Complications of peptic ulcer

Perforated peptic ulcer Clinical features The patient, who may have a history of peptic ulceration, develops sudden severe generalised abdominal pain. Bacterial peritonitis supervenes over a few hours, usually accompanied by a deterioration in the patient’s condition. O/E: the patient may be shocked with a tachycardia . The abdomen does not move with respiration, the abdomen tender and exhibits a boardlike rigidity and the patient is disinclined to move because of the pain.

Small duodenal perforation with slowley leaking fluid cause pain in the epigastrium and right iliac fossa as the fluid may track down the right paracolic gutter. The most common site of perforation is the anterior aspect of the duodenum. However, gastric ulcers may perforate into the lesser sac, which can be particularly difficult to diagnose.

Investigations An erect plain chest radiograph will reveal free gas under the diaphragm in 85 per cent of cases with perforated peptic ulcer, but CT imaging is more accurate. All patients should have serum amylase performed, as distinguishing between peptic ulcer perforation and pancreatitis can be difficult.

Treatment The initial priorities are resuscitation, analgesia and systemic antibiotics, Laparotomy is performed, usually through an upper midline incision. Closure of the perforation with thorough peritoneal lavage. Gastric ulcers should, if possible, be excised and closed, so that malignancy can be excluded. Occasionally, a Billroth II gastrectomy is useful operations. Following operation, gastric antisecretory agents should be started immediately. The stomach is kept empty postoperatively by nasogastric suction.

HAEMATEMESIS AND MELAENA Condition % Ulcers 60 Oesophageal 6 Gastric 21 Duodenal 33 Erosions 26 Oesophageal 13 Gastric 9 Duodenal 4 Mallory–Weiss tear 4 Oesophageal varices 4 Tumour 0.5 Vascular lesions, e.g. Dieulafoy’s disease 0.5 Others

Management In these circumstances, resuscitation, diagnosis and treatment should be carried out simultaneously intravenous access should be established. For those with severe bleeding, CVP monitoring should be set up. bladder catheterisation performed. Blood transfused as clinically indicated. Upper gastrointestinal endoscopy should be carried out after the patient has been stabilised.

Anti secretory drugs either H2-antagonist or a proton pump antagonist. Tranexamic acid, an inhibitor of fibrinolysis, may reduce overall mortality. Therapeutic endoscopy can achieve haemostasis in approximately 70 per cent of cases, with the best evidence supporting a combination of adrenaline injection with heater probe , laser or clips. Angiography with transcatheter embolisation may offer a valuable alternative to surgery in expert centres.

Surgical treatment A patient who continues to bleed requires surgical treatment. Patients with a visible vessel in the ulcer base, a spurting vessel or an ulcer with a clot in the base are likely to require surgical treatment to stop the bleeding. The duodenum, and usually the pylorus, is opened longitudinally as in a pyloroplasty, with under-running of the ulcer. The pyloroplasty is then closed with interrupted sutures in a transverse direction as in the usual fashion.

The principles of management of bleeding gastric ulcers are essentially the same. The stomach is opened at an appropriate position anteriorly and the vessel in the ulcer under-run. If the ulcer is not excised then a biopsy of the edge needs to be taken to exclude malignant transformation.

Stress ulceration This commonly occurs in patients with major injury or illness, or who have undergone major surgery. Many such patients are found in intensive care units. Antiacid drugs and the oral administration of Sucralfate are required. Gastric erosions Erosive gastritis has a variety of causes, especially NSAIDs. Fortunately, most such bleeding settles spontaneously. but sometimes surgery is necessary.

Mallory–Weiss tear This is a longitudinal tear at the gastro-oesophageal junction, which is induced by repetitive and strenuous vomiting. Occasionally, these lesions continue to bleed and require surgical treatment. Dieulafoy’s disease This is essentially a gastric arterial venous malformation. The lesion itself is covered by normal mucosa. Treatment by injection of sclerosant agent or endoscopic clips. If it is identified at operation, local excision is necessary.

Tumours All of the gastric tumours may present with chronic or acute upper gastrointestinal bleeding. Portal hypertension and portal gastropathy Fortunately, most bleeding from varices is oesophageal, which is much more amenable to sclerotherapy, banding and balloon tamponade. The gastric balloon of the Sengastaken– Blakemore tube can be used to arrest the haemorrhage. Octreotide, Glypressin is also said to be of use. TIPSS procedure (transjugular intrahepatic portosystemic shunt), can be useful.

GASTRIC OUTLET OBSTRUCTION The two common causes of gastric outlet obstruction are gastric cancer and pyloric stenosis secondary to peptic ulceration. gastric outlet obstruction should be considered malignant until proven otherwise. However, in recent years, the most common cause of gastric outlet obstruction has been gastric cancer. In this circumstance the metabolic consequences may be somewhat different from those of benign pyloric stenosis because of the relative hypochlorhydria found in patients with gastric cancer.

Clinical features A long history of peptic ulcer disease. The pain may become unremitting. The vomitus is totally lacking of bile. Very often it is possible to recognise foodstuff taken several days previously. The patient commonly complains of losing weight, and appears unwell and dehydrated. O/E: It may be possible to see the distended stomach and a succussion splash may be audible.

Metabolic effects The vomiting of hydrochloric acid results in hypochloraemic alkalosis. Initially, the sodium and potassium may be relatively normal. Bicarbonate is excreted along with sodium, and so with time the patient becomes progressively hyponatraemic and more profoundly dehydrated. Because of the dehydration, a phase of sodium retention follows and potassium and hydrogen are excreted in preference. This results in the urine becoming paradoxically acidic and hypokalaemia ensues. Alkalosis leads to a lowering in the circulating ionised calcium, and tetany can occur.

Management The patient should be rehydrated with intravenous isotonic saline with potassium supplementation. Replacing the sodium chloride and water allows the kidney to correct the acid–base abnormality. Correction of anaemia The patient should also have a gastric antisecretory agent, initially given intravenously to ensure absorption. The stomach should be emptied using a wide-bore gastric tube. A large nasogastric tube and lavage the stomach until it is completely emptied.

Investigation of the patient with endoscopy and contrast radiology with biopsy of the area around the pylorus is essential to exclude malignancy. Treatment: by gastroenterostomy rather than a pyloroplasty. Endoscopic treatment with balloon dilatation has been practised and may be useful in early cases. Occasionally, duodenal stent insertion will be considered in specialist centers.

GASTRIC POLYPS A number of conditions manifest as gastric polyps. Their main importance is that they may actually represent early gastric cancer. Biopsy is essential. The most common type of gastric polyp is metaplastic. These are associated with H. pylori infection and regress following eradication therapy. Inflammatory polyps are also common.They seem to be associated with the use of proton pump inhibitors and are also found in patients with familial polyposis. True adenomas: have malignant potential and should be removed, but they account for only 10 per cent of polypoid lesions. Gastric carcinoids arising from the ECL cells are seen in patients with pernicious anaemia and usually appear as small polyps.