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.
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
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.