Pyloric stenosis (or infantile hypertrophic pyloric stenosis or pylorostenosis)[1] is a condition that

causes severe projectile non-bilious vomiting in the first few months of life. There is narrowing
(stenosis) of the opening from the stomach to the first part of the small intestine known as
the duodenum, due to enlargement (hypertrophy) of the muscle surrounding this opening
(the pylorus, meaning "gate"), which spasms when the stomach empties. This hypertrophy is felt
classically as an olive-shaped mass in the middle upperpart or right upper quadrant of the infant's
abdomen. In pyloric stenosis, it is uncertain whether there is a real congenital narrowing or
whether there is a functional hypertrophy of the pyloric sphincter muscle. This condition
typically develops in male babies in the first 26 weeks of life.
Pyloric stenosis also occurs in adults where the cause is usually a narrowed pylorus due to
scarring from chronic peptic ulceration. This is a different condition from the infantile form

Summary
Pyloric stenosis, also known as chronic hypertrophic pyloric gastropathy, is a
narrowing of the structure required for passage of partially digested food from the stomach into
the small intestine (the pylorus, a stomach valve of sorts). It occurs primarily in dogs and is rare
in cats. This aberration of the stomachs normal emptying mechanism is caused by physical
obstruction of the pylorus. Hence, the inability of food to pass down to the rest of the
gastrointestinal tract for further digestion, nutrient absorption and normal waste excretion. This
obstruction can occur for one of two different reasons:
1. A congenital thickening of the smooth muscle of the pylorus. In other words, pets are born
with an abnormal muscle in this sensitive location. Animals with this form usually show signs
after weaning and up to a year of age.
2. A gradually acquired form of the disease in which either the smooth muscle, the delicate lining
of the stomach (the mucosa), or both, become thickened, thereby obstructing the pylorus. Its
cause is unknown but its believed that high gastrin levels (a hormone) may lead to this abnormal
thickening process. These animals tend to be older when diagnosed. They tend to be about ten
years old when symptoms arise.

Symptoms and Identification

The most common symptoms include chronic, intermittent vomiting and regurgitation
(because the mechanical obstruction means food cant get down to where it needs to go), weight
loss (because nutrients arent reaching the intestines for absorption) and respiratory problems
(because aspiration of stomach contents can occur as foods are brought back up). Diagnosis of
the problem can be difficult if the complete closing down of the pylorus is intermittent, but it
usually relies on X-rays after barium administration. These barium studies often show a thin
line of minimal amounts of this contrast material getting through the pylorus into the intestines,
thus strongly suggesting the diagnosis of pyloric stenosis. Endoscopy (using a fiberoptic device
to view the area) will assist the diagnosis by visualizing the thickness of the pylorus and by
allowing for tissue sampling of the affected area. Fluoroscopy is another technique used to
visualize the motion of material as it passes through the area. Surgery is sometimes required to
establish the definitive diagnosis. Certain blood test findings will also point to the presence of the
disease.
Affected Breeds
For the congenital form of the disease, brachycephalic breeds (short nosed dogs) are
primarily

affected.

This

includesBoxers, Boston

Terriers and Bulldogs.

Among

cats,

the Siamese is most affected. For the acquired form, the Lhasa Apso, Shih Tzu, Pekingese and
poodle are documented to be the most predisposed breeds.
Treatment
Treatment of the condition is typically surgical. A widening of the pylorus is typically
accomplished through one of various methods, depending on the degree of the diseases severity
and the potential for it to worsen. Heres a list of the most common procedures.
1. Pyloromyotomy (opens the area by incising throug the muscle layer)
2. Pyloroplasty (opens the area with a flap procedure)
3. Gastroduodenostomy (bypasses the pylorus)
4. Gastrojejunostomy (bypasses the pylorus and the first section of the small intestine)

The latter two procedures are typically selected for the most severe cases, in which repair of the
pyloric mechanism proves an inadvisable option.
Prevention
Its been proposed that high levels of gastrin (a hormone) in pregnant females may
predispose dogs to the development of the acquired form of this disease. Pre-pubertal spaying
(before the first heat) of non-breeding females within predisposed breeds is therefore considered
wise. Because chronic stress, undiagnosed gastric ulcers and other forms of chronic gastritis are
predisposing factors for gastrin increases, treating these processes early may well prevent pyloric
stenosis. Because of its hereditary nature, removing all affected animals from their breeding
programs and preventing their reproduction is considered a fundamental course of action. This is
true for both acquired and congenital forms of pyloric stenosis.
Diagnosis
Diagnosis is via a careful history and physical examination, often supplemented by
radiographic studies. There should be suspicion for pyloric stenosis in any young infant with
severe vomiting. On 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', and is sometimes
evident after the infant is given formula to drink. It is an elusive diagnostic skill requiring much
patience and experience. There are often palpable (or even visible)peristaltic waves due to the
stomach trying to force its contents past the narrowed pyloric outlet.
Most cases of pyloric stenosis are diagnosed/confirmed with ultrasound, if available, showing the
thickened pylorus. Although somewhat less useful, an upper GI series (x-rays taken after the
baby drinks a special contrast agent) can be diagnostic by showing the narrowed pyloric outlet
filled with a thin stream of contrast material; a "string sign" or the "railroad track sign". For
either type of study, there are specific measurement criteria used to identify the abnormal results.
Plain x-rays of the abdomen are not useful, except when needed to rule out other problems.
Blood tests will reveal hypokalemic, hypochloremic metabolic alkalosis due to loss of gastric
acid (which contains hydrochloric acid and potassium) via persistent vomiting and exchange of
extracellular potassium with intracellular hydrogen ions, in an attempt to correct the pH

imbalance; these findings can be seen with severe vomiting from any cause. The potassium is
decreased further by the body's release of aldosterone, in an attempt to compensate for
the hypovolaemia due to the severe vomiting.
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. The exact cause of the hypertrophy
remains unknown.[3]
The vomited material does not contain bile because the pyloric obstruction prevents entry of
duodenal contents (containing bile) into the stomach.
This

results in loss of gastric acid (hydrochloric acid). The chloride loss results

in hypochloremia which impairs the kidney's ability to excrete bicarbonate. This is the significant
factor that prevents correction of the alkalosis.
A secondary hyperaldosteronism develops due to the hypovolemia. 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 hypokalaemia).
The body's compensatory response to the metabolic alkalosis is hypoventilation resulting in an
elevated arterial pCO2.

Epidemiology
Males are more commonly affected than females, with firstborn males affected about four
times as often, and there is a genetic predisposition for the disease. It is commonly associated
with people of Jewish ancestry, and has multifactorial inheritance patterns. [Pyloric stenosis is
more common in Caucasians than Hispanics, Blacks, or Asians. The incidence is 2.4 per 1000
live births in Caucasians, 1.8 in Hispanics, 0.7 in Blacks, and 0.6 in Asians. It is also less
common amongst children of mixed race parents.[10] Caucasian babies with blood type B or O are
more likely than other types to be affected.

Infants exposed to erythromycin are at increased risk for developing hypertrophic pyloric
stenosis, especially when the drug is taken around two weeks of life.

References
1. DeNovo R. Antral pyloric hypertrophy syndrome. In: Kirk R, ed. Current veterinary
therapy X. Philadelphia: WB Saunders, 1989.
2. Matthiesen D. Chronic gastric outflow obstruction. In: Slatter D, ed. Textbook of small
animal surgery. 2nd ed. Philadelphia: WB Saunders, 1993.
3. Stanton M. Gastric outlet obstruction. In: Bojrab MJ, ed. Disease mechanisms in small
animal surgery. 2nd ed. Philadelphia: Lea and Febiger, 1993.
4. Hulka F, Campbell TJ, Campbell JR, Harrison MW (1997). "Evolution in the recognition
of infantile hypertrophic pyloric stenosis". Pediatrics 100 (2):
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E9.doi:10.1542/peds.100.2.e9. PMID 9233980.

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a b
Askew, Nathan (October 2010). "An overview of infantile hypertrophic pyloric
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2012.
7. Kerry Brandis, Acid-Base Physiology. Retrieved December 31, 2006.
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"Medical News:Laparoscopic Repair of Pediatric Pyloric Stenosis May Speed Recovery - in
Surgery, Thoracic Surgery from". MedPage Today. 2009-01-16. Retrieved 2012-02-21.
Sola JE, Neville HL (August 2009). "Laparoscopic vs open pyloromyotomy: a systematic
review and meta-analysis". J. Pediatr. Surg. 44 (8): 1631
7.doi:10.1016/j.jpedsurg.2009.04.001. PMID 19635317.
a b

Dowshen, Steven (November 2007). "Pyloric Stenosis". The Nemours Foundation. Retrieved

2007-12-30.

Fried K, Aviv S, Nisenbaum C (November 1981). "Probable autosomal dominant infantile

pyloric stenosis in a large kindred". Clin. Genet. 20 (5): 32830.doi:10.1111/j.13990004.1981.tb01043.x. PMID 7333028.
Pediatrics, Pyloric Stenosis at eMedicine
Maheshwai, Nitin (March 2007). "Are young infants treated with erythromycin at risk for
developing hypertrophic pyloric stenosis?". Archives of Disease in Childhood 92 (3): 271
3. doi:10.1136/adc.2006.110007. PMC 2083424. PMID 17337692. Retrieved 30 August 2012.
Elizabeth LaFond, DVM, Diplomate ACVS, Gert J. Breur, DVM, PhD, Diplomate ACVS and
Connie C. Austin, MPH, PhD; Department of Veterinary Clinical Sciences, School of Veterinary
Medicine, Purdue University, West Lafayette, Indiana 47907.