PYLORIC STENOSIS (GASTRIC OUTLET OBSTRUCTION)

Pyloric stenosis is rarely due to stenosis at the pylorus. More commonly, the obstruction is on one side of the pylorus, either in the first part of the duodenum due to chronic scarring from a duodenal ulcer or in the antrum due to a carcinoma. True pyloric stenosis can arise from a pyloric channel ulcer or very rarely from a congenital web or adult hypertrophic pyloric stenosis. Some instances of gastric stenosis are caused by inflammatory oedema surrounding an active ulcer and these often resolve with conservative treatment. The common causes of gastric outlet obstruction are:

•         chronic duodenal ulceration/fibrosis;

•         antral gastric carcinoma;

•         carcinoma of the head of the pancreas.

Barium meal showing gastric outlet obstruction caused by fibrosis following healing of chronic duodenal ulcer.

Barium meal showing hour-glass deformity caused by a lesser curve ulcer in the middle third of the stomach. The deformity resolved with medical treatment. However, some of these deformities are fibrotic in nature (contractures) when obstructive symptoms persist depite ulcer healing. These require dilatation or surgical treatment.

Rare causes include a variety of benign tumours, lymphomas, Crohn's disease, duodenal haematoma, adult pyloric hypertrophy, annular pancreas and mucosal diaphragm. Benign pyloric stenosis usually occurs in a patient with long-standing symptoms of ulceration. Vomiting and anorexia supervene. The typical vomiting of pyloric stenosis is projectile and the vomitus is characterized by an absence of bile and the presence of partially digested food eaten hours or even days previously. With repeated vomiting and failure to eat, the patient often becomes constipated, although in some cases diarrhoea may develop. Examination usually shows an underweight patient, dehydration and often a degree of iron-deficiency anaemia. A succussion splash may be present and visible contractions passing across the upper abdomen from left to right may be observed on inspection. Prolonged vomiting of gastric contents results in characteristic electrolyte disturbances. Initially, the major loss is fluid rich in hydrogen and chloride ions so that dehydration is accompanied by hypochloraemic alkalosis. At this stage the serum sodium is usually normal and hypokalaemia may not be obvious. More marked metabolic changes supervene as a result of continued losses and secondary changes in renal function. Initially, the urine is characterized by a low chloride content and is appropriately alkaline because of enhancedbicarbonate excretion compensating for the metabolic alkalosis but at the expense of sodium. If gastric losses continue, the patient becomes progressively hypovolaemic and hyponatraemic. In an attempt to conserve circulating volume, sodium is retained by the kidneys and exchanged for hydrogen ions and potassium. At this late stage, the patient has a metabolic alkalosis and, paradoxically, an acid urine. As a secondary effect of the alkalosis, the concentration of plasma ionized calcium may fall so that disturbances of consciousness and tetany may be apparent. The priority in management of the advanced case of pyloric stenosis is correction of the fluid and electrolyte

CT showing pyloric obstruction by an antral carcinoma.

disturbances. Rehydration is achieved by saline infusions with potassium supplements as indicated by electrolyte determinations. Gastric lavage is performed with a widebore tube using isotonic saline daily until the returning

fluid becomes clear. The surgical treatment of pyloric stenosis caused by duodenal ulceration/fibrosis is truncal vagotomy and posterior gastroenterostomy. In western countries the majority of cases of gastric outlet obstruction are caused by distal gastric cancer.