The etiologies of acute necrotizing pancreatitis are probably not yet completely recognized. Biliary tract disease, gastrointestinal
tract disease, ischemia, pancreatic ductal obstruction, infection, trauma, organophosphate poisoning, and lipodystrophy all
have known associations with the development of acute necrotizing pancreatitis in the cat. Hypercalcemia, idiosyncratic drug
reactions, and nutritional causes are suggested but poorly documented causes of the disease.
Concurrent Biliary Tract Disease – Concurrent biliary tract pathology has a known association with acute necrotizing pancreatitis in the cat. Cholangitis
is the most important type of biliary tract disease for which an association has been made, but other forms of biliary tract
pathology (e.g., stricture, neoplasia, and calculus) have known associations. Epidemiologic studies have shown that cats
affected with suppurative cholangitis have significantly increased risk for pancreatitis. The pathogenesis underlying this
association is not entirely clear but relates partly to the anatomic and functional relationship between the major pancreatic
duct and common bile duct in this species. Unlike the dog, the feline pancreaticobiliary sphincter is a common physiological
and anatomic channel at the duodenal papilla. Mechanical or functional obstruction to this common duct readily permits bile
reflux into the pancreatic ductal system.
Concurrent Gastrointestinal Tract Disease – Like concurrent biliary tract disease, inflammatory bowel disease (IBD) is an important risk factor for the development
of acute necrotizing pancreatitis in the cat. Several factors appear to contribute to this association: (1) High incidence
of inflammatory bowel disease – IBD is a common disorder in the domestic cat. In some veterinary hospitals and specialty
referral centers, IBD is the most common gastrointestinal disorder in cats. (2) Clinical symptomatology of IBD – Vomiting
is the most important clinical sign in cats affected with IBD. Chronic vomiting raises intra-duodenal pressure and increases
the likelihood of pancreaticobiliary reflux. (3) Pancreaticobiliary anatomy – The pancreaticobiliary sphincter is a common
physiological and anatomic channel at the duodenal papilla, thus reflux of duodenal contents would perfuse pancreatic and
biliary ductal systems. (4) Intestinal Microflora – Compared to dogs, cats have a much higher concentration of aerobic, anaerobic
and total (109 vs. 104 organisms/ml) bacteria in the proximal small intestine. Bacteria readily proliferate in the feline
small intestine because of differences in gastrointestinal motility and immunology. If chronic vomiting with IBD permits
pancreaticobiliary reflux, a duodenal fluid containing a mixed population of bacteria, bile salts, and activated pancreatic
enzyme would perfuse the pancreatic and biliary ductal systems.
Ischemia – Ischemia (e.g., hypotension, cardiac disease) is a cause or consequence of obstructive pancreatitis in the cat. Inflammation
and edema reduce the elasticity and distensibility of the pancreas during secretory stimulation. Sustained inflammation increases
pancreatic interstitial and ductal pressure which serves to further reduce pancreatic blood flow, organ pH, and tissue viability.
Acidic metabolites accumulate within the pancreas because of impaired blood flow Ductal decompression has been shown to restore
pancreatic blood flow, tissue pH, and acinar cell function.