Mucosal lesions in the stomach include benign polypoid lesions, such as post-inflammatory, adenomatous, and hamartomatous polyps (Fig. 9.8). Post-inflammatory polyps are most common. They are typically small (<1 cm), of smooth and sessile morphology, and multiple in number. They have no malignant potential but may be associated with atrophic gastritis and gastric cancer. Adenomatous polyps are usually larger (>2 cm) and solitary, unless associated with familial polyposis syndromes, in which case colonic polyps are also seen. These include familial adenomatous polyposis, as well as Gardner’s syndrome (associated with osteomas and extraintestinal soft tissue tumors) and Turcot’s syndrome (associated with cerebral gliomas). Morphologically, adenomatous polyps are lobulated with a sessile or pedunculated base. Adenomas also have malignant potential [3, 14]. Gastric hamartomas are seen in the setting of Peutz-Jeghers, juvenile polyps, Cowden’s syndrome, and Cronkhite-Canada syndrome. Despite the lack of malignant potential in hamartomas, Peutz-Jeghers syndromes and Cowden’s syndrome are associated with extraintestinal malignancies, while juvenile polyps are associated with gastrointestinal cancer [15].

Early gastric adenocarcinoma usually presents as a mucosal lesion with limited invasion. These cancers are classified by according to morphology (Fig. 9.9): type I lesions are polypoid lesions extending >5 mm beyond the normal gastric wall, whereas Type IIa lesions protrude <5 mm. Type IIb are flat lesions appearing as mucosal irregularities. Type IIc lesions are depressed but confined to the mucosa, while type III lesions are frankly ulcerated lesions disrupting the muscularis mucosa but confined to the submucosa [3]. Early diagnosis of subtle lesions, especially type II and III lesions, may require more sophisticated tools, like VG [8].

Gastric cancer may continue to grow in mass-like fashion (Fig. 9.10), or further involvement may be in the form of segmental of diffuse gastric wall involvement [5]. Focal, eccentric, or prominent wall thickening (>1 cm) may suggest a malignant lesion, but no combination of these is both sensitive and specific for cancer [16]. More advanced gastric cancers penetrate the muscularis propria and beyond. Accurate assessment of local disease is key to effective therapy. Thus, CT criteria for local staging closely parallel the American Joint Committee on Cancer’s TNM staging (Fig. 9.11). Most important is detection of serosal invasion, which is a poor prognostic indicator. Hazy, linear, or reticular densities at the perigastric fat interface suggest such involvement (Fig. 9.12) [17]. Aside from the common presentation of a mucosal lesion or gastric mass, gastric adenocarcinoma may commonly present as a malignant ulcer or wall thickening, possibly with linitis plastica (Tables 9.2 and 9.3).

Perigastric and extraperigastric lymphadenopathy may be considered when lymph node short-axis reaches >6 mm and >8 mm, respectively, or when lymph nodes have eccentric or absent fatty hila, increased or heterogeneous enhancement, or round shape (longitudinal-transverse diameter ratio <1.5).

Extraperigastric lymphadenopathy (stations 12p-16) (Fig. 9.13) is considered distant metastasis, but the liver is the most common site of hematogenous spread. Less commonly, gastric adenocarcinoma metastasizes to the lungs, adrenal glands, kidneys, bones, and brain [3, 7]. Clues to peritoneal metastasis include ascites, peritoneal soft tissue lesions, peritoneal thickening, and hyperenhancement (Fig. 9.14) [3].

Spread via the peritoneum can also lead to “drop metastases” involving small bowel, sigmoid colon, and rectum, as well as ovaries. Ovarian metastases typically from a gastrointestinal source, but also from other primary tumors, such as the breast or lung, are known as Krukenberg tumors (Fig. 9.15). Krukenberg tumors may be seen as unilateral or bilateral mixed cystic and solid ovarian lesions with diameters ranging from 1 to 20 cm [2]. Metastases to uterus can rarely occur.

Detection of extraperigastric lymph nodes and distant solid organ metastases may be enhanced with the use of FDG-PET (Fig. 9.16). Small, but hypermetabolic lesions may be better detected with FDG-PET. Distant metastases outside the abdominopelvic coverage of CT may be detected by whole-body FDG-PET. Diffuse or multifocal abdominopelvic FDG uptake may suggest peritoneal metastases [7].

Predominantly submucosal processes such as gastric lymphoma and gastrointestinal stromal tumors can uncommonly have a nodular or polypoid appearance [18, 19]. Similarly, hematogenous metastases like malignant melanoma and Kaposi’s sarcoma typically grow intramurally but may have a nodular appearance that mimics mucosal lesions (Fig. 9.17). These two entities may be distinguished by their hyperenhancement, however [6].

Benign submucosal tumors typically present as small, smooth, hyperenhancing intramural soft tissue lesions (Figs. 9.18 and 9.19). These include mesenchymal tumors, most commonly gastrointestinal stromal tumors (GIST). GIST expresses KIT (CD117), a tyrosine kinase receptor, which is what distinguishes it from other mesenchymal tumors. The diagnosis typically requires histopathologic evaluation to assess for malignant GIST. Hemangiomas, leiomyomas, neural tumors, such as schwannomas or neuromas, and neuroendocrine tumors, such as carcinoids, are less common benign entities [5, 6, 19]. Pancreatic rests may have similar characteristics. These may be indistinguishable on CT or MRI.

Lipomas have characteristic features on CT and MRI with a typical fat density on CT (Fig. 9.20), T1 hyperintensity on nonfat-suppressed pulse sequences, and hypointensity following fat suppression [6].

Hyperdensity on non-contrast CT may also suggest an intramural hematoma, particularly in the setting of trauma or bleeding diathesis.

Hypertrophic pyloric stenosis (HPS) is known as a congenital lesion that presents in infancy [20]. In adults, idiopathic HPS may also present as focal wall thickening. More commonly, adult pyloric stenosis results secondary to other causes of wall thickening, such as peptic ulcer disease. Regardless of the cause, this condition may mimic gastric cancer on CT [5, 21].