Common Gastrointestinal Syndromes in Cats

5. Common Gastrointestinal Syndromes in Cats

Dysphagia

Dysphagia is a difficulty in swallowing. It may be due to an obstruction, a painful oropharyngeal or esophageal disorder, or it may be a motility problem (Washabau, 2005). The main sign is regurgitation.

Regurgitation is defined as the passive expulsion of saliva or non-digested food. It often occurs very soon after the ingestion of food, although in the event of saliva regurgitation it may occur less rapidly. Contrary to vomiting, regurgitation occurs suddenly, without prodromal signs or abdominal contractions (Guilford & Strombeck, 1996b).

An esophageal disorder produces other clinical signs:

• Ptyalism
• Halitosis
• Dysorexia or anorexia
• Odynophagia (painful swallowing)
• Polypnea
• Coughing and/or discharge in the event of secondary pneumonia.

Complementary Tests

Plain Radiography

Physiologically, the esophagus cannot be visualized by radiography. Its appearance on a plain radiograph may be due to localized or generalized dilatation, or to the retention of liquids or solids. These images enable the identification of a radiodense foreign body or suggest the presence of a foreign body based on indirect signs (localized dilatation, localized air densification, pneumomediastinum) (Konde & Pugh, 2003).

Radiography with Contrast Medium

This confirms any dilatation if the plain radiographs are insufficient. The use of barium is contraindicated if parietal perforation is suspected due to the risk of mediastinitis. The presence of image subtraction suggests a foreign body or an endoluminal mass.

Fluoroscopy

This dynamic test is worthwhile when a functional problem is suspected. It may be beneficial when evaluating the extent of stenosis (Figure 6).

Figure 6. Radiograph with contrast medium that indicates esophageal stenosis. (©V. Freiche).

Esophagoscopy

The endoscopic examination (Figure 7), which is conducted under general anesthesia, is the examination of choice to explore all esophageal disorders of anatomical, inflammatory or neoplastic origin. It enables immediate macroscopic evaluation of the surface of the mucosa, biopsies, extraction of foreign bodies or enables dilatation of post-inflammatory or post-traumatic stenosis.

Figure 7. Esophagoscopy. Normal aspect of the distal esophagus of a cat showing characteristic rings. (©V. Freiche).

Vomiting

Vomiting is defined as the active reflexive rejection of the stomach content preceded by prodromal signs (nausea, ptyalism, abdominal contractions). The dietary behavior and lifestyle of carnivores mean that occasional vomiting is not considered alarming. In its more acute and more frequent form however, it is one of the main reasons among cats for a visit to the veterinarian.

There are a huge number of disorders that can cause vomiting. Therefore, the etiological diagnosis, when justified, is based on a number of tests, which must be conducted as part of a logical approach. The digestive causes of acute or chronic vomiting are considered after the exclusion of all other potential causes in cats: viral infections, hernias, neoplasia, metabolic diseases, kidney failure, neuroendocrine diseases, intoxication and others (Moore, 1992; Gaschen & Neiger, 2004; Simpson, 2005).

Vomiting with a digestive origin may be due to stomach problems. The most common are: inflammatory diseases, neoplasia, the presence of hairballs, pyloric obstruction, ulceration or foreign bodies (Figure 8). Primary gastric motility problems may be suspected with chronic vomiting, however, they are more common in dogs than in cats. In the absence of a specific disorder, there may be a problem with stomach emptying (Hall & Washabau, 1999).

Figure 8. 5 year old female cat who presented with anorexia. The abdominal ultrasound shows loops of the small intestine that are abnormally collapsed due to the presence of a linear foreign body. (©V. Freiche).

In cats, vomiting may also be a sign of a more distal disorder, even in the absence of any other sign. This is a peculiarity of the species. Major causes of vomiting not situated in the stomach include pancreatic diseases, inflammatory diseases or cholecystitis (Strombeck & Guilford, 1996b).

Signs of Vomiting

The aspect or chronology of vomiting with respect to the ingestion of food sometimes provides some pointers. Some criteria are reliable:

• Uncontrollable or unpredictable vomiting suggests an occlusive syndrome, peritonitis, pancreatitis, cholangiohepatitis, a metabolic, or a severe viral disorder;
• The presence of undigested food well after meal time suggests a gastric retention syndrome (functional or anatomical in origin) or pancreatitis;
• Vomiting in the morning before eating is common with chronic gastritis (or reflux gastritis);
• A large volume is common with an occlusive syndrome or delayed gastric emptying.

However, the nature or time of vomiting with respect to meal time commonly provides no pointers as to the cause:

• The presence of blood may be evidence of an underlying disorder with a very poor prognosis (neoplasia) or conversely an entirely benign and reversible inflammatory state.
• Some neoplastic diseases are expressed by crude, non-specific symptoms, that emerge slowly;
• Chronic sub-occlusive states are difficult to characterize, especially if they are caused by the ingestion of a linear foreign body.

Clinical Examination

There must be a precise and complete clinical examination as part of an internal medicine approach (Tams, 1996). If the cat is not cooperative, moderate sedation will make the examination easier.

• An inspection of the oral cavity (Figure 9) must always be conducted. It may reveal the ingestion of a linear foreign body or ulcers caused by uremia.
• Abdominal palpation is likely to provide pointers, such as the identification of a compressive digestive or extra-digestive mass, or palpation of a foreign body. The pressure generated by palpation may reveal induration or the presence of isolated sources of pain. Indirect signs are also seen, such as the accumulation of gas or fluid in front of a digestive lesion.
• If the cat is not obese, the presence of hyperplastic lymph nodes must always be palpated.
• A rectal swab (which generally necessitates tranquilization) enables evaluation of the rectal mucosa and the acquisition of a fecal sample (traces of fresh or digested blood).
• The hydration state of the cat.

Figure 9. Foreign body in the oral cavity. The inspection of the oral cavity is part of the clinical examination. A linear foreign body attached to the base of the tongue can be extracted. (©V. Freiche).

Diagnosis

Table 2 lists the benefits of complementary tests that may be conducted in the evaluation of a vomiting patient.

Gastric Retention Syndrome

Gastric retention syndrome is defined as the stomach’s incapacity to evacuate its content within the physiological time. This may be due to digestive lesions or functional disorders (primary or secondary digestive motor disturbances). Although more common in dogs, this syndrome has been reported in cats. The clinical signs include vomiting of partially digested food well after mealtime.

Etiology of Gastric Retention Syndrome

Obstructive Digestive or Extra-digestive Compressive Lesions

Some form of pyloric stenosis is the most common cause of gastric retention syndrome in domesticated carnivores. If they are intrinsic, they may be the result of several pathophysiological mechanisms.
- Congenital pyloric stenosis (Figure 10): found in young animals, is due to hypertrophy of the smooth muscle fiber. In cats, it is described in Asiatic breeds, specifically the Siamese (Strombeck, 1978)
- Secondary gastric retention syndrome with hairball (Figure 11), which can be lodged chronically and generate repetitive intermittent vomiting.
- Post-inflammatory pyloric stenosis (Figure 12): healed pyloric lesions (old ulcerations, chronic inflammatory lesions causing major parietal fibrosis, foreign bodies trapped in the antral-pyloric mucosa) sometimes cause acquired stenosing lesions.
- Extrinsic digestive compression (much less common): by adjacent abdominal organs (liver tumor, lymphadenopathy).

Figure 10. Pyloric stenosis in a young European cat a few months of age. The pyloric diameter compared to biopsy forceps (2.8 mm). (©V. Freiche).

Figure 11. Hairball secreted by a Japanese Bobtail (length: 5.5 cm) Hairballs are the primary cause of gastric retention in cats. (© C. Tournier).

Figure 12. Post-inflammatory pyloric stenosis in a European cat who historically had gastritis. Edema is visible in the mucosal antral area. (©V. Freiche).

Digestive Motor Disturbances

Digestive motor disturbances leading to slower gastric emptying may be caused by hypomotility or dysregulation of the contraction rhythm. Either primary or secondary in origin, their pathogenesis is thought to be related to dysfunction of the gastric pacemakers. This leads to gastric "arrhythmia", as observed in the event of repetitive hairballs in cats (Washabau, 2003). A gastric emptying disorder must be determined by studying the transit of solid food (Wyse et al., 2003). This exclusion diagnosis is suspected when other examinations are within normal limits.

There are secondary motor disturbances:

• Excessive sympathetic stimulation (stress, pain, deep abdominal lesions: peritonitis, pancreatitis, major parasitism): a very long gastric retention is observed with pancreatitis
• Post-surgery iatrogenic trauma
• Medical treatment: anticholinergic agents, opiates, non-steroidal anti-inflammatory drugs (NSAID)
• Metabolic disorders: acidosis, uremia, hyperkalemia, hypo- or hypercalcemia, endocrinopathies
• Neoplastic process or ulceration (pain inhibiting transit by sympathetic stimulation).

When Should the Gastric Retention Syndrome Should Be Suspected?

The characteristic clinical sign of the gastric retention syndrome is vomiting of undigested food well after mealtime. However, owners also often describe vomiting of gastric juice. These signs are due to chronic gastric distension and inflammation of the mucosa, respectively.

Digestive motor disturbances associated with gastric retention syndrome may cause signs of dyspepsia, such as intermittent ptyalism, antalgic gait, gas bloat, very painful spastic crises and yawning. Abdominal palpation confirms the presence of gastric distension. The clinical signs are more alarming when motor disruptions are secondary to metabolic alterations or a septic state (peritonitis, pancreatitis).

Diagnosis

Table 3 lists the benefits of the complementary tests that may be conducted to assist in the diagnosis of the gastric retention syndrome.

Figure 13. Male cat, 3 year old, presented for lethargy and vomiting. The echocardiographic picture shows an abnormal gastric retention. (©V. Freiche).

Treatment

This ensues from the etiology when it can be identified, of the gastric retention syndrome.

Medical Treatment

In the event of metabolic problems, treatment includes management of the underlying disorder and administration of prokinetic agents (Hall & Washabau, 1999) (metoclopramide, domperidone, ranitidine, etc). The administration of prokinetics entails a potential risk of occlusive syndromes.

Surgical Treatment

Depending on the case, pyloroplasty, extraction of a foreign body, excision or the biopsy of polyps or neoplastic lesions may be indicated.

Dietary Measures

Depending on the etiology, diet can be a significant adjunctive therapy (Hall & Washabau, 1999). Dietary treatment can support gastric emptying. Small meals of a liquid or moist diet are the best recommendation for the initial therapy. If small foreign bodies or trichobezoars (hair balls) have been identified, lubricants such as paraffin that facilitate the propulsion through the gut, maybe beneficial. Bromelain, a cysteine protease contained in pineapple juice, has been suggested as a dietary treatment. In one study, bromelain was able to degrade trichobezoars to a variable extent (Reed et al., 2004). However, more in vivo data are needed for the assessment of efficacy.

Dietary fiber plays an important role in preventing gastric retention. Dietary fiber significantly affects fecal hair excretion in cats and a high-fiber diet (12 - 15% total dietary fiber [TDF] as fed) is useful in the prevention of hairball formation (Tournier et al., 2005) (see Royal Canin Nutritional Information at the end of the chapter).

Diarrhea

Diarrhea is characterized by the increased frequency of evacuation, moisture content and often volume of fecal matter. The owner will not always immediately identify diarrhea if the cat excretes outdoors.

In cats, the moisture content in a normal stool usually varies between 55% and 70%, depending on the food (internal data from Royal Canin Research Center). It can go as low as 40% in constipation and as high as 90% with diarrhea (Williams & Guilford, 1996).

Diarrhea is mainly caused by intestinal diseases, but other systemic diseases may affect intestinal function and can induce hypersecretion or malabsorption (Battersby & Harvey, 2006). It can be due to diseases of the small or large intestine or it may affect both (Tams, 2004). Acute cases can be caused by dietary indiscretion, infections with enteropathogenic viruses, bacteria or parasites. In chronic cases, lymphoplasmacytic or eosinophilic inflammatory bowel disease (IBD), bacterial dysbiosis or dietary allergy or sensitivity can often be the underlying problem. Exocrine pancreatic insufficiency is reported in the cat. It is certainly under-diagnosed in this species (Williams, 2005). Drug intolerance and acute or chronic systemic diseases can induce diarrhea. Digestive tumors are also a common cause of chronic diarrhea in aging cats.

Origin in the Digestive System

There are far fewer clinical criteria to differentiate small intestinal diarrhea from large intestinal diarrhea in cats compared with dogs. This is due to the fact that disorders of the digestive walls are typically diffuse in cats.

Table 4 lists the criteria for differentiating small intestinal diarrhea and large intestinal diarrhea in domesticated carnivores.

Pathophysiological Reminders

Several mechanisms are involved in the increased water content of stools (Freiche, 2000). When the small intestine is injured three types of physiological disturbance may occur separately or collectively to lead to the clinical expression of diarrhea:

• Increased secretion of water and electrolytes
• Decreased absorption of nutrients (mainly carbohydrates and lipids)
• Decreased absorption of water and electrolytes (Figure 14)

When the colonic mucosa is responsible, failure of the reabsorption function of the colon and excessive secretory activity of the parietal mucus glands are observed.

Figure 14. Digestive factors that may affect stool consistency.  

Coherence of Diagnosis

Importance of the History and Clinical Examination

A very large number of diseases may cause chronic diarrhea. There is no general diagnostic plan that can be used in all cases, so the cat’s history and a detailed clinical examination are essential.

At the end of these two steps the clinician must attempt to answer two questions that have a significant impact on the choice of treatment:

• Does the diarrhea have a strictly digestive origin or could the cause be metabolic?
• Is it small intestinal diarrhea or large intestinal diarrhea? (Table 4)

Sequence of Complementary Tests and Differential Diagnosis

In its specific context, each clinical case demands a logical sequence of complementary examinations. Various tests are possible:

• Hemato-biochemical analyses, serological assays
• Fecal examination
• Biochemical exploration of malassimilation (folate and vitamin B12)
• Digestive tract imaging: radiography, ultrasound, gastrointestinal endoscopy. These different techniques have radically transformed knowledge of gastroenterology over the past decade.

Therapeutic Consequences

Current Therapies

Specific therapeutic plans are provided below for the most common diarrheal disorders in the cat:

• Infectious gastroenteritis
• Characteristics of diarrhea in kittens
• Dietary intolerance
• Chronic inflammatory bowel diseases (IBD)
• Colonic diseases
• Digestive neoplasia.

Dietary Treatment

Dietary treatment is more of an adjunctive type of therapy in many cases of chronic small intestinal disease. As undigested food compounds are fermented by the colonic microflora and can have negative effects (such as gas formation and flatulence, and perhaps also promote further diarrhea), the diet should be highly digestible.

Highly Digestible Diets

Diets for patients with suspected intestinal dysbiosis, to be characterized either as "small intestinal bacterial overgrowth" or as a disturbed micro-ecology in the upper or lower gastrointestinal tract, should be based on high quality ingredients. They support the patient by providing available carbohydrates and proteins that facilitate nutrient absorption in the small intestine. Highly digestible diets typically present dry matter digestibility values that exceed 85 - 88% and protein digestibility that exceeds 92%. These diets require less gastric, pancreatic, biliary and intestinal secretions for digestion. This results in almost complete digestion and absorption in the upper small intestine so that minimal residue is presented to the lower bowel (Figure 15). Minimal residue reduces bacterial byproducts that may contribute to inflammation and osmotic diarrhea.

The passage of unabsorbed nutrients into the lower gut is reduced, as is the potential load of antigenic material. As long as dietary sensitivity or allergy cannot be excluded, an antigen-limited hypoallergenic diet is advantageous. These diets contain either highly digestible protein sources (e.g., protein hydrolyzates, low-ash poultry, fish) or other meats that are unusual in commercial diets (e.g., venison, duck, rabbit etc).

Figure 15. Improving digestibility to limit fermentation in the colon.  

Carbohydrates

Mucosal atrophy typically leads to a decreased availability of disaccharidases and carbohydrate malabsorption. Bacterial overgrowth and decreased transport of monosaccharides by malfunctioning enterocytes can also contribute to carbohydrate malabsorption, which in turn contributes to osmotic diarrhea. Therefore, diets formulated for cats with gastrointestinal disease should contain reduced quantities of highly digestible carbohydrate. Rice has long been considered the ideal carbohydrate for gastrointestinal disease. Rice is very highly digestible because it has a limited branched starch structure (amylopectin) and a very low dietary fiber content. Rice does not present any crossed antigenicity with wheat gluten and has rarely been implicated in adverse food reactions.

Furthermore, rice improves the digestibility of dry diets, and contains soluble factors that inhibit secretory diarrhea.

Dietary fiber may benefit from an increased concentration or modified type of dietary fiber despite low-fiber diets (< 10% TDF) often being recommended. When indicated based on the clinical outcome, it can be worthwhile increasing fiber concentration by adding small amounts of insoluble or soluble fiber sources.

- On contact with water, soluble fiber such as pectin forms a gel (gelling capacity) or solution that can be more or less viscous (thickening capacity). Due to this viscosity, such fibers tends to slow down gastrointestinal transit by simply increasing resistance to the flow. Soluble fiber sources are also important regulators of the intestinal microbiota due to their high fermentability (Table 5).
- Insoluble fiber such as cellulose increases fecal bulk, fecal water content, absorbs toxins and normalizes both segmental and propulsive motility.

Both insoluble and soluble dietary fiber may be beneficial in the symptomatic treatment of certain large bowel diarrheas. In homemade diets, adequate supplements are 0.5 tablespoons of:

• Cellulose or wheat bran when insoluble types of fiber are desired
• Psyllium when soluble fiber sources are more promising. In commercial diets designed for intestinal disorders, various sources of fermentable fiber should already be included (e.g., beet pulp, fructo- oligosaccharides [FOS], mannan-oligosaccharides [MOS]).

Energy Density

Fat is often regarded critically as a compound in diets for patients with small intestinal disease: when fat digestion is impaired, the bacterial conversion of non-absorbed fatty acids and bile acids into hydroxylated fatty acids and deconjugated bile acids can increase fluid secretion and aggravate clinical signs of diarrhea.

On the other hand, weight loss and poor coat and skin quality can be major problems in cats with small intestinal problems. As high fat diets help provide energy and fat soluble vitamins to debilitated cats, the prescription of high fat diets is advocated. Fat digestibility is generally extremely high (up to 99%). In addition, a high-energy diet (> 20% on DMB) enables a reduction of the volume of the diet and decreases the intestinal load.

Therefore, the level of fat tolerated by cats with small intestinal disorders needs to be individually evaluated when increased dietary fat levels are warranted. It is justified to use increased fat intakes when weight loss is a prominent clinical sign and when a steatorrhea is not present.

Probiotics and Prebiotics

Probiotics and prebiotics have been suggested as treatment options for patients with intestinal problems.

Data on the efficacy and the presumed “stabilizing” effect of probiotics on digestive diseases are scarce. Often enough, products have not been evaluated with regards to efficacy or may not be suitable for cats and the specific conditions in the diseased intestinal tract. L. acidophilus (DSM 13241 strain) used as a probiotic increased the lactobacilli counts in feces and decreased numbers of Clostridium spp. and Enterococcus faecalis (Marshall Jones et al., 2006).

Prebiotics are non-digestible carbohydrates that are fermented by gut bacteria in the small and large intestine. The basic idea is to offer a substrate to "beneficial" members of the gut flora and to promote a shift in the composition of the gut bacteria in favor of the "healthy" microbiota, such as lactobacilli and bifidobacteria. Through inhibitory process, these bacteria prevent the proliferation of potentially pathogenic bacteria (i.e., Clostridium perfringens). These bacteria produce the short chain fatty acids (SCFA) butyrate, acetate and propionate, which provide fuel for the colonocytes. SCFA enhance sodium and water absorption, increase mucosal blood flow and increase gastrointestinal hormone release. These mechanisms contribute to the trophic effect that SCFA have on the intestinal mucosa, stimulating enterocyte and colonocyte proliferation.

Different prebiotic carbohydrates have been used, mainly inulin and various oligosaccharides (fructo-oligosaccharides, galacto-oligosaccharides, mannan-oligosaccharides). Some gastrointestinal changes can be expected, including pathogen control and reduced putrefactive compound production (Hesta et al., 2001; Flickinger et al., 2003). The efficacy of these additives needs to be studied more in clinical patients to evaluate whether such feed additives and feed compounds are beneficial in cats with intestinal disease (Sparkes et al., 1998).

Protein-losing Enteropathy

Protein-losing enteropathy (PLE) results from a range of gastrointestinal disorders that lead to non-selective protein loss. They are characterized by a total serum protein content less than 5 g/dL and an albumin concentration lower than 2 g/dL. These values must be interpreted on the basis of the normal reference ranges for the laboratory.

Although lymphangectasia remains the primary cause of PLE, many parietal disorders of the digestive tract are likely to be expressed as hypoproteinemia. Forms of PLE continue to be exceptional in cats, in the event of either IBD or digestive neoplasia. Identification of hypoproteinemia in cats always worsens the prognosis of the underlying disorder.

Disorders involved in PLE are listed in Table 6.

Dietary Measures

Patients with PLE are often clinically fragile, and careful symptomatic therapy must be integrated with intensive dietary and medical management strategies in most cases (Peterson & Willard, 2003). The nutritional management of cats with PLE is mainly based on diets with a low fat concentration. Low fat (≤10%, as fed) diets have been proven to be supportive because they counteract the pathophysiological events in PLE.

Long chain fatty acids are transported through the intestinal lymphatics. This may increase lymphatic vessel distension and increase intestinal protein loss and eventually lipid exudation. Linoleic acid and arachidonic acid have to be provided in sufficient amounts to fulfill the requirements. Medium chain triglycerides have some value because of their ability to be absorbed by bypassing the lymphatic system. A general limitation for using this type of fat is its negative effect on palatability and potential for inducing vomiting and diarrhea in cats. Higher supplementation with fat-soluble vitamins would be required and there are anecdotal reports of improvement with glutamine supplementation.

Melena

Melena occurs when blood from the stomach or small intestine is passed in the feces. The color is black due to the degradation of hemoglobin. It occurs frequently in combination with coagulation disorders or in those cases when the structure of the gastrointestinal epithelium is severely compromised and if erosions or ulcerations have developed (Kohn et al., 2003; Dennis et al., 2006).

Fecal Incontinence

Anal, gastrointestinal, neural or muscular disorders can cause fecal incontinence in cats (Guilford, 1990). Intervertebral disc disease or tumors can also be associated with the condition (Munana et al., 2001).

Flatulence

Gas formation in the intestinal tract is a normal process related to the activity of the intestinal microflora. Around 200 volatile compounds are formed as the bacteria break down the digestive content in the large intestine. The main compounds are alcohols (such as methanol, ethanol etc), sulfur compounds (hydrogen sulfide, methyl/ethyl mercaptans etc), nitrogen compounds (ammonia, indole, phenol, skatole etc), volatile fatty acids (acetic/propionic/butyric/valeric acids, etc.) and other organic compounds.

Some of the substances produced in the intestinal tract are highly unpleasant (Figure 16), such as sulfur compounds, ammonia, biogenic amines, indoles and phenols (Lowe & Kershaw, 1997).

• Ammonia is formed mainly from the deamination of amino acids.
• Biogenic amines (cadaverin, histamine, putrescine, tyramine etc) are produced essentially by the decarboxylation of amino acids.
• Indole and phenolic compounds result from the decomposition of aromatic amino acids (tyrosine and phenylalanine)
• Sulfur compounds (hydrogen sulfide, mercaptans) from that of methionine and cystine.

Figure 16. Correlations between fecal odor and the emission of hydrogen sulfide (H2S) and methyl mercaptan (CH3SH) by fecal matter. (Source: Royal Canin data).  

The different components of an odor can be identified by gas chromatography together with mass spectrometry. It is also possible to judge the intensity of the odor by comparing it with increasing concentrations of 1-butanol (Sorel et al., 1983).

Avoidance of dietary ingredients that favor intestinal gaseousness is of primary importance. Many legumes and other vegetable ingredients contain more or less non-digestible and microbially fermentable fractions. Some flatulence cases may be proof either of the poor quality of the food (generally mediocre protein quality) or the existence of a digestive function disorder (Williams & Guilford, 1996). Flatulence is common in cases of dietary hypersensitivity. However, the problem is not well understood: some cases respond to dietary changes, and hence dietary treatment has to be adjusted according to the individual case. An eviction diet or an hydrolysed diet can help to manage dietary hypersensitivity cases.