Page 676 - Clinical Small Animal Internal Medicine

644 Section 7 Diseases of the Liver, Gallbladder, and Bile Ducts

Coagulopathy
VetBooks.ir The liver is involved in the manufacture of the majority

of the coagulation factors, including fibrinogen (factor I),
prothrombin (factor II) and factors V, VII, IX, X, XI, and
XIII. The site of factor VIII production is controversial,
but it is likely that the liver plays an important role in its
production. It is also the site of the vitamin K‐dependent
activation of factors II, VII, IX, and X and protein C. In
addition to this, the liver is involved in the clearance of
activated clotting factors and the production of clotting
factor inhibitors (e.g., antithrombin and alpha‐1‐antit-
rypsin) and fibrinolytic proteins such as plasminogen.
Hence, in liver disease there is the potential for disrupted
production of coagulation factors and their inhibitors
along with impaired clearance of both activated coagula-
tion factors and the products of the fibrinolytic system.
The extent of the resulting abnormalities reflect the
severity of the underlying liver disease, ranging from
Figure 60.2 Dalmatian showing head pressing as a manifestation individual factor deficiencies to disseminated intravas-
of hepatic encephalopathy.
cular coagulation (DIC).
A study of 42 dogs with histologically confirmed liver
disease demonstrated that one or more coagulation
constellation of potential clinical signs ranging in sever-
ity from apathy and reduced awareness to coma and abnormalities was present in 57% of the dogs. These
unresponsiveness. The most commonly implicated toxin abnormalities ranged from single factor deficiencies in
in HE is ammonia, although there are some cases where four of the dogs to DIC in three dogs. An older study sug-
the plasma ammonia concentration is normal or only gested a figure of 93% of dogs with liver disease having
slightly raised despite signs of HE. Other potential abnormal coagulation parameters, although this study
triggers that have been studied include mercaptans, involved more severely affected cases. A study of 45 cats
manganese, systemic inflammation, altered gamma‐ with liver disease showed that 98% of the cats had one or
aminobutyric acid (GABA, an inhibitory neurotransmit- more abnormality detected. What is important to recog-
ter), benzodiazepine receptor signaling and altered nize clinically is that, whilst spontaneous hemorrhage
catecholaminergic signaling due to changes in branched may be rare in animals with hepatic disease, hemostatic
chain aromatic amino acid profiles. Whatever the abnormalities occur commonly. Hence, the clinician
underlying cause, the overall result is a disruption of needs to exercise caution when considering interven-
brain function, typically leading to waxing and waning tional diagnostic procedures and a coagulation profile
clinical signs. should be performed in all such cases.

Gastroduodenal Ulceration Signalment

Patients with hepatobiliary disease are predisposed to
gastric and duodenal ulceration for a number of reasons. Patient signalment is very important when approaching
Portal venous hypertension is an important risk factor the patient with hepatobiliary disease. There are a vari-
resulting in vascular stasis and venous congestion, which ety of known or suspected breed predispositions to
together increase the risk of mucosal ulceration due to hepatic disease which can be helpful to consider, particu-
reduced mucosal blood flow and secondarily reduced larly in view of the occult nature of many cases of early
bicarbonate and mucus secretion. This risk is further liver disease. Congenital portosystemic shunts (CPSS)
increased in anorexic animals or those exposed to non- have worldwide breed predispositions including Irish
steroidal antiinflammatory drugs or potentially corticos- wolfhounds, cairn terriers, Labrador retrievers, dachs-
teroids. Gastrointestinal ulceration and bleeding is an hunds, Yorkshire terriers, Australian cattle dogs, Maltese
important consideration in any patient with HE that terriers, and miniature schnauzers. In cats, the condition
suddenly deteriorates or in any patient with liver disease is seen most frequently in mixed‐breed cats, although
that becomes more subdued or develops a reduced Persian and Himalayan breeds are also overrepresented.
appetite. Additionally, copper‐associated hepatitis has been