Diet and Hepatic Disease
Hepatic disease is common in dogs and cats. Few cases were recognized thirty years ago. With current diagnostic procedures it is possible to identify nearly all hepatic disease early so treatment can be successful. The liver is damaged by many injuries and diseases elsewhere in the body. Thus, many different diseases need management to protect and heal the liver. Hepatic disease also develops that is unrelated to pathology outside the liver. A variety of toxins damage the liver. They include drugs, chemicals, and microbial toxins. Often drugs must be discontinued before the liver can recover. Most toxic chemicals enter orally with their primary source being food. Commercial pet foods contain chemicals that can be changed by intestinal bacteria to hepatotoxins. Pet foods also contain endotoxin, produced from bacteria, which can damage the liver. Many commercial pet foods contain little endotoxin while others contain large amounts. Endotoxin is often not injurious unless another chemical, such as a drug, is present. A synergistic action of the two cause liver damage. Commercial pet foods seldom contain substances that cause primary hepatic disease but their composition can interfere with its recovery. Pet food companies prepare no products for treating hepatic disease. They often recommend products for treating renal disease because they are low protein diets. Treatment of hepatic disease requires more, however. Feeding an owner-prepared diet is essential for managing hepatic disease. Feeding a specially prepared diet is more important than any other treatment. Very few forms of liver disease need drugs for recovery. As mentioned, most cases should be given no drugs. The liver must metabolize many drugs for excretion, a function that is often reduced by disease.
Evaluation of Dogs and Cats For Hepatic Disease1
Dogs and cats show few clinical signs with early hepatic disease. They include anorexia, depression, and often increased water consumption. Unfortunately, these signs are common with many problems. On waiting for these signs to disappear spontaneously, many cases of hepatic disease worsen. Some hepatic disease is difficult to treat when it is not recognized early. One also cannot seek some specific signs to suspect hepatic disease. No clinical signs are specific for hepatic disease. Hepatic disease is possible with any unexplained clinical signs. No physical findings are pathognomic for hepatic disease. Findings such as jaundice or ascites more commonly indicate nonhepatic problems. Blood screening tests help evaluate unexplained clinical findings caused by hepatic disease. Alanine aminotransferase (ALT)enzyme activity is restricted to liver cells. With damage ALT leaks out and its plasma activity increases. Other blood chemistry tests are not specific for hepatic injury. Reduced appetite is the earliest sign of hepatic disease. Other signs subsequently appear with worsening disease and loss of hepatic function. They include depression, weakness, and signs of hepatic encephalopathy. The most important cause of encephalopathy is increased blood ammonia. The normal liver removes ammonia and converts it to urea; ammonia is toxic and urea is not. Ammonia tolerance testing can be done to evaluate this function. No other test is reliable for determining whether hepatic disease is responsible for loss of appetite or any other signs. Many other tests can be done to evaluate for hepatic disease. Most do not provide useful information, however. For example, radiographs of the liver are almost never valuable in identifying hepatic disease. Liver biopsy is always useful in evaluating for liver damage. In many cases liver biopsy is not necessary, however, because disease outside the liver is responsible for hepatic damage. On recognizing and understanding a non-hepatic problem liver biopsy is often not needed because any secondary hepatic pathology is predictable and does not need to be proven with a biopsy. With primary liver disease liver biopsy is important for treatment and prognosis.
Management of Hepatic Disease1-6
Dogs and cats with hepatic disease and hepatic insufficiency should always be treated dietarily. Special consideration is usually important for caloric intake, carbohydrate supplementation, protein quantity and quality, fat quantity and quality, sodium restriction, potassium supplementation, and supplementation or restriction of vitamins and micronutrients. In addition, management may be necessary for hepatic encephalopathy, hepatic inflammation and fibrosis, toxins absorbed from the intestine, infection, fluid retention, altered drug metabolism, retention of bile acids, and complications such as gastric ulceration and hemorrhage. Portasystemic shunts are also managed surgically.
An initial goal in managing dogs and cats with hepatic insufficiency is to reduce intestinal toxin production and absorption. Such management includes defined-protein diets, antibiotics to reduce intestinal bacteria, and cathartics to minimize toxin absorption. Medical treatment for hepatic encephalopathy is generally unsuccessful.
Feeding is essential for management of hepatic disease. No drug helps recovery for hepatic damage; only feeding assists recovery. With anorexia there is no chance for recovery and hepatic damage worsens. Fasting depletes glutathione and other nutrients needed to protect hepatocytes and reduce further damage. Energy and a balanced supply of nutrients are needed for arresting degeneration and supporting hepatic regeneration.
Diets For Dogs and Cats With Hepatic Disease1,2
Carbohydrates
Dietary carbohydrates should be high-quality and highly digestible. Bacteria ferment undigested carbohydrates entering the colon. Such fermentation increases colonic bacteria that degrade proteins and urea to form ammonia. The colon absorbs ammonia and blood ammonia increases. Carbohydrates minimize amino acid catabolism for energy, especially the branched-chain amino acids which are used for energy and found at reduced levels. High dietary carbohydrate promotes insulin secretion and reduced glucagon release. That ratio favors anabolic conditions where amino acids absorbed from the intestine are converted to protein rather than metabolized to glucose. Catabolic conditions produce ammonia. Dietary carbohydrates are increased during management of episodic hypoglycemia and ammonia intolerance. Frequent feedings of simple and complex carbohydrates are of benefit. Simple and complex carbohydrates are provided by boiled white rice, potatoes, and vegetables. Simple carbohydrates are nearly completely digested and absorbed. Vegetables provide complex carbohydrates as fiber. Fiber reduces availability and absorption of such toxins as endotoxin, other bacterial toxins, and some bile acids. Fiber also promotes fecal excretion of ammonia, so less is absorbed. Fiber slows dietary carbohydrate absorption, which maintains normal blood glucose in patients intermittently hypoglycemic and hyperglycemic.
Proteins
Dietary proteins can be reduced but only with signs of protein intolerance. Hepatic regeneration requires maintained protein intake; protein requirements are greater during recovering from hepatic disease. In general, feed as much protein as can be tolerated. Giving too much causes hepatic encephalopathy to appear or worsen.
Ammonia Intoxication
Ammonia is probably the most important
toxin absorbed from the intestine. Approximately one-half is derived from
bacterial activity and the other half from glutamine metabolism. The colon
produces most ammonia from bacterial activity. Intestinal bacteria produce
ammonia by urease activity or by deaminating peptides. Urea diffuses from
extracellular fluid into the intestine in amounts determined by dietary
nitrogen levels. Dietary levels and kinds of protein and any unusual loss of
blood or plasma protein into the intestine determine colonic peptide levels.
With appropriate dietary protein, digestion and absorption are optimal, so
little dietary nitrogen enters the colon. Protein also enters the colon in
desquamated mucosal cells and plasma proteins. Desquamation of small
intestinal mucosa is minimal when intestinal contents are scanty. Low
roughage diets minimize desquamation. Protein-losing enteropathy can cause
entry of excess plasma proteins into the colon. Hypoproteinemia is most
commonly caused by protein-losing enteropathy and infrequently caused by
hepatic disease impairing protein synthesis.
Protein Restriction
Because hyperammonemia causes
the earliest and most important signs of hepatic disease, treatment is
sometimes necessary to reduce blood ammonia. Because all ammonia comes
directly or indirectly from dietary protein, hepatic disease is often
managed with low-protein diets. Adequate protein is needed to restore normal
hepatic structure and function, however. The liver also produces and exports
proteins such as for plasma. Reducing protein intake can compromize hepatic
function so the liver cannot recover. Proper management of hepatic disease
includes feeding as much protein as can be tolerated. Greater success is
evident when only high-quality proteins are fed. Proteins with high
biological value are used completely leaving little for conversion to
ammonia. Commercial pet foods contain little high-quality protein so they
are not useful for managing hepatic disease. The following diets contain
only high-quality proteins. When little or no protein is given and calories
are supplied by glucose, nitrogen metabolism remains abnormal, as reflected
in the ratio of plasma amino acids. Thus, a protein-free diet may reduce
blood ammonia levels and be beneficial in improving signs of hepatic
encephalopathy but does not correct amino acid imbalances. Protein
restriction can worsen other problems by causing low plasma protein
concentrations to decrease further. Dietary effects on hepatic protein
synthesis can be evaluated by plasma protein measurements. Hepatic metabolic
functions require protein to support their structures. Dietary protein
restriction compromises the liver’s ability to synthesize proteins. Protein
restriction is indicated only with unmanageable hepatic encephalopathy. In
others, dietary protein is not restricted but is adjusted to meet needs for
synthesizing proteins and to prevent signs of hepatic encephalopathy, which,
except in the acute case, may be of lesser importance. If possible, protein
intake should be maintained at a minimum of one gram per 20 calories of food
intake.
Protein Source
The source of protein is important to survival and clinical signs in
dogs with hepatic insufficiency. Dogs with experimentally produced disease
and fed commercial dog food develop signs of hepatic encephalopathy and die
within two to three months. Dogs with similar diseases and fed diets with
protein from milk or soy beans develop no clinical signs and survive many
months.3,4 This study is similar to others showing survival time and clinical
signs to be worse when meat rather than milk protein is fed. At one time it
was believed that survival as due to improved metabolism of branched-chain,
aromatic, and sulfur-containing amino acids. Abnormalities persist in amino
acid metabolism on any diet, however. Moreover, when amino acid
abnormalities are worsened by feeding excess aromatic amino acids, clinical
signs do not worsen. Also, milk proteins and soy bean protein have
sulfur-containing amino acid contents similar to meat proteins in commercial
dog foods. Milk protein and soybean protein diets could have lower ammoniagenic amino acids such as threonine, glycine, serine, histidine,
tryptophan, and lysine, but meat proteins have similar amounts of these
amino acids. Glutamine and glutamic acid comprise up to 20% of protein amino
acid nitrogen. Following absorption, a high percentage of glutamine is
converted to glutamate, releasing ammonia that represents one-half of portal
blood ammonia. Controlling glutamine intake may benefit dogs with hepatic
insufficiency, but the glutamine-glutamate content of milk protein is
relatively high, which suggests that glutamine is unimportant. A number of
other suggestions have been made to explain the beneficial effects of milk
or soy bean protein diets. The most important may be that a high ratio of
carbohydrate to protein is essential in order to see a benefit. The diet
should contain minimum methionine. Excess methionine escapes intestinal
absorption and enters the colon where bacteria change it to a toxin.
Absorption of this toxin worsens brain abnormalities seen with hepatic
disease. Methionine-rich foods are avoided. Sometimes other amino acids are
helpful in reducing signs of liver disease. Arginine and citrulline are two
that directly or indirectly accelerate conversion of ammonia to urea. This
can reduce ammonia’s toxic effects on brain function.
Fats
Dietary fat is essential as a source of calories and essential fatty acids;
it also enhances palatability. A number of studies have shown that dogs and
cats with hepatic disease (even cats with hepatic lipidosis) do well on
diets containing 20 percent to 25 percent fat. In contrast to this tolerance
of triglycerides, free fatty acids interfere with ammonia metabolism and
contribute to hyperammonemia. They also contribute directly to hepatic
encephalopathy. Most dietary fat is resynthesized into triglycerides and
formed into chylomicrons before leaving intestinal epithelial cells. Thus,
dietary fat does not increase plasma free fatty acids. Plasma fatty acids
increase during fasting when adipose triglycerides are catabolized for
energy.
Vitamins and Minerals
Some
nutrients can worsen liver damage. Vitamin A can be hepatotoxic. Small
amounts of vitamin A interacts with other substances, such as endotoxin or
copper, to damage the liver. Dietary vitamin A is restricted with hepatic
disease. The liver stores dietary copper and normally excretes it in bile.
When hepatic disease reduces bile excretion, hepatic copper increases.
Excess copper is hepatotoxic.
Copper is ten times higher in dog liver than in human liver. That is not
necessarily a species difference. More than likely the difference reflects
the amount of copper consumed, being much greater in the dog. Before dogs
ate commercial pet food, the content of copper in their liver was much lower
than it is today. The hepatic concentration of copper increased during the
last 60 years from less than 10 micrograms copper per gram dry weight of
liver to over 200 today. That twenty fold increase results from a dietary
level of copper in commercial pet foods that is much higher than needed. Copper levels in pet food are important because
copper can be toxic and cause both acute and chronic hepatic disease.7-9 Chronic toxicity is frequent in dogs. The liver normally excretes copper in
bile. Hepatic disease reduces excretion of copper in bile, and hepatic
copper levels increase. Greater copper levels damage the liver further and
worsen its ability to excrete copper. It is likely that the increasing
hepatic copper concentrations act with other insults to damage the liver and
cause hepatic disease to be more common today. Dietary copper should be
minimal with hepatic disease.
Many animals with hepatic disease are deficient in zinc. Zinc salts can be given to replace the deficit. Zinc is also useful because it competes with copper for intestinal absorption. Zinc supplements reduce copper absorption. Zinc supplements reduce copper absorption. Vitamins E and K are useful with hepatic disease. Vitamin E protects against lipid peroxidation in cell membranes. Vitamin K is essential for normal blood clotting which is often abnormal with hepatic disease. Dogs with hepatic disease can be deficient in ascorbic acid. Dogs make ascorbic in the liver and it can be deficient with hepatic disease. Ascorbic is also useful in protecting against liver damage. As an antioxidant it protects against lipid peroxidation.
Pet Food Contaminants
The diet should contain only minimal amounts of endotoxin and be free of chemicals. Diets prepared from wholesome foods accomplish that. As mentioned earlier, commercial pet foods can be high in endotoxin. (Endotoxin levels reflect the degree of bacterial contamination before or during processing.) Small amounts of endotoxin damage the liver. Very small amounts are usually not harmful unless another chemical interacts with endotoxin to cause damage. Often these chemicals alone cause no hepatic damage.
Management with Drugs
Very few drugs are needed to treat hepatic disease. If possible, all drugs should be discontinued. Many drugs can damage the liver and many others require hepatic conversion for their excretion. Hepatic drug conversion requires energy and nutrients that are needed for recovery of hepatic damage. Chronic hepatic inflammation (hepatitis) requires corticosteroid treatment; inflammation persists without such treatment. Cortisone causes hepatic degeneration that is not serious or life threatening, however. Thus, when inflammation disappears corticosteroids are discontinued and any drug damage disappears. Corticosteroids are not given when there is no hepatic inflammation. Antibiotics are often useful for managing animals with hepatic disease. Drugs selected should not require metabolism by the liver. Such drugs include penicillins and aminoglycosides. Other drugs are sometimes used for treating hepatic disease in humans. No other drugs are shown to be effective for hepatic disease in dogs and cats, however.
Diet Formulation For Dogs
A diet containing cottage cheese or tofu and a readily digested starch such as polished rice meets the nutritional requirements of dogs with hepatic disease. Fats, preferably animal, are added to enhance palatability and to provide essential fatty acids, and, if the diet cannot be completely balanced, additional vitamins and minerals are given. Meat is not recommended since hepatic encephalopathy and shortened survival times are problems when dogs with hepatic insufficiency are fed meat-based diets. Supplementation with mixtures of branched-chain amino acids offer no proven benefit. The protein content of the diet can be as low as 10 percent on a dry basis but should be increased with evidence of protein deficiency, such as hypoalbuminemia. As an alternative, meat-free prescription diets containing approximately 14 percent protein are sometimes fed. Diets for hepatic disease are balanced as necessary with vitamin and minerals. Requirements for B vitamins are determined by caloric intake. With complete anorexia there is no requirement; with resumption of food intake after a period of anorexia there is a greater than maintenance need for these vitamins. Such animals should receive a doubled dose of water soluble vitamins each day. Vitamin C supplementation may be necessary even when feeding a diet containing standard amounts of ascorbic acid. An important part of a dog's ascorbic acid is produced in the liver. With hepatic insufficiency plasma ascorbic acid can be lower than normal even when the patient is given recommended additions of a standard vitamin‑mineral supplement. Ascorbic acid can be given up to 25 mg/kg per day. Ascorbic acid can cause release of stored hepatic copper and that can worsen hepatic pathology. Vitamin E can be given at levels of 500 mg/day to dogs and 100 mg/day to cats. Vitamin E is an antioxidant that protects against lipid peroxidation and protects against such injury produced by copper. Vitamin A is not given because it can interact synergistically with chemicals and toxins such as endotoxin to injure the liver. That happens with levels of vitamin A that are normally not hepatotoxic. Mineral supplementation can include zinc (3 mg/kg/day of zinc gluconate or 2 mg/kg/day zinc sulfate, each divided into three doses; zinc acetate may be tolerated better with less chance of gastrointestinal irritation), based on studies that zinc inhibits intestinal copper absorption and its deposition in the liver. Hepatic copper accumulates in some dogs with hepatic disease, and high hepatic copper is toxic. The owner-prepared diets in this section are low copper. If a low copper intake is desired, supplements containing copper are not given. Dogs with hepatic disease causing copper retention should also not be fed commercial dog foods. It seems logical, as well, to restrict the supply of dietary copper to affected dogs by avoiding commercially prepared dogs foods inasmuch as all contain 5 to 10 mg copper/kg, as recommended by the National Research Council.
Diet Formulation for Cats
Cats must be fed a relatively high protein diet. They are fed a balanced diet providing 65 to 90 Kcal/kg body weight per day. Protein amounts should provide 12 percent to 20 percent of caloric needs, which is roughly twice that needed by dogs. There is little information on feeding cats with hepatic insufficiency. They are probably similar to other mammals in that feeding meat-protein diets worsens clinical signs and progression of hepatic pathology. However, it is difficult to find cats that accept meat-free diets, especially when they are anorectic due to hepatic disease. Diets containing milk or soybean protein offer little advantage because of their amino acid composition.
Although non-meat diets may be beneficial in containing only small amounts of sulfur-containing amino acids which can produce toxins, they are deficient in taurine, whose chronic lack can result in ocular and cardiac problems. Milk has little taurine, and vegetable proteins have essentially none, so a diet based on these proteins must be supplemented with 50 mg taurine per day for an adult cat. That can be provided by supplementing the diet with clams, which have taurine amounts that are up to seven times greater than for fish, beef or chicken. Protein-restricted diets can be owner-prepared and are also commercially available, such as the prescription diet Feline k/d.
Because most hepatic pathology is secondary to primary disease in nonhepatic tissue, dietary management is supportive or directed at the primary problem. In either case cats are fed 80 to 100 Kcal/kg body weight per day, and 12 percent to 20 percent of their caloric needs must be provided by protein. The diet must also contain adequate amounts of arginine and taurine.
Anorectic cats should be managed by feeding enteral diets via nasogastric or gastrostomy tube. Liquid enteral diet can be given slowly which minimizes the possibility of vomiting or diarrhea often seen with enteral diets. Tube feeding eliminates a need for benzodiazepines or anabolic steroids to stimulate appetite. These drugs, like many, have side effects that are unwanted with hepatic disease. The enteral diets are ideal because they are meat‑free, being formulated from milk and soy bean proteins. Most diets are high in fat, approximating 30 percent or more. There may be theoretical reasons for a high fat diet contributing to hepatic encephalopathy, but that is not seen. If most of dietary calories are provided by carbohydrates, large volumes of enteral diets would be required. Enteral diets based on milk and soy bean proteins require taurine supplementation; 150 mg is added to 8 oz of diet. Supplementation with branched‑chain amino acids is of no benefit.
Owner-prepared diets can be used for cats with hepatic disease. Such diets are similar to ones prepared for dogs, but they need more protein and taurine. No commercial diets are produced for cats with hepatic disease. The prescription diet k/d is recommended for that use because of its protein quality and content. There are no studies showing any benefits for that diet in cats with hepatic disease, however. In general, many species of animals with hepatic insufficiency do poorer and pathology worsens when they are fed commercially prepared animal foods. Feeding such a diet is probably unimportant in most cats with hepatic pathology, but any commercial diet is likely to be less effective than an enteral diet in cats with serious hepatic disease.
Diets for cats should be supplemented with B vitamins, especially thiamine because cats become deficient quite soon during anorexia. Recommendations for supplementation with fat‑soluble vitamins is the same as for dogs. No recommendations can be given for supplementation with ascorbic acid and zinc because nothing is known on requirements for cats with hepatic disease.
Feeding Frequency For Dogs and Cats
Small meals are fed often to minimize hepatic encephalopathy caused by excess ammonia formed from glutamine metabolism and from excess protein entering the colon. Large single daily feedings of protein that exceed nitrogen needs are catabolized for energy or converted to triglycerides. Following deamination of proteins, additional ammonia must be converted to urea. Frequent feedings also reduce the time during which body protein is catabolized for energy. During fasting, muscle protein is catabolized to amino acids, which are deaminated and converted to glucose, and peripheral triglycerides are catabolized to free fatty acids, which are metabolized to ketone bodies for energy. Protein catabolism produces additional ammonia and perpetuates amino acid imbalances. The branched-chain amino acids and alanine are used primarily for energy, whereas the aromatic amino acids are metabolized in the liver and their rate of utilization is reduced with hepatic disease. The potential toxic effects of free fatty acids appear during fasting, the time when their levels are highest. Long-chain fatty acids are incompletely oxidized in the liver, forming octanoic acid which contributes to encephalopathy. Frequent feedings also benefit carbohydrate metabolism. Dogs with portasystemic shunts can have low normal blood glucose. Hypoglycemia, manifested during fasting, is due to reduced glucose availability and is prevented by frequent feedings. Since oral glucose tolerance is impaired in dogs with shunts, frequent feedings maintain above-normal glucose levels. However, the derangement is not severe enough to produce significant hyperglycemia.
Dietary Management of Dogs With Shunts
Dietary management of dogs with portasystemic shunts is not successful long-term treatment, with most not having normal life expectancy. Liver function deteriorates because of progressive hepatic atrophy. Clinical signs of depression often persist despite optimum dietary management. The long-term prognosis is poor for animals managed with controlled diets. Nonsurgical management of dogs with portasystemic shunts results in at least two-thirds dying or being euthanized. Of the remainder, 7 percent survive and do well on medical management; the outcome of some is unknown.
Diets for Dogs with Hepatic Disease
Cottage Cheese, Tofu, and Rice Diet (moderate sodium)
1 1/2
cups white rice, cooked (240 grams)
1/2
cup cottage cheese, 1% fat (113 grams)
2/3 cup tofu, raw firm (169 grams)
1
tablespoon chicken fat (14 grams)
1/3 teaspoon
bone meal powder (2 grams)
1/4
multiple vitamin tablet for humans
1/4
teaspoon potassium chloride (salt substitute)
provides 651 calories, 36.9 g protein, 21.8 g fat, .280% sodium
supports caloric needs of a 20 pound dog
Two to 3 ounces or more of raw potato (23 kcalories/ounce)
can be used to increase bowel movement frequency
Cottage Cheese and Rice Diet (high sodium)
1 1/2
cups white rice, cooked (240 grams)
1 cup
cottage cheese, 1% fat (226 grams)
1
tablespoon chicken fat (14 grams)
1/3 teaspoon
bone meal powder (2 grams)
1/4
multiple vitamin tablet for humans
1/4
teaspoon potassium chloride (salt substitute)
provides 598 calories, 34.5 g protein, 17.1 g fat, .647% sodium
supports caloric needs of a 18 pound dog
Two to 3 ounces or more of raw potato (23 kcalories/ounce)
can be used to increase bowel movement frequency
Tofu and Rice Diet (low sodium)
1 1/2
cups white rice, cooked (240 grams)
1 1/3
cup tofu, raw firm (335 grams)
2
teaspoons chicken fat (10 grams)
1/3 teaspoon
bone meal powder (2 grams)
1/4
multiple vitamin tablet for humans
1/4
teaspoon potassium chloride (salt substitute)
provides 700 calories, 43.1 g protein, 24.1 g fat, .012% sodium
supports caloric needs of a 22 pound dog
Two to 3 ounces or more of raw potato (23 kcalories/ounce)
can be used to increase bowel movement frequency
Diets for Cats with Hepatic Disease
Cottage Cheese, Tofu, and Rice Diet (moderate sodium)
1/3
cups white rice, cooked (53 grams)
1/2
cup cottage cheese, 1% fat (113 grams)
2/3
cup tofu, raw firm (169 grams)
1
ounce clams, chopped in juice (29 grams)
1
tablespoon chicken fat (14 grams)
1/4- teaspoon
bone meal powder (1 grams)
1/4
multiple vitamin tablet for humans
provides 466 calories, 40.9 g protein, 22.6 g fat, .416% sodium
a 10
pound cat needs 318 calories per day (286 calories for 9 pound and 350
calories for 11 pound cat)
One to 2 ounces or more of raw potato (23 kcalories/ounce)
can be used to increase bowel movement frequency
Tofu and Rice Diet (low sodium)
1/3
cups white rice, cooked (53 grams)
1 cup
tofu, raw firm (252 grams)
1
ounce clams, chopped in juice (29 grams)
1
tablespoon chicken fat (14 grams)
1/4- teaspoon
bone meal powder (1 grams)
1/4
multiple vitamin tablet for humans
provides 463 calories, 36.3 g protein, 25 g fat, .036% sodium
a 10
pound cat needs 318 calories per day (286 calories for 9 pound and 350
calories for 11 pound cat)
Turkey and Rice Diet (low to moderate sodium)
1/3
cups white rice, cooked (53 grams)
1/3
pound (raw weight) turkey, cooked (152
grams)
1/4- teaspoon
bone meal powder (1 grams)
1/4
multiple vitamin tablet for humans
provides 321 calories, 28.3 g protein, 15.4 g fat, .133% sodium
a 10
pound cat needs 318 calories per day (286 calories for 9 pound and 350
calories for 11 pound cat)
One to 2 ounces or more of raw potato (23 kcalories/ounce)
can be used to increase bowel movement frequency
References
1. Guilford, W. Grant. 1996. Approach to Clinical Problems in Gastroenterology. In Strombeck’s Small Animal Gastroenterology, edited by W. Grant Guilford, Sharon A. Center, Donald R. Strombeck, David A. Williams and Denny J. Meyer, 50-76. Philadelphia: W.B. Saunders.
2. Rutgers H C Carolien and John G. Harte. 1994. Hepatic Disease. In The Waltham Book of Clinical Nutrition of the Dog and Cat. edited by J. M. Wills and K. W. Simpson, 239-276. Oxford: Pergamon Press.
3. Marks Stanley L., Quinton R. Rogers and Donald R. Strombeck. 1994. Nutritional Support in Hepatic Disease. Part I. Metabolic Alterations and Nutritional Considerations in Dogs and Cats. Compendium Continuing Education Practicing Veterinarians, 16:971-979.
4. Marks Stanley L., Quinton R. Rogers and Donald R. Strombeck. 1994. Nutritional Support in Hepatic Disease.Part II. Dietary Management of Common Liver Disorders in Dogs and Cats. Compendium Continuing Education Practicing Veterinarians,16:1287-1296.
5. Guilford, W. Grant. 1996. Nutritional Management of Gastrointestinal Diseases. In Small Animal Gastroenterology, edited by W. Grant Guilford, Sharon A. Center, Donald R. Strombeck, David A. Williams and Denny J. Meyer, 889-910. Philadelphia: W.B. Saunders.
6. Biourge, Vincent, Paul Pion, Julia Lewis, James G. Morris and Quinton R. Rogers. 1993. Spontaneous Occurrence of Hepatic Lipidosis in a Group of Laboratory Cats. Journal Veterinary Internal Medicine 7:194-197.
7. Twedt, David C., Irmin Sternlieb and Steven R. Gilbertson. 1979. Clinical, morphologic, and chemical studies on copper toxicosis of Bedlington Terriers. Journal American Veterinary Medical Association 175:269-275.
8. Su, LeChu, Charrles A. Owen, Paul Zollman and Robert Hardy, 1982. American Journal of Physiology 243 (Gastrointestinal Liver Physiology 6) G231-G236.
9. Center, Sharon A. 1996. Chronic Hepatitis, Cirrhosis, Breed-Specific Hepatopathies, Copper Storage Hepatopathy, Suppurative Hepatitis, Granulomatous Hepatitis, and Idiopathic Hepatic Fibrosis. In Small Animal Gastroenterology, edited by W. Grant Guilford, Sharon A. Center, Donald R. Strombeck, David A. Williams and Denny J. Meyer, 705-765. Philadelphia: W.B. Saunders