Diet plays a key role in the management of all aspects of diarrhoea. Inappropriate diet, for example, may be the primary cause, but it may also prolong the duration of diarrhoea even if the underlying cause is not diet-related. Conversely, careful consideration of diet can speed recovery and in some cases is an essential component of therapy. Mechanisms of Diarrhoea Large quantities of water enter the gastrointestinal tract every day, through a combination of oral intake and endogenous secretions. Approximately 95% of this water is reabsorbed from the colon, so a relatively small decrease in absorption (or increase in secretion) can readily result in increased colonic water content and diarrhoea. A relatively small change in faecal water content from about 70% (normal faeces) to 80% (very loose faeces) can result in a very marked change in faecal character. Diarrhoea occurs as the result of one or more mechanisms: Interference with the digestion or absorption of nutrients. Retained nutrients exert an osmotic effect within the intestinal lumen leading to the retention of water and diarrhoea. Osmotic diarrhoea is most commonly seen with nutritional overload, but it is also associated with any condition in which there is a deficiency of enzymes or enterocytes, including exocrine pancreatic insufficiency (EPI), small intestinal disease and brush border enzyme (such as lactase) deficiency. Increased secretion of fluid into the intestine by cells in the crypts of Lieberkühn (secretory diarrhoea), which maybe stimulated by bacterial toxins and by the products of bacterial degradation of bile acids and dietary fat (deconjugated bile acids and hydroxy fatty acids, respectively). Increased intestinal permeability due to mucosal damage, which can result from severe inflammation or conditions (cardiac disease, lymphatic obstruction) that increase intestinal hydrostatic pressure. If the pore size is large, fluid and plasma proteins escape into the intestinal lumen, creating a protein-losing enteropathy and diarrhoea. Altered intestinal motility. Contrary to popular belief, most cases are due to a reduction in segmentation contractions (designed to mix chyme and aid absorption of nutrients) rather than increased peristalsis. Loss of segmentation results in stagnation of intestinal contents, bacterial proliferation and degradation of nutrients. The increased faecal volume stimulates secondary peristaltic contractions, which may give the impression of hypermotility. Acute Diarrhoea The aetiology of acute diarrhoea in the dog is diverse and can be multifactorial. It is unclear what factors are most important, but one report has noted that enteropathogenic bacteria are responsible for less than 5% of acute diarrhoeal episodes in dogs. Dietary indiscretion, such as scavenging, overfeeding or sudden dietary change, is probably the major cause of acute diarrhoea in the dog, but these episodes are generally self-limiting and do not result in significant dehydration. In the dog as in humans, it is probable that viral infection may be an important cause of acute diarrhoeal episodes that are of sufficient severity to require treatment for dehydration. In most cases of acute diarrhoea, a definitive diagnosis is not established because symptomatic treatment is effective in reversing the clinical signs. Along with any specific therapy, such as antibiotics or anthelmintics, acute diarrhoea is typically managed by providing a short period (24 hours) of dietary rest and rehydration therapy followed by the introduction of a ‘bland’ diet once fluid and electrolyte balance is restored. There has been some controversy as to whether or not total dietary rest is, in fact, necessary in non-vomiting patients. Studies in human infants suggest that ‘feeding through diarrhoea’ speeds the healing process by maintaining better mucosal barrier integrity, by providing energy for active electrolyte uptake and by minimising malnutrition. The amino acid glutamine is major energy source for enterocytes and appears to be particularly important in maintaining intestinal health. However, although the duration of diarrhoea is not prolonged by ‘feeding through’, it increases the volume of stool production, especially in cases of osmotic diarrhoea. To many dog owners, an initial deterioration of diarrhoea is unacceptable, so short term dietary rest is usually indicated. Oral Rehydration Therapy Appropriate fluid therapy is important in cases of acute diarrhoea if there is excessive loss of fluids, since this can cause dehydration and electrolyte depletion with subsequent acidosis. Fluids and electrolytes may be provided orally in mild disease or parenterally in more severe cases. In the normal healthy gut, chloride ions are secreted into the lumen by crypt cells during the process of digestion, which prompts a parallel flow of water and other ions (including sodium) from the blood to the gut. Subsequently, sodium and chloride are actively reabsorbed by a co-transport system in the villus cells of the small intestine, resulting in the passive reabsorption of water. A number of diarrhoea-causing enterotoxins increase the chloride-secreting activity of crypt cells or impair the absorption of sodium by villus cells, or both. These actions have the net effect of promoting sodium and water secretion and inhibiting sodium-chloride reabsorption. Despite this biochemical chaos, a second carrier system, which co-transports sodium only in the presence of glucose, is unimpaired. In the dehydrated individual, active absorption of sodium with glucose (and other solutes) promotes the absorption of water from the intestinal lumen to the blood, thereby reversing the process of dehydration. The ability of the glucose-sodium co-transport system to function during enterotoxin-induced acute diarrhoea is the principle on which oral rehydration solutions have been formulated. In contrast, certain other aetiological agents (such as rotavirus) cause morphological damage to the small intestine with substantial villus cell loss and villus cell shortening. Despite the damage to the small intestinal epithelium, sufficient absorptive function remains to effect sodium-glucose transport and enable effective rehydration with oral rehydration solutions. The World Health Organisation (WHO) has recommended a standard formulation for oral rehydration solutions, which has enjoyed considerable success in both the developing and the developed world, for the treatment of dehydration associated with acute diarrhoea. Although the essential ingredients of oral rehydration solutions are well established, the optimal composition is a source of much debate. The major controversies surround the glucose and sodium concentrations and thus osmolality of the solution, to which these are the major contributors. Sodium is an essential constituent of oral rehydration solutions because of the substantial intestinal secretion and subsequent stool losses of sodium in individuals with acute diarrhoea. In the developing world, cholera and E. Coli enterotoxins are important causative factors in acute diarrhoeal episodes and oral rehydration solutions for humans are formulated with a sodium content of 90mmol/L, in line with WHO recommendations. However, viral causes of acute diarrhoea, which are more commonly implicated in the developed world, are usually associated with lower stool losses of sodium.For this reason, and because the high sodium formulation has occasionally been associated with hypernatraemia and periorbital oedema, the sodium concentration of oral rehydration solutions used in the developed world tend to be lower (35-75mmol/L). Oral rehydration solutions with the lower sodium concentration may be most appropriate for the treatment of acute diarrhoea in the dog, in which viral infection appears to be an important aetiological factor. Glucose is an essential element in oral rehydration solutions, since the glucose-sodium co-transport system is often the only route of sodium absorption that is able to function during acute diarrhoeal episodes. The WHO-oral rehydration solution has a glucose concentration of 111mmol/L, whereas those formulated for use in the developed world, have a considerably higher glucose concentration (200-277mmol/L) and, consequently, a higher osmolality. Solutions with high concentrations of glucose provide additional energy, but are considered hypertonic and may reduce net water absorption, increase luminal osmolality thus contributing to osmotic diarrhoea and, potentially, damage the intestinal mucosa. Use of highly hypertonic solutions should be avoided, particularly in cases with reduced absorptive capacity due to villus atrophy, where the possibility of glucose overload is increased. Inclusion of a glucose polymer in place of monomeric glucose will decrease osmolality, which may have a beneficial effect on water absorption. Although considerable debate continues to surround the area of optimal glucose concentration and osmolality for oral rehydration solutions, it appears that hypotonic solutions containing glucose polymers may be more beneficial than isotonic or hypertonic solutions. Potassium is an important component of oral rehydration solutions since in most acute diarrhoeal diseases, potassium losses in the stool are substantial. Paradoxically, some individuals with acute diarrhoea, concurrent with substantial stool losses of potassium, may develop hyperkalaemia. This is a result of acidosis, which causes a shift of potassium from intracellular to extracellular compartments and is not an indication for restricting potassium intake. Current recommendations suggest that a potassium concentration in the range of 20-30mmol/L is normally adequate to replace existing losse. Substantial stool losses of chloride are known to occur during acute diarrhoeal episodes. Chloride is normally included in oral rehydration solution as the anion of the sodium and, occasionally, potassium salts. Consequently, in most oral rehydration solutions the chloride and sodium concentrations are approximately equivalent. Citrate is included in oral rehydration solutions primarily for the correction of acidosis, which is commonly associated with dehydrating diseases. Furthermore, citrate and other base precursors (bicarbonate and acetate) have been shown to promote sodium and water absorption in normal mammalian intestine, although this effect has not been demonstrated in individuals with enterotoxin-mediated diarrhoea. In many cases, acidosis will be corrected once renal perfusion is restored following rehydration, but a number of clinical studies have shown that in acute diarrhoea, the inclusion of a base in oral rehydration solutions results in a more rapid correction of acidosis compared with base-free formulations. Inclusion of glycine in oral rehydration solutions may be of benefit since additional absorption of this amino acid may enhance sodium and water absorption and thereby reduce stool output. Although clinical studies with oral rehydration solutions containing amino acids have produced conflicting results, there is no evidence to suggest that inclusion of glycine is detrimental and, in certain cases, it may have a beneficial effect. ‘Bland’ Diets A bland diet can be defined as a high quality, highly digestible, non-spicy diet containing components that pose a low risk of adverse reactions, such as a protein source that is novel to the animal. Following an acute bout of diarrhoea, this type of diet helps to ensure that the enterocytes are presented with minimal digestive challenge, and that the likelihood of acquired food allergies or intolerance is minimised. Acquired sensitivities may develop as a result of increased permeability of the inflamed gut, which facilitates the uptake of dietary antigens that can then initiate a hypersensitivity response. Potentially, hypersensitivity could develop to one or more protein sources that are fed during this critical period. Although the response is normally short lived, it may be sustained following repeated presentation of these allergens. If the animal’s normal diet contains the protein(s) to which it is now sensitised, return to normal feeding would provide continual exposure to the antigen, resulting in chronic diarrhoea. To reduce the risk of possible complications, a minimal number of protein sources should be fed during, and following, a period of acute diarrhoea. Preferably, the protein source should be novel to the animal and should not form part of the maintenance diet that will be used following recovery. It is important that the diet is nutritionally complete and balanced and that the actual level of protein is not compromised, since this may hinder enterocyte repair. High digestibility of the protein will help to reduce the amount of luminal antigen available for absorption and, hence, the risk of sensitisation. Chronic Diarrhoea Successful management of chronic diarrhoea requires a definitive diagnosis and the implementation of specific therapy for the condition. A systematic approach to diagnosis should be adopted. A detailed history will provide information about the duration and severity of the diarrhoea; faecal characteristics; appetite; body weight changes; and predisposing factors including breed, age, diet and environment. This should help the clinician to identify the problem as being large or small intestinal in origin. Subsequently, a thorough physical examination will help to differentiate primary gastrointestinal disease from systemic conditions which may give rise to gastrointestinal signs, including cardiac, renal and hepatic disease, hypoadrenocorticism and infectious disease. A series of further evaluations may be conducted to try to establish a precise diagnosis. For small intestinal diarrhoeas, these may include faecal evaluation; imaging; serum chemistry tests; sugar absorption tests to evaluate enterocyte function and intestinal permeability; breath hydrogen testing; and endoscopy. Using an appropriate diagnostic protocol, the cause can be established in most cases. Techniques of particular value in the investigation of large intestinal diarrhoea include faecal examination for parasites and bacteria; endoscopy and biopsy followed by histological examination of biopsy samples; radiography and ultrasonography. Small Intestinal Disease Specific causes of small intestinal diarrhoea include exocrine pancreatic insufficiency (EPI), dietary sensitivity, neoplasia, bile acid deficiency and short bowel syndrome. Small intestinal bacterial overgrowth (SIBO) is a common problem that may occur as a complication in up to 50% of dogs with chronic diarrhoea. Idiopathic disorders include inflammatory bowel disease (IBD), which is characterised most commonly by infiltration with lymphocytes and plasmacytes, or occasionally by eosinophils. Lymphangiectasia is a chronic condition characterised by insufficiency and marked dilation of the intestinal lymphatics, which may result in protein losing enteropathy and fat malabsorption with diarrhoea (and steatorrhoea). Diet plays an important role in the management of many small intestinal diseases, generally in conjunction with appropriate pharmacological therapy. Although no single diet is appropriate for every condition, it is generally accepted that diets for the management of conditions involving the small intestine should be highly digestible since many diseases are likely to interfere with digestive and absorptive function. In most circumstances, therefore, high fibre diets are contraindicated for the management of small intestinal disease. Fat Fat is the most complex of the macronutrients to digest and absorb and is therefore most vulnerable when gastrointestinal function is suboptimal. Hydrolysis of fat is dependent mainly on the activity of pancreatic lipase (although some lipolysis occurs in the stomach through the action of lingual lipase) and is facilitated by pancreatic co-lipase and bile salts. Bile salts also interact with the products of fat digestion to form mixed micelles, which is the form in which fat is most efficiently absorbed across the intestinal cell wall. After re-esterification within the enterocyte, fat is discharged into the lacteals and transported via the lymphatics to the systemic circulation. There are several aspects of this process that may be disrupted in disease. Restriction of dietary fat thus reduces the challenge to an already compromised gastrointestinal tract and is recommended in a range of small intestinal diseases: exocrine pancreatic insufficiency (EPI), in which impaired fat digestion and absorption is a feature because of decreased production of pancreatic lipase (and co-lipase). Bacterial overgrowth is also a common complication of EPI small intestinal bacterial overgrowth (SIBO), because bacteria can deconjuge bile salts and metabolise dietary fat to hydroxy-fatty acids. This not only diminishes fat absorption (by interfering with micelle formation) and impairs bile acid recycling, but by-products of microbial metabolism of undigested fat may also stimulate secretory diarrhoea. lymphangiectasia, because obstruction of the lymphatic vessels results in fat malabsorption. some inflammatory conditions, if they result in fat malabsorption due to a reduction in surface area of functional enterocytes. As a guide, diets are considered low in fat if they contain approximately 12-20% of metabolisable energy (ME) from fat. Moderate fat diets would contain approximately 20-30% of ME as fat. In some cases, medium chain triglycerides (MCTs) may form a useful supplemental source of energy, since some MCTs can be absorbed intact from the gastrointestinal tract and can reach the circulation via portal rather than lymphatic channels. Furthermore, they may be hydrolysed by gastric lipase more readily than long chain fatty acids. Protein Moderate to high quantities of good quality protein are recommended for small intestinal diseases since protein malabsorption or protein-losing enteropathy may be a feature of some cases of chronic small intestinal diarrhoea. Protein deficiency can further compromise a diseased intestinal tract through impairment of immune function and the luminal barrier, and through decreased formation of brush border enzymes. Protein is also important in relation to dietary sensitivity since most ‘allergens’ are proteins or glycoproteins. Dietary sensitivity most commonly manifests as skin disease, but gastrointestinal signs of vomiting and/or diarrhoea may also be present. Gluten, a protein in wheat and other cereals such as barley (not maize), is responsible for a particular enteropathy of Irish setters in which poor weight gain or weight loss is usually accompanied by chronic diarrhoea. Sensitivity to dietary protein may also play a part in some cases of inflammatory bowel disease (IBD). Where dietary sensitivity is the cause of diarrhoea, sources of dietary protein should be minimised to one or two ingredients, which are not normally associated with sensitivity reactions. Carbohydrate Carbohydrate digestion and absorption can be impaired in conditions that reduce villus height or result in enterocyte damage, including IBD and lymphosarcoma. Damage to brush border enzymes may occur with SIBO. Nevertheless, starch presents a relatively low digestive challenge in comparison with fat and may provide a greater contribution to the energy content of diets that are restricted in fat. Highly digestible sources of carbohydrate, such as rice, are recommended. Mono- and disaccharides, particularly lactose, should be avoided because they provide an osmotic load in the gut. In addition, lactase and other disaccharidases are amongst the brush border enzymes that may be lost. Dietary Fibre Although dietary fibre is commonly used in the non-specific therapy of acute diarrhoeas, it is generally contraindicated in chronic diseases. Pectin, for example, is a gel-forming soluble fibre, which may improve faecal consistency. In chronic cases, however, dietary fibre may interfere with digestion and absorption, thereby further compromising an impaired gastrointestinal tract. Specifically, soluble fibre is contraindicated in EPI since this may interfere with pancreatic enzyme activity. In healthy individuals, the potential of soluble fibre to reduce pancreatic enzyme activity by up to 60% has no adverse effects but in patients with EPI, even a small reduction in pancreatic enzyme activity can result in a marked increase in fat malabsorption. Vitamins and Minerals Several small intestinal diseases can result in deficiencies of water soluble B-complex vitamins. Patients with EPI are particularly susceptible to cobalamin (vitamin B12) deficiency due to binding of the vitamin by bacteria; decreased pancreatic intrinsic factor, which is essential for cobalamin absorption in the ileum; and decreased production of pancreatic proteases to release cobalamin from R-proteins. The bioavailability of cobalamin is poor following oral ingestion, so parenteral therapy may be required to correct deficiency states. Cobalamin deficiency can also occur secondarily to any other cause of bacterial overgrowth or malabsorption affecting the distal small intestine. In contrast, folate is absorbed in the proximal small intestine, so folate deficiency may occur in any condition affecting this part of the small intestinal tract, including inflammatory bowel disease. Diets for small intestinal disease are, therefore, supplemented with B-complex vitamins, although additional parenteral administration of cobalamin may be necessary in cases of EPI. Malabsorption of fat-soluble vitamins, particularly tocopherol (vitamin E), can occur in EPI. Treatment with pancreatic enzyme replacer may not always fully correct the problem and in some cases, additional oral supplementation with fat soluble vitamins may be necessary. Absorption of zinc and, possibly, copper may also be adversely affected in EPI so supplementation with these nutrients is recommended. Management of EPI Exocrine pancreatic secretions are reduced or absent in EPI, leading to impaired digestion and absorption of fat and, to a lesser extent, carbohydrate and protein. This results in weight loss, despite a ravenous appetite, and diarrhoea with steatorrhoea. Management of the condition involves the provision of a low fat, highly digestible diet along with the appropriate amount of pancreatic enzyme replacer. Counsel the client about the need for compliance and the expected time frame of therapy Feed a highly digestible, low fat diet in amounts based on the dog’s current (not ideal) body weight Divide food allowance into two meals per day Prescribe the appropriate amount of enzyme replacer If poor results, consider using H2 receptor antagonist (cimetidine) 30 minutes before feeding Once faecal character is restored, gradually increase food allowance and enzyme replacer to allow body weight gain over a period of weeks As body weight increases, expect a reduction in ravenous appetite and improvement in other clinical signs If diarrhoea recurs because of access to other food, or if the food allowance is increased too quickly, fast the animal for 24 hours before gradually reintroducing the regimen Use only the low fat diet during the period of stabilisation For long term maintenance, alternative (low or moderate fat) diets may be tried but all dietary changes should be made gradually and only after the dog has been stable for some time. Any diet changes may necessitate a change in dose of the enzyme supplement. Large Intestinal Disease Specific causes of large intestinal diarrhoea include parasitism, neoplasia and Clostridium perfringens. In other cases, inflammatory changes characterised by infiltration with lymphocytes and plasmacytes or, less commonly, eosinophils may be seen on endoscopic examination of histological evaluation of biopsy samples. Some idiopathic cases of large intestinal diarrhoea may respond to dietary supplementation with fibre and are termed ‘fibre-responsive’ whereas others may be classified as functional diarrhoea, often known as ‘irritable bowel syndrome’. Dietary modification is a key element in the management of most large intestinal disorders. In contrast to small intestinal diseases, dietary fibre plays a major part in the management of diarrhoea of large intestinal origin. However, sensitisation to certain dietary proteins appears to have a role in the aetiology of a number of chronic inflammatory conditions, including idiopathic chronic colitis, which may be more effectively managed using a highly digestible diet based on a restricted number of novel protein sources. Dietary Fibre Therapy of large intestinal diarrhoea using dietary fibre has been evaluated to some extent in dogs. Adding a fibre source providing both insoluble and soluble forms may be beneficial in the symptomatic treatment of some large bowel diseases, as fibre helps to normalise transit time and faecal water content. In addition, fibre can act as a significant nutrient in the large bowel by virtue of its partial fermentation by bacteria to short chain fatty acids (SCFA). These SCFA have three major effects: they are absorbed from the colon and contribute to the energy balance of the host; they acidify the colonic environment; and by virtue of their osmotic action they draw water into the stool, increasing bulking. SCFA, particularly butyrate, contribute significantly to colonocyte nutrition, and a reasonable supply should be beneficial for colonocyte health. Theoretically, therefore, dietary fibre (particularly soluble, fermentable fibre) has a role to play in the regeneration of damaged mucosa. Although the clinical signs of ‘irritable bowel syndrome’ are indistinguishable from colitis, no pathological changes are found on endoscopic examination or biopsy evaluation. The condition is thought to be associated with stressful situations that lead to altered intestinal motility. Treatment is aimed at identifying and removing the underlying stress factor although drug therapy with motility modifiers, spasmolytics or sedatives may also be required. Dietary fibre supplementation may be beneficial in some cases through its physical properties, which help to normalise colonic contractility. One study of dogs with idiopathic large bowel diarrhoea observed improvement in seven of eight animals using a bland diet with fibre supplementation Clostridium perfringens is a normal inhabitant of the canine distal small intestine and colon in its vegetative form but the spore coat contains an enterotoxin and may cause clinical signs if sporulation occurs. One factor, which may cause sporulation is an alkaline environment in the large intestine. Although acute cases resolve spontaneously and chronic cases generally respond to antibiotic therapy, dietary fibre supplementation may be of benefit in intermittent cases which require long term therapy. This is thought to be due to the effects of soluble dietary fibre on the intestinal microbial population and the production of an acidic environment through the formation of short chain fatty acids Idiopathic Chronic Colitis Canine idiopathic chronic colitis (ICC) is considered to be one of the most common causes of chronic diarrhoea in the dog. As its name implies, the underlying aetiology of this inflammatory large bowel disease is unclear and proposed mechanisms are diverse. However, the body of evidence in support of the role of dietary hypersensitivity is growing. Commonly, therapy aims to treat the signs through control of inflammation. Anti-inflammatory drugs, motility modifiers, antibiotics and dietary manipulation have all been implemented with varying degrees of success. Amongst these approaches, dietary manipulation provides a non-pharmacological option for long term management, although medical therapy may be required in the initial stages. The specific nature of an appropriate diet has been the subject of considerable debate. Some investigators have reported minimal success with any diet. Others have had some success with highly digestible, relatively hypoallergenic diets and others have seen promising effects with predominately meat based, fibre-supplemented diets. It is clear that diet plays an important role in the pathogenesis of this condition and it seems that both digestibility and the allergen component of the diet are key factors in successful dietary management. The rationale behind the use of a highly digestible, ‘hypoallergenic’ diet can be based on three criteria: high digestibility of macro-nutrients reduces the digestive challenge to the terminal gut. For example, the colon may be physically irritated by coarse fibre particles low antigen content reduces the chance of an immunological reaction occurring the chance of dietary antigens entering the colon is minimised when digestibility of the diet is high, since most digestion occurs in the small intestine. The rationale for using high fibre diets in colitis is primarily related to the fact that some types of fibre can be fermented by bacteria in the colon. Bacterial fermentation of dietary fibre results in changes in colonic flora and production short chain fatty acids (SCFA). One of these SCFAs, butyrate, contributes significantly to colonocyte nutrition. It has been suggested that epithelial energy deficit may be partly responsible for progression of colitis. In dogs, however, high fibre diets have proven much less efficacious than ‘hypoallergenic’ diets in the management of ICC. Studies involving dogs with confirmed lymphocytic plasmacytic colitis have shown that the condition could be successfully managed using a commercial low residue, ‘hypoallergenic’ diet, in which the protein sources were limited to chicken and rice. Although, in most cases, previous attempts at drug and dietary therapy had failed, all dogs showed a marked improvement in clinical signs within a month of introducing the ‘hypoallergenic’ diet as the sole source of food. Sulphasalazine was used in the initial stages of management, but the requirement for this anti-inflammatory drug declined within a month. After one year, all dogs were still in remission and required no concurrent drug therapy, although temporary relapses were often associated with access to other foods. Similar studies with veterinary low fat or high fibre diets were less successful in the management of chronic colitis in dogs. Using these diets, a greater dependence on anti-inflammatory drugs was required to maintain a clinical improvement that was less marked than with the restricted antigen diet.     MAIN PAGE

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