Nonneoplastic Diseases of the Small Intestine: Clinical, Pathophysiologic, and Imaging Characteristics

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1 Residents Section Structured Review McLaughlin and Maher Nonneoplastic Diseases of the Small Intestine Residents Section Structured Review Residents inradiology Patrick D. McLaughlin 1,2 Michael M. Maher 1 McLaughlin PD, Maher MM Keywords: Crohn disease, differential diagnosis, nonneoplastic disease, small intestine DOI: /JR Received December 23, 2011; accepted after revision October 11, Departments of Radiology, University College Cork and Cork University Hospital, Wilton, Cork, Ireland. ddress correspondence to M. M. Maher (m.maher@ucc.ie). 2 Present address: Department of Emergency and Trauma Imaging, Vancouver General Hospital, Vancouver, C, Canada WE This is a web exclusive article. JR 2013; 201:W382 W X/13/2013 W382 merican Roentgen Ray Society Nonneoplastic Diseases of the Small Intestine: Clinical, Pathophysiologic, and Imaging Characteristics Key Points 1. lthough the imaging hallmark of celiac disease is jejunal fold atrophy (< 3 folds per inch) with secondary hypertrophy of the ileal folds (jejunoileal fold reversal) the most common imaging finding is a moderately dilated fluid-filled small bowel. 2. number of infectious pathogens may result in distal ileal imaging changes that mimic Crohn disease. The presence of superficial rather than deep ulceration and absence of luminal narrowing may aid in differentiation of Yersinia enteritis from Crohn disease, but Mycobacterium tuberculosis enteritis can be almost indistinguishable from Crohn disease because it often results in stenotic and transmural fistulating disease. 3. cute transmural small-intestine infarction typically results in mural thinning and small-intestine dilatation with reduced or absent mural enhancement, whereas nonocclusive mesenteric ischemia typically results in mural thickening and mucosal hyperenhancement. 4. Ischemia related to mesenteric venous thrombosis results in marked mural thickening, mucosal hyperenhancement, mesenteric stranding, and vascular engorgement. 5. Emerging evidence supports the role for CT in the evaluation of occult or low-grade gastrointestinal bleeding. Multiphasic contrastenhanced CT enterography complements wireless capsule endoscopy in identifying sources of occult gastrointestinal bleeding and may be particularly useful in identifying focal small intestinal masses. Compared with the upper gastrointestinal tract and large bowel, the small intestine is much less amenable to examination with endoscopy, and as a result, radiologic investigations play a pivotal role in the diagnosis of small-intestine pathology. cute inflammation of the small intestine typically results in segmental wall thickening, submucosal ede- ma, and mucosal hyperenhancement. These changes are commonly seen in Crohn disease, but many other nonneoplastic diseases of the small intestine can also produce these imaging findings. Clinical information is often vital in discriminating between potential mimics of Crohn disease, such as ulcerative jejunoileitis and infectious and eosinophilic enteritis, but the radiologist should also be aware of a number of imaging clues that may aid in the differentiation. First, a diagnosis of Crohn disease can be more specifically inferred when these changes are asymmetric and preferentially involve the mesenteric border of the bowel wall. Crohn disease typically results in multisegmental discontinuous disease, whereas graft-versus-host disease (GVHD), angioedema, and generalized intestinal ischemia typically result in more diffuse involvement of the small intestine. The presence of perienteric signs, such as mesenteric fibrofatty proliferation, is characteristic of Crohn disease. In this article, we review the important clinical, pathophysiologic, and imaging characteristics of a wide range of nonneoplastic disorders of the small intestine, including immune-mediated, infectious, and vascular-related disorders, some of which may occasionally mimic Crohn disease. Immune-Mediated Enteritis The intestinal immune system is composed of intestinal epithelial cells, mural lymphocytes, and aggregates of lymphoid tissue in the ileal mucosa known as Peyer patches [1]. The intestinal immune system is protective of both commensal bacteria and invasive pathogens, but disruption of this delicate balance is believed to cause a variety of immunerelated inflammatory syndromes [1]. Celiac Disease Celiac disease is a gluten-related immunemediated enteropathy in susceptible individ- W382 JR:201, September 2013

2 Nonneoplastic Diseases of the Small Intestine uals. The prevalence of celiac disease has increased dramatically over the past 50 years, largely due to increased detection attributable to improvements in endoscopy and serologic analysis [2]. lthough the imaging hallmark of celiac disease is jejunal fold atrophy (< 3 folds per inch) with secondary hypertrophy of the ileal folds (jejunoileal fold reversal) (Fig. 1), the most common imaging finding is a moderately dilated fluid-filled bowel [1, 3]. This excess luminal fluid results in characteristic findings on barium examinations, including air-fluid levels and disintegration of ingested barium. Flocculation represents the aggregation of coarse clumps of disintegrated barium, and this finding may be seen in greater than half of celiac patients but is also seen in patients with other malabsorption syndromes. In a single series of 44 patients undergoing CT enterography, jejunoileal fold reversal was found to be 100% specific but only 64% sensitive in the diagnosis of uncomplicated celiac disease [4]. Other imaging features in celiac disease include the presence of transient intussusceptions, which may occur in up to 20% of patients and splenic atrophy, which may occur in up to 50% of patients [1]. MRI is also useful in detecting celiac disease, and the presence of mesenteric fat stranding and bowel-wall thickening was found in one MR enteroclysis study to allow differentiation between uncomplicated (sensitive to gluten-free diet) and refractory (resistant to gluten-free diet) celiac disease [5]. Differentiation between uncomplicated and refractory celiac disease is important because patients with refractory celiac disease are more susceptible to the gastrointestinal complications of celiac disease, such as T-cell lymphoma and small-intestinal adenocarcinoma [5, 6]. The primary role of imaging in patients with celiac disease is evaluation for enteropathy-associated T-cell lymphoma, which should be clinically suspected when there is a history of abdominal pain or systemic - symptoms, such as weight loss, night sweats, and fever. CT is the first-line examination in most centers, but appearances of enteropathy-associated T-cell lymphoma are protean, ranging from multiple enhancing nodules to the more infiltrating form, which is associated with circumferential mural thickening (Fig. 2), destruction of the muscle wall, and myenteric plexus causing luminal dilation. Rarer imaging findings in patients with celiac disease include cavitary mesenteric lymph node syndrome, which results in enlarged fluid-attenuation mesenteric lymph nodes with thin peripherally enhancing rims [7] and ulcerative jejunoileitis. Ulcerative jejunoileitis results in diffuse mucosal ulceration, predominantly in the jejunum. The ulcers are typically of variable depth and may be visible as focal constrictions on barium followthrough examinations [8]. The appearance of ulcerative jejunoileitis on MDCT enteroclysis was best described by oudiaf et al. [9] who found, in an analysis of three cases, circumferential mural thickening with a bilaminar double halo configuration resulting from a high-attenuation inner halo of mucosal hyperenhancement and an outer halo of mural thickening with soft-tissue attenuation. Ulcerative jejunoileitis may closely simulate Crohn disease on imaging and on capsule endoscopy examinations [10]. Eosinophilic Gastroenteritis Eosinophilic gastroenteritis is a rare disease that may affect all age groups but typically presents in the third to fifth decades with a male predominance [11, 12]. The causative role of ingested food allergens is substantiated by patient response to dietary modification (with or without corticosteroids) and the fact that greater than 50% of cases occur in patients with a history of atopy [13]. The imaging manifestations of this disease vary depending on which layer (mucosa, muscle, or serosa) of the intestinal wall is involved [14]. ny portion of the gastrointestinal tract may be involved, but the small intestine and the stomach are the most common sites of disease [1]. Mucosal eosinophilic gastroenteritis results in fold thickening, polyps, and mucosal ulcers that are visible on both CT and barium examinations. Disease of the muscle layer results in small-intestine thickening (Fig. 3) with stricture formation, and serosal disease results in ascites, lymphadenopathy, omental thickening, and aggregation of small-intestine loops [1]. Initial treatment response to oral corticosteroids is often dramatic, but approximately 50% of patients develop chronic disease [13, 15]. Eosinophilic gastroenteritis should be suspected in any patient with smallintestine imaging changes accompanied by peripheral eosinophilia [15]. Graft-Versus-Host Disease Intestinal GVHD may involve any portion of the gastrointestinal tract, from the esophagus to the rectum. Signs and symptoms include a maculopapular skin rash, nausea, vomiting, abdominal pain, tenderness, and secretory diarrhea. The risk of developing GVHD depends on the graft type; degree of human leukocyte antigen matching; and donor and recipient characteristics, such as age, sex, and parity. cute GVHD is said to occur within 100 days and the small intestine is involved in GVHD in % of cases, with moderate mural thickening, mild bowel dilation, and mural stratification resulting from a combination of submucosal edema and mucosal hyperenhancement [16] (Fig. 4). part from key features in the clinical history, intestinal GVHD differs from other abnormalities, such as Crohn disease, due to the diffuse long length of bowel involvement, typically extending from the duodenum to the rectum, and bowel-wall thickening is typically mild. Infective differential diagnoses are more difficult to exclude, particularly when patients are immunocompromised. Stool cultures should be performed to evaluate for Clostridium difficile, but rectal biopsy is often required to differentiate GVHD from viral pathogens, such as cytomegalovirus (CMV). Infectious Enteritis Imaging is not routinely indicated in cases of acute infectious enteritis. history of acute rather than chronic diarrhea is typical and stool culture remains the best diagnostic approach. Nevertheless, the imaging manifestations of infectious enteritis may be encountered by the radiologist when imaging is performed for investigation of other suspected abnormalities, such as acute appendicitis or Crohn disease. Infectious enteritis may result from viral, bacterial, parasitic, or antibiotic-associated pathogens. Fever, diarrhea, and vomiting are often more prominent symptoms, but when acute abdominal pain with tenderness is a feature, acute yersiniosis should be suspected [17]. Yersinia enteritis commonly involves the terminal ileum and typically results in mild bowel-wall thickening with aphthous lesions and mucosal nodularity [18] (Fig. 5). M. tuberculosis infection may be transmitted by swallowing of infected sputum or hematogenous spread from active tuberculosis infection elsewhere. Ninety percent of gastrointestinal tuberculosis infections occur in the distal ileum or cecum because of the relative stasis and abundance of lymphoid tissue in this region [19]. Tuberculosis infection may be transmitted by swallowing of infected sputum or hematogenous spread from active tuberculosis infection elsewhere. oth Yersinia enteritis and tuberculosis may mimic Crohn disease in the appropriate clinical context; however, the relatively mild JR:201, September 2013 W383

3 McLaughlin and Maher severity of bowel-wall thickening, presence of superficial rather than deep ulceration on barium examinations, and absence of luminal narrowing may aid in differentiation of Yersinia enteritis from Crohn disease [20]. In contrast, M. tuberculosis enteritis can be almost indistinguishable from Crohn disease because it results not uncommonly in stenotic and transmural fistulating disease, classically resulting in a conical cecum on barium examinations [21]. Characteristic central low-attenuation mesenteric lymph nodes and absence of mesenteric fibrofatty proliferation in tuberculosis represent important clues in differentiating between abdominal tuberculosis and Crohn disease [22]. Infectious enteritis and bacterial or viral pharyngitis may precipitate a syndrome known as mesenteric adenitis, which is a common cause of right lower quadrant pain in children and has been found in one study to be the final diagnosis in approximately 16% of patients presenting with symptoms suspicious for acute appendicitis [23]. Mesenteric lymph nodes measuring greater than 5 mm in their shortest axis are present in almost two thirds of asymptomatic children; therefore, judicious clinical correlation and a short-axis size threshold of 10 mm are recommended in the literature [24]. Cross-sectional imaging reveals mesenteric lymph nodes measuring greater than 10 mm in the short axis, which may occasionally be accompanied by thickening of the ileal wall [25]. Extraintestinal infections such as acute pyogenic pelvic inflammatory disease may also disseminate within the peritoneal cavity, resulting in serosal thickening and reactive inflammation of the small intestine [26]. With the advent of highly active antiretroviral therapy the prevalence of opportunistic small-intestine infections in HIV patients has dramatically declined worldwide [27]. When small-intestine infection is suspected in HIV patients, a diverse range of pathogens, such as M. avium intracellulare, cryptosporidium, Cryptococcus species, CMV, and the HIV itself, should be considered [27, 28]. Cryptosporidiosis is the most common cause of enteritis in the patient with HIV and results in mild thickening of the bowel wall with a moderate amount of fluid within the lumen. The proximal small intestine is the most common site for M. avium intracellulare infection, which typically results in wall thickening and mesenteric lymphadenopathy [29]. CMV more commonly involves the cecum but may also result in a terminal ileitis [29]. Neutropenic enterocolitis is a life-threatening necrotizing enterocolitis occurring in non-hiv immunocompromised patients resulting from polymicrobial invasion of the cecum and terminal ileum [30]. Neutropenic enterocolitis, otherwise known as typhlitis (from the Greek typhlon meaning cecum), occurs in profoundly neutropenic patients and is most commonly seen in patients with hematologic malignancies days after undergoing chemotherapy [31]. Vascular and Circulatory Related Diseases of the Small Intestine Small-Intestine Ischemia cute intestinal ischemia typically results from thrombosis of the mesenteric arteries or veins but also may result from strangulation or pronounced overdistention of bowel or from a broad range of abnormalities that result in a global or regional reduction of intestinal perfusion, such as acute hypovolemia, cardiac failure, and substance abuse [32 34]. recent meta-analysis found that MDCT has high sensitivity and specificity (93% and 96%, respectively) for the detection of acute mesenteric ischemia [35], but the MDCT imaging manifestations of small-intestine ischemia are protean and vary according to the nature and severity of vascular insufficiency [32]. cute transmural small-intestine infarction typically results in mural thinning and small-intestine dilatation with reduced or absent mural enhancement [32] (Fig. 6). In contrast, nonocclusive mesenteric ischemia typically results in mural thickening and mucosal hyperenhancement, and ischemia related to mesenteric venous thrombosis results in marked mural thickening, mucosal hyperenhancement, mesenteric stranding, and vascular engorgement [32] (Fig. 7). scites is present in approximately two thirds of patients with acute intestinal ischemia but is a more prominent feature in cases of mesenteric venous thrombosis [32]. Pneumatosis intestinalis and superior mesenteric or portal venous gas were once considered ominous signs in cases of acute intestinal ischemia; however, a wide range of nonischemic causes are now known, including infection, inflammation, neoplastia, and even respiratory causes, such as asthma [32, 36]. Pneumatosis intestinalis and portal venous gas may be seen after investigations of the gastrointestinal tract, such as endoscopy or barium studies because of gaseous distention and raised intraluminal pressure. Systemic vasculitis should be suspected when there are imaging signs of intestinal ischemia involving young patients or atypical sites such as the stomach, duodenum, or rectum [32]. Vasculitis should also be suspected when there is recurrent involvement in different small-bowel segments, particularly when there is evidence of improvement over time or additional signs of systemic vasculitis, such as solid visceral infarcts [37]. The mesenteric and renal vessels should be scrutinized for aneurysms, which are most commonly seen in polyarteritis nodosa but may also be found in systemic lupus erythematosus, Wegener granulomatosis, rheumatoid vasculitis, and Churg-Strauss syndrome. Systemic lupus erythematosus may result in serositis causing ascites, lymphadenopathy and more diffuse bowel-wall thickening. The presence of solid visceral infarcts should also prompt suspicion for a cardioembolic cause of intestinal ischemia. Knowledge of the patient s cardiac rhythm is important because there is a wide spectrum of CT findings in mesenteric ischemia related to atrial fibrillation. These signs are dependent on the size and location of the embolus but include segmental bowel dilatation, wall thickening, altered mural enhancement, mesenteric stranding, and ascites [38]. Henoch Schönlein Purpura Henoch Schönlein purpura (HSP) is an Ig-mediated postinfectious vasculitis typically occurring in children between 3 and 15 years old. HSP clinically manifests as colicky abdominal pain with palpable purpura and arthralgia. Imaging often reveals discontinuous segmental small and large bowel thickening related to submucosal hemorrhage and edema, which may mimic Crohn disease. The clinical presentation of HSP, including arthralgia and skin manifestations, may also mimic Crohn disease, with the skin lesions being mistaken for pyoderma gangrenosum [39, 40]. scites is a more prominent feature on imaging in cases of HSP, and purpuric lesions may be seen on endoscopy involving the duodenum, stomach, and colon, allowing differentiation from Crohn disease. ngioedema ngioedema may present with acute abdominal pain and infrequently the segmental small-intestine involvement may mimic the skip lesions more commonly seen in Crohn disease [20]. ngioedema is caused by abnormal leakage of serum into the extravascular spaces and results in long-segment or diffuse small-intestine imaging changes. These W384 JR:201, September 2013

4 Nonneoplastic Diseases of the Small Intestine changes include small-intestine thickening with submucosal edema and mucosal hyperenhancement creating the target sign, often with prominent mesenteric vessels and associated ascites [41]. Small-intestine angioedema may be idiopathic or hereditary, but it also is recognized, with similar imaging features, in patients receiving angiotensin-convertingenzyme (CE) inhibitor therapy [42]. CE inhibitor induced small-intestine angioedema is estimated to occur in % of patients undergoing CE inhibitor therapy, but radiologists may play an important role in the detection of this rare complication because of the nonspecific clinical presentation that is often remote from the commencement of CE inhibitor therapy [43, 44]. Submucosal Hemorrhage lmost two thirds of complications related to systemic anticoagulation occur in the gastrointestinal tract [38]. Submucosal hemorrhage is often related to systemic anticoagulation but may also be a feature of acute mesenteric venous thrombosis, small-vessel vasculitis, and mesenteric arterial ischemia [45]. Unenhanced imaging may reveal a homogeneously hyperdense submucosal collection and marked wall thickening, often resulting in luminal stenosis [33] (Fig. 8), but after rapid bolus iodinated IV contrast administration, images typically show relative hypodensity of the submucosa, giving a characteristic target appearance [20]. Occult Gastrointestinal leeding MDCT angiography has an undisputed role in the diagnosis of acute gastrointestinal bleeding and, importantly, also successfully guides interventional management by facilitating selective catheterization and embolization of bleeding vessels [46, 47]. Emerging evidence now also defines a role for CT in the evaluation of occult or low-grade gastrointestinal bleeding. Multiphasic contrast-enhanced CT protocols with neutral enterographic oral contrast material improve the visualization of focal masses, discrete foci of active extravasation, or, in the case of angiodysplasia, enhancing dilated intramural vessels (Fig. 9). One recent study comparing multiphasic contrast-enhanced CT enterography with wireless capsule endoscopy found significantly greater sensitivity with CT enterography than with capsule endoscopy (88% vs 38%) in identifying a source of occult gastrointestinal bleeding [48]. The primary benefit of CT enterography over capsule endoscopy in this study was its superior ability in identifying focal smallintestine tumors. However, in clinical practice, CT enterography and capsule endoscopy are complementary, particularly in the investigation of benign causes of blood loss, such as angiodysplasia and mucosal inflammation. Conclusion Knowledge of the key pathophysiologic characteristics of immune-mediated, vascular and infectious causes of small-intestine disease provides a framework for rational and appropriate differential diagnosis because their imaging appearances may commonly overlap. Diagnostic pitfalls may arise because of the protean appearances of smallintestine ischemia, which range from mural thinning, hypoenhancement, and smallintestine dilatation seen in acute transmural infarction to mural thickening and mucosal hyperenhancement seen in nonocclusive mesenteric ischemia. nother common pitfall includes the many infectious and inflammatory processes that may result in distal ileal imaging changes mimicking Crohn disease. 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6 Nonneoplastic Diseases of the Small Intestine Fig year-old woman with refractory celiac disease., xial contrast-enhanced CT image shows mild dilatation of small intestine with jejunal fold atrophy (arrow) and secondary hypertrophy of ileal folds (arrowhead)., xial contrast-enhanced CT image shows focal circumferential thickening of ileum (arrow) with mesenteric adenopathy, which was subsequently found to represent enteropathy-associated T-cell lymphoma of distal ileum. Fig year-old woman with history of eosinophilic enteritis who presented with acute abdominal pain., xial CT image shows marked thickening of segment of jejunum (arrows) with mild proximal dilation., Coronal reformatted image shows multisegmental involvement of jejunum (arrows) and marked thickening and edema of lower esophagus (arrowheads). JR:201, September 2013 W387

7 McLaughlin and Maher Fig year-old woman with history of recurrent lymphoma who presented with acute diarrhea 6 weeks after bone marrow transplantation. and, xial CT images show thickening, submucosal edema, and mucosal hyperenhancement of entire small bowel, giving rise to target sign. There also is thickening, submucosal edema, and mucosal hyperenhancement of large bowel (arrows), consistent with acute graft-versus-host disease. C Fig year-old boy who presented with right iliac fossa pain and diarrhea secondary to biopsy-proven Yersinia enterocolitis., Transverse ultrasound image shows segmental thickening of distal ileum (arrowheads). and C, xial () and coronal reformation (C) CT images show irregular mural thickening (arrowheads) and many enlarged mesenteric lymph nodes (arrow, C), consistent with adenitis. W388 JR:201, September 2013

8 Nonneoplastic Diseases of the Small Intestine Fig year-old man with history of atrial fibrillation., Sagittal oblique reformatted CT image shows occlusive filling defect in superior mesenteric artery (arrow). and C, xial CT images show mild dilatation, mural thinning, and absent mural enhancement, consistent with acute transmural small-intestine infarction (arrowheads). Mural thickening and mucosal hyperenhancement of some posterior loops indicate nonocclusive mesenteric ischemia due to collateralization (arrow, C). C Fig year-old man with primary non- Hodgkin lymphoma of distal jejunum. and, xial () and coronal reformatted () CT images show smallintestine wall and fold thickening (arrows, ) and ascites related to thrombosis of superior mesenteric vein (arrows, ). JR:201, September 2013 W389

9 McLaughlin and Maher Fig year-old man undergoing anticoagulation therapy for atrial fibrillation who presented with acute abdominal pain. and, xial CT images obtained at presentation show marked thickening of segment of jejunum (arrowheads, ) with associated hemoperitoneum (arrow, ), consistent with intramural hemorrhage. C and D, Follow-up CT images after 1 week (C) and 2 weeks (D) show gradual resolution of bowel-wall thickening (arrowheads). C D Fig year-old man who presented with chronic anemia 2 years after total colectomy and radiation therapy for colorectal carcinoma. and, CT angiograms show numerous dilated enhancing intramural vessels in jejunum, consistent with angiodysplasia (arrows). W390 JR:201, September 2013