Omental cakes: unusual aetiologies and CT appearances

The greater omentum is a derivative of the dorsal mesogastrium, brought anteriorly by the counterclockwise rotation of the gut at 6 weeks of gestation. From the greater curvature of the stomach, two layers of peritoneum join and form an apron-like structure that hangs inferiorly anterior to the small bowel, then doubles back upon itself to fuse with the superior layer of the transverse mesocolon (Fig. 1) [2]. Laterally it extends to the pylorus or first portion of the duodenum on the right, and on the left is continuous with the gastrosplenic ligament. These four layers of variably apposed peritoneum may act either as an actual or potential anatomic space [3].

The size of the greater omentum and its correlative CT appearance are largely dependent on the amount of fat it contains. The greater omentum also contains gastroepiploic vessels, lymphatics, and “milky spots”, or accumulations of immune cells that are comprised predominantly of macrophages [4]. These “milky spots” are involved in the clearance of pathogens from the peritoneum and serve as part of the “abdominal policeman” role of the greater omentum. They also are potential traps for intraperitoneal metastases, particularly by intraperitoneal seeding [5]. These areas are located throughout the peritoneum and are seen in the highest concentration in the greater omentum, explaining the high frequency of omental involvement in intraperitoneal disease processes (Fig. 2).

On CT, the normal greater omentum appears as a band of fatty tissue with variable width. The CT appearance of omental pathology is dependent on the extent and duration of disease involvement. Early omental disease manifests as a smudged or permeated appearance of the omental fat (Fig. 3a). Enhancing soft tissue nodules form within the omentum as the disease progresses. An omental cake arises when these nodules coalesce to form a diffusely thickened mass and replace the normal fat (Fig. 3b) [6]. Depending on the cause of the omental cake and the extent of intraperitoneal disease, ascites may be an accompanying feature.

While 100–150 cc of non-ionic iodinated intravenous contrast material (1.5-2 cc/s) is desirable to increase the intrinsic contrast of the images, it may not be necessary to diagnose the extent of an omental cake, unless knowledge of the extent is important to surgical planning. Frequently, however, intravenous contrast material is administered, mostly to evaluate coexisting liver or other solid organ disease. Oral contrast material is valuable to avoid confusing unopacified bowel loops with omental pathology and to define the extent of the omental findings [7].

The presence of associated intraabdominal and intrahepatic findings, such as hepatic metastases and lymphadenopathy, may be the only clues as to the origin of omental disease if the diagnosis is unknown; the appearance of the omental cake itself is non-specific with respect to the diagnosis [6]. As there are many conditions that can produce an omental cake, the need for a specific diagnosis relies on percutaneous biopsy of the cake if the aetiology is unknown.

Ultrasound (US) and magnetic resonance imaging (MRI) also have been used to evaluate the greater omentum [8, 9]. US serves an alternative to CT in guiding biopsy of omental cakes [8]. MRI demonstrates omental cakes and other peritoneal implants, but unless a gastrointestinal contrast agent is administered, there is inferior contrast resolution relative to CT [9]. Thus, CT is the mainstay modality to image the greater omentum. Nevertheless, MRI may be utilized in patients with contraindications to CT (contrast sensitivity, pregnancy) or as an adjunct in patients with inconclusive CT findings. Delayed enhancement after gadolinium improves detection of peritoneal metastases [10]. Furthermore, the use of diffusion-weighted MRI is emerging as a potential technique for omental and peritoneal metastases [11].

Metastatic involvement is the most common cause of omental cakes [6]. Along with peritoneal fluid (74%) and peritoneal thickening with enhancement (62%), omental involvement is a frequently encountered finding with peritoneal carcinomatosis on CT [12]. While ovarian carcinoma is the most common cause of omental cakes, colonic, pancreatic, and gastric cancers are other common malignancies that may result in omental metastases [13]. However, virtually any tumour capable of intraperitoneal spread, such as endometrial or bladder cancer, may cause an omental cake (Figs. 4, 5, 6, 7) [13].

Metastases gain access to the greater omentum by any of four principal routes: (1) direct extension of tumour along peritoneal ligaments, (2) intraperitoneal seeding, or via (3) haematogeneous or (4) lymphatic spread of disease [7]. Hepatobiliary malignancies, such as gallbladder carcinoma and cholangiocarcinoma, are unusual causes of omental cakes that often are the result of direct extension of tumour along the hepatoduodenal ligament and lesser omentum (Figs. 8, 9, 10) [7]. Metastatic renal cell carcinoma to the omentum may break through the renal capsule, the anterior renal fascia, and the closely apposed posterior parietal peritoneum to spread along the peritoneal surface [14]. Unusual gynaecologic (fallopian tube and endometrium), genitourinary (prostate and urothelium), small bowel, and appendiceal primary cancers also may result in intraperitoneal seeding (Figs. 11, 12, 13, 14). Melanoma, lung, and breast cancers can cause omental cakes, typically by haematogenous spread. Metastases from breast cancer to the stomach may extend directly into the greater omentum (Figs. 15 and 16). Non-Hodgkin’s lymphoma, and, very rarely, Hodgkin’s disease, can develop omental cakes, often with associated diffuse peritoneal and retroperitoneal disease, and ascites from lymphatic spread (Fig. 17) [15].

With regards to imaging findings, obvious careful search for the primary malignancy is important to determine the aetiology if the cause of the omental cake is unknown. Metastatic omental involvement occasionally may be heralded by abdominal pain secondary to bowel obstruction or intussusception in cases of gastrointestinal malignancies that metastasise to the small bowel.

Primary malignancies and benign tumours of the peritoneum and omentum are rare. Typically of mesenchymal origin, they include: abdominal mesothelioma, haemangiopericytoma, leiomyoma, leiomyosarcoma, gastrointestinal stromal tumour (GIST), lipoma, liposarcoma, neurofibroma, fibrosarcoma, and small round cell tumours (Figs. 18, 19, 20, 21) [16, 17]. While these primary lesions are rare, these should be considered in the absence of a known or suspected primary organ-based malignancy [17]. With respect to differentiating imaging findings for benign versus malignant neoplastic cakes, benign lesions usually are well circumscribed, while malignant cakes commonly have indistinct margins and invade surrounding structures [13].

Infectious diseases are rare causes of omental cakes. Typically, these diseases are the result of haematogenous, lymphatic, or direct spread of infectious organisms into the peritoneum.

Tuberculous peritonitis commonly exhibits omental manifestations, albeit this condition is rare in developed countries. The appearance frequently is similar to peritoneal carcinomatosis. Nevertheless, there are several findings that can help distinguish tuberculous peritonitis from peritoneal carcinomatosis. These include: mesenteric macronodules, irregularity of the infiltrated omentum, an omental line, i.e. a fibrous wall covering the infiltrated omentum, and/or splenomegaly or splenic calcification [18]. The “fibrotic-fixed” form of tuberculous peritonitis produces an omental mass that may mimic metastatic disease (Fig. 22) [19]. Furthermore, the presence of associated enlarged and necrotic mesenteric lymph nodes may be a coexisting finding to narrow the differential diagnosis towards tuberculosis.

Actinomycosis produces an infiltrative solid or cystic omental mass that invades normal anatomic barriers, usually with dense inhomogeneous contrast enhancement [20]. Due to nonspecific clinical findings of actinomycosis, the diagnosis often is not suspected. If there is an omental mass along with clinical signs of leukocytosis and fever without an attributable source, biopsy/aspiration can determine the aetiology (Fig. 23). Attention to the appendix and colon should also be made, as these are the most common intraabdominal organs involved with actinomycosis [20].

Coccidioidomycosis rarely involves the peritoneum and omentum, but also can exhibit an omental cake that mimics peritoneal malignancy (Fig. 24) [21]. In another report [22], CT showed peripherally enhancing deposits in the peritoneal cavity in a patient with systemic coccidioidomycosis. In patients with omental masses and systemic infection geographically in the San Joaquin Valley in California or in Arizona, endemic coccidioidomycosis should be considered. A differentiating feature of coccidioidomycosis is that the gastrointestinal manifestations of coccidioidomycosis are usually preceded by pulmonic, neurological, and musculoskeletal involvement.

Non-tuberculous mycobacterial infection, histoplasmosis, and omental paragonimiasis all have been reported to cause omental cakes [23, 24]. A unique feature of omental paragonimiasis is the multiple, irregularly shaped, conglomerate calcifications that sometimes occur [24].

Various rare benign processes can infiltrate the omentum to such a degree that an omental cake may develop. Extramedullary haematopoiesis, secondary to a number of conditions such as myelofibrosis, is another rare cause of omental caking (Fig. 25). Along with hepatosplenomegaly and multiple masses in various organs in the abdomen, mesenteric and omental masses should raise the suspicion of extramedullary haematopoiesis [23].

Sclerosing omentitis and amyloidosis both may involve the greater omentum and contain scattered calcifications that mimic the appearance of metastatic ovarian cancer or treated peritoneal mesothelioma [25]. Associated calcifications in the subcutaneous tissues, kidneys, and urethra may be additional clues of the presence of amyloidosis [25].

Due to the non-specific CT appearances of omental cakes, biopsy is important to diagnose the etiology if unknown. The superficial location of omental cakes is ideally suited for both image-guided fine-needle (20 g or smaller) and large needle core biopsy (19 g or larger) under either CT or US guidance (Fig. 26).

One study reported a sensitivity of 89.5%, specificity of 100%, and accuracy of 92% in the detection of malignancy in 25 percutaneous CT-guided large-needle core biopsies of omental lesions. Furthermore, they were able to obtain a specific diagnosis of the malignancy in 78.9% (15/19) of cases [26]. In another study of 111 percutaneous image-guided peritoneal and omental biopsies, the overall diagnostic rate was 89%, with a sensitivity of 93% and specificity of 86% [26]. Moreover, the authors concluded that a second malignancy was revealed in approximately 10% of patients with a known primary cancer (8/79), such as non-Hodgkin’s lymphoma [27].

The risk of serious complications is minimal with these relatively superficial omental biopsies. It should be noted, however, that although omental involvement can be both conspicuous and relatively straightforward to biopsy, early cases may be subtle and challenging both to visualize and to biopsy.

If there is any question of where the cake-bowel interface is, bowel opacification with oral contrast should be administered to avoid inadvertent needle puncture of the gastrointestinal tract. US also may be used in cases of unexplained ascites with a thickened omentum. One study showed that of 258 patients with nodules in the greater omentum, definitive diagnoses were achieved in 94.57% of cases by US-guided biopsy [8].