Pancreatitis in the Dog and Cat
WSAVA 2002 Congress
Colin Burrows, BVetMed, PhD, MRCVS, Diplomate ACVIM
College of Veterinary Medicine, University of Florida
Gainesville, Florida, USA

The major function of the exocrine pancreas is to secrete an enzyme-rich fluid that degrades dietary proteins, lipids and polysaccharides and prepares them for further digestion and absorption. Proteolytic pancreatic enzymes are secreted in an inactive state and activated in the lumen of the small intestine by the action of the brush border enzyme enterokinase, which converts trypsinogen to trypsin. Trypsin in turn initiates separation of the other proteolytic enzymes from their inactive precursors.

Etiology and Pathogenesis. The cause of acute pancreatitis in dogs and cats is usually unknown. Potential risk factors, however, include obesity, high fat diets, malnutrition, hypertriglyceridemia, some drugs (thiazide diuretics, furosemide, azathioprine, L-asparaginase, corticosteroids, sulfonamides and tetracycline), toxins (organophosphates), hypercalcemia, duct obstruction, reflux of duodenal content into the pancreatic duct, pancreatic trauma, parasites (flukes) and pancreatic ischemia/reperfusion injury. There is also an apparent hereditary predisposition to pancreatitis in the miniature Schnauzer and possibly a few other miniature breeds.

In cats, pancreatitis may be a single disease entity but may also be associated with cholangiohepatitis, hepatic lipidosis, diabetes, pulmonary thrombosis, and inflammatory bowel disease.

Pancreatitis develops when the pancreas inappropriately begins to digest itself. Since proteolytic pancreatic enzymes are synthesized, stored and secreted in the inactive state, pancreatitis can only develop with the intraductal or intracellular activation of these enzymes. A variety of protective mechanisms normally guard against intrapancreatic enzyme activation and pancreatitis develops only when one or more of these are inhibited or overcome.

History and Clinical Signs. There are no pathognomonic signs of pancreatitis; indeed, the disease is characterized by the wide range of clinical signs that may be observed as well as in their varying severity.

Dogs: The disease occurs usually in middle aged to older dogs, and overweight dogs are at a higher risk. Miniature Schnauzers, Yorkshire and Silky Terriers, and Miniature poodles are at a higher risk. There is no sex predisposition. The history may reveal recent dietary indiscretion, drug administration or trauma. Common signs include anorexia, lethargy and vomiting. Diarrhea may also be reported; mild fever and abdominal pain may be detected in some dogs with a history of recurrent bouts of pancreatitis. Most afflicted animals exhibit signs of mild to moderate dehydration. Less common signs include jaundice, respiratory distress and hypovolemic shock.

Cats: There is a wide age range and no sex predisposition. Siamese may be over-represented. There is no sex predisposition. Clinical signs include lethargy, anorexia and weight loss. Vomiting, diarrhea, icterus, dehydration and dyspnea are less common.

The most common differential diagnoses are 1) acute gastroenteritis, 2) exacerbations of inflammatory bowel disease, 3) intestinal obstruction, 4) peritonitis and 5) acute renal failure.

Hematologic Findings. Leukocytosis is relatively common in dogs with acute pancreatitis. A left shift may be noted if the patient has severe disease and the hemogram is examined when the disease process is advanced. Toxic white cells are seldom reported but when seen, indicate a guarded to poor prognosis. Other hematologic changes reflect fluid loss and hemoconcentration.

Biochemical Findings. These may include azotemia, elevated liver enzymes, hyperbilirubinemia hyperglycemia, hypocalcemia and hyperlipemia.

Urinalysis differentiates azotemia into pre renal or renal.

Pancreatic Enzymes. Elevated amylase and lipase are certainly compatible with the disease but are not necessarily diagnostic. Dogs with normal amylase and lipase may have pancreatitis. Amylase and lipase are of no value in the cat. Radioimmunoassay of serum trypsinogen-like activity in dogs with pancreatitis may be useful in some patients. Measurement of pancreas specific lipase activity (cPLI and fPLI) may have the greatest diagnostic value.

Imaging Techniques. Radiographic signs associated with pancreatitis include: increased density, diminished contrast and possibly, granularity in the right cranial abdomen, displacement of the stomach to the left. Other signs include widening of the angle between the pyloric antrum and the proximal duodenum, displacement of the descending duodenum to the right, presence of a mass medial to the descending duodenum, static gas pattern in, or thickened walls, of the descending duodenum and possibly the transverse colon, gastric distension suggestive of outlet obstruction, and delayed passage of barium through the stomach and proximal duodenum. The most common ultrasonographic observation is a loss of echodensity that is compatible with edema. Other ultrasonographic findings include: increased echodensity suggestive of fibrosis, nonhomogeneous masses, and less commonly, fluid filled cyst-like structures.

Histologic Diagnosis. the "gold standard" for diagnosis of pancreatitis is microscopic examination of a pancreatic biopsy specimen. Since few animals are likely to be subjected to laparotomy and biopsy except as a therapeutic strategy for severe disease, diagnosis of pancreatitis is at best almost always tentative and is based primarily on the elimination of differential diagnoses that require specific, rather than supportive therapy.

The basic treatment for acute pancreatitis is the maintenance of fluid and electrolyte balance, limiting bacterial translocation, and placing the pancreas in a state of physiologic rest.

Acute pancreatitis is usually a self-limiting disease and with appropriate supportive care most patients should improve within 24-48 hrs. Severely afflicted patients, however, need more intensive and prolonged supportive measures that are designed to prevent shock, control vomiting and pain, prevent secondary infection and coagulation defects, and provide appropriate nutrition during the recovery phase.

Fluid Therapy. Conventional parenteral fluid therapy using a balanced electrolyte solution should be given to replace deficits and provide maintenance requirements. Peripancreatic sequestration of fluid can be extreme in pancreatitis and vital signs, urine output, packed cell volume and total protein should be monitored closely to ensure that adequate maintenance fluid volumes are administered. Replacement fluids should be routinely supplemented with potassium chloride (20-30 mEq/L) if hyperkalemia due to renal failure is not present.

Supportive Care. Evidence for primary or secondary infection in pancreatitis is rare; nevertheless, it is common practice to give broad-spectrum parenteral antibiotics to patients with acute pancreatitis to guard against development of secondary infection and pancreatic abscesses. Translocation of bacteria from the gut lumen is enhanced in pancreatitis and it is possible that antibiotics also help to reduce bacteremia. Secondary development of a pancreatic abscess is rare, however, regardless of whether antibiotics are administered or not. Injectable antibiotics are preferred since the patient is usually receiving nothing by mouth and gastric emptying may be unpredictable. Intravenous enrofloxacin, cephalosporin or amoxicillin are acceptable. Vomiting usually diminishes once food and water are withheld. Antiemetics (metoclopramide or chlorpromazine) and H2 blockers (e.g., ranitidine) may be prescribed. Analgesics should be administered to provide relief on an as needed basis. Buprenorphine or oxymorphone are good choices and a fentanyl patch may also be prescribed. Hyperglycemia is rare but in some cases frank diabetes may develop and require treatment with insulin. Respiratory distress, neurological problems, cardiac arrhythmias, bleeding disorders and acute renal failure are all poor prognostic signs but should be treated aggressively and appropriately. Transfusion of plasma or whole blood to replace "-macroglobulin can be life saving and has the benefit of maintaining plasma albumin concentrations. Hetastarch can also be used if plasma is unavailable, but this only maintains blood volume and does nothing to replace diminished "- macroglobulin stores. Surgery may be indicated in the presence of sepsis or prolonged bile duct obstruction. An exploratory laparotomy may be diagnostic in cats, especially if other diseases such as IBD or cholangiohepatitis are present. Pre-surgical coagulation tests should be performed and vitamin K given if necessary. Plasma transfusion before intervention should be routine. A jejunostomy tube should also be placed at surgery. Nutritional support of the patient with severe disease is critical. Fasting can be tolerated for 5-7 days in most patients, but if signs of recovery are delayed, nutritional supplementation, either via total parenteral nutrition or with an elemental diet given through a jejunostomy tube is very important.

Convalescence. Most patients with acute pancreatitis will recover if given appropriate supportive care. Oral liquids may be instituted after a 24 to 72-hour fast if the animal shows clinical improvement. After water is tolerated for 24 hours the patients should be offered a small quantity of carbohydrate based food such as crackers with beef or chicken bouillon. If these are tolerated without vomiting or apparent abdominal distress then the patient may be offered a low fat, low protein diet. Small amounts of oral liquids and food should then be offered every 3 to 4 hours. Feeding should be withheld again at any time if the patient vomits or exhibits abdominal distress. The patient may then be slowly returned to its original diet. High fat diets are best avoided.

Conclusion

Pancreatitis is an unpredictable disease of widely varying severity, and it is difficult to give a prognosis even when a diagnosis is definitively established. Life-threatening signs accompanying acute fulminating pancreatitis are usually followed by death in spite of supportive measures, but some dogs recover fully following an isolated severe episode. In other cases, relatively mild or moderate chronic or recurrent pancreatitis persists despite all therapy, and the patient either dies in an acute severe exacerbation of the disease or undergoes euthanasia because of failure to recover or the expense of long-term supportive care. Most patients with uncomplicated pancreatitis probably recover spontaneously after a single episode and do well as long as high-fat foods are avoided. The presentation of pancreatitis in cats can be subtle and diagnosis can be difficult. The prognosis may be guarded if other diseases are present.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Colin F. Burrows, BVetMed, PhD, MRCVS, Dip ACVIM
College of Veterinary Medicine
University of Florida
Gainesville, Florida, USA


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