Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

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include edema, erythema, and an abnormal vascular pattern (78). The diagnosis rests on histopathologic findings.

images, and enhanced slightly after gadolinium (79); the authors postulated that intracytoplasmic siderocalcific inclusions accounted for the CT and MRI findings.

Diversion Colitis

After surgical bowel diversion and formation of an excluded segment, some patients develop inflammatory changes in the diverted bowel. These consist of aphthae, crypt abscesses, and easy friability. Large ulcerations develop in an occasional patient.

Malacoplakia

Colonic malacoplakia is rare, occurring both in isolation and in association with other diseases. Although not a neoplasm, malacoplakia is locally aggressive and invades surrounding tissues. At times it is multifocal. Kidney transplant patients, in particular, appear prone to develop colorectal malacoplakia; in some, malacoplakia appears related to immunosuppression therapy. It has developed in a colon adenoma, although more often it is associated with a carcinoma, where malacoplakia is located adjacent to the tumor.

Rare clinical manifestations of malacoplakia include massive hemorrhage and cecal perforation.

Imaging usually suggests a malignancy. Some develop multiple polyps. Malacoplakia in one patient was hyperdense on unenhanced CT, hypointense both on T1and T2-weighted MR

Other Colitides

A barium enema should be diagnostic of colitis cystica profunda. If large enough, the fluid-filled cysts are also visible with CT or endorectal US (if the rectum is involved).

Occasional reports describe a hot-water enema or some chemical inducing colitis (Fig. 5.14).

Xanthogranulomatous inflammation of the sigmoid colon has led to colonic obstruction.

Kawasaki disease (mucocutaneous lymph node syndrome) in a child can present with fever and focal colitis.

Neonatal Necrotizing Enterocolitis

Clinical

A disease more common in premature neonates, necrotizing enterocolitis (NEC) typically starts with bloody diarrhea or distention several days after birth. Although a number of factors have been postulated, epidemic outbreaks in newborn nurseries implicate an infectious role. The final common pathway is probably ischemia with subsequent mucosal or more severe damage. A condition similar to neonatal NEC occasionally develops in older infants. Many

have had prior major surgery, and underlying ischemia appears to be a factor.

Necrotizing enterocolitis carries a high mortality, averaging 50% in some centers, with mortality varying inversely with gestational age and birth weight. Extensive bowel resection may result in a short gut syndrome.

Imaging

Any part of the bowel can be involved, although the most common sites are distal small bowel and proximal colon. Involvement ranges from diffuse to segmental. Among neonates undergoing surgery, about a third have NEC totalis (80). Strictures,usually colonic,and more often in the left colon, develop as a late complication.

Conventional radiography early in the course of NEC reveals small bowel dilation, then colonic distention. In some neonates focal regions of bowel lumen narrowing and wall thickening are evident, nonspecific findings. Eventually pneumatosis intestinalis and portal venous gas develop in some, findings almost pathognomonic for NEC in neonates (it is a gas and not air as some of the literature claims). Although in adults portal venous gas carries a grave connotation, in these neonates such gas represents a more benign finding. Complicating the picture, some babies even with severe NEC do not develop pneumatosis or portal venous gas. Ascites is usually a sign of severe NEC, a finding difficult to detect with conventional radiography but readily apparent with US. Although these findings are useful as a guide, they are insensitive in predicting impending perforation.

In neonates with NEC and portal venous gas, venous gas developed within 24 hours of onset of abdominal distention, feeding intolerance, or a finding of rectal blood (80); pneumatosis intestinalis was identified in 80%, and 20% progressed to perforation. Venous gas initially was transient but recurred in some of these neonates.

Urine CT attenuation is increased after enteral iohexol in neonates with NEC; in normal neonates urine CT attenuation is slightly above water. A serial increase in urine CT attenuation coefficients after oral ingestion of iohexol is associated with clinical deterioration (81).

Complications of NEC include perforation, often early in the course. Serial conventional

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horizontal-beam radiographs are necessary to detect a subtle perforation. Perforation, or impending perforation, is an indication for surgery.

A contrast enema is usually not performed during the acute episode because of a perceived increased risk of perforation. Most strictures are detected with a barium enema later, after the acute insult has resolved. An occasional sequela is an enteroenteric or enterocolic fistula.

If an ileostomy or colostomy is necessary, study of the distal colon is worthwhile prior to ostomy takedown to ensure that no residual strictures exist.

Ischemic Colitis

Clinical

Bowel ischemia and various vasculitides are discussed in more detail in Chapter 17. Isolated colonic ischemia is relatively common, especially in the elderly, and its clinical and imaging manifestations are sufficiently discrete to warrant separate discussion. Colon ischemia is often included under the colitides. Especially when chronic in nature, ischemic colitis and some of the vasculitides tend to mimic inflammatory bowel disease. Some of the conditions associated with colonic ischemia are listed in Table 5.3.

A typical clinical presentation is sudden onset of abdominal pain, distention, and bloody maroon-colored diarrhea. Atypical presentations are relatively common; in a study of patients with eventually proven ischemic colitis, ischemia was initially not suspected clinically in 30% (82). Underlying atherosclerosis, shock, and congestive heart failure are common but not universal findings in these often elderly patients. Sequelae range from a mild, selflimiting condition to major bowel infarction and death.

Most common sites for colonic ischemia are at the splenic flexure and sigmoid.At the splenic flexure a branch of the middle colic artery forms an anastomosis with an ascending branch of the inferior mesenteric artery, feeding the marginal artery of Drummond. This marginal artery is present in less than half the population; the tenuous splenic flexure blood supply only becomes worse with onset of arteriosclerotic disease.

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Table 5.3. Conditions associated with ischemic colitis

Arteriosclerotic vascular disease Venous thrombosis

Low flow states (hypotension, stasis) Emboli

Atherosclerotic emboli Cholesterol emboli

Vasculitides

Behçet’s syndrome Cocaine-use colitis Polycythemia in a smoker

Polycythemia vera and extensive extramedullary hematopoiesis

Takayasu’s arteritis

Thromboangiitis obliterans (Bürger’s disease) Systemic lupus erythematosus

Polyarteritis nodosa Dermatomyositis

Allergic granulomatous vasculitis (Churg-Strauss syndrome)

Other

Associated with oral contraceptives Massive caustic ingestion

A late complication of hemolytic-uremic syndrome Familial dysautonomia (Riley-Day syndrome) During a-interferon therapy

Isolated rectosigmoid ischemia is uncommon, presumably because of collateral blood supply. Occasionally sigmoid colectomy leads to rectal infarction; presumably the superior rectal arteries, which are sacrificed at resection, provide major rectal blood flow.

Colonic infarction in one patient led to transient gastric emphysema (83).

Ischemia after hemorrhagic shock is more common in the small bowel than colon. In the large bowel, the right colon is most often involved, even to the point of ischemic necrosis. Resection in some of these patients reveals no vascular thrombi or emboli, and nonocclusive ischemia is presumably responsible.

A type of ischemic colitis warranting separate mention is that occurring proximal to a colonic obstruction. Also called obstructive colitis, it is similar to inflammatory bowel disease. Ischemia in this condition is due to an impaired venous blood flow secondary to a combination of increased endoluminal pressure, underlying atherosclerotic disease that otherwise would be asymptomatic, and other possible factors. The

prevalence is about 1% to 5%, mostly in elderly patients. The most common cause of associated obstruction is a carcinoma, less often a benign stricture or diverticulitis; the ischemic segment appears thickened, ulcerated, or even necrotic. At times pneumatosis is evident. Untreated, perforation ensues.

Imaging

The role of imaging during an acute ischemic attack is to confirm that a patient’s symptoms are indeed due to colon ischemia rather than to another etiology. Angiography has a lesser role in detecting colon ischemia than in the past. Often identified is atheromatous disease involving major vessels.

Imaging findings during the acute phase consist of bowel wall thickening, seen as thumbprinting, and ulcerations, eventually clearing or evolving into strictures or frank necrosis. An ischemic segment tends to have sharp margins, in distinction to most acute infective colitides, which have poorly defined margins. Computed tomography readily identifies colonic wall thickening; pericolonic stranding is common but is nonspecific. Occasionally seen is a “halo” sign, consisting of an inner hypodense ring surrounded by a hyperdense outer ring, a nonspecific sign also found in some other colitides.

Computed tomography reveals the involved colonic wall to range from a heterogeneous appearance suggesting edema in about two thirds and homogeneous thickening in one third, with occasional intramural gas; wall thickening and segmental involvement are common.

Isolated cecal ischemia or infarction is rare. Clinically, appendicitis is suspected but CT should differentiate these two entities.

Doppler US aids in differentiating between inflammation and ischemia of thickened bowel wall. The absence of color Doppler flow and absence of arterial signal suggests ischemia; in fact, the absence of arterial flow in the wall of an ischemic colon predicts an unfavorable outcome (84).

In-111–labeled leukocyte imaging detects bowel activity in ischemic colitis. Normally In111 activity is not identified in bowel.A primary purpose of Tc-99m-HMPAO leukocyte scan is to detect inflammation rather ischemia, but in an

occasional patient, this scan reveals marked uptake within an ischemic sigmoid colon.

Conventional radiography in three patients revealed vascular calcifications close to the right hemicolon, a barium enema showed thumbprinting and right colic lumen narrowing, and CT detected colon wall thickening and venous calcifications (85); the authors termed this condition phlebosclerotic colitis.

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Amyloidosis

Amyloidosis ranges from localized to diffuse involvement. When localized, amyloidosis often mimics a benign stricture, rarely, a carcinoma (87). It does not predispose to cancer formation; a finding of localized amyloidosis and a coexistent carcinoma is probably fortuitous. Colonic amyloidosis does ulcerate and bleed; presumably blood vessel wall infiltration by amyloid leads to ischemia and ulceration.

Radiation Proctocolitis

Radiation proctocolitis is a disabling, often delayed manifestation of radiation injury and results in an obliterative endarteritis and ischemia. Because of its proximity to gynecologic structures, the rectum is a common site of involvement. These patients range from asymptomatic to having chronic bleeding, obstruction due to strictures, or fistulas. Bleeding typically develops months after completion of radiation therapy. Before ascribing rectal bleeding to proctitis, however, other causes of gastrointestinal bleeding should be excluded in these patients.

Computed tomography findings following radiation therapy vary. Detected are perirectal fascia thickening, increased perirectal fat density, and, less often, rectal wall swelling. Presacral space widening develops in a minority, increasing with dose. These changes develop soon after start of therapy.

Endorectal US shows thickening of perirectal connective tissue and obliteration of the rectal submucosal echogenic layer along the anterior rectal wall (86).

Magnetic resonance imaging identifies radiation fibrosis as irregular enhancement and high signal intensity, often even years later.

Clinically significant bleeding from radiationinduced proctitis has been managed successfully using a combination of endoscopic yttrium-aluminum-garnet (YAG) laser therapy and application of topical formalin dressings to the rectal mucosa.

The risk for future neoplasms with chronic radiation proctocolitis, even decades after pelvic radiation, is well known to most physicians. Both flat (nonpolypoid) adenomas and rectal carcinomas develop. Imaging is not reliable in detecting small neoplasms in the presence of radiation changes.

Epiploic Appendagitis

Appendices epiploicae are mostly fat-containing structures arising from colonic serosal surface. They exist throughout the colon. Normally they are not detected with imaging except if surrounded by fluid.

The sudden onset of localized acute abdominal pain is a common presentation for torsion (infarction) of an epiploic appendix. These patients are afebrile, and laboratory findings are normal. Depending on the location, clinically and with imaging the condition mimics acute appendicitis or diverticulitis. Although epiploic appendagitis is a nonsurgical cause of an acute abdomen, it is not uncommon for the diagnosis to be made by either the surgeon or pathologist. Untreated, spontaneous resolution in a week or so is the usual outcome.

Most often epiploic appendagitis occurs in either the ascending or descending portions of the colon and tends to be located anteriorly rather than posterior in the bowel wall circumference (Fig. 5.15). A CT finding of a focal inflammatory tumor or edema adjacent to the colon, especially at sites uncommon for diverticulitis, should suggest this condition. A fat density or almost fat density tumor is a common but not universal finding. Computed tomography in six patients identified a fatty tumor containing a hyperdense rim along the anterolateral colonic wall, together with infiltration of adjacent pericolic fat (88).

Ultrasonography often reveals a small, solid, focal noncompressible hyperechoic tumor at the site of maximum tenderness.

Computed tomography and US findings are strongly suggestive of the diagnosis. Similar findings are seen with segmental omental infarction, although usually these are in a dif-

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Figure 5.15. Epiploic appendagitis. A barium enema reveals focal extravasation (arrow). The appearance is atypical for diverticulitis.

ferent location. In either case, therapy is similar and surgery is avoided if the condition is suspected.

Follow-up CT shows resolution of inflammation, and although a lesion may still be identified, it should be decreasing in size (88). An occasional infarcted epiploic appendage eventually calcifies; some become detached and float within the peritoneal cavity. One such peritoneal loose body measured 6cm in diameter (89). The differential diagnosis of calcified peritoneal loose bodies includes gallstones lost during surgery and, unless their mobility is confirmed by imaging with different patient positioning, a calcified leiomyoma or similar tumor.

Tumors

A polyp is an intraluminal growth. It can be benign or malignant, neoplastic, inflammatory, or hyperplastic. It is a descriptive term having a specific morphologic meaning and does not imply a particular histologic connotation. The practice of some authors in using this term synonymously for an adenoma only leads to confusion and should be condemned.

Among colonic polyps <5mm in diameter, in adults, about 40% to 50% are adenomatous, 40% hyperplastic, and the rest a mix of mucosal tags, lymphoid tissue, and other benign causes. About half are located in the rectosigmoid. In children juvenile polyps predominate. In adults, the percent of adenomatous and carcinomatous polyps increases with an increase in polyp size.

Nonneoplastic Tumors

Hyperplastic Polyps

Small hyperplastic polyps (also called metaplastic polyps) are the most common nonneoplastic lesion in the colon and rectum. They tend to be sessile, often are multiple, generally <5mm in diameter, and most commonly in the rectosigmoid.

A relationship between hyperplastic polyps and the subsequent development of adenomas is controversial. Both share similar lifestyle risk factors. Most colonic hyperplastic polyps are not considered to have a neoplastic potential and are not directly involved in the adenomacarcinoma cycle, but some larger hyperplastic polyps do develop dysplasia and progress to a cancer. An occasional patient with multiple hyperplastic colonic polyps harbors a colon adenocarcinoma. In addition, follow-up of patients who had hyperplastic polyps suggests that they are more likely to develop adenomas than those without initial polyps (90). An occasional hereditary nonpolyposis colorectal cancer family patient develops colorectal cancers, adenomas, and hyperplastic polyps.

The radiologic and endoscopic appearance of adenomas and hyperplastic polyps <5mm in diameter is similar. A central umbilication tends to develop with further growth. Some of these small umbilicated tumors, at times called inverted hyperplastic polyps by pathologists, are difficult to detect even with a double-contrast barium enema and mimic the appearance of a flat adenoma and adenocarcinoma (91), and thus excision is warranted.

Rare instances of hyperplastic polyposis have been reported. These polyps tend to be larger than isolated ones and the overall appearance mimics multiple adenomatous polyps. Complicating the picture is the occasional patient with hyperplastic polyposis but with some of the polyps containing foci of adenomatous tissue or even an adenocarcinoma.

18F-fluoro-deoxy-D-glucose PET is negative for hyperplastic polyps; FDG does not accumulate in these polyps.

Juvenile Polyp

This polyp is known as a retention polyp, and it consists of inflammatory tissue, fibrosis, and a cystic component. No consensus exists about

whether it is inflammatory or hamartomatous in origin. It is the most common colonic polyp in the pediatric age group, although some are first detected in adults. It is more common in the distal colon and rectum, and most are solitary. A juvenile polyposis syndrome is rare.

Juvenile polyps are not believed to be premalignant; polypectomy of a solitary juvenile polyp does not predispose to future new juvenile polyps and is not associated with a future increased risk of colorectal cancer. Nevertheless, occasional reports describe both an adenoma and an adenocarcinoma associated with juvenile polyps.

Especially in children, a not uncommon presentation is hematochezia. An occasional juvenile polyp intussuscepts.

The polyps’ barium enema appearance is similar to that of an adenomatous polyp. Most have a smooth and oval outline. Compression gray-scale US shows them to be hypoechoic, contain small cysts and have an adjacent hyperechoic layer corresponding to the submucosa (92); their color Doppler findings range from hypoto hypervascular.

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Figure 5.16. Inflammatory fibrous polyp (arrows and arrowheads) in a man with rectal bleeding. Initially a carcinoma was suspected.

These tumors tend to invade and require resection with wide margins.

Inflammatory Fibroid Polyp

Inflammatory fibroid polyps are uncommon in the colon. Some are found in a setting of inflammatory bowel disease or chronic infections. Most manifest through rectal bleeding. Biopsy simply reveals inflammation.

Similar to an inflammatory pseudotumor, their appearance on a barium enema or colonoscopy suggests a malignancy. They range from a sessile, plaque-like, to a pedunculated polyp in appearance (Fig. 5.16).

Inflammatory Pseudotumor (Fibrosarcoma)

An occasional resected polyp or infiltrating tumor is termed an inflammatory pseudotumor (variously called inflammatory fibrosarcoma or plasma cell granuloma). These tumors are discussed in more detail in Chapter 14. They originate either in the colon or adjacent soft tissues, including presacral space. Their aggressive nature often suggests a malignancy.

Hamartoma

Retrorectal hamartomas consist of soft tissue and cysts lined by ciliated epithelium. Also called tail-gut syndrome, they are detected due to their mass-like effect, and occasionally one becomes infected.

Hemangioma

Colon hemangiomas range in size from small, focal submucosal lesions to large, diffuse, infiltrating tumors involving long colonic segments. Most manifest through chronic bleeding and anemia. Even when large, lumen obstruction is rare with a hemangioma (Fig. 5.17).

The full extent of a large hemangioma is evaluated by contrast-enhanced CT or MRI. Rectal cavernous hemangiomas and their surrounding structures are best evaluated by MRI using an endorectal surface coil. These often diffuse rectosigmoid cavernous hemangiomas produce colonic wall thickening and a hyperintense signal on T2-weighted MR images.

Occasionally a hemangioma is detected with a Tc-99m–red blood cell scan.