Nutrition in Disease Management in Small Animals

Food reactions are classified using specific terminology. An adverse reaction to a food is a clinically abnormal response to any type of food ingested. Food intolerance is a type of adverse reaction that does not involve the immune system, eg, food poisoning. A food allergy is a type of adverse reaction that does involve the immune system, eg, colitis or atopic dermatitis. (Also see Food Allergy and see Systemic Anaphylaxis (Generalized Anaphylactic Reactions).)

Dogs and cats with food allergy usually have GI signs (eg, vomiting or diarrhea, or both) or a pruritic skin condition, especially in the regions of the ears, rear, and feet. The prevalence of true food allergies is very small. Some dogs and cats with nonseasonal pruritus are having an adverse reaction to food. Unfortunately, food allergy cannot be differentiated from food intolerance, and skin testing for food allergies is unreliable. Blood tests are also an unreliable way to diagnose food allergies in dogs and cats. Hence, given all the possible etiologies and limited diagnostics available, any animal suspected of having an adverse reaction to food should undergo a food trial. The length of time needed for a food trial depends on the condition being managed. Food trials for adverse reactions to food associated with clinical signs involving the GI tract should continue for ≥2 wk, whereas food trials for clinical signs involving dermatologic conditions should continue for ≥10–12 wk.

During a food trial, the only item fed should be a diet containing a single novel protein source or a hydrolyzed protein diet. A careful dietary history must be obtained from the pet owner before selecting the type of diet. If the owner elects to feed a commercially prepared food, several products are available for dogs that use single novel protein sources (eg, kangaroo, venison, rabbit, duck, or fish). Commercially available diets available for cats use protein sources consisting of rabbit, duck, venison, and lamb. Fish is not a novel option for most cats, and there is a possible, but yet unclear, relationship between adverse food reactions in cats fed foods containing scombroid fish and histamine content. Most importantly, the formulation of whatever product or diet is fed must be fixed to ensure that the ingredient composition is consistent from batch to batch. These products are more expensive not only because of their unique and limited sources of protein but also because of the quality control procedures required to ensure fixed formulations and to eliminate cross-contamination with previous production batches of different foods.

A newer alternative diet commercially available for use in dogs and cats with suspected adverse reactions to food is a hydrolyzed protein diet. Protein is the most common nutrient associated with adverse reactions to food, because it is needed to bridge two IgE molecules together to cause the release of histamine. The protein in hydrolyzed diets is broken down into smaller peptide fragments that are too short to bridge two IgE molecules. Although these diets are helpful in many dogs and cats with adverse reactions to food, they are expensive, and some animals with allergies to the protein sources in these diets will still react to the typical hydrolyzed protein diet. Therefore, a novel protein diet is often tried first; if clinical signs do not resolve, then a hydrolyzed protein diet can be used.

Simplified homemade diets are also possible using the same protein sources suggested above (or other ingredient sources the owner wants to test). Homemade diets actually allow for a wider selection of source ingredients. Beef, wheat, and dairy products should be discouraged for use as a protein source in dogs, and beef, fish, and dairy products should be discouraged for use in cats, because animals have likely been exposed to these sources if previously fed foods with an open formulation. The basic recipe should closely resemble “complete and balanced,” but single sources of protein can be sequentially tested and replaced. The owner is responsible for quality control and consistency and must be willing to make such a diet for ≥2 wk for GI conditions and ≥10–12 wk for dermatologic conditions. On average, there is no price advantage in making a homemade diet over using commercially prepared foods. Formulating a homemade diet containing hydrolyzed protein is both very difficult and expensive.

The trial diet should be exclusively fed for the recommended length of time, and all treats, snacks, and table foods eliminated unless they are made of the exact same ingredients as the trial diet or contain a hydrolyzed protein source. All chewable medications and supplements must be eliminated from the trial diet, because most contain the same protein and additive ingredients as pet foods and treats. Other therapies such as hyposensitization and flea control are necessary in animals with concurrent disease. Testing various suspect ingredients by reintroducing them to the diet one at a time followed by recurrence of clinical signs is affirmation of an adverse reaction to that ingredient. Dietary ingredients reintroduced may reproduce clinical signs as early as 12 hr after ingestion but can take as long as 10 days. Lifelong treatment is dietary avoidance, which may be difficult if the offending ingredients are not positively identified.

Iron or copper deficiency (or both) is the major cause of hypochromic, microcytic anemia. A folic acid and B₁₂ (cobalamin) deficiency also produces anemia. Most commercial diets have more than required amounts of iron, copper, and vitamins; therefore, secondary causes such as inadequate food intake, malabsorption, hemorrhage, or heavy parasite infection should be investigated. Feeding an unbalanced homemade diet may also result in anemia.

Rarely can severe iron deficiency be corrected with diet alone, and feeding large quantities of liver in an attempt to correct iron deficiency is usually ineffective and can result in vitamin A toxicosis. Most animals require a supplemental source of iron administered either PO or IM to correct severe iron deficiency and, depending on the underlying cause, may need to continue receiving a supplemental source of iron indefinitely. If the underlying cause of iron deficiency is related to hemorrhage, parasitism, consuming an unbalanced diet, or consuming too little of a complete and balanced diet, once the underlying cause is eliminated and the iron deficiency is corrected, longterm supplemental iron may not be necessary.

Folic acid and vitamin B₁₂ are necessary to support normal cell division, and treatment for vitamin B₁₂ deficiency usually requires parenteral administration of vitamin B₁₂. Vitamin B₁₂ deficiency develops most commonly from intestinal malabsorption; however, it can also result from short-gut syndrome. Vitamin B₁₂ absorption in the GI tract is limited to the ileum, and surgical removal of large portions of the ileum may result in the need for lifelong parenteral B₁₂ supplementation.

Partial anorexia is seen when the animal is eating some food but not enough to provide at least 30 kcal/kg body wt in dogs and 40 kcal/kg body wt in cats. Complete anorexia occurs when the animal does not consume any food for ~3 days.

Anorexia (partial or complete) accompanies many underlying disorders, including drug reactions or reactions to environmental changes. Pain may also be a significant contributor to anorexia, and in most cases when the pain is adequately controlled, the anorexia resolves. Learned food aversions may also contribute to anorexia. This occurs most commonly when animals are started on a therapeutic diet while they are ill, eg, offering a therapeutic diet to manage renal failure while the animal is still in a uremic crisis. Food aversions can also occur as a result of force-feeding. Obviously, therapeutic diets do not help if they are not consumed. Eating some of a diet that is less than optimal is better than none of the “right” one. Assuming that an animal will eat a therapeutic diet when it gets hungry enough is inappropriate, and allowing an animal to starve in an attempt to stimulate its appetite is never recommended. If a particular diet is refused, an alternative(s) should be tried until one that the animal will eat is identified. Anorectic dogs and cats can sometimes be persuaded to eat by adding highly flavored substances to the diet (eg, animal fat, meat drippings, fish [fish juices or oils for cats]) or by hand-feeding. If these are not successful, nutritional support intervention may be necessary.

Nutritional support can be provided by either enteral or parenteral routes. Unless there is a contraindication to using the gut, enteral support is usually preferred over parenteral support. Enteral support is more physiologic, cheaper, and safer than parenteral support. In addition, more dietary options are available for enteral support than for parenteral support.

Many options for feeding tubes are available, including esophagostomy tubes, nasogastric or nasoesophageal tubes, gastrostomy tubes, and jejunostomy tubes. Both esophagostomy tubes and nasogastric or nasoesophageal tubes can be placed without the need for any specialized equipment. Nasogastric tubes are used more commonly for short durations (1–7 days) or when sedation or anesthesia are contraindicated. Esophagostomy tubes and gastric tubes are more commonly used when nutritional support is required for longer durations (weeks or months). Dogs and cats can be maintained at home with tube feedings (except in the case of jejunostomy tubes) after the procedure has been accepted by the animal and fully explained to the owner and if the frequency of feeding is something the owner can reasonably manage and the animal can tolerate.

It is advisable to take a stepwise approach to reintroduction of calories, and multiple small meals are often tolerated better than large meals. Vomiting, diarrhea, or refeeding syndrome can be a consequence of being too aggressive with reintroduction of calories. The size of the tube determines what dietary options can be used. Sizes 5 or 8 French tubes usually limit feeding to liquid enteral diets. Larger esophagostomy or gastrostomy tubes can also accommodate critical care diets and blenderized therapeutic diets. If use of a feeding tube is contraindicated or a tube cannot be placed, dogs and cats can be maintained by IV solutions that provide adequate calories, protein, electrolytes, B vitamins, and selected trace minerals until access to the small intestine is possible. Unfortunately, the parenteral route is more expensive and is associated with a higher incidence of complications, including catheter problems, infection, and electrolyte abnormalities.

Cachexia is most commonly associated with cases of neoplasia or chronic renal or cardiac disease. Cachexia appears to be a response to increased catabolism with either normal or decreased appetite. The deterioration of the animal’s condition clearly indicates that nutritional requirements are not being met, and the dietary goal is to increase the caloric density and palatability of the food while meeting the animal’s requirements for protein and other nutrients. The usual management of cachexia is to feed smaller amounts of a more calorically dense (ie, higher fat content), complete and balanced diet more frequently (3–6 meals/day). The form of food (dry or canned) that the dog or cat prefers should be fed. Tube feeding and partial or complete parenteral nutritional support (see above) should also be considered if the dog or cat continues to lose weight and condition.

Diarrhea can result from numerous GI diseases and can also occur secondary to disease outside the GI tract. Primary causes of GI disease are numerous and include adverse reaction to food, infections (bacterial, parasitic, fungal, and viral), inflammatory bowel disease, neoplasia, and toxin- or drug-induced. Certain breeds of dogs are predisposed to GI disease. German Shepherds are at increased risk of developing antibiotic-responsive diarrhea (formerly known as small-intestinal bacterial overgrowth), Doberman Pinschers and Rottweilers are at increased risk of parvoviral enteritis, and Yorkshire Terriers are at increased risk of lymphangiectasia.

Clinical signs associated with diarrhea are different in small-bowel versus large-bowel diarrhea (see Table: Characteristics of Small-bowel and Large-bowel Diarrhea). Dietary recommendations may vary depending on where the diarrhea is localized and the underlying cause.

Animals with small-bowel diarrhea usually benefit from a highly digestible diet, whereas those with large-bowel diarrhea often benefit from prebiotics (see Fiber). Small, frequent meals (3–6/day) should be offered. Probiotics are an additional tool available for management of small- or large-bowel diarrhea. Probiotics are defined as nutritional supplements containing live, viable, beneficial bacteria in sufficient numbers to provide a health benefit. Not all probiotics are created equal—a probiotic effective in one species may be ineffective in another. Probiotic bacteria provide many of the same benefits to the host as prebiotics. Synbiotics are a mixture of prebiotics and probiotics in which the prebiotic increases the survival of and nourishes the probiotic bacteria. Although clinical studies of probiotics in dogs and cats are limited, probiotics have been helpful in numerous causes of diarrhea.

Constipation results from impaired peristalsis or increased water absorption from the large intestine. The objective of dietary management is to provide a balanced diet with increased amounts of insoluble fiber (10%–25% dry-matter basis to effect) or moderately fermentable fiber in dogs or a highly digestible balanced diet containing prebiotics in cats. Constipated cats tend to do poorly on diets supplemented with insoluble fiber. Animals should be fed 2–4 times/day. In dogs, adding canned pumpkin or psyllium to the diet is also sometimes effective in mild cases of constipation.

One objective in managing CHF is to reduce water retention; restricting sodium intake and lowering sodium levels encourage diuresis. Typical commercial dog and cat foods have a sodium content of 0.45%–0.9% (450–900 mg sodium/100 g diet dry matter). Dietary sodium restriction is classified as mild (400 mg sodium/100 g diet dry matter) to severe (240 mg sodium/100 g diet dry matter). In view of these values, commercial dog and cat diets cannot even be classified as mild sodium restriction. Therefore, commercially prepared low-sodium diets or recipes that use low-sodium foods must be substituted. Sodium restriction often requires a special diet, although some manufacturers provide veterinary therapeutic diets for heart disorders. When using a home-prepared diet, all processed meats, cheeses, bread, heart, kidney, liver, salted fats, whole eggs, and snack foods should be avoided. Foods reasonably low in sodium include beef, rabbit, chicken, horsemeat, lamb, freshwater fish, oatmeal, corn, and rice.

Failed cardiac contractility may contribute to CHF, and taurine supplementation should be used to exclude a possible depletion of this amino acid in cardiac muscle. Both dogs and cats can develop dilated cardiomyopathy secondary to taurine deficiency. Some breeds of dogs with dilated cardiomyopathy may respond favorably to carnitine supplementation, which has also been beneficial in some breeds of dogs with CHF (including Boxers and Cocker Spaniels), in dogs with cystine or urate urolithiasis, and in dogs consuming a protein-restricted diet. Because obesity can be a contributing factor in CHF, a weight management program is needed in obese animals in addition to sodium restriction. In some instances, edema may give the appearance of obesity and mask emaciation. The edema should first be resolved, so that body weight and condition can be evaluated. If the animal is underweight, the food intake should be increased or the caloric content of the diet increased. If renal failure is also present, protein and phosphorus intake must be restricted.

Most DM in dogs is type I (insulin dependent) due to immune-mediated destruction of pancreatic islet cells (see Diabetes Mellitus). Although insulin sensitivity remains high in most diabetic dogs, no residual insulin production is left in the pancreas, and exogenous insulin therapy is required. Some dogs develop DM as a result of chronic pancreatitis causing widespread destruction of both endocrine and exocrine pancreatic tissue. Obesity does not appear to be a risk factor for developing DM in dogs, although obese dogs can have insulin resistance. Type 2 DM has not been reported in dogs, although some dogs may develop diestrus-associated diabetes that results in insulin resistance secondary to progesterone production. Remission of diabetes is possible when dogs are spayed or diestrus ends.

Some diabetic dogs have concurrent diseases, such as hyperadrenocorticism, and they may be very difficult to regulate if the hyperadrenocorticism remains untreated. Underlying urinary tract infection can also result in poor regulation and insulin resistance until the infection is cured. For diabetic dogs receiving insulin therapy, the nutritional requirements of any concurrent disease may take precedence over the dietary therapy for diabetes. Dietary recommendations for diabetic dogs without concurrent disease include feeding a diet that contains a moderate amount of a blend of soluble and insoluble fiber (3.5 g/100 kcal), such as a mixture of beet pulp and cellulose. Independent of the type of diet chosen, dietary intake should be consistent from day to day. Diabetic dogs usually require insulin twice a day, and it is recommended that dogs be fed first to ensure they eat before administering insulin.

Cats most commonly develop type 2 DM, although some cats may develop type 1, often secondary to chronic pancreatitis. The most common risk factors for DM in cats are obesity and increasing age. Most of these cats develop amyloid-mediated destruction of pancreatic islets. Although residual insulin capacity remains in most type 2 diabetic cats, insulin resistance is a characteristic of this form of DM.

Feline DM is similar to type 2 DM in people, and the main goals of therapy for diabetic cats are to control excess body weight and maintain optimal body condition, to reduce postprandial hyperglycemia and glucose toxicity, and to stimulate endogenous insulin secretion. Transient DM occurs in ~20% of diabetic cats, and these cats go into spontaneous remission usually within 1–4 mo after starting therapy for DM. The most likely reason for this is that untreated diabetic cats may develop glucose toxicity, and hyperglycemia decreases pancreatic β-cell function. When the cat is treated for DM and hyperglycemia is controlled, the glucose toxicity interfering with pancreatic islet cell function is removed.

Traditionally, diabetic cats have been fed fiber-supplemented diets similar to those recommended for diabetic dogs, and some cats have done well. However, more recently it has been shown that feeding diabetic cats a diet high in protein (>45% of calories) and low in carbohydrates (<20% of calories) improves glucose regulation and increases incidence of spontaneous remission. Nonetheless, some diabetic cats may have concurrent diseases for which the dietary management takes precedent.

FLUTD (see Feline Lower Urinary Tract Disease) has many possible underlying causes, including urolithiasis, urethral plugs, urinary tract infection, neoplasia, neurologic abnormalities, feline idiopathic cystitis (FIC), and anatomic defects, The underlying cause of FLUTD must be determined, because treatment for one cause may be contraindicated for other causes. The most common cause of FLUTD is FIC, followed by urolithiasis. Urethral plugs are most commonly composed of either mucus or mucus and struvite crystals. Urinary tract infections in cats without renal failure or diabetes mellitus is uncommon.

Urine dilution appears to be helpful in the treatment of FIC, because it decreases the concentration of substances in the urine that may be irritating to the bladder mucosa. Numerous ways to dilute urine have been investigated in cats, but one of the safest and most effective is to feed a canned-food diet. Other dietary modifications have been used to dilute urine, including sodium supplementation. Although sodium-supplemented diets are helpful in cats with FIC, they are contraindicated in cats with underlying renal disease. Highly acidic diets are not recommended, because highly acidic urine may increase sensory nerve fiber transmission in the bladder and increase pain perception. Regardless of treatment, clinical signs of FIC usually spontaneously resolve in 2–7 days. Unfortunately, FIC recurs within 12 mo in approximately half of the cats that experience spontaneous remission, and multiple recurrences are possible.

The two most common uroliths in the lower urinary tract of cats are magnesium ammonium phosphate (struvite) and calcium oxalate, although other mineral types are possible. Dietary management varies depending on the specific mineral composition of the urolith; however, regardless of composition, diluting the urine is important. Medical dissolution is an option for struvite uroliths but not for calcium oxalate uroliths. Producing a dilute urine reduces the concentration of minerals and crystals that form uroliths. Feeding a canned-food diet and encouraging water intake, eg, with water fountains, are safe and simple ways to dilute urine. Three major pet food companies have formulated diets for cats to manage both struvite and calcium oxalate. Two of these diets have high levels of sodium and, therefore, are contraindicated in cats with underlying renal disease. Diets reduce risk factors for developing uroliths but unfortunately do not prevent recurrence, which is common for calcium oxalate.

Fever increases energy requirements because of increased metabolic activity—a 1°F (0.5°C) rise causes an increase in caloric need of ~7 kcal/kg body wt/day. A highly palatable diet should be fed in quantities that can be consumed easily, and the caloric content should be increased by feeding a higher fat diet, if such a diet is not contraindicated. Because animals with fever generally have a decreased appetite, offering smaller meals more frequently with personal attention and encouragement may help stimulate intake. Feeding a feline growth diet or a calorically dense recovery-type diet also increases protein and energy intake in smaller feedings.

Currently, there is little evidence to suggest that certain specific nutrients in the diet, such as soy protein, lead to the development of gastric dilatation in susceptible dogs (see Gastric Dilation and Volvulus in Small Animals). The most common risk factors for developing gastric dilatation and volvulus (GDV) include breed risks (ie, large breeds with a deep chest), eating only one meal/day, elevated feeding bowls, and vigorous exercise 1 hr before or 2 hr after eating. Prophylactic gastropexy has been shown to prevent GDV if performed at the time of elective surgical neutering, and owners of high-risk breeds should be so advised. Other recommendations to prevent GDV include feeding multiple small meals/day and avoiding vigorous exercise before and after eating.

It is unknown whether the metabolic effects and energy expenditure in dogs and cats with severe head trauma, burns with ≥50% loss of skin, or prolonged dyspnea are the same as those in people with similar conditions. However, it is a reasonable supposition. The brain is one of the most metabolically active tissues; thus, providing aggressive nutritional support early is essential. Head trauma significantly alters neurologic control of metabolic rate, which is usually increased. Burns and other causes of significant areas of skin loss increase heat and water loss to the environment, thereby increasing energy needs. Increased respiratory rate and dyspnea are deceptively intense work that also result in increased energy needs. If a dog or cat is in an oxygen cage for >1 day, nutritional support (feeding IV or via feeding tube) should be instituted.

Brain trauma, burns, and sepsis are all conditions with high metabolic demands, and the amount of energy needed varies among animals. In all cases, energy is provided minimally at 30 kcal/kg body wt (dogs) or 40 kcal/kg body wt (cats) and increased in increments of 5 kcal/kg as the condition progresses and if weight loss is apparent. The energy source should be predominantly fat (60%–90% calories from fat, 10%–40% from glucose), because the body metabolism is predominantly lipolytic under these conditions, with the liver utilizing fat better than glucose during response to burns or trauma. Protein intake must also be matched with the energy intake to avoid net protein and muscle catabolism. Food that is 30%–45% protein and 25%–30% fat (dry-matter basis) and that is complete and balanced for all other nutrients should be fed using tube feeding. Human baby foods are not suitable for this purpose. These nutritional goals can also be met by parenteral (IV) nutrition, remembering that enteral and parenteral support are not mutually exclusive.

Dietary recommendations for dogs vary depending on the underlying cause and severity of liver dysfunction, and care must be taken to avoid overwhelming the metabolic capacity of the liver. In contrast, it is equally important not to unnecessarily restrict protein intake, because protein requirements are as high or higher in dogs with liver disease than in dogs without liver disease. Therefore, in dogs without encephalopathy, providing adequate intake of energy and a high-quality protein is essential to ensure a positive protein and energy balance and enable hepatic regeneration. Dietary antioxidants, such as vitamins C and E, as well as taurine, may also help minimize oxidative damage. Dietary copper restriction is recommended in dogs with documented increased copper levels in the liver.

In dogs with hepatic encephalopathy, reduced levels of high-quality protein may be necessary to reduce the accumulation of ammonia and other hepatic toxins. Soluble fiber or moderately fermentable fiber is helpful; colonic fermentation of these fibers produces short-chain fatty acids, which reduce both the intraluminal pH of the colon and the absorption of ammonia. Short-chain fatty acids also increase the blood supply to the colon and the amount of ammonia transported into the colon.

Frequent feeding of small meals (4–6/day) lowers the amount of nutrients or metabolites that require hepatic processing at a single time, thereby imposing less metabolic demand on the liver. Animals with liver disorders are frequently anorectic. Thus, food consumption and body weight and condition should be monitored.

Feline hepatic lipidosis is the most common liver disease in cats. It usually occurs in obese cats that are anorectic. This life-threatening condition requires aggressive nutritional support to reverse the changes in the liver. Most cats require a feeding tube. Energy-dense, high-protein diets, such as critical care diets, are usually selected for cats without encephalopathy. A step-wise reintroduction to calories is necessary to prevent complications, such as vomiting or electrolyte abnormalities. Hypokalemia is the most frequent electrolyte abnormality, and it can be exacerbated by too aggressive reintroduction to calories. Carnitine supplementation is also beneficial. Fluid needs must be met, and parenteral fluid support may be needed in many cats, at least initially. In encephalopathic cats with hepatic lipidosis, dietary protein may need to be restricted but should not be severely so. These cats usually have protein malnutrition secondary to anorexia, and providing too little dietary protein can interfere with hepatic repair and regeneration.

Also see Hepatic Disease in Small Animals.

Hyperlipidemia in dogs can be primary or secondary to hypothyroidism, pancreatitis, hepatic disease, diabetes mellitus, nephrotic syndrome, hyperadrenocorticism, or high-fat diets. Hyperlipidemia is present when blood lipids are increased with or without gross lipemia and probably results from abnormalities in the synthesis or use of plasma lipoproteins. In primary hyperlipidemia, the abnormalities can be familial and might be genetic, as has been suggested in Miniature Schnauzers. Some dogs with hyperlipidemia are asymptomatic. Clinically affected dogs may have recurrent seizures, depression, recurrent pancreatitis, vomiting, acute blindness, corneal opacity, and xanthogranulomas.

The goal of dietary management is to decrease the digestion and absorption of fat by feeding a diet restricted in fat (<10% dry-matter basis). The use of fish oil capsule supplements at a dosage of 1 g/4.5 kg body wt either once a day or in divided doses, depending on the number of capsules needed, helps reduce serum triglyceride concentrations. Although fish oil supplements generally do not return serum triglycerides to normal values, partial reduction is believed to mitigate the risk of pancreatitis or other problems related to marked increases of this lipid.

Diseases of the small intestine and pancreas often lead to a vague clinical syndrome characterized by weight loss, vomiting, diarrhea (with or without steatorrhea), and changes in appetite. In such cases, a highly digestible diet low in fiber (0–5%), moderate in fat (10%–15%) and protein (20%–25%), and containing carbohydrate from noncereal byproduct sources is recommended. Supplemental water-soluble vitamins should also be used. Malabsorption and maldigestion are often secondary to other underlying GI disease, such as inflammatory bowel disease. Appropriate management of the underlying disease may reverse malabsorption and maldigestion. Exocrine pancreatic insufficiency (EPI) is one of the most common causes of malabsorption/maldigestion in dogs. Certain breeds of dogs, eg, German Shepherds, are at increased risk of developing EPI. EPI can also result from severe or chronic pancreatitis. In EPI, supplementation with a powdered enzyme supplement, mixed with the food a few minutes before feeding, should be considered. Parenteral administration of vitamin B₁₂ (cobalamin) is also required in some animals with EPI, especially cats. (Also see Malabsorption Syndromes in Small Animals.)

Obesity is the most common nutritional health problem in dogs and cats, and obesity-associated health risks continue to increase. Obesity is the excessive accumulation of adipose tissue—for dogs and cats, >20% above ideal body weight. Dogs and cats 10%–20% above ideal body weight are considered overweight. It is estimated that 24%–44% of dogs and 25%–30% of cats seen by veterinarians are overweight or obese, and ~50% of dogs 5–10 yr old are overweight or obese.

Obesity occurs when energy intake exceeds energy expenditure. Risk factors for developing obesity include 1) lack of exercise, 2) breed predisposition (breeds with an increased risk include Labrador Retrievers, Miniature Schnauzers, Dachshunds, Shetland Sheepdogs, Cocker Spaniels, Beagles, Basset Hounds, and Cairn Terriers), 3) increasing age (metabolic rate decreases with age as lean muscle mass decreases and fat mass increases, 4) neutering, 5) certain endocrine disorders, and 6) certain drugs, such as corticosteroids and phenobarbital.

Health problems associated with obesity include decreased life expectancy, impaired quality of life, chronic inflammation, pulmonary and cardiovascular problems, exercise and heat intolerance, joint and musculoskeletal problems (eg, arthritis), compromised immune function, pancreatitis (dogs), diabetes mellitus and hepatic lipidosis (cats), and increased morbidity and mortality during and after anesthesia.

Adipose tissue was long considered metabolically inert, and its primary role in disease was attributed to stress on the joints caused by increased weight bearing and increased workload on the heart. However, it is now known that adipose tissue is not inert, but rather a major endocrine organ that produces hormones and protein factors and signals called adipokines. The expression, production, and release of many adipokines are increased in obesity, which results in persistent, low-grade inflammation and increased oxidative stress that plays a role in many chronic diseases, such as osteoarthritis and diabetes mellitus.

Treatment for obesity should include both short- and longterm goals. Short-term goals are to lose weight and reach an ideal body condition score. Longterm goals are to maintain ideal body condition score. Both of these goals require modification of behaviors that resulted in the dog or cat becoming overweight. Recommendations for lifestyle changes should be done in the context of maintaining the owner-animal bond. If this is ignored, owner compliance is unlikely.

The most successful weight loss programs include a combination of caloric restriction and exercise. The first step is to obtain a thorough diet history, followed by calculating the caloric intake appropriate to induce weight loss. Determining 60% of MER for dogs and 70% of MER for cats is one way to calculate starting caloric intake for a weight management program. Regardless of the formula used, the calculated caloric intake is only a starting point and may require modification based on response.

The next step is to decide on a diet for the weight loss program. Maintenance diets are generally not recommended for weight loss programs, because they are formulated to meet the nutritional needs of moderately active adults. Restricting caloric intake using maintenance diets may result in inadequate intake of some nutrients. Therapeutic weight loss diets are formulated to be restricted in calories while providing other nutrients in appropriate amounts. Adequate protein levels are important in any weight loss diet chosen. Most diets formulated for weight loss also have increased levels of dietary fiber. It is better to divide total daily caloric intake into multiple meals rather than one large meal. If giving treats is an important owner-pet interaction, providing the owner with low-calorie treat options is important. Most treats are not complete and balanced, so they should be restricted to <10% of the total caloric intake to avoid causing nutrient imbalances.

The next step is to decide on a rate of weight loss: a reasonable goal is loss of ~1% of body wt/wk. If the animal is losing weight at a slower rate than that chosen but is doing well otherwise and the owner is satisfied, then it may be best to allow weight loss to continue at the slower rate. The animal’s weight should be monitored every 2 wk and the program modified if needed based on response. Any weight loss is good weight loss, and celebrating successes with the owner helps maintain motivation.

Obese cats undergoing weight loss are at increased risk of developing hepatic lipidosis. Cats must continue to consume adequate calories and nutrients. If a cat does not like the weight loss diet chosen, then an alternative should be found. Starvation is never a safe or humane way to cause weight loss.

The goal in treating pancreatitis is to minimize stimulation of the exocrine function of the pancreas until inflammation has decreased. Often, the dog has multiple episodes of vomiting. A standard treatment is nothing per os (NPO) until vomiting ceases, which can last 3–15 days. Antibiotic, fluid, and electrolyte therapy during NPO treatment is essential, and IV nutritional support (total parenteral nutrition) should be instituted if NPO therapy continues for ≥3 days. Adult and young dogs can be nutritionally maintained by IV parenteral solutions that provide adequate calories, protein, electrolytes, B vitamins, and selected trace minerals until oral feeding is possible. If the dog appears painful or uncomfortable, medications to manage pain as well as plasma transfusions should be administered.

Unfortunately, total parenteral nutrition does not provide any nutrients to the enterocytes, and atrophy of the gut occurs as in starvation. The amino acid glutamine provides ~40% of the energy needs to the small-intestinal epithelial cells; it can be provided orally in very small quantities every 8 hr to provide some nutrition for the enterocytes.

When oral feeding can be resumed, a commercially prepared, easily digestible diet that has moderate fiber (10%–15% dry-matter basis) and is low in fat (5%–10%) can be fed in small, frequent meals (3–6 times/day). Because recurrent episodes of pancreatitis are common, feeding a complete and balanced low-fat diet is recommended for longterm management. Obesity and hyperlipidemia are common concurrent problems and should be investigated and resolved.

Parvovirus enteritis is most common in puppies 6–24 wk old. It is extremely infrequent in adult dogs. It is characterized by vomiting, diarrhea (often bloody), and weight loss. Severe cases can result in sepsis and disseminated intravascular coagulation. IV fluids, antiemetics, and antibiotic therapy are important. Fluid rates must be sufficient to account for maintenance needs as well as ongoing losses. Crystalloid therapy or plasma transfusions may be necessary in hypoalbuminemic dogs. Food and water are usually withheld until vomiting ceases. Severe cases may require total parenteral nutrition. Once vomiting has ceased, small amounts of water are offered first. If there is no vomiting, then small amounts of an easily digestible diet should be fed until the dog recovers. (Also see Canine Parvovirus.)

Numerous metabolic abnormalities that may alter an animal’s nutritional status develop in progressive renal failure. These include impaired clearance of nitrogenous products of protein metabolism; impaired regulation of sodium, potassium, and phosphorus; acidosis; impaired vitamin D metabolism; and often anorexia. The objective of dietary management in renal failure is to lessen the metabolic demands on the kidneys and to diminish metabolic end-products that cannot be readily excreted. The first consideration is to ensure normal water homeostasis. Regardless of whether the animal is polyuric, oliguric, or anuric, water should always be readily available. In addition, dietary management remains the mainstay of therapy for animals with CKD. Therapeutic renal diets are formulated to address many of the metabolic abnormalities associated with CKD. Any therapeutic renal diet should be phosphorus restricted, supplemented with omega-3 fatty acids (EPA/DHA) that come from fish oil, alkalinizing, supplemented with B vitamins, and in cats supplemented with potassium. In addition, feeding moderately fermentable fiber can facilitate enteric dialysis and provide a nonrenal route of urea excretion. Newer research has also shown the benefits of antioxidants in the management of CKD in dogs. The rate of decline of glomerular filtration rate by use of both dietary omega-3 fatty acids and antioxidants were additive. In addition, research in dogs is also showing that higher protein levels than what are typically used in most therapeutic renal diets is beneficial as long as the diets are phosphorus restricted. Energy should be supplied primarily via feeding relatively more digestible fat and carbohydrates.

The criteria used (eg, serum creatinine concentration, BUN) to define when dietary modifications should be made are under debate. However, it is easier to change the diet when the animal is feeling reasonably well than when it is anorectic. There is good evidence that animals with International Renal Interest Society (IRIS) Stage 3 and 4 CKD benefit from dietary management, and there is likely to be benefit in changing the diet early in the course of renal disease, such as that associated with IRIS Stage 2 CKD. Additional symptomatic and supportive care, such as H₂-blockers, antiemetics, medications to treat hypertension, intestinal phosphate binders, calcitriol, erythropoietin, and potassium gluconate (in cats) may be necessary as the disease advances.

The most common mineral composition for uroliths in dogs are primarily struvite (magnesium-ammonium-phosphate) and calcium oxalate, followed by urate and cysteine. Regardless of the type of stone, diluting the urine (eg, by encouraging water consumption) is warranted.

Struvite stones are more common in females than males. Most struvite stones in dogs are induced by infection with urease-producing bacteria. Although diet can be used to try to dissolve these stones, the most important therapy is to treat the urinary tract infection. Struvite stones can be medically dissolved, after which calculolytic therapeutic diets are usually unnecessary. Preventing a recurrence of the urinary tract infection and prompt treatment of a recurrence are important.

Calcium oxalate stones are not amenable to medical dissolution and must be removed through voiding, urohydropropulsion, surgery, or laser lithotripsy in symptomatic dogs. Two approaches are used for dietary management: 1) feeding an alkalinizing, protein-restricted diet low in oxalate, or 2) feeding a diet supplemented with sodium to encourage water consumption and production of dilute urine. Despite dietary management, the recurrence rate is high (33% in the first year and 50% by the third year).

Urate uroliths can occur in cases of liver disease, most commonly portosystemic shunts. However, two breeds of dogs, Dalmatians and English Bulldogs, are predisposed to developing urate uroliths without overt liver dysfunction. Medical dissolution is an option and consists of using a protein-restricted diet low in purines and alkalinizing the urine in combination with treatment with allopurinol, a xanthine oxidase inhibitor. The use of low-dose allopurinol as a strategy to prevent recurrences is discouraged. Instead, water should be added to the diet in the maximal amount the dog can tolerate without needing to urinate overnight. Recurrence rates are high, especially in dogs 1–6 yr old; however, this stone type becomes much easier to manage once the dogs reach middle age.

Cystine urolithiasis is due to a renal tubular defect. It is most common in Dachshunds, English Bulldogs, French Bulldogs, and Newfoundlands. Medical dissolution is an option using dietary management and thiola. However, protein-restricted diets should be used with caution, because some of these dogs also have aminoaciduria and carnitinuria. (Also see Urolithiasis in Small Animals.)

Steatitis (pansteatitis, yellow fat disease) is seen most often in kittens fed exclusively large amounts of unsaturated fatty acids, oily fish such as tuna or mackerel (packed in oil not water), diets that do not have an appropriate balance of antioxidants relative to polyunsaturated fats, or diets that have gone rancid. Clinical signs are anorexia, fever, pain over the thorax and abdomen, neutrophilia, and subcutaneous nodules of necrotic fat. Cats with steatitis should be fed diets restricted in polyunsaturated fatty acids (monounsaturated and saturated fats are permitted) and given vitamin E supplementation at 10–20 mg, bid for 5–7 days. The diet of choice is a commercial food to which vitamin E (α-tocopherol) or other antioxidants have been added.