The Perils of Acute Pancreatitis in the Dog and Cat
World Small Animal Veterinary Association World Congress Proceedings, 2005
Michael Schaer

Acute pancreatitis usually affects the middle-aged and older dog and cat. The severity of this condition can range from mild as seen in some forms of edematous pancreatitis to life-threatening as seen in the hemorrhagic necrotic form. Some of the known or suspected causes of this condition in the dog and cat include accidental or surgical trauma, pancreatic ischemia, and hypercalcemia (dog). Postprandial hyperlipidemia can stimulate pancreatic secretion in the dog and perhaps this explains why the ingestion of a fatty meal is often suspected as a predisposing cause of acute pancreatitis. The use of certain drugs such as glucocorticoids and azathioprine have been implicated as causative factors as well. In most cases the cause of acute pancreatitis in the dog and cat is listed as idiopathic. The basic pathophysiologic change involves a premature activation and release of pancreatic hydrolases followed by inflammation and autodigestion of the gland and the surrounding tissues.

History and Physical Examination Findings

The usual signs are acute vomiting, anorexia, and depression. Rarely, vomiting will be absent, especially in cats. Diarrhea can occasionally occur. The duration of these complaints can range from fulminating with severe forms of pancreatitis to mild and intermittent with the more mild form.

The physical examination findings again will vary depending on the severity of the problem. The abnormalities accompanying mild pancreatitis might be restricted to slight mental depression and equivocal abdominal tenderness. Those associated with hemorrhagic necrotic pancreatitis can include marked mental depression, fever, hypotension, tachypnea and sinus tachycardia, abdominal pain, and variable amounts of dehydration. Clinically detectable icterus does not accompany the peracute phase of this disorder, but it can appear in the subacute stages due to cholangiostasis with or without bile duct obstruction that occurs from fibrous adhesions. A reddish-brown colored ascitic fluid can sometimes accumulate with acute hemorrhagic necrotic pancreatitis.

Radiographic and Clinicopathological Findings

Abdominal radiographic findings are normal in mild pancreatitis. However, those accompanying the severe forms include: (1) a regional peritonitis involving the anterior and midabdominal regions and (2) lateral displacement of the duodenum. Patients with hemorrhagic necrotic pancreatitis can rarely also show pleural effusion and pulmonary fluid accumulation on their thoracic radiographs. Ultrasonography can reveal a heterogeneous pancreatic tissue pattern reflecting edema and inflammation. Peripancreatic mineralization can be seen as a bright hyperechoic density. Free abdominal fluid can also be evident.

The hemogram characteristically shows hemoconcentration and an elevated total protein due to intravascular volume depletion. The serum protein levels might decrease after plasma volume expansion with crystalloid fluid administration. The leukogram has a leukocytosis characterized as a neutrophilia. A left shift is commonly seen with the more severe forms of pancreatitis.

The BUN and serum creatinine levels can be mildly elevated and reflect pre-renal azotemia due to the dehydration associated with mild pancreatitis. However, with the more severe forms, these elevated parameters can reflect acute renal failure as well.

The serum electrolyte levels will vary. Mild hypernatremia (serum sodium > 147 mEq/l) reflects dehydration, while hyponatremia might be spuriously due to hyperlipidemia and/or hyperglycemia. Decreased serum sodium levels can also represent actual depletion from gastrointestinal loss. Hypochloremia reflects gastric chloride ion loss. Serum potassium levels are usually normal initially; however, hypokalemia might occur by the second or third day if the patient does not receive intravenous potassium ion supplementation. A low serum potassium level can also be due to metabolic alkalosis. Hyperkalemia suggests oliguric or anuric renal failure. Hypocalcemia is seen in hemorrhagic necrotic pancreatitis and is due to a decrease in the amount of protein bound calcium and saponification of the abdominal fat.

Elevated serum liver enzyme levels (AST, ALT, and alkaline phosphatase) are due to cholangiostasis and hepatocellular damage. These changes are usually self-limiting and of no clinical significance so long as there is no common bile duct obstruction. Hyperbilirubinemia and bilirubinuria can accompany cholangiostasis with or without extrahepatic biliary tract obstruction.

Serum glucose levels will range from low to marked elevations. Hyperglycemia may be transient due to temporary serum increases in glucagon, cortisol, and catecholamine hormones along with simultaneous impaired insulin secretion. If a substantial destruction of pancreatic B cells occurs, the animal might acquire permanent diabetes mellitus. Hypoglycemia can occur with hemorrhagic pancreatitis because of the accompanying enterotoxemia or sepsis.

Hyperlipemia due to hypertriglyceridemia can occur with acute pancreatitis. It can be due to an underlying metabolic disorder such as hypothyroidism or primary hyperlipidemia.

Hyperamylasemia frequently occurs with acute pancreatitis. It is important to remember that the degree of elevation does not necessarily parallel the severity of the disease and that decreased glomerular filtration will elevate and sustain the serum amylase level. Furthermore, hyperamylasemia in the absence of acute pancreatitis can occur with other abdominal abnormalities such as bowel obstruction or perforation and liver inflammation.

Hyperlipasemia is a more dependable laboratory test for the diagnosis of acute pancreatitis according to several authors. This author essentially agrees with this observation, but has seen several cases of acute pancreatitis where the animal had marked hyperamylasemia but an absent or only minimally elevated serum lipase level. Therefore, both of these parameters are recommended, with the test results interpreted in light of the patient's other clinical findings. A pancreas-specific isoenzyme for lipase is available for the dog and cat, but there is a delay of 1-2 weeks until this and other outside run tests result are received.

Some of the Newer Diagnostic Tests for Pancreatitis in the Dog and Cat

 CPLI--Canine pancreatic lipase immunoreactivity--80% sensitivity when > 200 µg/L.

 FPLI--Feline pancreatic lipase immunoreactivity--> 10 µg/L. Suggestive.

 TLI--Trypsinogen like immunoreactivity. Sensitivity is 33% in dogs and 30-60% in cats.

 Abdominal ultrasound--65% sensitivity.


Patients who present with mild historical and physical signs with unremarkable laboratory test results can often be treated conservatively with food intake restriction for 1-2 days and periodic offerings of water. If vomiting continues, complete oral intake restriction should be extended for 3-5 more days, and the animal's fluid requirements should be met with the administration of parenteral fluids.

The most important aspect of treatment with the more severe types of pancreatitis is appropriate parenteral fluid therapy. Hypotension should be treated with rapid volume expansion consisting of lactated Ringer's or 0.9% saline solutions at an initial dosage rate of 70-90 ml/kg over the first 1-2 hours of treatment. Once the vital signs are stabilized, a maintenance fluid rate of 15-25 ml/kg can be given over the remaining 24-hour period. The fluid dose for the cat should be one-half that for the dog. Maintenance IV fluid volume infusions usually consist of 2 1/2-5% dextrose in 0.45% saline solution; these should be supplemented with potassium chloride (3-5 mEq/kg BW/day) and soluble vitamin B complex. Any acid-base abnormalities should be recognized and appropriately treated. Hypoproteinemic animals should receive fresh plasma. This will increase the plasma oncotic pressure and consequently help prevent edema formation, pleural effusion, pulmonary edema, and renal failure.

Urine output should be closely observed after the patient is adequately volume expanded. Oliguria or anuria should prompt a furosemide-induced diuresis so long as the patient is rehydrated. Osmotic diuresis should be avoided if the animal's plasma is already hyperosmotic. Maintenance parenteral fluid volumes during the impaired urine output period should consist of the volume of urine produced plus any insensible fluid losses. Unsuccessful forced fluid diuresis attempts during anuria will cause potentially fatal pulmonary edema.

Historically, various gastrointestinal drugs such as atropine and propantheline bromide were commonly used. However their adverse side effects often exceeded the benefits. Therefore, the current recommendation calls for withholding parasympatholytic drug treatment so long as restriction of food and water suppresses vomiting. Metoclopramide can be used without the para-sympatholytic effects typical of many antiemetics. The recommended dose is 0.2-0.4 mg/kg q 6-8 h SQ or 1 mg/kg/24 hrs by continuous IV infusion. Cimetidine, ranitidine, or famotidine have been of purported benefit because of their antacid effects. Although there are theoretical justifications for its use, there are no well controlled clinical trials that substantiate any proven benefit. Acute pancreatitis commonly causes a paralytic ileus which can be corrected with cisapride given orally (0.5 mg/kg) or by J-tube bid-tid.

Antibiotics are usually reserved for the moderately or severely sick patient. A bactericidal antimicrobial effective against gram negative bacteria is preferred. Aminoglycoside antibiotics are not recommended due to their potential nephrotoxicity in a clinical setting where renal function might already be impaired.

Providing adequate nourishment is probably the most difficult aspect of treatment. Although 5% dextrose solutions will provide a small amount of calories that might suffice for the first few days of treatment, this form of treatment falls far short of providing the patient's caloric needs over the one to two week period of complete oral intake restriction that is sometimes required to inhibit pancreatic proteolytic enzyme secretion. Hopefully most animals will be able to resume the intake of liquids and then solids after the first 5-7 days of "nothing per os" (NPO).

Intravenous parenteral nutrition should be considered when the patient resumes vomiting after oral feedings are begun. This procedure is risky because there is evidence that the intravenous infusion of amino acid and lipid solutions can stimulate pancreatic secretion in the dog. Some of the problems associated with intravenous hyperalimentation include catheter-induced phlebitis, septicemia, plasma hyperosmolarity, meticulous preparation requirements, and expense. This feeding technique is therefore usually reserved for large medical facilities that can afford the expense and the manpower requirements. A tube jejunostomy (J-tube) and the infusion of elemental nutrients is an efficacious way of nourishing an animal that has protracted acute pancreatitis. Vivonex and Clinicare can be used to provide enteral nutrition.

Analgesic treatment should be reserved for the animal that has severe and intractable pain. Buprenorphine (0.1 mg/kg SQ Q8H) is very safe and effective. Fentanyl patches can also be used as can epidural morphine.

Insulin treatment is indicated when the blood glucose level exceeds 300 mg/dl. Regular crystalline zinc insulin (1/2 unit/kg) is preferred because its short duration of action is advantageous if the hyperglycemia is transient. If the patient shows a continued need for insulin treatment, it should then be managed similar to other diabetics.

Surgical peritoneal lavage was a recommended treatment for acute hemorrhagic necrotic pancreatitis in the 1970's. Because pancreatic exudate contains many potentially harmful substances that can be absorbed into the circulation and cause cardiovascular and respiratory instability, peritoneal lavage was advocated as a logical way to rid the body of these toxic substances. Although some patients appear to benefit from this treatment, several studies in humans have failed to statistically support the recommendation for its routine use. This author will use peritoneal lavage when the animal fails to respond to medical treatment after the first 5-7 days or when severe hemorrhagic necrotic pancreatitis is present. Lavage-induced hypoproteinemia and electrolyte deficiencies should be replaced with plasma and balanced electrolyte solutions. The surgical exploratory is also helpful for debriding necrotic debris, removing accumulations of pus, and allowing for the insertion of a J-tube.

Complications and Long-Termed Medical Management

There are several complications of acute pancreatitis. These include: diabetes mellitus, pancreatic abscess, bowel infarction and perforation, bowel obstruction, renal failure, bile-duct obstruction, septicemia, pancreatic fibrosis with exocrine insufficiency, consumption coagulopathy, relapsing acute pancreatitis, and death.

Returning the Patient to Feeding

Feeding and drinking will be resumed only when the patient has not shown any evidence of vomiting, regurgitation, or nausea for five consecutive days.

The protocol that has worked well for me is:

Day 1:

Offer free choice ice cubes to lick. If no vomiting...

Day 2:

Offer 5-10 laps of water every 2 hours. If no vomiting...

Day 3:

Offer water free choice and begin offering 10 laps of beef or chicken bouillon every 2-4 hours. If no vomiting...

Day 4:

Add 3-4 saltine crackers to the bouillon and feed every 4-6 hours. If no vomiting...

Day 5:

Feed Reducing Diet and send home on long-term reducing diet.

The long-termed medical management in the dog should include a low fat containing diet; the effect of this recommendation is not known in the cat. The animal's total food intake should be divided into 2-3 small feedings. Diabetes mellitus and pancreatic exocrine insufficiency should be treated according to standard recommended protocols.

Speaker Information
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Michael Schaer, DVM, DACVIM, ACVECC
University of Florida, College of Veterinary Medicine
Gainesville, FL

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