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Basics

Basics

Definition

Pyloric stenosis or chronic hypertrophic pyloric gastropathy is an obstructive narrowing of the pyloric canal resulting from varying degrees of muscular hypertrophy or mucosal hyperplasia.

Pathophysiology

  • Can result from a congenital lesion composed primarily of hypertrophy of the smooth muscle or be one of three types of acquired form-primarily circular muscle hypertrophy (type 1), a combination of muscular hypertrophy and mucosal hyperplasia (type 2), or primarily mucosal hyperplasia (type 3).
  • The cause is unknown; proposed factors include increased gastrin concentrations (which have a trophic effect on the muscle and mucosa) or changes in the myenteric plexus that lead to chronic antral distension and its associated effects.

Systems Affected

  • Gastrointestinal-chronic intermittent vomiting; regurgitation has also been reported.
  • Musculoskeletal-weight loss.
  • Respiratory-possible aspiration pneumonia.

Genetics

Inheritance pattern unknown

Incidence/Prevalence

Uncommon

Geographic Distribution

N/A

Signalment

Species

  • More common in dog
  • Rare in cat

Breed Predilections

  • Congenital-brachycephalic breeds (boxer, Boston terrier, bulldog); Siamese cats
  • Acquired-Lhasa apso, Shih Tzu, Pekingese, poodle

Mean Age and Range

  • Congenital-shortly after weaning (introduction of solid food) and up to 1 year of age.
  • Acquired-9.8 years of age.

Predominant Sex

Twice as many males as females

Signs

General Comments

  • Clinical signs are related to the degree of pyloric narrowing.
  • Projectile vomiting is generally not a presenting complaint. Animals are generally in good body condition.

Historical Findings

  • Chronic intermittent vomiting of undigested or partially digested food (rarely containing bile) often several hours after eating.
  • Congenital lesions associated with clinical signs shortly after weaning.
  • Frequency of vomiting increases with time.
  • Lack of response to antiemetic agents or motility modifying agents.
  • Occasional anorexia with weight loss.
  • Regurgitation.

Physical Examination Findings

Most dogs are generally in good physical condition.

Causes

  • Congenital or acquired
  • May be influenced by infiltrative mural diseases
  • Chronic elevations in gastrin concentrations
  • Neuroendocrine factors may play a role

Risk Factors

Chronic stress, inflammatory disorders, chronic gastritis, gastric ulcers, and genetic predispositions influence the disease process in humans and may play a role in small animals.

Diagnosis

Diagnosis

Differential Diagnosis

  • Gastric neoplasia
  • Gastric foreign body
  • Granulomatous fungal disease (e.g., pythiosis)
  • Eosinophilic granuloma
  • Motility disorders
  • Cranial abdominal mass-pancreatic or duodenal

CBC/Biochemistry/Urinalysis

  • Findings vary, depending on the degree and chronicity of obstruction.
  • Hypochloremic metabolic alkalosis (characteristic of pyloric outflow obstruction) or metabolic acidosis (or mixed acid-base imbalance).
  • Hypokalemia.
  • Anemia-if concurrent GI ulceration.
  • Prerenal azotemia-if dehydration present.

Other Laboratory Tests

N/A

Imaging

Abdominal Radiographs

Normal to markedly distended stomach.

Upper GI Barium Contrast Study

  • May display a “beak” sign created by pyloric narrowing, allowing minimal barium to pass into the pyloric antrum.
  • Retention of most of the barium in the stomach after 6 hours indicates delayed gastric emptying.
  • Intraluminal filling defects or pyloric wall thickening.

Fluoroscopy

  • Normal gastric contractility.
  • Delayed passage of barium through the pylorus.

Abdominal Ultrasound

Measurable thickening of the wall of the pylorus and antrum.

Diagnostic Procedures

Endoscopy-allows evaluation of the mucosa for ulceration, hyperplasia, and mass lesions; specimens can be obtained for histopathologic evaluation.

Pathologic Findings

  • Include focal to multifocal mucosal polyps, diffuse mucosal thickening, and pyloric wall thickening, with variable degree of pyloric narrowing.
  • Changes range from hypertrophy of the circular smooth muscle to hyperplasia of the mucosa and associated glandular structures; a wide spectrum of inflammatory cell infiltration exists.

Treatment

Treatment

Appropriate Health Care

  • Depends on severity of clinical signs.
  • Patients should be evaluated and surgery scheduled at the earliest convenience.

Nursing Care

  • Appropriate parenteral fluids to correct any electrolyte imbalances and metabolic alkalosis or acidosis.
  • Isotonic saline (with potassium supplementation) is the fluid of choice for hypochloremic metabolic alkalosis.
  • Consideration of postoperative nutritional support is important.
  • In severe cases treated with gastroduodenostomy or gastrojejunostomy, surgical placement of a jejunostomy tube for enteral nutrition may be advantageous.

Activity

Restrict

Diet

Highly digestible, low-fat-until surgical intervention is feasible.

Client Education

  • Surgical treatment is highly successful.
  • If clinical signs recur postoperatively, more aggressive surgical procedures may be indicated.

Surgical Considerations

  • Surgical intervention is the treatment of choice.
  • Goals involve establishing a diagnosis with histopathologic samples, excising abnormal tissue, and restoring GI function with the least-invasive procedure.
  • Surgical procedures depend on the extent of obstruction-pyloromyotomy (Fredet-Ramstedt), pyloroplasty (Heineke-Mikulicz or antral advancement flap), gastroduodenostomy (Billroth 1), gastrojejunostomy (Billroth 2).

Medications

Medications

Drug(s) Of Choice

  • Antiemetics and motility modifiers are generally ineffective.
  • H2-antagonists and proton pump inhibitors may provide symptomatic relief.

Contraindications

  • Evidence of complete pyloric obstruction precludes the use of promotility drugs.
  • Avoid anticholinergic agents because of their inhibitory effects on GI motility.

Precautions

N/A

Possible Interactions

N/A

Alternative Drug(s)

N/A

Follow-Up

Follow-Up

Patient Monitoring

Postoperatively for recurrence of clinical signs because of poor choice of surgical procedure.

Prevention/Avoidance

N/A

Possible Complications

Postoperative surgical complications include recurrence of clinical signs, gastric ulceration, pancreatitis, bile duct obstruction, and incisional dehiscence with peritonitis.

Expected Course and Prognosis

  • 85% of dogs show good-to-excellent results with resolution of clinical signs upon proper surgical intervention.
  • Poor prognosis if gastric neoplasia (especially adenocarcinoma) is an underlying cause.

Miscellaneous

Miscellaneous

Associated Conditions

Gastric ulceration

Age-Related Factors

Intermittent vomiting in young brachycephalic breeds upon weaning is suggestive of congenital stenosis.

Zoonotic Potential

None

Pregnancy/Fertility/Breeding

High gastrin concentrations in pregnant females may predispose to development of the syndrome.

Synonyms

  • Chronic hypertrophic antral gastropathy
  • Hypertrophic gastritis
  • Acquired antral pyloric hypertrophy
  • Congenital pyloric stenosis

Abbreviation

GI = gastrointestinal

Author Steven L. Marks

Consulting Editor Stanley L. Marks

Suggested Reading

Bellenger CR, Maddison JE, Macpherson GC, Ilkiw JE. Chronic hypertrophic pyloric gastropathy in 14 dogs. Aust Vet J 1990, 67:317320.

Fossum TW. Surgery of the digestive system. In: Fossum TW, ed., Small Animal Surgery. St. Louis: Mosby, 2013, pp. 433436.