The incidence of exocrine pancreatic disorders is quite large in both dogs and cats. In a large retrospective study of necropsy
findings 1.5% of 9,342 canine and 1.3% of 6,504 feline pancreata showed significant pathological lesions. However, recently,
it has been suggested that the true prevalence of pancreatitis is by far greater. In one study 208 dogs undergoing necropsy
at the Animal Medical Center in New York City were enrolled and more than 21% had macroscopic lesions suggesting pancreatitis.
Pancreata from all dogs were sectioned every 2 cm and a total of 64% had histological lesions of acute and/or chronic pancreatitis.
In another study 25.6% of 200 un-selected dogs submitted to necropsy through a group of first-opinion practices in the UK
showed evidence of chronic pancreatitis and 2% showed evidence of acute pancreatitis. These data suggest that pancreatitis
is far more common in dogs than previously suspected. However, the data also suggest that infiltration of the pancreas with
inflammatory cells is not necessarily clinically significant and more research is needed to better characterize clinically
significant disease. Similar data have recently been reported for cats. In a study of 115 cats submitted for necropsy at the
University of California in Davis that had 3 biopsies collected (i.e., one from the left limb, one from the right limb, and
one from the body of the pancreas), 75.7% showed lesions suggestive of acute and/or chronic pancreatitis. This would suggest
that, similarly to dogs, feline pancreatitis is far more common than previously expected, but also that more work is needed
to clearly characterize clinically significant disease. Approximately 50% of all canine and feline patients with exocrine
pancreatic disorders have pancreatitis. According to the current classification system of human pancreatitis acute pancreatitis
is an inflammatory condition of the pancreas that is completely reversible after removal of the inciting cause. Chronic pancreatitis
is characterized by irreversible histopathologic changes of the exocrine pancreatic tissue, such as atrophy or fibrosis. Both
forms can be mild or severe. Mild forms of pancreatitis are associated with no or little pancreatic necrosis and systemic
effects and often allow recuperation of the patient. In contrast, severe forms of pancreatitis are associated with extensive
pancreatic necrosis, multiple organ involvement, and often a poor prognosis.
Several diseases and risk factors have been associated with pancreatitis. Traumatic pancreatitis (due to road traffic accidents
in both dogs and cats or falling from heights in cats) has been reported. Surgical trauma can also cause pancreatitis, but
many human patients that undergo surgery of organs distant from the pancreas have also been shown to be at an increased risk
for pancreatitis, suggesting that hypoperfusion of the exocrine pancreas during anesthesia may be of bigger concern than surgical
handling of the organ itself. Infectious agents have been shown to cause feline pancreatitis, with the strongest causal relationship
for Toxoplasma gondii, and rare cases of Amphimerus pseudofelineus infestation in cats. Babesia canis has been reported to be associated with pancreatitis in dogs. Weaker evidence has been presented for feline panleukopenia
virus infections in kittens and infections with feline herpesvirus I and feline infectious peritonitis virus. Two cases of
feline pancreatitis after topical use of fenthion, an organophosphate cholinesterase inhibitor, have been reported. Many other
pharmaceutical compounds have been implicated in causing pancreatitis in human beings and dogs. Chronic hepatitis in dogs
and cholangitis in cats coexist in patients with pancreatitis, but there is no evidence that they play a causative role. Hypertriglyceridemia
and hypercalcemia can also cause pancreatitis. Finally, more than 90% of all cases of canine or feline pancreatitis are idiopathic.
According to a generally accepted pathogenic principle, pancreatic acinar cells ultimately respond in a common fashion to
a variety of harmful stimuli, leading to inappropriate intracellular activation of trypsin, and subsequently activation of
other digestive zymogens. These activated digestive enzymes cause local changes, such as inflammation, hemorrhage, acinar
cell necrosis, and peripancreatic fat necrosis. Pancreatitis, when severe, is also associated with a variety of systemic complications,
such as systemic inflammatory changes, systemic vasodilatation leading to hypotension, pulmonary edema, disseminated intravascular
coagulation, central neurologic deficits, respiratory failure, renal failure, and multiorgan failure. Traditionally, it was
hypothesized that these changes, similarly to local changes are caused by prematurely activated pancreatic enzymes. However,
more recently, cytokines are believed to play a more important role in the progression of pancreatitis and the development
of these systemic complications.