ARTERIAL SUPPLY

CARCINOMA
STOMACH
DR AAMIR HELA
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

RISKS FACTORS (AETIOLOGY)

 Helicobacter pylori Infection 6 times

 Dietary Factors – High salt foods, smoked meats that

contain high levels of nitrate.

 Fresh fruits and vegetables contain ascorbic acid are

protective against gastric cancer.
 Hereditary and Genetic Factors –

 Gene mutation for cell adhesion molecule E-cadherin. 90% risk

 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.
 Pernicious anemia – Achlorhydria occurs due to destruction of
chief and parietal cells by an autoimmune reaction. 6 times

 Adenomatous polyps > 2cms.

 Blood group ‘A’.

 Gastric remnant – after gastrectomy and GJ. 10-15 yrs later

 Smoking

 Agammaglobulinaemia.

 Chronic benign gastric ulcer.

 Menetrier’s disease.

 Obesity.

 Occupational – rubber workers, coal workers.

 Zinc, talc, lead, asbestos.

CLASSIFICATIONS
BORDER’S CLASSIFICATION
 Well differentiated

 Moderately differentiated

 Poorly differentiated

 Anaplastic
 LAUREN
Intestinal type Diffuse type
WHO PATHOLOGICAL CLASSIFICATION
 Adenocarcinoma
 Adenosquamous cell carcinoma
 Squamous cell carcinoma
 Undifferentiated carcinoma
 Unclassified carcinoma

Adenocarcinoma is further subdivided into 4 types-

 Papillary
 Tubular PTMS
 Mucinous
 Signet ring
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
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

TNM STAGING
 .

Nx No
N1 1 – 2 LN
N2 3 – 6 LN
N3a 7 – 15 LN
N3b >16 LN
Distant metastasis (M)

 Mx distant metastasis cannot be assessed

 M0 no distant metastasis

 M1 distant metastasis
Lymph node Stations

Japanese Research Society of Gastric Cancer

 N 1 Group ( First tier of lymph nodes )

•1 Right paracardial LN
•2 Left paracardial LN
•3 LN along the lesser curvature
• 4sa LN along the short gastric vessels
• 4sb LN along the left gastroepiploic vessels
• 4d LN along the right gastroepiploic vessels
•5 Suprapyloric LN
•6 Infrapyloric LN
 N 2 Group (Second tier of lymph nodes )
•7 LN along the left gastric artery
• 8a LN along the common hepatic artery
(Anterosuperior group)
• 8p LN along the common hepatic artery(Posterior
group)
•9 LN around the celiac artery
• 10 LN at the splenic hilum
• 11p LN along the proximal splenic artery
• 11d LN along the distal splenic artery
• 12a LN in the hepatoduodenal ligament (along the
hepatic artery)
• 12b LN in the hepatoduodenal ligament (along the
bile duct)
• 12p LN in the hepatoduodenal ligament (behind the
portal vein)
• 13 LN on the posterior surface of the pancreatic head
• 14v LN along the superior mesenteric vein
• 14a LN along the superior mesenteric artery
• 15 LN along the middle colic vessels
• 16a1 LN in the aortic hiatus
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).
Blood spread
 It occurs to the liver (most common) Multiple hard nodules
with umblication
 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.
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.
 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.
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.
 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.

 Haematemesis, melaena.

 Perforation.

 Sister Mary Joseph nodules.

 Cutaneous secondaries.

 Krukenberg tumors.
 Investigations
• Flexible Endoscopy
• Contrast radiology
• Ultrasonography ( Endoscopic USG – EUS )
• CT Scan and MRI
• PET – CT
• Laparoscopy
 To confirm the diagnosis
• Flexible Upper GI Endoscopy with directed
biopsy followed by histopathological
examination of the sample.
 Flexible Upper GI Endoscopy
EGD (esophago gastro duodenoscopy)
• Visual examination of the upper intestinal tract using a
lighted, flexible fiberoptic or video endoscope
• Gold standard
• More sensitive than conventional radiology ( 95% accuracy )
• Advantages
– Outpatient procedure
– No radiation Exposure
–Targeted biopsy from the lesion can be taken at the same setting.
– Diagnosis can be made more accurately
 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.
Gastric Carcinoma – Intestinal Type Gastric Carcinoma – Diffuse Type
Cancer in the Antrum of Stomach Antral cancer bleeding into the
cavity
Prepyloric Carcinoma
 Contrast Radiology
• Single Contrast/ Double Contrast
• Barium Meal
• Advantages
– Sensitivity comparable to endoscopy
– Non Invasive procedure
Stomach – Carcinoma of the gastric antrum
Normal Duble contrast barium study
Gastric Carcinoma of the body and Carcinoma along the greater curvature
proximal antrum ( Ulcerative lesion with filling defect )
(Multiple small ulcerations )
Distal GC Proximal GC Linitis plastica
 Findings in Carcinoma Stomach
• Irregular filling defect
• Loss of rugosity
• Delayed emptying
• Dilatation of stomach in carcinoma pylorus
• Decreased stomach capacity in linitis plastica
• Carmanns meniscus sign (margins of leison
project into lumen)
 Ultrasonography
• Endoscopic / Endoluminal Ultrasound is useful
to detect the involvement of layers of the
stomach, nodal status and to differentiate
early from advanced cancer.
• Excellent at determining the T- Stage ( 90% )
• High frequency probes used to differentiate
T1-2 stage
• Nodal status can also be assessed
• Limited use in advanced disease
The white arrow indicates the tumour invasion
The black arrow indicares the muscularis propria

A – TI stage – Tumour localized to the mucosa and sub mucosa

B – T2 stage – Tumour invades the muscularis propria
C – T3 stage – Tumour invades subserosa and abuts the surrounding structures
( here Aorta )
 Chest X-ray
• Look for
– Lung metastases
– Pleural Effusion

USG abdomen
• Liver metastases
 Computed tomography and MRI
• Every patient with a histological diagnosis of
gastric Carcinoma should undergo a Ct of the
chest and abdomen.
• Provides information about
– M stage ( Liver, Lung, Peritoneum and distant
nodes )
– T4 stage ( involvement of the adjacent structures )
Localized versus Diffuse thickening
Secondaries from Carcinoma Stomach in the Liver and the Lung
 Laproscopy
• To stage the disease especially in locally
advanced tumours
– Peritoneal secondaries
– Occult metastases
– Organ invasion
– Peritoneal lavage for cytology
– Biopsy of peritoneum and nodes
 Signs of inoperability
• Peritoneal deposits
• Fixity
• Liver secondaries
• Fixed iliac nodes
• Para aortic nodes
• Ascitic fluid positivity
• Sister Mary Joseph Nodule
• Left axillary lymph node secondaries
 Other tests
• Left Supraclavicular Node biopsy
• Tetracycline flourescence test
• CA 72-4 in relapse, CEA, CA 19-9, CA 12-5
• Combined PET – CT
• Sentinel Node biopsy
• HB, Hematocrit, LFT, PT
 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.
TREATMENT
TREATMENT OF LOCALIZED DISEASE
STAGE I DISEASE(EARLY GASTRIC CANCER)
Treatment options for patients with EGC include

 EMR

 Limited surgical resection,

 Gastrectomy.
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.
 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
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
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
 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.
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).
 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.
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
MID BODY TUMOURS
 Midbody tumours comprise 15% to 30% of tumours

 Generally require total gastrectomy to achieve adequate

margins.
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
“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.
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.

OPERATIVE PROCEDURE
PARTIAL GASTRECTOMY
SUB TOTAL GASTRECTOMY
TOTAL GASTRECTOMY
TOTAL GASTRECTOMY WITH
SPLENECTOMY & DISTAL
PANCREATECTOMY
TECHNIQUE OF OPERATION
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
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
A MID LINE UPPER ABDOMINAL
INCISION IS PREFERED
UPPER ABDOMEN EXPOSED
GREATER OMENTUM MOBILISED
ALLOWING ELEVATION OF STOMACH,
EXPOSURE OF LESSER SAC
LESSER CURVATURE IS MOBILISED BY INCISING
GASTRO HEPATIC LIGAMENT,
DIVISION OF GASTRODUODENAL ARTERY AND
VEIN
DUODENUM IS DIVIDED DISTAL TO
PYLORIC VEIN OF MAYO
FOR TOTAL GASTRECTOMY OESOPHAGEAL
RESECTION LINE IS DEFINED
RESULTANT DEFECT AFTER TOTAL
GASTRECTOMY WITHOUT SPLEENECTOMY
D1 RESECTION- DISTAL STOMACH
D2 RESECTION- DISTAL STOMACH
D1 RESECTION- MID STOMACH
D2 RESECTION- MID STOMACH
 Reconstruction procedures
• In case of sub total or partial gastrectomy,
Billroth II Anastomosis may be tried.
Roux-en-Y Oesophagojejunostomy
• Bypasses the stomach
• Done in cases of subtotal or total gastrectomy
SURGICAL COMPLICATIONS
OF GASTRECTOMY

Balasankar S
 INTRA-OPERATIVE
COMPLICATIONS:

Hemorrhage

Acute ischemia of Left lobe of Liver

(aberrant Left Hepatic artery)

Injury to Spleen, Pancreas, Common Bile

duct.

Disruption of Ampulla of Vater.

 POST- OPERATIVE
COMPLICATIONS:

IMMEDIATE (within 30 days of Surgery)

EARLY ( within 6 months)

LATE ( after 6 months)

 IMMEDIATE COMPLICATIONS:

Atelectasis(12-20%)
Pneumonia(9%)
Respiratory Failure(3%)
Pulmonary Embolism(0.05%)
Venous thrombosis of Lower limbs
Wound infection
Sub-phrenic abscess
Acute Pancreatitis
 EARLY COMPLICATIONS:

Post operative Anastomotic Hemorrhage

Anastomotic Leak
Duodenal Stump Leak
Small Bowel Obstruction
Stomal Obstruction
 Post Operative Anastomotic Hemorrhage:

It can be
*Intra-abdominal
*Intra-luminal
Bloody fluid from drain, tachycardia, fall in
Hb level, haemetemesis, melena.
Substantial: Open/ Laparoscopic re-
exploration
Remove clots; identify & control site of
bleeding.
Anastomotic Leak:

Frequently at Gastro-jejunal anastomosis.

Intra-abdominal leak > peritonitis > sepsis >

multi-organ failure.

Early signs: Fever, persistent tachycardia

>120/min, worsening abdominal pain.
Testing integrity:

*Instillation of
methylene blue

*Air insufflation
Meticulous repair of anastomosis remains
primary method of prevention.

IV Antibiotic therapy

Percutaneous drainage

Fully/ Partially covered Self Expanding

Metal Stents( SEMS) help in sealing of the
leaks.

Persistent : Abdominal washout and repair

of anastomosis.
Duodenal Stump Leak:
 ‘Blown’/Difficult Duodenal Stump.
 Follows Billroth II Gastrectomy.
 Incidence: 3-5%.
 Commonest cause: excessive dissection of
duodenal stump; compromises blood supply.
 Other causes include
*ischemia and necrosis (over zealous
suturing)
*increased tension on duodenal
stump caused by acute afferent loop
obstruction.
4 th or 5 th post-operative day with severe
Right upper quadrant
pain, fever, tachycardia, jaundice, bile-
stained discharge from incision; Biliary
Peritonitis.
Prevention:
*Duodenostomy- Foley catheter

*Nissen or Bancroft closure.

*Purse-string suturing.
Conservative:
*Per-cutaneous drainage
* Afferent loop decompression by
Nasogastric tube.
*Broad-spectrum antibiotics.
Surgical:
Thorough peritoneal
lavage, duodenostomy.
 Small Bowel Obstruction:

Internal Hernias through potential

mesenteric defects.
Retrocolic > Antecolic
Colicky abdominal
pain, nausea, vomiting, distension
Risk of strangulation & perforation.
Diagnosed by CT / serial small bowel
contrasts.
Laparoscopic repair.
Stomal Obstruction:

Obstruction of efferent stoma

Inflammatory adhesions
Dysphagia, nausea, vomiting, abdominal
pain.
Options:
-Endoscopic balloon dilatation
-Surgical release of adhesions.
 LATE COMPLICATIONS:

Anastomotic Stricture
Marginal Ulcer Bleeding
Gastro-gastric Fistula
Post Gastrectomy Syndrome
Small stomach syndrome
Remnant carcinoma
Anastomotic Stricture:

Gastro-jejunal anastomosis

Tension / Ischemia

Progressive dysphagia, vomiting, minimal

abdominal pain.

Endoscopic dilatation.
Marginal Ulcer Bleeding(MUB):

Ulceration around gastro-duodenal or

gastro- jejunal anastomotic site.
Chronic irritation by suture materials at the
anastomosis, use of
electrocautery, ischemic injury and
anastomotic stricture.
Epigastric pain
Endoscopy is diagnostic
PPIs, discontinue NSAIDs
Endoscopic coagulation or clipping.
Gastro- gastric Fistula(GGF):

Abnormal connection between gastric pouch

and excluded stomach.
Incomplete gastric transection

Inadequate Weight gain

Asymptomatic: PPIs

Symptomatic: Surgical correction

POST GASTRECTOMY SYNDROME:

3 main types:

1.Gastric reservoir dysfunction

2. Vagal dennervation
3. Aberrations in surgical reconstruction.
Gastric Reservoir Dysfunction:

DUMPING SYNDROME

METABOLIC ABERRATIONS
 Dumping Syndrome:

Frequently attributed to the rapid emptying

of gastric content into the small bowel.

2 types
• Early
• Late
Early Dumping Syndrome:

15 minutes to 1 hour after a meal.

 due to rapid release of hyperosmolar food

into small bowel > rapid shift in extracellular
fluid > systemic hypotension.

Nausea, vomiting, epigastric

fullness, abdominal cramping and
diarrhea, palpitation, diaphoresis.

Relieved by lying down.

Late Dumping Syndrome:

1 to 3 hours after a meal.

Carbohydrates absorbed quickly > blood

sugar level rises > hyper-insulinemia and
consequent hypoglycemia.

Fainting, tremor, prostration, decreased

consciousness.

Relieved by food.
 Management:
• CONSERVATIVE
Low carbohydrate diet (prefer complex
carbohydrate)

Small meal with solid and liquid food

Somatostatin analogues; Octreotide100 mcg

IV 15-60 minutes before meal to slow transit
time.
Alpha glucosidase inhibitor medication in late
dumping
• SURGICAL:

Iso/anti peristaltic segment of jejunum

interposed between stomach and small
bowel (10-20 cm)
 Conversion to Roux-en-Y gastro-
jejunostomy.
Metabolic Aberrations:
Anemia:
*Iron Deficiency( reduced absorption)
*Pernicious anemia( reduced intrinsic
factor)
*Folate deficiency (malabsorption).

Metabolic Bone disease( decreased Vit.D &

Ca absorption)
* Unexplained aches and pains in back or
long bones
*Rx : Ca and Vit D supplements.
 Vagal Denervation:

Diarrhea

Gastric stasis

Gallstone
Diarrhea:
Uncontrolled bowel movement >>
increased stool frequency .
Conservative Rx :
Cholestyramin
Codeine
Loperamide
Surgical : 10 cm segment of reversed
jejunum anastomosis placed 70-100 cm
from ligament of Treitz .
Gastric Stasis:

Conservative Rx :

Metoclopramide
Domperidone
Erythromycin

Naso jejunal tube feed

Gall Stone:

Division of hepatic branches of anterior

Vagal trunk.
Gallbladder dysmotility
Surgery indicated only if pathological.
No indication for prophylaxis
cholecystectomy.
Alkaline Reflux Gastritis:

Reflux of alkaline secretions into gastric

remnant.
Reflux symptoms: epigastric pain, bilious
vomiting
Clinical + evidence of bile reflux on
endoscopy.
Roux en Y Gastro- jejunostomy with
afferent limb measuring at least 40cm.
Afferent and Efferent Loop Obstruction:

Loop of bowel passing through the hiatus

between anastomosis in front &
transverse colon behind.
Severe postprandial epigastric pain(30-
60 mins),projectile vomiting & dramatic
clinical relief after vomiting.
Avoid excess length of afferent loop
Release trapped loop.
Roux Syndrome:
Symptom complex characterized by chronic
postprandial epigastric pain, fullness, and
vomiting after gastric reconstructive surgery
with vagotomy and Roux-en-Y
gastroenterostomy.
Post Vagotomy gastric atony.
 Medical treatment is successful in only
about half of cases.
Surgical :remove most or all of the gastric
remnant is usually successful.
TO SUMMARIZE…

High index of suspicion

DO NOT skeletonize >2cm of Duodenum:

simple duodenostomy

Late Complications >6months

Counsel properly to prevent Dumping

syndrome & nutritional deficiencies.
Thank You