general has declined, the number of
Perforated Peptic Ulcer
Introduction
The treatment of peptic ulcer disease
(PUD) that involves duodenal bulb and
prepyloric ulcers continues to evolve
because of recent advances in
pharmacology, bacteriology, and operative
techniques.
The first major change occurred after the
introduction of H2-receptor antagonists for
gastric acid suppression in the late 1970s,
followed by proton pump inhibitors in the
late 1980s. In addition, the discovery that
Helicobacter pylori is present in 75-85% of
these patients revolutionized the
pathophysiologic understanding of peptic
ulcer disease.
Elective peptic ulcer surgery has been
virtually abandoned. In the 1980s, the
number of elective operations for peptic
ulcer disease dropped more than 70%, and
emergent operations accounted for more
than 80%.
Etiology
Peptic ulcer disease (PUD) results from an
imbalance of acid secretion and mucosal
defenses that resist acid digestion.
Moreover, studies have confirmed the
strong association between gastric antral
infection with H pylori and peptic ulceration.
More than 90% of patients with peptic ulcer
disease are infected with H pylori, and
eradication of this infection not only heals
most uncomplicated ulcers but also
significantly decreases the likelihood of
recurrent ulceration.
Most peptic ulcer disease not associated
with H pylori is secondary to the use of
NSAIDs. Steroid use, cigarette smoking,
rapid gastric emptying, and defective
duodenal acid defense mechanisms also
contribute to the pathophysiology of peptic
ulcer disease. Patients with high gastrin
levels (eg, those with Zollinger-Ellison
syndrome) are at increased risk of
developing peptic ulcer disease and
subsequent perforations. Importantly,
although the frequency of ulcer disease in
patients affected by bleeding and
perforation has not changed significantly.
Pathophysiology
Most gastric acid is produced by parietal
cells, which are located in the fundus and
body of the stomach. The acid is then
secreted into a gastric pit, which is a
common lumen for small groups of gastric
glands located in the lamina propria of the
gastric wall. Parietal cells (which secrete
both hydrochloric acid and intrinsic factor),
mucous cells, and chief cells (which secrete
pepsinogen) comprise these gastric glands.
Numerous tubular vesicular membranes
thought to contain the proton-potassium-
adenosine triphosphatase (H+-K+-
adenosine triphosphatase [ATPase]) pump,
or proton pump, are located inside a resting
parietal cell.
Theoretically, when the cell is stimulated to
secrete acid, these tubular vesicular
membranes bind to the apical plasma
membrane, substantially increasing the
surface area of the microvilli. The proton
pumps, now fused with the apical plasma
membrane, can secrete hydrochloric acid
directly into the lumen of the gastric pits. 5
Stimulating factors for parietal cells include
histamine, acetylcholine, and gastrin.
Because many surgical procedures for
peptic ulcer disease (PUD) entail some
type of vagotomy, a discussion concerning
the vagal innervation of the abdominal
viscera is also appropriate. The left
(anterior) and the right (posterior) branches
of the vagus nerve descend along either
side of the distal esophagus. As they enter
the lower thoracic cavity, they can
communicate with each other through
several cross-branches that comprise the
esophageal plexus. However, below this
plexus, the 2 vagal trunks again become
separate and distinct before the anterior
trunk branches to form the hepatic, pyloric,
and anterior gastric (also termed the
anterior nerve of Latarjet) branches. The
posterior trunk branches to form the
posterior gastric branch (also termed the

posterior nerve of Latarjet) and the celiac
branch.
The parietal cell mass of the stomach is
segmentally innervated by terminal
branches from each of the anterior and
posterior gastric branches. These terminal
branches are divided during a highly
selective vagotomy. The gallbladder is
innervated from efferent branches of the
hepatic division of the anterior trunk.
Consequently, transection of the anterior
vagus trunk (performed during truncal
vagotomy) can result in a dilated
gallbladder with inhibited contractility and
subsequent cholelithiasis. The celiac
branch of the posterior vagus innervates
the entire midgut (with the exception of the
gallbladder). Thus, division of the posterior
trunk during truncal vagotomy may
contribute to postoperative ileus.
Presentation
Deep, penetrating ulcers on the anterior
duodenal surface may perforate into the
abdominal cavity. Lesions on the posterior
surface penetrate into the pancreas and
present as bleeding lesions rather than free
perforations. During the past decade, a
slightly increased peptic ulcer incidence has
been attributed to widespread use of
nonsteroidal antiinflammatory drugs
(NSAIDs). These agents damage the
gastroduodenal barrier by a variety of
mechanisms. NSAID use invariably results in
peptic ulcers. Gastroduodenal ulcer
perforations have two major presentations.
Young patients present with acute onset of
severe, intolerable abdominal pain. Generally,
patients can precisely identify the exact time
the pain began because of the sudden onset
and its severe intensity. The pain is
unremitting and exacerbated by any
movement. Nausea and vomiting may be
present. Abdominal wall rigidity with diffuse
tenderness can be expected. Posterior
perforations present with substantial bleeding
and not very much pain. Posterior
perforations induce pancreatitis, manifested
by acute abdominal pain. Elevated amylase
occurs with both anterior and posterior
perforations and, therefore, is not reliable for
2
the differentiation between these two. Free air
is common with anterior perforations, but
may be absent in as many as 20% of cases.
Thus, the absence of free air does not reliably
exclude a duodenal perforation. When the
suspicion is high for duodenal perforation, the
best approach is immediate exploration.
Chronically ill, elderly patients have a more
subtle presentation. Abdominal pain is vague
and poorly localized. The pain may develop
over the course of days to weeks. Patients
typically present with fever and leukocytosis,
the etiology of which is very difficult to
discern. Free air in the peritoneum is unusual,
and CT scanning of the abdomen often makes
the diagnosis.
Patients with perforated peptic ulcer
disease (PUD) usually present with a
sudden onset of severe, sharp abdominal
pain. Most patients describe generalized
pain; few present with severe epigastric
pain. As even slight movement can
tremendously worsen their pain, these
patients assume a fetal position. Abdominal
examination findings are usually consistent
with generalized tenderness, rebound
tenderness, guarding, and rigidity.
However, the degree of peritoneal findings
is strongly influenced by a number of
factors, including the size of perforation,
amount of bacterial and gastric contents
contaminating the abdominal cavity, time
between perforation and presentation, and
spontaneous sealing of perforation.
These patients may also demonstrate signs
and symptoms of septic shock, such as
tachycardia, hypotension, and anuria. Not
surprisingly, these indicators of shock may
be absent in elderly or
immunocompromised patients or in those
with diabetes. Patients should be asked if
retching and vomiting occurred before the
onset of pain. Obtaining the medical
history, especially for peptic ulcer disease,
H pylori infection, ingestion of NSAIDs, or
smoking, is essential in making the correct
diagnosis.
Indications

Traditionally, perforated peptic ulcers have
been treated surgically with urgent surgical
repair, with or without an ulcer-curative
operation, depending on the patient's
hemodynamic status. However, several
studies have demonstrated that perforated
peptic ulcers can be treated nonoperatively.
Each study has demonstrated different
indications to operate; however, the general
consensus is that any patient with a
perforated peptic ulcer who has peritoneal
signs should undergo exploratory
laparotomy.
Wangensteen et al believed that, in a
patient with perforation but without
evidence of pneumoperitoneum, one can
safely assume that perforation has sealed
off on its own.6 He advocated a
nonoperative approach for such patients.
However, he too agreed with operative
treatment in patients with perforated ulcer
and evidence of pneumoperitoneum. Berne
and Donovan emphasized the use of a
water-soluble upper GI study to
demonstrate spontaneous sealing of the
perforation.7 They demonstrated that as
many as 40% of perforated peptic ulcers
had no evidence of leak on upper GI
contrast study.
Berne and Donovan concluded that these
patients can be observed safely as long as
peritonitis does not develop.7 Mortality rates
were 6% and 3% in the operative and
nonoperative groups, respectively. In 1998,
in another study by Donovan et al, the
authors proposed to divide the patients
based on their H pylori infection status and
recommended nonoperative treatment in all
patients except those without H pylori
infection and those in whom prior treatment
of H pylori infection had failed.8
Despite strong arguments favoring
nonoperative treatment of patients with
perforated peptic ulcer disease (PUD),
delaying the initiation of surgery more than
12 hours after presentation was
demonstrated to worsen the outcome in
patients with perforated peptic ulcer
disease. Therefore, when definitely
indicated, a laparotomy should be
performed as soon as possible.9
3
Workup
Laboratory Studies
 CBC count (Leucocytosis with left
shift is found in most cases.)
 Serum gastrin levels: Gastrin levels
greater than 1000 pg/mL are
suggestive of gastrinoma.
 H pylori infection testing 
o Serum H pylori antibody
detection: Antibodies
(immunoglobulin G [IgG]) to
H pylori can be measured in
serum, plasma, or whole
blood. However, results from
whole blood tests using
finger sticks are less reliable.
o Urea breath tests: Urea
breath tests are used to
detect active H pylori
infection by testing for the
enzymatic activity of bacterial
urease. In the presence of
urease produced by H pylori,
labeled carbon dioxide
(heavy isotope, carbon-13, or
radioactive isotope carbon-
14) is produced in the
stomach, absorbed into the
bloodstream, diffused into the
lungs, and exhaled.
o Fecal antigen tests: Fecal
antigen testing is used to
identify active H pylori
infection by revealing the
presence of H pylori antigens
in stools. This test is more
accurate than antibody
testing and less expensive
than urea breath tests.
Imaging Studies
 Upright chest radiography or lateral
abdominal decubitus radiography
reveals evidence of free air
(pneumoperitoneum).
 Upper GI contrast study with water-
soluble contrast: Extravasation of
contrast is evidence of gastric
perforation.

 CT scanning is not used in the
diagnosis of peptic ulcer disease.
CT of the abdomen may
demonstrate free air in the presence
of a perforated ulcer. CT with oral
contrast may also demonstrate
extravasation of contrast in the
presence of a perforated ulcer. If
history and physical
examination raise the possibility
of perforation, upright chest
radiography and an upper GI
contrast study with water-soluble
contrast are the diagnostic studies of
choice. Do not perform CT scanning
in this situation.
Staging
Gastric ulcers are classified according to
the Johnson classification.  found with a 7-day course of levofloxacin,
Type I gastric ulcers are typically located
near the angularis incisura on the lesser
curvature, close to the border between the
antrum and the body of the stomach.
Patients with type I gastric ulcers usually
have typical or decreased gastric acid
secretion.
Type II gastric ulcers are a combination of
stomach and duodenal ulcers, and type III
gastric ulcers are prepyloric. Both type II
gastric ulcers and type III gastric ulcers are
associated with normal or increased gastric
acid secretion.
Type IV gastric ulcers occur near the
gastroesophageal junction, and gastric acid
secretion is normal or below normal.
Treatment
Medical Therapy
Nonoperative treatment is the rational
choice for a selected subgroup of patients
who meet the criteria discussed in
Indications. Treatment of these patients
includes the following10:
 Nasogastric decompression
 Fluid resuscitation with replacement
of fluid and electrolytes
 Proton pump inhibitor
 Broad-spectrum antibiotics
4
Initial treatment typically requires triple
therapy with 2 antibacterial agents and an
acid inhibitor, typically a proton-pump
inhibitor (PPI). Drug regimens most often
include 2 weeks of antibacterial therapy
with 4 weeks of acid suppression. 
Several second-line regimens are available
for adults; a regimen of ranitidine, bismuth
citrate, metronidazole, and tetracycline has
an eradication rate similar to that of PPI
with amoxicillin and metronidazole.
Omeprazole, furazolidone, and
clarithromycin demonstrated a high
eradication rate (90%) similar to that of
standard Maastricht triple therapy (ie,
omeprazole, amoxicillin, clarithromycin).
High eradication rates (85%) were also
clarithromycin, and a PPI.
Indications to abandon nonoperative
treatment in favor of surgery include the
following:
 Failure of symptoms to improve over
12-24 hours
 Peritoneal signs and an increase in
abdominal tenderness
 Hemodynamic instability
Surgical Therapy
Surgery is recommended in patients who
present with the following:
 Hemodynamic instability
 Signs of peritonitis
 Free extravasation of contrast on
upper GI contrast studies
Preoperative Details
Fluid resuscitation should be initiated as
soon as the diagnosis is made. Essential
steps include insertion of a nasogastric
tube to decompress the stomach and a
Foley catheter to monitor urine output.
Intravenous infusion of fluids is begun, and
broad-spectrum antibiotics are
administered. In select cases, insertion of a
central venous line or a Swan-Ganz artery
catheter may be necessary for accurate

fluid resuscitation and monitoring. As soon
as the patient has been adequately
resuscitated, emergent exploratory
laparotomy should be performed.
Intraoperative Details
The patient is placed in the supine position.
A midline incision provides the most
expeditious entry into the abdominal cavity.
The incision can be extended to the
symphysis pubis if necessary. Once the
abdomen is entered, the stomach and
duodenum are carefully examined to
determine the site of perforation. If the
anterior surface of the stomach and
duodenum shows no abnormalities, the
gastrocolic ligament is serially divided
between clamps to allow entrance into the
lesser sac and inspection of the posterior
surface of the stomach. The choice of
operative procedure depends on variables,
such as the presence of shock, life-
threatening comorbid conditions, the
degree of contamination of the upper
abdomen, the amount and duration of
perforation, and whether the patient has a
history of or currently has intraoperative
evidence of chronic peptic ulceration.
In the presence of life-threatening comorbid
conditions and severe intra-abdominal
contamination, the safest technique for an
acute anterior duodenal perforation is a
simple closure with a Graham patch using
omentum. Several full-thickness simple
sutures are placed across the perforation
using 2-0 or 3-0 silk sutures. A segment of
omentum is placed over the perforation.
The silk sutures are secured. If
contamination of the upper abdomen is
minimal and the patient is stable, a
definitive ulcer procedure can be
performed. For a perforated duodenal ulcer,
this may include a highly selective
vagotomy, a truncal vagotomy and
pyloroplasty, or vagotomy and antrectomy.
For a perforated gastric ulcer, the
procedure performed depends on the
patient's condition. If the patient is
moribund, the ulcer is best excised by
grasping it with multiple Allis clamps and
using a GIA-60 linear stapler. Alternatively,
5
the ulcer can be excised with
electrocautery, and the defect is
approximated with a 2-layer closure with
inner continuous 3-0 absorbable sutures
and outer interrupted Lambert sutures
using 2-0 or 3-0 silk sutures. In a stable
patient, the ulcer is excised and sent for
frozen section analysis to exclude
malignancy. For a benign gastric ulcer, a
distal gastrectomy with either a Billroth I
gastroduodenostomy or a Billroth II
gastroduodenostomy is performed.
Truncal vagotomy and drainage
To obtain access to the esophageal hiatus,
the left triangular ligament is sharply
divided with electrocautery, and the left
lateral lobe of the liver is carefully retracted
or folded. A transverse incision is made in
the peritoneum overlying the esophagus at
the hiatus in the diaphragm. This opening is
then widened on each side of the
esophagus by sharply dividing the adjacent
lesser omentum and the esophagophrenic
ligament. Blunt dissection is continued until
2 or 3 fingers can be comfortably passed
around the esophagus.
Using a large, right-angle Mixter clamp, a
one-half-inch Penrose is passed around the
esophagus. The anterior (left) vagal trunk is
then sought. The anterior trunk is separated
from the esophagus with the aid of a right-
angle Mixter clamp or a nerve hook. The
posterior vagus is usually felt as a stout
cord lying behind and to the right of the
esophagus. The nerve is carefully freed.
After the vagal trunks are transected, the
distal 5-6 cm of the esophagus must be
cleared by meticulously dissecting and
dividing all strands of nerve fibers, small
blood vessels, and fascia.
The criminal nerve of Grassi, which is a
branch of the posterior vagus to the fundus,
must be sought diligently and divided in the
usual fashion. After completion of this
extensive periesophageal dissection, only
the longitudinal esophageal fibers should
be visible. Such meticulous dissection is
essential to ensure complete vagotomy and
subsequent low incidence of recurrent

ulceration. If a selective vagotomy is to be
performed, the hepatic branch of the
anterior vagus nerve and the celiac division
of the posterior vagus nerve are preserved.
The type of drainage procedure performed
depends on the condition of the duodenum.
Typically, a pyloroplasty is considered
standard practice; however, if the
duodenum is scarred and inflamed, a
gastrojejunostomy is a suitable alternative.
Pyloroplasty
A Kocher maneuver is first performed to
mobilize the second part of the duodenum.
Two 2-0 silk stay sutures are placed at the
superior and inferior aspects of the pylorus.
A 6- to 10-cm transverse incision is made
starting from the antrum and extending
across the pylorus and into the first part of
the duodenum. This incision is closed
longitudinally with an inner layer of
interrupted 3-0 absorbable sutures
encompassing all layers, followed by a
seromuscular layer of 3-0 silk Lembert
sutures. Alternatively, a stapled closure can
be performed. In this case, the edges of the
incision are grasped in a longitudinal
fashion with several Allis clamps. The
incision is closed with a TA-55 stapler
containing 4.8-mm staples.
Gastrojejunostomy
To construct a gastrojejunostomy, a loop of
jejunum approximately 12-15 cm from the
ligament of Treitz is first selected and
brought through an opening in the
transverse mesocolon, usually to the left of
the middle colic vessels. The stoma should
be placed in the prepyloric region or at the
most dependent portion of stomach. Using
3-0 silk, a posterior layer of seromuscular
Lembert sutures is placed. Before the
bowel is opened, noncrushing Doyen
clamps are placed on both sides of the
proposed anastomosis to occlude the
jejunum. The area of the anastomosis is
isolated with moist laparotomy pads in case
spillage of jejunal contents occurs. In
addition, the suction catheter must be
readily available to contain any spillage.
6
The stomach and the adjacent jejunum are
opened. Using 3-0 absorbable sutures, the
full-thickness inner layer is started
posteriorly and completed anteriorly using
inverting Connell sutures. An anterior
seromuscular layer of interrupted 3-0 silk
Lembert sutures is placed to complete
theanastomosis.
For a stapled anastomosis, the jejunum is
first aligned to the dependent portion of the
stomach with 2-0 silk stay sutures at each
end. A stab incision is made in the stomach
and jejunum, and the anastomosis is
performed using a GIA-60 stapling device.
The staple line is inspected for hemostasis.
The combined stab incision is closed with
an inner layer of continuous 3-0 absorbable
sutures and an outer layer of interrupted 3-
0 silk Lembert sutures. Finally, the
transverse mesocolon is carefully closed
around the anastomosis to avoid herniation.
Billroth I and II gastrectomy
If antrectomy is to be performed as part of
the antiulcer procedure, dissection is
commenced along the distal half of the
greater curvature. First, the greater
omentum is separated from the proximal
half of the transverse colon. Next, the
branches from the gastroepiploic arcade to
the greater curvature are divided and
ligated. As this dissection proceeds toward
the duodenum, the small, fragile vessels
are ligated in continuity with 3-0 silk sutures
and divided.
With gentle dissection, the posterior wall of
the first part of the duodenum is freed from
the pancreas and divided with a GIA-60
linear stapler. The right gastric artery is
identified above the pylorus, divided, and
ligated with 2-0 silk sutures. With
electrocautery, the gastrohepatic ligament
is divided proximally along the lesser
curvature. Just proximal to the incisura
angularis, the left gastric vessels lying
along the lesser curvature are carefully
isolated with a right-angle Mixter clamp.
These vessels are individually ligated in
continuity with 2-0 silk sutures and divided.
Proximally, these vessels are suture ligated

with 3-0 silk sutures. After the nasogastric
tube is withdrawn proximally, the stomach
is divided with a GIA-90 linear stapler.
If adequate length of supple duodenum is
available, a Billroth I gastroduodenal
anastomosis can be constructed. The
staple line along the transected duodenum
is sharply excised and hemostasis is
controlled. A 2-layer anastomosis, with an
outer layer of interrupted Lembert 3-0 silk
sutures and an inner layer of full-thickness
continuous 3-0 absorbable sutures, is
performed. The gastric staple line from the
lesser curvature is inverted with 3-0 silk
interrupted Lembert sutures until the angle
of sorrow of the gastroduodenal
anastomosis is reached. A crown suture is
placed there.
If a Billroth II gastrojejunostomy (Polya-
Hoffmeister type) is to be constructed, a
loop of proximal jejunum is selected and
brought in an antecolic or retrocolic fashion
toward the transected stomach. The loop of
jejunum is aligned along the lower half of
the gastric staple line with 3-0 silk stay
sutures. For a hand-sewn anastomosis, a
posterior layer of interrupted 3-0 silk
Lembert sutures is placed, approximating
the posterior wall of the stomach and
jejunum. Noncrushing bowel clamps are
placed on the small bowel. With
electrocautery, a longitudinal enterotomy is
made in the loop of jejunum, and the
appropriate length of adjacent gastric staple
line is sharply excised. An inner layer of
continuous 3-0 absorbable sutures is
placed. Finally, the anterior interrupted
Lembert 3-0 silk sutures are placed to
complete the anastomosis.
Next, the gastric staple line from the lesser
curvature is inverted with 3-0 silk
interrupted Lembert sutures until the angle
of sorrow of the gastrojejunal anastomosis
is reached. A corner crown suture is placed
there. For additional security at this
location, the adjacent jejunal wall can be
used to cover the angle of sorrow. For a
stapled Billroth II anastomosis, stay sutures
are placed to hold the loop of jejunum
adjacent to the gastric remnant. A small
7
stab incision is made in the jejunum and at
the adjacent posterior wall along the
greater curvature of the stomach. The limbs
of the GIA stapler are inserted and fired. At
least 2 cm of posterior gastric wall is
needed between the gastric staple line and
the gastrojejunostomy to avoid necrosis.
Highly selective vagotomy
The position, incision, and initial exploration
are as described for truncal vagotomy and
pyloroplasty. First, the anterior nerve of
Latarjet is identified, which may be
observed leaving the gastroesophageal
junction and running downward in the
lesser omentum parallel to the lesser
curvature and terminating at the incisura
angularis (5-7 cm from the pylorus) as
several branches resembling a crow's foot.
These terminal branches and the branches
from the nerve of Latarjet to the body of the
stomach are accompanied by the blood
vessels. The posterior vagal trunk also runs
downward within the lesser omentum as
the posterior nerve of Latarjet, and its
course and distribution to the posterior
aspect of the stomach are similar to those
of the anterior nerve of Latarjet.
Before the anterior dissection is begun,
inspect the lesser sac for adhesions to the
pancreas that could be inadvertently
avulsed during dissection, which can lead
to bleeding. To enter the lesser sac, the
gastrocolic ligament is sharply divided, but
the gastroepiploic arcade is kept intact. Any
avascular congenital adhesions between
the stomach and pancreas are divided with
electrocautery. A nasogastric tube is placed
by the anesthesiologist and should be
directed toward the antrum to be used to
grasp the greater curvature and provide
downward traction.
The dissection commences at the site just
proximal to the crow's foot on the anterior
aspect of the stomach. The objective is to
divide the lesser omentum from the lesser
curvature, between the incisura angularis
and the esophagus, by dividing all the
blood vessels and the accompanying
nerves that enter the lesser curvature. The

anterior layer of the lesser omentum,
adjacent to the neurovascular bundle, is
sharply incised. With the use of a fine
Schnidt clamp, the neurovascular branches
are carefully dissected, ligated in continuity
with 3-0 or 4-0 silk sutures, and divided.
This dissection proceeds proximally up
along the lesser curvature until the left side
of the gastroesophageal junction is
reached.
Next, the stomach is turned upward, and,
again, the nasogastric tube is used to grasp
the greater curvature. The posterior
denervation is conducted in a similar
fashion. Attention is then turned to careful
and meticulous dissection of the lower 5 cm
of the esophagus, which involves ligating
and dividing all blood vessels and nerve
fibers entering the esophagus, particularly
on its right lateral and posterior aspects. By
dividing close to the wall of the upper
stomach and lower esophagus, damage to
the main vagal trunk and its celiac and
hepatic branches is avoided.
The two critical components of achieving a
successful, complete highly selective
vagotomy include (1) completely separating
the lesser curvature of the stomach from
the lesser omentum, extending from the
incisura angularis to the cardia, and (2)
skeletonizing the lower 5-7 cm of the
esophagus.
Postoperative Details
The nasogastric tube can be discontinued
on postoperative day 2 or 3, depending on
the return of GI function, and diet can be
slowly advanced. Patients who are found to
have H pylori infection should receive the
appropriate antibiotic regimen. Patients with
high serum gastrin levels should undergo
an evaluation for Zollinger-Ellison
syndrome. Patients should undergo upper
endoscopy to evaluate the area of ulcer
and healing of the perforation site 4-6
weeks after surgery.
Complications
Possible complications include the
following:
8
 Pneumonia (30%)
 Wound infection, abdominal abscess
(15%)
 Cardiac problems (especially in
those >70 y)
 Diarrhea (30% after vagotomy)
 Dumping syndromes (10% after
vagotomy and drainage procedures)
 Gastric outlet obstruction
 Recurrent peptic ulcer
Outcome and Prognosis
Conservative treatment may be possible in
60% of patients. Approximately 30% of
patients with perforated peptic ulcer
disease (PUD) undergo surgery
immediately. In the first group of patients,
approximately 10% of patients fail to
improve with conservative treatment and
must undergo secondary surgery.
Emergency operations for peptic ulcer
perforation carry a mortality risk of 6-30%. 9
Factors that affect the prognosis include the
following:
 Shock at the time of admission
 Renal insufficiency
 Delaying the initiation of surgery
more than 12 hours after
presentation
 Concurrent medical illness (eg,
cardiovascular disease, diabetes
mellitus)
 Age older than 70 years
 Cirrhosis
 Immunocompromised state
 Location of ulcer (Mortality
associated with perforated gastric
ulcer is twice that associated with
perforated duodenal ulcer.)
Future and Controversies
Successful treatment of perforated peptic
ulcer with the laparoscopic approach was
first reported in 1990.11 Since then, various
institutions have used this technique to
treat patients with perforated peptic ulcer.
Studies have shown that the conversion
rate from a laparoscopic approach to an
open approach varies from 0-25%.
 9
Compared with the open approach, the
following results were observed with the
laparoscopic method:

 Increased operative time

 Reduced requirement for
postoperative analgesia
 Reduced time to return to a normal
diet
 Shorter hospital stay
 Earlier return to work12
 No difference was found in blood
loss, stress response (as
determined by endotoxemia,
bacteremia, and inflammatory
markers), postoperative gastric
emptying, or morbidity or mortality.13

Only one prospective randomized trial has

compared laparoscopic surgery with open
surgery for perforated ulcer. The study
found that the only difference between the
two groups was a reduced need for
analgesia and an increased operative time
in the laparoscopic group.14
Contraindications for laparoscopic repair for
perforated peptic ulcer include large
perforations, a posterior location of the
perforation, and a poor general state of
health.