Page 627 - Small Animal Internal Medicine, 6th Edition

CHAPTER 36 Hepatobiliary Diseases in the Dog 599

are listed in Box 36.5, but any drug could cause idiosyncratic mean that the dog has a thrombus or DIC. More marked
hepatic necrosis in an individual dog. A case of destructive elevations are suggestive of DIC. Diagnostic imaging is not
VetBooks.ir cholangitis (termed disappearing bile duct syndrome) was usually helpful in dogs with acute hepatitis. There may be
hepatomegaly and a diffuse change in hepatic echogenicity;
reported in a dog as a suspected drug reaction to amoxicillin-
clavulanate, amitraz, and milbemycin oxime or a combina-
but these changes are not specific and do not help define the
tion of these (Gabriel et al., 2006); the author has seen this in some cases there may be splenic congestion and/or ascites,
in a clinical case likely caused by an idiosyncratic reaction cause or extent of the damage. In some patients, the ultraso-
to amoxicillin-clavulanate. nographic examination is unremarkable.
Clinical Features Treatment and Prognosis
The clinical features of acute fulminating hepatitis, indepen- Treatment of acute fulminant hepatitis in dogs is largely sup-
dent of the cause, relate to the acute loss of hepatic function portive, outlined in Box 36.4. Every attempt should be made
together with the effects of generalized cell necrosis and to identify and treat the primary cause at the same time that
release of inflammatory cytokines and tissue factors. Dogs supportive therapy is instituted. Corticosteroid treatment is
usually present with an acute onset of one or more of the not indicated in these cases and may worsen the prognosis
following—anorexia, vomiting, PD-PU, dehydration, HE by increasing the risk of GI ulceration and thrombosis. DIC
with depression progressing to seizures and/or coma, jaun- is a high risk in these cases, and the treatment of DIC is dif-
dice, fever, cranial abdominal pain, coagulopathy with pete- ficult and usually unsuccessful. The most effective treatment
chiae and possible hematemesis and melena, and, in some is to remove the inciting cause, which in acute liver failure
cases, ascites and splenomegaly resulting from acute portal in humans means rapid liver transplant. Without this option
hypertension. In dogs and cats with severe acute liver disease, in dogs and cats, the mortality in DIC of acute fulminant
spontaneous bleeding may result from depletion of clotting hepatitis is likely to be 100%. Recommended therapies
factors or from DIC. Renal failure is a severe complication include plasma transfusion to replace depleted clotting
in some cases, with both prerenal and intrinsic renal com- factors and careful heparin therapy during the hypercoagu-
ponents. In humans with acute hepatic failure, hypotension, lable phase. However, the efficacy of heparin therapy in DIC
cardiac arrhythmias, cerebral and pulmonary edema, and has recently been called into question in humans, and there
pancreatic inflammation also have been reported; these may are no clinical data supporting its use in dogs and cats (see
occur in some dogs, although they have not been specifically Chapter 87).
reported. The owner should be warned of the poor prognosis for
recovery in spite of intensive support, and in severe cases,
Diagnosis early referral to an intensive care unit should be considered.
The diagnosis is usually made on the basis of history, clinical However, dogs that recover from the acute phase have a good
signs, and clinicopathologic findings. Liver histopathology chance of complete recovery. Some research in humans and
should be confirmatory, but results are often not obtained animals has suggested that chronic liver lesions are less likely
until recovery (or postmortem) because of the severe, acute to develop if a single-protein milk or soybean-based diet is
nature of the disease. A history of recent drug or toxin expo- fed during the recovery phase.
sure is important in implicating these as a cause; vaccination
status is an important consideration for infectious causes.
On clinical pathology, dogs with acute hepatitis often BILIARY TRACT DISORDERS
have early marked increases in hepatocellular enzyme ALT
and AST activities (10-fold to >100-fold). Jaundice and Biliary tract disorders are less common in dogs than in cats,
increases in markers of cholestasis may also occur; the rare but primary biliary tract disorders and extrahepatic bile duct
cases of destructive cholangitis are characterized by early obstruction (EBDO) are recognized in dogs. In addition,
severe jaundice, marked increases in ALP activities, and destructive cholangitis caused by drug reactions leading to
hyperbilirubinemia. Hypoglycemia and hypokalemia are severe cholestasis and icterus has been recognized occasion-
common in dogs with acute hepatitis, and azotemia is seen ally in dogs but not cats. Dogs occasionally develop con-
in some cases as a result of both prerenal and renal causes. genital hepatic and renal cysts, similar to Caroli’s disease in
Hemostatic abnormalities, with prolonged clotting times and humans, which are discussed in the section on ductal plate
thrombocytopenia, are frequently present and can be a sign disorders later.
of developing DIC (see Chapter 87). In patients with DIC,
APTT and OSPT may be prolonged, but it is impossible to CHOLANGITIS AND CHOLECYSTITIS
distinguish this from reduced hepatic production of clotting Primary cholangitis has been considered to be less common
factors. However, measurement of increased D-dimers and/ in dogs than in cats, although recent reports suggest it has
or fibrin degradation products, combined with decreases in been underestimated (Tamborini et al., 2016; Harrison et al.,
platelet count and schistocytosis, increases the index of sus- 2018). Histologically, cholangitis is defined as inflammation
picion for DIC. D-dimer concentrations are often mildly to confined to the portal region with either inflammatory cell
moderately increased in dogs with liver disease because of infiltration of the bile duct wall or within the lumen of the
reduced clearance in the liver, and this does not necessarily bile duct. The clinical signs and diagnostic evaluation are