Inflammatory changes in the fat generally provide reliable evidence of an underlying acute intra-abdominal process. Disproportionate fat stranding in the pericolic region with mild colonic wall thickening suggests a pericolonic inflammatory process, including diverticulitis, appendicitis, epiploic appendagitis, and omental infarction, as opposed to colonic wall thickening centered on the colon, typical of infection, ischemia, and inflammatory bowel disease . Occasionally, the underlying pathologic process is in the fat itself, involving the omentum, mesentery, or epiploic appendages.
Appendices epiploicae arise in two rows from the serosal surface of the colon, from the cecum to the rectosigmoid junction (Figure 52.1). Pedunculated and with tenuous blood supply, they are prone to torsion, infarction, and subsequent inflammation.
Imaging of epiploic appendagitis reveals an ovoid or lobular lesion of fat density less than 5 cm in size (usually 1–4 cm) adjacent to the anterior colonic wall (Figures 52.2 and 52.3) . There is typically a well-defined hyperattenuating rim and surrounding inflammatory change. As with other pericolic processes, wall thickening of adjacent colon is mild compared with the degree of fat stranding.
Epiploic appendagitis can occur anywhere along the colon, but is most common adjacent to the sigmoid . The “central dot sign” has been described as a specific sign for epiploic appendagitis and reflects thrombosed or obstructed central vessels within the torsed appendage.