Page 1131 - Small Animal Clinical Nutrition 5th Edition

Hepatobiliary Disease 1177

VetBooks.ir Table 68-10. General therapy for patients with hepatobiliary disease.*
Fluid therapy
Maintain hydration
Prevent hypokalemia Give appropriate parenteral fluid therapy
Add KCl to maintenance fluids
Maintain acid-base balance Use potassium-replete food or potassium supplement
Prevent or control hypoglycemia Avoid alkalosis in patients with hepatic encephalopathy
Add dextrose to parenteral fluids as needed
Nutritional support
Maintain caloric intake Ensure that daily energy requirement is being met; if not, begin assisted feeding
Provide adequate vitamins and minerals Add B vitamins to fluids or give as injection
Modify feeding plan to control complications Use complete and balanced food
See specific complications below
Control hepatic encephalopathy
Modify food and prevent formation and absorption Avoid excess dietary protein
of enteric toxins Use retention enemas q6h containing lactulose or povidone iodine solution
Give lactulose orally
Control GI hemorrhage Treat GI parasites, treat gastric ulcers, avoid drugs that exacerbate
GI hemorrhage (e.g., aspirin, glucocorticoids)
Correct metabolic imbalances See fluid therapy above
Avoid drugs or therapies that exacerbate hepatic Do not administer sedatives, analgesics, anesthetics, diuretics, stored blood or
encephalopathy methionine-containing products
Control seizures Use appropriate anticonvulsant drugs (e.g., potassium bromide)
Control infection Give systemic antimicrobials (see below)
Control ascites and edema Avoid excess dietary sodium chloride
Administer diuretics (e.g., furosemide, spironolactone)

Control coagulation defects and anemia Give vitamin K parenterally
1
Give fresh plasma or blood transfusion as needed
Control GI ulceration Give H blockers (e.g., ranitidine) or cytoprotective agents (e.g., sucralfate)
2
Control infection and endotoxemia Give systemic antibiotics (e.g., penicillin, ampicillin, cephalosporins,
aminoglycosides, metronidazole)
Give intestinal antibiotics (e.g., neomycin)

Manage cholestasis Give bile “altering” or choleretic drugs (e.g., ursodiol)
Correct extrahepatic bile duct obstruction
*Adapted from Johnson SE, Sherding RG. Diseases of the liver and biliary tract. In: Birchard SJ, Sherding RG, eds. Manual of Small
Animal Practice. Philadelphia, PA: WB Saunders Co, 1994; 730.

synthetic failure (3/22), indeterminate (3/22) and disseminated FEEDING PLAN
intravascular coagulation (1/22). Increased AP activity was the
only biochemical abnormality statistically correlated with coag- The universal goals for dietary management of hepatobiliary
ulation abnormalities (p = 0.23). Cats with marked increases in disease are directed at clinical manifestations of the disease
AP activity were more likely to have coagulation abnormalities rather than the specific cause itself. The goals of nutritional
than those with only mild increases in AP activity (Lisciandro management for hepatobiliary disease include: 1) maintaining
et al, 1998). Despite the common presence of coagulation test normal metabolic processes and homeostasis, 2) avoiding and
abnormalities, spontaneous hemorrhage in liver disease patients managing HE, 3) providing substrates to support hepatocellu-
is rare. However, it should be assumed that liver disease patients lar repair and regeneration, 4) decreasing further oxidative
have a higher than normal risk of bleeding. damage to liver tissue and 5) correcting electrolyte disturbances
At the very least, foods for patients with liver disease should (Blackburn and O’Keefe, 1989; Center, 1998).
contain the minimum recommended allowance of vitamin K The therapeutic goals for patients with HE also include: 1)
(menadione) for foods for normal adult dogs and cats: 1.63 and recognizing and correcting precipitating causes of enceph-
1.0 mg/kg DM, respectively (NRC, 2006). Supplementing alopathy (e.g., hypokalemic alkalosis), 2) reducing intestinal
foods with active vitamin K (vitamin K ) is expensive and the production and absorption of neurotoxins, with special em-
1
vitamin would likely not survive the heat of processing. The phasis on ammonia and 3) finding the balance between pro-
water-soluble form of menadione, menadione sodium bisulfite, viding too much and too little protein, both of which increase
is much less expensive, is heat stable and is passively absorbed ammonia generation.
from the small intestine and colon. However, menadione is bio- Dietary therapy is only beneficial when performed in con-
logically inactive, as is vitamin K , and requires alkylation by junction with proper medical and surgical management of the
1
gut microorganisms or animal tissues to biologically active specific hepatobiliary disease involved. Medical management
menaquinone-4 (NRC, 2006). often includes use of antiinflammatory agents, immunomodu-