Gastric outlet obstruction

The two common causes of gastric outlet obstruction are gastric cancer (see below) and pyloric stenosis secondary to peptic ulceration. Previously the latter was more common. Now, with the decrease in the incidence of peptic ulceration and the advent of potent medical treatments, gastric outlet obstruction should be considered malignant until proven otherwise, at least in the West. The term pyloric stenosis is normally a misnomer. The stenosis is seldom at the pylorus. Commonly, when the con­dition is due to underlying peptic ulcer disease, the stenosis is found in the first part of the duodenum, the most common site for a peptic ulcer. True pyloric stenosis can occur due to fibrosis around a pyloric channel ulcer. 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

In benign gastric outlet obstruction there is usually a long history of peptic ulcer disease. Nowadays, as most patients with peptic ulcer symptoms are treated medically, it is easy to understand why the condition is becoming much less com­mon. In some patients the pain may become unremitting and in other cases may largely disappear. The vomitus is characteristically unpleasant in nature and is totally lacking in 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. Examin­ing the patient it may be possible to see the distended stomach and a succussion splash may be audible on shaking the patient’s abdomen.

Metabolic effects

These are most interesting, as the metabolic consequences of benign pyloric stenosis are unique. The vomiting of hydro­chloric acid results in hypochloraemic alkalosis. Initially the sodium and potassium may be relatively normal. However, as dehydration progresses more profound metabolic abnor­malities arise, partly related to renal dysfunction. Initially the urine has a low chloride and high bicarbonate content reflecting the primary metabolic abnormality. This 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

Treating the patient involves correcting the metabolic abnormality and dealing with the mechanical problem. 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. Following rehydration it may become obvious that the patient is also anaemic, the haemoglobin being spuriously high on presentation.

It is noteworthy that the metabolic abnormalities may be less if the obstruction is due to malignancy as the acid—base disturbance is less pronounced.

The stomach should be emptied using a wide-bore gastric tube. A large nasogastric tube may not be sufficiently large to deal with the contents of the stomach and it may be necessary to pass an orogastric tube and lavage the stomach until it is completely emptied. This then allows investigation of the patient with endoscopy and contrast radiology. Biopsy of the area around the pylorus is essential to exclude malignancy. The patient should also have a gastric antisecretory agent such as ranitidine, given initially intravenously to ensure absorption.

Early cases may settle with conservative treatment, pre­sumably as the oedema around the ulcer diminishes as the ulcer is healed. Traditionally severe cases are treated surgi­cally, usually with a gastroenterostomy rather than a pyloro­plasty. The addition of a vagotomy in these circumstances may be appropriate. Endoscopic treatment with balloon dilatation has been practised and may be most useful in early cases. This treatment is, however, not devoid of problems. Dilating the duodenal stenosis may result in perforation. The dilatation may have to be performed several times and sometimes may not be successful in the long term.

Other causes of gastric outlet obstruction

Adult pyloric stenosis

This is a rare condition and its relationship to the childhood condition unclear, although some patients have a long history of problems with gastric emptying. It is commonly treated by pyloroplasty rather than pyloromyotomy.

Pyloric mucosal diaphragm

The origin of this rare condition is unknown. It usually does not become apparent until middle life. When found simple excision of the mucosal diaphragm is all that is required.