{"id":31762,"date":"2022-10-10T20:20:45","date_gmt":"2022-10-10T20:20:45","guid":{"rendered":"https:\/\/todaysveterinarypractice.com\/?p=31762"},"modified":"2026-01-27T20:53:59","modified_gmt":"2026-01-27T20:53:59","slug":"dietary-requirements-for-patients-with-portosystemic-shunts","status":"publish","type":"post","link":"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/nutrition\/dietary-requirements-for-patients-with-portosystemic-shunts\/","title":{"rendered":"Dietary Requirements for Patients with Portosystemic Shunts"},"content":{"rendered":"

Portosystemic shunts (PSS), which are vascular liver disorders, lead to derangements in blood flow through the liver, which allow blood from the gastrointestinal tract direct access to the systemic circulation, bypassing the liver. PSS can result in hepatic insufficiency, allowing toxic substances, such as ammonia, to build up in the systemic circulation, leading to hepatic encephalopathy (HE) if not properly managed. <\/span><\/p>\n

PSS can be categorized as congenital or acquired. Congenital PSS is the most common congenital vascular disorder, and acquired vascular disorders (also known as multiple acquired PSS) are usually a consequence of chronic liver disease and portal hypertension. <\/span><\/p>\n

Congenital PSS can be further subdivided into extrahepatic or intrahepatic shunts. Extrahepatic shunts are more usually from the portal vein or a tributary outside the liver and more commonly affect small and toy breeds (e.g., Yorkshire terriers, Cairn terriers, Maltese, miniature schnauzers), whereas intrahepatic shunts arise from an intrahepatic portal vein branch within the liver parenchyma and more commonly affect large-breed dogs (e.g., Doberman pinschers, Old English sheepdogs, Irish wolfhounds). Congenital PSS leads to many clinical signs, most commonly in the neurologic, gastrointestinal, and urinary systems (<\/span>TABLE 1<\/b><\/span>).<\/span><\/p>\n

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Clinical signs of PSS can decrease quality of life and survival times, and the recommended treatment and management options include various methods of surgical attenuation (e.g., acute suture ligation, ameroid constrictors, cellophane banding, endovascular coils) and medical management (e.g., dietary management, synthetic disaccharide administration, antimicrobial administration).4-6<\/sup> For most patients, surgical attenuation is recommended and is associated with a significantly better survival rate than medical management.4<\/sup> However, for some patients, the location of the shunt and the cost of surgery make medical management the only viable long-term option. Medical management is crucial for all patients, including those undergoing future surgical treatment, to help minimize the potential for postoperative seizures1<\/sup> and for postoperative monitoring and management as complete attenuation is gradually and not always completely achieved.7<\/sup> Medical management can be implemented and monitored by primary veterinarians and clients together and can lead to a good quality of life if proper steps are taken to minimize the potential build-up of ammonia and other toxic substances that lead to the negative signs of PSS, mainly HE, although another consequence of PSS can be ammonium urate urolithiasis. <\/span><\/p>\n

Brief Pathogenesis of Hepatic Encephalopathy<\/h2>\n

The liver is an essential organ that is involved in many metabolic functions, including metabolism of protein, fat, and carbohydrate; metabolism and storage of vitamins and minerals; and detoxification and excretion of nitrogenous waste. The liver is the main site of ammonia detoxification, which occurs either in periportal hepatocytes in the urea cycle or in perivenous hepatocytes, synthesizing glutamine from glutamate and ammonia.2<\/sup> Ammonia is produced in 2 ways: urease-producing gastrointestinal microbial organisms produce ammonia by breaking down nitrogenous products (e.g., urea), and gastrointestinal enterocytes metabolize glutamine to produce ammonia.2<\/sup> Patients with PSS may experience inadequate ammonia detoxification, and successive increased circulating ammonia concentration (hyperammonemia) can lead to neurologic signs and severe skeletal muscle atrophy. For these patients, appropriate nutrition is crucial.<\/span><\/p>\n

The goals of therapy for patients with HE include recognizing and correcting the precipitating causes (e.g., gastrointestinal bleeding, constipation, hypokalemia<\/a>), reducing intestinal production and absorption of toxic substances, and providing symptomatic and supportive care.8,9<\/sup><\/span><\/p>\n

Role of Diet and Nutrition<\/h2>\n

The ideal diet for management of PSS should be complete and balanced, highly palatable, and highly digestible; should contain appropriate protein, both in quantity and type; and should supply appropriate quantities of vitamins and minerals, to provide essential nutrients to perform the many functions of the liver (<\/span>TABLE 2<\/b><\/span>).<\/span><\/p>\n

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Energy and Protein<\/h3>\n

Meeting energy and protein needs is critical as protein and energy malnutrition can lead to substantial problems (e.g., muscle loss). Patients with liver disease, such as those with PSS, may experience inadequate ammonia detoxification and a gradual increase of hyperammonemia, which can lead to severe skeletal muscle atrophy, increased apoptosis, and reduced protein synthesis, all of which are further detriments to muscle size and strength.10<\/sup> Thus, appropriate amounts of energy and protein must be provided. <\/span><\/p>\n

Energy requirements for individual patients should ideally be based on a complete diet history; however, for ease, calculations are often used. Many formulas exist to determine energy needs, but the author\u2019s preference for calculating resting energy requirement (RER) for dogs is to use the patient\u2019s body weight (BW) in kg to the power of 0.75 (RER dogs = 70 \u00d7 BWkg<\/sub>0.75<\/sup>) and for cats the same formula to the power of\u00a00.67 (RER cats = 70 \u00d7 BWkg<\/sub>0.67<\/sup>). Daily energy requirements or maintenance energy requirements (MER) are usually calculated by using a factor multiplied by RER (<\/span>TABLE 3<\/b><\/span>). The factor used depends on the animal\u2019s age, spay\/neuter status, and activity level. Hospitalized animals are typically fed to meet their RER (MER factor of 1); however, for young animals, the factor used should be appropriate to their age. For dogs that are not hospitalized, the factor used should better meet their energy needs, depending on their age, spay\/neuter status, and activity level. Sample calculations for 2 typical PSS patients are shown in <\/span>TABLE 4<\/b><\/span>.<\/span><\/p>\n

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Protein is of the utmost importance in the dietary management of patients with PSS. The appropriate amount of protein is not so excessive that it causes HE but not so restricted that it impedes the many functions of the liver. Patients with PSS may have increased protein requirements, and dietary protein should not be restricted in patients that are not encephalopathic.8<\/sup> In addition, providing the right type of protein can significantly affect a patient with PSS. Vegetable and dairy protein sources are often recommended to help mitigate the possibility of HE.8,11<\/sup> The most common causes of HE in animals with severe liver disease or PSS are ingestion of a meat-based high-protein diet, gastrointestinal bleeding, and azotemia.8<\/sup> For dogs with experimentally created PSS that were fed a dairy-based diet compared with a meat- or fish-based diet, survival times were significantly prolonged, weight loss was less, <\/span>and signs of encephalopathy were fewer and less severe.12<\/sup> It is thought that heme and other nitrogenous bases in meat diets contribute to exacerbation of HE, leading to shorter survival times.8,12<\/sup> Dogs experiencing urate stones or HE should be fed protein below its \u201cthreshold,\u201d which includes treats. Clients should be counseled to provide vegetable-based treats rather than meat-based treats whenever possible. Protein contents of veterinary therapeutic diets can be compared to determine appropriately controlled protein diets for dogs and cats (<\/span>TABLES 5 AND 6<\/b><\/span>).<\/span><\/p>\n

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Bacterial metabolism of dietary protein from meats is rich in aromatic amino acids (tryptophan, tyrosine, phenylalanine), whereas vegetable proteins are richer sources of branched-chain amino acids (leucine, isoleucine, valine) and produce less ammonia when fermented.1<\/sup> Many veterinary therapeutic diets capitalize on the potentially favorable amino acid profiles of vegetables. <\/span><\/p>\n

Traditionally, veterinary therapeutic renal diets have been considered as potential options for management of patients with PSS due to the protein restriction; however, the source of protein and the degree of protein restriction in renal diets may not be the best management approach for all patients with PSS. However, for some dogs that have severe HE and require severe protein restriction, renal diets may help mitigate encephalopathy. <\/span><\/p>\n

More appropriate are veterinary therapeutic diets that have been formulated for management of many liver diseases, including PSS but also copper storage disease. For some dogs, however, even these diets may be too protein restrictive and alternative options can be considered. For patients that do not improve with an appropriate therapeutic diet, have multiple diseases, or have issues of palatability, consulting a board-certified veterinary nutritionist is recommended. Diets that contain egg or vegetable-based proteins are available as veterinary therapeutic diets and may provide more protein as well as additional fiber that can help manage PSS. <\/span><\/p>\n

Dogs with underlying liver disorders are predisposed to urate urolithiasis due to the hyperammonuria and hyperuricosuria that result from the liver\u2019s reduced ability to convert ammonia to urea and uric acid to allantoin.13<\/sup> Management of urate stone\u2013producing patients should always include increasing water intake, ideally to achieve a urine specific gravity of <1.02 for dogs or <1.025 for cats, and providing a low-purine diet, although vegetarian diets have also been used to manage these patients.<\/span><\/p>\n

Fiber<\/h3>\n

Dietary fiber can reduce the availability and production of nitrogenous waste in the gastrointestinal tract. Fiber, whether from a higher-fiber content in the diet or supplemented in addition to the diet, can also affect the microbiome by acting as a prebiotic. <\/span><\/p>\n