Surgical Anatomy of

Stomach and Peptic

Ulcer Disease
Dr Jeet Vaghasiya
Gross Anatomy
• Derived from the tubular embryonic foregut and begins as a dilation
during the fifth week of gestation in the caudal portion.

• Two mesenteries invest the embryonic stomach:

• Dorsal (which becomes the gastrosplenic, gastrocolic, and gastro-phrenic
ligaments) and,

• Ventral (which becomes the hepatoduodenal and gastro-hepatic ligaments of

the lesser omentum and the falciform ligament)
Stomach bed
Arterial Supply
Venous Drainage
Lymphatic Drainage
Peptic Ulcer Disease
• Peptic ulcers are erosions in the GI mucosa that extend through the
muscularis mucosae.

• The most common symptom of peptic ulcer disease (PUD) is

dyspepsia, although the majority of patients with peptic ulcers are
asymptomatic
Epidemiology
• Much of this decline in ulcer incidence and the need for
hospitalization have stemmed from increased knowledge of ulcer
pathogenesis.

• Specifically, the role of H. pylori has been clearly defined, and the risks
of long-term NSAID use have been better elucidated.

• The need for surgery in the treatment of ulcer disease has also
decreased primarily as a result of a marked decline in elective surgical
therapy for chronic disease
 Pathogenesis
• Peptic ulcers are caused by decreased defensive factors, increased
aggressive factors, or both.

• Protective (or defensive) factors include mucosal bicarbonate secretion,

mucus production, adequate blood flow, growth factors, cell renewal, and
endogenous prostaglandins.

• Damaging (or aggressive) factors include hydrochloric acid secretion,

pepsins, ethanol ingestion, smoking, duodenal reflux of bile, ischemia,
NSAIDs, hypoxia, and, most notably, H. pylori infection.
Helicobacter pylori infection
• Infection with H. pylori has been shown to temporally precede ulcer
formation, and when this organism is eradicated as part of ulcer
treatment, ulcer recurrence is extremely rare.

• H. pylori is a spiral-shaped, flagellate, gram-negative bacteria that

resides in gastric-type epithelium within or beneath the mucus layer

• The exact mechanisms responsible for H. pylori-induced GI injury are

still not fully understood
Potential mechanisms
1. Production of toxic products that cause local tissue injury
• Mediators like urease,mucinase, cytotoxins, phospholipases, and platelet-
activating factor(lead to mucosal injury and thrombosis in microcirculation)

2. Induction of a local mucosal immune response

• Attracts pro-inflammatory cytokines and ROS.
3. Increased gastrin levels and changes in acid secretion

• Antral H.Pylori inf leads to inhibition of antral D cell release of somatostatin which in
turn leads to high basal and simulated gastrin release and acide secretion is reduced
in the acute phase

• In chronic phase, H.Pylori has trophic effect on ECF cells and G cells, leading to acid
hypersecretion. If chronic infection destroy the oxyntic cells hypoacidity will release

4. Gastric metaplasia occurring in the duodenum

• Duodenal mucosa is replaced with gastric epithelium in a protective response which
allows it to colonize these areas of duodenum leading to duodenitis
Associations of H.Pylori
• Most are asymptomatic
• Most patients with gastric cancer have current or past H. pylori
infection
Types of peptic ulcer
• Duodenal ulcer
• Gastric ulcer
Duodenal ulcer
• Most common site of peptic ulcer – D1
• More than 90% associated with h.pylori
• Associated with acid hypersecretion therefor duodenal ulcer respond
to acid reducing surgery or vagotomy or PPI

COMPLICATION OF DUODENAL ULCERS

• Most common complication is bleeding
• Peptic ulcers are the most common cause of the upper GI hemorrhage
• Posterior ulcers bleed vessel implicated – gastroduodenal artery
Gastric ulcer
• 60-70% are associated with h.pylori
• All gastric ulcers should be biopsied to rule out cancer
• Diagnosis – endoscopy
• Classifications of the gastric ulcer : johnson’ classifications
• type 1- ulcer along the lesser curvature close to incisura(most common
type of gastric ulcer)
• type 2 - ulcer in prepyloric region + ulcer in duodenam
• type 3 - only prepyloric
• type 4 – high up in the body along the lesser curvature
• type 5- diffuse ulcer due to NSAIDS
• Type 2 and 3 due to acid huypersecretion respond to vagotomy/PPI
• Mc gastric ulcer to bleed type 4
• mc complication perforation
Medical management of peptic
ulcer
• Antacids
• Sucralfate
• H2receptor antagonists
• Proton pump inhibitors
Treatmet of helicobacter pylori
infection
• After it became clear that the increased majority of cases were due to H. pylori
infection, there was a paradigm shift that saw PUD as an infectious disease, rather
than a consequence of pathologic acid secretion
• Current therapy is twofold in its approach, combining antibiotics against H. pylori
with acid-reducing medications.
• H. pylori eradication helps with initial healing, but its primary efficacy is in
preventing recurrence
• The treatment of H. pylori–positive peptic duodenal ulcer disease is triple or
quadruple therapy aimed at the eradication of H. pylori, along with acid suppression
. This triple therapy includes a PPI and two antibiotics, with the addition of bismuth
representing quadruple therapy. The choice of antibiotics should be guided by risk
factors for macrolide resistance and the presence of a penicillin allergy. R
• Clinical guidelines generally recommend treatment with a 14- day
course of triple therapy and a 10- to 14-day course of bismuth
quadruple therapy.
COMPLICATIONS OF PEPTIC
ULCER DISEASE
• HEMORRHAGE
- Upper GI bleeding is a relatively common problem, with an annual incidence of
approximately 19 to 57 cases per 100,000 individuals.9 Patients with upper GI
bleeding from PUD can present with hematemesis, melena, or both.
- The use of NSAIDs is the major risk factor for peptic ulcer bleeding.
- The initial approach to an upper GI bleed is similar to the approach to other patients
presenting with acute hypovolemic blood loss.
- Upper flexible endoscopy is the best initial procedure for diagnosis of the source of
upper GI bleeding and for therapeutic intervention, including in the setting of
bleeding ulcers. Almost all patients with a potentially substantial acute upper GI bleed
should undergo endoscopy within 24 hours.
- All patients undergoing endoscopic examination should be tested for H. pylori status.
• PERFORATION
• Perforation complicates 2% to 10% of PUD and has the highest mortality
rate of any complication of ulcer disease, reported as high as 30%.
• Perforation necessitates emergent surgical consultation
• The perforation usually can easily be accessed through an upper midline
incision. Perforations smaller than 1 cm can generally be closed
primarily and buttressed with a well-vascularized omentum.
• For larger perforations or ulcers with fibrotic edges that cannot be
brought together without tension, a Graham patch repair with healthy
omentum is performed.
• For very large perforations (>3 cm), control of the duodenal defect can
be difficult. The defect should be closed by the application of healthy
tissue, such as omentum or jejunal serosa from a Roux-en-Y type limb
GASTRIC OUTLET OBSTRUCTION
• Acute inflammation of the duodenum or pylorus can lead to mechanical
obstruction, with a functional gastric outlet obstruction manifested by early
satiety, anorexia, weight loss, nausea, and vomiting.
• . Gastric outlet obstruction from PUD is not a surgical emergency, and full
diagnostic workup prior to any surgical intervention is necessary.
• Endoscopic dilation (with or without stenting) and H. pylori eradication are the
mainstays of initial therapy
• Patients with refractory obstruction are best managed with primary antrectomy
and reconstruction along with vagotomy.
• when there is significant inflammation or scarring present, is vagotomy with a
drainage procedure, typically either a Jaboulay gastroduodenostomy or a
gastrojejunostomy
INTARACTABLE PEPTIC ULCER
DISEASE
• e. Intractability is defined as failure of an ulcer to heal after an initial
trial of 8 to 12 weeks of therapy or if patients relapse after therapy
has been discontinued; it is estimated to occur in 5% to 10% of
patients.
• Benign gastric ulcers that persist must be evaluated for malignancy as
well as other less common sources of ulceration such as ZES, Crohn
disease, or sarcoid. For any intractable ulcer, adequate duration of
antisecretory therapy, H. pylori eradication, and elimination of NSAID
use must be confirmed.
SURGICAL PROCEDURES FOR
PEPTIC ULCERS
• Elective operative intervention for PUD has become rare as medical therapy
has improved. The recognition of H. pylori and its eradication suggest that
the intractability indication for surgery may apply only to patients in whom
the organism cannot be eradicated, who cannot be taken off NSAIDs, or who
have a rarer cause of PUD
• The goal of operative ulcer therapy is to reduce gastric acid secretion. This
can be accomplished by removing vagal stimulation via vagotomy, gastrin-
driven secretion by performing an antrectomy, decreasing the number of
parietal-cells with a subtotal gastrectomy, or a combination procedure.
Vagotomy decreases peak acid output by approximately 50%, whereas
vagotomy plus antrectomy decreases peak acid output by approximately
85%. These surgeries can be performed open or laparoscopicall
• Truncal vagotomy
- truncal vagotomy is performed by division of the left and right vagus
nerves above the hepatic and celiac branches, just above the GE
junction.
- Pyloric relaxation is mediated by vagal stimulation, and a vagotomy
without a drainage procedure can cause delayed gastric emptying.
Truncal vagotomy in combination with a Heineke-Mikulicz
pyloroplasty
- When the duodenal bulb is scarred, a Finney pyloroplasty or Jaboulay
gastroduodenostomy may be a useful alternative.
• Selective vagotomy
- Selective vagotomy divides the main right and left vagus nerves just
distal to the celiac and hepatic branches, and a pyloric drainage
procedure is also performed.
- However, selective vagotomy results in higher ulcer recurrence rates
than truncal vagotomy, with no advantage in terms of decreased
postgastrectomy symptoms.
- . For these reasons, selective vagotomy has largely been abandoned.
• Highly selective vagotomy
- Highly selective vagotomy is also called parietal cell vagotomy or
proximal gastric vagotomy.
- This procedure was developed after recognition that truncal
vagotomy, in combination with a drainage procedure or gastric
resection, adversely affects the pyloral antral pump function. A highly
selective vagotomy divides only the vagus nerves supplying the acid-
producing portion of the stomach within the corpus and fundus. This
procedure preserves the vagal innervation of the gastric antrum and
pylorus, so there is no need for routine drainage procedures.
- Consequently, the incidence of postoperative complications is lower.
- Recurrence rates are higher than truncal vagotomy procedure.
• Truncal vagotomy and antrectomy
- Antrectomy is generally not performed for duodenal ulcers and is more
commonly performed for gastric ulcers.
- 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.
- When done in combination with truncal vagotomy, it is more effective at
reducing acid secretion and recurrence than truncal vagotomy in
combination with a drainage procedure or highly selective vagotomy.
- The recurrence rate for ulceration after truncal vagotomy and antrectomy
is 0% to 2%. However, this low recurrence rate needs to be balanced
against the 20% rate of postgastrectomy and postvagotomy syndromes in
patients undergoing antrectomy, longer operative times, and increased
postoperative morbidity