CT Imaging of Large Bowel Wall Thickening

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Patients commonly present to both primary care physicians and the emergency department with symptoms related to the gastrointestinal tract. As the clinical symptoms are often nonspecific with significant overlap between the myriad of potential underlying pathologies, clinicians often resort to computed tomography (CT) imaging to establish a diagnosis or direct patient management. With the increased utilization of CT, radiologists must be intimately familiar with the clinical and imaging manifestations of a variety of gastrointestinal pathologies. A more common imaging finding encountered in a general radiology practice is the presence of large bowel wall thickening. Although typically nonspecific, certain clinical and imaging manifestations may assist in narrowing the list of differential considerations or even lead to a specific diagnosis. This article will review some of the more common causes of large bowel wall thickening encountered in general radiology practices, which can often be categorized as inflammatory, infectious, ischemic, or neoplastic.

Inflammatory Bowel Disease

Inflammatory bowel disease includes Crohn disease and ulcerative colitis.

Crohn Disease

Crohn disease (CD) is a chronic idiopathic relapsing inflammatory bowel disease. CD has a prevalence of 1-2 per 1,000 people and affects approximately 500,000 individuals in North America.1 The exact etiology is not known, but thought to be multifactorial, with genetic, immunologic, vascular, and possibly lifestyle and environmental factors.1 CD is also known as granulomatous colitis and classically referred to as terminal ileitis. The age of onset is typically early adulthood, most commonly the third decade of life. However, late onset has also been reported up to the seventh decade of life.2 Crohn patients usually present with abdominal pain, tenesmus (rectal urgency), small volume stools, incomplete evacuation, and blood per rectum.2

CD most commonly affects the right colon and terminal ileum, but can involve any part of the bowel with development of aphthoid ulcers.1-3 Aphthoid ulcers have a discontinuous distribution (skip lesions), which produces the classic cobblestone appearance on barium studies (Figure 1).3 Complications and associations of CD include bowel obstruction, toxic colitis, abscess formation, fistulas, phlegmon, fibrofatty proliferation of mesentery, colon carcinoma, and lymphoma.1-3 Histologically, there is expansion of the lamina propria with chronic inflammatory cells, crypt distortion with crypt abscesses, ulcers, noncaseating granulomas, transmural lymphoid aggregates, thickened muscularis mucosa, and submucosal fibrosis.3

Imaging evaluation may be performed with barium fluoroscopy, CT, or MRI. CT and MRI enterography techniques provide more relevant information than barium secondary to visualization of the bowel wall and mesentery, which are not visible on x-ray or fluoroscopic studies. Due to its ease of access, CT is often used in the initial diagnosis when patients present acutely. CT enterography has been shown to be more accurate in evaluation of the bowel wall, which utilizes neutral oral contrast agents, as opposed to traditional positive contrast agents that may obscure bowel detail. CD usually has significant bowel wall thickening, > 10 mm (Figure 2).2 Another associated finding includes foci of increased attenuation within the surrounding fat, due to fibrofatty proliferation. This finding is known as creeping fat and results from the body’s attempt to confine the chronic inflammatory process (Figure 3).3 With transmural ulceration, fistula formation may occur between the bowel loops, urinary bladder, vagina or abdominal wall and skin (Figure 4).

Ulcerative Colitis

As one of the major etiologies classified under inflammatory bowel disease, ulcerative colitis (UC) is a disease characterized by a relapsing course of colonic inflammation and extra-intestinal manifestations.4 The intestinal inflammation is limited to the colonic mucosal layer and typically involves the rectum. UC may extend proximally and contiguously to affect the remaining colon as well.5 The pathogenesis of ulcerative colitis is relatively undetermined and is likely related to both genetic and environmental influences.4

Patients with ulcerative colitis can have gradually worsening episodes of diarrhea or bloody diarrhea, frequent small bowel movements with tenesmus or urgency, colicky lower abdominal pain, fever, and weight loss.5 Other manifestations include arthritis, which is the most common extra-intestinal presentation, uveitis, episcleritis, erythema nodosum, and liver disease.6 Long-term UC patients have an increased risk of developing colorectal cancer that is directly dependent on the extent and duration of disease.4 Another common complication is colonic stricture, which develops from repeated episodes of inflammation and muscular hypertrophy, placing the patient at risk for colonic obstruction.7 Considering the overlap in signs, symptoms, and radiographic findings between Crohn disease and ulcerative colitis, endoscopic biopsy with histologic confirmation may be required to determine the definitive diagnosis.

CT characteristics to suggest ulcerative colitis over Crohn disease or other inflammatory conditions on CT is difficult, but it may be inferred by location and caliber of the bowel wall thickening. Bowel wall thickening averaging 8 mm is more suggestive of UC, whereas CD tends to be > 10 mm (Figure 5). Due to its predilection to affect the rectum with extension into the left colon and rarely the right colon, left-sided diffuse and contiguous large bowel thickening is more likely to be ulcerative colitis.4 However, backwash ileitis with a dilated terminal ileum resulting from gaping patulous ileocecal valve can present with right-sided UC.1 Crohn disease preferentially involves the right colon and terminal ileum; isolated left colonic involvement is rare. Another differentiating feature is the asymmetric and segmental involvement of the bowel with skip regions characteristic for CD, in contrast to the contiguous nature of UC.1

Other than bowel wall thickening, chronic cases of ulcerative colitis demonstrate perirectal fat proliferation, and a low-attenuating ring within the bowel wall as a result of submucosal fat deposition called the halo sign.8 A serious known complication of UC is toxic megacolon, which is nonobstructive dilation of the colon > 6 cm, and is associated with systemic toxicity. This process is associated with high morbidity secondary to fluid loss, hemorrhage, and risk of bowel perforation. The development of this complication may arise at any time during the course of UC, but most commonly occurs within the first 3 months after initial diagnosis.4

Infectious Colitis

Infectious colitis may result from secondary spread of an adjacent process, such as appendicitis or diverticulitis, or may primarily involve the large bowel in either immunocompetent or immunosuppressed patients.


Historically ignored as an incidental appendage, acute appendicitis was definitively identified as a cause of right lower quadrant (RLQ) pain by Reginald Fitz in 1886, at which time clinical symptoms were described and surgical removal was suggested.3 Since that time, surgical treatment of appendicitis has become an important public health advancement in the past 150 years.9 Approximately 12% of men and 25% of women will experience acute appendicitis in their lifetime, making it one of the most common causes of abdominal pain requiring emergent surgery.8,9

Appendicitis occurs when the lumen of the appendix becomes obstructed, most often by a fecalith, but occasionally due to lymphoid hypertrophy, seeds, or infections. Obstruction of the appendiceal lumen increases intraluminal pressure causing disruption of the blood supply, which in turn results in ischemia and necrosis of the appendix.8-12 Almost all patients with appendicitis present with abdominal pain and anorexia. Classically, the abdominal pain starts periumbilically and then migrates to the RLQ; however, migratory pain occurs in only 50% to 60% of appendicitis cases.12,13 Other symptoms, such as nausea and vomiting, may follow pain onset. Laboratory findings in acute appendicitis include leukocytosis, often occurring with bandemia (increased immature neutrophils).9,14

Since appendicitis has significant clinical overlap with other causes of acute abdominal pathology, use of CT has increased over time to help elucidate the diagnosis. Key CT findings for acute appendicitis include an appendix dilated > 6 mm, wall thickening > 3 mm, and enhancement with surrounding inflammatory changes (Figure 6). A hallmark finding of appendicitis is inflammatory thickening of surrounding fat, described as a hazy, ill-defined increased density of the peri-appendiceal fat.1,8 Additionally, cecal apical thickening, the cecal bar sign, or arrowhead sign may also be observed on CT. Cecal apical thickening occurs due to contiguous spread of inflammation to the cecal tip, while a cecal bar is a curved strip of cecal wall thickening between the cecal lumen and an appendicolith. The arrowhead sign is seen when oral contrast material in the cecal tip produces an arrowhead-shaped collection near the occluded appendiceal opening.1,15 An additional suggested new criterion includes intraluminal appendiceal fluid > 2.6 mm in thickness on CT.16 As mentioned, once diagnosis is confirmed with CT, treatment is surgical removal of the appendix.


First described in 1700 by Alexis Littre, diverticular disease is common in developed countries, with left-sided diverticulosis highest in Western countries, and right-sided disease more common in Asia.17 An estimated 50% of people older than 50 years have diverticulosis, with the sigmoid colon most commonly affected. Of those with diverticulosis, an estimated 10% to 25% will develop diverticulitis.18

Diverticulosis is thought to develop from a lack of dietary fiber, which leads to small stool volumes requiring high pressures to move stool through the colon. Increased pressure in the colon leads to herniation of the mucosa and muscularis through the colonic wall, resulting in a diverticulum.8 With diverticulitis, the neck of a diverticulum becomes occluded, leading to microperforation and inflammation of surrounding fat.18,19 Diverticulitis can be complicated by abscess formation, colonic obstruction, peritonitis, or fistulas.18 Typical symptoms include several days of constant abdominal pain, most commonly in the left lower quadrant. Patients may also present with nausea, vomiting, low-grade fever, and/or change in bowel habits.20 Laboratory evaluation often reveals mild leukocytosis, but may be normal in up to 45% of cases.15

CT is the primary imaging modality used for diagnosing suspected diverticulitis. Diverticulosis appears as small, round to oval, air- or fecal-filled outpouchings of the colonic wall, with the highest incidence involving the sigmoid colon.1,18 The affected colonic wall may appear thickened due to muscular hypertrophy. In acute diverticulitis, segmental wall thickening and hyperemia with pericolonic fat stranding are identified (Figure 7). Identifying diverticula in the affected segment differentiates diverticulitis from other inflammatory bowl conditions. Sequelae or complications of diverticulitis, such as abscess, fistula, and/or perforation, may also be visualized (Figure 7). An abscess is identified as a fluid collection adjacent to the affected segment that may contain air or fecal debris.1,18 Fistulas, most often occurring within the urinary bladder, can be identified by air or contrast material in the bladder with associated wall thickening.1,18 Perforated diverticulitis is identified by small pockets of air or contrast material adjacent to the affected segment; frank pneumoperitoneum is uncommon in perforated diverticulitis.1,18

Uncomplicated diverticulitis is treated with bowel rest and oral antibiotics. Complicated diverticulitis with small abscesses may be treated with IV antibiotics, while large abscesses may require percutaneous drainage or laparotomy. Fistula formation requires resection of the affected colonic segment and repair of involved organs.

Neutropenic Enterocolitis (Typhlitis)

Occurring in neutropenic patients, typhlitis is a serious life-threatening enterocolitis. Patients are most often undergoing chemotherapy for hematologic malignancies, such as acute leukemia, lymphoma, multiple myeloma, myelodysplastic syndromes, or aplastic anemia. Typhlitis has also been noted as a complication in patients with cyclic or drug induced-neutropenia, AIDS, and those on postrenal transplant immunosuppressants.21 Pathologically, it is characterized by intramural infection by multiple microorganisms, leading to edematous thickening and induration of the cecal wall.22 This inflammatory process specifically affects the cecum due to its distensibility and stasis of bowel contents and may extend into the ascending colon and terminal ileum.21 In most cases, typhlitis leads to transmural necrosis, perforation with risk of septicemia, and possibly death if not diagnosed and treated appropriately. Patients typically present with fever, right lower quadrant abdominal pain, nausea, vomiting, and sometimes watery or bloody diarrhea. These symptoms arise approximately 3 weeks following cytotoxic chemotherapy when absolute neutropenia < 500 cells/microL is most profound.23

CT evaluation of typhlitis mirrors its pathogenesis and most commonly includes circumferential cecal wall thickening, measuring approximately 1-3 cm (Figure 8). The wall thickening can be isodense or hypoattenuating, which is indicative of edema, hemorrhage, or necrosis.22 The cecum may also demonstrate distension or dilatation with hyperattenuating adjacent fat and thickening of fascial planes, indicating pericolonic and mesenteric inflammation.21,24 Complications of typhlitis on CT include pneumatosis, pneumoperitoneum, and pericolic fluid collections, which carry a poorer prognosis and typically require urgent surgical intervention. Since this condition can be life-threatening, typhlitis should be suggested in any neutropenic patient with cecal wall thickening and inflammation. Medical management with bowel rest, nasogastric suction, aggressive fluid resuscitation, blood product administration, and broad spectrum antibiotics is reserved for patients without acute complications.25 Even with medical and surgical intervention, mortality rates in acute typhlitis remain > 50%, with most deaths resulting from transmural bowel necrosis with perforation and subsequent sepsis.26

Pseudomembranous Colitis

Pseudomembranous colitis is the leading cause of nosocomial diarrhea, with infection severity ranging from diarrhea to fulminant colitis.18,27,28 Pseudomembranous colitis is caused by Clostridium dificile, which occurs in the large intestines of up to 20% of hospitalized patients.29,30 Infection with Clostridium dificile is associated with antibiotic use, resulting in depletion of normal colonic flora and allowing for overgrowth of the bacterium.18,31,32 Production of toxin A (enterotoxin) causes inflammation, leading to fluid secretion and mucosal injury.33 Toxin B (cytotoxin) is essential for virulence and causes inactivation of regulatory pathways involved in cytoskeleton structure, leading to cell apoptosis.34 Although first associated with clindamycin, use of almost any antibiotic can lead to C. dificile colitis and, in some cases, even a single dose can lead to overgrowth of the bacteria.1,18,35 Symptoms of pseudomembranous colitis include profuse watery diarrhea, abdominal pain, cramping, and low-grade fever.35 Diagnosis is often made by identifying toxins in a stool sample, or by demonstrating pseudomembranes on endoscopy.28,36

Although usually a laboratory diagnosis, CT findings can aid detection of pseudomembranous colitis. Classically, pseudomembranous colitis is a pancolitis; however, it may also appear as isolated segments of colonic wall thickening.1 On CT, wall thickening can be circumferential or eccentric and is generally greater than the degree of wall thickening seen in other inflammatory states (Figure 9).1,37 Colonic wall thickening is also often more irregular with a shaggy appearance, distinguishing it from CD.1,37 Furthermore, there is often disproportionately mild colonic dilatation and pericolonic fat stranding compared to the degree of wall thickening.

Other imaging findings suggestive of pseudomembranous colitis include the accordion sign and target sign. The accordion sign appears when oral contrast is trapped between thickened haustral folds, and is highly indicative of pseudomembranous colitis; however, it is typically only seen in advanced disease.1,27 The target sign, identified by increased enhancement within the inner and outer rings of the bowel wall, is due to mucosal and serosal hyperemia and appears after administration of IV contrast (Figure 10).37 Treatment includes ceasing the antibiotic and beginning oral metronidazole or vancomycin therapy.18 Recurrent episodes may benefit from probiotics. In fulminant cases, colectomy may be lifesaving.18

Ischemic Colitis

Ischemic colitis (IC) is the most common colitis in patients > 50 years old.38 While it can occur in younger individuals, it is thought to be more common in the elderly secondary to underlying risk factors, including relative hypotension, heart failure, and arrhythmias.39 IC is part of a spectrum of bowel injury due to ischemia with involvement limited to the mucosa and submucosa and sparing the muscularis layer of the large bowel.38 While there are numerous causes, the pathogenesis is broken down into 3 categories: occlusive disease, which can be arterial or venous resulting from either thrombus or emboli; nonocclusive disease, which includes inflammatory states such as vasculitis and low-flow states as with shock; and mechanical disease, which is due to obstruction.40

With correction of the underlying etiology, IC is often self-limited and does not require surgical intervention. Rare complications include sepsis and perforation due to superinfection of the bowel.38 Abdominal pain, especially with eating, is the most common presenting complaint.39 Additional clinical signs and symptoms may include GI bleeding, diarrhea, abdominal distention and tenderness, tachycardia, pyrexia, and leukocytosis.40 Diagnosis is most commonly made usg CT imaging, elevated lactate levels, and direct visualization via colonoscopy.

CT sensitivity in diagnosing bowel ischemia is reported at 82%, which approaches that of angiography, the current gold standard for diagnosis.38 Due to the invasive nature of angiography, however, CT has become the imaging modality of choice in the initial workup and diagnosis of IC.1 The vascular distribution ischemia will determine which segments of bowel exhibit characteristic CT findings. Watershed areas are most frequently affected and include the splenic flexure and rectosigmoid junction.1 On CT, the most common finding of ischemic bowel is bowel wall thickening (> 3-5 mm), although this is also the least specific.38 Wall thickening can be due to edema, hemorrhage, and/or superinfection.40 When submucosal edema is present, the wall appears homogeneously hypoattenuated, which is referred to as the target sign.40 When wall thickening is due to hemorrhage or venous occlusion, it will often appear heterogeneous or hyperattenuated.

Although more rare, IC may result in dilation of the large bowel, in which case the bowel wall may appear normal in thickness secondary to the intraluminal exertion of increased pressure. Thus, lack of wall thickening does not exclude ischemic colitis from the differential. Other CT findings of IC include focal submucosal mural thickening (thumbprinting), mesenteric fat stranding, ascites, pneumatosis, and portal venous or mesenteric gas.38,40 When seen in the dependent portion of the bowel wall, pneumatosis almost always represents IC, especially when accompanied by portal venous gas (Figure 11).

Although IC is usually self-limited, when pneumatosis is definitively seen, close follow-up should be considered, as the IC may rapidly progress to involve a large segment of the bowel. CT angiography (CTA) may be helpful in identifying the underlying etiology so the correct treatment can be implemented. Strictures may develop due to fibrosis formation during healing.1

Colonic Adenocarcinoma

Approximately 132,700 people are diagnosed with colorectal cancer in the United States each year with 93,000 deaths, making it the third most common cause of cancer-related death.41 Colon cancers are thought to develop from colonic adenomas, with the villous type carrying the greatest risk.42 Risk is also associated with polyp size, ranging from minimal risk for polyps > 0.5 cm to < 40% risk for polyps > 2 cm.42 Other risk factors include diet, genetic predisposition, and environmental influences.42 Individuals are most often diagnosed between the sixth and seventh decades of life.43 Depending on the cancer’s location, the initial presentation will differ. Hematochezia and change in bowel habits or caliber of stool more commonly occur with left-sided and rectosigmoid cancers; whereas, melena and iron deficiency anemia are seen more often with right-sided malignancies.44 Lesions are also often found incidentally with screening or in association with signs and symptoms attributable to metastatic disease.44 Metastatic disease is most commonly seen in the liver, but may also present in lymph nodes, lungs, adrenal glands, and bones.45 Definitive diagnosis is made via biopsy. Depending on disease severity and location, treatment can consist of any combination of surgical resection, chemotherapy, and radiation therapy.

With increased use of CT in the initial evaluation of gastrointestinal complaints, radiologists are more commonly becoming the first to identify colon cancer.45 On CT, primary adenocarcinoma typically appears as a discrete soft tissue mass or focal, asymmetric colonic wall thickening, resulting in narrowing of the colonic lumen (Figure 12).45 Additionally, large masses may have areas of central low attenuation with or without air due to central necrosis. Local extension may be seen as an extracolic mass or thickening of the pericolic fat due to infiltration. Loss of fat planes between the adjacent organs can also be seen.45 Complications visualized on CT include bowel obstruction, perforation, and fistula formation.45 In addition to primary identification, CT is also used in evaluation for preoperative staging and identification of tumor recurrence. Colonography, also known as virtual colonoscopy, is under investigation as a screening method for colon cancer and has shown promising results with sensitivity rates for identifying lesions > 1 cm and reported as high as 90%.45


In summary, radiologists need to have a working knowledge of the clinical and imaging manifestations of various causes of large bowel wall thickening when reviewing abdominal CTs. The majority of underlying pathology encountered in general radiology practices can be categorized as inflammatory, infectious, ischemic, or neoplastic, with overlap in the imaging appearances among different entities. Clinical history and specific imaging findings, when present, may help narrow the list of differential considerations or even lead to a single diagnosis. As treatment options vary greatly between underlying pathologies, the radiologist’s role is critical in helping to guide appropriate patient management and follow-up.


  1. Thoeni RF, Cello JP. CT imaging of colitis. Radiology 2006;240(3):623-638.
  2. Furukawa A, Saotome T, Yamasaki M. Cross-sectional imaging in Crohn disease. Radiographics 2004;24:689-702.
  3. Williams GR. Presidential address: a history of appendicitis. With anecdotes illustrating its importance. Ann Surg 1983;197(5):495-506.
  4. Roggeveen MJ, Tismenetsky M, Shapiro R. Best cases from the AFIP: ulcerative colitis. RadioGraphics 2006;26:947‐
  5. Silverberg MS, Satsangi J, Ahmad T, et al. Toward an integrated clinical, molecular, and serological classification of inflammatory bowel disease: report of a Working Party of the 2005 Montreal World Congress of Gastroenterology. Can J Gastroenterol 2005;19SupplA:5A.
  6. Das KM. Relationship of extraintestinal involvements in inflammatory bowel disease: New insights into autoimmune pathogenesis. Dig Dis Sci 1999; 44(1):1-3.
  7. De Dombal FT, Watts JM, Watkinson G, Goligher JC. Local complications of ulcerative colitis: stricture, pseudopolyposis, and carcinoma of colon and rectum. Br Med J 1966;1(5501):1442-1447.
  8. Horton KM, Frank MC, Fishman EK. CT evaluation of the colon: inflammatory disease. RadioGraphics 2000;20:399‐
  9. Jaffe BM, Berger DH. Chapter 30: The appendix. In: Brunicardi FC, Andersen DK, Billiar TR, et al, eds. Schwartz’s Principles of Surgery, Ninth Edition. New York, NY: McGraw Hill Professional; 2009:1074-1091.
  10. Nitecki S, Karmeli R, Sarr MG. Appendiceal calculi and fecaliths as indications for appendectomy. Surg Gynecol Obstet 1990;171(3):185-188.
  11. Jones BA, Demetriades D, Segal I, Burkitt DP. The prevalence of appendiceal fecaliths in patients with and without appendicitis. a comparative study from Canada and South Africa. Ann Surg 1985;202(1):80-82.
  12. Birnbaum BA, Wilson SR. Appendicitis at the millennium. Radiology 2000;215(2):337-348.
  13. Chung CH, Ng CP, Lai KK. Delays by patients, emergency physicians, and surgeons in the management of acute appendicitis: retrospective study. Hong Kong Med J. 2000;6(3):254-259.
  14. Tehrani HY, Petros JG, Kumar RR, Chu Q. Markers of severe appendicitis. Am Surg 1999;65(5):453-455.
  15. Ambrosetti P, Robert JH, Witzig JA, et al. Acute left colonic diverticulitis: a prospective analysis of 226 consecutive cases. Surgery 1994;115(5):546-550.
  16. Moteki T, Horikoshi H. New CT criterion for acute appendicitis: maximum depth of intraluminal appendiceal fluid. AJR Am J Roentgenol 2007;188(5):1313-1319.
  17. Matrana MR, Margolin DA. Epidemiology and pathophysiology of diverticular disease. Clin Colon Rectal Surg 2009;22(3):141-146.
  18. Bullard Dunn KM, Rothenberger DA. Chapter 29: Colon, rectum, and anus. In: Brunicardi FC, Andersen DK, Billiar TR, et al, eds. Schwartz’s Principles of Surgery, Ninth Edition. New York, NY: McGraw Hill Professional; 2009:1038-1041.
  19. Rege RV, Nahrwold DL. Diverticular disease. Curr Probl Surg 1989;26(3):133-189.
  20. Konvolinka CW. Acute diverticulitis under age forty. Am J Surg 1994;167(6):562-565.
  21. Gayer G, Zissin R. Typhlitis: a computed tomography diagnosis. IMAJ 2002;4:146‐
  22. Frick MP, Maile CW, Crass JR, Goldberg ME, Delaney JP. Computed tomography of neutropenic colitis. AJR Am J Roentgenol 1984;143:763-765.
  23. Nesher L, Rolston KV. Neutropenic enterocolitis, a growing concern in the era of widespread use of aggressive chemotherapy. Clin Infect Dis 2013;56(5): 711-717.
  24. Kirkpatrick ID, Greenberg HM. Gastrointestinal complications in the neutropenic patient: characterization and differentiation with abdominal CT. Radiology 2003;226(3):668-674.
  25. Mullassery D, Bader A, Battersby AJ, et al. Diagnosis, incidence, and outcomes of suspected typhlitis in oncology patients—experience in a tertiary pediatric surgical center in the United Kingdom. J Pediatr Surg 2009;44(2)381.
  26. Gorschlüter M, Mey U, Strehl J, et al. Neutropenic entercolitis in adults: systematic analysis of evidence quality. Eur J Haematol 2005;75(1):1-13.
  27. Kelly CP, Lamont JT. Clostridium difficile—more difficult than ever. N Engl J Med 2008;359(18):1932-1940.
  28. Bagdasarian N, Rao K, Malani PN. Diagnosis and treatment of Clostridium difficile in adults: a systematic review. JAMA 2015;313(4):398-408.
  29. Zacharioudakis IM, Zervou FN, Pliakos EE, Ziakas PD, Mylonakis E. Colonization with toxinogenic C. difficile upon hospital admission, and risk of infection: a systematic review and meta-analysis. Am J Gastroenterol 2015;110(3):381-390.
  30. Riggs MM, Sethi AK, Zabarsky TF, Eckstein EC, Jump RL, Donskey CJ. Asymptomatic carriers are a potential source for transmission of epidemic and nonepidemic Clostridium difficile strains among long-term care facility residents. Clin Infect Dis 2007;45(8):992-998.
  31. Thomas C, Stevenson M, Riley TV. Antibiotics and hospital-acquired Clostridium difficile-associated diarrhoea: a systematic review. J Antimicrob Chemother 2003;51(6):1339-1350.
  32. Loo VG, Bourgault AM, Poirier L, et al. Host and pathogen factors for Clostridium difficile infection and colonization. N Engl J Med 2011;365(18):1693-1703.
  33. Sears CL, Kaper JB. Enteric bacterial toxins: mechanisms of action and linkage to intestinal secretion. Microbiol Rev 1996;60(1):167-215.
  34. Lyras D, O'connor JR, Howarth PM, et al. Toxin B is essential for virulence of Clostridium difficile. Nature 2009;458(7242):1176-1179.
  35. Deshpande A, Pasupuleti V, Thota P, et al. Community-associated Clostridium difficile infection and antibiotics: a meta-analysis. J Antimicrob Chemother 2013;68(9):1951-1961.
  36. Kufelnicka AM, Kirn TJ. Effective utilization of evolving methods for the laboratory diagnosis of Clostridium difficile infection. Clin Infect Dis 2011;52(12):1451-1457.
  37. Kawamoto S, Horton KM, Fishman EK. Pseudomembranous colitis: spectrum of imaging findings with clinical and pathologic correlation. Radiographics. 1999;19(4):887-897.
  38. Wiesner W, Khurana B, Ji H, Ros PR. CT of acute bowel ischemia. Radiology 2003;226(3):635-650.
  39. Theodoropoulou A, Sfiridaki A, Oustamanolakis P, et al. Genetic risk factors in young patients with ischemic colitis. Clin Gastroenterol Hepatol 2008;6(8):907-911.
  40. Rha SE, Ha HK, Lee SH, et al. CT and MR imaging findings of bowel ischemia from various primary causes. Radiographics 2000;20(1):29-42.
  41. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2015. CA Cancer J Clin 2015;65(1):5-29.
  42. Iyer RB, Silverman PM, Dubrow RA, Charnsangavej C. Imaging in the diagnosis, staging, and follow-up of colorectal cancer. AJR Am J Roentgenol 2002;179(1):3-13.
  43. Steele SR, Park GE, Johnson EK, et al. The impact of age on colorectal cancer incidence, treatment, and outcomes in an equal-access health care system. Dis Colon Rectum 2014;57(3):303-310.
  44. Majumdar SR, Fletcher RH, Evans AT. How does colorectal cancer present? Symptoms, duration, and clues to location. Am J Gastroenterol 1999;94(10):3039-3045.
  45. Horton KM, Abrams RA, Fishman EK. Spiral CT of colon cancer: imaging features and role in management. Radiographics 2000;20(2):419-430.
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Boyd SK, Cameron-Morrison JD, Hobson JJ, Saenz R.  CT Imaging of Large Bowel Wall Thickening.  J Am Osteopath Coll Radiol.  2016;5(2):14-22.

About the Author

Sara K. Boyd, D.O., Julia D. Cameron-Morrison, D.O., Julia J. Hobson, D.O., Rocky Saenz, D.O.

Sara K. Boyd, D.O., Julia D. Cameron-Morrison, D.O., Julia J. Hobson, D.O., Rocky Saenz, D.O.

Dr. Boyd, Dr. Cameron-Morrison, Dr. Hobson, and Dr. Saenz work with the Department of Radiology, Botsford Hospital, Farmington Hills, MI


Copyright © The American College of Osteopathic Radiology 2017