laparoscopic anterior seromyotomy with posterior truncal vagotomy ...

laparoscopic anterior seromyotomy with posterior truncal vagotomy ... laparoscopic anterior seromyotomy with posterior truncal vagotomy ...

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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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....<br />

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 />

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...<br />

. ..,


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gastric acid." Gastroenterology 100: 627, 1991. (quoted from<br />

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zt Buck SH, and Burks TF. (1986):<br />

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"A test for pyloric regurgitation" Lancet 2: 621, 1966. (quoted from<br />

Griffith,1995).<br />

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"Anatomy of the stomach and duodenum". Surgery of the Esophagus,<br />

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40 years." J Forrnos Med Assoc 95: 675, 1996.(quoted from Alan G.<br />

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28- Christine F. KoUmorgen, Seval Gunes, John B. Donohue,<br />

Geoffrey B. Thompson, and Michael G. Sarr (1996):<br />

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methods in the canine model". Annals of Surgery, vol. 224, No. 1,1996,<br />

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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 />

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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 />

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Results of application in two medical centers". Zentralbl Chir 1987;<br />

122(19), pp:1208-1215.<br />

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publishers 139- 173, 1985. (quoted from Henry L. Laws, and J. Barry<br />

McKeman, 1993)<br />

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"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 />

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Personal communications, 1956, 1961, 1963, 1968. (quoted from<br />

Griffith, 1995)<br />

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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 />

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(quoted ffom Griffith, 1995).<br />

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"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 />

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"Recurrence after parietal cell Vagotomy for peptic ulcer disease". The<br />

American Journal of Surgery, vol. l SO, September 1985. pp: 336-340.<br />

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vol. 217, No. 5, May 1993, pp: 548-556.<br />

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"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 />

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"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 />

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ulcer." Langenbecks Arch. Klin. Chir. 330: 197, 1972. (quoted from<br />

Alan G. Johnson, 2000.)<br />

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"Digestive disease: The changing scene." Br Med J 2: 689, 1972. (quoted<br />

from Christopher Wastell, and J.H. Baron, 1995).<br />

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"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 />

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"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 />

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(quoted from Alan G. Johnson, 2000.)<br />

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..,.


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+


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t


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><br />

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