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 treatment with either gastric antisecretory agents or, in the past, elective surgery. Although other factors exist, and multi­ple other factors may be involved in transition between the superficial and the deep penetrating chronic ulcer, they are of lesser importance.

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 often infirm patients suffering these complications. This latter trend can be explained not only by the H. pylori cohort effect but also by the increased use of NSAIDs in the elderly. In Eastern Europe the disease remains common and, from having been uncommon in some developing nations, it is now observed more frequently. Again, the relationship with H. pylori appears compelling.

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. In the stomach any abnormal lesion should be multiply biopsied, and in the case of a suspected benign gastric ulcer numerous biopsies must be taken in order to exclude, as far as possible, the presence of a malignancy. Commonly biopsies of the antrum will be taken to see whether there is histologi­cal evidence of gastritis and a CLO test performed to deter­mine the presence of H. pylori. A ‘U’ manoeuvre should be performed to exclude ulcers around the gastro-oesophageal junction. This is important as the increasing incidence of cancer at the gastro-oesophageal junction requires that all mucosal abnormalities in this region should undergo multiple biopsy. Similarly, if a stoma is present, for instance after gastroenterostomy or Billroth II gastrectomy, it is important to enter both afferent and efferent loops. Almost all stomal ulcers will be very close to the junction between the jejunal and gastric mucosa. Attention should be given to the pylorus to note whether there is any prepyloric or pyloric channel ulceration and also whether it is deformed, which is often the case with chronic duodenal ulceration. In the duodenum care must be taken to view all of the first part. It is not infrequent for an ulcer to be just beyond the pylorus and easily overlooked.

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 commonly employed for the complicated ulcer and, in addi­tion, many patients are left suffering from the consequences of the more destructive operations.

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 is to all intents and purposes unnecessary, there is now little interest in developing operations further. 

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 normally be diagnostic in both conditions, although this is seldom necessary.

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 surgeons have difficulty in understanding how a patient who is ill with widespread peritonitis and who has food debris widely distributed through the abdominal cavity will improve without an operation. However, there are undoubtedly patients who have small leaks from perforated peptic ulcer and relatively mild peritoneal contamination who may be managed with intravenous fluids, nasogastric suction and antibiotics. These patients are in the minority.

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 vagotomy is highly surgeon dependent. Cigarette smoking has been convincingly associated with an increased incidence of recurrent ulceration, and it has been shown that patients who had ulcers that are resistant to treatment with pharmacological agents before operation are more likely to develop recurrence afterwards.

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.