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39 Cards in this Set

  • Front
  • Back
What is the differential diagnosis of ahaustral colon?
- Ulcerative colitis
- Crohn’s disease
- Cathartic abuse (proximal to splenic flexure)
- Scleroderma
- XRT
1. What are the imaging findings in ulcerative colitis?
2. What is included in the DDX?
3. What are some extraintestinal manifestations of UC?
4. Which types of polyps can be present in pts with UC?
1. Mucosa has a granular (sandpaper like) or stippled appearance. The distribution of the disease is usually one of rectal involvement with disease affecting the more proximal colon in a continuous manner without skip areas. +/- involvement of the TI (backwash ileitis). Circumferential bowel wall symmetry is maintained. Colon may become ahaustral in chronic disease.
2. Infectious colitis
3. Erythema nodosum, pyoderma gangrenosum, PSC, cholangioCA, arthritis, sacroilitis, spondylitis, and iritis.
4.
- Pseudopolyps: occur in pts with severe acute inflammation that leads to islands of normal colonic mucosa surrounded by denuded ulcerative mucosa.
- Inflammatory polyps: regenerative mucosa on a background of denuded mucosa. Can be sessile or pedunculated.
1. What is toxic megacolon?
2. What are the imaging findings of toxic megacolon?
1. Serious complication of UC (more common) or Crohn colitis which occurs during a severe episode of acute inflammation.
2.
- Dilation (>6cm) AND adynamic ileus.
- 2/2 extension of inflammatory changes into the muscular layers and usually to the serosa of the colon.
- Submucosal edema (nodularity and polypoid changes w/n colonic wall)
- Pts are at high risk of rupture (intramural pneumatosis or pneumoperitoneum).
- DO NOT DO barium enema in these pts.
1. Where does UC start in the colon?
2. What is the healing pattern?
1. UC starts in the rectum and progresses proximally in a continuous manner.
2. Healing begins in the rectum and progresses proximally in a continuous manner. Therefore with healing, the rectum nearly always appears normal first, with variable degress of inflammation present in the more proximal colon. Also, pts using corticosteroid enemas may have normal appearing rectal mucosa with active disease in the more proximal colon.
1. What is ddx of a focal colonic stricture in a pt with UC?
2. What is the precursor of carcinoma and what is its appearance?
3. What are the features of colon carcinoma associated with UC?
1. Post-inflammatory stricture vs. annular carcinoma.
2. Mucosal dysplasia. It can appear as a solitary or multiple nodules. Most commonly, look for a close grouping of nodules.
3. Usually presents as an ANNULAR mass resulting in stricturing. Multiple cancers are common. Polypoid masses are rare.
1. What are the imaging features of chronic UC?
2. What does the presence of submucosal fat indicate?
1. Loss of normal haustral markings resulting in a diffusely shortened and often narrowed colonic lumen.
2. Fat attenuation in the wall of the colon indicates long standing disease that is inactive.
1. What is the most common location for ischemic colitis in the elderly?
2. What are the possible etiologies of ischemic colitis?
1. Splenic flexure.
2. Low flow states with superimposed chronic mesenteric ischemia, arterial emboli, or venous thrombosis.
1. What are the earliest changes of Crohn's disease as seen on DCBE?
2. What leads to aphthous ulcerations?
3. Are aphthous ulcers specific for Crohn disease?
1. Enlarged lymphoid follicles are the earliest finding of Crohn disease. However, it is normally seen in 10-15% of adults.
2. Aphthous ulcers develop from enlarged lymphoid follicles that ulcerate centrally.
3. No. They can be seen with infectious colitides, such as Yersinia and amebic colitis.
1. What is the distribution of Crohn diseae in the colon?
2. Does Crohn disease affect the retum? anus?
3. What is cobblestoning?
1. Discontinuous and asymmetric diease.
2. Spares the rectum. However, fistulas and perianal disease is characteristic.
3. Mucosal ulcerations can be longitudinal and transverse and can crisscross producing a cobblestone mucosal appearnce.
1. What are the imaging findings of diverticulitis on BE?
2. How do you differentiate intramural tracking of contrast from diverticulitis from Crohn disease?
3. How do you differentiate diverticulitis from colon cancer?
1.
- Narrowing of the colonic lumen (usually a longer segment is involved than in colon cancer)
- Thickening of the mucosal folds (from adjacent inflammation).
- Mass effect with an intact overlying mucosa (due to abscess). Note: abscesses can be intramural or within the sigmoid mesentery.
- Extravasation of contrast material into the abscess cavity. Before this occurs, there is extension of contrast from the lumen to the wall of the colon (intramural).
2. Both diseases can result in intramural tracking of contrast. However, Crohn disease will present with ulcerated, nodular mucosa whereas, the mucosa in diverticulitis is intact.
3. Diverticulitis usually causes longer segment ( > 10 cm) narrowing, more pericolonic inflammation, and no lymphadenopathy. Expect to see diverticula, infiltration of sigmoid mesocolon, and mesenteric hyperemia.
Colon carcinoma usually affects a short segment, without much pericolonic infiltration. Regional lymphadenopathy has a strong association with carcinoma, rarely seen in diverticulitis. Acute symptoms may be due to colonic obstruction with or without colitis, proximal to the obstructing mass.
1. What is the etiology of a giant sigmoid diverticulum?
2. Why is it resected?
1. Giant sigmoid diverticulum develops as a result of diverticulitis with pericolic abscess. A persistent tract forms b/w the colonic lumen and the abscess cavity. The cavity develops a fibrous well-defined capsule over time.
2. The cyst can reach gigantic proportions and cause mass effect. It can also perforate, torse, and undergo infarction.
1. What is the primary abnormality in radiation colitis?
2. What are the imaging findings of acute radiation colitis?
3. What are the imaging findings of chronic radiation colitis?
4. Why is surgery associated with high morbidity in these patients?
1. Occlusive endarteritis
2. Edema and mucosal ulceration. Bowel has a shaggy appearance with fold thickening and luminal narrowing.
3. Stricture formation usually with tapered margins.
4. Surgical treatment is difficult due to adherent loops, adhesion, poor tissues, and impaired healing.
1. What is the most commonly affected segment of colon affected by amebiasis?
2. What are the imaging findings and what can they be confused with?
3. Is the terminal ileum usually involved?
4. What are the complications?
1. Cecum, followed by sigmoid colon.
2. Look for a non-distensible and conical shaped cecum. On BE, pts may mucosal ulcerations, granular mucosa, and thickened, edematous haustra which can be confused with UC.
3. No, the terminal ileum is usually spared.
4. Ulcerations develop at site of bowel wall penetration. Hepatic abscess can develop and erode into the diaphgram resulting in pleural, pericardial, or lung infection. Penetration of an ulcer through the bowel weall can result in a pericolonic abscess, fistula, peritonitis.
1. What is the colon cut-off sign?
2. What part of the colon is most affected by pancreatitis? What can it be complicated by?
1.
- Classic radiographic findings of acute pancreatitis
- Gaseous distention of the right and transverse colon with little gas visible beyond the splenic flexure
2.
- Splenic flexure is involved with inflammatory changes b/c of its proximity to the pancreatic tail.
- COMPLICATION: Fistula formation between the pancreatic bed and splenic flexure resulting in a pancreatic abscess.
1. What are the imaging findings of scleroderma affecting the colon?
2. What is the main differential consideration?
1.
- Patchy replacement of the muscular layers of colon with collagen and elastin.
- Localized areas of narrowing seen as a result of ischemia from intimal hyperplasia.

- Sacculations (wide mouthed diverticula) arising from the antimesenteric border of the colon.
2. The main differential consideration is Crohn disease with multiple asymmetric bowel wall involvement and pseudodiverticula. The pseudodiverticula in Crohn disease affect both the mesenteric and antimesenteric border of the colon.
1. What is the most common location of epiploic appendagitis?
2. How is epiploic appendagitis differentiated from diverticulitis?
3. What is the location of mesenteric panniculitis?
4. Is omental torsion more common on the right or the left?
1. Most common part of the colon involved by acute appendagitis is the sigmoid colon.
2. Epiploic appendagitis is differentiated from diverticulitis by:
- absence of bowel wall thickening
- epicenter of the inflammatory process centered away from the colon
3. Inflammatory changes are centered in the root of the small bowel mesentery. The spectrum also includes retractile and sclerosing mesenteritis.
4. Omental torsion is more commonly seen in the right side of the abdomen.
What are imaging findings of Gardner Syndrome?
- Variant of familial polyposis with numerous extra-intestinal manifestations
- Desmoid tumors
- Osteomas in the skull, mandible, and maxilla.
What layers of the bowel are seen with endoscopic US?
1. Innermost echogenic layer respresents the mucosa.
2. Next hypoechoic layers is the muscularis mucosa.
3. Middle echogenic layers is the submucosa
4. Fourth hypoechoic layer is the muscularis propria.
5. Outer echogenic ring is the serosa.
What are the causes of pneumatosis coli?
Same underlying causes of pneumatosis intestinalis.
- Ischemic colitis is the most important condition to exclude as it requires an emergency operation to prevent perforation.
- Benign causes include corticosteroid treatment, collagen vascular disease, COPD, colonoscopy with biopsy.
1. What is pneumatosis cystoides coli?
2. Is the right or left colon more commonly affected?
3. How do you differentiate pneumatosis cystoides coli from colitis cystica profunda?
1. Intramural endothelial lined gas filled cysts seen w/n the bowel wall which do not communicate with the lumen. These gas filled cysts vary in size and can cause obstruction. They look like clusters of grapes.
2. The left side of the colon is more commonly affected than the right.
3. Colitis cystica profunda usally affects the rectum and the filling defects are not the lucency of gas.
How do you differentiate between appendicitis and an appendiceal mucocele?
APPENDICITIS:
- associated with INFLAMMATORY changes
- WALL THICKENING

APPENDICEAL MUCOCELE:
- THIN WALLED, cystic, and tubular structure with internal low density contents.
- WALL CALCIFICATIONS
- ABSENCE of inflammatory changes
1. What is the differential diagnosis of filling defect in the cecum?
2. What is a common presentation of pts with appendiceal tumors?
3. What is pseudomyxoma peritonei?
1. Prominent ileocecal valve (lipomatous hypertrophy), Appendicitis, appendiceal abscess, appendiceal mucocele, appendiceal adenoCA, lymphoma, lipoma, endometrioma.
2. Pts with appendiceal tumors may present with sx of acute appendicitis.
3. Metastatic mucinous cystadenoCA of the appendix produces large amounts of mucin that can calcify.
1. What are the differential considerations of narrowing of the sigmoid colon along its inferior border?
2. How does endometrial tissue cause colonic filing defects?
1.
- Diverticulitis and colon cancer are common.
- However when there is narrowing from the INFERIOR aspect of the sigmoid colon, look for disease arising from organs of the pelvis. In females, consider endometriosis and ovarian cancers.
2.
- Endometrial tissue is extruded from the fallopian tubes and can implant on the peritoneal surface in the pouch of Douglas or on the inferior aspect of the sigmoid colon.
- Endometrial implants invade the muscular and submucosal bowel layers stimulating local smooth muscle proliferation of the colon, secondary inflammatory changes, and variable degree of fibrosis.
1. What is the DDX of benign causes of filling defects in the colon?
1. Adenomas, lipomas, and endometriomas.
1. What is the DDX of numerous filling defects in the colon?
1. Polyposis syndrome
2. IBD with pseudopolyps and/or inflammatory polyps.
3. Crohn's disease resulting in aphthuous ulcers.
4. Diffuse lymphoma
5. Normal lymphoid pattern: seen more commonly in kids but can be seen in upto 15% of adutlts. Look for small size of filling defects that are uniformally distributed in the colon. Umbilication of the lymphoid nodules may be seen.
1. What is the etiology of post-inflammatory polyps?
2. What is filliform polyposis?
1. Post-inflammatory polyps develop during the healing phase in patients inflammatory processes such as UC and Crohn disease. The inflammation leads to a denuded mucosa. With healing, the mucosa starts to regenerate in a patchy manner simulating polyps.
2.
- Inflammatory polyps (regenerative mucosa) can be long and thin (wormlike) and may branch.
- May involve the colon diffusely or locally.
- Local collection of filliform polyps can simulate a villous adenoma.
1. What is colitis cystica profunda?
2. What is the DDX of multiple filling defects in the rectum?
1. Multiple mucin filled cyst within the mucosa and submucosa of the rectum and rarely the sigmoid colon.
2.
- Polyposis syndrome (look for polyps elsewhere in the colon)
- UC with postinflammatory polyps
- Lymphoma
1. What are the imaging findings of lymphoma affecting the colon?
2. What is a common complication of lymphoma that usually does not occur with other tumors?
3. What are the most common sites of colonic lymphoma?
1. Lymphoma may cause focal or diffuse bowel wall thickening.
LOCALIZED lymphoma may present as:
- polypoid mass (indistinguishable from a polypoid adenoCA)
- annular narrowing without obstruction
- aneurysmal dilatation.
DIFFUSE disease presents as:
- innumerable diffuse filling defects with associated haustral fold thickening.
2. PERFORATION is an important complication of lymphoma because of the LACK of the usual DESMOPLASTIC reaction that occurs with most other tumors.
3. Cecum and rectum
What is the pattern of involvement of the transverse colon in gastric and pacreatic malignancies?
- GASTRIC malignancies cause narrowing, mass effect, and tethering of the SUPERIOR aspect of the transverse colon.
- PANCREATIC malignancies usually involve the INFERIOR aspect of the transverse colon.
1. How does recurrent colorectal carcinoma present?
2. What is the recurrence rate of colon carcinoma that has undergone curative resection?
1.
- Expanding PRESACRAL soft tissue mass with indistinct margins.
- Mass/thickening at the level of the ANASTAMOSIS.
- At previous site of endoscopic removal
- DISTANT mets
2. 30-50% of pts have recurrence w/n 2 years after curative resection.
1. What are the most common causes of large bowel obstruction?
2. What are the findings in sigmoid volvulus?
3. What are the findings in cecal volvulus?
4. What finding favors obstruction over ileus?
1. Large bowel obstruction is most commonly caused by carcinoma. It can also be caused by diverticulitis, volvulus, extrinsic mass, fecal impaction, hernia, or adhesions.
2. Inverted U-shaped loop extending into the upper abdomen. If you do barium enema to confirm you will see beaking at the level of the obstruction.
3. Dilated viscus extending into the left upper quadrant. The colon distal to obstruction is decompressed.
4. Absence of gas in the rectum is suggestive of colonic obstruction rather than ileus. Perform decubitus or prone views to confirm that there is absence of air in the rectum.
1. What are the findings in adynamic ileus?
2. What is cecal ileus?
3. Why is it important to recognize this finding?
1.
- Distended air and fluid filled colon with a continuous column to the rectum.
- Sometiems the descending colon and sigmoid colon are not air-filled in ileus as a result of their dependent location.
- Radiographs with the pt in decubitus or prone positioning can be helpful in demonstrating gas filled portions of the colon.
- Often seen after surgery or with narcotic meds.
2. Cecal ileus develops in pts with a MOBILE CECUM and an underlying colonic ILEUS. The mobile cecum rotates anteromedially and gradually distends out of proportion to the remaining of the colon.
3. Excessive cecal distention longer than 2-3 days has a high risk of cecal perforation (higher than cecal volvulus and obstruction). Colonoscopic decompression may be needed until the ileus resolves.
1. What disorders are seen with pelvic floor relaxation?
2. What is rectal prolapse?
3. What is rectocele, enterocele, cystocele, peritoneocele?
4. What disorders predispose to rectal ulcerations?
1. Rectal prolapse
2. Rectal prolapse is protrusion of rectal mucosa through the anus. It starts off as rectal intussusception and when the intussusception crosses the anal sphincter, it becomes rectal prolapse.
3.
- Rectocele: abnormal bulge of the wall of the rectum into the vagina.
- Cystocele = posterior bulge of the bladder into the vagina.
- Peritoneocele = protrusion of pelvic fat into the rectovesical space.
- Enterocele = sigmoid colon, omentum, small intestines
4. Rectal ulcerations can occur with rectal prolapse and spastic pelvic floor syndrome.
1. What is the normal anorectal angle?
2. What is spastic pelvic floor syndrome?
Spastic pelvic floor syndrome involves the inability to relax the puborectalis muscle and thus the anorectal angle never straightens to allow evacuation.
What are the imaging features of cathartic colon?
- Lack of haustrations (most common in the right colon).
- Walls remain distensible whereas in UC the colon shortens and becomes less distensible due to chronic inflammation.
Infectious colitides
- Tuberculosis and amebic colitis can cause "apple core" lesions exactly like carcinoma.
- Lymphogranuloma venereum (caused by Chlamydia trachomatis) may affect the rectosigmoid colon leading to luminal narrowing, mucosal ulceration, perirectal abscess, and rectal fistula.
- Other infectious colitides, including Clostridium difficile and Campylobacter colitis, usually involve the entire colon, but may be segmental.
Ascending colonic wall thickening
Typhlitis
- Luminal narrowing and wall thickening of the cecum and ascending colon.
- 2/2 polymicrobial infiltration of the colonic wall.
- encountered only in severely neutropenic patines (leukemia, bone marrow transplant recipient).

Infectious colitis:
- could result from a variety of infectious agents (viral, bacterial, protozoan).

Cecal diverticulitis

Ischemic colitis
- rarely limited to the ascending colon, except with arterial embolization.

Pseudomembranous colitis:
usually pancolonic but can be segmental.
Large bowel dilatation
Toxic megacolon
- colon (especially transverse) loses normal transverse folds.
- surface irregularity represents ulceration, sloughed mucosa, and inflammatory pseudopolyps.
- wall may be thin or thickened.
- medical/surgical emergency as it may perforate.

Diverticulitis:
- pericolonic inflammatory changes on CECT would also be seen in diverticulitis.

Colonic ileus and Ogilvie syndrome
-disproportionate dilation of colon, especially in the cecum to transverse colon, without obstruction.
- The usual preceding causes are trauma, major surgical procedures, or metabolic or neurologic disorders. Even in the absence of obstruction, the colon must be decompressed to avoid the complication of ischemia due to mucosal ischemia, resulting from the luminal distention. Rectal tube placement and pharmacologic interventions, such as neostigmine, often result in decompression. Correction of the underlying metabolic abnormality, if present, is also essential.

Colon carcinoma
- look for obstructing colonic lesion.

Cecal volvulus
Incorrect: In cecal volvulus, the ascending colon twists on mesentery and becomes obstructed, dilated, and displaced toward the left upper quadrant.
1. What is colonic urticaria?
1. Reticular mucosal pattern in a markedly dilated colonic segment (almost looks like mottled gas density from fecal material).
- 2/2 mucosal/submucosal edema.
- represent mild ischemia of the affected segment and can progress to frank ulceration and perforation.