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Гастроэнтерология (анг,рус)

Complications of gastric resection or vagotomy 

Some degree of disability is seen in up to 50% of patients following peptic ulcer surgery. In most, the effects are minor but in 10% of cases they significantly impair quality of life. 

Early satiety and vomiting. Rapid gastric emptying leads to distension of the proximal small intestine as the hypertonic contents draw fluid into the lumen. This leads to abdominal discomfort and diarrhoea after eating. Autonomic reflexes release a range of gastrointestinal hormones which lead to vasomotor features such as flushing, palpitations, sweating, tachycardia and hypotension ('early dumping'). Patients should therefore avoid large meals with high carbohydrate content. 

Bile reflux gastritis. Duodenogastric bile reflux leads to chronic gastritis. This is usually asymptomatic but dyspepsia can occur. Symptomatic treatment with aluminium-containing antacids or sucralfate may be effective. A few patients require revisional surgery with creation of a Roux-en-Y loop to prevent bile reflux into the stomach. 

Late dumping syndrome. Symptoms of dumping occur 90-180 minutes after eating. The pathogenesis is broadly similar to early dumping, but in addition reactive hypoglycaemia occurs and may cause mental confusion. Rapid emptying of carbohydrates into the proximal small intestine results in an exaggerated release of insulin with subsequent reactive hypoglycaemia. Other gut hormones and enteric peptides may also be involved. Treatment is similar to that of early dumping syndrome. 

Diarrhoea and maldigestion. Diarrhoea may develop after any peptic ulcer operation and usually occurs 1-2 hours after eating. Poor mixing of food in the stomach, with rapid emptying, inadequate mixing with pancreatic biliary secretions, reduced small intestinal transit times and bacterial overgrowth, may lead to malabsorption. 

Diarrhoea often responds to dietary advice to eat small, dry meals with a reduced intake of refined carbohydrates. Antidiarrhoeal drugs such as codeine phosphate (15-30 mg 4-6 times a day) or loperamide (2 mg after each loose stool) are often helpful. 

Weight loss. Most patients lose weight shortly after surgery and 30-40% are unable to regain all the weight which is lost. The usual cause is reduced intake because of a small gastric remnant, but diarrhoea and mild steatorrhoea also contribute. 

Anaemia. Anaemia is common many years after subtotal gastrectomy. Although iron deficiency is the most common cause, folic acid and B12 deficiency are also seen. Inadequate dietary intake of iron and folate, lack of acid and intrinsic factor secretion, mild chronic low-grade blood loss from the gastric remnant and recurrent ulceration are responsible. 

Metabolic bone disease. Both osteoporosis and osteomalacia occur as a consequence of calcium and vitamin D malabsorption. 

Gastric cancer. An increased risk of gastric cancer has been reported from several epidemiological studies. The risk is highest in those with hypochlorhydria, duodenogastric reflux of bile, smoking and H. pylori infection. Although the relative risk is increased, the absolute risk of cancer remains low and endoscopic surveillance is not indicated following gastric surgery. 


Complications of peptic ulcer disease 

These are perforation, gastric outlet obstruction and bleeding. 


When free perforation occurs, the contents of the stomach escape into the peritoneal cavity, leading to peritonitis. Perforation occurs more commonly in duodenal than in gastric ulcers, and usually in ulcers on the anterior wall. About one-quarter of all perforations occur in acute ulcers and NSAIDs are often incriminated. 

Clinical features. Perforation is often the first sign of ulcer, and a history of recurrent epigastric pain is uncommon. The most striking symptom is sudden, severe pain; its distribution follows the spread of the gastric contents over the peritoneum. Pain initially develops in the upper abdomen and rapidly becomes generalised; shoulder tip pain is due to irritation of the diaphragm. The pain is accompanied by shallow respiration due to limitation of diaphragmatic movements, and by shock. The abdomen is held immobile and there is generalised 'board-like' rigidity. Intestinal sounds are absent and liver dullness to percussion decreases due to the presence of gas under the diaphragm. After some hours symptoms may improve, although abdominal rigidity remains. Later the patient's condition deteriorates as general peritonitis develops. 

In at least 50% of cases an erect chest radiograph shows free air beneath the diaphragm. If not, a water-soluble contrast swallow will confirm leakage of gastroduodenal contents. 

Management and prognosis. After resuscitation, the acute perforation is treated surgically, either by simple closure, or by converting the perforation into a pyloroplasty if it is large. On rare occasions a 'Polya' partial gastrectomy is required. Following surgery H. pylori is treated (if present) and NSAIDs are avoided. 

Perforation carries a mortality of 25%. This high figure reflects the high age and comorbidity of this population. 


Gastric outlet obstruction 

The causes are shown in Box 17.34. The most common is an ulcer in the region of the pylorus. 

Clinical features. Nausea, vomiting and abdominal distension are the cardinal features of gastric outlet obstruction. Large quantities of gastric content are often vomited, and food eaten 24 hours or more previously may be recognised. 

Physical examination frequently shows evidence of wasting and dehydration. A succussion splash may be elicited 4 hours or more after the last meal or drink. Visible gastric peristalsis is diagnostic of gastric outlet obstruction. 

Investigations. Loss of gastric contents leads to dehydration with low serum chloride and potassium, and raised serum bicarbonate and urea concentrations. This results in enhanced renal absorption of Na+ in exchange for H+ and paradoxical aciduria. Nasogastric aspiration of at least 200 ml of fluid from the stomach after an overnight fast suggests the diagnosis. 

Endoscopy should be performed after the stomach has been emptied by a wide-bore nasogastric tube. Endoscopic balloon dilatation of benign stenoses may be possible in some patients. In gastroparesis the pylorus is normal and the endoscope can be passed easily into the duodenum. 

Barium studies are rarely advisable because they cannot usually distinguish between peptic ulcer and cancer. Moreover, barium remains in the stomach and is difficult to remove. 



Management. Nasogastric suction and intravenous correction of dehydration are undertaken. In severe cases at least 4 litres of isotonic saline and 80 mmol of potassium may be necessary during the first 24 hours. Correction of metabolic alkalosis is not required. In some patients proton pump inhibitor drugs heal ulcers, relieve pyloric oedema and overcome the need for surgery. In others partial gastrectomy is necessary although this is best done after a 7-day period of nasogastric aspiration which enables the stomach to return to normal size. A gastroenterostomy is an alternative operation but patients will then require long-term proton pump inhibitor therapy to prevent stomal ulceration unless a vagotomy is also carried out. 




Gastroduodenal ulcers have a manyfold greater incidence, admission rate and mortality in older people.

This results from the high prevalence of H. pylori and NSAID use, and impaired defence mechanisms.

Pain and dyspepsia are frequently absent or atypical so older people develop complications such as bleeding or perforation more frequently.

When bleeding does occur, older patients require more intensive management (including central venous pressure measurement) than younger patients because they tolerate hypovolaemic shock poorly.