Colon and Appendix

The aganglionic segment is usually located in the upper rectum or rectosigmoid junction, with the proximal large bowel becoming grossly dilated over many years of partial obstruction. The diagnosis is usually best made by contrast enema studies (Fig. 5-2), even in the neonate, but definitive diagnosis requires rectal biopsy. The stricture is usually identified at contrast enema in the rectosigmoid regions with variable colonic distention proximal to the stricture. The aganglionic segment may not appear as an abrupt transition but rather as an irregular serrated or “sawtooth” appearance, which is characteristic of the disease (Fig. 5-3). Some patients develop an associated colitis, termed “Hirschsprung-associated enterocolitis,” that is characterized by foul-smelling diarrhea. These patients are at risk of perforation because of acute colitis, but subacute forms exist, and contrast enema studies may show the characteristic rectal sawtooth finding.

Ultrasound (US) sometimes shows a hypoechoic cystic mass with a thick wall, which has an echogenic outer layer and hypoechoic inner layer. On BE the cyst produces a mass effect of adjacent bowel and on CT appears as a nonenhancing mass, compressing or displacing the adjacent bowel, which may contain simple fluid, hemorrhage, or proteinaceous fluid (Fig. 5-4). On MRI the enteric cysts are usually hyperintense on T2-weighted imaging, reflecting their cystic nature (Fig. 5-5). Because many duplication cysts contain ectopic gastric mucosa, a Tc-99m pertechnetate radionuclide study can often show radionuclide uptake, which can also be observed within a Meckel diverticulum for the same reason.

The colonic mucosal disease always starts in the rectum and extends proximally to a variable degree, sometimes affecting the whole colon (pancolitis) and sometimes even a short segment of ileum, so-called backwash ileitis. The extent of colonic involvement typically directs the symptoms and seriousness of the disease. Some patients have only one short episode confined to the rectum, and others have recurring disease, sometimes with a life-threatening toxic megacolon. This usually necessitates aggressive medical or surgical therapy, often requiring an emergency total colectomy as the diffusely involved colonic mucosa becomes so thickened, friable, and distended that perforation is imminent.

The imaging features depend on the stage of the disease (Table 5-2), and many of these features are shared by Crohn disease (Table 5-3). They can sometimes be identified by plain abdominal radiography as thickened haustra, particularly when caused by a pancolitis (Fig. 5-5). Severe disease can almost certainly be recognized on plain radiography as can toxic megacolon, with marked colonic distention resulting from ileus (Fig. 5-6) and wall and mucosal thickening (Fig. 5-7). The wall thickening is sometimes referred to as “thumb-printing” because of the polypoid soft tissue nature of the mucosal edema and thickening. BE demonstrates typical features but has largely been replaced by optical colonoscopy for diagnosis. When BE is performed, the features depend on the severity and acuity of disease. In acute disease a variable length of colon (starting in the rectum) shows a granular mucosal pattern representing edema and ulcer formation, sometimes of the whole colon (Fig. 5-8), which may also affect the last few centimeters of the terminal ileum (“backwash ileitis”) (Fig. 5-9). “Collar-button ulcer” formation has been described, which represents acute ulceration of the colon with submucosal extension (Fig. 5-10), with further ulceration prevented by the relatively impermeable bowel wall. This sign is three times as common in UC as in Crohn disease. Pseudopolyp formation, which can also be recognized in Crohn disease, can occur with more chronic disease and represents areas of reparative mucosa between areas of ulceration (Fig. 5-11). As the disease progresses, the affected length of colon becomes featureless and shortened, termed “lead piping” (Fig. 5-12).

The presence and extent of disease are more readily evaluated by CT than by contrast enema, whose features also mirror the clinical disease. These include bowel wall thickening and luminal narrowing with a variable amount of pericolonic edema and mesenteric vascular hyperemia (Fig. 5-13). The degree of inflammation may be reflected by ¹⁸F-fluorodeoxyglucose (FDG) uptake at PET imaging (Fig. 5-13). Mural stratification or double-halo sign, which is common with an acute presentation, is a nonspecific sign for inflammatory bowel disease representing hyperemic mucosa and serosa with intervening submucosal edema (Fig. 5-14). If the acute disease worsens, the mucosa becomes progressively thickened and inflamed (Fig. 5-15), which can ultimately lead to a toxic megacolon, whose CT features include a distended colon with profusely thickened mucosal tissue, sometimes referred to as an “accordion pattern” (see Fig. 5-52).

More chronic features of the disease at CT are similar to those observed at BE with colonic shortening and luminal fibrotic narrowing. However, CT may identify widening of the presacral fat space and a characteristic “fat halo” sign consisting of inner mucosal and outer muscularis enhancement with a nonenhancing middle submucosal ring. This ring is composed of increased submucosal fat deposition (Fig. 5-16). There may be mesenteric adenopathy, but this is less common in UC than in Crohn disease. Stricture formation may be seen but is also less common than in Crohn disease (Figs. 5-12 and 5-17).

In addition to perforation from toxic megacolon, the greatest risk to patients with chronic UC is the late development of adenocarcinoma of the colon, for which they have an increased risk of 5% to 30% over the general population (Fig. 5-18). The risk increases by 10% for each decade of disease. Patients with more extensive disease may therefore undergo prophylactic colectomy.

As in the small bowel, transmural inflammation and thickening of the bowel wall occur during the acute phase with pericolonic inflammatory change, which can be almost impossible to distinguish from other forms of acute colitis, especially if a large segment of colon is involved. Repetitive inflammatory disease causes deep ulceration with localized perforation and abscess formation or fistulization with adjacent small bowel. Because these repetitive bouts of acute disease heal, luminal narrowing and stricture formation often occur. Perianal disease with fistula and abscess formation is common in Crohn disease.

The imaging features are similar to those described in the small bowel, although the imaging of colonic Crohn disease can, at times, mimic those of UC. However, there are a number of distinguishing features that help to differentiate the two diseases (Table 5-3). Plain radiography may demonstrate mucosal thickening (Fig. 5-19) or toxic megacolon. Contrast enema studies (usually barium) may demonstrate involvement of the whole colon (which is therefore difficult to distinguish from UC), but this is uncommon. More commonly a variable segment of the colon is affected (Fig. 5-20, A), and the disease may or may not involve the rectum. Acute disease at CT may present with mural stratification similar to that in the small bowel, representing mucosal and serosal hyperemia with submucosal inflammation or simple mural thickening and mesenteric edema (Fig. 5-20, B). Aphthous ulceration is characteristic of Crohn disease (Fig. 5-21). As in the small bowel, the mucosa in active disease enhances avidly after the administration of IV gadolinium. Although CT is easier and faster to perform, many patients with Crohn disease are young and may require repetitive assessment of the extent of their disease, so avoiding the radiation dose from multiple CT images is preferable. Therefore MRI is often advised, and newer MR enterographic techniques, particularly of the small bowel, have proved highly effective for evaluating the extent of disease (Fig. 5-22). Furthermore, the extent of perianal disease is best imaged with MRI, which can outline the relationship of inflammatory disease to the internal and external anal sphincters; this is important to determine whether surgical repair is needed.

Other differentiating features of UC include a propensity for Crohn disease to fistulize with the small bowel, with adjacent organs, or to the skin. This can be assessed by CT (Fig. 5-23), BE (Figs. 5-24 and 5-25), or MRI (Fig. 5-26). Abscess formation is also recognized in Crohn disease rather than UC (Fig. 5-27). An increased risk of small and large bowel malignancies, predominantly adenocarcinomas, is associated with Crohn disease (Fig. 5-28).

Typhlitis is readily identified at CT by circumferential cecal wall thickening, sometimes marked, that is thought to be caused by a combination of infection, hemorrhage, and ischemia. Bowel wall enhancement in common with other colitides is present, and there is often pericolonic inflammatory change (fat-stranding). Typhlitis may affect a variable length of the ascending colon, and the adjacent terminal ileum or appendix may be affected (Fig. 5-33).

Most disease is segmental in the colonic “watershed” areas, with the splenic flexure (i.e., arterial vascular transition between the superior mesenteric and inferior mesenteric arteries) and rectosigmoid region (i.e., junction between the inferior mesenteric and hypogastric arteries) most at risk. More extensive disease is, however, well recognized, particularly if the superior mesenteric artery is also affected and a pancolitis ensues, which is difficult to differentiate from other colitides.

Plain radiography may demonstrate an ileus, sometimes confined to the left colon. As the disease progresses, bowel wall thickening develops (Fig. 5-34) with a toxic megacolon if severe (Fig. 5-35). BE is now rarely performed, but results demonstrate thickened folds and ulceration, either linear or with mucosal sloughing. Healing can lead to stricture formation (Fig. 5-36). The findings are now usually made by CT and are similar to other forms of colitis (inflammatory bowel disease, infectious colitides, and radiation colitis if the radiation field included the colon). The disease is suggested in the appropriate clinical setting and by the left-sided distribution of the colonic changes (Fig. 5-37). Severely affected patients show colonic pneumatosis as the gas permeates the damaged mucosa, which can then enter the mesenteric venous system and be recognized as mesenteric venous gas (particularly at CT) and ultimately intrahepatic portal venous gas. Occasionally, ischemia occurs proximal to an obstructing colonic stricture, such as colonic adenocarcinoma. The obstruction causes marked distention of the proximal colon, compromising its vascular supply or directly invading mesenteric vasculature (Fig. 5-38).

The findings are most often visualized by CT, particularly because patients are often serially imaged to evaluate for any local cancer recurrence or metastatic disease, although MRI often detects more subtle changes (Fig. 5-40). Associated inflammatory changes are often observed in the surrounding mesentery (fat-stranding). This is commonly seen in the presacral region after radiation for rectal cancer preceding attempted surgical removal of the tumor. Radiation changes can sometimes be difficult to differentiate from local recurrence, but awareness that the patient has undergone radiation should alert the radiologist that the changes are benign rather than malignant recurrence. Increasingly, PET imaging is used to differentiate postradiation changes from recurrent disease (Fig. 5-41).

The imaging findings may lag behind the clinical features, and patients may have pronounced clinical disease without obvious imaging findings. When observed, the imaging features are similar to most other colitides. Plain radiography often demonstrates ileus and, as the disease progresses, nodular haustral thickening, often over a long segment because the disease usually presents as a pancolitis. There may be polypoid mucosal thickening representing the pseudomembranes, but this is not often observed (Fig. 5-45). The disease can progress readily to frank toxic megacolon. However, it is optimally evaluated by CT, which demonstrates bowel wall thickening, mucosal enhancement, often with a mural stratification (or target sign representing unenhanced thickened submucosa surrounded by enhancing mucosa and muscularis propria), pericolonic edema, and mild ascites. The bowel wall thickening is often pronounced, more so than in other colitides, with the thickened haustra giving the appearance of an accordion pattern (also found with CMV colitis) over a relatively long segment of bowel (Fig. 5-52), representing oral contrast material trapped between the bulbous-thickened haustra.

Mycobacterium avium intracellulare (MAI) infection is an atypical mycobacterial infection most commonly seen in patients in the latter stages of acquired immunodeficiency syndrome (AIDS). It can also be a multisystem disease, often producing multiple enlarged hypoattenuating nodes in the abdomen and retroperitoneum. MAI can be difficult to distinguish from the more common forms of TB but should be strongly considered in a patient with AIDS.

TB most commonly affects the ileocecal region when involving the GI tract. In the acute phase, there is an edematous thick-walled inflammatory mass of the terminal ileum and cecum, which can be identified at BE or CT imaging (Fig. 5-54). Because TB is a chronic disease, there may be fibrotic changes with contraction and distortion of colonic mucosa and wall, producing focal right-sided colonic strictures (Fig. 5-55). The fibrotic process may cause a fixed, distorted, or narrowed cecum, a so-called coned cecum (Fig. 5-56; Table 5-4). CT usually demonstrates associated regional adenopathy.

In the bowel, Actinomyces usually occurs in the appendix or cecum, although any part of the GI tract may be affected. Acute disease leads to ulceration and multiple small and larger abscess formation, which can be recognized by CT (Fig. 5-51). As the disease progresses, numerous small sinus tracts can develop, and the healing process with the granulation tissue can cause stricture formation.

The imaging features are not specific to amebiasis and include mucosal thickening, sometimes severe with “thumb-printing” (Fig. 5-57). The disease may progress to toxic megacolon. Unless amebiasis is considered, the disease may be mistakenly diagnosed as IBD, which has a very different treatment regimen. The diagnosis is readily made by identifying stool cysts or by antibody detection at serological testing. Amebomas are recognized at CT as heterogeneous masses, either single or multiple, and are one of the recognized causes of a “coned” cecum, in which the cecum takes on the shape of an inverted cone because of circumferential diffuse inflammation. Other causes of a coned cecum are listed in Table 5-4.

A coned cecum refers to a conical cecal shape that results from the inflammatory and fibrotic response to a number of limited right lower quadrant diseases (Table 5-4). The most common cause worldwide is TB (Figs. 5-56 and 5-61) and in the West is Crohn disease (Fig. 5-62). Occasionally, neoplastic infiltration of the cecum produces a coned cecum (Fig. 5-63).

Toxic megacolon is a progression beyond simple thumb-printing and is a serious clinical finding, potentially fatal if not treated urgently and appropriately. The diagnosis is usually straightforward when x-ray or CT demonstrates gross colonic distention (often >9 cm), particularly of the transverse colon, which is the most anterior colonic structure in the supine position and readily distends with the nondependent colonic gas. The haustra are markedly thickened and nodular (and some even slough off) and are better appreciated on CT, particularly on “lung window” contrast settings (Fig. 5-64).

At imaging, diverticula are readily identified by either contrast enema technique (Fig. 5-65) as numerous gas- or contrast-filled outpouches from the normal colonic wall. With CT the diverticula are easy to identify (Fig. 5-66). There is no pericolonic edema in simple diverticulosis. Mucosal hypertrophy and a focally thickened colonic wall are often present (Fig. 5-66). Sometimes the diverticula are isolated and few in number and can be difficult to differentiate from small mucosal polyps at BE, especially if viewed end on. Polyps and diverticula, however, can be differentiated using the “bowler hat” sign at BE. With polyps, the apex of the bowler hat points into the lumen if viewed en face (i.e., sideways) (Fig. 5-67), whereas if the apex points outward from the colonic wall, it represents a diverticulum (Fig. 5-68). If viewed end on, polyps and diverticula can be almost impossible to differentiate from one another. Here the outer margin with a barium ring can help because a sharper outer barium margin suggests a diverticulum, whereas a less well-defined border suggests a polyp. Furthermore, when barium pools in the colon, polyps are less dense within the pool (negative shadow), and they do not show fluid levels when the patient is upright, as do diverticula. Very large diverticula are termed “giant diverticula.” They are uncommon, but characteristic on plain radiography or CT (Fig. 5-69).

Although simple diverticula are of little significance for the majority of patients, some may develop diverticulitis in a mode similar to the development of appendicitis in the appendix. A stool pellet becomes impacted in a diverticulum and sets up a local inflammatory reaction and often a microperforation. The resulting inflammatory changes lead to colonic spasm with luminal narrowing, wall thickening, and pericolonic edema (stranding) (Figs. 5-70 and 5-71). These findings can be subtle and confined to one diverticulum or multiple (Fig. 5-72). The inflammatory reaction may cause a larger local perforation, which can be identified at BE by contrast tracking outside the colonic lumen, often in a linear “tram-track” fashion (Fig. 5-73). The perforation, however, is preferably imaged by CT and visualized as a linear gas pocket or fluid collection outside the colonic wall, representing an abscess, which can be either small or large, depending on the degree of perforation (Fig. 5-74). More distant effects may include mesenteric and portal venous gas and hepatic abscess formation after seeding via the mesenteric venous system (Fig. 5-75). Larger abscesses generally do not respond to antibiotic treatment alone, and percutaneous image-guided catheter placement is often required.

Hemorrhage is relatively common with diverticulitis because of mural inflammation and vascular erosion with consequent rectal bleeding, which at times can be profuse, requiring emergency surgery to prevent further profound blood loss. This occurs more frequently with the less commonly observed right-sided diverticula (Fig. 5-76). Severe diverticulitis can cause such an inflammatory reaction that fistulas with adjacent bowel, bladder, or vagina can form. This can be observed with BE (Fig. 5-77), but because of the risk of peritoneal barium leakage (although slight) and the greater ease of CT imaging, it is better evaluated by CT (Fig. 5-78). Giant diverticula are also at risk of diverticulitis (Fig. 5-79) and its complications (hemorrhage, abscess, and fistula formation).

On occasion, an attack of diverticulitis can mask an underlying adenocarcinoma (Fig. 5-80), and the radiologist should always consider the possibility of underlying colon cancer in the presence of diverticulitis. Features that suggest an underlying malignancy include a short segmental mass, shouldering (abrupt cutoff of colonic wall thickening), a large mass, pericolonic soft tissue extension of the mass, and regional lymphadenopathy. In practice, it can be very difficult to differentiate between the two (Figs. 5-71 and 5-80), and the radiologist should have a relatively low threshold for recommending repeat imaging after antibiotic treatment or follow-up endoscopy.

Because of the well-recognized risk that polyps will transform into adenocarcinoma, colonic screening with fecal occult blood after the age of 40 years and colonoscopy after the age of 50 years are recommended to reduce the incidence of colorectal cancers in the general population. Computed tomographic colonoscopy (CTC) has performed well in clinical trials compared with optical colonoscopy, although the latter is performed far more often. However, substantial numbers of the population are still not screened, and it is hoped that CTC might increase the number of patients who undergo colonic screening to prevent the development of larger polyps and malignant degeneration. Once a polyp is discovered by CTC, the patient is referred for optical colonoscopy and polyp removal.

The primary imaging investigation for colonic abnormalities was formerly DCBE but has now been largely superseded by optical colonoscopy. However, the imaging features are well described. Good colonic preparation and fluoroscopic technique are critical to reduce the number of false-positive findings, primarily because of stool residue. This requires good distention at DCBE and multiple views to evaluate the whole colonic wall. Polyps are recognized as filling defects, and the larger they are, the better they are appreciated. As with any contrast fluoroscopic technique, once an abnormality is detected, it is vital to take spot views in multiple planes to maximize the radiologist’s ability to classify the lesion. All features of the polyps can be identified, from sessile to pedunculated. Tubular adenomatous polyps usually have a smooth surface with or without polypoid features and are pedunculated (i.e., arise from a stalk). This stalk can be hard to identify unless orthogonal views are obtained, which will increase the chance of its detection. The stalk can be short (Fig. 5-83) or long (Fig. 5-84). When the tubular stalk is seen end-on, a characteristic “Mexican hat” sign is noted, representing the outer ring of the polyp and the inner ring of the stalk (Fig. 5-85). Most tubular polyps are not identified with conventional CT but can be with CTC (Fig. 5-86).

Sessile polyps are typically radiolucent when visualized on the dependent wall but when on a nondependent wall may demonstrate a barium-coated barium ring. A “bowler hat” sign, representing the base and tip of the polyp, may be seen when the polyp is viewed en face or side on (Fig. 5-66). Most sessile polyps larger than 5 mm can be detected with CTC (Fig. 5-87).

Villous polyps are almost always sessile and are usually multilobulated (frond or cauliflower like) on DCBE (Fig. 5-88) or CTC (Fig. 5-89). They can be carpet like where they “coat” the mucosal lining (Fig. 5-90). Tubulovillous polyps are a combination of tubular and villous adenomas and so have a stalk of variable length and a villous frond-like tip. Adenomatous polyps are occasionally detected by CT or MRI (Fig. 5-91), but most are not unless they are large enough (Fig. 5-92) or unless FDG avidity (some adenomas are hypermetabolic) points the radiologist to what was otherwise thought to be normal bowel (Fig. 5-93).

Patients with familial adenomatous polyposis (FAP) usually undergo prophylactic colectomy because of the sheer number of colonic polyps, all of which are at risk of malignant transformation. The polyps are readily identifiable by BE, CTC, and OC and may even be found with conventional CT (Fig. 5-94). Detection of malignant transformation can be harder because of the overwhelming number of polyps, which may easily obscure early malignant colon cancer, although larger lesions should be detected (Fig. 5-95).

Gardner syndrome is now considered a variant of FAP because there are numerous colonic adenomatous polyps, but not as many as are observed in FAP. They are more commonly identified in the stomach (unlike those of FAP). The disease is also associated with desmoid tumors, osteomas, epidermoid and sebaceous cysts, fibromas, and thyroid cancer. With imaging, Gardner adenomatous polyps generally cannot be distinguished from those of FAP, except perhaps that they are usually fewer in number (Fig. 5-96).

Other polyposis syndromes can produce hamartomatous colonic polyps, but they are far more common in the small bowel and only very rarely cause colonic polyps (see Chapter 4).

Most tumors (95%) are adenocarcinomas (approximately 5% of tumors are squamous cell), usually mucinous, and develop secondary to the adenoma-carcinoma sequence. All adenomas, whether acquired or congenital, are at risk for the development of adenocarcinoma. Other predisposing factors include IBD (both Crohn disease and UC). There is an increased risk in patients with hamartomatous syndromes (but not because of the hamartoma itself) and rarely in cystic fibrosis. Metachronous and synchronous adenocarcinomas are well recognized. The cumulative risk for metachronous disease (presentation of another tumor at a later date) is approximately 0.3% to 0.5% per year. Risk of synchronous disease (the presence of a second primary adenocarcinoma at the initial primary diagnosis) is approximately 5% (Fig. 5-102).

Squamous cell carcinoma, while representing the minority of colorectal tumors, are mostly found in the rectum. Predisposing factors include HIV and HPV infection and a rare form of rectal cancer arising from the remnant of the cloacal membrane at the anorectal junction. These tumors are usually aggressive and have metastasized at the time of presentation.

The location of the tumor usually dictates patient presentation. Tumors arising from the right side of the colon are more insidious, perhaps because the colon is wider and therefore tumors less often cause obstructive symptoms. This premise does not hold for cecal tumors that involve the ileocecal valve, which can cause early small bowel obstruction (Figs. 5-63 and 5-103). Patients may present with pain, but it is more likely that the tumor will bleed intermittently, often asymptomatically, and that the patients ultimately present with the symptoms of anemia rather than the direct local effects of the tumor. Left-sided colon tumors, in contrast, present more commonly with symptoms of obstruction because luminal narrowing is more prevalent (Fig. 5-104). Occasionally tumors are so indolent that the patient presents with a very large mass that has not yet declared itself with bleeding or obstruction.

Lesions in the rectosigmoid region commonly present with rectal bleeding (often bright red) and a change in bowel habit. They therefore tend to present earlier and consequently are associated with better survival statistics. Rarely tumors from any location in the colon can present because of perforation and peritonitis or abscess formation (Fig. 5-105). A very occasional tumor can present with intussusception, with a predominantly intraluminal mass acting as the lead point (Fig. 5-106).

The majority of colorectal cancers are now detected by optical colonoscopy, and patients are then referred for a screening metastatic CT. Less commonly, cancer might first be detected by CT if it is performed for symptoms associated with the disease (abdominal pain, weight loss, anemia, change in bowel habit) or as an incidental finding when CT is performed for other reasons. Small tumors (<2 cm) are often missed on CT because they are easily mistaken for normal stool. Masses at the ileocecal valve may be missed because the valve often has a mass-like appearance, particularly if the cecum is decompressed. A clue that a malignant mass is present at the ileocecal valve is the degree of soft tissue thickening of the cecal wall (Fig. 5-111). Multiplanar imaging can be helpful in these circumstances. Other tumors will be detected with CT based on their size (Fig. 5-112). Sometimes a CT “apple-core” equivalent can be identified (Figs. 5-104 and 5-113). Tumors may present with a more inflammatory-type mass that can be difficult to differentiate from diverticulitis (Fig. 5-114). In the diagnosis of simple diverticulitis by CT imaging, it is critical to consider any underlying carcinoma as the cause. Signs that suggest an underlying malignancy include the degree of wall thickness and regional adenopathy (Fig. 5-71). More sinister features include extension of the tumor beyond the cecal wall, with edematous changes (fat-stranding) in the surrounding mesentery or retroperitoneum or local metastatic deposits and regional lymphadenopathy (Fig. 5-112). Sometimes the tumor may perforate, usually locally, with a walled-off abscess (Fig. 5-105) or fistulize with adjacent viscera (Fig. 5-115). Ideally, however, these tumors should be detected before they have metastasized either locally or distant. Given that colorectal cancer is relatively common and early detection is critical, radiologists should evaluate the colon and rectum carefully on every CT image to exclude subtle early tumors.

Experience with CTC is sufficiently widespread that all the features identified on conventional cross-sectional CT can now be observed (Fig. 5-116). However, the main role of CTC is screening, ideally to detect adenomatous polyps before they degenerate into malignant lesions. Therefore large tumors are identified only uncommonly.

PET and PET/CT are used primarily for staging and monitoring of metastatic disease, but primary colorectal tumors, if large enough, should also be visualized (Fig. 5-117). Small tumors may not be identified, either because FDG uptake is insufficient to be visible at PET or because the normal bowel can also have some FDG activity. Determination of what constitutes normal versus abnormal uptake is also aided by PET/CT fusion software, whereby the PET uptake findings can be correlated with the anatomical CT findings. Extracolonic spread of the tumor, including spread to regional nodes or distant metastatic disease, can also be identified with PET imaging. Some adenomatous polyps are also strongly FDG avid but cannot be identified with CT alone because they are small or obscured by feces (Fig. 5-93).

Preoperative staging is increasingly being performed using MRI, particularly using an endorectal coil, which has shown benefit in determining the TNM staging of rectal adenocarcinoma. It is important preoperatively to determine whether the disease extends into the mesorectal fascia because chemoradiation treatment may be required before the surgeon contemplates total mesorectal excision. The normal rectal submucosa has a T2 intermediate signal and hypointense serosa (Fig. 5-118). With T2 invasion, the brighter submucosa is replaced by tumor that is hypointense (Fig. 5-119). Further progression to T3 obliterates the distinction between the muscularis and serosa and extends into the perirectal fascia (Fig. 5-120). Differentiation between T2 and T3 disease can be difficult (Fig. 5-121).

The imaging findings are usually straightforward, with fecal impaction, sometimes severe, noted on plain radiography (Fig. 5-139). Fecal impaction also is commonly identified at CT.

Pneumatosis cystoides coli is to be distinguished from the more common secondary forms of pneumatosis intestinalis resulting from chronic obstructive airway disease and necrotic conditions of the bowel wall, which affect the small bowel much more often than the large bowel. Any inflammatory large bowel disease can result in colonic pneumatosis once the mucosa has been breached. On plain radiography and CT, the gas is more linear or curvilinear (Fig. 5-142) than the gas cysts seen in pneumatosis cystoides coli (Fig. 5-143), and gas is often identified in the mesenteric venous system or liver or both (Fig. 5-144).

Most rectal perforation with BE rectal tubes is confined below the peritoneal reflection, so diffuse peritonitis is unlikely. Colonic perforation caused by overdistention with gas, whether iatrogenic or obstructive, is most likely to occur in the cecum because this region distends the most with equal pressure applied throughout the colon (Laplace’s^∗ law).

Other colonic trauma may result from self-induced trauma caused by objects inserted into the rectum, which can perforate and lead to either local abscess formation or more diffuse peritonitis if the peritoneal reflection is perforated.

MR imaging of the anal sphincter is best performed with an endorectal coil to provide better spatial resolution, but diagnostic images can be obtained with a body coil. Defecography or evacuation proctography can be used to evaluate functional abnormalities of defecation by visualizing the pelvic floor descent after the insertion of either barium paste at fluoroscopy or gel at MRI. In the former test, using video fluoroscopy, the patient is analyzed while seated upright during the process of defecation. Spot views show anatomical pelvic floor descent, but diseases are usually diagnosed by review of the fluoroscopic video. The examination has three stages: preevacuation, evacuation, and postevacuation. A line joining the posterior pubic bone margin to the lower coccyx (pubococcygeal line) defines the lower border of the pelvic floor in the healthy individual.

A rectocele is an anterior bulge of the rectal wall during evacuation (Fig. 5-148). Rectal prolapse may be internal or external. Internal prolapse is confined to the rectum and anal canal and is really a mucosal or full-thickness intrarectal intussusception. An external prolapse occurs when the rectal prolapse is visible externally beyond the anal canal. Small bowel prolapse (enterocele) occurs when the small bowel enters the rectogenital space, usually at the end of the examination from the increased intraabdominal pressure induced by the defecation process. A cystocele occurs when the bladder base descends below the inferior border of the pubic symphysis. Therefore defecography is sometimes preceded by voiding cystourethrogram to evaluate for any concomitant bladder disease.

Pelvic floor descent is defined as descent of the entire pelvic floor below the pubococcygeal line and is defined at the resting anorectal junction as greater than 3.0 cm below the ischial tuberosities or anorectal descent greater than 3.5 cm during evacuation (Fig. 5-148).

Pelvic floor descent is also observed using rapid sequence T2-weighted MRI obtained predominantly in the sagittal plane (Fig. 5-149). The pubococcygeal line (Fig. 5–149A) is used to define the pelvic floor, which extends from the inferior border of the pubic symphysis to the last joint of the coccyx. At rest, the anorectal junction normally lies at or just above this plane. Pelvic organ descent below this line generally indicates pelvic floor descent, and if it is greater than 2 cm, the patient may benefit from corrective surgery. Other lines may be drawn, including the H line (representing the anteroposterior width of the levator hiatus) from the interior pubic symphysis to the posterior rectal wall at the level of the anorectal junction and the M line (vertical descent of levator hiatus), which represents a perpendicular line drawn from the pubococcygeal line to the posterior margin on the H line. These lines are sometimes useful to confirm pelvic floor laxity. Imaging can also demonstrate levator ani abnormalities, which contribute to pelvic floor descent (Fig. 5-150).