Pyloric Stenosis

Pyloric Stenosis in Rabbits

From: National Center for Biotechnology Information:

DUODENAL/PYLORIC STENOSIS AND PYLOROSPASM

Alternative names - congenital hypertrophic pyloric stenosis; hypertrophic pyloric stenosis (HPS); functional pyloric stenosis (FPS); gastric outlet obstruction.
Description - Increase in size (thickening, hypertrophy) of the circular sphincter muscle of the pylorus (cone-shaped constriction in the gut at end of stomach/beginning of small intestine which prevents intestinal contents from reentering the stomach when the small intestine contracts, regulates passage of food into the duodenum). Pyloric stenosis often begins as prolonged spasms, the frequency increases, this may lead to muscular hypertrophy and complete obstruction. Occurs primarily in human infants 2-8 weeks old, young puppies, and foals.

In Functional Pyloric Stenosis (FPS) the physical appearance of the pyloric valve is normal. However, the muscle doesn't relax to allow food material to pass into the small intestine. The loss of function may be due to inflammation of the area or even a loss of normal nerve control. These cases can be frustrating to figure out.
Symptoms - Distended upper abdomen, apparent abdominal pain, gastric peristaltic waves (muscular contractions), vomiting (in humans) which becomes more frequent and projectile, dehydration, diarrhea/constipation, weight loss, constant hunger, fretfulness, apathy.
Diagnosis - Upper GI barium x-ray series or ultrasound (preferred) reveals: (1) elongation of the pyloric channel (2) little fluid entering the duodenum (3) persistent thickening of the pyloric muscle. There is no peristalsis through the pylorus. In plain abdominal films, the stomach develops a "caterpillar" appearance due to the rigorous peristaltic waves. There might be evidence of a gastric outlet obstruction with a large dilated stomach. Although the stomach emptying time may be evaluated to some degree, it is not definitive in each individual case. Sedation with endoscopy exam and tissue biopsy of the pyloric region is another option. A palpable olive-shaped mass (in humans) in the abdomen to the right of the umbilicus is sometimes detected.
Imaging Findings - Upper GI signs which indirectly image the pyloric mass include: (1) shoulder = mass effect on the lesser curvature of the gastric antrum, (2) teat = peristaltic waves encroaching on the mass and the shoulder, (3) beak = barium entering only the entrance of the pyloric canal, (4) string = barium extending into the narrowed and elongated pyloric canal, (5) U = upturned course of the pyloric canal towards the duodenum (6) track = parallel columns of barium in the pyloric canal produced by longitudinal infolding of the pyloric mucosa, (7) caterpillar = gastric contour distorted by multiple deep peristaltic waves, (7) mushroom = encroachment of the base of the duodenal bulb by the hypertrophic muscle mass, (8) US signs, which directly image the pyloric mass, include an anechoic ring of hypertrophied pyloric muscle surrounding the echogenic central mucosa.
Chemistry panel - the classic electrolyte picture is one of metabolic alkalosis accompanied by severe potassium depletion. Hemoconcentration may be reflected by elevated hemoglobin and hematocrit values. The serum chloride is low and the renal response to alkylosis causes the urine to be concentrated and alkaline (pH>7.4) because significant amounts of bicarbonate are excreted in the urine. The plasma bicarbonate concentration is decreased, thereby compensating for the alkylosis. Up to 30% of patients will have an indirect reacting hyperbilirubinemia which as yet remains unexplained. Electron microscopy of liver biopsy specimens has shown, in a small number of patients, dilatation of the endoplasmic reticulum.
Causes - Largely unknown, congenital (genetic, occurs in members of the same family or family cluster), cancer (malignant neoplasm) of the pyloric valve area, infiltrative mycosis, foreign bodies, scarring from peptic ulcer disease, or secondary to duodenal ulceration. Males are affected 4-5 times more often than females.

Sometimes the onset of signs is related to a change in diet (when solid food is first introduced). Acquired stenosis due to masses in the wall of the pyloric antrum has also been seen in young horses, possibly secondary to ulcers, and a mass of unknown cause was found at the pyloroduodenal junction in a horse. Gasterophilus (bot) larvae has also been reported to cause stenosis in very rare cases. In the boxer and Boston terrier breeds of dogs, it is congenital. There are some reports of a similar condition in cats, particularly Siamese.
Prevention - There is no known prevention.
Treatment - One of the following: (1) Pyloromyotomy (surgical procedure to split the over-developed musculature of the pylorus). Rehydration with IV fluids prior to surgery. A small incision is made into the abdomen. The surgeon then finds the enlarged pylorus and divides the muscle, leaving the lining of the stomach intact. Only the muscular band around the opening is incised. The muscle then shrinks and heals. The operation is fairly simple and has a high success rate. (2) Pyloroplasty (endoscopic "through the scope" balloon dilatation) is also extremely effective. (3) Highly selective vagotomy (HSV) plus dilatation of the stenosis. Since the stenosis is usually distal to the pylorus rather than truly pyloric, such dilatation does not damage the pyloric ring, although it may on occasion lead to perforation of the first part of the duodenum. (4) Endoscopic gastric drainage, followed by oral omeprazole (an inhibitor of gastric parietal cells' hydrogen pump) or cimetidine. [Caution: the incidence of gastric and duodenal bacterial overgrowth, which frequently occurs in conditions where diminished acid secretion is present, is considerably higher in patients treated with omeprazole compared with cimetidine because omeprazole inhibits acid secretion more effectively than cimetidine.]

Note: Oral triple therapy (bismuth subsalicylate, metronidazole, tetracycline) plus ranitidine or high-dose omeprazole (as an alternative to amoxycillin) is highly effective in eradicating Helicobacter pylori infection in patients with active peptic/duodenal ulcer disease and duodenal (bulbar) stenosis. A triple combination of omeprazole, clarithromycin, and tinidazole, given for 1 week, has also been shown to be highly tolerable and effective in treating ulcers caused by Helicobacter pylori infection, achieving a success rate of >90% in the adult population.

Expectations (prognosis) - Small, frequent glucose and saline feedings are usually well tolerated several hours after the surgery. The complete relief of symptoms occurs after adequate surgical repair. Recurrence is very unlikely.

From "Biology of the Laboratory Rabbit", ISBN 0-12-469235-4, 2nd Edition (1994), page 340:

IV. PYLORIC STENOSIS/PYLOROSPASM

Congenital pyloric stenosis with muscular hypertrophy was first reported in a rabbit by Cardy in 1973. A preweanling Flemish Giant male died suddenly, and gastric dilatation with complete closure of the pylorus was observed at postmortem examination. Histologically, the external muscularis layer of the pylorus was extremely thickened. Weisbroth and Scher (1975) reported three cases of hypertrophic pyloric stenosis in rabbits, all of which were older than 12 weeks of age. The rabbits had similar clinical histories of anorexia, listlessness, weight loss, and constipation. Hypertrophy of the muscularis was noted in all three cases, and postmortem measurements indicate that the pylorus was thickened at the expense of the lumer as pyloric circumference was normal. It was not known if the three cases were exacerbations of congenital pyloric stenosis, whether they arose de novo in adulthood, or whether they were secondary to pylorospasm.

Pylorospasm has been reported twice in the domestic rabbit by Klarenbeek in 1946 and by Blount in 1957. Both cases occurred in Europe and involved substantial numbers of post-weaning or young adult animals. Although a satisfactory cause was not established, the cases were assumed to be associated with some noxious substance ingested with the food. In the report by Klarenbeek (1946), anorexia, gastric and cecal tympany, constipation, and grinding of the teeth were the most consistent signs, with death usually resulting in 1-5 days. Barium sulfate meals failed to pass through the pylorus during diagnostic radiographic examinations owing to spasmodic contraction of the pylorus. Gastric or pyloric lesions (such as hypertrophy) were not reported, although secondary hypertrophy is known to be a result of pylorospasm (Flatt et al., 1974). A variety narcotic and sympathomimetic relaxants were used in unsuccessful attempts to treat the condition.

NOTE: The "noxious substance ingested with the food", which may cause delayed emptying of the stomach and painful stomach/GI ulceration, could be mycotoxins (invisible corrosive poisons produced by molds) which may occur as "hot spots" in the hay or pellets. Have your feed tested for mycotoxins at an agricultural food safety laboratory. Be sure to ask for numerical results down to 100 parts per billion, if possible, because even low concentrations can be harmful/deadly to rabbits.