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452 Part IV Stomach and Duodenum
TABLE 21-4: REBLEEDING RATES BY
PROCEDURE FOR BLEEDING PEPTIC ULCER
Ulcer Suture
or Excision (%)
10–30 0–30 0–10
Data from Legrand MJ, Jacquet N. Surgical approach in severe bleeding peptic
ulcer. Acta Gastroenterol Belg . 1996;59:240–244.
Truncal
Vagotomy and
Pyloroplasty (%)
Truncal
Vagotomy and
Antrectomy (%)
e e cacy of endoscopy diagnosis and therapy depends
on timing. Early endoscopy correctly classi es patients as
low risk for recurrent hemorrhage and permits safe avoidance of hospitalization. Early endoscopy also bene ts highrisk patients by directing speci c, active hemostatic therapy.
Patients with early endoscopy have been demonstrated to
have fewer episodes of rebleeding, lower rates of operation,
31
less resource consumption, and shorter hospitalizations.
Operative intervention is indicated for the following:
Massive hemorrhage leading to shock or cardiovascular
instability
Prolonged blood loss requiring continuing transfusion
Recurrent bleeding during medical therapy or after endo-
scopic therapy
Recurrent hemorrhage requiring hospitalization
e need for emergency intervention signi cantly increases
surgical risks, and not surprisingly, mortality is increased
10-fold. Emergent operative therapy should consist of duodenotomy with direct suture ligation of the bleeding vessel in
the ulcer base ( Table 21-4 ). Postoperatively, patients should
receive proton pump inhibitors and antibiotics directed against
H.pylori . is treatment approach is based on the observation,
in medically treated patients, that peptic ulcer hemorrhage
recurs in 20% of patients when H. pylori is not eradicated,
while rebleeding is reduced to 3% in patients who receive
31–34
H. pylori antibiotic therapy.
is recommendation is an
extrapolation; the studies that support this practice were not
designed to evaluate postoperative hemorrhage ( Table 21-5 ).
PERFORATION
e lifetime risk for perforation in patients with duodenal
ulceration not receiving therapy approximates 10%, while
ulcer perforation is unusual if initial ulcer healing has been
achieved. Duodenal ulcer perforation is followed by sudden
and severe epigastric pain. e pain is caused by contact of
the peritoneum with highly caustic gastric secretions. Pain
is often instantaneous and remains constant. Peritoneal irritation is usually intense and causes most patients to avoid
movement.
Physical examination reveals fever, diminished bowel
sounds, rigidity of the abdominal musculature, and guarding.
TABLE 21-5: ERADICATION OF
H. PYLORI
AND ULCER REBLEEDING
Treatment Group
No. of Patients Eradication Rate (%) Rebleeding (%)
133 83 6
Control Group
No. of Patients Eradication Rate (%) Rebleeding (%)
129 4 28
Data from Sharma VK, Sahai AV, Corder FA, et al. Helicobacter pylori eradication
is superior to ulcer healing with or without maintenance therapy to prevent
further ulcer hemorrhage. Aliment Pharmacol er . 2001;15:1939–1947.
Upright abdominal radiographs demonstrate pneumoperitoneum in 80% of cases. If free air is not present, computed
tomography of the abdomen is very sensitive for demonstrating perforation.
Occasional reports have described nonoperative treatment of
this complication, but this approach is not appropriate for the
large majority of patients with perforated peptic ulcer. Perforation is a strong indication for surgery in most circumstances.
Laparotomy or laparoscopy a ords the opportunity to relieve
intraperitoneal contamination and to close the perforation.
e results of surgical treatment of duodenal perforation in
the era preceding the recognition of H. pylori are instructive.
Signs of preexisting duodenal ulceration, in terms of history of
prior symptoms and anatomic evidence of duodenal scarring,
should be sought, but a lack of antecedent symptoms is not
protective. Patients without antecedent symptoms are at substantial risk for recurrent ulceration. By 5–6 years, symptomatic ulcer recurrence in patients with acute ulcer perforation
is similar to that for patients with chronic disease. Before the
role of H. pylori was appreciated, simple omental closure of
duodenal perforation had not provided satisfactory long-term
results; up to 80% of patients so treated had recurrent ulceration and 10% experienced reperforation. It is now known
that four- fths of all patients with perforation have H. pylori
infestation and therefore are at risk of recurrent disease.
e mortality of emergency operation for ulcer perforation
is most clearly correlated with the existence of preoperative shock, coexisting medical illness, and the presence of
35
perforation beyond 48 hours.
For stable patients who receive
prompt surgical attention, the operation can be performed
36
with safety.
Proximal gastric vagotomy with omental patch
closure of the perforation is one option in this circumstance.
is procedure has been shown to be both safe and e ective in preventing ulcer relapse. Incorporation of the site of
perforation as part of a pyloroplasty or resection of the perforation during antrectomy can also be combined with truncal
vagotomy. e performance of these operations has declined
signi cantly, however, with the focus on H. pylori as the cause
of most ulcer recurrences.
Chapter 21 Benign Gastric Disorders 453
Several investigators advocate omental patch closure
37–41
alone with postoperative anti–H. pylori therapy.
Omental
patching can also be accomplished laparoscopically in select
42
patients.
is approach rests upon three assumptions: (1)
that most perforated duodenal ulcers are caused by H. pylori;
(2) that the duodenal perforation is small enough that secure
closure can be obtained; and (3) that further surgical therapy
will be obviated by the eects of postoperative antibiotic therapy and acid suppression. Minimally invasive approaches are
becoming frequently performed.
OBSTRUCTION
Gastric outlet obstruction can develop either acutely or chronically in patients with duodenal ulcer disease. Surprisingly, the
incidence of H. pylori infection in this subgroup of patients
may not be as high as that seen in patients presenting with
hemorrhage or perforation.
and inammation, is associated with ulcers in the pyloric channel and the rst portion of the duodenum. Pyloric obstruction
causes recurrent vomiting and dehydration. Hypochloremic
alkalosis, due to loss of hydrochloric acid in gastric secretions,
is distinctive of gastric obstruction. Hypokalemia may develop
as a secondary renal compensation for alkalosis. Acute gastric
outlet obstruction is treated by nasogastric suction, rehydration, and intravenous administration of antisecretory agents.
Acute obstruction due to pyloric inammation resolves with
supportive measures within a few days.
Repeated episodes of ulceration can lead to pyloric scarring
and a xed stenosis with chronic gastric outlet obstruction.
In cases of recurrent duodenal ulceration, the lifetime risk of
chronic pyloric stenosis approximates 10%.
Initial investigation begins with upper GI endoscopy to
conrm the site of obstruction and to exclude intrinsic or
extrinsic obstruction due to malignancy, the most common
cause of gastric outlet obstruction in the modern era. Endoscopic balloon dilation of the area of peptic ulcer obstruction
can also be attempted; with success obtained in up to 85% of
44
patients.
Most treated patients note immediate symptomatic
improvement, but only 40% have sustained improvement by
3 months after balloon dilation. Recurrent symptoms are presumed due to residual scarring in the pyloric channel. In most
cases, operative correction is required. is should include
treatment of the underlying ulcer disease and relief of the
anatomic abnormality. Truncal vagotomy with antrectomy
and parietal cell vagotomy with gastrojejunostomy have both
been used with success in this circumstance.
43
Acute obstruction, due to edema
duodenal ulceration. e opposite is found in Japan where
gastric ulcers are 5–10 times more common. Gastric ulcer is
more common in men than women and occurs in a patient
cohort approximately 10 years older than that of duodenal
ulceration. In symptomatic patients, upper GI endoscopy is
the preferred method for diagnosing gastric ulceration. e
visual appearance of benign and malignant gastric ulcers may
be identical, and dierentiation may be made only by biopsy.
Benign gastric ulcers appear smooth and at and are often
covered by a gray, brous exudate. e margin is often raised
and erythematous. e ulcer margin is friable and may bleed
with manipulation. All gastric ulcers should undergo multiple
biopsies, obtained from the perimeter of the lesion. e addition of endoscopic brushings to multiple biopsies increases
diagnostic accuracy to approximately 95%.
Although benign gastric ulcers may occur in any location
in the stomach, more than half are located along the lesser
curvature proximal to the incisura angularis. Fewer than 10%
of benign ulcers are located on the greater curvature. Most
benign gastric ulcers lay within 2 cm of the histologic transition between fundic and antral mucosa.
Similar to duodenal ulceration, H. pylori infection is the
key to the pathogenesis of benign gastric ulcers. Antibiotic
treatment regimens useful for duodenal ulcer have also been
used for benign gastric ulceration. e response of gastric
ulcers to antibiotic therapy is equivalent to that of duodenal
ulcers. Recurrence of gastric ulcers after H. pylori eradication
is equal to the rate of reinfection.
In addition to H. pylori infection, alterations in gastric
motility have been demonstrated in some patients with
benign gastric ulcers. Motility defects include delayed gastric
emptying, abnormal pyloric sphincter function, prolonged
high-amplitude gastric contractions, duodenogastric reux,
and alterations in the gastric migrating motor complex.
ese alterations have not been denitively demonstrated
to be pathogenic, and their relevance to gastric ulceration is
unsettled. A denite association between chronic NSAID use
and benign gastric ulceration has been recognized. As with
duodenal ulceration, cigarette smoking is associated with
development of gastric ulceration, and continued smoking
impairs medical therapy. Gastric and duodenal ulcers may
occur in patients who receive hepatic artery chemotherapy
if improper placement of the catheter permits perfusion of
gastric and duodenal mucosa. A variety of agents, including 5-uorouracil, cisplatin, doxorubicin, and mitomycin C,
have been implicated.
Therapy
GASTRIC ULCER DISEASE
Diagnosis
In the United States, benign gastric ulcers are found in approximately 90,000 new patients a year, about one-fth that of
e primary therapy for benign gastric ulceration is antibiotic
treatment of H. pylori infection using treatment protocols
similar to those for duodenal ulceration. Antibiotic response
rates are similar. Cessation of NSAID therapy is required
to improve results. Operative treatment is reserved for
complications of gastric ulcer, including hemorrhage and
perforation. Unlike duodenal ulcer, failure of a recurrent
454 Part IV Stomach and Duodenum
ulcer to respond to medical therapy may be an indication for
operation, usually because nonhealing raises concerns about
malignant disease.
For benign gastric ulcers, the elective operation of choice
is usually a distal gastrectomy with either gastroduodenal
(Billroth I) or gastrojejunal (Billroth II) anastomosis. e
ulcer should be excised with the gastrectomy specimen ( Fig.
21-5 ). Performed electively, operative mortality approximates
2–3%, and ulcer recurrence rates are less than 5%. Inclusion
of vagotomy does not improve recurrence rates, which is not
surprising given the variability of acid secretion in patients with
gastric ulcers. e occurrence of a benign ulcer near the gastroesophageal junction (type IV ulcer) represents a di cult surgical problem. e ulcer may be excised via a distal gastrectomy
with an extension along the lesser curvature and reconstruction with gastrojejunostomy. Emergency treatment of hemorrhage or perforation requires ulcer excision. Distal gastrectomy,
including the site of perforation or bleeding, is usually the procedure of choice. Operative mortality rates average 10–20% in
the presence of hemorrhage or perforation.
Intractability or Nonhealing Ulcers
is should indeed be a rare indication for surgery performed
today. Arguably, the patient referred for surgical evaluation of
intractable peptic ulcer disease should raise red ags for the
A
B
d
FIGURE 21-5 Points of transection for distal gastrectomy performed
to resect a gastric ulcer along the lesser curvature. d, the approximate
diameter of the duodenum.
TABLE 21-6: DIFFERENTIAL DIAGNOSIS OF
INTRACTABILITY OR NONHEALING PEPTIC
ULCER DISEASE
Cancer
Gastric
Pancreatic
Duodenal
Persistent H. pylori infection
Tests may be false negative
Consider empiric treatment
Noncompliant patient
Failure to take prescribed medication
Surreptitious use of nonsteroidal anti-in ammatory drugs
Motility disorder
Zollinger-Ellison syndrome
Brunicardi FC, Anderson DK, Billiar TR, et al. Schwartz’s Principles of Surgery .
8th ed. New York, NY: McGraw-Hill; 2005:969.
surgeon. Acid secretion can be totally blocked and H. pylori
eradicated with modern medication; therefore, the question
remains: “Why does the patient have a persistent ulcer diathesis?” e surgeon should review the di erential diagnosis
of nonhealing ulcer prior to any consideration of operative
treatment ( Table 21-6 ).
Surgical treatment should be considered in patients with
nonhealing or intractable peptic ulcer disease who have
multiple recurrences, large ulcers (>2 cm), complications
(obstruction, perforation, or hemorrhage), or suspected gastric cancer. Surgery should be approached most cautiously in
the thin or marginally nourished individual.
It is important that the surgeon not fall into the trap of
performing a large, irreversible operation on these patients,
based on the unproven theory that if all other methods have
failed, a larger operation is required. Today’s patients are different than those of three or four decades ago. One might
argue that modern medical care has healed the minor ulcer,
and that patients presenting with true intractability or nonhealing will be more di cult to treat and are likely to have
chronic problems after a major ulcer operation. If surgery is
necessary, less is often better. It is the practice of the authors
never to perform a gastrectomy as the initial elective operation
for intractable duodenal ulcer in the thin or asthenic patient.
Instead, the preferred operation for this group of patients is
HSV. In patients with nonhealing gastric ulcer, wedge resection with HSV should be considered in thin or frail patients.
Otherwise distal gastrectomy (to include the ulcer) is recommended. It is unnecessary to add a vagotomy in patients with
type I gastric ulcer.
Juxtaesophageal gastric ulcers (type IV) are pathophysiologically akin to type I gastric ulcers (ie, associated with
gastric acid hyposecretion) but are often di cult to resect
as part of a distal gastrectomy. A variety of techniques
have been used to treat these ulcers surgically, including
the Csendes operation, the Pauchet gastrectomy, and the
Kelling- Madlener procedure ( Fig. 21-6 ).
Chapter 21 Benign Gastric Disorders 455
Ulcer excision Antrectomy Pauchet procedure
Kelling-Madlener
procedure
FIGURE 21-6 Operations for gastric ulcer. (Reproduced with permission from Seymour NE. Operations for peptic ulcer and their complications. In: Feldman M,
Scharschmidt BF, Sleisenger MH, eds. Gastrointestinal and Liver Disease, 6th ed. Philadelphia, WB Saunders; 1998.)
Roux-en-Y esophagogastrojejunostomy
POSTGASTRECTOMY SYNDROMES
Subtotal gastrectomy
Forpatients who experience mild dumping symptoms in the
Csendes procedure
early postoperative period, dietary alterations, and time bring
A number of syndromes have been described after gastric
operations performed for peptic ulceration as well as gastric
neoplasm. e occurrence of permanent disabling postoperative symptoms is uncommon, occurring only in about 1–3%
of cases, and unpredictable. e two most common postgastrectomy syndromes are dumping and alkaline re ux gastritis.
improvement in all but approximately 1–2%. For those who
remain persistently symptomatic, the long-acting somatostatin analogue, octreotide, improves dumping symptoms when
45
administered subcutaneously before a meal.
e e ects of
somatostatin on the vasomotor symptoms of dumping are
summarized below ( Table 21-7 ).
Dumping
Dumping is de ned as a postoperative clinical syndrome
with gastrointestinal and vasomotor symptoms. e cause
of dumping is uncertain but is likely related to unregulated
entry of ingested food into the proximal small bowel following resection, bypass, or division of the pyloric sphincter.
Early dumping symptoms occur within 1 hour of ingestion
of a meal and include nausea, epigastric discomfort, tremulousness, and sometimes dizziness or syncope. Late dumping
symptoms follow a meal by 1–3 hours. Late symptoms are
usually due to reactive hypoglycemia.
Most patients who undergo vagotomy or gastrec-
tomydo not experience dumping symptoms postoperatively.
TABLE 21-7: MECHANISMS OF ACTION OF
OCTREOTIDE IN DUMPING SYNDROME
Delay in the accelerated gastric emptying
Delay in small intestine transit time
Inhibition of enteral hormone secretion
Inhibition of insulin release
Inhibition of postprandial vasodilation/splanchnic vasoconstriction
Increase in intestinal absorption of water and sodium
Ukleja A. Dumping syndrome: pathophysiology and treatment. Nutr Clin Pract .
2005 Oct;20:517–525.
456 Part IV Stomach and Duodenum
Alkaline Re ux Gastritis
Alkaline re ux gastritis is a postoperative syndrome characterized by postprandial epigastric pain associated with nausea
and bilious vomiting. Endoscopic examination reveals re ux
of bile into the stomach, and biopsy demonstrates histologic
evidence of gastritis.
Alkaline re ux gastritis is a diagnosis of exclusion. e differential diagnosis of postoperative epigastric pain includes
recurrent ulceration, calculous biliary disease, pancreatic in ammation, a erent loop obstruction, and esophagitis. Upper endoscopic examination is essential to exclude recurrent ulcer. e
gastric mucosa appears in amed, friable, and edematous. Gastric in ammation is often uneven and nonulcerative. Histologic
examination shows glandular atrophy, mucosal and submucosal
edema, and the presence of acute and chronic in ammatory cells
in the lamina propria. Intestinal metaplasia may be present.
Postoperative alkaline re ux gastritis is resistant to medical treatment. Antacids, proton pump inhibitors, and dietary
manipulations have not been de nitively demonstrated to be
bene cial. e most e ective treatment for persistent alkaline re ux gastritis is operative diversion of intestinal contents from contact with the gastric mucosa. is solution
usually requires conversion of a Billroth I or II gastrectomy
to a Roux-en-Y gastrojejunostomy with an intestinal limb of
50–60 cm ( Fig. 21-7 ). e length of the Roux limb prevents
re ux of intestinal contents. is procedure is very e ective
in eliminating bilious vomiting. However, persistent pain
is reported in up to 30% of patients, and 20% of patients
develop postoperative delayed gastric emptying.
STRESS ULCER DISEASE
Gastritis and gastric ulceration can be induced by physiologic
stress. Usually occurring in hospitalized patients with critical
illness, stress gastritis can be demonstrated endoscopically in
the majority of patients recovering from shock. While occult
bleeding in this population is common, clinically signi cant hemorrhage de ned by the need for blood transfusion,
hypotension, or alteration in other vital signs occurs in only
0.5–5% of patients. In four recent surgical series comprising more than 28,000 patients, the incidence of clinically
signi cant stress ulceration was 0.4%.
16,612 hospitalized patients, the incidence of overt stress
47
bleeding was only 0.1%.
In a review of patients admitted
to both surgical and medical intensive care units (ICUs), the
incidence of clinically signi cant and endoscopically proven
48
stress ulceration was 0.17%.
Major trauma, especially if accompanied by hypotension,
sepsis, respiratory failure, hemorrhage, or multiple injuries,
predisposes to acute stress gastritis ( Table 21-8 ). Acute stress
gastritis is also common after thermal injury with greater
than 35% total body surface area burned. A form of gastritis similar to that following trauma may complicate central
nervous system injury or intracranial hypertension. When
viewed endoscopically, multiple ulcerations are observed in
the proximal, acid-secreting portion of the stomach. Fewer
lesions are found in the antrum, and only rare ulcerations in
the duodenum.
e major complication of stress gastritis is hemorrhage.
Patients with coagulopathy and those requiring mechanical
ventilation are at increased risk of hemorrhage. Patients
without these two risk factors have been reported to have an
overall risk of hemorrhage of only 0.1%, while those with
both demonstrate clinically signi cant bleeding in 3.7% of
46
In another series of
60 cm
FIGURE 21-7 Roux-en-Y gastrojejunostomy used to treat alkaline
re ux gastritis.
Operations . 9th ed. Stamford, CT: Appleton & Lange; 1989:716.)
(Redrawn from Schwartz SI, Ellis H. Maingot’s Abdominal
TABLE 21-8: RISK FACTORS FOR STRESS
ULCER BLEEDING
Respiratory failure
Coagulopathy
Hypotension
Sepsis
Hepatic failure
Renal failure
Steroids
Injury Severity Score > 16
Spinal cord injury
Age >55 y
Chapter 21 Benign Gastric Disorders 457
cases. Respiratory failure is dened as greater than 48 hours
on a mechanical ventilator. Coagulopathy is dened as a plate-
3
let count less than 50,000/mm
, an international normalized
ratio greater than 1.5, or a partial thromboplastin time greater
than two times control.
Admission to an ICU by itself does not place patients
at risk for hemorrhage, and patients undergoing major GI
surgery do not have an increased risk of stress-related bleeding
in the absence of complications. Increased patient age, emergency surgery, need for reoperation, and the occurrence of
hypotension are risk factors for postoperative gastric bleeding.
e occurrence of sepsis and respiratory failure are also risk
factors. Multiple regression analysis has shown that mechanical ventilation and coagulopathy impart the greatest risk.
e diagnosis of stress ulceration requires endoscopic
examination. Acute mucosal ulcerations may be observed as
early as 12 hours postinsult; lesions appear as multiple shallow areas of erythema and friability, accompanied by focal
hemorrhage. Histologically, the lesions consist of coagulation
necrosis of the supercial endothelium with inltration of
leukocytes into the lamina propria. Signs of chronicity, such
as brosis and scarring, are absent. With resolution of injury
or sepsis, healing is accomplished by mucosal restitution and
regeneration.
A survey of Society of Critical Care Medicine members
showed that ranitidine, famotidine, sucralfate, and cimetidine were the drugs used most commonly for prophylaxis.
e presence of bright red blood in the nasogastric tube was
considered by most to dene prophylaxis failure, and the
addition of a second drug from a dierent therapeutic class
was the preferred mode of treatment.
49
Because hemorrhage does not occur in all patients, studies
that use bloody nasogastric discharge as a sign of stress gastritis
underestimate the true incidence in critically ill patients. In
one endoscopically controlled study, 100% of patients with
life-threatening injuries had evidence of gastric erosions by 24
hours. A high prevalence of gastric erosions is also noted in
burn patients, while GI hemorrhage occurs in only 25–50%
of patients with burn wound infection. Barium contrast
examinations have no role in the diagnosis of stress gastritis
and interfere with endoscopic examination.
It is important to distinguish stress ulceration from
other causes of postoperative hemorrhage. Several recent
studies have demonstrated that duodenal ulceration and
gastric ulcers are common in postoperative patients. In one
series, sources of clinically signicant bleeding included
duodenal ulcer in 26%, gastric ulcer in 13%, esophagitis
in 18%, and esophageal varices in 7%. Similar results have
been reported in other series, emphasizing the need for
specic diagnosis.
UPPER GASTROINTESTINAL BLEEDING
Acute upper gastrointestinal (GI) hemorrhages are frequent
medical events occurring at a rate of approximately 50 cases
per 100,000 persons per year. Acute GI hemorrhage still
has a signicant associated mortality, approximating 10%.
Although urgent endoscopy has been used for the past 20
years for the diagnosis and management of acute upper GI
hemorrhage, the mortality rate has not substantially declined
even with the introduction of endoscopic intervention.
Patients with acute upper GI hemorrhage are increasingly of
advanced age and have preexisting medical comorbidities.
Endoscopy has become the preferred method for diagnosis in patients with acute upper GI bleeding. is method
is informative in most patients, correctly identifying the site
and source of bleeding in 90% of cases. While the ecacy of
upper endoscopy has been established for diagnosing acute
upper GI tract hemorrhage, optimal timing has been controversial. e majority of existing studies support the claim that
early endoscopy is both safe and eective for all risk groups.
For low-risk patients, the current evidence demonstrates
that early endoscopy promotes safe patient disposition. In
many instances, these patients can avoid hospitalization with
a very low risk of recurrent bleeding. For high-risk patients,
there is benet of early endoscopy for outcomes, including
transfusion requirements, rebleeding rate, and the need for
emergency surgery. Early endoscopy directs therapy and signicantly reduces length of hospitalization relative to delayed
endoscopy without evidence of cost shifting to the outpatient
setting. In this sense, early endoscopy provides prompt diagnosis and assists in decision making regarding clinical triage
and subsequent management. Current evidence does not
demonstrate, however, that early endoscopy decreases overall mortality. ere is no evidence that the practice of early
endoscopic intervention results in patient harm.
Based on current information, gastroduodenal ulceration
accounts for approximately 40% of cases of acute upper
GI hemorrhage. Other diagnoses, in decreasing frequency,
include acute gastritis, esophageal variceal bleeding, esophagitis, duodenitis, Mallory-Weiss tears, and upper GI tract
malignancies.
Initial treatment of upper GI tract hemorrhage begins
with restoring intravascular volume. Hemodynamic monitoring is crucial. Unstable patients should be initially
treated in an ICU setting. Interestingly, although numerous
trials have examined the ecacy of H
-receptor antagonists
2
in patients with bleeding peptic ulcers, none of these have
demonstrated consistent therapeutic benet either individually or when examined by meta-analysis. Sixteen prospective
trials have also examined the use of proton pump inhibitors
in the setting of acute ulcer bleeding. Only 7 of these 16
trials have demonstrated a statistically signicant benet in
terms of rebleeding or need for urgent surgical intervention.
None of the trials showed a reduction in mortality. Over
half (9 of 16) of the studies did not demonstrate reduction
in any of the primary outcomes that included rebleeding,
surgery, or mortality.
In addition to providing diagnostic information, aggressive endoscopy also presents an opportunity for therapeutic
intervention. Relative to medical therapy alone, patients with
stigmata of active bleeding, visible vessels, and nonbleeding
adherent clots benet from endoscopic ulcer hemostasis.
458 Part IV Stomach and Duodenum
e major modalities used include bipolar electrocautery
probes, heater probes, and epinephrine injection.
Mechanisms by which epinephrine injections cause ulcer
hemostasis have been examined experimentally. Epinephrine
causes intense vasoconstriction, platelet aggregation, and vessel
sclerosis. ese combined eects permit permanent control of
arterial hemorrhage in most patients. Absolute alcohol has
also been used for injection therapy with good results.
Potential complications of endoscopic therapy include
bowel perforation and incitement of active bleeding from a
nonbleeding vessel. e rate of perforation is low and has
been reported to approximate 0.7%. New bleeding is induced
by therapy in fewer than 1% of patients.
Under selective circumstances, repeated attempts at endoscopic therapy may also be used. In a prospective randomized
trial, investigators evaluated whether emergency surgery or
repeated endoscopic therapy resulted in better outcomes for
patients with severe ulcer hemorrhage. Endoscopic therapy
consisted of a combination of epinephrine injection and
heater probe application. Denitive hemostasis was signicantly higher in surgically treated patients (93 vs 73%), but
the complication rate was signicantly higher in the surgery
group (36%) relative to the endoscopy group (15%).
Acute therapy of variceal bleeding may also be directed
endoscopically. Major approaches have included variceal
injection with sclerosants and band ligation. Because of
ecacy and safety, endoscopic variceal ligation has largely
replaced sclerotherapy as the endoscopic method of choice
50
for acute variceal hemorrhage.
is method has also been
used for secondary prevention of esophageal variceal hemorrhage. Prospective randomized trials indicate that prophylactic variceal ligation decreases the risk of rst variceal bleeding
relative to no treatment or to treatment with propranolol. In
addition, ligation decreases the risk of recurrent bleeding and
associated mortality relative to no treatment. In this circumstance, however, relative to propranolol therapy, ligation does
not improve mortality.
In patients with acute peptic ulcer as a cause for upper
GI hemorrhage, H. pylori is a common etiology. After initial
control of hemorrhage, eradication of infection should be a
treatment imperative. Because eradication of H. pylori eliminates ulcer recurrence, it is logical to assume that it would
also decrease the rate of recurrent ulcer bleeding. Randomized
trials demonstrate that recurrent hemorrhage usually occurs in
patients who have persistent or recurrent H. pylori infection.
Without antibiotic treatment, recurrent hemorrhage occurs in
as many as 20% of patients. e risk of recurrent hemorrhage
can be reduced to approximately 3% in individuals treated
with an eective antibiotic regimen after hemorrhage.
pancreas). e most common gastric polyp (~75% in most
series) is the hyperplastic or regenerative polyp, which frequently occurs in the setting of gastritis and has a low but
real malignant potential. Adenomatous polyps may undergo
malignant transformation, similarly to adenomas in the
colon. ey constitute about 10–15% of gastric polyps.
Hamartomatous, inammatory, and heterotopic polyps have
negligible malignant potential. Polyps that are symptomatic,
larger than 2 cm, or adenomatous should be removed, usually
by endoscopic snare polypectomy. Consideration should also
be given to removing hyperplastic polyps, especially if large.
Repeat esophagogastroduodenoscopy (EGD) for surveillance
should be done following removal of adenomatous polyps.
A fourfold rise in the incidence of nonfamilial fundic
gland polyps has been noted due to the increased use of proton pump inhibitors. However, no increased risk of dysplasia
has been noted.
51
LIPOMA
Lipomas are benign submucosal fatty tumors that are usually asymptomatic, found incidentally on upper GI series
or EGD. Endoscopically they have a characteristic appearance; there also is a characteristic appearance on endoscopic
ultrasound. Excision is unnecessary unless the patient is
symptomatic.
BEZOARS
Bezoars are collections of undigestible matter that accumulate
in the stomach and small bowel. ey are the most common
foreign body found in the stomach and may be seen in
patients who have undergone prior gastric surgery, includ-
52–54
ing after bariatric surgery.
e most common bezoar is
composed of hair (trichobezoars). It occurs most commonly
in young women. Phytobezoars are composed of vegetable
matter and are usually seen in association with gastroparesis
or gastric outlet obstruction. Other types of bezoars include
lactobezoars (concentrated milk formula), mixed medica-
55
tion bezoars, and food bolus bezoars.
Bezoars may pres-
ent with obstruction, ulceration or bleeding, and rarely as
56
intussusception.
Diagnosis is suggested by upper GI series
and conrmed by endoscopy. Enzyme therapy with papain,
cellulase, or acetylcysteine may be used, but most patients
will need endoscopic or surgical disruption and extraction.
DIEULAFOY’S LESION
POLYPS
Gastric epithelial polyps are the most common benign tumor
of the stomach. ere are essentially ve types of benign
epithelial polyps: adenomatous, hyperplastic (regenerative),
hamartomatous, inammatory, and heterotopic (eg, ectopic
Dieulafoy’s lesion is a congenital arteriovenous malformation
of the proximal stomach, typically on the lesser curve where it
derives its supply from branches of either the left or right gastric artery. It is seen in middle-aged or elderly men and characterized by an unusually large tortuous submucosal artery.
Prior to widespread endoscopy, Dieulafoy’s lesions were
Chapter 21 Benign Gastric Disorders 459
diagnosed postoperatively but are now becoming diagnosed
57
and treated routinely via endoscopy.
It clinically presents as
an upper GI bleed if eroded and on endoscopy appears as a
stream of arterial blood emanating from what appears grossly
to be a normal gastric mucosa. Patients may also present with
intermittent episodes of mild upper GI bleeding, and endoscopy can miss the lesion if it is not actively bleeding. Most
lesions are now treated via endoscopic therapy (injection of
epinephrine or other sclerosants, electrocoagulation, hemoclipping, rubber band ligation, and photocoagulation) or via
angiographic embolization. Surgery is sometimes necessary,
at which time the lesion may be oversewn or resected.
Dieulafoy’s lesions may occasionally be seen in the duode-
58–60
num and jejunum, as well as in the colon.
also been successfully managed via endoscopy or surgery.
ese lesions have
61
DIVERTICULA
Gastric diverticula are typically solitary and may either be
congenital or acquired. Congenital diverticula are rare, true
diverticula that typically occur near the gastroesophageal
junction and are found on the lesser curve or in the posterior
area. ey will demonstrate all three layers of the gastric wall
62
on endoscopic ultrasound.
Acquired or pseudodiverticula
usually have a negligible outer muscle layer and are due to
either pulsion or traction and most are found in the antrum.
Symptoms are due to inammation and may produce pain or
bleeding but perforation is rare. Symptomatic lesions should
be removed and can be done laparoscopically.
Foreign Bodies
Ingested foreign bodies are usually asymptomatic, but
removal of sharp or large objects should be considered to
avoid bleeding, perforation or obstruction. is can usually be done endoscopically. Aspiration of the foreign body
during removal may occur, as well as potential rupture of
drug-containing bags in “body packers.” Both complications
can be fatal. In body packers as well as in patients with large
jagged objects, surgical removal is recommended.
Mallory-Weiss Tear
e Mallory-Weiss lesion is a longitudinal tear in the mucosa
of the GE junction, usually due to forceful vomiting and/or
retching, and is commonly seen in alcoholics. It typically presents with impressive upper GI bleeding. Endoscopy conrms
the diagnosis and may be useful in controlling the bleeding,
but 90% of patients stop bleeding spontaneously. In patients
who continue to bleed, balloon tamponade; angiographic
embolization; or selective infusion of vasopressin, systemic
vasopressin, and surgery are other treatment options. At surgery, the bleeding lesion is oversewn via a long gastrotomy.
VOLVULUS
Gastric volvulus occurs when the stomach twists around one
of its axes, usually seen with a large hiatal hernia. It can also
occur in the unusually mobile stomach without a hiatal hernia.
Typically, the stomach twists along its long axis (organoaxial
volvulus), and the greater curvature ips up. Less frequently, it
occurs around the transverse axis, called mesoaxial volvulus. It
is usually a chronic condition that can be surprisingly asymptomatic and expectant nonoperative management is usually
advised, especially in the elderly. e risk of strangulation and
infarction has been overestimated in asymptomatic patients.
Surgery is recommended for symptomatic patients, especially if these are severe and/or progressive. ese patients
complain of pain and pressure related to the intermittently
distending and poorly emptying twisted stomach. Dyspnea,
palpitations, and dysphagia may be seen due to compressive
eects of the distended stomach on the surrounding organs.
Symptoms are often relieved with vomiting or, if possible, passage of a nasogastric tube. e patient who presents moribund
most likely has an infarcted stomach and is a case of surgical
emergency requiring resection. Elective operation may often
be done laparoscopically and usually involves reduction of the
stomach and repair of hiatal hernia, with or without gastropexy.
Gastropexy alone may be considered for high-risk patients.
GASTROPARESIS
Gastroparesis is a chronic gastric motility disorder dened by
delayed gastric emptying of solids without evidence of mechan-
63
ical obstruction.
Primary gastroparesis aects mostly young
and middle-aged women who present with nausea, abdominal
pain, early satiety, vomiting, fullness, bloating, anorexia, and
weight loss, with nausea and vomiting being the most disquieting of all the symptoms. e condition is diagnosed by symptom assessment and delayed gastric emptying of a solid meal.
Gastric retention of more than 10% of the standard low-fat
meal at 4 hours is indicative of delayed emptying.
Severe gastroparesis might result in recurrent hospitalizations, malnutrition, and signicant mortality. Patients failing
medical therapy are often considered for a variety of surgical
interventions, the ecacy of which is not well studied. ese
procedures include gastrostomy, jejunostomy, gastric pacing/
stimulation, and gastrectomy or surgical drainage procedures.
Completion gastrectomy seems to provide symptom relief in
postsurgical gastroparesis.
64
LAPAROSCOPIC GASTRIC
OPERATIONS
Perhaps the most common laparoscopic gastric operations
performed today are for gastroesophageal reux disease
and obesity. Most of the procedures described in this chapter can be performed with minimally invasive techniques.
460 Part IV Stomach and Duodenum
Some (eg, partial or total gastric resection) are technically
dicult or are of debatable merit (eg, laparoscopic resection
for cancer).
e operations, described previously, that lend themselves
most readily to minimally invasive techniques are highly
selective vagotomy, vagotomy and gastrojejunostomy, and
gastrostomy. Laparoscopic wedge resection, combined with
either intra-operative endoscopic or radiologic localization,
often is possible for most localized, benign lesions such as
lipomas, or gastric diverticula, although the incision required
to retrieve the specimen may be larger than the initial port
65,66
incisions.
niques have also been described.
Combined endoscopic and laparoscopic tech-
67
Diagnostic laparoscopy
may prevent a futile laparotomy in some patients with gastric
cancer. e number as well as the location of ports is determined by triangulating around the target organ, and most
procedures can be performed using four to ve ports. e
benets of laparoscopic surgery (less post-op pain, quicker
recovery, and decreased hospital stay) are all realized without
compromising surgical principles of adequate resection and
tension-free anastomosis.
REFERENCES
1. Marshall BJ, Warren JR. Unidentied curved bacilli in the stomach of
patients with gastritis and peptic ulceration. Lancet. 1984;1:1311–1315.
2. Atherton JC, Blaser MJ. Co-adaptation of Helicobacter pylori and hu-
mans: ancient history, modern implications. J Clin Invest. 2009;119(9):
2475–2487.
3. National Institutes of Health. Helicobacter pylori in peptic ulcer disease.
NIH Consensus Statement. 1994;12:1–18.
4. Suerbaum S, Michetti P. Helicobacter pylori infection. N Engl J Med.
2002;347:1175–1186.
5. Kokoska ER, Kauman GL, Jr. Helicobacter pylori and the gastroduodenal
mucosa. Surgery. 2001;130:13–16.
6. Blaser MJ. Helicobacter are indigenous to the human stomach: duodenal
ulceration is due to changes in gastric microecology in the modern era.
Gut. 1998;43:721–727.
7. Atherton JC. e clinical relevance of strain types of Helicobacter pylori.
Gut. 1997;40:701–703.
8. Gisbert JP, Pajares JP. Stool antigen test for the diagnosis of H pylori infection:
a systematic review. Helicobacter. 2004;9(4):347–368.
9. Malfertheiner P, Megraud F, Bazzoli F, et al. Current concepts in the
management of Helicobacter pylori infection: the Maastricht III Consensus
Report. Gut. 2007;56:772–781.
10. Gisbert JP, Bermejo F, Castro-Fernandez M, et al. Second-line rescue therapy
with levooxacin after H. pylori treatment failure: a Spanish multicenter
study of 300 patients. Am J Gastroenterol. 2008;103:71–76.
11. Lassen AT, Pedersen FM, Bytzer P, et al. Helicobacter pylori test-and- eradicate
versus prompt endoscopy for management of dyspeptic patients: a randomized
trial. Lancet. 2000;356:455–460.
12. Moayyedi P, Soo S, Deeks J, et al. Eradication of Helicobacter pylori for non-
ulcer dyspepsia [review]. Cochrane Database Syst Rev. 2006;2:CD002096.
13. Laine L, Schoenfeld P, Fennerty MB. erapy for Helicobacter pylori in
patients with nonulcer dyspepsia. Ann Intern Med. 2001;134:361–369.
14. Moayyedi, P, Soo S, Deeks J, et al. Eradication of Helicobacter pylori for non-
ulcer dyspepsia [review]. Cochrane Database Sys Rev. 2006;2:CD002096.
15. Logan RPH, Hirschl AM. Epidemiology of Helicobacter pylori infection.
Curr Opin Gastroenterol. 1996;12:1–5.
16. Wang, YR, Ritcher JE, Dempsey DT. Trends and outcomes of hospitaliza-
tions for peptic ulcer disease in the United States, 1993–2006. Ann Surg.
2010;251(1):51–58.
17. Parasher G, Eastwood GL. Smoking and peptic ulcer in the Helicobacter
pylori era. Eur J Gastroenterol Hepatol. 2000;12:843–853.
18. Sontag S, Graham DY, Belsito A, et al. Cimetidine, cigarette smoking, and
recurrence of duodenal ulcer. N Engl J Med. 1984;311:689.
19. Cryer B. Mucosal defense and repair. Gastroenterol Clin North Am.
2001;30:877–894.
20. Peskar BM, Maricic N, Gretzer B, et al. Role of cyclooxygenase-2 in gastric
mucosal defense. Life Sci. 2001;69: 2993–3003.
21. Huang JQ, Sridhar S, Hunt RH. Role of Helicobacter pylori infection
and non-steroidal anti-inammatory drugs in peptic-ulcer disease: a
meta-analysis. Lancet. 2002;359:14–22.
22. Hopkins RJ, Girardi LS, Turney EA. Relationship between Helicobacter
pylori eradication and reduced duodenal and gastric ulcer recurrence: a
review. Gastroenterology. 1996;110:1244–1252.
23. Johnson AG. Proximal gastric vagotomy: does it have a place in the future
management of peptic ulcer? World J Surg. 2000;24:259–263.
24. Klee J, Friess H, Büchler MW. How Helicobacter pylori changed the life
of surgeons. Dig Surg. 2003;20:93–102.
25. Houben MHMG, Van De Beek D, Hensen EF, et al. A systematic review of
Helicobacter pylori eradication therapy—the impact of antimicrobial resistance on eradication rates. Aliment Pharmacol er. 1999;13:1047–1055.
26. Espat NJ, Ong ES, Helton WS, et al. 1990–2001 U.S. General Surgery
chief resident operative experience: analysis of paradigm shift. J Gastroin-
test Surg. 2004;8:471–477.
27. Bustamante M, Stollman N. e ecacy of proton-pump inhibitors in acute
ulcer bleeding. A qualitative review. J Clin Gastroenterol. 2000;30:7–13.
28. Gisbert JP, Calvet X, Faust F, et al. Eradication of Helicobacter pylori for the
prevention of peptic ulcer rebleeding. Helicobacter. 2007;12:279–286.
29. Millat B, Fingerhut A, Borie F. Surgical treatment of complicated duodenal ulcers: controlled trials. World J Surg. 2000;24:299–306.
30. Machicado GA, Jensen DM. ermal probes alone or with epinephrine
for the endoscopic haemostasis of ulcer haemorrhage. Baillieres Best Pract
Res Clin Gastroenterol. 2000;14:443–458.
31. Hepworth CC, Swain CP. Mechanical endoscopic methods of haemostasis
for bleeding peptic ulcers: a review. Baillieres Best Pract Res Clin Gastroenterol.
2000;14:467–476.
32. Spiegel BMR, Vakil NB, Ofman JJ. Endoscopy for acute nonvariceal
upper gastrointestinal tract hemorrhage: is sooner better? Arch Intern Med.
2001;161:1393–1404.
33. Gisbert JP, Khorrami S, Carballo F, et al. H. pylori eradication therapy vs.
antisecretory non-eradication therapy (with or without long-term maintenance antisecretory therapy) for the prevention of recurrent bleeding from
peptic ulcer [review]. Cochrane Database Syst Rev. 2004;2:CD004062.
34. Sharma VK, Sahai AV, Corder FA, et al. Helicobacter pylori eradication is
superior to ulcer healing with or without maintenance therapy to prevent
further ulcer haemorrhage. Ailment Pharmacol er. 2001;15:1939–1947.
35. Leivonen MK, Haglund CH, Nordling SFA. Helicobacter pylori infection
after partial gastrectomy for peptic ulcer and its role in relapsing disease.
Eur J Gastroenterol Hepatol. 1997;9:369–374.
36. Boey J, Wong J, Ong GB. A prospective study of operative risk factors in
perforated duodenal ulcers. Ann Surg. 1982;195:265.
37. Matsuda M, Nishiyama M, Hanai T, et al. Laparoscopic omental patch
repair for perforated peptic ulcer. Ann Surg. 1995;221:236–240.
38. Lau W-Y, Leung K-L, Kwong K-H, et al. A randomized study comparing
laparoscopic versus open repair of perforated peptic ulcer using suture or
sutureless technique. Ann Surg. 1996;224:131–138.
39. Dubois F. New surgical strategy for gastroduodenal ulcer: laparoscopic
approach. World J Surg. 2000;24:270–276.
40. Lagoo S, McMahon RL, Kakihara M, et al. e sixth decision regarding
perforated duodenal ulcer. JSLS. 2002;6:359–368.
41. Donovan AJ, Berne TV, Donovan JA. Perforated duodenal ulcer: an alternative therapeutic plan. Arch Surg. 1998;133:1166–1171.
42. Matsuda M, Nishiyama M, Hanai T, et al. Laparoscopic omental patch
repair for perforated peptic ulcer. Ann Surg. 1995;221:236–240.
43. Gibson JB, Behrman SW, Fabian TC, et al. Gastric outlet obstruction
resulting from peptic ulcer disease requiring surgical intervention is infrequently associated with Helicobacter pylori infection. J Am Coll Surg. 2000
Jul;191(1):32–37.
44. Hogan RB, Hamilton JK, Polter DE. Preliminary experience with hydrostatic balloon dilation of gastric outlet obstruction. Gastrointest Endosc.
1986;32:71.
45. Lamers CBHW, Bijlstra AM, Harris AG. Octreotide, a long-acting somatostatin analog, in the management of postoperative dumping syndrome.
Dig Dis Sci. 1993;38:359.
Chapter 21 Benign Gastric Disorders 461
46. Hiramoto JS, Terdiman JP, Norton JA. Evidence-based analysis: postoper-
ative gastric bleeding: etiology and prevention. Surg Oncol. 2003;12:9–19.
47. Wijdicks EF, Fulgham JR, Batts KP. Gastrointestinal bleeding in stroke.
Stroke 1994;25:2146–2148.
48. Lam N, Lê PD, Crawford S, et al. National survey of stress ulcer prophy-
laxis. Crit Care Med. 1999;27(1):98–103.
49. Pimental M, Roberts DE, Bernstein CN, et al. Clinically signicant
gastrointestinal bleeding in critically ill patients in an era of prophylaxis.
Am J Gastroenterol. 2000;95:2801–2806.
50. Imperiale TF, Chalasani N. A meta-analysis of endoscopic variceal ligation
for primary prophylaxis of esophageal variceal bleeding. Hepatology.
2001;33:802–807.
51. Jalving M, Koornstra JJ, Wesseling J, et al. Increased risk of fundic gland
polyps during long-term proton-pump inhibitor therapy. Aliment Pharm
er. 2006 Nov;24(9):1341–1348.
52. Pinto D, Carrodeguas L, Soto F, et al. Gastric bezoar after laparoscopic
Roux-en-Y gastric bypass. Obes Surg. 2006;16:365–368.
53. Ionescu AM, Rogers AM, Pauli EM, et al. An unusual suspect:
coconut bezoar after laparoscopic Roux-en-Y gastric bypass. Obes Surg.
2008;18:756–758.
54. White NB, Gibbs KE, Goodwin A, et al. Gastric bezoar complicating
laparoscopic adjustable gastric banding and review of literature. Obes Surg.
2003;13:948–950.
55. Erzurumlu K, Malazgirt Z, Bektas A, et al. Gastrointestinal bezoars: a retrospective analysis of 34 cases. World J Gastroenterol. 2005;11(12):1813–1917.
56. Dalshaug GB, Wainer S, Hollaar GL. e Rapunzel syndrome (trichobezoar) causing atypical intussusception in a child: a case report. J Pediatr
Surg. 1999;34(3):479–480.
57. Schmulewitz N, Baillie J. Dieulafoy lesions: a review of 6 years of experience
at a tertiary referral center. Am J Gastroenterol. 2001;96(6):1688–1694.
58. Matuchansky C, Babin P, Abadi JC, et al. Jejunal bleeding from a solitary
large submucosal artery. Gastroenterology. 1978;75(1):110–113.
59. Goldenberg SP, DeLuca VA, Marignani P. Endoscopic treatment of Dieula-
foy’s lesion of the duodenum. Am J Gastroenterol. 1990;85(4):452–454.
60. Barbier P, Luder P, Trinek J, et al. Colonic hemorrhage from a solitary
minute ulcer. Gastroenterology. 1985;88:1065–1068.
61. Meister TE. Varilek GW, Marsano LS, et al. Endoscopic management of
rectal Dieulafoy-like lesions: a case series and review of literature. Gastroin-
test Endosc. 1998;48(3):302–305.
62. Simon M, Zuber-Jerger I, Schölmerich J. True gastric diverticulum. Dig Liver
Dis. 2009;41:370.
63. AGA Clinical Practice Committee. American Gastroenterological Association Technical Review on the Diagnosis and Treatment of Gastroparesis.
Gastroenterology. 2004;127:1592–1622.
64. Jones MP, Kalyani M. A systematic review of surgical therapy for gastroparesis. Am J Gastroenterol. 2003;98(10):2122–2129.
65. Buyske J, McDonald M, Fernandez C, et al. Minimally invasive management
of low-grade and benign gastric tumors. Surg Endosc. 1997;11:1084–1087.
66. Cugat E, Hoyuela C, Rodriguez-Santiago JM, et al. Laparoscopic ultrasound
guidance for laparoscopic resection of benign gastric tumors. J Laparoendosc
Adv Surg Tech A. 1999;9(1):63–67.
67. Omori T, Nakajima K, Ohashi S, et al. Laparoscopic intragastric surgery
under carbon dioxide pneumostomach. J Laparoendosc Adv Surg Tech A.
2008;18(1):47–51.