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C linical M anagement .......................................................................................................................... 69
encouraging results of this operation have not been sustained over time.
C
HRONIC ANEMIA
Iron-deficiency anemia commonly
occurs several years after gastrectomy, but it can also
develop following truncal vagotomy. The causes may
include chronic occult blood loss from gastritis and poor
absorption of dietary iron. Megaloblastic anemia, due to
vitamin B
12
deficiency, may be seen after radical gastrectomy, indicating insufficient secretion of intrinsic factor.
It can be successfully treated with monthly vitamin B
12
administration parenterally.
M
ALABSORPTION Postgastrectomy patients often
undergo weight loss and sometimes show signs of malabsorption of fat, carbohydrates, vitamins, and metals. Mild
steatorrhea tends to occur after Bilroth II gastrectomy.
Vitamin deficiencies may be related to blind-loop syndrome. Lactose intolerance is unmasked in patients who
have a mild preoperative lactase deficiency. A significant
long-term complication of gastric surgery is calcium
malabsorption, which over years may lead to osteoporosis,
particularly in women.
P
OSTGASTRECTOMY CARCINOMA
A higher incidence of
carcinoma of the stomach is seen in patients who had gastrectomy 20 years or more previously.
9
The cause is
unknown but may be related to hypoacidity favoring
bacterial overgrowth and a generation of carcinogenic
nitrosamines from food.
NON-PEPTIC ULCER CAUSES OF UPPER
GASTROINTESTINAL BLEEDING
Peptic ulcer and erosive gastritis are the most common
causes of upper gastrointestinal hemorrhage, accounting
for 85% of cases. But upper gastrointestinal bleeding may
also be caused by lesions of the esophagus, stomach, and
duodenum other than peptic ulcer or erosive gastritis.
Esophageal Causes
Esophageal Varices
Esophageal varices represent the most important cause of
bleeding from the esophagus. Portal hypertension and
esophageal varices are covered more fully in later chapters.
Suffice it to say here that esophageal varices must be
excluded whenever upper GI hemorrhage is encountered.
A history of alcoholism, cirrhosis, or hepatitis is suggestive. The presence of jaundice and other stigmata of
chronic liver disease (e.g., spider nevi, palmar erythema,
gynecomastia, hepatosplenomegaly, dilated collateral veins
around the umbilicus or caput medusae, ascites, testicular
atrophy, and encephalopathy) make the diagnosis of
variceal hemorrhage more likely, but do not prove it. Only
upper GI endoscopy can verify that esophageal varices are
present and that they are the source of bleeding. As many
as 30% to 40% of patients with proven esophageal varices
may bleed from another source, most commonly a peptic
ulcer or erosive gastritis. The management of variceal
hemorrhage is discussed in Chapter 6.
Gastroesophageal Reflux Disease
Gastroesophageal reflux disease (GERD) can cause bleeding, either from erosive esophagitis or from development
of Barrett’s ulcer. Bleeding from erosive esophagitis can be
significant but is rarely massive unless a coagulopathy
coexists. Bleeding from a Barrett’s ulcer, on the other hand,
can be massive. The cause is development of a typical
peptic ulcer in Barrett’s epithelium in the esophagus. Both
conditions are nearly always associated with a sliding
hiatal hernia. The topic is covered in more detail in
Chapter 1.
Paraesophageal Hernia
The cause of bleeding in paraesophageal hernia is almost
always venous congestion of the mucosa caused by
mechanical obstruction of venous outflow from the herniated segment of the esophagus. Bleeding tends to be slow
but is occasionally severe enough to present as hematemesis and/or melena. The treatment is surgical correction of
the hernia.
Miscellaneous Causes
Malignancy and aortoesophageal fistula are rare causes of
bleeding. Bleeding from aortoesophageal fistula can be
exsanguinating and must always be suspected in the
patient who has had an aortofemoral graft.
Non-Peptic Causes of Gastric Bleeding
Mallory–Weiss Syndrome
A mucosal tear at the gastroesophageal junction can lead
to arterial bleeding at the base of the tear. The cause is
usually mechanical and precipitated by retching and
vomiting. The patient usually indicates that he or she
had retched repeatedly or vomited non-blood–containing
fluid before vomiting blood. The diagnosis is made with
endoscopy, and the bleeding can usually be controlled
with endoscopic coagulation. If endoscopic control fails,
the bleeding is readily controlled surgically using an
abdominal approach. The gastroesophageal junction is
mobilized and a gastrotomy is performed adjacent to the
gastroesophageal junction. Brisk arterial bleeding is seen
coming from the base of a mucosal tear that usually
straddles the gastroesophageal junction. The bleeder is
under-sewn using 00-silk sutures.
70 ..................................................................................................................... Stomach and Duodenum
Dieulafoy Syndrome
Dieulafoy syndrome involves bleeding through apparently
normal gastric mucosa from localized angiodysplasia in
the submucosa. The bleeding is from a single vessel and is
easily controlled by endoscopic injection of adrenaline
around the site of bleeding.
Gastric Tumors
Benign or malignant tumors of the stomach occasionally
cause upper GI bleeding. These include both mesenchymal tumors (leiomyoma and leiomyosarcoma) and epithelial tumors (adenocarcinoma and carcinoma).
Hemangioma
Gastric hemangiomas can be single or multiple and may
occur as isolated gastric lesions or as hemangiomatosis
syndromes that affect other parts of the gastrointestinal
tract.
Gastric Varices
Gastric varices are most commonly associated with splenic
vein thrombosis. Although nonsurgical techniques may
control the bleeding temporarily, the definitive treatment
is splenectomy. Acutely bleeding varices may require
suture control via gastrotomy prior to splenectomy.
Duodenal Causes
Non-peptic ulcer bleeding from the duodenum is rare and
is associated with pancreatic tumors that have eroded into
the organ.
Liver and Pancreas Causes
Liver and pancreas are exceedingly rare causes of upper GI
bleeding and are considered when all other causes are
excluded. There may be bleeding into the bile ducts or
pancreatic duct and then into the duodenum through the
ampulla of Vater. When the liver is the source, hepatic
trauma is the usual cause, and bleeding originates from
branches of the hepatic artery. The bleeding site may be
identified angiographically and controlled by angiographic embolization. Bleeding into the pancreatic duct is
exceedingly rare and may result from either trauma or
acute pancreatitis.
Small Intestinal Causes
Upper GI bleeding caused by lesions in the small intestine
is discussed in Chapter 8. The three important causes are
Meckel’s diverticulum, tumors, and hemangioma. Bleeding distal to the ligament of Treitz does not present as
hematemesis but as rectal bleeding or melena.
MOTOR DISORDERS OF THE STOMACH
Gastroparesis
Gastroparesis represents one of the most difficult management problems in gastroenterology. Patients are usually
referred for surgical opinion when all forms of medical
therapy have failed. Many of these patients have had previous ulcer surgery.
Nonsurgical Management
Medical treatment for motor disorders of the stomach
includes the administration of dopamine antagonists,
cholinergic agonists, or acetylcholine releasers to improve
gastric emptying. Metoclopramide, domperidone, and cisapride may improve gastric emptying, but in true gastroparesis, and particularly in patients who have had previous
ulcer surgery, the effectiveness of these drugs is neither
impressive nor long-lived.
Surgical Management
Gastroparesis presents a special challenge, as the surgeon
is being asked to perform a major operation with an
uncertain outcome. On the other hand, extensive experience now exists to suggest that total gastrectomy with
Roux-en-Y esophagojejunostomy is the best surgical
option. When this operation is performed, a feeding
jejunostomy should be provided because the patient may
require a long adaptive phase to learn to eat without a
stomach.
Dumping Syndrome
The syndrome has been described above. Fortunately,
most cases are mild. When the syndrome is severe,
however, no adequate treatment exists. Hence, prevention
is important.
Prevention
The best way to prevent dumping syndrome is to avoid,
whenever possible, performing operations that are likely
to cause it, including gastrectomy and truncal vagotomy
and drainage. Pharmacologic and bacteriologic advances
have nearly eliminated the need for elective ulcer surgery.
In an emergency situation, the surgeon must decide
whether to perform the quickest and safest operation at
that moment as opposed to a lengthier operation with less
undesirable side effects. Whenever the condition of the
patient allows, particularly in young patients and women,
PGV is a better choice than truncal vagotomy and
drainage. In the setting of hemorrhage, control of bleeding is accomplished through duodenotomy, leaving the
pyloric sphincter intact. When perforation is the indica-
C linical M anagement .......................................................................................................................... 71
tion for emergent surgery, PGV is again preferred if an
acid-reducing procedure is to be done.
Nonsurgical Management
Dietary measures often effectively control dumping syndrome. These include avoiding a high carbohydrate diet;
eating small, frequent meals; not ingesting fluids with the
meals; and lying down for about 60 minutes after eating.
Patients with severe symptoms have been successfully
treated with the long-acting somatostatin analogue
octreotide. The problem with this form of treatment is
cost and the long-term need for injection therapy.
Surgical Management
As always, surgical treatment for the dumping syndrome
is a last resort. Some operative approaches are simple and
have a chance to succeed. These include pyloric sphincter
reconstruction when a pyloroplasty is present, or takedown of gastrojejunostomy when the stomach is otherwise
intact. Other surgical options are more complex and
should be undertaken only in extreme cases. These include
conversion of Bilroth II gastrectomy to Bilroth I, and interposition of jejunum between the stomach and the duodenum. The latter procedures have had variable success.
GASTRIC MALIGNANCIES
Information regarding premalignant conditions and other
factors of gastric malignancy is summarized in Table
2.14.
Premalignant Conditions
Helicobacter pylori
Patients with H. pylori infection have a six- to nine-fold
increased risk of gastric cancer. The pathogenesis is
thought to proceed from gastritis to dysplasia to cancer
(Figure 2.24). The incidence of mucosa-associated lymphoid malignancy is higher than adenocarcinoma.
Atrophic Gastritis and Pernicious Anemia
The risk of developing adenocarcinoma is increased nearly
six-fold in patients with atrophic gastritis and pernicious
anemia. In a longitudinal prospective study, 1 in 80
patients with pernicious anemia developed cancer.
10
The
achlorhydria that accompanies this condition favors
bacterial proliferation, which generates carcinogenic
nitrosamines from nitrates in food.
Gastric Polyps
Adenomatous polyps, which represent about 10% of all
gastric polyps, pose significant risk for cancer. The cancer
risk in small adenomatous polyps (<2 cm) is 2%, but the
risk rises to 24% in polyps 2 cm or larger.
Gastric Ulcer
The incidence of malignant degeneration of a benign
gastric ulcer is probably no higher than 1% to 2%. On the
other hand, malignant lesions can masquerade as benign
ulcers more frequently.
Hypergastrinemia
Hypergastrinemia can be caused by gastrinoma, by prolonged achlorhydria that occurs as a result of atrophic gastritis, and by long-term therapy with proton-pump
inhibitors. Hypergastrinemia results in hyperplasia of the
ECL cells and a tendency to cause carcinoid tumors.
Gastric carcinoids occur more frequently in patients with
atrophic gastritis and the Zollinger–Ellison syndrome.
Long-term therapy with proton-pump inhibitor has
caused carcinoid tumors in mice, but there has been no
TABLE 2.14. Essentials: Gastric Malignancy
Premalignant conditions
H. pylori infection
Atrophic gastritis and pernicious anemia
Gastric polyps
Gastric ulcer
Hypergastrinemia
Blood group A
Previous gastric resection
Ménétrier’s disease
Carcinoma of the stomach
Falling incidence
Gross appearance: Polypoid, ulcerative, colloid, or infiltrative
Surgical treatment: Bilroth II or total gastrectomy
Early gastric cancer
䊏
No invasion of muscularis
䊏
10% of gastric cancers in U.S.
䊏
5-year survival of 70%–95%
Advanced gastric cancer
䊏
Invasion of muscularis and/or lymph node metastasis
䊏
80% of cases in U.S.
Gastric carcinoid tumors
Classification
䊏
Type I: Associated with atrophic gastritis
䊏
Type II: Associated with MEN-I syndrome
䊏
Type III: Sporadic; most are malignant and metastasize to
liver
Treatment
䊏
Tumors <2 cm: Endoscopic excision
䊏
Tumors >2 cm: Resection with 1-cm margin
Gastric lymphoma
Non-Hodgkin’s lymphoma of B-cell type
Significant association with MALT and H. pylori infection
40% present with bleeding, perforation or obstruction
Cure rate of 65%–75% after curative resection and
neoadjuvant therapy
Treatment
䊏
Responsive to chemotherapy and radiotherapy
䊏
When confined to stomach: Curative resection followed by
adjuvant chemo- or radiotherapy
Abbreviations: MALT, mucosa-associated lymphoid tissue; MEN-1,
multiple endocrine neoplasia-1.
FIGURE 2.24. Helicobacter pylori and genesis of gastric cancer.
reported incidence of carcinoid tumors in humans on
long-term therapy. The clinical effects of long-term hypergastrinemia are listed in Table 2.15.
surgically. A few patients with gastric polyposis (Figure
2.25) require total gastrectomy to prevent cancer.
Stromal Tumors
Leiomyomas are common stromal neoplasms of the
gastric smooth muscle. Most are asymptomatic and found
only at autopsy. Nearly 50% occur in the gastric corpus.
They usually protrude into the lumen but can also grow
outwardly. A central ulceration of the overlying mucosa
may develop and may cause upper GI bleeding (Figure
2.26). Symptomatic lesions or those 3cm or more in diameter should be surgically excised with a 2 to 3cm margin
of normal gastric wall.
Some 50% of unresectable malignant stromal tumors
have been shown to respond to treatment with imatinib
mesylate (Gleevec®), a selective tyrosine kinase inhibitor.
The tumors that respond express CD117, a marker for
KIT-receptor tyrosine kinase, an enzyme critical in the
pathogenesis of gastrointestinal stromal tumors including
leiomyosarcoma.
Ménétrier’s Disease (Hypertrophic Gastritis)
11
Blood Group A
A strong association exists between gastric cancer and
individuals with blood Group A.
Previous Partial Gastrectomy
Patients who had partial gastrectomy 20 or more years ago
have an increased risk of developing adenocarcinoma in
the gastric stump.
Ménétrier’s Disease
An undefined risk of gastric cancer exists in Ménétrier’s
disease.
Benign Neoplasms
Adenomatous Polyps
Adenomatous polyps, the most common benign neoplasms, are premalignant lesions. They may be single or
multiple. They can cause bleeding or intussusception into
the pylorus, causing gastric outlet obstruction. Lesions 2
cm or greater should be resected either endoscopically or
TABLE 2.15. Essentials: Clinical Effects of Long-Term
Hypergastrinemia in Humans
Ménétrier’s disease is diffuse gastric mucosal hypertrophy
that can lead to massive enlargement of rugal folds, usually
sparing the antrum. No unanimity of opinion exists about
the microscopic diagnostic criteria, but the disease
involves expansion of the glandular stomach with elongated and branched gastric pits, often with focal cystic
dilatation (Figure 2.27). The gastric hypertrophy can
Known effects
Increased ECL cells
Increased parietal cells
Thickening of gastric mucosa
Probable risks
Development of gastric carcinoids
Accelerated growth of colonic neoplasms
Abbreviations: ECL, enterochromaffin-like.
FIGURE 2.25. Gastric polyposis (arrows) is demonstrated with a
barium upper GI series. If the polyposis is extensive, total gastrectomy may be required to prevent cancer. (Courtesy of Henry
I. Goldberg, MD.)
72 ..................................................................................................................... Stomach and Duodenum
A
B
FIGURE 2.26. Gastric leiomyomas. These are common benign neoplasms of the gastric smooth muscle
that are usually asymptomatic. (A) They may be detected by endoscopy and barium upper GI x-rays as
a large round smooth mass (arrows), especially when they degenerate into leiomyosarcoma. (B) The
partial gastrectomy surgical specimen shows a leiomyosarcoma that projects into the lumen as a polypoid mass. (Courtesy of Linda D. Ferrell, MD, and Henry I. Goldberg, MD.)
C linical M anagement .......................................................................................................................... 73
A
B
FIGURE 2.27. Ménétrier’s disease. (A) Gross appearance of Ménétrier’s disease shows hyperplastic,
hypertrophic giant rugal folds involving mostly the body of the stomach. (B) Microscopic examination
shows hypertrophic gastritis, with replacement of the normal mucosa by hyperplastic surface epithelial
cells forming convoluted or cystic structures extending to the muscularis. (Reprinted with permission
from Fenoglio-Preiser CM, Lantz P, Listrom M, et al., eds. Gastrointestinal Pathology Plus. 2nd ed.
Philadelphia: Lippincott Williams & Wilkins, 1999.)
74 ..................................................................................................................... Stomach and Duodenum
FIGURE 2.28. Gross classification of gastric cancer. Gastric cancer can be polypoid, ulcerating, or infiltrating. Linitis plastica is the infil-
trating type with the poorest survival outcome. (Adapted from Douglass HO, Nava HR. Gastric adenocarcinoma—management of the
primary disease. Semin Surg Oncol 1985;12:32–45.)
mimic that seen in the Zollinger-Ellison syndrome, but
there is no associated hypergastrinemia or acid hypersecretion. The hypertrophic mucosa may secrete proteins
and lead to hypoalbuminemia. The primary clinical symptoms are abdominal pain, malnutrition, edema, and
weight loss.
Antisecretory therapy (anticholinergics, H
blockers,
2
proton-pump inhibitors) is used to decrease acid and fluid
loss and thereby to limit protein loss. In rare circumstances, when symptoms are severe and uncontrollable,
total gastrectomy with Roux-en-Y esophagojejunostomy is
necessary.
Pseudolymphoma
In pseudolymphoma, lymphocytic infiltration of the
gastric mucosa leads to diffuse thickening or enlargement
of rugal folds. Microscopically, lymphoid follicles have
clearly reactive germinal centers.
Carcinoma of the Stomach
Incidence
There is wide geographic variation in the incidence of
gastric cancer. The number of cases per 100,000 population varies from 8 in the United States to 18 in England
and Wales, 49 in Chile, over 50 in Japan and Russia, and
78 in Costa Rica.
decline in the incidence of gastric cancer has occurred over
the past 70 years, from 40 per 100,000 men in the 1930s,
to about 8 per 100,000 in the 1990s.
accounted for 20% to 30% of all cancer deaths 50 years
ago. Today, it accounts for only 3%.
partly by the higher standard of living achieved, changing
dietary habits, and perhaps the reduction in H. pylori
12
In the United States, a remarkable
13
Gastric cancer
14
This can be explained
infections as a result of improved sanitation and food
handling and increased use of antibiotics. Clearly, the incidence of gastric cancer is inversely related to the socioeconomic status of the populations it affects.
Pathology
Four macroscopic appearances (Figure 2.28) are seen in
stomach cancer:
1. Malignant ulcer;
2. Polypoid tumor growing into the lumen;
3. Colloid tumor, which is gelatinous and capable of
massive growth; and
4. Linitis plastica, a scirrhous cancer that infiltrates the
submucosa to cause “leather-bottle stomach.”
Microscopically, tumors are identified as adenocarcinoma
with various degrees of differentiation. Linitis plastica is
particularly anaplastic, manifesting clumps of bizarrelooking cells with surrounding fibrosis. Signet-ring cell
carcinoma is particularly malignant in its behavior. Signetring cells result from intracellular mucus secretion (Figure
2.29).
Depth of Invasion
The depth of invasion has great prognostic significance in
gastric cancer and is the basis for classifying gastric cancer
as “early” or “advanced.”
ARLY GASTRIC CANCER Cancer detected in patients
E
early involves only the mucosa and submucosa and does
not penetrate the muscularis propria (Figure 2.27). Even
the presence of lymph node metastasis does not severely
C linical M anagement .......................................................................................................................... 75
A
B
FIGURE 2.29. Gastric adenocarcinoma. Microscopic appearance of two types of gastric adenocarcinoma:
(A) Superficial carcinoma with keratin stain demonstrates a tumor that has not invaded the muscularis
mucosa and has an excellent prognosis. (B) By contrast, linitis plastica with signet-ring cells has a very
poor prognosis but, fortunately, accounts for only 10% of gastric cancer. (Courtesy of Linda D. Ferrell,
MD.)
76 ..................................................................................................................... Stomach and Duodenum
A
FIGURE 2.30. Late gastric cancer. (A and B) Once the muscularis propria is involved, the prognosis is
considerably worsened. Even an apparently superficial malignant ulcer, seen on a double-contrast
upper GI series (arrows in A), may be found to penetrate the muscularis propria when surgical resection is performed (arrows in B). (Courtesy of Henry I. Goldberg, MD.)
B
affect the good prognosis of early gastric cancer. The 5-year
survival rate is 70% to 95%, depending on whether or not
lymph nodes are involved.
15
Unfortunately, only 10% to
15% of all gastric carcinomas are early cancers at diagnosis. Endoscopic screening to diagnose gastric cancer at this
early stage is too expensive and has a low yield, even in
incidence of proximal gastric cancers has been increasing,
and some 25% of these patients present with dysphagia.
Approximately 10% of the patients present with disseminated disease as evidenced by an enlarged left supraclavicular node (Virchow’s node), rectal shelf (Bloomer’s shelf),
hepatomegaly, jaundice, or ascites.
countries like Japan, where the disease is endemic.
DVANCED GASTRIC CANCER Once the invasion pene-
A
trates the muscularis propria, prognosis declines (Figure
2.30). Unfortunately, more than 80% of all gastric cancers
encountered in the United States are advanced at the time
of diagnosis.
Investigations
A double-contrast barium meal test is the most economical preliminary examination in patients with nonspecific
symptoms (Figure 2.31). About 15% of those so examined
require endoscopy. Endoscopy with multiple biopsies and
brushing is the most specific way to establish the diagno-
Clinical Presentation
Symptoms are insidious. Abdominal pain and weight loss
are seen in 50% and 60% of patients, respectively. Other
symptoms include anorexia and early satiety. The relative
C linical M anagement .......................................................................................................................... 77
sis. Endoscopic ultrasonography indicates the depth of
wall invasion with 80% to 90% accuracy, but its ability to
detect involved lymph nodes is less than 70%.
Computed tomography is a useful examination. It may
not only show the gastric lesion and thickening of the
TABLE 2.16. TNM Classification of Carcinoma of the Stomach
Primary tumor (T)
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
Tis Carcinoma in situ: intraepithial tumor without
T1 Tumor invades lamina propria or submucosa
T2 Tumor invades muscularis propria or subserosa
T2a Tumor invades mucularis propria
T2b Tumor invades subserosa
T3 Tumor penetrates serosa (visceral peritoneum)
T4 Tumor invades adjacent structures
Regional lymph nodes (N)
NX Regional lymph node(s) cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in 1 to 6 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
Source: Reprinted with permission from the American Joint Committee on
Cancer (AJCC), Chicago, Illinois. The original source for this material is the
AJCC Cancer Staging Manual, Sixth Edition (2002) published by SpringerVerlag New York, www.springer-ny.com.
invasion of the lamina propria
without invasion of adjacent structures
FIGURE 2.31. Barium meal test for gastric cancer. Nonspecific
symptoms that may be indicative of gastric cancer are best and
most economically evaluated at the outset with a doublecontrast barium meal test. This double-contrast upper GI
radiography demonstrates a Type I, slightly raised, lobulated
early gastric cancer (arrows) in the body of the stomach.
(Courtesy of Henry I. Goldberg, MD.)
stomach wall but indicates the presence of extragastric
extension. Its most important role, however, is to detect
the presence of metastases in the liver and in other abdominal organs.
Staging
Accurate staging is possible only after surgery. The use of
laparoscopy to stage the disease is promising but its role is
yet undefined. The most widely used staging method is the
TNM classification and clinical staging (Tables 2.16 and
2.17).
Surgical Treatment
Surgical resection provides the only hope for curing gastric
cancer. Even then, some patients show criteria of inoperability at the time of presentation. These include the presence of Virchow’s node, obvious liver metastasis, rectal
shelf, and ascites.
The type of gastric resection needed depends on location of the tumor (Figure 2.32). In all cases, proximal and
distal surgical margins should be clear of tumor for at least
TABLE 2.17. Relating TNM Classification to Clinical Staging of
Gastric Cancer
Stage TNM classification
0 T1S N0 M0
IA T1 N0 M0
IB T1 N1 M0
T2 N0 M0
II T1 N2 M0
T2 N1 M0
T3 N0 M0
IIIA T2 N2 M0
T3 N1 M0
T4 N0 M0
IIIB T3 N2 M0
T4 N1 M0
IV T4 N2 M0
Any T Any N M1
78 ..................................................................................................................... Stomach and Duodenum
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