The Role of Fiber

To understand the pathogenesis of diet-related and GI diseases of the rabbit, a thorough knowledge of the normal anatomic and physiologic aspects of rabbit digestion must be appreciated. Details of this are discussed in Chapter 14. In summary, rabbits have a unique digestive physiology. They are strict herbivores, but their digestive strategy differs from those of other hindgut or cecal fermenters (e.g., horses) and ruminants. Being a prey species of small size, rabbits rely on a high energy intake while at the same time having the ability to quickly eliminate fibrous waste that would otherwise have to be carried in the digestive tract. To accomplish this, the rabbit’s cecum and colon have a well-developed mechanism for separating out the digestible and readily fermentable components of the diet while allowing the crude fiber components to be purged. The main driving force for this mechanism is the presence of large quantities of indigestible fiber. Lack of this fiber, either due to dietary inadequacies or conditions that cause anorexia, is the major cause of GI disease in rabbits.¹²

Digesta are separated in the colon in a process of selective retention of fluid and small particles. Normal peristaltic movements propel the larger fiber particles through the colon, while contractions of the haustra in the colon move the fluid and small particles retrograde to the cecum. Small particles and fluid are retained in the cecum, allowing for extensive fermentation. Cecal contents are expelled at regular intervals and reflexively consumed directly from the anus. Fiber stimulates cecocolic motility, either by a distention effect of the bulk, or directly. For example, diets high in fiber promote the production of specific volatile fatty acids in the cecum that directly promote peristalsis.¹²

Inadequate ingestion of coarse, nondigestible fiber will inhibit normal GI peristalsis. Rabbits will ingest hair routinely in the process of grooming. However, unlike many other mammalian pets, rabbits cannot vomit to eliminate accumulated hair. If GI motility is normal, ingested hair moves along with food out of the stomach at regular intervals and is ultimately expelled in the feces. If GI motility is impaired, either as a result of inadequate fiber intake or ileus secondary to anorexia (stress, concurrent disease), hair and normal ingesta accumulate in the stomach. With this accumulation, fluid is absorbed from the stomach, further compacting the contents. Compacted ingesta may cause discomfort to the rabbit, contributing further to anorexia and exacerbating GI hypomotility. A vicious cycle can result, until large amounts of hair and compacted ingesta accumulate in the stomach. This accumulation is erroneously referred to as a “hairball,” “wool block,” or “trichobezoar.” These terms imply, incorrectly, that the hair accumulation is the cause of disease in the rabbit rather than simply being the consequence or a symptom of impaired intestinal motility.

The Effect of Diet and Cecocolic Motility

Cecal bacteria are vital to health. The cecum acts as a fermentation chamber and contains large populations of anaerobic organisms, such as Bacteroides species, and large anaerobic metachromatic staining bacteria (LAMB).^9,17,31 Other bacteria normally present include gram-negative oval and fusiform rods, along with several nonpathogenic species of protozoa and amoeba.³¹ A rabbit-specific ascosporogenous yeast (Cyniclomyces guttulatus), in the Saccharomyces family, resides in the normal rabbit cecum.²⁰ Veterinarians unfamiliar with rabbit fecal flora commonly mistake this yeast for coccidia on fecal examinations. This combined microflora is responsible for the processing of food particles entering the cecum into digestible nutrients, which are then reingested as cecotrophs.

An inappropriate diet or GI stasis can disrupt the balance of this complex cecal microflora and the environment in which it grows. Diets low in fiber cause cecocolic hypomotility, prolonging the retention of digesta in the cecum and ultimately producing changes in cecal microflora. Populations of potentially pathogenic bacteria, primarily Clostridium species and coliform species such as Escherichia coli, are normally present in small numbers in the cecum.^9,17,21 A slowing of cecocolic motility leads to the production of abnormal cecal fermentation products and alterations in the cecal pH. Even mild alterations in cecal pH will cause an increase in these pathogens as the populations of normal organisms decrease. Similarly, a decrease in peristalsis in the small intestine will allow normally small populations of potentially pathogenic bacteria to proliferate. Overgrowth of these pathogens can cause a range of pathology from mild diarrhea to death from enterotoxemia. Other effects of fiber consumption are indirect. High-fiber diets have a low level of available carbohydrates and thus decrease the risk of enterotoxemia caused by carbohydrate overload of the hindgut. Carbohydrates provide an environment in which pathogens such as E. coli and Clostridium species proliferate. Glucose, a byproduct of carbohydrate digestion, is necessary for the production of iota toxin by Clostridium species. Thus, diarrhea and enterotoxemia in pet rabbits is often caused by this disruption in microflora, commonly referred to as dysbiosis.

Feeds high in fiber, such as long-stemmed hay, can also protect rabbits from infectious bacterial enteritis. Rabbits have highly acidic stomachs, with the normal pH of 1 to 2. This acidic environment destroys most ingested bacterial pathogens, resulting in nearly sterile gastric contents. Ingested large-particle fibers, such as hay, mix with other foodstuffs to form a lattice-like ball of food in the stomach. The lattice-like structure of this ball of food allows gastric acid to fully penetrate the ingesta and destroy bacteria. However, if a rabbit is fed primarily pelleted foods, a dense, compacted mass of food is formed in the stomach. The compacted nature of this food protects ingested bacteria from degradation by gastric acid, thus allowing potentially pathogenic bacteria to enter the small intestine. The combination of ingestion of pathogenic bacteria and slowing of intestinal motility as described above can result in clinical bacterial enteritis.

History and Clinical Signs

Obtain a complete dietary history, including the type and amount of commercial pelleted ration, hay, fresh leafy greens, and treats. Rabbits whose regular diet consists primarily of pelleted rations are at higher risk of developing GI stasis. The pelleted diets fed exclusively to feeder rabbits are high in calories (high in digestible carbohydrates), low in fiber, high in protein, and highly digestible, designed to increase weight gain in growing rabbits raised for their meat or fur. Commercial pellet formulations available for pet rabbits vary significantly in their protein, carbohydrate, and fiber contents. Formulations that contain a mix of dried fruits, vegetables, seeds, nuts, grains, and pellets generally have the lowest fiber content and the highest content of fat and carbohydrates. As the previous discussion indicates, there is significant potential for GI complications in a rabbit fed these diets. Similarly, rabbits routinely fed large amounts of high-carbohydrate, high-fat treats such as nuts, seeds, baked goods, and fruits are also predisposed to GI stasis. Acute episodes of GI stasis and dysbiosis are common following ingestion of a large volume of these treats. Rabbits at lowest risk are fed diets of unlimited grass or timothy hay, a moderate amount of fresh leafy greens, minimal commercial pellets, and occasional treats (see Chapter 14).

Question the owner about recent potentially stressful events or underlying disease processes that may cause anorexia. Most rabbits with episodes of GI stasis have such a history, even if fed an excellent diet. Examples of stressful events include changes in housing, introduction of new rabbits or other pets, recent illness, trauma, or surgery. Common underlying disorders that may cause anorexia include dental disease, chronic upper respiratory tract disease, neurologic disorders, lower urinary tract disease, and renal or hepatic disorders. Many affected rabbits will also have a history of little or no routine exercise.

The most common presenting complaint in rabbits with GI stasis is a gradual decrease in appetite and subsequent decrease in fecal production. Appetite usually decreases over a period of 2 to 7 days. Most rabbits will first stop eating pellets, then greens, hay, and finally treats. Left untreated, they stop eating all foods. Water consumption is often decreased as well. Feces become scant, dry, and small, eventually ceasing altogether. Owners may report a corresponding decrease in activity, usually as a result of abdominal pain. Rabbits in pain are reluctant to move, appear less social, may grind their teeth, may dig or scratch, and sit in a hunched position. Weight loss may also be noted, either due to anorexia or underlying disease.

Physical Examination Findings

Affected rabbits generally appear alert and quiet, exhibiting little or no sign of depression. Palpate the abdomen, with careful attention to the stomach contents, intestines, and cecum. The size of the stomach can vary with the duration of disease, but it always contains ingesta. The stomach usually feels firm and doughy and remains pitted on compression. Occasionally, stomach contents are severely dehydrated and solid. No fluid and little or no gas is palpable within the stomach of affected rabbits. This contrasts sharply with rabbits suffering from acute GI dilation (bloat), discussed below. The intestines and cecum frequently contain large amounts of gas. Little or no feces are palpable in the colon. Auscultate the abdomen, listening for borborygmus. Rabbits with GI stasis have few or no gut sounds. The remainder of the physical examination is usually unremarkable except for those findings related to any underlying disorder. Perform a thorough oral examination in all anorectic rabbits to look for underlying dental disease.

Diagnostic Testing

In many cases, the history and physical examination are sufficient for a diagnosis of GI stasis. It is very important, however, to look for an underlying cause. As discussed above, GI stasis occurs secondary to dietary or husbandry deficiencies, stress, pain, or underlying disease and will quickly recur if these are not addressed. Obtain additional diagnostics as indicated to rule out suspected underlying disorders. Radiography may or may not be helpful for diagnosis because the mass of food and hair appears similar to normal ingesta, even with contrast radiography. Visualization of a large, ingesta-filled stomach in a rabbit that has been anorexic for several days is suggestive (Fig. 15-1). This contrasts sharply with the dilated gas and/or fluid-filled stomach observed radiographically in rabbits with acute GI dilation (bloat) (Fig. 15-2) and can be helpful to differentiate the two disorders. Other common radiographic features seen in rabbits with GI stasis include moderate to severe distention of the intestines and cecum and scant fecal pellets. Radiographs may also be helpful to identify underlying causes of GI stasis.

Fig. 15-1 Lateral radiograph of a rabbit with gastrointestinal stasis secondary to ureteral and renal calculi. Note the distention of the stomach with ingesta (arrows) and large amounts of gas within the intestines and cecum (arrowheads), characteristic of gastrointestinal stasis.

Fig. 15-2 Survey lateral (A) and ventrodorsal (B) radiographs of a rabbit with acute gastrointestinal obstruction. Note the severely distended gas- and fluid-filled stomach and the lack of gas within the gastrointestinal tract distal to the stomach. This is consistent with an acute proximal small intestinal obstruction.

Treatment

The key principles in the treatment of GI stasis are to rehydrate the patient and stomach contents, alleviate pain, provide nutrition, and treat any underlying disorders. Fluid therapy is essential to recovery. Administer fluids via either the intravenous or subcutaneous route, depending on the severity of dehydration. If they are anorexic for more than 1 to 2 days, affected rabbits are usually significantly dehydrated and generally require hospitalization for intravenous fluid therapy. Rehydrate the stomach contents by assisted feeding with a syringe or placing a nasogastric feeding tube (see Chapter 13) if the rabbit will not accept feeding slurries orally. A commercial product (Critical Care for Herbivores, Oxbow Pet Products, Murdock, NE) is available for this purpose, and most rabbits will readily accept this product when offered via a syringe. This formula is relatively high in fiber and will provide nutrition needed to stimulate GI motility in addition to rehydrating the stomach contents. If this formula is not available, blenderized pellets soaked with water or an oral electrolyte solution can be used. Feeding these slurries will also help to prevent hepatic lipidosis, which can develop rapidly in a rabbit with a negative energy balance. In addition to assisted feeding, offer rabbits water, plenty of fresh hay, and a variety of greens to provide every opportunity to self-feed. Ingestion of food is critical to reestablishing GI motility.

Rabbits with GI stasis have mild to severe gut pain, especially if the intestines are distended with gas. Most will not begin to eat until this pain is alleviated. If the rabbit appears to be much in pain (reluctant to move, hunched posture, bruxism), administer buprenorphine (0.01-0.05 mg/kg SC, IV q6-12h) and a nonsteroidal anti-inflammatory drug (NSAID) such as meloxicam (Boehringer Ingelheim Vetmedica, Inc., St. Joseph, MO) (0.3-0.5 mg/kg SC q12-24h) or carprofen (1.0-2.2 mg/kg PO q12h). Rabbits feeling less pain may respond well to NSAIDs alone. Be certain that the rabbit is fully hydrated and no underlying renal disorders are present prior to administering NSAIDs. If intestinal motility is severely impaired, parenteral administration is indicated.

Other treatments include GI prokinetics and antibiotics. The use of intestinal prokinetic agents is somewhat controversial; however, anecdotal evidence suggests that they may be beneficial. Cisapride (0.5 mg/kg PO q8h) is readily absorbed from the GI tract and is available through compounding pharmacies. Metoclopramide (0.2-1.0 mg/kg PO, SC, IM q6-8h) has also been used. Antibiotics may be indicated if evidence of dysbiosis is present. If an overgrowth of Clostridium species is suspected, administer metronidazole (20 mg/kg PO q12h). Antibiotics generally effective against other potential pathogenic bacteria include enrofloxacin (15-20 mg/kg PO q12h) and trimethoprim-sulfamethoxazole (30 mg/kg PO q12h).

Continue treatment for 3 to 5 days. Most rabbits will begin to eat and pass stool within 24 to 48 hours of treatment. Feces passed initially may look abnormal in shape, size, and consistency and may contain mucus or hair. Rabbits not responding to treatment should be reevaluated to identify underlying disorders contributing to anorexia. When treatment is successful, instruct owners to feed a diet that contains large amounts of grass or timothy hay, fresh leafy greens, and limited pellets and treats.

Other popular remedies of questionable value include the use of lubricants (e.g., petroleum laxatives), protein-digesting enzymes (e.g., pineapple for bromelain and papain), and simethicone. These treatments alone will have no beneficial effect as they do nothing to return function to the intestinal tract. Many rabbit associations and websites promote the use of simethicone, and it appears to have no ill effects. Caution owners against the use of protein-digesting enzymes, as these can be very irritating to oral mucosa and potentially gastric mucosa. The risk of gastric ulceration is increased in anorexic rabbits, and use of these enzymes may exacerbate this.

Very rarely, the mass of material in the stomach is so dehydrated that it forms a solid, immovable mass and the rabbit fails to respond to medical treatment. In this case, surgical intervention may be necessary. However, the prognosis for a successful outcome is greatly reduced in rabbits that are treated surgically. Anesthesia, pain, stress, and manipulation of the intestinal tract all exacerbate GI stasis. Complications of hepatic lipidosis are a common cause of death in these patients.

History and Physical Examination Findings

A sudden onset of anorexia and depression is the hallmark feature of acute GI obstruction. Some rabbits are found acutely moribund or discovered dead with no premonitory signs. Unlike rabbits with GI stasis, there is no history of a recent stressful or painful event, and dietary history does not play a role. Affected rabbits suddenly refuse all food and quickly stop producing feces. Most demonstrate signs of severe pain, such as reluctance to move, hunched posture, and bruxism. As metabolic derangements and shock develop, affected rabbits become severely depressed, listless, laterally recumbent, and minimally responsive to external stimuli. With stomach rupture, they may suddenly cry out and die. On physical examination, a large, fluid-filled or tympanic stomach is palpable in the cranial abdomen. Pain is elicited on palpation of the stomach. If examined early, affected animals are alert but quiet, tachypneic, and tachycardic. Later, they become hypothermic, bradycardic, and hypotensive.

Diagnostic Testing

Obtain radiographs to confirm the diagnosis. The radiographic appearance of a rabbit with acute GI obstruction differs sharply from that of a rabbit with GI stasis or that of a normal rabbit. The stomach will appear severely distended with gas, fluid, or both (see Fig. 15-2). Gas distention of intestinal loops proximal to the obstruction are noted, especially with obstructions occurring in the midduodenum or ileocecocolonic junction. Pneumoperitoneum indicates that the stomach has ruptured and carries a grave prognosis. Obtain blood for a complete blood count (CBC) and biochemical profile. Results may demonstrate dehydration and a variety of acid-base and electrolyte disorders.

Initial Medical Treatment

Begin treatment immediately, as this is a life-threatening disorder. Initial treatment goals are to decompress the stomach, treat shock, correct any fluid and electrolyte imbalances, and control pain. To control pain, administer buprenorphine (0.02-0.05 mg/kg SC, IV q6-12h). Sedation is necessary to decompress the stomach in most cases. Sedate with midazolam (0.5-1.0 mg/kg IM, IV) and/or mask with isoflurane or sevoflurane. A well-lubricated 16- to 18-Fr red rubber catheter works well as an orogastric tube. It may be necessary to cut additional holes in the end of the tube to allow larger volumes of gas and fluid to pass. Measure the distance from the nose to the last rib (the distance to the stomach) and mark the tube. Lubricate the tube well and pass it gently per os into the stomach. Remove all gas and air from the stomach. Percutaneous trocharization of the stomach is not recommended as a method of decompression, since this will likely cause rupture of the stomach. While the stomach is being decompressed, place an intravenous catheter and begin treatment with a shock dose (90 mL/kg per hour) of isotonic crystalloid fluids. When dehydration is corrected and shock is controlled, reduce administration to a maintenance rate. Correct any electrolyte imbalances. In most instances, surgery is immediately necessary to remove the obstruction. However, in a small number of cases, the foreign object will pass following medical treatment. Monitor these rabbits closely to determine if the obstruction is passing. Palpate the abdomen frequently, monitor for signs of pain, and repeat radiographs. The gas pattern will change, and gas will be visible in the distal intestines if the rabbit is passing the obstruction. These rabbits will appear comfortable and begin eating, drinking, and defecating.