Page 557 - Small Animal Internal Medicine, 6th Edition

CHAPTER 33 Clinical Manifestations of Hepatobiliary and Pancreatic Disease 529

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FIG 33.10
Acholic feces from a 7-year-old spayed female Collie dog
with a strictured bile duct and complete bile duct obstruction
3 weeks after recovery from severe pancreatitis.

BOX 33.4

Coagulation Proteins and Inhibitors Synthesized
by the Liver
FIG 33.11
Proteins C and S English Cocker Spaniel with chronic pancreatitis showing
Antithrombin loss of body weight and poor coat as a result of developing
Fibrinogen exocrine deficiency. Weight loss is slow and insidious, and
Plasminogen often not recognized initially by owner or vet.
Vitamin K–dependent factors
II (prothrombin)
VII melena are common bleeding presentations and a common
IX cause of death in dogs with chronic liver disease. In contrast
X to human patients, in whom fragile esophageal varices
Factor V develop and can burst, causing severe and often fatal hemor-
Factor XI rhage, the mechanism of GI hemorrhage in companion
Factor XII animals is unknown but is suspected to be related to poor
Factor XIII mucosal perfusion and reduced epithelial cell turnover asso-
ciated with portal hypertension and splanchnic pooling of
blood.
in plasma clotting factor concentrations without spontane-
ous hemorrhage. Having severe hepatic parenchymal disease
predisposes a dog or cat not only to changes in coagula- PROTEIN-CALORIE MALNUTRITION
tion factor activity from hepatocellular dysfunction but also
to DIC, particularly in those with acute disease. In dogs Pathogenesis
with acute hepatic necrosis, some clinicians have observed Protein-calorie malnutrition is very common in dogs with
thrombocytopenia, thought to be associated with increased chronic hepatitis and dogs and cats with chronic pancreatitis
platelet use or sequestration. Splenic sequestration of plate- as a result of reduced intake caused by anorexia, vomiting,
lets is common in humans with chronic liver disease and and diarrhea, and increased loss/wastage of calories caused
portal hypertension but has not been not reported in dogs by hypermetabolism and poor liver function or (in the case
and cats. of chronic pancreatitis) lack of digestive enzymes. In chronic
Other than noticeable imbalances in coagulation factor pancreatitis, the development of exocrine pancreatic insuf-
activity, the only other mechanism whereby bleeding might ficiency is progressive and insidious, and it may not be ini-
occur in a cat or dog with severe hepatic disease is portal tially recognized (Fig. 33.11). In human medicine, anyone
hypertension–induced vascular congestion and fragility. In with confirmed chronic pancreatitis is assumed already to
such cases, which are expected considerably more often in have some degree of exocrine insufficiency and is given
dogs than in cats because of the types of hepatobiliary dis- enzyme supplementation. A more proactive approach to
eases that they acquire, the common site affected is the upper supplementation would also be wise in dogs and cats because
GI tract (stomach, duodenum); therefore hematemesis and protein-calorie malnutrition in both liver and pancreatic