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Inflammatory bowel disease imaging Dr Karam Manzalawi
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Inflammatory bowel disease (IBD)  is a chronic idiopathic disease affecting the gastrointestinal (GI) tract.  Crohn’s disease (CD) and ulcerative colitis (UC).  ? an exaggerated and inappropriate immune response to gut luminal microbes.  peak age of onset between 15-30 years of age .  up to 20% of people with IBD are diagnosed during childhood.
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Classification  Crohn's disease and ulcerative colitis (UC).  other forms of IBD  Microscopic colitis subdivided into collagenous colitis and lymphocytic colitis  Diversion colitis  Behçet's disease  Indeterminate colitis
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IBD clinical manifestations and treatment strategies  Symptoms of IBD often wax and wane, defining periods of “flare” and “remission”, respectively.  Clinical manifestations of UC include diarrhea, with or without blood, abdominal pain, tenesmus, and fecal Urgency.  manifestations of CD are more variable depending on the extent and location of the GI inflammation. CD with predominantly colonic involvement often presents in similar fashion to UC  whereas in small bowel CD, diarrhea and rectal bleeding are seen less frequently and symptoms such as fever,fatigue and weight loss are common.
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Extraintestinal manifestations  Extraintestinal manifestations, such as arthritis/arthralgias, skin and ocular involvement and hepatobiliary conditions like primary sclerosing cholangitis, occur in more than 1/3 of IBD patients  Linear growth attenuation and pubertal delay are common among children with IBD. Up to 30% of children with CD.  Laboratory abnormalities such as anemia, hypoalbuminemia and elevation in erythrocyte sedimentation rate and C-reactive protein (CRP) can be supportive but are not specific for IBD and are normal in up to 50% of IBD patients at the time of diagnosis
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 The diagnosis of IBD =clinical features +findings on endoscopy and histopathology.  There is no medical cure for CD or UC, but medical therapy is effective in many cases, both at reducing symptoms and at reducing intestinal inflammation.  The classes of medications most commonly used to treat IBD include corticosteroids, antibiotics, anti-inflammatory agents (5-aminosalicylates), immunomodulators (6-mercaptopurine, azathioprine and methotrexate) and newer biologic therapies.
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Surgery  Surgery in IBD is typically reserved for medically refractory cases.  In UC, total colectomy with ileal pouch-anal anastomosis is often performed for medically refractory cases or for patients with IBD-associated dysplasia or colorectal cancer but is associated with complications including pouchitis and pouch malfunction/dysfunction.  Intestinal resections in CD are also frequently performed in medically refractory cases but disease recurrence is common if not nearly universal.
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treatment  While treatment goals in practice have traditionally focused on an improvement in clinical symptoms, this improvement alone may not predict underlying disease activity. In CD in particular, the discrepancy between clinical symptoms and active inflammation can potentially lead to unnecessary treatments for patients whose symptoms are not due to active inflammation and to asymptomatic progression of disease and disease-related complications in patients who are without clinical symptoms despite active inflammation.  This discordance has led to a search for additional targets that can be used in combination with clinical symptoms to help guide treatment decisions.
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 Candidate targets include CRP, fecal calprotectin, intestinal appearance on cross-sectional imaging modalities like CT enterography (CTE) and MRE, and mucosal healing based on endoscopic findings, which is becoming a preferred objective measure of disease activity as it correlates well with improved clinical outcomes
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Current role of imaging in IBD evaluation  (1) at the time of initial diagnosis to distinguish UC from CD;  (2) to assess and track progression of extraintestinal IBD manifestations;  (3) to visualize penetrating complications of disease that extend outside the bowel wall;  (4) to assess disease activity in patients with known IBD during symptomatic recurrence,
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Crohn disease vs ulcerative colitis
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bowel involved  CD: small bowel 70-80%, only 15-20% have only colonic involvement  UC: rectal involvement 95%, with terminal ileum only involved in pancolitis (backwash ileitis)
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Distribution  CD: skip lesions typical.  UC: continuous disease from rectum up.
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Gender  CD: no gender preference  UC: male predilection
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colonic wall  fat halo sign seen in 61% of chronic UC cases, but only in 8% of CD  bowel wall is thicker in CD than in UC (when colon involved)  serosal surface smooth in UC (95%), irregular in CD (80%)
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perianal involvement  UC: although rectal involvement is very common, perianal complications are not as frequently seen  CD: common, seen in 82% of patients  stranding of ischiorectal fossa/perirectal fat (73%)  fistulas/sinus tracts (22%)
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mesenteric creeping fat  CD: common in chronic cases.  UC: not seen, as small bowel not involved.
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abscess formation  CD: common, eventually seen in 15-20% of patients  UC: uncommon
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extraintestinal complications  gallstones: seen in 30-50% of CD patients  primary sclerosing cholangitis: more common in UC  hepatic abscess: seen in CD  pancreatitis: more common in CD
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Crohn disease" regional enteritis"  Epidemiology  Clinical presentation
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Radiographic features  The characteristic of Crohn disease is the presence of skip lesions and presence of discrete ulcers
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ULTRASOUND limited role, it has been evaluated as an initial screening tool Typically examination is limited to the small bowel and wall thickness assessed: Bowel wall thickness should be <3 mm, normally thickness < 3 mm helps exclude the disease in a low risk patient. thickness > 4 mm helps establish the diagnosis in a high risk patient. Ultrasound in the assessment of extraintestinal manifestations.
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features on ultrasound:  non-compressible, rigid, fixed bowel wall  perienteric fluid  creeping fat - echogenic area (representing proliferation of adipose tissue that extends around active inflammation) separating bowel loops  gut signature - lost or preserved  strictures - fibrotic (maintains gut signature) or inflammatory (loss of gut signature)  abscess  fistula
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US image - stricture in a patient with active Crohn's disease
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Advanced Intestinal Mucosal Manifestations of Crohn’s Disease  coarsened and granular appearance of the mucosa  nodular thickening of the valvulae conniventes.  Aphthous mucosal lesions  dilution and/or flocculation of the intraluminal contrast column.
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 Aphthous lesions. 34-year-old woman with diarrhea.  Double contrast barium enema demonstrates diffuse aphthae throughout the colon ( arrowheads ) manifesting as shallow erosions surrounded by a zone of edema
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Advanced Intestinal Mucosal Manifestations of Crohn’s Disease  the ulcers take on a linear conformation, typically only 1–2 mm wide and extending up to 15 cm in length. (along the mesenteric margin)  because it maintains its pliability, the antimesenteric side may appear sacculated when compared to the contracted and rigid mesenteric side
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 Crohn’s disease of the duodenum, with sacculations. 30-year-old woman with diarrhea.  Upper GI study demonstrates  a diffusely diseased duodenum with areas of focal dilation ( arrows ) consistent with sacculations.  Additionally, there are several ulcers ( arrowheads ) and discontinuous segments offocal narrowing
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 deep longitudinal, oblique, and transverse linear ulcers intersect  islands of edematous mucosa, commonly referred to as “pseudopolyps,” may mimic the appearance of nodules protruding beyond the mucosal surface
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 Pseudopolyps should be distinguished from true inflammatory polyps, which occur when focal inflammatory cellular infiltrate and edema cause the involved mucosa to project above the level of the neighboring mucosa.  On contrast fluoroscopy, inflammatory polyps will appear as multiple small, rounded luminal filling defects
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 The coexistence of regional mucosal denudation and pseudopolyps gives rise to the characteristic “cobblestone” appearance of advanced Crohn’s disease.  cobblestoning appears as large and irregular regions of mucosal ulceration with interspersed pseudopolyps of variable size and shape. The involved segment of bowel may demonstrate reduced pliability and luminal narrowing
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 Crohn’s ileitis with cobblestone confi guration.  23-year-old woman with chronic diarrhea, malnourishment, and evidence of enteric blood loss. Small bowel follow- through shows loop separation due to severe mural edema as well as transverse ( arrowhead ) and linear ( arrow ) ulcerations involving the distal ileum. The coexistence of pseudopolyps produces the characteristic cobblestone appearance
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 Frayed string appearance. 22-year-old woman with chronic diarrhea diagnosed with Crohn’s disease.  Small bowel follow-through shows contrast traversing a diffusely narrowed segment of distal ileum, resembling the appearance of a frayed string ( arrow ). Note the eccentric involvement of the bowel wall, with sacculations along the antimesenteric margin ( arrowheads )
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Fibroinflammatory Stenosis in Advanced Crohn’s Disease  Intestinal pliability may be compromised in advanced Crohn’s disease by any combination of fibrosis, inflammatory infiltration, and spasm.  Because inflammatory stenosis and spasm may be amenable to medical therapy, whereas fibrous stricture generally requires surgical repair, the radiologist is often called upon to help distinguish between these entities.
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 On contrast fluoroscopy, both inflammatory stenosis and fibrous stricture will appear as luminal narrowing; the classic “string sign” describes a thin column of intraluminal barium within the narrowed segment of bowel that resembles a frayed string.  The key to differentiating stricture :monitoring of luminal distensibility  in fibrous stricture, luminal distensibility is lost ,  in spasm, dispensability is preserved;  in inflammatory stenosis,distensibility should remain at least partially intact
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Mesenteric Involvement and Perforating Disease  “creeping fat” may be suspected when bowel loops appear abnormally separated.  fibrosis in the mesentery may result in kinking and fixation of the neighboring small bowel loops.  fistulae and/or sinus tracts :extension of contrast agent beyond the expected boundaries of the intestinal Lumen.  “internal” fistula.  “external” fistula.  Sinus tracts
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 Colovesical internal fistula. 52-year- old woman with diffuse Crohn’s disease status post multiple prior small bowel resections resulting in short bowel syndrome.  This image from a single contrast barium retrograde rectal enema demonstrates a narrowed and irregular rectosigmoid colon, with a fistula communicating from the inferior aspect of the sigmoid colon to the bladder ( arrow )
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 Terminal ileal deep ulcers and abscess formation.  This 25-year-old woman with Crohn’s ileocolitis underwent ileocecal resection 4 years prior to this study.  The patient presented with a non-resolving right lower quadrant mass for over a year. Small bowel followthrough shows active infl ammation involving the distal ileum just proximal to the ileocolic anastomosis. There  are deep ulcers ( arrowheads ) with medial perforation into an abscess demonstrated by irregular collections of contrast material ( arrow )
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 Fistulogram. 20 mL of water-soluble iodinated contrast was injected through a percutaneous tube into a fistulous tract. It demonstrates ramifying fi stulae, communicating with the distal ileum ( arrows ) and the rectosigmoid ( arrowheads )
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APTHOUS ULCERS First sign of chron’s disease on barium
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APHTHOUS ULCER
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APHTHOUS ULCER
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Cobblestone appearance: due to deep fissuring ulcers around inflammed mucosa
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Fissuring ulceration in Crohn'sdisease - graphically called `raspberrythorn' ulcers.
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COBBLESTONE- LONGITUDNAL & CIRCUMFERENTIAL FISSURES AND ULCERS SEPARATE ISLANDS OF MUCOSA, GIVING IT AN APPEARANCE REMINISCENT OF COBBLESTONES.
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A SMALL BOWEL ENEMA SHOWING EXTENSIVE JEJUNAL DISEASE CHARACTERIZED BY LOSS OF DISTENSIBILITY, (THE CAPABILITY OF BEING STRETCHED OR DISTENDED), THICKENING OF THE SMALL-BOWEL WALL AND GROSS DISRUPTION OF THE CIRCULAR HAUSTRAL FOLD PATTERN, WHICH IS LARGELY REPLACED BY A MARKED COBBLESTONE EFFECT. CD OF THE JEJUNUM
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COBBLESTONE CROHN DISEASE. THIS IS A MAGNIFIED IMAGE FROM THE RIGHT ILIAC FOSSA PERFORMED AS PART OF A SMALL BOWEL FOLLOW THROUGH. IT SHOWS THE CLASSIC APPEARANCE OF CROHN DISEASE IN THE TERMINAL ILEUM – SO-CALLED ‘COBBLESTONING’. THIS IS CAUSED BY EXTENSIVE FISSURES AND ULCERATION IN BETWEEN AREAS OF INTACT BUT OEDEMATOUS MUCOSA, RESEMBLING COBBLESTONES (ARROWS).
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ROSE THORN THE DEEP, LINEAR ULCERS (ARROWS) THAT HAVE FILLED WITH BARIUM IN THIS STENOSED TERMINAL ILEUM ARE KNOWN AS ‘ROSE-THORN ULCERS’ AND ARE TYPICAL OF CROHN DISEASE.
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String sign: spasm/fibrosis of bowelwall
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ILEOILEAL FISTULA: long standing chron’s
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 spatial and temporal with good luminal distention
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CT features of active Crohn disease  mucosal hyperenhancement(most sensitive indicator of active Crohn disease )  wall thickening (thickness > 3 mm)  mural stratification with a prominent vasa recta (comb sign)  mesenteric fat stranding,  reactive lymphadenopathy  complications such as fistulas and abscesses
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stratification  mural stratification denotes the visualization of bowel wall layers at CT  At CT enterography, the edematous bowel wall has a trilaminar appearance, with enhanced outer serosal and inner mucosal layers and an interposed submucosal layer of lower attenuation
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Findings in inactive Crohn disease  submucosal fat deposition  pseudosacculation  surrounding fibrofatty proliferation  fibrotic strictures.
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 pseudosacculation of the antimesenteric border, Involvement of the mesenteric border of the affected bowel segment in the inflammatory process, with associated asymmetric fibrosis.  Fibrofatty proliferation in the surrounding mesentery is thought to play a role in sustaining the inflammatory process related to the production of tumor necrosis factor a .  bowel strictures occurring as a complication.  Submucosal fat deposition is commonly associated with longstanding disease
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Reversible vs irreversible stricture  Reversible strictures produced by active disease demonstrate  mucosal hyperenhancement,  mural stratification,  fat stranding,  engorgement of the vasa recta  lack of enhancement and loss of stratification might be seen in the presence of transmural fibrosis  Is It important to differentiate?
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 Submucosal fat deposition in longstanding Crohn disease. Axial CT enterographic section shows abnormally low attenuation of the bowel wall (arrow-heads), a finding consistent with submucosal fat deposition. Submucosal fat deposition in longstanding Crohn disease. Axial CT enterographic section shows abnormally low attenuation of the bowel wall (arrow-heads), a finding consistent with submucosal fat deposition.
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Recurrent Crohn disease after bowel resection.
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 Large bowel involvement in Crohn disease. Axial CT enterographic sections obtained in three different patients show luminal narrowing and dilatation in a segment of the ascending colon (arrow in a), a perianal abscess (arrow in b), rectosigmoid involvement (black arrowhead in c), and a comb sign (white arrowheads in c).
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 Capsule impaction in bowel stricture due to Crohn disease. Anteroposterior radiograph (a) and axial CT enterographic section (b) demonstrate the impaction of an endoscopic capsule (black arrow) within the lumen of a thick-walled diseased ileal segment (white arrow in b).
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 Fistula formation in Crohn disease. Coronal volume-rendered CT enterographic sections obtained in two patients depict ileo-ileal fistulas (arrowheads in a) and an ileocolonic fistula (arrow in b).
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 Abscess formation in Crohn disease. Axial (a) and coronal volume- rendered (b) CT enterographic sections show a large fluid collection (arrows) with attenuation similar to that of enteric contrast material. Lack of communication between the collection and the bowel, as well as the marked difference in caliber between the two, helps confirm an extraluminal location of the collection. Note the evidence of active Crohn disease (* in a) in the terminal ileum
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Fat halo sign in chron’s disease Transverse CTscan shows the central fatty submucosal layer of low attenuation (*) surrounded by higher-attenuation inner (long arrow) and outer(short arrow) layers grossly corresponding to the mucosa and muscularis propria and serosa of the descending colon, respectively.
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COMB SIGN:Hypervascular appearance of the mesentery in active Crohn's disease. Fibrofatty proliferation and perivascular inflammatory infiltration outline the distended intestinal arcades. This forms linear densities on the mesenteric side of the affected segments of small bowel, which give the appearance of the teeth of a comb.
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CECTimage, coronalsection, venous phase - enterocecal fistula with secondary traction of the cecum and right psoas muscleabscess
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Bowel distention  There are two techniques to acquire distension of the small bowel:  MR enterography: oral administration of contrast.  MR enteroclysis: administration of contrast via a nasojejunal tube.  We routinely perform MR enterography as it suffices in the large majority of patients while being less burdensome and more time efficient.
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Oral contrast  For oral contrast several options are available. Mannitol in water solution (2%), which provides good contrast between lumen and bowel wall on both T1 and T2 sequences and is well accepted by patients. There is one precaution: no colonoscopy with electrocoagulation should be performed directly after the MRI because of methane resulting from Mannitol breakdown.
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MRI sequences  Balanced FFE (axial and/or coronal) in breath-hold  T2 with fat sat (axial) in breath-hold  T1 pre- and post-contrast (axial/coronal) in breath-hold Optional sequences:  T2-FSE without fat sat for additional overview and comparison with T2 with fat sat.  Diffusion Imaging (DWI).  Balanced FFE cine-study for motility.
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MRI signs of Crohn’s disease.
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Bowel wall thickness  With adequate distension the normal bowel wall has a thickness of 1-3 mm.  A common categorization is 3-5 mm for mild thickening, 5- 7 mm for moderate thickening and > 7 mm for marked thickening of the bowel wall.  T1 weighted post-contrast images or non fatsat T2 weighted images (if available) are preferable for measurement of bowel wall thickness.
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 The image is a coronal post-contrast T1 weighted image showing disease activity in the transverse colon with marked wall thickening of more than 7 mm and deep ulceration (arrow).
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 Increased bowel wall thickness is one of the most common signs of inflammatory activity, but not specific for Crohn's disease.  Bowel wall thickness correlates well with the severity of the disease activity.  Measurements are best performed on the sequence with good luminal distension.  Black border artifacts on balanced FFE sequences can distort thickness measurements.
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 Balanced FFE image shows marked bowel wall thickening and luminal narrowing of the terminal ileum. Measurement on the balanced FFE sequence can be less accurate due to the black border artifact (arrows).dc
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Enhancement  Abnormal bowel wall enhancement after administration of gadolinium is the result of increased vascular permeability and angiogenesis.  It is seen both in active disease and fibrosis.  Enhancement can be graded by comparing to the precontrast images, to normal bowel loops and nearby vascular structures.  No abnormal enhancement Equivalent to normal bowel wall Minor increased enhancement More than normal bowel wall, but significantly less than nearby vascular structures  Moderate enhancement Somewhat less than nearby vascular structures  Marked enhancement Equal or more intense than nearby vascular structures
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 Thickened terminal ileum segment with marked enhancement on axial post-contrast T1W image with fatsat.
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 The latter two enhancement patterns can only be appreciated when the wall is thickened.  There is some discussion about the value of the enhancement pattern.
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Homogeneous enhancement  Strong homogeneous enhancement is seen in active inflammation.  The image shows a terminal ileum with a homogeneous enhancement pattern with moderate (green arrow) and marked (red arrow) enhancement on an axial post- contrast T1 image.
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Mucosal enhancement  This is seen as bowel wall thickening with increased enhancement of the mucosal layer relative to the outer layers.  The image is a post-contrast T1 image with a mucosal enhancement pattern in the terminal ileum (arrow).  There is relatively low enhancement of the middle and outer layers
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Layered enhancement pattern  This pattern suggests severe disease activity or longstanding chronic disease.  The three-layered appearance is caused by strong enhancement of the mucosa and the serosa with no enhancement of the middle layer, which is the submucosa and the muscular layer.  This middle layer can consist of fat, edema or fibrotic tissue.  This can be distinguished using a fat sat T2 sequence.
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 Layered enhancement pattern of the rectum with some surrounding fat stranding on an axial post-contrast T1 image (arrow). Continued inflammation with a homogeneous enhancement pattern can be seen in the sigmoid colon (green arrow). Also, a right- sided adnexal cyst is present with enhancing rim (arrowheads).
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T2 mural signal intensity  Increased mural signal intensity on fat-saturated T2 images indicates the presence of mural edema, suggesting active disease.  Presence of bowel wall thickening with a low mural T2 signal intensity is more suggestive of fibrotic disease.  The psoas muscle can be used as a reference when assessing mural T2 signal.  Fat suppression is routinely used to differentiate between mural fat depositions and mural edema. Fat depositions are the result of chronic bowel inflammation and therefore quite common in Crohn's disease.  However, its presence does not indicate active disease.  Perimural edema or fluid can be identified as well and is associated with active disease .
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T2 mural signal intensity can be graded as follows using a T2 sequence with fat sat:  No increase normal bowel wall  Minor increase bowel wall appears dark gray  Moderate increase bowel wall appears light gray  Marked increase bowel wall contains areas of white high signal approaching that of luminal content.
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 Actively inflamed terminal ileum with marked thickening and moderate mural signal intensity (mural edema) on an axial T2 with fat sat.
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 inflamed small bowel showing wall thickening and mild mural T2 signal (arrow) on an axial T2 with fat sat. Prestenotic dilatation can be seen proximally of the diseased segment.
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 Fat suppression is routinely used to differentiate between mural fat depositions and mural edema.  Fat depositions are a result of chronic bowel inflammation, but not typical of active disease.  These fat depositions can be diffuse but can also present as a layered pattern.  The CT equivalent for this pattern is the 'fat-halo sign'.
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 Wall thickening of the terminal ileum in a 67-year-old male with Crohn's disease since 11 years. Layered enhancement is seen on an axial post-contrast T1 image with fat sat (left). T2 with fat sat (middle) shows the same pattern with a middle layer of low intensity. T2 without fat sat shows an increased signal in the middle layer, suggesting fat depositions. Endoscopy showed only superficial disease
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Ulceration  Moderate to deep ulceration can be seen on T1 and T2 images, but small ulcerations can be difficult to distinguish from mucosal folds depending on the degree of luminal distension.  Ulcerations are active spots of inflammation and usually there is increased enhancement on the post-contrast T1 images.
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 Coronal post-contrast T1 and T2 fat sat images show multiple small ulcerations in the terminal ileum.
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Loss of haustration  When the colon is involved in Crohn's disease a decrease of haustral folds can be seen.  A complete loss of haustration results in a smooth surface.  This is also a common finding in ulcerative colitis and known as 'lead pipe' colon.  The coronal post-contrast T1 image shows loss of haustral folds throughout the colon in a patient with chronic Crohn's disease.
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Comb sign  Increased vascularity of the mesentery is seen in active inflammation.  The engorged vessels have a linear appearance, resembling the teeth of a hair comb (comb sign).
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Creeping fat  Creeping fat, also called fibrofatty proliferation or fat wrapping, are different names for hypertrophy of the subserosal fat.  It is a common finding in longstanding Crohn's disease.  The image shows creeping fat surrounding the descending colon. It isolates the colon from surrounding bowel loops.
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Skip lesions  Skip lesions and patchy inflammation are a typical finding in Crohn's disease, in contrast to the continuous inflammation, which is seen in ulcerative colitis.  Skip lesions refers to the interspersed inflammation "skipping" parts of the bowel, which are left unaffected (green arrows).
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 The coronal T1 post- contrast image (left) and the T2 image (right) show skip lesions in the terminal ileum. The affected lesions show increased enhancement with a layered pattern (yellow arrows), while another part is unaffected or skipped (green arrows).
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Stenosis  Stenosis can present as bowel wall thickening combined with lumen narrowing. The presence of a prestenotic dilatation increases the likelihood of a stenosis  Abnormal contrast enhancement of the affected bowel segment is usually present.  In the grading system, only severe stenosis is included as a complication, which is defined as a stenosis with prestenotic dilatation and a moderate-to- marked increase in mural T2 signal.
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 Coronal post-contrast T1 image with a stenosis at the ileocecal junction (left). No obvious pre- stenotic dilatation is seen. The stenosis was non-passable using endoscopy (right).
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Infiltrate  Infiltrate can be seen as creeping fat between bowel loops with replacement of the fat signal intensity and tethering and kinking of bowel loops.  Obstructive symptoms due to adhesions, inflammatory narrowing or fibrosis are common.  Fistulas and abscesses are often present. Due to the complex structure, the exact path of a fistula can be difficult to define.
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Fistula  Sinus tracts and fistulas are common complications in patients with Crohn's disease. Both show marked enhancement on T1 images after administration of gadolinium. A fistulous track can present with a layered 'tram track' configuration or as a linear enhancing structure.  It can be seen going from one bowel loop to another bowel loop, to another hollow organ or to the skin.
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Abscess  Abscesses are often seen in patients with severe active Crohn's disease.  Abscesses are characterized by rim enhancement on post-contrast T1 images and central high signal intensity on T2 images.  The abscess is frequently surrounded by fat stranding.
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Causes superficial ulceration of colon and rectum. It starts from rectum and retrogradely involves whole colon  continuously. In total colitis- back wash ileitis. More common in DR2 relatedgenes. More female predilection, age group 30-40 yrs. Clinical symtoms- diarrhoea, tenesmus, bleeding per rectum, passage ofmucus, crampy abdominal pain. ULCERATIVECOLITIS
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MILD DISEASE: fine granularity MODERATE: marked erythema, coarse granularity, contactbleeding and no ulceration. SEVERE:spontaneous bleeding,edematous and ulcerated Long standing cases epithelialregeneration- pseudopolyps, pre cancerous condition Eventually shortening and narrowing of colon FULMINANT DISEASE: toxic colitis/megacolon PATHOGENESIS
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Acute UC – descending colon has irregular outline. No fecal residue in colon S/O total colitis
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Mucosal inflammation-granular appearance to the surface of the bowel. Mucosal ulcers are undermined -button-shapedulcers Islands of mucosa remain giving it a pseudo-polyp appearance In chronic cases the bowel becomes featureless with loss of normal haustral markings, luminal narrowing and bowel shortening- lead pipe sign BARIUM ENEMA
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FINE MUCOSAL GRANULARITY- FIRSTSIGN NARROWING OFLUMEN
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COLLAR BUTTON ULCERS
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LEAD PIPECOLON
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Back wash ileitis : patulous ICvalve and dilated granular terminal ileum
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COLLAR BUTTON ULCERS- CLASSICALLY SEEN IN THE COLON ASSOCIATED WITH ACTIVE UC. THE COLLAR BUTTON APPEARANCE IS FORMED BY MUCOSAL ULCERATION WITH ASSOCIATED UNDERMINING OF THE EDGE BY LATERAL SUBMUCOSAL EXTENSION.
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LEAD PIPE COLON DOUBLE CONTRAST BARIUM ENEMA IN LONG STANDING ULCERATIVE COLITIS CASE SHOWS CLASSIC ‘LEAD PIPE’ SIGN. THE IMAGE DEMONSTRATES DESCENDING COLON AND SIGMOID COLON TO BE FEATURELESS WITH LACK OF HAUSTRA AND NARROWING.
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PSEUDOPOLYPS THIS DOUBLE CONTRAST BARIUM ENEMA REVEALS AN IRREGULAR MUCOSA AND NUMEROUS SMALL FILLED NODULES OR POLYPOIDS THROUGHOUT THE ENTIRE COLON REPRESENTATIVE OF INFLAMMATORY PSEUDOPOLYPS IN LONG STANDING ULCERATIVE COLITIS. ALSO VISIBLE ARE SMALL WORM LIKE STRUCTURES THAT ARE SMALL GROUPS OF RESIDUAL MUCOSA CALLED FILIFORM POLYPS.
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CTFINDINGS Inflammatory pseudopolyps Inflamed and thickened bowel - target appearance, due concentric rings of varying attenuation- mural stratification In chronic cases, submucosal fat deposition is seen particularly in the rectum fathalo sign Extramural deposition of fat, leads to thickening of the perirectal fat, widening of the presacral space Marked muscularis mucosa hypertrophy-lead pipe sign.
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INFLAMMATORY PSEUDOPOLYPS
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Wall Thickening- median wall thickeness of colon ranges from 4.7 to 9.8 mm, more severe the disease more thicken the wall Increased Enhancement- enhancement of themucosa with no or less enhancement of the submucosa Loss of haustralmarkings MRI
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Mri image reveals thickening of colon with loss of haustral markings
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