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.