Stomach Neoplasms

Professor Ravi Kant

FRCS (England), FRCS (Ireland),
FRCS(Edinburgh), FRCS(Glasgow), MS, DNB,
FAMS, FACS, FICS,
Professor of Surgery
Stomach Neoplasm
 Maltoma
 Lymphoma
 GIST
 CA stomach
 Gastric Lymphoma

Most common primary GI Lymphoma .

It’s increasing in frequency.

Presentation:
Similar to gastric carcinoma.
May reveal peripheral adenopathy, abdominal mass
or splenomegaly.
Diagnosis:
1.EGD 2.contrast GI x-ray.
3.CT guided fine needle biopsy.
Treatment :
Gastric Lymphoma Rx is Surgery
(Other organs- preferred Rx of Lymphoma
is Chemotherapy or Radiotherapy)
Maltoma

Mucosa associated lymphoid

tumour
MALTOMA
 Aetiology= H Pylori
 Rx = Rx of H Pylori
 = Triple drugs
 What are GIST…??
 Gastrointestinal Stromal Tumors are
uncommon mesenchymal tumors that
arise in the wall of the
gastrointestinal tract
 It is believed to originate from an
intestinal pacemaker cell called the
interstitial cell of Cajal.
Cajal cell
 An intestinal pacemaker cell, has been
proposed the cellular origin of GISTs.
It has characteristics of both smooth
muscle and neural differentiation on
ultrastructural examination
KIT
 role of the KIT and platelet-derived
growth factor receptor (PDGFR)
tyrosine kinase receptors
 KIT receptor tyrosine kinase (KIT RTK)
KIT
 approximately 5% of GIST cells show not
activation and aberrant signaling of the
KIT receptor, but rather mutational
activation of a structurally related kinase,
PDGFR- (PDGFRA).
 90% rate of mutations seen in a more
recent series searching for potential
mutations in each of exons 11, 9, 13,
and 17
 CD117 CD34 Actin & S-100
Desmin

+ - -

GIST +
Desmoid - + - -
tumor

True - - + -
leiomyosarc
oma

Schwanoma - - - +
Diagnosis
 CT is the common mode of diagnosis

FDG PET is mandatory
►PET CT scan is ideal
 MR
GIST & chemoresistance
 ▲ P-glycoprotein [the product of the
multidrug resistance-1 (MDR-1) gene]
 ▲ MDR protein
Distribution…
 Stomach 50-60%
 Small bowel 20-30%

 Large bowel 10%

 Esophagus 5%

 Else where in abdomen 5%

Symptoms…
 Abdominal pain
 Dysphagia

 Gastrointestinal bleeding

 Symptoms of bowel obstruction

 Small tumors may be

asymptomatic
 Cytologically…
1. Spindle cell GISTs
2. Epithelioid cell GISTs
 Although GISTs can differentiate
along either or both cell types,
some show NO significant
differentiation at all
Diagnosis…
MUST BE DONE
IMMUNOCHEMICALLY
 The CD34 antigen (70-78%)
 The CD117 antigen (72-94%)
 Malignant Versus Benign
Size Mitotic count
Very Low risk <2 cm <5/50 HPF
Low risk 2-5 cm <5/50 HPF
Intermediate <5 cm 6-10/50 HPF
risk 5-10 cm <5/50 HPF
High risk >5 cm >5/50 HPF
>10 cm Any count
Any size >10/50 HPF
predictors of survival
 Male sex, significant
on
 Tumor size > 5cm
multivariate
 Incomplete resection analysis
 Treatment…
 Surgical excision is primary treatment
option but recurrence rates are high
 Resistant to standard chemotherapy
regimens due to over-expression of
efflux pumps
 Radiation therapy limited by large
tumor sizes and sensitivity of adjacent
bowel

IMATINIB
Since activation of Kit played a crucial
role in the pathogenesis of GIST,
inhibition of Kit would be therapeutic

IMATINIB
 Orally bioactive tyrosine kinase
inhibitor
 Shown to be effective against GIST
tumors in two trials in the US and
Europe reported in 2001 & 2002
Gastrointestinal Stromal Tumor ‘GIST’

 Previously leiomyoma & leiomyosarcoma.

 <1 %
 Rarely cause bleeding or obstruction.
 The origin: Intestinal Cells of Cajal ‘ICC;s’
autonomic nervous system.
 The distinction b\w benign & malignant is
unclear. In general terms, the larger the tumor
& greater mitotic activity, the more likely to
metastases.
 The stomach is the most common site of GIST.
 Usually are discovered incidentally on
endoscopy or barium meal
 The endoscopic biopsies may be
uninformative as the overlying mucosa is
usually normal
 Small tumorswedge resection
 Larger onesgastrectomy
35
36
 GIST
 Case history-  Rx
submucosal  Surgery
 Cajal Cell  Chemoresistance
 Gene KIT  Imatininb

 PGDRF  Sumanitib
 Diagnosis  Prognosis
 CT  Predictor factors
 PET 37
GASTRIC CARCINOMA
 GASTRIC NEOPLASM
Benign Malignant

Epithelial 1.Primary
Mesenchymal Adenocarcinoma
Gastrointestinal stromal tumors
‘GIST’
Lymphoma

2. Secondary:
invasion from adjacent tumors.
 Gastric Carcinoma
Epidemiology
DEFINITION &Malignant
Risk Factors
lesion of the stomach.

55 year old Japanese male who is living in

Incidence of Gastric
Japan & working in industry.
Carcinoma:
Japan 70 in100,000/year
Europe 40 in 100,000/year Twice more common
UK 15 in 100,000/year In world
Japan has the male than in female
dust ingestion
Can occur
USA 10 in at any agehighest Rate of
100,000/year from a variety
Studies
But Peak have confirmed
incidence
It is decreasing
thatyears worldwide.
incidence gastric cancer. of industrial
Is 50-70 old. decline in
Japanese
It is more immigrant to
aggressive processes
America.
In younger ages. may be a risk.
 Gastric Carcinoma:
Risk Factors

Predisposing : Environmental: Genetic:

1. Pernicious anaemia 1.H.pylori infection 1.Blood group A

& atrophic gastritis Sero(+)patients 2.HNPCC:
(achlorhydra) have 6-9 folds risk Hereditary non-
2. Previous gastric 2.low polyposis colon
resection socioeconomic cancer.
3. Chronic peptic ulcer Status
(give rise to 1%) 3. nationality
4. Smoking. (JAPAN)
5. Alcohol. 4. Diet (prevention)
 Clinical Presentation
Most patients present with advanced stage..
why?
They are often asymptomatic in early stages.

Common clinical Presentation:

The patient complained of loss of appetite that was
epigastric pain
followed by weight loss of 10Kg in 4 weeks.
Bloating
Heearly
hadsatiety
notice
nausea & vomiting*
epigastric
dysphagia* discomfort & postprandial fullness.
He presented to theDyspepsia
anorexia ER complaining of vomiting of
weight quantities
large loss of undigested food & epigastric
upper GI bleeding
distension.
(hematemesis, melena,
iron deficiency anemia)
signs
-Anemia.
-Wt. loss ( cachexia)
-Epigastric mass, Hepatomegaly, Ascitis
-Jaundice.
-Blumer’s shelf
-Virchow's node
-Sister Mary Joseph node
-Krukenberg tumor
-Irish node
 Pathology
DIO Classification
Lauren Classification:
1. Intestinal Gastric ca.
It arises in areas of intestinal metaplasia to form
polypoid tumors or ulcers.

2. Diffuse Gastric ca.

It infiltrates deeply in the stomach without
forming obvious mass lesions but spreads widely in
the gastric wall “Linitis Plastica”
& it has much more worse prognosis

3. Mixed Morphology.
 Morphology
• Polypoid
• Ulcerative
• Superficial spreading
• Linitis plastica
Gastric cancer can be divided into:

 Early:
 Limited to mucosa & submucosa with or without
LN (T1, any N)
 >> curable with 5 years survival rate in 90%.

 Advanced:
 It involves the Muscularis.
 It has 4 types( Bormann’s classification). Type III
& IV are incurable.
 Spread
Stagingof
ofGastric
gastric Cancer
cancer

T1 lamina propria & submucosa

Direct Spread Lymphatic spread
T2 muscularis & subserosa
Tumor penetrates the
T3 serosa
muscularis, serosa &
What is important here is
Virchow’s node
T4 Adjacent
Adjacent organs organs (Trosier’s sign)
(Pancreas,colon &liver)
N0 no lymph node
Blood-bornenode
N1 Epigastric Transperitoneal
metastasis spread
N2 main arterial trunk
Usually with extensive This is common
M0Disease
No distal metastasis
where liver 1st Anywhere in peritoneal cavity
(Ascitis)
M1Involved
distal then lung &
metastasis
Bone Krukenberg tumor (ovaries)
Sister Joseph nodule
(umbilicus)
 Complications
 Peritoneal and pleural effusion

 Obstruction of gastric outlet or small bowel

 Bleeding

 Intrahepatic jaundice by hepatomegaly

 Differential Diagnosis
1.Gastric ulcer
From history,
Cancer is not relieved by antacids
Not periodic
Not relieved by eating or vomiting.

2.Other gastric neoplasms

3.Gastritis
4.Gastric Polyp
5.Crohns disease.
INVESTIGATIONS
Full blood count –IDA-
LFT,RFT
Amylase & lipase.
Serum tumor markers (CA 72-4,CEA,CA19-9)
not specific
Stool examination for occult blood
CXR ,Bone scan.
Specific:
UGI endoscopy with biopsy
Double contrast study
CT, MRI & US
Laparoscopry
EGD esophagogastroduodenoscopy
Diagnostic accuracy is 98%
if up to 7 biopsies is taken.

Diagnostic study of Choice

Double Contrast barium upper GI x-ray

Diagnostic accuracy 90%
WHY?
1.Early superficial gastric mucosal lesion
can be missed.
2. can’t differentiate b/w benign ulcer &
Ulcerating adenocarcinoma.
 X-ray showing Extensive
carcinoma involving
X-ray showing Gastric ulcer the cardia & Fundus
With symmetrical radiating
Mucosal folds.
By histology, no evidence of
Malignancies was observed.

Pyloric stenosis
 CT,MRI & US:

Help in assessment of wall thickness,

metastases (peritoneum ,liver & LN)

 Laparoscopy:
Detection of peritoneal
metastases
UGI ENDOSCOPY
THE GOLD STANDARD
 It allows taking biopsies
 Safe (in experienced hands)
UGI ENDOSCOPY,contd.
 You may see an ulcer (25%),
polypoid mass (25%), superficial
spreading (10%),or infiltrative
(Linitis plastica)-difficult to be
detected-
 Accuracy 50-95% it depends on
gross appearance, size, location &
no. of biopsies
 IF YOU SEE ULCER ASK UR SELF…
BENIGN OR MALIGNANT?
BENIGN MALIGNANT
Round to oval punched out Irregular outline with
lesion with straight walls & necrotic or hemorrhagic
flat smooth base base
Smooth margins with Irregular & raised margins
normal surrounding
mucosa
Mostly on lesser curvature Anywhere

Majority<2cm Any size

Normal adjoining rugal Prominent & edematous

folds that extend to the rugal folds that usually do
margins of the base not extend to the margins
 Management
• Surgery

• Chemotherapy
NO PROVEN BENEFIT

• Radiotherapy
 Treatment
Initial treatment:
1.Improve nutrition if Preoperative Care
needed by Preoperative Staging is
parenteral or enteral important because we
feeding. don’t want to subject
the patient to radical
2.Correct fluid
surgery that can’t help
&electrolyte
him.
& anemia if they are
present.
PRE-OPERATIVE CARE
 Careful preoperative staging
 Screen for any nutritional deficiencies &
consider nutritional support
 Symptomatic control
 Blood transfusion in symptomatic anemia
 Hydration
 Prophylactic antibiotics
 ABO & cross match
 Ask about current medications & allergies
 Cessation of smoking
BASIC SURGICAL PRINCIPLES

3 TYPES:
TOTAL,SUBTOTAL,PALLIATIVE
 ANTRAL DISEASESUBTOTAL
GASTRECTOMY
 MIDBODY & PROXIMAL TOTAL
GASTRECTOMY
TOTAL (RADICAL) GASTRECTOMY

o Remove the stomach +distal part

of esophagus+ proximal part of
duodenum + greater & lesser
omentum + LN
o Oesophagojejunostomy with roux-
en-y .
SUBTOTAL GASTRECTOMY

 Similar to total one except that the

PROXIMAL PART of the stomach
is preserved
 Followed by reconstruction &
creating anastomosis
 ( by gastrojejunostomy, Billroth II )
PALLIATIVE SURGERY
• For pts with advanced (inoperable)
disease & suffering significant
symptoms e.g. obstruction,
bleeding.
• Palliative gastrectomy not
necessarily to be radical, remove
resectable masses & reconstruct
(anastomosis/intubation/stenting/
recanalisation)
POSTOPERATIVE ORDERS

• Admit to PACU
• Detailed nutritional advise (small
frequent meals)
Post-Operative Complications

1.Leakage
1. from
duodenal stump.

2.Secondary
2.
hemorrhage.

3.Nutritional
3.
deficiency in long
term.
2.Chemotherapy:
Responds well, but there is no effect on survival.
Marsden Regimen
Epirubicin, cisplatin &5-flurouracil (3 wks)
6 cycles
Response rate : 40% .
3. Radiotherapy:
Postperative-radiotherpy: may decrease the
recurrence.
 Preventive measures
By diet
Convincing:
vegetable & fruits.
Early diagnosis remains the Key
Probable:
Vit. C &E
Problem
Possible
Carotenoids, whole grain cereals and green tea.
Smoking cessation
Cessation of alcohol intake
PROGNOSTIC FEATURES
2 important factors influencing survival in
resectable gastric cancer:
 depth of cancer invasion
 presence or absence of regional LN
involvement
• 5yrs survival rate:
10% in USA
50% in Japan
Bailey & Love’s short practice of
surgery E-medicine web site
Clinical surgery ( A. Cuschieri). The Washington Manual of Surg