The greater omentum is a large peritoneal fold that is continuous with the visceral peritoneal layers of the stomach and transverse colon. It contains fat and blood vessels and often serves to contain the spread of intraperitoneal infections [6].
Torsion of the omentum is the main reason for infarction and two different forms have been described: primary torsions (without other pathologic intra-abdominal findings) and secondary torsions (tumors, cysts, inflammatory changes, adhesions, hernias). Predisposing factors for torsion are anomalies of the omentum, such as a small root, irregular vascular anatomy, abdominal trauma, cough, and physical strain [7, 8].
The etiology of omental infarction without torsion remains uncertain but several mechanisms have been proposed, such as an anomaly of venous vessels. Other possible causes for primary infarctions could be disorders of hemostasis or vascular diseases. It is known that hematologic changes occur during pregnancy and the puerperium and that hypercoagulability leads to an increased risk of thromboembolic events. The exact mechanism leading to infarction in this case remains unclear [9,10,11].
Our patient was on treatment with tibolone for over 24 months to treat perimenopausal symptoms. However, data of the effects of tibolone on the coagulatory system as well as the risk of venous thromboembolism in postmenopausal women are not univocal [12, 13]. Therefore, unless future studies, in our case tibolone seems to be not involved.
Both primary and secondary omental infarction, with or without torsion, result in venous stasis and thrombosis leading to congestion and edema, pathologically with hemorrhagic necrosis and extravasation of serosanguineous peritoneal fluid. In our patient, no obvious anatomic and pathologic reasons or precipitating factors for the omental infarction were found, so we were dealing with a case of omental infarction without torsion [10, 11].
The great majority of cases of omental infarction reported in the literature were segmental involving the right side of the omentum with right lower quadrant or right para-umbilical pain mimicking perforated duodenal ulcer, acute appendicitis, acute cholecystitis, cecal diverticulitis or epiploic appendagitis [1, 2]. Left-sided omental infarction is unusual but has been described [14].
Since the great majority of patients present with acute abdomen, a CT scan of the abdomen is the examination of choice and can assist in the exclusion of various other conditions presenting a similar clinical setting. However, the incidence of omental infarction is low and the clinical features often non-specific; thus, it is not included in the clinical differential diagnosis in most of cases on initial evaluation [1, 2].
By showing CT findings suggestive of diverticulitis such as visualization of the inflamed diverticulum, marked wall thickening, and formation of paracolic abscess, the CT scan will help in narrowing the differential diagnosis. In fact, in omental infarction there is no or only subtle local wall thickening, although a case of omental torsion with transient thickening of the wall of the transverse colon has been recently reported [6, 7].
Differentiating appendagitis from omental torsion is more subtle. Thickening of the adjacent bowel wall is not a constant feature of primary epiploic appendagitis. However, the larger size and the location of the mass relative to the ascending or descending colon favor omental abnormality rather than primary epiploic appendagitis [15, 16].
The CT findings of fatty mass in the omentum may also suggest other diagnoses including lipoma, liposarcoma, angiomyolipoma, teratoma, mesenteric lipodystrophy, pseudomyxoma peritonii, and peritoneal mesothelioma or metastatic peritoneal seeding (commonly from ovarian cancer). All of these conditions clearly present in a different clinical setting so that diagnostic confusion is unlikely [17,18,19,20].
CT findings of omental infarction without torsions, as in our case, include a well circumscribed, oval, or cake-like fatty mass with heterogeneous attenuation, containing strands of soft-tissue attenuation corresponding to hemorrhage and necrosis. Focal fat stranding surrounding the lesion is often associated. The mass is most often located deep to the rectus abdominis and anterior to the colon. It appears adherent to inflamed, thickened parietal peritoneum. A small to moderate amount of free peritoneal fluid may be present [21, 22].
In these cases, gross pathologic examination reveals the presence of an omental mass with areas of hemorrhagic infarction. The earliest microscopic finding is hemorrhagic infarction; later, varying degrees of inflammatory infiltrate are seen. The most advanced stage is characterized by the presence of a fibroblastic reaction [11].
The importance of making the correct CT diagnosis of acute omental infarction is especially important to avoid unnecessary surgical intervention. Traditionally, surgery has been the treatment of choice. Nevertheless, most recent literature shows a disunity between authors regarding the designated treatment. Arguments in favor of conservative medical management are the often self-resolving character of omental infarction, especially since omental infarction is described to be self-limiting (proven with CT) even after 1–3 years follow-up, as well as the safety and effectiveness of conservative treatment, which protects patients from unnecessary surgical intervention. Arguments in favor of surgical intervention are a shorter length of hospitalization time compared with conservative treatment, which save money. In addition, (laparoscopic) treatment is favored by some because it allows for confirmation of the radiologic findings [23].
Thus, a conservative initial approach seems justified, but it should be done with caution and followed up by clinical and imaging evaluation until complete resolution occurs. Intervention is required when the patient’s condition worsens or when there are doubts on the diagnosis [1, 2].
