Gastric and duodenal peptic

ulcer disease
• Gastric ulcers are most
often caused by NSAIDs
or H. pylori infection.
• There are four major
complications of peptic
ulcer disease (PUD):
bleeding, perforation,
penetration, and
obstruction. Complications
can occur in patients with
peptic ulcer of any
etiology.
Duodenal ulcer
Medical treatment of uncomplicated duodenal ulcer disease is usually
successful.
a. Avoidance of aspirin, caffeine, alcohol, and tobacco is recommended.
b. Stress reduction may be beneficial.
c. Eradication of H. pylori
d. Pharmacologic therapy is the mainstay of treatment of peptic ulcer
disease. H2-receptor antagonists and proton pump inhibitors are used most
commonly for initial treatment and then are decreased to a single bedtime
dose for maintenance therapy. Most duodenal ulcers heal in 6-8 weeks with
such therapy. Maintenance therapy is recommended because ulcer
recurrence after discontinuing medical therapy occurs in 50%-80% of
patients.
Surgical treatment of duodenal ulcer is reserved for patients who have
ulcers that fail to respond to medical therapy or who have
complications, such as perforation or bleeding. There are a number of
surgical options. The goal of each is to reduce acid secretion; therefore,
most approaches concentrate on interrupting vagal stimulation, antral
gastrin secretion, or both.
a. Vagotomy with antrectomy is the procedure associated with the
lowest recurrence rate.
b. Vagotomy with drainage is associated with a recurrence rate of 6%-7%. After
vagotomy, the
motility of the stomach and pylorus is impaired, creating a functional obstruction.
For this reason, a drainage procedure, such as a pyloroplasty or gastrojejunostomy,
is required.
c. Parietal cell vagotomy , also known as highly selective vagotomy, is gaining in
popularity, especially when the indication for surgical intervention is intractable
pain. Only the gastric branches of the vagus nerve are divided. Because innervation
of the pylorus is maintained, a drainage procedure is not necessary. Recurrence
rates with this procedure are somewhat higher (approximately 10%), but the
morbidity is less as compared with truncal vagotomy with antrectomy. This
procedure is often performed laparoscopically, further decreasing its morbidity.
 Perforated peptic ulcer EPIDEMIOLOGY
Despite the widespread use of gastric
antisecretory agents and eradication therapy,
the incidence of perforated peptic ulcer has
changed little. However, there has been a
considerable change in the epidemiology of
perforated peptic ulcer in resource-rich
countries over the last two decades.
Previously, most patients were middle aged,
with a ratio of 2:1 of male:female. With time
there has been a steady increase in the age
of the patients suffering this complication
and an increase in the numbers of females,
such that perforations now occur most
commonly in elderly female patients. NSAIDs
appear to be responsible for most of these
perforations.
 CLINICAL FEATURES
The classical presentation of perforated duodenal ulcer is instantly
recognizable. The patient, who may have a history of peptic ulceration,
develops sudden-onset severe generalised abdominal pain due to the
irritant effect of gastric acid on the peritoneum. Although the contents of
an acid-producing stomach are relatively low in bacterial load, bacterial
peritonitis supervenes over a few hours, usually accompanied by a
deterioration in the patient’s condition. Initially, the patient may be
shocked with a tachycardia but a pyrexia is not usually observed until
some hours after the event. The abdomen exhibits a board-like rigidity
and the patient is disinclined to move because of the pain. The abdomen
does not move with respiration. Patients with this form of presentation
need an operation, without which the patient will deteriorate with a
septic peritonitis.
 This classical presentation of the perforated peptic ulcer is observed
less commonly than in the past. Very frequently the elderly patient who
is taking NSAIDs will have a less dramatic presentation, perhaps because
of the use of potent anti-inflammatory drugs (steroids). The board-like
rigidity seen in the abdomen of younger patients may also not be
observed and a higher index of suspicion is necessary to make the
correct diagnosis. In other patients, the leak from the ulcer may not be
massive. They may present only with pain in the epigastrium and right
iliac fossa as the fluid may track down the right paracolic gutter.
Sometimes perforations will seal owing to the inflammatory response
and adhesion within the abdominal cavity, and so the perforation may be
selflimiting. All of these factors may combine to make the diagnosis of
perforated peptic ulcer difficult.
 By far the most common site
of perforation is the anterior
aspect of the duodenum.
However, the anterior or incisural
gastric ulcer may perforate and,
in addition, gastric ulcers may
perforate into the lesser sac,
which can be particularly difficult
to diagnose. These patients may
not have obvious peritonitis.
 INVESTIGATIONS
An erect plain chest radiograph will reveal free gas under the diaphragm
in excess of 50% of cases with perforated peptic ulcer but CT imaging is
more accurate. All patients should have serum amylase performed, as
distinguishing between peptic ulcer, perforation and pancreatitis can be
difficult. Measuring the serum amylase, however, may not remove the
diagnostic difficulty. It can be elevated following perforation of a peptic
ulcer although, fortunately, the levels are not usually as high as the levels
commonly seen in acute pancreatitis. Several other investigations are
useful if doubt remains. A CT scan will normally be diagnostic in both
conditions.
TREATMENT
The initial priorities are resuscitation and analgesia. Analgesia should
not be withheld for fear of removing the signs of an intra-abdominal
catastrophe. In fact, adequate analgesia makes the clinical signs more
obvious. It is important, however, to titrate the analgesic dose.
Following resuscitation, the treatment is principally surgical.
Laparotomy is performed, usually through an upper midline incision if
the diagnosis of perforated peptic ulcer can be made with confidence.
This is not always possible and hence it may be better to place a small
incision around the umbilicus to localise the perforation with more
certainty. Alternatively, laparoscopy may be used.
 The most important component of the operation is a thorough
peritoneal toilet to remove all of the fluid and food debris. If the
perforation is in the duodenum it can usually be closed by several well-
placed sutures, closing the ulcer in a transverse direction as with a
pyloroplasty. It is important that sufficient tissue is taken in the suture to
allow the edges to be approximated, and the sutures should not be tied
so tight that they tear out. It is common to place an omental patch over
the perforation in the hope of enhancing the chances of the leak
sealing. If the perforation is difficult to close primarily it is frequently
possible to seal the leak with an omental patch alone, and many
surgeons now employ this strategy for all perforations.
 When securing the omental patch
it is important not to tie the sutures
too tight so as to obliterate the
omental blood supply. Gastric ulcers
should, if possible, be excised and
closed, so that malignancy can be
excluded. Occasionally a patient is
seen who has a massive duodenal or
gastric perforation such that simple
closure is impossible; in these
patients a distal gastrectomy with
Roux-en-Y reconstruction is the
procedure of choice.
 All patients should be treated with systemic antibiotics in addition to
a thorough peritoneal lavage. In the past, many surgeons performed
definitive procedures such as either truncal vagotomy and pyloroplasty
or, more recently and probably more successfully, highly selective
vagotomy during the course of an operation for a perforation. Studies
show that in well-selected patients and in expert hands this is a very
safe strategy. However, nowadays, surgery is confined to first-aid
measures most commonly, and the peptic ulcer is treated medically.
Following operation, gastric antisecretory agents should be started
immediately. H. pylori eradication is mandatory.
 Perforated peptic ulcers can often be managed by minimally invasive
techniques if the expertise is available. The principles of operation are,
however, the same; thorough peritoneal toilet is performed and the
perforation is closed by intracorporeal suturing. Whatever technique is
used, it is important that the stomach is kept empty postoperatively by
nasogastric suction, and that gastric antisecretory agents are
commenced to promote healing in the residual ulcer.
A number of factors have been associated with poor outcome after
perforated peptic ulcer, including:
● delay in diagnosis (>24 hours);
● medical comorbidities;
● shock;
● increasing age (>75).
There is little evidence to advocate the conservative management of
patients who exhibit any of these characteristics. Patients who have
suffered one perforation may suffer another one. Therefore, they should
be managed aggressively to ensure that this does not happen. Lifelong
treatment with proton pump inhibitors is a reasonable option especially
in those who have to continue with NSAID treatment.
 HAEMATEMESIS AND MELAENA

Upper gastrointestinal hemorrhage remains a major medical problem

with an incidence over 100/100 000 per year in western practice that
increases with increasing age. Hemorrhage is strongly associated with
NSAID use. Despite improvements in diagnosis and the proliferation in
treatment modalities over the last few decades, an in-hospital mortality
of 5–10% can be expected. This rises to 33% when bleeding is first
observed in patients who are hospitalised for other reasons. In patients
in whom the cause of bleeding can be found, the most common causes
are peptic ulcer, erosions, Mallory–Weiss tear and bleeding esophageal
varices
 Whatever the cause, the principles of management are identical.
First, the patient should be adequately resuscitated and, following this,
the patient should be investigated urgently to determine the cause of
the bleeding. Only then should treatment of a definitive nature be
instituted. For any significant gastrointestinal bleed, intravenous access
should be established and, for those with severe bleeding, central
venous pressure monitoring should be set up and bladder
catheterization performed. Blood should be cross-matched and the
patient transfused as clinically indicated, usually when >30% of blood
volume has been lost. There is no evidence for the use of intravenous
proton pump inhibitors prior to endoscopy.
 As a general rule, most gastrointestinal bleeding will stop, albeit
temporarily, but there are sometimes instances when this is not the
case. In these circumstances, resuscitation, diagnosis and treatment
should be carried out simultaneously. There are occasions when life-
saving manoeuvres have to be undertaken without the benefit of an
absolute diagnosis. For instance, in patients with known esophageal
varices and uncontrollable bleeding, a Sengstaken–Blakemore tube may
be inserted before an endoscopy has been carried out. This practice is
not to be encouraged, except in extremis. In some patients, bleeding is
secondary to a coagulopathy. The most important current causes of this
are liver disease and inadequately controlled warfarin therapy. In these
circumstances the coagulopathy should be corrected, if possible, with
fresh-frozen plasma or concentrated clotting factors.
 Upper gastrointestinal endoscopy should be carried out by an
experienced operator as soon as practicable after the patient has been
stabilised. In patients in whom the bleeding is relatively mild,
endoscopy may be carried out on the morning after admission; this is
usually guided by local policy. In all cases of severe bleeding it should
be carried out immediately. A number of scoring systems have been
advocated for the assessment of rebleeding and death after upper
gastrointestinal hemorrhage. Perhaps the most useful of these is the
Rockall score. This can be used in a pre-endoscopy format to stratify
patients to safe early discharge and postendoscopy it can relatively
accurately predict rebleeding and death.
 Bleeding peptic ulcers
The epidemiology of bleeding peptic ulcers exactly mirrors that of
perforated ulcers. In recent years, the population affected has become
much older and the bleeding is commonly associated with the ingestion
of NSAIDs. Diagnosis can normally
be made endoscopically, although
occasionally the nature of the
blood loss precludes accurately
identifying the lesion. However,
the more experienced the
endoscopist, the less likely this is
to be a problem.
 Medical and minimally interventional
treatments
Medical treatment has limited efficacy. All patients are commonly
started on either an H2-antagonist or a proton pump antagonist, and
recent evidence confirms the benefit of proton pump inhibitor
administration to prevent rebleeding after endoscopy. Furthermore,
meta-analysis of studies suggests that tranexamic acid, an inhibitor of
fibrinolysis, may reduce overall mortality.
 Therapeutic endoscopy can achieve hemostasis in approximately
70% of cases, with the best evidence supporting a combination of
adrenaline injection with heater probe and/or clips. Therapeutic
endoscopy will probably never be effective in patients who are
bleeding from large vessels and with which the majority of the
mortality is associated.
 In patients where the source of bleeding cannot be identified or in
those who rebleed after endoscopy, angiography with transcatheter
embolisation may offer a valuable alternative to surgery in expert
centers. The risk of significant ischemia following embolisation is low
because of the rich collateral blood supply of the stomach and
duodenum. The surgeon should be mindful that rescue surgery after
failed embolisation is associated with poor outcome and it may be
advantageous to proceed directly to surgery.
 Surgical treatment
Criteria for surgery are well worked out. A patient who continues to
bleed requires surgical treatment. The same applies to a significant
rebleed. The only exception applies in expert centers with 24-hour
interventional radiology and experience of angiographic embolisation
where attempts may be made to arrest bleeding and avoid surgery. The
surgical team should care for these patients and an operation should not
be delayed if any concerns remain. Patients with a visible vessel in the
ulcer base, a spurting vessel or an ulcer with a clot in the base are
statistically likely to require surgical treatment to stop the bleeding.
Elderly and unfit patients are more likely to die as a result of bleeding
than younger patients. Ironically, they should have early surgery. A patient
who has required more than six units of blood in general needs surgical
treatment.
 The aim of the operation is to stop the bleeding. The advent of
endoscopy has greatly helped in the management of upper
gastrointestinal bleeding as a surgeon can usually be confident about the
site of bleeding prior to operation. The most common site of bleeding
from a peptic ulcer is the duodenum. In tackling this, it is essential that
the duodenum is fully mobilised. This should be done before the
duodenum is opened as it makes the ulcer much more accessible and
also allows the surgeon’s hand to be placed behind the gastroduodenal
artery, which is commonly the source of major bleeding. Following
mobilisation, the duodenum, and usually the pylorus, is opened
longitudinally as in a pyloroplasty. This allows good access to the ulcer,
which is usually found posteriorly or superiorly.
 Accurate hemostasis is important and can be achieved initially by
direct pressure. It is the vessel within the ulcer that is bleeding and this
should be controlled using well-placed sutures on a small round-bodied
needle that under-run the vessel. The placing of more and more
inaccurately positioned sutures is counterproductive. Following under-
running, it is often possible to close the mucosa over the ulcer. The
pyloroplasty is then closed with interrupted sutures in a transverse
direction as in the usual fashion. In a giant ulcer the first part of the
duodenum may be destroyed making primary closure impossible. In this
circumstance one should proceed to distal gastrectomy with Roux-en-Y
reconstruction. The duodenal stump may then be closed using the
Nissen technique with T-tube drainage.
 The principles of management of bleeding gastric ulcers are
essentially the same. The stomach is opened at an appropriate position
anteriorly and the vessel in the ulcer under-run. If the ulcer is not
excised then a biopsy of the edge needs to be taken to exclude
malignant transformation. Sometimes the bleeding is from the splenic
artery and if there is a lot of fibrosis present then the operation may be
challenging. However, most patients can be managed by conservative
surgery. Gastrectomy for bleeding has been widely practised in the past,
but is associated with a high perioperative mortality even if the
incidence of recurrent bleeding is less.
Stress ulceration
This commonly occurs in patients with major injury or illness, who
have undergone major surgery or who have major comorbidity. Many
such patients are found in intensive care units. There seems little doubt
that the incidence of this problem has reduced in recent years due to
the widespread use of prophylaxis. Acid inhibition and the nasogastric
or oral administration of sucralfate has been shown to reduce the
incidence of stress ulceration. There is no doubt that it is far better to
prevent this condition than to try to treat it once it occurs. Endoscopic
means of treating stress ulceration may be ineffective and operation
may be required. The principles of management are the same as for the
chronic ulcer.
 Gastric erosions
Erosive gastritis has a variety of
causes, especially NSAIDs.
Fortunately, most such bleeding
settles spontaneously, but when it
does not it can be a major problem
to treat. In general terms, although
there is a diffuse erosive gastritis,
there is one (or more) specific
lesion that has a significant-sized
vessel within it. This should be
dealt with appropriately,
preferably endoscopically, but
sometimes surgery is necessary.
 Mallory–Weiss tear
This is a longitudinal tear at the gastro-
esophageal junction, which is induced by
repetitive and strenuous vomiting. Doubtless,
many such lesions occur and do not cause
bleeding. When it is a cause of hematemesis,
the lesion may often be missed as it can be
difficult to see as it is just below the gastro-
esophageal junction, a position that can be
difficult for the inexperienced endoscopist.
Occasionally these lesions continue to bleed
and require surgical treatment.
 Dieulafoy’s disease
This is essentially a gastric arterial venous malformation that has a
characteristic histological appearance. Bleeding due to this malformation
is one of the most difficult causes of upper gastrointestinal bleeding to
treat. The lesion itself is covered by normal mucosa and, when not
bleeding, it may be invisible. If it can be seen while bleeding, all that may
be visible is profuse bleeding coming from an area of apparently normal
mucosa. If this occurs, the cause is instantly recognisable. If the lesion
can be identified endoscopically there are various means of dealing with
it, including injection of sclerosant and endoscopic clips. If it is identified
at operation then only a local excision is necessary.
 GASTRIC OUTLET OBSTRUCTION
The two common causes of gastric
outlet obstruction are gastric cancer
and pyloric stenosis secondary to
peptic ulceration. Previously, the latter
was more common. Now, with the
decrease in the incidence of peptic
ulceration and the advent of potent
medical treatments, gastric outlet
obstruction should be considered
malignant until proven otherwise, at
least in resource-rich countries.
Gastric outlet obstruction
●● Gastric outlet obstruction is most commonly associated with longstanding
peptic ulcer disease and gastric cancer;
●● The metabolic abnormality of hypochloraemic alkalosis is usually only seen with
peptic ulcer disease and should be treated with isotonic saline with potassium;
●● Endoscopic biopsy is essential to determine whether the cause of the problem
is malignancy;
●● Aggressive medical therapy for peptic ulcer disease often leads to resolution;
●● Endoscopic dilatation of the gastric outlet may be effective in less severe cases
of benign stenosis;
●● Operation is frequently required, with a drainage procedure being performed
for benign disease and appropriate resectional surgery if malignant;