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World J. Surg. 24, 299 –306, 2000
DOI: 10.1007/s002689910048 WOR L D
Journal of
SURGERY
© 2000 by the Socie´te´
Internationale de Chirurgie
Surgical Treatment of Complicated Duodenal Ulcers: Controlled Trials
Bertrand Millat, M.D.,
1
Abe Fingerhut, M.D.,
2
Frede´ric Borie, M.D.
1
1
Hoˆpital St. Eloi, Rue Bertrand Sans, 34295 Montpellier, France
2
Centre Hospitalier Intercommunal, Rue du Champs Gaillard, 78303 Poissy, France
Abstract. Indications for surgery of duodenal ulcer (DU) have changed
radically because of the efficacy of H
2
-antagonists, endoscopic procedures,
and eradication of Helicobacter pylorus. The aim of this study was to
analyze the current literature to determine if definitive surgery is still
relevant for complicated DU (bleeding, perforation, gastric outlet ob-
struction). Two studies have compared early to late surgery in terms of
bleeding. One recommended early surgery (significant reduction in mor-
tality) in the elderly, but no statistically significant difference was found
when analyzed with “intention to treat.” In the other, mortality with early
surgery was five times higher than with expectant therapy (when it was
possible). Two studies comparing different surgical techniques for bleed-
ing favored the radical procedure. Of at least 15 studies comparing
endoscopic treatments, however, none has compared endoscopic therapy
to surgical intervention for bleeding DU. One trial, comparing nonopera-
tive to surgical treatment for perforation, found similar rates of morbid-
ity, intraabdominal abscess, and mortality; but the hospital stay was
longer (p < 0.001). Nonoperative treatment failed more often (p < 0.05)
in patients over age 70. In three trials, postoperative morbidity (excepting
wound sepsis in one) was not significantly increased by definitive surgery,
with less ulcer recurrence (p < 0.05) compared with simple closure.
Laparoscopy (versus laparotomy) was shown to take longer (p < 0.001)
but required less postoperative analgesics (p < 0.03); there were no
statistically significant differences as concerns the duration of nasogastric
aspiration, intravenous drips, hospital stay, time to resume normal diet,
Visual Analogous Scale pain scores for the first 24 hours after surgery,
morbidity, reoperation rate, or mortality. Of 48 laparoscopic patients, 11
(23%) underwent conversion to open surgery. Three surgical techniques
[highly selective vagotomy (HSU) ⴙ gastrojejunostomy (group 1), HSV ⴙ
Jaboulay gastroduodenostomy (group 2), or selective vagotomy (group
3) ⴙ antrectomy) for gastric outlet obstruction (GOO)] showed that
although postoperative results were similar (except wound sepsis in one
trial), long-term Visick scores were significantly (p < 0.01) better in group
1 than in group 2, but not in group 3. Further studies are needed to
determine the exact prevalence of Helicobacter pylori in complicated DU
and to compare (1) definitive to minimal surgery (stop the bleeding or
close the perforation) combined with antisecretory drugs and eradication
of H. pylori; (2) surgery to endoscopic treatment combined with eradica-
tion of H. pylori; and (3) for GOO, surgery to balloon dilatation combined
with eradication of H. pylori.
Peptic ulceration is an infectious disease. Helicobacter pylori, a
motile flagellar bacillus that dwells in the mucous layer of the
stomach, is found in more than 90% of patients with duodenal
ulcer (DU). When the bacteria are eradicated, ulcer recurrence is
dramatically reduced [1].
Complications of peptic ulcer disease are seen in an estimated
11% of patients [2]. Indications for surgery of DU have changed
radically during the last decades, essentially because of the efficacy
of antisecretory drugs [3]. As several controlled trials have deter-
mined that radical or definitive surgical treatment was indicated
for bleeding or perforated duodenal ulcers, and as new pathogenic
aspects of peptic ulceration (H. pylori infection) surface, a new
outlook is needed. The aim of this report was to determine if the
results of these controlled surgical trials are still relevant in view
of the infective pathogenesis of peptic ulceration.
Bleeding Peptic Ulcers
Upper gastrointestinal (GI) bleeding, occurring at an annual in-
cidence estimated at 100 per 100,000 people [4], is often a life-
threatening emergency with a 10% mortality rate [5] despite
modern advances in endoscopic and pharmacologic intervention.
Persistent or recurrent bleeding, occurring in 20% to 33% [6] of
patients, is associated with a mortality rate between 10% and 14%
when rebleeding occurs without treatment and 10% and 44%
when rebleeding occurs despite treatment [7].
Alternative to Surgical Treatment: Endoscopic Hemostasis
Approximately 80% of patients with clinically probable peptic
ulcer bleeding stop bleeding spontaneously [8]; surgical or endo-
scopic intervention is not necessary for these patients. On the
other hand, another 80% of patients with active bleeding at
endoscopy continue to bleed or rebleed in hospital [9], and 50%
of those who have a nonbleeding visible vessel also rebleed [9].
Endoscopic injection treatment stops active bleeding and prevents
further hemorrhage in most of these patients. The mechanism of
action is heterogeneous, comprised of tamponade, vasoconstric-
tion, sclerosis, tissue dehydration, and thrombogenesis; sub-
stances injected include epinephrine, sclerosants, alcohol, throm-
bin, or a combination thereof. Although trials often define the
need for surgery as the result of injection treatment failure, an
alternative view is that endoscopic control may facilitate safe,
early elective surgery [9]. No studies to date have compared
surgery with endoscopic therapy.
In 1995 the cumulative meta-analysis by Lau et al. [10] was
highly in favor of the reduction of overall mortality by endoscopic
treatment of upper GI hemorrhage. Kubba and Palmer reviewed
Correspondence to: A. Fingerhut, M.D.
the literature on controlled trials of endoscopic injection therapy
for bleeding peptic ulcer in 1995 [9]. Epinephrine was used with
success for the first time by Chung et al. [11]. Four studies
compared epinephrine plus sclerosant versus conservative treat-
ment in nearly 300 patients [12–15], and all four found that
epinephrine plus sclerosant was effective, reducing the need for
emergency surgery. Three other studies compared epinephrine
injection alone to epinephrine plus a sclerosant [16–18] without
finding any significant difference in results. At least three other
studies [19–21] compared alcohol injection and reported reduced
mortality rates [21] and a reduced need for surgery [20]. Direct
injection of thrombin has been shown to be effective as well
[22–24], but the number of patients in these studies was relatively
small, and the studies therefore lacked power [9]. According to
another study by the same team [25] endoscopic interventional
treatment should be offered to all high risk bleeding ulcer pa-
tients. A posterior location of the ulcer, however, was significantly
more often associated with failed endoscopic therapy than when it
was in an anterior location [25]. At least two controlled trials
indicated that repeat injection could increase the success rate [26,
27].
Results of Surgical Trials
In one of the earliest studies on record, Morris et al. [28] con-
ducted a randomized study to determine the optimal timing of
operation for bleeding peptic ulcer. In this study [28] a total of 142
patients with a proved duodenal or gastric ulcer, hospitalized
between October 1980 and September 1983, were randomized to
early (aggressive) or delayed (conservative) surgical management.
Operation was carried out in each group whenever specific oper-
ative criteria were attained. The limits of these criteria were 4
units of blood or plasma expander required to correct acute blood
loss in 24 hours, one rebleed, endoscopic “red” stigmata (active
bleeding, visible vessel, adherent clot, spots), previous upper GI
hemorrhage plus 2-year history of dyspepsia) for the “early, ag-
gressive” policy compared with 8 units of blood, two rebleeds,
persistent hemorrhage requiring transfusion of 12 units in 48
hours or 16 units in 72 hours for “late, conservative” surgical
management. The type of operation in each group was decided by
the surgeon (vagotomy ⫹ underrunning of the ulcer in 44, gastric
resection with Billroth I reconstruction in 8, with Polya recon-
struction in 3 and total gastrectomy in 1). Significantly more
operations (n ⫽ 42, 60%) were performed in the early surgery
group than in the delayed surgery group (n ⫽ 9, 20%) (p ⬍ 0.01).
There were no deaths among the 42 patients under age 60. The
overall mortality in the 100 patients aged 60 was 10%. Operative
mortality in the elderly was 7% in the early group compared with
43% in those treated by the delayed policy. The authors con-
cluded that for patients over age 60 an aggressive surgical policy
is associated with a significant reduction in mortality. This was the
case overall when one death due to bleeding colonic polyp was
excluded and in the group of elderly patients with gastric ulcer
disease. The difference in patients with DU was not found to be
statistically significant. Moreover, when analyzed on an “intention
to treat” basis, there was no longer any difference between early
and delayed surgery.
Saperas et al. [29] compared early surgery (suture of the bleed-
ing lesion plus truncal vagotomy and pyloroplasty in all patients
within 4 hours of admission) to expectant management. They
studied patients for whom endoscopy revealed active nonarterial
bleeding or evidence of recent hemorrhage from a duodenal ulcer
without a visible vessel in 69 of 305 patients over 50 years old seen
during a 3-year period. Overall mortality was 8.6%. Mortality in
patients undergoing early surgery was five times higher than in
those allocated to expectant therapy (14.7% vs. 2.9%; risk ratio
5.07). These results suggest that expectant management is advis-
able in patients with a bleeding duodenal ulcer that is not bleeding
massively and in whom endoscopy does not disclose spurting
arterial bleeding or a visible vessel.
Millat et al. [30] compared oversewing the ulcer and vagotomy
(O⫹V) with distal gastric resection (GR) in patients undergoing
emergency surgery for massive, persistent bleeding or recurrent
bleeding from a bulbar peptic ulcer. Of 202 patients with bleeding
duodenal ulcer during a 10-year period, 120 were enrolled in a
prospective randomized trial, 59 being assigned to O⫹V and 61 to
distal GR. One patient in each group was excluded after random-
ization. The two groups were well matched with respect to clinical
and prognostic factors. The rate of postoperative bleeding recur-
rence was 17% after O⫹V compared with 3% after GR (p ⬍
0.05). The duodenal leak rate was higher after GR (13%) than
after O⫹V (3%) (p ⬍ 0.01) but was not statistically significantly
different when the morbidity of reoperations for bleeding recur-
rence after O⫹V was considered on an intention-to-treat basis
(12% vs. 13%). Overall mortality was similar (22% for O⫹V vs.
23% for GR). Postoperative mortality was not different between
O⫹V (27%) and GR (30%). Of 82 nonrandomized patients seen
during the same period, 10 were not analyzed. Of the remaining
72, bleeding recurrence, duodenal leakage, and postoperative
mortality rates were consistent with the results of the randomized
study. The authors concluded that GR with ulcer excision is the
procedure of choice for emergency surgical treatment of bleeding
duodenal ulcer because postoperative bleeding recurrence is
lower and the overall rates of mortality and duodenal leakage
were the same in the two groups. In both randomized and non-
randomized groups, there was only one bleeding recurrence
among 20 patients undergoing oversewing and vagotomy associ-
ated with gastroduodenal and right gastroepiploic artery ligation.
Although this so-called Weinberg procedure [31] was not random-
ized in this study, it might be an appropriate alternative when GR
cannot be performed.
Of the 202 patients with bleeding duodenal ulcers requiring
emergency surgical hemostasis, 145 ulcers (72%) were located on
the posterior duodenal wall. According to univariate analysis, the
posterior (compared with anterior) localization was significantly
associated with older age (p ⬍ 0.001), a higher proportion of
women (p ⬍ 0.02), a lower preoperative red blood cell count (p ⬍
0.05), higher preoperative blood requirements (p ⬍ 0.001), and
higher postoperative mortality (p ⬍ 0.02). With multivariate anal-
ysis, however, when age and blood requirements were taken into
consideration, the posterior localization was no longer an inde-
pendent predictor of mortality. The authors concluded that the
posterior location of duodenal ulcers was a poor prognostic factor
only because these ulcers have a strong tendency to bleed and are
associated with aged and poor risk patients.
In one multicenter study published in 1991 [5], the outcomes of
62 patients allocated to minimal surgery (underrunning the vessel
or ulcer excision and adjuvant rantidine) were compared to that of
67 undergoing conventional surgery (vagotomy and pyloroplasty
or partial gastrectomy). Among them, 29 patients died: 16 (26%)
300 World J. Surg. Vol. 24, No. 3, March 2000
after minimal therapy and 13 (19%) after conventional opera-
tions. The only significant difference between the groups was the
incidence of fatal rebleeding, which occurred in six patients after
minimal surgery compared with none after conventional surgery
(p ⬍ 0.02, Fisher’s exact test). There was no correlation between
rebleeding and ulcer site or size, duration of symptoms, status of
the surgeon or anesthesiologist, or age of the patient. Subcutane-
ous heparin did not predispose to rebleeding. The trial was dis-
continued in view of the high rates of rebleeding after minimal
surgery in this interim analysis.
Helicobacter pylori and Bleeding
Eradication of H. pylori in patients with uncomplicated ulcers
results in recurrence rates of ⬍ 10%, suggesting that eradication
of H. pylori in patients with bleeding ulcers may virtually prevent
recurrence of both the disease and its complications. Several
randomized trials clearly show that in patients with bleeding H.
pylori-positive ulcers cure of the infection prevents both the re-
currence of the ulcer and bleeding [32–35]. In a study from Spain
[36], 6 of 84 patients (7.1%) in whom H. pylori was eradicated had
recurrence, two with rebleeding (2.3%), compared with 13 of 41
patients (31.7%) receiving ranitidine maintenance therapy, five
with rebleeding (12.5%). Although the difference between ulcer
recurrence rates was statistically significant (p ⬍ 0.01), the differ-
ence between the two rebleeding rates was not. In another ran-
domized study from Germany [37], one (5%) patient had recur-
rence without rebleeding in the eradicated group compared with
six with recurrence (21%), three with rebleeding, in the ranitidine
(150 mg) maintenance group. In both of these studies, however,
half of the recurrences occurred in patients who did not follow
their treatment correctly. In one study from Turkey [38] the
incidence of H. pylori was studied in 50 patients admitted for
bleeding duodenal ulcer compared with 64 patients with a non-
bleeding duodenal ulcer. H. pylori was detected by both the rapid
urease (CLO) test and biopsies in 44 (88%) patients with bleeding
duodenal ulcer compared with 43 (67.2%) duodenal ulcer patients
without a bleeding history (p ⬍ 0.05). Although there remains
doubt as to whether H. pylori infection can be incriminated in the
bleeding tendency in duodenal ulcer patients, the authors con-
cluded that eradication therapy should be applied to all H. pylori-
positive duodenal ulcer patients to prevent bleeding episodes.
Although the prevalence of H. pylori infection approaches
100% in duodenal ulcer patients (and 80–90% of gastric ulcer
patients) not using nonsteroidal antiinflammatory drugs
(NSAIDs) [39], the prevalence of the organism in bleeding ulcers
is still not well defined. It has been reported to be lower than that
of noncomplicated ulcers, ranging from 40% to 90%. The reasons
for this might be multiple: (1) Many ulcer bleeding episodes
reported in the literature are due to NSAIDs or aspirin, which are
known to cause ulcers in the absence of H. pylor [40]; (2) the
optimal number of biopsy specimens for diagnosis of H. pylori
infection cannot be obtained because the procedure is performed
under emergency conditions [41]; or (3) the presence of blood
leads to false-positive results with the rapid urease test [42, 43].
Two randomized trials in 1995 [33, 35] concerning the treat-
ment of H. pylori infection in patients recovering from duodenal
ulcer hemorrhage showed that these patients experienced a 0%
rate of recurrent bleeding during the year following randomiza-
tion. This figure contrasted with the 33% and 27% rates of
recurrence in the control groups in these studies. When the results
of the two studies were combined, Howden [44] calculated the
relative risk reduction (1.0, or 100%), the absolute risk reduction
(0.3, or 30%), and the number of patients required to treat in
order to prevent one (bleeding) event [45, 46], which was only 3.3.
Perforated Duodenal Ulcers
The operative mortality for perforated DU is approximately 5%
[47], although figures higher than 30% of in-hospital mortality
have been reported, notably in the elderly [48, 49]. Mortality is
related to patient condition and the adequacy of intensive care,
rather than to the procedure used to repair the perforation. Risk
factors predicting mortality include concurrent major medical
illness, the presence of shock on admission to hospital, and a
presentation delayed of more than 24 hours [47, 49]. Mortality
rates of less than 1% can be expected in patients with none of
these risk factors.
Nonoperative treatment for perforated DU consists of resusci-
tation with intravenous fluids, intravenous antibiotics, and naso-
gastric suction. Simple closure through laparotomy, with perito-
neal lavage, is the standard and quickest operation. Laparoscopic
repair of perforated DU was proposed as an alternative to the
open approach as early as 1989 by Mouret et al. [50]. The high
rate of symptomatic relapse after simple closure, however, has led
to advocacy of immediate definitive surgery of peptic ulcer disease
in the emergency setting. Nonoperative treatment was evaluated
in one randomized controlled trial [51] and immediate definitive
surgery in three [52–54]. One surgical team has compared lapa-
rotomy to laparoscopic procedures [55].
Arguments favoring a nonsurgical approach were advanced by
Taylor [56] nearly 50 years ago, at a time when the mortality rate
for surgical treatment was close to 20%. The fall in the overall
mortality rate for patients treated surgically since then, together
with advances in ulcer treatment and antibiotic therapies, justified
a comparative evaluation [51]. Over a 13-month period patients
with a clinical suspicion of perforated peptic ulcer were randomly
assigned to conservative treatment (n ⫽ 40) or to emergency
surgery (n ⫽ 43). In the surgically treated group, 40 patients had
DU, 2 had gastric ulcers, and one had a perforated gastric carci-
noma. The operations performed were 24 simple omental patch
repairs, 15 vagotomies plus pyloroplasty, and four partial gastrec-
tomies. Eleven patients (27.5%), including three with an errone-
ous diagnosis (two perforated gastric carcinomas, one perforated
sigmoid cancer), who had no improvement within 12 hours of
conservative treatment underwent operation (eight omental patch
repairs, one vagotomy plus pyloroplasty, and one partial gastrec-
tomy). Morbidity was similar in the nonsurgical and surgical
groups (20 vs. 17 patients); intraabdominal abscesses developed in
six and two patients, respectively. Two deaths occurred in each
treatment group, for an overall mortality rate of 4.8%. The dura-
tion of the hospital stay was significantly longer (p ⬍ 0.001) in the
nonsurgical group (12.0 days) than in the surgically treated group
(7.8 days). Failures of the nonoperative policy were significantly
(p ⬍ 0.05) more frequent in patients over 70 years of age (6/9,
67%) than in the younger patients (5/31, 16%).
Simple closure of a perforated DU was compared to definitive
surgery in three randomized trials [52–54]. Patients with risk
factors were not included in two of these studies [52, 54]. In truth,
only one postoperative death was reported among the 328 pa-
Millat et al.: Complicated Duodenal Ulcers 301
tients included in these three randomized trials. Postoperative
morbidity was not significantly increased by definitive surgery,
except for wound sepsis in one trial [53]. Chest infection was the
most frequent complication (36/328, 11%). In two trials, patients
were eligible for entry only if they had a history of chronic ulcer
[52, 54]. With a mean follow-up of 20 months [52] and 39 months
[54], ulcer recurrence was reported in 61% (38/62) and 6% (6/92)
of cases following simple closure and definitive treatment, respec-
tively.
Operation for perforated peptic ulcer is required in an emer-
gency setting when laparoscopic facilities and surgical staff trained
in laparoscopic procedures are not available. Within these limita-
tions, Lau et al. [57] analyzed a total of 100 consecutive patients
with perforated duodenal ulcers treated by laparotomy and omen-
tal patch repair (group 1, n ⫽ 44), laparoscopic suture patch
repair (group 2, n ⫽ 35), or laparoscopic fibrin glue repair (group
3, n ⫽ 21). Patients in the three groups were comparable as
regards the Acute Physiology And Chronic Health Evaluation
(APACHE-II) score and as regards risk factors such as shock on
admission, delayed presentation, and associated underlying med-
ical illness. Operative mortality and morbidity data were identical
in all groups. The mean operating time was significantly longer in
the two laparoscopic groups. Conversion to laparotomy was nec-
essary in 6 of 35 patients and in 1 of 21 patients in groups 2 and
3, respectively. Postoperative analgesic requirements were less
with the laparoscopic repair compared with the open repair.
Intraabdominal abscess or leakage of repair was reported in 1 of
44 patients (2%) in the laparotomy group (group 1) versus 5 of 56
patients (9%) in the laparoscopic groups (groups 2 and 3). A
randomized study was then undertaken when the on-call surgeons
had acquired sufficient experience in laparoscopy to perform the
procedure. From August 1992 to December 1994 a series of 134
patients with a clinical diagnosis of perforated peptic ulcer were
considered for inclusion [55]. Patients with a history of chronic
ulcer (n ⫽ 13), uncertain clinical diagnosis (n ⫽ 10), poor pre-
morbid state (n ⫽ 4), or refusing to consent to randomization
(n ⫽ 4) were not included. Altogether 103 patients were randomly
allocated to laparoscopic or open repair and, inside each group,
between suture and sutureless repair (plug of gelatin sponge and
fibrin glue). Four patients in the laparoscopic group and six in the
open repair groups were excluded after randomization, either
because the ulcer closed spontaneously (n ⫽ 5) or an incorrect
diagnosis (n ⫽ 5). Of 48 patients in the laparoscopic group, 11
(23%) were converted to open surgery. Partial gastrectomy for
gastric ulcers was performed in two and four patients randomized
for laparoscopic or open surgery, respectively. Definitive ulcer
surgery was performed in seven patients with laparotomy. Lapa-
roscopic repair of perforated peptic ulcer took significantly (p ⬍
0.001) longer than open repair (94 vs. 54 minutes, respectively).
Patients who had laparoscopic repair required fewer analgesic
doses postoperatively than those who had open surgery (p ⬍ 0.03).
There were no statistically significant differences noted between
the laparoscopic and open groups as concerns the duration of
nasogastric aspiration, intravenous drips, hospital stay, time to
resume normal diet, and Visual Analogous Scale pain scores for
the first 24 hours after surgery. There was no significant difference
in morbidity, reoperation rate, or mortality between patients who
underwent laparoscopic and open repair. One patient in each
group underwent repeat operation for leakage. Three patients in
the study died: one due to multiorgan failure 17 days after open
repair and two due to heart failure following laparoscopic surgery.
Controversy exists regarding the relation between H. pylori and
perforated DU. The H. pylori infection rate demonstrated by
intraoperative and antral biopsies in 73 patients was 70% in one
Hong Kong study and rose to 80% if NSAID users were excluded
[58]. This prevalence was not much higher than the 55% preva-
lence of infection in the local population and lower than would be
expected among all patients with DU. The urea breath test carried
out 8 days after simple closure of the perforation was positive in
24 of 29 patients in a study from the United Arab Emirates [59].
The urease test performed on mucosal biopsy samples was posi-
tive in 12 of 14 patients with upper GI endoscopy 6 weeks after
discharge. Seven of these twelve patients had persisting duodenal
ulceration. In contrast with these studies, Reinbach et al. [60], in
a series of patients of whom 40% were taking NSAIDs, claimed
that acute perforated DU was not associated with H. pylori infec-
tion. No correlation was found between the incidence of H. pylori
infection in perforated DUs detected by enzyme-linked immu-
nosorbent assay (ELISA) and polymerase chain reaction (PCR)
and control (nonsurgical gastroduodenal) groups, as 47% of per-
forated DUs were positive for H. pylori detected by ELISA,
similar to the value of 50% in control patients in the United
Kingdom [60]. However, only 9 of 23 (39%) had a history of peptic
ulcer or acid inhibitory drug therapy [61]. H. pylori and NSAIDs
are the two major causes of perforated DU and are independent
risk factors of peptic ulceration with different ulcerogenic mech-
anisms [62].
According to what is now known regarding H. pylori, few sur-
geons would embark on definitive ulcer operation in the emer-
gency setting, notably if this definitive ulcer operation was to be
performed laparoscopically. In the present-day setting, however,
one must not forget that the previous controlled trials [52–54]
established and confirmed a high recurrence rate when only sim-
ple repair was performed. Younger patients (⬍ 40 years) without
NSAIDs are the most prone to be infected [58] and should
theoretically benefit from a nonoperative approach [51] with H.
pylori eradication. Patients ⬎ 40 years of age should undergo
operation. The attractive laparoscopic sutureless procedure using
a plug of gelatin sponge with fibrin glue is feasible and appears to
be easier and quicker than suture procedures; as yet, however, no
clinically demonstrable benefit for the patient has been shown
[55]. In patients not receiving NSAIDs, proton pump inhibitors
should be given postoperatively in association with H. pylori erad-
ication, either as a routine or depending on the operative or
postoperative demonstration of infection. The patient with intrac-
table recurrent symptoms of DU despite adequate medical treat-
ment, but without H. pylori infection (a patient using NSAIDs), is
probably the only remaining indication for elective definitive sur-
gical treatment of peptic ulcer disease. Patients with risk factors
should be treated with simple closure.
Gastric Outlet Obstruction
Gastric outlet obstruction (GOO) has been reported to occur in
6% to 8% of patients with DUs [63]. The double aim of proposed
operations include relieving obstruction while controlling peptic
ulcer disease [64, 65]. Evaluation of the effectiveness of surgical
treatment was based on recurrence and restenosis rates.
302 World J. Surg. Vol. 24, No. 3, March 2000
Surgical Trials
Three surgical techniques for the treatment of GOO secondary to
duodenal ulcer were compared in a prospective randomized study
[66]. After laparotomy, patients underwent either highly selective
vagotomy (HSV) ⫹ gastrojejunostomy (n ⫽ 30), HSV ⫹ Jaboulay
gastroduodenostomy (n ⫽ 30), or selective vagotomy (SV) ⫹
antrectomy (n ⫽ 30). There were no differences in the postoper-
ative course of the groups. One patient died after HSV ⫹ Jabou-
lay gastroduodenostomy. With a mean follow-up of 98 months
(range 30–156 months) the clinical state of all patients was graded
using the Visick classification. Outcome was significantly (p ⬍
0.01) better after HSV ⫹ gastrojejunostomy (80% Visick I) than
after Jaboulay anastomosis (70% Visick I) but not after SV ⫹
antrectomy (75% Visick I). When compared with pyloroplasty,
gastrojejunostomy was recommended as the drainage procedure
of choice after vagotomy [67]; but unlike patients in Csendes et
al.’s study [66], those in Kenedy et al.’s study [67] did not show any
evidence of GOO.
Endoscopic balloon dilatation has been proposed as an alter-
native to surgical treatment [68–70]. In the latter study, however,
only 50% of patients treated with balloon dilatation remained
without recurrent ulceration and outlet obstruction at 3 years [70].
Helicobacter pylori and GOO
There is little information available on the relation between H.
pylori infection and GOO. In unpublished data found in the
editorial by Chung and Li [71], 50% of patients with pyloric
stenosis in the Department of Surgery of the Chinese University
of Hong Kong were infected with H. pylori. Reversal of GOO after
eradication of H. pylori infection has been reported [72]. This
observation suggests that oral eradication of H. pylori might be
indicated as a first-line treatment in patients with GOO and those
with H. pylori-associated gastritis and peptic ulcer, and it could
decrease the risk of recurrence if endoscopic balloon dilation is
indicated. In the future, surgery might be compared to balloon
dilatation combined with eradication of H. pylori.
Conclusions
With bleeding duodenal ulcers, even if it can be shown that H.
pylori is responsible for bleeding, endoscopic or surgical hemosta-
sis is still necessary in certain cases. The major aim of urgent
surgery for a severely bleeding DU is to stop life-threatening
hemorrhage and to prevent rebleeding during the immediate
postoperative period. The goal of gastric resection with ulcer
excision in this setting is to stop bleeding but should no longer be
performed as definitive treatment of peptic disease. Eradication
of H. pylori is, at best, expected to decrease the number of patients
requiring elective and emergency surgery.
Whether a radical definitive treatment operation at the time of
perforation is necessary, however, remains to be shown. More-
over, we need to know whether minimal surgical treatment (to
stop the bleeding or to close the perforation) combined with
antisecretory drugs and eradication of H. pylori is sufficient for
these patients and, if so, for how long. Second, we need to know
whether this treatment (antisecretory drugs plus eradication of H.
pylori) also works when bleeding or perforation has warranted a
surgical procedure.
Re´sume´
Les indications de la chirurgie pour ulce`re duode´nal ont change´
radicalement en raison de l’efficacite´ des antagonistes H2, des
proce´de´s endoscopiques et de l’e´radication d’Helicobacter pylori.
Le but de cette e´tude a e´te´ d’analyser la litte´rature actuelle pour
de´terminer si la chirurgie de´finitive a toujours un roˆle dans les
complications de la maladie ulce´reuse complique´e (he´morragie,
perforation, ste´nose pylorique). Deux e´tudes ont compare´la
chirurgie pre´coce a` la chirurgie retarde´e pour he´morragie. L’une
e´tait en faveur de la chirurgie pre´coce (re´duction significative de
la mortalite´) chez le sujet aˆge´, mais e´tait sans aucune diffe´rence
statistiquement significative lorsque les re´sultats e´taient analyse´s
en «intention de traiter». Dans l’autre, la mortalite´ apre`s chirurgie
pre´coce e´tait cinq fois plus e´leve´e que pour l’abstention,
applique´e chaque fois que possible. Deux e´tudes, comparant de
diffe´rentes techniques chirurgicales he´mostatiques ont conclu en
faveur du proce´de´ radical. Parmi les 15 e´tudes comparant les
diffe´rentes me´thodes endoscopiques, aucune n’a compare´ cette
me´thode a` la chirurgie dans le cadre de l’ulce´re gastroduode´nal
he´morragique. Dans un seul essai pour perforation, comparant le
traitement non chirurgical au traitement chirurgical, les taux de
morbidite´, d’abce`s intra-abdominal et de mortalite´e´taient
similaires, mais la dure´e d’hospitalisation e´tait plus longue (p ⬍
0.001). Il y avait plus d’e´checs avec le traitement non-ope´ratoire
(p ⬍ 0.05) chez les patients de 70 ans et plus. Dans trois essais, la
morbidite´ postope´ratoire (excepte´ le taux d’abce`s de paroi dans
un) n’e´tait pas augmente´e de fac¸on significative par la chirurgie
de´finitive, la re´cidive e´tant moindre (p ⬍ 0.05) compare´e aux
re´sultats de la simple fermeture de la perforation par suture. Par
rapport a` la laparotomie, la laparoscopie prenait plus de temps (p
⬍ 0.001), mais ne´cessitait moins d’analge´siques en pe´riode post-
ope´ratoire (p ⬍ 0.03), cependant, sans diffe´rence statistiquement
significative en ce qui concerne la dure´e d’aspiration nasogas-
trique, la dure´e de perfusion intraveineuse, la dure´e d’hospital-
isation, la dure´e du temps avant la reprise d’une alimentation
normale, le score d’e´chelle visuelle analogue pour les 24 heures
post-chirurgicales, la morbidite´, le taux de re´ope´ration ou de
mortalite´. Onze des 48 patients du groupe laparoscopique (23%)
ont ne´cessite´ une conversion a` la chirurgie ouverte. En ce qui
concerne la comparaison de trois techniques chirurgicales pour la
ste´nose d’origine ulce´reuse, a` savoir, 1) la vagotomie ultra-
se´lective (VUS) ⫹ anastomose gastroje´junale (groupe 1), 2) la
VUS ⫹ anastomose gastroduode´nale selon Jaboulay (groupe 2),
ou 3) la vagotomie se´lective ⫹ antrectomie (groupe 3), les scores
de Visick a` long terme e´taient significativement (p ⬍ 0.01)
meilleurs dans le groupe 1 que dans groupe 2, mais pas dans
groupe 3. Par contre, les re´sultats postope´ratoires e´taient
similaires (excepte´ l’abce`s de paroi dans un essai). Conclusions:
D’autres e´tudes sont ne´cessaires pour de´terminer la pre´valence
exacte de l’H. pylori dans l’ulce`re duode´nal complique´ et pour
comparer : 1) la chirurgie de´finitive a` la chirurgie a` minima
(arreˆter l’he´morragie ou fermer la perforation) combine´e a` des
me´dicaments antisecre´toires et l’e´radication de l’H. pylori; 2) La
chirurgie versus le traitement endoscopique combine´a`
l’e´radication de l’H. pylori, et 3) dans la ste´nose du pylore, la
chirurgie versus la dilatation au ballonnet combine´e a`
l’e´radication de l’H. pylori.
Millat et al.: Complicated Duodenal Ulcers 303
Resumen
La indicacio´n quiru´rgica en el tratamiento de la u´lcera duodenal
(DU) se ha modificado radicalmente como consecuencia de la
eficacia de los antagonistas H2, de los procedimientos endo-
sco´picos y de los tratamientos erradicadores del “H. pylori”. El
objetivo de este estudio fue analizar la bibliografı´a actual, con
objeto de determinar si la cirugı´a desempen˜a algu´n papel en el
tratamiento de las u´lceras duodenales complicadas (sangrantes,
perforadas, con estenosis pilo´rica). Dos estudios comparan los
resultados precoces y tardı´os de la cirugı´a en u´lceras sangrantes.
Uno, recomienda un tratamiento quiru´rgico precoz, sobre todo en
pacientes an˜osos, pues la mortalidad es significativamente menor;
sin embargo, no se encontraron diferencias estadı´sticamente
significativas, por lo que se refiere a la intencio´n curativa del
tratamiento. En el otro trabajo, la mortalidad con cirugı´a precoz
fue 5 veces mayor que con terapia conservadora, siempre que e´sta
estuviese indicada. Dos estudios que comparan las diferentes
te´cnicas quiru´rgicas para el tratamiento de la u´lcera sangrante,
postulan un procedimiento radical. Existen al menos 15 trabajos,
que comparan los resultados que se obtienen con diferentes
tratamientos endosco´picos. Sin embargo, no hay un solo estudio
comparativo entre el tratamiento endosco´pico vs. quiru´rgico en la
u´lcera duodenal sangrante. Un ensayo efectuado comparando, en
u´lceras perforadas, el tratamiento quiru´rgico vs. conservador,
demostro´ tasas semejantes de morbilidad, abscesos intraabdomi-
nales y mortalidad; sin embargo, la estancia hospitalaria fue
mayor con el tratamiento conservador (p ⬍ 0.001). La eficacia del
tratamiento conservador es menor en pacientes mayores de 70
an˜os (p ⬍ 0.05). En 3 ensayos, la morbilidad postoperatoria
(excepcio´n hecha de una infeccio´n de la herida) no aumento´
significativamente con la cirugı´a radical vs. a la simple sutura de la
perforacio´n. Sin embargo, la racidiva ulcerosa fue menor con
cirugı´a radical (p ⬍ 0.05). La cirugı´a por vı´a laparosco´pica vs.
laparoto´mica requiere un mayor tiempo (p ⬍ 0.001), mientras que
las necesidades analge´sicas postoperatorias fueron menores (p ⬍
0.03); por el contrario, no se encontraron diferencias estad-
ı´sticamente significativas por lo que se refiere: a la duracio´n de la
aspiracio´n nasoga´strica, de la infusio´n intravenosa, estancia
hospitalaria, tiempo transcurrido hasta la reanudacio´n de una
ingesta normal, dolor durante las primeras 24 horas tras cirugı´a
valorado mediante la escala Analo´gica Visual, morbilidad, tasas
de reintervenciones o mortalidad. Once (23%) de 48 pacientes
intervenidos laparosco´picamente hubieron de ser reconvertidos a
cirugı´a abierta. Tres te´cnicas quiru´rgicas: 1) Vagotomı´a
supraselectiva (HSV) ma´s gastroyeyunostomı´a (grupo 1); 2) HSV
ma´s gastroduodenostomı´a a lo Jaboulay (grupo 2) y 3) Vagotomı´a
selectiva ma´s antrectomı´a (grupo 3). Estas tres te´cnicas
empleadas como tratamiento de la estenosis pilo´rica (GOO)
demostraron, que si bien los resultados postoperatorios fueron
similares, excepcio´n hecha de una infeccio´n de la herida en un
ensayo, los resultados a largo plazo, utilizando la escala de Visick
fueron significativamente mejores (p ⬍ 0.01) en le grupo 1 que en
el grupo 2, pero no en relacio´n al grupo 3. Conclusiones: Se
precisan ma´s estudios para averiguar con exactitud la prevalencia
del “H. pylori” en las u´lceras duodenales complicadas, ası´ como
para comparar lo siguiente: 1) Cirugı´a radical definitiva o cirugı´a
mı´nima (sutura del vaso sangrante o de la perforacio´n) asociada
a drogas antisecretoras y erradicadoras del “H. pylori”. 2) Cirugı´a
vs. tratamiento endosco´pico combinado con la erradicacio´n del
“H. pylori” y 3) En la estenosis pilo´rica cirugı´a vs. dilatacio´n con
balo´n, combinada con erradicacio´n del “H. pylori”.
References
1. Forbes, G.M., Glaser, M.E., Cullen, D.J., Christiansen, K.J., Marshall,
B.J., Collins, B.J.: Duodenal ulcer treated with Helicobacter pylori
eradication: seven-year follow-up. Lancet 343:258, 1994
2. Elanshoff, J.D., Van Deventer, G., Reedy, T.J., Ippoliti, A., Samloff,
I.M., Kurata, J., Billings, M., Isenberg, M.: Long-term follow-up of
duodenal ulcer patients. J. Clin. Gastroenterol. 5:509, 1983
3. Feliciano, D.V.: Do perforated duodenal ulcers need an acid-decreas-
ing surgical procedure now that omeprazole is available? Surg. Clin.
North Am. 72:369, 1992
4. Longsteth, G.F.: Epidemiology of hospitalisation for acute upper
gastrointestinal hemorrhage: a population-based study. Am. J. Gas-
troenterol. 90:861, 1995
5. Poxon, V.A., Keighley, M.R.B., Dykes, P.W., Heppinstall, K., Jader-
berg, M.: Comparison of minimal and conventional surgery in patients
with bleeding peptic ulcer: a multicentre trial. Br. J. Surg. 78:1344,
1991
6. Inadomi, J., Koch, J., Cello, J.P.: Long-term follow-up of endoscopic
treatment for bleeding gastric and duodenal ulcers. Am. J. Gastroen-
terol. 90:1065, 1995
7. Kuttila, K., Havia, T., Pekkala, E., Ali-Melkkila¨, T.: Surgery of acute
peptic ulcer hemorrahage. Ann. Chir. Gynaecol. 80:26, 1991
8. Clason, A.E., MacLeod, D.A.D., Elton, R.A.: Clinical factors in the
prediction of further haemorrhage or mortality in acute upper gastro-
intestinal haemorrhage. Br. J. Surg. 73:985, 1986
9. Kubba, A.K., Palmer, K.R.: Role of endoscopic injection therapy in
the treatment of bleeding peptic ulcer. Br. J. Surg. 83:461, 1996
10. Lau, J., Schmid, C.H., Chalmers, T.C.: Cumulative meta-analysis of
clinical trials builds evidence for exemplary medical care. J. Clin.
Epidemiol. 48:45, 1995
11. Chung, S.C.S., Leung, J.W.C., Steele, R.J.C., Crofts, T.J., Li, A.K.C.:
Endoscopic injection of adrenaline for actively bleeding ulcers: a
randomised trial. B.M.J. 296:1631, 1988
12. Balanzo, J., Sainz, S., Such, J., Espinos, J.C., Guarner, C., Cusso, X.,
Mone´s, J., Vilardell, F.: Endoscopic hemostasis by local injection of
adrenaline and polidocanol in bleeding ulcer: a prospective random-
ized trial. Endoscopy 20:289, 1988
13. Oxner, R.B.G., Simmonds, N.J., Gertner, D.J., Nightingale, J.M.D.,
Burnham, W.R.: Controlled trial of endoscopic injection treatment for
bleeding from peptic ulcers with visible vessels. Lancet 339:966, 1992
14. Panes, J., Viver, J., Forne, M., Garcia-Oliveres, E., Marcos, C., Garau,
J.: Controlled trial of endoscopic sclerosis in bleeding peptic ulcers.
Lancet 2:1292, 1987
15. Rajgopal, C., Palmer, K.R.: Endoscopic injection sclerosis: effective
treatment for bleeding peptic ulcer. Gut 32:727, 1991
16. Choudari, C.P., Palmer, K.R.: Endoscopic injection therapy for bleed-
ing peptic ulcer: a comparison of adrenaline alone with adrenaline
plus ethanolamine oleate. Gut 35:608, 1994
17. Chung, S.C.S., Leung, J.W.C., Leong, H.T., Lo, K.K., Li, A.K.C.:
Adding a sclerosant to endoscopic epinephrine injection in actively
bleeding ulcers: randomised trial. Gastrointest. Endosc. 39:611, 1993
18. Villaneuva, C., Balanzo, J., Espinos, J.C.: Prediction of therapeutic
failure in patients with bleeding peptic ulcer treated with endoscopic
injection. Dig. Dis. Sci. 38:2062, 1993
19. Chiozzini, G., Bortoluzzi, F., Pallini, P., Bettot, G., Castaqntini, R.,
Costa, F.: Controlled trial of absolute ethanol vs epinephrine as
injection agent in gastroduodenal bleeding. Gastroenterology 96:A86,
1989
20. Lazo, M.D., Andrade, R., Medina, M.C., Garcia-Fernandez, G.,
Sanchez-Cantos, A.M., Franquelo, E.: Effect of injection sclerosis with
alcohol on the rebleeding rate of gastroduodenal peptic ulcers with
non-bleeding visible vessels: a prospective controlled trial. Am. J.
Gastroenterol. 87:843, 1992
21. Pascu, O., Draghici, A., Acalovchi, I.: The effect of endoscopic hemo-
stasis with alcohol on the mortality rate of non variceal upper gastro-
intestinal hemorrhage: a randomized prospective study. Endoscopy
21:53, 1989
22. Balanzo, J.C., Villaneuva, C., Sainz, S., Espinos, J.C., Mendez, C.,
304 World J. Surg. Vol. 24, No. 3, March 2000
Guazner, C., Vilardell, F.: Injection therapy of bleeding peptic ulcer:
a prospective randomized trial using epinephrine and thrombin. En-
doscopy 22:157, 1990
23. Benedetti, G., Sablish, R., Lacchin, T.: Endoscopic injection sclero-
therapy in non-variceal upper gastrointestinal bleeding: a comparative
study of polidocanol and thrombin. Surg. Endosc. 5:28, 1991
24. Moreto, M., Zaballa, M., Suarez, M.J., Ibanez, S., Ojembarrena, E.,
Castillo, J.M.: Endoscopic injection therapy of ethanolamine oleate
and thrombin as an effective treatment for bleeding duodenal ulcer: a
controlled trial. Gut 33:456, 1992
25. Choudari, C.P., Rajgopal, C., Elton, R.A., Palmer, K.R.: Failures of
endoscopic therapy for bleeding peptic ulcer: an analysis of risk
factors. Am. J. Gastroenterol. 89:1968, 1994
26. Saeed, Z., Cole, R.A., Schneider, F.E., Rodman, D.Y., Graham, V.A.:
Retreatment 24 hours after successful initial endoscopic hemostasis of
bleeding ulcers improves outcome: a prospective randomized trial
[abstract]. Gastrointest. Endosc. 40:293, 1995
27. Villaneuva, C., Balanzo, J., Torras, X., Soriano, G., Sainz, S.,
Vilardell, F.: Value of second-look endoscopy after injection therapy
for bleeing peptic ulcer: a prospective and randomized trial. Gastro-
enterol. Endosc. 40:34, 1994
28. Morris, D.L., Hawker, P.C., Brearley, S., Simms, M., Dykes, P.W.,
Keighley, M.R.B.: Optimal timing of operation for bleeding peptic
ulcer: prospective randomized trial. B.M.J. 288:1277, 1984
29. Saperas, E., Pique, J.M., Perez Ayuso, R., Bordas, J.M., Teres, J.,
Pera, C.: Conservative treatment of bleeding duodenal ulcer without
a visible vessel: prospective randomized trial. Br. J. Surg. 7:784, 1987
30. Millat, B., Hay, J.M., Valleur, P., Fingerhut, A., Fagniez, P.L., French
Associations for Surgical Research: Emergency surgical treatment for
bleeding duodenal ulcer: oversewing plus vagotomy versus gastric
resection; a controlled randomized trial. World J. Surg. 17:568, 1993
31. Weinberg, J.A.: Treatment of the massively bleeding duodenal ulcer
by ligation, pyloroplasty and vagotomy. Am. J. Surg. 102:158, 1981
32. Graham, D.Y., Hepps, K.S., Ramirez, F.C., Lew, G.M., Saeed, Z.A.:
Treatement of Helicobacter pylori reduces the rate of rebleeding in
peptic ulcer disease. Scand. J. Gastroenterol. 28:939, 1993
33. Jaspersen, D., Koerner, T., Schorr, W., Breenestuhl, M., Raschka, C.,
Hammar, C.H.: Helicobacter pylori eradication reduces the rate of
rebleeding in ulcer hemorrhage. Gastrointest. Endosc. 41:5, 1995
34. Labenz, J., Borsch, G.: Role of H. pylori eradication in the prevention
of peptic ulcer bleeding relapse. Digestion 55:19, 1994
35. Rokkas, T., Karameris, A., Mavrogeorgis, A., Rallis, E., Giannikos,
N.: Eradication of Helicobacter pylori reduces the possibility of re-
bleeding in peptic ulcer disease. Gastrointest. Endosc. 41:1, 1995
36. Santander, C., Gravalos, R.G., Cedenilla, A.G., Parares, J.M.: Main-
tenance treatment vs Helicobacter pylori eradication in preventing
rebleeding of the peptic ulcer disease: a clinical trial and follow-up for
two years [abstract]. Gastroenterology 108:A208, 1995
37. Maier, M., Schilling, D., Dorlars, D., Wegener, K., Kohler, B., Benz,
C., Riemann, J.F.: Eradication of Helicobacter pylori or H
2
blocker
maintance therapy after peptic ulcer bleeding: a prospective random-
ized trial [abstract]. Gastroenterology 108:A156, 1995
38. Kadayifei, A., Simsek, H.: Do Helicobacter pylori-positive duodenal
ulcers have an increased risk of bleeding? Am. J. Gastroenterol.
90:1901, 1995
39. Vaira, D., Holton, J., Miglioli, M., Menegatti, M., Mule`, P., Barbara,
L.: Peptic ulcer disease and Helicobacter pylori infection. Curr. Opin.
Gastroenterol. 10:98, 1994
40. McColl, K.E.L., el-Nujumi, A.M., Chittajullu, R.S., Dahill, S.W., Dor-
rian, C.A., el-Omar, E., Pennan, I., Fitzsimmons, E.J., Drain, J.,
Graham, H., Ardill, J.E.S., Bessert, R.: A study of the pathogenesis of
Helicobacter pylori-negative chronic duodenal ulceration. Gut 34:762,
1993
41. Veldhuyzen van Zanten S.J.O.: Bleeding ulcers, interaction between
NSAIDs and Helicobacter pylori infection, and nonulcer dyspepsia.
Gastroenterology 113:S90, 1997
42. Buckley, M., Lee, J., O’Morain, C.: The problem ulcer: bleeding,
perforation, H. pylori-negativity and intractability. In: Helicobacter
pylori: Basic Research to Clinical Cure, vol. 1, R.H. Hunt, editor,
London, Klu¨wer Academic, 1996, ch. 30
43. Lai, K.C., Hui, W.M., Lam, S.K.: Bleeding ulcers have high false
negative rates for antral H. pylori when tested with urease test [ab-
stract]. Gastroenterology 110:A167, 1996
44. Howden, C.W.: How many patients must we treat for H. pylori
infection to prevent a recurrent duodenal ulcer hemorrhage [letter]?
Gastrointest. Endosc. 43:175, 1996
45. Cook, D.J., Guyarr, G.H., Salena, B., Laine, L.: Endoscopic therapy
for acute nonvariceal upper gastrointestinal hemorrhage: a meta-
analysis. Gastroenterology 102:139, 1992
46. Laupacis, A., Sackett, D.L., Roberts, R.S.: An assessment of clinically
useful measures of the consequences of treatment. N. Engl. J. Med.
318:1728, 1988
47. Boey, J., Choi, S.K.Y., Alagaratnam, T.T., Poon, A.: Risk stratification
in perforated duodenal ulcers: a prospective validation of predictive
factors. Ann. Surg. 205:22, 1987
48. Blomgren, L.G.M.: Perforated peptic ulcer: long-term results after
simple closure in the elderly. World J. Surg. 21:412, 1997
49. Irvin, T.T.: Mortality and perforated peptic ulcer: a case for risk
stratification in elderly patients. Br. J. Surg. 76:215, 1989
50. Mouret, P., Franc¸ois, Y., Vignal, J., Barth, X., Lombard-Platet, R.:
Laparoscopic treatment of perforated peptic ulcer. Br. J. Surg. 77:
1006, 1990
51. Crofts, T.J., Park, K.G.M., Steele, R.J.C., Chung, S.S.C., Li, A.K.C.L.:
A randomized trial of nonoperative treatment for perforated peptic
ulcer. N. Engl. J. Med. 320:970, 1989
52. Boey, J., Lee, N.W., Koo, J., Lam, P.H.M., Wong, J., Ong, G.B.:
Immediate definitive surgery for perforated duodenal ulcers: a pro-
spective controlled trial. Ann. Surg. 196:338, 1982
53. Hay, J.M., Lacaine, F., Kohlmann, G., Fingerhut, A.: Immediate
definitive surgery for perforated duodenal ulcer does not increase
operative mortality: a prospective controlled trial. World J. Surg.
12:705, 1988
54. Tanphiphat, C., Tanprayoon, T., Na Thalang, A.: Surgical treatment
of perforated duodenal ulcer: a prospective trial between closure and
definitive surgery. Br. J. Surg. 72:370, 1985
55. Lau, W.Y., Leung, K.L., Kwong, K.H., Davey, I.C., Robertson, C.,
Dawson, J.J.W., Chung, S.C.S., Li, A.K.C.: A randomized study com-
paring laparoscopic versus open repair of perforated peptic ulcer
using suture or sutureless technique. Ann. Surg. 224:131, 1996
56. Taylor, H.: Aspiration treatment of perforated ulcers. Lancet 1:7,
1951
57. Lau, W.Y., Leung, K.L., Zhu, X.L., Lam, Y.H., Chung, S.C.S., Li,
A.K.C.: Laparoscopic repair of perforated peptic ulcer. Br. J. Surg.
82:814, 1995
58. Ng, E.K.W., Chung, S.C.S., Sung, J.J.Y., Lam, Y.H., Lee, D.W.H.,
Lau, J.Y.W., Ling, T.K.W., Lau, W.Y., Li, A.K.C.: High prevalence of
Helicobacter pylori infection in duodenal ulcer perforations not
caused by non-steroidal anti-inflammatory drugs. Br. J. Surg. 83:1779,
1996
59. Sebastian, M., Prem Chandran, V.P., El Ashaal, Y.I.M., Sim, A.J.W.:
Helicobacter pylori infection in perforated peptic ulcer disease. Br. J.
Surg. 82:360, 1995
60. Reinbach, D.H., Cruickshank, G., McColl, K.E.L.: Acute perforated
duodenal ulcer is not associated with Helicobacter pylori infection.
Gut 34:1344, 1993
61. Matsukura, N., Onda, M., Tokunaga, A., Kato, S., Yoshiyuki, T.,
Hasegawa, H., Yamashita, K., Tomtitchong, P., Hayashi, A.: Role of
Helicobacter pylori Infection in perforation of peptic ulcer: an age-
and gender-matched case-control study. J. Clin. Gastroenterol.
25(suppl.):S235, 1997
62. Taha, A.S., Dahill, S., Nakshabendi, I., Lee, F.D., Sturrock, R.D.,
Russell, R.I.: Duodenal histology, ulceration, and Helicobacter pylori
in the presence or absence of non-steroidal anti-inflammatory drugs.
Gut 34:1162, 1993
63. Ellis, H.: Pyloric stenosis complicating duodenal ulceration. World
J. Surg. 11:198, 1987
64. Mentes, A.S.: Parietal cell vagotomy and dilatation for peptic duode-
nal stricture. Ann. Surg. 212:597, 1990
65. White, C.M., Harding, L.K., Keighley, M.R.B., Dorricott, N.J., Alex-
ander-Williams, J.: Gastric emptying after treatment of stenosis sec-
ondary to duodenal ulceration by proximal vagotomy and duodeno-
plasty or pyloric dilatation. Gut 19:783, 1978
66. Csendes, A., Maluenda, F., Braghetto, I., Schutte, H., Burdiles, P.,
Diaz, J.C.: Prospective randomized study comparing three surgical
techniques for the treatment of gastric outlet obstruction secondary to
duodenal ulcer. Am. J. Surg. 166:45, 1993
Millat et al.: Complicated Duodenal Ulcers 305
67. Kenedy, J., Johnston, G.W., Lowe, A.H.G., Connell, A.M., Anne
Spencer, E.F.: Pyloroplasty versus gastrojejunostomy. Br. J. Surg.
76:145, 1989
68. DiSario, J.A., Fennerty, B., Tietze, C.C., Huston, W.R., Burt, R.W.:
Endoscopic balloon dilatation for ulcer induced gastric outlet obstruc-
tion. Am. J. Gastroenterol. 89:868, 1994
69. Krevsky, B.: Endoscopic management of gastric outlet obstruction.
Gastroenterology 101:553, 1991
70. Lau, J.Y.W., Chung, S.C.S., Sung, J.J.Y., Chan, A.C., Ng, E.K., Suen,
R.C., Li, A.K.: Through-the-scope balloon dilatation for pyloric ste-
nosis: long-term results. Gastrointest. Endosc. 43:98, 1996
71. Chung, S.C.S., Li, A.K.C.: Helicobacter pylori and peptic ulcer sur-
gery. Br. J. Surg. 84:1489, 1997
72. De Boer, W.A., Driessen, W.M.: Resolution of gastric outtlet obstruc-
tion after eradication of Helicobacter pylori. J. Clin. Gastroenterol.
21:329, 1995
306 World J. Surg. Vol. 24, No. 3, March 2000
