FURTHER PATIENT EVALUATION
Once you decide to pursue additional diagnostic testing, the next step is diagnostic imaging. If diagnostic imaging fails
to show any abnormalities that dictate a specific diagnostic or therapeutic approach (e.g. surgery in the case of gallbladder mucoceles, choleliths, or portosystemic vascular anomaly), then consider obtaining a hepatic
Abdominal radiographs allow assessment of liver size and abdominal detail and may reveal choleliths (50% are visible radiographically).
Hepatomegaly is typically associated with any vacuolar hepatopathy (e.g. hyperadrenocorticism, adrenal hyperplasia syndromes, and hypothyroidism), phenobarbital hepatopathy, and acute and chronic
inflammatory hepatobiliary disease. Microhepatia may be seen with portosystemic vascular anomalies (with the exception of
microvascular dysplasia) or cirrhosis. Choleliths can be associated with cholecystitis and may indicate a subclinical hepatobiliary
Ultrasonography is helpful in differentiating focal (abscess, hepatobiliary neoplasia), multifocal (nodular hyperplasia, metastatic
disease), or diffuse lesions. In cases of nodular hyperplasia, homogenous hypoechoic masses or mixed hypoechoic to hyperechoic
lesions may be noted but cannot be differentiated from primary or secondary neoplasia.13 Ultrasonography can also reveal changes in liver echogenicity; unfortunately, no change is classic for a specific disease.
Both a corticosteroid hepatopathy and hepatic lipidosis are characterized by a diffusely hyperechoic liver. Normal liver parenchyma
does not rule out hepatic disease.
The gallbladder and biliary tree can also be evaluated ultrasonographically. Gallbladder mucoceles, choleliths, and intrahepatic
or extrahepatic bile duct dilatation can be identified ultrasonographically. Hepatic portal vasculature can also be evaluated
to identify small, single or multiple acquired shunts. Extrahepatic causes for liver enzyme elevations may also be evaluated,
including pancreatitis, hyperadrenocorticism (assessment of adrenal glands), and gastrointestinal tract disease.
Before the hepatic biopsy, perform a coagulation profile to assess the prothrombin time, partial thromboplastin time, and
platelet count. Hepatic biopsy samples can be obtained with ultrasound guidance (Tru-Cut biopsy) or exploratory surgery (see the article) or laparoscopy (wedge biopsy). A wedge biopsy is the gold standard, and studies suggest that discordance occurs on histopathologic
assessment of wedge vs. Tru-Cut biopsy samples from the same liver.14 The results of any hepatic biopsy, however, need to be interpreted in light of sampling error.
The method by which to obtain a biopsy sample may be influenced by the suspected diagnosis. In some diseases, such as microvascular
dysplasia and nodular hyperplasia, a wedge biopsy is often necessary to obtain a definitive diagnosis. In other cases, such
as with a diffuse vacuolar hepatopathy, inflammatory disease, or neoplasia, a diagnostic sample can likely be obtained by
performing a Tru-Cut biopsy. In the case of focal or diffuse neoplasia, a fine-needle aspiration biopsy may yield diagnostic
samples. In most cases, however, fine-needle aspiration biopsy is inadequate for diagnostic purposes.
Cholecystocentesis can also be performed to obtain bile for culture in cases in which subclinical infection is suspected.
This procedure should be performed with ultrasonographic guidance by an experienced ultrasonographer.
DIAGNOSTIC FINDINGS FOR SPECIFIC CAUSES OF ELEVATED HEPATIC ENZYME ACTIVITIES
Causes of elevated liver enzyme activity in asymptomatic dogs can generally be divided into extrahepatic and hepatobiliary
Your diagnostic test findings may point to three extrahepatic causes—hyperadrenocorticism, hypothyroidism, and gastrointestinal
Hyperadrenocorticism is associated with mild to moderate increases in total serum ALP activity in about 85% of cases. Similar
degrees of elevation may be seen with GGT activity, and in 50% to 80% of dogs a mild increase in ALT activity is noted.15 Other clinicopathologic changes that might provide clues to the presence of hyperadrenocorticism are mild polycythemia,
a stress leukogram, mild thrombocytosis, hypercholesterolemia, hypertriglyceridemia, and isosthenuria.15