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    Ezekiel T. Arteta

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    PLAIN FILM

    Detects colonic obstruction, colonic ileus, and the toxic megacolonsyndrome in IBD

    SINGLE CONTRAST

    Demonstrates anatomy and tonus (contraction) of colon, along with mostabnormalities

    DOUBLE CONTRAST

    Allows visualization of lumen with any polyps or lesions

    CT

    Determines the presence and extent of extracolonic disease

    UTZ

    Rarely used because of intraluminal gas

    Imaging

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    Anatomy

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    Function

    Formation, transport, and evacuation of feces

    Water absorption by the right colon

    Physiology

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    Filling Defect radiolucency in a barium pool caused by a protruding mass lesion.

    May be caused by polyps, tumors, air bubbles, feces, mucus, or foreign objects.

    Polyp

    Protrusions from the mucosa

    Does not imply a histologic diagnosis

    Colon Filling Defects/ Mass Lesions

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    Most common malignancy of the GI tract

    Location:

    Rectum and Rectosigmoid area (50%)

    Sigmoid Colon (25%)

    Most developed from preexisting adenomasMost are annular constricting lesions, with raised everted edges andulcerated mucosa.

    Spreads through

    Colorectal Adenocarcinoma

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    Colorectal Adenocarcinoma

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    Spreads through: Direct Invasion into pericolonic fat and adjacent organs

    Lymphatic Invasion to regional nodes

    Hematogenous Invasion through the portal veins to the liver and the systemic

    circulation

    Most common complication is obstruction

    Colorectal Adenocarcinoma

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    Risk factors: Ulcerative colitis

    Crohns disease

    Familial Adenomatous Polyposis

    Peutz-Jeghers syndrome

    Clinical Features

    Peak age 50-70 years

    Weight loss

    Blood in stool

    Loss of appetite

    Change in bowel habits

    Colorectal Adenocarcinoma

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    Imaging Methods Transrectal or Colononoscopic US: Local disease staging

    CT and MR: For more advanced disease and to detect recurrence

    CT is the method of choice for tumor recurrence because it can survey the whole

    abdominal cavity

    Colorectal Adenocarcinoma

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    Cross-Sectional Findings

    Polypoid Primary Tumor (usually >1 cm)

    Apple-core lesions

    Cystic, necrotic, and hemorrhagic areas within the tumor mass

    Linear soft tissue stranding into the pericolonic fat

    Enlarged regional lymph nodes

    Distant metastases, especially in the liver

    Thickening of the wall of the uninvolved colon proximal to the tumor

    Colorectal Adenocarcinoma

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    Annular Adenocarcinoma(Single Contrast Study)

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    Localized mass that projects from the mucosa into the lumen.

    Presence is a major indication for barium studies of the colon

    Rules of Thumb:

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    Hyperplastic polyps Nonneoplastic; round and sessile, nearly all are smaller than 5

    mm

    Adenomatous polyps Distinctly premalignant; major risk for developing

    adenocarcinoma

    Neoplasms with a core of connective tissue

    Hamartomatous polyps (juvenile polyps) common cause of rectal bleeding in children

    Inflammatory polyps

    usually multiple; associated with inflammatory bowel disease

    Polyps

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    Polyp

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    Bowler Hat Sign

    Polyp

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    Polyp

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    2/3 inherited, 1/3 spontaneous

    Autosomal dominant

    Tubulovillous adenomas that becomes prominent at age 20

    Colorectal cancer will eventually develop in nearly all patients

    Tx: total colectomy with rectal mucosectomy and ileoanal pouchconstruction

    Familial Adenomatous PolyposisSyndrome

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    Familial Adenomatous PolyposisSyndrome

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    Less commonly involved than the stomach or small bowel Anal and rectal lymphoma= frequent in AIDS patients

    Morphology

    Multinodular (lymphomatous polyposis)

    Solitary (resemble a polypoid carcinoma)

    Lymphoma

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    Rectal Lymphoma

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    Most common submucosal tumor of the colon

    Most frequent in the cecum and ascending colon

    Nearly 40% present with intussusception

    Appearance:

    Barium: smooth, well-defined, elliptic filling defect, usually 1 to 3 cm in diameter

    CT: fat-density tumor (definitive)

    Lipoma

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    Ulcerative Colitis

    Crohns Disease

    Infectious Colitis

    Toxic Megacolon

    Pseudomembranous Colitis

    Amoebiasis

    Colon Inflammatory Diseases

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    Idiopathic inflammatory disease involving primarily the mucosa andsubmucosa of the colon

    Peak age: 20 to 40 years, onset after age 50 is common.

    Superficial ulcerations, edema, and hyperemia

    Granular mucosa, confluent shallow ulcerations, symmetry of diseasearound the lumen, and continuous confluent diffuse involvement.

    Ulcerative Colitis

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    Radiographic Hallmarks:

    Granular mucosa

    Confluent shallow ulcerations

    Symmetry of disease around the lumen

    Continuous confluent diffuse involvement

    Morphology:

    Collar button ulcers: deeper ulcerations of thickened edematous mucosa with crypt abscesses

    extending in the submucosa

    Coarse granular pattern by replacement of diffusely ulcerated mucosa with granulation tissue

    Ulcerative Colitis

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    Collar Button Ulcers

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    Late Changes:

    Pseudopolyps= mucosal remnants in areas of extensive ulceration

    Inflammatory polyps= small islands of inflamed mucosa

    Postinflammatory polyps= mucosal tags that are seen in quiescent phases of the disease

    Filiform polyps= postinflammatory polyps with a wormlike appearance

    Hyperplastic polyps= may during healing after mucosal injury

    Ulcerative Colitis

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    CT Findings Halo sign: low-density submucosal edema with wall thickening

    Narrowing of the lumen of the colon

    Pseudopolyps

    Pneumatosis coli with megacolon

    Complications:

    Strictures

    colorectal adenocarcinoma

    Ulcerative Colitis

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    Complications: Strictures

    Colorectal adenocarcinoma

    Toxic megacolon

    Massive hemorrhage

    Ulcerative Colitis

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    Strictures

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    Lead Pipe Sign

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    Involves the colon in two thirds of cases

    Isolated to the colon in approximately one third of all cases

    Hallmarks:

    Early aphthous ulcers

    Later confluent deep ulcerations

    Predominant right colon disease

    Discontinuous, asymmetric involvement

    Strictures, fistulas, and sinus formation

    Crohns Disease

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    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 casesConfluent 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

    Ulcerative Colitis vs. Crohns Disease

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    Etiologic Agents:

    Bacteria (Salmonella, Shigella, E. coli)

    Parasites

    Viruses (CMV, Herpes)

    Fungi (Histoplasmosis, Mucormycosis)

    Most cause a pancolitis with edema and inflammatory wall thickening withinfiltration of pericolonic fat

    Pericolonic fluid and intraperitoneal fluid may be present.

    Infectious Colitis

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    CMV Colitis

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    Potentially fatal

    Marked colonic distension and risk of perforation

    Complication of fulminant colitis

    Radiographic Findings:

    Marked dilatation of the colon (transverse colon >6 cm) with absence of haustral markings

    Edema and thickening of the colon wall

    Pneumatosis coli

    Evidence of perforation

    Barium studies must be avoided

    Toxic Megacolon

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    Inflammatory disease characterized by the presence of a pseudomembraneof necrotic debris and overgrowth ofClostridium difficile

    Radiographic Findings:

    Dilated colon

    Nodular thickening of the haustra

    Ascites

    Pseudomembranous Colitis

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    CT findings:

    marked wall thickening up to 30 mm (average 15 mm) with halo or target appearance

    characteristic stripes of intraluminal contrast media trapped between nodular areas of wall

    thickening (accordion sign)

    Mild pericolonic fat inflammation disproportionate with the marked colonic wall inflammation

    ascites

    Pseudomembranous Colitis

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    Pseudomembranous Colitis

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    Infection by the protozoan parasite Entamoeba histolytica

    Barium studies demonstrate a disease that closely mimics Crohn colitis

    Primary areas: cecum and rectum (terminal ileum is characteristically notinvolved)

    Amoebiasis

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    Diverticulosis

    Diverticulitis

    Diverticular Diseases

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    Acquired condition

    Mucosa and muscularis mucosae herniate through the muscularis propria ofthe colon wall, producing a saccular outpouching

    False diverticula

    Common with age over 75 years oldMajor risk factor: low-residue diet

    Most common site: sigmoid colon

    Diverticulosis

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    Severely affected portions of bowel are usually shortened in length, resulting incrowding of the thickened circular muscle bundles.

    Diverticulosis without diverticulitis is a cause of painless colonic bleeding

    Radiographical Findings:

    gas-filled sacs parallel to the lumen of the colon Barium studies show diverticula as barium or gas-filled sacs outside the colon lumen

    Diverticulosis

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    CT Findings Thickened colon wall and distorted luminal contour

    diverticula are shown as well-defined gas-, fluid-, or contrastfilled sacs outside the

    lumen

    Diverticulosis

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    Diverticulosis

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    inflammation of diverticula, usually with perforation and intramural orlocalized pericolic abscess

    Complications:

    Bowel obstruction

    Bleeding

    Peritonitis

    Sinus tract and fistula formation

    Diverticulitis

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    inflammation of diverticula, usually with perforation and intramural orlocalized pericolic abscess

    Complications:

    Bowel obstruction

    Bleeding

    Peritonitis

    Sinus tract and fistula formation

    Diverticulitis

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    Barium Studies deformed diverticular sacs

    demonstration of abscess

    extravasation of barium outside the colon lumen

    CT Findings

    localized wall thickening

    inflammation of pericolonic fat

    pericolonic abscess

    diverticula at or near the site of inflammation

    Diverticulitis

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    Diverticulitis

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    Filling of the appendix is attained most reliably by single-contrast bariumenema examination

    Failure to fill the appendix with barium on barium enema examination is notdefinitive evidence of appendiceal disease.

    Both CT and US have proven extremely useful in the diagnosis of

    appendiceal disease, especially acute appendicitis

    Appendix

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    arises from the posteromedial aspect of the cecum at the junction of the taeniacoli, approximately 1 to 2 cm below the ileocecal valve.

    blind-ended tube that is 5 to 10 mm in diameter (on barium studies) andapproximately 8 cm in length, although it may be up to 30 cm long.

    mucosa is heavily infiltrated with lymphoid tissueOn CT and US, the normal appendix appears as a thin-walled tube less than 6 mmin diameter

    Anatomy

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    Anatomy (CT Scan)

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    most common cause of acute abdomenresults from obstruction of the appendiceal lumen

    Bacterial infection causes gangrene and perforation with abscess

    Most periappendiceal abscesses are walled off, but free perforation and

    pneumoperitoneum occasionally occur

    Acute Appendicitis

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    Plain films will demonstrate an appendiceal calculus (appendicolith orfecalith) in approximately 14% of patients

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