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Pathology and Pathways of Spread
The terms gastric cancer and stomach cancer usually refer to adenocarcinoma, which accounts for 90% to 95% of all gastric malignancies. Other histologic types include lymphoma (usually intermediate- or high-grade histologic types), leiomyosarcoma, carcinoid, adenoacanthoma, and squamous cell carcinomas. The site of origin within the stomach has changed in frequency in the United States over recent decades, with more proximal lesions now being diagnosed and treated. The largest percentage of gastric cancers still arises within the antrum or distal stomach (around 40%), are least common in the body of the stomach (around 25%), and are of intermediate frequency in the fundus and esophagogastric junction (around 35%).47
Gastric carcinomas have been categorized by using both microscopic (Fig. 75-1) and gross pathological features. The Lauren classification system includes an intestinal type with improved prognosis that predominates in regions with high prevalence of gastric cancer, as well as a diffuse histologic type, with poor prognosis, which occurs more commonly in countries with low prevalence of stomach cancer.48 Grossly, gastric cancers can be categorized according to Borrmann’s49 five types: I, polypoid or fungating; II, ulcerating lesions surrounded by elevated borders; III, ulceration with invasion of the gastric wall; IV, diffusely infiltrating (linitis plastica); and V, unclassifiable. The Japanese Research Society for Gastric Cancer has a classification system that divides lesions into protruded (I); superficial (II) with elevated (IIa), flat (IIb), and depressed (IIc) subtypes; and excavated (III) types.50
Pathways of Tumor Spread
The stomach is surrounded by a number of organs and structures that can be involved by direct extension once a lesion has extended beyond the gastric wall. These structures include the omenta, pancreas, diaphragm, transverse colon or mesocolon, duodenum, jejunum, spleen, liver, superior mesenteric and celiac vessels, abdominal wall, left adrenal gland, and kidney. Adherence from inflammatory conditions can mimic direct extension of tumor, but all adhesions between a gastric carcinoma and adjacent structures must be regarded as malignant.
Abundant lymphatic channels are present within the submucosal and subserosal layers of the gastric wall. Microscopic or subclinical spread well beyond the visible gross lesion (intramural spread) occurs via these lymphatic channels. Accordingly, frozen sections of the gastric resection margins should be obtained intraoperatively to ensure that margins of resection are uninvolved microscopically. The submucosal lymphatic plexus is also prominent in the esophagus and the subserosal plexus in the duodenum, allowing both proximal and distal intramural tumor spread.
Because of the numerous pathways of lymphatic drainage from the stomach, it is difficult to perform a complete nodal dissection (E-Fig. 75-2). Although initial drainage is usually to lymph nodes along the lesser and greater curvatures (perigastric or N1 nodes using the Japanese Research Society for Gastric Cancer designation), primary node drainage includes nodes along all three branches of the celiac axis (common hepatic, splenic, left gastric) and the celiac artery itself (Japanese N2 nodes).50 Node groups that are more distal include hepatoduodenal, peripancreatic, root of mesentery (N3), periaortic, and middle colic (N4). When proximal gastric lesions extend into the distal esophagus, the paraesophageal nodal system is at risk for involvement.
For malignancies confined to the stomach, venous drainage is primarily to the liver via the portal system. At initial exploration, liver involvement is found in up to 30% of patients, predominantly as a result of hematogenous metastases but sometimes because of direct tumor extension. For lesions that extend proximally to involve the esophagus or posteriorly, the lung may be at risk for distant metastases.
Because the stomach is an intraperitoneal organ, peritoneal dissemination is possible once a lesion extends beyond the gastric wall to a free peritoneal (serosal) surface. Peritoneal spread may initially be a localized process limited by surrounding organs and ligaments (gastrohepatic, gastrosplenic, and gastrocolic).