Page 925 - Cote clinical veterinary advisor dogs and cats 4th

Hepatitis (Chronic, Idiopathic) of Dogs 453

• Immune-mediated mechanisms: poorly • Coagulation tests: prothrombin time (PT), TREATMENT
documented in the dog. Studies measuring activated partial thromboplastin time (aPTT; Treatment Overview
VetBooks.ir responses in affected cases fail to determine penia, and proteins induced by vitamin K If an underlying cause can be identified, it Diseases and Disorders
most common abnormality), thrombocyto-
liver-associated antibodies or cell-mediated
should be addressed directly. Otherwise, treat-
if the response is primary or a secondary
antagonism (PIVKA) may become abnormal
phenomenon. Expression of dog lymphocyte
of ongoing inflammation, providing optimal
(TEG) may demonstrate a hypercoagulable
antigen (DLA) class II in some dogs suggests in advanced disease. Thromboelastography ment is aimed at halting/slowing progression
a role for the immune system in chronic or hypocoagulable state. nutrition and hepatic support, and treating
hepatitis. • Abdominal ultrasonography: variable hepatic complications as they occur.
• Drug-associated: anticonvulsants, NSAIDs, parenchymal changes. Microhepatica,
trimethoprim-sulfadiazine, lomustine, or nodular liver, and ascites occur in late-stage Acute General Treatment
potentially almost any drug disease (cirrhosis/hepatic failure). Decreased Complications of chronic hepatitis should be
• Copper-associated liver disease: defective portal flow and evidence of acquired shunt treated as they occur. Commonly used treat-
copper metabolism or increased dietary formation are seen with portal hyperten- ments during acute management of idiopathic
copper intake sion. Ultrasound findings may be normal chronic hepatitis:
• Other conditions: aflatoxins, chemicals, or or nonspecific, even in advanced disease. • Fluid therapy to correct deficits and electrolyte
other environmental factors • Ultrasound-directed fine-needle aspiration losses: supplemental dextrose 2.5%-5% is
and cytology cannot accurately diagnose recommended; limit sodium with ascites
DIAGNOSIS chronic hepatitis, but can identify some (e.g., switch to low-sodium, isotonic main-
other causes of hepatic dysfunction (e.g., tenance fluid when patient is hydrated, such
Diagnostic Overview neoplasia). as Plasma-Lyte 56 plus 5% dextrose, with
The diagnosis is suspected in any dog with • Serologic testing as indicated by geography or potassium supplementation).
historical, physical, biochemical, or imaging- other clinical signs: potentially includes tests • Dextrans, hetastarch, plasma, or albumin
identified signs of hepatobiliary disease. for leptospirosis, bartonellosis, leishmaniasis, infusions if necessary to improve oncotic
Confirmation is achieved by histologic analysis and antinuclear antibody (ANA) titer for pressure during administration of IV crystal-
of a liver biopsy specimen. Unexplained immune-mediated disease. loid fluids
persistent abnormal liver enzyme activities • Abdominocentesis (pp. 1056 and 1343) in • Gastric ulceration (p. 380): omeprazole
should initiate investigation of possible chronic patients with ascites demonstrates a pure or 0.7-1 mg/kg PO q 12-24h and sucralfate
hepatitis. modified transudate. 0.5-1 g PO q 8h; avoid cimetidine because
• Surgery or laparoscopy (p. 1128): grossly, of hepatic metabolism
Differential Diagnosis liver may appear normal (subclinical disease) • HE treatment (p. 440): lactulose, antibiotics
• Acute hepatitis or may be small, nodular, and fibrotic/firm • Coagulopathies are treated with fresh-frozen
• Hepatic neoplasia (advanced disease). plasma or fresh whole blood (p. 1169) if there
• Pancreatitis • Liver biopsy and histopathologic evaluation is evidence of overt bleeding and anemia.
• Reactive hepatopathies secondary to systemic, ○ Assess coagulation before biopsy, and Stored blood should be avoided due to high
metabolic, or GI disease consider pre-biopsy plasma transfusion ammonia concentrations.
• Congenital portosystemic shunts (HE) if indicated. • If ascites causes discomfort or respiratory
• Cholecystitis or extrahepatic bile duct ○ Large biopsies (obtained by laparoscopy or compromise, treat with abdominocentesis
obstruction (icterus) laparotomy) are preferred over needle-core (p. 1056). Diuretics are less effective and
biopsies because of superior diagnostic possibly associated with greater side effects
Initial Database accuracy. in the acute stages of mobilizing ascitic fluid
• CBC: nonregenerative anemia, stress leuko- ○ Obtain liver samples for quantitative (see below).
gram possible copper and iron analysis and for culture • Sepsis (p. 907): if present, appropriate
• Serum biochemistry profile: increased and sensitivity. antibiotics immediately
liver enzyme activities, including alanine ○ Subclinical disease is associated with
aminotransferase (ALT), aspartate amino- infiltration of mononuclear inflamma- Chronic Treatment
transferase (AST), alkaline phosphatase tory cells into portal and parenchymal All therapy discussed below lacks critical
(ALP), and gamma-glutamyltransferase areas. scientific review in dogs but reflects the
(GGT), are extremely common. In ○ Clinical disease is associated with evidence current consensus of a number of veterinary
advanced disease, hyperbilirubinemia and of active hepatitis, with areas of piecemeal gastroenterologists:
decreased albumin, glucose, blood urea and bridging necrosis. • Antiinflammatory therapy using prednisolone
nitrogen, and/or cholesterol concentrations ○ In cirrhosis, extensive fibrosis and nodular 1-2 mg/kg PO q 24h; maximum dose 60 mg/
may occur. Hyperglobulinemia is often regeneration are also present. day. Dosage is often tapered to 0.5 mg/kg q
observed. ○ Histochemical staining for copper and 24-48h after there is clinical improvement.
• Urinalysis: bilirubinuria, variable specific iron are often positive. Corticosteroids cause a secondary vacu-
gravity, and sometimes ammonium biurate • Hepatic metal quantitative analysis: hepatic olar (steroid) hepatopathy; monitoring of
crystalluria associated with hyperammonemia copper can accumulate secondary to the liver ALP is not helpful, but there should be a
• Abdominal radiographs: normal or small disease; concentrations often range from decline in serum bilirubin, ALT, and AST
liver ± signs of ascites in advanced disease 600-1500 mcg/g dry weight liver (normal concentrations and often an increase in
(cirrhosis/hepatic failure) < 400 mcg/g). Values > 1000 mcg/g can be serum albumin concentration during effective
associated with a primary copper-associated treatment.
Advanced or Confirmatory Testing hepatopathy (p. 458). Hepatic copper can ○ If ascites present, dexamethasone 0.2 mg/
• Elevated serum bile acid concentrations also be determined with computer-assisted kg PO q 24-48h is used instead to avoid
suggesting altered hepatic function or portal digital analysis of copper-stained hepatic mineralocorticoid effect.
shunting biopsy specimens. Hepatic iron is often ○ For corticosteroid-intolerant animals or
• Elevated plasma ammonia concentrations or elevated > 1200 mcg/g dry weight and is for additional immunomodulation, aza-
ammonia tolerance test (often associated with thought to accumulate in macrophages from thioprine 2 mg/kg PO q 24h for 1 week,
portosystemic shunting). hepatic parenchymal death. then q 48h, or mycophenolate mofetil

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