PYLORIC STENOSIS

Pyloric stenosis

Other Pylorostenosis, infantile

names hypertrophic pyloric stenosis

Pyloric stenosis is a narrowing of the opening from the stomach to the first part of
the small intestine (the pylorus).

Signs and symptoms

Babies with this condition usually present any time in the first weeks to 6 months of life
with progressively worsening vomiting. It is more likely to affect the first-born with males
more commonly than females at a ratio of 4 to 1.
 A "projectile vomiting",and non-bile stained ("non bilious") vomitus noticed.
 Some infants present with poor feeding.
 weight loss but others demonstrate normal weight gain.
 Dehydration.
 epigastric fullness.
 visible peristalsis in the upper abdomen from the infant's left to right.
 Constant hunger.
 Belching.
 colic.

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Cause
Rarely, infantile pyloric stenosis can occur as an autosomal dominant condition. It is
uncertain whether it is a congenital anatomic narrowing or a functional hypertrophy of
the pyloric sphincter muscle.
Pathophysiology
The gastric outlet obstruction due to the hypertrophic pylorus impairs emptying of gastric
contents into the duodenum. As a consequence, all ingested food and gastric secretions can
only exit via vomiting, which can be of a projectile nature. While the exact cause of the
hypertrophy remains unknown, one study suggested that neonatal hyperacidity may be
involved in the pathogenesis. This physiological explanation for the development of
clinical pyloric stenosis at around 4 weeks and its spontaneous long term cure without
surgery if treated conservatively, has recently been further reviewed.
Persistent vomiting results in loss of stomach acid (hydrochloric acid). The vomited
material does not contain bile because the pyloric obstruction prevents entry of duodenal
contents (containing bile) into the stomach. The chloride loss results in a low blood
chloride level which impairs the kidney's ability to excrete bicarbonate. This is the factor
that prevents correction of the alkalosis leading to metabolic alkalosis.
A secondary hyperaldosteronism develops due to the decreased blood volume. The
high aldosterone levels causes the kidneys to avidly retain Na+ (to correct the
intravascular volume depletion), and excrete increased amounts of K+ into the urine
(resulting in a low blood level of potassium). The body's compensatory response to the
metabolic alkalosis is hypoventilation resulting in an elevated arterial pCO
Diagnosis.
Diagnosis is via a careful history and physical examination, often supplemented by
radiographic imaging studies.
Pyloric stenosis should be suspected in any young infant with severe vomiting.
On physical exam, palpation of the abdomen may reveal a mass in the epigastrium.
This mass, which consists of the enlarged pylorus, is referred to as the 'olive',[14] and
is sometimes evident after the infant is given formula to drink.]
Ultrasound,
An x- ray.

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Treatment

Infantile pyloric stenosis is typically managed with surgery; very few cases are mild enough
to be treated medically.
Intravenous and oral atropine may be used to treat pyloric stenosis. It might be an
alternative to surgery in children who have contraindications for anesthesia or surgery, or
in children whose parents do not want surgery.
Surgery
The definitive treatment of pyloric stenosis is with surgical pyloromyotomy known as
Ramstedt's procedure (dividing the muscle of the pylorus to open up the gastric outlet).

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