This document provides information on carcinoma of the stomach, including: - Risk factors include H. pylori infection, diet, genetics, smoking. - Types include intestinal and diffuse. Staging uses TNM and other classifications. - Common symptoms are weight loss, abdominal pain, vomiting. Investigations include endoscopy and biopsy. - Treatment depends on stage but commonly includes surgery such as gastrectomy along with lymph node dissection. Endoscopic resection may be used for early stages. Adjuvant therapy is sometimes used for later stages.

1. CARCINOMA
STOMACH
Dr. Rushabh Shah R3 S/E
Dr. Manan Shah R3 S/E

2. ANATOMY

3. ARTERIAL SUPPLY

4. VENOUS DRAINAGE

5. NERVE SUPPLY

6. CARCINOMA STOMACH
Introduction
 More common in Japan – 70 per 1 lakh population.
 More common in males 2:1.
 Peak incidence in the seventh decade of life.
Incidence
 3% of total
 6%: cardia and fundus
 27%: body
 64%: pyloric and prepyloric region

7. RISKS FACTORS (AETIOLOGY)
 Helicobacter pylori Infection
 Dietary Factors – High salt foods, smoked meats that
contain high levels of nitrate.
 Fresh fruits and vegetables contain ascorbic acid and are
protective against gastric cancer.

8.  Hereditary and Genetic Factors –
 Gene mutation for cell adhesion molecule E-cadherin.
 Li – Fraumeni syndrome
 HNPCC or Lynch syndrome
 Mutation in tumor suppressor genes p53 and p16
 Adenomatous polyposis coli gene mutations.
 Also c-met proto-oncogene, k-sam and c-erbB2
oncogenes may be overexpressed.

9.  Pernicious anemia – Achlorhydria occurs due to destruction of
chief and parietal cells by an autoimmune reaction.
 Adenomatous polyps > 2cms.
 Blood group ‘A’.
 Gastric remnant – after gastrectomy and GJ.

10.  Smoking
 Agammaglobulinaemia.
 Chronic benign gastric ulcer.
 Menetrier’s disease.
 Obesity.
 Occupational – rubber workers, coal workers.
 Zinc, talc, lead, asbestos.

11. CLASSIFICATIONS
PATHOLOGICAL CLASSIFICATION:
 BORDERS
 LAUREN
 WHO
CLINICAL CLASSIFICATION:
 BORRMANN
 TNM (AJCC)

12. BORDER’S CLASSIFICATION
 Well differentiated
 Moderately differentiated
 Poorly differentiated
 Anaplastic

13. LAUREN
Intestinal type Diffuse type

14. WHO PATHOLOGICAL CLASSIFICATION
 Adenocarcinoma
 Adenosquamous cell carcinoma
 Squamous cell carcinoma
 Undifferentiated carcinoma
 Unclassified carcinoma
Adenocarcinoma is further subdivided into 4 types-
 Papillary
 Tubular
 Mucinous
 Signet ring

15. GROWTH PATTERN (MING)
Expanding type
 Grow en mass and by expansion resulting in the
formation of discrete tumor nodules with relatively good
prognosis
Infiltrative type
 Invades individually
 Poor prognosis

16. BORRMANN CLASSIFICATION
 Type I: Polypoid or Fungating
 Type II: Ulcerating lesions with
elevated borders
 Type III: Ulceration with invasion of
wall
 Type IV: Diffuse infiltration (Linitis
Plastica)
 Type V: Cannot be classified

17. TNM STAGING
 TX Primary tumour cannot be
assessed
 T0 No evidence of primary
tumour
 Tis Carcinoma in situ:
intraepithelial tumour without
invasion of the lamina propria

18.  T1 Tumour invades lamina propria or sub mucosa
 T2 Tumour invades muscularis propria or sub
serosa
 T2a Tumour invades muscularis propria
 T2b Tumour invades sub serosa
 T3 Tumour penetrates serosa
 T4 Tumour invades adjacent structures

19. Regional Lymph Nodes (N)
 NX Regional lymph node(s) cannot be assessed
 N0 No regional lymph node metastasis
 N1 Metastasis in 1 to 2 regional lymph nodes
 N2 Metastasis in 3 to 6 regional lymph nodes
 N3a Metastasis in 7 to 15 regional lymph nodes
 N3b Metastasis in 16 or more lymph nodes

20. LN group
1 R cardiac
2 L cardiac
3 Lesser curvature
4 Greater curvature
5 Suprapyloric
6 Infrapyloric
7 L gastric artery
8 Common hepatic artery
9 Celiac artery
10 Splenic hilar
11 Splenic artery
12 Hepatic pedicle
13 Retroduodenal
14 Mesenteric root
15 Middle colic artery
16 Paraaortic
17 Around lower oesophagus
18 Supradiaphragmatic

21. Distant metastasis (M)
 Mx distant metastasis cannot be assessed
 M0 no distant metastasis
 M1 distant metastasis

22. Staging
 Stage 0 Tis N0 M0
 Stage 1A T1 N0 M0
 Stage IB T1 N1 M0
T2a/b N0 M0
 Stage II T1 N2 M0
T2a/b N1 M0
T3 N0 M0
 Stage IIIA T2a/b N2 M0
T3 N1 M0
T4 N0 M0
 Stage IIIB T3 N2 M0
 Stage IV T4 N1-3 M0
T1-3 N3 M0
Any T Any N M1

23. MODE OF SPREAD
Direct spread
 Horizontal submucosal spread
 Vertical spread by invasion across to adjacent structures
like- pancreas, colon, liver.
Lymphatic spread
 Spread occurs by permeation and embolisation through
lymphatics to subpyloric, gastric, pancreaticoduodenal,
splenic, coeliac, aortic, and later to left supraclavicular
lymph nodes (Virchow’s lymph node – Troisier’s sign).

24. Blood spread
 It occurs to the liver (most common)
 Later lungs and bones can get involved
Transperitoneal spread
 It can cause peritoneal seedlings leading to ascites and
also can cause Krukenberg’s tumor in ovary in
menstruating age group.
 Rectal secondaries (Blummer shelf), Sister Mary Joseph
umbilical secondaries are through transperitoneal spread.

25. PRESENTATIONS
 Asymptomatic in early gastric cancer.
 Nonspecific symptoms – indigestion, vague epigastric
discomfort, constant non radiating pain which is not
related to food intake.
 Specific symptoms depend on the site of tumour –
obstruction, dysphagia, mass.

26.  Metastatic disease – liver secondaries, ascites,
secondaries in ovary, rectovesical pouch, umbilicus,
supraclavicular nodes, lung and bone secondaries.
 Unusual presentations – acanthosis nigricans, Irish
nodes in the axilla.

27. CLINICAL FEATURES
 Loss of appetite and weight, early satiety, fatigue.
 Microcytic hypochromic anaemia.
 Upper abdominal pain.
 Vomiting with features of gastric outlet obstruction.
 Mass in pylorus lies above the umbilicus, nodular, hard,
with impaired resonance, mobile, moves with respiration,
all margins well defined.

28.  Dysphagia.
 Along with jaundice, liver may be palpable with
secondaries which are hard, nodular with umbilication.
 Ascites.
 Troisier’s sign positive.
 Rectovesical secondaries (Blummer shelf) on per rectal
examination.
 Trousseau sign positive – migrating thrombophlebitis.

29.  Haematemesis, melaena.
 Perforation.
 Sister Mary Joseph nodules.
 Cutaneous secondaries.
 Krukenberg tumors.

30. DIFFERENTIAL DIAGNOSIS
 Acid peptic disease, pyloric stenosis with gastric outlet
obstruction.
 Gastritis.
 Pancreatic mass.
 Transverse colon mass.
 Advanced fixed stomach mass may mimic
retroperitoneal or nodal mass.

31. INVESTIGATIONS
 Routine Blood Investigations
 Liver function tests
 Kidney function tests
 Flexible Fiber Optic Upper GI Endoscopy & Biopsy
 Endoscopic Ultrasonography
 CECT Abdomen

32.  Laparoscopy
 Laparoscopic Ultrasonography
 Rapid Urease Test
 Double Contrast Barium Meal
 Chest X Ray
 Fractional Test Meal (Gastric Acid Studies)
 Tumour markers (CEA, Ca19-9)
 Fecal occult blood test (FOBT)

33.  Flexible upper endoscopy is the diagnostic modality of
choice.
 During endoscopy, multiple biopsy samples (seven or
more) should be obtained around the ulcer crater to
facilitate histological diagnosis.
 Biopsy of the ulcer crater itself may reveal only necrotic
debris.

34.  When multiple biopsy specimens are taken, the
diagnostic accuracy of the procedure approaches 98%.
 The addition of direct brush cytology to multiple biopsy
specimens may increase the diagnostic accuracy of the
study.
 The size, location, and morphology of the tumour should
be noted and other mucosal abnormalities carefully
evaluated.

35. Cancer in the Antrum of Stomach Antral cancer bleeding into the
cavity

36. Prepyloric Carcinoma

37. ENDOSCOPIC ULTRASOUND
 EUS can gauge the extent of gastric wall invasion as well as
evaluate local nodal status
 EUS cannot reliably distinguish tumour from fibrosis.
Therefore, it is not a good modality for evaluating response
to therapy.
 Overall, staging accuracy with EUS is about 75%
 The diagnostic criteria for early or advanced gastric cancer
under endoscopy are based on Bormann’s classification

38. RADIOLOGIC DIAGNOSIS
Classic radiography signs of malignant gastric ulcer
 Asymmetric/distorted ulcer crater
 Ulcer on the irregular mass
 Irregular/distorted mucosal folds/loss of rugosity
 Mucosal rugae stop far away from the ulcer
 Nodularity, mass effect or loss of distensibility
 Margin of the lesion projects outward from the ulcer into
the gastric lumen – Carmanns meniscus sign.

39. Distal GC Proximal GC Linitis plastica

40.  US abdomen to see liver secondaries, ascites, lymph
nodes, ovaries.
 Often FNAC from left supraclavicular LN when it is
significantly palpable.

41. CECT SCAN
 In women, a pelvic CT scan or ultrasound is also
recommended to look for Krukenberg tumour.
 CT of the chest may be needed for proximal gastric
cancers.
 CT can readily detect the presence of visceral metastatic
disease as well as malignant ascites.

42. LIMITATIONS OF CT SCAN
 The major limitations of CT are in the evaluation of
early gastric primaries and in the detection of small (<5
mm) metastasis in the liver or on peritoneal surfaces.
 The reported accuracy for CT staging of lymph node
metastasis ranges from 25% to 86%.

43. LAPAROSCOPY
 Laparoscopy is recommended as the next step in the
evaluation of patients with loco regional disease.
 Inspect peritoneal surfaces, liver surface.
 Identification of advanced disease avoids non-therapeutic
laparotomy in 25%.
 Patients with small volume metastases in peritoneum or
liver have a life expectancy of 3-9 months, thus rarely
benefit from palliative resection.

44. CYTOLOGIC ANALYSIS
 Cytological analysis of peritoneal fluid or of fluid
obtained by peritoneal lavage may reveal the presence of
free intra-peritoneal gastric cancer cells, identifying
patients with otherwise occult carcinomatosis.
 Patients with positive findings on peritoneal cytology
have a poor prognosis, similar to that of patients with
macroscopic stage iv disease.

45.  Tetracycline fluorescence test – gastric cancer cells take
up tetracycline given orally which becomes yellow in
colour.
 Under UV light it shows yellow fluorescence.
 CA 72-4 is important tumor marker to evaluate the
relapse.
 CEA, CA 19-9, CA 12-5 are other markers.
 Combined PET-CT scan is useful to evaluate metabolic,
physiologic and functional activity.

46. TREATMENT

47. TREATMENT OF LOCALIZED DISEASE
STAGE I DISEASE(EARLY GASTRIC CANCER)
Treatment options for patients with EGC include
 EMR
 Limited surgical resection,
 Gastrectomy.

48. ENDOSCOPIC MUCOSAL RESECTION/
ENDOSCOPIC SUBMUCOSAL DISSECTION
 A subset of patients with EGC can undergo an R0
resection without lymphadenectomy or gastrectomy.
 This approach involves the sub mucosal injection of fluid
to elevate the lesion and facilitate complete mucosal
resection under endoscopic guidance
 Emerging variations of EMR techniques including the
cap suction and cut verses a ligating device.

49.  EMR-related complication rates, including bleeding and
perforation are less.
 Tumours invading the sub mucosa are at increased risk
for metastasizing to lymph nodes and are not usually
considered candidates for EMR
 EMR is emerging as the definitive management of
selected EGCs

52. LIMITED SURGICAL RESECTION
 Patients with small (less than 3 cm) intra mucosal
tumours and those with non-ulcerated intra mucosal
tumours of any size may be candidates for limited
resection.
 Gastrotomy with local excision may be done.
 This procedure should be performed with full-thickness
mural excision (to allow accurate pathologic assessment
of T status)
 Formal lymph node dissection is not required in these
patients

53. GASTRECTOMY WITH LYMPH NODE DISSECTION
 This procedure should be considered for patients with
EGC who cannot be treated with EMR or limited
surgical resection
 Patients who have intra mucosal tumours with poor
histological differentiation
 Size >3 cm

54.  Those who have tumour penetration into the sub mucosa
or beyond.
 There is no consensus on the extent of lymphadenectomy
that should be performed as part of gastrectomy for
EGC. Dissection of level I lymph nodes is a reasonable
minimum standard at this time.

55. STAGE II AND STAGE III DISEASE
 Surgical resection is the cornerstone of treatment for
patients with localized gastric cancer; indeed, surgical
resection can be curative in most patients with EGC.
 However, for stages II and III disease, surgery is
necessary but often not sufficient for cure.
 The general therapeutic goal is to achieve a micro- and
macroscopically complete resection (R0).

56.  The extent of gastric resection is determined by the need
to obtain a resection margin free of microscopic disease.
 A line of resection at least 5 cm from the tumour mass is
necessary to ensure a low rate of anastomotic recurrence.
 The appropriate surgical procedure should be determined
by the location of the tumour and the known pattern of
spread.

57. PROXIMAL TUMOURS OF THE STOMACH
 Resected by total gastrectomy or proximal subtotal
gastrectomy.
 Tumours of the GE junction may require
esophagogastrectomy with cervical or thoracic
anastomosis
 To avoid postoperative morbidity of reflux esophagitis
and impaired gastric emptying associated with proximal
subtotal gastrectomy.
 Total gastrectomy with Roux-en-Y esophagojejunostomy
is generally the preferred option

58. MID BODY TUMOURS
 Midbody tumours comprise 15% to 30% of tumours
 Generally require total gastrectomy to achieve adequate
margins.

59. DISTAL TUMOURS
 Distal tumours may be resected by distal subtotal
gastrectomy or total gastrectomy with no difference in
overall survival.
 Risks of specific sequelae of total gastrectomy are early
satiety, weight loss, and the need for vitamin B12
supplementation.
 Nutritional status and quality of life are superior
following subtotal gastrectomy.
 Making it the preferred option when adequate margins
can be obtained while maintaining an adequate gastric
remnant

60. “D” NOMENCLATURE
Describes extent of resection and lymphadenectomy.
 D1- removes all nodes within 3cm of tumor.
 D2- D1 plus hepatic, splenic, celiac, and left gastric
nodes.
 D3- D2 plus omentectomy, splenectomy, distal
pancreatectomy, clearance of porta hepatis nodes.

61. R STATUS-CARCINOMA STOMACH
 The term R status was first described by Hermanek in
1994, is used to describe the tumor status after resection.
 R0 describes a microscopically margin-negative
resection, in which no gross or microscopic tumour
remains in the tumour bed.
 R1 indicates removal of all macroscopic disease, but
microscopic margins are positive for tumour.
 R2 indicates gross residual disease.

62. LAPAROSCOPIC GASTRIC RESECTIONS
 Laparoscopic gastric resections have been reported for
the treatment of gastric cancer
 Advantages of reduced pain, shorter hospitalization, and
improved quality of life.
 Long-term outcome with respect to cancer recurrence
awaits.

63. LYMPH NODE DISSECTION
 AJCC: number rather than location of LN is prognostic.
 Extent of dissection controversial.
 Nodal involvement indicates poor prognosis, and more
aggressive approaches to remove them are taking favor.

64. ROLE OF SPLENECTOMY IN GASTRIC CANCER
 The purpose of splenectomy in gastric cancer, aside from
managing direct tumour extension, is for removal of
lymph nodes at the splenic hilus (station 10) as a part of
an extended lymph node resection (D2) for proximal
gastric cancer.
 Japanese surgeons perform splenectomy and partial
pancreatectomy during D2 resections for primaries
whose drainage includes these echelons
 Because of the increased morbidity in the patients
receiving these adjunctive resections, Western surgeons
do not typically resect the spleen or pancreas unless
involved by direct extension from a T4 tumour.

65.  Because the extent of resection can influence survival,
this R designation to complement the TNM system.
 Long-term survival can be expected only after an R0
resection; therefore, a significant effort should be made
to avoid R1 or R2 resections

66. STAGE IV DISEASE
 Because 20% to 30% of gastric cancer patients present
with stage IV disease - palliative treatment.
 Surgical palliation may include resection with
Gastrojejunostomy or bypass alone(Devines exclusion
procedure) or in conjunction with percutaneous,
endoscopic, or radiotherapy techniques.
 Endoscopic laser surgery or endo luminal stent
placement as palliative therapy to relieve symptoms and
improve the quality of life

67. OPERATIVE PROCEDURE

68. PARTIAL GASTRECTOMY

69. SUB TOTAL GASTRECTOMY

70. TOTAL GASTRECTOMY

71. TOTAL GASTRECTOMY WITH
SPLENECTOMY & DISTAL
PANCREATECTOMY

72. TECHNIQUE OF OPERATION

73. TECHNIQUE OF OPERATION
Beginning with laparoscopy allows for careful intra operative
staging of disease and inspection for
 the presence of ascites
 hepatic metastases
 peritoneal seeding
 Fixation to underlying structures
 disease in the pelvis- metastasis
 ovarian involvement

74. STRUCTURES REMOVED IN RADICAL
GASTRECTOMY
 Entire greater and lesser omentum
 Stomach along with growth {clearance of 5-7cm }
 Appropriate lymph node dissection{d1/d2/d3}
 Distal pancreas and spleen
 Continuity maintained by roux en y
esophagojejunostomy

75. A MID LINE UPPER ABDOMINAL
INCISION IS PREFERED

76. UPPER ABDOMEN EXPOSED

77. GREATER OMENTUM MOBILISED
ALLOWING ELEVATION OF STOMACH,
EXPOSURE OF LESSER SAC

78. LESSER CURVATURE IS MOBILISED BY INCISING
GASTRO HEPATIC LIGAMENT,
DIVISION OF GASTRODUODENAL ARTERY AND
VEIN

79. DUODENUM IS DIVIDED DISTAL TO
PYLORIC VEIN OF MAYO

80. FOR TOTAL GASTRECTOMY OESOPHAGEAL
RESECTION LINE IS DEFINED

81. RESULTANT DEFECT AFTER TOTAL
GASTRECTOMY WITHOUT SPLEENECTOMY

83. D1 RESECTION- DISTAL STOMACH

84. D2 RESECTION- DISTAL STOMACH

85. D1 RESECTION- MID STOMACH

86. D2 RESECTION- MID STOMACH

87. ADJUVENT CHEMO IMMUNO THERAPY
 The immune depression encourages the growth of tumor
cells in certain patients.
 Numerous immunomodulators have been found to
enhance T-cell function and stimulate natural killer cells.
 Immunotherapy alone has rarely been shown to be
effective against residual tumors.
 The advantages are greatest in patients with Stage III and
IV disease or patients who underwent R0 resection.

88.  Rationale is to provide additional loco-regional control.
 In unresectable patients, higher 5 year survival with
mutimodal tx, in comparison to chemo alone.
 Cetuximab is EGFR inhibitor and Transtuzumab which
is HER2 antagonist have also been used.
 Cetuximab is also used in combination therapy with
FOLFIRI ( 5-FU, levofolinic acid, and irinotecan) and
with DOCETUX (doxatel and cisplatin).

89.  Numerous randomized clinical trials comparing
combination chemotherapy in the adjuvant setting to
surgery alone did not demonstrate a consistent survival
benefit.
 The most widely used regimen is 5-FU, epirubicin and
cisplatin(ECF). The addition of leukovorin did not
increase response rates.

90.  Epirubicin 50 mg/m2 iv on day 1
 Cisplatin 60 mg/m2 iv on day 1
 Flurouracil 1200 mg/m2 iv continuous infusion over 24
hrs daily on days 1-3
 Cycled every 21 days.

91. ALTERNATIVE REGIMEN
 Mitomycin 6 mg/m2 iv on day 1
 Irinotecan 125 mg/m2 iv on day 2 and 9
 Cycled every 28 days

92. ADVANCED UNRESECTABLE DISEASE
AND RADIOTHERAPY
 Surgery is for palliation, pain, allowing oral intake
 Radiation provides relief from bleeding, obstruction and
pain in 50-75%. Median duration of palliation is 4-18
months
 EBRT (45 to 50.4 Gy) when used concurrently with
flurouracil improves survival.
 Intensity modulated radiotherapy (IMRT) has potential to
reduce radiation related toxicity by delivering large doses
to target tissues.

93. COMPLICATIONS OF GASTRECTOMY
 Leakage from esophago jejunostomy
 Fistula from wound / drain site
 Leakage from duodenal stump
 Para duodenal collections
 Biliary peritonitis
 Catastrophic secondary haemorhage

94. LONG TERM COMPLICATIONS
 Reduced capacity
 Dumping syndrome
 Diarrhorea
 Nutritional deficiencies
 Vitamin B12 deficiency

95. PROGNOSIS AFTER SURGICAL
TREATMENT
 IN JAPAN 75% OF PATIENTS WHO UNDERWENT
CURATIVE RESECTION 5yr SURVIVAL RATE IS 50-
70%
 IN WEST 25-50% OF PATIENTS WHO UNDERWENT
CURATIVE RESECTION 5yr SURVIVAL RATE IS 20-
30%

96. PROGNOSIS
 The TNM classification/staging of gastric cancer is the
best prognostic indicator
 The 5 years survival rate depends on the depth of gastric
cancer invasion
 Patients in whom tumors are resected for cure also have
good prognosis

97. PREVENTION
 Eradication of H. Pylori infection in those high risk
population
 Chronic gastritis with atrophy
 Family history of gastric cancer
 Gastric ulcer

98.  Management of dietary risk factor
 Intake adequate amount of fruits, vegetables
 Minimize their intake of salty/smoked foods
 Tightly follow up those with precancerous condition
 Endoscopic or radiologic screening