Fundamentals of Diagnostic Radiology
3rd Edition

Chapter 32
Colon and Appendix
William E. Brant
Imaging Methods
The primary imaging methods for detection and characterization of colon abnormalities have continued to evolve over time. The persistently expanding availability of colonoscopy has continued to reduce the role of barium enema in imaging the colon. On the other hand, the use of CT to image the abdomen and pelvis continues to increase, making CT often the preferred method for initial detection of colon disease. CT (virtual) colonography challenges the role of traditional colonoscopy for polyp and cancer detection. Once a possible neoplastic lesion is discovered, however, colonoscopy or proctoscopy is usually used for biopsy. The single-contrast barium enema is still occasionally used for the evaluation of colonic obstruction and fistulas and in old, seriously ill, or debilitated patients. The double-contrast (air-contrast) barium enema (Fig. 32.1) is favored for detection of small lesions (<1 cm), for documentation of inflammatory bowel disease, and for detailed imaging evaluation of the rectum (1). Colonoscopy is sporadically limited by occasional failure to reach the right colon. In such cases, barium enema or virtual colonoscopy is utilized to complete the examination. As elsewhere in the GI tract, CT complements colonoscopy and barium examinations by demonstrating intramural and extracolonic components of disease. It is excellent for demonstrating extrinsic inflammatory and neoplastic processes that affect the colon: abscesses, sinuses, and fistulas.
CT and MR imaging have been utilized for initial staging of colorectal carcinoma. However, both methods are limited in their ability to determine the extent of bowel wall tumor infiltration and involvement of regional lymph nodes. Transrectal US is more accurate than CT or MR in determining local tumor extent of rectal carcinomas, and it is used in the evaluation of other rectal and perirectal disease (2). For the initial staging of colorectal carcinoma, CT and MR should be reserved for patients with suspected widespread local or disseminated disease. CT is useful in screening for recurrence of colorectal carcinoma because it can provide a comprehensive examination of the liver, abdominal cavity, and entire colon. MR is sensitive but nonspecific for the detection of local recurrence of rectal carcinoma.
CT colonography (Fig. 32.2) is becoming a viable alternative to invasive colonoscopy to screen for colorectal cancer (3). The procedure begins with diligent bowel preparation, identical to that used for invasive colonoscopy. A rectal tube is inserted and the colon is insufflated with carbon dioxide or room air. Multidetector CT of the entire extent of the colon with the patient in supine position is obtained in a single breath-hold utilizing 1.25- to 2.5-mm collimation and a reconstruction interval of 1 mm. The scan is repeated with the patient in prone position. Commercially available software programs that provide endoluminal display and “fly-through” capabilities provide three-dimensional volume-rendering image processing. Image viewing and interpretation are usually performed using

both standard two-dimensional axial CT reconstructions and three-dimensional volume-rendered images on a computer workstation. The role of virtual colonoscopy in imaging the colon and screening for colorectal cancer is still being debated.
FIGURE 32.1. Double-Contrast Barium Enema. An upright radiograph from a double-contrast barium enema demonstrates normal colon anatomy. The appendix (larger white arrow) extends from the cecum (C). The ascending colon (AC) extends to the hepatic flexure (HF), the coils of which must be examined by multiple oblique views. The transverse colon (TC) extends to the splenic flexure (SF), which continues as the descending colon (DC). This patient has a long sigmoid colon (SC) that extends high into the abdomen. The transverse colon is relatively short. Patients with a short sigmoid colon usually have a long, redundant transverse colon. The distended balloon at the tip of the enema catheter causes a lucent filling defect (black arrowhead) in the rectum (R). A tiny intramural diverticulum (smaller white arrow) is seen in the proximal transverse colon.
The large intestine consists of the cecum and appendix, colon, rectum, and anal canal. It is approximately 1.5 m in length from the ileum to the anus. The large intestine is characterized by the taenia coli, three longitudinal bands of muscle that traverse the colon and shorten it to form haustra, the sacculations created by puckering of the bowel wall. The major functions of the large intestine are the formation, transport, and evacuation of feces. These functions require mobility, absorption of water, and secretion of mucus. Infrequent peristalsis transports feces from the ascending and transverse colon to the sigmoid colon, where fecal material is stored until defecation. The cecum and ascending colon absorb water from the highly liquid material received from the ileum. Mucus secreted by mucosal goblet cells protects the mucosa from injury and is secreted in profuse amounts when the mucosa is irritated or injured.
FIGURE 32.2. Polyp on Virtual Colonography. Three-dimensional reconstructed image shows a 7-mm polyp (straight arrow) extending into the lumen of the colon. Multiple normal-appearing folds (arrowhead) are evident. The white line (curvy arrow) shows the colon “fly-through” path. Images are usually reviewed in color on a computer workstation.
The cecum is the large blind pouch that extends below the level of the ileocecal valve. The cecum generally lies in the right iliac fossa but may be quite mobile. It is usually covered on all sides by peritoneum (intraperitoneal), but it may be fixed extraperitoneally and covered by peritoneum on its ventral surface only. The appendix is a long wormlike tube that hangs from near the apex of the cecum. The ileocecal valve consists of two lips that project into the cecum, forming a sometimes prominent mass.
The ascending colon is extraperitoneal, lying in the anterior pararenal space and covered by peritoneum on its ventral surface only. The hepatic flexure forms two curves. The proximal, more posterior curve is closely related to the descending duodenum and right kidney. The more distal anterior curve is closely related to the gallbladder.

The transverse colon is intraperitoneal and suspended from the transverse mesocolon, which arises from the peritoneum to cover the pancreas and sweep transversely across the upper abdomen. The transverse mesocolon limits the superior extent of the small bowel loops. The splenic flexure is closely related to the tail of the pancreas and the caudal aspect of the spleen. The splenic flexure is anchored to the diaphragm by the phrenicocolic ligament, which serves as a boundary between disease processes of the left subphrenic space and the left paracolic gutter.
The descending colon, like the ascending colon, is extraperitoneal within the anterior pararenal space and is covered by peritoneum only on its ventral surface. The sigmoid colon forms a redundant loop of variable length from the distal descending colon in the left iliac fossa to the rectum. The sigmoid colon is completely intraperitoneal and is suspended by the sigmoid mesocolon, which allows considerable mobility. The sigmoid colon penetrates the peritoneum at the level of vertebrae S2 to S4 to continue as the extraperitoneal rectum. The rectum extends for approximately 12 cm, in close relationship with the sacrum. Peritoneum forming the pouch of Douglas covers the ventral and lateral aspects of the rectum. The anal canal is 3 to 4 cm long and is invested by the sphincter ani and levator ani muscles. A series of vertical folds forms the rectal columns of Morgagni, beneath which are the veins that, when dilated, are hemorrhoids. The colon is recognized on imaging studies by its course, haustral markings, and fecal content. The thickness of the wall of the normal colon does not exceed 5 mm.
Colon Filling Defects/Mass Lesions
Filling defect refers to a radiolucency in a barium pool caused by a protruding mass lesion. On barium enema examinations, filling defects may be polyps, tumors, plaques, air bubbles, feces, mucus, or foreign objects. Polyps are protrusions from the mucosa that produce filling defects in pools of barium or are etched in white when coated by barium and outlined by air on double-contrast studies. Polyps may be pedunculated on a stalk (Fig. 32.3) or sessile. They may appear as “bowler hats” (Fig. 32.4) when viewed obliquely. The term polyp is generic for a protruding lesion and does not imply a histologic diagnosis. Air bubbles rise to the highest point of a contrast column (the “carpenter’s level” sign), but fecal material usually remains dependent. Plaques are flat lesions that barely rise above the mucosal surface.
Colorectal adenocarcinoma is the most common malignancy of the GI tract and the second most common malignant tumor in the United States. Approximately 50% arise in the rectum and rectosigmoid area. Another 25% occur in the sigmoid colon, and the remaining 25% are evenly distributed throughout the remainder of the colon. Nearly all cancers of the colon are adenocarcinomas arising from preexisting adenomas. Most tumors are annular constricting lesions, 2 to 6 cm in diameter, with raised everted edges and ulcerated mucosa (Fig. 32.5). Polypoid tumors are less common, with some having the frondlike appearance of villous carcinoma. Infiltrating scirrhous tumors—common in gastric carcinoma—are rare in the large intestine, unless the patient has ulcerative colitis. The tumor spreads by direct invasion through the bowel wall into pericolonic fat (Fig. 32.6) and adjacent organs, through lymphatic channels to regional nodes, and hematogenously through the portal veins to the liver and systemic circulation. Intraperitoneal seeding from a tumor that penetrates the colon wall may also occur. Obstruction is the most frequent complication. Other complications are uncommon but include perforation (Fig. 32.7), intussusception, abscess, and fistula formation. Up to 20% of patients have a second tumor of the large bowel at diagnosis, usually an adenoma or another carcinoma. Approximately 5% of patients will have a second colorectal carcinoma,

either simultaneously or diagnosed subsequently. Patients with ulcerative colitis, Crohn disease, familial adenomatous polyposis syndrome, and Peutz-Jeghers syndrome are at increased risk of colon carcinoma.
FIGURE 32.3. Pedunculated Polyp. Double-contrast barium enema demonstrates a long-stalked pedunculated polyp with a bulbous tip (straight arrow) arising (curved arrow) from the mucosa of the descending colon.
FIGURE 32.4. Bowler Hat Sign. The “bowler hat” sign is produced by barium coating both the body of the polyp (large arrow) and the recesses (small arrows) between the base of the lesion and the normal colonic mucosa.
Local disease staging is best evaluated with transrectal or colonoscopic US. CT and MR are used for more advanced disease and to detect recurrence (4). Microscopic invasion through the bowel wall and tumor involvement of normal-size lymph nodes are not detected by CT or MR. Cross-sectional imaging findings include: (1) polypoid primary tumor (usually >1 cm); (2) “apple-core” lesions, with bulky, irregular thickening of the colon wall and irregular narrowing of the lumen; (3) cystic, necrotic, and hemorrhagic areas within the tumor mass, especially when the tumor is large; (4) linear soft tissue stranding into the pericolonic fat, which is often indicative of tumor extension through the bowel wall; (5) enlarged regional lymph nodes (>1 cm) representing lymphatic spread of tumor; (6) distant metastases, especially in the liver (5). When tumors cause colonic obstruction, edema and/or ischemia may thicken the wall of the uninvolved colon proximal to the tumor.
Tumor recurrences are most common (1) at the operative site, near the bowel anastomosis; (2) in lymph nodes that drain the operative site; (3) in the peritoneal cavity; and (4) in the liver and distant organs. Because the entire abdominal cavity must be surveyed to detect tumor recurrence, CT is the current method of choice.
FIGURE 32.5. Colon Carcinoma. Radiograph of the sigmoid colon from a double-contrast barium enema demonstrates a characteristic “apple core” constricting lesion of colon carcinoma. The lumen is markedly narrowed (open arrow), and the shoulders of the tumor cause a mass impression on the adjacent distended lumen (solid arrow).
A polyp is defined as a localized mass that projects from the mucosa into the lumen. Because the majority of colorectal cancers are believed to arise from preexisting adenomatous polyps, the detection of colon polyps is a major indication for barium studies of the colon. The following “rules of thumb” can be applied. Polyps smaller than 5 mm are almost all hyperplastic, with a risk of malignancy less than 0.5%. Polyps between 5 and 10 mm are 90% adenomas, with a risk of malignancy of 1%. Polyps between 10 and 20 mm are usually adenomas, with a risk of malignancy of 10%. Polyps larger than 20 mm are 50% malignant.
Hyperplastic polyps are nonneoplastic mucosal proliferations. They are round and sessile. Nearly all are smaller than 5 mm.
Adenomatous polyps are distinctly premalignant and a major risk for development of colorectal carcinoma. Adenomatous polyps are neoplasms with a core of connective tissue. Approximately 5% to 10% of the population older than 40 years have adenomatous polyps.

Hamartomatous polyps (juvenile polyps) represent approximately 1% of colon polyps. They are a common cause of rectal bleeding in children. The Peutz-Jeghers polyp is a type of hamartomatous polyp.
FIGURE 32.6. Cecal Carcinoma. CT reveals a large mass (M) representing adenocarcinoma of the cecum. Note the asymmetric, irregular narrowing of the cecal lumen (arrow). Soft tissue stranding (arrowhead) extending well into the pericecal fat is indicative of tumor extension through the wall of the colon.
FIGURE 32.7. Rectal Carcinoma With Perforation. An aggressive rectal carcinoma (T) markedly thickens the wall of the rectum and narrows its lumen to a tiny channel (thin arrow). The tumor has perforated the wall of the rectum, resulting in a perirectal abscess (wide arrow); this is shown on CT as soft tissue and fluid density with air bubbles replacing the perirectal fat.
FIGURE 32.8. Postinflammatory Filiform Polyps. Detail view from an air-contrast barium enema in a patient with ulcerative colitis shows the characteristic wormlike appearance of postinflammatory filiform polyps (arrow). Numerous polyps are present.
Inflammatory polyps are usually multiple and associated with inflammatory bowel disease (Fig. 32.8). They account for less than 0.5% of colorectal polyps.
Familial adenomatous polyposis syndrome is approximately two thirds inherited and one third spontaneous. The inheritance pattern is autosomal dominant with high penetrance. The polyps are tubulovillous adenomas, which usually are evident by age 20. Colorectal cancer will eventually develop in nearly all patients, so total colectomy with rectal mucosectomy and ileoanal pouch construction is the current recommended therapy. Polyps typically carpet the entire colon (Fig. 32.9). Patients are at risk for numerous extracolonic manifestations, including carcinomas of the small bowel, thyroid carcinoma, and mesenteric fibromatosis. Patients with associated bone and skin abnormalities, including cortical thickening of the ribs and long bones, osteomas of the skull, supernumerary teeth, exostoses of the mandible, dermal fibromas, desmoids, and epidermal inclusion cysts, have been diagnosed as Gardner syndrome. Those with associated tumors of the CNS have been grouped as Turcot syndrome. These are variations of the same disease.
Hamartomatous Polyposis Syndromes
Hamartomatous polyps are nonneoplastic growths with a smooth

muscle core covered by mature glandular epithelium (6). The hamartomatous polyps associated with various syndromes have minor histologic differences. These lesions carry no risk of malignant transformation. However, patients with hamartomatous polyposis syndromes may also develop adenomatous polyps, which do carry a risk of malignancy.
FIGURE 32.9. Familial Adenomatous Polyposis Syndrome. Cone-down image from a double-contrast barium enema reveals the colonic mucosa to be carpeted with innumerable small polyps, seen as tiny filling defects (arrow).
Peutz-Jeghers syndrome predominantly involves the small bowel, but most cases have gastric and colon polyps as well. The condition is autosomal dominant with incomplete penetrance. Dark pigmented spots on the skin and mucous membranes are characteristic. Risk of carcinoma arising from coexisting adenomatous polyps is 2% to 20%. Patients are at risk for breast, uterine, and ovarian cancer and early age cancer of the pancreas.
Cowden disease is a syndrome of multiple hamartomas, including hamartomatous polyposis of the GI tract, with goiter and thyroid adenomas and increased risk of breast cancer and transitional cell carcinoma of the urinary tract. The syndrome is autosomal dominant and affects mainly Caucasians. All patients have mucocutaneous lesions with facial papules, oral papillomas, and palmoplantar keratoses.
Cronkhite-Canada syndrome is a disease of older patients with a mean age of onset of 60 years. Polyps are distributed throughout the stomach, small bowel, and colon. Associated skin findings include nail atrophy, brownish skin pigmentation, and alopecia. Patients present with watery diarrhea and protein-losing enteropathy.
Lymphoid hyperplasia may involve the colon. The normal lymphoid follicular pattern of diffuse tiny nodules 1 to 3 mm in diameter (Fig. 32.10) with characteristic umbilication is most common in the terminal ileum and cecum but may involve any portion of the colon. The nodular lymphoid hyperplasia pattern of diffuse nodules larger than 4 mm is associated with allergic, infectious, and inflammatory disorders.
FIGURE 32.10. Nodular Lymphoid Hyperplasia. Single-contrast barium enema in a young patient with hypogammaglobulinemia shows numerous small nodules (arrow) throughout the colon.
The colon is less commonly involved with lymphoma than the stomach or small bowel. Involvement of the cecum or rectum is most common with anal and rectal lymphoma, which is increasingly frequent in AIDS patients. Morphologic patterns include small to large nodules, which may ulcerate, excavitate, and perforate, and diffuse infiltration of the bowel wall, resulting in bulbous folds and thickened bowel wall (Fig. 32.11). As in the small intestine, marked narrowing of the lumen is uncommon, and aneurysmal dilation occurs when transmural disease destroys innervation. The diffuse multinodular form may be difficult to differentiate from nodular lymphoid hyperplasia. Lymphoma nodules vary in size, although lymphoid hyperplasia nodules are uniform in size. Non-Hodgkin lymphoma is most common.
GI stromal tumors (GISTs) account for nearly all mesenchymal tumors of the colon. True colonic leiomyomas and leiomyosarcomas are very rare (7). GISTs are much less common in the colon than in the stomach and small bowel, accounting for only 7% of the total. As in the remainder of the GI tract, they may appear as exophytic, mural, or intraluminal masses. Ulceration is relatively

frequent. Hemorrhage, cystic change, necrosis, and calcification are more common in larger tumors (Fig. 32.12).
FIGURE 32.11. Rectal Lymphoma. CT demonstrates a prominent mass of lymphoma (L) that causes irregular narrowing of the lumen (arrowhead) of the rectum. Note the homogeneous attenuation of the lymphomatous mass. The CT appearance is indistinguishable from adenocarcinoma of the rectum.
Lipoma is the most common submucosal tumor of the colon. It is most frequent in the cecum and ascending colon. Nearly 40% present with intussusception. Barium studies demonstrate a smooth, well-defined, elliptic filling defect, usually 1 to 3 cm in diameter. The tumors are soft and change shape with compression. CT demonstration of a fat-density tumor is definitive.
Extrinsic masses commonly cause mass effect on the colon that may simulate intrinsic disease (Fig. 32.13).
FIGURE 32.13. Serosal Metastases Involving the Colon. Metastases from carcinosarcoma of the uterus implanted on the serosal surface of the sigmoid colon (S) cause narrowing and spiculation (arrows) of the lumen.
Endometriosis commonly implants on the sigmoid colon and rectum (8). Defects are frequently multiple and of variable size. Lesions are commonly within the cul-de-sac. Barium studies demonstrate sharply defined defects that compress but do not usually encircle the lumen. CT demonstrates complex cystic pelvic masses with high-density fluid components. Multiple pelvic organs may be incorporated into the mass. MR demonstrates masses with signal characteristics of hemorrhage.
Benign pelvic masses such as ovarian cysts, cystadenomas, teratomas, and uterine fibroids produce smooth extrinsic mass impressions on the colonic wall. The colon is displaced but not invaded.
Malignant pelvic tumors and metastases may involve the colon by contiguous spread, by spreading along mesenteric fascial planes, by intraperitoneal seeding, through lymphatic channels, or by embolus through blood vessels. The involved colon demonstrates thickening of the wall, separation of folds, spiculation, angulations, narrowing, and serosal plaques. Metastases often cannot be differentiated

from primary tumors by imaging methods. Crohn disease and metastatic disease may also look exactly alike radiographically. CT and MR demonstrate contiguous involvement of the colon and rectum by pelvic tumors.
FIGURE 32.12. Malignant GI Stromal Tumor of the Rectum. A CT scan shows a large tumor (T) with an irregular low-density area of central necrosis arising exophytically from the wall of the rectum (arrowhead), which is displaced laterally and anteriorly. The tumor obstructed the bladder outlet, necessitating placement of a suprapubic Foley catheter (F).
Extrinsic inflammatory processes, such as appendicitis, pelvic abscess, diverticular abscess, and pelvic inflammatory disease, cause mass effect, asymmetric tethering, and spiculation.
Colon Inflammatory Disease
Ulcerative colitis is an uncommon idiopathic inflammatory disease involving primarily the mucosa and submucosa of the colon (9). The peak age for its appearance is 20 to 40 years, but onset of disease after age 50 is common. The disease consists of superficial ulcerations, edema, and hyperemia. The radiographic hallmarks of ulcerative colitis are granular mucosa, confluent shallow ulcerations, symmetry of disease around the lumen, and continuous confluent diffuse involvement (Table 32.1). An early fine granular pattern is produced by mucosal hyperemia and edema that precede ulceration. Superficial ulcers spread to cover the entire mucosal surface. The mucosa is stippled, with barium adhering to the superficial ulcers. Collar button ulcers (Fig. 32.14) are deeper ulcerations of thickened edematous mucosa with crypt abscesses extending in the submucosa. A coarse granular pattern is produced later by the replacement of diffusely ulcerated mucosa with granulation tissue. Late changes include a variety of polypoid lesions. Pseudopolyps are mucosal remnants in areas of extensive ulceration. Inflammatory polyps are small islands of inflamed mucosa. Postinflammatory polyps are mucosal tags that are seen in quiescent phases of the disease. Filiform polyps are postinflammatory polyps with a characteristic wormlike appearance (Fig. 32.8). They are typically seen in an otherwise normal-appearing colon. Hyperplastic polyps may occur during healing after mucosal injury. Involvement typically extends from the rectum proximally in a symmetric and continuous pattern. The terminal ileum is nearly always normal. Rare backwash ileitis may produce an ulcerated but patulous terminal ileum. CT findings include: (1) wall thickening, often with a “halo sign” of low-density submucosal edema; (2) narrowing of the lumen of the colon; (3) pseudopolyps; and (4) pneumatosis coli with megacolon. Complications of ulcerative colitis include: (1) strictures (Fig. 32.15), usually 2 to 3 cm or longer and commonly involving the transverse colon and rectum; (2) colorectal adenocarcinoma, with an approximate risk of 1% per year of disease; (3) toxic megacolon (2% to 5% of cases) as the initial manifestation; and (4) massive hemorrhage. Associated extraintestinal diseases include sacroiliitis mimicking ankylosing spondylitis (20% of cases), eye lesions including uveitis and iritis (10% of cases), cholangitis, and an increased incidence of thromboembolic disease.
TABLE 32.1 Ulcerative Colitis Versus Crohn Colitis
Ulcerative Colitis Crohn Colitis
Circumferential disease Eccentric disease
Regional (continuous disease) Skip lesions (discontinuous disease)
Predominantly left-sided Predominantly right-sided
Rectum usually involved Rectum normal in 50% of cases
Confluent shallow ulcers Confluent deep ulcers
No aphthous ulcers Aphthous ulcers early
Collar button ulcers Transverse and longitudinal ulcers
Terminal ileum usually normal Terminal ileum usually diseased
Terminal ileum patulous Terminal ileum narrowed
No pseudodiverticula Pseudodiverticula
No fistulas Fistulas common
High risk of cancer Low risk of cancer
Risk of toxic megacolon No toxic megacolon
FIGURE 32.14. Ulcerative Colitis. Double-contrast barium enema shows a pattern of continuous involvement of the colon with innumerable submucosal collar button ulcers (arrows).
Crohn disease involves the colon in two thirds of cases and is isolated to the colon in approximately one third of all cases. Hallmarks of Crohn colitis include early aphthous ulcers, later confluent deep ulcerations, predominant right colon disease, discontinuous involvement with intervening regions of normal bowel, asymmetric

involvement of the bowel wall, strictures, fistulas, and sinus formation (Fig. 32.16) (Table 32.1). Pseudodiverticula of the colon are formed by asymmetric fibrosis on one side of the lumen, causing saccular outpouches on the other side. Involvement of the rectum is characterized by deep rectal ulcers and multiple fistulous tracts to the skin.
FIGURE 32.15. Ulcerative Colitis Stricture. A long-segment stricture (arrow) is typical of inflammatory bowel disease rather than malignancy. Air-contrast barium enema shows irregular narrowing of the lumen of the descending colon.
FIGURE 32.16. Crohn Colitis. A. CT scan through the transverse colon (T) demonstrates the asymmetric thickening of the colon wall characteristic of Crohn colitis. The anterior wall (arrowhead) is normal, and the posterior wall (arrow) is thickened and nodular. B. A more caudal CT scan in the same patient demonstrates numerous air-containing perineal cutaneous fistulas (arrowheads) surrounding the rectum (R).
Infectious colitis may be caused by a variety of bacteria (Salmonella, Shigella, Escherichia coli); parasites; viruses (cytomegalovirus, herpes); and fungi (histoplasmosis, mucormycosis). Most cause a pancolitis with edema and inflammatory wall thickening with infiltration of pericolonic fat. Pericolonic fluid and intraperitoneal fluid may be present (Fig. 32.17).
Toxic megacolon is a potentially fatal condition characterized by marked colonic distension and risk of perforation. It occurs as a complication of fulminant colitis, often caused by ulcerative colitis, Crohn disease, pseudomembranous colitis, use of antidiarrheal drugs, and hypokalemia. Transmural inflammation causes deep ulcers that may extend to the serosa surface, large areas of denuded mucosa, and loss of muscle tone. Radiographic findings include: (1) marked dilatation of the colon (transverse colon >6 cm) with absence of haustral markings, (2) edema and thickening of the colon wall, (3) pneumatosis coli, and (4) evidence of perforation. Barium studies should be avoided because of risk of perforation.
Pseudomembranous colitis is an inflammatory disease of the colon (and occasionally the small bowel) characterized by the presence of a pseudomembrane of necrotic

debris and overgrowth of Clostridium difficile (10). There are many contributing causes, including antibiotics (any that change bowel flora), intestinal ischemia (especially following surgery), irradiation, long-term steroids, shock, and colonic obstruction. The disease presents as fulminant inflammatory bowel disease with diarrhea and foul stools. Plain radiographs may reveal: (1) dilated colon, (2) nodular thickening of the haustra, and (3) ascites. The colon may be greatly dilated, and toxic megacolon has been reported. Barium enema demonstrates an irregular lumen with thumbprint indentations similar to ischemic colitis. Superficial ulcers are common. Plaquelike defects on the mucosal surface are caused by the pseudomembranes. The colitis is frequently patchy in distribution, with sparing of the rectum. The condition is commonly first detected on CT, which shows: (1) marked wall thickening up to 30 mm (average 15 mm) with halo or target appearance, (2) characteristic stripes of intraluminal contrast media trapped between nodular areas of wall thickening (the “accordion sign”) (Fig. 32.18), (3) mild pericolonic fat inflammation disproportionate with the marked colonic wall inflammation, and (4) ascites (35%).
FIGURE 32.17. Infectious Colitis. CT demonstrates marked thickening of the wall (arrow) of the transverse colon. Pericolonic fat is diffusely infiltrated, and ascites (a) is present. This patient was proven to have colitis caused by Cytomegalovirus.
Amebiasis is an infection by the protozoan parasite Entamoeba histolytica. The disease exists worldwide but is particularly common in South Africa, Central and South America, and Asia. At least 5% of the population of the United States harbor amebae. Encysted amebae are ingested with contaminated food and water. The cyst capsule is dissolved in the small bowel, releasing trophozoites that migrate to the colon and burrow into the mucosa, forming small abscesses. The infection can spread throughout the body by hematogenous embolization or direct invasion. Amebic colitis produces dysentery with frequent bloody mucoid stools. Barium studies demonstrate a disease that closely mimics Crohn colitis, with aphthous ulcers, deep ulcers, asymmetric disease, and skip areas. The cecum and rectum are the primary sites of colonic disease. The terminal ileum is characteristically not involved. Complications include strictures, amebomas consisting of a hard fixed mass of granulation tissue that may simulate carcinoma, toxic megacolon, and fistulas, particularly following surgical intervention. Amebic liver abscess results from the spread of infection through the portal system and may be complicated by diaphragm perforation, pleural effusion, and thoracic disease.
FIGURE 32.18. Pseudomembranous Colitis. The wall of the transverse colon (arrow) is markedly and diffusely thickened, trapping intraluminal contrast between the folds and producing the “accordion sign” on this CT scan. This patient developed Clostridium difficile colitis caused by broad-spectrum antibiotic therapy.
Typhilitis is a potentially fatal infection of the cecum and ascending colon usually seen in patients who are neutropenic and immunocompromised by chemotherapy. Concentric, often marked, thickenings of the wall of the cecum and ascending colon with prominent pericolonic inflammatory changes are characteristic (Fig. 32.19). Patients are at risk for colon ischemia.
Ischemic colitis mimics ulcerative colitis and Crohn colitis, both clinically and radiographically (11). The causes of ischemic colitis include arterial occlusion caused by arteriosclerosis, vasculitis, or arterial emboli; venous thrombosis owing to neoplasm, oral contraceptives, and other hypercoagulation conditions; and low-flow states such as hypotension, congestive heart failure, and cardiac arrhythmias. The pattern of involvement generally follows the distribution of a major artery and is the clue to

diagnosis. The superior mesenteric artery supplies the right colon from the cecum to the splenic flexure. The inferior mesenteric artery supplies the left colon from the splenic flexure to the rectum. The splenic flexure region and descending colon are watershed areas and most susceptible to ischemic colitis. Early changes include thickening of the colon wall, spasm, and spiculation. As blood and edema accumulate within the bowel wall, multiple nodular defects are produced in a pattern called “thumbprinting” (Fig. 32.20). Progression of the disease results in ulcerations, perforation, scarring, and strictures. CT demonstrates symmetric or lobulated thickening of the bowel wall, with an irregularly narrowed lumen. Submucosal edema may produce a low-density ring bordering on the lumen (target sign). Air in the abnormal bowel wall (pneumatosis) is highly suggestive of ischemia. Thrombus may occasionally be demonstrated within the superior mesenteric artery or vein.
FIGURE 32.19. Typhilitis. The wall of the cecum (arrow) is markedly thickened and edematous, demonstrating the target sign. The pericecal fat is infiltrated with fluid. The mucosa enhances weakly, indicating ischemia. This patient was neutropenic because of chemotherapy.
AIDS-associated colitis occurs most commonly in AIDS patients with CD4 lymphocyte counts below 200. Causative organisms are most commonly Cytomegalovirus or Cryptosporidium, although HIV itself may cause ulceration and colitis. Right colon disease is most common, with wall thickening and ulceration.
Radiation colitis may be indistinguishable radiographically from early ulcerative colitis. The diagnosis is made by confirmation that the involved colon is within an irradiation field. The rectosigmoid region is most commonly involved, owing to radiation of pelvic malignancy. Colitis is produced by a slowly progressive endarteritis that causes ischemia and fibrosis. Radiographic findings include thickened folds, spiculation, ulceration, stricture, and occasionally fistula formation. Fibrosis results in a rigid, featureless bowel. Healing may include formation of pseudopolyps and postinflammatory polyps.
FIGURE 32.20. Ischemic Colitis. Double-contrast barium enema shows thumbprinting pattern (arrows) involving the proximal portion of a redundant transverse colon (T). H, hepatic flexure.
Cathartic colon is caused by chronic irritation of the mucosa by laxatives, including castor oil, bisacodyl, and senna. The involved colon may be dilated and without haustra, or narrowed. The right colon is most commonly affected. Bizarre contractions are often observed. The diagnosis is made by clinical history.
Diverticular Disease
Colon diverticulosis is an acquired condition in which the mucosa and muscularis mucosae herniate through the

muscularis propria of the colon wall, producing a saccular outpouching. Colon diverticula are classified as false diverticula because the sacs lack all of the elements of the normal colon wall. The condition is rare in those younger than 25 but becomes more common with age thereafter to affect 50% of the population over age 75. The major risk factor for diverticulosis is a low-residue diet. The condition is very uncommon in cultures where a high-residue diet is the norm, such as African native populations. The formation of diverticular sacs is usually associated with thickening of the muscularis propria, including both the circular muscle and the taenia coli. Severely affected portions of bowel are usually shortened in length, resulting in crowding of the thickened circular muscle bundles. Muscle dysfunction associated with diverticulosis may result in pain and tenderness without evidence of inflammation. Diverticulosis without diverticulitis is a cause of painless colonic bleeding that may be brisk and life threatening. Plain abdominal radiographs demonstrate diverticula as gas-filled sacs parallel to the lumen of the colon. Barium studies show diverticula as barium or gas-filled sacs outside the colon lumen. Sacs vary in size from tiny spikes to 2 cm in diameter. Most are 5 to 10 mm in diameter. They may occur anywhere in the colon but are most common and usually most numerous in the sigmoid colon. Some sacs are reducible and may disappear with complete filling of the lumen. Others may contain fecal residue. The associated muscle abnormality is seen as thickening and crowding of the circular muscle bands with spasm and spiked irregular outline of the lumen. CT demonstrates the muscle hypertrophy as a thickened colon wall and distorted luminal contour. The diverticula are shown as well-defined gas-, fluid-, or contrast-filled sacs outside the lumen (Fig. 32.21).
Diverticulitis is inflammation of diverticula, usually with perforation and intramural or localized pericolic abscess (12). Diverticulitis eventually complicates approximately 20% of the cases of diverticulosis. Clinical signs include painful mass, localized peritoneal inflammation, fever, and leukocytosis. Complications of diverticulitis include bowel obstruction, bleeding, peritonitis, and sinus tract and fistula formation. Diverticulitis is a less common cause of colon obstruction than is colon carcinoma. Obstruction caused by diverticulitis is often temporarily relieved by smooth muscle relaxants such as glucagon. Colon bleeding is more often associated with diverticulosis than diverticulitis. Most diverticular abscesses are quickly walled off and confined, but free perforation with pus and air in the peritoneal cavity and diffuse peritonitis may occur. Sinus tracts may lead to larger abscess cavities in the peritoneal or retroperitoneal compartments. Fistulas are most common to the bladder (Fig. 32.22), vagina, or skin, but they may develop to any lower abdominal organ, including fallopian tubes, small bowel, and other parts of the colon. Diverticulitis of the right colon may

be mistaken clinically for acute appendicitis. Diverticulitis is efficiently diagnosed radiographically by barium enema or CT. Barium enema examination is considered safe, except when signs of free intraperitoneal perforation or sepsis are present. Hallmarks of diverticulitis on barium enema include deformed diverticular sacs, demonstration of abscess, and extravasation of barium outside the colon lumen. The smooth outlines of the involved sacs are deformed by inflammation and perforation. The resulting abscess causes extrinsic mass effect on the adjacent colon. The colon lumen is narrowed but tapers at the margins of narrowing, in contrast to the abrupt narrowing of carcinoma. Barium leaks into the abscess cavities or it may form tracks paralleling the colon lumen and often connecting multiple perforated sacs (the “double track” sign). CT excels at demonstrating the paracolic inflammation and abscess associated with diverticulitis, as well as complications such as colovesical fistula. CT findings are: (1) localized wall thickening (Fig. 32.23), (2) inflammation of pericolonic fat, (3) pericolonic abscess, and (4) diverticula at or near the site of inflammation.
FIGURE 32.21. Diverticulosis. A noncontrast CT scan demonstrates air-filled outpouchings (arrowhead), representing diverticula in the sigmoid colon. Note the absence of soft tissue stranding or fluid in the adjacent fat, indicating that no inflammation is present.
FIGURE 32.22. Diverticular Abscess and Colovesical Fistula. Single-contrast barium enema demonstrates barium filling a diverticular abscess (A) and opacifying the bladder (B). Thin columns of barium (arrowheads) outline fistulous tracts extending from the bowel lumen to abscess and from abscess to the bladder. The lumen of the sigmoid colon (S) is irregularly narrowed by the inflammatory process.
FIGURE 32.23. Diverticulitis. A CT scan demonstrates focal, marked thickening of the wall (arrow) of the sigmoid colon. Stranding into the adjacent fat (arrowhead) is indicative of inflammation. Because of the close resemblance of diverticulitis to colon carcinoma on CT, this patient must be followed to confirm complete resolution.
Lower GI Hemorrhage
Although upper GI hemorrhage is usually readily diagnosed by gastric aspirate and endoscopy, lower GI hemorrhage is difficult to localize, even during surgery. The common causes of lower GI hemorrhage are listed in Table 32.2. Radionuclide imaging studies are often selected as the screening examination of choice for confirming the presence of, and often localizing, lower GI bleeding. Technetium-99m-sulfur colloid or technetium-99m-red blood cell studies are capable of detecting bleeding at rates below 0.1 mL/min. A negative scintigraphic study usually precludes the need for urgent angiography. Angiography requires bleeding rates of 0.5 mL/min or greater; however, angiography is more specific than scintigraphy in demonstrating the anatomic cause of bleeding and offers the possibility of nonoperative treatment by embolization. Colonoscopy is usually unrewarding because of the large quantities of sticky, melanotic stool. Barium enema is not used to evaluate acute hemorrhage, because it usually cannot locate the source of bleeding and will interfere with any subsequently needed angiographic procedure. Multidetector CT performed without intraluminal contrast shows promise in the detection of hemorrhage by documenting intraluminal extravasation of intravenously administered contrast (13).
TABLE 32.2 Causes of Lower GI Hemorrhage
Cause Percentage of Cases
Colon diverticula 40
Angiodysplasia 17–30
Colon carcinoma 7–16
Polyps 8
Rectal trauma/fissure/hemorrhoids 7
Duodenal ulcer Rare
Meckel diverticulum Rare
Bowel ischemia Rare
Angiodysplasia refers to ectasia and kinking of mucosal and submucosal veins of the colon wall. The condition results from a chronic, intermittent obstruction of the veins where they penetrate the circular muscle layer. A maze of distorted, dilated vascular channels replaces the normal mucosal structures and is separated from the bowel lumen only by a layer of epithelium. Angiodysplasia is acquired and probably related to aging. The average age of affected patients is 65 years. Bleeding is usually chronic, resulting in anemia, but may be acute and massive. Angiography demonstrates a tangle of ectatic vessels without an associated mass.

Imaging Methods
Filling of the appendix is attained most reliably by single-contrast barium enema examination. The appendix is also frequently visualized on abdominal films obtained 6 to

48 hours following oral administration of barium. Failure to fill the appendix with barium on barium enema examination is not definitive evidence of appendiceal disease. Both CT and US have proven extremely useful in the diagnosis of appendiceal disease, especially acute appendicitis (14).
The appendix arises from the posteromedial aspect of the cecum at the junction of the taenia coli, approximately 1 to 2 cm below the ileocecal valve. The appendix is a blind-ended tube that is 5 to 10 mm in diameter (on barium studies) and approximately 8 cm in length, although it may be up to 30 cm long. Its mucosa is heavily infiltrated with lymphoid tissue. The appendix is quite variable in position: it may be pelvic, retrocecal, or retrocolic, and it can be intraperitoneal or extraperitoneal in location. The appendix always arises from the cecum on the same side as the ileocecal valve. A posterior position of the ileocecal valve indicates a posterior position of the appendix. On CT and US, the normal appendix appears as a thin-walled tube less than 6 mm in diameter (Fig. 32.24).
Acute Appendicitis
Acute appendicitis is the most common cause of acute abdomen. Frequently the clinical diagnosis is straightforward. However, patients with atypical presentations cause diagnostic problems. The most difficult patients are women of childbearing age, in whom ruptured ovarian cysts and pelvic inflammatory disease may mimic acute appendicitis. Acute appendicitis results from obstruction of the appendiceal lumen. Continued mucosal secretions cause dilation and increased intraluminal pressure that impairs venous drainage and results in mucosal ulceration. Bacterial infection causes gangrene and perforation with abscess. Most periappendiceal abscesses are walled off, but free perforation and pneumoperitoneum occasionally occur.
FIGURE 32.24. Normal Appendix. A noncontrast CT image shows a normal appendix (arrow) as a small gas-filled tubular structure with a blind end.
Plain films will demonstrate an appendiceal calculus (appendicolith or fecalith) in approximately 14% of patients with acute appendicitis. An appendicolith is formed by calcium deposition around a nidus of inspissated feces. The resultant calcification is usually laminated, with a radiolucent center. Appendiceal abscess or periappendiceal inflammation may result in a visible soft tissue mass in the right lower quadrant. The lumen of the cecum, as outlined by gas, will be deformed; localized ileus may be evident. Barium enema examination is frequently nonspecific. Complete filling of the appendix to its bulbous tip is strong evidence against appendicitis. However, nonfilling of the appendix, as would be expected with luminal obstruction, has no diagnostic value of its own. Mass impression on the cecum has many causes besides appendicitis.
US, using the graded compression technique, is quite accurate in providing a definitive diagnosis and is commonly the imaging technique of choice in women of childbearing age and in children. Slow graded compression is applied with a near-focus transducer to the area of maximum tenderness (14). The normal appendix has a diameter of less than 6 mm when compressed. US signs of acute appendicitis are: (1) a noncompressible appendix larger than 6 mm in diameter, measured outer wall to outer wall (Fig. 32.25), and (2) visualization of a shadowing appendicolith. With perforation, sonography demonstrates a loculated pericecal fluid collection, a discontinuous wall of the appendix, and prominent pericecal fat. When the US examination is negative for appendicitis, an alternate diagnosis can frequently be suggested based on visualized abnormalities.
CT is the imaging method of choice in men, in older patients, and when periappendiceal abscess is suspected (15). Definitive CT diagnosis of acute appendicitis is based on finding: (1) an abnormally dilated (>6 mm), enhancing appendix (Fig. 32.26); (2) enhancing appendix surrounded by inflammatory stranding or abscess; or (3) pericecal abscess or inflammatory mass with a calcified appendicolith (16,17). A inflammatory mass is seen as indurated soft tissue with a CT density greater than 20 H. A liquified mass less than 20 H in CT density is evidence of abscess (Fig. 32.27). Abscesses larger than 3 cm generally require

surgical or catheter drainage. Smaller abscesses commonly resolve on antibiotic treatment alone.
FIGURE 32.25. Acute Appendicitis: US. Graded compression US demonstrates a distended appendix with a diameter (between arrowheads) of 10 mm. The mucosal interface produces a bright echogenic line (thin arrow). The blunt tip (wide arrow) confirms identification of this tubular structure as the appendix. Inflammation of the periappendiceal fat (asterisk) increases its echogenicity. Surgery confirmed an acutely inflamed and focally necrotic appendix.
Mucocele of the Appendix
Mucocele refers to distension of all or a portion of the appendix with sterile mucus (18). The lumen is obstructed by appendicolith, foreign body, adhesions, or tumor. Some cases are caused by mucinous cystadenomas or cystadenocarcinomas of the appendix. Continued secretion of mucus produces a large (up to 15 cm), well-defined, cystic mass in the right lower quadrant (Fig. 32.28). Peripheral calcification may be present. Rupture of the mucocele may result in pseudomyxoma peritonei. Gelatinous implants spread throughout the peritoneal cavity, causing adhesions and mucinous ascites.
FIGURE 32.26. Acute Appendicitis: CT. CT image shows a dilated appendix (wide arrow) measuring 8 mm in diameter with irregularly thickened and indistinct walls. Marked stranding (arrowheads) in the periappendiceal fat is indicative of inflammation. An appendicolith (thin arrow) is seen in the lumen of the appendix.
Appendiceal Tumors
Carcinoid is the most common tumor of the appendix, accounting for 85% of all tumors (18). The appendix is the most common location for carcinoid tumor, accounting for 60% of all carcinoids. Most occur near the tip and are round, nodular tumors up to 2.5 cm. Most are solitary

and have fewer tendencies to metastasize than carcinoids elsewhere in the GI tract. Carcinoid syndrome is rare, and the mesenteric reaction seen with small bowel carcinoid is usually absent.
FIGURE 32.27. Appendiceal Abscess. CT demonstrates a thick-walled fluid collection (arrow) adjacent to the cecum (C). Inflammatory stranding is seen in the nearby fat. The appendix was not visualized. Surgery revealed a ruptured appendix with a focal abscess.
Adenomas occur in the appendix, usually in association with familial multiple polyposis. Isolated adenomas are usually mucinous cystadenomas associated with mucocele of the appendix.
Adenocarcinoma of the appendix is rare and is usually discovered in the clinical setting of suspected appendicitis in an older adult. Imaging demonstrates a soft tissues mass within or replacing the appendix (18).
FIGURE 32.28. Appendiceal Mucocele. CT reveals a tubular cystic mass (arrow) with calcification in its wall (arrowhead) in the right lower quadrant of the abdomen.
1. Levine MS, Rubesin SE, Laufer I, Hermlinger H. Diagnosis of colorectal neoplasms at double-contrast barium enema examinations. Radiology 2000;216:11–18.
2. Bipat S, Glas AS, Slors FJM, et al. Rectal cancer: local staging and assessment of lymph node involvement with endoluminal US, CT and MR imaging–a meta-analysis. Radiology 2004;232:773–783.
3. Macari M, Bini EJ, Jacobs SL, Lange N, Lui YW. Filling defects at CT colonography: pseudo- and diminutive lesions (the good), polyps (the bad), flat lesions, masses, and carcinomas (the ugly). Radiographics 2003;23:1073–1091.
4. Iyer RB, Silverman PM, DuBrow RA, Charnsangave C. Imaging in the diagnosis, staging, and follow-up of colorectal cancer. AJR Am J Roentgenol 2002;179:3–13.
5. Horton KM, Abrams RA, Fishman EK. Spiral CT of colon cancer: imaging features and role in management. Radiographics 2000;20:419–430.
6. Harned RK, Buck JL, Sobin LH. The hamartomatous polyposis syndromes: clinical and radiologic features. AJR Am J Roentgenol 1995;164:565–571.
7. Levy AD, Remotti HE, Thompson WM, Sobin LH, Mietten M. Gastrointestinal stromal tumors: radiologic features with pathologic correlation. Radiographics 2003;23:283–304.
8. Szucs RA, Turner MA. Gastrointestinal tract involvement by gynecologic diseases. Radiographics 1996;16:1251–1270.
9. Chen MYM, Anthony EY, Ott DJ, Scharling ES, Gelfand DW. Colitis: causes, pathology, and imaging. Radiologist 2001;8:119–128.
10. Kawamoto S, Horton KM, Fishman EK. Pseudomembranous colitis: spectrum of imaging findings with clinical and pathologic correlation. Radiographics 1999;19:887–897.
11. Balthazar EJ, Yen BC, Gordon RB. Ischemic colitis: CT evaluation of 54 cases. Radiology 1999;211:381–388.
12. Horton KM, Corl FM, Fishman EK. CT evaluation of the colon: inflammatory disease. Radiographics 2000;20:399–418.
13. Tew K, Davies RP, Jadun CK, Kew J. MDCT of acute lower gastrointestinal bleeding. AJR Am J Roentgenol 2004;182:427–430.
14. Abu-Yousef MM. Ultrasonography of the right lower quadrant. Ultrasound Q 2001;17:211–225.
15. Levine CD, Aizenstein O, Lehavi O, Blachar A. Why we miss the diagnosis of appendicitis on abdominal CT: evaluation of imaging features of appendicitis incorrectly diagnosed by CT. AJR Am J Roentgenol 2005;184:855–859.
16. Vaswani KK, Seth SK, Vitellas KM, Reader DW, et al. Normal appendix, appendicitis, and complications: CT evaluation—a practical approach and challenges for diagnostic radiologists. Radiologist 2002;9:31–45.
17. Rao PM. Technical and interpretative pitfalls of appendiceal CT imaging. AJR Am J Roentgenol 1998;171:419–425.
18. Pickhardt PJ, Levy AD, Rohrmann CA Jr, Kende AI. Primary neoplasms of the appendix: radiologic spectrum of disease with pathologic correlation. Radiographics 2003;23:645–662.