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Cirrhotic/Fibrosing Liver Disease 175

• Serum biochemistry panel TREATMENT with cleansing and/or retention enemas
○ Elevated hepatic enzyme activities (alkaline Treatment Overview (povidone-iodine diluted 1 : 10 with tap
VetBooks.ir aspartate aminotransferase, gamma- Very few treatment options are proven to water) to decrease ammonia production/ Diseases and Disorders
phosphatase, alanine aminotransferase,
water or lactulose diluted 1 : 3 with tap
absorption in cases of HE. Generally, patients
glutamyl transferase) typical
directly impact the progression of this con-
○ Hyperbilirubinemia
stage) (depending on dition unless a specific cause (e.g., copper with advanced disease requiring this level of
accumulation, drug-induced condition) can be
therapy have a grave prognosis.
○ Low blood urea nitrogen (BUN) (variable) targeted. Fortunately, very few of the myriad • Ursodiol 10-15 mg/kg PO q 24h as a
○ Hypoalbuminemia and hyperglobulinemia of potentially beneficial nonspecific treatments choleretic in cases of cholestasis
(variable) (e.g., antioxidants, liver protectants) are thought • Alpha-tocopherol (vitamin E) 200-600 IU
○ Hypocholesterolemia (variable) to have significant adverse effects. PO q 24h, S-adenosylmethionine 20 mg/
○ Hypoglycemia (variable) kg PO q 24h, and milk thistle/silymarin
○ Electrolyte abnormalities (hypokalemia, Acute General Treatment (optimal dose unknown) may act as hepa-
hyponatremia) • Intravenous fluids (balanced electrolyte toprotective antioxidants.
• Urinalysis solution) as needed • Spironolactone 1-2 mg/kg PO q 12h or
○ Isosthenuria ○ Avoid 0.9% NaCl with ascites and furosemide 1-2 mg/kg PO q 12h in cases
○ Ammonium biurate crystalluria (variable) hypoalbuminemia of ascites
○ Avoid lactate if hepatic failure • Vitamin K 1 1-2 mg/kg SQ or IM if overt
Advanced or Confirmatory Testing ○ Potassium (20-40 mEq/L or more, based clinical bleeding is identified or if PT or
• Abdominocentesis and fluid analysis of on serum potassium concentration) and aPTT are prolonged > 2 × normal
ascites (pp. 1056 and 1343): pure transudate dextrose (2.5%-5%) supplementation may • Sucralfate 1 g/25 kg PO q 8-12h, omeprazole
(hypoalbuminemia) or modified transudate be necessary. 1 mg/kg PO q 12h as gastrointestinal ulcer
(portal hypertension) ○ Dextrans, hetastarch, or plasma transfusion therapy
• Coagulation studies: prolonged activated for oncotic pressure support. Plasma
clotting time (ACT), partial thromboplastin advantages include presence of albumin Nutrition/Diet
time (PT), activated partial thromboplastin (contributes positively to protein balance), • Most commercial geriatric, liver, or renal
time (aPTT), fibrinogen concentration, presence of clotting factors, and persis- diets are appropriate. Copper restriction
proteins induced by vitamin K antagonism tence in circulation (vs. protein-losing appropriate for copper-associated hepatic
or absence (PIVKA), buccal mucosal bleed- enteropathy or nephropathy, in which the disease (p. 459)
ing time, and thromboelastography (TEG). transfused proteins may be lost quickly). • Adjust protein consumption in the face of
It has not been shown that any of these • Therapeutic abdominocentesis when neces- HE (decreased/optimal quantity, replace meat
studies will help predict bleeding after hepatic sary (i.e., respiratory compromise, significant proteins with dairy and/or vegetable protein).
biopsy. abdominal discomfort) Protein restriction is not warranted in the
• Serum bile acids: elevated (fasting and absence of encephalopathy.
postprandial). Bile acids are abnormal Chronic Treatment • Fermentable fiber in cases of HE
(and therefore an unnecessary test) in cases See HE (p. 440). • Water-soluble vitamin supplementation
where the total bilirubin concentration is • Antibiotics • Avoid mineral supplements containing
elevated. ○ Specific to infectious agent if identified copper.
• Radiographs: small liver (dogs), large liver as underlying cause (rarely in dogs)
(cats), loss of abdominal detail ○ For signs of hepatic encephalopathy, consider Drug Interactions
• Abdominal ultrasound ■ Metronidazole 10-15 mg/kg PO q 12h, • Animals with hepatic failure are anesthetic
○ Nodular hyperechoic/mixed echogenicity or risks. Barbiturates should be avoided,
of hepatic parenchyma with abdominal ■ Amoxicillin-clavulanate 12-25 mg/kg and benzodiazepines should be used with
effusion PO q 12h, or care. Isoflurane or sevoflurane are the gas
○ +/− Acquired portosystemic shunt(s) ■ Ampicillin 20-40 mg/kg PO q 8h, or anesthetics of choice. Propofol, although
○ +/− Ascites ■ Neomycin 20 mg/kg PO q 8h hepatically metabolized, may be administered
• Laparoscopy or laparotomy • Antiinflammatory: with histopathologic to effect (usually requiring a small fraction of
○ Small, firm, irregular liver confirmation of chronic noninfectious normal dosages) for controlling seizures due
• Liver biopsy (p. 1128) for histopathologic inflammation, consider prednisolone 1-2 mg/ to HE.
analysis: confirmatory kg PO q 24-48h (taper if possible) and/or • Lidocaine, theophylline, propranolol, cap-
○ Fibrosis: inflammatory (bridging) or azathioprine 2 mg/kg PO q 24h initially, topril, and tetracyclines should be avoided.
noninflammatory (sinusoidal, triads). tapered to 1 mg/kg. Other immunosup- • Diuretics may worsen HE, promote dehy-
Request reticulin and Masson’s trichrome pressive agents used for chronic hepatitis dration or metabolic alkalosis, and should
stains (or Sirius Red stain). are discussed on p. 452. be used only in otherwise stable patients
○ Cirrhosis, nodular regeneration, loss of • Antifibrotic: colchicine 0.03 mg/kg PO q for the long-term delay of return of
normal hepatic architecture 24h, although no published data support its ascites.
○ NOTE: suspicion of cirrhotic/fibrosing liver use or clearly demonstrate a beneficial effect; • Glucocorticoids should be avoided in animals
disease should prompt the consideration veterinary data regarding safety and efficacy with active infection, may precipitate hepatic
of wedge biopsy of the liver rather than are lacking at present. Telmisartan 0.5-1 mg/ failure and/or gastric ulceration, and cause
ultrasound-guided needle-core biopsy kg PO q 12h and phosphatidylcholine sodium retention (may use dexamethasone
because biopsies from a firm, severely 20-70 mg/kg/day PO decrease stellate cell [no mineralocorticoid activity] as an alterna-
fibrotic liver often yield small pieces of activation and may be beneficial. Prednisone tive to prednisone).
fragmented tissue, and it may be dif- (antiinflammatory) and D-penicillamine • Nonsteroidal anti-inflammatory drugs may
ficult to penetrate the liver safely with (copper chelator) 10-15 mg/kg PO q 12h exacerbate gastrointestinal ulceration.
needle-core biopsy instruments, especially also have weak antifibrotic properties. • Avoid medications that rely solely or
if ascites is present. Needle-core biopsies • Lactulose 0.25-0.5 mL/kg PO q 8h predominantly on hepatic metabolism for
are often inaccurate in cirrhotic livers. (titrated to achieve loose fecal consistency) effectiveness or clearance.

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