Rabbits, chinchillas, and guinea pigs are monogastric, hind-gut fermenters; all have a functional cecum and require a high-fiber
diet. Fiber is broken down in the cecum by a variety of microorganisms which are nourished by a constant supply of water and
nutrients from the stomach and small intestine. These same microorganisms produce volatile fatty acids (VFAs) which, in turn,
affect appetite and gut motility. Any disturbance in this mutually beneficial relationship can result in gastrointestinal
hypomotility—increased GI transit time characterized by decreased frequency of cecocolonic segmental contractions. In severe
cases, this leads to ileus with little to no caudal movement of ingesta, known in practice as gastrointestinal stasis.
Gastrointestinal stasis is not a disease but a symptom that one or more of the factors governing GI motility are out of order.
There are no breed or gender predilections for GI stasis, and it can occur at any age. Proper hind-gut fermentation and GI
tract motility are dependent on the ingestion of large amounts of roughage, long-stemmed hay, and water. Diets that contain
inadequate amounts of long-stemmed, course fiber predispose the patient to gastrointestinal stasis. Hypomotility of the GI
tract can alter cecal fermentation, pH, and substrate production such that enteric microflora populations are altered.
Diets low in course fiber typically contain high simple carbohydrate concentrations, which provide a ready source of fermentable
products. This alters the large bowel ecology in a way that threatens favorable microorganisms and promotes bacterial pathogens
(e.g. E. coli and Clostridium), and toxin production. Bacterial dysbiosis can cause acute diarrhea, chronic intermittent diarrhea, enterotoxemia, ileus,
or gas accumulation ("bloat"). As nausea and gastrointestinal discomfort lead to anorexia, fiber and water intake are further
reduced, and the process becomes self-perpetuating. If prolonged, GI stasis often leads to hepatic lipidosis, dehydration,
and other secondary complications.
Rabbits, guinea pigs, and chinchillas can not vomit. In the healthy digestive tract, a moderate amount of gas is normally
produced by the fermentation process and eliminated by peristalsis. With GI stasis, however, there can be excessive gas production
and, without normal motility, the stomach and intestines can overfill with gas and become distended, a condition commonly
Gastrointestinal stasis is often the result of insufficient dietary fiber and/or excessive stress. It is most commonly associated
with inappropriate diet. A diet high in roughage such as grasses and long-stemmed hay is ideal. Rabbits, guinea pigs, and
chinchillas that do not receive enough fiber often suffer from subclinical hypomotility, and are thus more susceptible to
other risk factors for GI stasis, whereas those that have adequate fiber intake are more resistant.
GI hypomotility is promoted by a diet consisting primarily of commercial pellets, especially those containing seeds, oats,
or other high-carbohydrate treats. Feeding cereal products (bread, crackers, and breakfast cereals) and foods high in simple
carbohydrates (fruits, yogurt drops, other treats) further increases the risk. Because intestinal microflora depend on a steady
flow of water and nutrients, and the digestive tract depends of fiber for normal motility, any event leading to inappetence
or anorexia (pre-surgical fasting, sudden changes in the diet, concurrent illness, starvation) or dehydration (sipper malfunction,
bad tasting water, careless mistake) can trigger an episode of GI stasis.
Stressful conditions have a negative effect on gut motility. GI motility is regulated in part by the autonomic nervous system;
stress increases the adrenal output of epinephrine and inhibits peristalsis. Common causes of stress include dental disease
(malocclusion, molar elongation, odontogenic abscesses), metabolic disease (renal disease, liver disease), pain (oral, trauma,
postoperative, urolithiasis), anxiety (dyspnea, fear, fighting, lack of hide box), neoplasia, infection, parasitism, and environmental
changes (boarding, new pets, unfamiliar noises).
Other factors that can contribute to GI stasis include toxin ingestion, foreign material (scoopable cat litter, hair, carpet
fiber), obesity, inactivity, confinement, and certain drugs (anesthetics, anticholinergics, opioids, antibiotics). Inappropriate
antibiotics can damage enteric microflora, promote the growth of pathogens associated with GI stasis, and lead to antibiotic-associated