are similar. A role for ischemia is occasionally postulated. Its relationship to extraperitoneal fibrosis (discussed below) is uncertain. Retractile mesenteric is associated with a number of neoplasms and immunosuppression therapy. Numerous reports describe sclerosing peritonitis developing in association with a luteinizing thecoma. A rare association exists between retractile mesenteritis and a mesothelioma.
Excessive fatty infiltration of the mesentery, or lipomatosis, may be idiopathic, part of generalized obesity, or associated with steroid therapy. Most lipomatosis is diffuse and tends to infiltrate rather than displace adjacent structures. It is the occasional focal collections of fat that suggest a fat-containing neoplasm in the differential diagnosis.
Mesenteritis presents either as an acute abdomen or, more often, evolves as a chronic condition of diffuse abdominal pain, at times intermittent. Large fibrofatty tumors develop in the abdomen. Histology reveals a fibrofatty infiltrate containing inflammation, fat necrosis, and fibrosis. Multiple mesenteric lymphatic cysts develop in this entity. Mesenteric fat necrosis, or lipodystrophy, also occurs with pancreatitis and some infections. Mesenteric infiltration has led to a protein-losing enteropathy; in fact, enteropathy can be the first manifestation of this condition.
Exuberant small bowel mesenteric fibrosis predominates in some individuals. This variant, often called retractile mesenteritis, also leads to some degree of inflammation, but the primary finding is mesenteric foreshortening and resultant mesenteric and small bowel distortion. Less often the mesocolon or sigmoid mesentery are affected. Normally little omental involvement is found. Rarely, a similar inflammatory process involves primarily the omentum rather than mesentery.
The differential diagnosis of retractile mesenteritis includes mesenteric and other peritoneal neoplasms. In some patients an open biopsy is necessary for diagnosis and to exclude a malignancy.
Imaging
Usually the small bowel mesentery is involved and ranges from a diffuse infiltrate, a focal soft tissue tumor, to discrete inflammatory nodules. The infiltrate typically also involves adjacent small bowel and results in a spiculated, irregu-
ADVANCED IMAGING OF THE ABDOMEN
lar outline to contrast-filled bowel. Valvulae conniventes are thickened and distorted but not destroyed, thus differentiating this condition from most malignant infiltrations. At times the appearance mimics Crohn’s disease, which also results in mesenteric inflammation and fibrosis. Occasionally mesenteric calcifications develop, probably within necrotic tissue.
Primarily retractile mesenteritis and panniculitis have separate and distinct CT appearances (23): patients with retractile mesenteritis show a mostly homogeneous soft tissue infiltrate denser than fat that distorts bowel loops. Those with panniculitis have a heterogeneous fat-density infiltrate typically involving the mesenteric root but with preserved fat around the greater vessels (fat ring sign), and a loss of the usual sharp outline of enclosed arteries; at times soft-tissue nodules are evident.
Ultrasonography identifies hypoechoic mesenteric tumors, occasionally containing a cystic component.
Magnetic resonance of lipomatosis reveals a fat signal intensity with all imaging parameters. T1-weighted fat-suppressed SGE images are useful to confirm that a focal collection is indeed fat. T1-weighted images of panniculitis (inflammation) reveal hypointense stranding traversing the hyperintense fat.
Sclerosing peritonitis manifests by thickening of the peritoneal lining, diffuse or loculated fluid collections, peritonitis and resultant small bowel obstruction, or simply disordered small bowel motility. Dense adhesions develop. Extensive fibrosis can involve the liver capsule. Peritoneal calcifications develop eventually. Imaging of patients on chronic ambulatory peritoneal dialysis and sclerosing peritonitis detects peritoneal thickening and calcifications; most also have loculated fluid collections and small bowel tethering or dilation.
Aside from calcifications, the imaging appearance of sclerosing peritonitis is similar to that of ovarian carcinoma with carcinomatosis. Both tend to develop adnexal tumors. In carcinomatosis, however, only the peritoneal surface is involved and it has an irregular outline due to malignant nodules; in sclerosing peritonitis not only does the peritoneal thickening have a smooth outline, but also the small bowel and colon walls are thickened. The differential for sclerosing peritonitis also includes diffuse mesothelioma, some chronic infections, and primary and secondary amyloidosis.