FRANK J. MILNE STATE-OF-THE-ART LECTURE


pulp with molasses. Pre-cecal digestibility of pro- cessed oats is higher than unprocessed corn and barley.272,273 Palatability of the feeds must be con- sidered, given that it is important to keep the horse eating something (even if it is not the ideal feed). Only small amounts of the high-glycemic feeds ( 1.0 g/kg) should be fed at a time to improve small intestinal starch digestibility as well as prevent hy- perglycemia, extreme insulin surges, and small in- testinal overload, which could result in excessive starch passing undigested into the cecum271,274,275 The amount fed may need to be modified based upon appetite of the horse, blood glucose concentrations, and consideration of individual metabolic condi- tions, e.g., presence of any insulin dysregulation. Structural carbohydrates that are converted to vol- atile free fatty acids (VFAs) in the large bowel are an important source of energy for the horse and should be fed to supplement the energy potential obtained from sugars and hydrolysable starches digested in the small intestine. Some of the VFAs (i.e., ace- tate) may be used directly for energy,276 whereas others such as propionate and lactate that undergo hepatic gluconeogenesis277 may be of less value with a severely diseased liver. A highly palatable grass or grass hay (legumes may be too high in protein for horses with liver failure) should be fed at approxi- mately 1.5% of body weight dry matter basis for hay if the horse will eat this amount, in addition to the small feedings of a grain-based feed as described above depending upon blood glucose levels. Palat- ability of fresh grass may be higher than hay or even some concentrates and horses ill with severe liver disease may only be willing to ingest grass. If the horse with severe liver disease has markedly dimin- ished appetite for grain and hay, grazing a nonle- gume grass should be offered as long as the grazing is monitored (gorging while grazing/eating too much too quickly would likely be harmful) and grazing should be performed at night or in shaded pastures to prevent photosensitization in predisposed horses. Horses with severe liver disease and concurrent in- sulin dysregulation or those prone to laminitis should not have uncontrolled grazing on potentially high water-soluble carbohydrate (fructan and sim- ple sugars) pastures unless appetite is poor. As- suming the horse with liver disease is still eating, the above outlined combination of grains and for- ages might be able to maintain glucose within a normal range, decrease hepatic work necessary for glycogenolysis and gluconeogenesis, and hopefully allow the horse to maintain body condition. Horses with liver failure that are anorexic may need to be supplemented by forced enteral feeding (especially ponies, miniature horses, and donkeys with hepatic lipidosis) or by continual intravenous administra- tion of 5% glucose with potassium chloride, B vita- mins, and supplemental protein.178 There are no evidence-based guidelines available


for dietary protein feeding in horses with liver fail- ure. In horses with liver failure and neurologic


96 2015  Vol. 61  AAEP PROCEEDINGS


signs of HE, it can be assumed that the amount of protein in the diet should initially be restricted. The old concept of providing a low protein diet to all animals with chronic liver failure with no evidence of HE is no longer believed to be standard of care in other species and should be considered in horses as well. With HE, it can be assumed that the amount of protein in the diet should initially be restricted in hopes of preventing or decreasing hyperammone- mia. Feeding a low-protein feed to horses with hy- perammonemia may decrease enteric production of ammonia and concentration of proteins that may be metabolized to ammonia or other neurotoxins, which are believed to contribute to HE. It is, however, important to maintain adequate energy supply by feeding carbohydrates (as discussed above) and fat (except with hyperlipemic conditions) to horses with liver failure, or there could be sufficient breakdown of muscle protein to cause an increase in blood am- monia. It is also very important that horses with liver disease have adequate fluid volume (either self- drinking or interventional fluids) to maintain hydra- tion and sufficient dietary potassium which may decrease resorption of ammonia from the kidneys.255 The gut, liver, muscle, and kidney are all involved in regulating blood ammonia concentrations! There is some evidence that feeding BCAAs (va-


line, leucine, and isoleucine) and increasing the BCAA-to-aromatic-amino-acid ratio (AAA) can be helpful with the treatment of liver disease, liver failure, and HE in humans.278 The rationale for recommending BCAA in the treatment of liver fail- ure is based on their unique metabolic and pharma- cologic properties; muscle metabolism for energy and stimulatory effect on ammonia detoxification to glutamine by muscle rather than hepatic metabo- lism.269 In horses with PA toxicity or in foals with toxic hepatopathy there was an increase in concen- tration of AAA without increases in BCAA.150,279 Although BCAA treatment for severe liver disease is often recommended, there is no published data to confirm their benefit in treating horses with liver disease and in humans with HE the evidence is relatively low.269 A proper dose of BCAA in horses with liver disease is also not known and excessive amounts could actually enhance ammonia produc- tion from excessive glutamine breakdown in the in- testine and the kidneys, worsening HE.269 I have, therefore, generally taken a conservative approach with BCAA supplementation, recommending 10 g/adult horse every 12 hours. The BCAA can be given as a commercial paste product or if the horse is still eating, sorghum and soaked beet pulp can be fed as these concentrate sources have a relatively high BCAA:AAA ratio. Corn also has a high BCAA: AAA ratio but if unprocessed has a decreased pre- cecal carbohydrate digestibility compared with the other two products. Sugar supplemented beet pulp can be offered to diminish total protein intake, yet provide a high BCAA:AAA ratio and a digestible energy equal to oats, but with less fluctuation in


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