Peptic ulcer
Peptic ulcers are so named because, in
addition to acid being a requirement for their occurrence, pepsin is probably
also required. Certainly, it is clear that patients with duodenal ulcers tend to
have a higher than average pepsin level within the gastric juice. However, this is of
little practical importance as in the absence of acid, for instance in type A
gastritis with atrophy, peptic ulcers do not occur. All peptic ulcers can be
healed by using proton pump inhibitors, such as omeprazole, that can render a
patient virtually achlorhydric.
Common
sites for peptic ulcers are the first part of the duodenum and the lesser curve
of the stomach, but they also occur on the stoma following gastric surgery, the
oesophagus and even in a Meckel’s diverticulum, which contains ectopic gastric
epithelium. In general, the ulcer occurs at a junction between different types
of epithelia, the ulcer occurring in the epithelium least resistant to acid
attack.
In
the past much distinction has been made between acute and chronic peptic ulcers,
but this difference can sometimes be difficult to determine clinically. It is
probably best to consider that there is a spectrum of disease from the
superficial gastric and duodenal ulceration, frequently seen at endoscopy, to
deep chronic penetrating ulcers. This does not minimise the importance of acute
stress ulceration. These ulcers can both perforate and bleed (see ‘Stress
ulceration’ later).
For
many years and despite enormous research endeavour the cause of peptic
ulceration remained an enigma. Acid, which is so easy to measure, was studied
incessantly, such studies being particularly beloved by gastric surgeons. However,
it is clear that although acid levels are higher comparing groups of patients
with duodenal and prepyloric peptic ulcers with normal subjects the overlap is
very considerable. Patients with gastric ulceration have normal levels of
gastric acid secretion or, in the view of some, lower levels. As peptic
ulceration will occur in the presence of very high acid levels, such as those
found in patients with a gastrinoma (Zollinger—Ellison syndrome, see the
section on ‘Duodenal tumours’ later), and as all ulcers can be healed in the
absence of acid it is clear that acid is important. In some cases it may be the
only aetiological factor. This is clearly not the case in the majority of
patients. As with most diseases there clearly are genetic components as
exemplified by the often quoted and clinically irrelevant finding that patients
with blood group 0 are over-represented amongst the duodenal ulcer population.
Similarly, social stress has also been implicatated, falsely (Asher).
It
is now widely accepted that infection with H.
pylori is the most important factor in the development of peptic ulceration.
The other factor of major importance at present is ingestion of NSAIDs.
Cigarette smoking predisposes to peptic ulceration and increases the relapse
rate after
Duodenal
ulceration
Incidence
There have been marked changes in the last two
decades in the demography of patients presenting with duodenal ulceration in the
West. First, even before the introduction of H2-receptor antagonists,
the incidence of duodenal ulceration and the frequency of elective surgery for
the condition were falling. This trend has continued and now, in the West,
dyspeptic patients presenting with a duodenal ulcer at gastroscopy are
uncommon. In part, this may relate to the liberal prescription of gastric
antisecretory agents and eradication therapy for patients with dyspepsia.
Secondly, the peak incidence is now in a much older age group than previously
and, although it is still more common in men, the difference is less marked.
These changes, at least in part, mirror the changes in the epidemiology of H. pylori infection. A cohort effect can be demonstrated (Susser),
the age group in whom Helicobacter infection
was prevalent in the early part of the twentieth century was ageing and
suffering the complications of the infection late in life. This probable
relationship with H. pylori can also be
seen in relation gastric to ulceration and, indeed, gastric cancer. Similarly,
the incidence of perforation and bleeding duodenal ulcers in young and
middle-aged patients appears to be falling but, by contrast, there is currently
a marked increase in the numbers of elderly and
Pathology
Most occur in the first part of the duodenum (Figs 51.14 and 51.15). A chronic
ulcer penetrates the mucosa and into the muscle coat leading to fibrosis. The
fibrosis causes deformities such as pyloric stenosis. When an ulcer heals a
scar can be observed in the mucosa. Sometimes there may be more than one
duodenal ulcer. The situation in which there is both a posterior and an anterior
duodenal ulcer is referred to as ‘kissing ulcers’. Anteriorly placed ulcers
tend to perforate and, by contrast, posterior duodenal ulcers tend to bleed,
sometimes by eroding a large vessel such as a gastroduodenal artery.
Occasionally the ulceration may be so extensive that the entire duodenal cap is
ulcerated and devoid of mucosa. With respect to the giant duodenal ulcer,
malignancy in this region is so uncommon that under normal circumstances
surgeons can be confident that they are dealing with benign disease even though
from external palpation it may not appear so. In the stomach the situation is
different.
Histo pathology
Microscopically, destruction of the muscular
coat is observed and the base of the ulcer is covered with granulation tissue,
the arteries in this region showing the typical changes endarteritis obliterans.
Sometimes the terminations of nerves can be seen amongst the fibrosis. The
pathological appearances of the healing ulcer must be carefully interpreted as
some of the epithelial down-growths can be misinterpreted as invasion. This is
unlikely to be important in duodenal ulcers when malignancy rarely, if ever,
occurs but it is much more important with gastric ulcers.
Gastric ulcers
Incidence
As with duodenal ulceration, H.
pylori and NSAIDs are the important aetiological factors. Gastric ulceration
is also associated with smoking, other factors are of lesser importance.
There
are marked differences between the populations afflicted by chronic gastric
ulceration compared with duodenal ulceration. First, gastric ulceration is
substantially less common than duodenal ulceration. The sex incidence is equal
and the population with gastric ulcers tends to be older. It is more prevalent
in low socioeconomic groups and is considerably more common in the developing
world than in the West.
Pathology
This is essentially similar to that of a duodenal ulcer, except that gastric ulcers tend to be larger. Fibrosis, when it occurs, may result in the now rarely seen hour-glass contraction of the stomach. Large chronic ulcers may erode posteriorly into the pancreas and on other occasions into major vessels such as the splenic artery. Less commonly, they may erode into other organs such as the transverse colon. Chronic gastric ulcers are much more common on the lesser curve, especially at the incisura angularis (Figs 51.16 and 51.17), than the greater curve, and even when high on the lesser curve they tend to be at the boundary between the acid-secreting and the non acid-secreting epithelia. With atrophy of parietal cell mass nonacid-secreting epithelium migrates up the lesser curvature
Malignancy in gastric ulcers
Chronic duodenal ulcers are not associated
with malignancy and, by contrast, gastric ulcers are. Widely varying estimates
are made of the incidence of gastric malignancy in gastric ulcers. The reason
for this is that the authors reporting such diverse incidences are describing
different clinical situations. Two clinical extremes must be distinguished to
understand this problem properly. First, there is the situation in which a
benign chronic gastric ulcer undergoes malignant transformation. This is known
to happen, albeit rarely, and can be observed histologically in specimens in
which there are the classical histological features of benign gastric ulceration
associated with an area of malignant transformation. It is impossible to
estimate the incidence of such an occurrence but it is uncommon. The contrasting
clinical extreme is the patient identified as having an ulcer in the stomach,
either endoscopically or on contrast radiology, which is assessed as benign but
biopsies reveal malignancy. In this situation the patient does not have, and
probably never has had, chronic peptic ulceration in the stomach but has
presented with an ulcerated cancer. This situation is common, although whether a
lesion found in the stomach is described as being benign or malignant on
clinical grounds depends very much on the skill and experience of the
endoscopist or radiologist.
It
is fundamental that any gastric ulcer should be regarded as being malignant no
matter how classical the features of a benign gastric ulcer. Multiple biopsies
should always be taken, perhaps as many as 10 well-targeted biopsies, before an
ulcer can be tentatively accepted as being benign. Even then it is important
that further biopsies are taken whilst the ulcer is healing and when healed.
Modern antisecretory agents can frequently heal the ulceration associated with
gastric cancer but clearly are ineffective in treating the malignancy
itself. At operation even experienced surgeons may have difficulty
distinguishing between the gastric cancer and a benign ulcer. Operative
strategies differ so radically that it is essential, if at all possible, that a
confident diagnosis be made before operation. The patechial haemorrhages found
on the serosa of the patient with peptic ulceration are a useful sign but not entirely reliable. If, at
operation, it are determined that the ulcer is probably benign it should, none
the less, be excised, in totality if possible, and submitted for histological
examination. It is not known whether a patient’s survival is compromised by
this approach if the ulcer turns out to be malignant on biopsy as convincing
data are not available.
Other peptic
ulcers
Prepyloric gastric ulcers require special
mention. In terms of acid secretion they are similar to duodenal ulcers and in
the past have proved to be more difficult to treat, a problem overcome with the
advent of proton pump inhibitors. Pyloric channel ulcers are similar to duodenal
ulcers. Both prepyloric and pyloric ulcers may be malignant, and biopsy is
essential. Stomal ulcers occur after a gastroenterostomy or a gastrectomy of
the Billroth II type. The ulcer is usually found on the jejunal side of the
stoma.
Clinical
features of peptic ulcers
Whilst many textbooks try and create
differences in the clinical feature of gastric and duodenal ulceration, detailed
analysis has shown that they cannot be differentiated on the basis of symptoms.
Certainly, the demographic characteristics of groups of patients with gastric
and duodenal ulceration do differ but this does not allow discrimination.
Pain
The pain is epigastric, often described as
gnawing and may radiate to the back. Eating may sometimes relieve the
discomfort.
The pain is normally intermittent rather than intractable.
Periodicity
One of the classical features of untreated
peptic ulceration is periodicity. Symptoms may disappear for weeks or months to
return again. This periodicity may be related to the spontaneous healing of
the ulcer.
Vomiting
Whilst this occurs, it is not a notable
feature unless the stenosis has occurred.
Alteration in weight
Weight loss or, sometimes, weight gain may
occur. Patients with gastric ulceration are often underweight but this may
precede the occurrence of the ulcer.
Bleeding
All peptic ulcers may bleed. The bleeding may
be chronic and presentation with anaemia is not uncommon. Acute presentation
with haematemesis and melaena is discussed later.
Clinical
examination
Examination of the patient may reveal
epigastric tenderness but except in extreme cases (for instance gastric outlet
obstruction) there is unlikely to be much else to find.
Investigation
of the patient with suspected peptic ulcer
In the investigation of such patients,
imaging, preferably with flexible gastroduodenoscopy, is required.
Gastroduodenoscopy
This is the most sensitive investigation in
the management of suspected peptic ulceration and in the hands of a well trained
operator is highly sensitive and specific.
Treatment of
peptic ulceration
The vast majority of uncomplicated peptic
ulcers is treated medically. Surgical treatment of uncomplicated peptic ulceration
has decreased markedly since the 1960s and in the West is now seldom performed.
Surgical treatment was aimed principally at reducing gastric acid secretion and,
in the case of gastric ulceration, removing the diseased mucosa. When originally
devised medical treatment also aimed to reduce gastric acid secretion, initially
using the highly successful H2-receptor antagonist and subsequently
proton pump inhibitors. This has now largely given way to eradication therapy
Medical treatment
It is reasonable that a doctor managing a
patient with an uncomplicated peptic ulcer should suggest modifications to the
patient’s lifestyle, particularly the cessation of cigarette smoking. This
advice is rarely followed and pharmacological measures form the mainstay of
treatment.
H2-receptor
antagonists
H2 antagonists (Black)
revolutionised the management of peptic ulceration. Most duodenal ulcers and
gastric ulcers can be healed by a few weeks of treatment with these drugs
provided that they are taken and absorbed. There remained, however, a group of
patients who were refractory to conventional doses of H2-receptor
antagonists. This is largely now irrelevant as proton pump inhibitors can
effectively render a patient achlorhydric and all benign ulcers will heal using
these drugs. The problem with H2-receptor antagonists alone, as with
other gastric antisecretory agents, is that relapse is virtually inevitable once
treatment is discontinued.
Proton pump inhibitors
All ulcers will heal on proton pump
inhibitors, such as omeprazole, the majority within 2 weeks. Symptom relief is
impressively rapid, most patients being asymptomatic within a few days. Like H2
antagonists, omeprazole is safe and relatively devoid of serious side
effects. As with H2-receptor antagonists relapse following cessation
of therapy is almost universal.
Eradication therapy
Eradication therapy is now routinely given to
patients with peptic ulceration, and this is described earlier in this chapter.
Evidence suggests that if a patient has a peptic ulcer and H. pylon is the principal aetiological factor (essentially the
patient not taking NSAIDs) then complete eradication of the organism will cure
the disease and reinfection as an adult is uncommon. Eradication therapy is
therefore the mainstay of treatment with peptic ulceration. It is extremely
economical by comparison with prolonged courses of antisecretory agents or
surgery. It is also considerably safer than surgical treatment.
There
are some patients with peptic ulcers in whom eradication therapy may not be
appropriate and this includes patients with NSAID -associated ulcers. Such
patients should avoid these drugs if possible and if not they should be
co-prescribed with a potent antisecretory agent. Similarly, patients with Stomal
ulceration are not effectively treated with eradication therapy and require
prolonged prescription of antisecretory agents. Patients with Zollinger—
Ellison syndrome should be treated long term with omeprazole, unless the tumour
can be adequately managed by surgery.
Surgical
treatment of uncomplicated peptic ulceration
From its peak in the 1960s the incidence of
surgery for uncomplicated peptic ulceration has fallen markedly, to the extent
that peptic ulcer surgery is now of little more than historical interest. A
description of operations used in the treatment of peptic ulcers is still
necessary because surgery is
Operations for
duodenal ulceration
Duodenal ulcer surgery —
rationale
Procedures devised for the treatment of
duodenal ulcers have the common aim of excluding the damaging effects of acid
from the duodenum. This has been achieved by diversion of the acid away from the
duodenum, reducing the secretory potential of the stomach, or both. It has long
been known that patients with duodenal ulceration have higher than average
levels of gastric secretion. All of the operations devised achieved their aim to
some extent, but with varying degrees of morbidity, mortality and postoperative
side-effects. The operations are described in historical sequence.
Billroth II gastrectomy
The first successful gastrectomy was performed
by Billroth in January 1881 (Fig. 51.18) and Wolfer performed the first
gastroenterostomy in the same year. The original Billroth operations consisted
of a gastric resection with gastroduodenal anastomosis (Billroth I technique)
(Fig. 51.18). The Billroth II operation was devised more by accident than design
(Fig. 51.19).
A gastroenterostomy (Fig. 51.20) was performed on a gravely ill patient with a pyloric cancer who
was not expected to survive. Contrary to expectations the patient improved and
the stomach distal to the anastomosis was resected. It soon became evident that
the use of gastrojejunal anastomosis after gastric resection could be safer
and easier than the Billroth I procedure, and it became popular and effective in
the surgical treatment of duodenal ulcer. Because of its disadvantages, such as
higher operative mortality and morbidity, it has not been used for many years
in the patient with an uncomplicated ulcer but it is still used occasionally in
the treatment of a complicated ulcer with a ‘difficult’ duodenum. In
Billroth II gastrectomy, or its close relation Polya gastrectomy, the antrum and
distal body of the stomach are mobilized by opening the greater and lesser omentum
and dividing the gastroepiploic arteries, (right) gastric artery and the (left)
gastric artery arcade at the limit of the resection. The duodenum is closed off
either by suture or using staples, sometimes with difficulty in patients with a
very deformed duodenum. Various techniques are available to close the difficult
duodenum and in extremis
a catheter
may be placed in the duodenal stump, the duodenum closed around it and a
catheter brought out through the abdominal wall. Following resection the distal
end of the stomach is narrowed by the closure of the lesser curve aspect of the
remnant. The greater curve aspect is then anastomosed, usually in a retrocolic
fashion, to the jejunum leaving as short an afferent loop as feasible (Fig. 51.19).
Even when well performed this procedure has an operative mortality rate of a
few per cent and morbidity is not unusual. A common cause of morbidity is
leakage from the duodenal stump, which is particularly associated with kinking
of the afferent loop. Leakage from the gastrojejunal anastomosis is unusual
unless either it is under tension or the stomach has been devascularised
during the mobilisation. The incidence of side effects following gastrectomy is
considerable, as shown in Table 51.2.
Recurrence
of the ulcer at the stoma is uncommon but can occur, especially as this
procedure is traditionally not combined with the vagotomy.
Gastrojejunostomy
Because of the potential for mortality after
gastrectomy the use of gastrojejunostomy alone in the treatment of duodenal
ulceration was developed (Fig. 51.20).
Reflux
of alkali from the small bowel into the stomach reduced duodenal acid exposure
and was often successful in healing the ulcer. However, because the jejunal
loop was exposed directly to gastric acid stomal ulceration was extremely
common, hence the procedure in isolation was ineffective.
Truncal vagotomy and drainage
Truncal vagotomy was first introduced in 1943
by Dragstedt, and for many years this truncal vagotomy combined with drainage
was the mainstay in the treatment of duodenal ulceration. The principle of the
operation is that section of the vagus nerves, which are critically involved in
the secretion of gastric acid, reduces the maximal acid output by
approximately 50 per cent. This is similar to the effect of conventional doses
of H2-receptor antagonists. Because the vagal nerves are motor to the
stomach, denervation of the antro-pyloroduodenal segment results in gastric
stasis in a substantial proportion of patients on whom truncal vagotomy alone
is performed. This was first noted by Dragstedt who, when he first introduced
the operation, did not perform a drainage procedure.
In
performing truncal vagotomy the lower oesophagus is exposed by division of the
overlying peritoneum. By gentle blunt dissection the oesophagus, which should
contain a nasogastric tube, is encircled and slung with a tape. The posterior
vagal trunk can be felt as a tight cord posteriorly and is divided between
ligatures as it may be accompanied by blood vessels. On the front of the
oesophagus the anterior vagus consists of a plexus which is divided. The lower 7
cm of oesophagus should be completely cleared of nerve fibres to achieve an
adequate vagotomy (Fig. 51.21).
The
most popular drainage procedure is the Heineke—Mikulicz pyloroplasty (Fig.
51.22).
It is simple to perform and
involves the longitudinal section of the pyloric ring. This need not be an
extensive excision when performed in the elective situation. The incision is
closed transversely, usually with a single layer of interrupted sutures.
Gastrojejunostomy (Fig. 51.20) is the alternative drainage procedure to
pyloroplasty. This is performed through opening the lesser sac and an
anastomosis performed between the most dependent part of the antrum and the
first jejunal loop. An isoperistaltic anastomosis is most commonly performed.
The operation of truncal
vagotomy and drainage is substantially safer than gastrectomy (Table 51.2).
However, the side effects of surgery are, in fact, little different from
those that follow gastrectomy.
Selective vagotomy and drainage
In an attempt to reduce the side effects of
truncal vagotomy, selective vagotomy was developed. In contrast to truncal
vagotomy, where a complete vagal denervation is performed, in selective vagotomy
the hepatic and coeliac nerves are preserved but the stomach is still completely
vagally denervated. Drainage is required and, as this operation had all the
disadvantages of truncal vagotomy but not the merit of simplicity, it was
abandoned in favour of highly selective vagotomy.
Highly selective vagotomy
In 1968 Johnston and Amdrup independently
devised the operation of highly selective vagotomy in which only the parietal
cell mass of the stomach was denervated. This proved to be the most
satisfactory operation for duodenal ulceration with a low incidence of side
effects and acceptable recurrence rates when performed to a high technical
standard.
This operation became the gold standard for operations on duodenal ulceration
in the 1970s. The operative mortality was lower than any other definitive
operation for duodenal ulceration, in all probability because the gastrointestinal
tract is not opened during this procedure. The untoward effects of peptic ulcer
surgery are largely avoided, although loss of receptive relaxation of the
stomach does occur, leading to epigastric fullness and sometimes mild dumping.
However, the severe symptoms that occur after other more destructive gastric
operations do not occur. It is often said that recurrent ulceration is the
Achilles’ heel of this operation, although when performed well recurrence
should be no more common than after truncal vagotomy.
In
highly selective vagotomy the nerves of Latarjet supplying the antrum are
preserved and a complete neurovascular clearance of the proximal lesser curve is
carried out (Fig. 51.23).
This is
achieved by commencing the dissection from the anterior aspect and then opening
the lesser sac through the greater omentum to perform the posterior dissection.
Dissection is continued up to the oesophagogastric junction and the lower 7 cm
of oesophagus cleared of nerve fibres. Particular attention must be paid to the
nerve of Grassi which passes posteriorly to the greater curve, but the greater
curvature itself need not be cleared. Attention must also be given to
‘adhesions’ within the lesser sac as these may carry nerve fibres. Using
24-hour pH-monitoring studies it has been demonstrated that this operation will
achieve a reduction in the 24-hour intragastric acidity greater than can be
obtained with conventional doses of H2-receptor antagonists.
The
advent of laparoscopic surgery renewed some interest in the surgery for duodenal
ulceration but the technical difficulties in performing a full highly selective
vagotomy laparoscopically are considerable. For this reason some centres adopted
the procedure of anterior highly selective vagotomy and posterior truncal
vagotomy as an alternative. However, as surgery for uncomplicated duodenal
ulceration
Truncal vagotomy and antrectomy
For completeness this operation should be
mentioned as it was at one stage popular in the USA. In addition to a truncal
vagotomy, the antrum of the stomach is removed thus removing the source of
gastrin, and the gastric remnant joined to the duodenum. The recurrence rates
after this procedure are exceedingly low. However, the operative mortality
is higher than after vagotomy and drainage
(Table 51.2) and the incidence of unpleasant side effects is
similar.
Operations for
gastric ulcer
By contrast with duodenal ulcer surgery, where
the principal objective is to reduce duodenal acid exposure, in gastric
ulceration the diseased tissue is usually removed as well. This has the
advantage that malignancy can then be confidently excluded. Although levels of
gastric acid secretion are not abnormally high in the patients with gastric
ulceration, acid is still a prerequisite and hence operations to lower acid
secretion have been commonly employed.
Billroth I gastrectomy
This was the standard operation (Fig. 51.18) for gastric ulceration until medical treatments became prevalent. The distal stomach is mobilised and resected in the same way as in the Billroth II gastrectomy. This resection should include the ulcer that is usually situated on the lesser curve. The cut edge of the remnant is then partially closed from the lesser curve aspect leaving a stoma at the greater curve aspect which should be similar in size to the duodenum. Reconstruction may be facilitated by mobilising the duodenum using Kocher’s manoeuvre. The incidence of recurrent ulceration after this operation is low, but it carries with it the morbidity and mortality associated with any gastric resection.
Billroth II gastrectomy
This may be used for the high and lesser curve
gastric ulcer where a gastroduodenostomy is technically difficult.
Vagotomy, pyloroplasty and ulcer excision
Truncal vagotomy, drainage and ulcer excision
was developed because of the concerns about morbidity and mortality following
gastric resection for gastric ulcer. Highly selective vagotomy and gastric
excision has a similar rationale, although is much more favourable in terms of
side effects compared with truncal vagotomy and drainage. As with duodenal ulcers, most operations for
uncomplicated gastric ulcers are of historical significance.
The
complications of peptic ulceration
The common complications of peptic ulcer are
perforation, bleeding and stenosis. Bleeding and stenosis are considered below
in the relevant sections on ‘Haematemesis and melaena’ and ‘Gastric outlet
obstruction’.
Perforated
peptic ulcer
Epidemiology
Overall and despite the widespread use of
gastric antisecretory agents and eradication therapy, the incidence of
perforated peptic ulcer has changed little. There has, however, been a
considerable change in the epidemiology of perforated peptic ulcer 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 now perforations most commonly occur 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 recognisable (Fig. 51.24). 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. 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 self-limiting. 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 per cent of cases with perforated
peptic ulcer (Fig. 51.25).
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 water soluble contrast
swallow will show a free peritoneal leak. Diagnostic peritoneal lavage will
usually easily distinguish between perforation and pancreatitis, and a CT scan
will
Treatment
The initial priorities are resuscitation and
analgesia. Analgesia should not be withheld for fear of removing the signs of
an intra-abdominal catastrophe. If anything, adequate analgesia makes the
clinical signs more obvious. It is important, however, to titrate the analgesia
so that the patient is not rendered unconscious. Following resuscitation and the
diagnosis being established 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 employed. 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. 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 and in these patients a Billroth II gastrectomy is
a useful operation.
All
patients should be treated with systemic antibiotics and there may be some
advantage in washing out the abdominal cavity with tetracycline, 1 g in 1 litre
of isotonic saline. 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, most commonly nowadays surgery is
confined to first-aid measures and the peptic ulcer treated medically as
described earlier in this chapter. Following operation gastric antisecretory
agents should be started immediately.
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 closed by
intracorporeal suturing. Whatever technique is used it is important that the
stomach be kept empty postoperatively by nasogastric suction, and gastric
antisecretory agents commenced to promote healing in the residual ulcer.
A
great deal has been written about the conservative management of perforated
ulcer. Some writers say that virtually all patients can be managed
conservatively, whereas most
Patients
who have suffered one perforation may suffer another one. They should therefore
be managed aggressively to ensure that this does not happen. In patients with Helicobacter-associated
ulcers, eradication therapy is appropriate. Patients on NSAIDs, who now form
the majority of such patients, should have the drug withdrawn and another
analgesic substituted. If it is necessary to continue the NSAIDs the patient
should have concomitant treatment with a proton pump inhibitor such as
omeprazole.
Sequelae of
peptic ulcer surgery
There is a number of sequelae of peptic ulcer
surgery which include recurrent ulceration, small stomach syndrome, bilious
vomiting, early and late dumping, diarrhoea and malignant transformation.
These sequelae principally follow from the more destructive operations that are
now seldom performed. However, a substantial number of patients suffers from
side effects from operations undertaken in the past. Approximately 30 per cent
of patients can expect to suffer a degree of dysfunction following peptic ulcer
surgery, and in about 5 per cent of
such patients the symptoms will be intractable.
Recurrent ulceration
Although mentioned first, this is by far the
easiest problem to treat. Just as all peptic ulcers will heal with potent anti-secretory
agents so will ulcers that are recurrent after ulcer surgery. The incidence of
recurrent ulceration after the various operations is shown in Table 51.2.
The
recurrent ulcer normally presents with pain, although some may develop a
complication without any prior warning. Following an operation such as highly
selective vagotomy the ulcer is in a similar position to the original ulcer,
usually the first part of the duodenum. In patients with gastrojejunostomy,
recurrent ulcer will commonly be at the anastomosis but on the jejunal side.
Jejunal mucosa is much more sensitive to acid digestion compared with the
stomach. Similarly, following gastrectomy the recurrent ulcer will be normally
found on the jejunal side of the stoma.
A
number of factors has been convincingly related to the development of recurrent
ulceration. First and foremost, if the original operation was technically
inadequate, such as the vagotomy being incomplete, then the incidence of
recurrent ulceration is much higher. In this respect it is noteworthy that
recurrent ulceration after, for instance, highly selective
If
recurrent ulceration is diagnosed electively then long-term antisecretory agents
are probably the treatment of choice if the patient has had an anatomically
destructive operation. In patients with recurrent ulcer after highly selectively
vagotomy, then eradication therapy may be effective. As with other peptic
ulcers, recurrent ulcers may present with complications, particularly bleeding
and perforation. In this respect the complication of gastrojejunal colic fistula
requires a particular mention. In this rare condition the anastomotic ulcer
penetrates into the transverse colon. The patient suffers from diarrhoea that is
severe and follows every meal. They have foul breath and may vomit formed faeces.
Severe weight loss and dehydration are rapid in onset, and for this reason the
condition may be mistaken for malignancy. The major factor producing the
nutritional disturbance is the severe contamination of the jejunum with colonic
bacteria. A number of imaging techniques can be used to detect the flstula. A
barium enema will normally demonstrate the problem, and CT scanning is also
accurate. Endoscopy may not convincingly demonstrate the fistula and, in about
half of such cases, the barium meal will not reveal the problem. The treatment
of gastrocolic fistula consists of, first, correcting the dehydration and
malnutrition and then performing revisional surgery.
Small stomach syndrome
Early satiety follows most ulcer operations to
some degree, including highly selective vagotomy. In this latter circumstance,
although there is no anatomical disturbance of the stomach there is loss of
receptive relaxation. Fortunately, this problem does tend to get better with
time and revisional surgery is not necessary.
Bile vomiting
Bile vomiting can occur after any form of
vagotomy with drainage or gastrectomy. Commonly, the patient presents with
vomiting a mixture of food and bile or sometimes some bile alone after a meal.
Often eating will precipitate abdominal pain and reflux symptoms are common.
Bile chelating agents can be tried but are usually ineffective. In intractable
cases revisional surgery may be indicated. The nature of that revisional
surgery depends very much on the original operation. Following gastrectomy
Roux-en-Y diversion is probably the best treatment. In patients with a
gastroenterostomy, this can be taken down and in most circumstances a small
pyloroplasty performed. In patients with a pyloroplasty, reconstruction of the
pylorus has been attempted but in general terms the results of this operation
have been rather poor. Antrectomy and Roux-en-Y reconstruction may be the better
option.
Early and late dumping
Although considered together because the
symptoms are similar, early and late dumping have different etiologies (Table
51.3). A common feature, however, is early rapid gastric emptying. Many patients
have both early and late dumping.
Early dumping.
Early dumping consists of abdominal and vasomotor symptoms that are
found in about 10 per cent of patients following gastrectomy or vagotomy and
drainage. It also affects a few per cent of patients following highly selective
vagotomy due to the loss of receptive relaxation of the stomach. The small bowel
is filled with foodstuffs from the stomach which have a high osmotic load and
this leads to the sequestration of fluid from the circulation into the
gastrointestinal tract. This can be observed by the rise in the packed cell
volume while the symptoms are present. All of the symptoms shown in Table 51.3
can be related to this effect on the gut and the circulation.
Treatment.
The
principal treatment is dietary manipulation. Small dry meals are best, and
avoiding fluids with a high carbohydrate content also helps. Fortunately, with
time following operation the syndrome tends to improve. For some reason,
however, there is a group of patients who suffer intractable dumping regardless
of any of these measures. The somatostatin analogue octreotide given before
meals has been shown to be useful in some individuals and the long-acting
preparation may also be useful. However, this treatment can lead to the
development of gallstones and it does not help the diarrhoea from which many
patients with dumping also suffer.
Revisional
surgery may be occasionally required. In patients with a gastroenterostomy, the
drainage may be taken down or, in the case of a pyloroplasty, repaired.
Alternatively, antrectomy with Roux-en-Y reconstruction is often effective,
although the procedure is of greater magnitude. Following gastrectomy it is the
revisional procedure of choice.
Late dumping.
This is reactive hypoglycaemia. The carbohydrate load in the small
bowel causes a rise in the plasma glucose which in turn causes insulin levels to
rise causing a secondary hypoglycaemia. This can be easily demonstrated by
serial measurements of blood glucose in a patient following a test meal. The
treatment is essentially the same as for early dumping. Octreotide is very
effective in dealing with this problem.
Postvagotomy diarrhoea
This can be the most devastating symptom to
afflict patients having peptic ulcer surgery. Most patients will suffer some
looseness of bowel action to some degree (with the exception of highly selective
vagotomy) but in about 5 per cent it
may be intractable. In spite of much investigation the precise etiology of the
problem is uncertain. It is related, to some degree, to rapid gastric emptying.
In all probability, the denervation of the upper gastrointestinal tract as a
result of the vagotomy is also important. Exaggerated gastrointestinal peptide
responses may also aggravate the condition.
The
diarrhoea in postvagotomy patients may take several forms. It may be severe and
explosive, the patient experiencing a considerable degree of urgency. The
patients sometimes describe the diarrhoea as feeling like passing boiling water.
At the other extreme some patients only have minor episodes of diarrhoea which
are not as directly related to food.
Many
authors regard diarrhoea and dumping as being essentially the same problem.
However, many patients with severe diarrhoea do not have any of the other
symptoms of dumping, and likewise some patients with dumping do not experience
any significant diarrhoea.
The
condition is difficult to treat. The patient should be managed as for early
dumping and antidiarrhoeals may be of some value. Octreotide is not effective in
this condition and the results of revisional surgery are too unpredictable to
make this an attractive treatment option.
Malignant transformation
Many large studies now confirm that operations
such as gastrectomy or vagotomy and drainage are independent risk factors for
the development of gastric cancer. The increased risk appears to be
approximately four times compared with the control population. It is interesting
to note that this phenomenon is seen only in areas with already a significant
incidence of gastric cancer; in areas such as Scandinavia with a low incidence
it is difficult to observe such a phenomenon.
It
is not difficult to understand the increased incidence of gastric cancer as bile
reflux gastritis, intestinal metaplasia and gastric cancer are linked. The lag
phase between operation and the development of malignancy is at least 10 years
Highly selective vagotomy does not seem to be associated with an increased
incidence of gastric cancer in the long term.
Nutritional consequences
Nutritional disorders are more common after
gastrectomy than after vagotomy and drainage. Weight loss is common after
gastrectomy and the patient may, in fact, never return to their original weight.
Nutritional advice advising the taking of small meals is often more useful.
Anaemia may be due to either iron or B12 deficiency.
Iron
deficiency anaemia occurs after both gastrectomy and vagotomy and drainage and
is probably multifactorial in origin. Reduced iron absorption is probably the
most important factor, although the loss of blood from the gastric mucosa may
also be important. B12 deficiency is prone to occur after total
gastrectomy. However, because of the very large B12 stores that most
patients have, this may be very late in occurring. B12 supplementation
after total gastrectomy is, however, sensible. B12 deficiency may
rarely occur after lesser forms of gastrectomy. In such patients the cause is
probably a combination of reduced intrinsic factor production and also the fact
that some patients have bacterial colonisation which results in the destruction
of the B12 in the gut.
Bone
disease is seen principally after Polya gastrectomy and mainly in women. The
condition is essentially indistinguishable from the osteoporosis commonly seen
in post-menopausal women. It is only the frequency and magnitude of the disorder
that distinguish it. Treatment is by dietary supplementation, with calcium and
vitamin D, and exercise.
Gallstones
The development of gallstones is strongly
associated with truncal vagotomy. Following truncal vagotomy the biliary tree,
as well as the stomach, is denervated leading to stasis and, hence, stone
formation. Patients developing symptomatic gallstones will require
cholecystectomy. This, however, may induce or worsen other postpeptic ulcer
surgery syndromes such as bilious vomiting and postvagotomy diarrhoea.