PEPTIC ULCER

By DR.A.VIJAY ANAND
Dept. of Surgery
Pathogenesis
Caused by increased aggressive factors, decreased
defensive factors or both
Leads to mucosal damage and subsequent ulceraion
Protective factors
Mucosal bicarbonate secretion
Mucus secretion
Blood flow
Growth factors
Cell renewal
Endogenous prostaglandin
Damaging factors
HCl
Pepsin
Ethanol
Smoking
Duodenal reflux of bile
Ischemia
NSAIDs
Hypoxia
H. pylori infection
H. pylori infection
It is now believed that 90% of duodenal ulcers and
roughly 75% of gastric ulcers are associated with H.
pylori infection
The organism was found to be a spiral or helical gram
negative rod with 4 to 6 flagella that resided in gastric-
epithelium within or beneath the mucus layer
Micro-aerophyllic organism
It is one of the most potent producers of urease of any
bacteria yet described.
This enzyme is capable of splitting urea into ammonia
and bicarbonate, creating an alkaline microenvironment
in the setting of an acidic gastric milieu.
Three potential mechanisms for H. pylori–induced
gastrointestinal injury have been proposed:
(1) production of toxic products to cause local tissue injury;
(2) Induction of a local mucosal immune response; or
(3) Increased gastrin levels with a resultant increase in acid
secretion.
Antral gastritis – strongly associated with peptic
ulcer
H.pylori induced chronic gastritis – intestinal
metaplasia – gastric cancer
H.pylori – induces MALT – Lymphoma
Regression of these lymphomas has been
demonstrated following eradication of the
organism
H.pylori eradication reduces ulcer recurrence
NSAIDs
Upper GI bleeding increased with NSAIDs
Increased in > 50 yrs and use of steroids or anti
coagulants,
Mucosal injury or ulceration due to anti
inflammatory effect – ulcer formed in stomach
Gastritis is not frequently found with an NSAID-
induced ulcer
Acid
Plays an important role in formation of ulcer
Type I and IV gastric ulcer – not associated with
excessive acid secretion
Type II and III gastric ulcers – associated with gastric
acid hypersecretion – behave like duodenal ulcers
Duodenal ulcer –
Acid and pepsin secretion with H.pylori infection or
NSAIDs
Clinical manifestations
Abdominal pain –
Sudden onset severe epigastric pain, episodic ,
seasonal, may relapse during periods of emotional stress
When the pain becomes constant, this suggests that
there is deeper penetration of the ulcer, and referral
of pain to the back is usually a sign of penetration into
the pancreas.
Diffuse peritoneal irritation is usually a sign of free
perforation.
Diagnosis
Routine lab investigations
Complete blood count
LFT
Serum creatinine
Sr. amylase
Calcium levels
Sr. gastrin levels should also be obtained in patients with ulcers
that are refractory to medical therapy or require surgery
An upright chest radiograph to rule out perforation.
Upper gastrointestinal radiographs and
Fiberoptic endoscopy
Helicobacter pylori Testing
Diagnosed by mucosal biopsy.
The invasive tests available are the rapid urease test,
histology, and culture
SEROLOGY
ELISA – 90% sensitive and specific
Antibodies can be high for 1yr or longer. Cannot be used to
assess eradication after therapy
UREA BREATH TEST
4 weeks after therapy
Document eradication
Carbon labelled urea – H.pylori – urease converts urea into
CO2 & ammonia
Rapid urease test – detects urease in gastric biopsy
specimen
Histology – from biopsy samples
Culture – 3 to 5 days . Diagnosis requires up to 3 to 5
days. Nevertheless, it does provide the opportunity to
perform antibiotic sensitivity testing
Upper GI radiography
Demonstration of barium within the ulcer crater,
which is usually round or oval and that may or may not
be surrounded by edema.
Useful to determine the location and the depth of
penetration of the ulcer as well as the extent of
deformation from chronic fibrosis
Double -contrast studies 80% to 90% of ulcer
craters can be detected.
 Fiberoptic endoscope –
Most reliable for duodenal ulcer
Endoscopy provides the ability to sample tissue for
H. pylori testing and may also be used for
therapeutic purposes in the setting of gastrointestinal
bleeding or in the therapy of obstruction
Treatment
Three categories
1. Targeted against H.pylori
2. Reduced acid level by reducing secretion or
chemical neutralization
3. Increase mucosal protective barrier
Antacids
Antacids reduce gastric acidity by reacting with hydrochloric
acid, forming a salt and water to inhibit peptic activity by
raising pH.
Magnesium antacids tend to be the best buffers but can cause
significant diarrhea.
Aluminum acids precipitate with phosphorous and can
occasionally result in hypophosphatemia and sometimes
constipation.
They are most effective when ingested 1 hour after a meal. If
taken on an empty stomach, the antacids are emptied rapidly
and have only a transient buffering effect.
H2 receptor antagonists
Famotidine is probably the most potent
Healing upto 90%
All undergo hepatic metabolism and excreted by kidney
PPI’s
Most potent
More complex and prolonged inhibition by H2 receptor
antagonist
Healing rate – 85% - 4 weeks, 96% - 8 weeks
Require an acidic environment within the gastric lumen to
become activated
Sucralfate
It is an aluminum salt of sulfated sucrose that disassociates
under the acidic conditions in the stomach.
sucrose polymerizes and binds to protein in the ulcer crater
to produce a kind of protective coating that can last as long as 6
hours.
It has also been suggested that it may bind and concentrate
endogenous basic fibroblast growth factor, important in
mucosal healing.
 Duodenal ulcer healing after 4 to 6 weeks of treatment with
sucralfate (1 g four times daily) is superior to placebo and
comparable to H2 -receptor antagonists such as cimetidine.
Treatment of H.pylori infection
Triple therapy
1. Antisecretory agents – mostly PPI
2. Two anti biotics – Amoxicillin with
clarithromycin or metronidazole for two weeks
Side effects – mild nausea vomiting diarrhoea rash and
altered taste
 10% refractory – Quadruple therapy – addition of
bismuth
Complications
Hemorrhage
Perforation
Obstruction
Intractable peptic ulcer

Hemorrhage:
Non variceal bleeding
Most bleeding stops spontaneously
Mortality 6-8 % in those who persistently bleed
Increased mortality seen in
1. Increased age
2. Decreased Hb <10gm/dl
3. Shock
4. Melena
5. Need for blood transfusion

Endoscopy within – 24 hrs

Initial management – Resuscitation
1. Large bore IV access
2. Restoration of intra vascular volume with fluids and blood
products
3. Close monitoring for signs of rebleeding
4. NG lavage –
Bright red blood – endoscopic intervention
Clear or coffee ground
Endoscope findings –active bleeding, arterial jet or oozing
adherent clot or visible vessel
Without active bleeding – no visible vessel – clean ulcer base
Endoscopic control –
Injection of vasoconstrictor at the site of bleeding – 30%
rebleeding
Second vasoconstrictor or sclerosing agent
Thermal coagulation
Placement of clips

Dual approach – best results

Thermal coagulation and mechanical clips

Complications – necrosis , perforation

High risk – monitor until bleeding slops for 24 hrs
IV PPI – initial bolus followed by continuous infusion or
intermittent dose upto 72 hrs lowers bleeding rate
5-10% persistent bleeding seen – surgical intervention
needed
Vessel most likely to bleed – Gastro duodenal artery
Duodenum opened longitudinally, incision carried across
pylorus.
Three point V stitch technique. Ligate the main vessel
Avoid CBD into the stitch
Duodenotomy closed transversly
Perforation
Sudden onset – severe epigastric pain – first symptom
Localised peritoneal sign or diffuse peritonitis may occur
Mortality 15%
Plain x ray chest – free air in the peritoneal cavity
Surgery – perforation closure – usually I part of duodenum
<1cm closes primarily with well vascularised omentum
Large perforation – Grahms patch repair with a tongue of healthy
omentum
>3cm perforation – closure difficult
Closed by healthy omentum or jejunal serosa
Duodenostomy tube
Wide drainage
Antrectomy with Billroth II reconstruction
Laparoscopic closure – less painful – early discharge
No difference in pulmonary complications or abdominal
septic complications
If patients with chronic NSAID’s negative for H.pylori
cannot discontinue / failed medical therapy – acid reducing
procedure can be added at end of repair
Decompression of stomach until bowel activity returns
Drain until patient has eaten without a change in drain
output or quality (leak)
All H,pylori patients – triple therapy
GOO
Acute inflammation – mechanical obstruction –
functional GOO – delayed gastric emptying – anorexia,
nausea, vomiting
Prolonged vomiting – dehydration – hypochloremic
hypokaelemic metabolic acidosis
Chronic inflammation – recurrent healing with
fibrosis – stenosis of duodnal lumen – obstruction –
painles vomiting – large gastric contents - metabolic
alkalosis – dehydration – dilated stomach – loss of
muscular tone
Malnutrition
Cancer must be ruled out by endoscopy
Treatment - Endoscopic dilatation (5 times)
H.pylori eradication
Anti secretory drugs
Refractory obstruction – primary gastrectomy and
reconstruction along with vagotomy
Intractable peptic ulcer – initial trial of 8-10 weeks
Relapse after therapy
Benign gastric ulcer persists – rule out malignancy
Serum gastrin level to rule out gastrinoma
Elimination of NSAIDs – if unable to discontinue
Acid reducing operation –
Truncal or high selective v agotomy wih or without
antrectomy
Surgical procedure for peptic ulcer
Goal – to reduce gastric acid secretion
1. Remove vagal stimulation – vagotomy
2. Gastrin induces secretion – antrectomy
3. Or both
Vagotomy decreases peak acid output by
approximately 50%
Vagotomy plus antrectomy, which removes the
gastrin-secreting portion of the stomach, decreases
peak acid output by approximately 85%.
Truncal vagotomy is performed by division of the
left and right vagus nerves above the hepatic and celiac
branches just above the GE junction.
The classic truncal vagotomy in combination with a
Heineke-Mikulicz pyloroplasty
When the duodenal bulb is scarred, a Finney
pyloroplasty or Jaboulay gastroduodenostomy
may be useful alternatives
Heineke-Mikulicz pyloroplasty
Side-effects
Bile reflux – common after gastro enterostomy
Diarrhoea – common in pyloroplasty
Dumping for both
Highly selectve vagotomy
The highly selective vagotomy is also called the parietal cell vagotomy
or the proximal gastric vagotomy
This procedure divides only the vagus nerves supplying the acid-
producing portion of the stomach and preserves the vagal
innervation of the gastric antrum so that there is no need for routine
drainage procedures.
Consequently, there are fewer postoperative complications.
In general, the nerves of Latarjet are identified anteriorly and
posteriorly, and the crow’s feet innervating the fundus and body of
the stomach are divided.
These nerves are divided up to a point approximately 7 cm proximal to
the pylorus or the area in the vicinity of the gastric antrum.
Superiorly, division of these nerves is carried to a point
at least 5 cm proximal to the GE junction on the
esophagus
Ideally, two or three branches to the antrum and
pylorus should be preserved.
The “criminal nerve of Grassi” represents a very
proximal branch of the posterior trunk of the vagus, and
great attention needs to be taken to avoid missing this
branch in the division process because it is frequently
cited as a predisposition for ulcer recurrence if left
intact.
Truncal vagotomy and antrectomy
The most common indications for antrectomy or
distal gastrectomy are
duodenal ulcer disease,
gastric ulcer, and
large benign gastric tumors.
Relative contraindications include cirrhosis,
extensive scarring of the proximal duodenum that
leaves a difficult or tenuous duodenal closure, and
previous operations on the proximal duodenum such as
choledochoduodenostomy.
Recurrence – 0-2%
20% - post vagotomy, post gastrectomy syndrome
Reconstruction following antrectomy
Billroth I –
For benign diseases, gastroduodenostomy is usually
favored because it avoids the problem of
retained-antrum syndrome,
duodenal stump leak, and
afferent loop obstruction associated with
gastrojejunostomy following resection.
Billroth II –
If the duodenum is significantly scarred,
gastroduodenostomy may be technically more
difficult, necessitating gastrojejunostomy.
The retrocolic anastomosis minimizes the length of
the afferent limb and decreases the likelihood of
twisting or kinking that could potentially lead to
afferent loop obstruction and predispose to the
devastating complication of a duodenal stump leak
Mortality 2%
 Gastric ulcer
 Can occur in any location in the stomach.
Usually in the lesser curvature near the incisura
angularis.
 Approximately 60% of ulcers are located in this
location and are classified as type 1 gastric
ulcers. These ulcers generally are not associated
with excessive acid secretion and may, in fact,
have low-to-normal acid output.
 Type 2 gastric ulcers are located in the body of
the stomach in combination with a duodenal
ulcer.
 These types of ulcers usually are associated with
excess acid secretion
 Type 3 gastric ulcers are prepyloric ulcers and
account for about 20% of the lesions. These
ulcers also behave like duodenal ulcers and are
associated with hypersecretion of gastric acid.
 Type 4 gastric ulcers occur high on the lesser
curvature near the GE junction. The incidence
of type 4 gastric ulcers is less than 10%, and they
are not associated with excessive acid secretion.
Gastric ulcer types
Type Location Acid level

I Lesser curvature Low to normal

II Gastric body with DU Increased

III Pre pyloric Increased

IV High on lesser curvature Normal

V Anywhere Normal, NSAID induced

Gastric ulcers rarely develop before 40 years of age, and the
peak incidence occurs between 55 and 65 years of age.
They are more likely to occur in lower social economic
classes
Some conditions that may predispose to gastric ulceration
are
age older than 40 years,
sex (female:male, 2:1),
Ingestion of barrier-breaking drugs such as aspirin or
NSAIDs,
abnormalities in acid and pepsin secretion,
gastric stasis through delayed gastric emptying,
coexisting duodenal ulcer,
duodenal gastric reflux of bile,
gastritis, and
infection with H. pylori.
Some clinical conditions that may predispose to
gastric ulceration include
chronic alcohol intake,
smoking,
long-term corticosteroid therapy,
infection, and
intra-arterial therapy
Clinical manifestations
Pain – bleeding – obstruction – perforation
Recurrent episodes of quiscence and relapse
Challenge – to rule out malignancy
Hemorrhage – 35-40%
Less likely to stop bleeding spontaneously
Higher mortality and morbidity
Most common in type II III and IV
Perforation – Anterior aspect of lesser curvature
Mortality and morbidity more
GOO – Type II and III ulcers
Diagnosis / treatment
malignancy must be ruled out with multiple biopsies
Acid supression and H.pylori eradication
Type I & IV – acid normal
No vagotomy
Type I gastric ulcer – Excision of ulcer
Distal gastrectomy without vagotomy
Morbidity 3-5 %, mortality 1-2%
Recurrence <5%
Gastrectomy is not superior to resection
Type II & III gastric ulcer – Acid level increased
Distal gastrectomy with truncal vagotomy
High selective vagotomy – laparoscopy – recurrence –
resection
Type IV ulcer - The surgical treatment depends on the ulcer
size, the distance from the GE junction, and the degree of
surrounding inflammation
Excision or gastrectomy (total or subtotal) followed by Roux-En-
Y oesophagojejunostomy or Roux-en-y gastrojejunostomy
Bleeding gastric ulcers –
Resuscitation and monitoring
Endoscopic control – biopsy to rule out malignancy –
H.pylori status – eradication
If not controlled – surgery
Excision of ulcer – vagotomy in type II orIII ulcer, type
IV – who cannot discontinue NSAIDs
Perforation –
Type I –distal gastrectomy with Billroth I
Patch closure of the duodenum can be performed by
either a laparoscopic or open procedure
Biopsy – H.pylori positive – eradication
Type II and III – patch closure with/without truncal
vagotomy and pyloroplasty

Giant Gastric ulcers

>3 cm or more
Lesser curvature – malignancy 10%
Medical therapy – healing 80% - surveillence with EGD
Complication – failure to heal
Gastrectomy with vagotomy for types II & III
Stress gastritis
Stress gastritis has been referred to as stress ulcerations,
stress erosive gastritis, and hemorrhagic gastritis.
These lesions may lead to life-threatening gastric bleeding
and by definition occur after physical trauma, shock, sepsis,
hemorrhage, respiratory failure, or severe burns.
Multiple , superficial (nonulcerating) erosions that begin
in the proximal or acid-secreting portion of the stomach and
progress distally
CNS disease such as that seen with a Cushing ulcer or as a
result of thermal burn injury involving more than 30% of the
body surface area (Curling ulcer).
Early lesions - appear within the first 24 hours.
These early lesions are typically multiple, shallow,
and discrete areas of erythema along with focal
hemorrhage or an adherent clot
On microscopy, these lesions appear as wedge-
shaped mucosal hemorrhages with coagulation
necrosis of the superficial mucosal cells
Late lesions (24-72) - appear identical to those of
regenerating mucosa around a healing gastric ulcer.
 Pathophysiology
Impaired mucosal defense mechanisms against luminal acid such
as a reduction in blood flow, a reduction in mucus, a reduction in
bicarbonate secretion by mucosal cells, or a reduction in
endogenous prostaglandins. Leads to hemorrhagic gastritis
Stress (trauma, shock,sepsis, hemorrhage, respiratory failure)

 Mucosal ischaemia

 Defense mechanism failure

 Hemorrhage

 Gastritis
Presentation and diagnosis
More than 50% of patients develop their stress gastritis
within 1 to 2 days following a traumatic event.
The only clinical sign may be painless upper
gastrointestinal bleeding that may be delayed at onset.
 The bleeding is usually slow and intermittent and may
be detected by blood in the NG tube or an unexplained
drop in the hemoglobin
Hypotension
Melena, hematochezia - rare
Endoscopy is required to confirm the diagnosis
Treatment
Fluid resuscitation
Correction of coagulation/platelet abnormalities
Treat sepsis
Endoscopic electrocautery or heat probe coagulation
Selective infusion of vasopressin into sphlanchnic circulation through
left gastric artery
Vasopressin is administered by continuous infusion through the
catheter at a rate of 0.2 to 0.4 IU/min for a maximum of 48 to 72 hours.
Decreases blood loss but doesn’t improve survival
If the patient has underlying cardiac disease or liver disease, vasopressin
should not be used
Embolization of the left gastric artery – not as successful
Indication for therapy
Bleeding that recurs or persists requiring more than 6
units of blood (3000 mL) is an indication for operation
Surgery –
Antral gastrectomy – ligating the bleeding vessel –
Truncal vagotomy with pyloroplasty
Partial gastrectomy with vagotomy
Total gastrectomy
Prophylaxis
Antacids
H2 receptor antagonists
Sucralfate – 1gm every 6 hrs – stomach maintains
normal pH – prevents bacterial overgrowth – and
subsequent nosocomial pneumonia
Post gastrectomy syndromes
Gastric surgery results in a number of physiologic
derangements due to
loss of reservoir function,
interruption of the pyloric sphincter mechanism,
the type of gastric reconstruction, and
vagal nerve transection.
Dumping syndrome
Early dumping -20 – 30 min after eating
Late dumping – 2 or 3 hrs after eating

Early dumping - accompanied by both gastrointestinal

and cardiovascular symptoms.
The gastrointestinal symptoms include
nausea and vomiting,
a sense of epigastric fullness,
eructations,
cramping abdominal pain, and
often explosive diarrhea.
The cardiovascular symptoms include
palpitations,
tachycardia,
diaphoresis,
fainting,
dizziness,
flushing, and
occasionally blurred vision
It occurs because of the rapid passage of food of high
osmolarity from the stomach into the small intestine.
(normally, stomach delivers food in the form of small
particles in isotonic solution)
Hypertonic food bolus passes into the small intestine,
which induces a rapid shift of extracellular fluid into the
intestinal lumen to achieve isotonicity.
Following this shift of extracellular fluid, luminal distention
occurs and induces the autonomic responses listed earlier.
Symptoms of early dumping due to several humoral agents –
serotonin, bradykinin, neurotensin, enteroglucagon
Late dumping

The basic defect in this disorder is also rapid gastric emptying;

however, it is related specifically to carbohydrates being delivered
rapidly into the proximal intestine.
When carbohydrates are delivered to the small intestine, they are
quickly absorbed, resulting in hyperglycemia that triggers the
release of large amounts of insulin to control the rising blood
sugar.
This results in an actual “overshooting” such that a profound
hypoglycemia occurs in response to the insulin.
This activates the adrenal gland to release catecholamines,
which results in diaphoresis, tremulousness, lightheadedness,
tachycardia, and confusion.
The symptom complex is indistinguishable from insulin or
hypoglycemic shock.
Treatment
Dietary measures
Avoid food containing large amounts of sugars
Frequent small meals rich in proteins and fats
Separate liquids from solids during meals

Long acting octreotide agonists inhibit gastric

emptying- affect small bowel mobility – intestinal
transit of ingested meal is prolonged
Metabolic distrbances
Anemia
1. Iron deficiency
2. Vitamin b12 deficiency

Iron deficiency anemia –

1. decreased iron intake,
2. impaired iron absorption,
3. chronic subclinical blood loss secondary to the hyperemic,
friable gastric mucosa primarily involving the margins of the
stoma where the stomach connects to the small intestine
 Treatment – suppliment iron
Vitamin b12 deficiency
occurs secondary to poor absorption of the substance due
to lack of intrinsic factor secretion in the gastric juice
Both osteoporosis and osteomalacia have also been
observed following gastric resection and appear to be
caused by deficiencies in calcium.
If fat malabsorption is also present, the calcium
malabsorption is further aggravated as fatty acids bind
calcium
Treatment – Calcium ( 1-2g/day) with vit D( 500-
5000U/day)
Afferent loop syndrome –
Afferent loop obstruction – accumulation of pancreatic, hepatobiliary
secretion with distention – epigastric discomfort and cramping
Pressure increases to forcefully empty its contents into the stomach,
resulting in bilious vomiting that is often projectile but offers
immediate relief of symptoms
Long time obstruction – blind loop syndrome – bacterial overgrowth
– bind with vit B12 and deconjugated bile acids
This results in a systemic deficiency of vitamin B12 with the
development of megaloblastic anemia
Investigations – UGI endoscopy
Radionucleotide imaging
Surgical correction – Billroth II to Billroth I
Entero-enterostomy below stomach
Roux-en-Y procedure

Efferent loop obstruction

Rare. The most common cause of efferent loop obstruction is
herniation of the limb behind the anastomosis in a right-to-
left fashion.
This can occur with both antecolic and retrocolic
gastrojejunostomies.
Colicky abdominal pain
Bilious vomiting
Distention
Investigations – contrast barium study of the stomach with
failure of barium to enter the efferent limb
Operative intervention is almost always necessary and consists of
reducing the retroanastomotic hernia and closing the
retroanastomotic space to prevent recurrence of this condition.

Alkaline reflux gastritis

Reflux of bile is associated with severe epigastric abdominal pain
accompanied by bilious vomiting and weight loss. It is usually not
relieved by food or antacids.
Investigations – HIDA scan
UGI scopy – friable inflamed mucosa
Treatment – Billroth II to Roux-en-Y anastamosis gastrojejunostomy
in which the Roux limb has been lengthened to 40cms.
Gastric atony
Persistent gastric stasis
Retention of food in stomach
Feeling of fullness
Abdominal pain
GOO obstruction
Investigations – scintigraphic assessment of gastric emptying
other causes of delayed gastric emptying such as diabetes
mellitus, electrolyte imbalance, drug toxicity, and
neuromuscular disorders must also be excluded
Rule out GOO
Treatment – prokinetics
Metoclopramide - Metoclopramide exerts its
prokinetic effects by acting as a dopamine
antagonist and by cholinergic-enhancing effects as
a result of facilitation of acetylcholine release from
enteric cholinergic neurons
Erythromycin markedly accelerates gastric
emptying by binding to motilin receptors on
gastrointestinal smooth muscle cells, where it acts as a
motilin agonist