Etiology

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.

Pancreatic Ductal Obstruction

Obstruction of the pancreatic duct (e.g., neoplasia, pancreatic flukes, calculi, and duodenal foreign bodies) is associated with the development of acute necrotizing pancreatitis in some cases. Pancreatic ductal obstruction has marked effects on pancreatic acinar cell function. During ductal obstruction, ductal pressure exceeds exocytosis pressure and causes pancreatic lysosomal hydrolases to co-localize with digestive enzyme zymogens within the acinar cell.

History

Siamese cats were initially reported to be at increased risk for the disease in one of the first retrospective studies of feline pancreatitis. Clinical case surveys of the past 10 years suggest that most cases of feline pancreatitis are seen in the Domestic Short Hair breed. Anorexia (87%) and lethargy (81%) are the most frequently reported clinical signs in cats with acute pancreatitis, but these clinical signs are not pathognomonic for pancreatitis. Anorexia and lethargy are the most important clinical signs in many feline diseases. Gastroenterologic signs are sporadic and less frequently reported in the cat. Vomiting and diarrhea are reported in only 46% and 12% of cases, respectively. In dogs, vomiting (90%) and diarrhea (33%) appear to be more important clinical signs.

Physical Examination Findings

Physical examination findings in cats with acute necrotizing pancreatitis include dehydration (54%), hypothermia (46%), icterus (37%), fever (25%), abdominal pain (19%), and abdominal mass (11%). These findings suggest that a "classic textbook" description of acute pancreatitis (e.g., vomiting, diarrhea, abdominal pain, and fever) is not consistently seen in the domestic cat. Many of these physical examination findings are more commonly reported in canine acute pancreatitis. Abdominal pain (58% in dogs; 19% in cats) and fever (32% in dogs; 25% in cats), for example, are more commonly reported in dogs with acute pancreatitis.

Diagnosis

Laboratory Findings

In cats affected with acute necrotizing pancreatitis, laboratory abnormalities have included: normocytic, normochromic, regenerative or non-regenerative anemia (38%), leukocytosis (46%), leukopenia (15%), hyperbilirubinemia (58%), hypercholesterolemia (72%), hyperglycemia (45%), hypocalcemia (65%), hypoalbuminemia (36%), and elevations in serum alanine aminotransferase (57%) and alkaline phosphatase (49%) activities. Changes in red blood cell counts, serum activities of liver enzymes, and serum concentrations of bilirubin, glucose, and cholesterol are fairly consistent findings in feline acute necrotizing pancreatitis, just as they are in dogs. Important differences between cats and dogs appear to be reflected in white blood cell counts and serum calcium concentrations. Leukocytosis is a more important clinical finding in the dog (62% in dogs; 46% in cats). Leukopenia is sometimes seen instead of leukocytosis in cats, and a worse prognosis has been attributed to leukopenia in the cat. Hypocalcemia also appears to be a more frequent finding in cats (3-5% in dogs; 45-65% in cats). Hypocalcemia (total and serum ionized) may result from several mechanisms, including acid-base disturbances, peripancreatic fat saponification, and parathormone resistance. Regardless of the mechanism, hypocalcemia appears to confer a worse clinical prognosis in cats. This finding suggests that cats should be monitored fairly closely for the development of hypocalcemia and treatment should be initiated, accordingly.

Special Tests of Pancreatic Function

Lipase and Amylase Activity Assays--Serum lipase activities are elevated in experimental feline pancreatitis, but serum lipase and amylase activities do not appear to be elevated or of clinical value in the diagnosis of clinical pancreatitis. Serum lipase activity may still have some clinical utility in the diagnosis of acute necrotizing pancreatitis in the dog. Assays of serum lipase activity are complicated by the fact that there may be as many as five different isoenzymes circulating in the blood, consequently general serum lipase activity assays have been superseded by the development of pancreatic lipase immunoreactivity assays (e.g., cPLI, fPLI).

Trypsin-like Immunoreactivity (TLI)--Serum TLI mainly measures trypsinogen but also detects trypsin and some trypsin molecules bound to proteinase inhibitors. TLI assays are species-specific, and different assays for feline (fTLI) and canine (cTLI) have been developed and validated. Serum TLI concentration is the diagnostic test of choice for feline exocrine pancreatic insufficiency because it is highly sensitive and specific for this disease in the cat. The use of this test in the diagnosis of feline acute necrotizing pancreatitis is less clear. Serum trypsinogen-like immunoreactivity (TLI) concentrations are transiently elevated in experimental feline acute pancreatitis, but elevations in clinical cases are less consistently seen. The poor sensitivity (i.e., 33%) of this test precludes its use as a definitive assay for feline acute necrotizing pancreatitis.

Pancreatic Lipase Immunoreactivity (PLI)--A radioimmunoassay for the measurement of pancreatic lipase immunoreactivity (fPLI) has been developed and validated in the cat. fPLI elevations have been cited in preliminary reports of experimental and clinical feline acute necrotizing pancreatitis. Multi-institutional prospective clinical studies will be required to determine the true sensitivity and specificity of fPLI in the diagnosis of feline ANP.

Imaging Findings

Radiography: The radiographic findings of feline acute necrotizing pancreatitis have not been very well characterized. The radiographic hallmarks of canine acute pancreatitis (e.g., increased density in the right cranial abdominal quadrant, left gastric displacement, right duodenal displacement, and gas-filled duodenum/colon) have not been substantiated in the cat. Indeed, in several recent reports, many of these radiographic findings were not reported in cats with documented acute pancreatic necrosis.

Ultrasonography: Enlarged, irregular, and/or hypoechoic pancreas, hyperechogenicity of the peripancreatic mesentery, and peritoneal effusion have been observed with abdominal ultrasonography in many cats with spontaneous acute pancreatitis.^3-8,10 The specificity of this imaging modality appears to be high (>85%), but the sensitivity has been reported as low as 35% in some studies. The low sensitivity suggests that imaging the pancreas in cats with pancreatitis is technically more difficult than imaging the pancreas in dogs or that the ultrasonographic appearance of pancreatitis in cats differs from that reported for dogs. New diagnostic criteria may be needed if abdominal ultrasonography is to be a more effective tool in the diagnosis of pancreatitis in cats.

Therapy

 Supportive care

 H₁ and H₂ histamine antagonists

 Relief of pain

 Broad spectrum antibiotics

 Anti-emetic agents

 Ductal decompression

 Calcium gluconate supplementation

References

1.  Washabau RJ. Feline acute necrotizing pancreatitis. In, August JR, ed. Consultations in Feline Internal Medicine. 5th ed. Philadelphia: WB Saunders Co., 2005, 109-116.