UPPER GASTROINTESTINAL

BLEED
Dr Muhammad Hanif bin Khairudin
PPS HSM

 Acute upper gastrointestinal bleeding is a common medical emergency that

has a 10% hospital mortality rate
remains a common cause of hospitalization
defined as bleeding derived from a source proximal to the ligament of Treitz

Classification
VARICEAL BLEED
Esophageal Varices
Gastric Varices

NON VARICEAL BLEED

Peptic Ulcers
Erosions
Esophagitis
Mallory-Weiss tear
Malignancy

Clinical Presentation
History findings: weakness, dizziness, syncope associated with
hematemesis , and melena
Occasionally, a brisk UGIB manifests as hematochezia (fresh red
stools)
Patients may have a history of dyspepsia, ulcer disease, early
satiety, and NSAID or aspirin use.
Patients may present in a more subacute phase, with a history of
dyspepsia and occult intestinal bleeding manifesting as a positive
fecal occult blood test result or as iron deficiency anemia.
A history of chronic alcohol use of more than 50 g/d or chronic
hepatitis (B or C) increases the risk of variceal hemorrhage
The presence of postural hypotension indicates more rapid and
severe blood loss.

Varices
Esophageal varice are dilated veins of the esophagus that
form as a consequence of portal hypertension, preferentially
in the submucosa of the lower esophagus.
collateral veins within the wall of the esophagus that project
directly into the lumen
Rupture and bleeding from esophageal varices are major
complications of portal hypertension and are associated with
a high mortality rate.
Gastric varices are dilated submucosal veins in the stomach
Variceal bleeding accounts for 1030% of all cases of upper
gastrointestinal bleeding

Pathophysiology
Portal System
Conducts venous return
from gut and associated
organs to the liver
Much of the system is
retroperitoneal but some
tributaries are within
mesentery

Pathophysiology
1) Increased Vascular Resistance
Blood vessel radius significantly reduced
in liver dz that produce an increase in
portal vascular resistance
In cirrhosis increase in hepatic
microcirculation

2) Endothelin&Nitric Oxide(NO)
A vasodilator synthesised by the sinusoidal
endothelial cells
Cirrhotic liver reduced NO production,
causing hepatic vasoconstriction
Concomitant splanchnic arteriolar
vasodilation causing increased portal
venous inflow

Presentation
Vomiting blood
Black, tarry or bloody stools
Shock (in severe case)
Abdominal pain.
Features of liver disease and specific underlying condition
Dysphagia/odynophagia (pain on swallowing; uncommon)
Confusion secondary to encephalopathy (even coma)
Pallor.
Hypotension and tachycardia (ie shock).
Reduced urine output.
Reduced Glasgow Coma Scale.
Signs of sepsis may also commonly be present.

Investigation
Endoscopy is required at an early stage
FBC - haemoglobin may be low; MCV may be high, normal or low;
platelets may also be low; WCC may be raised.
Clotting including INR.
Renal function.
LFTs.
Group and cross-match.
CXR - patients may have aspirated or have chest infection.
Ascitic tap may be needed if bacterial peritonitis is suspected.

Management
1) Prophylaxis
Reducing pressure in the portal vein - beta blockers[propranolol (Inderal,
Innopran) and nadolol (Corgard)] markedly reduced risk of variceal bleeding as
well as slowing the progression of small varices into larger ones.
Banding - Using an endoscope, the doctor snares the varices and wraps them with
an elastic band, which essentially "strangles" the veins so they can't bleed.
Esophageal band ligation carries a small risk of complications, such as scarring
of the esophagus.

Management
2) Management of active variceal bleed
Resuscitation and initial management
Resuscitate A,B,C. Look for early signs of shock(tachycardia, postural HPT)
Assess mental state (if altered such as in encephalopathy protect airway)
Correct fluid losses (place two wide-bore cannulae and also send bloods at the
same time).
Transfuse patients with massive bleeding with blood, platelets and clotting
factors
Offer platelet transfusion to patients who are actively bleeding and have a
platelet count of less than 50 x 109/litre.
Offer fresh frozen plasma to patients who have either:
a fibrinogen level of less than 1 g/litre, or
a prothrombin time (international normalised ratio) or activated partial
thromboplastin time greater than 1.5 times normal
Offer prothrombin complex concentrate to patients who are taking warfarin
and actively bleeding.

Emergency endoscopy- Timing of Endoscopy

Offer endoscopy to unstable patients with severe acute upper
gastrointestinal bleeding immediately after resuscitation.
Offer endoscopy within 24 hours of admission to all other patients with
upper gastrointestinal bleeding.
Urgent endoscopy is necessary for variceal haemorrhage - confirms
the diagnosis and source of bleeding, allowing the bleeding point to be
visualised and treated: Band ligation is the first choice of treatment

Vasoactive drugs
The use of vasoactive agents (terlipressin, octreotide or somatostatin) is
associated with a significantly lower risk of acute all-cause mortality and
transfusion requirements, and improved control of bleeding and shorter
hospital stay.
Terlipressin is an analogue of vasopressin and is considered the vasoactive
agent of choice in acute variceal bleeding. It should be given to all patients
presenting with suspected variceal bleeding prior to endoscopy and
following confirmation.
*Vasopressin and terlipressin should not be used in severe hypovolaemic
shock and patients with severe cardiac disease.
Variceal obturation with glue
This involves embolisation of varices with a glue-like substance (N-butyl-2cyanoacrylate).
It is particularly good for gastric or gastro-oesophageal variceal bleeding.
However, there is a risk of embolisation to the lung, spleen or brain.

Balloon tube tamponade (Sengstaken-Blakemore tube)

Balloon tamponade should be considered as a temporary salvage treatment for

uncontrolled variceal haemorrhage.
The Sengstaken tube is inserted through the mouth and into the stomach.
The gastric balloon is inflated with air and the gastric balloon in then pulled up
against the oesophagogastric junction, compressing submucosal varices.
If bleeding continues, it may be that the tube is wrongly positioned or bleeding is from
another source.

Indication for sengtaken blakemore

- Before referral to endoscopy centre
- For patient not fit for endoscopy/massive bleed

Transjugular intrahepatic portosystemic shunt (TIPS)- recommended as the

treatment of choice for uncontrolled variceal haemorrhage.
The hepatic vein is cannulated percutaneously via the internal jugular vein, using a
needle under ultrasound or fluoroscopic guidance.
A tract is created through the liver from the hepatic to the portal vein - thus reducing
portal pressure. This is dilated and an expandable metal stent inserted to create a
shunt.
This has a high success rate but encephalopathy is found in 25% of cases (as portal
blood diverted from the liver) and shunt occludes within one year in up to 50% of
cases.

Non Variceal Bleed

PEPTIC ULCER DISEASE (PUD)
-spectrum of disease characterised
by ulceration of the stomach or
proximal duodenum due to an
imbalance between the acid
secretion and mucosal defense
mechanisms
Modified Johnson Classification
Type 1 Lesser curvature
Type 2 Lesser curvature and
duodenal 15%
Type 3 Prepyloric 20%
Type 4 Proximal stomach/cardia
Type 5 Anywhere in stomach

Anatomy

Pathophysiology
Peptic ulcers are defects in the
gastric or duodenal mucosa that
extend through the muscularis
mucosa.
The epithelial cells of the stomach
and duodenum secrete mucus in
response to irritation and as a
result of cholinergic stimulation.
The superficial portion of the
gastric and duodenal mucosa
exists in the form of a gel layer.
Other gastric and duodenal cells
secrete bicarbonate, which aids in
buffering acid that lies near the
mucosa.

Prostaglandins of the E type (PGE)

have an important protective role,
because PGE increases the
production of both bicarbonate
and the mucous layer.
In the event of acid and pepsin
entering the epithelial cells,
additional mechanisms(ion
pumps, the process of restitution,
mucosal blood flow) are in place
to reduce injury.
Under normal conditions, a
physiologic balance exists
between gastric acid secretion
and gastroduodenal mucosal
defense.
Mucosal injury and, thus, peptic ulcer
occur when the balance between
the aggressive factors and the
defensive mechanisms is
disrupted.

Helicobacter pylori
When H pylori colonizes the gastric mucosa, Most patients with duodenal ulcers have impaired
duodenal bicarbonate secretion, which has also proven
inflammation usually results.
to be caused by H pylori

In patients infected with H pylori, high levels

The combination of increased gastric acid secretion
of gastrin and pepsinogen and reduced
and reduced duodenal bicarbonate secretion lowers
levels of somatostatin have been measured.
the pH in the duodenum, which promotes the
development of gastric metaplasia (ie, the presence of

In infected patients, exposure of the

gastric epithelium in the first portion of the
duodenum to acid is increased. Virulence
duodenum).
factors produced by H pylori, including
urease, catalase, vacuolating cytotoxin, and H pylori infection in areas of gastric metaplasia
induces duodenitis and enhances the susceptibility to
lipopolysaccharide, are well described.
acid injury, thereby predisposing to duodenal ulcers.

Etiology
Peptic ulcer disease (PUD) may be due to any of the
following:
H pylori infection
Drugs NSAIDs impair mucosal prostaglandin
production (non selective COX inhibition)
Lifestyle factors cigarette smoking
Severe physiologic stress Type A personality
Hypersecretory states (uncommon)

Presentation
Symptoms
Symptoms of dyspepsia
Epigastric pain, usually 1 to 3 hours postprandial - it may sometimes wake the
patient in the night and be relieved by food(duedenal ulcers), exacerbated by intake
for gastric ulcers.
Nausea.
Oral flatulence, bloating, distension and intolerance of fatty food
A posterior ulcer may cause pain radiating to the back.
Symptoms are relieved by antacids (very nonspecific).
Signs
In uncomplicated cases there is very little to find on examination:
There is often epigastric tenderness.
If gastric emptying is slow, there may be a succussion splash
Perforation sudden generalised abdominal pain, aggravated by the slightest
movements, boardlike rigidity, guarding on examination. An erect CXR air under
right hemi-diaphragm(pneumoperitoneum- left is fundus gas)

Investigation
FBC may show evidence of iron-deficiency anaemia.
Testing for H. Pylori urea breath test or serology antibody testing, stool
test , biopsy
H Pylori breakdown urea to ammonia and carbon dioxide, co2 detect and
recorded
Endoscopy, for:

Diagnosis

Bleeding risk

Endotherapy: - Injection with adrenaline, coagulation, hemostatic

clipping

Management
Conservative - PPI
Modification of behaviour
If drugs are the cause then they should be stopped or replaced but
this may not be possible. Being more meticulous about the
instructions for taking alendronate or taking NSAIDs including
aspirin after food may be required.
Cessation of smoking should be advised if applicable.
Healing ulcers - H. pylori-positive
Treatment for H. pylori-associated ulcer disease is mainly directed
at eradication of infection. 1 acid reducing medication + 2
antibiotics

Healing ulcers - H. pylori-negative, NSAID-induced

The NSAID should be stopped. More than 90% of gastric or duodenal
ulcers heal with eight weeks of standard-dose H2-receptor
antagonists, eg ranitidine 150 mg twice a day if NSAID is
discontinued.
PPIs are better than standard-dose H2-receptor antagonists and
misoprostol for prevention of duodenal ulcers.

H. pylori-negative NSAID-negative ulcer

Ulceration of the gastric or duodenal mucosa in the absence of H.
pylori infection and NSAID or aspirin usage is rare. A careful history
of the use of NSAIDs and aspirin is very important in any patient
presenting with gastroduodenal ulceration in the absence of H.
pylori infection. The patient might be unaware that several drugs
obtainable over the counter as well as some herbal medications
contain NSAIDs or aspirin.
To exclude the rare conditions that may cause this, such as
Zollinger-Ellison syndrome, samples should be taken from the ulcer
and surrounding mucosa.

Surgical therapy
Truncal vagotomy with pyloroplasty

Truncal vagotomy with antrectomy and

Billroth I or Billroth II reconstruction

Highly selective vagotomy

Gastric ulcers are treated with either wedge excision or antrectomy

with inclusion of the ulcer, depending on the ulcer location.

Management of recurrence and its prevention

For gastric ulcer with H. pylori infection, NICE recommends eradication therapy followed by proof of
eradication and repeat endoscopy. For patients who have relapses, intermittent therapy and
annual review is recommended.
Repeat endoscopy may be required for:
Failure to eradicate symptoms in a duodenal ulcer.
Failure to have eradicated H. pylori.
Follow-up of a gastric ulcer - this requires repeat endoscopy to confirm healing at 6 to 8 weeks along
with confirmation of eradication of H. pylori.
NSAID-induced ulcers - these should be treated according to whether they are gastric or duodenal.
If a gastric ulcer persists, referral to secondary care is required. If it is healed but symptoms persist,
a course of acid suppression for a limited duration may be in order but, if symptoms persist,
referral is necessary.

GERD
Gastro-oesophageal reflux disease

Lower oesophageal sphincter (LOS) is a physiological

sphicter that help to prevent reflux
GERD result from various pathophysiological factors
1.loss of LOS function
(decrease tone, hiatal hernia)
2.Delayed gastric emptying (Diabetes -> damage to
vagus nerve)
3. increased intraabdominal pressure
(obesity, tight garment,pregnancy)
4.motor failure of oesophagus with loss of peristalsis
(achalasia)
5.Drugs that cause smooth muscle relaxation : calcium
channel blocker, beta agonist, coffee and smoking

Reflux esophagitis
Reflux esophagitis develops when gastric
contents are passively regurgitated into the
esophagus.
where acid reflux from the stomach is
persistent, the result is damage to the
esophagus, causing symptoms(heartburn)
Gastric acid, pepsin, and bile irritate the
squamous epithelium
leading to inflammation, erosion, and
ulceration of the esophageal mucosa.

Symptoms
Heartburn- burning feeling, rising from the
stomach or lower chest up towards the neck
Acid brash : reflux of sour gastric juices back into
mouth
Symptoms occur usually after food, particularly a
heavy meal and are aggrevated by lying flat
Long standing disease can lead to dysphagia
due to stricture formation
Pulmonary symptoms (aspiration) : chronic
cough, chest infections

Oesophagitis
Reflux is prolonged or excessive it may cause
breakdown of this protection with inflammation
of the oesophagus.

video
http://www.sciencedirect.com/science/article/pi
i/S2212097113700463

Endoscopic grading of oesophagitis

The Savary-Miller grading system is commonly used
Grade 1: single or multiple erosions on a single fold. Erosions may be
exudative or erythematous.
Grade 2: multiple erosions affecting multiple folds. Erosions may be
confluent.
Grade 3: multiple circumferential erosions.
Grade 4: ulcer, stenosis or oesophageal shortening.
Grade 5: Barrett's epithelium. Columnar metaplasia in the form of circular
or non-circular (islands or tongues) extensions.
The more recent and more objective Los Angeles grades A to D
classification is also used
Grade A: one or more mucosal breaks no longer than 5 mm, none of
which extends between the tops of the mucosal folds.
Grade B: one or more mucosal breaks more than 5 mm long, none of
which extends between the tops of two mucosal folds.
Grade C: mucosal breaks that extend between the tops of two or more
mucosal folds, but which involve <75% of the mucosal circumference
Grade D: mucosal breaks which involve 75% of the mucosal
circumference

VIDEO
https://www.youtube.com/watch?
v=9bnIuKiHdDE

Treatment
Medical
Acid suppressuon therapy : proton pump inhibitor (omemprazole) / H2
receptor antagonist (ranitidine)
Prokinetics to increase LES pressure metoclpramides
Surgical
Indication
Failure of medical therapy
Oesophagitis with frank ulceration or stricture
Complication of reflux oesophagitis barrets oesophagus
Severe symptoms or pregressive disease
Goal of surgery
Increase pressure at gastrooesophageal junction
FUNDOPLICATION
Nissen fundoplication 360 degree wrap of the fundus around the gastro
oesophageal junction
Complication
Perforation of oesophagus
Excessive tight wrap resulting in dysphagia

Barretts oesophagus

 a/w long term reflux

Intestinal metaplasia
of oesophageal
epithelial lining
( stratified squamous
epitelium convert to
mucus secreting
columnar epithelium
with goblet cell)
Adaptation
mechanism where
intestinal epthelium
withstand exposure to
acidic reflux better
than oesophageal
epithelium

Diagnosed on endoscopy and histology

The squamocolumnar junction (Z line) is visible of
endoscope as gastric and intestinal type epithelium is pink
and granular in appearance but stratified squamous
epithelium is smooth and pale.
If squmocolumnar junction is above gastro-oesophageal
junction ( gastric fold begin) and biopsy of junction shows
intestinal metaplasia-> diagnose barretts oesophagus

Short segment Barretts is defines as

squamocolumnar junction being <3cm above
gastro-oesophageal junction, while long
segment barretts is >3cm
Risk of development of adenocarcinoma is
about 10-15% in 10years

Squamocolumnar
junction
Gastro-oesophageal
junction

Management
1. Treatment of underlying reflux
2. Endoscopic surveillance
- to pick up dysplasia
3. Treatment of high-grade dysplasia
-endoscopic therapies to ablate the dysplastic
tissue eg photodynamic therapy, laser therapy,
argon plasma coagulation -> will not remove all
dysplastic cells thus potential for malignancy still
remaims
-oesophagectomy is the only definitive
treatment to remove all dysplasia

video
https://www.youtube.com/watch?
v=VsbbZ8_nTaE

Mallory-weiss syndrome
Longitudinal tear in the
oesophagus at oesophagogastic
junction

 Binge drinking with subsequent severe retching and

vomitting leading to heamatemasis
Acute illness with severe vomitting
Presumed pathogenesis is inadequate relaxation of
musculature of lower oesophageal sphicter during
vomitting with stretching and tearing of
oesophagogastric junction at the moment of propulsive
explusion of gastric content
Hiatal hernia is found in 75% of patient with mallory
weiss tear
50% have no antecedent history of
nausea,retching,abdominal pain or vomitting
Account for 5-10% of Upper GI bleed
Most often bleeding is not profuse and ceases without
surgical intervention (90%) , but life treatening
heamatemesis may occur

Endoscopy
the procedure of choice for both diagnosis and
therapy of these lesions.
Endoscopic diagnosis of a Mallory-Weiss tear is
readily made by identifying active bleeding, an
adherent clot, or a fibrin crust over a mucosal split
within or near the gastroesophageal junction.
Epinephrine injection,
Balloon tamponade,
band ligation,multipolar
electrocoagulation (MPEC)

GASTRITIS
Inflammation of the gastric mucosa
ACUTE GASTRITIS
Acute mucosal inflammatory process usually of a
transient nature
CHRONIC GASTRITIS
Presence of chronic mucosal inflammatory changes
leading eventually leading to mucosal atrophy and
epithelial metaplasia

Source : Robbins Basic pathology

 Acute gastritis can be broken down into 2 categories: erosive (eg,

superficial erosions, deep erosions, hemorrhagic erosions) and
nonerosive (generally caused by Helicobacter pylori).
Risk Factors:
Heavy use of NSAIDS esp aspirin (rheumatoid arthritis)
Excessive alcohol consumption
Heavy smoking
Treatment with cancer chemotherapeutic drugs
Ischaemia and shock
Suicide attempts with acids and alkali
Ureamia
Pathophysiological factor
Disruption of adherent mucous layer
Stimulation of acid secretion with hydrogen ion back-diffusion into
superficial epithelium
Decrease production of bicarbonate buffer by superficial epithelial cells
Decreased mucosal blood flow
Direct damage to the epithelium

NSAID
reduction in prostaglandin synthesis in
cyclooxygenase pathway (COX 1)
Prostaglandins are chemicals responsible for
maintaining mechanisms that result in the
protection of the mucosa from the injurious effects
of the gastric acid.

CLINICAL FEATURES
Asymptomatic
Upper abdominal discomfort/epigastric pain
Nausea & vomiting
Hematemesis/malaena (acute gastritis)
COMPLICATION
Peptic ulcer disease
Gastric carcinoma

Malignancy
-accounts for less than 3% of
all UGIB cases
-bleeding usually occur at a
late stage of malignancy
resulting in diffuse mucosal
ulceration or erosion into an
underlying vessel

Esophageal carcinoma
9th most common cancer in the world
15th most common cancer in Malaysia(2.1%)
Disease of mid to late aduldhood, uncommon before
the age of 50, M>F
6% 5 year survival
Squamous cell cancer & adenocarcinoma

a) Squamous cell carcinoma

Squamous cell cancer is the predominant type
Located in middle 3rd of esophagus. May ulcerate
or diffuse infiltration into surrounding structures.
Risk factors
Alcohol & tobacco use, poverty, achalasia,
Plummer-Vinson syndrome, consumption of hot
beverages, exposure to radiation.

Large ulcerated squamous cell

carcinoma of the esophagus.

Squamous cell carcinoma of the

esophagus: low-power microscopic view
showing invasion into the submucosa

Endoscopy and radial endoscopic

ultrasound images of submucosaltumour in
mid-esophagus

b) Adenocarcinoma
Arises in the background of Barrett esophagus &
chronic GERD.
Increased risk in those who smoke,obesity & prior
radiation therapy.
Lower risk by diets rich in fresh fruits & vegetables

Transition from Barrett esophagus to

adenocarcinoma

Clinical feature
Dysphagia is the first symptom in most patients-obstructive
symptom
Develop insidiously, having trouble with solid food then liquid
Odynophagia may be present
Weight loss
Haematemesis
Hoarseness
Nausea and vomiting
Indigestion and heartburn

Investigation
Oesophagogastroduodenoscopy (OGDS)-Biopsy
taken & examined histologically
Endoscopic ultrasound (depth of tumour penetration
through the oesophageal wall and regional lymph
node spread)
Barium swallow
CT-scan of chest
Blood investigation (FBC, LFT)
Ultrasound (assess spread to the liver)

Barium swallow
A barium swallow is a radiographic (X-ray)
examination of the upper gastrointestinal (GI) tract
The pharynx and esophagus are made visible on Xray film by a liquid suspension called barium sulfate
(barium).
Barium highlights certain areas in the body to create
a clearer picture.
To visualize any stricture or intraluminalmass on xray

Gastric Ca
Double-contrast barium swallow
Provides preliminary information that may help the
physician determine if a gastric lesion is present and
whether the lesion has benign or malignant features.
Look for suspicious filling defect

Filling defect in arrow

Staging

Metastasis
Direct spread occurs both laterally, through the
component layers of the oesophageal wall, and
longitudinally within the oesophageal wall
Thorasic, abdominal lymph node
Distant metastasis in the liver, lungs, bone, and
central nervous system

Principle of management
At the time of diagnosis, around two-thirds of all patients with
oesophageal cancer will already have incurable disease
Palliative care: advance stage
Surgery: confined to the oesophagus (T1, T2) without nodal
metastasis (N0)
Radical oesophagectomy is the most important aspect of curative
treatment
Neoadjuvant treatments before surgery may improve survival in a
proportion of patients to shrink the tumour
Useful palliation for dysphagia may be achieved by
chemo/radiotherapy or stenting/laser

Gastric carcinoma
One of the ten most common cancer in Malaysia

2nd most common cancer in the world

Rare under 50, male predominance (National Cancer Society

Malaysia)

Curable disease if detected at an appropriate stage and treated

adequately.

Nearly all are adenocarcinoma

Other are lymphoma and occasionally carcinoid
tumour or sarcoma
2 types: intestinal type (distal third of stomach)
and diffuse type (proximal third).
The 5-year survival rate for advanced gastric cancer
below 20%.

Etiologies
H.pylori infection
-

Colonise gastric mucosa over long periods and cause chronic gastritis and progresses to type B multifocal
atrophic gastritis [lead to intestinal and colonic metaplasia , dysplasia and cancer]

Pernicious anemia
Gastric polyps
Previous history of peptic ulcer surgery
Duodenogastric reflux and reflux gastritis
Cigarate smoking
Diets
-excessive salt intake, smoked meat, red meat
-deficiency of antioxidant (ascorbic acid)
-exposure to N-nitroso compound
Genetic factor
- blood group A, family history, familial adenomatous polyposis

Clinical feature
Dysphagia is the first symptom in most patients
Develop insidiously, having trouble with solid food then liquid
Odynophagia may be present
Weight loss
Haematemesis
Hoarseness
Nausea and vomiting
Indigestion and heartburn

Investigation

Oesophagogastroduodenoscopy (OGDS)-Biopsy taken & examined histologically

Endoscopic ultrasound (depth of tumour penetration through the oesophageal wall and
regional lymph node spread)

Barium swallow

CT-scan of chest

Blood investigation (FBC, LFT,)

Ultrasound (assess spread to the liver)

Tumour
T1 tumour involve lamina propia
T2 -invasion of muscularis or

subserosa

T3 -involve serosa
T4 -invasion of adjacent organ
Node
N0 -no regional lymph node
N1- 1-6 LN
N2- 7-15 LN
N3- >15 LN
Metastasis
M0- none
M1-present ( peritoneum and distant lymph
node)

TNM Staging

STAGING

IA

IB

IIIB

IV

1-3

1-3

ANY T

ANY N

MI

II

IIIA

TREATMENT
Multidisciplinary approach. It depend on the age, general
health, tumor staging.
Radical Surgery
Gastric resection

Subtotal gastrectomy for adenocarcinoma of the distal

and middle thirds of the stomach with a palpable 7-cm
free margin from the oesophagogastric junction

A total gastrectomy was performed for adenocarcinoma

involving the proximal third of the stomach.

Adjuvant and Neoadjuvant Therapies

Chemotherapy is an alternative for inoperable patient:

-Postoperative chemotherapy may be considered for patient with nodal
positive and tumour invasion disease.

-Chemotherapy regime:
Epirubacin, cisplatin and infusional 5-fluorouracil(ECF)

Neoadjuvant chemotherapy have shown to downstage the T and N

stage and improve overall survival (5-FU and cisplatin)

Radiation therapy alone shown no advantage in clinical trial.

Radiotherapy not routinely use in gastric CA, more to palliation

 Palliative gastrectomy
- if tumour bleeding , necrosis or encroachment on gastric lumen
resulting in nausea , vomiting , anorexia or symptoms of anemia
Stenting gastric outlet obstruction

Others
Stomach
Lymphoma, Gastric polyp, Hereditary haemorrhagic telangiectasia,
Dieulafoy lesion,Gastric Antral Vascular Ectasia(GAVE) ,Angiodysplasia
Duodenum
Duodenal ulcer, Vascular malformation, Aorta-duodenal fistula
Polyps (including Peutz-Jeghers syndrome and other polyposis syndromes)
Carcinoma of ampulla, Carcinoma of pancrease, Haemobilia

Management
Vascular Malformations (Including Telangiectasia
and GAVE)
Multiple sessions of Argon plasma coagulation
(APC) or heater probe therapy may be required to
achieve haemostasis
Dieulafoy Lesion
Band ligation injection and thermal methods