Cats, even those with severe pancreatitis, present with less specific clinical signs than do dogs. In a recent review of 159
cats with pancreatitis, clinical signs reported included anorexia in 87%, lethargy in 81%, dehydration in 54%, weight loss
in 47%, vomiting and hypothermia in 46%, icterus in 37%, fever in 25%, abdominal pain in 19%, diarrhea in 12%, and a palpable
abdominal mass in 11%.9 Especially remarkable in this report is the low incidence of vomiting and abdominal pain in cats with pancreatitis.
Clinical signs in patients with pancreatitis are due either to prematurely activated pancreatic enzymes or to systemic effects
of the inflammatory response to pancreatic autodigestion. Recent experimental data in rats and mice suggest that the exocrine
pancreas responds to many different noxious stimuli in a similar fashion.10 The first common change reported is decreased pancreatic enzyme secretion.10 This change is followed by the formation of giant cytoplasmic vacuoles in acinar cells, visible only by electron microscopy.10 Biochemical studies have shown that these vacuoles are the product of co-localization of zymogens of digestive enzymes and
lysosomal enzymes, which are normally strictly segregated.10 The ensuing decrease in pH in the giant cytoplasmic vacuoles, the presence of the lysosomal enzymes such as cathepsin B,
or both lead to premature trypsinogen activation. Trypsin in turn activates other zymogens, leading to local effects such
as inflammation, pancreatic edema and hemorrhage, pancreatic necrosis, and parapancreatic fat necrosis. These local effects
are associated with clinical signs such as vomiting and abdominal pain.
Until recently it was thought that systemic signs seen in patients with pancreatitis, like local effects, are a direct result
of circulating pancreatic enzymes. While there is little doubt that some of these systemic effects, such as systemic lipodystrophy,
are caused by circulating pancreatic enzymes, recent data suggest that other systemic sequelae are a consequence of the release
of inflammatory mediators in response to pancreatic inflammation.11 Systemic effects seen in patients with severe pancreatitis include fever, systemic vasodilation leading to hypotension and
sometimes acute renal failure, pulmonary edema leading to respiratory failure, disseminated intravascular coagulation, and
in some cases multiorgan failure. A few patients also develop systemic lipodystrophy. Neurologic signs such as disorientation
have been seen in people, dogs, and cats with severe pancreatitis and are sometimes referred to as pancreatic encephalopathy.
While clinical signs are not specific for pancreatitis, vomiting, anorexia, and cranial abdominal pain are key clinical signs
in dogs with pancreatitis. Cats display these key clinical signs less frequently, making it more difficult for veterinary
clinicians to suspect pancreatitis.
GENERAL CLINICAL PATHOLOGY
Complete blood count and serum chemistry profile results often show mild and nonspecific changes in both dogs and cats with
pancreatitis.6,7 In a study of 70 dogs with fatal acute pancreatitis, complete blood count abnormalities included a neutrophilia with a left
shift in 55% of the cases, thrombocytopenia in 59%, and anemia in 29%.7 Similarly, complete blood count abnormalities in 40 cats with severe pancreatitis included anemia in 26% of the cases, hemoconcentration
in 13%, leukocytosis in 30%, and leukopenia in 15%.6 While these findings may help in the overall assessment of a patient's health status, they are not useful for arriving at
a specific diagnosis of pancreatitis in either dogs or cats.
Serum chemistry profiles in dogs or cats with pancreatitis may show mild elevations of hepatic enzymes.6,7 Electrolyte abnormalities are common in severe cases and may be due to dehydration or severe vomiting. Azotemia can be seen
and may be due to dehydration or acute renal failure.6,7 Hypoalbuminemia may also occur. Hypocalcemia can be seen in severe cases and may be present because of hypoalbuminemia or
the formation of calcium salts with fatty acids secondary to fat necrosis. In one study, a decreased plasma ionized calcium
concentration was common in cats with acute pancreatitis and was significantly lower in cats with fatal disease.12 However, there was great overlap between the groups,12 and the plasma ionized calcium concentration lacked sensitivity for identifying fatal disease.
Urinalysis often reveals an elevated urine specific gravity secondary to dehydration. However, in severe cases acute renal
failure may ensue; consequently, the urine specific gravity may drop and casts may be seen in the sediment.