WELCOME

STOMACH

Lt Col Ashim Kumar Dutta

Classified Specialist in Surgery
CMH Cumilla
 Surgical Anatomy
•Stomach is an irregular pyriform shape, tapering towards the duodenum. It is
divisible into 4 parts—
1. Cardia---Located at the cardio-oesophageal junction.
2. Fundus---Lies left to the oesophagus, cephaloid to gastro-oesophageal
junction.
3. Body----It is the capacious central part.
4. Pyloric region---From angular notch on the lesser curvature to the pyloric
sphincter, subdivided into
a. Pyloric antrum---proximal tapering section.
b. Pyloric canal---distal tubular part.
•Stomach bed---the stomach rest on the stomach bed consisting of spleen,
diaphragm, left kidney & adrenal, pancreas, splenic artery, transverse colon
and mesocolon.
 FUNCTION

1. It acts like a hopper ie initial reservoir of ingested food.

2. Food is mixed, triturated & delivered into the duodenum in
amounts regulated by its chemical nature & texture
(osmolality)
3. First stage of protein and carbohydrate digestion are
carried out in the stomach.
4. A few substance are absorbed across the gastric mucosa.
 ARTERY SUPPLY

1. left gastric artery —branch of celiac artery

2. Right gastric artery---branch of common hepatic artery
3. Left gastroepiploic artery---branch of splenic artery
4. Right gastroepiploic artery----branch of gastroduodenal artery
5. Short gastric artery (vasa brevia) -----branch of splenic artery
 Venous drainage.

•In general, the veins of stomach parallel the arteries.

1. Left gastric vein(coronary vein)----drain into portal vein.
2. Right gastric vein-----drain into portal vein.
3. Left gastroepiploic vein----drain into splenic vein.
4. Right gastroepiploic vein -----drain into mesenteric vein
 Lymph Drainage

•This is exceedingly complex but has considerable importance in the surgery

of gastric cancer.
1. Right cardiac nodes—right side of abdominal oesophagus.
2. Left cardiac node-----left side of abdominal oesophagus.
3. Nodes along lesser curvature.
4. Nodes along greater curvature.
5. Supra pyloric nodes
6. Sub pyloric nodes

•All drains to celiac group of node—then to thoracic duct.

Japanese society for gastric cancer mapped the lymph node into numbered
station that form the basis of various types of gastric resection for cancer -------
1. Right cardiac nodes
2. Left cardiac nodes
3. Nodes along lesser curvature
4. Nodes along greater curvature
5. Supra pyloric nodes
6. Sub pyloric nodes
7. Nodes along left gastric artery
8. Nodes along common hepatic artery
9. Nodes along celiac axis
10.Nodes at the splenic hilum
11. Nodes along splenic artery
12.12 to18 are not mentioned here
19.Infradiaphragmatic nodes
20.Nodes in the oesophageal hiatus
 INNERVATION
•Parasympathetic innervation through left and right vagus nerve.
Left vagus gives off the hepatic branch to the liver and then continues
along the lesser curvature as anterior nerve of Latarjet. The right
vagus also gives a branch off to the celiac plexus and the continues
posteriorly along the lesser curvature as posterior nerve of latarjet.
The parasympathetic fibers sub-serve secretory & motor function.

•Sympathetic supply is through the splanchnic nerves (T6-T10) with

preganglionic efferent fibers ending in the celiac plexus and then the
post-ganglionic fibers travel in the periarterial plexuses along the
arteries to the stomach. The sympathetic fibers sub-serve visceral
sensation and pain.
 Gastric glandular organization

• Gastric mucosa consist of columnar glandular epithelia. The function

of the glands and the cells lining the glands vary according to the
region of the stomach in which they are found. Each gastric pit drain
3-7 gastric glands. Following cells are present.
• Mucous cell (40%)--------Luminal end of gastric gland and pits down
to neck of the gland for variable distance. It secret viside mucous.
• Chief cell (44%)--------Present in the distal part of the gland which
are mainly located in the body of stomach, few in the antrum, none
in the cardia& pyloric canal. It secret pepsinogen-1.
 Continue……..

• Parietal cell (13%)-----Also called oxyntic cell, present in the

proximal part of gastric gland located in the body few in the
antrum and none in the cardia& pyloric canal. It secret
hydrochloric acid and intrinsic factor.
• Endocrine cell (3%)------It comprises
– G cell---present in the gastric gland located in the gastric antrum and
produce gastrine, which evoke parietal cell to secret hydrochloric acid.
– D cell---present in the gastric glands located throughout the stomach
and produce somatostatin which inhibit parietal cell to secret
hydrochloric acid.
– ECL (enterochromafine like cell)-----these cells are present in gastric
gland located in the body of stomach and produce histamine which
plays a key role in gastric acid secretion.
 Gastric acid secretion mechanism
• Acid secretion by parietal cell is regulated by 3
stimuli.
• Gastrin-------It is secreted in response to the
presence of food in the stomach.
• Gastrin stimulate parietal cell through G cell
receptor to secret hydrochloric acid.
• Gastrin also stimulate ECL to secret histamine,
which stimulate parietal cell to secret HCL
• Actylcholine------It is secreted by vagal
stimulation in response to sight, smell, thought
or taste of food.
 Inhibition of gastric acid secretion
• Gastrin secretion is inhibited by intraluminal excess acid milieu through
negative feedback mechanism
• Somatostatin produced by D cell in response to luminal acid ( PH 3 ) causes
• Inhibition of gastrin release from G cell.

• Inhibition of histamine release from ECL

TO REMEMBER
• [PPI (proton pump inhibitor) totally abolish gastric acid production.
Significant hypergastrenemia ensue.
• Histamine receptor blocker markedly reduce acid production. Less
hypergastrenemia ensue.
• Prolong use of PPI causes benign tumour of ECL in animal]
 Phases of gastric acid secretion
• Cephalic phase----mediator is acetylcholine—released by vagal
stimulation in response to sight, smell, thought or taste of food.
• Gastric phase----mediator is acetylcholine and gastrin---
released by distention of stomach and interaction of digestion
product respectively.
• Intestinal phase----mediator is secretin released in response to
the presence of acid chime in the duodenum and small bowel
to inhibit gastric acid secretion
 Gastric mucosa and gastric mucosal barrier
• 1. Outer surface of gastric mucosa is covered by mucous gel which is
hydrophobic and chemically high molecular weight glycoprotein secreted by
mucus cell. Mucous is in a constant state of flux to replenish the constant loss
due to degradation effect by luminal peptic digestion. Gastric acid is thought to
enter the lumen through thin spot in the mucous overlying the gastric gland.
• Mucous secretion is stimulated by vagal stimulation, cholinergic drug,
prostaglandin, luminal acid.
• Mucous secretion is inhibited by anticholinergic drug, NSAID.
• 2. The gastric mucosal cells extract bicarbonate from the mucosal blood and
secret into the mucous, maintain high pH on the surface while low pH in the
lumen. Enhanced secretion of bicarbonate is induced by
prostaglandin ,theophylin. In contrast secretion reduced by smoking, alcohol,
certain drug( cyclooxygenase inhibitor) and somatostatin.
• 3. Mucosal defect produced by mechanical or chemical trauma are rapidly
repaired by adjacent normal cell that spread to cover the defect.
 SUMMARY

• Damaging factor--------Hydrochloric acid, Pepsin,

Alcohol, Smoking, NSAID, Hypoxia, Helicobacter
pylori.
• Protective factor------Ability to secret mucous,
bicarbonate, Rapid repair of mucosal cell, blood flow
to mucosa
 HELICOBACTER PYLORI
• It is previously called as campylobacter pylori, is a
spiral or helical shaped gm-vemicroaerophilic,
fastidious, flagellate bacillus
• Found only in gastric mucosa or metaplastic gastric
mucosa in duodenum due to presence of adherence
receptor (adhesin)
• 90% duodena ulcer, 75% gastric ulcer are associated
with H-pylori infection.
 Pathogenesity
• By elaboration of various enzyme & toxin, local mucosal immune response
• Endopeptidase.
• Mucinase—powerful mucolytic action.

• Phospholipase----damage epithelial cell.

• Urease-- split urea to produce ammonia which is a strong alkali, stimulate G
cell to release gastrin and ultimately results in gastric acid hyper secretion.
• Cytotoxin---Vacuolizingcytotoxin...vacuolization of affected cell
• Weak haemolysis---
• Local mucosal immune reponse-----organism insite a classical inflammatory
reaction to produce chemotactic factors that attract nutrophil& monocyte
and intern produce a number of proinflamatory cytokine & reactive oxygen
metabolite.
 Investigation
Invasive.
• Via flexible endoscpe three mucosal specimen is taken
• Rapid ureas test (CLO)------Commercially available kit containing urea & indicator
is brought in contact with mucosal specimen. If H-pylori present, its enzyme
urease split urea to ammonia, which is indicated by indicator
• For microscopic examination------By special stain (warthin-starry silver stain) to
identify the organism.
• For culture--Columbia agar media, incubated for 5 days under microaerophilic
condition. False –ve high
Non invasive
• Serology---ELISA for antibody against H-pylori
• UBT (urea breath test)---Urea leveled with radioactive carbon (C13,14) is given
orally. After 30 minute radioactive carbon is looked for in the breath by gamma
counter. If radioactive carbon found in breath , it must have been comes from
ingested urea by the splitting effect of urease elaborated by H-pylori.
 GASTRTIS
•Inflamatory condition of gastric mucosa is called gastritis.

 Acute gastritis is a transient mucosal inflammatory process that may be

asymptomatic or cause variable degree of epigastricpain , nausea and
vomiting.. In more severe cases there may be mucosal
erosion ,haemorrhage, haematemesis, malena or rarely massive blood loss.

 Chronic gastritis the symptoms nausea, vomiting, upper abdominal

discomfort are less severe but more persistent and may progress to
dysplasia and development of gastric cancer.
•From histologic point of view the histopathologist
graded them into
Mild gastritis
 Moderate gastritis
Severe gastritis
 TYPES OF GASTRITIS
 Type-A Gastritis( Atrophic gastritis/ autoimmune gastritis)
• This type of gastritis affects mainly the corpus ( body ) where
parietal cell predominant and appears to be autoimmune
aetieology with the presence of circulating parietal cell
antibody. There is associated pernicious anaemia due to lack
of intrinsic factor. There is hypergastraenemia and this may
lead to development of endocrine tumor ( ECL). There is an
increased risk of gastric cancer which is usually diffuse type
and screening such patient endoscopically may be
appropriate.
 Cont…
 Type-B Gastritis
• This type of gastritis is the result of infection of antral mucosa by H.
pylorie and eradication of the infection is followed by documented
histological improvement.The changes always begin distally in the
pyloric region and subsequently spread to the antrum and body of
the stomach to a variable extent. There is significant risk of
development of gastric cancer.
 Comparison of Type-A & Type-B
Gastritis
Type A gastritis Type B gastritis

Location Body Antrum

Inflammatory cells Lymphocyte, macrophages Neutrophil, plasma cells

Acid production Decreased Increased to slightly dereased

Gastrin Increased Normal to decreased

Serology Antibody to parietal cells Antibody to H. pylori

Association Autoimmune disease—graves disease Low socio-economic status

Sequelae Pernicious amaemia, adenocarcinoma Peptic ulcer, adenocarcinoma

 Erosive Gastritis( Reactive gastritis )

• This is the result of gastric mucosal damage by exogenous or

endogenous irritant. Histologically there is foveolar hyperplasia,
severe congestion, oedema and fibrosis of the lamina propria with a
paucity of inflammatory cells. Reactive gastritis is commonly
caused by drugs, e.g, NSAIDS and alcohol. The usual locations of
drug-induced damage are the antral and pre-pyloric regions.
 Reflux Gastritis
• It is a form of reactive gastritis due to enterogastric reflux of
bile with a dinstinctive pathological change consisting of
subnuclear vacuolization of the foveolar epithelium. It is
particularly common after gastric surgery.
 Eosinophilic Gastritis

 This occurs as part of eosinophilicgastroenteropathy in infants

and children and has an allergic basis. The pyloric region and adjacent
duodenum become diffusely thickened due to oedema of the
submucosal and the muscle layers, which are also infiltrated with
eosinophils and occasional giant cells.
 Lymphocytic Gastritis
• This type of gastritis is seen rarely. It is characterized by the
infiltration of the gastric mucosa by T cells and is probably associated
with H. pylori infection. The pattern of inflammation resembles that
seen in coeliac disease or lymphocytic colitis.
 Granulomatous Gastritis

• Granulomatous gastritis is seen rarely in crohn,s disease. The

microscopic features are similar to those of intestinal crohn,s and non
caseating granulomas are present . In addition there is focal chronic
active ulceration with erosion of the epithelium.
 AIDS Gastritis

• It is secondary to infection with cryptosporidium.

 TREATMENT
 The treatment depends on the effect of the gastritis (e.g, bleeding,
chronic symptoms),
 The removal of the underlying cause when applicable, or specific
therapy when indicated.
 When the chronic gastritis is accompanied by dysplasia, surveillance
by endoscopy is indicated
 If dysplasia becomes severe, then gastric resection is indicated.
 PEPTIC ULCER

 The term peptic ulcer refers to the development of ulcer due to

erosive action of acid gastric juice on vulnerable epithelium.
 When the term peptic ulcer was first used , it was thought that
most important factor was peptic activity in gastric juice.
 Since then evidence has implicated acid as the chief injurious
agent.
 Thereby aimed at reduction of acid secretion depending on
circumstances.
 PEPTIC ULCER

Ulcer may occur at

1. Oesophagus—in case of GORD/ GERD.
2. Duodenum
3. Stomach
4. Jejunum---after gastroenterostomy
5. Ileum—in relation to ectopic gastric mucosa in Meckel`s diverticulum
•Ninety percent (90%) duodenal ulcer and seventy percent (70%) gastric
ulcer are associated with H. pylori colonization, which weaken the mucosa
before acid is able to do the damage. This has lead many experts to
conclude that PUD is in reality, as infectious disease..
 Causes of PUD
1. Helicobacter pylori
2. NSAID-Aspirin, clofenac, indomethacin
3. Smoking
4. alcohol
5. Sever physiological stress—burn, multiorgan failure, CNS
trauma
6. Endocrine
i) Zollinger-Ellison syndrome
ii) Multiple adenoma syndrome
iii) Hyperparathyroidism
 DUODENAL UCER

 Occur at any age but most common in young & middle age (20-45 )
 Men more common than women
 95% are situated within 2cm of pylorus (1st part of duodenum)
 Mostly in anterior wall of 1st part of duodenum
 Sometimes posterior wall
 Rarely both are present called Kissing ulcer
 Anteriorly placed ulcer usually perforate
 Posteriorly placed ulcer bleed because of eroding of underlying
gastroduodenal artery.
 CAUSES
1. Infection by H. pylori
2. Parietal cell hyperplasia
3. Chronic use of NSAID----direct chemical irritation and reduced PG2
secretion
4. Cigarette smoking—impair mucosal blood flow and impair healing
5. High dose steroid—reduces PG secretion and impair healing
6. Hyper parathyroidism—hypercalcemia stimulate gastrin secretion
7. Zollinger Ellison syndrome—G cell hyperplasia
 MORPHOLOGY OF ULCER
1. Usually solitary ulcer
2. Size < .3cm dia are shallow ulcer
3. Size > .6cm dia are deep ulcer
4. Round or oval in shape
5. Sharply punched out
6. Floor is smooth and clean as a result of peptic digestion f exudates.
7. Malignant transformation is rare.
 GASTRIC ULCER
 Peak incidence 40 – 60 yrs
 Male female ratio equal.
 Infection by H. pylori, use of NSAID, smoking are the aetiologic factors
 Ulcers are more common in lesser curvature especially at
incisuraangularis
 Ulcer tends to be larger
 Ulcer may erode posteriorly into pancreas, occasionally into splenic
artery
 Ulcer less commonly erode into transverse colon.
 It is fundamental that any gastric ulcer should be regarded as being
malignant, no matter how classically it resembles a benign gastric ulcer.
Multiple biopsies should always be taken, perhaps as many as 10 well-
target biopsies, before an ulcer can be tentatively accepted as
being benign..
 CLASSIFICATION OF GASTRIC
ULCER
1. Type I---present on lesser curvature near incisuraangularis……60%
2. Type II—present in the body of stomach…………………………..<15%
3. Type III—present in pre-pyloric region…………………………......20%
4. Type IV---present high on lesser curvature near gastroesophageal
junction ….<10%
 CLINICAL FEATURE OF PUD
•C/F of Gastric & Duodenal ulcer can,t be differentiated on basis of
symptoms
1. Pain in epigastrium, which is burning, gnawing, or aching in nature.
2. Pain tends to occur 1-3 hour after meal during day, is worse at night and is
relieved by alkali or food.
3. Periodicity is a classical feature i.e symptoms disappear for weeks or
month to return again. ( this periodicity may be related to the spontaneous
healing of the ulcer )
4. Nausia, vomiting, bloating, belching may present.
5. Weight loss or sometimes weight gain may occur.
6. Bleeding in the form of haematemesis or malena may occur.
 Gastric ulcer vs Duodenal ulcer

Features Gastric ulcer Duodenal ulcer

Onset of pain Soon after eating 2-3 hour after eating
Periodicity of pain 2-3 months cycle 4-6 months cycle
Relieving factor Vomiting Eating
Precipitating factor Eating Missing a meal, anxiety,
Duration of attack Few weeks stress
Body weight Loss Few months
Gain
 COMPLICATION OF PUD
 Perforation
 Bleeding
 Scarring and deformity(pyloric stenosis, tea pot deformity, hour glass
deformity)
 Malignancy
 INVESTIGATION
1. Gastroduodenoscopy is the investigation of choice to visualization & biopsy
specimen for histology and H. pylori
2. Upper GI radiography to demonstrate
1) barium in ulcer crater or niche which is round or oval in shape.
2) extent of deformity due to chronic fibrosis.
3) deformity of duodenal bulve.
3. Gastric juice analysis
 Basal acid output (BAO)—measurement of acid production by the
unstimulated stomach under basal fasting conditions and expressed in
meq/l.
 Maximal acid output (MAO)---measurement of acid production during
stimulation by histamine or pentagastrin given in a dose maximal for this
effect and expressed in meq/l.
 DIFFERENTIAL DIAGNOSIS OF PUD
• Chronic cholecystitis
• Chronic pancreatitis
• Reflux oesophagitis
 TREATMENT

MEDICAL MANAGEMENT------Vast majority of uncomplicated peptic ulcer are treated medically

1. Inhibition of acid secretion by H2 receptor blocker or by proton pump inhibitor(PPI)
2. Eradication of H. pylori by combination antibiotic. It is given routinely in PUD patient.
• H. pylori is sensitive to Tetracyclin, Azithromicine, Amoxicillin, Metronidazol, Chlarithromicine.
• Use of single antibiotic---eradication rate up to 30%.
• Combination antibiotic-there is effective eradication rate.
• Standard combination—Amoxicillin 1000mg and Clarithromicine 500mg ---twice daily for 2
weeks.or Metronidazole 400mg and clarithromiine 500mg---twice daily for 2 weeks. In both cases
PPI is added. PPI is continued for 6-12 weeks.
1. Change of life style----stop smoking, alcohol, NSAID, asprin, discontinuation of coffee (coffee
stimulate acid secretion)

SURGICAL MANAGEMENT------Indication for surgical treatment

2. Intractable ulcer (very difficult to deal with)
3. Perforation of ulcer
4. Haemorrhage from ulcer
5. Obstruction of gut
 Duodenal ulcer----
1. Intractable ulcer---Parietal cell vagotomy (highly selective vagotomy) or
Truncalvagotomy / selective vagotomy with drainge procedure ( pyloroplast y /
gastrojejunostomy )
2. Bleeding ulcer---Oversewing of bleeding vessel with truncalvagotomyanpyloroplasty.
3. Obstruction---- Vagotomy of any form with gastrojejunostomy
4. Perforating ulcer--
 Patch closure of perforation with or without parietal cell vagotomy
 Truncal/selective vagotomy with pyloroplasty at perforation site.

 Gastric ulcer----
1. Intractable ulcer---Type-I, II & III gastric ulcer…distal gastrectomy with truncalvagotomy
and Billroth II procedure.
2. Bleeding ulcer----Type-I, II & III gastric ulcer------same as above
3. Perforation--- same as above
4. Obstruction—Antrectomy with vagotomy and Billroth-II procedure.
 COMPLICATION OF PEPTIC ULCER SURGERY
a.Early complication
1. Stump leakage
2. Gastric retention
3. Haemorrhage.
A. Late complication
1. Recurrent ulceration (marginal ulcer/stomal ulcer/anastomotic ulcer)----
 Develop immediate adjacent to anastomosis on intestinal side
 Present with upper abdominal pain which aggravate by eating and improve
by antacid
 Often present with GI haemorrhage
 Rarely present with free perforation r fistula formation to adjacent viscus
 Treatment-----same as original ulcer
 Continue….
1. Billius vomiting ( alkaline reflux gastritis )
 Reflux is associated with severe epigastric pain accompanied by
bilious vomiting
 Pain not relieved by food or antacid
 Marked weight loss
 Treatment by revision surgery---convertBilroth-II to Roux-en- Y
gstrojejunostomy
 Small stomach syndrome
i. Early satiety
ii. Gets better in course of time
 Continue….
1. Post vagotomy diarrhea
 Treated by antidiarrhoeal agent
 Usualy disappear by 3 to 4 months
 In intractable case, surgery---to interpose a 10 cm segment of reverse
jejunum 70 to 100 cm from ligament of Treitz . This has led to sustained
relief of diarrhea.
1. Dumping syndrome—Dumping syndrome refers to a symptom complex
that occurs following ingestion of a meal when a portion of the stomach
has been removed. There re 2 types of dumping, Early & Late dumping
 Continue….
 Early dumping syndrome---
 This usually occurs within 20 to 30 minutes after ingestion of a meal
 It is accompanied by both GI symptoms like nausea, vomiting, epigastric
fullness, eructation, cramping abdominal pain, often explosive diarrhea and
cardiovascular symptoms like palpitation, tachycardia, diaphoresis, fainting,
dizziness, flushing and occasionally blurred vision.
 This is because of the rapid passage of food of high osmolality from the
stomach into the small intestine, which induces a rapid shift of extracellular
fluid into the intestinal lumen to achieve isotonicity.
 This shift of fluid causes luminal distention and induces the autonomic
responses listed previously.
 Dietary measure to treat the syndrome include avoiding food containing large
amount of carbohydrate, frequent feeding of small meals rich in protein & fat.
  Late dumping syndrome—
 This usually occurs 2 to 3 hours after meal and less common than
early dumping syndrome.
 The basic defect is rapid delivary of carbohydrate in to the small
intestine.
 They are quickly absorbed, resulting hyperglycemia, which
triggers the release of large amount of insulin.
 Subsequently hypoglycemia results due to overshooting of insulin.
 Hypoglycemia activates the adrenal gland to release
catecholamine which results in diaphoresis, light-headedness,
tachycardia and confusion.
 The patients are advised to take frequent small meal poor in
carbohydrate.
 Continue….

1. Metabolic disturbance
 Amaemia--Two types have been identified, one is related to iron deficiency
& other to vit B12 deficiency
 Steatorrhea---Due to impaired fat absorption.
 Osteoporosis and osteomalasia----caused by calcium deficiency
1. Malignant transformation-------
 Operation such as gastrectomy or vagotomy and drainage are independent
risk factors for the development of gastric cancer.
 The increased risk appears to be approximately four times that of the
control population.
 It is not difficult to understand the increased incidence of gastric cancer, as
bile reflux gastritis, intestinal metaplasia and gastric cancer re linked.
 The lag phase between operation and the development of malignancy is at
least 10 year
 CARCINOMA STOMACH

•INTRODUCTION
 Carcinoma of the stomach is a major cause of cancer mortality worldwide.
 Gastric cancer is actually an eminently curable disease provided that it is detected at
an appropriate stage and treated adequately.
 The only treatment modality able to cure the disease is resectional surgery.

•INCIDENCE
 There are marked variations in the incidence of gastric cancer worldwide.
 In USA 10 cases per 100000 population per year.
 In UK 15 cases per 100000 population per year.
 In Eastern Europe 40 cases per 100000 population per year.
 In Japan 70 cases per 100000population per year.
 In certain part of China incidence is double that of Japan.
 AETIOLOGY
There are various factors causing gastric cancers. The important
factors are
 Dietary factors
 H. pylori infection
 Following peptic ulcer surgery
 Pernicious anaemia
 Cigarette smoking
 Ulcer cancer— The incidence is 0.1%
 Genetic factor
 SITE OF CANCER IN THE STOMACH

 In the west the proximal stomach is now the most common site for
gastric cancer.
 Japan and rest of the world distal cancer is predominant
 Pyloric region— 47 %
 Body— — 23%
 Cardia— — 21%
 Fundus— — 2%
 Linitis plastic —7%
 MACROSCOPIC TYPES OF
CARCINOMA STOMACH
There are four principal varieties of gastric cancer
 Proliferative type—Cauliflower type of growth projecting into the lumen
of the stomach
 Ulcerative type— most common type. Ulcer has rolled out everted
edge with surrounding induration
 The colloid or mucoid type— appear as a massive tumor of gelatinous
apparence
 Linitisplastica— the tumor infiltrate submucosa and subserosa without
protruding into the lumen. Desmoplastic reaction give rise to extensive
fibrous tissue and stomach become contracted and rigid like a leather
bottle
 HISTOLOGIC TYPE OF GASTRIC CANCER

 Adeno carcinoma— This is the commonest type of carcinoma. There are

two types of adenocarcinoma (Lauren`s classification)
 Intestinal type of gastric carcinoma—
 Gastric carcinoma cell derived from metaplastic gastric cell.
 Metaplastic cell exhibit a striated (brush) border and generally resemble
intestinal cell.
 They grow along broad cohesive fronts to form either an exophyticmass or
ulcerated lesion and frequently surrounded by intestinal metaplasia.
 Neoplastic cell contain apical mucin vacuole and abundant mucin may be
present in gland lumen.
HISTOLOGIC TYPE OF GASTRIC
CANCER
 Diffuse gastric type---
 Carcinoma arising from normal gastric mucosa.
 Carcinoma composed of discohesive cell that do not form glands.
 Neoplastic cell contain large mucin vacuole pushing nucleus to the
periphery giving signet ring appearance.
 Lesion infiltrate the gastric wall without forming a mass
&evokedesmoplastic reaction that stiffens the gastric wall
 Squamous cell carcinoma
 Adenosquamous
 Carcinoid
 CONTRAST BETWEEN INTESTINAL AND DIFFUSE
GASTRIC CANCER

Intestinal Diffuse gastric

Histogenesis Area of intestinal metaplasia Normal gastric mucosa
Early cancer Protruding type Flat, Depressed or excavated
Infiltration Localized Diffuse
Peritoneal dissemination Infrequent Frequent
Hepatic metastasis Nodular Diffuse
Sex incidence Common in male Common in female
Age incidence Common in elderly Common in young
Prognosis Better Dismal
 SPREAD OF CANCER

 Direct spread to adjacent organ

 Lymphatic spread—By permeation and emboli to the affected tiers of nodes.
Unlike breast malignancy , nodal involvement does not imply systemic
dissemination (except N4 node)
 Blood born metastasis— Liver , lung, bone.
 Transplantation— During surgery cancer cell may implant at the site of
incisions.
 Transperitoneal spread—
 Common mode of spread once the tumor has reached the serosa of the
stomach.
 Affect anywhere in the peritoneal cavity and commonly give rise to ascites.
 Advanced tumor palpated rectally as a tumor `shelf``.
 Krukenberg`stumour when ovary affected
 Sister joseph`s nodule when umbilicus affected.
 CLASSIFICATION OF GASTRIC
CANCER
A. Early gastric cancer— Cancer limited to the mucosa and submucosa with or without lymph
node involvement.
• Further classified by Japanese into three varieties
a. protruding
b. superficial
c. excavating
A. Advanced gastric cancer— Cancer involves the muscularispropria.

Further classified by Bormann into four varieties.

a. Type1 polypoid well demarcated
b. Type2 Ulcerated with sharply demarcated margins
c. Type3 Ulcerated without definite limits, infiltratring the surrounding margin.
d. Type 4 Diffusely infiltrating without significant ulceration
 CLINICAL FEATURE
•Symptoms
 Dyspepsia— In early gastric cancer it is indistinguishable from benign dyspepsia
 Recent dyspepsia in a patient over 45 yrs
 Loss of appetite
 Early satiety
 Bloating, distension
 Epigastric fullness, vomiting
 Dysphagia if cardia involved
 GOO if pylorus involved

•Sign
 Epigastric mass
 Ascities
 Troiseir`s sign— Virchow`s node
 Trousseau`s sign— thrombophlebitis, deepvein thrombosis
 Hepatomegaly
 Blumer shelf
 Sister joseph`s nodule
 DYSPEPSIA WITH ALARM FEATURES

 Weight loss
 Anaemia
 Vomiting
 Haematamesis and / or malena
 Dysphagia
 Palpable abdominal mass
 INVESTIGATION
 Upper GI endoscopy is the investigation of choice.
 Multiple biopsies from the edge and base of the gastric ulcer.
 Barium meal is a poor alternative
 USG of abdomen
 Further imaging (CT & MRI ) is necessary for accurate staging and
resectability
 Laparoscopy is the only reliable modality to detect peritoneal spread.
 Tumour marker
 CEA
 CA-19-9
 CA-74-4 (most important marker fo cancer stomach)
 TREATMENT
 Curative treatment

 Surgery— surgical resection offers the only hope of cure which can be
achieved in 90% with early gastric cancer. For majority who have locally
advanced disease radical and total gastrectomy with lymphadenectomy is
the operation of choice.
• Sign of incurability
 Haematogenous distant metastasis
 Involvement of distant peritoneum
 N4 nodal disease
 Fixation to structure that can not be removed
• Resection are of two types depending on site of tumour. Lymph
node resection include one tier advance than the 9 tier involved.
 Continue….
 Total gastrectomy—Indications
 Proximal gastric cancer involving the cardia
 Diffuse gastric cancer (boreman type 4)
 Growth involving the two or all 3 sectors of the stomach
 Generalized linitisplastica
 Partial gastrectomy
• For tumour distally placed in the stomach are suitable for
partial gastrectomy. Resection margin should be 2cm in early
gastric carcinoma and 5cn in advanced gastric carcinoma.
•
 Neoadjuvantchemotheraphy— ECF (epirubicin, cisplatin and
fluorouracil) improves the survival rate.
 Palliative treatment-
 If there are sign of incurability / inoperable then palliation of symptoms
are done
 Carcinoma at cardia—endoscopic dilatation---recanalisation with
laserlaser ---insertion of stent.
 Carcinoma at pylorus— gastrojejunostomy
 Endoscopic laser ablation to control bleeding. Or palliative resection to
control bleeding.
 Palliation also be achieved for inoperable tumour with chemotherapy
like ECF or FAM( fluorocil, doxorubisin and mitomycin).
 INFANTILE HYPERTROPHIC
PYLORIC STENOSIS
•INTRODUCTION
 Pyloric stenosis is the most common surgical disorder producing
emesis in infancy

•AETIOLOGY
 Not known
 Genetic basis may be present
 INFANTILE HYPERTROPHIC
PYLORIC STENOSIS
•INCIDENCE
 1: 400 live birth
 Male : female ratio 4:1, particularly first born male baby.

•PATHOLOGY
 It results from hypertrophy of circular and longitudinal muscularis of the
pylorus and the distal antrum of the stomach with progressive
narrowing of the pyloric canal.
 Oedema and inflammatory changes in the mucosa and submucosa
may aggravate the narrowing.
 CLINICAL FEATURE
 Typically , the affected infant is full term when born and feeds and grows
well until 2—4 weeks after birth., at which time occasional regurgitation of
some of the feedings occur.
 Several days later , however, the vomiting becomes more frequent and
forceful.
 The vomitus contains the previous feeding and no bile. Blood may be
seen in vomitus in 5% of cases.
 With dehydration infants often have sunken fontanelles, dry mucous
membrane, and poor skin turgor.
 Weight loss follows progressive feeding intolerance.
 Gastric peristalsis waves can usually be seen moving from left costal
margin to the area of pylorus.
 When infant is relaxed, the pyloric tumour( often called olive) can be
palpable.
•METABOLIC ABNORMALITY
 Metabolic abnormality is same as adult patient.
 Metabolic alkalosis with hyponatremia, hypochloremia and
hypokalemia. Mechanism as follows

•IMAGING
 Abdominal ultrasonogram is the most sensitive and specific test
 A contrast upper gastrointestinal series is indicated if efficient
sinologist is not available or in diagnostic confusion.
a. Outlining of the narrow pyloric channel by a single “string sign”
b. A pyloric “”beak” where the pyloric entrance from the antrum occurs.
c. The “shoulder sign” in which the pyloric mass bulges into the antrum
d. Complete obstruction of the pylorus
 DIFFERENTIAL DIAGNOSIS

 Over feeding
 Intracranial lesion
 Pylorospasm
 Antral wave
 Gastroesophageal reflux
 Duodenal stenosis
 Malrotation of bowel.
 TREATMENT

A. Correction of the metabolic abnormalities by dextrose saline and potassium

(2.5% dextrose plus 0.45% sodium chloride plus 1gm of potassium chloride per
500 ml of fluid.
B. Next is the surgical treatment known as Ramstedt`spyloromyotomy, which splits
and widely separates the hypertrophic muscle at the submucosalplane , from
stomach to duodenum.
 Anaesthesia general or local
 Skin is opened through a transverse incision placed in the upper abdomen over
the right rectus sheath
 Rectus sheath is opened in the same line.
 The rectus muscle is then split along the line of its fiber and posterior rectus
sheath is opened in the line of skin incision.
 .
 Continue……..
 Hypertrophied pylorus is delivered and rotated so that its superior surface
comes into views.
 Incision is made through the serosa only over the hypertrophied pylorus and
muscle is then split by blunt dissection.
 The pyloric mucosa bulges into the cleft, great care to be taken not to
perforate the mucosa.
 If accidental perforation occur, it is to be closed with a omental patch.
 Post operatively feeding start after recovery from anaesthesia.
 In case of mucosal perforation feeding delayed for 3 days.
•OUTCOME
 In complete pyloromyotomy— pyloric stenosis never recurs and there is a
uniformly excellent outcome
 In incomplete pyloromyotomy – vomiting persist beyond 2 weeks post
operatively
 GASTRIC OUTLET OBSTRUCTION

•INTRODUCTION
 Two common causes of gastric outlet obstruction are gastric cancer and pyloric stenosis secondary to
peptic ulceration.
 Now pyloric stenosis is decreasing due to decrease incidence of peptic ulcer with the advent of potent
medical treatment.
 The term pyloric stenosis is normally a misnomer as the stenosis is seldom at the pylorus.
 Stenosis is found in the first part of the duodenum , the common site for a peptic ulcer.
 True pyloric stenosis is can occur as a result of fibrosis around a pyloric channel ulcer.

•PATHOGENESIS
 The cycle of inflammation and repair in peptic ulcer disease may cause obstruction of the
gastroduodenl junction as a result of scarring, oedema and muscular spasm .
 If oedema and muscular spasm are involved , the obstruction may be reversible with medical
treatment.
 A few gastric ulcers that obstruct, are close to the pylorus.
 Malignant tumour of antrum or pancreas is now the leading cause of obstruction with decline of peptic
ulcer disease.
 METABOLIC CHANGE

• In vomiting there is huge water and electrolyte loss leading to

hypovolumia,hypochloremia, hypokalemia and loss of HCL, all of which contribute
metabolic alkalosis. Parietal cells secret HCL into the lumen of stomach, for every
H+secretion one HCO3 – is added to the blood, so loss of HCL directly contributes
to metabolic alkalosis.
 This bicarbonate is excreted along with sodium and so, with time, the patient
becomes progressively hyponatraemic and dehydrated.
 Hypovolumia and hyponatraemia will stimulate Renin-angiotensin-aldosterone
system to secrete aldosterone which causes retention of sodium in exchange of
potassium. In extreme hypokalemia, sodium will be reabsorbed in exchange of
hydrogen ion.This results in urine becoming paradoxically acidic. This is called
paradoxicaciduria.
 Alkalosis leads to a lowering of the circulating ionized calcium, and tetany can
occur.
 CLINICAL FEATURE

 In benign gastric outlet obstruction there is usually a long history of peptic

ulcer disease.
 Tenderness in upper abdomen.
 Abdominal distention , nausea, vomiting.
 Large quantities of gastric content are often vomited and food eaten 24
hours or more may be recognized which are not bile stained.
 Vomiting is projectile in nature.Often patient induces vomiting to get relief
of abdominal discomfort.
 Dehydration and malnutrition are obvious.
 Peristalsis may be visible.
 Succession splash may be audible on shaking the patient`s abdomen.
 INVESTIGATION

 Upper gastrointestinal endoscopy.

 Barium meal x-ray
 Plain x-ray may reveal large gastric fluid level.
 Serum electrolyte shows— hypochloremia, hypokalemia, hyponatremia
and increased bicarbonate.
 200ml gastric aspiration after overnight fasting is suggestive of GOO.
 TREATMENT
A. Medical treatment
 Stomach should be emptied using a wide-bore gastric tube.
 Gastric lavage with normal saline twice daily.
 Intravenous correction of dehydration by normal saline infusion along with potassium
supplement.
 In some patient PPI drugs heal ulcers, relieve pyloric oedema and overcome the need
for surgery.
 Gradual resumption from liquid to solid food is permitted as tolerated.

A. Surgical treatment
 If 5-7 days of medical treatment do not results in relief of the obstruction , the patient
should be treated surgically.
 Surgical treatment may consist of a truncal or parietal cell vagotomy and drainage
procedure in the form of pyloroplasty or gastrojejunostomy.
 PERFORATION OF PEPTIC ULCER

•INTRODUCTION
 Perforation is a common complication of peptic ulcer.
 But its incidence is declining with the widespread use of gastric
antisecretory agents and H. pylori eradication therapy.

•SITE OF PERFORATION
 This is more common in duodenal than in gastric ulcer.
 Anteriorly placed duodenal ulcer tends to perforate than the posteriorly
placed ulcer because of the absence of protective viscera.
 1/4th of all perforations occur in acute ulcer and NSAIDs are often
incriminated.
 CLINICAL FEATURE

 The classical presentation is instantly recognizable.

 The patient, who may have a history of peptic ulceration, develops sudden
onset, severe, generalized abdominal pain as a result of the irritant effects
of gastric acid on the peritoneum.
 Clinical picture is described in 3 stages.
 First stage is known as peritonism—
 It is due to the leakage of gastric juice in to the peritoneal cavity (chemical
peritonitis).
 This stage usually last for about 6 hours.
 The pain initially develops in the upper abdomen, then gravitate along the
paracolic gutter to right iliac fossa and rapidly becomes generalized.
 Shoulder tip pain is due to irritation of the diaphragm.
 Respiration is shallow due to the limitation of diaphragmatic movement.
 Abdomen is held immobile and there is generalized board like rigidity.
 Bowel sounds are absent
 Continue…
 Second stage is known as the stage of reaction( stage of illusion)—
 The irritant fluid becones diluted with the peritoneal exudate.
 The intensity of symptoms dwindles.
 Abdominal rigidity continues. Rectal examination may elicit
tenderness in the rectovesical or rectouterine pouch.
 Third stage is the stage of diffuse bacterial peritonitis—
 The pinched and anxious face, sunken eye and hollow cheeks— the
so called facieshippocratica.
 Rising pulse rate , persistent vomiting, rigidity and increasing
distention of the abdomen .
 INVESTIGATION

 Plain x-ray of abdomen

 In upright position reveals free air in subdiaphragmatic region.
 Left lateral decubitous position—In uncomfortable patient because of
shock or disability.
 If finding are questionable, 400 ml of air can be insufflated into the
stomach through nasogastric tube & films are repeated.
 Contrast x-ray—If no free air is demonstrated but clinical picture
suggestive, then contrast x-ray done with water soluble dye
(gastrografin). If perforation has not been sealed, the diagnosis is
established.
 Leukocytosis is common
 Mild rise in serum amylase is probably caused by absorption of enzyme
from duodenal secretion within the peritoneal cavity.
 TREATMENT

 Initial management consists of resuscitation.

 Nasogastric tube insertion and decompression of stomach
 Intravenous fluid. Intravenous antibiotic of 3rd generation cephalosporin
and metronidazole. Adequate analgesics.
 Urinary catheterization to monitor unine out-put
 Surgical treatment— Through peritoneal toileting done and respective
ulcer is dealt as follows.
 Duodenal ulcer
 Simple closure whereby the ulcer is underrun with suture and use of
omentalpatch.
 It can be done by open or laparoscopic method.
 Followed by PPI medication and eradication therapy.
 If scarring present then vagotomy and pyloroplasty is preferred.
 Gastric ulcer— excision and closure is done so that malignancy could be
excluded.
 UPPER GI HAEMORRHAGE
•INTRODUCTION
 Upper gastrointestinal haemorrhage is the most common gastrointestinal
emergency.
 Upper GI haemorrhage accounts for nearly 80% of of significant GI
haemorrhage.
 Despite improvement in diagnosis and treatment modalities, mortality rate is
still about 5 %.

•WHAT IS UPPER GI HAEMORRHAGE

• Upper GI bleeding refers to bleeding that arises from the GI tract proximal
to ligament of Treitz
 CAUSES

 Ulcers— 60%
 Duodenal ulcer
 Gastric ulcer
 oesophageal
 Erosion— 26 %

 Oesophageal erosion
 Gastric erosion
 Duodenal erosion
 Mallory-Weiss tear— 4 %
 Oesophagealvarices— 4 %
 Angiodysplasia— 2 %
 Tumors— rare
 Others (Dieulafoy`s disease)
 PRESENTATION
 Sign of blood loss— hypotension, tachycardia, pallor
 Sign of liver disease and portal hypertension— spider naevi,
portosystemic shunting, bruising.
 History of peptic ulcer disease
 History of drug intake most importantly anticoagulant, NSAIDs

•Haematemesis— Bright coloured blood vomiting often associated with clot,

when profuse bleeding.
— Black coffee ground vomiting when less severe bleeding

•Malena — Passage of black tarry stool containing altered blood, where

bleeding is not profuse.
—The characteristic color and smell are the result of the action of
digestive enzymes and of bacteria upon haemoglobin.
 MANAGEMENT

• Principle of treatment are

1. First resuscitation
2. Then investigated urgently to determine the cause of bleeding
3. Only then definitive treatment be instituted

•Resuscitation
 Intravenous access is obtained— volume expand with colloidal or crystalloid
solution
 Nasogastric tube is passed to monitor the bleeding and prevent aspiration
 Urinary catheter is inserted
 Central line is often used to help to monitor central venous pressure
 Blood transfusion, to replace the loss
 Oxygen inhalation
 Drug— PPI, Propranolol, antibiotics
 Basic investigation

 Full blood count

 Blood urea and electrolyte
 Liver function test
 Prothrombin time
 Cross-matching
 Definitive treatment

 Endoscopic method
 Once resuscitation has stabilized the patient endoscopy is used to
detect the site of bleeding, as well as therapeutic purpose.
 Bleeding from an ulcer can effectively be stopped by injection of diluted
adrenaline (epinephrine), ethanol, cautery using heated probe, leser,
application of metallic clips
 Balloon tamponade by Sangstaken tube— oesophagealvarices
 Angiography— in whom endoscopy does not identify the bleeding point
(bleeding must be >1ml/min)
 Continue…
 Surgical method
 Emergency surgery is indicated if endoscopy reveals bleeding from a major
artery or unable to control bleeding directly
 Duodenal ulcer—
 Open the anterior wall of the pylorus by pyloromyotomy.
 Bleeding duodenal ulcer may simply be underrun with non absorbable
suture.
 If gross scarring is present then pylorus be closed transversely.
 Gastric ulcer—
 Open the stomach anteriorly (anterior gastrotomy).
 Ulcer should be excised completely by undertaking a partial gastric
resection for biopsy to exclude malignancy.
 If not then a smaller wedge resection taken for biopsy and bleeding
controlled by underrunning of the ulcer .
 Continue…
 Mallory-Weiss tear—
 This is the longitudinal tear below the gastro-oesophageal junction,
induced by repetitive and strenuous vomiting
 Stomach is opened by longitudinal gastrostomy
 Underrunning of the tear that all is required.
 Dieulafoy`s disease—
 Large tortuous submucosal artery normally found in the body of stomach,
often missed endoscopic examination.
 Local excision of the artery is required.
 Continue…
 Oesophagealvarices—
 Oesophageal transection and reanastomosis
 Emergency shunt can also be done.
 Selective shunt—Splenorenalshunt→splenic vein to left renal vein
• ( Less chance of encephalopathy ).
 Non-selective shunt ( More chance of encephalopathy )
i. Portocaval—Portal vein to inferior vena cava
 End to side portocaval
 Side to side portocaval
i. Mesocaval—Superior mesenteric vein to inferior vena cava
 BEZOAR

•DEFINATION
• Bezoar are the concretions formed in the stomach

•TYPES
1. Trichobezoar—
 It is composed of hair
 Usually found in female psychiatric patient often young girl who pick at their hair
and swallow it.
1. Phytobezoar—
 It is composed of agglomerated vegetable fiber.
 Usually found principally in patient who have gastric stasis often following
gastric surgery.
 Orange segments or other fruits that contain a large amount of cellulose have
been implicated in most cases.
 Improper mastication of food is a contributing factor
•CLINICAL FEATURES
 Upper abdominal pain
 Haematemesis
 Malena
 Features of GOO

•INVESTIGATION
 Upper GI endoscopy

•TREATMENT
 Bezoar can be broken up and disperse by endoscope
 Removal of bezoar by endoscope
 May require open surgical removal.
THANK YOU