The condition may be due to abnormal pyloric motor function, or from congenital or acquired stenosis of the pylorus. Focal hypertrophic gastritis also causes outflow obstruction.
Congenital cases are seen most in brachiocephalic dogs and Siamese cats (). Symptoms occur at an early age associated with commencement of solid feeding and are progressive. The acquired form has no breed or sex predisposition and occurs in mid and old aged animals.
Aetiology is not known but may be due to high levels of gastrin which stimulates smooth muscle hypertrophy causing hypertrophy of the circular fibres. When food is retained by outlet obstruction this causes distention of the stomach which leads to release of gastrin. Gastrin, in addition to effects on smooth muscle, also causes release of hydrochloric acid and pepsin which can induce ulceration often observed in pyloric stenosis.
Abnormal pyloric motor function develops because of a reduction in the nerves of the myenteric plexus in the pyloric antrum so there is antral dilation and muscle hypertrophy together with nerve degeneration in the pylorus.
Gastric retention results in vomiting food hours after eating. Vomiting is often projectile, occurring abruptly without warning or without salivation or retching preceding the act of vomiting. Vomiting may occur at varying periods from minutes to hours after eating and frequently contains undigested or partially digested food. Bile is never found in the vomitus while saliva and gastric secretion may be observed. Young animals with the congenital form are otherwise healthy, except for vomiting, and failure to gain weight. Vomiting starts just after weaning and is progressive. There may be dehydration, anorexia and abdominal distention.
Normally the stomach will empty in 4—6h. A tentative diagnosis is made where there is a delay in gastric emptying. Vomiting of undigested food when the stomach should be empty is another diagnostic sign.
The gastric emptying time is that time required for the stomach to start emptying not the time for complete emptying. It should be less than 30 min in normal dogs and is often nearer 5 to 10 min. Barium retained for 12 to 24 h is abnormal. However it is a crude method of estimating gastric function. Drugs, stress and excitement will all influence the rate of emptying, together with the actual composition of the barium itself. It may be possible for liquid barium to pass through the pylorus without difficulty while barium mixed with food is retained in pyloric stenosis.
There may be failure of the pyloric canal to fill with barium, and the so-called ‘pyloric beak’ at the entry to the canal may be seen. Fluoroscopy is useful in assessing motility. Usually there is a loss of antral contractions, but initially there may be hypermotility then hypo motility in pyloric stenosis.
Endoscopy is of little value although it will detect hypertrophic gastritis, ulceration or tumour if they are involved in the aetiology. Exploratory laparotomy is an important diagnostic procedure where outflow obstruction is likely. It will also allow immediate surgical correction to be carried out at the same time.
Pyloric stenosis: Treatment
A knowledge of foods which empty fastest will allow good dietary management. For example low fat and high carbohydrate liquid diets are most effective. They should be given as frequent small meals.
Where pylorospasm is thought to be present drugs such as atropine, propanthelene bromide are useful as are parasympathomimetics such as bethanechol. Metaclopramide (Emequell; SmithKline Beecham) at 0.5 mg to 1 mg/kg orally 3/4 h before food is the most effective drug. It restores gastric tone and contractions and also relaxes the pyloric sphincter so improving gastric emptying.
Pyloric stenosis generally requires surgical correction. Either pyloromyotomy or pyloroplasty should be carried out depending on the extent of the changes observed. The muscle should always be biopsied in case there is a lesion such as a tumour present. The operation is good for improving the emptying of liquids and to some extent solids. Generally the prognosis is good in uncomplicated cases where there is no serious underlying cause. The prognosis is more guarded where tumour or destructive lesion is detected.
Selections from the book: “Digestive Disease in the Dog and Cat” (1991)