Most colonic diverticula are acquired herniations of the mucosa and submucosa (false diverticula) through the muscularis propria at weak points where vasa recta pass through the submucosa. Although the majority of colonic diverticula occur in the distal descending colon and sigmoid colon, they can occur anywhere throughout the colon. However, in Asian populations, right side involvement is more prominent (Almeida et al. 2009). Stasis or obstruction of diverticular neck by inspissated stool or food particles may cause inflammation, bacterial overgrowth, and localized ischemia, ultimately leading to microperforation of the diverticulum and pericolic inflammation which results in acute diverticulitis (Thoeni and Cello 2006). On CT, diverticula appear as small outpouchings of the colonic wall that contain air, contrast material, or fecal material. The involved colonic wall may show circumferential undulating thickening due to the thickening of circular muscle. Typical CT findings of diverticulitis include colonic diverticula with pericolic fat stranding or abscess and with adjacent colonic wall thickening that extends more than 5 cm. Other CT findings include engorged vessels supplying the affected segment, fluid in the mesenteric root, free intraperitoneal or extraperitoneal air, fistulae, and sinus tracts (Thoeni and Cello 2006; Almeida et al. 2009; Singh et al. 2005). On US, inflamed diverticula are shown as hypoechoic or hyperechoic outpouching of the colonic wall with focal disruption of the normal layer continuity and accompany increased peridiverticular fat echogenicity and segmental colonic wall thickening (Pradel et al. 1997). The most important differential diagnosis is colon cancer, especially in sigmoid diverticulitis with significant muscular thickening. CT features that indicate diverticulitis are inflamed diverticula (enhancement of thickened diverticular wall surrounded by the area of peridiverticular inflammation), layered enhancement pattern, long-segment involvement (>10 cm), and inflammatory changes in pericolic area and mesentery (Thoeni and Cello 2006; Jang et al. 2000). However, perforated colon cancer can be associated with inflammation or abscess, thus mimicking diverticulitis. When CT findings are equivocal, barium enema or colonoscopy should be performed to exclude colon cancer after treatment of diverticulitis. On barium enema, partial colonic obstruction, gradual zone of transition, preservation of mucosal folds, and associated diverticula indicate diverticulitis (Laufer 2008).

Acute appendicitis occurs when the appendiceal lumen is obstructed from any cause such as fecalith, lymphoid hyperplasia, foreign bodies, parasites, and tumors. Obstruction leads to luminal distention, tissue ischemia, bacterial overgrowth, transmural inflammation, and finally perforation. CT findings of non-perforated acute appendicitis include outer appendiceal diameter greater than 6 mm, symmetric appendiceal wall thickening greater than 2 mm, appendiceal wall hyperenhancement, mural stratification, cecal apical thickening, and inflammatory changes in the periappendiceal area and contiguous structures including the terminal ileum. There is a wide variation in the diameter of the appendix in normal patients (up to 1 cm). Therefore, when the appendix measures between 6 and 10 mm on CT, other CT findings as well as clinical findings should be considered for the diagnosis. CT findings suggesting perforated appendicitis include a defect in enhancing appendiceal wall, periappendiceal abscess, extraluminal appendicolith, and extraluminal air (Birnbaum and Wilson 2000; Pinto Leite et al. 2005). US is recommended as an initial imaging study in children, thin young women, and pregnant women. A graded compression technique should be performed throughout the entire length of the appendix. US criteria for acute appendicitis are outer transverse appendiceal diameter greater than 6 mm, non-compressibility, circumferential color Doppler signal in the wall, increased periappendiceal fat echogenicity, intraluminal fluid, and the absence of gas in the appendix. When ischemic or gangrenous change prior to perforation occurs, a loss of wall layers and decreased or no color Doppler signal can be seen. Although CT demonstrates higher sensitivity, accuracy, and negative predictive value for the diagnosis than US, CT and US complement each other when the results of initial examination are equivocal or suboptimal (Birnbaum and Wilson 2000). MRI can be a good alternative to CT in patients with a risk of contrast-induced nephropathy or during pregnancy. MRI features of acute appendicitis include appendiceal diameter greater than 7 mm, appendiceal wall thickening greater than 2 mm, hyperintense luminal contents, and hyperintense periappendiceal fat stranding and fluid on T2WI (Spalluto et al. 2012).

Primary epiploic appendagitis is a rare, self-limited inflammation of epiploic appendages (also known as appendices epiploicae) that are peritoneal pouches arising from the serosal surface of the colon, to which they are attached by a vascular stalk. Torsion or spontaneous venous thrombosis of the epiploic appendages with resultant infarction and inflammation is a cause of primary epiploic appendagitis. The most common site is the area adjacent to the sigmoid colon followed by the descending colon and right hemicolon (Singh et al. 2005). A unique CT finding is an oval fatty lesion less than 5 cm in diameter surrounded by inflammatory changes that abuts the anterior colonic wall (Almeida et al. 2009; Singh et al. 2005). Associated colonic wall thickening is usually absent. The presence of a hyperattenuating rim representing the thickened visceral peritoneum surrounding an inflamed epiploic appendix is a diagnostic finding. A central hyperattenuating area corresponding to central thrombosed vessels, hemorrhage, or fibrosis is sometimes seen. Omental infarction may have a similar CT appearance, but it appears as a larger, cake-shaped lesion centered in the omentum and lacks the hyperattenuating rim and central hyperattenuating area (Almeida et al. 2009; Singh et al. 2005). The characteristic US finding is a non-compressible hyperechoic mass with hypoechoic halo at the site of maximal tenderness, adjacent to the colon, with no central blood flow depicted on color Doppler US images (Almeida et al. 2009; Singh et al. 2005). The absence of color Doppler signal and lengthy colonic wall thickening are useful findings to differentiate primary epiploic appendagitis from secondary epiploic appendagitis due to acute diverticulitis (Singh et al. 2005).

Ulcerative colitis is one of the main subtypes of inflammatory bowel disease that primarily affects the mucosa. It begins in the rectum with variable degrees of continuous, circumferential, and proximal extension throughout the colon. In an acute phase, mucosal granularity attributable to mucosal edema, hyperemia, and abnormal mucin production is the earliest radiographic finding on double-contrast barium enema (DCBE). As inflammation worsens, continuous and symmetric wall thickening often with water halo sign can be seen on CT. Ulcerations through the mucosa and submucosa with lateral spread in the submucosal layer results in characteristic collar button ulcers on DCBE. Extensive ulcerations leave islands of mucosal remnants, creating inflammatory pseudopolyposis which may be seen in a well-distended colon on CT as well as on DCBE. In chronic phase, mural thickening with fat halo sign, luminal narrowing, and widening of presacral space are commonly seen on CT due to the hypertrophy of the muscularis mucosa and fat deposition in the submucosa and perirectal area. On DCBE, the involved colon shows a narrowed, ahaustral, and shortened appearance often with postinflammatory pseudopolyposis (abnormal proliferation of inflamed mucosa) (Gore et al. 1996; Lichtenstein 1987). Toxic megacolon, a potentially fatal complication, is characterized by both nonobstructive colonic dilatation of at least 6 cm and evidence of systemic toxicity (Sheth and LaMont 1998). Typical findings are marked colonic dilatation with an ahaustral pattern often associated with thin wall and ill-defined, nodular inner margin on plain radiograph and CT (Thoeni and Cello 2006). Pancolitis or chronic ulcerative colitis is associated with an increased colorectal cancer risk. These cancers with flat or infiltrating type are difficult to diagnose early by DCBE and even by colonoscopy. On CT, features of asymmetric marked mural thickening and loss of mural stratification suggest associated malignancy (Thoeni and Cello 2006; Gore et al. 1996).

Ischemic colitis represents partial mural ischemia mainly affecting the mucosa and submucosa that is usually seen in elderly patients. With disease progression, necrosis of the muscle layer can lead to the fibrotic stricture or transmural infarction. It is caused by mesenteric vascular occlusion, low flow or vasospasm, as well as strangulated colonic obstruction or overdistention. Watershed segments such as the splenic flexure and the rectosigmoid colon are commonly affected in nonocclusive ischemia. However, any part of the colon can be involved if small vessel disease and/or reperfusion injury occurs. Intramural necrosis is always followed by intramural edema and/or hemorrhage often with superinfection (Wiesner et al. 2003). Therefore, common CT findings include segmental mural thickening, water halo sign, pericolic fat stranding, and ascites. The colonic wall is thin and unenhanced, associated with luminal dilatation when the involved colon becomes infarcted due to total vascular occlusion without reperfusion (Thoeni and Cello 2006; Wiesner et al. 2003). Pneumatosis coli and portomesenteric venous gas are infrequent but ominous findings indicating transmural infarction. The diagnosis is dependent on the history and clinical findings, and colonoscopy is needed for definitive diagnosis (Thoeni and Cello 2006).

Radiation colitis is characteristically localized to the radiation port, which is commonly in the pelvis for treatment of genitourinary tract neoplasms. The sigmoid colon and rectum are most commonly affected. In acute stage, radiation damages the actively proliferating mucosa. Wall thickening with edema and inflammatory standing can be seen. Chronic injury is due to radiation-induced endarteritis. This chronic ischemia leads to fibrosis of the bowel wall, often manifesting as stricture, fistula, and sinus tract. Increased mural and perirectal fat and thickening of perirectal fibrous tissue can be seen in the chronic stage. The CT appearance is nonspecific, but the clinical history will help suggest the diagnosis (Capps et al. 1997).

The colonic wall can be involved by adjacent extrinsic diseases. Among these, actinomycosis is a chronic infection characterized by formation of well-enhancing abscesses or masses rich in granulation and fibrous tissues and extensive infiltration across the adjacent tissue planes. It is caused by Actinomyces israelii and commonly associated with bowel perforation, surgery, trauma, and intrauterine device. The sigmoid colon is the most common segment of the colon involved (Lee et al. 2001). Endometriosis is defined as the presence of endometrial glands and stroma outside the uterus. The rectosigmoid colon is the most common segment of intestinal endometriosis. Implants are usually attached to serosal surface but can eventually erode through the subserosal layers and cause marked thickening and fibrosis of the muscularis propria (Woodward et al. 2001).