed Tomography and Magnetic Resonance Enterography Findings”).

Diagnostic Tools

There are many examinations available for diagnosing, staging, and following Crohn’s disease of the small bowel. These include ileocolonoscopy with direct inspection and biopsy of the terminal ileum, push enteroscopy to examine the proximal and mid small bowel, video capsule endoscopy, conventional small bowel follow-through, conventional enteroclysis, CT with (CTE) or without enterography or enteroclysis, MR enterography (MRE) or enteroclysis, ultrasonography, and lately positron emission tomography (PET), PET/CT, and PET/MRI. These studies are used to do the following:

Demonstrate the early changes of Crohn’s disease.
Depict the full extent of involvement and the possible presence of skip lesions if surgery is contemplated.
Determine the cause of any clinical deterioration in previously stable patients with Crohn’s disease.
Distinguish between spasm (active inflammatory disease), mixed active and fibrostenotic disease, and fibrostenotic disease (stricture formation); increasingly used to dictate medical versus surgical therapy, especially with MRE.
Investigate postoperative complications of Crohn’s disease.
Definitively rule out the presence of Crohn’s disease in the small bowel, especially in patients with an indeterminate colitis.

BARIUM CONTRAST EXAMINATIONS

Barium–fluoroscopic barium examination of the small bowel for Crohn’s disease has been largely supplanted by CTE and MRE. However, there are patients who have medical conditions that preclude the use of CTE or MRE with contrast enhancement (e.g., severe chronic kidney disease) who have known or suspected Crohn’s disease. These patients must be evaluated with a barium examination using fluoroscopy.

There are two methods of examining the small bowel with barium using fluoroscopy—the standard small bowel series and enteroclysis. For accuracy, both require meticulous fluoroscopic technique using patient rotation and graded compression with a lead glove, inflatable paddle, or wooden spoon. Enteroclysis is available only in certain centers and requires intubation of the proximal small bowel via the nose or mouth. This is uncomfortable for most patients, and conscious sedation is used in some centers to improve patient tolerance.

As a general rule, the key radiographic finding in Crohn’s disease is asymmetry ( Figs. 27.1 – 27.6 ). Radiologists usually think of asymmetry as skip disease in the z direction. However, the asymmetry of Crohn’s is also in the xy direction. Crohn’s disease always affects the mesenteric more than the antimesenteric border. The normal undulating fold pattern on the mesenteric border will become ulcerated, effaced, flattened, and foreshortened, whereas there is relative sparing of the antimesenteric border, giving rise to the pseudodiverticulosis sometimes associated with the disease. This classic feature is better portrayed with barium examinations but can be seen with CTE or MRE.

Fig. 27.1, Early active inflammatory Crohn’s disease: Enlarged lymphoid follicles.

Fig. 27.2, Early active inflammatory Crohn’s disease: Aphthoid ulcerations.

Fig. 27.3, Active inflammatory Crohn’s disease: Cobblestone mucosa.

Fig. 27.4, Deep ulcerations of fistulizing-perforating Crohn’s disease.

Fig. 27.5, Sacculations in Crohn’s disease.

Fig. 27.6, Fibrostenotic Crohn’s disease.

Marshak’s 10 principles of Crohn’s disease are worth remembering because they assist the radiologist in detecting and characterizing disease. Initially presented in 1973, these principles have generally held very true. The principles most helpful for the radiologist include principle 3 (the string sign is the most pathognomonic barium manifestation and does not represent fibrosis but spasm secondary to ulceration), principle 8 (following surgery, recurrence is common), and principle 9 (look for recurrence at anastomotic and strictureplasty sites).

Early Radiographic Active Inflammatory Disease

The pathologic and radiologic findings correlate well in early Crohn’s disease. The earliest histologic changes consist of hyperplasia of the lymphoid tissue (see Fig. 27.1 ) and obstructive lymphedema in the submucosa. Because the submucosa extends into the core of mucosal folds, the folds may thicken at this stage in a smooth, symmetric manner. However, in general, symmetric fold thickening in Crohn’s disease is an uncommon finding and is identified only early in the disease. When the disease advances, the folds become much more asymmetrically thickened, giving a macronodular polygonal appearance; the macronodules vary in size (at this point, the main differential is lymphoma; see later).

Hyperplasia of lymphoid follicles (see Fig. 27.1 ) in the lamina propria can be associated with shallow, 1- to 3-mm mucosal erosions surrounded by a small halo of edema, also known as aphthoid ulcers (see Fig. 27.2 ).

Intermediate Radiographic Active Inflammatory Disease

As the disease gradually extends transmurally, further changes take place in the mucosa and submucosa. Progressive submucosal edema may cause the base of the folds to widen until some folds are partially or completely obliterated or effaced, especially on the mesenteric side. This process is similar to the thumbprinting that occurs in patients with bowel ischemia. In patients with ischemia, however, the fold abnormalities change over a period of days to weeks, whereas in patients with Crohn’s disease, the fold abnormalities persist and are usually associated with changes of more advanced Crohn’s disease elsewhere in the small bowel. The mucosal inflammatory infiltrate tends to vary focally in intensity. This infiltrate, together with patchy submucosal fibrosis, leads to a distortion and interruption of folds. The fold pattern in this stage can be described as macronodular (>1 cm), with the nodules asymmetric in size, location, and appearance.

Some aphthoid ulcers may enlarge and deepen, producing a stellate or rose thorn appearance. Other aphthoid ulcers may fuse with adjacent ulcers, producing crescentic or linear shapes. A typical finding is that of a long linear ulcer on the mesenteric border, which may be accentuated by a parallel radiolucency caused by fusion of thickened, transaxially oriented folds. The mesenteric border ulcer is associated with thickening, sclerosis, and retraction of the adjacent mesentery and of the straightened mesenteric border of the involved bowel. At the same time, the unaffected, or relatively unaffected, redundant antimesenteric border becomes pleated, scalloped, or sacculated, giving a pseudodiverticular-like pattern (distinct from the pseudodiverticular pattern present in scleroderma, in which the outpouchings are much closer together because of the foreshortening of the bowel).

An inflammatory cellular infiltrate with focally pronounced edema and granulation tissue can give rise to localized mucosal elevations or inflammatory polyps. These lesions are common in the colon but infrequent in the small bowel. Inflammatory pseudopolyps usually occur in small numbers in an area of mucosa that is denuded of folds. Occasionally, a bowel segment contains many inflammatory pseudopolyps (≤1 cm in diameter), separated from one another by curving lines of barium occupying the crevices between the elevations. When seen in profile, the polyps appear as notches demarcated by protrusions of barium. The diameter of these bowel segments is not reduced. This is called the nodular pattern of Crohn’s disease to underscore its essential difference from the ulceronodular, or cobblestone, pattern of advanced, fissuring, ulcer-related Crohn’s disease (see Fig. 27.3 ).

Advanced Radiographic Active Inflammatory Disease

In advanced Crohn’s disease, the process has extended transmurally to the serosa and beyond. Deep linear clefts of ulceration, or fissures, are typical of this stage of the disease (see Fig. 27.4 ). Islands of surviving mucosa surrounded by extensive ulceration give the appearance of elevations above the ulcerated background. These islands of mucosa are, therefore, known as pseudopolyps. The deep fissures characteristic of this advanced stage may be manifested by a combination of axial and transaxial fissuring, which separates the pseudopolyps from one another. This finding is always associated with luminal narrowing; it is referred to as the ulceronodular or cobblestone pattern of advanced Crohn’s disease (see Fig. 27.3 ). This pattern should not be confused with the nodular pattern of less advanced Crohn’s disease.

Changes associated with linear mesenteric ulceration advance in a caudad direction as the disease progresses. Antimesenteric redundancy of the opposite bowel wall gradually disappears as it is incorporated in the transaxial extension of ulcerated Crohn’s disease (see Fig. 27.5 ). The bowel wall is now thickened by a combination of fibrosis and inflammatory infiltrate. Another feature of transmural disease is the so-called fat wrapping that occurs as the hypertrophied subperitoneum is tethered toward the bowel wall by mesenteric perivascular fibrosis.

Quiescent or Inactive Disease

Very little has been written about the barium findings of quiescent disease. Presumably, the mucosa is normal in these patients. Thus, the fold pattern should be normal.

Fibrostenotic Disease

The strictures of small bowel Crohn’s disease (see Fig. 27.6 ; Fig. 27.7 ) are caused by collagen deposition, predominantly in the submucosa. It is important to differentiate fibrostenotic strictures from the luminal narrowing that can result from spasm. The classic string sign of Crohn’s is primarily caused by spasm in segments of active inflammatory disease. Fluoroscopically, the lumen, coated with barium, appears initially narrowed, with no or only mild upstream dilation. Then, when a peristaltic wave propels the barium through the lumen, the lumen expands to a near-normal caliber. A fibrostenotic predominant stricture will not change its caliber with peristalsis, and the upstream, nonaffected lumen will be dilated, regardless of the state of peristalsis. It should be noted that in many if not most cases of the string sign, the lumen of the affected bowel never fully distends, and there is often some degree of upstream ballooning or dilation during peristalsis. This suggests that more than spasm is occurring in the affected segment (Crohn’s is a progressive process; at sites of active disease, there is often active proliferation of the smooth muscle and collagen that restricts compliance).

Fig. 27.7, Aneurysmal dilation of fibrostenotic small bowel in Crohn’s disease.

These strictures are an important cause of small bowel obstruction (SBO), often necessitating surgery. Strictures or stricture-like findings are reported in 21% of patients with small bowel Crohn’s disease. Multidetector CT (MDCT), magnetic resonance imaging (MRI), CTE, CT enteroclysis, and MR enteroclysis are valuable techniques for differentiating fibrotic strictures from the lumen narrowing by spasm or active ulcerated stenotic disease. It is important to note that active inflammation is present in many, if not most, fibrostenotic strictures (see later). Obstruction by a fibrous stricture may require surgery; whenever possible, it should consist of strictureplasty to avoid bowel resection. Some patients with Crohn’s disease may develop high-grade SBO; this complication is reliably documented by CT and MR.

Other patients with Crohn’s disease may have multiple strictures, representing advanced skip lesions. Stasis related to strictures can be associated with bacterial overgrowth. This is especially true in patients who develop aneurysmal dilation of the small bowel (see Fig. 27.7 ), usually between two strictures. Strictures are generally well shown by barium study.

Resection of bowel in patients with Crohn’s disease is followed by a high frequency (85%) of disease recurrence. Recurrent inflammation has been detected within 8 days of surgery, provided that exposure to the fecal stream had been reestablished. Multiple resections have made Crohn’s disease of the small bowel a major cause of the short bowel syndrome.

Fistulizing or Penetrating Disease

Fistulizing or penetrating disease is manifest by sinus tracts, fistulae, abscess, and uncommonly free perforation. Abscesses develop in some 20% of patients with Crohn’s disease, and most can be treated with percutaneous drainage. Inflammatory lesions may remain closely related to a diseased segment of the bowel or may extend beyond the bowel, occasionally into the psoas muscle. In some cases, barium may enter an abscess cavity, a collection of tracts, or multiple small spaces within an inflammatory mass. However, CT, ultrasonography, and MRI are preferred diagnostic methods for evaluating abscesses in patients with Crohn’s disease.

Fistulae are abnormal communications between two epithelial surfaces or an epithelial surface and the skin, which occur in 6% to 33% of patients with Crohn’s disease. Fistulae occur in the presence of, and likely as a result of, stricture formation (fistulae are only rarely found in isolation, only 4% to 7% of the time; Fig. 27.8 ). Ileocecal, ileosigmoid, and enteroenteric fistulae are the most common and are often multiple. An enterocolic fistula may lead to bacterial overgrowth and is one of the causes of malabsorption associated with Crohn’s disease. Enterocutaneous fistulae can be well shown by barium studies, CT, and MRI.

Fig. 27.8, Fistulizing-perforating Crohn’s disease.

Because the attachment of the transverse mesocolon crosses the mid-descending duodenum, Crohn’s-related fistulae between the transverse colon and duodenum are not unusual. Recurrent Crohn’s disease in the neoterminal ileum after ileotransverse colonic anastomosis may be associated with such a fistula. Ileosigmoid fistulae are encountered more often. These may serve a useful purpose by bypassing strictures in the ileocecal area. In most cases, the entry site of these fistulae into the sigmoid colon shows only nonspecific inflammatory changes. If surgery is contemplated, it is usually adequate to resect the diseased ileum and stricture, leaving the sigmoid colon intact.

ULTRASOUND

Ultrasound has been increasingly used to assess Crohn’s disease, especially in the pediatric population. The examination requires meticulous, systematic scanning of all parts of the bowel using graded compression and a high-frequency transducer after the administration of oral contrast. Recently, investigations have shown the added benefit of contrast-enhanced ultrasound in assessing Crohn’s disease, especially in differentiating fibrosis from active inflammation. Mural thickening ( Fig. 27.9 ) is the most common abnormality seen in patients with Crohn’s disease of the small bowel. ^, It is typically concentric, and the mural echogenicity depends on the degree of inflammatory infiltration and fibrosis. In early acute disease, mural stratification is retained. With long-standing disease, a target or pseudokidney appearance may be identified. In patients with burned out, long-standing disease, fat deposition in the submucosa may be present.

Fig. 27.9, Crohn’s disease: Sonographic features.

Actively inflamed gut appears rigid and fixed, with decreased or absent peristalsis. ^, Color Doppler imaging typically shows hyperemia. Findings on spectral Doppler analysis include increased superior mesenteric and/or inferior mesenteric artery blood flow, increased pulsatility index, decreased resistive index, and increased portal vein velocity. Increased systolic and diastolic flow through the superior mesenteric artery may also be seen, attesting to disease activity. Creeping fat of the mesentery manifests as a uniform echogenic halo around the mesenteric border of the encased gut. As with barium study, MDCT, and MRI, this abnormal fat causes separation of bowel loops.

Prominent lymph nodes are seen in most patients with the active inflammatory phase of Crohn’s disease. These perienteric lymph nodes, which are located in the subperitoneal space of the small bowel mesentery, present as focal hypoechoic masses that are spherical and have lost their normal echogenic streak emanating from the nodal hilum. These nodes are typically hyperemic, moderate in size, and tender. Abnormal lymph nodes are not commonly seen in quiescent Crohn’s disease. ^,

Crohn’s disease strictures show mural thickening of the gut, with the luminal surfaces of the involved segments in apposition. The lumen may appear as a narrow, linear, echogenic central region within the thickened segment of small bowel. Dilated hyperperistaltic segments can be seen proximal to the strictured segments. Aneurysmal dilation and sacculation may be seen proximal to the involved segments.

Fistula appear as linear bands of varying echogenicity, extending from the gut to the bladder, another segment of bowel, or bladder. Gas within the fistula will appear echogenic and may show the so-called ring-down artifact. An empty or partially closed tract will appear as a hypoechoic segment of bowel or bladder. Abscesses on ultrasound manifest as a fluid-filled or complex mass, which may contain gas. ^,

MAGNETIC RESONANCE IMAGING

MRI (see Chapter 40) has become a well-established technique in evaluating patients with known or suspected Crohn’s disease by virtue of its ability to help confirm the diagnosis; localize lesions; assess their severity, extent, and inflammatory activity; and identify extraintestinal complications that may require surgical intervention. ^, MR enteroclysis is an emerging diagnostic tool that combines the advantages of conventional enteroclysis and MRI. However, MRE is the most practical method of evaluating patients with Crohn’s disease.

MRE has two major advantages over CTE. No ionizing radiation is used; as a result, multiple pulse sequences with and without contrast enhancement can be performed. Static imaging can help identify wall edema and lymphatic distention, and contrast-enhanced imaging can be performed long after the injection has been given, potentially allowing for further characterization. The major disadvantage is a long examination time, requiring relatively long breath holding. Furthermore, magnet time is at a premium in many institutions and is used for many other disease states. Bowel motion remains a problem; glucagon and hyoscyamine (Levsin) are the only antiperistaltic agents approved in the United States (Buscopan or hyoscine butylbromide is an excellent agent but only approved in countries other than the United States). Finally, spatial resolution, even with 3-T magnets, does not approach the resolution of MDCT with its near-isotropic imaging. Nevertheless, MRE is equivalent to CTE for the evaluation of Crohn’s disease. Adequate distention of the bowel lumen is ideal in MRE because collapsed bowel loops can potentially hide lesions or mimic pathology. However, in general, the small bowel affected by Crohn’s disease can almost always be detected unless there is significant bowel motion or no distention of a large amount of small bowel. Different methods have been used to achieve adequate distention. MR enteroclysis provides distention of the entire small bowel, visualizes mucosal abnormalities, and can show functional information about small bowel mobility.

Regardless of the pulse sequence, it is important to obtain imaging in orthogonal planes, often axial and coronal. These planes should be obtained in all patients on static and postcontrast scans. As with CTE, disease presence, strictures, and especially fistulae and sinus tracts are best elucidated with orthogonal imaging.

Many T2-weighted pulse sequences are available on modern scanners. New, fast, T2-weighted spin-echo sequences can be obtained in a single breath-hold. These include T2-weighted, half-Fourier rapid acquisition with relaxation enhancement, turbo spin-echo, fast spin-echo, half-Fourier acquisition single-shot turbo spin-echo (HASTE), single-shot turbo spin-echo, EXPRESS, and the newest sequence, called BLADE, which uses periodically rotated overlapping parallel lines with enhanced reconstruction (PROPELLER). These T2-weighted sequences are obtained with and without fat saturation. Fat saturation helps identify and characterize increased T2 signal in abnormal loops of bowel (increased T2 signal in the wall can result from increased fluid from edema or lymphatic distention or from fat deposition). T1-weighted, gadolinium-enhanced, spoiled gradient-echo sequences are also important in evaluating the location, extent, and severity of Crohn’s disease. T1-weighted gadolinium-enhanced MRI has been the most investigated pulse sequence in Crohn’s disease. A variety of 2D and 3D techniques are available; the most common use a fast, 3D, fat-saturated gradient-echo sequence acquired in a single breath-hold lasting 15 to 20 seconds. These sequences have various names, such as VIBE, FAME, THRIVE, and 3D QUICK. ^, T1 acquisition in regard to contrast enhancement varies, with acquisition commonly at 30, 60, and 90 seconds postinjection start. More delayed imaging of up to8 minutes postcontrast may be helpful.

Multiple coronal, true fast imaging with steady-state precession (FISP), cine motility sequences have been reported to differentiate between a high-grade and low-grade partial SBO. These sequences give an MR “fluoroscopic” depiction of peristalsis above a stricture, showing the progressive dilation of bowel proximal to the stricture. Some believe that static imaging may not be able to make this distinction. However, in our experience, most significant strictures (predominantly fibrostenotic) demonstrated dilated loops of the small bowel (>3 cm) proximally.

Magnetization transfer has been shown to help detect fibrosis in an animal model of Crohn’s disease.

COMPUTED TOMOGRAPHY

There are three major CT techniques used for the evaluation of Crohn’s disease of the small bowel—conventional positive intraluminal contrast studies, CTE, and CT enteroclysis. ^, Conventional CT using positive intraluminal contrast agents is generally reserved for postoperative patients in whom a bowel leak is suspected. In a patient with an acute exacerbation of symptoms, one might argue that identifying an abscess is the most important question. Thus, conventional CT with positive oral agents should be used. However, many patients with acute symptoms do not have an abscess but have exacerbation of the disease, obstruction or progressive stricture formation with or without fistulization. We have found that CTE, even in these acutely ill patients, can confidently distinguish an abscess using neutral oral contrast agents. CT enteroclysis is a rarely used technique and is reserved for those institutions in which it is performed routinely. Finally, the assessment of mural enhancement is hindered by the presence of positive intraluminal contrast because this contrast obscures inner wall hyperenhancement.

CTE uses MDCT with a narrow section thickness and reconstruction interval, vis-à-vis (IV) contrast material, and large volumes of neutral contrast agent to distend the lumen in an effort to improve the detection of small bowel inflammation and extracolonic complications. CT can be performed during the enteric phase (45 seconds after injection) and portal venous phase (70 seconds after injection). Regardless of the technique used, there is no significant difference in detecting Crohn’s disease. Jejunal attenuation is greater than ileal attenuation, and collapsed bowel loops demonstrate greater attenuation than distended bowel loops. CT enteroclysis uses contrast material infused through a nasojejunal tube. Both positive (dilute barium) and neutral contrast (water, methylcellulose, VoLumen) agents may be administered. CT enteroclysis uses the same technique as standard fluoroscopic enteroclysis, except that imaging is performed with contrast-enhanced MDCT, as in CTE. All MDCT datasets should be reconstructed in at least two planes, typically axial and coronal. Occasionally, sagittal or oblique planes are helpful in identifying fistulae.

Every effort should be made to limit radiation exposure in patients, especially if they have had multiple CT scans in the past. Several studies have shown that some patients with Crohn’s disease can receive large cumulative doses (>100 mSv) over the course of their disease, and often are examined with CT two to three times a year.

The most effective strategy for reducing ionizing radiation exposure in patients with Crohn’s disease is to shift imaging to MRE from CTE. Our strategy is first to perform CTE on all patients with Crohn’s disease if they have not had one performed. This serves as the baseline examination, establishing the location and extent of disease. The study is fast, the spatial resolution is superb, and there is little to no bowel motion artifact. We favor CTE or MRE as the initial study because bowel motion remains a problem for MRE in the United States. Furthermore, the spatial resolution of MRE is still not equivalent to that of CTE. As a result, the risk of missing disease on an initial MRE image is relatively high. However, every other examination, except for patients who are acutely ill or perioperative, should be MRE. Acutely ill patients should be examined with CTE, especially if abscess detection and potential drainage is relatively likely. Once detected, the abscess can be rapidly drained using CT guidance. Postoperative patients should be examined after the ingestion of positive oral contrast medium and the administration of rectal contrast medium if there is a colonic anastomosis because a leak may be present.

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