Chapter 8

OPERATION ON THE STOMACH AND DUODENUM

8.1. ANATOMY AND PHYSIOLOGY

The stomach and duodenum may be considered logically logically as a unit, since
many physiologic functions and certain disorders are either shared by these two
segments of the gut, or interact on each other.
For gross description, the stomach can be divided into fundus, body and antrum
(Fig. 8.1). The cardia is located at the esophagogastric junction.The pyiorus is the
boundary between the stomach and the duodenum, which may be palpated as a thick
ring of muscle and is externally marked by the prominuent vein (prepyloric vein).The
incisure, approximately 5–6 cm proximal to the pylorus on the lesser curvature, is called
the angular incisre.The fundus is the dome of the stomach that lies cephalad to the
esophagogastric junction.

Figure. 8.1. The stomach and duodenum.

 The area distal to a line drawn from the angular incisure to the greater curvature
and proximal to the pylorus is the gastric antrum.The body of the stomach is the
capacious central part, lying between the fundus and the antrum.
The cardiac gland area is the small segment located at the esophagogastric
junction. Histologically, it contains principally mucus–secreting cells, athough a few
parietal cells are somethimes present. The oxyntic gland area is the portion containing
parietal cells and chief cells that secrete acid peptic juice. The pyloric gland area
constitutes the distal 30%of the stomach and contains the G–cells that secrete a
hormone, gastrin. Mucous cells, which secrete relatively alkaline mucus, are common in
both the oxyntic and pyloric gland areas.
Blood supply Blood supply of the stomach is particularly rich and the wall of the
stomach contains a rich submucosal vascular plexus. The left gastric artery (a branch of
celiac trunk) andright gastric artery (a branch of the common hepatic artery) supply the
area of the lesser cuvature and connects each other.The greater curvature is supplied by
the right gastroepiploic artery.The mid portion of the greater curvature corresponds to a
point at which the gastroduodenal artey and the left gastroepiploic artery. The fundus of
the stomach along the greater curvature is supplied by the short gastric arteries, branches
of the splenic. The gastroduodenal artery may sends small branches to the area of the
pylorus. In 60% of persons, a posterior gastric artery arises off the middle third of the
splenic artery and terminates in branches on the posterior surface of the body and the
fundus.
The blood supply to the duodenum is from the superior and inferior
pancreaticoduodenal arteries provide blood supply to the superior portion of duodenum.
Venous blood from the stomach drains into the coronary, gastroepiploic, and
splenic veins before entering the portal vein.
Nerve supply. The parasymapthetic nerves to the stomach is from the vagal
nerve. About 90% of the vagal fibers are sensory a afferent, the remaining 10% are
efferent. The efferent fibers of the vagal nerves stimulate the motility of the stomach and
the secretion of acid, pepsin and gastrin. As a rule, 2 major vagal trunks pass through the
esophageal hiats in cose approximation to the esophageal muscle. In the region of the
gastroesophageal junction, each trunk bifurcates. The left or anterior vagal trunk sends
to the liver a division at travels in the lesser momentum. The bifurcation of the right or
posterior trunk gives rise to fibers that enter the celiac plexus and supply the
parasympathetic innervation to the remainder of the gastrointestinal tract. Both trunks,
after giving rise to their extra gastric divisions, send some fibes directly onto the surface
of the stomach. “The anterior vagal trunk supply innervation to the anterior wall of the
stomach (anterior nerves of Latarjet), the posterior vagal trunk supply innervation to the
posterior wall of the stomach (the posterior nerves of Latarjet).
The sympathetic nerve fibers pass along the arterial vessels from the celial plexus
to the stomach.
GASTRIC SECRETION
The output of gastric jujce in a fasting subject varies between 500 and 1500ml/d.
After each meal, about 1000 ml are secreted by the stomach.
 The components of gastric juce are as follows:
1. Pepsinogen. Pepsinogen are synthesized in the chief cells of the oxyntic gland
area (and to a lesser extent in the pyloric area) and are stored as visible granules.
Cholinergic stimuli are the most potent for secretions of pepsinogen, gastrin and
secretin. The precursor zymogen is activated when pH fals below 5.0 a process that
entails severance of a polypeptide fragment from the farger molecule. Pepsin cheaves
peptide bonds, especialy those containing phenylalanine, tyrosine, or leucine. Its optimal
pH is about 2.0 Pepsin activity is abolished at pH greater that 5.0, and the molecule is
irreversibly denatured at pH greater than 8.0.
2. Electrolytes. The uniqe characteristic of gastric secretion is its high
concentration of hydrochloric acid,a product of the parietal cells. As the concentration of
H2–rises during secretion, the concentration of Na drops in a reciprocal fashion.
Kremains relatively constant at 5–10 m Eq/L. Chloride concentration remains near 150
mEq/L, and gastric juice maintains its isotonicity and varying secretory rates.
3. Mucus. Mucus is a heterogeneous mixture of glycoproteins manufactured in
the mucous cells of the oxyntic and pyloric gland areas. Mucus provides a weak barrier
to the diffusion of H2 and protects the mucosa. It also acts as a lubricant and impedes
diffusion of pepsin.
4. Intrinsic factor. Intrinsic factor, a mucoprotein seceted by the parietal cells,
binds with vitamin B12 of dietary origin and greatly enhances absorption of the vitamin.
Deficiency in intrinsic factor may decrease vitamin B12 absorption from gut and result in
megaloblastic anenmia.
5. Blood group substances. 75% of people secrete blood group antigens into
gastric juice. The trait is genetically determined and is associated with a lower incidence
of duodenal ulcer than in nonsecretor.
The onset of secretion is accompanied by striking morphologic changes in the
apical membranes. Resting parietal cells are characterized by an infolding of the apical
membrane, called the secretory canaliculus, with is lined by short microvilli. Multiple
membrane–bound tubulovesicles and mitochondria are present in the cytoplasm. With
stimulation, the secretory canaliculus expand, the microvilli become long and narrow
and filled with microfilaments, and the cytoplasmic tubulovesicles disappear. The proton
pump mechanism for acid secretion is located in the tubulovesicles in the resting state
and in the secretory canaliculus in the stimulared state.
The basal lateral membrane contains the receptors for secretory stimulants and
transfers HCO3 out of the cell to balance the H2 output at the apical membrane. Active
uptake of Cl and K+ conduction also occur at the basal lateral membrane. Separate
membrane bound receptors exist for histamine (H2–receptor), gastrin, and acetylcholine.
The intracellular second messengers are thought to be cAMP for histamine and CaCl +
forgastrin and acelylcholine.
Acid secretion at the apical membrane is accomplished by a membrane –bound
H /K –ATPase (the proton pump); H2 is secreted into the lumen in exchange for K+.
+ +

The regulation of acid secretion may be deserlbed by considering separately those

factors that enhance gastric acid production and those that depress it. The interaction of
these forces is what determines the levels of secretion observed during fasting and after
meals.
Gastric secretion may be classified as spontaneous secretion (interdigestive
secretion), and stimulated secretion. Spontaneous acid secretion, occurring without.
Stimulated acid secretion is usually described as the result of 3 phases that are exeied
simultaneously after a meal.
1. Cephalic phase. Stimuli, such as sight, smell, taste, or even thought of
appetizing food, the vagal nuclei of the brain lead to increased vagal efferent activity.
The vagal stimuli release acetylcholine that have a direct effect on the parietal cells to
increase acid output. The effect is entirely vagal mediated and is abolished by vagotomy.
2. Gastric phase. Food in the stomach (principally protein hydrolysate and
hydrophobic amino acids) stimulates gastrin release rome the antrum. Gastric distention
has a simialar but less intense effect. Gastrin effects on the parietal cells to increase acid
secretion.
3. Intestinal phase. The role of the intestinal phase in the small bowel releases a
humoral factor, may named enter–oxyntin, that evokes acid secretion from the stomach.
pH below 2.5 in the antrum inhibits the release of gastrin, then remove gastrin stimulus
for acid secretion. When the pH–reaches 1.0, gastrin release is almost completely
blocked. If the normal relationship of parietal cell mucosa to antral mucose is changed to
that acid does not flow past the site of gastrin production, serum gastrin may increase to
high levels, with marked acid stimulation. Somatostatin in gastric antral cells serves a
physiolonic role as an inhibitor of gastrin release.
Fat in the intestine (duodenum) is the most effective inhibitor, which affect gastrin
release and acid secretion. The intestine may participates in controlling acid secretion by
liberating some hormones, secretin, or a still unidentified hormone that inhibit both the
release of gastrin and its effects on the parietal cells, and blocks acid secretion. The most
remarkable physiological action of gastrin is its ability to stimulate gastric acid
secretion. In addition to this action, gastrin also stimulates pepsin secretion, increase the
gastric mucosal blood flow, and stimulate pancreatic enzyme secretion.
Gastrin is synthesized, stored by G cells in the pyloric glands of antral mucosa,
and released from G cells. Carrying by the blood, gastrin stimulates the receptors in
various organs of the gut. Gastrin has been shown to exist in a variety of sizes.
The initial form of gastrin was composed of 17 linearly arranged L–amino acids with a
molecular weight of around 2100 (G–17), which is known as little gastrin. Minigastrin
(G–14) consists of the 14 C–terminal amino acid residues of G–17. G–17 can be split
enzymatically from big gastrin, that consists of 34 amino acids (G–34) and is the
predominant from in circulation. Big–big gastrin has been shown to pwssess the full
physiologic action of the parent molecule. This material is now available as pentagastrin.
With the development of specific and sensitive radioimmunoassay technique, it
has been possible to measure directly the concentration of serum gastrin. Depending on
the laboratory and technique, the normal basal level of serum gastrin is 50–100
picograms/ml (pg/ml).The level over 200 pg/ml can almost always be considered high.
Many patients with Zollinger–Englison syndrome have serum gastrin levels greater than
1,000–10,000 pg/ml.

8.2. DEFINITION OF ULCER

Ulcers are crater–like sores (generally 1/4 inch to 3/4 inch in diameter, but
sometimes 1 to 2 inches in diameter) which form in the lining of the stomach (called
gastric ulcers), just below the stomach at the beginning of the small intestine in the
duodenum (called duodenal ulcers) or less commonly in the esophagus (called esophageal
ulcers).
In general, ulcers in the stomach and duodenum are referred to as peptic ulcers.
It is known that the stomach is a bag of muscle that crushes and mixes food with
the digestive “juices” – hydrochloric acid and pepsin. If the lining of the stomach (or
duodenum) is damaged in one place or another, the acid and pepsin go to work on the
lining as they would on food, breaking it down as though to digest it.

Aggressive factors: Defensive factors:

H. pylori; Mucus, bicarbonate layer;
Drugs (NSAIDs); Blood flow, cell renewal;
acid, pepsin; Prostaglandins;
Bile salts. Phospholipid.

Figure 8.2. Pathogenesis of ulcers.

An ulcer is the result of an imbalance between aggressive and defensive factors

(Fig. 8.2).
On one hand, too much acid and pepsin can damage the stomach lining and cause
ulcers. On the other hand (and more commonly), the damage comes first from some other
causes, making the stomach lining susceptible to even an ordinary level of gastric acid.
The stomach defends itself from hydrochloric acid and pepsin by creating a mucus
coating (that shields stomach tissue), by producing bicarbonate and by circulating blood to
the stomach lining to aid in cell renewal and repair. If any of these functions are impaired it
can lead to the formation of an ulcer.
The primary cause of ulcers is the bacterium called Helicobacter pylori (H. pylori)
(Fig. 8.3). H. pylori is a spiral–shaped bacterium found in the stomach. Unlike other
bacterium, H. pylori is able to twist through the layer of mucous that protects the stomach
cavity and attach to cells on the surface of the stomach wall, where it produces urease, an
enzyme that generates ammonia.
 Figure 8.3. Transmission electron micrograph of Helicobacter pylori.

The Nobel Prize

in Physiology or
Medicine
(2005)

Barry J. Marshall J. Robin Warren

Helicobacter pylori Research Laboratory, QEII Medical Centre; University of Western
Australia, Nedlands, Australia.
Figure 8.4. Barry J. Marshall and J. Robin Warren.
 On October 3, 2005, Sweden Karolinska Medical School announced to grant
Australian scientists Barry J. Marshall and J.Robin Warren the Nobel Prize in
Physiology or Medicine 2005 for their discovery of pylori helicobacter pylori, a
bacterium caused gastritis and gastric ulcer. Owing to their discovery in 1982, the
chronic and incorrigible gastric ulcer could be cured by simply administering antibiotics
and other drugs (Fig. 8.4).
Non–steroidal anti–inflammatory drugs (NSAIDs) such as aspirin, ibuprofen,
naproxen, or piroxicam interfere with the stomach's ability to produce mucus and
bicarbonate (a chemical produced in the stomach that neutralizes and breaks down the
hydrochloric acid and pepsin into substances less harmful). NSAIDs also affect blood flow
to the stomach, hinder cell repair and cause the stomach's defense mechanisms to fail.
Lifestyle factors such as smoking, drinking caffeine, consuming alcohol and stress
are also associated with ulcers.
Smoking slows the healing of ulcers and makes them likely to recur.
Caffeine stimulates acid secretion in the stomach, thus aggravating the pain of an
existing ulcer.
Studies on alcohol consumption and ulcers have been less conclusive, although
alcoholic cirrhosis has been linked to an increased risk of ulcers, and heavy drinking has
been shown to delay the healing of ulcers.
Although emotional stress is no longer thought to be a cause of ulcers, people with
ulcers often report that emotional stress increases ulcer pain. However, physical stress
increases the risk of developing gastric ulcers.

8.3. GASTRIC ULCERS

Modified Johnson Classification

For many years ulcers of the stomach and duodenum were classified as a single
disease. As a result some of their differing features cancelled out and were concealed in
consideration of peptic ulcer as a whole. They are now generally recognized as distinct
entities, and considered by many to have different pathogeneses.
Dragstedt's theory that duodenal ulcers are caused by neurogenic acid
hypersecretion, and gastric ulcers by acid hypersecretion of hormonal origin, ignores
the fact that less than 50 per cent of gastric ulcer subjects are acid hypersecretors.
In the classification of gastric ulcers proposed by H. D. Johnson (1965), gastric
ulcer associated with duodenal ulcer represents a separate entity often featuring
increased acid secretion, like prepyloric gastric ulcer (Table 8.1).
Type 1. This is an ulcer in the body of the stomach without abnormality of the
duodenum, pylorus or prepyloric region (Fig. 8.5).
Type 2. This is an ulcer in the body of the stomach combined with, and probably
secondary to, an ulcer or its scar in the duodenum or at the pylorus. Although patients
with ulcers of this type usually exhibit well–marked or even gross acid hypersecretion,
in many the rate of secretion is low. These ulcers have a bad prognosis. They are very
resistant to medical treatment and have a strong tendency to bleed.
 Type 3. This is a gastric ulcer close to the pylorus. Lesions in this position which
were combined with duodenal ulcers, or with a Type 2 ulcer proximal to them, were all
classified as Type 3. Patients with prepyloric gastric ulcers, like those with duodenal
ulcers, usually have acid hypersecretion.
Type 4. This is an ulcer in the body near gastroesophageal junction of the
stomach.
Table 8.1.

The types of gastric ulcers

Type Location Acid hypersecretion
I Lesser curvature, incisura No
II Body of stomach, incisura, and duodenal ulcer (active or Yes
healed)
III Prepyloric Yes
IV High on lesser curve, near gastroesophageal junction No
V Anywhere (medication induced) No

Figure 8.5. The types of gastric ulcer (modified Johnson classification).

 Hypersecretion ulcers. Type 2 and 3: Gastric ulcers occurring as a complication
of duodenal ulcers, and juxtapyloric gastric ulcers, both tend to occur – as do duodenal
ulcers – in, hypersecreting individuals, though the onset of pyloric obstruction often
modifies these findings in late cases. However, though antral ulcers, like duodenal
ulcers, may be caused by hypersecretion, other factors must be considered in ulcers of
Type 2.
Hyposecretion ulcers. Type 1: excessive hormonal stimulation may occur in the
presence of gastric retention and may help to promote a gastric ulcer of Type 2 as a
complication of a duodenal ulcer. Many researchers have shown that prepyloric ulcers
occur in patients whose acid secretion averages more than that of healthy people. The
mean secretion rate for patients with gastric ulcers of any kind, however, is below
normal, for this average has been influenced by the consistently low rate of acid secre
tion in patients with primary ulcers in the body of the stomach.
Several factors may promote ulcers in persons with acid hyposecretion: 1) as-
sociated hyposecretion of mucus, 2) prolonging of the acid attack when gastric retention
is present and 3) local slowing of the already–critical rate of mucus secretion which
must result when submucosal arteriovenous shunts are opened.
Clinical features
The symptoms and complications of gastric ulcer closely resemble those of
duodenal ulcer. The complications would be discussed separately in this chapter.
The principal symptom is epigastric pain. Epigastric tenderness is a variable
finding. Compared with duodenalulcer, the pain in gastric ulcer tends to appear earlier
after eating, often within 30 minutes. Vomiting, anorexia, and aggravation of pain by
eating are also more common with fastric ulcer. However, the overlap of symptoms
between the 2 diseases is so great that historical information does not permit an accurate
diagnosis without barium z–rays examination.
If gastric ulcer is accompanied by signs of active or old duodenal ulcer, gastric
analysis may show hypersecretion. If gastric ulcer is unrelated to duodenal disease,
basal and maximal acid secretion will be low or normal. Achlorhydria is defined as no
acid after pentagastrin stimulation. Achlorhydria is incompatible with the diagnosis of
bnign peptic ulcer and suggests a malignant gastric ulcer.
Standard gastric analysis. The standard gastric analysis consists of the
following: 1) measurement of acid production by the unstimulated stomach under basal
fasting conditions; the result is expressed as H+ secretion in mEq/h and is termed the
basal acid output (BAO); 2) measurement of acid production during stimulation by
histamine (0.04 mg/Kg) or rentagastrin given (6 ug/Kg).The result is expressed as H 2
secretion in mEq/h and is termed the maximal acid ouput (MAO).Usually the normal
upper limit of BAO is 6 mEq/h in man,and 4 mEq/h in women, MAO is 40 mEq/h in
man, and 30 mEq/h in women.
Both BAO and MAO is more high that the normal upper limits in the most
patients with duodenal ulcer, while it is normal or little lower than normal in the patients
with gastric ulcer.
 The term achlorhydria denotes no acid (pH>6.0) after maximal stimulation.
Achlorhydria is incompatible with a diagnosis of benign peptic ulcer. In whom X–ray
examination have demonstrated gastric ulcer, this finding would indicate the presence of
underlying gastric cancer.
In Zollinger–Ellison synderome, basal acid secretion is ofter greater than 15
mEq/h, and the ratio of BAO to MAO is characteristically 0.6 or greater. But
confirmation of the diagnosis requires direct measurement of elevated serum gastrin
levels by immunoassay.
Hollander insulin gastric analysis. Hollander test involves the intravenous
administration of regular insulin and measurement of gastric acid secretion. The
intravenous injection of regular insulin in dose of 0.2 u/Kg may cause hypoglycemia
(blood sugar less than 50 mg %). The hypoglycemia stimulate vagal activity, which
results in acid secretion by gastric parietal cells. The procedure is based on the
assumption that increased acid found after insulin hypoglycemia is entirely the result of
vagal inpulses arising from central nervous system stimulation .The Hollander test was
used principally to test for completeness of vagotomy postoperatively.
Upper gastrointestinal X–ray (Fig. 8.6) will show an ulcer niche usually on the
lesser curvature in the pyloric area. In the absence of a tumor mass, the following
suggest that the ulcer is malignant 1) the deepest penetration of the ulcer is not beyond
the expected border of the gastric wall; 2) the meniscus sign is present, a prominent rim
of radiolucency surrounding the ulcer, caused by heaped–up edges of tumor; and 3)
ulcer niche is greater than 2 cm in diameter. Coexistence of duodenal deformity or ulcer
favors a diagnosis of benign ulcer in the stomach.

Figure 8.6. Xray: gastric ulcer, type I (arrow).

Gastroscopy and biopsy. Gastroscopy should be performed as part of the initial
workup of patients with gastric ulcer to attempt to find malignant lesions (Fig. 8.7).
 Figure 8.7. Gastroscopy: gastric ulcer, type I (arrow).

The rolled–up margins of the ulcer can be distinguished from the flat edges
characteristic of a benign ulcer. Multiple (preferably 5–6) biopsy specimens and brush
biopsy should be routinely obtained from the edge of the lesion.
The characteristic symptoms of gastric ulcer are ofter clouded by numerous
nonspecific complaints. Atrophic gastritis, chronic cholecystitis, irritable colon
syndrome, and undifferentiated functional problems are needed to be distinguishable
from peptic ulcer through X–rays, and gastroscopy. These examinations should be
always required before making the diagnosis of gastric ulcer. Besides these, one must
always consider whether the noncharacteristic complain or a ulcer niche seen on X–ray
represent an ulcerated malignant tumor rather than a simple benign ulcer.

8.4. DUODENAL ULCERS

Duodenal ulcers may occur in any age group but are most common in the young
and middeaged (20–35 years). They appear in men more often than women. About 95%
of duodenal ulcers are situated within 2 cm of the pylorus, in the duodenal bulb.
Physiologic abnormalities found in patients with duodenal ulcer include the
following: 1) increased numbers of parietal and chief cells, resulting in increased acid
and pepsin secretion; 2) increased sensitivity of parietal cells to stimulation by gastrin;
3) increased gastric response to a meal; 4) decreased inhibition of gastricn release from
the antral mucosa in response to acidification of gastric contents; 5) increased rate of
gastric emptying, including decreased inhibition of emptying in response to a specific
acid load in the duodenum; and 6) decreased bicarbonate productionin the duodenum.
Not all abnormalities are found in every patient, and other unknown factors must be
important in some cases.
Another theoretic cause of peptic ulcer is decreased resistance of the duodenal
mucosa to the action of gastric acid and pepsin. Several other clinical factors are known
to be associated with cnhanced susceptibility to duodenal ulcer. The disease is more
common in individuals with blood group O and in those who fail to secrete blood group
antigens A, or B in their gastric juice. Antral gastritis associated with Helicobacter
pylori infection is present in a majority of patients with duodenal ulcer. Chronic liver
disease, chronis lung diseases and chronic pancreatitis have all been implicated as
increasing the possibility of duodenal ulceration.
Clinical features
Pain, the presenting symptom in most patients, is usually located in the
epigastrium and is variably described as aching, burning, or gnawing. The daily cycle of
the pain is often characteristic. The patient usually has no pain in the moring until an
hour or more after breakfast. The pain is relieved by the noon meal, only to recur in the
later afternoon. Pain may appear again in the evening, and in about half of cases it
arouses the patient during the night. Food, milk, or antacid preaparations give temporary
relief. When the ulcer penetrates the head of the pancreas posteriorly, back pain is noted;
conconmitantly, the cyclic pattern of pain may change to a more steady discomfort, with
less relief from food and antacids. Varying degrees of nausea and vomiting are common.
Vomiting may be a major feature even in the absence of obstruction.
The abdominal examination may reveal localized epigastric tenderness to the right
of the midline, but in many instances no tenderness can be elicited.
The activity of duodenal ulcer and its accompanying symptoms typically remit and
recur at intervals of several years. Reapses last for 2–4 months, but the variation is great.

Figure 8.8. Gastroduodenoscopy: duodenal ulcer (arrow).

 Gastric analysis. Both basic acid output (BAO) and maximal acid output (MAO)
are increased.
Upper gastrointestinal series. The changes induced by duodenal ulcer consist of
duodernal deformities and an ulcer niche.
Gastroduodenoscopy. It is useful in evaluating patients with an uncertain
diagnosis and peptic ulcer those with bleeding from the upper intestine, and those who
have obstrucion of the gastroduodenal segment and for assessing response to therapy
(Fig. 8.8).

8.5. ULCER PENETRATION

Ulcer penetration refers to penetration of the ulcer through the bowel wall
without free perforation and leakage of luminal contents into the peritoneal cavity.
Surgical series suggest that penetration occurs in 20 percent of ulcers, but only a small
proportion of penetrating ulcers become clinically evident. Penetration occurs in
descending order of frequency into the pancreas, gastrohepatic omentum, biliary tract,
liver, greater omentum, mesocolon, colon, and vascular structures.

Fig. 8.20. The scheme of penetration of gastric ulcer.

Antral and duodenal ulcers can penetrate into the pancreas. Penetration can also
involve pyloric or pre pyloric ulcers penetrating the duodenum, eventually leading to a
gastroduodenal fistula evident as a “double’ pylorus. A long–standing ulcer history is
common but not invariable in patients who develop penetration.
The scheme of penetration of stomach ulcers is presented in drawing (Fig. 8.20).
Clinical features
Intense persistent pain. Penetration often comes to attention because of a change
in symptoms or involvement of adjacent structures. The change in symptom pattern may
be gradual or sudden; it usually involves a loss of cyclicity of the pain with meals, and
loss of food and antacid relief. The pain typically becomes more intense, of longer
duration, and is frequently referred to the lower thoracic or upper lumbar region.The
diagnosis of penetrating ulcer is suspected clinically when an ulcer in the proper region
is found. Mild hyperamylasemia can develop with posterior penetration of either gastric
or duodenal ulcer, but clinical pancreatitis is uncommon. Penetration can be associated
with a wide array of uncommon complications including perivisceral abscess (evident
on CT or ultrasonography), erosion into vascular structures leading to exsanguinating
hemorrhage (aortoenteric fistula) , or erosion into the cystic artery . Rare biliary tract
complications include erosion into the biliary tree with choledochoduodenal fistula,
extra hepatic obstruction, or hematobilia. Fistulization into the pancreatic duct has also
been reported with penetrating duodenal ulcer fistulae are seen with greater curvature
gastric ulcers, particularly marginal ulcers. Typical features of this complication include
pain, weight loss, and diarrhea; feculent vomiting is an uncommon, but diagnostic
symptom. A duodenocolic fistula can also occur.
Diagnosis confirmed by X–Ray (Fig. 8.21), endoscopy (Fig. 8.22), CT or MRI.

Fig. 8.21. X–ray: gastric ulcers (barium collects in ulcer crater).

Fig. 8.22. Endoscopic view of ulcer.

 8.6. PYLORIC STENOSIS

Piloric stenosis is a narrowing of the outlet stomach (Fig. 8.23). Stenosis of

pyloric part of the stomach and duodenum due to ulcers arise as a result of scarring
and morphological changes around an ulcer. Narrowing, disturbance of the
coordinated motility of pylorus as a result of ulcer creates an obstacle to the normal
movement of stomach content to the duodenum.

Fig. 8.23. Pyloric stenosis.

The pyloric orifice is 0,5–0,7cm in diameter. The mucosa of pyloric part of
stomach is thickened with rough folds. Muscular fibers are hypertrophied and solid.
During decompensation stage the muscular layer of stomach becomes thinner
and the pyloric orifice narrows to a few millimeters. Microscopically atrophy of
mucosa and muscular fibers, vessels sclerosis is seen.
Clinical stages of stenosis are distinguished:
1. Compensation stage.
2. Subcompensation stage .
3. Decompensation stage.
Clinical features
The first signs of stenosis can be seen eight–ten years after the onset of the
peptic ulcer disease, there is mainly narrowing, rigidity and disturbance of the activity of
the pylorus, which creates a barrier for transition of stomach content to the duodenum.
At the compensation stage, the hypertrophy of the wall of stomach develops.
Thereupon gastric content does pass through the narrowed area of stomach but passes
slowly. In this stage, patient usually complains of a feeling of discomfort in the
epigastric area after food intake with periodic vomiting of sour gastric contents. X–ray –
on an empty stomach in the stomach is determined 200–300 ml of fluid; the stomach is
of normal size or slightly enlarged. The evacuation of barium suspension is timely or
slowed down to 6–12 hours.
At the subcompensation stage muscular layer of stomach becomes thinner.
Evacuation disorders are increased. In this stage of the disease patients usually complain
of permanent feeling of discomfort in epigastric region, nausea and vomiting. Vomiting
becomes systematic (once or twice on a day). When examined at this stage, the symptom
of "splash noise" is often detected, diagnosed on an empty stomach or a few hours after
eating. X–ray: the tone of the stomach is reduced, its capacity is increased, the peristalsis
is sluggish. An empty stomach in the stomach with more than 500 ml of liquid.
Evacuation of the barium suspension is slowed down to 10–12 hours.
At the decompensation stage, the clinical signs appear quickly. There are
disturbances in the general condition of the patient, considerable loss of weight (30–
40%), acutely expressed dehydration, hypoproteinemia, hypocalcaemia, azotemia and
alkalosis. In case of prolonged disease, as a result of progression of disturbances of
metabolism, there can be convulsive syndrome (gastric tetany). Vomiting in this stage is
not always considered to be a typical sign, in fact patients often stop eating, and the
stomach considerable increases in size and atrophy of wall is seen. In such patients, it is
possible to define the contours of the stretched stomach in the epigastric region, which
has slow peristalsis. 1.5–2litres of food with a putrid smell are removed with a gastric
tube. There can be considerable disturbances of electrolyte metabolism. X–ray: there is
an increase in the size of the stomach and its lowering, a decrease in tone, a sluggish
peristalsis. Evacuation is dramatically slowed down to 24 hours or more.
In the decompensated stage of stenosis, the stomach is not completely absorbed
from food. Vomiting becomes systematic, pain is permanent. The severity and raspiranie
in the epigastric region disappear only after vomiting or rinsing of the stomach. The
general condition deteriorates sharply, exhaustion and dehydration increase, seizures and
symptoms of azotemia (weakness, headache, loss of appetite, thirst, stench from the
mouth, oliguria, seizures, etc.) appear. Determined constant "noise splash" on an empty
stomach, develops a humoral syndrome: hypochloremia, hyperazotemia, alkalosis; there
is a thickening of the blood.
As a result of repeated and profuse vomiting, in which hydrochloric acid is
removed from the body, and with it a chlorine component, chlorine ions are drawn from
the blood to form hydrochloric acid. The released sodium ions enter into a compound
with bicarbonates, alkalosis develops. Alkalosis, azotemia, a violation of calcium
metabolism contribute to an increase in the excitability of the neuromuscular system.
With increased muscular excitability, positive are: Khvostek’s sign – reduction of facial
muscles of the face when struck by a hammer in the projection of the trunk of the facial
nerve or its branches; Goffman’s sign – unbearable pain when tapping a hammer in the
region of the exit of branches of the trigeminal nerve; Trusso’s sign – convulsive
evidence of fingers under pressure on the median nerve on the shoulder or forearm in the
form of "hand of an obstetrician"; Bechterew's sign is the flexion of the fingers when
striking the back surface of the foot in the region of III and IV metatarsus. Sometimes
there is diplopia due to cramps in the eye muscles; myotonia – the patient cannot flex
and unbend the hands and feet. With the growth of the hypochloraemia clinic, painful
tonic spasms of skeletal muscles arise, spontaneous reduction of the fingers in the form
of the "hand of an obstetrician" (Poole's sing), tonic convulsions of the whole body with
opisthotonus and trismus. In severe cases, a deep coma develops.
The methods of investigations
Laboratory studies
 CBC count (leucocytosis with left shift is found in most cases.); biochemical
parameters of blood, blood and urine analysis; coagulogramm; Ht (hematocrit, parity of
volumes of uniform elements and plasmas of blood); blood group, rhesus–factor (Rh–
factor);
 Serum gastrin levels (gastrin levels greater than 1000 pg/mL are suggestive of
gastrinoma).
 H. pylori infection testing: 
 Serum H. pylori antibody detection: Antibodies (immunoglobulin G [IgG])
to H. pylori can be measured in serum, plasma, or whole blood
 Urea breath tests: Urea breath tests are used to detect active H. pylori
infection by testing for the enzymatic activity of bacterial urease. In the presence of
urease produced by H. pylori, labeled carbon dioxide (heavy isotope, carbon–13, or
radioactive isotope carbon–14) is produced in the stomach, absorbed into the
bloodstream, diffused into the lungs, and exhaled.
 Fecal antigen tests: Fecal antigen testing is used to identify active H. pylori
infection by revealing the presence of H. pylori antigens in stools. This test is more
accurate than antibody testing and less expensive than urea breath tests.
 Hypochloremia is a relatively rare but severe and life–threatening complication of
peptic ulcer of the stomach and duodenum, found in 0.5–1.5% of cases.

Fig. 8.24. X–ray: normal gastric anatomy.

 Fig. 8.25. Pyloric stenosis is seen in newborns within the first months. There is a
4:1 male ratio and is due to hypertrophied musculature at the pylorus.
X–ray examination (Fig. 8.24). In the compensation stage, the size of
stomach is normal, its peristalsis is deep, increased, evacuation of contents occurs in
not more than 6 hours. In the stage of subcompensation the size of stomach increases,
peristalsis is decreased; evacuation takes up to 12 hours. During decompensation stage
the stomach is considerably dilated like a sack and deformed, the contrast stays for long
(more than 24–48 hours) (Fig. 8.25).
Gastroscopy with biopsy is a very informative method of examina tion of
such patients. By this method it is possible to determine the reason and degree of
stenosis and also the state of mucosa of the stomach (Fig. 8.26).

Figure 8.26. Gastroscopy examination degree of stenosis.

 Differential diagnosis
Functional gastrostasis is more frequently seen in women. In that there, is
absence of some organic changes in the area of pyloric part of stomach or in a
duodenum, that can be exposed during gastroscopy.
Carcinoma of the stomach as a rule also does not cause special difficulties. A
diagnosis is finally confirmed by histological examinations of the biopsy material taken
during endoscopy.
Conservative and surgical treatment. Treatment for chronic ulcers involves
conservative therapy and surgical intervention according to the indications.
Conservative treatment of peptic ulcers, basically, includes three components:
 Antibiotic usually includes amoxicillin or clarithromycin, sometimes tetracycline.
 Antimicrobial drug usually includes metranidazole.
 Proton pump inhibitors (omeprazole, rabeprazole, etc.) or bismuth preparations.
This treatment regimen is used for 7–14 days and allows to achieve destruction
of Helicobacteria in 90% of patients. The patient should know that he must perform the
prescribed treatment in full. Patients are also assigned physiotherapeutic treatment and
recommended sanatorium treatment in sanatoria with medicinal mineral waters.
Particular qualities:
1. Rare; most uncomplicated ulcers heal within 12 weeks.
2. If don’t, change medication, observe addition 12 weeks.
3. Check serum gastrin (antral G–cell hyperplasia or gastrinoma).
4. Esofogogastrodoudenscopy: biopsy all 4 quadrants of ulcer (rule out cancer)
if refractory.
Absolute indications for surgical treatment are urgent: perforation of the ulcer,
profuse bleeding, not docking conservatively, and delayed: decompensated stenosis of the
outlet of the stomach, unstable hemostasis or recurrent bleeding.
Relative indications: refractory ulcers to conservative therapy or often recurrent
(more than 2 times a year for complex treatment), with complications in the history, as
well as ulcers in the cardia, large curvature and in the pyloric part of the stomach, which
can not be conservatively treated during 8 weeks.
Surgical treatment of peptic ulcer
In 1881, Theodor Billroth successfully performed the first gastric resection with
gastroduodenostomy for gastric carcinoma complicated with pyloric obstruction in
Vienna. In 1882, von Rydigier performed the same procedure firstly for peptic ulcer. By
1940, the term “subtotal gastrectomy” was interpreted as denoting removal of the distal
two–thirds or three–fourths of the stomach.
After resection of the stomach, the continuity of the gut can be restored by
anastomosis of the remaining portion of the stomach to the duodenum
(gastroduodenostomy, or Billroth I anastomosis) or by anastomosis, there are different
choices for gastrojejunostomy, the surgeon may bring the jejunal loop up to the gastric
remnant either anterior to the transverse colon (Moynihan’s operation, and V.
Eishlsberg’s operation) or posteriorly through a hole in the transverse mesocolon
(Hoffmeister’s operation, and Ploy’s operation).
 For duodenal ulcer, Billroth II anastomosis may be preferable, because the
recurrent rate of Billroth I is higher than Billroth II. Billroth I is the first choice for
gastric ulcer. When creating a Billroth II anastomosis, which kind of gastrojejunostomy
should be elected is depended on surgeon’s personal experiences since another methods
is satisfactory.
Physiologically, subtotal gastrectomy removes the antrum which is the major
sorce of gastrin secretion. As result, it decreases the gastric acid secretion stimulated by
gastrin. The procedure removes the part of the parietal cell mass by excision of the half
ara of the gastric body. As result, it decreases the gastric acid secretion stimulated
directly by vagus nerve.
In 1943 and 1949, Drapanas reported his idea that pathogenesis of duodenal ulcer
was associated with increased acid secretion and vagus section would be beneficial
experience about vagotomy. After long period of development, vagotomy has been
accepted in widely use in the western. In general, vagotomy include three basic types,
truncal vagotomy, selective vagotomy and superselective vagotomy (Fig. 8.27).

Fugure 8.27. Types of vagotomy: 1 – truncal vagotomy; 2 – selective

vagotomy; 3 – superselective vagotomy.

Truncal vagotomy. Truncal vagotomy consists of resection of 2 cm segment of

each vagal trunk as it enters the abdomen on the distal esophagus. Resection of truncal
vagus causes a great reduction of gastric acid secretion, but it also greatly suppresses
gastric motility due to vagal enervation of the entire stomach, and produces the
disturbances of the remainder of the ahdominal viscera due to denervating these organs,
which often present as diarrhea and gallstones. The method of drainage must be performed
for–delayed emptying of the stomach. Because the denervation of the vagal fibers in other
abdominal viscera is stil a big problem, this operation is not used very often.
The most common types of surgery for ulcers are vagotomy, antrectomy and
pyloroplasty. Vagotomy involves cutting the vagus nerve that transmits messages from the
brain to the stomach. This interruption reduces acid secretion. Antrectomy removes the
lower part of the stomach (antrum) which produces a hormone that stimulates the stomach
to secrete digestive juices. This enlarges the opening into the duodenum and small intestine
(pyloris), enabling contents to pass more freely from the stomach. Pyloroplasty may be
performed with a vagotomy.
Selective vagotomy. In selective vagotomy, each abdominal vague is transected
at a point just beyond its bifurcation into gastric and extra gastric divisions. Thus, the
hepatic branch of the anterior vagus and the celiac branch of the posterior vagus are
maintained. The drainage procedure is still necessary in selective vagotony. Two kinds
of drainage procedures can be chosen, pyloroplasty and gastrojejunostomy.
The pyloroplasty, originally introduced by Heiineke (1886) and Mikulicz (1888),
can provide a large gastric outlet and enhance emptying of the stomach. There are
multiple techniques for pyloroplasty, Heineke–Mikulicz technique and Finney technique
are most commonly in use today. If gastroenterostomy is chosen for delayed emptying
of the stomach, the anastomosis should be perofrmed in the distal antrum, immediately
proximal to the pylorus.
Superselective (highly selective) vagotomy. The newer operation was developed
for the treatment of peptic ulcer. The technique spares the main nerves of Latarjet but
divides al vagal branches that terminate on the proximal two–thirds of the stomach. The
denervation of the vagal fibers is limited to only the proximal stomach (roughly to the
area of parietal cells mass ) with preservation of the innervation of the antrum. Since
antral innervation is preserved, gastric emptying is relatively unimpaired, and a drainage
procedure is unnecessary. Physiologically, all typess of vagotomy eliminate direct vogal
stimulation of the parietal cells, as the result, gastric acid secretion stimulated by vagus
is decreased; gastric acid secretion stimulated by gastrin is also decreased since gastrin
release from antrum is diminished resulting from vagus resection. Basal and
postprandial serm gastrin levels are increased because of the rise in gastric pH. Basal
and stimulated acid secretion are both reduced to about one–thired of preservation of the
entire gastric reservoir capacity. The principal disadvantage is recurrent ulceration in
about 10% of patients. The reason mainly is incomplete vagotomy, which lead to great
emphasis on this procedure. In addition to the problems of surgical technique, variations
in the vagus at the esophageal hiatus and adjacent to the abdominal esophagus and on
the stomach make complete interruption of al vagel fibers impossible in some patients.
Antrectomy and vagotomy. This operation entails a distal gastrectomy of 50% of
the stomach, with the line of gastric transection carried high on the lesser curvature to
conform with the boundary of the gastrinproducing mucosa. Excision of the antrum
removes gastric acid secretion stimuated by gastrin; vagotomy eliminates direct vagal
stimlation of the parietal cells. The procedure combines gastrectomy and vagotomy in
both surgical technique, and effects to peptic ulcer. The procedure of antrectomy and
vagotomy is associated with a low incidence of marginal ulceration and a generally good
overall outcome.

Figure 8.29. Billroth I procedure.

The terms antrectomy and hemigastrectomy are loosely synonymous. The

proximal remnant may be reanastomosed to the dodenum (Bilroth I anastomosis, Fig. 8.29)
or to the side of the proximal jujunum (Billroth II anastomosis, Fig. 8.30). The Billroth I
technique is most popular, but there is no conchusive evidence that the results are superior.
When creating a Billroth II anastomosis, the surgeon may bring the jejunal loop up to the
gastric remnant either anterior to the transverse colon or posteriorly throgh a hole in the
transverse mesocolon. Since either method is satisfactory, and antecolic anastomosis is
elected in most cases because it is simpler.

Type IV gastric ulcer:

Figure 8.30. Billroth II (1) and R–Y limb gastrectomy (2) procedures.
  Least common (5% of all gastric ulcers).
 Ulcers 2–5cm from cardia can be treated with distal gastrectomy, extending
resection along the lesser curvature and Billroth I (Pauchet–Shoemaker’s procedure) (Fig.
8.27).
 Ulcers closer to GEJ, tongue–shaped resection high onto lesser curve (Csende’s
procedure with Roux–en–Y reconstruction) (Fig. 8.31).

Figure 8.31. Csendes resection (line of transection; Roux–en–Y anastomosis).

Giant Gastric Ulcer

 Giant gastric ulcer: >3cm; 30% malignancy risk.
 Subtotal gastrectomy with Roux–en–Y (high morbidity and mortality).
 Kelling–Madlener procedure: less aggressive, antrectomy, Billroth I reconstruction,
bilateral truncal vagotomy, leave ulcer, multiple biopsies, cautery of ulcer.
Surgical treatment of penetration ulcer
1. Reduce gastric acidity:
 Antisecretory drugs (proton pump inhibitors, H2  receptor antagonists etc.):
reduce histamine production, which also blocks effects of acetylcholine, and gastrin.
 Antibiotics to get rid of H. pylori infection.
 Discontinue smoking.
2. Surgery (Figs. 8.29–8.30):
 Last resort.
 Most applicable to complications that don’t respond to drug therapy.
 Procedure involves reduction of acid secretion while ensuring gastric drainage.
Duodenal ulcers
The main task of routine surgical treatment for peptic ulcer is the creation in the
postoperative period of conditions for the elimination of aggression factors in the
gastroduodenal region with a simultaneous decrease in mortality and the maximum
reduction of side effects. With ulcer of the duodenum – this effect on the acid–producing
zone, the effectiveness of the operation is determined by the level of suppression of gastric
secretion; with gastric ulcer – the effect on the zone of ulcerative infiltrate, which further
allows to normalize trophic disorders and create conditions for stabilizing histostructural
changes in the gastric mucosa. In the structure of surgical interventions in duodenal ulcer,
the most justified in the dominance of the nervous mechanism of acid regulation are
selective proximal vagotomy, selective or truncal vagotomy (Fig. 8.32) with removal of
the ulcerous substrate or its excretion in the lumen of the digestive tract and various
variants of duodeno– or pyloroduodenoplasty in depending on the performed vagotomy.

Figure 8.32. Removal of ulcer (A), pyloroplasty and truncal vagotomy (B).

Figure 8.32. Antrectomy with Billroth I and truncal vagotomy.

 The prevalence of the humoral link of the regulatory mechanisms, which is
expressed by the hyperplasia of the gastrin–producing cells of the antral part of the
stomach and the simultaneous decrease in the amount of somatostatin–producing cells,
serves as an indication for performing subdiaphragmatic truncal vagotomy with
antrumectomy as an operation that acts simultaneously on two mechanisms of acid
regulation in the stomach: the nervous and humoral (Fig. 8.33).
Surgical treatment of ulcerative stenosis of the outlet stomach
Preparation of patients for operation: correction of metabolic disturbances, such
patients must receive transfusion of fluids up to 2,5–3 1 per day which contain the ions
K+, Na+, Ca++, amino acid and glucose; plasma, albumin. Twice daily decompression
and washing of stomach with anti–ulcer therapy is done. Effective preoperative
preparation in such patients requires 5–7 days, sometimes even more.
The choice of operation method depends on many factors: degree of stenosis,
secretory and motility functions of stomach, age of patient, presence of accompanying
diseases etc. In the compensated and subcompensated stages of stenosis and when
functions of stomach are preserved, it is possible to perform organ–saving drainage
operations or minimal resection of stomach. With increase in the signs of stenosis and
disturbance of basic functions of stomach, the volume of operation must be increased to
resection by the Bilroth's methods.
Stomach resections and vagotomy:
 Billroth I – gastro–duodenoanastomosis end–to–end.
 Billroth II – gastro–jejunoanastomosis end–to–side with blind closure of
duodenum.
 Selective or highly selective vagotomy – denervation of parietal gastric cells.
Postoperative complications:
 Gastric atony  50%.
 Alkaline gastritis.
 Recurrent ulcers  2%.
 Diarrhea  16%.
 Dumping syndrome  14%.
 Bilious vomit  10%.
 Anemia  12%.
 B12 deficiency  14%.
 Folate deficiency  32%.
Postvagotomy complications:
 Diarrhea  2%.
 Dumping syndrome  2%.
 Bilious vomiting < 2%.
 8.7. POSTOPERATIVE COMPLICATIONS OF SURGERY FOR PEPTIC
ULCER

Postoperative complications after gastrectomy

In our clinics, we use to the following classification of postresection syndromes:
I. Functional disorders.
II. Organic disorders.
Functional disorders include: dumping syndrome, functional syndrome leading
and withdrawal hinge syndrome, hypo– and hyperglycemic syndrome, and post–
resection dystrophy; to organic – disorders due to mechanical causes (operation
defects): a) mechanical syndrome of the resulting loop, b) anastomoses; 2) disorders,
which are based on inflammatory processes: a) cholecystitis, b) hepatitis, c) pancreatitis,
d) enterocolitis, e) peptic ulcers of stump of the stomach and jejunum. In addition, we
single out early and late postoperative complications.
Early complications: postoperative hemorrhage, duodenal stump leakage,
anastomosis leakage, obstruction, and gastric retention may develop in the immediate
postoperative period.
Postoperative hemorrhage. Within 24 hours after operation, small voume of
dark red or coffee grounds’ gastric juice may be sucked from nasogastric tube. The
volume usually is less than 100–300 ml/d. It should disappear during the second to third
days after operation.Massive blood sucked from nasogastric tube, or severe melena is
the indication of postoperative hemorrhage, which may be due to bleeding at the sutre
line of gastrojejunostomy of gastroduodenostomy, or may be due to failure to control
bleeding from ulcer if lesion is left in the place. Most patients with this complication can
be cured by nonoperative mangements including prolonged fasting, hemostatic, and
blood transfusion. But reoperation is indicated if blood loss is more than 1500 ml in 24
hours, or shock occurs.
Doodenal stump leakage. Blowout of the duodenal stump is the most common
cause of death after Billroth II gastrectomy. This complication can be mininimized by
resorting to catheter drainage of the duodenum if the duodenal closure is not satisfied
due to duodenal scarring and intiammation. Equally important is selection of vagotomy
with drainage proccedure in preference to gastric rescction in patients with a badly
danmaged or inflamed duodenum. Obstruction of the afferent limb of the
gastrojejunostomy may contribule to this complication by increasing intraluminal
pressure in the duodenum.
The cliniacal picture is characterized by sudden severe upper abdominal pain
during the third to sixth days after sugery. The pain often radiates to the shoulder, and
the patient develops abdominal rigidity, high fever, and leukockytosis.
Immediate reoperation is mandtory. A sump device should be placed in the
ragion of the leaking duodenal closure. Spontaneous closure usually occurs if the patient
survives the acute phase; if it does not, the fistula should be surgically closed after the
patient has been stable for 4–6 weeks.
 Anastomosis leakage. Anastomosis leakage usually occurs during the fifth to
seventh days after operation, and it may occur at the gastrojejunstomy (Billroth II
anastomosis) or at gastroduodenostomy (Billroth I anastomosis). Both result in
peritoneal soilage with gut contents and are associated with peritonitis. Leakage form
the suture line is most commonly caused by ischemia or by problems of suture techniqe.
Nonoperative managements are considered firstly.Some patients may need reoperation
to repair leakage.
Postoperative obstructions. According to the anatomic position, postoperative
obstruction can be divided into anastomotic obstruction, afferent loop obstruction and
efferent loop obstruction.
Anastomotic obstruction. Anastomotic obstruction occurs following Billroth I
gastrectomy (gastroduodenostomy). The diameter of anastomosis between the remaining
portion of the stomach and the duodenum is limited by the lumen of the duodenum. The
problems of surgical suture and tissue edema may cause the obstruction of the
anastomosis. The clinical features are the gastric stasis and vomiting after eating, the
vomitus usually does not contain bile. Barium x–ray examination may demonstrate the
diagnosis. If consevative treatment for short period does not relief obstruction,
reoperation and re–anastomosis is indicated.
Afferent lop obstruction. Afferent loop obstruction occurs only after Billroth II
gastrectomy (gastrojejunostomy). It may occur as an acute complete obstruction, or as a
chronic incomplete problem. Obstruction can result from sharp angulation or kink at the
gastrojejunstomy, inflammation secondary to an anastomotic leak, fat necrosis. If the
transected edge of the stomach is sewn to the jejunum on a line that is not parallel to the
antimesenteric border of the jejunum, the anastomosis is likely to twist and obstruct.
Acute omplete obstruction of the afferent loop is a closed–loop obstruction,
characterized by sudden and severe epigastric pain, frequent vomiting withot bile, and
severe tenderness of right upper quadrant. In chronid incomplete obstruction of the
afferent loop, bile and pancreatic juices distend the partially obstructed afferent part,
especially after eating. The feature is that abdominal pain and vomiting with bile occur
at 15–30 mintes after eating. The meal itself is usually niot vomited because it enters the
efferent part of loop without difficulty. Chronic incomplete obstruction of the afferent
loop is also termed afferent loop syndrome.
All patients with acute complete obstruction should undergo emergency
operation. But medical management may be considered for afferent loop syndrome.
Reoperation is indicated if symptoms are severe and persistent. The afferent and efferent
parts of loop may be anastomosed side to side. A Billtroth II anastomosis can be
converted to a Billroth I anastomosis or a Roux–en–Y gastrojejunostomy.
Efferent loop obstruction. Obstuction of the efferent part of gastrojejunostomy
may be due to the same causes responsible for the afterent part obstruction. In addition,
obstruction of the efferent part of loop may be due to herniation of small bowel through
the space behind the gastrojejunostomy untess this space is obliterated. The clinical
manifestations are the presentation of high jejunum obstruction, and vomitus contains
bile. Emergency operation should be considered if symptoms do not relief.
 Gastric retention. An occasional patient is unable to tolerate oral feedings when
they are started 4 or 5 days after surgery. If this condition is due to edema of the stump,
resolution will usually occur if the stomach is decompressed for several more days. If
improvement is slow, balloon dilatation by an endoscopy may be helpful.
Late complications. Late complications may occur at several months or years
after operation.
Anastomotic ulcer. Anastomotic ulcer is recurrent ulcers, which is nearly
always locates immediately adjacent to the anastomosis on the intestinal side (marginal
ulcer). More than 90% develops after Billroth II subtotal gastrectomy for duodenal ulcer,
and it is unusual after gastrectomy for gastric ulcer.
The usual complaint is upper abdominal pain, which is often aggravated by
eating and improved by antacids. About a third of patients with anastomotic ulcer will
experience massive gastrointestinal hemorrhage. The common cause of anastomotic
ulcer after gastrectomy is inadequate gastric resetion. Another common cause found in
patient received Billroth II gastrectomy is too long afferent loop, which prduces
considerable absorption of alkaline pencreatic and biliary secretions before these juices
reach the anastomosis. H2 receptor blocker (cimetidine) or proton pump blocker
(omeprazole, etc. )will cause most marginal ulcers to heal, but recurrences are common,
re–gastrectomy will be indicated in the most cases.
Dumping syndrome. Early dumping syndrome occurs within 10–20 minutes of
eating and seem to be most common after milk with suger or a carbohydrate meal.
“Symptoms of the dumping syndrome” are noted to some extent by most patients who
have an peration that impairs the ability of the stomach to regulate its rate of demptying .
The sudden emptying of hyperosmotie material into jejunum may bring about a large
inflow of extracellular fluid into the jejunum. This rapid fluid shift may result in
decreased blood volume, increased splanchnic blood folw, decreased blood pressure,
and increased hematocrit. Patients may experience palpitation, weakness, sweating ,
dyspnea, naused and vomiting, diarrhea, abdominal cramps, even synocpe. The degree
of severity varies widely, and not all symptoms are reported by all patients. The patient
must lie down for 30–40 minutes until the discomfort passes. Within several months to
one year, however, dumping correlates loosely with the size of the gastronintestinal
anastomosis, and preoperative psychologic instability.
Diet therapy to reduce jejunal osmolality is successful in all but a few cases. The
diet should be low in carbohydrate and high ih fat and protein content. Meals should be
taken dry, with restricting all intake of fluid during meals. Anticholinergic drugs may be
of help in some patients. If dumping symptoms are refractory to dietary and drugs
therapy, further surgery may be considered. Good results have been reported following
cnversion of Billroth II into Billroth I anastomosis and with the insertion of a reversed
10 cm segment of small intestine at the gastric outlet.
The late dumping syndrome occurs in 2–4 hours after eating. This condition
mimics early dumping syndrome, but the clinical featres are caused by hypoglycemia.
The etiology may be the same as early dumping syndrome. After eating, large amont of
food flow into jejunum rapidly, resulting in rapid absorption of sugar and
hyperglycemia. Hyperglycemia stimulates more insulin, which produce hypoglycemia.
The patient obtains relief by eating sugar immediately after the symptoms of
hypoglycemia occurs.
Alklige reflux gastritis. Reflux of duodenal juices into the stomach is an
invariable and usually innocuous situation after operations that interfere with pyloric
function, but in some patients, it may cause marked gastritis. Bile salts may destroy
gastric mucosal barrier. The principal symptons are:
1. Persistent epigastric burning pain, which is getting worse after meal, antacids
do not relief pain.
2. Vomiting with bile.
3. Weight loss, stools may be positive when tested for occult blood,but melena
or hematemesis is rare. The diagnosis is depended on endoscopic and biopsy
demonstration of an edematous inflamed gastric mucosa. Since a minor degree of
gastritis is found in most patients after gastrectomy, the endoscopic lindings are to some
degree nonspecific. There appears to be a correlation between the amout of bile reflex
and a way to select patients for corrective operation.
Roux–en–Y gastrojejunostomy with a 40 cm efferent jejunal loop is the
treatment of choice. About 75–95% of patients experience a satisfying result.
Nutritional disturbances
Weight loss and malabsorption. Some patients gain weight when gastrectomy
relieves ulcer discomfort, but on the average, a 5–10% of patients have weight loss. The
major factors than can contribute to malnutrition after gastrectomy are as follows; small
gastric reservoir after the most area of stomach is removed, a decreased fat absorption
caused by uncoordinated mixing of food and pancreatic enzymes in the bowel, and blind
loop syndrome. Diet therapy and oral nutritional support may be needed in the patients.
Anemia. Anemia after gastrectomy is due to a nutritional deficiency of iron,
vitamin B12 or folate. Iron deficiency plays the most important role in the development
of chronic anemia, but anemia may be the result of any combination of iron, vitamin
B13, and folate deficiencies. Before this diagnosis is acccepted, the patient should be
checked for blood loss, marginal ulcer, or an unsuspected tumor. Iron deficiency anemia
develops in about 30% of patients within 5 years after gastrectomy. It is caused by
failure to absorb food iron bound in an organic molecule.Inorgain ironm, ferrous sulfate
or ferrous gluconate, is indicated for treatment and organic molecule. Inorganic iron,
ferrous sulfateor, ferrous gluconate is indicated for treatment and is absorbed normally
after gastrectomy. Megaloblastic anemia is due to deficiency absorption of vitamin B12,
which is the result of a deficiency of the intrinsic factor after gastrectomy. Vitamin B12
can be given to cure megaloblastic anemia.
Steatorrhea. Steatorrhea is the loss in the stool of more than 7% of the total
amount of fat ingested, which is occasionally seen after Billroth II gastrectomy. In this
situation, bypass of duodenum may interfere with mixing of bile and pancreatic lipase
with ingested fat. Some patients have afferent loop stasis, overgrowth of bacteria in the
afferent limb may cause the blind loop syndrome, resulting in malabsorption and
steatorrhea.
 Bone Disease. Bone disease usually occurs in 5–10 years after gastrectomy, and
is more commonly observed in women than men. Osteomalacia and osteoporosis are
common findings. Malabsorption of vitamin D or calcium rather than their decreased
dietary intake is responsible for these postoperative bone diseases.
Postoperative complications after vagotomy
Postvagotomy diarrhea. The daily frequency of bowel movements is increased
in about two thirds of patients who have had a truncal vagotomy. But only about 5–10%
of patients who have severe diarrhea and require treatment with antidiarrheal agents at
some time. The diarrhea may occr two or three times every week or may be episodic, in
which case the onset is unpredictable after symptom free intervals of weeks to months.
An attack may consist of only one or 2 watery movements or, in severe cases, may last
for a few days. Other patients may continually produce 3–5 loose stools per day.
Postvagotomy diarrhea is probably due to increased gastrie emptying (following
the drainage procedure) and the effects of vagal denervation on intestinal motility, but
the pathophysiology has not been fully understood. This complication may be avoided
by parietal cell vagotomy.
Necrosis of gastric lesser curvature. Necrosis of gastric lesser curvature is a
rare early complication seen in patients with superselective vagotomy. It may be caused
by devascularization and injury achieved incidentally in the process of denervating the
lesser curvature. If this complication is suspected, gastroscopy may be used for a prompt
diagnosis. Emergency reoperation and excision of necrotic area of the stomach are
indicated.
Gastric retention. The mechanism of gastric retention after vagotomy is
different from that aftr gastrectomy. But this complication occurs only in truncal and
selective vagotomy without drainage procedure. Gastric emptying is brought about in
large part by contraction of the antral musculature. The vagal denervation of the stomach
including the antrum produces delayed gastric emptying. After drainage procedures
(pyloroplasty and gastrojejunostomy) have been addded in vagotomy, gastric retention
did not occur commonly. Superselective vagotomy has been developed also for
avoidance of delayed gastric emptying by preservation of the vagal innervation of the
antrum.
Stress upper gastrointestinal mucosal injurier (SUGMI)
The term “stress ulcer” has been used classicaly for long time to refer to a
heterrogeneous group of acte upper gaastrointestinal ulcers or acute mucosal injury that
develop following physiolgicaly stressful illnesses, such as shock, sepsis, burns, and
central nervous system tumors and trauma, or occurs in the patients who are critically ill
for long periods. It may also develop following some drugs ingestion (aspirin,
cortisone). This pathological conditions were termed variedly, for example, acute
gastritis, Curling’s ulcer (following burns), or Cushing’s ulcer (following central
nervous system tumors and trauma). But non of these including stress ulcer can exactly
present and describe the pathological and clinical features for this conditions. The term
“stress upper gastrointstinal mucosal injuries” may be more preferable. The reasons are
the following (1) although the lesions are found most commonly in the stomach, but
they are not linited within the gastric mucosa, the duodenum, the lower portion of the
esophagus and the upper portion of the jejunum may be evolved, so “upper
gasrointestinal mucosal” has to be used; (2) lesions may be superficial erosions, or acute
ulcer deep into the muscular layer not correct; (3) lesions usually occur in the streased
patients or lesions result stress condition, so term “stress” should not be abandoned.
Gastroduodenal endoscopy performed early in traumatized or burned patients has
shown acute gastric erosions in the majority of patients within 72 hours of the injury.
Such studies illustrate how frequently the disease process remains subcilinical; clinically
apparent lesions develop in about 20% of susceptible patients. In fact, the real incidence
of SUGMI would be more high than the incidence of masssive hemorrhage and acute
perforation, because it is difficult to be found if SUGMI occurs without complication of
masssive hemorrhage or perforation.
Iiemorrhage is the major clinical problem and usually is the first manifestation in
severe stressed patients, although perforation occurs in about 10% of cases Acute
gastroduodenal perforation is the second common symptom.Clinically evident bleedfing
is usually seen 3–5 days after the injury, and massive bleeding generally does not appear
unitl 4–5 days later.
Physical examination is not econtributory except to reveal gross or occult fecal
blood or signs of shock.
SUGMI should be considered whenever acute gastrointestinal bleeding or
perforation occurs after major trauma or during the course of critically ill. Gastroscopy
is the most important diagnostic procedure available. It is usually possible to
demonstrate acute, superficial, bleeding gastrivc erosions if gastroscopy is performed
during the period of bleeding. Upper gastrointestinal x–ray series are rarely helpful since
the erosion lesions are quite superficial. The diagnosis of perforated ulcer is depeneded
on the clinical features, (the sudden severe epigastric pain, signs of peritonitis).
Initial management should consist of gastric lavage with iced Normal Saline
solution, antacids, H2  receptor antagonists and proton pump inhibitors. Blood
transfusion may be indicated in some patients.
In the sickest patients, if facilities and trained personnel are available, the
selective infusion of vasoconstricting agents (eg, vasopressin) into the left gastric artery
through a percutaneously placed catheter catheter should probably be attempted befor
operation is considered.
Emergency laparotomy should be considered if the nonoperative management
fails to control the bleeding. Surgical treatment consist of subtotal gastrectomy, or
vagotomy and pyloroplasty with sture of the bleeding points. Most experts recommend a
high subtotal gastrectomy excising as much ulcerated parietal cell mucosa as possible, if
the patients’s condition permits. When it occurs, rebleeding is nearly always from an
lesions left behind at the initial procedure. Rarely, total gastrectomy has had to be used
because of the extent of erosions and severity of bleeding.
 8.8. ENDOCRINE DISEASES THAT CAUSE PEPTIC ULCERS
8.8.1.PRIMARY HYPERPARATHYROIDISM
Primary hyperparathyroidism causes hypercalcemia (elevated blood calcium
levels) through the excessive secretion of parathyroid hormone (PTH), usually by an
adenoma (benign tumors) of the parathyroid glands. Its incidence is approximately 42
per 100,000 people. It is almost exactly three times as common in women as men.

Figure 8.33. Thyroid and parathyroid gland.

The parathyroid glands are four pea–sized glands located on the thyroid gland in
the neck (Fig. 8.33). Occasionally, a person is born with one or more of the parathyroid
glands embedded in the thyroid, in the thymus, or located elsewhere around this area. In
most such cases, however, the glands function normally.
Though their names are similar, the thyroid and parathyroid glands are entirely
different glands, each producing distinct hormones with specific functions. The
parathyroid glands secrete PTH, a substance that helps maintain the correct balance of
calcium and phosphorus in the body. PTH regulates the level of calcium in the blood,
release of calcium from bone, absorption of calcium in the intestine, and excretion of
calcium in the urine.
When the level of calcium in the blood falls too low, the parathyroid glands
secrete just enough PTH to restore the blood calcium level.
Signs and Symptoms
The signs and symptoms of primary hyperparathyroidism are those of
hypercalcemia. They are classically summarized by the mnemonic “stones, bones,
abdominal groans and psychic moans.”
 “Stones” refers to kidney stones, nephrocalcinosis, and diabetes insipidus
(polyuria and polydipsia). These can ultimately lead to renal failure.
 “Bones” refers to bone–related complications. The classic bone disease in
hyperparathyroidism is osteitis fibrosa cystica, which results in pain and sometimes
pathological fractures. Other bone diseases associated with hyperparathyroidism are
osteoporosis, osteomalacia, and arthritis.
  “Abdominal groans” refers to gastrointestinal symptoms of constipation,
indigestion, nausea and vomiting. Hypercalcemia can lead to peptic ulcers and acute
pancreatitis.
 “Psychic moans” refers to effects on the central nervous system. Symptoms
include lethargy, fatigue, depression, memory loss, psychosis, ataxia, delirium, and
coma.
 Left ventricular hypertrophy.
 Increased all cause mortality.
Diagnosis
Blood tests – hyperparathyroidism is diagnosed based upon levels of blood
calcium and parathyroid hormone. In most people with hyperparathyroidism, both levels
are higher than normal. Occasionally, a person may have an elevated calcium level and a
normal or minimally elevated PTH level. Since PTH should normally be low when
calcium is elevated, a minimally elevated PTH is considered abnormal and indicates
hyperparathyroidism.
Bone density testing – bone density testing is usually recommended for people
with hyperparathyroidism. This test can help determine if the bones have become
weakened as a result of abnormal blood calcium levels. Dual x–ray absorptiometry
(DXA) testing is the most commonly used method for measuring bone density. This test
is described in detail separately.
Kidney stone testing – testing for “silent” kidney stones is not recommended
when you are first diagnosed with hyperparathyroidism. Testing is recommended,
however, if you have had a kidney stone previously. Testing usually involves an
ultrasound or CT scan of the kidneys. Further testing is not needed after the initial
screening unless a person develops signs or symptoms of a stone.
Causes
The most common cause of primary hyperparathyroidism is a sporadic, single
parathyroid adenoma resulting from a clonal mutation (~ 97%). Less common are
parathyroid hyperplasia (~ 2.5%), parathyroid carcinoma (malignant tumor), and
adenomas in more than one gland (together ~ 0.5%).
Primary hyperparathyroidism is also a feature of several familial endocrine
disorders: multiple endocrine neoplasia type 1 and type 2A (MEN type 1 and MEN type
2A), and familial hyperparathyroidism.
Complications
The classic bone disease in hyperparathyroidism is osteitis fibrosa cystica, which
results in pain and sometimes pathological fractures. Other bone diseases associated
with hyperparathyroidism are osteoporosis, osteomalacia, and arthritis.
Treatment
Treatment is usually surgical removal of the gland(s) containing adenomas.
Medications
Medications include estrogen replacement therapy in postmenopausal women
and bisphosphonates. Bisphosphonates may improve bone turnover. Newer medications
termed “calcimimetics” used in secondary hyperparathyroidism are now being used in
Primary hyperparathyroidism. Calcimimetics reduce the amount of parathyroid hormone
released by the parathyroid glands. They are recommended in patients in whom surgery
is inappropriate.
Surgery
Surgery is often recommended for people whose blood calcium is moderately
elevated. Surgery is also recommended for people who are excreting a significant
amount of calcium through their urine and for people with signs of impaired kidney
function or decreased bone density.
It is also recommended if the person is less than 50 years old or if periodic
follow–up would be difficult (eg, if a person lived a great distance from a healthcare
provider or travels to places where it is difficult to find medical care).
Traditional surgery. The surgery is usually performed while the person is under
anesthesia. An incision is made in the lower neck measuring 5 to 10 cm (2 to 5 inches).
All four parathyroid glands are examined; usually, at least one abnormal–appearing
gland is removed while the normal–appearing glands are left in place.
Minimally invasive surgery. Minimally invasive surgery can be performed in
cases where one abnormal parathyroid gland has been located by a pre–operative
imaging study.
The surgery can be performed under local nerve block, and is an alternative
when one abnormal gland has been localized pre–operatively. This procedure is also a
good alternative for patients who are at high–risk for general anesthesia. During the
surgery, a small incision (2 to 4 cm or 0.8 to 1.8 inches) is made in the neck and the
abnormal tissue is removed. The patient's blood level of PTH is tested before and
immediately after removal to confirm that the PTH level drops significantly after the
abnormal tissue is removed.
The advantage of minimally invasive surgery compared to traditional surgery is
that it requires a smaller incision, less time under anesthesia, and a shorter hospital stay.
This procedure is only available for people with certain characteristics and it requires an
experienced surgeon and medical center.
Effectiveness of surgery. With an experienced endocrine surgeon, surgical
treatment is effective in curing hyperparathyroidism in about 95 percent of patients. The
complication rate associated with surgery is very low.
Complications could include temporary or permanent damage to the other
parathyroid glands resulting in low calcium levels and/or temporary or permanent
hoarseness. Patients are hospitalized for a short time after surgery, usually for less than
two days.
Occasionally, some abnormal parathyroid tissue goes undetected and is not
removed during the first operation. In this case, high calcium levels and symptoms of
hyperparathyroidism persist after surgery. Imaging studies are required to locate the
abnormal parathyroid tissue. In some patients, parathyroid glands may be present in
unusual locations, such as in the chest or in other regions of the neck. A second surgical
procedure is usually required to remove remaining abnormal tissue.
 Follow up care after surgery. Six to eight weeks after surgery, most clinicians
recommend a blood test to measure the blood level of calcium and PTH. These tests are
then repeated once per year to ensure that they remain normal and that abnormal tissue
has not regrown. A bone density test may be recommended one year after surgery to
guide treatment of bone loss (osteopenia or osteoporosis).

8.8.2. ZOLLINGER–ELLISON SYNDROME

Zollinger–Ellison syndrome (ZES) is a rare disorder characterized by one or

more tumors in the pancreas, duodenum, or both. The tumors cause the stomach to make
too much acid, leading to peptic ulcers in the duodenum. The tumors are sometimes
cancerous and spread to other areas of the body.
Causes ZES
ZES is caused by tumors called gastrinomas, which release the hormone gastrin.
Normally, cells in the stomach produce and control gastrin so only the right
amount is released. Gastrin travels through the bloodstream to signal other cells in the
stomach to release gastric acid to help break down food. Gastrinomas release abnormal
amounts of gastrin, resulting in excess gastric acid in the stomach and duodenum. The
excess acid eventually causes sores called peptic ulcers to form in the lining of the
duodenum.
Scientists are unsure what causes the majority of gastrinomas, which appear
sporadically. About 25 percent of gastrinoma cases are caused by an inherited genetic
disorder called multiple endocrine neoplasia type 1 (MEN1). MEN1 can cause a variety
of hormone–releasing tumors such as prolactinomas and insulinomas. Prolactinomas
form in the pituitary gland in the brain and cause excess prolactin – a hormone that
influences milk production, fertility, and bone strength. Insulinomas form in the
pancreas and cause excess insulin – a hormone that helps control blood glucose. Signs
and symptoms of MEN1 include increased hormone levels in the blood, kidney stones,
diabetes, muscle weakness, and weakened bones and fractures.
Anyone can get ZES, but the disease is more common among men 30 to 50 years
old. People with MEN1 have a 20 to 61 percent chance of developing ZES. Children
who have a parent with MEN1 have a 50 percent chance of inheriting the MEN1 gene
and are, therefore, also at increased risk of ZES.
Symptoms of ZES
ZES symptoms are similar to those of peptic ulcers and include:
 burning abdominal pain;
 nausea and vomiting;
 weight loss;
 diarrhea;
 severe gastroesophageal reflux – a condition where gastric acid and food from the
stomach backs up into the esophagus
Diagnostics ZES:
 assessing symptoms;
  measuring stomach acid and the amount of gastrin circulating in the blood;
 conducting imaging tests to look for gastrinomas.
A doctor may suspect ZES if diarrhea accompanies peptic ulcer symptoms or if
treatment for peptic ulcers fails. Most peptic ulcers are caused by bacteria called
Helicobacter pylori (H. pylori) or the use of nonsteroidal anti–inflammatory drugs
(NSAIDs) such as aspirin and ibuprofen. Peptic ulcers in the absence of H. pylori
infection or NSAIDs usage or severe peptic ulcers that bleed or cause perforation of the
duodenum are possible indicators of ZES. A MEN1 diagnosis in the patient or the
patient’s family or the presence of MEN1 signs and symptoms strongly suggests ZES.
Multiple ulcers in the duodenum – seen during upper gastrointestinal (GI)
endoscopy –may cause a doctor to suspect ZES. Upper GI endoscopy, however, rarely
reveals gastrinomas, which grow in tissue layers beneath the visible surface.
A procedure called somatostatin receptor scintigraphy (SRS) – sometimes called
OctreoScan – is used to find gastrinomas in the duodenum, pancreas, and other parts of
the body. SRS uses a radioactive compound called a radiotracer that, when injected into
the bloodstream, selectively labels tumor cells. The labeled cells light up when scanned
with a device called a gamma camera.
Other imaging procedures used to find gastrinomas include the following:
Angiography is sometimes used to find tumors in the pancreas.
Endoscopic ultrasonography is sometimes used to look for tumors in the
pancreas.
A computerized tomography (CT) scan takes hundreds of cross–sectional x–ray
images in a few seconds. A computer assembles the images to produce three–
dimensional views of internal organs and tissues. While not good at finding tumors in
the pancreas or duodenum, this technique is more useful in finding gastrinomas that
have spread to the liver.
Treatment
ZES is treated with medications to relieve ulcer symptoms and surgery, if
appropriate, to remove tumors. Chemotherapy is sometimes used when tumors are too
widespread to remove with surgery.
A class of drugs called proton pump inhibitors effectively reduces gastric acid
secretion in the stomach and includes: esomeprazole; lansoprazole; pantoprazole;
omeprazole.
Reducing stomach acid allows peptic ulcers to heal and relieves ZES symptoms.
Surgical removal of gastrinomas is the only cure for ZES. Some gastrinomas
behave like cancers and spread to other parts of the body, especially the liver and bones.
Finding and removing all gastrinomas is often challenging.
Gastrinomas that cannot be surgically removed are sometimes treated with
chemotherapy drugs, including: streptozotocin; 5–fluorouracil; doxorubicin.
The outcome for people with ZES largely depends on the nature and extent of
the gastrinomas. About 25 percent of gastrinoma cases are considered cancerous, with
an estimated 10–year survival rate of around 30 percent. The remaining cases are
considered slow–growing, with an estimated 10–year survival rate of around 95 percent.
If peptic ulcer symptoms are well controlled, however, most patients – even those with
tumors that spread – will feel well until the late stages of the disease.

8.9. BEZOARS AND FOREIGN BODIES

Bezoars are tightly packed collections of partially digested or undigested

material stuck in the stomach or other parts of the digestive tract. Foreign bodies are
small ingested objects that can also get stuck in the digestive tract and sometimes
perforate (pierce) it.
 Masses of undigestible materials can get stuck in various parts of the digestive
tract.
 Most bezoars and foreign bodies cause no symptoms.
 The diagnosis is based on x–rays and sometimes on a visual examination of the
digestive tract by using a flexible viewing tube (endoscopy).
 Most bezoars and foreign bodies pass without treatment, but some need to be
broken down manually or removed surgically.
The stomach is a common collection site for hardened, partially digested or
undigested masses of food or other materials (bezoars) or for foreign objects (bodies).
Reasons include the curved shape of the stomach and the narrow opening (pyloric
sphincter) that the stomach's contents must pass through to enter the first segment of the
small intestine (duodenum). Bezoars or foreign bodies larger than 3/4 of an inch (about
2 centimeters) in diameter are rarely able to pass out of the stomach.
Bezoars may consist of partially digested hair, fiber from fruits or vegetables,
even hardened blocks of drugs (such as antacids), which accumulates most often in the
stomach but sometimes elsewhere in the digestive tract (Fig. 8.34, 8.35).

INCLUDEPICTURE "http://nmhm.washingtondc.m
useum/exhibits/virtual/543344.jpg" \* MERGEFO
RMATINET

Figure 8.34. Bezoar from the craw of Figure 8.35. Trichobezoar from a human.
a chicken.
 These hairballs or foodballs cannot pass through narrow openings or spaces and
thus get stuck in the digestive tract. Foreign bodies are sometimes swallowed by
children and even adults, especially intoxicated adults. If these undigestible objects are
small, they pass through the digestive system until they are excreted with stool.
However, larger objects or sharp ones, such as fish bones, may get stuck in the
esophagus or stomach or, less often, in other parts of the digestive tract. Sometimes
foreign bodies are swallowed purposely, as when smugglers swallow balloons filled
with illegal drugs to get through customs.
Food or other materials can collect in anyone but do so more often under certain
circumstances. People who have undergone surgery to their digestive tract, particularly
if they have had part of their stomach or intestines removed, are particularly prone to
bezoars and foreign bodies becoming stuck. People with diabetes sometimes develop a
condition in which the stomach does not empty properly, resulting in problematic
collections of food.
Symptoms and diagnosis
Most bezoars and foreign bodies cause no symptoms.
A small blunt object that is swallowed may produce the sensation of something
being stuck in the esophagus. This feeling may persist for a short time even after the
object has passed into the stomach. A small sharp object that is swallowed may become
lodged in the esophagus and cause pain, even though the person is able to swallow
normally. When the esophagus is completely blocked, the person is unable to swallow
anything, even saliva, and drools and spits constantly. The person may try to vomit, but
nothing comes up. If a sharp object pierces the esophagus, consequences may be serious.
Sometimes bezoars or foreign bodies lead to blood in the stool. If they are
partially or completely obstructing the stomach, the small intestine, or, rarely, the large
intestine, they cause cramps, bloating, loss of appetite, vomiting, and sometimes fever. If
a sharp object has pierced the stomach or intestines, stool spills into the area around the
intestines, causing severe abdominal pain, fever, fainting, and sometimes shock. Such a
leakage is a medical emergency because it can cause peritonitis. If a person has
swallowed a drug–filled balloon, the balloon may rupture, which can then lead to an
overdose of the drug.
Often, an obstructing object can be seen on x–rays of the abdomen. Sometimes,
endoscopy (a visual examination of the digestive tract using a flexible tube called an
endoscope is performed to determine the nature of the obstructing object and to exclude
a tumor as the cause. Rarely, computed tomography (CT) and ultrasound scans are used
to identify the problem.
Treatment
Most bezoars and foreign bodies require no treatment. Even a small coin is likely
to pass without problem. A doctor advises the person to check the stool to see when the
object is excreted. Sometimes a doctor recommends that the person consume a liquid
diet to help excrete the object.
 To help break down a bezoar, a doctor may prescribe a regimen of cellulase or
meat tenderizer, which is dissolved in a liquid and taken by mouth for several days.
Sometimes doctors use forceps, a laser, or other instruments to break up bezoars so that
they can pass through or be removed more easily.
When a doctor suspects that a blunt foreign body is stuck in the esophagus, the
drug glucagon may be given intravenously to relax the esophagus and allow the object to
pass through the digestive tract. Other drugs such as metoclopramide taken by mouth
can help bezoars or blunt foreign objects pass through the digestive tract by causing
muscles to contract.
Doctors can remove some objects that are stuck in the esophagus with forceps or
a basket passed through an endoscope.
Because sharp objects may pierce the wall of the esophagus, they must be
removed, either by endoscopy or surgery. Batteries are also removed from the esophagus
because they can cause internal burns. When an object suspected of being a drug–filled
balloon is detected, it is removed to prevent the drug overdose that can occur if such a
balloon ruptures.

8.10. MALLORY–WEISS SYNDROME

Mallory–Weiss syndrome or gastro–esophageal laceration syndrome refers to

bleeding from tears (a Mallory–Weiss tear) in the mucosa at the junction of the stomach
and esophagus, usually caused by severe retching, coughing, or vomiting. It is often
associated with alcoholism and eating disorders and there is some evidence that presence
of a hiatal hernia is a predisposing condition.
In 1929, Kenneth Mallory and Soma Weiss first described a syndrome
characterized by esophageal bleeding caused by a mucosal tear in the esophagus as a
result of forceful vomiting or retching. The initial description was associated with
alcoholic bingeing; however, with the advent of endoscopy, Mallory–Weiss tears have
been diagnosed in many patients with no antecedent history of alcohol intake. Although
the tear typically occurs after repeated episodes of vomiting or retching, it may occur
after a single incident.
Causes
Many underlying disorders that cause vomiting and retching result in a Mallory–
Weiss tear.
 Gastrointestinal disease.
 Infectious gastroenteritis.
 Gastric outlet obstruction.
 Ulcers.
 Hiatal hernias.
 Malrotation.
 Volvulus.
 Inflammatory conditions of the stomach and intestine.
  Pregnancy: Some women develop hyperemesis gravidarum, a syndrome
characterized by persistent severe vomiting and retching, in the first trimester of
pregnancy. Gastric dysrhythmias and prolonged small–bowel motility cause the
development of hyperemesis gravidarum. Some women lose as much as 10% of their
body weight during this period.
 Hepatitis: acute inflammation of the liver causes vomiting in 10–20% of patients.
 Cirrhosis.
 Cholecystitis.
 Biliary cirrhosis.
 Renal disease: vomiting is often associated with diseases affecting the kidneys,
including the following:
 urinary tract infections;
 kidney stones;
 uteropelvic junction (UPJ) obstruction;
 renal failure.
 Increased intracranial pressure: Intracranial lesions that cause hydrocephalus or
increased intracranial pressure may lead to vomiting in children. Most common causes
of hydrocephalus include tumors, cysts, and congenital abnormalities. Other causes of
increased intracranial pressure consist of trauma, infections (eg, meningitis),
medications, and pseudotumor cerebri.
 Iatrogenic causes: complications of endoscopy may cause esophageal tears and
are almost always associated with a patient who is retching or struggling during the
procedure. The use of polyethylene glycol lavage, when used for ingestions, severe
constipation, or preparation for colonoscopy, may cause severe vomiting.
 Other causes:
 severe diabetic ketoacidosis;
 toxins;
 drugs (eg, chemotherapeutic agents).
Pathophysiology
Any disorder that initiates vomiting may result in the development of a Mallory–
Weiss tear, which develops as a linear laceration at the gastroesophageal junction
because the esophagus and stomach are cylindrical. The cylindrical shape allows
longitudinal tears to occur more easily than circumferential tears. These tears have been
postulated to occur either by a rapid increase in intragastric pressure and distention,
which increases the forceful fluid ejection through the esophagus, or secondary to a
significant change in transgastric pressure (ie, difference in pressure across the gastric
wall) because negative intrathoracic pressure and positive intragastric pressure leads to
distortion of the gastric cardia, resulting in a gastric or esophageal tear.
Although most cases of Mallory–Weiss tears are self–limiting, patients with
severe or recurrent episodes of bleeding that require intensive care therapy and
interventional endoscopy have been reported. Typically these patients have underlying
conditions, including portal hypertension and hepatic insufficiency. Although upper
gastrointestinal bleeding is generally assumed to be secondary to varices in these
patients, the physician must also be aware of the potential for Mallory–Weiss tears.

Figure 8.36. Mallory–Weiss tear.

Typical longitudinal mucosal tear with Figure 8.37. Mallory–Weiss tear.
overlying fibrinous exudate extending from the Retroflexed view of the cardia showing the
distal esophagus to the gastric cardia (arrow). typical location of the tear with a clean base
(arrow).

Presentation
Mallory–Weiss syndrome often presents as an episode of vomiting up blood
(hematemesis) after violent retching or vomiting, but may also be noticed as old blood in
the stool (melena), and a history of retching may be absent.
In most cases, the bleeding stops spontaneously after 24–48 hours, but
endoscopic or surgical treatment is sometimes required and rarely the condition is fatal.
Diagnosis
Definitive diagnosis is by endoscopy (Fig. 8.36, 8.37).
Treatment
Treatment is usually supportive as persistent bleeding is uncommon. However
cauterization or injection of epinephrine to stop the bleeding may be undertaken during
the index endoscopy procedure.
Very rarely embolization of the arteries supplying the region may be required to
stop the bleeding.
8.11. MENETRIE’S DISEASE

Menetrie’s disease causes the ridges along the inside of the stomach wall –
called rugae – to enlarge, forming giant folds in the lining of the stomach. The rugae
enlarge because of an overgrowth of surface mucous cells of the stomach. In a normal
stomach, rugae release protein–containing mucus. Enlarged rugae release too much
mucus, causing a leakage of protein from the blood into the stomach. This shortage of
protein in the blood is known as hypoproteinemia. Ménétrie’s disease also causes a
decrease in stomach acid resulting from a reduction in acid–producing parietal cells.
Menetrie’s disease is rare and more common in men, usually appearing between
the ages of 30 and 60.
People with Menetrier disease suffer from severe stomach pain, nausea, frequent
vomiting, and other symptoms. They also have a higher risk of developing stomach
cancer, also called gastric cancer.
Menetrie’s disease is also called hypoproteinemic hypertrophic gastropathy.
Other conditions that can cause enlarged rugae but are not Menetrie’s disease
include:
 Zollinger–Ellison syndrome – a condition in which tumors in the pancreas cause
the stomach to make too much acid.
 Syphilis – a type of sexually transmitted bacterial infection.
 Cytomegalovirus – a type of viral infection.
 Histoplasmosis – a type of fungal infection.
 Linitis plastica – a type of gastric cancer.
 Gastric lymphoma – a type of cancer originating in the stomach.
Causes
What causes Menetrie’s disease is unclear; however, it is thought to be an
acquired disorder with no known genetic component. Recent studies suggest people with
Ménétrie’s disease have stomachs that make abnormally high amounts of a protein
called transforming growth factor–alpha (TGF–α). Growth factors are proteins in the
body that tell cells what to do, such as grow larger, change shape, or divide to make
more cells. A cause for the overproduction of TGF–α has yet to be found.
Symptoms
Possible signs and symptoms of Menetrie’s disease include:
 severe pain in the top middle part of the abdomen;
 nausea and frequent vomiting;
 swelling of the face, abdomen, limbs, and feet;
 loss of appetite;
 extreme weight loss;
 malnutrition;
 low blood protein;
 anemia;
 diarrhea.
Diagnosis
Menetrie’s disease is diagnosed through x rays, endoscopy, and biopsy of
stomach tissue. Endoscopy involves looking at the inside of the stomach using a long,
lighted tube inserted through the mouth. During a biopsy, the doctor removes a small
piece of tissue and examines it with a microscope for signs of disease.
 Menetrie’s disease causes the ridges along the inside of the stomach wall – called
rugae – to enlarge, forming giant folds in the lining of the stomach.
 Menetrie’s disease is rare and more common in men, usually appearing between
the ages of 30 and 60.
 Recent studies suggest people with Menetrie’s disease have stomachs that make
abnormally high amounts of transforming growth factor alpha (TGF–α) – a protein that
tells cells what to do.
 Menetrie’s disease is diagnosed through x rays, endoscopy, and biopsy of stomach
tissue.
 Treatment for Menetrie’s disease may include medications to relieve nausea and
pain and surgery to remove part or all of the stomach.
Treatment
Treatment may include medications to relieve nausea and pain. A high–protein
diet is prescribed to offset the loss of protein from enlarged rugae. Part or all of the
stomach may need to be removed if the disease is severe.
The anticancer drug cetuximab (Erbitux) blocks the action of TGF–α and is
being investigated as a promising new treatment for Ménétrier disease.

8.11. OSLER–WEBER–RENDU SYNDROME

Osler–Weber–Rendu syndrome, also known as hereditary hemorrhagic

telangiectasia (HHT), is an autosomal dominant disorder typically identified by the triad
of telangiectasia, recurrent epistaxis, and a positive family history for the disorder. The
major cause of morbidity and mortality due to this disorder lies in the presence of
multiorgan arteriovenous malformations (AVMs) and the associated hemorrhage that
may accompany them. The disease has a wide spectrum of presentations; patients may
be asymptomatic or have multiple organ involvement presenting at any age.
Pathophysiology
The clinical manifestations of Osler–Weber–Rendu disease are caused by the
development of abnormal vasculature, including telangiectasias, AVMs, and aneurysms.
The genetic defect largely involves either one of two genes: ENG or ALK–1. Both of
these genes transcribe proteins that are highly expressed on endothelial cells and play
important roles in tissue repair and angiogenesis through their common function as
receptors for transforming growth factor beta. Defects in the endothelial cell junctions,
endothelial cell degeneration, and weakness of the perivascular connective tissue are
thought to cause dilation of capillaries and postcapillary venules, which manifest as
telangiectasias. Most commonly, telangiectasias involve the mucous membranes, as well
as the skin, the conjunctiva, the retina, and the gastrointestinal tract tract. AVMs are
abnormal tortuous vessels with both arterial and venous components. The larger AVMs
can cause left–to–right shunting and, if sufficiently large, may contribute to high–output
heart failure. Loss of the muscularis layer and disturbance of the elastic lamina of vessel
walls may also give rise to aneurysms in multiple organ systems. AVMs are found in the
lungs, brain, and liver.
The disease is caused by genetic defects with an autosomal dominant
inheritance. So far, two primary loci have been identified associated with Osler–Weber–
Rendu syndrome: one on chromosome arm 9q33–34 (HHT1) and a second on
chromosome arm 12q11–14 (HHT2). Two more genes have been implicated; MADH4
gene mutation in patients with a combined syndrome of Osler–Weber–Rendu syndrome
and juvenile polyposis and an unidentified HHT3 gene linked to chromosome 5.
 Chromosome arm 9q33–34 (HHT1) harbors the endoglin gene, which encodes for
a homodimeric integral membrane glycoprotein expressed at high levels on human
vascular endothelial cells. Over 150 mutations of the endoglin gene have been reported
in family members with Osler–Weber–Rendu syndrome. The vast majority of these
mutations create premature stop codons and subsequently reduce levels of functional
endoglin protein, the likely cause of Osler–Weber–Rendu syndrome type 1.
 Chromosome arm 12q11–14 (HHT2) contains the activin receptorlike kinase 1
(ALK1), which encodes for a surface receptor for the transforming growth factor (TGF)–
beta superfamily of ligands. The TGF–beta multifunctional protein plays an important
role in angiogenesis and vascular remodeling. Over 120 mutations have been reported in
the ALK1 gene, yet unlike Osler–Weber–Rendu type 1, more than 50% of the mutations
contributing to type 2 are missense substitutions.
 In patients with the HHT1 genotype, the prevalence of pulmonary AVMs and
cerebral AVMs was shown to be higher than that of patients with the HHT2 genotype.
Also, oral and nasal mucosal telangiectasias present earlier in life in patients with the
HHT1 genotype. The prevalence of hepatic AVMs is higher in patients with HHT2 than
in patients with HHT1. Patients with the HHT2 genotype also present earlier in life with
dermal lesions.
Mortality/Morbidity
Patients are at risk for hemorrhage from both mucosal and visceral sites, as well
as high–output cardiac failure, cerebral abscess, ischemic stroke, migraines and further
sequelae. Studies show that life expectancy appears to be significantly lower in patients
with Osler–Weber–Rendu syndrome compared with the general population.1 The
mortality of these patients revealed an early peak at age 50 years and a later peak at 60–
79 years due to acute complications.
 Hemorrhage: recurrent epistaxis is observed in as many as 90% of patients. In one
half of patients, the epistaxis becomes more serious with age, and blood transfusions are
required in 10–30% of patients. Patients with pulmonary AVMs and telangiectasis of the
gastrointestinal tract are at risk for life–threatening hemorrhage of the lungs and
gastrointestinal tract.
 CNS complications: cerebral abscess due to impaired function of pulmonary
vasculature is the most common neurologic manifestation of Osler–Weber–Rendu
syndrome. Also, patients with this disease suffer from strokes, which may be either
hemorrhagic or ischemic. Ischemic strokes likely due to pulmonary AVMs are common,
whereas hemorrhagic strokes due to cerebral AVMs are far less common. Of patients
who have pulmonary AVMs, 2% per year are estimated to have a stroke and 1% per
year are estimated to develop a brain abscess.
 High–output cardiac failure: due to the presence of large AVMs and blood loss,
high–output cardiac failure may occur. This known complication of HHT has recently
been linked with the onset of severe and recurrent epistaxis in a small sample of patients.
Clinical
Because Osler–Weber–Rendu syndrome is an autosomal dominant disease, a
family history of telangiectasia and recurrent bleeding in other family members is
usually present. Symptoms vary depending on the area of involvement. The main areas
of involvement are nasal mucosa, skin, the gastrointestinal tract, pulmonary vasculature,
and the brain.
Diagnostic criteria are based on 4 components. The diagnosis is considered
definite if 3 criteria are present and is considered possible if 2 criteria are present. The
diagnosis is unlikely if fewer than 2 criteria are present. The criteria are as follows:
 Nosebleeds – spontaneous and recurrent.
 Telangiectasias – multiple sites including the lips, oral cavity, fingers, and nose
 Presence of internal lesions – gastrointestinal telangiectasia, pulmonary
arteriovenous malformations (AVMs), hepatic AVMs, cerebral AVMs, spinal AVMs.
 Family history – a first–degree relative with Osler–Weber Rendu syndrome
according to these criteria.
Other symptoms that may be reported include the following:
Nasal mucosa: epistaxis is the most common manifestation of the disease and
occurs in as many as 90% of affected patients. Bleeding may occur as often as every day
or as infrequently as once a month. Patients with epistaxis usually present before the
second decade of life. Blood transfusions are required in 10–30% of patients, and as
many as 50% of patients require surgical treatment.
Gastrointestinal tract: recurrent painless gastrointestinal bleeding occurs in 10–
40% of patients and generally occurs later in life than epistaxis. Patients may report
abdominal pain that may be due to thrombosis of gastrointestinal AVMs.
Pulmonary vasculature: Pulmonary AVMs are present in 15–33% of patients
with the disease. Dyspnea and exercise intolerance are often presenting
symptoms; however, recent studies reveal that most patients with pulmonary AVM have
no significant respiratory symptoms. Pulmonary AVMs may cause enough right–to–left
shunting to cause cyanosis, hypoxemia, and secondary polycythemia. Pulmonary AVMs
also increase the incidence of infection due to septic emboli formation in the pulmonary
vasculature.
Hemoptysis results from either telangiectasia of the trachea and bronchi or
pulmonary arteriovenous (AV) fistulas. Patients usually present around the third or
fourth decades of life.
Migraine headaches are present in 13–50% of patients with Osler–Weber–Rendu
syndrome. Although the reason is unclear, the headaches are more prevalent in patients
with pulmonary AVMs.
CNS involvement:
  Neurologic involvement occurs in 8–12% of patients with Osler–Weber–Rendu
syndrome. A history of headache, seizures, and focal neurologic symptoms (eg,
paraplegia, paralysis) may be presenting symptoms.
 Stroke and brain abscess are more common in patients with Osler–Weber–Rendu
syndrome compared with the healthy population. This is due to loss of the normal
filtering function of the pulmonary vasculature in patients with pulmonary AVMs. These
AVMs allow thrombotic and septic emboli to travel to the brain. Untreated patients have
a 2% risk of stroke and a 1% risk of brain abscess per year.
Fatigue: fatigue may be elicited on history and may be due to an iron deficiency
anemia caused by recurrent blood loss.
Visual disturbances: visual disturbances may be noted, possibly caused by
intraocular hemorrhage. Patients may notice bloody tears, which are due to conjunctival
telangiectases.
Liver involvement: liver involvement (often asymptomatic) is reported in as
many as 40% of patients. Symptoms may include right upper quadrant pain, jaundice,
symptoms of high–output cardiac failure, and bleeding from esophageal varices. The
complication of cardiac failure is caused by a large left–to–right shunt that can occur
between the hepatic arteries and veins. Occasionally, patients with Osler–Weber–Rendu
syndrome may present with atypical cirrhosis.
Physical
The areas involved dictate the signs that may be found on physical examination.
Skin
 The most obvious finding on physical examination is telangiectasias. These
lesions may be found on the oral mucosa, nasal mucosa, skin, and conjunctiva.
 Cyanosis and clubbing may be present in patients with pulmonary AVMs. These
signs develop due to right–to–left shunting.
 Liver involvement may cause jaundice.
 CNS: if a previous stroke, brain abscess, or intracerebral hematoma has occurred,
patients may present with focal neurologic signs.
 Respiratory system: in the presence of pulmonary AVMs, the patient may be
tachypneic, cyanotic, and have clubbing. A pulmonary bruit may be heard best on
inspiration.
 Cardiovascular system: patients may be cyanotic because of right–to–left
pulmonary shunting or pale because of anemia. Patients may have a hyperdynamic
circulation if they have hepatic involvement and a large left–to–right shunt.
Hyperdynamic circulation may be exacerbated by anemia.
 Gastrointestinal system:
 Examination of the oral mucosa reveals telangiectasias in 58–79% of
patients.
 Rectal examination may reveal frank blood.
 Signs of liver involvement include jaundice, hepatomegaly, and a right
upper quadrant bruit or thrill.
  Eyes: funduscopic examination may reveal retinal telangiectasias and
hemorrhages. Bloody tears may be present because of conjunctival telangiectasias.
Investigations
Capillary microscopy (examining the capillary pattern of the fingernail; this can
be useful in screening for HHT, as most patients have detectable abnormalities before
development of other signs). CT, MRI scanning and angiography (for example,
pulmonary and cerebral angiography) are used to identify lesions.
Diagnosis
The diagnosis is made if at least three of the following are present:
 Epistaxes.
 Telangiectasia.
 Visceral lesions.
 Appropriate family history
Genetic testing can be undertaken to identify the specific mutation in the index
case. This can then be used to investigate other family members.
Management
Optimal management is improved with early diagnosis, based on clinical
findings.
Acute haemorrhage may require treatment including blood transfusion and
attempts to stem the flow.
Surgical or laser ablation may be required as an emergency or elective
procedure. AVMs may need embolisation, ligation of the blood supply or resection.
Septoplasty of the nose may be required.
Liver transplantation or stereotactic intracranial radiosurgery may be indicated.
Prognosis
Usually there is no effect on lifespan unless there is severe haemorrhage,
although cirrhosis may shorten life.