DOI: 10.1148/rg.233025127
(Radiographics. 2003;23:625-644.)
© RSNA, 2003
Dedicated Multidetector CT of the Stomach: Spectrum of Diseases1
Ahmed Ba-Ssalamah, MD,
Mathias Prokop, MD,
Martin Uffmann, MD,
Peter Pokieser, MD,
Bela Teleky, MD and
Gerhard Lechner, MD
1 From the Departments of Radiology (A.B.S., M.P., M.U., P.P., G.L.) and Surgery (B.T.), University of Vienna, Währinger Gürtel 18–20, A-1090 Vienna, Austria. Recipient of a Certificate of Merit award for an education exhibit at the 2001 RSNA scientific assembly. Received July 15, 2002; revision requested September 6; final revision received January 3, 2003; accepted January 15. Address correspondence to A.B.S. (e-mail: ahmed.ba-ssalamah@univie.ac.at).
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Abstract
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Multidetector computed tomography (CT) offers new opportunities in imaging of the gastrointestinal tract. When thin collimation is used, near-isotropic imaging of the stomach is possible, allowing high-quality multiplanar reformation and three-dimensional reconstruction of gastric images. Proper distention of the stomach and optimally timed administration of intravenous contrast material are required to detect and characterize disease. In contrast to gastroscopy and double-contrast studies of the stomach, CT provides information about both the gastric wall and the extragastric extent of disease. Preoperative staging of gastric carcinoma appears to be the main clinical indication for multidetector CT. In addition, multidetector CT allows detection of other gastric malignancies (lymphoma, carcinoid tumors, metastases, gastrointestinal stromal tumors) and benign gastric tumors (neural tumors, polyps). Gastric inflammation (gastritis, ulcers, Ménétrier disease) and miscellaneous gastric conditions (emphysema, gastric outlet obstruction, varices) can also be visualized with multidetector CT. Multidetector CT is a valuable tool for the evaluation of gastric wall disease and serves as an adjunct to endoscopy.
© RSNA, 2003
Index Terms: Emphysema, gastrointestinal, 72.782 • Gastritis, 72.291 • Gastrointestinal stromal tumor (GIST), 72.3119 • Menetrier disease, 72.292 Stomach, neoplasms, 72.30, 72.34, 72.316, 72.33, 72.311 • Stomach, stenosis or obstruction, 72.74 • Stomach, ulcer, 72.25 • Stomach, varices, 72.75
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LEARNING OBJECTIVES FOR TEST 2
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After reading this article and taking the test, the reader will be able to:
- Describe the spectrum of common and uncommon multidetector CT findings of gastric diseases.
- Identify the multidetector CT features and criteria that help distinguish between the various gastric diseases.
- Discuss the usefulness of optimizing CT examination protocols by using two-phase multidetector CT with water as an oral contrast agent to demonstrate gastric diseases.
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Introduction
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Multidetector computed tomography (CT) offers new opportunities for imaging of gastrointestinal organs. When thin collimation is used, imaging of the stomach becomes possible and allows high-quality multiplanar reformation and three-dimensional visualization. Adequate distention of the stomach by using water as a negative contrast agent is a prerequisite for assessing the stomach wall. While such techniques have already been used with single-section spiral CT to improve staging of gastric malignancies, single-section scanning was substantially limited by a relatively large section thickness (1–3). Because of a substantial decrease in scanning time, optimization of intravenous contrast material injection is necessary with multidetector scanning. Proper contrast material injection techniques (4) offer improved differentiation of tumor tissue from normal mucosa. Thus, the combination of water-enhanced CT with near-isotropic multidetector imaging offers improved diagnosis of a large variety of gastric diseases. In comparison with endosonography, multidetector CT is able to demonstrate not only the immediate vicinity of the stomach but also more distant regions, such as paraaortic lymph nodes or abdominal organs. It can be expected that multidetector CT will be helpful in deciding between conservative and surgical therapy in selected patients.
This article reviews the applications of multidetector CT in a large variety of diseases of the stomach. Specific topics discussed are CT technique, gastric adenocarcinoma, other gastric malignancies, benign gastric tumors, gastric inflammation, miscellaneous conditions, and the clinical value of multidetector CT.
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CT Technique
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An optimum CT technique requires high spatial resolution, proper gastric distention, and proper timing of contrast media injection to detect subtle changes in the gastric wall and to accurately stage tumors. Table 1 provides an overview of techniques for various multidetector CT scanner types.
We performed CT examinations on a four–detector row CT scanner with a 0.5-second tube rotation (Somatom Volume Zoom; Siemens, Forchheim, Germany). To acquire a near-isotropic data set, we chose 4 x 1-mm collimation and reconstructed 1.25-mm-thick sections every 0.7 mm. For diagnostic viewing, we reconstructed 3–4-mm-thick axial sections either directly from the scanning data or from the thin-section volumetric data set (the secondary raw data set) using the multiplanar reformation function of the scanner console. In addition, we routinely performed coronal and sagittal reformation in the region of the stomach. Because of high image noise on the original 1.25-mm-thick sections, the width of these reformatted sections was increased to 3–5 mm, depending on the size of the patient. Interactive reformation is helpful whenever diagnostic questions remain unresolved at standard multiplanar reformation. We performed interactive reformation on a dedicated CT workstation (MagicView 1000; Siemens).
Contrast material injection for the stomach was timed in a manner that ensured portal phase imaging. If tumor staging was required, an additional arterial phase examination of the liver was added to the protocol. In such cases, the scanning range included only the liver and stomach in the arterial phase and the upper abdomen down to the iliac crest for the portal venous phase (Table 1). We used 125 kVp and 150 mAseff as the exposure settings. The resulting volume CT dose index, as an indicator of average local dose, was 17.1 mGy for each multidetector acquisition. This number may be varied with patient size: 125 kVp and 10 mGy appear sufficient for slim patients, but for very obese patients, 140 kVp and up to 30 mGy should be used for optimal image quality.
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Gastric Adenocarcinoma
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Gastric cancer remains a deadly disease, with overall 5-year survival rates of less than 20%. However, early gastric cancers are curable lesions, with 5-year survival rates of more than 90%. The peak prevalence is between 50 and 70 years of age (5). Gastric carcinoma has striking geographic variations, with the highest prevalences reported in Japan. Conditions that predispose patients to the development of gastric carcinoma include atrophic gastritis, pernicious anemia, gastric polyps, partial gastrectomy, and Ménétrier disease (6). About 30% of cancers are located in the antrum, 30% in the body, and 30% in the fundus or cardia region. The remaining 10% are diffusely infiltrating lesions that involve the entire stomach. Most gastric cancers are adenocarcinomas of mucous cell origin (7). Signet-ring cell carcinomas account for 5%–15% of all gastric cancers and typically cause scirrhous infiltration of the gastric wall (8). Scirrhous carcinomas frequently involve the distal half of the stomach, arise near the pylorus, and gradually extend upward from the antrum into the body and fundus. In advanced cases, the entire stomach is infiltrated by tumor.
Tumor Detection and Classification
Gastric carcinomas may manifest as a focal area of mural thickening with or without ulceration, as a polypoid lesion, or as generalized mural thickening.
In early gastric cancers, malignant invasion is limited to the mucosa or submucosa, regardless of the presence of lymph node metastases (9). Early cancers are classified into three types (10) (Fig 1), and type I lesions can be better detected than type II and III lesions (Fig 2).
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Figure 1a. Types of early gastric cancer. Thin straight line = mucosa, jagged line = muscularis mucosae, thick straight line = muscularis propria. (a) Type I lesions are elevated and protrude more than 5 mm into the lumen. (b) Type IIa lesions are elevated but protrude less than 5 mm into the lumen. (c) Type IIb lesions are essentially flat. (d) Type IIc lesions are slightly depressed but do not penetrate the muscularis mucosae. (e) Type III lesions are true mucosal ulcers that penetrate the muscularis mucosae but not the muscularis propria. (Adapted and reprinted, with permission, from reference 10.)
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Figure 1b. Types of early gastric cancer. Thin straight line = mucosa, jagged line = muscularis mucosae, thick straight line = muscularis propria. (a) Type I lesions are elevated and protrude more than 5 mm into the lumen. (b) Type IIa lesions are elevated but protrude less than 5 mm into the lumen. (c) Type IIb lesions are essentially flat. (d) Type IIc lesions are slightly depressed but do not penetrate the muscularis mucosae. (e) Type III lesions are true mucosal ulcers that penetrate the muscularis mucosae but not the muscularis propria. (Adapted and reprinted, with permission, from reference 10.)
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Figure 1c. Types of early gastric cancer. Thin straight line = mucosa, jagged line = muscularis mucosae, thick straight line = muscularis propria. (a) Type I lesions are elevated and protrude more than 5 mm into the lumen. (b) Type IIa lesions are elevated but protrude less than 5 mm into the lumen. (c) Type IIb lesions are essentially flat. (d) Type IIc lesions are slightly depressed but do not penetrate the muscularis mucosae. (e) Type III lesions are true mucosal ulcers that penetrate the muscularis mucosae but not the muscularis propria. (Adapted and reprinted, with permission, from reference 10.)
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Figure 1d. Types of early gastric cancer. Thin straight line = mucosa, jagged line = muscularis mucosae, thick straight line = muscularis propria. (a) Type I lesions are elevated and protrude more than 5 mm into the lumen. (b) Type IIa lesions are elevated but protrude less than 5 mm into the lumen. (c) Type IIb lesions are essentially flat. (d) Type IIc lesions are slightly depressed but do not penetrate the muscularis mucosae. (e) Type III lesions are true mucosal ulcers that penetrate the muscularis mucosae but not the muscularis propria. (Adapted and reprinted, with permission, from reference 10.)
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Figure 1e. Types of early gastric cancer. Thin straight line = mucosa, jagged line = muscularis mucosae, thick straight line = muscularis propria. (a) Type I lesions are elevated and protrude more than 5 mm into the lumen. (b) Type IIa lesions are elevated but protrude less than 5 mm into the lumen. (c) Type IIb lesions are essentially flat. (d) Type IIc lesions are slightly depressed but do not penetrate the muscularis mucosae. (e) Type III lesions are true mucosal ulcers that penetrate the muscularis mucosae but not the muscularis propria. (Adapted and reprinted, with permission, from reference 10.)
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Figure 2a. Early gastric cancer (pathologic stage T1). (a) Sagittal reformatted image shows a type I tumor as an enhancing polypoid lesion (arrow) that protrudes more than 5 mm into the lumen. (b) Coronal reformatted image shows a type IIa tumor as an elevated lesion in the greater curvature that protrudes less than 5 mm into the lumen. There is marked focal enhancement of the inner layer of the gastric wall (arrows). (c) Coronal reformatted image shows a type IIb tumor as focal thickening of the gastric wall with marked enhancement but an essentially flat surface (arrows). The other nodular protrusions of the gastric wall correspond to normal folds, which are stretched out because of gastric dilatation. (d) Oblique sagittal reformatted image shows a type III tumor as focal thickening of the gastric wall with a central ulcer (arrow).
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Figure 2b. Early gastric cancer (pathologic stage T1). (a) Sagittal reformatted image shows a type I tumor as an enhancing polypoid lesion (arrow) that protrudes more than 5 mm into the lumen. (b) Coronal reformatted image shows a type IIa tumor as an elevated lesion in the greater curvature that protrudes less than 5 mm into the lumen. There is marked focal enhancement of the inner layer of the gastric wall (arrows). (c) Coronal reformatted image shows a type IIb tumor as focal thickening of the gastric wall with marked enhancement but an essentially flat surface (arrows). The other nodular protrusions of the gastric wall correspond to normal folds, which are stretched out because of gastric dilatation. (d) Oblique sagittal reformatted image shows a type III tumor as focal thickening of the gastric wall with a central ulcer (arrow).
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Figure 2c. Early gastric cancer (pathologic stage T1). (a) Sagittal reformatted image shows a type I tumor as an enhancing polypoid lesion (arrow) that protrudes more than 5 mm into the lumen. (b) Coronal reformatted image shows a type IIa tumor as an elevated lesion in the greater curvature that protrudes less than 5 mm into the lumen. There is marked focal enhancement of the inner layer of the gastric wall (arrows). (c) Coronal reformatted image shows a type IIb tumor as focal thickening of the gastric wall with marked enhancement but an essentially flat surface (arrows). The other nodular protrusions of the gastric wall correspond to normal folds, which are stretched out because of gastric dilatation. (d) Oblique sagittal reformatted image shows a type III tumor as focal thickening of the gastric wall with a central ulcer (arrow).
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Figure 2d. Early gastric cancer (pathologic stage T1). (a) Sagittal reformatted image shows a type I tumor as an enhancing polypoid lesion (arrow) that protrudes more than 5 mm into the lumen. (b) Coronal reformatted image shows a type IIa tumor as an elevated lesion in the greater curvature that protrudes less than 5 mm into the lumen. There is marked focal enhancement of the inner layer of the gastric wall (arrows). (c) Coronal reformatted image shows a type IIb tumor as focal thickening of the gastric wall with marked enhancement but an essentially flat surface (arrows). The other nodular protrusions of the gastric wall correspond to normal folds, which are stretched out because of gastric dilatation. (d) Oblique sagittal reformatted image shows a type III tumor as focal thickening of the gastric wall with a central ulcer (arrow).
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Advanced gastric cancer invades the muscularis propria. Advanced cancer (9) may manifest as large, segmental (Fig 3a), or diffuse wall thickening with irregular lobulation and, often, ulcer-ation (Fig 3b). Signet-ring cell cancer usually manifests as a scirrhous tumor of the stomach that leads to obliteration of gastric folds and diffuse thickening of the gastric wall (linitis plastica) (Fig 3c). Gastric carcinoma can manifest as large, polypoid, fungating lesions (Fig 4a).
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Figure 3a. Advanced gastric cancer (pathologic stage T2). (a) Coronal reformatted image shows focal wall thickening in the antrum with marked enhancement of the mucosal layer (arrows). At histologic analysis, the outer layers of the muscularis propria were intact, whereas the inner layers were infiltrated. The subtle irregularities of the mucosal surface corresponded to ulcers at histologic analysis. Note the clear fat plane around the tumor. (b) Axial CT scan shows a large carcinoma at the lesser curvature. Note that there is an area of irregular distinction of the tumor from the surrounding fat (arrowhead), which corresponded to a desmoplastic reaction at histologic analysis. There are two slightly hyperenhancing lymph nodes adjacent to each other (arrow). Both proved to be metastasis positive at histologic analysis. (c) Sagittal reformatted image shows diffuse thickening of the gastric wall in the fundus and body regions due to linitis plastica. Note the lack of gastric folds and the decreased distention in the affected region.
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Figure 3b. Advanced gastric cancer (pathologic stage T2). (a) Coronal reformatted image shows focal wall thickening in the antrum with marked enhancement of the mucosal layer (arrows). At histologic analysis, the outer layers of the muscularis propria were intact, whereas the inner layers were infiltrated. The subtle irregularities of the mucosal surface corresponded to ulcers at histologic analysis. Note the clear fat plane around the tumor. (b) Axial CT scan shows a large carcinoma at the lesser curvature. Note that there is an area of irregular distinction of the tumor from the surrounding fat (arrowhead), which corresponded to a desmoplastic reaction at histologic analysis. There are two slightly hyperenhancing lymph nodes adjacent to each other (arrow). Both proved to be metastasis positive at histologic analysis. (c) Sagittal reformatted image shows diffuse thickening of the gastric wall in the fundus and body regions due to linitis plastica. Note the lack of gastric folds and the decreased distention in the affected region.
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Figure 3c. Advanced gastric cancer (pathologic stage T2). (a) Coronal reformatted image shows focal wall thickening in the antrum with marked enhancement of the mucosal layer (arrows). At histologic analysis, the outer layers of the muscularis propria were intact, whereas the inner layers were infiltrated. The subtle irregularities of the mucosal surface corresponded to ulcers at histologic analysis. Note the clear fat plane around the tumor. (b) Axial CT scan shows a large carcinoma at the lesser curvature. Note that there is an area of irregular distinction of the tumor from the surrounding fat (arrowhead), which corresponded to a desmoplastic reaction at histologic analysis. There are two slightly hyperenhancing lymph nodes adjacent to each other (arrow). Both proved to be metastasis positive at histologic analysis. (c) Sagittal reformatted image shows diffuse thickening of the gastric wall in the fundus and body regions due to linitis plastica. Note the lack of gastric folds and the decreased distention in the affected region.
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Figure 4a. Advanced gastric cancer (pathologic stage T3). (a) Axial CT scan shows a large, polypoid carcinoma with gross infiltration of the perigastric fatty tissue (arrows). (b) Oblique coronal reformatted image, tilted posteriorly to display the body and fundus of the stomach and the distal esophagus, shows a large tumor (T) that protrudes from the posterior wall into the lumen and appears as a filling defect within the water-filled stomach. Note the high-attenuation stranding in the perigastric fat (arrow) and the oval lymph node (arrowhead), which was hyperplastic at histologic analysis.
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Figure 4b. Advanced gastric cancer (pathologic stage T3). (a) Axial CT scan shows a large, polypoid carcinoma with gross infiltration of the perigastric fatty tissue (arrows). (b) Oblique coronal reformatted image, tilted posteriorly to display the body and fundus of the stomach and the distal esophagus, shows a large tumor (T) that protrudes from the posterior wall into the lumen and appears as a filling defect within the water-filled stomach. Note the high-attenuation stranding in the perigastric fat (arrow) and the oval lymph node (arrowhead), which was hyperplastic at histologic analysis.
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Carcinoma of the gastric cardia may be difficult to appreciate at CT because of the normal soft-tissue thickening that occurs at the gastroesophageal junction due to the reflections of the phrenoesophageal ligament and the attachments of the gastrohepatic ligament on the adjacent lesser curvature. Proper distention of the stomach helps distinguish a focal tumor from the normal gastroesophageal junction.
T Staging.—
Criteria for differentiating the various T stages are given in Table 2 (11). In early advanced gastric cancers (T2), malignant invasion is limited to the muscularis propria or serosa and the outer border may be smooth (Fig 3a) or show a few small linear strands of soft tissue extending into the fat plane, as is the case with a desmoplastic or inflammatory reaction (Fig 3b). The probability of transmural extension of the tumor (T3) is directly correlated with mural thickness. In transmural extension, the serosal contour becomes blurred and strandlike areas of increased attenuation may be seen extending into the perigastric fat (Fig 4). Tumor spread frequently occurs via ligamentous and peritoneal reflections to adjacent organs (T4) (Fig 5). The liver may be invaded via the gastrohepatic ligament, the pancreas via the lesser sac (Fig 5a), and the transverse colon via the gastrocolic ligament (Fig 5b). The distal esophagus is directly involved by carcinoma of the cardia in about 60% of patients (Fig 5c), whereas the duodenum is involved by carcinoma of the antrum in 13%–18% of patients. It is often difficult to distinguish infiltration into the transverse mesocolon (T4) from infiltration of the mesenteric fat. Coronal or sagittal reformatted images are best suited for this purpose (Fig 5b).
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Figure 5a. Advanced gastric cancer (pathologic stage T4). (a) Axial CT scan shows an advanced cancer of the posterior wall of the gastric body that infiltrates the pancreatic tail (arrow). (b) Coronal reformatted image of the posterior portions of the abdomen shows a large gastric cancer with obliteration of the fat plane and thickening of the colonic wall (arrow). At histologic analysis, the transverse colon was infiltrated. (c) Oblique coronal reformatted image obtained through the esophagus and the fundus and body of the stomach shows circumferential thickening of the gastric wall with loss of gastric folds due to linitis plastica. The tumor extends into the distal esophagus (arrow).
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Figure 5b. Advanced gastric cancer (pathologic stage T4). (a) Axial CT scan shows an advanced cancer of the posterior wall of the gastric body that infiltrates the pancreatic tail (arrow). (b) Coronal reformatted image of the posterior portions of the abdomen shows a large gastric cancer with obliteration of the fat plane and thickening of the colonic wall (arrow). At histologic analysis, the transverse colon was infiltrated. (c) Oblique coronal reformatted image obtained through the esophagus and the fundus and body of the stomach shows circumferential thickening of the gastric wall with loss of gastric folds due to linitis plastica. The tumor extends into the distal esophagus (arrow).
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Figure 5c. Advanced gastric cancer (pathologic stage T4). (a) Axial CT scan shows an advanced cancer of the posterior wall of the gastric body that infiltrates the pancreatic tail (arrow). (b) Coronal reformatted image of the posterior portions of the abdomen shows a large gastric cancer with obliteration of the fat plane and thickening of the colonic wall (arrow). At histologic analysis, the transverse colon was infiltrated. (c) Oblique coronal reformatted image obtained through the esophagus and the fundus and body of the stomach shows circumferential thickening of the gastric wall with loss of gastric folds due to linitis plastica. The tumor extends into the distal esophagus (arrow).
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N Staging.—
Lymphatic spread is found in 74%–88% of patients with gastric carcinoma because of the abundant lymphatic vessels in the stomach (12). The frequency of lymphatic metastases is related to the size and depth of penetration of the tumor. According to the American Joint Committee on Cancer (13), N staging depends on the number of positive perigastric lymph nodes (N1 = one to five, N2 = six to 15, and N3 = >15 affected lymph nodes) (Figs 6, 7). Lymph node assessment for metastatic spread remains a challenge even with multidetector CT. However, improved evaluation appears possible if both morphologic and enhancement criteria are used (Table 2).
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Figure 6a. Normal lymph nodes in gastric cancer. (a) Axial CT scan shows a small, slightly oval lymph node 4 mm in diameter without significant enhancement (arrow). (b) Coronal reformatted image obtained through the gastric fundus shows a large gastric cancer of the cardia (pathologic stage T2) with multiple lymph nodes. Note the two inhomogeneous enhancing nodes greater than or equal to 8 mm in diameter (arrows), as well as the multiple nodes less than 6 mm in diameter (arrowheads). At histologic analysis, all of the nodes were metastasis negative.
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Figure 6b. Normal lymph nodes in gastric cancer. (a) Axial CT scan shows a small, slightly oval lymph node 4 mm in diameter without significant enhancement (arrow). (b) Coronal reformatted image obtained through the gastric fundus shows a large gastric cancer of the cardia (pathologic stage T2) with multiple lymph nodes. Note the two inhomogeneous enhancing nodes greater than or equal to 8 mm in diameter (arrows), as well as the multiple nodes less than 6 mm in diameter (arrowheads). At histologic analysis, all of the nodes were metastasis negative.
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Figure 7a. Lymph node metastases in gastric cancer (pathologic stages N1-N3). (a) Axial CT scan shows an ulcerated gastric cancer of the antrum with multiple hepatic metastases (pT2 pN1 pM1). Compare the metastasis-positive lymph node (diameter, 8 mm) (small arrow) with the metastasis-negative lymph node (diameter, 6 mm) (arrowhead). The hemiazygos vein (large arrow) may mimic a hyperenhancing lymph node in the retrocrural position. (b) Axial CT scan shows a moderately large ulcerated carcinoma of the lesser curvature that extends into the antrum (pT2). There are multiple round, hyperattenuating, metastasis-positive lymph nodes (pN2) (arrows) in the perigastric fat close to the left gastric artery. Note the group of hyperplastic lymph nodes smaller than 6 mm in diameter (arrowhead). (c) Coronal reformatted image shows multiple round and enlarged perigastric and paraaortic lymph nodes (pN3) (arrows) and multiple hepatic metastases (pM1) (arrowheads). Note the irregular contours of the organ borders due to continuous breathing in this dyspneic patient.
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Figure 7b. Lymph node metastases in gastric cancer (pathologic stages N1-N3). (a) Axial CT scan shows an ulcerated gastric cancer of the antrum with multiple hepatic metastases (pT2 pN1 pM1). Compare the metastasis-positive lymph node (diameter, 8 mm) (small arrow) with the metastasis-negative lymph node (diameter, 6 mm) (arrowhead). The hemiazygos vein (large arrow) may mimic a hyperenhancing lymph node in the retrocrural position. (b) Axial CT scan shows a moderately large ulcerated carcinoma of the lesser curvature that extends into the antrum (pT2). There are multiple round, hyperattenuating, metastasis-positive lymph nodes (pN2) (arrows) in the perigastric fat close to the left gastric artery. Note the group of hyperplastic lymph nodes smaller than 6 mm in diameter (arrowhead). (c) Coronal reformatted image shows multiple round and enlarged perigastric and paraaortic lymph nodes (pN3) (arrows) and multiple hepatic metastases (pM1) (arrowheads). Note the irregular contours of the organ borders due to continuous breathing in this dyspneic patient.
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Figure 7c. Lymph node metastases in gastric cancer (pathologic stages N1-N3). (a) Axial CT scan shows an ulcerated gastric cancer of the antrum with multiple hepatic metastases (pT2 pN1 pM1). Compare the metastasis-positive lymph node (diameter, 8 mm) (small arrow) with the metastasis-negative lymph node (diameter, 6 mm) (arrowhead). The hemiazygos vein (large arrow) may mimic a hyperenhancing lymph node in the retrocrural position. (b) Axial CT scan shows a moderately large ulcerated carcinoma of the lesser curvature that extends into the antrum (pT2). There are multiple round, hyperattenuating, metastasis-positive lymph nodes (pN2) (arrows) in the perigastric fat close to the left gastric artery. Note the group of hyperplastic lymph nodes smaller than 6 mm in diameter (arrowhead). (c) Coronal reformatted image shows multiple round and enlarged perigastric and paraaortic lymph nodes (pN3) (arrows) and multiple hepatic metastases (pM1) (arrowheads). Note the irregular contours of the organ borders due to continuous breathing in this dyspneic patient.
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M Staging.—
Hematogenous metastases from gastric carcinoma most commonly involve the liver because the stomach is drained by the portal vein (Fig 7c). Other less common sites of hematogenous spread include the lungs, adrenal glands, kidneys, bones, and brain. Lymph node involvement outside the perigastric location is considered M1 disease. Advanced cancers can develop peritoneal metastases (Fig 8). Some patients with signet-ring cell gastric carcinomas may have intraperitoneally seeded metastases to the ovaries, which are known as Krukenberg tumors.
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Figure 8. Spread of gastric cancer. Oblique coronal reformatted image obtained to display the fundus, body, and antrum of the stomach shows an advanced cancer in the gastric body with ascites and peritoneal carcinomatosis (arrowheads). The cancer was surgically proved.
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Follow-up after Partial Gastrectomy
A gastric "stump" cancer is defined as a primary carcinoma of the gastric remnant that occurs after latent periods of 15–25 years from the time of gastrectomy for gastric ulcers or other benign disease (Fig 9a). Affected individuals usually have undergone a Billroth II procedure rather than a Billroth I procedure. These tumors tend to be located in the distal portion of the gastric remnant near the gastrojejunal anastomosis. It has been postulated that recurrent bile reflux above the anastomosis causes chronic gastritis, intestinal metaplasia, and eventually gastric carcinoma. Not all thickening of the anastomotic region is due to tumor involvement (Fig 9b). Gastric surgery, such as a Nissen procedure for gastric reflux, can sometimes lead to marked fold thickening (Fig 9c) or postoperative complications such as seroma (Fig 9d).
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Figure 9a. Postoperative findings. (a) Oblique coronal reformatted image, obtained to display the gastroesophageal junction as well as the gastroenterostomy after partial gastrectomy for adenocarcinoma of the stomach, shows a large recurrent tumor (arrows) in the region of the anastomosis that infiltrates the remaining portions of the lesser curvature up to the gastroesophageal junction. The tumor was histologically proved. (b) Oblique axial image, tilted laterally to display the gastrojejunostomy after a Billroth II resection, shows substantial thickening of the anastomotic region (arrow). However, there was no evidence of malignancy in multiple biopsy specimens. (c) Axial CT scan obtained after fundoplication shows marked fold thickening at the gastroesophageal junction (arrows). (d) Coronal reformatted image, obtained through the gastric fundus after a Billroth II resection, shows a round, homogeneous seroma (arrow) adjacent to the lesser curvature. The seroma was biopsy proved.
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Figure 9b. Postoperative findings. (a) Oblique coronal reformatted image, obtained to display the gastroesophageal junction as well as the gastroenterostomy after partial gastrectomy for adenocarcinoma of the stomach, shows a large recurrent tumor (arrows) in the region of the anastomosis that infiltrates the remaining portions of the lesser curvature up to the gastroesophageal junction. The tumor was histologically proved. (b) Oblique axial image, tilted laterally to display the gastrojejunostomy after a Billroth II resection, shows substantial thickening of the anastomotic region (arrow). However, there was no evidence of malignancy in multiple biopsy specimens. (c) Axial CT scan obtained after fundoplication shows marked fold thickening at the gastroesophageal junction (arrows). (d) Coronal reformatted image, obtained through the gastric fundus after a Billroth II resection, shows a round, homogeneous seroma (arrow) adjacent to the lesser curvature. The seroma was biopsy proved.
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Figure 9c. Postoperative findings. (a) Oblique coronal reformatted image, obtained to display the gastroesophageal junction as well as the gastroenterostomy after partial gastrectomy for adenocarcinoma of the stomach, shows a large recurrent tumor (arrows) in the region of the anastomosis that infiltrates the remaining portions of the lesser curvature up to the gastroesophageal junction. The tumor was histologically proved. (b) Oblique axial image, tilted laterally to display the gastrojejunostomy after a Billroth II resection, shows substantial thickening of the anastomotic region (arrow). However, there was no evidence of malignancy in multiple biopsy specimens. (c) Axial CT scan obtained after fundoplication shows marked fold thickening at the gastroesophageal junction (arrows). (d) Coronal reformatted image, obtained through the gastric fundus after a Billroth II resection, shows a round, homogeneous seroma (arrow) adjacent to the lesser curvature. The seroma was biopsy proved.
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Figure 9d. Postoperative findings. (a) Oblique coronal reformatted image, obtained to display the gastroesophageal junction as well as the gastroenterostomy after partial gastrectomy for adenocarcinoma of the stomach, shows a large recurrent tumor (arrows) in the region of the anastomosis that infiltrates the remaining portions of the lesser curvature up to the gastroesophageal junction. The tumor was histologically proved. (b) Oblique axial image, tilted laterally to display the gastrojejunostomy after a Billroth II resection, shows substantial thickening of the anastomotic region (arrow). However, there was no evidence of malignancy in multiple biopsy specimens. (c) Axial CT scan obtained after fundoplication shows marked fold thickening at the gastroesophageal junction (arrows). (d) Coronal reformatted image, obtained through the gastric fundus after a Billroth II resection, shows a round, homogeneous seroma (arrow) adjacent to the lesser curvature. The seroma was biopsy proved.
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Other Gastric Malignancies
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Gastric Lymphoma
Lymphoma involves the stomach more frequently than any other portion of the gastrointestinal tract (14). Primary gastric lymphomas are confined to the stomach and regional lymph nodes (about 35% of gastrointestinal lymphomas) and are predominantly non-Hodgkin lymphomas of B-cell origin (14). Lymphoma of mucosa-associated lymphoid tissue (MALT) is a distinct type of extranodal lymphoma that is characterized by a relatively indolent clinical course and has a much better prognosis than gastric carcinoma, with overall 5-year survival rates of 50%–60% (15). There is evidence linking Helicobacter pylori gastritis with the development of lymphomas of the MALT type (16). It is thus proposed that H pylori infection may trigger the acquisition of MALT and that the subsequent inflammatory response may be a prerequisite for the development of MALT lymphoma. It has further been proposed that MALT lymphoma may be a precursor of high-grade B-cell non-Hodgkin lymphoma in gastric tissue and that most high-grade lymphomas follow this evolutionary pathway (17). However, high-grade B-cell gastric lymphoma may also arise de novo (18). Although the clinical symptoms in high-grade lymphoma and MALT lymphoma may be similar, they differ in several aspects. High-grade B-cell lymphoma has a relatively aggressive course as opposed to the more indolent and favorable outcome of MALT lymphoma (19). In high-grade gastric lymphomas, the extent of disease is usually greater at presentation, with involvement of adjacent organs and perigastric lymph nodes (19).
Lymphomas may involve any portion of the stomach. Transpyloric spread of tumor into the duodenum occurs in about 30% of patients (20). Despite extensive lymphomatous infiltration, the stomach usually remains pliable and distensible without significant luminal narrowing.
Early gastric lymphoma is confined to the mucosa and submucosa (Fig 10a), with an average size of only 3.5 cm at diagnosis (21). Gastric lymphomas are usually advanced lesions with a mean diameter of 10 cm (Fig 10b). Most cases involve the antrum and body, although the entire stomach can be involved.
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Figure 10a. Gastric lymphoma (biopsy proved). (a) Coronal reformatted image shows an early gastric lymphoma as focal thickening of the antral wall (arrows). (b) Sagittal reformatted image shows an advanced B-cell lymphoma as bulky disease.
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Figure 10b. Gastric lymphoma (biopsy proved). (a) Coronal reformatted image shows an early gastric lymphoma as focal thickening of the antral wall (arrows). (b) Sagittal reformatted image shows an advanced B-cell lymphoma as bulky disease.
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There are four gross pathologic types of gastric lymphoma (22): Infiltrative gastric lymphomas manifest as focal or diffuse enlargement of gastric folds due to submucosal spread of tumor (Fig 11a). One or more ulcerated lesions characterize ulcerative gastric lymphoma (Fig 11b). Polypoid gastric lymphomas are characterized by intraluminal masses that may simulate polypoid carcinomas (Fig 11c). Multiple submucosal nodules ranging in size between several millimeters and several centimeters characterize nodular gastric lymphoma (Fig 11d).
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Figure 11a. Morphologic types of gastric lymphoma (biopsy proved). (a) Axial CT scan shows an infiltrative gastric lymphoma as large areas of gastric wall thickening (arrows) with enlarged lymph nodes (arrowhead). (b) Coronal reformatted image shows a polypoid advanced gastric lymphoma with ulceration (arrow) and extensive extension into the mesenteric root (arrowhead). (c) Coronal reformatted image shows a polypoid advanced gastric lymphoma as segmental thickening (arrowhead) and a large polypoid filling defect arising from the posterior wall of the stomach (arrow). (d) Coronal reformatted image shows a nodular gastric lymphoma as nodular thickening of the gastric wall.
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Figure 11b. Morphologic types of gastric lymphoma (biopsy proved). (a) Axial CT scan shows an infiltrative gastric lymphoma as large areas of gastric wall thickening (arrows) with enlarged lymph nodes (arrowhead). (b) Coronal reformatted image shows a polypoid advanced gastric lymphoma with ulceration (arrow) and extensive extension into the mesenteric root (arrowhead). (c) Coronal reformatted image shows a polypoid advanced gastric lymphoma as segmental thickening (arrowhead) and a large polypoid filling defect arising from the posterior wall of the stomach (arrow). (d) Coronal reformatted image shows a nodular gastric lymphoma as nodular thickening of the gastric wall.
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Figure 11c. Morphologic types of gastric lymphoma (biopsy proved). (a) Axial CT scan shows an infiltrative gastric lymphoma as large areas of gastric wall thickening (arrows) with enlarged lymph nodes (arrowhead). (b) Coronal reformatted image shows a polypoid advanced gastric lymphoma with ulceration (arrow) and extensive extension into the mesenteric root (arrowhead). (c) Coronal reformatted image shows a polypoid advanced gastric lymphoma as segmental thickening (arrowhead) and a large polypoid filling defect arising from the posterior wall of the stomach (arrow). (d) Coronal reformatted image shows a nodular gastric lymphoma as nodular thickening of the gastric wall.
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Figure 11d. Morphologic types of gastric lymphoma (biopsy proved). (a) Axial CT scan shows an infiltrative gastric lymphoma as large areas of gastric wall thickening (arrows) with enlarged lymph nodes (arrowhead). (b) Coronal reformatted image shows a polypoid advanced gastric lymphoma with ulceration (arrow) and extensive extension into the mesenteric root (arrowhead). (c) Coronal reformatted image shows a polypoid advanced gastric lymphoma as segmental thickening (arrowhead) and a large polypoid filling defect arising from the posterior wall of the stomach (arrow). (d) Coronal reformatted image shows a nodular gastric lymphoma as nodular thickening of the gastric wall.
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CT is the primary imaging modality for pretreatment evaluation of abdominal lymphoma. In patients with suspected gastric lymphoma, multidetector CT may allow both depiction of a stomach lesion and staging of generalized lymphoma in the abdomen and chest. Furthermore, multidetector CT may aid in early diagnosis of disease progression in patients undergoing therapy and follow-up for low-grade MALT lymphoma, which may progress to high-grade B-cell lymphoma. However, the CT appearances of lymphoma and gastric carcinoma may be very similar (Table 3).
Carcinoid Tumors
Carcinoid tumors of the stomach are rare (prevalence, approximately 0.3%) (23). Clinicopathologic characterization of gastric carcinoid tumors has revealed three subtypes, which have unique endoscopic appearances, predisposing conditions, and clinical outcomes.
Type 1 gastric carcinoid tumors are associated with enterochromaffin-like cell hyperplasia, hypergastrinemia, and chronic atrophic gastritis, with or without pernicious anemia. Type 1 tumors generally represent benign disease. Nodal and hepatic metastases are very rare (24).
Type 2 tumors are the least common type, representing 5%–10% of gastric carcinoid tumors. They are seen in the hypergastrinemic state of Zollinger-Ellison syndrome in association with multiple endocrine neoplasia (MEN) type 1. Approximately 30% of patients with MEN 1 have gastric carcinoid tumors (25). Type 2 tumors also arise from enterochromaffin-like cells in the setting of hyperplasia. These tumors are multicentric and variable in size but are prone to developing local lymph node metastases. Tumor-related death is rare, as is carcinoid syndrome. The appearance of these tumors on CT scans and radiographs of the upper gastrointestinal tract can be striking because there are multiple masses in the setting of diffuse gastric wall thickening (26).
Type 3 gastric carcinoid tumors are sporadic tumors and are not associated with a hypergastrinemic state. They represent about 13% of gastric carcinoid tumors (24). Unlike type 1 and 2 tumors, type 3 tumors are large, solitary tumors that may show ulceration and are more likely to be invasive with distant metastases (Fig 12). The likelihood of metastasis is dependent on tumor size (25). Carcinoid syndrome may be seen in patients with hepatic metastases. The prognosis is poor, with 20% of patients surviving 5 years (24,25).
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Figure 12. Carcinoid tumor. Coronal reformatted image shows a gastric carcinoid tumor as an ulcerated mass. The tumor was biopsy proved. Note the thickened rim of the ulcer (arrows). Also note the presence of two hepatic metastases.
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The improved understanding of gastric carcinoid tumors has important implications for radiologic evaluation of patients. When these tumors are suspected, contrast material and water enhanced multidetector CT should be used to detect small mucosal masses. The discovery of polyps in a patient known to have chronic atrophic gastritis should alert the radiologist to the possibility of type 1 gastric carcinoid tumors. Multidetector CT is necessary to properly assess type 2 (MEN 1 associated) and type 3 (sporadic) gastric carcinoid tumors, given the increased predisposition for nodal and hepatic metastases (26).
Metastases
Gastric metastases are found at autopsy in less than 2% of patients who die of carcinoma. The majority of lesions are hematogenous metastases from malignant melanoma or carcinoma of the breast or lung. Furthermore, metastases from ovarian (Fig 13a), esophageal (Fig 13b), and hepatic (Fig 13c) carcinomas can occur.
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Figure 13a. Metastases to the stomach. (a) Coronal reformatted image of the gastric antrum and body shows rounded, calcified metastases from ovarian cancer in the antrum. At histologic analysis, all layers of the gastric wall were infiltrated and psammoma bodies were found. (b) Coronal reformatted image shows gastric metastases from esophageal carcinoma, which were biopsy proved. Note the submucosal location. (c) Coronal reformatted image of a patient with cholangiocellular carcinoma shows two subserosal metastases to the stomach. The metastases were histologically proved.
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Figure 13b. Metastases to the stomach. (a) Coronal reformatted image of the gastric antrum and body shows rounded, calcified metastases from ovarian cancer in the antrum. At histologic analysis, all layers of the gastric wall were infiltrated and psammoma bodies were found. (b) Coronal reformatted image shows gastric metastases from esophageal carcinoma, which were biopsy proved. Note the submucosal location. (c) Coronal reformatted image of a patient with cholangiocellular carcinoma shows two subserosal metastases to the stomach. The metastases were histologically proved.
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Figure 13c. Metastases to the stomach. (a) Coronal reformatted image of the gastric antrum and body shows rounded, calcified metastases from ovarian cancer in the antrum. At histologic analysis, all layers of the gastric wall were infiltrated and psammoma bodies were found. (b) Coronal reformatted image shows gastric metastases from esophageal carcinoma, which were biopsy proved. Note the submucosal location. (c) Coronal reformatted image of a patient with cholangiocellular carcinoma shows two subserosal metastases to the stomach. The metastases were histologically proved.
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Continuous tumor invasion into the stomach may occur from tumors that arise in neighboring structures, such as the pancreas (Fig 14a), esophagus (Fig 14b), gallbladder, liver, colon, and kidney.
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Figure 14a. Direct invasion of the stomach by a neighboring tumor. (a) Oblique coronal reformatted image obtained through the pancreas shows direct invasion of the stomach by an adenocarcinoma of the pancreatic tail (arrow). There is a splenic infarct (white arrowhead) and splenic malperfusion (black arrowhead) due to obstruction of the splenic artery and splenic vein by the tumor. (b) Parasagittal reformatted image obtained through the gastroesophageal junction shows direct infiltration of the stomach by an esophageal carcinoma (arrows). The tumor invasion was surgically proved.
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Figure 14b. Direct invasion of the stomach by a neighboring tumor. (a) Oblique coronal reformatted image obtained through the pancreas shows direct invasion of the stomach by an adenocarcinoma of the pancreatic tail (arrow). There is a splenic infarct (white arrowhead) and splenic malperfusion (black arrowhead) due to obstruction of the splenic artery and splenic vein by the tumor. (b) Paras | |
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Abstract
LEARNING OBJECTIVES FOR TEST...
