16-Oct-19

GROSS ANATOMY OF THE STOMACH

AND DUODENUM

Stomach and
duodenum

 The gastroduodenal artery, which is also a

branch of the hepatic artery, passes behind
the first part of the duodenum, highly
relevant with respect to the bleeding
duodenal ulcer.
 On the lesser curve, the coronary vein is
particularly important. It runs up the lesser
curve towards the oesophagus and then
passes left to right to join the portal vein.
This vein becomes markedly dilated in portal
hypertension

 Posterior vagus gives criminal nerves of  Highly selective vagotomy (HSV) nerve
Grassi, which supply lower oesophagus and of Latarjet is retained so as to retain antral
fundus of stomach, which,if not cut properly pump and no drainage is required.
during vago tomy, may lead to recurrent
ulcer.
 Truncal vagotomy with posterior
gastrojejunostomy is done for chronic
duodenal ulcer with pyloric stenosis.
 In selective vagotomy splanchnic branches
are retained but it is presently not done.

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Gastric acid secretion Gastric mucus and the gastric mucosal barrier
 The gastric mucous layer is essential to the
integrity of the gastric mucosa. It is a viscid layer
of mucopolysaccharides produced by the mucus-
producing cells of the stomach and the pyloric
glands.
 Gastric mucus is an important physiological
barrier to protect the gastric mucosa from
mechanical damage, and also the effects of acid
and pepsin.
 Its considerable buffering capacity is enhanced
by the presence of bicarbonate ions within the
mucus.

 Many factors can lead to the breakdown of INVESTIGATION OF THE STOMACH AND
this gastric mucous barrier. These include DUODENUM
bile, non-steroidal anti-inflammatory drugs  Flexible endoscopy
(NSAIDs), alcohol, trauma and shock.

1. For diagnosing any pathology Therapeutic procedures done are:

 Gastric ulcer.  Variceal injection or ligation or glueing or
 Duodenal ulcer. banding
 Gastritis.  Stenting of pseudocyst of pancreas through
 Stomal ulcer. gastroscopy
 Carcinoma stomach.  Polyp removal
 Oesophagitis.  Submucosal resection
 Varices.
 For ERCP diagnostic and therapeutic proced
 Biopsies from the suspected cases of ures
malignancy or for Helicobacter pylori can be
taken.  Percutaneous gastrostomy (PEG)

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BARIUM MEAL STUDY
 Barium sulphate solution is used [Barium is
neurotoxic, but in sulphate media it will not
get absorbed and so barium sulphate is used
(Barium phosphate is not used)].
 About 300 ml solution is given to the patient
to drink and its flow down to the stomach is
observed under fluoroscopic guidance. Films
are taken as required. Commonly oblique
views are taken.
Pathogenesis (the manner of development of a disease.)
 It is the most common bacterial infection in
the world. Rhesus monkey is the only natural
reservoir. Its incidence increases with age.
 One of the characteristics of the organism is
its ability to hydrolyse urea, resulting in the
production of ammonia, a strong alkali.
 The effect of ammonia on the antral G cells is
to cause the release of gastrin via the
negative feedback loop.
 Up to 50 per cent of the world’s population
may be infected with helicobacter.
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Gastric outlet obstruction—the cause may be
chronic duodenal ulcer with pyloric stenosis
or carcinoma pylorus. Features are:
 Enormous dilatation of stomach.
 Greater curvature below the level of iliac
crest.
 Absence of duodenal cap.
 No filling of dye in 2nd part of duodenum.
 Mottled appearance of stomach because of
retained food particles.
 Evidence of gastritis.
Carcinoma stomach—irregular filling defect.
HELICOBACTER PYLORI
 It is gram –ve spiral like flagellated organism,
first studied by Warren and Marshall (both
got Nobel prize), which is commonly present
in stomach.
 This is probably responsible for the modest,
but inappropriate, hypergastrinaemia in
patients with peptic ulcer disease, which, in
turn, may result in gastric acid
hypersecretion.
 H. pylori impair mucosal healing, cause
degranulation of eosinophils. It releases
various protease and lipases that break
mucus and so strong protective mucus
barrier.
 Even though normal duodenum cannot
harbour the Helicobacter
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 The means of spread has not been
identified, but the organism can occur in the
faeces and faecal–oral spread seems most
likely.
 It is more common in lower socioeconomic
group.
PEPTIC ULCER
 Most peptic ulcers are caused by H. pylori or
NSAIDs and changes in epidemiology mirror
changes in these principal aetiological factors
 Duodenal ulcers are more common than gastric
ulcers, but the symptoms are indistinguishable
 Gastric ulcers may become malignant and an
ulcerated gastric cancer may mimic a benign
ulcer
 Gastric antisecretory agents and H. pylori
eradication therapy are the mainstay of
treatment, and elective surgery is very rarely
performed
Clinical features of peptic ulcers
 Pain : The pain is epigastric, often described
as gnawing and may radiate to the back.
Eating may sometimes relieve the discomfort.
The pain is normally intermittent rather than
intractable.
 Periodicity : One of the classic features of
untreated peptic ulceration is periodicity.
Symptoms may disappear for weeks or
months to return again. This periodicity may
be related to the spontaneous healing of the
ulcer.
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Tests for H. pylori
 Rapid urease test—90% sensitivity, 98%
specificity (CLO test)
 C13/ C14 breath tests—95% sensitivity and
specificity—'gold standard‘
 Serology to identify IgG antibody—ELISA test
with 90% sensitivity and specificity
 Detected histologically using the Giemsa or the
Ethin–Starey silver stains, and cultured using
appropriate media.
 PCR products of H. pylori—urease gene, 165
rRNA identified using specialised probes when
organisms are in less number
 The long-term complications of peptic ulcer
surgery may be difficult to treat
 The common complications of peptic ulcers are
perforation, bleeding and stenosis
 The treatment of the perforated peptic ulcer is
primarily surgical, although some patients may
be managed conservatively
 Common sites for peptic ulcers are the first part
of the duodenum and the lesser curve of the
stomach, but they also occur on the stoma
following gastric surgery, the oesophagus and
even in a Meckel’s diverticulum, which contains
ectopic gastric epithelium.
 Vomiting : While this occurs, it is not a
notable feature unless stenosis has occurred.
 Alteration in weight : Weight loss or,
sometimes, weight gain may occur. Patients
with gastric ulceration are often underweight
but this may precede the occurrence of the
ulcer.
 Bleeding : All peptic ulcers may bleed.
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Duodenal ulceration Sites:

Aetiology a. In the bulb (bulbar)—95%.
 Common in people with blood group O +ve. b. Post-bulbar (5%).
 Stress, anxiety—‘hurry, worry, curry’.  An anterior ulcer perforates commonly,
 Helicobacter pylori infection is an important posterior ulcer bleeds or penetrates
aetiology for duodenal ulcer (90%). commonly.
 NSAIDs, steroids.
 Endocrine causes: Zollinger-Ellison syndrome,
MEN syndrome, hyperparathyroidism.
 Other causes: Alcohol, smoking, vitamin
deficiency.

Gastric ulcers
 Gastric ulcer is large in size, usually lies in the
lesser curvature,its floor being formed by the
muscular layer.
 Gastric ulceration is substantially less
common than duodenal ulceration.
 The sex incidence is equal and the population
with gastric ulcers tends to be older.
 It is more prevalent in low socioeconomic
groups and is considerably more common in
the developing world than in the West.

Differential Diagnosis
 Hiatus hernia.
 Cholecystitis.
 Chronic pancreatitis.
 Chronic gastritis.
 Dyspepsia.
 Carcinoma stomach.

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 H2-receptor antagonists and proton pump
inhibitors (The problem with all gastric
antisecretory agents is that following
cessation of therapy relapse is almost
universal.)
 Eradication therapy (Evidence suggests that if
a patient has a peptic ulcer and H.pylori is the
principal aetiological factor , then complete
eradication of the organism will cure the
disease and reinfection as an adult is
uncommon. Eradication therapy is therefore
the mainstay of treatment for peptic
ulceration.
 It binds to ulcer bed and stays for 12 hours;
prevents back diffusion of hydrogen ion;
raises endogenous prostaglandin level in
tissues; binds bile acid and pepsin;prevents
colonisation of gastric mucosa by bacteria.
Misoprostol
 (200 mg tid) is the only prostaglandin agonist
accepted.
 PG E1 (mesoprostol) and E2 increase mucus
and bicarbonate secretion, improves mucosal
blood flow, but reduces acid secretion.
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Treatment of peptic ulceration
 Medical treatment
 Surgical treatment
Medical treatment
 Modifications to the patient’s lifestyle,
particularly the cessation of cigarette
smoking.
 This advice is rarely followed and
pharmacological measures form the mainstay
of treatment.
Antacids
 Neutralises the HCl to form water and salt and
also inhibits peptic activity.
 Aluminium hydroxide and magnesium
trisilicate are commonly used.
Sucralfate
 It is an aluminium salt of sulfated sucrose
which provides a protective coat to ulcer crater
thereby promotes healing. It inhibits peptic
activity.
Ulcers that fail to heal
 Endoscopic re-evaluation should be regarded
as mandatory to confirm healing of gastric
ulcers.
 The most common cause of failed healing is
persistent H. pylori infection.
 Biopsies should be repeated at the time of
endoscopy as false-negative results with
breath tests may be expected soon after
eradication therapy and serum antibody titres
may not fall for six months after successful
eradication.
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 Failure of eradication is usually due to poor Surgical treatment

compliance or bacterial resistance and
bacteriological culture will guide further
attempts at H. pylori eradication.
 Zollinger–Ellison syndrome

 Truncal vagotomy and drainage Sequelae of peptic ulcer surgery

 Highly selective vagotomy  Recurrent ulceration

 Truncal vagotomy and antrectomy Recurrent ulcers may present with

complications, particularly bleeding and
perforation. The complication of gastrojejuno-
colic fistula requires a particular mention.
 Small stomach syndrome
Early satiety follows most ulcer operations to
some degree, including highly selective
vagotomy due to loss of receptive relaxation.
 Bile vomiting

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 Early and late dumping
 It is related, to some degree, to rapid gastric
emptying and Exaggerated gastrointestinal
peptide responses may also aggravate the
condition.
 It may be severe and explosive, the patient
experiencing a considerable degree of urgency.
The patients sometimes describe the diarrhoea
as feeling like passing boiling water.
 In most patients the diarrhea resolves 3 to 8
months postoperatively
 The condition is difficult to treat. The patient
should be managed as for early dumping and
antidiarrhoeal preparations may be of some
value.
 Nutritional consequences
 Weight loss is common after gastrectomy and
the patient may, in fact, never return to their
original weight.
 Anaemia may be due to either iron or vitamin
B12 deficiency. Iron-deficiency anaemia.
 Bone disease is seen principally after
gastrectomy, and mainly in women. Both
osteoporosis and osteomalacia have also
been observed after gastric resection and
appear to be caused by deficiencies in
calcium.
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 Postvagotomy diarrhoea
– This can be the most devastating symptom to
afflict patients having peptic ulcer surgery.
– Patients with truncal vagotomy develop
diarrhea more than those with selective
vagotomy.
– It is estimated that 30% to 70% of the
patients will report an increased frequency of
bowel movements following truncal
vagotomy or selective vagotomy and 2% to
5% of them will develop disabling diarrhea.
– About 5% , it may be intractable.
 Malignant transformation
 The increased risk appears to be
approximately four times that of the control
population.
 The lag phase between operation and the
development of malignancy is at least ten
years.
 Highly selective vagotomy does not seem to
be associated with an increased incidence of
gastric cancer in the long term.
 Gallstones
 The development of gallstones is strongly
associated with truncal vagotomy.
 The biliary tree, as well as the stomach, is
denervated, leading to stasis and hence stone
formation.
 Mechanical complications
 Afferent/efferent loop obstruction ,
Jejunogastric intussusceptions , Gastro-
oesophageal reflux
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Complications of peptic ulceration PERFORATED PEPTIC ULCER

 Pyloric stenosis: Due to scarring and
cicatrisation of first part of the duodenum.
 Bleeding (10%).
 Perforation (5%). Both acute and chronic
ulcers can perforate. Anterior ulcers
perforate.
 Residual abscess.
 Penetration to pancreas.
 Chronic duodenal ulcer will not turn into malignancy.
 Ulcer which is more than 2 cm is called as giant
duodenal ulcer.
 It is the terminology used for perforation of
duodenal ulcer or gastric ulcer or stomal ulcer
 Perforation is common in duodenal ulcer (75% of
perforated peptic ulcers).
 Mortality is more in gastric ulcer perforation and
perforation in elderly.
 NSAIDs appear to be responsible for most of
these perforations.
 Commonly ulcer in the lesser curve near the
antrum perforates.
 Malignancy should always be suspected and so
biopsy from the edge is a must.

Clinical Features  Vomiting

 Presents with severe persistent pain in the
epigastrium initially, later in the right side
abdomen (as the inflammatory fluid spills
along the right paracolic gutter) and finally
becomes generalised.
 Pain is of sudden in onset, is due to contact
of expelled gastric contents with the parietal
peritoneum.
 Pain often radiates to right scapular region.
 Painbecomes more on movements.
 Abdominal distension occurs.
 Tenderness and rebound tenderness is seen
(Blumberg sign) all over the abdomen.
 Fever, dehydration, oliguria occurs.
 Patient is toxic, with tachycardia,
hypotension, tachypnoea.
 Guarding and rigidity, initially in the
epigastrium but later all over the abdomen.
 Dullness over the flank because of fluid.
 Silent abdomen with absence of bowel
sounds.

 Obliteration of liver dullness—as a result of

collection of escaped gas under the
diaphragm.
 The board-like rigidity
 Tenderness felt on per rectal examination.
 Hippocratic facies (sunken eyes, cold
periphery and shallow rapid breathing, ill
look)

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Investigations
 Plain X-ray abdomen (erect posture): Shows
gas under diaphragm in 70% of cases. In 30%
of cases, there is no gas under diaphragm. It
may be due to, either the gas leak is less than
1 ml or due to previous surgery causing
adhesions between liver and diaphragm, or
sealed peptic ulcer.
 U/S abdomen shows free fl uid and often gas.
 CT scan abdomen is very sensitive
investigation whenever there is absence of gas
under diaphragm.

Treatment
 The initial priorities are resuscitation and
analgesia.
 Analgesia should not be withheld for fear of
removing the signs of an intra-abdominal
catastrophe. In fact, adequate analgesia
makes the clinical signs more obvious.
 Treatment is Initial and surgical treatment

Initial Management
 Patient is advised admission.
 IV fluids—Ringer lactate, normal saline,
dextrose saline.
 Antibiotics—Cefotaxime, metronidazole,
amikacin.
 Catheterisation.
 Ryle’s tube aspiration.

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Surgery
 Emergency laparotomy or Lapaoscopy
 Emergency laparotomy through upper
midline incision is done.
 The most important component of the
operation is a thorough peritoneal toilet to
remove all of the fluid and food debris.
 Perforation is identified and closed with
interrupted , horizontal sutures using either
vicryl.
 Primary closure with an edge biopsy is
commonly used in Gastric perforation.
 Patients who have suffered one perforation
may suffer another one. Therefore, they
should be managed aggressively to ensure
that this does not happen.
 In patients with Helicobacter associated
ulcers, eradication therapy is appropriate.
Life-long treatment with proton pump
inhibitors is a reasonable option,
16-Oct-19
 Omental patch is placed before suturing—it is
called as Rosoe-Graham Operation.
Because of its adhesion property it seals
perforation; good vascularity and lymphatics
promote the healing effectively.
 Peritoneal wash (toilet) using 5-10 litres of
saline is given. Drain is placed and abdomen
is closed.
 Drain is removed in 3-5 days.
 During discharge, patient is advised to take
H2 blockers or proton pump inhibitors for 6-
12 weeks.
 Highly selective vagotomy during the course
of an operation for a perforation.
 There are patients who have small leaks from
a perforated peptic ulcer and relatively mild
peritoneal contamination, who may be
managed with intravenous fluids, nasogastric
suction and antibiotics. These patients are in
the minority.
 Poor outcome after perforated peptic ulcer,
including: delay in diagnosis (>24 hours) ,
medical comorbidities , shock , increasing
age (>75).
PYLORIC STENOSIS DUE TO CHRONIC
DUODENAL ULCER
 Chronic DU after many years undergoes
scarring and cicatrisation causing total
obstruction of the pylorus, leading to
enormous dilatation of stomach.
Clinical Features
 Pain is severe, persistent, in epigastric region,
and also with feeling of fullness.
 Loss of periodicity.
 Loss of appetite and weight
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 Vomiting—large quantity, foul smelling and Pyloric stenosis , causes :

frothy, vomitus contains food consumed on
 Congenital
previous day (partially digested or undigested
food).  Chronic DU—fi brosed/cicatrised
 Visible gastric peristalsis (VGP)—may be  Carcinoma pylorus
elicited by asking the patient to drink a cup of  Adult pyloric stenosis—it is treated by
water. pyloroplasty (not by pyloromyotomy)
 Positive succussion splash which is done with 4  Pyloric mucosal diaphragm—it should be
hours empty stomach excised surgically or endoscopically
 Electrolyte changes : hypochloraemic,
hyponatraemic, hypokalaemic,
hypocalcaemic,hypomagnesaemic alkalosis
occurs. It causes para doxical aciduria.

Investigations
 Barium meal study:
– Absence of duodenal cap.
– Dilated stomach where greater curvature is
below the level of iliac crest.
– Mottled stomach.
– Barium will not pass into duodenum.
 Gastroscopy to rule out carcinoma stomach
and to visualise the stenosed area.
 Electrolyte study for correction of
electrolyte imbalance.
 ECG to check for hypokalaemia.

Treatment
 Correction of dehydration and electrolytes by
IV fluids , normal saline or double strength
saline, calcium, potassium, magnesium.
 Blood transfusion is given if there is anaemia.
 TPN support.
 Stomach wash to clean the stomach contents
(using normal saline) is given using stomach
tube like Eswald’s. It also reduces the oedema
of stomach wall and improves gastric
emptying time by increasing the gastric
muscle tone.

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 HSV with gastrojejunostomy  To control alkalosis, kidney secretes excess

 Truncal vagotomy along with gastrojejuno bicarbo nate (Inalkalosis without
stomy hyponatraemia, bicarbonate is secreted along
with sodium). Here, due to hyponatraemia,
body conserves sodium and so bicarbonate is
ELECTROLYTE CHANGES IN PYLORIC secreted along with hydrogen ion.
STENOSIS  So urine becomes acidic. It is called as
 Because of severe vomiting which contains paradoxical aciduria.
acid as well as undigested retained food,
sodium, chloride, potassium, magnesium
levels drop, causing metabolic alkalosis.
Alkalosis can lead to hypocalcaemia causing
tetany. It is called as gastric tetany

HAEMATEMESIS Causes of upper gastrointestinal bleeding

Hematemesis or haematemesis is the  Ulcers
vomiting of blood. The source is generally the  Erosions
upper gastrointestinal tract, typically above  Mallory–Weiss tear
the suspensory muscle of duodenum. Patients
 Oesophageal varices
can easily confuse it with hemoptysis
(coughing up blood)  Tumour
 Vascular lesions, e.g. Dieulafoy’s disease
 Others

Risk factors for UGIB : Examination

 Alcohol abuse.  Pallor and signs of anaemia should be
 Chronic renal failure. sought.
 Non-steroidal anti-inflammatory drug  Pulse and blood pressure.
(NSAID) use.  Postural hypotension may be detected and
 Age. usually indicates a blood loss of 20% or
 Low socio-economic class. more.
 Coagulopathy  Other signs of shock : Cool extremities ,
Confusion , Delirium.
 Evidence of dehydration (dry mucosa,
sunken eyes, skin turgor reduced).

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 Stigmata of liver disease may be present
(jaundice, gynaecomastia, ascites, spider
naevi, flap, etc.).
 Signs of a tumour may be present (nodular
liver, abdominal mass, lymphadenopathy).
 Subcutaneous emphysema and vomiting
suggests Boerhaave's syndrome
(oesophageal perforation).
 Urine output should be monitored (oliguria
is a sign of shock).
Laboratory tests
 FBC: haemoglobin is measured serially (4-6
hourly in the first day) to help assess trend.
The requirement for transfusion is based on
initial haemoglobin and a clinical assessment
of shock.
 Crossmatch blood (usually between 2 and 6
units according to rate of active bleeding).
 Coagulation profile: prothrombin time with
activated partial thromboplastin time and an
international normalised ratio (INR),
fibrinogen level.
Imaging
 CXR: may identify aspiration pneumonia;
pleural effusion, perforated oesophagus.
 Erect and supine abdominal X ray to exclude
perforated viscus and ileus.
 CT scan and ultrasound can identify:
– Liver disease.
– Cholecystitis with haemorrhage.
– Pancreatitis with haemorrhage and
pseudocyst.
– Aortoenteric fistulae
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Investigations
 Endoscopy should be undertaken
immediately after resuscitation for unstable
patients with severe acute UGIB.
 Endoscopy should be undertaken within 24
hours of admission for all other patients with
UGIB.
 LFTs to detect underlying liver disease
 Renal function tests and electrolytes; BUN-
to-creatinine ratio (greater than 36 in renal
insufficiency suggests UGIB).
 Calcium level should be assessed to detect
hyperparathyroid patients and to monitor
the effect of citrated blood transfusions.
 Gastrin levels can identify the rare
gastrinomas causing UGIB.
Principle of management
 Resuscitation, diagnosis and treatment
should be carried out simultaneously.
 Intravenous access should be established
and, for those with severe bleeding, central
venous pressure monitoring should be set up
and bladder catheterisation performed.
 Blood should be cross-matched and the
patient transfused as clinically indicated,
usually when >30 per cent of blood volume
has been lost.
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Resuscitation and initial management :
 Correct fluid losses : (place two wide-bore
cannulae and also send bloods at the same
time). Either colloid or crystalloid solutions
may be used to achieve volume restoration
prior to administering blood products.
 Transfuse patients with massive bleeding with
blood, platelets and clotting factors in line
with local protocols for managing massive
bleeding.
Specific management
Management of non-variceal bleeding
 Endoscopy is now the method of choice for
controlling active peptic-ulcer related UGIB.
 For the endoscopic treatment of non-variceal
UGIB, one of the following should be used :
 A mechanical method (eg clips) with or without
adrenaline (epinephrine).
 Thermal coagulation with adrenaline
(epinephrine).
 Fibrin or thrombin with adrenaline
(epinephrine).
 Angiography with transcatheter embolisation
Management of bleeding for NSAIDs, aspirin
or clopidogrel
 Continue low-dose aspirin for secondary
prevention of vascular events in whom
haemostasis has been achieved.
 NSAIDs should be stopped
 Discuss the risks and benefits of continuing
clopidogrel with the appropriate specialist
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 Fresh frozen plasma should be used for
patients who have either a fibrinogen level
of less than 1 g/litre, or a prothrombin time
(INR) or activated partial thromboplastin
time greater than 1.5 times normal.
Management of variceal bleeding
 Terlipressin should be offered to patients
with suspected variceal bleeding at
presentation.
 Prophylactic antibiotic therapy
 Balloon tamponade should be considered as
a temporary salvage treatment for
uncontrolled variceal haemorrhage.
 Band ligation , Transjugular intrahepatic
portosystemic shunts (TIPS) , Endoscopic
injection of N-butyl-2-cyanoacrylate
Surgical intervention
 A patient who continues to bleed requires
surgical treatment.
 visible vessel in the ulcer base, a spurting
vessel or an ulcer with a clot in the base are
statistically likely to require surgical
treatment to stop the bleeding.
 A patient who has required more than six
units of blood in general needs surgical
treatment.
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MELAENA
 Melena or melaena refers to the dark black,
tarry feces that are associated with upper
gastrointestinal bleeding.
 The black color and characteristic strong odor are
caused by hemoglobin in the blood being altered by
digestive enzymes and intestinal bacteria.
 Iron supplements may cause a grayish-black stool
that should be distinguished from melena.
 Hematochezia Bleeds that originate from the lower
gastrointestinal tract (such as the sigmoid
colon and rectum) are generally associated with the
passage of bright red blood, or hematochezia.
Mallory–Weiss tear
 This is a longitudinal tear at the gastro-
oesophageal junction, which is induced by
repetitive and strenuous vomiting.
 Carcinoma of the distal stomach and body of
the stomach is most common in low
socioeconomic groups, whereas the increase
in proximal gastric cancer seems to affect
principally higher socioeconomic groups.
 Proximal gastric cancer does notseem to be
associated with H. pylori infection, in contrast
with carcinoma of the body and distal
stomach.
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Causes
 Peptic ulcer disease
 Anticoagulant medications, such as warfarin
 Malignant tumors affecting the esophagus,
stomach or smallintestin
 Hemorrhagic blood diseases, such
as thrombocytopenia and hemophilia, gastris
, esophageal varices, Meckel's
diverticulum and Mallory-Weiss syndrome
GASTRIC CANCER
 Its prognosis tends to be poor, with cure
rates little better than 5–10 per cent,
although better results are obtained in Japan,
which has a high population incidence,
screening programmes and a highquality
surgical treatment
 Men are more affected by the disease than
women and, as with most solid-organ
malignancies, the incidence increases with
age.
Aetiology
 Gastric cancer is a multifactorial disease.
 A significant role played by H. pylori
 Patients with pernicious anaemia and gastric
atrophy are at increased risk
 Gastric polyps.
 Patients who have had peptic ulcer surgery,
particularly those who have had drainage
procedures such as Billroth II or Polya
gastrectomy, gastroenterostomy or
pyloroplasty, are at approximately four times
the average risk
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 Diet appears to be an important factor Site

 Alcohol
 Excessive salt intake
 Deficiency of antioxidants and exposure to
N-nitroso (processed meat) compounds are
also related.
 Genetic factors
 Fruits and vegetables rich in vitamin ‘C’
protect from carcinoma stomach.
 The proximal stomach is now the most
common site for gastric cancer in the West.
 Because so many malignancies occur at the
oesophagogastric junction, and because the
lower oesophagus is also a very common site
of adenocarcinoma

Pathology
Gross types
 Cauliflower type
 Ulcerative type
 Leather-bottle (Linitis plastica)

Lauren’s classification
 Intestinal type (53%)
 Diffuse type (33%)
 Others—Unclassifi ed (14%).

Depending on the depth of invasion

 Early gastric cancer
 Advanced gastric cancer

Japanese’s classification of Early

gastric cancer
 Protruded.
 Superficial—elevated, flat , depressed.
 Excavated.

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 Early gastric cancer is defined as involvement of Advanced carcinoma , Borrmann classification

mucosa and/or submucosa only with or without
involvement of lymph nodes – T1 + any N.
 Advanced gastric cancer is defined as
involvement of muscularis and/or serosa with or
without involvement of lymph nodes.
Borrmann’s classification
I. Single, polypoid carcinoma.
II. Ulcerated carcinoma with clear cut margin.
III. Ulcerated carcinoma without clear cut margin.
IV. Diffuse carcinoma—linitis plastica.

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Spread (Biological Behaviour)
Direct spread
 Horizontal submucosal spread along stomach
wall.
 Vertical spread by invasion across to adjacent
structures like—pancreas, colon, mesocolon,
liver.
Transperitoneal spread
 It can cause peritoneal seedlings (leading to
ascites) and also can cause Krukenberg’s
tumours in ovary in menstruating age group.
Krukenberg’s tumour can arise from carcinoma
breast (lobular), other abdominal organs also.
 Rectal secondaries (Blumer shelf), Sister Mary
Joseph umbilical secondaries are through
transperitoneal spread.
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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 liver (most common) , Later
lungs and bones can get involved.
Presentations of Carcinoma Stomach
 Asymptomatic in early gastric cancer or often
in cancer of body of stomach.
 Nonspecific symptoms—indigestion/vague
epigastric discomfort, constant nonradiating
pain which is not related to food intake.
 Specific symptoms depend on the site of
tumour—obstruction, dysphagia, mass, etc.
 Metastatic disease—liver secondaries,
ascites, secondaries in ovary, rectovesical
pouch, umbilicus, supraclavicular nodes, lung
and bone secondaries.
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Clinical Features
 Recent onset of loss of appetite and weight,
early satiety, fatigue. Microcytic, hypochromic
anaemia (irondeficiency) is common (40%).
 Upper abdominal pain.
 Vomiting with features of gastric outlet
obstruction
 Mass abdomen: Mass in pylorus lies above
the umbilicus,nodular, hard, with impaired
resonance, mobile, moves with respiration, all
border well made out.
 Haematemesis (15%), melaena.
 Occasionally carcinoma stomach can present
as perforation to begin with (4%).
 Rarely as secondaries in the liver with silent
primary in stomach.Secondaries in umbilicus,
as Sister Joseph’s nodules (spread through
ligamentum teres).
 Krukenberg tumours.
Barium meal Styudy
 Irregular filling defect
 Loss of rugosity
 Delayed emptying
 Dilatation of stomach in carcinoma pylorus
 Decreased stomach capacity in linitis plastica
 Margin of the lesion projects outward from
the ulcer/lesion into the gastric lumen—
Carmanns meniscus sign
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 Dysphagia with mass in upper epigastrium.
 When it arises from the body of stomach, it
may present as only mass abdomen.
 Along with jaundice, liver may be palpable
with secondaries which are hard, nodular
 Ascites.
 +ve rectovesical secondaries. (Blumer shelf)
on per rectal examination.
 +ve Trousseau sign—migrating
thrombophlebitis, also seen in carcinoma
pancreas.
 Anaemia, cachexia.
Investigations
 Laboratory Findings : Complete Blood Count ,
Anemia is present in 40% of patients.
Carcinoembryonic antigen (CEA) levels are
elevated in 65%, usually indicating extensive
spread of the tumor.
 Gastroscopy and Biopsy : Large gastric
carcinomas can usually be identified as such
by their gross appearance at endoscopy. All
lesion examined by taking multiple biopsy
during endoscopy. Minimum of six biopsies is
necessary for greatest accuracy.
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Staging
 CT scan : thorax, abdomen and pelvis to
determine the presence of metastatic disease,
the extent of lymph node involvement and
local tumour invasion.
 USG of abdomen to see liver secondaries,
ascites, nodes, ovaries. It is not as sensitive
as EUS and CT scan.
 Endoscopic ultrasound
 Staging laparoscopy
 PET scan

Treatment
 Surgery is the treatment of choice for
carcinoma stomach
 Adjuvant Therapy : Chemotherapy ,
Chemoradiotherapy
 Palliative Treatment : To palliate pain , To
palliate vomiting , When there is bleeding
,To improve appetite, Partial gastrectomy
(palliative) is the best method
 Multidisciplinary team

Preoperative preparation Surgery

 Correction of anaemia, nutrition, fluid and  Total gastrectomy
electrolyte
 Sub Total gastrectomy
 Cardiac, respiratory and renal status
 Distal gastrectomy
assessment
 Stomach wash using normal saline
 Prophylactic antibiotic as achlorhydria in
gastric lumen allows colonisation of
Streptococcus faecalis, E. coli, bacteroides,
Staphylococcus ablus
 Blood/FFP may be needed preoperatively
and for surgery

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 The standard surgical procedure for
clinically node positive or T2 to T4a
tumours is either total or distal
gastrectomy.
 Distal clearance towards duodenum is 1
cm from tumour end.
Metabolic features of GOO
Initially, the major loss is fluid rich in
hydrogen and chloride ions so that the
dehydration is accompanied by
hypochloraemic alkalosis. 》 continued
losses and secondary changes in renal
function 》In the early stages, the urine is
characterized by low chloride content
and is appropriately alkaline because of
enhanced bicarbonate excretion
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Extent of gastric resection
 A proximal margin of at least 3 cm is
recommended for T2 or deeper tumours
 5 cm is recommended for those with
expansive growth pattern types III and IV.
 When tumours invade the gastro-
oesophageal junction a 5 cm margin may not
be achieved, and therefore frozen section is
recommended to ensure R0 resection.
Chemotherapy
 Perioperative chemotherapy : a treatment
plan of three cycles of preoperative and
postoperative epirubicin , cisplatin and 5-
fluorouracil (ECF) significantly improved 5
year survival from 23% with surgery alone to
36.3%.
》This tends to compensate for the metabolic
alkalosis, but it does so at the expense of
sodium loss 》If the gastric losses continue,
the patient becomes progressively more
dehydrated and hyponatraemic 》In an
attempt to conserve the circulating blood
volume, sodium is retained by the kidneys and
hydrogen ions and potassium are excreted in
exchange 》
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patient with a metabolic alkalosis will have,
paradoxically, acid urine 》As a secondary
effect of the alkalosis, the concentration of
plasma ionized calcium may fall such that
disturbances of the conscious level and
tetany may be apparent.
Diagnosis
 Endoscopy : Dye based image enhanced
endoscopy (chromoendoscopy ) , Narrow
band imaging endoscopy.
 Endoscopic ultrasound
This type of cancer is eminently curable, and
even early gastric cancers associated with
lymph node involvement have five-year
survival rates is 90%.
 Endoscopic mucosal resection has been
accepted as a curative modality for early
gastric cancer.
Dumping Syndrome
This symptom complex can develop after
any operation on the stomach but is more
common after partial gastrectomy with the
Billroth II reconstruction. It is much less
commonly observed following the Billroth I
gastrectomy or after vagotomy and drainage
procedures.
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Early gastric cancer
 Gastric cancer can be divided into early
gastric cancer and advanced gastric
cancer.
 Early gastric cancer is defined as cancer
limited to the mucosa and submucosa with
or without lymph node involvement (T1,
any N).
 Post endoscopic resection management and
surveillance :
 Patients undergo annual endoscopic surveillance,
in addition to half-yearly abdominal computed
tomography or endoscopic ultrasonography, for
at least 3 years in order to detect lymph node or
distant metastasis.
 When the pathological examination indicates
noncurative resection, additional surgery
including lymph node dissection is strongly
recommended.
 Early detection and early treatment are vital,
improving the prognosis of gastric cancer.
Dumping syndrome can be :
 Early (20 to 30 minutes after eating) :
Early dumping is more common, with
more GI and fewer cardiovascular
effects.
 Late (2 or 3 hours after a meal).
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Presentation
 GI symptoms include : nausea and
vomiting, a sense of epigastric fullness,
cramping abdominal pain, and often
explosive diarrhea.
 Cardiovascular symptoms include :
palpitations, tachycardia, diaphoresis,
fainting, dizziness, flushing, and
occasionally blurred vision.
 When carbohydrates are delivered to the
small intestine, they are quickly absorbed,
resulting in hyperglycemia, which triggers
the release of large amounts of insulin to
control the rising blood sugar level. This
results in an overcompensation so that a
profound hypoglycemia occurs in response
to the insulin. This activates the adrenal
gland to release catecholamines, which
results in diaphoresis, tremulousness,
light-headedness, tachycardia, and
confusion. The symptom complex is
indistinguishable from insulin shock.
Clinical Features
 Common in fi rst born males (4:1).
 Incidence is 4 in 1000 births.
 It is familial.
 It is seen between 3rd and 6th weeks of age
of an infant, the time taken by the
hypertrophied muscle to cause complete
obstruction.
 Vomiting—forcible, projectile and non-bilious.
 Visible gastric peristalsis (VGP).
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Pathophysiology
 Dumping occurs because of the rapid
passage of food of high osmolarity from
the stomach into the small intestine
which induces a rapid shift of
extracellular fluid into the intestinal
lumen to achieve isotonicity. After this
shift of extracellular fluid, luminal
distention occurs and induces the
autonomic responses listed earlier.
CONGENITAL HYPERTROPHIC PYLORIC
STENOSIS
 It is hypertrophy of musculature of pyloric
antrum, especially the circular muscle fi bres,
causing primary failure of pylorus to relax.
Duodenum is normal.
 Palpable lump of hypertrophied pylorus
which is better felt from left side, as a
mobile, smooth, firm mass, with all borders
well made out, moves with res piration, with
impaired resonance on percus sion. It is the
most important clinical feature (95%).
 Constipation.
 Dehydration and loss of weight.
 Electrolyte imbalance—hypokalaemic
metabolic alkalosis.
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Differential Diagnosis Treatment

 Duodenal atresia (Bilious vomiting is
present).
 High intestinal obstruction (e.g. volvulus
neonator um).
 Intracranial haemorrhage.
 Correction of dehydration and electrolyte
imba lance.
 Surgery: Ramstedt’s operation—After
laparotomy, hypertrophied muscle is cut
along the whole length adequately until the
mucosa bulges out. Mucosa should not be
opened (pyloromyotomy).

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