In acute upper gastrointestinal haemorrhage, gastroscopy is almost mandatory, as described in Chapter 19. Gastroscopy can identify the site of the bleeding and is particularly useful if gastro-oesophageal varices are suspected to be the source of bleeding but are found not to be. Gastroscopy also allows recognition of features which can help stratify patients into low or high risk of rebleeding and it provides an important means of treating bleeding sites by injection of vasoconstrictors or sclerosants.

Contrast radiology

Contrast radiography of the upper gastrointestinal tract is used largely to determine swallowing function, to define anatomy, particularly with large hiatus hernias, and to give an idea of the effectiveness of gastric emptying. It involves the patient swallowing barium suspension (barium meal). During the investigation, the patient is tilted and rolled in various directions to demonstrate the whole region of interest. Effervescent tablets are given to produce gaseous distension of the stomach and duodenum and spread the contrast in a thin, even layer over the mucosal surface. This standard double contrast technique improves the imaging of mucosal detail.

Presenting features of peptic ulcer disease

The various ways in which peptic inflammation affects the oesophagus, stomach and duodenum are summarised in Table 21.1.

Table 21.1

Clinical consequences of peptic ulcer disease in different anatomical sites

Epigastric pain (usually described as ‘boring’, ‘gnawing’ or ‘burning’) is the principal presenting symptom and is common to peptic disorders whatever the site. Pain is often accompanied by other forms of discomfort, often described by the patient as ‘indigestion’ or ‘dyspepsia’. A more specific description may suggest particular diagnostic entities. Retrosternal pain (‘heartburn’) and bitter regurgitation (‘waterbrash’) suggests reflux oesophagitis. Nausea or vomiting, anorexia (loss of appetite) and abdominal fullness or bloating are common in gastric ulcer and pyloric stenosis, but may also occur in a variety of other upper gastrointestinal disorders, e.g. gallstone disease and irritable bowel syndrome.

The relationship of symptoms to food intake may help to distinguish gastric from duodenal ulceration; gastric ulcer pain is typically exacerbated by food and duodenal ulcer pain relieved by it.

Peptic ulcers may be virtually asymptomatic, particularly those caused by NSAIDs. Diagnosis may then only occur on acute presentation with bleeding or perforation or on investigation of iron deficiency anaemia.

Non-acute presentations of peptic ulcer disease

Peptic disorders of the oesophagus

All peptic disorders of the oesophagus are associated with reflux of gastric contents. These disorders range from mild reversible inflammation, through moderate acute inflammation with superficial ulceration (reflux oesophagitis), to severe persistent inflammation which may lead to fibrotic scarring and stenosis (see Fig. 21.3) and sometimes chronic peptic ulceration. In many patients, reflux is associated with hiatus hernia (see Ch. 22).

On gastroscopy, reflux oesophagitis is characterised by mucosal reddening and, in more severe cases, by typical linear superficial ulceration (see Fig. 21.4). Peptic strictures occur in the distal oesophagus and are usually located just above the oesophago-gastric junction, which itself often lies above the diaphragm because of inflammatory shortening of the oesophagus. The normal oesophago-gastric junction is about 40 cm from the incisor teeth when seen on endoscopy. Specialised intestinal metaplasia, dysplasia and carcinoma must be excluded by biopsies because the visual appearances may not be characteristic. Occasionally, a deep chronic ulcer occurs in the lower oesophagus; this looks and behaves like an often linear gastric or duodenal ulcer. When squamous oesophageal epithelium is repeatedly damaged by reflux, it may be replaced by metaplastic columnar epithelium. This is known as Barrett’s oesophagus and there is strong evidence that it predisposes to malignant change. If found, it should be biopsied to exclude dysplasia. When dysplasia is severe, there is about a 1% annual risk of malignant change and endoscopic resection or surgery is necessary. Standard protocols are usually employed for surveillance of Barrett’s oesophagus with repeated endoscopy every 2–3 years.

Peptic disorders of the stomach

Peptic disorders of the stomach range from mild inflammation (gastritis) to chronic gastric ulcers and most often occur in the antral region and along the lesser curve beyond the incisura.

Chronic gastric ulcers must be distinguished from malignant ulcers. The site may aid recognition of a benign ulcer, but carcinoma may occur in any part of the stomach, with the region of the gastro-oesophageal junction now the most common. Malignancy can only be excluded by histological examination of multiple representative biopsies taken from around the ulcer circumference (not the base). In most cases, carcinoma probably arises de novo but occasionally a benign ulcer may undergo malignant transformation.

Gastritis: Gastritis appears as widespread reddening of the mucosa. If biliary reflux from the duodenum into the stomach is evident, the condition is sometimes referred to as ‘biliary gastritis’ on the assumption that it is caused by the irritant effect of biliary and pancreatic secretions. Acute gastritis, often caused by alcohol (chronic alcoholism or single alcoholic binges) or aspirin/NSAID ingestion, can cause symptoms of sufficient severity to warrant gastroscopy. The mucosa often exhibits patchy shallow ulceration (erosive gastritis) and is friable and easily traumatised, causing bleeding.

Stress ulcers: Acute ‘stress’ ulcers are single or multiple small discrete superficial lesions that may develop rapidly in seriously ill patients, often in intensive care units. The condition may be a complication of extensive burns, systemic sepsis (possibly via visceral hypoperfusion), multiple trauma, major head injuries, uraemia or terminal illness. Stress ulcers typically present with haemorrhage (haemorrhagic gastritis), which is sometimes catastrophic, and occasionally with perforation. There is minimal mucosal inflammation around the ulcers and the aetiology may be primarily mucosal ischaemia rather than peptic. The risk of this life-threatening complication can be minimised in vulnerable patients by prophylactic treatment with proton pump inhibitors.

Chronic gastric ulceration: Chronic gastric ulcers vary greatly in size but the majority are small (less than 2 cm in diameter). Giant ulcers (up to 10 cm) are occasionally seen in the elderly; if posteriorly situated, they may erode through the stomach wall, obliterating the lesser sac and adhering to the surface of the pancreas. In these cases, the ulcer base or floor is composed of pancreatic tissue and erosion may cause catastrophic haemorrhage.

Benign gastric ulcers are typically regular in outline with a base consisting of white fibrinous slough. The ulcer gives the impression of having been punched out of the gastric wall, and there is no heaping-up of the mucosal margin as seen in malignant ulcers. The surrounding mucosa is surprisingly normal, although there may be radiating folds resulting from chronic fibrotic contractures. The typical endoscopic appearance of a gastric ulcer is shown in Figure 21.5a.

Fig. 21.5 Peptic ulcers
(a) Lesser curve benign gastric ulcer as seen through a gastroscope. At the original examination, the ulcer could be viewed from several directions and biopsies taken of the edge to exclude malignancy. (b) Photograph taken at emergency laparotomy for bleeding duodenal ulcer. The pylorus has been opened longitudinally and a deep chronic posterior ulcer crater is identified (arrowed). Thrombus T overlying an eroded artery is visible. A bleeding artery in the ulcer crater was under-run with sutures to arrest the haemorrhage

Case History

Fig. 21.3 Peptic stricture of the oesophagus
(a) A barium swallow in a 60-year-old woman who complained of burning retrosternal pain when lying flat (present for several years) and the recent onset of pain and difficulty when swallowing solid foods. The X-rays show the lower end of the oesophagus O and stomach St, part of which lies above the level of the diaphragm (position arrowed), forming a sliding hiatus hernia H. There is a tight stenosis in the last 2 cm of the oesophagus due to a peptic stricture S. (b) At greater magnification, barium can be seen filling the crater of a chronic peptic ulcer U immediately above the stricture

Peptic disorders of the stomach typically cause severe, often disabling, epigastric pain which tends to be exacerbated by food, especially if acidic or spicy. The pain may be so severe that patients lose weight and develop a fear of food. Symptoms tend to persist for weeks or months, fluctuating in intensity and then disappearing completely, only to recur weeks or months later. Symptoms are a poor guide to disease activity or response to treatment. Indeed, major ulcers may be silent. Both can be monitored only by repeated gastroscopy until healing. A rare complication of peptic disease is perforation of a gastric ulcer into the transverse colon. The resulting gastro-colic fistula causes true faecal vomiting.

Peptic disorders of the duodenum

Duodenitis: Duodenitis, a non-ulcerative form of duodenal inflammation, has a similar endoscopic appearance to gastritis. It is commonly discovered in patients suspected of having duodenal ulceration, and probably represents a mild form of peptic disease.

Case History

Fig. 21.4 Reflux oesophagitis
Gastroscopic view of the lower end of the oesophagus in a woman of 62 with a long history of reflux. Note the patchy ulceration U and the irregular fibrotic cardia caused by recurrent ulceration and attempts at healing. Further scarring may cause stricture formation

Chronic duodenal ulceration: Chronic duodenal ulcers almost exclusively occur in the pyloric channel and the first part of the duodenum. The latter area is known endoscopically as the ‘duodenal bulb’ and radiologically as the ‘duodenal cap’. On endoscopy, duodenal ulcers have a range of appearances similar to chronic gastric ulcers. There is usually a single ulcer but two or more ulcers at one time are common (‘kissing ulcers’ occur on opposing walls of the duodenum). Malignancy is very rare in the duodenal bulb, so biopsy of the ulcer for this purpose is seldom necessary; biopsy of the gastric antrum for confirmation of H. pylori infections is, however, indicated. The endoscopic characteristics of a duodenal ulcer are shown in Figure 21.6.

Duodenal ulcer symptoms follow the same general pattern as gastric ulcer but with important exceptions. The pain tends to appear several hours after a meal (‘hunger pain’) and is relieved by eating. A typical history includes episodic early morning waking (often around 2 a.m.) with epigastric pain; this pain is relieved by drinking milk and eating bland foods. Consequently, undiagnosed patients tend to gain weight from the increased intake of food and milk. This is in contrast to the weight loss often associated with gastric ulcer. Symptoms in duodenal ulcer are more useful as a guide to disease activity and response to treatment than in gastric ulcer.

Management of chronic peptic ulcer disease

Both the nature and the management of peptic ulcer disease have undergone extraordinary changes over the past four decades. Back then, medical management was relatively ineffective and was largely confined to simple antacid drugs, bland diets and bed rest. The only definitive treatment was major surgery and it was widely employed, often after a long period of chronic symptoms. Surgery was deferred as long as possible in the hope of spontaneous remission, and patients often had to ‘earn’ their operations by years of suffering! Partial gastrectomy offered the best cure rate and was thus the most common operation despite its mortality of 2–10% and its serious long-term complication rate. Later, various versions of surgical vagotomy were shown to be almost equally effective, but with fewer complications.

The principles of modern management of peptic disorders are summarised in Box 21.1.

Box 21.1 Principles of management of peptic disorders

Control of predisposing or aggravating causes

• Modify diet, reduce alcohol intake, cease smoking, avoid irritant and ulcer-provoking drugs (aspirin and other NSAIDs), avoid stress, reduce oesophageal reflux by losing weight and attention to posture

Elimination of proven H. pylori infection

• Combined therapy with anti-acid and antibiotic combinations

Diminishing of irritant effects of acid–pepsin

• Simple antacid drugs, alginate preparations, liquorice derivatives, bismuth preparations

Administration of mucosal protective agents

• Sucralfate

Reduction of acid secretion

• H₂-receptor-blocking drugs (cimetidine, ranitidine), proton pump inhibitors (PPIs, e.g. omeprazole), surgical vagotomy (rarely employed nowadays)

Surgical removal of intractable ulcers and gastrin-secreting tissue

• Partial gastrectomy

Correction of secondary anatomical problems

• Dilatation of oesophageal strictures, operations for pyloric stenosis and hiatus hernia

Control of predisposing or aggravating causes: The patient’s history may reveal adverse factors which can be easily eliminated. These are summarised at the start of Box 21.1. Radical dietary modification is unnecessary; patients should merely be advised to avoid food which they find aggravates the symptoms. Spicy or acidic foods are often blamed.

Case History

Fig. 21.6 Duodenal ulceration
Endoscopic view of lesser curve gastric ulcer. This ulcer has probably only been present for about 4 months. It does not show surrounding scarring and distortion of the gastric wall that would be characteristic of longstanding ulcers

Aspirin and other NSAIDs should be avoided, although this is often difficult in patients with arthritic disorders. The ulcerogenic effect of these drugs is directly proportional to their effectiveness and relates largely to their systemic anti-cyclooxygenase (COX1) activity, an agent protective of gastro-duodenal mucosa. There is therefore little to be gained from changing drugs within the group or by using them in enteric-coated or suppository form. If NSAIDs cannot be avoided in patients with a predisposition to peptic ulceration, concurrent use of cytoprotective drugs may be indicated.

Patients with oesophageal reflux, especially if associated with hiatus hernia, can minimise the damage by simple mechanical measures such as losing weight, elevating the head end of the bed and being aware of posture in daily activities.

Elimination of proven H. pylori infection: Once H. pylori has been confirmed, treatment involves a course of acid inhibition combined with antibiotic treatment. Eradication usually produces long-term ulcer remission, and H. pylori reinfection is rare. A triple regimen including a proton pump inhibitor (e.g. omeprazole) and two antibiotics (clarithromycin plus either amoxicillin or metronidazole) given for 1 week eliminates Helicobacter in over 90% of cases, although increasingly strains of H. pylori are demonstrating antibiotic resistance and local antibiotic protocols should be followed. Longer courses give potentially higher elimination rates but produce more side-effects and lower compliance. Confirmation of eradication can be achieved by re-endoscopy and rapid urease testing (Fig. 21.7), or by breath testing.

Fig. 21.7 Proprietary urease testing kit for H. pylori
Biopsies of gastric or duodenal mucosa are placed in the well and the result read after a set period. A positive result is indicated by the colour change seen here in (b)

Diminishing of irritant effects of acid–pepsin: An array of proprietary antacid preparations is available over the counter and on prescription. When used assiduously, they promote ulcer healing almost as effectively as any other drug, although more slowly. They all utilise a few main active ingredients. Sodium bicarbonate offers rapid but temporary relief of symptoms, while magnesium trisilicate or aluminium hydroxide promotes ulcer healing. Some of these agents, however, interfere with proton pump inhibitors. Colloidal bismuth compounds have been in use for many years. They have an antacid action and have been found to be active against H. pylori.

Alginate preparations form a foamy layer on the surface of gastric contents, coating the upper stomach and lower oesophagus and protecting it from oesophageal reflux.

Administration of mucosal protective agents: Sucralfate is a complex of aluminium hydroxide and sulphated sucrose that is minimally absorbed from the gastrointestinal tract. It is believed to act by binding to denuded areas of mucosa and protecting them from acid–pepsin attack. It has been shown to be as effective as H₂-blockers in providing symptom relief and healing when given in the dose of 2 g twice daily. It does not interfere with other drugs and is safe in pregnancy. It is also effective for preventing stress ulcers in seriously ill patients.

Reduction of acid secretion: Acid secretion by the gastric mucosa is normally controlled by two mechanisms:

• Direct cholinergic stimulation of parietal cells mediated via the vagus nerve. This is under reflex control originating in the cerebral cortex triggered by the sight and taste of food

• Gastrin is secreted by APUD cells in the gastric antrum and promotes acid secretion via histamine released from mast cells in the vicinity of the parietal cells. The histamine receptors on the parietal cells are distinct from those elsewhere in the body and are designated as type 2 (H₂) receptors; these receptors are not blocked by standard ‘antihistamine’ drugs such as chlorphenamine. Gastrin secretion is partly controlled by the vagus and partly by local (vagally independent) reflexes initiated by gastric distension and the presence of food or alcohol in the stomach

From this, two practical methods have been found to reduce acid secretion: drugs which selectively block H₂-receptors or the proton pump mechanism (described earlier), and surgical division of the vagus nerve.

H₂-receptor blockade and proton pump antagonists: H₂-receptor blocking drugs were developed in the 1970s and were the first ‘medical’ revolution in the management of peptic disorders. Cimetidine was the first but was joined by ranitidine, which has a few minor advantages but is no more effective for healing ulcers. H₂-receptor antagonists are highly effective in reducing gastric acid secretion. Symptomatic response is rapid, usually within a day or two, and healing follows within a few weeks in 70–90% of cases. Recurrence rates, however, are high even with maintenance therapy, with 50–75% of patients developing further symptoms within 2 years.

A newer group of drugs, the substituted benzimidazoles, are extremely potent and reduce acid production to near zero by direct inhibition of the proton pump. Omeprazole and other variants are now often the first line treatment for most peptic ulcer disorders. In all cases where H. pylori infection is present, the use of these drugs must be combined with eradication antibiotic therapy.

Vagotomy: Vagotomy was first performed in the 1920s and popularised by Dragstedt from 1943. It gradually superseded classic partial gastrectomy as the surgical treatment of choice for chronic duodenal ulcer. The vagotomy operations illustrated in Figure 21.8 are now only of historical interest. The simplest involved dividing the anterior and posterior vagal trunks close to the abdominal oesophagus just below the diaphragm (truncal vagotomy). The operation is effective in promoting ulcer healing but paralyses gastric motility and slows pyloric emptying. A surgical drainage procedure, usually pyloroplasty (‘V & P’), or less commonly gastro-jejunostomy, was therefore a necessary part of the operation.

Fig. 21.8 The vagotomies and gastric drainage procedures (rarely performed nowadays but of historical interest)
(a) Truncal vagotomy is followed by a drainage procedure, either pyloroplasty (Heinecke–Mikulicz is illustrated) or gastro-jejunostomy. In gastro-jejunostomy an anastomosis is created to the most dependent part of the stomach; a short efferent loop of jejunum is brought up either in front of the transverse colon and sutured to the anterior wall of the stomach (antecolic), or behind the transverse colon via an incision in the mesocolon and sutured to the posterior wall of the stomach (retrocolic). (b) Highly selective vagotomy does not require a drainage procedure. Only the parietal cell mass is denervated, preserving the innervation of the pylorus and antrum plus the rest of the abdominal viscera

Attempts to reduce the gastric emptying complications of truncal vagotomy led to operations designed to preserve the innervation of the distal antrum and pylorus whilst denervating the proximal acid-secreting portion of the stomach. Highly selective vagotomy preserved the nerves of Latarjet and avoided the need for a gastric drainage procedure. Early postoperative side-effects were fewer but ulcer recurrence rates were higher than for truncal vagotomy.

Surgical removal of intractable ulcers and gastrin-secreting tissue: Partial gastrectomy was occasionally used for patients where medical management had failed to heal a benign gastric ulcer or to treat repeated recurrences. The operation had the dual role of removing the ulcer and the gastrin-secreting mucosa. The classic gastrectomy for chronic gastric ulcer was known as the Billroth I type (Billroth, 1881) and involved removing the distal two-thirds of the stomach. The gastric remnant was then anastomosed to the first part of the duodenum (see Fig. 21.9).

Fig. 21.9 Types of partial gastrectomy formerly performed for peptic ulcer disease

The standard partial gastrectomy for duodenal ulcers was a Polya-type gastrectomy (Polya, 1911), also involving resection of the distal two-thirds of the stomach but anastomosing the cut end of the stomach to the side of a loop of proximal jejunum (gastro-jejunostomy). This is also known as a Billroth II operation. The cut end of the duodenum (duodenal stump) was closed and the ulcer left in situ to heal (see Fig. 21.9). Numerous variations on gastrectomy have been described over the years, but the essential difference is whether the gastric remnant is anastomosed to the duodenum (Billroth I-type) or to a jejunal loop (Polya-type).

In general, partial gastrectomy was highly effective in relieving symptoms and preventing recurrence of peptic disease, but long-term side-effects were a serious problem affecting 30–40% of patients.

Complications and side-effects of partial gastrectomy: The main complications of partial gastrectomy occur in the long term and may not become manifest for years (see Box 21.2). Recurrent ulceration after partial gastrectomy was rare and occurred in the gastric remnant or at the stomal margin. The usual reason was that insufficient stomach had been removed, but occasionally malignant change was responsible (3% risk over 15 years). Abnormally high acid production was another cause, sometimes due to Zollinger–Ellison syndrome or hyperparathyroidism.

Box 21.2 Side-effects of partial gastrectomy

• Inability to eat normal-sized meals due to reduced gastric capacity

• ‘Dumping’ due to rapid emptying of stomach contents—common but most patients adapt with time

• Episodic bilious vomiting due to reflux of bile into stomach via the anastomosis

• Tendency to bolus obstruction of the gastric outlet stoma

• Weight loss due to a combination of above factors and malabsorption—especially common in women

• Vitamin B₁₂ deficiency due to loss of gastric intrinsic factor; may present as macrocytic anaemia or subacute combined degeneration of the spinal cord—potentially catastrophic, occurring many years after operation and preventable by regular vitamin B₁₂ (hydroxycobalamin) injections

• Iron deficiency anaemia due to reduced iron absorption—common but easily prevented by taking iron tablets, e.g. once weekly

• Malignant change in gastric remnant possibly due to bacterial production of carcinogens—rare

Correction of secondary anatomical problems: The main anatomical problems secondary to peptic disease are oesophageal stricture and pyloric stenosis.

Oesophageal strictures can usually be managed by periodic dilatation and medical or surgical treatment of the underlying cause. With the patient intravenously sedated, a guide-wire is inserted across the stricture endoscopically, and then metal, plastic or balloon dilators are inserted over it. Occasionally, reflux continues to cause damage and stricturing; it may then become necessary to perform anti-reflux surgery.