Page 739 - Clinical Small Animal Internal Medicine

65 Cirrhosis and its Consequences 707

Signalment elevated liver enzymes, including alanine aminotrans­
VetBooks.ir Signalment of an animal with cirrhosis largely depends on ferase (ALT), aspartate aminotransferase (AST), alkaline
phosphatase (ALP), and gamma­glutamyl transpepti­
dase (GGT). However, in occasional cases of severe
the underlying cause of liver disease, but cirrhosis is much
more common in dogs than in cats. This may be due to a hepatocellular loss, liver enzymes may be within normal
slower accumulation of fibrosis in cats, or development of limits simply due to the low number of remaining hepat­
more severe complications of hepatic failure before ocytes. Liver pseudofunction tests may also be abnor­
advanced fibrosis occurs. Males and females are likely to be mal, and suggest some degree of liver dysfunction. It is
equally affected, and dogs with breed‐related risk of CH estimated that a reduction of approximately 70–80% of
are more likely to be affected. For further details of dog overall hepatic function must be present before these
breed predilections to CH, the reader if referred to alterations occur. Pseudofunction tests include decreased
Chapter 62. Dogs with idiopathic CH and copper‐associ­ albumin, BUN, cholesterol, and/or glucose, and an
ated CH are often middle‐aged to older, while dogs with increase in bilirubin. All of these pseudofunction com­
lobar‐dissecting hepatitis are usually young, around 2 years pounds are produced or metabolized normally by the
of age. Dogs or cats with a history of hepatotoxicity sec­ liver, and will be altered in states of liver dysfunction.
ondary to environmental toxins or drugs may be of any age. On a complete blood count, microcytosis may be noted
in patients with acquired or congenital PSS, secondary to
a deficiency in mobilization of iron stores. Anemia may
History and Clinical Signs occur from GI ulceration and blood loss or bleeding sec­
ondary to coagulopathy. Mild thrombocytopenia may be
The presenting clinical signs in chronic liver disease are present due to decrease in hepatic synthesis of throm­
often vague in nature, and include a history of inappe­ bopoietin. Leukocytosis is nonspecific, but may occur
tence, lethargy, vomiting, polyuria/polydipsia, weight loss, secondary to stress, inflammation, or infection.
and/or diarrhea. Melena may be observed if GI ulceration Urinalysis is often normal in patients with cirrhosis,
is present. Ascites and icterus are more specific clinical but may demonstrate dilute urine as a result of decreased
signs that may be noted. Neurologic abnormalities such as BUN concentration. Urea is a major component of the
depressed mentation, circling, ptyalism in cats, star‐gaz­ renal medullary concentration gradient, and, when
ing, seizures, stupor or coma may also occur secondary to decreased, may lead to the development of dilute urine.
HE. These neurologic changes may be intermittent in Bilirubinuria may be observed, and is always significant
nature, and frequently occur shortly following ingestion of in the cat, and if 2+ or greater is also significant in the
a meal containing protein. Signs have usually been present dog. Urate crystals may be observed in as many as
for weeks to months, and are often progressive in nature. 40–70% of dogs with canine PSS, and secondary urinary
Physical examination findings are also often nonspe­ tract infections are possible as a result of dilute urine.
cific, and may only include weight loss or muscle wast­ Coagulation testing should be undertaken if hepatic
ing. If ascites is present, abdominal distension and a biopsy is to be performed, or if any clinical signs of
palpable fluid wave may be apparent. Splenomegaly may bleeding are observed. Prothrombin time (PT) and partial
also occur in the presence of PH and pooling of blood in thromboplastin time (PTT) may be increased, and anti­
the spleen. Icterus may be visualized on the skin, sclera, thrombin, fibrinogen, and protein C levels are decreased
or mucous membranes as a result of accumulation of in dogs and cats with cirrhosis due to poor production of
bilirubin. Less commonly, petechiae or ecchymosis may coagulation factors and/or decreased recycling of vitamin
be observed on the skin or mucous membranes second­ K. Vitamin K deficiency may be especially important in
ary to thrombocytopenia or thrombocytopathy. Melena cats with severe liver disease. Evaluation of platelet func­
may be observed on rectal examination. If HE is present, tion testing via buccal mucosal bleeding time may also be
neurologic examination abnormalities localizing to the abnormal secondary to a thrombocytopathy.
forebrain may be present. Hepatic function testing can be performed by measur­
ing pre‐ and postprandial bile acid concentrations or
blood ammonia levels. Both tests may be elevated in the
Diagnosis face of significant liver dysfunction or aPSS secondary
to cirrhosis. Postprandial bile acids are considered to
be more sensitive for detection of PSS but elevated
Laboratory Testing
ammonia may be more specific. Additionally, ammonia
The most common laboratory abnormalities in patients is currently the only measureable HE toxin, so the find­
with cirrhosis are alterations of liver‐related enzymes. ing of hyperammonemia may also suggest a higher risk
Patients with cirrhosis will often have a known history of of clinical signs related to HE. However, ammonia sam­