10. Surgical Anatomy
–Arterial blood supply
Left gastric artery
Right gastric artery
Right gastroepiploic artery from gastroduodenal artery
left gastroepiploic artery a branch of splenic artery.
short gastric arteries from splenic artery
11.
12. Venous drainage
right & left gastric veins drain into
portal vein
left gastro epiploic vein & vasa
brevia join splenic vein
right gastro epiploic vein join
superior mesenteric vein
13. Nerve supply
1-Intrinsic
a- myenteric plexus of Auerbach
b- submucosal plexus of Meissner
2-Extrensic
parasympathetic
ant. Vagus
post. vagus
Sympathetic T5 – T10
14.
15. Epidemiology
of peptic ulcer disease
The incidence and prevalence of peptic
ulcer disease (PUD) has severely
decreased over the last four decades
but still represents a significant health
problem.
Although the recent advances in
pharmacologic therapy (antisecretory
agents and Helicobacter pylori treatment
regimens) have not eliminated the disease
process,
16. Outpatient symptomatology has been
successfully treated and therefore there
has been a dramatic decline, by
approximately 85% over the last three
decades, in the need for elective operative
therapy for PUD.
These treatments have not changed the
complication rate of PUD and thus the
number of emergency surgeries performed
for bleeding, perforation, and obstruction
has remained the same.
17. Complications occur in all types of
gastrointestinal (GI) ulcers but are much
more common in duodenal ulcers.
Hemorrhage occurs in 20–30%
gastric outlet obstruction in 5%,
and perforation in 2–10%.
Perforated gastric ulcers have a much
higher mortality rate than perforated
duodenal ulcers
18. Gastric ulcers account for approximately
5% of all PUD but require operation much
more frequently than duondenal ulcers.
95% of gastric ulcers are benign. Ulcers in
the fundus are rare but are almost always
malignant.
Giant gastric ulcers, those greater than 2
cm in diameter, which were previously
thought to be malignant, are benign 90% of
the time.
Duodenal ulcers are almost always benign.
19. PHYSIOLOGy of
ACID SECRETION
The normal human stomach contains
approximately 1 billion parietal cells,
and total gastric acid production is
proportional to parietal cell mass.
Gastrin, acetylcholine, and
histamine stimulate the parietal cell
to secrete hydrochloric acid
Food ingestion is the physiologic
stimulus for acid secretion
three phases: cephalic, gastric, and
intestinal.
20.
21. Acid secretion is controlled by several types of
specialized cells.
G cells in the gastric antrum release gastrin.
Gastrin activates enterochromaffin cells in the
body of the stomach and these secrete histamine.
Histamine, in turn, stimulates parietal cells to
secrete acid.
Gastrin also directly promotes the growth of
parietal cells and enterochromaffin cells.
Antral D cells secrete somatostatin which inhibits
gastrin production.
22. pathophysiology of
peptic ulcer disease
Peptic ulcers occur when there is an alteration in the balance
between acid production and mucosal protective mechanisms.
There are two major etiologies of this imbalance:
H. pylori infection and NSAID use.
H. pylori infection is present in 75% of gastric ulcers and greater
than 90% of duodenal ulcers, Several recent meta-analyses
demonstrated that there is a definite synergism between H.
pylori infection and NSAID use
and between H. pylori and cigarette smoking in the formation of
complicated PUD.
More than half of patients with complications of PUD
report recent use of NSAIDs
24. In 35% of patients with duodenal ulcers, the basal
acid output (BAO) and the maximum acid output (MAO) are
increased.
BAO greater than 15 mEq/h puts one at greatest risk.
The increased BAO is frequently observed in patients with
increased parietal cell mass (increase acid production to any
stimulus) and in patients with accelerated gastric emptying
(increased acid load in the first portion of the duodenum).
High levels of BAO and MAO are seen in
Type II (gastric and duodenal) and
Type III (prepyloric) gastric ulcers,
but not in
Type I (lesser curvature at the incisura),
Type IV (juxtaesophageal), and
Type V (anywhere secondary to medication) ulcers.
25. The epithelial cells of the stomach and duodenum secrete
mucus in response to an acid load and to cholinergic
stimulation.
This mucus form a gel layer that is impermeable to acid and
pepsin.
Other gastric and duodenal cells secrete bicarbonate to aid in
buffering acid near the mucosal cells. Prostaglandin E increases
the production of both bicarbonate and the gel layer.
When acid does penetrate the protective layers and enters
the epithelial cells, ion pumps in the basolateral cell membranes
are activated to remove excess hydrogen ions and restore
intracellular pH.
26. Role of helicobacter pylori
infection in peptic ulcer disease
Unlike other bacteria, H. pylori is able to survive in
the acidic environment of the stomach because of
its urease enzyme which converts urea into
ammonia and bicarbonate and creates a buffered
environment for its own survival.
The bacteria lives in the mucus layer above the
epithelium and causes PUD by
altering acid secretion
and by inducing gastroduodenal mucosal damage.
The bacteria causes an inflammatory response
which results in cytokine stimulation of G cells
and parietal cells and inhibits the production of
somatostatin.
27. The hypergastrinemia has two major effects.
It causes an acid hypersecretion that overwhelms
the duodenal protective mechanisms and it leads to
parietal cell hyperplasia/metaplasia in the duodenum.
The metaplasia creates a mucus layer in the duodenum
that allows H. pylori to colonize the area and reduces
duodenal bicarbonate secretion.
This infection, just like any other infection, stimulates an
inflammatory response with host cells that further
damages the mucosa.
H. pylori secretes toxins that act locally on the
epithelium and it produces proteases that degrade the
mucus layer.
29. Role of NSAIDs in the
development of peptic ulcer disease
The chronic use of NSAIDs significantly increases the risk of
complications of PUD and is the most common cause of PUD
in patients who do not have H. pylori.
Age over 60 years, prior GI complication, high NSAID dose,
and concurrent steroid and/or anticoagulant use, greatly
increase the risk of ulcer complications.
The cyclooxygenase-1B inhibitor (COXIB) drugs have a
slightly lower risk of upper GI complications than the traditional
NSAIDs but only at lower doses,
the cyclooxygenase- 2 inhibitor (COX2) drugs have not been
found to change the overall outcome of GI complications
when compared to traditional NSAIDs.
30. NSAIDs have a local topical irritative
effect on gastric mucosa which cause
submucosal erosions.
They also inhibit the formation of
prostaglandins and thus inhibit their
mucosal protective effects such as the
production of bicarbonate and the increase
in mucosal blood flow.
All of these effects are intensified with the
coexistence of H. pylori infection.
31. Other causes of peptic
ulcer disease
• Crohn’s disease,
• Zollinger–Ellison Syndrome
• hyperparathyroidism,
• steroid use,
• cigarette smoking, and
• Cocaine use
32. Zolllinger–Ellison
Syndrome
ZES, or gastrinoma, is caused by a tumor of the
pancreatic islet cells that produce gastrin.
These tumors can arise sporadically from
mutations in oncogenes such as Her-2/Neu
or as part of the Multiple Endocrine Neoplasia
Type 1 (MEN 1) syndrome.
These are responsible for 0.1–1.0% of duodenal
ulcers.
ZES frequently causes ulcerations in atypical
locations such as the distal duodenum or jejunum.
50% of ZES ulcers are solitary and 50% are
considered malignant (as they have lymph node
and/or hepatic involvement).
33. Cigarette Smoking
Smoking increases
the gastric acid secretion and
duodenogastric reflux.
It inhibits
prostaglandin production and
decreases pancreaticoduodenal
bicarbonate secretion.
34. Cocaine Use
• Recent literature has identified crack
cocaine with juxtapyloric
peptic ulcers that have an increased
propensity to perforate.
• The etiology has not yet been elucidated
but many speculate that
these ulcers are secondary to a local
ischemia from the drug induced
vasoconstriction rather than from an acid
imbalance.
35.
36. Presentation of
noncomplicated PUD
The typical symptoms of noncomplicated PUD include episodic
burning pain in the epigastrium relieved by antacids, or
antisecretory agents.
A small proportion of patients will have vomiting, heartburn,
or intolerance to fatty foods. Patients with duodenal ulcers will
be more likely to have pain relieved by food intake than patients
with gastric ulcers.
Weight loss secondary to fear of food intake is more common
with gastric ulceration than with duodenal ulceration.
patients with ZES are more likely to present with diarrhea
as part of their symptomatology.
Physical examination in noncomplicated PUD is unreliable.
37. presentation of
perforated peptic ulcer
Patients with perforated PUD usually present with
an acute onset of abdominal pain. Often, they can
tell you the exact timeof the perforation.
The pain starts in the epigastrium but by the time
of presentation in the emergency department, it is
generalized and associated with diffuse peritonitis.
it is important to ascertain whether the patient has
a history consistent with chronic PUD,
either by prior treatment, current medications or
pre-existing symptoms of noncomplicated disease.
38. Diagnosis of perforated
peptic ulcer disease
History and physical examination
Upright chest radiographs will show pneumoperitoneum
(“free air”) in 80–90% of the cases.
If pneumoperitoneum is identified on plain radiographs, there is
no need for further studies.
Ultrasound is less sensitive for detecting free air but could be
used to identify other indirect findings of perforation such as
free fluid and decreased peristalsis when the diagnosis remains
in question.
Computerized tomography (CT) scans are more sensitive
for detecting pneumoperitoneum than the other modalities
but should ideally be performed at least 6 h following the onset
of symptoms.
the use of oral contrast medium with CT scanning to identify
the site of perforation and the presence of ongoing leakage.
39.
40.
41. Test
for h. pylori infection
Every patient diagnosed with PUD should be screened for H.
pylori infection.
All patients with complicated PUD should be treated for H. pylori
infection.
The gold standard test is the histologic examination of a
mucosal biopsy using special stains. Thus, all gastric ulcers
should be biopsied at the time of operation or endoscopy.
Other tests for H. pylori infection include a serologic test,
a urea breath test, a rapid urease test, and a fecal antigen test.
The serologic test is noninvasive and has a sensitivity > 80%
and a specificity of 90%. It is not reliable if the patient has
already received antibiotic therapy for H. pylori and it cannot
be used to confirm disease eradication because the serum
will remain positive for an indeterminate length of time.
42. The urea breath test is a newer modality and involves
the ingestion of radio-labeled urea with subsequent
analysis of expired air.
This test has a high sensitivity and specificity
but is used mostly to confirm cure following treatment
rather than to make the primary diagnosis.
The rapid urease test requires a biopsy specimen and is a
simple laboratory test but has a high false-negative rate
(especially after PPIs or antibiotics have been given).
The fecal antigen test that detects active infection is
a very simple test and can be used for diagnosis or
confirmation of cure.
43. Indications for surgery in
patients with peptic ulcer disease
The indications for surgery for PUD have
recently been limited to the treatment of
complicated PUD.
because of the high mortality rate
following emergency surgery for perforated
PUD, many are suggesting nonoperative
management rather than surgical
management in high-risk patients.
High risk is defined as
the presence of severe comorbidities,
perforation greater than 24 h,
and hypotension on presentation.
44. Crofts et al. determined that nonoperative
management with nasogastric suction,
fluid resuscitation, and antibiotics
can be effective in the treatment of
perforated PUD if the site of perforation
has sealed.
Failure to improve within 24 h should then
prompt an operation.
Each case must be individualized, and
nonoperative management should not be
undertaken if a contrast study of the upper
gastrointenstinal tract shows continuing
free perforation.
45. Treatment options for
perforated peptic ulcer disease
Surgery for PUD has a long history with
many surgical options.
Many procedures have gone out of favor
due to complications, side effects, and
inadequacy, leaving
highly selective vagotomy (HSV) or
Truncal vagotomy with pylorplasty or
gastrojejunosotomy,
Vagotomy with antrectomy, and
Omental patch closure
as the current options.
46. Omental patch closure
Omental patch closure is a quick and simple procedure that is
very useful in perforated PUD.
It has long been the recommended treatment in patients with
multiple comorbidities, those that are
hemodynamically unstable and
those with exudative peritonitis.
It is not useful in Type IV gastric ulcers and may not be the
optimal treatment in a stable patient with a perforated Type I
gastric ulcer
Numerous authors in recent years have prospectively
investigated peptic ulcer recurrence rates after simple patch
closure and H. pylori eradication and have reported high success
rates
47.
48.
49. Highly selective
vagotomy
HSV is a tedious but safe operation , that
can be performed laparoscopically,
with minimal side effects.
It has a higher recurrent ulcer rate than
the other procedures (10–20%).
It is not useful for Type II or Type III
gastric ulcers or for complicated PUD.
50.
51. Truncal vagotomy
Truncal vagotomy and drainage
procedure is very useful in
complicated ulcer disease.
It reduces peak acid secretion
by 50%.
It has a significant side effect
profile and has a recurrent
ulcer rate of 10%.
54. Vagotomy with
antrectomy
Vagotomy with antrectomy is most effective at reducing
acid secretion and has a recurrence rate of 0–2%.
But, this operation has a 20% rate of post-gastrectomy
and post-vagotomy syndromes and has a significant
associated mortality.
The mortality risk increases with patient comorbidities
and with emergency surgery for complicated PUD.
It should be avoided in hemodynamically unstable
paitents and those with extensive inflammation since the
anastamosis may be compromised.
55.
56. postoperative morbidity and mortality associated
with repair of a perforated peptic ulcer disease
Despite current advances in medical and surgical
therapy, the morbidity and mortality associated
with perforated PUD remains very high and
this area has remained a topic of current research
efforts.
Comorbidities and preoperative shock are well-
established independent risk factors for a poor
outcome following emergency surgery.
Kocer et al. added age, time before surgery, and
performance of a definitive operation to the list
of significant risk factors.
57. Adjunctive medical treatments
following operation for perforated PUD
Proton Pump Inhibitors
Discontinuation of
Nonsteroidal Anti-
inflammatory Drugs
Medications for Mucosal
Cytoprotection
Treatment of Helicobacter
pylori and verification of
eradication
58. Proton Pump
Inhibitors
Patients with perforated PUD who do not undergo an acid
reducing operation should be placed on acid suppression therapy
for life.
80 – 90 % of peptic ulcers will heal with
the chronic use of antacid medications.
Several randomized control trials have demonstrated that ulcer
healing occurs faster and in a higher percentage when PPIs
are used in place of H2 blockers.
PPIs must be taken on a regular basis (not as needed) and
should be administered before the first meal of the day.
59. Discontinuation of
Nonsteroidal Anti-
inflammatory Drugs
Cessation of all NSAIDs is highly recommended in
all patients with complicated PUD.
This recommendation includes the discontinuation
of cardio-protective doses of aspirin therapy.
There are, however, certain patient populations
that require chronic anti-inflammatory medications
(i.e., rheumatoid arthritis, transplant patients). In
these patients, the traditional NSAIDs can be
substituted with the more specific but potentially
cardiotoxic COX2 inhibitors and supplemented
with cytoprotective agents.
60. Medications for Mucosal
Cytoprotection
Rostom et al. performed a meta-analysis of randomized control
trials and concluded that misoprostol, PPIs, and double-dose H2
blockers are equally effective in preventing PUD from NSAID use.
They also showed that sulcralfate is not effective.
Although the theory of enhancing the weakened mucosal barrier
seems worthwhile, there has been no added benefit
identified in patients with complicated PUD.
Misoprostol is a prostaglandin E2 analog that decreases
mucosal injury but that has severe GI side effects secondary to its
potent stimulation of smooth muscle. This has severely limited
its clinical use.
61. Treatment of Helicobacter pylori
and verification of eradication
Treatment of H. pylori with a 2-week course of either a triple
regimen or quadruple drug regimen results in 90–98% eradication
rate.
Because the recurrence rate of ulceration without complete
eradication is high, 38–70% versus 5% with eradication ,
endoscopic reexamination to confirm cure is necessary.
Triple therapy for H. pylori eradication includes a PPI and two
antibiotics, commonly metronidazole and amoxicillin
and clarithromycin.
Quadruple therapy adds bismuth to one of the triple therapy
and is used in areas where there is high metronidazole
resistance or triple therapy treatment failures
62. After completion of drug therapy, at least 1 month’s time
should pass before testing for cure is attempted.
Testing for cure can be accomplished by any of the
methods for H. pylori detection that were discussed in
the diagnosis but repeat endoscopy is most accurate.
According to Ng et al. endoscopy performed at 8 weeks
following treatment showed ulcer cure rate > 80% in
both the H. pylori treatment group and the PPI
alone group.
But, at 1 year following treatment, the ulcer recurrence
rate was 4.8% in the H. pylori group versus 38.1%
in the PPI alone group.
64. If eradication has not been achieved at the
time of retesting, a second course of
therapy should be initiated.
Quadruple drug therapy should be
used at this time regardless of which
regimen was used during the initial
treatment phase.
As for the future, research on H. pylori
vaccine continues.
65. Treatment Regimens
for Helicobacter
pylori
PPI + clarithromycin 500 mg bid
+ amoxicillin 1000 mg bid
10–14d
PPI + clarithromycin 500 bid
+ metronidazole 500 bid
10–14 d
PPI + amoxicillin 1000 mg bid,
then
PPI + clarithromycin 500 mg
bid + tinidazole 500 mg bid
5 d
5 d
66. Salvage regimens for patients who fail
one of the above initial regimens:
Bismuth subsalicylate 525
mg qid + metronidazole 250
mg qid + tetracycline 500
mg qid + PPI
10–14 d
PPI + amoxicillin 1000 mg
bid + levofloxacin 500 mg
daily
10 d
67. Confirmation of cure in
complicated PUD
Stool antigen test
Urea breath test
Endoscopic biopsy if being done
for other reason
Serology (not recommended)
68.
69. keypoints to remember in managing
patients with perforated PUD
Biopsy of all perforated gastric ulcers is required.
No single approach is ideal for all patients.
Surgeons must be prepared to individualize
all treatment plans
Any patient admitted to a hospital because of
peptic ulcer disease should be placed on lifelong
acid suppression.
Patients who regularly take NSAIDs or aspirin
should take concomitant acid suppressive
medication if they are more than 60 years old.
Lifelong acid suppressive medication may be
equivalent to surgical vagotomy in preventing
recurrent peptic ulcer or ulcer complications.
