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The stomach andduodenum 225
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• Steatorrhoea: in the presence of a long afferent
loop, food passing into the jejunum traverses the
bowel without mixing adequately with pancreatic
and biliary secretions. Calcium deficiency and
osteomalacia may occur.
• Stomal ulceration complicates about 2% of gas-
trectomies for duodenal ulcer; it is extremely
rare after resection for gastric ulcer. It may be
due to inadequate removal of the acidarea of the stomach or, rarely, because of the
Zollinger–Ellison syndrome. A stomal ulcer, like
any other peptic ulcer, may perforate, stenose,
invade
treated by either vagotomy or higher gastric
resection.
surrounding structures or bleed. It is
secreting
Post- vagotomy syndromes
The following sequelae may occur after truncal
vagotomy.
Steatorrhoea and diarrhoea: frequently transient
•
or episodic, they may be severe and persistent in
about 2% of patients. The incidence is reduced in
patients subjected to highly selective vagotomy
without drainage.
• Stomal ulceration may occur if vagotomy is
incomplete.
Complications ofpeptic
ulceration
Peptic ulcer at any site may undergo the following
complications:
•
Perforation either into the peritoneal cavity or into
adjacent structures, for example the pancreas,
liver or colon.
•
Stenosis.
Haemorrhage.
•
•
Chronicity due to formation of fibrous tissue in the
ulcer base.
• Malignant change, which does not occur in duo-
denal ulcers but may rarely take place in a gastric
ulcer; a long history does not necessarily mean
that the ulcer was not malignant de novo. Both
benign gastric ulcer and gastric carcinoma are
common conditions and there may merely be a
chance association between the two. Around 1%
of all gastric carcinomas arise in a gastric ulcer.
Perforated peptic ulcer
Pathology
Perforation of a peptic ulcer is a relatively common
and important emergency, and the incidence of peptic ulcer perforation is decreasing due to early diagnosis and effective medical management. Male
preponderance, once very high, is now about 2:1.
Until recently, perforation occurred particularly in
young adults, but now the shift is towards the older
age groups, especially in patients who are on either
steroids or NSAIDs.
Clinical features
A previous history of peptic ulceration is obtained in
about half the cases, although this may be forgotten
by the patient in agony. Typically, the pain is of sudden onset and of extreme severity; the patient can
often recall the exact moment of the onset of the pain.
Subphrenic irritation may be indicated by referred
pain to one or both shoulders, usually the right. The
pain is aggravated by movement and the patient lies
rigidly still. There is nausea, but only occasionally
vomiting. Sometimes, there is accompanying haematemesis or melaena.
Examination reveals a patient in severe pain, cold
and sweating with rapid, shallow respirations. In the
early stages (hours), there may be no clinical evidence
of true shock: the pulse is steady and the blood
pressure normal; the temperature is either normal or
a little depressed. The abdomen is rigid and silent,
although in some instances an occasional bowel
sound may be heard. Liver dullness is diminished in
about half the cases owing to escape of gas into the
peritoneal cavity. Rectal examination may reveal pelvic tenderness.
In the delayed case, after 12 hours or more, the
features of generalized peritonitis with paralytic
ileus become manifest; the abdomen is distended,
effortless vomiting occurs and the patient is in
septic shock.
226 The stomach andduodenum
Suture closu
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Special investigations
• Chest X- ray, with the patient erect, shows free gas
below the diaphragm in over 70% of cases.
Computed tomography (CT) scan is more sensitive
•
in the detection of free intraperitoneal gas, and
can exclude common differential diagnoses such
as pancreatitis when doubt exists.
Differential diagnosis
The four conditions with which perforated ulcer is
most commonly confused are:
•
Perforated appendicitis.
• Acute cholecystitis.
•
Acute pancreatitis.
• Myocardial infarction.
Treatment
Indications forsurgery
• Generalized peritonitis and typically, but not
always, free gas under the diaphragm on erect
chest X-
ray (CXR).
• Failed conservative management in selected
patients. Conservative management can be chosen in patients with a confirmed diagnosis of peptic perforation who are haemodynamically stable
and have no, or localized, signs of peritonitis.
Preoperative management
A nasogastric (NG) tube is passed to empty the
stomach and diminish further leakage. This is an
essential preis given to relieve pain and intravenous fluid resuscitation is started. Antibiotics are given to contend
with the peritoneal infection, and an intravenous
proton pump inhibitor commenced. Most surgeons
are in favour of immediate operative repair of the
perforation.
Operative management
Perforations usually occur on the anterior wall of
the first part of the duodenum. Surgery involves
suturing an omental plug to seal the perforation,
together with lavage of the peritoneal cavity
(Figure23.3). In addition, a gastric ulcer is biopsied
at all four quadrants to exclude malignancy; an
anaesthetic measure. Opiate analgesia
(a) Suture closure of duodenal perforation
(b) Omental patch technique
Figure23.3 Techniques to close a perforated ulcer.
obviously malignant gastric ulcer is removed by
partial gastrectomy.
Laparoscopic closure of the peptic ulcer should be
considered in all cases. Advantages of laparoscopic
surgery include similar results as open surgery with
the additional advantage of decreased postoperative
pain, hospital stay, wound infections and incisional
hernia. However, the procedure can be technically
more challenging and time-
consuming.
Prognosis
The mortality for perforated peptic ulcer lies between
5% and 10%. Most deaths are in patients incorrectly
diagnosed, with consequent delay in correct treatment,
or in those who are too ill for operation. The subjects
who die are typically either over the age of 70 years or
reach hospital 12 hours or more after the time of perforation or are shocked on admission. The long- term
prognosis following perforation depends on whether or
not the ulcer is chronic, and whether a treatable cause,
such as H. pylori or NSAIDs, is present.
Pyloric stenosis
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This is an inaccurate term when applied to duodenal
ulceration, as the obstruction is in the first part of the
duodenum.
Pathology
At first, fibrotic scarring is compensated by dilation
and hypertrophy of the stomach muscle. Eventually,
failure of compensation occurs, much like the failure
of a hypertrophied ventricle of the heart with valvular
stenosis.
Clinical features
During the phase of compensation, there is nothing
in the history to suggest stenosis. Once failure
occurs, there is characteristic profuse vomiting,
which is free from bile. The vomitus may contain
food eaten days previously and appears and smells
faeculent. Because of copious vomiting, there is
associated loss of weight, constipation (because of
dehydration) and weakness because of electrolyte
disturbance.
On examination, the patient may appear dehydrated and wasted. Progressive dilation and hypertrophy of the stomach occurs. At first, a gastric
splash (succussion splash) can be elicited by shaking
the patient’s abdomen several hours after a meal. As
the stomach enlarges, visible peristalsis can also be
seen, passing from left to right across the upper
abdomen. Finally, the grossly dilated, hypertrophied stomach, full of stale food and fluid, can actually be palpated.
Gastric aspiration normally yields a morning
resting juice of over 100 mL. In advanced cases of
pyloric stenosis, it may amount to several litres of
foul- smelling gastric contents.
Special investigations
• Gastroscopy following decompression of the stom-
ach with a nasogastric tube will identify the cause
in most cases.
• CT scan will provide further anatomical informa-
tion about the diagnosis and its aetiology.
• Arterial blood gases and electrolyte estimation may
show a hypochloraemic alkalosis, with hypokalaemia and uraemia.
The stomach andduodenum 227
Biochemical disturbances
Pyloric obstruction with copious vomiting results in
not only dehydration from fluid loss but also alkalosis
due to loss of hydrogen ions from the stomach. The
alkalotic tendency is compensated by the renal
excretion of sodium bicarbonate, which may keep
the blood pH within normal limits. During this phase,
the dehydration results in diminished volume and
increased concentration of urine, the chloride content of which is first diminished and then disappears
and the pH of which is alkaline. If vomiting continues, a large sodium deficit becomes manifest. This
loss of sodium is partly accounted for by loss in the
vomitus but it is mainly the result of urinary excretion consequent upon the bicarbonate lost in the
urine as sodium bicarbonate. As the body’s sodium
reserves become depleted, hydrogen and potassium
ions are substituted for sodium as the cations that are
excreted with the bicarbonate. This results in the
paradox that the patient with advanced alkalosis now
excretes an acid urine.
The blood urea rises, partly because of dehydration
and partly because of renal impairment secondary to
the electrolyte disturbances. Eventually, the patient
may develop tetany as a result of a shift of the ionized,
weakly alkaline calcium phosphate to its unionized
state, in attempted compensation for the alkalosis.
The concentration of calcium ions in the plasma,
therefore, falls, although the total calcium concentration is not affected.
The metabolic disturbances may be summarized as
follows:
•
The patient is dehydrated and the haematocrit
level is raised.
• The urine is scanty, concentrated, initially alka-
line, but later acid; the chloride content of the
urine is reduced or absent.
•
Serum chloride, sodium and potassium are low-
ered and the plasma bicarbonate and urea are
raised.
Differential diagnosis
• Carcinoma of the pylorus.
Other causes of pyloric obstruction are unusual in the
adult:
• Scarring associated with a benign gastric ulcer
near the pylorus.
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• Carcinoma of the head of the pancreas infiltrating
the duodenum and pylorus.
Chronic pancreatitis.
•
•
Invasion of the pylorus by malignant nodes.
The differential diagnosis from a pyloric carcinoma
cannot always be established until endoscopy and
biopsy, or even laparotomy, but a reasonable attempt
can be made on the following points.
Length of history: a history of several years of char-
•
acteristic peptic ulcer pain is in favour of benign
ulcer. Cancer usually has a history of only months
and indeed may be painless.
• Gross dilation of the stomach favours a benign
lesion, as it may take several years for this to
develop.
•
The presence of a mass at the pylorus indicates
malignant disease, although, rarely, a palpable
inflammatory mass in association with a large
duodenal ulcer can be detected.
Treatment
The treatment of established pyloric obstruction is
invariably surgical. Before operation, dehydration and
electrolyte depletion are corrected by intravenous
replacement of saline together with potassium. Daily
gastric lavage is performed to remove the debris from
the stomach. In addition, this often restores function
to the stomach and allows fluid absorption to take
place by mouth. Vitamin C is given, as the patient with
a chronic duodenal ulcer is often
acid. This may be a direct effect of H. pylori or it may
be the result of a diet low in fruit and vegetables.
Surgical correction is carried out after a few days of
preoperative preparation. Surgery usually involves an
antrectomy with a Roux-
en- Y gastroenterostomy.
deficient in ascorbic
Assessment ofthe patient
An initial appraisal of the patient’s airway and
breathing is undertaken; oxygen is administered
when necessary. Indicators of severe blood loss are
the features of shock, namely pallor, cold, clammy
and peripherally shut down, with a tachycardia and a
systolic blood pressure below 100mmHg. It should be
remembered that patients on β- blockers tend not to
become tachycardic, and if the patient is known to
have hypertension a systolic pressure well above
100mmHg does not rule out shock.
The presence of shock is an indication for immediate fluid replacement with normal saline or compound sodium lactate (Hartmann’s) solution; at the
same time, blood should be taken for crossAdditional evidence of significant bleeding is a
marked difference between lying and standing blood
pressure (postural hypotension) and a low central
venous pressure. Every patient presenting with GI
haemorrhage should have blood taken for grouping
and cross-
should be taken to establish the possible aetiology of
the bleeding.
matching.
Once resuscitation is under way, a further history
matching.
Aetiology
In considering the aetiology of the bleeding, both
general and local causes should be borne in mind
(see Box23.1).
General bleeding diatheses seldom cause bleeding
by themselves, they alter the course of bleeding from
a local lesion. About 55% of patients in the UK with
upper GI bleeding of an acute form have a peptic
ulcer or erosion of the stomach or duodenum. About
5% of patients have oesophageal varices, and the
remainder are accounted for by the other causes
listed above.
Gastrointestinal
haemorrhage
Management
The management of patients presenting with haematemesis and/or melaena is threefold:
1
Assessment and resuscitation of the patient.
2 Diagnosis of the source of the bleeding.
3 Treatment and control of the source of bleeding.
Bleeding peptic ulcer
Overview
Gastrointestinal bleeding is the most common
complication associated with peptic ulcer disease.
Vomiting of fresh blood, or haematemesis,
indicates that bleeding originates from a site
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Box 23.1 Cause ofgastrointestinal
haemorrhage
Local causes
1
Oesophagus:
a Reflux oesophagitis (associated with hiatus
hernia).
b Oesophageal varices (associated with portal
hypertension, see Chapter32).
c Peptic ulcer.
d Tumours (benign and malignant).
2 Stomach:
a Gastric ulcer.
b Acute erosions (small ulcers <5mm; associated
with aspirin, other NSAIDs and corticosteroids).
c Gastritis (generalized inflammation, appearing
as red dots through the endoscope).
d Mallory–Weiss
chapter).
e Vascular malformation (e.g. Dieulafoy lesion
f Tumours (benign and malignant).
3 Duodenum:
a Duodenitis.
b Duodenal ulcer.
c Erosion of the duodenum by a pancreatic tumour.
d Aortoduodenal fistula, usually in patients with
previous aortic graft.
4 Small intestine:
a Tumours.
b Meckel’s diverticulum.
c Angiodysplasia.
d Aortoenteric fistula.
5 Large bowel:
a Tumours (benign and malignant, commonly
adenocarcinomas).
b Diverticular disease.
c Angiodysplasia.
d Colitis (ulcerative colitis, ischaemic colitis and
infective colitis).
General causes
Haemophilia.
a
b Leukaemia.
c Anticoagulant therapy.
d Thrombocytopenia.
10
George Kenneth Mallory (1900–1986), Professor of
Pathology, Boston University, Boston, MA, USA. Soma
Weiss (1898–1942), Professor of Medicine, Harvard
University, Boston, MA, USA.
11
Paul Georges Dieulafoy (1839–1911), Physician, Paris.
e lesion is a submucosal artery running abnormally
close to the mucosa, typically occurring in the gastric
fundus near the oesophagogastric junction and a cause
of recurrent bleeding.
10
syndrome (see later in this
11
proximal to the duodenal- jejunal flexure (ligament
of Treitz
12
).
A history of fresh haematemesis usually implies a
significant bleed and the patients may go into haemodynamic instability due to hypovolaemia. ‘Coffee
ground’ vomiting, usually arising from altered black
blood, often indicates that active bleeding may have
ceased.
Melaena is the passage of black tarry stool. It occurs
when haemoglobin in the gut is converted to haematin by bacterial degradation. As little as 200 mL of
bleeding inside the digestive tract can produce melaena. Although melaena generally denotes bleeding
proximal to the duodenal-
jejunal flexure, bleeding
from small bowel or proximal colon may also cause it,
especially when colonic transit is slow.
Haematochezia, passage of pure red blood or blood
mixed with the stool, generally occurs when bleeding
).
comes from the lower GI tract. It can also present due
to massive upper GI bleeding. When a substantial
amount of blood is lost into the GI lumen, tachycardia
and hypotension develop. The haemoglobin concentration at this stage may not reflect the actual amount
of blood loss before haemodilution sets in. A close
monitoring of vital signs and estimation of volume of
vomitus offer a better prognostic indicator of the
severity of the illness.
Management (Table23.1)
Bleeding from a peptic ulcer can be life- threatening.
Urgent endoscopy is performed to identify the site
and cause of bleeding, and also to institute appropriate therapeutic intervention. Early endoscopy within
24 hours of admission has been shown to reduce
blood transfusion and length of hospital stay.
Bleeding vessels may be managed by endoscopic
clipping or adrenaline injection and most, but not all,
bleeding can be controlled in this way. Urgent interventional radiology with embolization of the bleeding
vessel or surgical intervention may occasionally be
required.
Indications forsurgery
• Failure of endoscopic control.
• Rebleeding after successful endoscopic therapy.
12
Václav Treitz (1819–1872). Professor of Pathological
Anatomy, Prague.
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Table23.1 Summary ofRecommendations forgastroduodenal ulcer disease
Clinical problem Operative risk Recommended approach
Perforated duodenal ulcer Low or high Laparoscopic or open repair with omental or
Perforated gastric ulcer Low Open or laparoscopic excision of ulcer and
Perforated gastric ulcer High Open or laparoscopic excision of ulcer and
Bleeding duodenal or gastric
ulcer refractory to endoscopic
management
Bleeding duodenal or gastric
ulcer refractory to endoscopic
management
Gastric outlet obstruction
refractory to endoscopic dilation
Refractory gastroduodenal ulcer
disease positive for gastrinoma
or other hypersecretory state
Refractory gastroduodenal ulcer
disease
Low Open exploration, biopsy of gastric ulcer with
High Angioembolization with open surgery and suture
Low Gastric resection and reconstruction with
Low Resection of gastrinoma.
High Truncal vagotomy with antrectomy and
falciform patch. Postoperative management with
evaluation for H. pylori infection, acid suppression
therapy, management of risk factors (NSAIDs,
alcohol, tobacco).
closure. Gastric resection if obviously malignant
ulcer.
closure. Postoperative management as above.
suture ligation of all branches of arteries feeding
the ulcer bed. Consider truncal vagotomy and
pyloroplasty or highly selective vagotomy (if
appropriately experienced) or gastric wall closure
and postoperative management.
ligation of bleeding vessel if this fails.
postoperative therapy.
reconstruction if medical therapies fail.
• Elderly and unfit patients may not tolerate
bleeding– consider early surgery.
• Patients with ongoing blood transfusion
requirements.
In some patients, particularly those unfit for major
surgery, radiological embolization of the gastroduodenal artery may be preferred to surgery for duodenal
ulcer haemorrhage.
Gastroparesis
Gastroparesis is a motility disorder defined by the
manifestations of chronic upper GI symptoms and
prolonged gastric emptying in the absence of
mechanical obstruction. It affects predominantly
females with an incidence of 14–25in 100 000.
Symptoms
Symptoms can be mild to severe, tend to be intermittent and include: early satiety (fullness), nausea,
vomiting that may lead to dehydration, loss of
appetite, weight loss, malnutrition, bloating, abdominal pain or discomfort, gastroesophageal reflux disease (GORD) and unpredictable blood sugars in
people with diabetes.
Causes
Gastroparesis may be without obvious cause
(idiopathic), or the result of problems with nerves
and muscles controlling the emptying of the stomach. Other causes include: poorly controlled diabetes, bariatric surgery, gastrectomy, medication such
as opioids, scleroderma, Parkinson’s disease and
amyloidosis.
Special investigations
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• Barium X- ray.
Gastric emptying scan using scintigraphy: food
•
containing a very small amount of a radioactive
substance is ingested with a subsequent scan.
•
Endoscopy to exclude any intrinsic or extrinsic
cause.
Capsule endoscopy.
•
The stomach andduodenum 231
Gastric volvulus
Gastric volvulus is a rare condition whereby the stomach rotates more than 180°, creating a closedobstruction that can result in strangulation. It can
manifest either as an acute abdominal emergency or
as a chronic intermittent problem.
loop
Treatment
There is no cure for gastroparesis. Symptoms can be
reduced/resolved with dietary changes such as eating
small and frequent meals, eating soft and liquid foods
that are easier to digest, chewing food well before
swallowing, drinking non- fizzy liquids with meals
and avoiding or reducing certain foods such as highfibre and foods high in fat.
Other treatments include:
•
Gastroelectrical stimulation (GES): surgical
implantation of a battery- operated device, to
deliver electrical impulses to stimulate the muscles involved in controlling the passage of food
through the stomach (often inappropriately
referred to as a ‘gastric pacemaker’).
• Botulinum toxin injected endoscopically into the
pyloric sphincter offers temporary relief, and may
need repeating.
•
Transpyloric stenting, but effectiveness limited by
risk of stent migration.
Laparoscopic or endoscopic pyloromyotomy and
•
gastrectomy.
•
Symptomatic control with antiemetics and
antibiotics.
Alternative feeding methods: nasojejunal tube or
•
jejunostomy feeding, or parenteral nutrition.
• A gastric bypass procedure (gastroenterostomy or
gastrojejunostomy) may benefit some patients,
releasing gas and relieving bloating.
The latest guidelines from the European Society of
Gastrointestinal Endoscopy recommend against the
use of botulinum toxin injection, balloon dilations,
and transpyloric stenting in unselected patients
with gastroparesis, while a gastrectomy is seldom
currently performed due to the appearance of minimally invasive procedures, including different
modalities of pyloromyotomy and GES. The optimum intervention option for gastroparesis remains
elusive.
Classication ofgastric volvulus
The most frequently used classification system of gastric volvulus relates to the axis around which the
stomach rotates and includes the following three
types:
•
Organoaxial: the stomach rotates around an
axis that connects the gastro- oesophageal junction (GOJ) and the pylorus. The antrum rotates
in the opposite direction to the fundus of the
stomach. This is the most common type of gastric volvulus, occurring in approximately 59% of
casesand it is usually associated with diaphragmatic defects.
•
Mesenteroaxial: the mesenteroaxial axis bisects
the lesser and greater curvatures. The antrum
rotates anteriorly and superiorly so that the posterior surface of the stomach comes to lie anteriorly.
The rotation is usually incomplete and occurs
intermittently. Vascular compromise is uncommon. This aetiology accounts for approximately
29% of cases of gastric volvulus.
•
Combined: is a rare form in which the stomach
twists both mesenteroaxially and organoaxially.
This type of gastric volvulus makes up the remainder of cases and is usually observed in patients
with chronic volvulus.
In aetiologic terms, gastric volvulus can be classi-
fied as either:
•
Type 1 (idiopathic): makes up two- thirds of cases
and is presumably due to abnormal laxity of the
gastrosplenic, gastroduodenal, gastrophrenic and
gastrohepatic ligaments. This allows approximation of the cardia and pylorus when the stomach is
full, predisposing to volvulus.
•
Type 2 (congenital or acquired): is found in one-
third of patients and is usually associated with
congenital or acquired abnormalities that result in
abnormal mobility of the stomach.
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Epidemiology
Males and females are equally affected. About 10–20%
of cases occur in children, usually before the age of
one year, but cases have been reported in children as
old as 15 years.
Symptoms
The presenting symptoms depend on the degree of
twisting and the rapidity of onset. The classic
Borchardt triad of features comprises:
•
Severe epigastric pain.
•
Retching without vomiting.
• Inability to pass a NG tube.
Acute gastric volvulus
The Borchardt triad is diagnostic of acute volvulus
and reportedly occurs in 70% of cases. Other symptoms are: hiccups, sudden onset of severe epigastric
or left-
upper- quadrant pain, sharp chest pain radiating to the left side of the neck, shoulder, arms and
back, progressive distention and nonretching follow the pain, while some patients present
with hematemesissecondary to mucosal ischaemia
and sloughing.
productive
Chronic gastric volvulus
Intermittent epigastric pain and abdominal fullness
after meals, early satiety, dyspnoea, chest discomfort
and dysphagia are the most common symptoms.
• CT scan is the imaging modality of choice, outlining the anatomy.
Upper GI endoscopy may be helpful in the diagno-
•
sis of gastric volvulus.
Contrast studies are less commonly performed
•
now.
•
Other investigations may be necessary to exclude
the differential diagnoses, which include gallstones, hiatus hernia, myocardial infarction and
peptic ulcer.
Management
In general, treatment of an acute gastric volvulus
involves emergency surgical repair. In patients who
are not surgical candidates, endoscopic reduction
may be attempted and may allow adequate resuscitation and medical optimization before definitive surgical repair. Chronic gastric volvulus may be treated on
emergency basis.
a non-
Gastric tumours
Classication
Benign
1 Epithelial: adenoma:
a Single.
b Multiple (gastric polyposis).
2 Connective tissue: gastrointestinal stromal tumour.
3
Vascular: haemangioma.
Complications
Strangulation and necrosis are the most feared
complications of gastric volvulus; they can be
life- threatening and occur most commonly with
organoaxial gastric volvulus (5–28% of cases). Gastric
perforation occurs secondary to ischaemia and necrosis and can result in sepsis and cardiovascular collapse;
it can also complicate endoscopic reduction.
Special investigations
• Chest X- ray: a retrocardiac gas- filled viscus may be
seen in cases of intrathoracic stomach, which confirms the diagnosis.
• Abdominal X- ray: reveals a massively distended
viscus in the upper abdomen.
Malignant
1 Primary:
a
Adenocarcinoma.
b Gastrointestinal stromal tumour.
c Lymphoma.
2 Secondary: invasion from adjacent tumours (pan-
creas or colon).
Epidemiology
Benign tumours of the stomach are uncommon, with
an incidence of 0.4% in autopsy series and 3–5% in
upper endoscopic series, most of them performed for
unrelated reasons. Polyps account for 3.1% of all
gastric tumours and their frequency increases to
almost 90% of benign gastric tumours. Age and sex
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distribution depend on the type of tumour. There is
no difference in distribution by race.
Many benign gastric tumours are found incidentally on gastroscopy. Small tumours are usually
asymptomatic, but larger tumours can ulcerate and
cause occult bleeding and anaemia. Large antral
tumours cause intermittent gastric outlet obstruction,
as manifested by nausea, vomiting and early satiety. If
ulcerated, these tumours may cause epigastric pain
similar to that caused by a peptic ulcer.
Gastric polyps
Gastric polyps are usually found incidentally during
endoscopy. According to the cell of origin, polyps can
be epithelial (fundic gland polyp, hyperplastic polyp,
adenomatous polyp), neuroendocrine, lymphohistiocytic (xanthelasma, lymphoid hyperplasia),
mesenchymal (gastrointestinal stromal tumour, neural or vascular tumours) or mixed. They can be sporadic or occur as part of a syndrome.
•
Fundic gland polyps are the most common type of
gastric polyps and were originally described in
patients with familial adenomatous polyposis
(FAP). The incidence of fundic gland polyps is low
in patients with Helicobacter pylori infection and
relatively high in patients taking proton pump
inhibitors. While lowin FAP patients with fundic gland polyps, dysplasia is rare in sporadic cases.
•
Hyperplastic polyps are composed of epithelial
and stromal components and are most frequently
found in the antrum of patients with inflamed or
atrophic gastric mucosa, and represent around
14% of gastric polyps. Removal of the underlying
cause, such as H. pylori infection, results in regression of the hyperplastic polyps in 70% of patients.
Hyperplastic polyps should be regarded as surrogate markers of cancer risk and synchronous or
metachronous gastric carcinomas have been
reported in up to 6% of cases.
• Adenomatous polyps are subdivided into classic
intestinaltype adenomas. Adenomatous polyps are precursors of gastric adenocarcinomas with the risk of
adenocarcinoma increasing with increasing size;
50% of adenomatous polyps > 2 cm harbour
malignancy.
type adenomas and non- intestinal-
grade dysplasia is frequent
• Polyposis syndromes. Hamartomatous polyps in
the stomach have been found in patients with
Jeghers syndrome, juvenile polyposis,
PeutzCronkhiteease. All patients with these polyposis syndromes
have an increased risk of developing gastric carcinoma, which appears to be highest in patients
with Peutz-
Canada syndrome and Cowden dis-
Jeghers syndrome, at 30%.
Symptoms
The majority of patients are asymptomatic.
Occasionally, polyps bleed, presenting as haematemesis or melaena. Rarely, large pedunculated polyps
can obstruct the pylorus, leading to nausea, abdominal distension and vomiting.
Special investigation
Upper GI endoscopy is indicated to elicit the cause.
Histological assessment of all polyps is essential
because early gastric cancers can look insignificant.
Treatment
Removal or resection of adenomatous polyps is
essential. Otherwise, treatment is related to symptoms and may include a polypectomy (polyp
removal). Polyps smaller than 2cm are easily snared
endoscopically and removed. Larger polyps or sessile
polyps are best removed operatively to obtain a clear
margin and complete removal. Occasionally, staged
piecemeal endoscopic removal can be performed in
patients with severe comorbidities.
Wide, local or segmental resection of the stomach
may be performed for multiple polyps, depending on
their histology and location. Gastrectomy is justified
in patients with diffuse involvement of the stomach
by polyps, which can make detection of a synchronous focus of cancer difficult.
Gastrointestinal stromal
tumours
Gastrointestinal stromal tumours (GISTs) are softtissue sarcomas of mesenchymal origin that arise in
the gastrointestinal tract; they are rare, representing
<3% of all gut tumours and 5% of all soft- tissue
sarcomas.
234 The stomach andduodenum
https://t.me/medicina_free
Pathology
GISTs were previously thought to arise from the muscular layer or from nerve cells in the gut wall; in fact,
they are now believed to arise from the interstitial
cells of Cajal
trointestinal tract. ICCs are part of the autonomic
nervous system and when the tumour has the appearance of neural tissue it is often called a gastrointestinal autonomic nervous tumour (GANT). Other
tumours may have an appearance more like smooth
muscle cells; hence, they were previously thought to
be leiomyomas.
GISTs may be malignant or benign, and, although
they may occur anywhere in the gastrointestinal tract,
they are most common in the stomach, but not infrequent in the rest of the small intestine. They appear as
small tumours within the muscular wall or larger
tumours growing out from the bowel wall. Large
tumours may outstrip their blood supply and become
partly cystic; sometimes, the cyst communicates with
the bowel lumen. GISTs typically present with either
intestinal bleeding or obstruction; some are found
during investigation of non- specific abdominal pain.
13
(ICCs), the pacemaker cells of the gas-
Aetiology
The aetiology of GISTs is unclear, but they are associated with type 1 neurofibromatosis in some cases.
Typically, patients are over 40 years and there is no
sex difference in incidence. The pathogenesis is a
spontaneous mutation in the c- kit gene, which codes
for a transmembrane receptor (c-
growth factor called stem cell factor. The c- kit muta-
tion results in a continuous signal for cell growth
which is mediated via a tyrosine kinase in the intracellular domain of the molecule. Some GISTs arise
from mutations in platelet- derived growth factor
receptor α (PDGFA); occasional cases demonstrate an
inherited predisposition.
kit/CD117) for a
detected during investigations or surgical procedures
for unrelated disease. The vast majority of these are of
low-
risk for malignancy. The most common symptom
is gastrointestinal bleeding which is present in around
half of patients. Patients with larger tumours may
experience abdominal discomfort or develop a palpable mass. GISTs are often clinically silent until they
reach a large size, bleed or rupture. Most duodenal
GISTs occur in the second part of the duodenum
where they can cause obstructive symptoms or infiltrate into the pancreas.
Special investigations
• Endoscopy usually detects the tumour, which
appears as a submucosal polyp and which often
has an ulcerated surface.
CT scan may also identify the presence of a
•
tumour.
•
Endoscopic ultrasound (EUS) can be used to con-
firm the nature of the polyp and demonstrates
clearly the origin of the polyp from the muscular
layer of the stomach wall.
• Positron emission tomography (PET) is used both
for detection and for staging of the tumours.
Once a tumour is found, diagnosis is by biopsy. Owing
to the polyp’s submucosal origin, mucosal biopsies
are frequently nonthe diagnosis relies on EUS appearances with or without EUSundertaken in the presence of metastases, but not
undertaken otherwise to avoid the risk of seeding
tumour cells along the biopsy track. The presence of
cdiagnostic. Most small GISTs (< 5 cm) have a low
mitotic rate and behave like benign tumours; larger
GISTs (> 5cm) have a more malignant phenotype and
require adjuvant chemotherapy.
guided biopsy. Percutaneous biopsies are
kit protein (CD117) on the cell surface is almost
diagnostic and confirmation of
Clinical features
The symptoms of GISTs are non- specific and depend
on the size and location of the lesion. Small GISTs
(2 cm or less) are usually asymptomatic and are
13
Santiago Ramóny Cajal (1852–1934), Histologist and
Professor, successively in Valencia, Barcelona and Madrid,
Spain. Awarded the Nobel Prize in 1906with Golgi for
studies of the neurone.
Treatment
• Surgical: complete resection by wide excision is
the treatment of choice, and is often possible
laparoscopically.
•
Endoscopic resection may be possible and effective
for smaller (≤ 4.0cm) GISTs originating from the
muscularis propria.
• Chemotherapy: molecular targeted chemotherapy
with imatinib mesilate (Glivec), an inhibitor of the
c- kit tyrosine kinase, is very effective. It can be
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