Introduction
Less than a century ago, gastric carcinoma was the most common cancer in the world.
Since then, the incidence and mortality rates of gastric carcinoma have been decreasing.
It is currently the fifth most common cancer worldwide and accounts for 8.2% of all
cancer-related deaths globally.[1] There is substantial geographic heterogeneity in the incidence of gastric carcinoma,
wherein the incidence can vary up to 10-fold between high-risk and low-risk countries.
There are several reasons why this difference persists such as differences in H. pylori
infection rates, cigarette smoking, and use of salt and salt-preserved foods, which
are established carcinogens associated with gastric carcinoma. Estimates from the
global burden of diseases, injuries, and risk factors study of 2017 suggest that Mongolia
and Afghanistan had the highest age-standardized incidence rates with 37.6 and 33.6
per 100,000 population. It is notable that high age-standardized incidence rate is
seen generally in the high-income Asia Pacific region (Japan, South Korea), with incidences
of 29.5 per thousand population, followed by Eastern Europe and Andean Latin America.
In contrast, India has relatively low rates of gastric carcinoma, with age-standardized
incidence rate of 7.5 per 100,000 population.[2]
Gastric carcinoma presents at an advanced stage and has a poor prognosis. Some countries
with high incidence of gastric carcinoma (such as Japan) have national screening programs.
These programs allow for more patients getting diagnosed with gastric carcinoma at
an early stage when the disease is potentially curable.[3] For localized gastric carcinoma, the best chance for durable disease control and
survival is curative surgery. The overall survival for gastric carcinoma is poor and
the 5-year survival rate with surgical treatment alone ranges between 23 to 25%. Hence,
multimodality therapy with either preoperative or postoperative chemoradiotherapy
is employed to improve rate of disease control and minimize disease recurrence.
Clinical Presentation
Signs and symptoms of gastric carcinoma are nonspecific. Hence, the diagnosis is often
late and patients generally have advanced disease at the time of presentation. Weight
loss and persistent abdominal pain are the most common symptoms at initial diagnosis.
Advanced cancer of the proximal stomach is a cause of pseudoachalasia, which may present
with dysphagia and mimic achalasia on upper gastrointestinal (GI) barium studies.
Nausea or early satiety may result from the tumor mass occupying the gastric lumen.
This symptom may also be seen in patients with diffuse gastric carcinoma (linitis
plastica), due to disruption of gastric peristalsis and loss of gastric distensibility.
Occult GI bleeding with or without iron deficiency anemia is seen in a few patients.
Some patients present with signs or symptoms related to distant metastatic disease
such as palpable left supraclavicular node (Virchow's node), periumbilical nodule
(sister Mary Joseph node), and left axillary node (Irish node). Peritoneal spread
can present with ascites and abdominal distention. Jaundice or clinical evidence of
liver failure can be seen in advanced metastatic disease involving the liver. Rarely,
patients with advanced gastric cancer may involve the adjacent transverse colon, causing
feculent emesis or severe diarrhea related to gastrocolic fistula. Nausea, vomiting,
and abdominal distention can occur due to large bowel obstruction or gastric outlet
obstruction (GOO). Gastric adenocarcinoma is also associated with deep venous thrombosis,
which when treated with anticoagulants may cause upper GI bleed from the gastric mass.
Anatomy
The stomach is a derivative of the foregut, and it is suspended at its location by
five ligaments: the gastrohepatic ligament, the hepatoduodenal ligament, the gastrosplenic
ligament, the splenorenal ligament, and the gastrocolic ligament. The gastrohepatic
and hepatoduodenal ligaments together form the lesser omentum, and they extend between
the liver hilum and the lesser curvature of the stomach and the proximal duodenum.
The gastrocolic ligament extends between the greater curvature of the stomach and
the transverse colon, and it forms the greater omentum. The gastrosplenic ligament
extends between the hilum of the spleen and the gastric fundus along with the greater
curvature of the stomach. The splenorenal ligament is a misnomer, and this ligament
extends between the hilum of the spleen and the anterior pararenal space, which contains
the pancreatic tail and splenic vessels.[4]
[5]
The gastric ligaments are covered by peritoneal lining, and they contain adipose tissue,
nerves, lymphatics and blood vessels. On CT, blood vessels that coarse through these
ligaments serve as landmarks to identify these ligaments. The arcade of the left and
right gastric arteries courses within the gastrohepatic ligament. The portal triad
(hepatic artery, portal vein, and common bile duct) passes through the hepatoduodenal
ligament. The arcade of the right and left gastroepiploic arteries courses within
the gastrocolic ligament. The gastrosplenic ligament is close to the splenic hilum,
and it contains the short gastric and left gastroepiploic arteries. The splenorenal
ligament contains the distal splenic artery and vein.[5]
Gastric cancer can spread though lymphatics contained within the gastric ligaments,
ultimately draining into the para-aortic lymph nodes. Alternatively, a tumor breaching
the subserosal connective tissue of the stomach can directly spread through the adipose
tissue of gastric ligaments without perforating its peritoneal lining, which is termed
subperitoneal dissemination. On cross-sectional imaging, subperitoneal dissemination
appears as sheet-like thickening or soft-tissue nodularity along the gastric ligaments.[5]
Classification
There are several classification systems proposed to describe gastric carcinoma. Clinically,
an important differentiation is the differentiation between cancers involving the
gastric cardia (gastroesophageal junction) and cancers involving the noncardia (more
distal) portions of the stomach. Rates of noncardia gastric cancer have been steadily
declining over the last several decades in most populations and are likely affected
by extrinsic factors such as H. pylori infection and food preservatives. Cancers of
the gastric cardia, on the other hand, have epidemiological characteristics similar
to esophageal adenocarcinoma like obesity and gastroesophageal reflux disease. Cancers
of the cardia are relatively more common in the West, whereas cancers of the distal
stomach are more common in high risk geographic regions. At MD Anderson Cancer Center,
41% of all upper GI cancers involve the gastroesophageal junction.[6]
Another important classification system which has stood the test of time is the Lauren
classification, which allows a better understanding of the pathology and pathophysiology
of this disease. The Lauren classification differentiates gastric carcinoma, based
on microscopic growth pattern into intestinal and diffuse types.[7] Diffuse cancers exhibit deep infiltration of the gastric wall and show little or
no gland formation, and they are associated with inflammation and desmoplasia with
relative sparing of the mucosa. The intestinal type shows glandular proliferation,
similar to that seen in the large intestine. These can be well- to poorly differentiated
and tend to show an expansile growth pattern rather than an infiltrative pattern.
Diffuse cancers are seen mainly in younger individuals likely secondary to genetic
predisposition.[8] Diffuse cancers are relatively more common in the West. Intestinal type cancer,
on the other hand, is believed to be related to environmental factors. It is relatively
more common in high-risk regions. The steady decline in the incidence of gastric carcinoma
incidence and mortality is attributed to the decrease in the incidence of intestinal
type of adenocarcinoma.[8]
[9]
In addition to environmental factors such as diet and Helicobacter pylori infection,
gastric carcinoma can occur as a part of hereditary nonpolyposis colon cancer syndrome
and other gastrointestinal polyposis syndromes such as Peutz–Jeghers syndrome and
familial adenomatous polyposis.[10] Mutations in the E-cadherin gene are a well-recognized cause of hereditary diffuse
gastric cancer.[11]
Another system of classification is based on histopathology and cell origin: epithelial,
mesenchymal, neuroendocrine tumors, and lymphoma. Malignant epithelial tumors constitute
most malignant tumors of the stomach, about 90% of which are adenocarcinomas. Gastric
carcinomas are pathologically further subclassified, based on histological appearance
into tubular, papillary, mucinous, and signet-ring cell carcinomas. Based on gross
macroscopic appearance, it is classified into four types. Type I is a polypoid and
fungating variety, type II is a polypoid tumor with central ulceration, type III is
an ulcerated tumor with infiltrative margins, and type IV is diffuse infiltrative
type or linitis plastica. This method of classification is called the Borrmann's classification
and is generally reserved for advanced cancers.[12] However, the most widely accepted and clinically used classification is the Lauren's
classification.
Staging
The tumor, node, and metastases (TNM) staging system is the most widely accepted method
for staging gastric carcinomas,[13] and it is depicted on [Table 1]. [Table 2] summarizes key radiologic imaging features that need to be described for staging
of gastric malignancies. Depth of tumor invasion is an important determinant of overall
survival. For example, T1 cancers have a 10-year survival rate of about 80%, which
drops to 55% in T2 cancers. T3 and T4 cancers have a 10-year survival of only 30%.[14]
[15]
[16]
[17]
Table 1
The AJCC TNM classification[13]
|
Abbreviations: AJCC, American Joint Committee on Cancer; TNM, tumor, node, and metastases.
|
|
Primary tumor (T)
|
|
Tx: Primary tumor cannot be assessed
|
|
T0: No evidence of primary tumor
|
|
Tis: Carcinoma in situ: intraepithelial tumor without invasion of the lamina propria
|
|
T1: Tumor invades the lamina propria or submucosa
|
|
T2: Tumor invades the muscularis propria or the subserosa
|
|
T2a: Tumor invades muscularis propria
|
|
T2b: Tumor invades subserosa
|
|
T3: Tumor penetrates the serosa (visceral peritoneum) without invading adjacent structures
|
|
T4: Tumor invading adjacent structures
|
|
Regional lymph nodes (N)
|
|
Nx: Regional lymph node(s) cannot be assessed
|
|
N0: No regional lymph node metastasis
|
|
N1: Metastasis in one to six regional lymph nodes
|
|
N2: Metastasis in 7 to 15 regional lymph nodes
|
|
N3: Metastasis in more than 15 regional lymph nodes
|
|
Distant metastasis (M)
|
|
Mx: Distant metastasis cannot be assessed
|
|
M0: No distant metastasis
|
|
M1: Distant metastasis
|
Table 2
Key imaging findings that need to be included while staging gastric carcinoma
|
Imaging radiology report keys
|
|
Primary tumor (T)
|
|
o Lesion morphology: polypoid, ulcerated or diffuse
o Location: cardia, fundus, body, antrum, pylorus, greater curvature, lesser curvature.
o Local extent: presence of any extraluminal extension into the adjacent ligaments,
direct invasion of nearby organs.
|
|
Lymph node (N)
|
|
o Presence, size location and number of lymph nodes in the expected nodal basins
draining the site of the primary tumor.
|
|
Metastases (M)
|
|
o Liver metastases.
o Peritoneal deposits (ascites is suggestive for peritoneal involvement).
o Special attention to nodes in the posterior to the head of pancreas, in the para-aortic
region and in the supraclavicular region. These are considered distant metastases.
|
The Japanese research society for gastric carcinoma has classified regional lymph
nodes, based on location into four compartments 1 to 4.[18] Compartment 1 consists of perigastric lymph nodes immediately adjacent to the stomach
along unnamed arteries. Compartment 2 are nodes along the left gastric artery, the
common hepatic artery, the celiac axis, and the splenic artery. Compartment 3 are
nodes along the hepatoduodenal ligament, nodes posterior to the head of the pancreas,
and nodes at the root of the small bowel mesentery. Compartment 4 includes para-aortic
lymph nodes. The extent of lymph node dissection in surgery is described, based on
surgical dissections of these compartments. D1 dissection includes compartment 1,
D2 dissection includes compartments 1 and 2, D3 dissection includes compartments 1,
2 and 3, whereas D4 dissection includes dissection of all four compartments. Surgical
practices vary widely and are mainly based on the extent of lymph node dissection.
The knowledge of nodal anatomy in gastric carcinoma in an attempt to stage these accurately
is one of the biggest contributions radiologists can make to triage gastric carcinoma
patients for appropriate treatment.
The international committee on gastric carcinoma recommends that for accurate staging
and prediction of prognosis, a minimum of 16 lymph nodes have to be included in the
surgical specimen.[19] The N stage is an independent variable for survival. N0 disease has a 10-year survival
of 70%, N1 has a survival of 41%, and N2/N3 have a 10-year survival rate of less than
30%.[20] Nodal involvement is discussed in more detail in this issue in the article “Lymph
node mapping in gastric carcinoma.”
Imaging Evaluation
Radiologic and endoscopic ultrasound staging are important in diagnosis and management
of gastric carcinoma patients. Various imaging techniques including double-contrast
upper gastrointestinal (UGI) barium examinations, multidetector CT (MDCT), MRI, positron
emission tomography-CT (PET-CT), and endoscopic ultrasound (EUS) are all used in the
diagnosis and staging of gastric carcinoma to varying degrees.
Optimal gastric distention is essential for imaging of stomach malignancy, and it
may be achieved through administration of effervescent granules or by consumption
of 800 mL of water as a negative contrast agent. Dynamic multiphasic CT scanning is
performed after injection of approximately 85 mL of intravenous (IV) contrast at a
rate of 2.5 to 3.0 mL/second. Arterial phase imaging is performed at 25 to 40 seconds
after starting the injection of IV contrast, the venous phase at 60 to 80 seconds,
and delayed phase at 3 to 4 minutes.[5]
[21] Despite the rapidly expanding role of MRI in cancer imaging, current guidelines
do not recommend this modality for local staging of gastric cancer.[22] However, MRI is a useful tool to characterize indeterminate liver lesions suspicious
for metastasis.
Double-contrast UGI examination can be used as a screening tool for gastric cancer.
It requires 6 hours of fasting, and it involves distending the gastric lumen using
effervescent granules and coating its mucosal lining with high-density (210–250% wt/vol)
barium suspension. Both functional and anatomic information of the esophagus, stomach,
and duodenum can be obtained from these studies. However, endoscopy is necessary for
tissue sampling and differentiating benign from malignant etiologies if an abnormality
is noted on UGI series.[5]
Tumor Detection and Staging
Screening programs for gastric cancer have been implemented in high-income east Asian
countries where there is a higher incidence of gastric cancer. Both endoscopy and
double contrast UGI barium studies were proven to be effective for gastric cancer
screening, and Japanese guidelines recommend these modalities for screening adults > 50
years of age. However, the utilization of double contrast UGI barium studies has been
declining.[23] Currently, endoscopy is the modality of choice to detect and diagnose gastric carcinoma
due to its high specificity, ability to diagnose the disease at an early stage, and
the added advantage of obtaining tissue samples. In addition, it provides access to
perform EUS, which offers a reliable way to T-stage the tumor at the time of diagnosis.[24]
Endoscopic ultrasound is superior to all other modalities in visualizing different
layers of the gastric wall and perhaps is the most accurate preoperative staging modality
of gastric carcinoma with an accuracy ranging between 78 to 94%.[25]
[26] The gastric wall is seen as layers of alternating hyper and hypoechoic bands: superficial
mucosa, deep mucosa, submucosa, muscularis propria, and serosa. Tumors are hypoechoic
or hyperechoic, and they disrupt this regular wall pattern, thereby allowing for staging.[27]
Gastric cancer has various imaging appearances on UGI barium examination, depending
on tumor morphology and on its location within the stomach. Disruption of the normal
mucosal pattern, known as the areae gastricae, can be a subtle sign for the presence
of a gastric mucosal lesion. Filling defects along gastric walls suggest a polypoid
lesion protruding from the mucosal surface ([Fig. 1]). Accumulation of barium within an ulcer niche along with a radiolucent rim surrounding
the niche is termed bull's eye appearance, and it is suggestive of an ulcer. Radiolucent
rim surrounding the ulcer niche and smooth gastric folds that extend to the periphery
of the ulcer are findings suggestive of a benign etiology. Findings suspicious for
a malignant ulcer include an eccentric/irregular ulcer and mucosal folds which do
not extend to the ulcer niche. Thick, irregular, or nodular mucosal folds in the vicinity
of the ulcer are suspicious for submucosal infiltration of the disease and are also
suspicious for malignancy. Rigidity and limited distensibility of the gastric lumen
are suspicious for linitis plastica. Abnormal peristalsis and GOO are also suggestive
of a malignant etiology ([Fig. 2]). However, in the presence of these radiographic findings, endoscopy is still required
for verification and tissue sampling.[5]
Fig. 1 Upper gastrointestinal barium examination showing an irregular polypoid mass protruding
into the gastric lumen along the greater curvature of the stomach (arrow). Image courtesy:
Dr Rajesh Gothi.
Fig. 2 Upper gastrointestinal barium examination narrowing and lack of distensibility of
the distal gastric lumen with irregular contours (arrow) suggestive of adenocarcinoma.
Image courtesy: Dr Rajesh Gothi.
Use of high-resolution CT scanning along with multiplanar reconstructions have improved
the ability of CT scan in the staging of gastric carcinoma; although, it remains inferior
to EUS. Normal gastric wall shows a two- to three-layered structure: a markedly enhancing
mucosa layer, a submucosal layer with lower attenuation, and an outer muscular layer
invested with serosa, showing moderate enhancement in the arterial and early portal
venous phase of contrast enhanced CT ([Fig. 3]).[28]
Fig. 3 Axial contrast-enhanced computed tomography of the abdomen showing alternating three
layers of normal stomach: the hypervascular mucosa (solid black arrow), the hypovascular
submucosa (solid white arrow), and the mildly hypervascular muscularis and serosa
(dotted black arrow).
Macroscopically, gastric adenocarcinoma can be classified as superficial, mass forming
([Fig. 4]), ulcerative ([Fig. 5]), diffuse infiltrative ([Fig. 6]) or unclassifiable.[29] Superficial tumors may be undetectable on cross-sectional imaging if they are flat,
but they may be visualized when they have a polypoid configuration. T1 and T2 lesions
are limited to the gastric wall ([Fig. 7]). T3 lesions may show slight blurring of the outer contour with stranding of perigastric
fat ([Figs. 8], [9]). T4 lesions are seen spreading via ligamentous attachments and peritoneal reflections
or directly invading adjacent structures.[30]
Fig. 4 An annular pyloric mass forming adenocarcinoma (arrow) causing gastric outlet obstruction
with upstream dilatation of the gastric body.
Fig. 5 A malignant ulcer along the greater curvature of the stomach (arrow) with the ulcer
crater filled with oral contrast.
Fig. 6 Diffuse thickening involving the submucosa and muscularis layers of the stomach (black
arrowheads) compatible with diffuse infiltrative gastric adenocarcinoma and linitis
plastica. There is also an enlarged retroperitoneal lymph node (black arrow). The
retroperitoneal node is considered a compartment 4 node in the Japanese surgical society
classification and is included in D4 lymph node dissection, but it is classified as
M1 disease according to the American Joint Committee on Cancer (AJCC) classification.
Fig. 7 Sagittal reconstruction of contrast-enhanced computed tomography scan showing a large
annular mass in the gastric body. The tumor is limited to the gastric wall without
evidence of blurring of the outer contour or stranding of the perigastric fat (arrow).
Fig. 8 Axial contrast-enhanced computed tomography scan of a patient with a tumor in the
gastric fundus. There is blurring of the outer contour with stranding of the perigastric
fat (arrow), indicating a T3 lesion.
Fig. 9 Axial contrast-enhanced computed tomography scan of the abdomen in a patient with
gastric adenocarcinoma, which is seen as a focal area of mucosal thickening and adjacent
fat stranding. At resection, this was found to be a T3 disease (Lauren intestinal
variety).
CT scans perform better at T-staging of advanced (T3 and T4) carcinomas (98% and 82%,
respectively) versus early (T1 and T2) carcinomas (23 and 15%, respectively).[21] Multiplanar reconstructions in coronal and sagittal planes slightly improve the
detection and staging. While MRI has an advantage of multiplanar capability and better
tissue contrast, the use of MRI in staging of the primary tumor is limited due to
respiratory, cardiac, and peristalsis motion artefacts.
Fluorodeoxyglucose (FDG) PET-CT performs inconsistently in the detection of gastric
carcinoma, as there is physiologic uptake of FDG in the gastric mucosa. In addition,
FDG uptake varies, according to the histologic subtype of gastric cancer. Signet ring
cell carcinoma and poorly differentiated adenocarcinoma show little or no radiotracer
uptake.[31]
[32]
Lymph Node Staging
Nodal staging in gastric carcinoma is challenging due to significant limitations in
detecting microscopic metastases by currently available imaging modalities. In practice,
nodes which are larger than 8 to 10 millimeters in short axis are considered as suspicious.
However, it is humbling to note that while 80% of the lymph nodes, which were less
than 5 millimeters in size, are benign, 55% of metastatic nodes are also less than
5 millimeter in short axis, clearly demonstrating the weakness of size criteria as
a parameter on imaging modalities.[33]
[34] The problems of CT scan are compounded on MRI, as it is subject to significant motion
artefacts from respiration, cardiac activity, and peristalsis. Although imperfect,
CT is marginally better at staging lymph nodes compared to MRI[34]
[35]
[36] EUS can detect metastatic nodes in the perigastric region. However, important nodal
stations, which are key to surgical planning (such as station 3, station 4 nodes),
cannot be staged using this modality ([Figs. 6], [10]
[11]
[12]
[13]). FDG avid nodes on PET-CT are likely malignant and hence PET-CT has a higher specificity
than CT or MRI ([Fig. 14]). However, PET-CT has a significant size limitation, and smaller nodes may not be
detectable.[37] In addition, signet cell carcinomas do not show FDG uptake and there is a possibility
of understaging lymph nodes on PET-CT.
Fig. 10 Metastatic left gastric lymph nodes (black arrows) seen in a patient with advanced
and diffuse gastric adenocarcinoma (asterisk). This belongs to compartment two in
the Japanese research society for gastric carcinoma classification.
Fig. 11 Metastatic celiac artery lymph node (black arrows) in a patient with gastric adenocarcinoma.
Fig. 12 Metastatic lymph node at the splenic hilum (white arrows) in a patient with gastric
adenocarcinoma. This is considered as compartment 2 lymph node, according to the Japanese
research society for gastric carcinoma classification. In patients with tumors of
the distal stomach, the metastatic lymph node at the splenic hilum is considered M1
disease in the American Joint Committee on Cancer (AJCC) classification.
Fig. 13 Axial contrast-enhanced computed tomography scan of the abdomen shows an enlarged
suspicious lymph node posterior to the pancreatic head (black arrows). This is classified
as compartment III, according to the Japanese research society for gastric carcinoma,
and it is considered as M1 disease according to American Joint Committee on Cancer
(AJCC) classification. Compartment 3 lymph nodes are included in D3 dissection.
Fig. 14 Axial computed tomography (CT) scan of the abdomen and fused positron emission tomography
(PET)-CT scan showing an enlarged left gastric lymph node, demonstrating avid radiotracer
uptake. Elevated metabolic activity increases the specificity for predicting nodal
metastasis.
Metastatic Gastric Carcinoma
According to the American Joint Committee on Cancer (AJCC) staging system, cancer
infiltration of the hepatoduodenal ligament ([Fig. 15]), retropancreatic, mesenteric or para-aortic lymph nodes are considered distant
metastases (i.e., M1 disease).[13] Hematogenous spread of gastric carcinoma is commonly seen in the liver due to its
portal venous drainage, and hepatic metastatic deposits are usually hypovascular,
and they are usually best seen on portal venous phase ([Fig. 16]). Lung metastases are less common, and they are best detected using CT. Lung metastases
appear on CT as solid lung nodules, which is a nonspecific imaging pattern ([Fig. 17]). Bone metastases are more common in advanced cases. On CT bone, metastases can
be sclerotic, lytic, or they may be isodense to bone marrow ([Fig. 18]). The latter imaging pattern is frequently missed on CT, but it may show avid FDG
uptake on PET/CT without a CT correlate. After chemotherapy, isodense can become sclerotic
and hence is visible on CT. Therefore, new sclerotic bone lesions that appear after
initiation of chemotherapy can be treated metastases, but new bone metastases cannot
be excluded. Involvement of distant lymph nodes such as left supraclavicular node
(Virchow's node) can also be seen.
Fig. 15 Soft-tissue density lesions (arrow) along the gastrohepatic ligament (A) and hepatoduodenal ligament (B) represent tumor infiltration.
Fig. 16 Axial computed tomography scan showing multiple hepatic metastases of gastric adenocarcinoma
(arrow). Adenocarcinoma metastases are typically hypoenhancing, and they are best
visualized on portal venous phase.
Fig. 17 Several bilateral lung nodules (arrows) suggestive of lung metastases.
Fig. 18 Several sclerotic bone metastases (arrows) in the right sacral wing and right iliac
bone.
Advanced gastric carcinoma frequently metastasizes to the peritoneum, typically involving
the omentum, the ovaries (Krukenberg tumor) ([Fig. 19]), and rectovesical pouch (Blumer's shelf tumor) ([Fig. 20]). The presence of ascites in a patient with gastric carcinoma is generally associated
with positive free tumor cells, which is suspicious for peritoneal carcinomatosis.
Fig. 19 A gastric adenocarcinoma patient with a left ovarian metastasis (white arrow), in
keeping with Krukenberg tumor. Note the adjacent uterine fibroid (asterisk).
Fig. 20 A gastric adenocarcinoma patient with peritoneal implants (broken arrows) involving
the rectouterine pouch (Blumer's shelf tumor) and along the dome of the urinary bladder.
Laparoscopy is superior to CT and all other imaging modalities for staging and detection
of small volume peritoneal disease. Its sensitivity for detection of peritoneal disease
reaches up to 96%. Some authors consider MRI to be superior to CT in detecting extragastric
metastases. This may be particularly true for detection of hepatic metastases, but
in the authors experience, CT is superior to MRI in detecting peritoneal metastases.
The value of PET-CT is limited and it is still under investigation.
Differential Diagnosis
The differential diagnosis of solid gastric masses mainly includes gastric lymphoma
and gastrointestinal stromal tumors (GIST). Rare causes of solid gastric tumors include
metastases, leiomyoma, schwannoma, neuroendocrine tumors, lipoma, hemangioma, and
glomus tumors.
Gastric lymphoma can mimic adenocarcinoma, and it may show polypoid, ulcerative or
diffuse infiltrative macroscopic appearances. Infiltrative gastric lymphoma can cause
extensive fold thickening and may mimic linitis plastica, but preservation of distensibility
of the stomach and patency of its lumen can distinguish this entity from adenocarcinoma
([Fig. 21]). Although GOO can occur in adenocarcinoma, it rarely occurs in gastric lymphoma.
The presence of several polypoid lesions or ulcerating lesions may suggest the diagnosis
of gastric lymphoma as opposed to adenocarcinoma. Absence of perigastric fat infiltration
can also suggest the diagnosis of gastric lymphoma, especially in the setting of a
large gastric mass ([Fig. 22]). Although enlarged lymph nodes can occur in both entities, the presence of bulky
lymph nodes or enlarged retroperitoneal lymph nodes, particularly below the level
of the renal veins, is suggestive of gastric lymphoma.[38]
Fig. 21 Axial contrast enhanced computed tomography (CT) (A) and fluorodeoxyglucose (FDG) positron emission tomography (PET)-CT image (B) show diffuse thickening of the gastric wall (arrows), extending from the cardia
to the antrum with elevated FDG uptake (SUVmax 22.5), mimicking infiltrative adenocarcinoma
and linitis plastica. Biopsy revealed low grade marginal zone lymphoma of mucosa-associated
lymphoid tissue (MALT) lymphoma.
Fig. 22 Axial computed tomography image showing annular homogenous soft-tissue mass involving
the gastric antrum (arrows). Despite extramural extension of the disease, there is
no stranding of the adjacent fat planes, a feature suggestive of lymphoma. Biopsy
revealed diffuse large B-cell lymphoma.
Gastric GISTs are characterized by exophytic growth pattern ([Figs. 23] and [24]). Although an intramural growth pattern can be frequently seen ([Fig. 25]), an intraluminal pattern of growth is uncommon. Most GISTs larger than 2 cm can
have ulceration of the overlying mucosa, which can cause a bull's eye appearance on
barium studies. Hemorrhagic or cystic degeneration can occur in GISTs ([Fig. 23]), but calcifications are rare. Although liver metastases can occur in half of malignant
GISTs, lymphatic dissemination and lymphadenopathy are uncommon.[39]
Fig. 23 Coronal (A) and sagittal reformatted computed tomography images (B) show a mass demonstrating exophytic growth along the greater curvature of the stomach
(arrows). Gastrointestinal (GI) stromal tumor is the main differential of exophytic
gastric masses, and it may have a homogenous or heterogenous texture on cross-sectional
imaging. Final surgical pathology revealed a gastric gastrointestinal stromal tumors
(GIST).
Fig. 24 Axial computed tomography image showing a homogenous exophytic gastric lesion, demonstrating
exophytic growth pattern (arrow). Final surgical pathology revealed gastric gastrointestinal
stromal tumor (GIST).
Fig. 25 Axial computed tomography image showing a small gastric mass, demonstrating intramural
growth pattern within the collapsed gastric wall at the cardia, which also contains
calcifications (arrow). Intramural growth pattern is uncommon in gastrointestinal
stromal tumors (GIST). Calcifications and intraluminal growth are rarely seen in GISTs.
