imaging in uc and chrons disease (1).pptx

nagasaipelala 36 views 50 slides Oct 14, 2024
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About This Presentation

imaging in chrons disease and ulcerative colitis


Slide Content

IMAGING IN ULCERATIVE COLITIS AND CHRONS DISEASE PRESENTER – DR. VENKATESH MODERATOR – DR. ANIL KUMAR

Introduction: Inflammatory bowel disease (IBD) is a fairly common enteropathy that occurs in one per 1000 people in developed countries. The peak incidence of IBD is between the ages of 15 and 40 years, with a possible second peak between 50 and 80 years. IBD is a heterogeneous group of chronic gastrointestinal disorders with two broad subtypes: Crohn disease (CD) and ulcerative colitis (UC).

Ulcerative colitis is characterized by relapsing and remitting episodes of inflammation limited to the colon’s mucosal layer. It almost invariably involves the rectum, typically extends in a proximal, and continues to involve other portions of the colon. Chron’s disease can involve any component of the gastrointestinal tract from the oral cavity to the anus and is characterized by trans-mural inflammation. Extensive involvement of the right colon and small intestine(Terminal ileum) is more common in CD.

Etiopathogenesis Highly complex and dependent on multiple factors. Occur in individuals who have aberrant genes which makes them abnormally susceptible to commensal bacteria which are normally present in the colon (intestinal microbiota) thus causing inflammation in the colonic mucosa. These interactions between the mucosa of the colon and colon commensals are triggered by exposure to risk factors in the environment.

Risk and Protective Factors for UC and CD Ulcerative Colitis Crohn’s Disease RISK FACTORS: RISK FACTORS: Higher socioeconomic status (hygiene hypothesis), Previous h/o enterocolitis, NSAIDs use, OC pills Higher socioeconomic status (hygiene hypothesis) NSAIDs use, OC pills, Antibiotic use in childhood, Smoking PROTECTIVE FACTORS: PROTECTIVE FACTORS: Breastfeeding, Smoking, Appendicectomy Breast feeding

Clinical presentation Diarrhea and rectal bleeding > 6 weeks (UC > CD). Tenesmus (Rectal inflammation). The severity of patient presenting with colitis can be graded as mild, moderate and severe based on the clinical presentation and physical signs.

Inflammatory markers : serum – ESR stool - Fecal cal protein.

Diagnostic algorithm for confirmation of IBD diagnosis

IMAGING MODALITIES

Two groups of imaging modalities are available for the evaluation of IBD. Imaging modalities that allow assessment of the bowel lumen, bowel wall, and the extraintestinal abdomen, represented by the cross-sectional imaging modalities: ultrasonography (US), CT enterography, and magnetic resonance (MR) enterography. Imaging modalities that evaluate exclusively the bowel lumen: small-bowel follow-through (SBFT) and barium enema examinations.

SBFT and Barium Enema Examinations ADVANTAGES Dynamic evaluation of the whole gastrointestinal tract Allows manual mobilization of the bowel DISADVANTAGES Ionizing radiation Limited in the evaluation of the intestinal wall It does not allow panoramic view of the abdominal cavity. ADVANTAGES Low cost Can be repeated as many times as necessary Absence of ionizing radiation or contrast medium DISADVANTAGES Operator dependent Limited because of intestinal gas distribution It does not allow panoramic view of the abdominal cavity. US Examination

CT ENTEROGRAPHY MR ENTEROGRAPHY ADVANTAGES Thin section Widely available The optimal method for depicting extraluminal bowel gas and complex abdominal fistulas DISADVANTAGES Ionizing radiation Lower contrast resolution of the bowel wall Intravenous iodinated contrast material necessary ADVANTAGES High contrast resolution Allows functional evaluations Can be performed without the use of intravenous contrast material The optimal method to evaluate perianal fistulas DISADVANTAGES Higher cost and less availability Contraindications related to the magnetic field and paramagnetic contrast material

Systemic approach I - Inflammatory mesentery B - Bowel wall changes D - Disease complications

B I D LYMPHADENOPATHY FAT CHANGES ENGORGED VESSELS Inflammatory Mesentery LUMINAL STRICTURES DILATATIONS CANCER EXTRALUMINAL FISTULA ABSCESS PERFORATION Disease Complications THICKENING STRATIFICATION PERMANENT STRUCTURAL CHANGES Bowel Wall Changes

INFLAMMATORY MESENTERY GROUP 1

FAT STRANDING: The sharp interface between bowel and mesentery is lost due to influx of inflammatory cells and fluid. The enhancement of perienteric fat is used as a severity marker of IBD in imaging-based indices ( MR imaging and Sailer index), and recent studies have shown that diffusion-weighted imaging is equivalent for the detection of small-bowel inflammation. Fat stranding: active inflammation marker .

FAT STRANDING:

FIBROFATTY PROLIFERATION Fibrofatty proliferation, also called creeping fat or fat wrapping, represents the asymmetric proliferation of fat usually along the mesenteric border, which is almost exclusively seen in CD. This mesenteric adipose tissue hypertrophy causes an asymmetric displacement of mesenteric vessels and isolation of the bowel from the surrounding bowel loops. Fibrofatty proliferation: inactive and chronic inflammation marker.

FIBROFATTY PROLIFERATION

ENGORGED VASA RECTA Engorged vasa recta represents vascular dilatation on the mesenteric side of the bowel. This is also known as the “comb” sign because the engorged vessels have a linear appearance, resembling the teeth of a hair comb. Engorged vasa recta: active inflammation marker

ENGORGED VASA RECTA

LYMPHADENOPATHY : Reactive mesenteric lymphadenopathy is characterized by hyperenhancing lymph nodes that typically range from 3 to 8 mm. Lymphadenopatathy is commonly found in patients with IBD, both CD and UC, although it is more commonly seen with CD. The lymph nodes may be detected more frequently at the mesenteric root, the mesenteric periphery, or in the right lower abdominal quadrant. When lymph nodes are multiple and larger than 10 mm, the possibility of tumor should be considered, mainly lymphoma and carcinoma. Mesenteric lymphadenopathy: a ctive inflammation marker

BOWEL WALL GROUP 2

HOMOGENEOUS THICKENING: Bowel wall thickening is defined as a small bowel wall thickness greater than 3 mm in a distended loop. In homogeneous bowel thickening, the parietal bowel wall is enlarged without mural stratification. It can be asymmetric with increased thickening on the mesenteric side of the bowel, mainly in CD. Homogeneous thickening without enhancement may represent active or inactive inflammation marker. Homogeneous thickening with enhancement: active inflammation marker

BILAMINAR STRATIFICATION: Bowel wall thickening with bilaminar stratification results from the association of mucosal hyperenhancement and submucosal edema. Submucosal edema is a severity marker used in imaging-based IBD indexes. It is not specific for IBD and may be seen in other small bowel inflammatory conditions, such as ischemia and radiation enteritis. Bilaminar stratification: active inflammation marker

TRILAMINAR TRILAMINAR :

FAT HALO SIGN: The “fat halo” sign represents infiltration of the submucosa with fat between the muscularis propria and the mucosa. It may be indicative of IBD, although it has been reported in cytoreductive therapy and graft-versus-host disease. In the absence of clinical or radiologic evidence of IBD, the presence of the fat halo sign may represent a normal finding. Inactive inflammation marker.

PERMANENT STRUCTURAL CHANGES:

GROUP 3 DISEASE COMPLICATIONS

COLORECTAL CANCER Colorectal cancer has a higher incidence in patients with long-standing IBD. The risk is related to the duration and anatomic extent of the disease.

PITFALL: inflammatory or malignant? When we need to think of malignant wall thickening When thickening of bowel wall can be described as Focal (<5 cm) Irregular or asymmetric Heterogeneous Perienteric fat stranding disproportionally less severe than the degree of wall thickening When thickening of bowel wall can be described as Segmental or diffuse ( 6–40 cm or >40 cm) Regular, circumferential, symmetric Homogeneous Perienteric fat stranding disproportionally more severe than the degree of wall thickening NEOPLASTIC CONDITION INFLAMMATORY CONDITION

STRICTURES AND DILATATIONS

TOXIC MEGACOLON Toxic megacolon is a potentially lethal complication of IBD that is characterized by total or segmental nonobstructive colonic dilatation associated with systemic toxicity. It can occur in colitis caused by UC and CD. The diagnosis is made by a combination of symptoms and clinical signs: Radiographic evidence of colonic dilatation Any three of the following: fever (>101.5 °F), tachycardia (>120 beats per minute), leukocytosis (>10.5 x 10 3 /µL), or anemia Any one of the following: dehydration, altered mental status, electrolyte abnormality, or hypotension Imaging findings include: bowel wall thickening, loss of haustra, and segmental or total colonic dilatation of at least 5 cm (CT) and 8 cm (supine radiograph

PERFORATION

FISTULA Fistula is a permanent abnormal passageway between two organs. The clinical course is variable and depends on the location and complexity. Fistulas may be external (arise from the intestine and communicate with the skin) or internal ( enteroenteric or between the bowel and adjacent organs). The most common fistulas are enterocutaneous and perianal. When compared with surgical findings, CT enterography has a reported accuracy of 86% for fistulas, with a false-negative rate of 8%.

ABSCESS

PERIANAL ABSCESS :

Dilatation of the vasa recta Fibrofatty proliferation Mural stratification Colonic wall thickening Mural thickening: 11–13 mm, eccentric and discontinuous Skip lesions (pathognomonic) Right colon and terminal ileum CHRONS DISEASE ULCERATIVE COLITIS I NFLAMMATORY MESENTERY B OWEL WALL CHANGES Dilatation of the vasa recta D ISEASE COMPLICATIONS Postinflammatory polyps Fistulas, abscesses Mural stratification Colonic wall thickening Mural thickening: 8 mm, symmetric and continuous Postinflammatory polyps Toxic megacolon

DIFFERENTIAL DIAGNOSIS: TUBERCULOSIS ISCHEMIC COLITIS

ANGIOEDEMA OF THE SMALL BOWEL PSEUDOMEMBRANOUS COLITIS

TYPHLITIS INFECTIOUS ENTEROCOLITIS

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