Page 506 - Problem-Based Feline Medicine

498 PART 7 SICK CAT WITH SPECIFIC SIGNS

toneum may occur with amyloidosis and peliosis
LIVER DISEASE**
hepatis.
Classical signs Coagulation abnormalities are more likely to be pres-
ent if there is concurrent pancreatitis.
● Lethargy, inappetence, weight loss,
vomiting, icterus.
● Spontaneous or excessive bleeding may
occur. Clinical signs
More than 80% of cats with liver disease may have a
See main reference page 421 (The Yellow Cat or Cat
coagulation abnormality, but abnormal clinical bleed-
With Increased Liver Enzymes).
ing is uncommon.
Excessive bleeding may occur following venepunc-
Pathogenesis
ture and liver biopsy.
The most common causes of liver disease in the cat are
Severity of coagulopathy correlates to some extent
lipidosis, cholangiohepatitis and lymphoma. Less
to increase in alkaline phosphatase value, likely due
common causes include congenital portosystemic shunts,
to cholestasis.
amyloidosis, non-lymphoid neoplasia, feline infectious
peritonitis, peliosis hepatis, toxoplasmosis and toxins In other species acute bleeding into the intestinal tract
(e.g. diazepam). may precipitate hepatic encephalopathy, but this has
not been documented in the cat.
Liver disease may cause bleeding tendencies by several
mechanisms including:
● Acquired platelet function defects (not proven in cats).
● Decreased synthesis of coagulation factors. Diagnosis
– Primary hepatocellular failure affecting syn-
Combining results of several studies, coagulation
thesis of all factors.
abnormalities may be categorized as follows:
– Vitamin K deficiency (contributing to coagu-
● Vitamin K deficiency: Normal platelet count, pro-
lopathy in about 50% of cases).
longed PT, ± prolonged aPTT, normal TT.
– Intrahepatic cholestasis and extrahepatic bile
● Synthesis failure: Normal platelet count, pro-
duct obstruction prevent release of bile acids
longed PT, prolonged aPTT, prolonged TT.
into the small intestine that are needed for
● Indeterminate: Normal platelet count, normal PT,
absorption of vitamin K1 and K2.
prolonged aPTT, normal TT.
– Anorexia and antibiotic therapy contribute to
● DIC: Low platelet count, prolonged PT, prolonged
vitamin K deficiency.
aPTT, prolonged TT; or 3 of the following: low
● Synthesis of abnormal prothrombin (not proven in
platelet count, prolonged PT or aPTT, prolonged
cats).
TT or hypofibrinogenemia, decreased antithrombin
● DIC causing consumption of platelets and coagula-
III (not routinely available), presence of FDPs, red
tion factors.
blood cell fragments.
● Decreased clearance of plasminogen activators
thus promoting fibrinolysis (not proven in cats). Vitamin K deficiency may also be identified by improve-
ment in coagulation following vitamin K1 therapy.
In general, fever decreases the half-life of coagula-
tion factors and wound healing increases consumption PIVKA time is more sensitive in identifying abnor-
of coagulation factors (e.g. after exploratory laparo- mal coagulation than are PT and aPTT. Cats may show
tomy). Both of these may be present with liver disease. a bleeding tendency with a prolonged PIVKA time and
normal PT and aPTT.
The liver may be more fragile with hepatic lipidosis,
amyloidosis and peliosis hepatis increasing the risk of More than one mechanism may contribute to coagu-
bleeding after liver biopsy. Spontaneous hemoperi- lopathy.