laparoscopic anterior seromyotomy with posterior truncal vagotomy ...
laparoscopic anterior seromyotomy with posterior truncal vagotomy ... laparoscopic anterior seromyotomy with posterior truncal vagotomy ...
- Page 4: List ofImages Image Image 1: ECRT s
- Page 9: With LOVE! DEDICATION To the soul o
- Page 14: -4- with medical treatments for thi
- Page 17 and 18: -7- However, if the same physiologi
- Page 20 and 21: Surgical Anatomy: -9- REVIEW OF LIT
- Page 22: Mucosal Typt"S: -11- Older histolog
- Page 25 and 26: 2_ Antral-Parietal Mucosal Junction
- Page 27: 3. Prepyloric Duodenal Ulcer: -16-
- Page 30: -19- muscle fibers of the pyloric s
- Page 33 and 34: -22- circulation within it than tha
- Page 35 and 36: -24- proximal duodenum. Its first b
- Page 37 and 38: -26- arteries may arise from the ce
- Page 39 and 40: -28- brevia and left gastroepiploic
- Page 41 and 42: NERVE SUPPLY A. SYMPATHETIC NERVES:
- Page 43: 2. Abdominal Vagi: a. The Anterior
- Page 47 and 48: -36- enough to cause recurrence aft
- Page 49 and 50: -38- postulated that intact hepatic
- Page 51 and 52: -40- mucosa (Poppen et al., 1976)_
List ofImages<br />
Image<br />
Image 1: ECRT showing black color change during PGV -----------------<br />
Image 2: ERCT showing disappearance ofthe black color -----------------<br />
Image 3: Large deep active DU ------------------------------------------------<br />
Image 4: Deformed duodenal cap ----------------------------------------------<br />
Image 5: Elevation ofthe liver -------------------------------------------------<br />
Image 6: Opening the lesser omentum ----------------------------------------<br />
Image 7: The two landmarks for <strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong> --------------<br />
Image 8: Traction of the white <strong>posterior</strong> vagus trunk -----------------------<br />
Image 9: Clipping the <strong>posterior</strong> vagus trunk ---------------------------------<br />
Image 10: A segment ofthe <strong>posterior</strong> vagus trunk resected ----------------<br />
Image 11: Ligation ofthe big vessels onto the stomach ---------------------<br />
Image 12: Marking the line of <strong>anterior</strong> <strong>seromyotomy</strong> ---------------------.-<br />
Image 13: The esophagogastric junction --------------------------------------<br />
Image 14: The crew's foot ------------------------------------------.-----------<br />
Image 15: Starting seromyotorny from below ---------.------.---------------<br />
Image 16: Seromyotomy using bipolar coagulating knife --------.---------<br />
Image 17: Seromyotomy using coagulating hook ----------------------------<br />
Image 18: Suturing <strong>seromyotomy</strong> -------------.--------------------------------<br />
Image 19: Chronic DU by intraoperative ECRT .-------------.--------------<br />
Image 20: Gastric outlet patency by intraoperative ECRT ------------------<br />
Image 21: Washing gastric ----------.-------------------------------------------<br />
Image 22: Spraying gastric mucosa <strong>with</strong> CR ---------------------------------<br />
Image 23: Gastric mucosa at the end of ECRT -----------------.--------------<br />
Page<br />
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ACKNOWLEDGEMENT<br />
First ofall I offer my great thankful prayer to Allah<br />
I wish to express my great thanks to my kind professor, Prof. Dr.<br />
Mohammad Abd AI-Bary Al-Sharabasy, Prof Dr. of general surgery, Faculty<br />
of Medicine, Zagazig University, for his great patiency, kind advises and help.<br />
And, I wish to express my great thanks to my kind professor, Prof. Dr.<br />
Ismaiel Abd AI-Rahman Koutb, Prof Dr. of general surgery, Faculty of<br />
Medicine, Zagazig University, for his great faithful sympathy and help.<br />
Also, I wish to express my great thanks to my kind professor, Prof. Dr.<br />
Nabiel Ali Gad AI-Hak, Prof Dr. of general surgery, Faculty of Medicine,<br />
Mansoura University, for his great advises and encouraging help.<br />
To, Dr. Samir Ibrahim Mohammad, Lecturer of general surgery, Faculty<br />
of Medicine, Zagazig University, I express many thanks and gratitude for his<br />
great cooperation in doing the intraoperative endoscopic Congo red test.<br />
Dr. Samy Shahwan
With LOVE!<br />
DEDICATION<br />
To the soul ofmy MOTHER,<br />
To my FATHER,<br />
To my WIFE,<br />
I dedicate this work.<br />
To my SONS & DAUGHTERS,<br />
To ALL WHO LOVED ME &<br />
To ALL WHO HELPED ME;<br />
Dr. Samy Shahwan<br />
,"
-2-<br />
increasingly encountering treatment 'failures. In a recent survey, United<br />
States physicians reported using 103 different eradication regimens; many<br />
were ineffective or ofunknown effectiveness (Freston, 2000).<br />
The era ofHi-receptor blocker treatment for peptic ulcer disease had<br />
already led to a sharp decline in the elective treatment of such disease.<br />
Yet, during era there did not appear to be any fall in the rates of peptic<br />
ulcer perforation. This seems surprising and means that we can not<br />
assume on a priori grounds alone that the rate of perforation will fall<br />
during the H. pylori era (Jamieson, 2000).<br />
The side effects ofantibiotic therapy can include digestive problems<br />
in 30% of patients, especially pseudomembranous colitis, that oblige<br />
patients to stop therapy (Mouiel et al., 1999).<br />
Medical therapy cures in just a few weeks over 95% of patients;<br />
however, when suspended, the rate of relapses varies from 10% after ]<br />
month's therapy to 65% after 18 months (Croce et aI., 1999). Once<br />
medication is stopped, however, ulcer recurrence is frequent, hence the<br />
need for maintenance treatment (Mouiel et al., 1999).<br />
The relation between H. pylori infection and gastroesophageal reflux<br />
disease (GERD), once thought to be non existent, has become a clinically<br />
relevant issue in light of reports suggesting that the presence ofH. pylori<br />
infection may in some way afford some protection against the<br />
development of GERD. Evidence suggests that H. pylori eradication may<br />
foster the development oferosive esophagitis (Freston, 2000).<br />
H. pylori eradication in duodenal ulcer patients was followed by a<br />
significant increase in the prevalence of erosive esophagitis after 3 years<br />
"-ro:
-4-<br />
<strong>with</strong> medical treatments for this benign, frequent and recurrent disease is<br />
often far from satisfactory (Mouie! et al., I 999).<br />
Yet, ulcer-related mortality remains a serious health problem, and its<br />
incidence has even risen in the elderly, surgical treatment, <strong>with</strong> its<br />
recognized long-term efficacy, may thus have a role to play in the<br />
prevention ofcomplications (Meuiel et aI., 1999).<br />
Despite this enormous success of medical therapy, there are several<br />
reasons why elective surgery for peptic ulcer disease is unlikely to<br />
disappear altogether. First is the fact that medical treatment still<br />
sometimes, fails, in such patients anti-ulcer surgery remains an<br />
appropriate option-more so since the advent of <strong>laparoscopic</strong> highly<br />
selective <strong>vagotomy</strong>. Second is the cost of treatment, particularly when<br />
that treatment is centered on anti-secretory drugs. This means that in less<br />
economically developed countries, elective <strong>laparoscopic</strong> anti-ulcer<br />
surgery is likely to continue and may even flourish (Jamieson, 2000).<br />
A parameter to be taken into account is the patient preference, i.e.<br />
the duly informed patient can select either prolonged medical therapy or<br />
minimally invasive surgical procedure (Mouiel et al., 1999).<br />
It must be noted that the percentage of operations being carried out<br />
in patients <strong>with</strong> peptic ulcer disease has sharply increased in regard to<br />
emergency surgery and there is no doubt that a large part of this increase<br />
has been due to the decrease in elective surgery (Jamieson, 2000).<br />
Regarding highly selective <strong>vagotomy</strong>, there are, however, several<br />
drawbacks: the operative technique is difficult, and training is required to<br />
successfully complete proximal denervation of the distal esophagus and<br />
distal denervation of the upper part ofthe crow's foot There is also a risk<br />
t 'or'
-6-<br />
denervation ofthe pancreas and the intestine. In particular, post-<strong>vagotomy</strong><br />
diarrhea is avoided and motility is maintained in the pyloric and antral<br />
regions. Similarly, <strong>anterior</strong> <strong>seromyotomy</strong> spares the pyloric branches of<br />
the vagus nerves, thereby preserving the antral pump and preventing<br />
pylorospasm. This in tum ensures physiological emptying to the stomach,<br />
obviating the need for an associated drainage procedure. The procedure<br />
combines the rapidity and effectiveness of <strong>truncal</strong> <strong>vagotomy</strong>, which has<br />
the advantage of maintaining the gastric antral pump; <strong>with</strong> ultraselective<br />
<strong>vagotomy</strong> (Mouiel et aI., 1999).<br />
An advantage of <strong>anterior</strong> <strong>seromyotomy</strong> <strong>with</strong> <strong>posterior</strong> <strong>truncal</strong><br />
<strong>vagotomy</strong> over PGV is a shorter operating time, Seromyotomy <strong>with</strong><br />
<strong>posterior</strong> <strong>vagotomy</strong> also appeared to give a more consistent and effective<br />
<strong>vagotomy</strong> than PGV (Chisholm er al., 1993).<br />
In the last 5 years, <strong>laparoscopic</strong> techniques have been reported for<br />
the management of uncompiicated peptic ulcer disease, including<br />
<strong>laparoscopic</strong> <strong>truncal</strong> <strong>vagotomy</strong>, proximal gastric <strong>vagotomy</strong>, and <strong>anterior</strong><br />
<strong>seromyotomy</strong> <strong>with</strong> <strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong> (Kollmorgen et al., 1996).<br />
This minimally invasive surgical approach has opened a new era in<br />
effective treatment of ulcer disease and from now on must represent an<br />
alternative to long-term medical therapy. The technique also has other<br />
undeniable technical advantages, which have been confirmed by other<br />
investigators: the procedure is easier, faster to perform, and gives constant<br />
results, even in obese patients, because the success of the operation is<br />
independent of anatomic variations in the vagus nerve (Mouiel et aI.,<br />
1999),
-7-<br />
However, if the same physiologic consequences can be obtained<br />
<strong>with</strong> less pain, shorter hospital stay, and faster recovery, the advantages<br />
ofa <strong>laparoscopic</strong> approach are obvious (Kollmorgen et al., 1996).<br />
To conclude, the advent of laparoscopy has made it possible, not<br />
only to surgically correct peptic diseases non-traumatically by reducing<br />
the complications of this pathology and releasing patients from the need<br />
for chronic medical therapy, but also to obtain functional results which<br />
can be overlapped <strong>with</strong> the traditional surgical ones (Croce et al., 1999).<br />
An approach to ensuring adequate <strong>vagotomy</strong> is to perform intra<br />
operative intra-gastric pressure monitoring or pH testing (Chisholm et al.,<br />
1993). An endoscopic test that uses Congo red as an indicator of acid<br />
production during PGV is recently modified. (Donahue et al.,(1987).
-8-<br />
AIl"d OF THE WORK<br />
This study aims at evaluation of the results of <strong>laparoscopic</strong> <strong>anterior</strong><br />
<strong>seromyotomy</strong> <strong>with</strong> <strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong> as a surgical treatment for<br />
chronic duodenal ulcer disease.
Surgical Anatomy:<br />
-9-<br />
REVIEW OF LITERATURE<br />
• Mucosa.<br />
• Musculature.<br />
• Arteries.<br />
• Nerve supply.<br />
SurgicalPhysiology.<br />
ChronicDuodenalUlcer Disease:<br />
• Definition.<br />
• Incidence.<br />
• Location.<br />
• Aetiology.<br />
• Pathologyand pathogenesis.<br />
• Clinical picture.<br />
• Diagnosis and investigations.<br />
• Complications.<br />
• Treatment ofchronic duodenal ulcer-
MUCOSA:<br />
-10-<br />
SURGICAL ANATOMY<br />
The stomach is divided into the traditional bJTOSS anatomic areas.<br />
However, if we define fundus as the stomach's dome, or that part above<br />
the esophageal inlet, and define pylorus as the part at the pyloric<br />
sphincter, then the fundus and pylorus are the only parts of the stomach<br />
we can accurately delineate by gross examination. We can not accurately<br />
delineate the cardia, corpus and antrum, because the stomach's gross<br />
configuration does not present any landmarks that allow to do so (Figure<br />
l.A). The incisura angularis ventriculi on the lesser curvature separates<br />
corpus from antrum in textbooks and in the dissecting laboratory but, in<br />
the operating room, this landmark either cannot be found or can be only<br />
vaguely located. Furthermore, the incisura angularis ventriculi may often<br />
be confused <strong>with</strong> peristaltic waves on radiographs. Even when an<br />
incisura angularis is thought to be identified, its position changes from<br />
an erect to a horizontal position (Griffith, 1995).
Mucosal Typt"S:<br />
-11-<br />
Older histologic terminology is both confusing and surgically<br />
meaningless. To impart more surgical meaning, the four distinct types of<br />
mucosa in the adult foregut are divided as follows (Fig. 1-8):<br />
1. Stratified squamous epithelium lines the esophagus. Mucous cells<br />
underliethe most distal esophageal epithelium.<br />
2. Parietal mucosa, which Kay of Glasgow first called the parietal<br />
cell mass and others the oxyntic mucosa, contains the parietal<br />
and chief cells that secrete acid and pepsin, respectively.<br />
3. Antral mucosa contains mucous cells and the G cells that secrete<br />
gastrin. Chief and parietal cells are scarce to absent. In contrast to<br />
the acid surface of the parietal II1UCOSa, the surface of the antral<br />
mucosa is neutral or slightlyalkaline.<br />
4 Duodenal mucosa is characterized by the presence of Brunner<br />
glands, which always extend distally as far as the papilla of Vater<br />
and, in most bodies, beyond the papilla but never as far as the<br />
jejunum. The alkaline mucus secreted by Brunner glands provides<br />
the proximal duodenum <strong>with</strong> more resistance to acid-peptic<br />
ulceration than jejunum (Griffith, 1995).
Mucosal Resistance and Ulceration:<br />
-13-<br />
The esophageal squamous epithelium is the least resistant to acid<br />
pepsin ulceration of the four mucosal types. Following; in order of<br />
increasing resistance, are the duodenal mucosa, the antral mucosa and<br />
the parietal mucosa. Because parietal mucosa is the most resistant to<br />
acid-peptic ulceration, gastric ulcer is rare. Careful histologic studies<br />
have shown that gastric ulcers in the parietal area occur either in ectopic<br />
islands of antral mucosa <strong>with</strong>in the parietal mucosa or in parietal mucosa<br />
that has become "intestinalized" or "antralized" by injury from duodenal<br />
reflux (Capper et al,1966). The surfaces of both the ectopic islands of<br />
antral mucosa and the antralized parietal mucosa are neutral or alkaline<br />
(Oi et at, 1969).<br />
Mucosal Junctions:<br />
1. Mucosal Esophagogastric Junction:<br />
The mucosal esophagogastric junction is readily seen as a sharp<br />
line on the gross mucosal surface. Microscopical sections through this<br />
junction reveal an abrupt transition from stratified squamous epithelium<br />
to gastric mucosa, <strong>with</strong> mucous glands underlying both types of<br />
epithelium (Griffith, 1995).
2_ Antral-Parietal Mucosal Junction:<br />
-14-<br />
No gross anatomic landmarks exist to locate the antral-parietal<br />
mucosal border. However, the border usually lies in the general area<br />
where the rugal folds of the corpus flatten out onto the smooth surface of<br />
the antrom(Landboe,1944). Microscopical sections reveal that the<br />
parietal mucosa gives way to the antral mucosa either abruptly or<br />
gradually in a zone of transition that rarely exceeds 1cm. The antral<br />
parietal border can also be clearly demonstrated by topical Congo red<br />
(CR) or intravenous neutral red. The distance from this border to the<br />
pylorus varies considerably (Pritchard et 81.,1968).<br />
3.Mucosal Gastroduodenal Junction:<br />
The mucosal gastroduodenal junction usually is <strong>with</strong>in the pyloric<br />
sphincter but may be either immediately proximal or immediately distal<br />
to it. Although the gastroduodenal junction may be seen, on close<br />
inspection, to be a straight or dentate line, this junction is not nearly so<br />
obvious as the gross esophagogastric junction. However, microscopical<br />
sections always reveal a sharp transition from antral to duodenal mucosa<br />
(Oi et aI., 1959)_<br />
--rl.
Surgical Applications:<br />
-15-<br />
1. Mucosal Junctions and Peptic Ulcer:<br />
Oi et al (1959) showed that ulcers occur adjacent to mucosal<br />
junctions. Reflux esophagitis and ulceration are most severe immediately<br />
proximal to the esophagogastric junction. With the unusual exception of<br />
postbulbar ulcer, duodenal ulcers occur just distal to the gastroduodenal<br />
junction. Gastric ulcers most commonly occur immediately distal to<br />
either the antral-parietal mucosal junction or the antralized parietal<br />
mucosal junction. Thus, peptic ulcers occur at or adjacent to junctions<br />
where the pH of the mucosal surface changes and always on the alkaline<br />
side ofthe junction (Capper, 1967).<br />
2. PYloric Ulcer:<br />
- Duodenal or Gastric ?'<br />
The antral-duodenal mucosal junction usually lies <strong>with</strong>in the<br />
pyloric channel but may lie proximal or distal to it. Thus, dependent on<br />
the specific variation present, a given channel ulcer may be either<br />
duodenal or gastric. This histologic differentiation mayor may not<br />
explainthe unique intractabilityofpyloric ulcer (Griffith, 1995).
3. Prepyloric Duodenal Ulcer:<br />
-16-<br />
In the unusual to rare patient the antral-duodenal mucosal border<br />
lies as far as 2cm proximal to the pylorus. In these patients, a prepyloric<br />
ulcer may therefore be duodenal rather than gastric (Landboe, 1944).<br />
4. High and Low Gastric Ulcers:<br />
The usual location of the antral-parietal mucosal border in the<br />
distal part of the middle third of the stomach explains the usual location<br />
of gastric ulcers. However, the location of the antral-parietal border<br />
varies considerably. When located in the proximal third of the stomach,<br />
accompanied by antralization of the parietal mucosa, the ulcer is high in<br />
the unusual to rare instance, as high as the cardia. In contrast, when the<br />
antral-parietal border is low, the ulcer is prepyloric (or, in Oi's (1959)<br />
terminology, juxtapyloric). Prepyloric ulcers are much more commonly<br />
gastric than duodenal (Griffith, 1995)<br />
S. The Antral Cell Mass:<br />
In most patients <strong>with</strong> gasstric ulcer and in patients <strong>with</strong>out ulcer but<br />
<strong>with</strong> dyspepsia of gastritis due to duodenal reflux through an
-18-<br />
oblique muscle and proximal to the circular muscle bundleTurtbermore,<br />
gastric ulcers occur most commonly when the circular muscle border<br />
underlies the antral-parietal mucosal border. When these two borders arc<br />
not in proximity to each other, gastric ulcer is rare but gastritis is not<br />
Thus, Oi et aL(1969) entitled their work "A possible dual control<br />
mechanism in the origin of peptic ulcer"; the paper proposes the theses<br />
of mucosal sensitivity and the kinetic strain of musculature activity. This<br />
dual control also influences the formation of duodenal ulcer just distal to<br />
the pylorus. The pyloric sphincter consists of a thickening of the middle<br />
circular muscle; <strong>with</strong> the rare exceptions previously described, this<br />
sphincteric border underlies the antral-duodenal mucosal border<br />
(Griffith, 1995)<br />
Pylorus:<br />
When the pylorus was not readily located because of edema or<br />
fibrosis, its identification would be described by a vein that is highly<br />
constant and has been called the pyloric vein of Mayo (Mayo,1907). The<br />
middle circular muscle thickens gradually to form the pyloric sphincter.<br />
This thickening ends abruptly on the duodenal side. Also, the circular
-19-<br />
muscle fibers of the pyloric sphincter converge on the lesser curvature to<br />
form a torus (Torgensen, 1942).<br />
ARTERIES:<br />
1.Submucosal plexus:<br />
The stomach receives its blood supply through its two mesenteric<br />
borders (the lesser and greater curvatures) (Fig. 2). The right and left<br />
gastric arteries run <strong>with</strong>in the lesser omentum adjacent to the lesser<br />
curvature, and the right and left gastroepiploic arteries and vasa brevia<br />
run <strong>with</strong>in the greater omentum adjacent to the greater curvature. These<br />
arteries supply the stomach by sending off specific <strong>anterior</strong> and <strong>posterior</strong><br />
gastric branches that penetrate the stomach's muscular coat <strong>anterior</strong>ly<br />
and <strong>posterior</strong>ly, close to the lesser and greater curvatures. On reaching<br />
the submucosa, these gastric branches ramify extensively throughout the<br />
entire submucosa. Maintaining a relatively large caliber, these<br />
submucosal ramifications anastomose frequently <strong>with</strong> one another to<br />
form the submucosal plexus, which consists of both the arteries and their<br />
venous-counterparts. Independent branches from the submucosal plexus<br />
supply the mucosa every where except in the lesser curvature, which<br />
receives delicate branches from the right and left gastric arteries<br />
(Griffith, 1955).
-.<br />
Ulceration ofthe Lesser Curvature:<br />
-21-<br />
The frequent incidence of gastric ulcer along the lesser curvature<br />
was once related to its distinctive circulation (Bentley et al., 1952). Now<br />
<strong>with</strong> Oi's dual control mechanism as an explanation, this distinctive<br />
circulation may be of concern only as a factor for the well-known<br />
intractability ofmany lesser curvature ulcers (Oi et at, 1969).<br />
Necrotic Perforation:<br />
Of more importance IS the occurrence of necrotic perforation<br />
along the lesser curvature after its blood supply is interrupted by parietal<br />
<strong>vagotomy</strong>. Although several reported and unreported instances of this<br />
frequently fatal complication occurred in the early and mid-1970s, it is<br />
now well known that necrotic perforation is best avoided by imbricating<br />
tile <strong>anterior</strong> and <strong>posterior</strong> gastric walls over the lesser curvature. In the<br />
absence of these imbrications, factors other than iatrogenic injury to the<br />
lesser curvature during parietal <strong>vagotomy</strong> (e.g. penetrating the curvature<br />
<strong>with</strong> a clamp or burning it <strong>with</strong> use of a cautery, as proposed by many<br />
surgeons) merit consideration. First of all, the gastric wall is thinnest<br />
along the lesser curvature by virtue of the absence of the inner oblique<br />
muscle. Of more importance are the vascular circumstances unique to the<br />
lesser curvature (Griffith, 1995). In an anatomic study by angiography<br />
in cadavers, it was shown that the left gastric arterial branches ligated<br />
during parietal <strong>vagotomy</strong> are more or less end arteries <strong>with</strong> weak<br />
connections to the underlying submucosal plexus (Agossou-Voyeme et<br />
at, 1990). Unfortunately, this part of the plexus has less collateral
-22-<br />
circulation <strong>with</strong>in it than that <strong>with</strong>in the rest of the submucosal plexus<br />
throughout the entire stomach. Also, the submucosal mucosa along the<br />
lesser curvature has relatively poor connections <strong>with</strong> the richer<br />
submucosal mucosa immediately adjacent to it. Thus, after parietal<br />
<strong>vagotomy</strong>, angiography shows a definite avascular band of the gastric<br />
wall 2cm wide coursing along the operated part of the lesser curvature.<br />
Ischemic petforations occur through this avascular band (Griffith,<br />
1995).<br />
CoUateral Circulation:<br />
The large volume of blood flowing through the submucosal plexus<br />
and the abundant anastomoses <strong>with</strong>in the submucosal plexus constitute<br />
the collateral circulation that permits extensive devascularization of the<br />
stomach <strong>with</strong>out causing necrosis (Griffith, 1995). A complete filling of<br />
all intramural vessels of the stomach is demonstrated by injecting any of<br />
the four major arteries after ligating all other extramural vessels. This<br />
confirms (I) the futility of controlling haemorrhage from gastric ulcer by<br />
ligating extrinsic arteries, (2) the viability of a stomach supplied by only<br />
the right gastroepiploic artery (plus or minus the right gastric) and<br />
mobilized to the chest or neck for anastomosis, (3) the viability of a<br />
gastric remnant supplied by only the left gastroepiploic artery and vasa<br />
brevia (after subtotal gasrectomy <strong>with</strong> ligation of the left gastric), and (4)<br />
the viability of a small gastric cuff supplied by only descending<br />
esophageal arteries anastomosing <strong>with</strong> the submucosal plexus after 90<br />
95 percent resection, in which all extrinsic vessels are ligated (Brown et<br />
al., 1952). Fatal ischemic necrosis of the gastric remnant after gastric<br />
resection, for example, is extremely rare, but it can and does occur. This
"<br />
-23-<br />
complication may be caused by atherosclerotic occlusion of the vasa<br />
brevia and left gastroepiploic artery (Jackson, 1949), but more<br />
commonly it is caused by insufficient blood descending from the<br />
esophagus into the submucosal plexus (Fell et aL, 1958).<br />
Hemorrhage:<br />
Because of its extensive submucosal plexus, the stomach is the<br />
most vascularized segment of the alimentary tract. The gastric mucosa<br />
requires a tremendous amount of blood (and energy) to form and secrete<br />
gastric juice. The smallest and most superficial erosions can hemorrhage<br />
profusely. Surgeons must take every precaution to prevent postoperative<br />
hemorrhage from the suture line after incising or transecting the stomach<br />
(Griffith, 1995).<br />
Arteriovenous Shunts:<br />
The submucosal plexus contains many arteriovenous<br />
shunts(Shennan et al., 1954). Vasopressin decreases bleeding from<br />
esophageal varices by closing these arteriovenous shunts and thereby<br />
lowering portal venous pressure(Eiseman et aI., 1960). The shunts close<br />
to supply a maximum of blood to the mucosa for the secretion of the<br />
gastric juice, and open to divert blood from the mucosa when the mucosa<br />
is at rest(Peters et aI., 1958).<br />
2. Pancreaticoduodenal Arcades:<br />
The gastroduodenal artery usually arises from the hepatic artery or<br />
its right and left branches and descends in a position dorsal to the most
-24-<br />
proximal duodenum. Its first branch is the posterosuperior<br />
pancreaticoduodenal (or retroduodenal) artery, which descends in close<br />
association <strong>with</strong> the common bile duct (it often spirals around the distal<br />
common duet) <strong>posterior</strong> to the head of the pancreas and <strong>posterior</strong><br />
duodenum. The retroduodenal artery is relatively large, and its injury by<br />
careless duodenal mobilization, common duct exploration, or<br />
sphincterotomy can cause brisk hemorrhage. After sending off its<br />
retroduodenal branch, the gastroduodenal artery curves <strong>anterior</strong>ly to run<br />
forward and medial to the duodenum, where the head of the pancreas<br />
becomes closely attached to the duodenum The gastroduodenal artery<br />
terminates by dividing into the right gastroepiploic and superior <strong>anterior</strong><br />
pancreaticoduodenal arteries (Griffith, 1995).<br />
The posterosuperior (retroduodenal) and <strong>anterior</strong> pancreatico<br />
duodenal arteries anastomose <strong>with</strong> their inferior <strong>anterior</strong> and <strong>posterior</strong><br />
pancreaticoduodenal counterparts, which anse from the supenor<br />
mesenteric artery (or its first jejunal branches, or its aberrant right<br />
hepatic branch, when present). The <strong>anterior</strong> pancreaticoduodenal arcade<br />
supplies the <strong>anterior</strong> head of the pancreas and <strong>anterior</strong> duodenum <strong>with</strong><br />
specific pancreatic and duodenal branches. The <strong>posterior</strong><br />
pancreaticoduodenal arcade supply the <strong>posterior</strong> head of the pancreas<br />
and <strong>posterior</strong> duodenum in a similar manner. The superior and inferior<br />
pancreaticoduodenal arteries may either branch into two to four vessels<br />
or remain as single trunks. In any event, the anastomosis between the<br />
superior and inferior vessels is direct and rich. This direct and rich<br />
anastomosis in the pancreaticoduodenal arcades represents the most<br />
important route of collateral circulation between the celiac and superior<br />
mesenteric arteries. In only 1 percent or so of instances is it lacking, <strong>with</strong><br />
f
-25-<br />
I, occurs when the gastroduodenal artery arises from the supenor<br />
mesenteric(Griflitb, 1995). This collateral circulation cocems us in the<br />
following respects: (1) it prevents fatal hepatic necrosis after resecting<br />
gastric carcinoma by excising the celiac axis and the hepatic artery<br />
proximal to the origin of the gastroduodenal artery(Clarke,I955); (2) it<br />
is one of the several routes to the liver that explain the unpredictable<br />
results of ligating the hepatic artery(Micbels,I953); and (3) it accounts<br />
for the futility of ligating the gastroduodenal or superior<br />
pancreaticoduodenal arteries to control bleeding from duodenal ulcer, for<br />
bleeding will continue from the inferior pancreaticoduodenal arteries<br />
(Griffith, 1995).<br />
Another anatomic aspect of hemorrhage from the gastroduodenal<br />
or superior pancreaticoduodenal artery cancers a selective decrease in<br />
hepatic arterial flow. Blood destined for the liver by way of the hepatic<br />
artery is diverted through the gastroduodenal artery and out the ulcer.<br />
Thus, blood flow to the liver is decreased by the same mechanism as that<br />
by which a hole in a garden hose decreases flow out of the nozzle. The<br />
result is hepatic anoxia more severe than that caused by the total blood<br />
loss per se (Lee Veen et at. 1952).<br />
3. Celiac Axis:<br />
Although the celiac artery USually trifurcates into the hepatic, left<br />
gastric and splenic arteries, any of these three main branches may arise<br />
independently from any of the other branches or they may branch<br />
independently from the aorta or superior mesenteric artery. Conversely,<br />
the superior mesenteric, middle and left colic, and dorsal pancreatic
-26-<br />
arteries may arise from the celiac axis or from one of its main branches.<br />
Thus, resecting the celiac axis may entail ligating more than one artery,<br />
and, more important, it may interrupt arterial flow to the small intestine,<br />
transverse colon, and pancreas (Appleby, 1953).<br />
4. Left Gastric Artery:<br />
As the left gastric artery ascends to the proximal lesser curvature,<br />
it may send off a large left hepatic branch just before it reaches the lesser<br />
curvature. The left hepatic artery runs <strong>with</strong>in the lesser omentum to the<br />
hilus of the liver. These aberrant left hepatic arteries carry either the<br />
entire or partial arterial supply to the left lobe of the liver (Michels,<br />
1955). Hence, ligating the left gastric artery proximal to the origin of its<br />
left hepatic branch (when present) may cause left lobar hepatic necrosis<br />
(Friesen, 1967). To emphasize the occurrence and importance of this left<br />
hepatic artery, the French refer to the left gastric as the hepatogastric<br />
artery. The occurrence of this aberrant left hepatic artery from the left<br />
gastric artery depends on the variable development of an artery which, in<br />
the embryo, runs across the lesser omentum to connect the left gastric<br />
<strong>with</strong> the hepatic artery in the hilus of the liver. Occasionally, this<br />
connecting artery persists, but usually it becomes oblitrated. When this<br />
artery loses only its connection <strong>with</strong> the hepatic artery, it persists as a left<br />
hepatic from the left gastric. When this artery loses only its connection<br />
<strong>with</strong> the left gastric, it persists as an accessory left gastric from the<br />
hepatic. Another source of an accessory left gastric is the splenic artery,<br />
which from any where along its course occasionally sends a large artery<br />
up to the <strong>posterior</strong> surface of the fundus (As a result of arteriography,<br />
this variation has been called the <strong>posterior</strong> gastric artery). On reaching
-27-<br />
the proximal lesser curvature, the left gastric artery bifurcates into an<br />
ascending esophageal branch (or branches) and a descending gastric<br />
branch, which immediately turns forward and then runs down the lesser<br />
curvature. Usually, this descending gastric artery divides into <strong>anterior</strong><br />
and <strong>posterior</strong> branches, which in tum send off branches to the <strong>anterior</strong><br />
and <strong>posterior</strong> aspects of the lesser curvature (Griffith, 1995). The<br />
descending left gastric artery, or its <strong>anterior</strong> descending branch,<br />
terminates on the lesser curvature by sending out "a crew's foot type<br />
cluster <strong>with</strong> both distal and proximal ramifications". This arterial crew's<br />
foot accompanies the terminal branches of the <strong>anterior</strong> nerve of Latarjet,<br />
which have also beencalled the crow's foot (payne, 1963).<br />
5. Gastroepiploic Arteries and Vasa Brevia:<br />
The right gastroepiploic artery usually anses from the<br />
gastroduodenal artery, but occasionally it branches from the superior<br />
mesenteric. It runs close to the greater curvature <strong>with</strong>in the gastrocolic<br />
ligament and supplies the stomach <strong>with</strong> independent gastric branches,<br />
each of which divides into <strong>anterior</strong> and <strong>posterior</strong> rami that run to the<br />
<strong>anterior</strong> and <strong>posterior</strong> aspects of the greater curvature respectively. The<br />
left gastroepiploic artery arises from the main splenic trunk or its<br />
terminal branches, runs adjacent to the tail of the pancreas and splenic<br />
hilus, and reaches the greater curvature by way of the gastrosplenic<br />
ligament. The vasa brevia usually arises from the splenic trunk or its<br />
terminal branches, but occasionally they anse from the left<br />
gastroepiploic artery. The vasa brevia run through the gastrosplenic<br />
ligament to the greater curvature from the level of the spleen to the<br />
cardia; some may reach the esophagus. Gastric branches from the vasa
-28-<br />
brevia and left gastroepiploic artery are significantly longer than those<br />
from the right gastroepiploic artery and, accordingly, can be more easily<br />
ligated and transected individually in freeing the greater curvature of<br />
omentum to remove the stomach or spleen- The pattern of anastomosis<br />
between the right and left gastroepiploic arteries varies from no gross<br />
connection outside the stomach to a connection so large that the exact<br />
area of anastomosis is difficult to locate. Usually, however, the site of<br />
anastomosis is readilyapparent (Griffith, 1995).<br />
Pylorus and Proximal Duodenum:<br />
The superior aspect of the pylorus and proximal duodenum is<br />
supplied by branches of the right gastric and supraduodenal arteries<br />
descending <strong>with</strong>in the hepatoduodenal ligament The right gatsric artery<br />
usually arises from the hepatic or left hepatic distal to the origin of the<br />
gastroduodenal artery. The supraduodenal artery is inconstant When<br />
present, it usually comes from the retroduodenal or gastroduodenal<br />
artery. Because of varying arterial patterns supplying the anterosuperior<br />
aspect of the duodenum just beyond the pylorus, the vascularity of this<br />
specific area may be weak(Griffith, 1995). This relative ischaemia is<br />
correlated to frequency of ulcer in this area(Reeves, 1920). However, as<br />
in gastric ulcer of the lesser curvature, Oi's dual control mechanism has<br />
replaced this thesis (Oi et al., 1969). Nevertheless, Mayo's "anaemic<br />
spot" may still pertain to intractability. The gastroduodenal artery or its<br />
pancreaticoduodenal and right gastroepiploic branches also send specific<br />
arteries to the inferior and medial aspect of the pylorus and proximal<br />
duodenum by way of the greater omentum. These arteries present<br />
variable patterns. The variations, plus a scanty submucosal plexus in the
-29-<br />
duodenum, may represent an underlying factor in necrosis and leak from<br />
a duodenal stump or anastomsis if the duodenum has been freed<br />
excessivelyfrom its mesenteric attachments (Griffith, 1995).
NERVE SUPPLY<br />
A. SYMPATHETIC NERVES:<br />
-30-<br />
Preganglionic efferent fibers destined for the stomach and<br />
duodenum leave the spinal cord (fifth or sixth to ninth or tenth thoracic<br />
segment), traverse their respective sympathetic ganglia <strong>with</strong>out synapse,<br />
and unite to join the greater splanchnic nerves. On reaching the celiac<br />
ganglia by way of the greater splanchnics, the preganglionic fibers form<br />
a synapse <strong>with</strong> the postganglionic fibers that go to the stomach and<br />
proximal duodenum by way of the various branches of the celiac artery.<br />
The afferent system consists of a single neuron that returns along the<br />
same pathways. In addition to these sympathetic fibers, the canine<br />
abdominal vagi contain adrenergic fibers arising primarily from the<br />
stellate ganglia (Ahlman et aI., (979). The stomach and duodenum<br />
receive most of their sympathetic innervation from the seventh and eight<br />
thoracic spinal segments. The pain of peptic ulcer is therefore most<br />
commonly perceived in the seventh and eight thoracic dermatomes (the<br />
epigastrium). Higher (fifth and sixth) or lower (ninth and tenth) thoracic<br />
segments, however, may also contribute many fibers to the stomach and<br />
duodenum. Thus, we encounter a few patients <strong>with</strong> peptic ulcer who<br />
complain of pain in the lower thorax and others whose pain is around the<br />
umbilicus(Griffith, (995).<br />
B. PARASYMPATHETIC NERVES:<br />
So far as is known, the vagus nerves are the sole source of<br />
parasympathetic innervation of the foregut and midgut The existence of<br />
a splanchnic parasympathetic system from the thoracolumbar spinal<br />
I ....
-31-<br />
segments in humans is only conjectural. Whereas the sympathetic system<br />
innervates the entire embryologic gut, the vagal system innervates only<br />
the foregut and midgut; the sacral parasympathetic system innervates the<br />
hindgut. The boundary between the midgut and hindgut is at the splenic<br />
flexure of the colon. At this boundary, vagal innervation ends and sacral<br />
innervation begins; also at this boundary the superior mesenteric artery<br />
ends and the inferior mesenteric artery begins. Preganglionic efferent<br />
vagal fibers reach the foregut directly. Those to the midgut traverse<br />
various autonomic ganglia <strong>with</strong>out synapse and accompany the arterial<br />
supply to the liver, biliary tract, and intestine. The preganglionic fibers<br />
synapse <strong>with</strong> the postganglionic fibers in the intramural plexuses of the<br />
gut (Griffith, 1995).<br />
1. Vagi from Thorax to Abdomen:<br />
Below each pulmonary hilus, the left and right vagus nerves<br />
descend on either side of the esophagus and, in the lower thorax, branch<br />
and communicate <strong>with</strong> each other as the esophageal plexus around the<br />
esophagus. Depending on the variable number of branches that each<br />
vagus nerve contributes to form this plexus, the complexity of the plexus<br />
varies from body to body. The branches of the esophageal plexus then<br />
unite to form two, and only two, vagal trunks-one <strong>anterior</strong> and the other<br />
<strong>posterior</strong> to the esophagus. The <strong>anterior</strong> vagal trunk divides into the<br />
<strong>anterior</strong> gastric and hepatic vagal divisions. The <strong>posterior</strong> trunk divides<br />
into the <strong>posterior</strong> gastric and celiac vagal divisions (Griffith, 1995).
2. Abdominal Vagi:<br />
a. The Anterior Vagus:<br />
-32-<br />
The <strong>anterior</strong> vagi are conceived in terms of three components: (1)<br />
the hepatic division, (2)the pyloric nerve of McCrea (McCrea, 1924),<br />
and (3) the <strong>anterior</strong> gastric division. The last was termed the principal or<br />
greater <strong>anterior</strong> gastric nerve by Latarjet (1921) and his student<br />
Wertheimer (1922); it is now commonly called the nerve of Latarjet,<br />
The pyloric nerve of McCrea is more often absent than present. When<br />
absent, its pyloric fibers are most commonly a part of the hepatic<br />
division and descend to the pylorus (and distal antrum and proximal<br />
duodenum) <strong>with</strong>in the hepatoduodenal ligament, usually in company<br />
<strong>with</strong> the right gastric artery. In its classic position, the pyloric nerve runs<br />
<strong>with</strong>in the lesser omentum midway between the hepatic and <strong>anterior</strong><br />
gastric divisions to the distal antrum and pylorus. In a lower position, the<br />
nerve of McCrea runs just above and parallel to the nerve of Latarjet. In<br />
this pattern, Loeweneck et al, (1967) called McCrea's pyloric nerve the<br />
antral nerve, and others have referred to the double nerve of Loeweneck.<br />
Finally, the nerves of McCrea and Latarjet may be incorporated into one<br />
nerve, which runs all the way to the pulorus and, rarely, onto the<br />
proximal duodenum (Fig. 3) The hepatic division is constant from the<br />
standpoint that it can always be seen <strong>with</strong>in the stretched-out lesser<br />
omentum just beneath the under surface of the liver in contrast against<br />
the dark background of the caudate lobe of the liver. Usually as a few<br />
small fibers in parallel, the hepatic vagi accompany the vestige of the left<br />
hepatic artery from the left gastric artery (or <strong>with</strong> this aberrant left<br />
hepatic artery when it is present) <strong>with</strong>in the lesser omentum to the
. The Posterior Vagus:<br />
-34-<br />
The <strong>posterior</strong> vagus runs down behind and separate from the<br />
esophagus and upper gastric wall to the level of the left gastric artery<br />
where it becomes closely applied to the lesser curvature (Taylor, 1979).<br />
The <strong>posterior</strong> vagi consist of the <strong>posterior</strong> gastric division (<strong>posterior</strong><br />
nerve of Latarjet) and the celiac division. No specific <strong>posterior</strong> pyloric<br />
nerve exists. Although the <strong>posterior</strong> nerve of Latarjet reaches the distal<br />
antrum in a few bodies, it is usually shorter and has fewer gastric<br />
branches than the <strong>anterior</strong> nerve. Aside from these differences, the<br />
<strong>posterior</strong> gastric nerve may be conceived as the counterpart of the'<br />
<strong>anterior</strong> nerve (Griffith, 1995). The celiac division is constant in two<br />
respects. First, it is the largest of the tour <strong>truncal</strong> divisions and may be<br />
conceived of as the continuation of the <strong>posterior</strong> trunk. Second, it always<br />
descends <strong>with</strong>in the pancreaticoduodenal fold as one large fiber to the<br />
celiac and superior mesenteric autonomic plexuses. Two variations are<br />
of surgical irnponanee. The first concerns its variable positions <strong>with</strong>in<br />
the pancreaticoduodenal fold. Second, as the <strong>posterior</strong> trunk-celiac<br />
division, some or all of the <strong>posterior</strong> gastric vagi may arise just above the<br />
celiac plexus and accompany the left gastric artery to the stomach<br />
(Jackson, 1949) (Fig. 4).
-36-<br />
enough to cause recurrence after conventional parietal <strong>vagotomy</strong>. When<br />
the gastroepiploic nerves are divided by ligating and transecting the<br />
gastroepiploic pedicles it is termed extended highly selective <strong>vagotomy</strong><br />
(Donahue et al., 1993).<br />
To the best of my knowledge, the anatomic routes of the<br />
gastroepiploic nerves have not yet been demonstrated by gross<br />
dissections. From their many experimental studies, Donahue et<br />
al.,(1993) infer that these nerves arise from the most distal branches of<br />
the nerves of Latarjet and pursue intramuscular courses through the<br />
pylorus and duodenum, but where and how they emerge into the greater<br />
omentum is unknown (Griffith, 1995). Others have proposed that the<br />
gastroepiploic nerves arise from some of the descending hepatic vagal<br />
fibers and reach the greater curvature in company <strong>with</strong> major arteries<br />
(the gastroduodenal and its gastroepiploic branch on the right and the<br />
common hepatic, splenic and its gastroepiploic branch on the<br />
left)(Berthoud et al., 1991). However, this proposal is at odds <strong>with</strong> all<br />
our experimental and clinical studies of selective gastric <strong>vagotomy</strong>,<br />
which show that neither the hepatic nor the celiac vagi send efferent<br />
motile or secretory fibers to the stomach (Griffith, 1995).<br />
Segmental Innervation ofThe Stomach:<br />
The fibers from each left and right vagus nerve are distributed<br />
diffusely throughout the parietal mucosa as a result of their intermingling<br />
<strong>with</strong> one another in the esophageal plexus. At the level of this plexus,<br />
however, innervation becomes segmental- Each branch of the esophageal<br />
plexus innervates a segment of parietal mucosa via the vagal trunk to<br />
which it contributes. The <strong>anterior</strong> and <strong>posterior</strong> gastric divisions from the
<strong>anterior</strong> and <strong>posterior</strong> trunks innervate the <strong>anterior</strong> and <strong>posterior</strong> mucosal<br />
surfaces, respectively, and each terminal branch from the gastric<br />
divisions (nerves of Latarjet) innervates its own small segment of<br />
parietal mucosa. Furthermore, by correlating the amount of innervated<br />
mucosa <strong>with</strong> the amount of the contractile response of the stomach, we<br />
showed that each end branch innervates its own small segment of<br />
muscle. Thus, the demonstration of segmental innervation of both the<br />
parietal mucosa and gastric muscle indicates that the innervation of the<br />
whole stomach is segmental (Jones et aI., 1970). The method using<br />
neutral red did not permit visualization of the exact pattern of<br />
innervation of the antral mucosa. However, this method did permit<br />
demonstration of two distinct anatomic routes for innervation of the<br />
antnun. The extramural route is from the end branches of the nerves of<br />
Latarjet. The intramural route is from more proximal branches of the<br />
nerves of Latarjet that run in the submucosa beneath the parietal mucosa<br />
to the antral mucosa (Legros et al., 1969).<br />
Anatomic Basis for Parietal Vagotomy:<br />
Both Dragstedt(1968) and Hollander(l956) rejected our initial<br />
experiments because, at that time, they and all other physiologists and<br />
surgeons believed that <strong>vagotomy</strong> obeyed the law of all or non. This law,<br />
as expressed by Dragstedt et al.,(1947), held that any single fiber<br />
remaining after an incomplete <strong>vagotomy</strong> "appears to be able to activate<br />
the entire glandular apparatus, acting presumably through the<br />
submucosal plexus of Meissner". It therefore followed that the intact<br />
vagal fibers to the antrum after parietal <strong>vagotomy</strong> would activate the<br />
corpus and fundus. They also objected to selective <strong>vagotomy</strong> and
-38-<br />
postulated that intact hepatic and celiac vagal fibers might reach the<br />
stomach by circuitous pathways through their respective autonomic<br />
plexuses (Griffith, 1995). Using methods of both motility and secretion,<br />
we showed that the hepatic and celiac vagi do not innervate the stomach<br />
and therefore, that selective <strong>vagotomy</strong> provides a complete gastric<br />
<strong>vagotomy</strong> (Stavney, 1963).<br />
Finally, after some 10 years of fiuitless effort, we proved that<br />
vagal innervation of the stomach is segmental. Although this finding<br />
revealed that the parietal mucosa could be selectively vagotomized, the<br />
question arose whether the residually innervated antral mucosa could<br />
reinnervate the denervated parietal mucosa by sprouting. Long-term<br />
experiments showed that this type of reinnervation is probably<br />
insignificant (Griffith, 1995).<br />
The Proximal Extent ofParietal Vagotomy:<br />
Dissection of the distal esophagus for parietal selective and total<br />
<strong>vagotomy</strong> concerns the proximal extent of parietal <strong>vagotomy</strong>, which<br />
even though complete, does not prevent recurrence (Amdrup, 1982).<br />
The fibers in question may lie <strong>with</strong>in or deep to the esophageal fascia<br />
propria but not deep the esophageal muscle. The latter fibers innervate<br />
the esophagus and not the stomach(Skandalakis, 1981). To accomplish<br />
a complete <strong>vagotomy</strong>, therefore, the esophagus need not be circumcised<br />
or perforated (Griffith, 1995).<br />
....
-39-<br />
The Distal Extent of Parietal Vagotomy:<br />
The distal extent of parietal <strong>vagotomy</strong> concerns two anatomic<br />
variations- the variable extent of the parietal mucosa distally and the<br />
variable lengths of the <strong>anterior</strong> nerve of Latarjet (Griffith, 1995). If the<br />
<strong>vagotomy</strong> is extended to a point on the lesser curvature 6cm from the<br />
pylorus (which is about as far as can go and still preserve enough antral<br />
motility to prevent gastric stasis), denervation of the distal parietal<br />
mucosa will be complete in most patients. In other patients, the<br />
<strong>vagotomy</strong> of the distal parietal mucosa is incomplete, but the area of<br />
incompleteness is not large enough to cause recurrence, and the<br />
<strong>vagotomy</strong> is therefore adequate. In smaller numbers of patients, perhaps<br />
5 percent or fewer, the parietal mucosa extends to distances, 4,3 and<br />
even less than 2cm from the pylorus. In these patients <strong>with</strong> a<br />
correspondingly and extremely small areas of antral mucosa, the area of<br />
the residually innervated distal parietal mucosa may be large enough for<br />
the incomplete <strong>vagotomy</strong> to be inadequate (Richter et aI., 1987).<br />
With regard to the variable length of the <strong>anterior</strong> nerve of Latarjet,<br />
at one extreme is the nerve that contains all the pyloric fibers from the<br />
hepatic division and the nerve of McCrea and runs all the way to and<br />
beyond the pylorus. At the other extreme is the considerably shorter<br />
nerve that contains no pyloric fibers, which in these instances, are carried<br />
in either or both the hepatic division and nerve of McCrea. These short<br />
nerves of Latarjet barely reach 6-cm point from the pylorus and, in a few<br />
bodies, end well proximal to this point (Skandalakis et aI., 1980). The<br />
shortest nerve of Latarjet ended a measured 8.5cm from the pyloric ring<br />
(Nielsen et al., 1981). Thus, there is no correlation between the distal<br />
extent of the <strong>anterior</strong> nerve ofLatarjet and the distal extent ofthe parietal
-40-<br />
mucosa (Poppen et al., 1976)_ The patients of concern are those who<br />
have extremely small antra and extremely short nerves of Latarjet and<br />
who, therefore, have sizable areas of residual innervation in the distal<br />
parietal mucosa after parietal <strong>vagotomy</strong>. The terminal branches of the<br />
<strong>anterior</strong> nerve of Latarjet on the lesser curvature have been termed the<br />
crow's foot and have been used as a landmark for the distal extent of the<br />
parietal <strong>vagotomy</strong>. Although not all that constant, the crow's foot<br />
landmark has proved workable in most patients (Griffith, 1995).<br />
/ .o(
PHYSIOLOGY<br />
GASTRIC PHYSIOLOGY:<br />
-41-<br />
The four basic functions of the stomach are to store, sterilize, mix<br />
and deliver ingested food in suitable form to the small intestine. The<br />
mechanisms by which the stomach achieves these functions depend on<br />
an integration of humoral, nervous electrophysiologic, and<br />
physicochemical activities. Although performing its function as an<br />
integrated organ, the stomach actually is two organs in series-namely,<br />
the gastric body and fundus and the gastric antrum, the former producing<br />
predominantly acidic secretions in the form of hydrochloric acid,<br />
enzymes, intrinsic factor and electrolytes, and being associated <strong>with</strong><br />
storage capacity, and the latter producing bicarbonate secretions and<br />
antral gastrin and being associated <strong>with</strong> the powerfull muscular activity<br />
that mixes and sieves the gastric chyme in preparation for its coordinated<br />
delivery to the duodenum and small intestine ( . 5) (Elder et at, 1995).<br />
A-Storage Function:<br />
The capacity to eat a meal, sometimes of several courses over a<br />
relatively short time, demands that the stomach achieve isometric<br />
adaptive relaxation to develop the storage capacity <strong>with</strong>out discomfort.<br />
This function depends on intact vagal pathways, whose cell bodies<br />
originate in the dorsal motor nucleus of the vagus in the floor of the<br />
fourth ventricle in the brain stem. Most vagal fibers (90 percent) arc<br />
afferent in carrying massages back from the stomach to the brain stem<br />
(Allen et al.,l980). In the stomach itself, these fibers originate from<br />
stretch receptors in the muscle wall as well as from nerve filaments
-42-<br />
adjacent to epithelial cells, and the rate of discharge increases on passive<br />
distention of the stomach during eating. This sets up long vagal reflex<br />
arcs via the brain stem, which are integral to the process of adaptive<br />
relaxation.<br />
Fig (5): Schematic representation of vagal pathways, gastrin effects, and<br />
local reflex arcs in stomach active in the control of gastric acid secretion.<br />
EeL :::: enterochromaffin-like ceUs (Elder et at, 1995).
-43-<br />
There are other slower-acting chemoreceptors originating from<br />
small nerves m the mucosa that probably ere involved in local<br />
submucosal and myenteric plexus reflexes. Many of the cells in these<br />
plexuses contain neuropeptides (Buck et al., 1986). Predominant among<br />
these is vasoactive intestinal peptide. It has a role in stimulating smooth<br />
muscle contraction in the arterioles adapting blood flow and is involved<br />
in the control of mucus and electrolyte secretion. The vagus nerve is<br />
involved also in inhibition of antral motility as part of a neurohumoral<br />
mechanism when fat, acid, peptides, or amino acids such as tryptophan<br />
enter into the duodenum and smallintestine (Mercer et al., 1990).<br />
The storage function of the stomach therefore is largely dependent<br />
on intact vagal nerve pathways and although some adaptation occurs<br />
after proximal gastric <strong>vagotomy</strong> in humans, impairment of this function<br />
has been noted. Predictably, <strong>vagotomy</strong> changes the pattern of muscle<br />
contraction and leaves the stomach atonic and dilated, retaining its<br />
content for a variable period of time, the procedure results in an<br />
incoordination of gastric emptying, necessitating a drainage procedure<br />
either pyloroplasty or gastroenterostomy after a <strong>truncal</strong> <strong>vagotomy</strong>. This<br />
is avoided after a highly S(;: ••.ctive <strong>vagotomy</strong> where vagal antral<br />
innervationis preserved (Madara, I 991).<br />
B. Acid Secretion: A Sterilizing Force:<br />
The stomach is a unique organ in that the glands in the body can<br />
achieve extremely high concentrations of protons (hydrogen ions) <strong>with</strong>in<br />
the parietal cells as well as in the lumen of the stomach, achieving a<br />
concentration gradient <strong>with</strong> respect to H+ ions of 2.5 million-fold. It<br />
... would seem that the main function of secreting such a powerful acid as
Hcl is to achieve a low pH that will sterilize the food. The stomach<br />
secretes approximately 2500 ml of gastric juice per day. The gastric<br />
glands of the fundus and body of the stomach contain both parietal and<br />
chief or peptic cells and, under appropriate stimulation, these glands can<br />
secrete a fluid containing Bel at a concentration approaching 150 mmol<br />
(Elder et at, 1995).<br />
Acid secretion results after cholenergic stimulation by<br />
acetylcholine, by gastrin and, perhaps most importantly, after histamine.<br />
Recently, it has been proposed that histamine is almost certainly the final<br />
common pathway for stimulation of parietal cells and is released from<br />
enterochromaffin-like cells. Histamine then is bound specifically to the<br />
H2 receptors at the basolateral membrane of the parietal cell and incites<br />
acid stimulation directly via an increase in and activity of basolateral<br />
adenylate cyclase adenosine 3':5'-cyclic phosphatase (Macdennott et<br />
al; 1991) (FiR 6).<br />
Acid secretion is incited initially by psychic stimuli mediated by the<br />
vagus nerves and triggered by the sight, smell, anticipation, and taste of<br />
food (Elder et al., 1995).<br />
...
-,<br />
..........v··<br />
-45-<br />
ECL-CELL<br />
PARIETAL CELL<br />
Fig. 6. Probable role of histamine in the final common pathway of<br />
stimulation of acid secretion. EeL = enterochromaffin-like (Elder et al.,<br />
1995).<br />
Postganglionic vagal nerve fibers innervate the antral G cells,<br />
releasing gastrin-releasing peptide as a transmitter; m addition, the<br />
products of protein digestion, chiefly amino acids m the stomach,<br />
stimulate G cells directly. Gastrin circulates through the portal and<br />
systemic routes to receptors on parietal ceUs and enterochromaffin-like<br />
cells (Le et til., 1987). As gastric pH decreases as a consequence of<br />
increased acid secretion, inhibition of gastrin release takes place when<br />
the lumenal pH reaches 3. There is, therefore, a "gastrin response" to<br />
each meal, which has been shown to be exaggerated in patients <strong>with</strong><br />
duodenal ulcer disease(Ritchie et at, 1991) (Fig. 7).
-48-<br />
The gastric fundus itself does not participate in active peristalsis (Elder<br />
et at, 1995).<br />
D. The Delivery System for Gastric Chyme:<br />
In general, the proximal stomach functions largely as reservoir,<br />
whereas the more muscular and distal antrum acts as a grinder, a sieve<br />
and is the propulsive part of the stomach for delivering chyme into the<br />
duodenum (Elder et 81, 1995).<br />
Gastric emptying is a complex result of several integrated<br />
responses, determined by the volume of the meal, the liquid and solid<br />
components, and individual characteristics of each of those components.<br />
Increasing concentrations of nutrients, salts and acids in a liquid meal<br />
results in fairly slow gastric emptying and conversely, nutrients or acids<br />
at low concentrations are emptied more quickly than those at high<br />
concentrations, the result being that the amount of nutrient or acid<br />
entering the duodenum over time remains constant (Davenport, 1972).<br />
The initial concentration of liquid nutrient entering the duodenum at the<br />
beginning of gastric emptying plays a v""ry important part in determining<br />
the pattern of emptying that follows. In general, there is a rapid initial<br />
and then a slower subsequent phase for the emptying of liquids. All<br />
forms of gastric denervation-that is, <strong>truncal</strong> <strong>vagotomy</strong>, selective gastric<br />
<strong>vagotomy</strong>, and proximal gastric <strong>vagotomy</strong>-accelerate the initial<br />
emptying phase for liquids, as does antral resection. Emptying of solids<br />
from the stomach follows a course different from that of liquids, and<br />
studies using radio-labeled foods or plastic markers have revealed a time<br />
course of gastric emptying that is more a segmoid pattern than linear,<br />
often accompanied by a long initial lag phase during which non of the<br />
•.
-..,.<br />
-49-<br />
, marker or the radio-labeled meat appears to empty. The two-component<br />
hypothesis describing liquid and solid emptying separately does not<br />
totally account for the observed patterns of gastric emptying in humans;<br />
it is likely that several mechanisms, such as proximal gastric tone, antral<br />
contractility, pyloric resistance, duodenal resistance, and gastroduodenal<br />
coordination, are all integrated in response to varying stimuli to produce<br />
the patterns seen in the intact human (Elder et at, 1995).<br />
The electrical stimulation of the <strong>anterior</strong> nerve of Latarjet<br />
produced contractile activity on both <strong>anterior</strong> and <strong>posterior</strong> surfaces of<br />
the antrum, indicating that axons of neurons from the front of the<br />
stomach cross over to the back, thereby essentially maintaining the<br />
potential for normal gastric emptying. This was true crossover<br />
innervation and was not due to the propagation of conduction of<br />
electrical response activity. They found that contractions induced locally<br />
by injection of acetylcholine into a small artery did not propagate. The<br />
cross-over innervation and the direct innervation were both segmental.<br />
This work suggests that the maintenance of the antral branches of the<br />
<strong>anterior</strong> nerve of Latarjet is all that is required for the full functional<br />
mobility ofthe antral musculature (Taylor et at, 1982).<br />
Johnston, (1970) decided that denervation to <strong>with</strong>in 6 cm of the<br />
pylorus on the lesser curve was likely to denervate nearly aU the parietal<br />
cells, Later studies <strong>with</strong> an intra-gastric pH probe confirmed this level,<br />
which usually meant that only one distal branch of the nerve of Latarjet<br />
remained (Johnson, 2000).
Physiologic Basis ofVagotomy:<br />
-50-<br />
Although <strong>vagotomy</strong> undoubtedly blocks the cephalic phase of<br />
gastric secretion, it also reduces the sensitivity of the parietal cells to<br />
circulating gastrin, reducing the acid response to pentagastrin or<br />
histamine by 65-70 percent (Christiansen et aI., 1981). Vagotomy, like<br />
atropine, completely abolishes the acid response to modified sham<br />
feeding in humans, while having no effect on gastrin release in either<br />
normal or DU patients (Konturek et al., 1979). In addition to acid<br />
secretion, the vagus nerve influences receptive relaxation of the stomach<br />
and antral motility as well as function of the liver, pancreas, and small<br />
intestine. It is surprising that TV has so few side effects and how well the<br />
other control mechanisms can compensate (Johnson, 1995).<br />
-Regeneration ofNerves?<br />
That there was an Increase in the recurrence of duodenal ulcer<br />
<strong>with</strong> time and an increase in the positive rate <strong>with</strong> insulin test suggested<br />
that divided nerves might regenerate (Johnson, 2000). Regeneration<br />
would require sprouting to occur across a 1-2cm gap and for the minority<br />
of efferent nerves to grow along the appropriate axon sheaths. Such<br />
efficient nerve regeneration would seem unlikely and indeed acid<br />
secretory studies perfurmed up to I year after myotomy do not show<br />
evidence of a major degree of regeneration. Amdrup et al., (1969)<br />
stated that in their experience the amount of mucosal reinnervation<br />
occurring as a result of the phenomenon of sprouting is insignificant<br />
(Taylor, 1979). The concept of nerves crossing large gaps by sprouting<br />
is not supported by the facts, but it is possible that a small nerve left in<br />
one part of the parietal cell mass could spread the innervation to other ....
-51-<br />
parts <strong>with</strong> time. Experimental studies show that it appears to take place<br />
in a proximal to distal manner rather than the other way around, so<br />
adequate denervation in the upper part of the stomach is particularly<br />
important (Johnson, 2000).<br />
-Adequacy ofincomplete <strong>vagotomy</strong>:<br />
Of principal concern is the process of sprouting, which can occur<br />
only if <strong>vagotomy</strong> is incomplete. Intact postganglionic fibrils at the<br />
cellular level in the residually innervated mucosa send out sprouts that<br />
reinnervate cells in the adjacent denervated mucosa (Murray, 1959).<br />
Another concern is vagal reinnervation by restoration of continuity of<br />
divided nerve ends. Specifically, no one has correlated any restoration of<br />
continuity of divided vagal fibers <strong>with</strong> a resultant return of increased<br />
gastric secretion in either animals or humans (Griffith, 1995).<br />
All types of <strong>vagotomy</strong> transect preganglionic fibers which are<br />
incapable of restoring end-to-end continuity <strong>with</strong> any return of function.<br />
Preganglionic fibers also can not sprout. Thus, the proposal, particularly<br />
after parietal <strong>vagotomy</strong>, that the proximal ends of the transected fibers<br />
may send out fibrils (or sprouts) that penetrate the gastric wall to<br />
reinnervate muscle and mucosa is based on unfounded speculation<br />
(Dragstedt et al., 1950). Sprouts grow only from postganglionic fibers<br />
innervated by intact preganglionic fibers. Sprouting is a microscopic<br />
process <strong>with</strong>in muscle submucosa at the periphery of areas of residual<br />
innervation and is limited in both time and extent to minimal<br />
reinnervation of the adjacent denervated tissue (Murray, 1959). Up to<br />
this point, I have stated that sprouting is probably insignificant and that
-52-<br />
an incomplete but adequate <strong>vagotomy</strong> remains permanently adequate<br />
(Griffith, 1995).<br />
When HoUander,(1956) devised his criteria for interpreting his<br />
insulin test, he believed <strong>vagotomy</strong> obeyed the law of all or none and<br />
assumed there were "no degrees of vagality". He therefore interpreted<br />
his results only as negative or positive. TIlls interpretation still is used in<br />
many centers, despite the fact that it denies the occurrence of various<br />
types of incomplete <strong>vagotomy</strong> <strong>with</strong> variable degrees of adequacy. We<br />
compared the insulin responses of an intact trunk <strong>with</strong> an intact fundic<br />
branch. There are indeed variable degrees of vagality Legros et al.,<br />
(1968). Consequently, as proposed by Ross et al., (1964), positive<br />
insulin responses are classified as adequate or inadequate. The former<br />
response is typically small and delayed and indicates adequate protection<br />
against recurrent ulcer; the latter is large and early and indicates<br />
inadequate protection against recurrence. These two examples of<br />
incomplete <strong>vagotomy</strong> represent the extremes of adequacy and do not<br />
include the shades of gray between. Nonetheless, these revised criteria<br />
have proved to work well in differentiating the incomplete <strong>vagotomy</strong><br />
that causes recurrence from that which does not and they arc much more<br />
useful than Hollander's original criteria (Bell, 1966).
-54-<br />
Peptic ulceration is a common disease in civilized countries and it has<br />
been estimated that about 10010 of aU people suffer from peptic ulceration<br />
during some stage oftheir life (Rifaat, 1988).<br />
Age Incidence:<br />
Duodenal ulcers are rare in people younger than 15 years, and their<br />
incidence reaches a peak between ages 35 and 44 in both men and<br />
women (Langman, 1974).<br />
Sex Ratio:<br />
In 1938, the male-female ratio was 4.5: I, and the ratio has<br />
progressively decreased year by year until currently it is approximately<br />
2: I (Monson et al., 1969).<br />
LOCATION:<br />
Most duodenal ulcers occur in the first part of the duodenum, but<br />
ulcers occurring in different locations must be considered also, in<br />
particular those occurring just proximal to the pyloric sphincter, those in<br />
the pyloric canal, and those distal to the pulb and in the descending and<br />
other portions ofthe duodenum (Kaufman et at, 1957).<br />
The ulcers. whether esophageal, gastric, or duodenal occur at<br />
mucsal junctions. The pyloroduodenai mucosal boundary was sharp and<br />
distinct and might extend for approximately 2 em on either side of the<br />
apex of the pyloric muscular ring (Oi et al., 1959). This provides an<br />
anatomic explanation for the prepyloric ulcer that has all the
-55-<br />
characteristics of a duodenal ulcer: the ulcer IS located III duodenal<br />
mucosa (Christopher et al., J995).<br />
AETIOLOGY:<br />
Most duodenal ulcers are due to gastric hypersecretion of acid and<br />
pepsin and only a few are due to extragastric factors (Rifaat, 1988)<br />
(A) Gastric Hyperacidity:<br />
Clinical and experimental observations indicate that a relative or<br />
absolute excess of acid - pepsin in the gastric secretion is the essential<br />
factor in the pathogenesis ofchronic duodenal ulcer (Rifaat, 1988).<br />
1. Large parietal-cell mass:<br />
The total number of parietal cells counted postmortem in the<br />
stomachs of duodenum ulcer patients is about twice that found in the<br />
stomachs <strong>with</strong>out ulcers, and it has been found that doudcnal ulcers do<br />
not occur below a threshold parietal-cell count of 10 9 (Rifaat, 1988). The<br />
stomachs of those who had duodenal ulcers were larger, thicker, and<br />
more densely populated <strong>with</strong> parietal cells than normal (Cox, 1952). The<br />
greater parietal cell mass may be a genetically inherited trait or may be<br />
the result of work hyperplasia in response to prolonged stimulation. It<br />
has been suggested that the predominance of duodenal ulcer in males<br />
may be due to the met that generally men have more parietal cells than<br />
females (Rifnt, 1988).
2_ Vagal over-activity:<br />
-56-<br />
The vagus nerve is to a great extent responsible for the secretion,<br />
tone and motility of the stomach and it has been suggested that increased<br />
vagal impulses of subconscious origin may be responsible for the<br />
hypersecretion accompanying duodenal ulcer- In duodenal ulcer patients,<br />
the vagal tone is usually abnormally high and the patient is nervous and<br />
irritable and often a heavy smoker (Rifaat, 1988).<br />
3. Hormonal over stimulation:<br />
Except in the Zollinger-Ellison syndrome, serum gastrin essays<br />
have shown that the fasting serum gastrin levels are not higher in ulcer<br />
patients than in control subjects. However, it is possible that dietetic<br />
indiscretions, such as alcoholic excess and ingestion of spiced foods,<br />
may cause excessive hormonal stimulation of gastric secretion (Ritaat,<br />
1988). It has been abundantly recorded that persons <strong>with</strong> chronic<br />
duodenal ulcers secrete, on average, more acid at night, while fasting,<br />
and in response to food and stimulants than do those <strong>with</strong>out such ulcers<br />
(Fordtran et al., 1973).<br />
4. Helioobacter pylori infection:<br />
Helicobacter pylori enhance the risk for ulcer disease and gastric<br />
cancer (Atherton, 2001)_ It has been established beyond reasonable<br />
doubt that infection <strong>with</strong> the spiral, motile organism Helicobacter pylori<br />
bears a causal relationship <strong>with</strong> gastric and duodenal ulcer. H pylori in<br />
metaplastic gastric mucosa in the duodenum causes duodenal ulcer.<br />
The familiality of duodenal ulcer may be cross-infection <strong>with</strong> II<br />
pylori in the family (Chrisopher et at, 1995).
-57-<br />
5. Usc ofnon-steroidal anti-inflammatory drugs:<br />
Most cases of peptic ulceration in the absence of Helicobacter<br />
pylori are associated <strong>with</strong> the use of NSALDs, particularly in the elderly.<br />
Many of these patients can not stop taking these drugs because they<br />
become incapacitated by their arthritis (Johnson, 2(00).<br />
(B)Extragastric Factors: (Rifaat, 1988)<br />
Certain genetic factors and disease states predispose to duodenal<br />
ulcer in a way not always related to gastric secretion.<br />
I. Genetic Factors:<br />
An excess of ulcer disease exists among siblings of ulcer patients<br />
and it has been found that subjects <strong>with</strong> blood group 0 are more<br />
prevalent among ulcer patients than in the control population. Another<br />
important genetic factor is the "secretory status of the individual.<br />
Approximately, 75% of human individuals arc "secretors", i.e. they<br />
secrete into their saliva, gastric juice and urine, water-soluble blood<br />
group antigens identical to those on their red blood cells. 'The remainders<br />
are "non-secretors" and instead of their major blood group antigen, they<br />
secrete the Lewis antigen. These "non- secretors" arc more liable to<br />
duodenal ulceration than secretors,
2, Hyperparathyroidism:<br />
-58-<br />
Primary hyperparathyroidism is associated <strong>with</strong> a higher incidence<br />
of duodenal ulcer In some cases, the ulceration is due to an associated<br />
gastrin-secreting panreatic tumour (Zollinger-Ellison syndrome) while in<br />
others it seems to be due to the hypercalcaemia which results in gastric<br />
hypersecretion,<br />
3. Chronic pancreatitis:<br />
Although patients <strong>with</strong> chronic pancreatitis do not secrete more acid<br />
than healthy subjects, they show an increased susceptibility to peptic<br />
ulceration, particularly duodenal. Because chronic pancreatitis IS<br />
associated <strong>with</strong> low bicarbonate content of the pancreatic juice, the<br />
ulceration is probably due to decreased buffering capacity of the<br />
duodenal secretions.<br />
4. Liver disease:<br />
Cirrhotics are particularly liable to acute erosrve gastritis and<br />
chronic peptic ulceration However, their gastric acidity is lower than in<br />
healthy individuals and much lower than the acidity usually<br />
accompanying duodenal ulcer,<br />
< Pulmonary disease:<br />
Peptic ulcer is at least 3 times more common m patients <strong>with</strong><br />
pulmonary emphysema than in the general population. Conversely,<br />
emphysema occurs 3 to 4 times more often in patients <strong>with</strong> peptic ulcer
-59-<br />
than would be expected from the usual incidence of emphysema in the<br />
general population. Probably, the hypercapnoea of chronic lung disease<br />
predispose to the peptic ulceration.<br />
PATHOLOGY and PATHOGENESIS:<br />
-Mucosal Protective Factors:<br />
Ulceration is inevitably the failure of the mucosa either to protect<br />
itself or to regenerate at a rate sufficient to replace lost cells. Various<br />
cytoprotective mechanisms exist that affect the duodenal epithelium.<br />
These include the mucous layer, which prevents acid and pepsin from<br />
coming into contact <strong>with</strong> the luminal aspect of the cell. Bicarbonate is<br />
secreted by the duodenal mucosa, is present in pancreatic juice, and has<br />
the effect of neutralizing hydrogen ions deep to the mucosal layer<br />
(Christopher et aI., 1995). Other factors include prostaglandin £2,<br />
which, in addition to inhibiting acid secretion, has another much less<br />
well-defined effect that can be demonstrated: Surface active<br />
phospholipids have been shown to protect the _gastric, and possibly<br />
duodenal as well as epithelial, cell in the experimental animal, but<br />
interference <strong>with</strong> this mechanism by ethanol and H. pylori may<br />
predispose to their damage (Hills, 1993). Mucosal blood flow is another<br />
important factor (Jacobson, 1992). Nitric oxide produce divergent<br />
effects, and its donators are concerned <strong>with</strong> the regulation of mucosal<br />
blood flow and, therefore, its protection (Lopez et at, 1993).
-60-<br />
- Characteristics of chronic duodenal'ulcer:<br />
Chronic duodenal ulcer is usually solitary and always situated in the<br />
supra-ampullary portion of the duodenum. Sometimes, two ulcers are<br />
present, one on the <strong>anterior</strong> surface and the other on the <strong>posterior</strong> surface<br />
of the first inch of the duodenum (kissing ulcers), and, occasionally, a<br />
duodenal ulcer is associated <strong>with</strong> a chronic gastric ulcer in the pyloric<br />
region of the stomach (combined ulcers). The ulcer is usually round or<br />
oval and small, measuring I inch or less in diameter. The edges are<br />
regular and sharply defined, extending steeply to the floor to produce a<br />
pouched-out appearance. The floor is deep and regular <strong>with</strong> an indurated<br />
fibrous base. Almost invariably, there is complete destruction of the<br />
muscle coat so that the floor is formed by the thickened subserous layer<br />
alone. The surrounding mucosa is often thrown into folds which<br />
converge on the ulcer as a result of scarring. The serosa is thickened and<br />
scarred when rubbed gently <strong>with</strong> a swab, it becomes stippled <strong>with</strong><br />
numerous capillary vessels and petechial haemorrhages (stippling sign).<br />
The related omentum is often thickened and scarred and there may be<br />
multiple adhesions to neighbouring organs (Rifaat, 1988). Gastric outlet<br />
stenosis incites dilatation of the stomach <strong>with</strong> hypertrophy of the gastric<br />
musculature and increased acid output, thus increasing the<br />
aggressivenessofthe process ofulceration (Taylor, 1995).<br />
- Mucosal Regeneration:<br />
The epithelial cells surrounding a duodenal ulcer replicate at a<br />
greater rate than normal. Those closest to the ulcer edge divide more<br />
rapidly than those further away (Smedley et at, 1988). The mechanism<br />
.I
-61-<br />
responsible for this almost certainly involves epidermal growth factors<br />
(EGFs) suggested by the demonstration of an increase of EGF receptor<br />
expression on cells at the edge of a peptic ulcer (Tarnawski et al.,<br />
1992). Epidermal growth factor has been shown to influence the rate of<br />
cell proliferation in the small intestine (Coodlad, 1989), and salivary<br />
EGF may promote healing of peptic ulcer (Konturek, 1990).<br />
Transforming growth factor alpha interacts <strong>with</strong> the same receptor as<br />
EGF and is also found in gastric mucosal cells (Polk et al., 1992). Basic<br />
fibroblast growth factor is responsible for angiogenesis and may be<br />
important in ulcer healing (Folkman et aI., 1991). Insulin-like growth<br />
factors are also found in the proliferating margin of crypt cells in the<br />
small intestine (Vanderhoffet al., 1992).<br />
- Helicobacter pylori:<br />
The organism is characterized by a powerful urease <strong>with</strong> resultant<br />
production of amonia from urea. It exists deep to the mucous layer of the<br />
stomach, its distribution being dependent on the acid-secreting<br />
characteristics. In high secretory states, the orgarusrn tends to be<br />
distributed more distally and, if acid secretion is low or inhibiu.,', the<br />
proximal area of infection migrates cephalad. Apart from the pH effects<br />
of infection, the organism has been shown to interfere <strong>with</strong> the surfactant<br />
effect of surface-active phospholipids, which protect the epithelial cell.<br />
There is also electron-microscopical evidence to suggest that H. pylori<br />
ingests these phospholipid, even perhaps employing them for self<br />
protection (Hills, 1993). More difficult to establish is the precise<br />
relationship <strong>with</strong> duodenal ulcer production. One suggestion is the<br />
gastrin mechanism: The release of ammonia ions in close association
-62-<br />
<strong>with</strong> the antrum tends to maintain a high pH favoring continual secretion<br />
of gastrin and, thereby, acid. Hypergastrinemia has been demonstrated in<br />
infected patients compared <strong>with</strong> controls. Eradication of H pylori has<br />
been shown to result in a reduction in gastrin level to normal (Prewett et<br />
at,I991).<br />
CLINICAL PICTURE:<br />
The cardinal symptom of duodenal ulcer is epigastric pain, located<br />
midway between the xiphisternum and umbilicus and slightly to the right of<br />
the midline. When the patient is asked to indicate the site of his pain, he can<br />
often localize the pain accurately <strong>with</strong> a fmger or group of fingers. A positive<br />
pointing test is the most valuable sign of chronic duodenal ulcer. Deep<br />
palpation usually reveals tenderness in the mid-epigastrium, either in the<br />
middle line or just to the right of it, but never to the left. During acute<br />
exacerbations, slight rigidity may be elicited over the upper part of the right<br />
rectus muscle (Rifaat, t 988). The pain commonly wakes the patient at night,<br />
often at approximately 2:00 AM (Christopher et al., 1995). The ulcer pain is<br />
relieved by anything that dilutes or buffers the gastric acid, e.g, plain water,<br />
milk, antacids or food. As a I esult, the patient often carries biscuits and<br />
alkaline tablets in his pockets and keeps a glass of milk by his bedside at night<br />
(Rifaat, 1988).<br />
Heartburn occurs in a number of patients, but it usually follows closely<br />
the development of the abdominal pain (Christopher et al., 1995). Acid<br />
eructations are common complaints but vomiting seldom occur spontaneously<br />
and when it does it relieves the patient so that it is frequently self-induced.
-63-<br />
Since the appetite is good and food apparently relieves the pain, no loss of<br />
weight occurs and the patient may even gain weight (Rifaat, 1988).<br />
When symptoms first occur, they usually arc troublesome for several<br />
hours each day for a period of I to 2 weeks. This experience is followed by a<br />
remission period, often extending for several months. The cycle then is<br />
repeated, <strong>with</strong> the difference that the episodes of pain become longer and the<br />
periods ofremission shorter (Christopher et al., 19(5).<br />
DIAGNOSIS & INVESTIGAnONS:<br />
The mainstays of objective diagnosis are the barium meal<br />
examination and endoscopy. Together these two procedures provide<br />
considerable accuracy (Barnes et al., 1974). The diagnosis can be made<br />
<strong>with</strong> absolute certainty only by endoscopy or direct inspection<br />
(Christopher et aI., 1995).<br />
COMPLICATIONS:<br />
In many countries, there is steady increase In the incidence of<br />
complications of peptic ulcer in patients of both sexes older than 65<br />
years (Johnson, 1995). Over four thousand people die annually in<br />
England and Wales from peptic ulcer disease(Taylor et aI., Dec. 1985).<br />
A possible explanation for the marked increase in ulcer-associated<br />
mortality in the elderly woman is the increased use of non-steroidal anti<br />
inflammatory drugs (NSAIDs) that has occurred in recent years. Other<br />
possibility that may be considered to account for this rise in mortality are<br />
the increased incidence of colonization of the stomach and duodenum by
-64-<br />
II. pylori and the marked reduction In use of peptic ulcer elective<br />
surgical procedures (Taylor, 1995).<br />
On reaching the age of 50 years, duodenal ulcer patients (both male<br />
and female) run a 25 percent risk of significant ulcer haemorrhage <strong>with</strong>in<br />
the next decade of their lives. The corresponding risk figures for<br />
perforation over the decade between the ages of 50 and 60 years are 9<br />
percent for men and 7 percent for women. With each subsequent decade<br />
thereafter, these incidences rise. The overall mortality for upper<br />
gastrointestinal bleeding remains today, as it has throughout this century,<br />
at 10 percent, and the mortality for ulcer perforation is at least 10 percent<br />
(Pulvertaft, 1968). Apart from perforation and hemorrhage, chronic<br />
duodenal ulcer may result in stenosis of the first part of the duodenum<br />
(Christopher et aL, 1995). Gastric outlet stenosis is produced by<br />
aggressive duodenal ulceration, which lays down dense fibrous tissue in<br />
the region of the ulcer. Gastric outlet stenosis incites dilatation of the<br />
stomach <strong>with</strong> hypertrophy of the gastric musculature and increased acid<br />
output, thus increasing the aggressiveness of the process of ulceration.<br />
The aggressive <strong>posterior</strong> duodenal ulcer, which may penetrate into the<br />
pancreas or <strong>posterior</strong> abdominal wall, sometimes giVing nse to<br />
pancreatitis or abscess formation (Taylor, 1995).
-65-<br />
TREATMENT OF CHRONIC DUODENAL ULCER:<br />
The massive changes in the treatment of duodenal ulcer disease that<br />
have taken place in recent years as a result of the availability of<br />
efficacious medical treatment have called into question the role of<br />
elective surgical intervention in the treatment of this condition (Taylor,<br />
1995). It is beyond dispute that a major decline has occurred in the<br />
number of patients undergoing elective duodenal ulcer surgery (Taylor<br />
et aI., 1990).<br />
Currently there are three options for medical therapy of ulcer<br />
disease: H2-receptor antagonists (H2-RAs), proton pump inhibitors, and<br />
triple therapy. Acid suppression either by blocking the H2-receptors or<br />
proton pump inhibitors has the intrinsic disadvantage of recurrence<br />
<strong>with</strong>out expensive, long-term maintenance therapy Triple therapy is<br />
designed to eradicate the underlying H pylori infection (Cuschieri,<br />
1995). The vast majority of ulcers can be healed by these acid-reducing<br />
drugs, but long-term continuous maintenance therapy is essential to<br />
avoid recurrence allll complications. The reduction in the incidence of<br />
serious complications (hemorrhage and perforation) by H2RA therapy<br />
appears to be of the same order at; that achieved by ulcer surgery. Some<br />
10-15 percent of patients prove refractory (non-healing after 2 months of<br />
therapy) to H2RAs (penston et aL, 1992),<br />
Omeprazol and lansoprazol produce covalent (reversible) inhibition<br />
of the acid proton pump. Acid secretion is suppressed, and the pH of the<br />
gastric contents remains above 3.0 for at least 16 hours per 24-hour<br />
period while the patient is on treatment. However, maintenance therapy<br />
is necessary to prevent recurrence and reduce complications (Bader et<br />
at, 1989). Long-term therapy <strong>with</strong> proton pump inhibitors has its
-66-<br />
problems. These are the consequence of the profound acid inhibition and<br />
include persistent hypergastrinemia <strong>with</strong> hyperplasia of the<br />
enterochromaffin cells, bacterial overgrowth of the upper gastrointestinal<br />
tract, and the risk of infections. Others are metabolic in nature:<br />
malabsorption of vitamin B12 <strong>with</strong> reduction of the body stores of this<br />
vitamin and reduction of the serum iron levels <strong>with</strong> development of iron<br />
deficiency anemia (Koop, 1992). Awareness of the limitations of triple<br />
therapy is, therefore, important since this therapeutic approach has<br />
several problems. There is a high noncompliance rate due to the side<br />
effects of therapy and persistence of ulcer symptoms during the<br />
treatment. Resistance to antibiotics develops in some patients and<br />
therapy fails to eradicate the infection in 20 percent of patients. Serious<br />
side effects including fungal infections, diarrhea and<br />
pseudomembraneous colitis occur in 30 percent of patients (Cuschieri,<br />
1995).<br />
Despite the large number of medical treatments, the recurrence rate<br />
of ulcers treated non-operatively is on the order of 90% at 1 year,<br />
regardless of which medication is used. Further, the widespread use of<br />
these agents for the past ]0 years has not diminished the mortality due to<br />
complications of ulcer disease, particularly in the elderly (Mouiel et al.,<br />
1993). Although ulcer healing can be achieved in some 90 percent of<br />
patients <strong>with</strong>in 2 months of starting medication, almost 90 percent of<br />
these patients will relapse by the end of t year of stopping treatment. Hr<br />
receptor antagonists have presumably had no appreciable beneficial<br />
effect on ulcer-associated mortality because immediately on stopping<br />
treatment <strong>with</strong> these drugs, the acid output returns to pretreatment levels<br />
and the ulcer diathesis still exists, leaving the elderly patient vulnerable
-67-<br />
to the potentially fatal complications of perforation and bleeding<br />
(Taylor, 1995). Duodenal ulcer has a natural cycle of healing and<br />
relapse; and treatment by acid-inhibitory drugs, whether H2-receptor<br />
antagonists or proton pump inhibitors, was effective only while they<br />
were being taken, <strong>with</strong> a high relapse rate when they were stopped<br />
(Johnson, 2000). It could be recommended, therefore, that those subjects<br />
<strong>with</strong> a well-established ulcer diathesis who frequently relapse after<br />
cessation of treatment <strong>with</strong> Hrreceptor antagonists should be considered<br />
for elective peptic ulcer operation at approximately the age of 50 or<br />
perhaps 60 years. Deferring elective ulcer treatment thereafter would<br />
increase the postoperative mortality in view of the increased incidence of<br />
coexisting medication problems, such as are encountered <strong>with</strong> therapy<br />
for coronary artery disease, hypertension, respiratory disease and the risk<br />
ofstroke (Taylor, 1995).<br />
Surgery has been the mainstay for the management of<br />
complications of peptic ulcer disease since the 1930s (Laws et al.,<br />
1993). Although the incidence of elective surgery for peptic ulcer has<br />
diminished dramatically in recent years, the number of operations for<br />
bleeding or perforation has changed liitlc. Indeed, it has increased in the<br />
elderly, many of whom are on NSAlDs and have no warning symptoms<br />
before the complicarion arises (i.e., the complication is the first<br />
presentation) (Chen, 1996).<br />
The primary aim of any long-term treatment of peptic ulcer is; first,<br />
to keep the ulcer healed to prevent life-threatening complications and,<br />
second, to relieve symptoms (Johnson, 2000). The only established way<br />
of maintaining ulcer healing is surgical repair of the ulcer (Jordan,<br />
1989).
-68-<br />
The other major consideration that will apply to the continued use<br />
of peptic ulcer operations is one of cost In these increasingly cost<br />
conscious times where health care must he assessed in financial terms,<br />
the alternative strategies of surgical therapy and drug therapy for ulcers<br />
will have to be compared, taking into account financial considerations in<br />
the long term. As operative treatment most commonly leads to life-long<br />
healing of peptic ulceration and overcomes the risks of perforation or<br />
bleeding from the ulcer, thus strategy may compare favorably to<br />
prolonged or repeated use of drug therapy, which in itself is increasingly<br />
expensive (Taylor, 1995).<br />
The main indication for elective surgery now is true failure of drug<br />
treatment, which takes two forms, the first is failure of the ulcer to heal<br />
after 8 weeks of full-dose treatment <strong>with</strong> drugs and the second as an<br />
alternative to long-term full-dose maintenance therapy <strong>with</strong> acid<br />
suppressing drugs. The patient should be given the choice of a lifetime of<br />
drugs or an operation. This decision would depend on social factors, the<br />
patient's age and temperament, and on economic factors In some<br />
countries, poor patients cannot afford the drugs but can have an<br />
operation free of charge (Johnson, 1995). Intractable pain, often<br />
producing loss of sleep and social or economic dislocation, used to be<br />
the major indication for elective surgical ulcer repair (Taylor, 1995).<br />
Gastric outlet stenosis produced by aggressive duodenal ulceration<br />
remams one of the absolute indications for surgical repair of ulcer<br />
(Keynes, 1965). Medical treatment is unlikely to influence the fibrosed<br />
duodenum, and so some form of therapeutic intervention is necessary<br />
(Kreel et al., 19(5). A further remaining indication for surgical<br />
treatment of ulcer is the aggressive <strong>posterior</strong> duodenal ulcer, which may
-69-<br />
penetrate into the pancreas or <strong>posterior</strong> abdominal wall, sometimes<br />
giving rise to pancreatitis or abscess formation. Under these<br />
circumstances, healing is much more difficult to achieve <strong>with</strong> drug<br />
therapy (Taylor, 1995). Perforation is an absolute indication for surgical<br />
treatment in the early hours following its occurrence (Kay, 1978).<br />
Operations for duodenal ulcer have ranged from radical forms of<br />
gastric resection to the conservative highly selective <strong>vagotomy</strong><br />
(Donicott et at, 1978). The more aggressive the approach, in tenus of<br />
acid reduction, the more likely is the ulcer to remain healed but at the<br />
price of some undesirable and often incurable side effects such as<br />
dumping and diarrhea. The more conservative the surgical procedure, the<br />
less likely it is to have undesirable side effects; however, there is a<br />
higher incidence of ulcer recurrence <strong>with</strong> the more conservative forms of<br />
operation (Jordan, 1976).<br />
In peptic-ulcer surgery there is a delicate balance between the<br />
expedients of operative safety, simplicity and speed and the problems of<br />
dumping, diarrhea, duodenogastric reflux, recurrent dyspepsia and death<br />
(Taylor et al., 1982). Thus, there is a potential for major reduction in<br />
ulcer-associated mortality by the carefuliy sei-cted application of<br />
elective surgical repair of peptic ulcer (Taylor, 1995). The operation of<br />
choice has progressively changed from gastroenterostomy to gastric<br />
resection to some form of <strong>vagotomy</strong> alone or combined <strong>with</strong> a drainage<br />
procedure (Laws et at, 1993).
-71-<br />
patients to relieve the symptoms of gastric stasis. Later, Dragstedt<br />
advocated the transabdominal, perihiatal approach to the vagal trunks,<br />
followed by a pyloroplasty or gastroenterostomy. Since 1943, <strong>vagotomy</strong><br />
of some type has become a standard operation for DU (Johnson, 1995).<br />
Virtually all operations for duodenal ulcer include some form of<br />
<strong>vagotomy</strong> (Laws et at, 1993). Since its introduction more than 10 years<br />
ago, parietal cell <strong>vagotomy</strong> has gradually become accepted as the<br />
method of choice in the surgical treatment of chronic duodenal ulcer<br />
mainly because of the well-documented low postoperative morbidity<br />
(GrafTner et al., 1985). The fact that <strong>vagotomy</strong> heals duodenal ulcers by<br />
reducing acid secretion is well known (J. Mouiel et aL, 1993).<br />
Vagotomy fulfilled Dragstedt's aim of being a safe alternative to<br />
gastrectomy; but it had a rather high recurrent ulcer rate, and some<br />
patients still suffered from dumping syndrome, diarrhoea, and bile reflux<br />
(Johnson, 20(0). Total <strong>truncal</strong> <strong>vagotomy</strong> leads to an almost total<br />
reduction of gastric acid secretion., which is often accompanied by<br />
pyloric spasm leading to gastric stasis (Moniel et aI., 1993). After<br />
<strong>truncal</strong> <strong>vagotomy</strong> and gastroenterostomy early emptying of both liquids<br />
and solids was increased and there was an overall increase in gastric<br />
emptying over the 2-h period. Rapid gastric emptying may be<br />
responsible, at least in part, for dumping and post<strong>vagotomy</strong> diarrhea; this<br />
is particularly the case for the early phase of emptying where gastric<br />
incontinence after <strong>vagotomy</strong> and drainage leads to the rapid emptying of<br />
both liquids and solids emphasizing the importance of the pylorus in<br />
controlling and monitoring gastric emptying (Caylor et aI., Aug. 1985).<br />
A gastric drainage procedure subsequently becomes complicated by a
-72-<br />
marginal ulcer which continues to require surgical intervention (Laws et<br />
a1.,1993).<br />
Proximal gastric <strong>vagotomy</strong> (PGV) is a modification of <strong>truncal</strong><br />
<strong>vagotomy</strong>, which was introduced by Dragstedt for the treatment of<br />
duodenal ulcer (DU) in 1943. It is a technically demanding operation;<br />
but when performed by an experienced surgeon, it is safe and gives a<br />
cure rate for DlJ of more than 90%, <strong>with</strong> minimal side effects (Johnson,<br />
2000). The main purpose of PGV is to avoid a pyloroplasty <strong>with</strong> its<br />
attendant side effects (Johnson, 1995).<br />
On the assumption that total <strong>vagotomy</strong> of the whole of the<br />
derivatives of fore-gut and mid-gut was the main cause of the side<br />
effects, a modification was devised by Griffith,(1960) in which only the<br />
stomach was denervated, leaving the nerves to the liver and intestine<br />
intact. This was named "selective <strong>vagotomy</strong>". However, because a<br />
pyloroplasty or gastroenterostomy was still required, the side effects<br />
remained (even if reduced to some extent), and this modification did not<br />
become generally used. In the meantime, Holle et al. had devised an<br />
even more selective operation in which the proximal part of the stomach,<br />
which contained the parietal cells, was denervated, leaving the muscular<br />
antrum, which is important for gastric emptying, still innervated.<br />
However, they still performed a pyloroplasty, which was responsible for<br />
some continued side effects (dumping and diarrhea) (Johnson, 2000).<br />
Johnson (1970) in England and Amdrup (1978) in Denmark<br />
completed the evolution of <strong>vagotomy</strong> by avoiding a drainage procedure<br />
altogether. This operation was initially called "highly selective<br />
<strong>vagotomy</strong>" to distinguish it from selective <strong>vagotomy</strong>, but other names<br />
include "proximal gastric <strong>vagotomy</strong>" and "parietal cell <strong>vagotomy</strong>". The
I<br />
I<br />
I<br />
I I<br />
I<br />
-73·<br />
anatomic and physiologic bases were sound in that gall bladder<br />
emptying, for example, is unaffected, but bile reflux into the stomach did<br />
not differ regardless of whether there was a pyloroplasty (Eriksson et<br />
aL,I990).<br />
Proximal gastric <strong>vagotomy</strong> was more technically demanding than<br />
<strong>truncal</strong> <strong>vagotomy</strong> and took longer to perform. The two challenges to the<br />
surgeon are (I) to ensure that the relevant part of the stomach is<br />
completely denervated and (2) that the junction between parietal cell<br />
mass and muscular antrum is correctly identified so the antral muscle<br />
remain innervated. The problem is that there is no visual demarcation<br />
line (Johnson, 1981). In conventional highly selective <strong>vagotomy</strong> it is the<br />
<strong>posterior</strong> parietal ceU mass. which is the most difficult area of the<br />
stomach to denervate, particularly because of fibers at the<br />
oesophagogastric junction and at the antral-corpus junction (T ylor et<br />
aI., 1990) (fig, 8).<br />
Fig. 8: Four areas are difficult to<br />
denervate during proximal gastric<br />
<strong>vagotomy</strong>. A: greater curve at<br />
antrallbody junction; B: <strong>posterior</strong><br />
aspect of lesser curve; C:<br />
<strong>posterior</strong> aspect of cardia; D:<br />
supenor aspect of fundus<br />
(Johnson, 2(00).
-74-<br />
It has been largely as a result of ulcer recurrence rates that<br />
operations for duodenal ulcer either stand or fall. Some recurrences are<br />
inevitable and are treatable by drugs or further surgical procedures,<br />
whereas the sequalae of dumping and diarrhoea are incurable.<br />
Gastrojejunostomy was safe, simple and had few postoperative sequalae,<br />
but floundered, almost half a century ago, on the grounds of high<br />
recurrence rates. Rates of recurrence exceeding 25 percent, which have<br />
been reported in the long term after highly selective <strong>vagotomy</strong>, have<br />
aroused particular concern (Koffman et aI., 1983). These rates are<br />
higher in the hands of the inexperienced surgeon (Blackett et aL, 1981).<br />
In view of the high rate of late recurrence following HSV, some<br />
surgeons extend the denervation lower on the lesser curvature, cutting<br />
one or two of the branches of the crow's foot. Such an HSV, <strong>with</strong><br />
extensive mobilization of the cardia and esophagus creates the risk of<br />
gastroesophageal reflux, whichrequirescorrection (Dubois, 2000).<br />
Highly selective <strong>vagotomy</strong> is not <strong>with</strong>out its disadvantages,<br />
namely that the operation is tedious and time-consuming to perform,<br />
damage to the nerve of Latarjet may produce gastric stasis and there is a<br />
risk of ischaemic necrosis which, when it does occur, is not uncommonly<br />
fatal. The major objection to highly selective <strong>vagotomy</strong> raised by<br />
surgeons is that the operation is tedious and time-consuming, as every<br />
nerve and blood vessel passing onto the lesser curve of the stomach,<br />
above the incisura, hasto be ligated and divided (Taylor, 1979).<br />
Elective peptic ulcer surgery has been affected not only by the<br />
availability of the H2-receptor antagonists but also by concern relating to<br />
the side-effects of <strong>truncal</strong> <strong>vagotomy</strong> and the high rates of recurrence<br />
after highly selective <strong>vagotomy</strong> (Taylor et al., 1990). Highly selective
-75-<br />
<strong>vagotomy</strong> may be associated <strong>with</strong> recurrence rates of less than 5%, but<br />
rates of over 20% have been recorded in some series because of<br />
inadequate denervation of the parietal cell mass (Taylor et al., 1982).<br />
Consequently, the operation of conventional highly selective <strong>vagotomy</strong><br />
was somewhat slow to gain acceptance in many centers. Over the last<br />
decade, it has become increasingly apparent that conventional highly<br />
selective <strong>vagotomy</strong> in the hands of many surgeons is an unsatisfactory<br />
procedure for chronic duodenal ulcer, largely because of ever-increasing<br />
incidences of recurrent peptic ulceration. These are reported to be as<br />
high as 30 per cent over follow-up periods of up to 18 years in the<br />
excellent center in Copenhagen from which the operation was first<br />
descnbed (Taylor, 1995).<br />
Lesser curve <strong>seromyotomy</strong> was devised <strong>with</strong> the intention of<br />
providing a simplified technique for denervating the parietal cell mass<br />
(Taylor et at, 1982). The main advantage of lesser curve myotomy is<br />
that it produces a highly selective <strong>vagotomy</strong> in an expeditiously and<br />
easily performed manner. There should be neither risk of damage to the<br />
nerve of Latarjet, which need not be identified, nor of ischaemic necrosis<br />
ofthe lesser curvature (Tavlor; 1979).<br />
In considering the structure and deposition of these branches of<br />
the nerve of Latarjet that pass along the <strong>anterior</strong> and <strong>posterior</strong> walls of<br />
the stomach and that innervate the parietal cell mass, there are three<br />
anatomic points of fundamental importance. First, there is no particular<br />
predilection for these nerves to run <strong>with</strong> blood vessels along the lesser<br />
curvature of the stomach. Second, the nerves can be traced for some<br />
distance beneath the serous coat before they penetrate the gastric<br />
musculature. Third, the vagus nerve branches always run superficial to,
-76-<br />
and more obliquely than the blood vessels along the lesser- curvature of<br />
the stomach. A fourth anatomic point worthy of consideration is that the<br />
main nerve of Laterjet often bifurcates, or even trifurcates, very high<br />
along the lesser curvature of the stomach and well proximal to the classic<br />
position ofthe CTOW'S foot at the incisura angularis (Fig. 9).<br />
Fig. 9: Anatomic relationship of the nerve of Latarjet, which lies<br />
superficial to the left gastric vessels. There is no particular predilection<br />
for the branches of the nerve of Latarjet to run <strong>with</strong> the vessels (Taylor,<br />
1995).<br />
Applying these anatomic considerations, lesser curvature <strong>seromyotomy</strong><br />
was devised. In this operation, the branches of the nerve of Latarjet are<br />
divided as they run intimately welded to the serosa close to the lesser<br />
curvature of the stomach . Division of the longitudinal and superficial<br />
circular muscle fibers produces wide separation of the divided nerve<br />
\ "'i
-77-<br />
bundles. The blood vessels running across the lesser curvature onto the<br />
<strong>anterior</strong> wall of the stomach are divided, but those that form the end<br />
arteries directly entering the lesser curvature are preserved, thus<br />
overcoming any possibility of ischemic necrosis of the lesser curvature<br />
of the stomach. This complication, which accounts for the major<br />
mortality associated <strong>with</strong> conventional highly selective <strong>vagotomy</strong>, has<br />
not been recorded after ASPTV in several thousand cases (Taylor,<br />
1995).<br />
Following <strong>vagotomy</strong>, intragastric pressure after a meal is increased.<br />
It is possible that by virtue of dividing the full thickness of the circular<br />
muscle of the corpus of the stomach in performing <strong>seromyotomy</strong> the loss<br />
of accommodation for a meal is to some extent compensated and that<br />
rapid early emptying does not occur. If this was true, not only should<br />
dumping and diarrhoea be reduced but also distension or epigastric<br />
fullness, present in up to 50 per cent of patients after <strong>vagotomy</strong>, should<br />
be less or absent. This would provide <strong>seromyotomy</strong> <strong>with</strong> a potential<br />
advantage over all existing forms of <strong>vagotomy</strong> including the<br />
conventional highlyselected procedure (Taylor et al, Aug. 1985)_<br />
Initially in humans, the <strong>seromyotomy</strong> was performed ?long both<br />
<strong>anterior</strong> and <strong>posterior</strong> walls of the stomach (Taylor, 1995). Although<br />
this operation is quick and easy to carry out, the <strong>posterior</strong> wall of the<br />
stomach is less accessible and therefore more difficult to denervate, in<br />
particular close to the gastro-oesophageal junction (Taylor et al., 1982).<br />
After performing some of these procedures, the author decided to modify<br />
the operation and carry out <strong>anterior</strong> lesser curvature <strong>seromyotomy</strong> <strong>with</strong><br />
<strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong>. The reasons for this were again technical.<br />
Experience soon showed that the addition of <strong>posterior</strong> trucal <strong>vagotomy</strong>
-78-<br />
to <strong>anterior</strong> lesser curvature <strong>seromyotomy</strong> did not appreciably increase<br />
the incidence of diarrhea when compared to highly selective <strong>vagotomy</strong>,<br />
and dumping did not occur (Taylor, 1995).<br />
Two major anatomical considerations are fundamental to the<br />
success of this procedure. First, that all vagal branches passing to the<br />
parietal cell area are divided and, secondly, that the divided nerves do<br />
not regenerate (Taylor, 1979). Anterior <strong>vagotomy</strong> is rapidly and easily<br />
performed by means of a <strong>seromyotomy</strong> paralleling the lesser curvature<br />
from the gastroesophageal junction to the crow's foot (Moniel et al.,<br />
1993). Division of the <strong>posterior</strong> vagus nerve trunk should reliably<br />
denervate the whole of the <strong>posterior</strong> wall of the stomach and thus<br />
overcome the propensity of some surgeons to leave intact areas of<br />
innervation of the <strong>posterior</strong> wall of the stomach at the esophagogastric<br />
junction and the antral-corpus junction. Retaining innervation of these<br />
two areas probably accounted tor a large number of recurrent ulcers that<br />
developed after this operation and may have facilitated reinnervation of<br />
the <strong>posterior</strong> wall of the stomach, which might have occurred by<br />
sprouting from the intact residual nerves (Taylor, 1995).<br />
Three factors may contribute to the dumping and diarrhea produced<br />
after <strong>truncal</strong> <strong>vagotomy</strong> and drainage These are (1) division of the<br />
hepatic branches of the <strong>anterior</strong> vagus, (2) division of the celiac branches<br />
of the <strong>posterior</strong> vagus, and (3) destruction of the pylorus by pyloroplasty.<br />
Of these, the latter would appear to be the most significant contributory<br />
factor to emptying problems following <strong>vagotomy</strong>. Clearly, the pylorus is<br />
controlled by a very intricate system of innervation that permits the<br />
emptying of liquefied gastric contents into the duodenum in a highly<br />
controlled and sophisticated way. Most of the innervation of the antrum
-79-<br />
and pylorus is afferent rather than efferent, and these afferent nerves<br />
probably coordinate the mechanism of gastric emptying. Clearly,<br />
division of the celiac branches of the <strong>posterior</strong> vagus nerve may<br />
contribute in part to post-<strong>vagotomy</strong> sequelae but, when the integrity of<br />
the pylorus and of the hepatic branches of <strong>anterior</strong> vagus are maintained,<br />
as in the operation of ASPTV, then it is unlikely that division of the<br />
celiac branches of the vagus will produce any significant clinical<br />
problems. Preservation of the pylorus could be justified from the<br />
observations of Daniel et at, (1973), who showed that stimulation of the<br />
<strong>anterior</strong> nerve of Latarjet produced contraction of the circular muscle in<br />
the <strong>anterior</strong> and <strong>posterior</strong> antral walls, the stimulus being conducted<br />
through vasovagal arcs to the <strong>posterior</strong> wall of the stomach (Taylor,<br />
1995). Following <strong>vagotomy</strong>, intragastric pressure after a meal is<br />
increased. It is possible that by Y; ..rtue of dividing the full thickness of the<br />
circular muscle of the corpus of the stomach in performing <strong>seromyotomy</strong><br />
the loss of accommodation for a meal is to some extent compensated and<br />
that rapid early emptying does not occur. If this was true, not only should<br />
dumping and diarrhoea be reduced but also distension or epigastric<br />
fullness, present in up to 50 per cent of patients after <strong>vagotomy</strong>, should<br />
be less or absent This would provide <strong>seromyotomy</strong> <strong>with</strong> a potential<br />
advantage over all exrstmg forms of <strong>vagotomy</strong> including the<br />
conventional highly selected procedure (Taylor et al., 1985).<br />
Anterior <strong>seromyotomy</strong> <strong>with</strong> <strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong> represent a<br />
greater degree of gastric denervation than highly selective <strong>vagotomy</strong>, the<br />
whole of the <strong>posterior</strong> wall of the stomach being denervated. This may<br />
obviate the risk of leaving areas of the parietal cell mass, at the antral<br />
corpus and gastro-oesophageal junctions innervated (Taylor et al., Dec.
-80-<br />
1985). We suggest that the expedients of peptic-ulcer surgery are that the<br />
parietal cell mass must be denervated; the pylorus should be preserved;<br />
gastric emptying should be near normal; the loss of adaptive relaxation<br />
should be compensated for; duodenogastric reflux should be minimised;<br />
the incidence of dumping and diarrhoea must be low, the operation must<br />
be safe, simple, and rapid; risks of ishaemic necrosis and of damage to<br />
the nerve of Latarjet must be overcome; the incidence of recurrent ulcer<br />
must be acceptably and competitively, in terms of other operations, low.<br />
The operation of <strong>anterior</strong> lesser curve <strong>seromyotomy</strong> <strong>with</strong> <strong>posterior</strong><br />
<strong>truncal</strong> <strong>vagotomy</strong> appears to fulfill many of these expedients (Taylor,<br />
1982).<br />
Apparently, the major cause of death after conventional highly<br />
selective <strong>vagotomy</strong> was ischemic necrosis of the lesser curvature, yet<br />
this complication has never been reported after ASPTV Preservation of<br />
the left gastric vessels to the <strong>posterior</strong> wall of the stomach and also of<br />
those end arteries that directly enter the lesser curvature would seem to<br />
obviate any potential risk that exists for ischemic necrosis (Taylor,<br />
1995).<br />
We have, in recent years, been performing the operation of <strong>anterior</strong><br />
lesser curve <strong>seromyotomy</strong> <strong>with</strong> <strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong> (ASPTV)_<br />
The operation is quick and simple to perform and denervates the parietal<br />
cell mass <strong>with</strong> the whole <strong>posterior</strong> wall of the stomach whilst obviating<br />
the need for a drainage procedure (Taylor et al., Aug. 1985). Such is the<br />
relative simplicity of <strong>anterior</strong> <strong>seromyotomy</strong> <strong>with</strong> <strong>posterior</strong> <strong>truncal</strong><br />
<strong>vagotomy</strong> that the operation takes no longer to perform than <strong>truncal</strong><br />
<strong>vagotomy</strong> and pyloroplasty, thus keeping the nonspecific risks of surgery
-81-<br />
to a minimum. In our own center the average total operating time is 40<br />
min (Taylor et at, Dec. 1985).<br />
The one complication directly attributable to the operation, that of<br />
gastric perforation, was considered to be due to a diathermy bum.<br />
Initially the muscle fibers were divided by diathermy; the use of<br />
diathermy is now confined to the incision m the serosa and the<br />
coagulation of small vessels running along the serosal surface, the<br />
muscle fibers are divided by blunt-ended dissecting scissors. The<br />
integrity of the mucosa is checked at the end of the operation by<br />
introducing air into the stomach and it is currently considered that the<br />
risk of perforation is entirely avoidable. The operation carries <strong>with</strong> it all<br />
the advantages associated <strong>with</strong> preservation of the innervated pylorus,<br />
the value of which has been shown <strong>with</strong> conventional highly selective<br />
<strong>vagotomy</strong> (Taylor, 1979). ASPTV was technically simpler and less<br />
time-consuming than conventional PGV, it would replace the latter<br />
procedure as the operation of choice in the surgical treatment of chronic<br />
duodenal ulcer (Taylor, 1995).<br />
Since the rnid-1985s, minimally invasive procedures and<br />
technology have changed the pattern of surgical thinking and patient care<br />
and, particularly <strong>with</strong> the introduction of laparoscopy into the practice of<br />
general surgeons, a revolution in surgical techniques and technology has<br />
occurred (MacFadyen, 1999). The last decade of the twentieth century<br />
probably will historically be high lighted as the period in which the<br />
widespread use of <strong>laparoscopic</strong> intra-abdominal surgery was shown to be<br />
feasibleand often advantageous (Taylor, 1995).<br />
There is no question that minimal access (also called minimally<br />
invasive) surgery has revolutionized the practice of many surgical
-82-<br />
disciplines. The shorter postoperative stay, decreased pain and<br />
discomfort, and faster return to daily activities are the most significant<br />
positive factors in its acceptance (Herd et at., 2000). The postoperative<br />
measures required after <strong>laparoscopic</strong> <strong>vagotomy</strong> are minimal (Dubois,<br />
2000). Laparoscopic procedures have begun to replace many<br />
conventional operations because of the avoidance of major surgery and<br />
the rapid recovery of the patient. The majority of these traditional<br />
operations will be performed <strong>laparoscopic</strong>ally in the future (Cuschieri,<br />
1992). The <strong>laparoscopic</strong> approach to conventional surgery is a<br />
burgeoning area of surgical practice, <strong>with</strong> new techniques and<br />
procedures introduced on a yearly if not monthly basis. This revolution<br />
has been fueled by the belief among surgeons, referring physicians, and<br />
the general public that <strong>laparoscopic</strong> procedures are "minimally invasive"<br />
and thus entail less pain (compared to traditional open surgery) and lead<br />
to a faster recovery (Velanovich, 2000).<br />
The <strong>laparoscopic</strong> approach is now a standard alternative option In<br />
abdominalsurgery (Lee et aI., 1999).<br />
One important factor that may relate to the use of surgical<br />
procedures is the duration of hospitalization and the period of time lost<br />
from active employment: an associated issue is the feasibility and<br />
increasing use of <strong>laparoscopic</strong> surgery. With the latter, inpatient times<br />
have fallen to 1-2 days, and periods lost from active employment are as<br />
brief as 2 weeks (Taylor, 1995).<br />
Laparoscopic management of duodenal ulcers is feasible. The<br />
various forms of <strong>vagotomy</strong>, omentopexy, and drainage procedures arc<br />
technically feasible VIa <strong>laparoscopic</strong> approach. The <strong>laparoscopic</strong>
-84-<br />
are laid out for traditional surgery should laparotomy be necessary<br />
(Mouiel et at, 1993).<br />
Pneumoperitoneum and Trocar Insertion:<br />
The pneumoperitoneum is created by insufflation of C02 and a<br />
pressure of 14 mmHg is maintained electronically. The puncture needle<br />
is usually introduced through the umbilicus. Once the abdominal wall is<br />
raised offthe viscera troears are introduced (Mouiel et al., 1993).<br />
Basic Laparoscopic Techniques:<br />
Exploration:<br />
The abdominal cavity is explored as soon as the video-laparoscpe is<br />
inserted. The surgeon should ascertain that the operation is feasible and<br />
particularly that the liver can be retracted so the area of operation is<br />
visible. If the operation is impossible or seems dangerous or difficult,<br />
open surgery is preferred (Moniel et aI., 1993).<br />
Dissection, Hemostasis, Tissue Approximation:<br />
As <strong>with</strong> open surgery, dissection may be "sharp", usmg scissors,<br />
the spatula, or the hook <strong>with</strong> or <strong>with</strong>out electrocautery; or it may be<br />
"blunt", using a probe or pledget swabs. For hemostasis, several methods<br />
arc used: (1) the hook coagulator is used <strong>with</strong> monopolar current to<br />
coagulate small-caliber vessels (2) the neodymium laser coagulates<br />
superficial surfaces <strong>with</strong> a contact fiber (3) Titanium clips are used for<br />
the short gastric, left gastric, and small accessory hepatic vessels after
Approack to the Hiatus:<br />
-86-<br />
The left lobe of the liver is retracted using a palpation probe placed<br />
through the xiphoid port. The pars flaccida is seized <strong>with</strong> grasping<br />
forceps, and the surgeon incises it <strong>with</strong> the hook coagulator and enters<br />
the lesser sac. The dissection is continued up to the right crus of the<br />
diaphragm. A coronary hepatic vein or accessory left hepatic artery may<br />
be encountered and must be divided between two clips (Mouiel et al.,<br />
1993).<br />
Posterior Truncal Vagowmy:<br />
The two primary landmarks during performance of a <strong>posterior</strong><br />
<strong>truncal</strong> <strong>vagotomy</strong> are the caudate lobe of the liver and the right crus of<br />
the diaphragm. The right crus is seized <strong>with</strong> the right-sided grasping<br />
forceps and retracted to the right to expose the pre-esophageal<br />
peritoneum. The peritoneum is incised along the length of the border of<br />
the right crus, allowing separation of the abdominal esophagus <strong>anterior</strong>ly<br />
and to the left, giving access to its <strong>posterior</strong> wall and mesoesophagus.<br />
Within the depths of this angle the <strong>posterior</strong> vagus can be easily<br />
recognized as a pearly white cord. It is gently grasped <strong>with</strong> a forceps<br />
while its vasa vasorum is stripped <strong>with</strong> the hook coagulator. The nerve is<br />
then transected between two clips (Mouiel et al., 1993) (Fig. 10).
-87-<br />
... --- -- .-<br />
Fig. 10. Posterior <strong>truncal</strong> <strong>vagotomy</strong> <strong>with</strong> the two essential landmarks:<br />
right diaphragmatic crus and caudate lobe of the liver (Mould et sl.,<br />
1991).<br />
Anterior Seromyotomy:<br />
The <strong>anterior</strong> surface of the stomach is stretched <strong>with</strong> the right and<br />
left grasping forceps. The outline of the <strong>seromyotomy</strong> is marked <strong>with</strong> the<br />
hook coagulator, beginning exactly I.5cm from the lesser curvature at<br />
the level of the gastroesophageal junction, and this distance is<br />
maintained paralleling the lesser curvature and stopping 5 to 7cm from<br />
t- the pylorus at the level of the trifurcation of the "crew's foot", respecting<br />
the integrity of the two inferior branches. The <strong>seromyotomy</strong> is performed<br />
<strong>with</strong> the electric hook coagulator using a blended monopolar current at a<br />
setting of medium wattage. The hook successively cuts through the<br />
serosa, the oblique muscular layers, and the superficial circular muscular<br />
layers. The two grasping forceps hold the edges, helping stretch the deep
-88-<br />
circular fibers, which eventually split as a result of the combined effect<br />
of mechanical traction and hook coagulation. After these last muscular<br />
fibers are split, the bluish mucosa protrudes, and it is possible to verify<br />
its integrity because of the magnification produced by the video<br />
laparoscope, as during microsurgery. The <strong>seromyotomy</strong> is continued<br />
proximally in the same fashion. During this part of the procedure one<br />
may encounter three to five short vessels, and they should be transeeted<br />
after hemostasis. Several approaches can be used: As described by<br />
Taylor,(1979), the vessels can be isolated in the seromuscularis by<br />
passing a hook underneath them and clipping and transecting them;<br />
alternatively, one can use sutures. It is essential to observe rigorously all<br />
the details of the exact anatomic location of the <strong>seromyotomy</strong> and<br />
hemostasis; otherwise, the <strong>seromyotomy</strong> may be ineffective. Once the<br />
<strong>seromyotomy</strong> is achieved, it appears as a slice 7 to 8mm wide (Fig. II).<br />
/<br />
)<br />
I<br />
/<br />
,.<br />
,I<br />
Fig. 11 . Anterior lesser curve <strong>seromyotomy</strong> (Mouiel et aL, 1993).<br />
....<br />
,
-90-<br />
In our expenence, this <strong>laparoscopic</strong> procedure has given the same<br />
results as open surgery <strong>with</strong>out mortality and <strong>with</strong> low morbidity.<br />
Operative time has ranged from 55 to 190 minutes, <strong>with</strong> a mean of 90<br />
minutes. The postoperative period has been relatively benign. Pain is<br />
generally trivial and is due to minimal parietal trauma and the use of<br />
local anaesthetic infilteration around the abdominal puncture points;<br />
systemic analgesics are unnecessary. The patients are ambulatory much<br />
earlier than after laparotomy owing to the lack of invasive postoperative<br />
care. A nasogastric tube is left in place for 24 hours, and oral fluids are<br />
resumed after its removal. The patient is discharged between the 3 m and<br />
5 th postoperative days and this period possibly may be shortened further<br />
(Mouiel et al., 1993). The postoperative course is usually surprisingly<br />
uneventful. The hospital stay varies from 3 to 5 days (Dubois, 2000).<br />
During follow-up of the <strong>laparoscopic</strong> Taylor procedure, no clinically<br />
significant bloating, diarrhea, or dumping has been observed.<br />
Postoperative upper endoscopy proved to heal the duodenal ulcer<br />
completely. No recurrence has been observed (Mouiel et al., 1993).<br />
There is good evidence that the success of POY (or any type of<br />
<strong>vagotomy</strong>) depends on the completeness of the denervation of the<br />
parietal cells. The problem is that the fine vagal branches arc hardly<br />
visible, and the area of the gastric parietal cell mass can not be seen by<br />
looking at the outside of the stomach. The vagus nerve, as its name<br />
implies, is variable (Johnson, 2000). There is an understandable desire<br />
to have a test that will tell the surgeon that the <strong>vagotomy</strong> is incomplete<br />
during the operation, when faults can be corrected. It is of little comfort<br />
to discover the incompleteness 10 days to 3 months postoperatively. Two<br />
groups of tests have been devised, one based on motility and the other on
-91-<br />
acid secretion. They can be used for all types of <strong>vagotomy</strong>. In the<br />
Burge,(1958) test, the rise in intragastric pressure is measured, using a<br />
nasogastric tube, in response to stimulation around the vagal trunks <strong>with</strong><br />
an electric current If there are no residual vagal fibers supplying the<br />
stomach, there will be no rise III pressure [Johnson, 1995).<br />
Grassi,(1971) test uses a pH probe inserted in the stomach through a<br />
gastrostomy after the surface of the stomach had been washed <strong>with</strong><br />
saline. Donahue,(1985) Congo red test sprays the mucosal surface <strong>with</strong><br />
Congo red dye, which turns black in acidic areas and can be viewed <strong>with</strong><br />
a gastroscope at the operation <strong>with</strong>out opening the stomach. Both tests<br />
depend on the physiologic phenomenon that the parietal cells becomes<br />
temporarily completely unresponsive to a circulating gastrum (.Johnson,<br />
2000). The intraoperative Congo red test has much appeal and we intend<br />
to incorporate it in our operations (Laws et al., 1993). Demonstrating the<br />
adequacy of a <strong>vagotomy</strong> by the endoscopic Congo fed avoids the futile<br />
effort of completing an incomplete but adequate <strong>vagotomy</strong> and indicates<br />
the need for other measures (Griffith, 1995) (Images 1,2).
-92-<br />
Image (1): Black color change along the greater curvature suggesting<br />
persisting vagal innervation despite completion of the standard<br />
dissection during PGV (Donahue et aI., 1987).<br />
Image (2): Disappearance of the black color change along the greater<br />
curvature after division of the right gastroepiploic nerve (Donahue et<br />
al., 1987).
,..--;.,<br />
i /j;<br />
'Ii<br />
I/ i<br />
, r<br />
'.../)<br />
/..-.--)
PATIENTS:<br />
-93-<br />
PATIENTS AND METHODS<br />
This work was conducted in the Department of General Surgery at<br />
Faculty of Medicine in Zagazig University and in the Center of Digestive<br />
System Surgery at Faculty of Medicine in Mansoura University. It was<br />
applied to 20 patients from the received 30 ones suffering from chronic<br />
duodenal ulcer disease.<br />
Patients asked for surgery because they could economically not<br />
tolerate the long periods of the expensive medical treatment which gave no<br />
permanent cure and relapses often occurred on stopping it, others because<br />
they got exhausted and afraid from the multiple attacks of haernatemesis and<br />
melena and others from the severe epigastric pain which could not be<br />
prevented by medical treatment.<br />
All patients were subjected to the following<br />
1- Full history taking.<br />
2- FuJI general and local examination.<br />
3- Routine investigations such as urine analysis, stool examination,<br />
hematological tests, plain chest x-ray and abdominal ultrasonography.
-94-<br />
4- Specific investigations such as fibrooptic upper GI endoscopy (Image 3)<br />
and barium meal (Image 4}<br />
5- Upper GI endoscopy of the received 30 patients revealed 7 patients were<br />
found suffering from marked pyloric stenosis and 3 from pyloric<br />
obstruction; all were excluded as contraindication to our procedure and<br />
bilateral <strong>truncal</strong> <strong>vagotomy</strong> <strong>with</strong> gastrojejunostomy was applied to them.<br />
6- Laparoscopic <strong>anterior</strong> <strong>seromyotomy</strong> <strong>with</strong> <strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong><br />
assessed by intraoperative endoscopic Congo red test was applied to 10 of<br />
the remaining 20 patients and <strong>laparoscopic</strong> <strong>anterior</strong> <strong>seromyotomy</strong> <strong>with</strong><br />
<strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong> alone was applied to the other 10 ones.<br />
7- The Hrreceptor antagonists and the PPIs therapy were stopped for 48 hrs<br />
before surgery to prevent interference <strong>with</strong> the Congo red test in the<br />
Congo red test group.<br />
8- Patients were reviewed after the first month and each three months after<br />
the operation. Questions were specifically asked a proforma regarding<br />
general well-being, pain, dyspepsia symptoms, dumping, vomiting and<br />
diarrhea, <strong>with</strong> special attention to symptoms suggestive of recurrent ulcer<br />
disease. Upper GJ endoscopy was performed when symptoms of recurrent<br />
ulcer were present, and only when an ulcer crater was endoscopically<br />
verified was the patient classified as having a recurrent ulcer. A recurrent<br />
ulcer was defined as an endoscopically proven, symptomatic relapse.<br />
9- The results offollow up were recorded and analysed.
METHODS:<br />
Preparation:<br />
-95-<br />
General anesthesia <strong>with</strong> endotracheal intubation and intra-operative<br />
monitoring was used. A nasogastric tube attached to a continuous very low<br />
suction was used to maintain complete deflation of the stomach. The patient<br />
was prepared and draped; and instruments were laid out for traditional open<br />
surgery should laparotomy might be necessary.<br />
Position:<br />
The operation was performed <strong>with</strong> the patient in the supine position<br />
<strong>with</strong> legs spread apart. The operating table should allow 15° elevation<br />
(reverse Trendelenburg position). We place a small support between the<br />
shoulder blades to elevate them approximately 1Ocrn.<br />
The operating surgeon stranded between the patient's legs. The first<br />
assistant was on the patient's left and the second assistant on the right. The<br />
video-endoscopic system <strong>with</strong> irrigation-suction were placed on the left A<br />
second video monitor was placed on the right, <strong>with</strong> the electrocoagulation<br />
unit<br />
Instrumentation:<br />
The standard instruments required for <strong>laparoscopic</strong> surgery were used.<br />
We routinely used a bipolar coagulating knife or an electro-surgical hook<br />
knife <strong>with</strong> a channel for smoke evacuation, a curved electro-coagulating
-97-<br />
performed <strong>laparoscopic</strong>ally. When difficulties were anticipated, open surgery<br />
was performed.<br />
Operative Technique:<br />
The procedure involved three steps: A) access to the hiatal region, B)<br />
<strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong>, and C) <strong>anterior</strong> seromyoromy.<br />
A- Acce.u to the hiatus:<br />
The left lobe of the liver was elevated <strong>with</strong> the help of the retractor<br />
(Image 5) and the surgeon gained access to the hiatal region by opening the<br />
lesser omentum (Image 6), which was stretched between two retracting<br />
dissectors at the level of the right crus of the diaphragm. Ibis division gave<br />
access to the upper part of the lesser sac, while respecting the gastrohepatic<br />
branches of the <strong>anterior</strong> vagus nerve. The incision was continued to the<br />
region ofthe right crus and was mobilized along its entire length.<br />
B- Posterior <strong>truncal</strong> <strong>vagotomy</strong>:<br />
The two landmarks for <strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong> are the caudate<br />
lobe of the liver on one side and the right crus of the diaphragm on the other<br />
(Image 7)_ The right crus was grasped by a dissector and drawn towards the<br />
right to expose the pre-esophageal peritoneum. Incision of the peritoneum<br />
along the border of the right crus provided access to the <strong>posterior</strong> aspect of<br />
the esophagus and the mesoesophagus where the abdominal esophagus could<br />
be tracted outwards.
-98-<br />
The white trunk of the <strong>posterior</strong> vagus nerve could easily be identified<br />
in this angle. The vagus was grasped by a dissector held taut (Image 8) and<br />
cleared ofany associated small vessels <strong>with</strong> electrocoagulating hook knife. A<br />
segment was resected between two clips (Image 9, I 0)<br />
c-Anterior <strong>seromyotomy</strong>:<br />
The <strong>anterior</strong> wall of the stomach was displayed <strong>with</strong> the help of<br />
graspers inserted through the right and left subcostal ports<br />
Three to five short vessels were encountered along the line of<br />
dissection. These vessels were divided between ligatures (Image II).<br />
Extreme care was taken to achieve adequate hemostasis during<br />
<strong>seromyotomy</strong>.<br />
The position of the seromyotorny was marked out <strong>with</strong> the coagulating<br />
hook (Image 12), from the esophagogastric j unction which is the upper limit<br />
of <strong>seromyotomy</strong> (Image 13) following the lesser curvature of the stomach at<br />
a distance of 1.5 em and this distance was maintained parallel to it and<br />
stopping about 6 em from the pylorus at the level of the trifurcation of the<br />
"crew's foot", which is the lower limit of scrornyotomy (Image 14),<br />
respecting the integrity of the two inferior branches.<br />
Seromyotorny was performed using bipolar coagulation knife (Image<br />
15) or coagulating hook (Image 16) starting from below (Image 17); the<br />
coagulating knife was used to successively incise the serosa, the oblique and<br />
circular muscle layers The two graspers were used to hold the edges of the<br />
incision, improving exposure of the deep circular muscle fibers which were
Image (3): Large deep<br />
active <strong>anterior</strong> superior<br />
duodenal ulcer revealed<br />
during preoperative<br />
upper GI endoscopy.<br />
Image (4): Preoperative<br />
barium meal revealing<br />
deformed duodenal cap.<br />
-101-
Li er<br />
-102-<br />
Image (5): Elevation of the liver using a fan-shaped liver retractor.<br />
Image (6): Opening the lesser omentum to gain access to the hiatal<br />
region.
-103-<br />
c<br />
l<br />
Image (7): The caudate lobe of the liver and the right crus of the<br />
diaphragm; the two landmarks for <strong>posterior</strong> <strong>truncal</strong> vaqotorny.<br />
Image (8): Traction of the white trunk of the <strong>posterior</strong> vagus nerve.
-104-<br />
Image (9): Clipping of the <strong>posterior</strong> vagus trunk.<br />
Image (10): A segment of the <strong>posterior</strong> vagus trunk resected between<br />
two dips.
-105-<br />
Image (11): The angle of His, at the esophaqoqastnc junction, the<br />
upper limit of the <strong>anterior</strong> <strong>seromyotomy</strong>.<br />
Image (12): The crow's foot, the lower limit of the <strong>anterior</strong><br />
<strong>seromyotomy</strong>.
-106-<br />
Image (13): Ligation of the big vessels running onto the <strong>anterior</strong> aspect<br />
of the stomach.<br />
Image (14): Marking the line of <strong>anterior</strong> <strong>seromyotomy</strong> using coagulating<br />
hook.
-107-<br />
Image (15): Starting <strong>anterior</strong> <strong>seromyotomy</strong> from below upward, at the<br />
level of the proximal branch of the crow's foot.<br />
Image (16): Anterior <strong>seromyotomy</strong> using bipolar coagulating knife.
-108-<br />
Image (17): Anterior <strong>seromyotomy</strong> using coagulating hook.<br />
Image (18): Suturing the <strong>anterior</strong> <strong>seromyotomy</strong> in an overtapping<br />
manner.
-109-<br />
Image (19): Chronic duodenal ulcer revealed during intraoperative<br />
endoscopic Congo red test.<br />
Image (20): Gastric outlet patency revealed during intraoperative<br />
endoscopic Congo red test.
Image (21): Washing the gastric<br />
mucosa <strong>with</strong> water during<br />
intraoperative endoscopic Congo<br />
red test.<br />
Image (22): Spraying the gastric<br />
mucosa <strong>with</strong> the Congo red<br />
solution during the intraoperative<br />
endoscopic Congo red test.<br />
Image (23): The gastric mucosa<br />
free of black spots after spraying<br />
<strong>with</strong> Congo red solution during the<br />
intraoperative endoscopic Congo<br />
red test.<br />
-110-
_.- -1<br />
1<br />
1<br />
1<br />
1<br />
1<br />
1<br />
1
-112-<br />
Two patients were converted to the open procedure; one of them<br />
due to perforation of the gastric mucosa <strong>with</strong> diathermy and the other<br />
was due to difficult dissection at the hiatal region.<br />
In the Congo red test group, nine patients showed grade I and one<br />
showed grade II. No patients had showed grade 1Ilor IV<br />
The operating time, i.e. time passed from induction of anesthesia to<br />
return of the patient to the recovery room, for <strong>laparoscopic</strong> ASPTV<br />
ranged from 70 to 80 minutes <strong>with</strong> mean of 75 minutes. The<br />
intraoperative endoscopic Congo red test increased the operative time<br />
<strong>with</strong> only 5 to 7 minutes <strong>with</strong> a mean of6 minutes (tables 8-9) (Fig. 16).<br />
Operative mortality, defined as death occurring during surgery or<br />
the subsequent 30 days, did not occur at any patient. The only<br />
intraoperative complication, related to the procedure, was the perforation<br />
of the gastric mucosa at one patient. Significant immediate postoperative<br />
complications did not occur.<br />
days.<br />
The hospital stay for the <strong>laparoscopic</strong> ASPTV ranged from 3 to 4<br />
Symptoms were classified as: absent, mild or severe. A side effect<br />
was considered severe if it interfered <strong>with</strong> the patient's life or<br />
necessitated repeated medication. Patients <strong>with</strong> diarrhea were classified<br />
according to the frequency of the attacks either <strong>with</strong> frequent diarrhea or<br />
<strong>with</strong> infrequent diarrhea.<br />
The patients were graded I-IV on a Goligher, (1978) modified<br />
Visick classification. According to this classification, patients <strong>with</strong>out<br />
recurrence symptoms were classified as Visick grade T, those <strong>with</strong> mild
-114-<br />
Table 3: The received patients presented <strong>with</strong> complication ofch.D.U<br />
Complication No. %<br />
Haematemesis and meleana 8 26.66<br />
Pyloric obstruction 3 10<br />
Marked pyloric stenosis 7 23.3<br />
Ulcer perforation 0 0<br />
Total No. ofthe received cases 30 100<br />
Ulcer perforation<br />
Marked pyloric<br />
stenosis<br />
Pyloric<br />
obstruction<br />
Haematemesls<br />
and meleana<br />
I<br />
I<br />
U<br />
o 5 10 15 20 25 30<br />
Fig. (13): Distribution ofthe received patients presented <strong>with</strong><br />
complication ofch.D.U<br />
u<br />
u
-115-<br />
Table 4: The excluded and the operated cases.<br />
Cases No. %<br />
Excluded cases:<br />
•<br />
Due to marked pyloric stenosis 7 23.3<br />
.<br />
• Due to pyloric obstruction 3 10<br />
Operated cases:<br />
• ASPTValone 10 33.3<br />
• ASPTV <strong>with</strong> ECRT 10 33.3<br />
Total No. ofthe received cases 30 100<br />
33.3%<br />
10.0%<br />
Fig. (14) : The excluded and the operated cases<br />
Due to mM'ked pyloric stenosls<br />
iJ Due to pyloric obstruction<br />
u ASPTV alone<br />
o ASPTV <strong>with</strong> ECRT
-119-<br />
Table 8: Timing ofthe operation<br />
Step Time (min)<br />
Induction ofanaesthesia 0.0<br />
Trapping 5<br />
Insertion ofports 5<br />
Exploration and liver elevation 2<br />
Annroach to the hiatus 2<br />
PTV 10<br />
Anterior seromvotomv 30<br />
Congo red test 6<br />
Suturing; 10<br />
Waldng; 5<br />
Total 75<br />
Waking<br />
Suturing<br />
Congo red test<br />
Anterior <strong>seromyotomy</strong><br />
PTV<br />
Approach to the hiatus<br />
Exploration and liver elevation<br />
Insertion of ports<br />
Trapping<br />
Induction of anaesthesia<br />
0<br />
=:J<br />
"1<br />
j<br />
I<br />
I<br />
I<br />
I<br />
o 5 10 15 20 25 30 35<br />
Fig. (18): Timing ofthe operation<br />
I
-122-<br />
m 1987 when <strong>laparoscopic</strong> cholecystectomy was first performed; and<br />
subsequently, minimal-access approaches have been used by general<br />
surgeons for multiple intra-abdominal operations, and that minimally<br />
invasive surgery revolutionized the practice of general surgery in the<br />
past decade. Lee et at, (1999) mentioned that the <strong>laparoscopic</strong> approach<br />
is now a standard alternative option in abdominal surgery. Kathouda<br />
and MouieJ(1991) were the first who applied the <strong>laparoscopic</strong> approach<br />
to chronic duodenal ulcer disease.<br />
In our study we evaluated the results of <strong>anterior</strong> <strong>seromyotomy</strong> <strong>with</strong><br />
<strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong> as a surgical treatment for chronic duodenal<br />
ulcer disease. Along the last two years we received 30 patients <strong>with</strong><br />
chronic duodenal ulcers, 20 males and 10 females <strong>with</strong> MIF ratio equals<br />
2/1 which is the same as estimated by Christopher et al., (1995), and<br />
this may be due to the fact the men usually have more active nervous life<br />
style <strong>with</strong> higher rates ofsmoking and drinking than women.<br />
The age of the patients ranged from 18 to 7() <strong>with</strong> a mean of 44<br />
years which corresponds Langman, (1974) range; 20 patients were<br />
heavy smokers and all of them were below the age of 60 years while 6<br />
ones were on NSAlDs and were below the age of 60 years; both smoking<br />
and NSAIDs are, as Johnson, (2000)said, factors which predispose to<br />
DO.<br />
All patients asked surgical treatment after trying vanous types of<br />
medical ones especially after being informed about the benefits and<br />
advantages of the <strong>laparoscopic</strong> surgery. All of them complained of being<br />
tired and exhausted from the repeated relapses of the disease which
-123-<br />
reached 10 times for 22 of them, and 8 patients were afraid from the<br />
recurrent attacks ofhaematemesis which reached 5 times for 6 ofthem.<br />
We depend mainly in our diagnosis of chronic duodenal ulcer, as<br />
Taylor et at, (1982), Christopher et al., (1995) and Mouiel et<br />
al.,(1999) did, on preoperative upper GI endoscopy and barium meal<br />
test. Upper GI endoscopy revealed 7 cases of marked pyloric stenosis<br />
and 3 cases of pyloric obstruction and all of them were excluded as<br />
contraindications to ASPTV and bilateral <strong>truncal</strong> <strong>vagotomy</strong> wit h<br />
gastrojejunostomy was applied to them. Fourteen of the remaining 20<br />
cases showed single I"" part DU, 2 cases showed two kissing 1!l part DU<br />
and the last 4 cases showed single 1"" part DU; all ulcers varied from 0.5<br />
to l.Scm in size.<br />
This study included the last 20 patients, 10 of them underwent<br />
<strong>laparoscopic</strong> ASPTV alone, while the other 10 underwent <strong>laparoscopic</strong><br />
ASPTV assessed by intraoperative ECRT.<br />
We preferred to perform the operation <strong>with</strong> the patient in the supine<br />
position <strong>with</strong> legs apart and thc operating surgeon standing between his<br />
or her legs which is the same position used by Mouiel et 1\1., (1993)<br />
because it is more accessing and comfortable for the surgeon and avoids<br />
pressure ischaemia of the patient's legs which occurs in the French<br />
preferred position described by Dubois,(2000) in which the patient lies<br />
in the lithotomy position <strong>with</strong> the operating surgeon standing between<br />
his or her legs resting his arms on the legs.<br />
We applied the technique applied by Mouiel et al.,(1991) <strong>with</strong> mild<br />
differences. In ]0 cases we placed a liver retractor port about I" below<br />
the xiphoid process, and in the other ones we placed it below the right
-124-<br />
costal margin. Also we used a fan-shaped liver retractor instead of<br />
MOllie' et al.,(1993) palpation probe and we found it more accessible,<br />
stable and easily handled when placed in the subxiphoid port<br />
In the FeRT group we used the second monitor to connect it <strong>with</strong><br />
the gastroscope to follow and evaluate the test<br />
Access to the hiatus and P'TV were so simple and fast the same as<br />
reported by both Taylor et al., (1979) and Mouiel et al., (1991), except<br />
in one patient who showed difficult dissection at the hiatal region due to<br />
vague anatomy which led to turn him to open surgery.<br />
To transect the large vessels on the <strong>anterior</strong> gastric wall Taylor et<br />
al., (1979) and Mouiel et at, (1993) used clipping before cutting them,<br />
but preferred to use ligation <strong>with</strong> sutures because ligatures are more<br />
secure and stable than clips which may slip during gastric contractions.<br />
For <strong>seromyotomy</strong> Mouiel et al.,(t993) used rnonopolar coagulation<br />
hook, while we used the monopolar coagulation hook, the bipolar<br />
coagulation knife and the harmonic ultrasonic knife. We found the latter<br />
two knives, especiaJly the last one, more easy, fast and safe than the<br />
former and the case of mucosal perforation happened during using the<br />
former.<br />
For the overlapping closure of the serornyotomy wound we.as<br />
Mouiel et al., (1993) and Taylor. (1995) did, preferred the continuous<br />
suture than the interrupted one because it is more secure, coapting, easy,<br />
rapid and close any unnoticed perforation ofthe gastric mucosa.<br />
Kusakari et al., (1972) and Saik et al., (1976) used HistaJog 50mg<br />
subcutaneously to stimulate maximum gastric acid secretion during
-125-<br />
intraoperative ECRT , Donahue et al., (1987) used both histalog and<br />
pentagastrin 6uglkg subcutaneously and Chisholm et at, (1993) used<br />
pentagastrin, but we used insulin 0.2 i.u./kg intravenously because of the<br />
unavailability of the previous substances and to avoid their hazards<br />
especially hypotension and shock and we found it giving the required<br />
response beside its easy availability<br />
In the intraoperative EeRT group, 9 patients showed G I tests, 1<br />
Patient G II test and no patients showed G lIT or G IV tests.<br />
As Chisholm et al., (1993) did we found the intraoperative ECRT,<br />
IS easy to perform, does not require specialized equipment. It added<br />
little to the operating time. We completed it in about 6 minutes, near the<br />
time consumed by Donahue et al., (1987) who completed it in less than<br />
5 minutes It was very beneficial as it revealed the degree of<br />
completeness of <strong>vagotomy</strong> while we were in situ and able to complete it<br />
if it was not complete and so ensuring a great guarantee against post<br />
operative recurrence. So we recommend the intraoperative endoscopic<br />
Congo red test to be an essential step of<strong>laparoscopic</strong> ASPTV<br />
This study revealed that the <strong>laparoscopic</strong> ASPTV is simple and fast<br />
technique. The operating time ranged from 70-80 minutes <strong>with</strong> a mean<br />
of 75 minutes which is shorter than that achieved by Mouiel et<br />
al.(I993), who recorded a mean operating time of90 minutes.<br />
The only one intra-operative complication related to the procedure,<br />
reported also by Taylor, (1979), was perforation of the gastric mucosa,<br />
due to burning <strong>with</strong> the electrocoagulation hook used to perform<br />
<strong>seromyotomy</strong> and we could avoid it by USIng a bipolar<br />
electrocoagulating knife scromyotomy.
-126-<br />
Mouiel et al., (1993) were not forced to convert a <strong>laparoscopic</strong><br />
procedure to a laparotomy while we did this in 2 cases, one due to<br />
difficult dissection at the hiatal region and the other due to perforation of<br />
the gastrie mucosa.<br />
We had no cases of operative death unlike Mouiel et al., (1993)<br />
who reported one operative death due to myocardial infarction, which is<br />
a cause away from the procedure.<br />
Mouiel et at, (1999) reported one case of postoperative<br />
pneumothorax treated by a chest drain for 24 hours, while we had one<br />
patient complained of early dysphagia which disappeared spontaneously.<br />
He was that patient <strong>with</strong> difficult dissection at the hiatal region; so early<br />
dysphagia may be due to excessive manipulation at this region.<br />
Otherwise the post-operative course showed no significant complications<br />
and was very eventful.<br />
Tay.or,(1995) reported a hospital stay which may fall to 1-2 days,<br />
while Mouiel et al., (1993) and Dubois. (2000) had a hospital stay<br />
vaned from 3 to 5 days, but in our study the hospital stay ranged from 3<br />
to 4 days<br />
During follow up Taylor et at. (1982) reported no severe<br />
post<strong>vagotomy</strong> diarrhea but only mild transient increases in bowel action,<br />
while Moniel et al., (1999) had one case of reflux esophagitis and 2/62<br />
cases of ulcer recurrence after 2 years and Oostvogel et al., (1988) had<br />
4/46 cases of recurrence after :::6 months During our follow up, which<br />
reaches 2years, no mortality occurred, no significant bloating or<br />
dumping were recorded and only one patient had infrequent diarrhea<br />
...
-127-<br />
which was successfully treated medically. We had no recurrence cases<br />
i.e 0120 cases,<br />
We had no cases of ischemic necrosis of the lesser curvature, the<br />
same as Taylor,(1995). Mouiel et al., (1999) did<br />
According to Visick grading, after 2-4 years follow up of 143<br />
patients, Taylor et al., (1982) had 81 patients G I, 53 patients G II, 7<br />
patients G III and 2 Patients G IV, Taylor et at. «1990) after 2 years<br />
follow up of 76 patients had 52 patients G I, 14 patients G II, 5 Patients<br />
G HI and 5 patients G IV while our 2 years follow up of 20 patients<br />
revealed 17 patients G I, 3 patients G II and no patients as G IV<br />
Lastly after this study, we agree <strong>with</strong> Cuschieri, (1992), Laws ct<br />
al., (1993),Taylor.(1995). Mouiel et al., (1999) and Leena et al., (2002)<br />
that a minimally invasive technique such as ASPTV, especially when<br />
assessed by intra-operative endoscopic Congo red test, is a safe speed<br />
economic and surely curing alternative to the life-long expensive not<br />
safe and not surely curing medical treatment
-128-<br />
SUMMARY AND CONCLlJSJ()N<br />
Chronic duodenal ulcer disease is a common disease nowadays and<br />
although benign, it causes a high rate of mortality which equals that of<br />
some dangerous diseases such as pancreatic and esophageal carcinomas.<br />
So there is a continuous need for a successful treatment for this disease.<br />
Many types of treatment either surgical or medical were devised in this<br />
way and they vary in either givmg high curing rates but <strong>with</strong> high<br />
mortality and complications rates, or gIvmg low mortality and<br />
complications rates but <strong>with</strong> low curing and high recurrence rates.<br />
OUf study, which included 20 patients <strong>with</strong> chronic DU, ASPTV<br />
alone was applied to 10 of them and ASPTV assessed by intraoperative<br />
ECRT was applied to the other 10 patients, revealed that <strong>laparoscopic</strong><br />
<strong>anterior</strong> <strong>seromyotomy</strong> <strong>with</strong> <strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong>, which was first<br />
introduced by Taylor <strong>with</strong> open surgery and by Mouiel et al. <strong>with</strong><br />
<strong>laparoscopic</strong> surgery, particularly when assessed by intra-operative<br />
endoscopic Congo red test, is overall a very safe, patient compliant. It<br />
has overall good recovery rates in terms of control of duodenal ulcer. It<br />
is technically easy and can be do..c in a short time. It has a rrummum<br />
post-operative morbidity and preserves near normal stomach when<br />
compared <strong>with</strong> other procedures for duodena! ulcer.<br />
After two years follow-up we had no recurrent cases and no cases<br />
ofischemic necrosis oflesser curvature were encountered.<br />
Also, we found that the intra-operative endoscopic Congo red test<br />
was very beneficial in the intra-operative assessment, so we recommend<br />
it as an essential step of<strong>laparoscopic</strong> ASPTV.
1- A. Cuscbieri (1992):<br />
-129-<br />
REFERENCES<br />
"The spectrum of <strong>laparoscopic</strong> surgery". World Journal of Surgery,<br />
vol.l 6, No.6, Nov.IDec.I992, pp:1089-1097.<br />
2- Agossou- Voyeme K.. et at (1990):<br />
"Arterial vascularization of the operated stomach" Surg Radiol Anat<br />
12:247, 1990. (quoted from Griffith,1995).<br />
3- Ahlman BDJ. et al (1979):<br />
"Origin of the adrenergic nerve fibers in the subdiaphragmatic vagus in<br />
the dog." Am J Surg 137: 116, 1979. (quoted from Griffith,1995).<br />
4- A. k. Siriwardena and A. A. Gunn (1988):<br />
"Anterior lesser curve scromyotomy and <strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong> for<br />
chronic duodenal ulcer: the results at five years". British Journal of<br />
Surgery, vol. 75, September 1988, pp: 866-868.<br />
5- Alan G. Johnson (1995):<br />
"Truncal <strong>vagotomy</strong>". Surgery of the Esophagus, Stomach, and Small<br />
Intestine'l.S" edition, voL I, 1995, pp:484-492.<br />
6- Alan G.Johnson (2000):<br />
''Proximal gastric <strong>vagotomy</strong>: Does it have a place in the future of peptic<br />
ulcer?". World Journal of Surgery, vol. 24, No.3, March 2000, pp: 259<br />
263.
7-Albertus M. (1940):<br />
-130-<br />
Systemea Jurisprudenit Medicae. Hale, 1727. (cited in 0 Jennings,<br />
"Perforated peptic ulcer: Changes in age, incidence and sex distribution<br />
in the last ISO years. Lancet I: 395, 1940). (quoted from Christopher<br />
Waste1l, and JH. Baron, 1995).<br />
8- Alfred Cuschieri (1995):<br />
"Minimal access surgery of the upper gastrointestinal tract". Surgery of<br />
the Esophagus, Stomach, and Small Intestine, SUi edition, vol. II, 1995,<br />
pp: 754-769.<br />
9- Allen A. and Gamer A. (1980):<br />
"Mucous and bicarbonate secretion in the stomach and their possible role<br />
in mucosal protection" Gut 21: 464, 1980. (Quoted from James B. Elder,<br />
and Mark Deakin, J995)<br />
10- Amdrup E. (1982):<br />
Personal communications, J980, 1982. (quoted from Griffith, 1995).<br />
11- Amdrup E., Andersen D., and Hostrup H. (1978):<br />
"ThcAarhus County Vagotomy Trial.I. An interim report on pnmary<br />
results and incidence of sequelae following parietal cell <strong>vagotomy</strong> and<br />
selective gastric <strong>vagotomy</strong> in 748 patients." World J Surg 2: 85, 1978.<br />
(quoted from Alan G. Johnson, 2000.)<br />
...<br />
. ..,
.;<br />
12- Appleby LH. (1953):<br />
-131-<br />
"The celiac axis in expansion of the operation for gastric carcinoma."<br />
Cancer 6: 704, 1953. (quoted from Griffith, 1995).<br />
13- Bader JP, Walan A (OOs). (1989):<br />
"Proceedings of the International Symposium on Omeprazole." Scand<br />
Gastroenterol166 (suppl): 24, 1989.(quoted from Alfred Cushieri,1995).<br />
14- Hager B. (1929):<br />
"Beitrag zur Kenntnis uber Vorkommen, Klinik und Behandlung von<br />
perforierten Magen und Duodenal-geschwuren nebst emer<br />
Undersuchung uber die Spatresultatie nach versciedenen Operations<br />
methoden." Acta Chir Scand 64(Suppl): 11, 1929. (quoted from<br />
Christopher Wastell, and JH. Baron,1995).<br />
15- Barnes RJ, Gear MWL, Nicola er aL (1974):<br />
"Study of dyspepsia in a general practice as assessed by endoscopy and<br />
radiology." Br Med J 4: 214, 1974. (quoted from Christopher Wastell,<br />
and IR Baron,1995).<br />
16- BeDPRF. (1966):<br />
"The insulin test after <strong>vagotomy</strong>." In TF Thompson, IE Gillespie (Eds),<br />
Postgraduate Gastroenterology. London: Bailliere, Tindall & Cox, 1966,<br />
241. (quoted from Griffith, 1995).
-132-<br />
17- Bentley FH, and Barlow TEo (1952):<br />
"Stomach- vascular supply in relation to gastric ulcer" In ER Carling, JP<br />
Ross (Eds), Surgical Process. London: Butterworth, 1952. (quoted from<br />
Griffith, 1995).<br />
1R- Berger EH. (1934):<br />
"The distribution of parietal cells in the stomach: A histopographic ,<br />
study" Am J Anat 54: 87, 1934. (quoted from Griffith, 1995).<br />
19- Berthoud RD, et al. (1991):<br />
"Abdominal pathways and central origin of rat vagal fibers that stimulate<br />
gastric acid." Gastroenterology 100: 627, 1991. (quoted from<br />
Griffith.l 995).<br />
20- Brown JR and Derr .JW. (1952):<br />
" Arterial blood supply of human stomach" Arch Surg 64: 616, 1952.<br />
(quoted from Griffith,1995),<br />
zt Buck SH, and Burks TF. (1986):<br />
"The neuropharmacology of capsaicin." Pharmacol Rev 38: 179, 1986.<br />
(Quoted from James B. Elder, and Mark Deakin, 1995)<br />
22- B. V. MacFadyen (1999):<br />
"Change is inevitable". Surgical Endoscopy, vol. 13, pp:1-2<br />
r<br />
...
23- Capper WM. (1967);<br />
-133-<br />
"Factors in the pathogenesis of gastric ulcer." Ann R el;!] Engl 40: 21,<br />
1967. (quoted from Griffith, 1995)<br />
24- Capper WM, et at. (1966):<br />
"A test for pyloric regurgitation" Lancet 2: 621, 1966. (quoted from<br />
Griffith,1995).<br />
25- Capper WM, et 31. (1966):<br />
"Variation in size of the gastric antrum." Ann Surg 163: 281, 1966.<br />
(quoted from Griffith,1995).<br />
26- Charles A. Griffith (1995):<br />
"Anatomy of the stomach and duodenum". Surgery of the Esophagus,<br />
stomach, and Small Intestine, s" edition, vol. I, 1995, pp: 388 - 417<br />
27- Chen c.x, Lee P."., Chang K.J., Wang S.M., Wei T.e., Chen<br />
K.M. (1996):<br />
"Surgical treatment of peptic ulcer disease: changing patterns in the past<br />
40 years." J Forrnos Med Assoc 95: 675, 1996.(quoted from Alan G.<br />
Johnson, 2000.)<br />
28- Christine F. KoUmorgen, Seval Gunes, John B. Donohue,<br />
Geoffrey B. Thompson, and Michael G. Sarr (1996):<br />
"Proximal gastric <strong>vagotomy</strong>-comparison between open and <strong>laparoscopic</strong><br />
methods in the canine model". Annals of Surgery, vol. 224, No. 1,1996,<br />
PP: 43-50.
29- Christiansen J, Jenserl HE, ~'jb~-~oulsen P, et al. (1981):<br />
"prospective controlled <strong>vagotomy</strong> trial for duodenal ulcer: primary<br />
results, sequelae, acid secretion, and recurrence rates two to five years<br />
after operation. Ann Surg 193: 49, 1981. (quoted fi-om Alan G. Johnson,<br />
30- Christopher Wastell and J. H. Baron (1995):<br />
'Chronic doudenal ulcer and gastric secretion tests". Surgery of the<br />
Esophagus, Stomach, and Small Intestine, 5& edition, vol. 1, 1995, pp:<br />
456468.<br />
"Hepatic necrosis following celiac artery ligation during gastric resection<br />
in man." Arch Swg 71: 171, 1955. (quoted from Griffith,1995).<br />
32- Cox AJ. (1952):<br />
"Stomac~l size and its relation to chronic peptic ulcer." Arch Pathol 54:<br />
407, 1952. (quoted horn Christopher Wastell, and J.H. Baron, 1995).<br />
33- Davenport HW. (1972):<br />
"'fhe gastric rnucosal barrier." Digestion 5. 162, 1972. (Quoted fiom<br />
Jarnes B. Elder, and Mark Deakiq 1995)<br />
34- Donahue PE, et al. (1993):<br />
"Experimental basis and clinical application of extended highly selective<br />
<strong>vagotomy</strong> for duodenal ulcer. " Surg Gynecol Obstet 1 76: 39, 1993.<br />
(quoted from Griffith, 1995).<br />
#
n P<br />
35- Donahue PE, Maroske D, Roeher HD and Nyhus LM (1987):<br />
'Xxperience: <strong>with</strong> the endoscopic test for completmas of <strong>vagotomy</strong>.<br />
Results of application in two medical centers". Zentralbl Chir 1987;<br />
122(19), pp:1208-1215.<br />
36 - Donahue PE, Tsai H, Yoshida J, and Nyhus LR (1%):<br />
"Proximal gastric <strong>vagotomy</strong>: the fist 26 years." Year Book Medical<br />
publishers 139- 173, 1985. (quoted from Henry L. Laws, and J. Barry<br />
McKeman, 1993)<br />
37- Donicot NJ, McNeish AR, Alexander-WWims J, et a1 (1978):<br />
"prospective randomized multicentre trial of proximal gastric <strong>vagotomy</strong><br />
or t d<br />
vagotorny and antrectomy for chronic duodenal ulcer: interim<br />
results" Br J Surg 65; 152-54, 1978.(quoted fiom T.V Taylor, D.A.D.<br />
Macleod, A A Gunn, and L MacLennan, 1982.)<br />
38- Dragsted t LR (1968):<br />
Personal communications, 1956, 1961, 1963, 1968. (quoted from<br />
Griffith, 1995)<br />
39- Dragsted t LR, et al. (1947):<br />
"Section of the nerves to the stomach in the treatment of peptic ulcer."<br />
Ann Surg 126: 687, 1947. (quoted fiom Griffith, 1995).<br />
40- Dragstedt LR, et al. (1950):<br />
"Question of the return of gastric secretion after complete <strong>vagotomy</strong>."<br />
I Arch Surg 6 1 775, 1950. (quoted from Griffith, 1995).
- 139-<br />
"Selective gastric <strong>vagotomy</strong>." iiiest Surg Obstet Gynecol 70: 107, 1962.<br />
(quoted ffom Griffith, 1995).<br />
59-Griff~tb CA and Harkins HN. (1957):<br />
"Parietal gastric <strong>vagotomy</strong>." Gastroenterology 32: 96, 1957. (quoted<br />
from Grifith, 1995).<br />
60- Eans 0. Graffner Gustav F. Liedberg and Jan E. A. Oscarson<br />
(1985):<br />
"Recurrence after parietal cell Vagotomy for peptic ulcer disease". The<br />
American Journal of Surgery, vol. l SO, September 1985. pp: 336-340.<br />
6 1 - Henry L. Laws and J. Barry McKernau (1993):<br />
"Endoscopic management of peptic ulcer disease". Annals of Surgery,<br />
vol. 217, No. 5, May 1993, pp: 548-556.<br />
62- Kills BA. (1993):<br />
"Gastric mucc-! barrier: Evidence for Helicobacter pylori ingesting<br />
gastric surfactant and deriving protection from it." Gut 34: 588, 1993.<br />
(quoted from Christopher Wastell, and J.H. Baron,1995).<br />
63- H. J. M. Ooshogel and Th. J. M. V. van Vroonhoven (1988):<br />
"Anterior lesser cun-e <strong>seromyotomy</strong> <strong>with</strong> <strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong><br />
versus proximal gastric <strong>vagotomy</strong>". British Journal of Surgery, vol. 75,<br />
February 1988, pp: 12 1 - 124.
64- Hollander F. (1956):<br />
-l An-<br />
Personal communication, 1956. (quoted from Griffith, 1995).<br />
65- Holle F., Bauer H., and Holle G. (1972):<br />
"Clinical results of selective proximal <strong>vagotomy</strong> in gastro-duodenal<br />
ulcer." Langenbecks Arch. Klin. Chir. 330: 197, 1972. (quoted from<br />
Alan G. Johnson, 2000.)<br />
66- Hunt T. (1972):<br />
"Digestive disease: The changing scene." Br Med J 2: 689, 1972. (quoted<br />
from Christopher Wastell, and J.H. Baron, 1995).<br />
67- Jackson RG. (1949):<br />
"Anatomy of the vagus nerves in the region of the lower esophagus and<br />
the stomach." Anat Res 103: l, 1949. (quoted from Griffith, 1995).<br />
68- James B. Elder and Mark Deakin (iP75):<br />
"Gastl-IC physiology". Surgery of the Esophagus, Stomach Small<br />
Intestine, 5Ih ~dition, vol. I, 1995, pp: 420 - 430.<br />
69- James W. Freston (2000):<br />
Management of peptic ulcers: Emerging Issues" World Jouma! of<br />
Surgery, vol. 24, No. 3, March 2000, PP: 250-255.<br />
"The chips are down for Helicobacter pylori". Gut, vol. 50, 2002, pp:<br />
293-294.
71- Jennings D. (1940):<br />
-/4! -<br />
"Perforated peptic ulcer: Changes in age, incidence and sex distribution<br />
in the last 150 years." Lancet 1: 395, 1940. (quoted from Christopher<br />
Wastell, and J.H. Baron.I 995)<br />
72- J. Mouiel and N. Katkhouda (1993):<br />
"Laparoscopic <strong>vagotomy</strong> for chronic duodenal ulcer disease". World<br />
Journal of Surgery, vol.l7, No. I, Jan.lFeb. 1993, pp: 34-39.<br />
73- J. Mouiel and N. Kathouda (1999):<br />
"Posterior <strong>vagotomy</strong> and <strong>anterior</strong> <strong>seromyotomy</strong> as elective surgery for<br />
duodenal ulcer disease". Hepato-gastroenterology, vol. 46, 1999, PP:<br />
1507-1516.<br />
74- Johnson A.G. (1982):<br />
"Areas difficult to denerv.v- " In Vagotomy in Modem Surgical<br />
Practice, J.H. Baron, 1. Alexander-Williams, M. Allgower, C. Muller, .J.<br />
Spencer.editors, Oxford, Burterworths Heinemann, 1982, pp 127-131.<br />
(quoted from Alan G. Johnson, 2000.)<br />
75- Johnston D., Wilkinson A.R. (1970):<br />
"Highly selective <strong>vagotomy</strong> <strong>with</strong>out a drainage procedure in the<br />
treatment of duodenal ulcer." Br J Surg 57: 289, 1970. (quoted from<br />
Alan G. Johnson, 2000.)
-143-<br />
82- Konturek SJ, Dwiecien N, Obtulowicz W, et al. (1979):<br />
"Cephalic phaseof gastric secretion in healthy subjects and duodenal<br />
ulcer patients: Role of vagal innervation." Gut 20: 875, 1979. (quoted<br />
from Alan G. Johnson, 1995).<br />
83- Konturek 55. (1990):<br />
"Role of growth factors in gastroduodenal protection and healing of<br />
peptic ulcers." Gastroenterol Clin North Am 19: 41, 1990. (quoted from<br />
Christopher Wastell, and J.H. Baron,1995).<br />
84- Koop H. (1992):<br />
"Metabolic consequences of long-term inhibition of acid secretion by<br />
omeprazole." Aliment Pharmacol Ther 6: 399, 1992. (quoted from<br />
Alfred Cushieri, 1995).<br />
85- Kreel L, and Ellis H. (1965):<br />
"Pyloric stenosis in adults: A clinical and radiological study of 100<br />
consecutive patients." Gut 6: 253, 1965. (quoted from Thomas V.<br />
Taylor, 1995)<br />
86- Kusakari K, Nyhus L, Gillison E, Rombeek CEo (1972):<br />
"An endoscopic test for completeness of <strong>vagotomy</strong>." Arch Surg 105:<br />
386, 1972. (quoted from Richard P.Saik, A. Gerson Greenburg, Jack M.<br />
Farris, and Gerald W. Peskin. Am .I Surg 132: Aug 1976.)
-144-<br />
87- Landboe-Christensen K (1944):<br />
"Extent of the pylorus zone in the human stomach" Acta Pathol<br />
Microbial Scand 54(Suppl): 671,1944. (quoted from Griffith, I 995).<br />
88- Landboe-Christensen E. (1944):<br />
"The Duodenal Glands of Brunner in man: Their Distribution and<br />
quantity. London: Humphrey Milford. Oxford Univeristy press, 1944.<br />
(quoted from Griffith,1995).<br />
89- Langman M. (1974):<br />
"The changing nature of the duodenal ulcer diathesis." In C Wastell (Ed),<br />
Westminster Hospital Symposium on Chronic Duodenal Ulcer. London:<br />
Butterworth, 1974. pp 3-12. (quoted from Christopher Waste!l, and J.H.<br />
Baron,1995).<br />
90- Latarjet A. (1921):<br />
"Prelirninaire sur l'innervation de l'estornac." Lyon \1ed 130: 166, 1921.<br />
(quoted from Griffith, 1(95).<br />
91- Latarjet A. (1922):<br />
"Resection des nerfs de l'estornac." Bu!1 Acad 0Jatl Med (Paris) 87: 681,<br />
1°22. (quoted from Griffith, 1995).<br />
92- Lars-Erik Hansson (2000):<br />
"Risk or stomach cancer in patients <strong>with</strong> peptic ulcer disease" World<br />
Journal of Surgery, vol. 24, No.3, March 2000, PP: 315-320.<br />
..,.
.<br />
-145-<br />
'" 93- Leena Khaitan and Michael D. Holzman (2002):<br />
"Laparoscopic advances in general surgery". JAMA, vol. 287. No. 12,<br />
March 27,2002. pp: 1502-1505.<br />
94- Legros G and Griffith CA. (1968):<br />
"The anatomic basis tor the variable adequacy of incomplete <strong>vagotomy</strong><br />
(partlf)." Ann Surg 168: ]035, 1968. (quoted from Griffith" 1995).<br />
95- Legros G and Griffith CA. (1969):<br />
"The anatomic pathways of the vagal fibers to the antral mucosa. "<br />
Surgery 66: 751, 1969. (quoted from Griffith,1995).<br />
96- Le J, and Vilcek J. (1987):<br />
"Tumor necrosis factor and interleukin 1: Cytokines <strong>with</strong> multiple<br />
overlapping biological activities" Lab Invest 56: 234, 1987. (Quoted<br />
from James B. Elder, and Mark Deakin, 1995).<br />
97- LeVeen HB, et aL (1952):<br />
"the physiological mechanism for death in massively bleeding peptic<br />
ulcer." Surg Gynecol Obstet 94: 433, 1952. (quoted from Griffith,1995).<br />
98- Loeweneck VB, et 31. (1967):<br />
"VahJUS and Cholinergisches system am magen des menschen." Munch<br />
Med Wochenschr 109: 1754, 1967. (quoted from Griffith,1995).
111- Moynihan BG. (1907):<br />
-148-<br />
"Report on 334 cases of operation for non-malignant disease of the<br />
stomach." Med Chir Trans 90: 393, ]907. (quoted from Christopher<br />
Wastell, and J.H. Baron,1995).<br />
I \2- Murray JG. (1959):<br />
"the consequences of injury and disease of nervous tissue." J R Coll Surg<br />
Edinb 4: 199, 1929. (quoted from Griffith,1995). ,<br />
113- Nielsen BO. et 81. (1981):<br />
"The antrum in duodenal ulcer patients: Relationship between antrum<br />
size, nerve of Latarjet, gastrin cell quantity, and gastric acid secretion."<br />
Scand J Gastroenterol16: 491, 1981. (quoted from Griffith,1995).<br />
114- N. J. Lygidakis (1984):<br />
"Posterior <strong>truncal</strong> <strong>vagotomy</strong> and <strong>anterior</strong> curve superficial <strong>seromyotomy</strong><br />
as an alternative for the surgical management of chronic ulcer of the<br />
duodenum". Surgery of Gynecology & Obstetrics, vol 158, March 1984,<br />
pp:251-254.<br />
115- Oi M, et aI. (1969):<br />
"A possible dual control mechanism in the ongm of peptic ulcer."<br />
Gastroenterology 57: 280,1969. (quoted from Griffith,1995).<br />
+
-149-<br />
116- Oi M, Hoshiko S,Fumatsu S. (1958):<br />
"A study of the distribution of parietal cells in the human stomach." Jikei<br />
Med J 5: 10, 1958. (quoted from Christopher Wastell, and lH.<br />
Baron,1995).<br />
117- Oi M, and Oshida K. (1959):<br />
"The association of esophageal, gastric, and duodenal ulcers. "<br />
Gastroenterology 36: 57, 1959. (quoted from Griffith, 1995).<br />
118- Oi M, Oshida K, and Sugimura S. (1959):<br />
"The location of gastric ulcer. I, Gastroenterology 36: 45, 1959_ (quoted<br />
from Christopher WasteU, and Ill. Baron,1995).<br />
119- Oi M, and Sakurai Y. (1959):<br />
"The location of duodenal ulcer." Gastroenterology 36: 60, 1959_<br />
(quoted from Griffith, 1995).<br />
120-Payne J1'. (1963):<br />
"The significance of vascular landmarks in gastric resection." West J<br />
Surg Obstet Gynecol 71: 161, 1963_ (quoted from Griffith, 1995)_<br />
121- Penston JG, Wonnsley KG. (1992):<br />
"Maintenance treatment <strong>with</strong> H2- receptor antagonists for peptic ulcer<br />
disease." Aliment Pharmacal 6: 3, 1992_ (quoted from Alfred<br />
Cushieri,1995).<br />
122- Peters RM, and Womack NA. (1958):
-150-<br />
"Hemodynamics of gastric secretion." Ann Surg 148: 537, 1958. (quoted<br />
from Griffith,1995).<br />
123- Philip E. Donahue, C. Thomas Dombeck, Yunichi Yoshida and<br />
Lloyd M Nyhus (1987):<br />
"Endoscopic Congo red test during proximal gastric <strong>vagotomy</strong>". The<br />
American Journal ofSurgery, vol. 153, March 1987, pp:249-255.<br />
124- Poppen D, et al. (1976):<br />
"Parietal cell <strong>vagotomy</strong>: Localization of the microscopical antral-fundic<br />
boundary in relation to the macroscopical." Acta Chir Scand 142: 251,<br />
1976. (quoted from Griffith,1995).<br />
125- Pritchard GR, et al. (1968):<br />
"A physiologic demonstration of the stomach. " Surg Gynecol Obstet<br />
126: 791, 1968. (quoted from Griffith,1995).<br />
126- Reeves TB. (1920):<br />
"A study of the arteries supplying the stomach and duodenum and their<br />
relation to ulcer." Surg Gynecol Obstet 30: 374, 1920. (quoted from<br />
Griffith,1995).<br />
127- Richard P. Saik, A. Gerson Greenburg, Jack M. Farris and<br />
Gerald W. Peskin (1976):<br />
"The practicality of the Congo red test, or is your <strong>vagotomy</strong> complete?".<br />
The American Journal ofSurgery, vol.132, August 1976, pp: 144-149.<br />
t
-154-<br />
«Mortality and morbidity after <strong>anterior</strong> lesser curve <strong>seromyotomy</strong> <strong>with</strong><br />
<strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong> for duodenal ulcer". British Journal of<br />
Surgery, vol, 72, December 1985, pp: 950-951.<br />
146- T. V. Taylor, D. A. D. Macleod, A. A. Gunn and L Maclennan<br />
(1982):<br />
«Anterior lesser curve <strong>seromyotomy</strong> and <strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong> m I<br />
the treatment of chronic duodenal ulcer". The Lancet, vol. 16, October<br />
1982, pp: 846-848.<br />
147- T. V. Taylor, J. P. Lythgoe, J. B. McFarland, I. T. Gilmore, P.<br />
E. Thomas and G. H. Ferguson (1990):<br />
«Anterior lesser curve <strong>seromyotomy</strong> and <strong>posterior</strong> <strong>truncal</strong> <strong>vagotomy</strong><br />
versus <strong>truncal</strong> <strong>vagotomy</strong> and pyloroplasty in the treatment of chronic<br />
duodenal ulcer". British Journal of Surgery, vol. 77, September 1990, pp:<br />
1007-1009.<br />
148- T. V. Taylor, S. Holt and R C. Heading (1985):<br />
"Gastric emptying after <strong>anterior</strong> lesser curve scromyotomy and <strong>posterior</strong><br />
<strong>truncal</strong> <strong>vagotomy</strong>". British Journal of Surgery, vol. 72, August 1985, pp:<br />
620-622.<br />
149- VanderhoffJA, McCusker RH. and Clark Ret at. (1992):<br />
"Truncated and insulin-like growth factor 1 enhance mucosal adaptation<br />
after jejuno-ileal resection." Gastroenterology 102: 1949, 1992. (quoted<br />
from Christopher Wastell, and LH. Baron,1995). '"<br />
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