INTRODUCTION,ANATOMY,CLASSIFICATION,STAGING,&MANAGEMENT OF GASTRIC CANCER

1. GASTRIC CANCER
DR.SUNIL KAMBLE
ASSISTANT PROFESSOR
DEPT.OF GEN.SURGERY
MNR MEDICAL COLLEGE,SANGAREDDY

2. Introduction
• Major cause of cancer mortality worldwide.
• Cure rate 5-10%
• Better results in Japan
• Rarely disseminates
INCIDENCE
• UK- 15/100 000 per year
• US-10/100 000 per year

3. • Eastern Europe-40/100 000 per year
• Japan-70/100 000 per year
• In some geographical areas of China incidence is
double than Japan
• Incidence is falling 1% per year
• Proximal gastric cancer more in high
socioeconomic group and not associated with
H.Pylori infection.

4. ANATOMY

5. Five layers
• Mucosa, submucosa, muscular layer,
subserosal layer, serosal layer.
• Peritoneum of greater sac covers anterior
surface
• A portion of lesser sac drapes posteriorly
over stomach.
• The GE junction has limited serosal
covering.

7. • The site of the lesion is classified on
basis of relationship to long axis of
stomach.
– 40% lower part
– 40% middle part
– 15% upper part
– 10% more than one part

10. • Zone I (inferior gastric)
drains into the subpyloric
and omental nodes
• Zone II (splenic) drains
into the
pancreaticosplenic nodes
• Zone III (superior gastric)
drains into the superior
gastric nodes
• Zone IV (hepatic) drains
into the suprapyloric
nodes

12. RISK FACTORS
H. Pylori
infection
• Cancers in the lower (distal) part of the stomach.
• Inflammation (chronic atrophic gastritis) and pre-cancerous
changes of the inner lining of the stomach.
Gender
• More common in men than in women.
• Men:Women  2:1
Aging
• Sharp increase in stomach cancer after the age of 50.
• Most people diagnosed are in their late 60s, 70s, and 80s.

13. Ethnicity
• Common in Asian/Pacific Islanders.
Diet
• Increased risk of stomach cancer -diets containing large
amounts of smoked foods, salted fish and meat, and pickled
vegetables.
• Nitrates and nitrites are substances commonly found in caned
meats. They can be converted by certain bacteria, such as H.
pylori, into compounds that have been found to cause stomach
cancer in animals.
• Eating fresh fruits and vegetables that contain antioxidant
vitamins (such as A and C) appears to lower the risk of stomach
cancer.

14. Tobacco
use
• Smoking increases stomach cancer risk,
particularly for cancers of the upper portion
of the stomach closest to the esophagus.
• Doubled in smokers.
Obesity
• Being very overweight or obese has emerged
as a possible cause of cancers of the cardia.

15. Previous
stomach
surgery
• Allows more nitrite-producing bacteria to be present. Acid
production goes down after ulcer surgery, and there may be
reflux of bile from the small intestine into the stomach.
• Risk continues to increase for as long as 15 to 20 years after
surgery.
Pernicio
us
anemia
• Certain cells in the stomach lining normally make intrinsic
factor (IF), which is a substance needed to absorb vitamin B12
from foods.
• People without enough IF may end up with a vitamin B12
deficiency, which affects the body's ability to make new blood
cells.
Menetri
er
disease
• Excess growth of the stomach lining leads to the formation of
large folds in the lining and to low levels of stomach acid.
• Disease is very rare.

16. Inherited
cancer
syndromes
• Hereditary diffuse gastric cancer is an inherited condition
that greatly increases the risk of developing stomach
cancer.
• Quite rare, but the lifetime stomach cancer risk among
affected people is about 70% to 80%.
• Gene (E-cadherin/CDH1) .
Inherited
cancer
syndromes
• Hereditary non-polyposis colorectal cancer (HNPCC, also
known as Lynch syndrome) and familial adenomatous
polyposis (FAP) are also inherited genetic disorders. Cause
increased risk of getting colorectal cancer and stomach
cancer in family members who have these gene
mutations.
• People who carry mutations of the inherited breast cancer
genes BRCA1 and BRCA2 may also have a higher rate of
stomach cancer.

17. Type A
blood
• For unknown reasons, individuals with Type A blood have
an increased risk of developing gastric cancer.
Family
history
of gastric
cancer
• People with several first-degree relatives who have had
stomach cancer are more likely to develop this disease
Epstein-
Barr
infection
• Epstein-Barr virus has been found in the stomach cancers
of 5% to 10% of people with this disease.
• Slower growing, less aggressive cancer with a lower
tendency to spread.

18. Histology
• 95% adenocarcinoma
• 4% lymphoma
• 1% leiomyosarcoma (GIST-malignant
gastrointestinal stromal tumors)
• Rare – carcinoid, angiosarcoma, squamous cell
carcinoma.
• As metastatic lesion from
– Colon/Pancreas
– Melanoma/Breast

19. GASTRIC ADENOCARCINOMA
Lauren System
• Diffuse Type
• Intestinal Type

20. Diffuse type
• Cell cohesion absent, with individual cells
infiltrating and thickening stomach wall
without forming a discrete mass.
• More often in younger age group.
• Develops throughout stomach, including
cardiac → loss of distensibility of gastric wall
(“linitis plastica” or "leather bottle"
appearance), with a far more ominous
prognosis.

21. • Above: low power view, with poorly
differentiated cancer arising from
mucosa and diffusely infiltrating all layers
of gastric wall
• Right: ↑ magnification, with effacement
of lamina propria of gastric mucosa

22. • Linitis plastica carcinoma diffusely infiltrates entire
gastric wall without forming an intraluminal
mass;wall typically thickened ~ 2-3 cm, with
leathery, inelastic consistency.

24. Intestinal Type
• Cohesive neoplastic cells forming gland - like
tubular structures
• Frequently ulcerative
• More commonly in antrum - prepylorus,
cardia - fundus and lesser curvature of
stomach, and often preceded by prolonged
pre - cancerous process

27. Bormann Classification
Polypoid
Ulcerating
Ulcerating / Infiltrating
Infiltrating
(Linnitus
Plastica)

28. Japanese Endoscopic Society (JES)
Classification

29. International Union Against
Cancer(UICC) staging of gastric cancer
Primary Tumour (T)
T1 – Tumor invades lamina propria/ submucosa
T1a- lamina propria
T1b-submucosa
T2 – Tumor invades muscularis propria
T3 – Tumor involves subserosa
T4a – Tumor perforates serosa
T4b – Tumor invades adjacent organs

30. Regional Lymph Nodes (N)
N0 : No lymph nodes
N1 : Metastasis in 1 - 2 regional nodes
N2 : Metastasis in 3 - 6 regional nodes
N3a : Metastasis in 7 - 15 regional nodes
N3b : Metastasis in more than 15 regional nodes

31. Distant Metastasis (M)
M0 : No distant metastasis
M1 : Distant metastasis (this includes peritoneum and
distant lymph nodes)

32. • A tumor may penetrate the muscularis propria
with extension into the gastrocolic or
gastrohepatic ligaments, or into the greater or
lesser omentum, without perforation of the
visceral peritoneum covering these structures.
• In this case, the tumor is classified T2.
• If there is perforation of the visceral
peritoneum covering the gastric ligaments or
the omentum, the tumor should be classified
T3.

33. • Positive peritoneal cytology is classified as M1.
• The adjacent structures of the stomach include
the spleen, transverse colon, liver, diaphragm,
pancreas, abdominal wall, adrenal gland, kidney,
small intestine, and retroperitoneum.

34. ANATOMIC STAGE / PROGNOSTIC GROUPS (STOMACH)
STAGE T N M
I A T 1 N0 M0
I B T2
TI
N0
N1
M0
M0
II A T3
T2
T1
N0
N1
N2
M0
M0
M0
II B T4a
T3
T2
T1
N0
N1
N2
N3
M0
M0
M0
M0
III A T4a
T3
T2
N1
N2
N3
M0
M0
M0
III B T4b
T4b
T4a
T3
N0
N1
N2
N3
M0
M0
M0
M0
III C T4b
T4b
T4a
N2
N3
N4
M0
M0
M0
IV ANY ANY M1

36. Residual tumour (R)
• The absence or presence of residual tumor after
treatment.
Rx – Presence of residual tumor cannot be
assessed
R0 – No residual tumor
R1 – Microscopic residual tumor
R2 – Macroscopic residual tumor

37. Histological Typing
– Ulcerated carcinoma (25%)
• Deep penetrated ulcer with shallow edges
• Usually through all layers of the stomach
– Polipoid carcinoma (25%)
• Intraluminal tumors, large in size
• Late metastasis
– Superficial spreading carcinomas (15%)
• Confinement to mucosa and sub-mucosa
• Metastasis 30% at time of diagnosis
• Better prognosis

38. – Linitis plastica (10%)
• Varity of SS but involves all layers of the
stomach
• Early spread with poor prognosis
– Advanced carcinoma (35%)
• Partly within and outside the stomach
• Represents advanced stage of most of the fore
mentioned carcinomas

39. Siewert Classification of EG
junction tumours

40. • The lymphatic drainage routes differ for type I
versus types II and III lesions.
• The lymphatic pathways from the lower
esophagus pass both cephalad (into the
mediastinum) and caudad (toward the celiac
axis).
• In contrast, the lymphatic drainage from the
cardia and subcardial regions is toward the
celiac axis, splenic hilus, and para-aortic nodes.

41. • Thus, the Siewert classification provides a
practical means for choosing among
surgical options.
• For type I tumors, esophagectomy is
required,
• Types II and III tumors can be treated by
transabdominal extended gastrectomy
(resection of the stomach and distal intra-
abdominal esophagus).

42. Clinical Course
• Directly, via lymphatics, or hematogenously
• Direct extension into omentum, pancreas,
diaphragm, transverse colon, and duodenum.
• If lesion extends beyond wall to a free peritoneal
surface, peritoneal involvement is frequent.

43. • Abundant lymphatic channels in submucosal and
subserosal layers allow for easy spread.
• The submucosal plexus is prominent in esophagus,
the subserosal plexus prominent in duodenum,
which allows for proximal and distal spread.
• Liver mets common, from hematogenous spread.

44. CLINICAL FEATURES
• Advanced disease – indigestion,
nausea, dysphagia, early satiety,
anorexia, weight loss.
• Weight loss, nausea & vomiting –
tumours of pylorus
• Dysphagia & early satiety – diffuse
lesions originating in cardia
• Upper abdominal discomfort (vague,
postprandial fullness to steady pain)
– extensive tumour

45. Physical Examination
• All physical signs are late events.
-Palpable stomach with succussion
splash
– Hepatomegaly
– Virchow nodes
– Sister Mary Joseph nodes
– Irish nodes
– Malignant ascites
– Weight loss
– Pallor from bleeding and anemia.

46. • Late complications include:
– Pleural effusions,
– Peritoneal effusions,
– Gastric outlet obstruction,
– GE obstruction,
– Small bowel obstruction,
– Bleeding,
– Jaundice,
– Cachexia.
• Unusual clinical features:
– Migratory thromboplebitis,
– Microangiopathic hemolytic anemia

47. INVESTIGATIONS
• Screening:
– Double Contrast Barium Study
– Diagnostic Endoscopy
– Serum Tumour markers
• Local assessment:
– Upper GI Endoscopy
– Endoscopic Ultrasound
• Assessment for distal disease:
– X-ray chest
– CT – Thorax/Abdomen/Pelvis
– MRI

48. Laboratory Studies
• Complete blood count identifies anemia, which may
be caused by bleeding, liver dysfunction, or poor
nutrition.
• 30% have anemia.
• Electrolytes and liver function tests.

49. Double Contrast Barium Study
• Useful alternative to endoscopy
• Has similar sensitivity in detection of gastric cancer
• Used as mass screening tool in Japan

51. Flexible Upper GI Endoscopy
• Obtains tissue for diagnosis.
• Detects large tumors, but only occasionally detects
extension into esophagus or duodenum, especially if
small or submucosal.

53. Imaging Studies
• CXR: done to evaluate for
metastases & pleural effusion
• CT scan or MRI of chest,
abdomen, pelvis: evaluate
local disease process, and
areas of spread.
• Unresectable or not
• Accurately predicts stage 66-
77%.
• Poor nodal status prediction.

54. Endoscopic Ultrasound
• Useful when CT fails to show T3, T4, or metastatic
disease.
• Used with neoadjuvant chemotherapy to stratify
patients
• Can achieve resolution of 0.1 mm.
• Cannot reliably distinguish between tumor and
fibrosis.
• Staging accuracy -75%
• Poor for T2 lesions (38%)
• Better for T1(80%), T3 (90%)

56. Diagnostic Laparoscopy
• Inspect peritoneal surfaces, liver surface.
• Peritoneal lavage & biopsy can also be taken.
• Identification of advanced disease avoids non-
therapeutic laparotomy in 25%.
• Indications for laparoscopy
– Lymphadenopathy on CT
– GE junction tumours
– Diffuse tumours

58. PET Scan
• Less sensitive but more specific than CT for
local LN metastases
• Potential role for early response assessment to
neo-adjuvant Rx.

60. Screening
Patients at risk for gastric cancer should undergo yearly
endoscopy and biopsy
1. Familial adenomatous polyposis
2. Hereditary nonpolyposis colorectal cancer
3. Gastric adenomas
4. Menetrier’s disease
5. Intestinal metaplasia or dysplasia
6. Remote gastrectomy or gastrojejunostomy

61. • Widely practiced in Japan (25% of gastric
cancers).
• The early screening programs used double-
contrast radiography
• 40%–60% of cancers diagnosed by the
screening programmes are early cancer with no
lymphatic metastasis.
• A low level of serum pepsinogen I significantly
associated with gastric cancer

62. • Pepsinogen I concentration of less than 70
ng/mL, and a ratio of pepsinogen I:pepsinogen
II of less than 3, are useful indicators, with a
sensitivity of 84.6% and a specificity of 73.5%.
• Although an elevated gastrin level of greater
than 200 ng/L appears to be specific, the
sensitivity is low (30%), which precludes its use
as a screening tool.

63. Prognostic Features
Stage –
Stage, invasion and lymph node involvement are
the most significant prognostic factors.
Clinical classification –
Superficial cancer > Focal cancer > Infiltrative
cancer.
Grade – high histologic grade – poor prognosis
Flow cytometry –
Diploid (18 months) > Aneuploid tumours (5
months)
Nature & extent of resection – R0 > R1 > R2

64. MANAGEMENT
• Smoking avoidance or cessation.
• Diets rich in fruit, vegetables and fibre.
• Avoidance of salted, smoked and poorly preserved
foods.
• Eradication of H. pylori.
• Mass screening is a viable strategy in high risk
populations.
• Antioxidants,Green Tea

65. • Risk for lymph node metastasis is important when evaluating
treatment options for patients with Early Gastric Cancer
(EGC).
• Thus, once tumors penetrate into the submucosa, the risk for
nodal metastasis increases with tumor size.
Tumor size Lymph node mets – Incidence
< 1 cm 7.9%
1.1 – 2.0 cm 13.3%
2.1 – 3.0 cm 15.55%
3.1 – 4.0 cm 23.3%
STAGE 1 DISEASE

66. Early Gastric Cancer – Treatement Options
• Endoscopic Mucosal Resection (EMR)
• Endoscopic Submucosal Dissection (ESD)
• Endoscopic Laser Ablation (ELA)
• Limited surgical resection
• Gastrectomy

67. Endoscopic Mucosal Resection
• Candidates for EMR:
– Tumors that have extremely low metastatic
potential
– Differentiated, superficial type IIa (slightly elevated
lesions), ≤ 2 cm in diameter.
– Differentiated, superficial type IIc (slightly
depressed lesions), without ulcer formation, ≤ 1
cm in diameter.
– Located in an easily manipulated area.
• Tumors invading the submucosa are at increased risk
for metastasizing to lymph nodes and are not usually
considered candidates for EMR.
• En bloc resection rate is significantly lower with
conventional EMR for tumors ≥11 mm than for
tumors ≤10 mm

69. Endoscopic Submucosal Dissection
• ESD has been developed for en bloc removal of large
(usually more than 2 cm), flat GI tract lesions.
• Superior to conventional EMR.

70. • Advantages of ESD over EMR
– For lesions ≥ 11 mm in size, en bloc resection rates were
significantly higher
– Possible to get histologically complete resection
– Reduced local recurrence rates
• Disadvantages of ESD over EMR
– Longer operating time
– Frequent intraoperative bleeding (can be reducer using
various knives).
– Higher risk of perforation in case of ulcerated lesion

71. Endoscopic Laser Ablation
• Photodynamic therapy (PDT)
• Uses meso-tetrahydroxyphenylchlorin (mTHPC)
as the photosensitiser in superficial gastric cancer.
• Types of Laser Coagulation used:
– Argon plasma coagulation (at 60 W for 15 s/cm2)
– contact Nd:YAG laser irradiation (40-60 joules)
• Day care procedure
• Useful for tumours situated in difficult areas
• Early gastric cancers that are obscurely
demarcated are good indicators for low output
laser therapy

72. Gastrectomy
• Patients who have intramucosal tumors with
– Poor histologic differentiation
– Size greater than 3 cm
– Tumor penetration into the submucosa
– Diffuse gastric cancer

73. STAGE II AND III DISEASE
To achieve a microscopically and macroscopically
complete resection (R0).

74. Treatement Modalities
• Surgery
• Perioperative chemotherapy
• Neoadjuvant chemotherapy
• Adjuvant chemotherapy
• Intraperitoneal chemotherapy
• Adjuvant radiotherapy
• Intraoperative radiotherapy
• Adjuvant chemoradiation

75. Mid & Distal Gastric Tumours
• 5-cm grossly negative margin around the tumor
• Microscopically negative surgical margins (R0)
• When gastrectomy is performed with curative intent,
frozen-section assessment of proximal and distal
resection margins.
• Distal Gastrectomy is comparable to Subtotal
Gastrectomy, in terms of morbidity, mortality &
oncologic outcome.

76. Mobilization of the greater curvature with omentectomy and
division of the left gastroepiploic artery

77. Infrapyloric mobilization with ligation of the right gastroepiploic
artery and vein as it enters the gastrocolic trunk

79. Suprapyloric mobilization with ligation of the right gastric
artery

80. Duodenal transection

82. Lymphadenectomy with dissection of the porta hepatis,
common hepatic artery, left gastric artery, celiac axis, and
splenic artery and ligation of left gastric artery

83. Gastric transection

88. Proximal Gastric Cancer
• Optimal surgical procedure for patients with localized
tumors of the esophagogastric junction and proximal
stomach is a matter of considerable debate
• Trans-abdominal approach with
1. Resection of lower esophagus and proximal
stomach
2. Total gastrectomy
• Abdominal + thoracic approach

94. R0 Resection
• Can be achieved by a gastric-preserving approach,
partial gastrectomy is preferred over total
gastrectomy.
• Gastric-preserving R0 approach may minimize the
risks of specific sequelae of total gastrectomy
– Early satiety,
– Weight loss, and
– Need for vitamin B12 supplementation.

95. Extent of Lymphadenectomy
N1 – 3 to 6 N2 – 1, 2, 7, 8 & 11 N3 – 9, 10 & 12
– N1 nodes are within 3cm of the tumor
– N2 nodes are along hepatic & splenic arteries
– N3 are more distant nodes
• To avoid under staging of gastric CA, a minimum of
15 nodes should be resected with the gastrectomy
specimen.

97. “D” Nomenclature
Describes extent of resection and lymphadenectomy
D1 – Removes tumour and all nodes within 3cm of
tumor (Tumour + N1).
D2 – D1 plus hepatic, splenic, celiac, and left
gastric nodes (Tumour + N1 + N2).
D3 – D2 plus omentectomy, splenectomy, distal
pancreatectomy, clearance of porta hepatis
nodes (Tumour + N1 + N2 + N3).
D1 dissection is the minimally accepted dissection.

98. • The Japanese surgeons define any lymph nodal
dissection less than a D2 dissection as
suboptimal.
• Surgeons in the western hemisphere are of the
opinion that there is no significant survival
difference between D1 and D2 dissection.

99. Indications for Splenectomy
• If macroscopic disease can be resected & the
operation is potentially curative then en bloc
splenectomy or pancreaticosplenectomy is
worthwhile.
• If it is more palliative then this benefit must be
weighed against the potential complications of
splenectomy and more extensive operation.

100. Distal Pancreatectomy
• Associated with marked increase in morbidity &
mortality with or without splenectomy
• Indications for pancreatectomy:
– Direct invasion of the tail of the pancreas
– Likelihood of splenic artery nodal involvement

101. Peri-operative Chemotherapy
Chemotherapy consisted of three preoperative and three
postoperative cycles of intravenous epirubicin (50 mg/m2
bsa) and cisplatin (60 mg/m2) on day 1, and a continuous
intravenous infusion of fluorouracil (200 mg/m2 meter per
day) for 21 days.

102. • As compared with the surgery group, the
perioperative‐chemotherapy group had a higher
likelihood of overall survival (five‐year survival rate,
36 percent vs. 23 percent) and of progression‐free
survival (0.53 to 0.81; P<0.001).
• Rates of postoperative complications were similar in
the perioperative‐chemotherapy group and the
surgery group (46 percent and 45 percent,
respectively), as was the 30 day mortality after
surgery.

103. Neo-adjuvant Chemotherapy
• Rationale –to downstage the disease and favor
an R0 resection and also to treat occult
micrometastases.
• No definite evidence of the effectiveness of
neoadjuvant chemotherapy in resectable gastric
cancer

104. Adjuvant Chemotherapy
• Meta‐analyses assessing the safety and efficacy
of different adjuvant chemotherapeutic
regimens in patients with gastric carcinomas
who have undergone gastrectomy have found
adjuvant chemotherapy to have a small survival
benefit.

105. Intraperitoneal Chemotherapy
• A significant improvement in survival was associated
with hyperthermic intraoperative intraperitoneal
chemotherapy (HIIC) alone or HIIC combined with
early postoperative intraperitoneal chemotherapy
(EPIC).
• HIIC with or without EPIC after resection of
advanced gastric primary cancer is associated with
improved overall survival at the cost of increased risk
of intra‐abdominal abscess and neutropenia .

106. Radiotherapy (RT)
• RT alone has not proved useful in treating gastric
cancer.
• RT (4000 cGy in 4 weeks) in combination with 5-FU
(15 mg/kg IV on first 3 days of RT), however, appears
to improve survival over RT alone in pts with
localized but unresectable cancers.

107. Intraoperative Radiation Therapy (IORT)
• IORT allows high dose of radiation to tumour
bed or residual disease while permitting the
exclusion of mobile radiosensitive normal
tissues from the area irradiated.
• Selected pts may benefit from IORT, particularly
when combined with supplemental external-
beam radiation and chemotherapy.

108. Adjuvant Chemoradiation
• A Dutch phase I/II study performed to determine the
maximal tolerated dose (MTD) and toxicity profile of
postoperative radiotherapy with concurrent daily
cisplatin and capecitabine treated patients.
• Capecitabine 1000 mg/m2 b.i.d. for 2 weeks.
• Subsequently, patients received capecitabine
(250‐650 mg/m2 orally b.i.d, 5 days/week) and
cisplatin (3‐6 mg/m2 i.v., 5 days/week) according to
an alternating dose‐escalation schedule.

109. • Radiotherapy was given to a total dose of
45 Gy in 25 fractions.
• Gastric cancer outcome could be improved
with more effective and intensified
postoperative chemoradiotherapy.

110. STAGE IV DISEASE
Therapeutic Goal
• Palliation
• Improved quality of life

111. Treatment Modalities
• Endoscopic palliation
• Surgical resection
• Intestinal bypass procedures
• Palliative chemotherapy
• Palliative radiotherapy

112. Endoscopic Palliation
• The tumour mass obstructing the
gastrointestinal lumen can either be
– Evaporated using lasers, or
– The tract opened using baloon dilators, or
– Self expanding stents can be placed across
the obstruction to restore the bowel
continuity.

114. Palliative Surgery
• Considered in circumstances such as tumor
obstruction, perforation, and bleeding.
• If gastrectomy is performed, gross disease
immediately adjacent to the stomach should be
removed.
• Leaving behind a primary tumor mass in the
stomach not only invites bleeding and
perforation but also diminishes the likelihood of
response to subsequent palliative chemotherapy.

115. • Alternatively, a bypass procedure or
gastrojejunostomy can be performed.
• However, gastric resection is not indicated in
patients with a poor chance of survival, and the
final decision is usually dictated by the overall
clinical conditions of the patients.

116. Palliative Chemotherapy
• Chemotherapy significantly improves survival in
comparison to best supportive care.
• In addition, combination chemotherapy improves
survival compared to single‐agent 5‐FU, but the
effect size is much smaller.

117. • Among the combination chemotherapy regimens
studied, best survival results are achieved with
regimens containing 5‐FU, anthracyclines and
cisplatin of which, ECF (epirubicin, cisplatin and
continuous infusion 5‐FU) is tolerated best.
• Regimens including FU as bolus exhibit a higher rate
of toxic deaths than regimens using a continuous
infusion of FU, such as epirubicin, cisplatin, and
continuous‐infusion FU.

118. Palliative Radiotherapy
• Gastric adenocarcinoma is relatively radioresistent &
requires high doses of radiation with toxic effects to
surrounding organs.
• RT may be useful for palliating pain, vomiting due to
obstruction, gastric haemorrhage, and metastasis to
bone and brain.

119. PROGNOSIS
• 5-year survival rate (%) for a curative resection is
• Recurrences continuing for at least 8 years after
surgery

120. Complications
• Mortality 1-2%
• Anastamotic leak, bleeding, ileus, transit failure,
cholecystitis, pancreatitis, pulmonary infections, and
thromboembolism.
• Late complications -dumping syndrome, vitamin B-12
deficiency, reflux esophagitis, osteoporosis.

123. References
• Textbook of Gastroenterology, Yamada,
5th edition
• Sleisenger and Fordtran’s Gastrointestinal
& Liver Diseases, 9th edition
• Principles and Practice of Oncology,
DeVita, 9th edition
• Mastery of Surgery, 6th edition

124. • Bailey and Love short practice of surgery-
26th edition
• Sabiston textbook of Surgery , 20th edition
• Schwartz textbook of Principles of
Surgery, 10th edition
• Gray’s Anatomy, 40th edition
• Skandalakis Surgical Anatomy, 2004