Peptic ulcer disease
A peptic ulcer is a break in the integrity of the stomach or duodenal mucosa.
15% of the population will suffer from a duodenal ulcer and 5% a gastric ulcer at some time during their life.
More common with increasing age.
Duodenal ulcers 4M : 1F.
In the United Kingdom duodenal ulcers are more common in North England and Scotland.
Factors involved include presence of H. pylori within the stomach, the use of nonsteroidal anti-inflammatory drugs (NSAIDs) and aspirin. Rarely pathological hyper-secretion of gastrin (Zollinger–Ellinson syndrome) may be the cause of multiple ulcers. Most duodenal ulcers occur in the proximal duodenum, most gastric ulcers occur on the lesser curve. Rare sites include the following:
· The oesophagus following columnar metaplasia due to gastrooesophageal reflux.
· The jejunum in Zollinger–Ellinson syndrome.
· A Meckel’s diverticulum containing ectopic gastric mucosa.
Ulceration results from an imbalance between the gastric secretion of acid and the ability of the mucosa to withstand such secretion. Normal protective mechanisms include mucous, bicarbonate and prostaglandins. Patients with H. pylori infection have elevated basal and stimulated concentrations of serum gastrin and a decreased concentration of somatostatin resulting in increased acid production. H. pylori also releases proteases which degrade mucous glycoproteins which normally protect the gastric mucosa.
Clinically patients present with dyspepsia, which they often describe as indigestion, nausea and occasionally vomiting. Gastric ulcers tend to cause pain that is worse during the day and after meals. Duodenal ulcers tend to cause well-localised epigastric pain that may radiate to the back. It occurs a few hours after meals or on an empty stomach and is often worse at night or in the early hours of the morning when circadian acid secretion is maximal.
Chronic ulcers have sharply defined borders, without any heaping up of the edges (which would be suggestive of a malignant ulcer). There is a break in the integrity of the epithelium extending down to the muscularis mucosa. Active inflammation is seen with granulation tissue and fibrosis.
Perforation occurs much more commonly with duodenal ulcers. It results in peritonitis and an acute abdomen, free air is seen under the diaphragm on plain erect chest X-ray. Patients require resuscitation and emergency surgery to locate and close the duodenal perforations, a partial gastrectomy may be required in gastric ulcers.
Haemorrhage may be slow and chronic presenting as anaemia. More rapid loss may cause melaena and haematemesis. Peptic ulcer disease is the most common cause of acute upper gastrointestinal haemorrhage and may cause hypovolaemia and shock. Acute bleeds require resuscitation to stabilise the patient and may require urgent endoscopic treatment. Early endoscopy can reduce the risk of rebleeding by injection or argon plasma coagulation of bleeding ulcers. Surgery may be needed if bleeding is uncontrollable or endoscopy is unsuccessful.
Scarring of the pyloric region results in gradual development of outflow obstruction (pyloric stenosis). The patient presents with upper abdominal distension after meals and projectile vomiting. X-ray reveals a distended stomach, barium meal is diagnostic. Fibrotic stenosis requires surgical intervention following treatment of any electrolyte imbalances resulting from copious vomiting.
Patients are investigated and managed as for dyspepsia, i.e. patients under the age of 55 years without ‘alarm symptoms and signs’ (see under section Dyspepsia) are treated without endoscopy. Older patients and those with suspicious features should undergo endoscopy to exclude malignancy prior to commencing treatment.
· H. pylori positive (90%): Patients should receive eradication therapy (see below). If asymptomatic following this treatment a further endoscopy is not necessary. If symptoms persist or recur (or in all patients initially presenting with complications) a urea breath test should be performed at 4 weeks and further eradication therapy used if positive. If negative clinical reevaluation is necessary.
· H. pylori negative (10%): Antisecretory therapy such as H2 receptor antagonists (first line) or proton pump
· inhibitors are used. If the patient is taking NSAIDs these should be stopped if possible.
· H. pylori positive (70%): Eradication therapy is used (see below) followed by antisecretory therapy for 2 months.
· H. pylori negative (30%): The majority of these are NSAID or aspirin induced. Standard antisecretory therapy should be given for 2 months and NSAIDs should be stopped if possible.
Repeat endoscopy with biopsies is essential in all gastric ulcers until completely healed, as there may be an underlying malignancy. If the ulcer does not heal within 6 months then surgery should be considered.
In all patients with peptic ulcer disease who continue to require NSAIDs, long-term treatment with a proton pump inhibitor (or misoprostol in gastric ulcers) should be considered. In patients with rheumatoid arthritis or osteoarthritis a COX2 specific antagonist may be considered in place of the NSAID.