Ulcerative and Granulomatous Colitis: Idiopathic Inflammatory Bowel Disease

Plain Abdominal Radiographs

Considerable information can be gained by carefully scrutinizing the abdominal radiographs of patients with ulcerative colitis. Although attention should be focused on the colon, other abnormalities, such as renal calculi, sacroiliitis, ankylosing spondylitis, and avascular necrosis of the femoral heads, must also be excluded.

Although the extent of ulcerative colitis is generally determined by barium enema and colonoscopy, these procedures carry a higher risk in severely ill patients. The following radiographic features can be used to assess the severity and extent of the colitis: (1) the extent of formed fecal residue; (2) the appearance of the mucosal edge; (3) alterations of the haustra; (4) colonic width; and (5) mural thickness.

Granular Pattern

The earliest pathologic changes of ulcerative colitis are hyperemia and the accumulation of inflammatory cells in the mucosa. ^, These changes are manifested by a loss of normal mucosal translucency and obscuration of the submucosal pattern on endoscopy. Subtle thickening of the mucosa or haustral edema may be present radiographically, but these findings are often appreciated only in retrospect. With progressive edema and hyperemia, the mucosa develops a granular pattern ( Fig. 41.2A ). The smooth, sharp, and distinct appearance of the colonic margin seen on normal double-contrast studies is replaced by an amorphous, thickened, and indistinct mucosal line. There is a gradual transition between the normal and abnormal mucosa that extends for several centimeters. This granularity should be distinguished from the granular appearance of chronic ulcerative colitis ( Fig. 41.2B ). In chronic ulcerative colitis, the mucosal surface pattern is coarser, and there are significant changes in colonic contour.

The granular pattern develops as a result of abnormalities in the quality and quantity of mucus produced by the involved mucosa. On histologic examination, there is a reduction in the number of goblet cells, which contain less than the normal complement of mucin. ^{, , ,} Normal mucus is essential to normal barium coating of the gut. Any process, whether benign or malignant, infectious or inflammatory, that alters mucin production affects mucosal coating and visualization.

Mucosal Stippling

During the granular phase of ulcerative colitis, inflammatory cells accumulate at the base of the mucosal crypts. ^{, ,} Cellular debris tends to block the crypts of Lieberkühn, which leads to the formation of microabscesses, better known as crypt abscesses. These crypt abscesses eventually erode into the lumen. ^, The ulcers deepen, and barium flecks become adherent to them, producing mucosal stippling ( Fig. 41.3 ). This stippling resembles white paint applied by dabbing a surface with the end of a fairly dry paintbrush.

“Collar Button” Ulcers

With disease progression, the ulcers of the crypt abscess breach the lamina propria and muscularis mucosae and cause undermining of the less resistant areolar tissue of the submucosa. The involved submucosa becomes necrotic, and the ulcers extend laterally, causing further undermining. This undermining is contained by the muscularis propria on the serosal side and by the muscularis mucosae on the luminal side of the colon. ^, The ulcers are frequently related to the taeniae. The mucosal defect is small relative to the degree of undermining and produces a flasklike, so-called collar button ulcer ( Fig. 41.4 ). As these ulcers enlarge and interconnect, the collar button ulcer configuration is lost; a network of residual islands of mucosa and inflammatory pseudopolyps is produced.

Polyps

A variety of different mucosal protrusions may be seen on barium studies in patients with IBD. ^, Their appearance and significance depend on the stage of disease and pathologic origin.

Inflammatory Pseudopolyps

In patients with severe ulcerative colitis, there is extensive mucosal and submucosal ulceration in which only small islands of mucosa and submucosa may survive. The inflamed edematous mucosa protrudes above the surrounding areas of ulceration, which gives a polypoid appearance ( Fig. 41.5 ). Because these represent merely the remnants of preexisting mucosa and submucosa rather than new growths, they are termed pseudopolyps. Inflammatory pseudopolyps are the natural progression of collar button ulcers: the ulcers extend and interconnect so that the pseudopolyp rather than the ulcers becomes the major radiographic finding. Inflammatory pseudopolyps usually occur in ulcerative colitis but may also be seen in Crohn’s disease. The cobblestoning pattern seen in Crohn’s disease is another type of pseudopolyp, in which larger islands of preserved mucosa are surrounded by linear and transverse ulcerations.

Postinflammatory Pseudopolyps

When IBD goes into remission, the denuded mucosa heals and is covered by granulation tissue that has a granular appearance similar to that observed in the early stages of ulcerative colitis. ^{, , ,} In some patients, the regenerated mucosa has a tendency to overgrow ( Fig. 41.6 ). This overgrowth often results in polypoid lesions that may be small and rounded, long and filiform, or proliferate into a bushlike structure simulating a villous adenoma. Because the regenerating mucosa is cytologically normal, it is not a true neoplasm but a pseudopolyp. Because this occurs during mucosal healing, it is termed a postinflammatory pseudopolyp . These polyps represent the aftermath of a severe attack of colitis and may be the only sign of previous disease. Mucosal bridges are also postinflammatory pseudopolyps, in which a bridge of mucosa survives between islands of mucosa surrounded by ulceration. With remission, the underside of the mucosal bridge and underlying ulcer reepithelialize. ^,

Postinflammatory pseudopolyps can also be seen after ischemia, after severe infection, and in Crohn’s disease. Filiform polyps have also been described in the esophagus, stomach, and small bowel in patients with Crohn’s disease.

Backwash Ileitis

In 10% to 40% of patients with chronic ulcerative pancolitis, the distal 5 to 25 cm of ileum is inflamed ( Fig. 41.7 ). This ileitis occurs only in the presence of pancolitis and usually resolves 1 to 2 weeks after colectomy. ^, Although small ulcerations may be present, this is not a primary inflammation of the ileum. The distal ileum can be used to form an ileostomy or pouch. The pathogenesis of this disorder is uncertain but may relate to the reflux of colonic contents into the small bowel, hence the term reflux or backwash ileitis.

Barium studies reveal a chronic pancolitis associated with a patulous and fixed ileocecal valve that easily refluxes and persistent dilation of the terminal ileum. The normal fold pattern is absent, and the mucosa is granular.

Blunting and Lost Haustra

In the course of ulcerative colitis, the haustral folds undergo two major changes: (1) early in the disease, they are edematous and thickened; (2) with chronic disease, they become blunted or may be completely lost. ^, This evolution of haustral changes can be understood by a brief review of haustral formation.

At birth, colonic haustra are usually absent, which explains why it is difficult to differentiate colonic from small bowel gas in neonates. As the colon grows, the circular muscle of the muscularis propria outgrows the longitudinal muscle, the taeniae coli. This differential growth rate causes the taeniae to shorten the colon in an accordion-like fashion, with production of saccular haustra that usually are first seen by the age of 3 years.

Haustra are fixed anatomic landmarks in the proximal colon because the circular muscle is fused to the taeniae. In the distal colon, haustra are created by active contraction of the taeniae. Consequently, the colon can normally be devoid of haustra distal to the midtransverse colon; loss of haustra in the proximal colon is always abnormal. ^,

In early ulcerative colitis, the haustra are deformed and thickened because of edema and may produce a corrugate outline to the colon, which has been called the indenture sign. ^, In chronic ulcerative colitis, the haustra are often lost for two reasons, alterations in the muscle tone of the taeniae ^, and the fact that the colon is shortened. In this disease, the taeniae coli become relaxed for some unknown reason. This relaxation is associated with abolition of the haustral pattern. With healing, the haustra may reappear as they gain tone. A second major factor is also at work in chronic ulcerative colitis—massive hypertrophy and fixed contraction of the muscularis mucosae, which causes foreshortening of the colon. Thus, the normal accordion-like array of colon on the relatively shorter taeniae is lost.