Page 626 - Small Animal Internal Medicine, 6th Edition

598 PART IV Hepatobiliary and Exocrine Pancreatic Disorders

kg PO q12h, 30 minutes before a meal. 2,3,2-Tetramine is Treatment focuses on providing supportive measures and
difficult to obtain. Penicillamine is not helpful in an acute allowing the liver to recover. Dogs with acute hepatitis are at
VetBooks.ir crisis because chelation takes weeks to months. However, it high risk of disseminated intravascular coagulation (DIC).
Severe loss of liver function is also fatal because it cannot be
should be noted that there is much less information available
about the pharmacokinetics, drug interactions, and toxicity
treatment as liver dialysis. However, because of the remark-
of trientine in dogs than there is for D-penicillamine. Re- replaced artificially while awaiting recovery; there is no such
ported adverse effects include nausea, gastritis, abdominal able regenerative capacity of the liver, animals that survive
pain, melena, and weakness. On recovery, the animal should the acute phase of the disease can recover completely, with
continue on long-term treatment, as outlined in the follow- no permanent hepatic injury, as long as they are fed and
ing sections. supported properly.
Treatment of dogs that already have high hepatic copper Most causes of acute fulminating hepatitis in dogs are
concentrations documented by biopsy but are not in an acute infectious or toxic (see Box 36.5). In unvaccinated dogs,
crisis consists of active copper chelation, zinc supplementa- CAV-1 and leptospira are important differential diagnoses.
tion once chelation is completed, and a low-copper diet and Dogs with copper storage disease can present acutely, often
additional supportive therapy. The chronic hepatitis second- associated with high serum copper concentration in addi-
ary to copper storage disease should be treated the same way tion to acute hepatic necrosis. Xylitol, an artificial sweet-
as in dogs with idiopathic chronic hepatitis, using antioxi- ener, has been reported to cause acute hepatic necrosis and
dants, ursodiol, and other supportive medication (see earlier, an associated coagulopathy in dogs (Dunayer et al., 2006),
“Idiopathic Chronic Hepatitis”). There is a particular role for with a high mortality. Aflatoxin in contaminated food has
antioxidants such as vitamin E and SAM-e in metal-induced also caused acute and subacute hepatitis with a high mor-
liver injury. Chelation can be achieved using D-penicillamine tality in dogs (Newman et al., 2007). The most common
or trientine. D-Penicillamine takes months to have a signifi- drugs implicated in causing acute hepatic necrosis in dogs
cant effect on the copper content of the liver but is easily
available and its pharmacokinetics and toxicity in dogs are
well documented; it also has weak antifibrotic and antiin- BOX 36.5
flammatory properties. The recommended dosage is 10 to
15 mg/kg PO q12h, 30 minutes before meals. Starting at the Potential Causes of Acute Fulminant Hepatitis in Dogs
lower end of the dosage range and increasing the dose after
1 week (or dividing the dose and giving it more frequently) Infections
can reduce the common adverse effects of vomiting and • Canine adenovirus type 1
anorexia. It has also been reported rarely to cause nephrotic • Neonatal canine herpesvirus
syndrome, leukopenia, and thrombocytopenia in dogs, so a • Leptospira interrogans (various serovars)
• Endotoxemia
complete blood count (CBC) and urine samples should be • Yersinia
monitored regularly during therapy. A decrease in liver • Sarcocystic hepatitis (neospora; sarcocystitis and
copper content of about 900 µg/g dry weight/year can be hammondia) rarely (Irvine et al., 2016).
anticipated in dogs treated with D-penicillamine. Trientine
(2,2,2-tetramine) is another efficacious copper chelator that Thermal
may be used; it can remove copper from the liver more • Heat stroke
rapidly than D-penicillamine. Details of dosage and potential
adverse effects have been presented earlier. Metabolic
Copper chelation treatment is continued until a normal • Acute necrosis associated with copper storage disease
liver copper concentration is reached; this is best determined in Bedlingtons, Dalmatians, and some Labradors and
Dobermans (see Box 36.1)
by liver biopsy and copper quantification or cytologic esti-
mate. An alternative is to monitor serum liver enzyme activi- Toxic or Drug-Induced
ties every 2 to 3 months until they return to normal. • Acetaminophen
Treatment should then be stopped to prevent copper defi- • Phenobarbital or primidone
ciency, which can occur after prolonged, overzealous copper • Carprofen (especially Labrador Retrievers)
chelation and can result in severe effects of copper deficiency, • Mebendazole
with weight loss and hematemesis. The regimen can then be • Thiacetarsamide
changed to a preventive protocol consisting of a copper- • Mercury
restricted diet and zinc administration throughout the ani- • Potentiated sulfonamides
mal’s life span. • Mebendazole
• Cyanobacteria (blue-green algae) in seawater and
ACUTE HEPATITIS fresh water
• Xylitol
Etiology and Pathogenesis • Aflatoxin
• Nitrofurantoin
Acute hepatitis is much less common than chronic hepatitis • Lomustine (CCNU)
in dogs but, when severe, carries a much poorer prognosis.