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.

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.