Page 914 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Liver disease 889

VetBooks.ir Dietary management appears little evidence of serious fat malabsorption
in most hepatic insufficiency cases.
Horses with liver disease, in the absence of hepatic
insufficiency, are unlikely to benefit significantly
Although concerns have often been expressed
from dietary changes. However, in a horse where the about dietary protein in cases of hepatic failure, it
liver is failing to perform its many nutritional and should be remembered that both a high and a low
metabolic functions, there may be some benefit from protein ration are equally harmful. Several protein-
supportive nutritional strategies. derived toxic principles are implicated in HE, includ-
Hepatic insufficiency will generally be associated ing ammonia, mercaptans, phenols, AAAs and ‘false
with weight loss as a result of protein-calorie mal- neurotransmitters’ leading to the common miscon-
nutrition. The liver has a central role in glycogen ception that dietary protein should be restricted in
storage and also controls both glycogenolysis and horses with hepatic failure. Indeed, well-controlled
gluconeogenesis to maintain plasma glucose during dietary studies in other species have shown that there
fasting. However, hepatic insufficiency is associated is no association between dietary protein concentra-
with low hepatic glycogen, thus requiring increased tion and HE, and that restriction of dietary protein
gluconeogenesis from amino acids even during inevitably promotes undesirable catabolism of endog-
short-term fasting. Poor appetite will only magnify enous proteins as a source of amino acids for gluco-
the problem, leading to further protein-calorie mal- neogenesis. It is also interesting and relevant that
nutrition. Therefore, a frequent supply of dietary vegetable protein, rather than meat or fish, is advo-
non-structural carbohydrates is beneficial to horses cated in human HE patients, which further detracts
with hepatic failure, such as cereal-based mixes from the need to manipulate dietary protein in
fed every 6–8 hours to provide up to 1 g/kg body equine cases. In the overall diet of horses with hepatic
weight (BWT) starch per meal. Whole or rolled oats insufficiency a crude protein intake of approximately
(typically 50% starch) are the preferred cereal type 1.2–1.5 g/kg BWT daily is likely to be optimal.
although processed maize (typically 70% starch) Although B vitamin supplementation appears popu-
may be used (starch in whole or cracked maize is lar practice in dietary management of liver disease,
largely indigestible). Commercial compounded con- there is no basis for this unless appetite and intake are
centrate mixes and ‘sweet feeds’ (typically 15–25% poor. Additionally, most such supplements are rich in
starch, 8–10 MJ/kg [1.9–2.4 Mcal/kg] digestible iron, which may promote further harm from haemo-
energy [DE] and 8–10% crude protein) may also be siderin accumulation in the liver. Supplementation
used. Alternatively, home- formulated rations can of the hepatic-stored fat-soluble vitamins is sensible
be made from sugar beet pulp and/or alfalfa chaff at perhaps 60 IU/kg vitamin A; 13 IU/kg vitamin D;
to provide good quality fibre, with a small amount 2 IU/kg vitamin E; and 0.2 mg/kg vitamin K. Zinc
of cereal or molasses to provide starch or sugars. supplementation (e.g. 0.5 mg/kg) may also be beneficial.
Where frequent meals are not practical, cereals Nutritional supplements, including s-adenyl
mixed with forage in large buckets may be especially methionine (SAMe) and also flavinolignans derived
useful to promote a constant slow intake of starch. from milk thistle (Silybum marianum), known collec-
Grazing should be encouraged, although this might tively as sylimarin, have become popular as adjunc-
be problematic when photosensitisation is a concern, tive aids for horses suffering from liver disease.
in which case ad libitum grass hay or haylage should These products are claimed to act as antioxidants
be provided. When horses are grazing it is impos- and to protect against the effects of hepatotoxins,
sible to accurately gauge intake, although when sta- although the evidence basis for these effects is very
bled and provided with forage and other feeds, a DE weak, especially at the low doses generally adminis-
intake of approximately 150–170 kJ/kg (35–40 kcal/ tered to horses.
kg) BWT should be anticipated but can be adjusted
up or down according to body condition. Addition Control of hepatic encephalopathy
of vegetable oil (0.1–0.5 ml/kg BWT) to increase The pathophysiology of HE is complex, although
the ration energy density may also be useful as there of primary importance in most cases will be