At least 80% of peptic ulcers occur in the duodenum.
Duodenal ulcers may occur at any age, but especial- ly in the thirties to forties; about 80% occur in men.
Women are relatively immune to duodenal ulceration before menopause and especially during pregnancy.
Gastric ulcers occur predominantly in men, but the sex preponderance is less marked – about 3:1 for men to women. Any age may be affected, but especially the forties to fifties (i.e. a decade later than the peak for duodenal ulceration).
Clinical features
Physical signs in the uncomplicated case are absent or confined to epigastric tenderness. Clinical diagno- sis depends on a careful history.
The pain is typically epigastric, occurs in attacks that last for days or weeks and is interspersed with pe- riods of relief. Pain that radiates into the back suggests a posterior penetrating ulcer. Peptic ulcer pain may come on immediately after a meal but more typically commences about 2 h after, so that the patient says it precedes a meal (‘hunger pain’). Characteristically, it wakes the patient in the early morning, so much so that the patient may adopt the habit of taking a glass of milk or an alkali preparation to bed. However, it is a myth to say that one can differentiate between a gas- tric and a duodenal ulcer merely on the time relation- ship of the pain. The pain is aggravated by spicy foods and relieved by milk and alkalis, although the relief is lost in deep and penetrating ulcers. There may be associated heartburn, nausea and vomiting. The pa- tient may lose weight because of the pain produced by food but often may gain weight because of the high intake of milk.
Special investigations
• Fibreoptic endoscopy: enables the oesophagus, stomach and duodenum to be examined. The ul- cer can be identified and, particularly in the case of a gastric lesion, biopsy material obtained to en- able differentiation between a benign and malig- nant ulcer.
• H. pylori detection.
– Endoscopic biopsy. Histological examination will confirm the presence of the organism and identify mucosal damage. A urease test, in which a biopsy sample is placed in a solution of urea together with a pH indicator, is highly
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The stomach and duodenum specific and sensitive for the organism. H.pylori splits urea, releasing ammonia, which changes the pH of the solution.
– 13C-labelled urea breath test. The patient in- gests a solution containing 13C-labelled urea (non-radioactive). The urease from the organ- ism cleaves the urea load and bicarbonate (HCO3−) is released into the blood and expired as 13CO2. Measurement of labelled CO2 in breath samples taken before and after inges- tion of the urea solution confirms the diag- nosis, and serial tests can be used to confirm eradication of the organism.
– Serological testing. Infection with H. pylori re- sults in generation of antibodies, which may be detected. Antibody titre falls slowly after eradi- cation.
• Faecal occult blood examination is often positive in the presence of an ulcer.
Treatment
Treatment of a peptic ulcer is medical in the first instance; surgery is indicated when complications supervene. The complications are chronicity, perfo- ration, stenosis, haemorrhage and, in the case of gas- tric ulcer, malignant change. They are considered in detail later in this chapter.
Principles of medical treatment
The main principles of treatment are to eradicate H. pylori and to reduce and neutralize (using alka- lis and milk) acid secretion. Failure to eradicate H.
pylori by giving antacid therapy alone results in high relapse rates.
• H. pylori eradication. A 2-week course of antimi- crobial therapy combined with acid reduction therapy will eradicate H. pylori. Acid reduction is usually afforded by a proton pump inhibitor (e.g. omeprazole, lanzoprazole) and the antimi- crobial therapy is based on either clarithromycin or amoxicillin, together with metronidazole. The combination of two antibiotics is recommended because of the high incidence of antibiotic resist- ance. Such protocols will eradicate H. pylori in over 90% of patients.
• Acid reduction. Acid reduction with a proton pump inhibitor such as omeprazole (or less com- monly a H2-receptor blocker such as ranitidine) alone results in the majority of ulcers healing within 1–2 months; the ulcers will recur if H. pylori has not been eradicated.
Violent gastric acid stimulants such as alcohol should be avoided. Rest, sedation, avoidance of smoking and dealing with underlying anxiety states are helpful. Aspirin and other NSAIDs should be avoided wherever possible.
Principles of surgical treatment
Surgical treatment is now reserved for those patients in whom complications of ulceration occur. In the emergency situation, minimal surgery is practised with the confidence that medical cure of the underly- ing disease may be effected. The most common indi- cations for emergency surgery are bleeding or perfo- ration (see later in this chapter).
• Gastric ulcers are treated by removing the ulcer together with the gastrin-secreting zone of the an- trum. Traditionally, this was done by the Billroth I gastrectomy7 (Figure 21.2), but is now more com- monly achieved by an antrectomy combined with a Roux-en-Y gastroenterostomy, the latter to limit bile reflux.
• Duodenal ulcers will heal providing the high acid production of the stomach is abolished. This can be effected by removing the bulk of the acid- secreting area of the stomach (the body and the lesser curve), and re-establishing gastric drain- age via a Roux-en-Y gastroenterostomy. The tra- ditional procedures involved a partial (Pólya8) gastrectomy with closure of the duodenum and a gastrojejunostomy, or division of the vagus nerves. As total vagotomy interferes with the mechanism of gastric emptying, this operation must be accompanied by a drainage procedure, either gastrojejunostomy or pyloroplasty. If the branches of the vagus that supply the pyloric sphincter (the nerves of Latarjet9) are left intact, the remaining vagal fibres can be divided with- out the necessity of gastric drainage (highly se- lective vagotomy), but nevertheless the goal of reduction in the vagal phase of acid secretion is achieved.
• Postgastrectomy syndromes. Even though about 85% of patients are well following Pólya partial gastrectomy for peptic ulcer, a large number of
7Theodor Billroth (1829–1894), Professor of Surgery, Vienna, Austria. He performed the first successful gastrectomy for cancer at the pyloric end of the stomach in 1881.
8Eugen Alexander Pólya (1876–1944), surgeon, St Stephen’s Hospital, Budapest, Hungary.
9André Latarjet (1876–1947), Professor of Anatomy, Lyon, France.
The stomach and duodenum
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Gastric ulcer Billroth I gastrectomy
Duodenal ulcer
Gastric or duodenal ulcer
Duodenotomy and pyloroplasty
Pólya gastrectomy
Roux-en-Y gastro- enterostomy
Entero- enterostomy
Figure 21.2 The principal operations once commonly performed for peptic ulcer. Surgery is still indicated in the presence of haemorrhage from an ulcer, and usually comprises a partial gastrectomy with drainage into a Roux-en-Y loop of jejunum. The more traditional procedures are also shown here: for a gastric ulcer, a Billroth I gastrectomy with gastroduodenal anastomosis was performed;
for a duodenal ulcer, a simple longitudinal duodenotomy, closed as a pyloroplasty, with under-running of the bleeding vessel, was performed, combined with acid suppression with a proton pump inhibitor (instead of the traditional vagotomy); a Pólya gastrectomy with under-running of the vessel was an alternative. Eradication of Helicobacter pylori should be undertaken when necessary. For gastric cancer, a gastrectomy with Roux-en-Y drainage is now preferred.
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The stomach and duodenum unpleasant sequelae may occur. These may be classified into the following.– Small stomach syndrome: a feeling of fullness after a moderate-sized meal.
– Bilious vomiting due to emptying of the affer- ent loop of a Pólya gastrectomy into the stom- ach remnant.
– Anaemia due usually to iron deficiency (HCl is required for adequate iron absorption) or, occa- sionally, vitamin B12 deficiency owing to loss of intrinsic factor with extensive gastric resection.
– Dumping: comprises attacks of fainting, verti- go and sweating after food, rather like a hypo- glycaemic attack. This is probably an osmotic effect due to gastric contents of high osmolar- ity passing rapidly into the jejunum, absorbing fluid into the gut lumen and producing a tem- porary reduction in circulating blood volume.
– Steatorrhoea: in the presence of a long afferent loop, food passing into the jejunum traverses the bowel without mixing adequately with pancreatic and biliary secretions. Calcium de- ficiency and osteomalacia may occur.
– Stomal ulceration complicates about 2% of gas- trectomies for duodenal ulcer; it is extremely rare after resection for gastric ulcer. It may be due to inadequate removal of the acid-secret- ing area of the stomach or, rarely, because of the Zollinger–Ellison syndrome (see Chapter 32). A stomal ulcer, like any other peptic ulcer, may perforate, stenose, invade surrounding structures or bleed. It is treated by either va- gotomy or higher gastric resection.
• Postvagotomy syndromes. The following sequelae may occur after truncal vagotomy.
– Steatorrhoea and diarrhoea: frequently tran- sient or episodic, they may be severe and per- sistent in about 2% of patients. The incidence is reduced in patients subjected to highly selec- tive vagotomy without drainage.
– Stomal ulceration may occur if vagotomy is in- complete.