Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_639_Библиотеки_им_академика_М_И_Перельмана.pdf
This page intentionally left blank
BENIGN GASTRIC DISORDERS
Ian S. Soriano • Daniel T. Dempsey
21
INTRODUCTION
e surgical management of benign gastric disorders has
evolved signi cantly over the past 30 years. Elective surgery
for ulcer disease has largely been abandoned in favor of medical management with surgery being utilized mainly for complications after failed medical treatment. Most elective (and
some emergent) gastric procedures can now be performed
with laparoscopy if local expertise is available, augmented by
either radiologic (mainly via intra-operative ultrasound) or
endoscopic guidance for more accurate localization. ese
techniques can help the surgeon perform a more targeted
resection because wide margins are not necessary.
HELICOBACTER PYLORI INFECTION
When Marshall and Warren elucidated the relationship
between Helicobacter pylori and peptic ulcer disease, a discov-
ery for which they were later awarded the Nobel Prize in Medicine, they rekindled the hypothesis that this common clinical
malady was an infectious disease.
spiral agellated organism that currently infects more than
half of the people in the world. e prevalence of H. pylori
infection varies among populations and is strongly correlated
with socioeconomic conditions. In a number of developing countries, H. pylori infection a ects more than 80% of
middle-aged adults. Infection rates are lower in industrialized
countries. Epidemiological data indicate that the prevalence
of infection in the United States has been declining since
the second half of the 19th century, with the decreases corresponding to improvements in sanitation. Nonetheless, H.
pylori infection is predicted to remain endemic in the United
States for the next century.
Human beings are the only reservoir for H. pylori . Infec-
tion is presumed to occur by oral ingestion of the bacterium. Direct transmission from person to person occurs via
saliva and feces, and infection also occurs through contact
with contaminated water. In developing countries, most
1
H. pylori is a gram-negative
individuals are infected during childhood. Family members
are at increased risk of infection. A number of occupations
also show increased rates of H. pylori infestation, notably
health care workers. Infection with H. pylori is a chronic
disease and does not resolve spontaneously without speci c
treatment.
H. pylori has evidently adapted to the hostile gastric
environment and displays a number of features that permit
its entry into the surface mucus layer, attachment to gastric
epithelial cells, evasion of immune responses, and persistent
colonization despite luminal acidity. Up to 15% of the protein
in a helicobacter organism is composed of cytoplasmic urease
that converts periplasmic urea into CO
latter bu ering the surrounding acid.
and ammonia, the
2
2
Host Response to H. Pylori
H. pylori infestation is followed by continuous gastric in am-
mation in virtually all individuals. Because spontaneous cure is
unusual for most infected individuals, this means that H. pylori
gastritis is a lifelong a iction. Worldwide, H. pylori –induced
gastritis accounts for 80–90% of all gastritis.
H. pylori infection is not invasive of the gastric mucosa,
and the host immune response is triggered by the attachment
of bacteria to surface epithelial cells. e initial in ammatory
response is characterized by recruitment of neutrophils, followed sequentially by T and B lymphocytes, plasma cells, and
macrophages. e resultant chronic gastric in ammation in
a ected individuals is characterized by enhanced expression
of multiple cytokines.
e relationship between H. pylori infection and ulcer-
ation is overwhelmingly strong; multiple observations establish H. pylori as a factor in the pathogenesis of duodenal
ulceration.
vaccine has not yet been developed.
pathogenesis of human duodenal ulceration include the
following:
3–7
Most of the evidence is inferential. An e ective
Observations that support H. pylori as a factor in the
443
443
444 Part IV Stomach and Duodenum
1. H. pylori infection is invariably followed by the development
of chronic gastritis, and the organism is the primary cause of
chronic active gastritis worldwide. e infectious response
to H. pylori is characterized by nonerosive in ammation of
the gastric mucosa. Antral gastritis is present histologically in
patients with duodenal ulcer, and H. pylori can be isolated
from gastric mucosa of ulcer patients.
2. H. pylori binds only to gastric-type epithelium. Gastric
metaplasia of the duodenal bulb is a nonspeci c response
to damage, which develops after infestation of the gastric
mucosa. Antral gastritis with H. pylori is preceded by active
chronic duodenitis. Metaplastic gastric epithelium is colonized by H. pylori from gastric sources. Gastric metaplasia
is extremely common in duodenal epithelium surrounding areas of ulceration.
3. Eradication of H. pylori with antibiotics that have no e ect
on acid secretion leads to ulcer healing.
4. erapy of peptic ulceration with bismuth compounds,
which eradicate H. pylori , is associated with reduced rates
of ulcer relapse relative to acid suppression therapy.
5. Relapse of duodenal ulcer after eradication of H. pylori
is preceded by reinfection of the gastric mucosa by the
organism.
However, infection by H. pylori alone does not cause peptic
ulceration in most individuals, suggesting the existence of other
pathogenetic factors. Half of patients evaluated for dyspepsia
have histologic evidence of bacterial infection. In developed
countries, one- fth of healthy volunteers harbor the bacteria,
and the incidence of bacterial infestation increases with age in
the healthy, asymptomatic population. e occurrence of peptic
ulcers in only a fraction of individuals who harbor the organism
suggests that other factors must also act to induce ulceration.
H. pylori infection can be diagnosed by both invasive and non-
invasive means. Noninvasive methods include the urea breath
test, serology, and detection of antigen in stool samples. e urea
breath test is based on production of urease by H. pylori in the
14
gastric mucosa. C
-labeled urea is ingested and C 14 -labeled CO 2
is produced and excreted in the breath. is test has a sensitivity and speci city of greater than 90% and indicates ongoing
infection. e urea breath test is useful for initial diagnosis of
infection and for follow-up after eradication therapy.
e stool antigen test is another noninvasive test to detect
both initial H. pylori infection as well as response to treatment.
Both polyclonal and monoclonal kits have been developed.
Likewise, di erent kits are available for both out- and inpatient settings. Overall results have been comparable to those
8
obtained using the urea breath test method.
Because H. pylori induces a strong immunologic response,
serological testing is useful but may not be as accurate as the
urea breath test or the stool antigen test. Validation with
either of the two tests is recommended. It may be used for
epidemiologic studies. Because H. pylori –induced serology
does not return to normal after bacterial eradication, this test
is not reliable in monitoring therapy.
H. pylori infection can also be diagnosed on the basis of
biopsies in patients undergoing upper endoscopic examination.
Individuals older than 50 years, or those with signi cant symptoms including gastrointestinal (GI) bleeding, anemia, and
weight loss, should undergo endoscopic diagnosis. During
endoscopy, antral biopsies can be obtained and the organism
cultured in agar containing both urea and a pH-sensitive colorimetric agent. H. pylori hydrolysis of urea causes a diagnostic
change in color. e sensitivity of this test varies from 80 to
100% and speci city exceeds 90%. e test is associated with
false-negative results in patients with active or recurrent bleeding and in those taking antibiotics or antisecretory compounds.
Biopsy also permits histologic examination with visualization
of the organism. Culture of H. pylori is not routine and is usu-
ally reserved for recurrent infection and for antibiotic sensitivity testing when second-line therapy has failed.
Complete eradication of H. pylori infection is the goal of
treatment, and recurrence of disease signi es reinfection in
most circumstances. An enormous worldwide experience has
developed relating to H. pylori eradication. More than 2000
articles report the results of antibiotic trials, and a large number of summary articles and meta-analyses are available. It
is important to note that none of the therapeutic regimens
reported to date cure H. pylori infection in 100% of patients.
To be e ective, antimicrobial drugs must be combined with
gastric acid secretion inhibitors or bismuth salts.
In the absence of treatment, eradication of H. pylori infec-
tion is very rare. ree consensus conference meetings as well
as numerous clinical guidelines in various regions have been
published in the past decade to further de ne the approach to
diagnosis and treatment of H. pylori . e Maastricht III Con-
sensus Report brought together a multidisciplinary group in
2007 from around the world to publish an update on the
initial guidelines published in 1996 (known then as the European Helicobacter Study Group) and subsequently revised in
2000 after including a review of published guidelines from
9
North America, Europe, China, and Japan ( Table 21-1 ).
Current evidence indicates that eradication therapy with
a proton pump inhibitor, metronidazole, and amoxicillin
TABLE 21-1: FIRST CHOICE TREATMENT
FOR
H. PYLORI
1. For PPI (standard dose BID) clarithromycin (500 mg BID),
amoxicillin (1000 mg BID), or metronidazole (400 or 500 mg
BID), 14-d treatment is more e ective than that of 7-d by 12%
(95% con dence interval 7–17%). A 7-d treatment may be
acceptable where local studies show that it is e ective.
2. PPI-clarithromycin-amoxicillin or metronidazole treatment is
the recommended rst-choice treatment in populations with
<15–20% clarithromycin resistance. In populations with < 40%
metronidazole resistance, PPI-clarithromycin-metronidazole
is preferable. Quadruple treatments are alternative rst-choice
treatments.
3. e same rst-choice H. pylori treatments are recommended
worldwide, although di erent doses may be appropriate.
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.
INFECTION
Chapter 21 Benign Gastric Disorders 445
decreases the prevalence of metronidazole-resistant H. pylori
strains. e prevalence of clarithromycin-resistant strains
varies greatly from country to country, with the highest rates
reported in southern Europe. In this region, clarithromycin
resistance now approximates 15%. is rate is predicted to
rise over the next several years with increasing use of macrolide
antibiotics. In patients failing therapy, culture of H. pylori
from gastric mucosa is possible for resistance testing. Also, a
recent multicenter trial in Spain demonstrated that a 10-day
regimen of levooxacin (500 mg BID), amoxicillin (1 g
BID), and omeprazole (20mg BID) had 97% compliance
13
and 77% eradication based on a negative
done 4–8 weeks after completion of therapy.
C urea breath test
10
NONULCERATIVE DYSPEPSIA
Dyspepsia is a very common symptom complex that is
characterized by pain and discomfort centered in the upper
abdomen. Dyspepsia is among the most common disorders
encountered by primary care physicians and gastroenterologists
in the United States and Western countries. It is estimated
that approximately 25% of the population will experience
dyspepsia and that this problem accounts for 5% of visits to
primary care providers.
Dyspepsia is characterized by symptoms that are focused in
the upper abdomen. Symptoms may include heartburn, but a
symptom complex limited to this complaint suggests gastroesophageal reux disease and excludes the diagnosis of dyspepsia. Nonulcerative dyspepsia is considered when no anatomic
or biochemical abnormality is discovered that explains the
patient’s symptoms. is common disorder is not associated
with increased morbidity or mortality. However, it is generally
long lasting and responsible for impaired quality of life. Investigation of nonulcerative dyspepsia and its treatment represent a
large economic burden. Optimal treatment is controversial.
Since the description of H. pylori as a cause of gastritis, its
association with nonulcerative dyspepsia has been disputed.
H. pylori infestation is always associated with histologic gastritis, but may be absent in cases of nonulcerative dyspepsia. A large number of studies have reported the ecacy of
therapy for H. pylori infection on symptoms of nonulcerative
11–13
dyspepsia.
A recent Cochrane review of the literature
showed a small but statistically signicant eect of H. pylori
treatment in nonulcer dyspepsia but recommended further
research before making any denitive recommendations.
14
For surgeons, the importance of nonulcerative dyspepsia
relates to its place in the dierential diagnosis of epigastric pain.
ere is no role for surgery in the treatment of this disorder.
PEPTIC ULCER DISEASE
Epidemiology
Peptic ulcer disease is a major public health problem in the United
States and a source of substantial health care expenditure.
15
Overall, peptic ulcer mortality and hospitalization rates have
declined for the past two decades from over 200,000 admissions
in 1993 down to a little over 150,000 in 2006. Hemorrhage
continues to be the most frequent presentation at admission,
followed by perforation and obstruction. A signicant shift was
also seen in the management of ulcer hemorrhage from surgery
(21% decrease) to endoscopy (59% increase). Although overall
mortality rates decreased slightly (2.7%, down from 3.8%), no
change was seen in the determinants of mortality, with perforation still being associated with the highest mortality, followed
by obstruction and then bleeding. e mortality from surgical
intervention decreased over the time period but remains high
compared to endoscopy and embolization.
16
In parallel with the discovery of H. pylori and the subse-
quent development of improved therapies for its eradication,
surgical treatment of peptic ulcer has changed dramatically,
with the virtual elimination of elective operations for ulcer
disease. Operative therapy is now used mostly for emergent
treatment of complicated disease. Antibiotics have become
primary antiulcer therapy with the realization that, in most
cases, peptic ulceration is an infectious disease. A wide variety
of antisecretory drugs are available for clinical practice. Endoscopic and surgical therapies are frequently integrated in the
care of individual patients.
Pathophysiology
e pathogenesis of peptic ulceration is multifactorial but
increasingly understood to be a consequence of H. pylori
infection. Before the recognition of the role of H. pylori, ulcer
disease was conceived as an imbalance between acid and pepsin
secretion and mucosal defense, with the balance shifted toward
peptic injury and disease. In groups of patients, increases in
acid secretion are well-documented, and, although gastric acid
is crucial in the development of ulcers, an acquired defect in
mucosal defense exists to tip the balance away from health.
Mucosal infestation with H. pylori is the factor that contributes
to ulceration in most patients; nonsteroidal anti-inammatory
drug (NSAID) use is the second most important factor in
ulcer pathogenesis.
OTHER FACTORS
Substantial evidence implicates cigarette smoking as an additive
risk factor in the development of duodenal ulcers. Smokers
appear to have an increased risk of developing H. pylori infection
relative to nonsmokers. Cigarette smoking impairs ulcer healing and increases the risk of recurrent ulceration. Continued
smoking blunts the eectiveness of active ulcer therapy. Cigarette smoking increases both the probability that surgery will
be required and the risks of operative therapy. When H. pylori
is eradicated in smokers, they appear to have no greater risk of
peptic ulceration than nonsmokers.
gests that smoking is probably not an independent risk factor
for ulcer disease but acts by increasing the harmful eects of
17,18
is observation sug-
446 Part IV Stomach and Duodenum
bacterial infection. Cessation of smoking is a key goal of antiulcer therapy.
Abnormalities of gastric acid secretion in patients with peptic
ulceration have been recognized for more than 50years. e formation of duodenal ulcers clearly depends on gastric secretion
of acid and pepsin. is association is emphasized by the dictum
“no acid-no ulcer.” H. pylori infection is now known to secondarily induce alterations in gastric acid secretion as a prerequisite
for ulcer development, and a more complete and accurate statement might be “no acid and no H. pylori–no ulcer.”
Abnormalities of mucosal function have been invoked as
contributing factors to peptic injury. In support of this concept, several agents that are used to treat peptic ulceration are
cytoprotective. Cytoprotective agents inhibit mucosal injury
at concentrations lower than threshold doses that suppress
19
acid secretion.
e ability of such agents to heal ulcers suggests that abnormalities in mucosal defense, in addition to
abnormalities in acid secretion, cause ulceration. Most cytoprotective agents act via mucosally secreted bicarbonate or on
mucosal prostaglandin production.
NSAIDs are a major risk factor for the development of
acute ulceration and for hemorrhagic complications of ulceration. NSAIDs produce a variety of lesions, ranging from
supercial mucosal erosions to deeper ulcerations. While the
mucosal injury caused by NSAIDs is more common in the
stomach than in the duodenum, ulcer complications occur
with equal frequency in these two sites. H. pylori and NSAID
use independently increase the risk of peptic ulcer and ulcer
bleeding. ese agents also act synergistically. In the duodenum, it appears likely that invasive H. pylori– associated ulcers
are compounded by the direct injurious eects of NSAIDs.
e injurious actions of NSAIDs are secondary to systemic
suppression of prostaglandin production. Numerous experimental models have demonstrated that NSAIDs injure the gastroduodenal mucosa. Ulcers resembling those occurring in humans
can be produced by administration of NSAIDs to animals, and
NSAID-associated gastric ulcers can be prevented by the coadministration of prostaglandin analogues. Ulcers associated with
NSAIDs heal rapidly when the drug is withdrawn, corresponding temporally to reversal of antiprostaglandin eects.
None of the currently available NSAIDs are free of the
19
hazard of gastroduodenal ulceration.
Clinically signicant
ulceration of the stomach and duodenum is estimated to occur
at a rate of 2–4% per patient-year. e risks of long-term
NSAID use are increased by H. pylori infection and cigarette
smoking. e incidence of NSAID-related ulcer complications is highest in older patients, as is attendant mortality rate.
Peptic ulcer disease is rare in individuals who are H. pylori–
negative and who do not receive NSAID medications.
20
head of the pancreas, referral of pain to extra-abdominal sites
is not common. Many patients report that pain is worsened by
fasting. Ingestion of antacids usually provides prompt relief. In
uncomplicated cases, physical examination is usually normal.
e dierential diagnosis includes a variety of diseases
originating in the epigastrium and upper GI tract. Common disorders to be distinguished include nonulcer dyspepsia, gastritis,
gastric neoplasia, cholelithiasis and related diseases of the biliary
system, neoplastic lesions of the liver, and both inammatory
and neoplastic disorders of the pancreas. In dyspeptic patients,
especially those older than 50 years of age, the most important
dierential diagnoses are peptic ulceration and gastric cancer.
e evaluation of patients with suspected peptic ulceration
usually involves endoscopic examination of the esophagus,
stomach, and duodenum. In most circumstances, contrast
radiography is not the preferred initial diagnostic method; endoscopy has become the standard to which other modalities are compared. Endoscopy eliminates the need for radiation, is safe, is tolerated by elderly patients, and permits both visual inspection and
biopsy of the esophagus, stomach, and duodenum. In controlled
trials, endoscopy was both more sensitive (92 vs 54%) and more
21
specic (100 vs 91%) than radiographic examination.
Endoscopy must be utilized with discretion because of the potential for
perforation (approximately 1 per 5000 cases) and cost.
Endoscopically, duodenal ulceration is characterized by
lesions that are erosive to the intestinal wall. When viewed
endoscopically, peptic ulcers have a typical appearance, with
edges that are usually sharply demarcated. e ulcer consists
of the exposed underlying submucosa. With chronic ulcers,
the base is usually clean and smooth. Acute ulcers and ulcers
with recent hemorrhage may demonstrate clot, eschar, or
adherent exudate. e surrounding duodenal mucosa may be
friable, but marked inammation is uncommon. e most
frequent site for peptic ulceration is the rst portion of the
duodenum, with the second portion less frequently involved.
Peptic ulceration of the third or fourth portions of the duodenum is distinctly unusual; occurrence of ulcers in these locations raises the possibility of gastrinoma. Peptic ulcers in the
pyloric channel or the prepyloric area are similar in appearance to duodenal ulcers. Endoscopic demonstration of a
duodenal ulcer does not require duodenal biopsy but should
prompt mucosal biopsy of the gastric antrum to demonstrate
the presence of H. pylori and guide subsequent therapy.
Contrast radiographs demonstrate retention of contrast
within the ulcer. When viewed tangentially, the ulcer projects
beyond the level of the duodenal mucosa. Distortion of the
duodenal bulb by spasm or scarring is a secondary sign of
current or previous ulceration.
Diagnosis
Duodenal ulceration is characterized by epigastric pain. e pain
is usually localized to the upper abdomen without radiation and
is described as burning, stabbing, or gnawing. In the absence
of complications such as perforation or penetration into the
OPERATIVE TREATMENT OF
ULCER DISEASE
e realization that peptic ulceration is an infectious disease has
fundamentally altered the role of surgery in ulcer treatment.
Indications for operative intervention have changed over the
past 20 years as a consequence, with the virtual elimination of
22,23
Chapter 21 Benign Gastric Disorders 447
elective operations.24 Operative intervention is now reserved for
the treatment of complicated ulcer disease. ree complications
are most common and constitute contemporary indications for
peptic ulcer surgery: hemorrhage, perforation, and obstruction.
Evolving indications are also reected in the forms of operative
therapy and in surgical training experience.
25,26
e rst goal of current surgical therapy is treatment of anatomic complications, such as pyloric stenosis or perforation. e
second major goal should be patient safety in the acute setting,
combined with freedom from undesirable chronic side eects.
e third goal in contemporary surgical treatment of complicated ulcer disease should be alteration of the ulcer diathesis so
that ulcer healing is achieved and recurrence is minimized. To
achieve these goals, the gastric surgeon can combine therapy
through endoscopic, radiologic, or operative means, the appropriate choice depending on the clinical circumstances.
Operative Procedures
ere is currently no indication for surgical treatment of uncomplicated ulcer disease. A number of operative procedures have
been developed to treat peptic ulcer but have been used with
decreasing frequency in the past decade. Operative treatment
of gastric outlet obstruction has decreased by approximately
50%. e majority of surgical patients are currently treated
emergently for the complications of bleeding or perforation.
Truncal vagotomy and drainage, truncal vagotomy and antrectomy, and proximal gastric vagotomy are the most widely
utilized procedures in the operative treatment of peptic ulcer
disease. However, surgical therapy of complicated peptic ulcer
disease is directed increasingly at correction of the immediate
problem without gastric denervation. e underlying cause of
the ulcer diathesis may then be addressed after recovery from
surgery by antibiotic therapy directed at H. pylori and by longterm acid suppression therapy. is approach is applicable to
most patients with peptic ulcer undergoing emergent operation
and is also reected by the fact that the use of gastrectomy and
vagotomy has decreased signicantly from 4.4 to 2.1% (gastrectomy) and 5.7 to 1.7% (vagotomy) over the last two decades.
Transection of both vagal trunks at the esophageal hiatus, termed truncal vagotomy, denervates the acid-producing
fundus of the stomach. e procedure also denervates the
remainder of the supplied viscera, including the liver and
biliary tree, pancreas, small bowel, and colon to the midtransverse portion. Because denervation impedes normal pyloric
coordination and impairs gastric emptying, truncal vagotomy
is usually combined with a procedure to eliminate or bypass
pyloric sphincter function. A pyloroplasty or gastrojejunostomy is performed for gastric drainage.
Several methods of pyloroplasty have been developed. e
Heineke-Mikulicz pyloroplasty (Fig. 21-1) consists of a longitudinal incision of the pyloric sphincter extending into the
antrum and the duodenum. e incision is closed transversely,
eliminating sphincteric closure and increasing the lumen of
the pyloric channel.
e Finney pyloroplasty (Fig. 21-2) extends the pyloric
incision 5 cm onto the duodenal wall forming an inverted
16
A
B
C
D
FIGURE 21-1 Heinecke-Mikulicz pyloroplasty. (Redrawn with permission
from Zinner MJ. Atlas of Gastric Surgery. New York, NY: Churchill Livingstone; 1992.
Illustrated after Gwynne Gloege.)
448 Part IV Stomach and Duodenum
Approximation suture
Pylorus
Gallbladder
Duodenum
Inverted
incision
Stomach
A
through & through
suture (1st ant. tier)
C
Connell
Stomach
Posterior
through &
through suture
B
FIGURE 21-2 Finney pyloroplasty (
Abdominal Operations. 10th ed. London, UK: Prentice Hall Inc.; 1997:Chap. 13.)
From Soybel DI, Zinner MJ. Stomach and duodenum: operative procedures. In: Zinner MJ, Schwartz SI, Ellis H, eds. Maingot’s
Duodenum
Cushing
seromuscular
suture (2nd ant. tier)
D
Chapter 21 Benign Gastric Disorders 449
U-shaped incision after the placement of superior and inferior
traction sutures. Once traction is applied, the two limbs of
the inverted U-shaped incision are lined up and sutured to
each other to complete the procedure, with the inferior suture
line forming the posterior wall and the superior suture line
forming the anterior wall of the pyloroplasty.
A Jaboulay gastroduodenostomy (Fig. 21-3) requires
more extensive dissection beginning with a Kocher maneuver
followed by corresponding incisions on the stomach and the
duodenum proximal and distal to the pylorus respectively.
Traction sutures are then placed between the stomach and
duodenum to approximate the two incisions, and the anastomosis is then performed.
FIGURE 21-3 Jaboulay gastroduodenostomy.
450 Part IV Stomach and Duodenum
Truncal vagotomy can be combined with resection of the
gastric antrum to further reduce acid secretion by removing
antral sources of gastrin. e limits of antral resection are
dened by external landmarks. e stomach is divided proximally along a line from a point above the incisura angularis to
a point along the greater curvature midway from the pylorus
to the gastroesophageal junction. Reconstruction via a gastroduodenostomy is called a Billroth I procedure. A Billroth II
procedure uses a gastrojejunostomy to restore GI continuity.
Proximal gastric vagotomy, also termed highly selective vag-
otomy (HSV), diers from truncal vagotomy in that only the
nerve bers to the acid-secreting fundic mucosa are transected
(Fig. 21-4). e hepatic and celiac divisions are not divided,
and vagal nerve bers to the antrum and pylorus remain
intact. e operation has also been called parietal cell vagotomy to emphasize the intended functional consequence.
Proximal gastric vagotomy is a safe operation. e procedure has a reported operative mortality rate of less than 0.05%,
lower than the reported mortality for any other gastric procedure for peptic ulcer. Truncal vagotomy and pyloroplasty has
an accepted mortality rate of 0.5–0.8%, whereas mortality
6–8 cm
7 cm
FIGURE 21-4 Technique of proximal gastric vagotomy. e distal
6 cm of the esophagus is skeletonized. Denervation spares the antrum
and pylorus by stopping 7 cm proximal to the pylorus.
with permission from Holle F, Anderson S. Vagotomy: Latest Advances. New York:
Springer; 1994.)
(Reproduced
after truncal vagotomy and antrectomy approximates 1.5%.
ese statistics require an important caveat; almost all large
series report the results of elective operations on patients with
peptic ulceration and may not accurately reect expected
results when similar procedures are performed emergently.
Postoperative Alterations
Division of vagal nerve bers alters gastric acid secretion by
reducing cholinergic stimulation of parietal cells. Vagal denervation also decreases parietal cell responsiveness to gastrin
and histamine. Basal acid secretion is diminished by approximately 80% in the immediate postoperative period and is
maintained over time. e maximal acid output in response
to secretagogues such as pentagastrin is reduced by approximately 70%. After 1 year, pentagastrin-stimulated maximal
acid output increases to 50% of prevagotomy values but
remains at this level on subsequent testing. Acid secretion due
to meal stimulation is reduced by 60–70% relative to normal
subjects. e inclusion of antrectomy to truncal vagotomy
further reduces acid secretion. Maximal acid output is reduced
by 85% relative to values recorded before antrectomy.
Both forms of vagotomy cause postoperative hypergastrinemia. Fasting gastrin values are increased to approximately
twice preoperative levels. Postprandial gastrin response is
exaggerated. Hypergastrinemia is due to decreased luminal acid, with loss of feedback inhibition of gastrin release.
Chronic hypergastrinemia is caused by mucosal gastrin
cell hyperplasia in addition to loss of inhibitory feedback.
When antrectomy is performed, circulating gastrin levels are
decreased. Basal gastrin values are reduced by approximately
half and postprandial gastrin levels by two-thirds.
Operations that involve vagotomy aect gastric emptying. Both truncal vagotomy and proximal gastric denervation
abolish vagally mediated receptive relaxation that normally
allows the ingestion of a meal with no increase in intragastric pressure. After vagotomy, the intragastric pressure rise is
greater for any given volume ingested, and the gastroduodenal
pressure gradient higher than in normal subjects. As a result,
emptying of liquids, which depends on the gastroduodenal
pressure gradient, is accelerated. Because nerve bers to the
antrum and pylorus are preserved with proximal gastric vagotomy, the function of the distal stomach to mix solid food is
preserved and emptying of solids is nearly normal. Truncal
vagotomy aects the motor activity of the distal stomach, and
solid and liquid emptying rates are usually increased when
truncal vagotomy is accompanied by pyloroplasty.
Dumping is dened by a postprandial symptom complex
of abdominal discomfort, weakness, and vasomotor symptoms of sweating and dizziness. Dumping occurs transiently
in 10–15% of patients after truncal vagotomy and antrectomy
and is persistent in 1–2%. Dumping is present initially in 10%
of patients undergoing truncal vagotomy and pyloroplasty, and
remains in approximately 1%. Permanent symptoms of dumping are unusual after proximal gastric vagotomy. e incidence
of diarrhea, presumably caused by denervation of the pylorus
Chapter 21 Benign Gastric Disorders 451
and small bowel and by elimination of pyloric function, parallels the incidence of dumping when truncal vagotomy is performed. Persistent and disabling diarrhea is present in fewer
than 1% of patients after proximal gastric vagotomy.
e largest surgical series examining ulcer recurrence rates
were reported at a time before the pathogenic role of H. pylori
was appreciated. With appropriate use of antibiotics directed
against H. pylori , ulcer recurrence rates as low as 0.22% have
27
been reported.
Although recurrence rates (without H. pylori
treatment) as low as 5% have been reported, a more generally representative gure is 10%. is rate is similar to that
of reinfection with H. pylori after successful eradication.
Ulcer recurrence rates after proximal gastric vagotomy can be
adversely a ected by the inclusion of prepyloric and pyloric
channel ulcers. Proximal gastric vagotomy is signi cantly less
e ective when used to treat ulcers in this position than when
used for duodenal ulceration.
Ulcer Hemorrhage
Hemorrhage continues to be a major source of morbidity
in patients with peptic ulceration. Bleeding is the leading
cause of death associated with peptic ulcer. e incidence of
hemorrhage has not changed since the introduction of H
23
receptor antagonists.
e lifetime risk of hemorrhage for
patients with duodenal ulcer who do not undergo speci c
therapy approximates 35%. Hemorrhage usually occurs during the initial episode of ulceration or during relapse; patients
who have bled previously have a higher risk of bleeding again.
Patients with recurrent bleeding and elderly patients are at
25,
greatest risk of death.
28
e risk of mortality from bleeding peptic ulcer is surprisingly high at 10–20%. When surgery is necessary, operative
risk is increased in patients who have shock at admission,
recurrent bleeding, delay in operative intervention, or comorbid illnesses. Surgical delay leads to recurrent hypovolemia
and subsequently multisystem organ failure.
Upper GI endoscopy is the appropriate initial diagnostic
test, following resuscitation, when hemorrhage from ulceration is suspected. Endoscopy identi es the site and source
of bleeding in over 90% of patients. An ulcer should be
accepted as the bleeding source only if it exhibits stigmata
of active or recent hemorrhage ( Table 21-2 ). Active hemorrhage is de ned by an arterial jet, active oozing, or oozing
beneath an adherent clot. Signs of recent hemorrhage include
adherent clot without oozing, adherent slough in the ulcer
base, or visible vessel in the ulcer. Up to 30% of patients
who have stigmata of recent hemorrhage experience rebleeding, and most of the patients who bleed recurrently require
emergency treatment. e signs are not su ciently accurate,
nor are rebleeding rates high enough, to be indications for
surgery. Endoscopic stigmata indicate that aggressive therapy
is needed and close follow-up mandatory. e occurrence of
hypovolemic shock, rebleeding during hospitalization, and a
posteroinferior location of the ulcer are clinical features that
are associated with increased risk of recurrent bleeding. Acute
-
2
TABLE 21-2: ULCER STIGMATA AND
REBLEEDING IN PEPTIC ULCERS
Prevalence (%) Rebleeding (%)
Active arterial bleeding 12 88
Nonbleeding visible vessel 22 50
Nonbleeding at clot 10 33
Oozing 14 10
Nonbleeding at spots 10 7
Clean ulcer base 32 3
Machicado G. ermal probes alone or with epinephrine for the endoscopic
haemostasis of ulcer haemorrhage. Baillières Clin Gastroenterol . 2000;14:442–458.
reduction of acid secretion by H
-receptor antagonists or
2
proton pump inhibitors is not su cient to prevent recurrent
hemorrhage. However, the continuous infusion of proton
26
pump inhibitors has been shown to decrease rebleeding.
e ability to visualize bleeding duodenal ulcers endoscopically permits endoscopic treatment. Methods of
endoscopic therapy include thermal coagulation by bipolar
electrocoagulation or direct application of heat through a
29
heater probe.
Injection of epinephrine into the base of the
bleeding ulcer is also an established method to control ulcer
hemorrhage.
Both reduced rebleeding rates and avoidance of operation
29,
have been demonstrated for endoscopic hemostasis.
30 Proof
of e cacy for endoscopic treatment of hemorrhage is complicated by the 70% rate of spontaneous, sometimes temporary,
cessation of bleeding without intervention ( Table 21-3 ). In
addition to endoscopic stigmata, hemodynamic instability,
continuing transfusion requirements, red stool or hematemesis, age older than 60 years, and medical comorbidity are
clinical features that mandate endoscopic therapy. Rebleeding
during hospitalization and the endoscopic ndings of visible
vessel, oozing, or bleeding associated with an adherent clot
are also indications for endoscopic hemostasis. Ulcers with
clean bases and no stigmata of recent hemorrhage require no
treatment.
Failure of endoscopic treatment is usually due to inaccessibility
of the ulcer that is caused by pyloric scarring, rapid active bleeding, or an obscuring clot. Patients treated endoscopically should
be observed closely for further hemorrhage. ose who rebleed
within 72 hours of initial endoscopic control may be success-
30
fully retreated without increased risk of mortality.
TABLE 21-3: FAILURE RATES FOR
ENDOSCOPIC HEMOSTASIS
Rebleed (%) Urgent Surgery (%) Mortality (%)
0–40 0–32 0–16
Data from Lundell L. Upper gastrointestinal hemorrhage—surgical aspects. Dig Dis .
2003;21:16–18.