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Veterinary Focus

Issue number 27.1 GI tract

Canine pancreatitis

Published 11/07/2019

Written by Melinda A. Wood and Craig Datz

Also available in Français , Deutsch , Italiano and Español

Pancreatitis in dogs is a common and debilitating disease that may be acute or chronic in nature; Craig Datz and Melinda Wood review various aspects of the condition, including the etiology, the preferred diagnostic tests, and the options for treatment.

Canine pancreatitis

Key Points

Pancreatitis in dogs may be acute or chronic in nature, and although several etiological factors have been suggested, the trigger for the onset of disease is typically idiopathic.

Pancreatitis develops because of premature activation of trypsinogen to trypsin within the pancreas, leading to pancreatic cell destruction. In some cases, the systemic effects can be severe and lead to multiorgan failure.

The clinical signs of pancreatitis may range from mild to severe and life-threatening; the most sensitive and specific serum marker currently available is the canine pancreatic lipase immunoreactivity assay.

Nutrition can play a key role in therapy; several studies have demonstrated the safety and efficacy of providing assisted enteral nutrition to dogs with pancreatitis.


Canine pancreatitis is an inflammatory disease of the pancreas that may be acute or chronic in nature. In acute cases, there are no permanent changes to the pancreas, whereas fibrosis and atrophy of the pancreas develop in the chronic scenario 1. Despite recent advances in available analytical tests, establishing a diagnosis can be challenging.

The cause for pancreatitis in an individual dog is typically idiopathic, but several risk factors have been suggested, including dietary indiscretion, obesity, and endocrine diseases such as diabetes mellitus, hyperadrenocorticism, and hypothyroidism and hypertriglyceridemia (2-5). Numerous drugs have been implicated as possible causes of pancreatitis, including potassium bromide, phenobarbital, thiazide diuretics and furosemide, L-asparginase, azathioprine and organophosphates 3 6 7, and babesiosis has also been reported to be a causative agent 7.

Several studies have shown Miniature Schnauzers and Yorkshire Terriers to be at increased risk for developing acute pancreatitis 2 3 4. A study of chronic pancreatitis in US dogs demonstrated an increased prevalence in toy and non-sporting breeds 8, but a UK study on the same condition reported an increased risk in Cavalier King Charles Spaniels, English Cocker Spaniels, Boxers and Collies 9.


Under normal conditions, several mechanisms protect the pancreas from autodigestion by digestive enzymes. Proteolytic enzymes synthesized within the pancreas are stored as inactive zymogens and are activated only once they have entered the duodenum. Pancreatic acinar cells synthesize and secrete pancreatic secretory trypsin inhibitor, and plasma contains several anti-proteases which both limit intra-pancreatic proenzyme activation and inactivate proteolytic enzymes if they have been released into the circulation 7 10.

Pancreatitis develops because of premature activation of trypsinogen to trypsin within the acinar cells of the pancreas, leading to pancreatic cell destruction. Trypsin activation triggers activation of all other pancreatic zymogens, causing pancreatic autodigestion, inflammation and necrosis, as well as a systemic inflammatory reaction. In some cases, the effects can be severe and lead to multiorgan failure 7 10.

Clinical signs and diagnosis

Clinical signs of pancreatitis in dogs may range from mild to severe and life-threatening, and can include vomiting, lethargy, anorexia or decreased appetite, diarrhea and abdominal pain 8 11. Patients with chronic pancreatitis generally present with low-grade, intermittent clinical signs, although they can present acutely 1. Dogs may assume the classic “prayer” position with forelimbs extended along the ground and raised hindlimbs (Figure 1). Physical exam findings will vary depending on the severity of disease, but may include abdominal pain (Figure 2), dehydration, fever, and icterus if secondary post-hepatic bile duct obstruction is present 8 11

Dogs with pancreatitis may assume the classic “prayer” position with their forelimbs extended along the ground and raised hindlimbs.
Figure 1. Dogs with pancreatitis may assume the classic “prayer” position with their forelimbs extended along the ground and raised hindlimbs. © E McNeill/S Kellam/J Daft
Physical exam findings will vary depending on the severity of the pancreatitis, but abdominal pain is often noted.
Figure 2. Physical exam findings will vary depending on the severity of the pancreatitis, but abdominal pain is often noted. © E McNeill/S Kellam/J Daft

Biochemical and hematologic findings in affected dogs are non-specific and can include elevated liver enzymes, hyperbilirubinemia, azotemia, hypoalbuminemia, hypocalcemia, hypokalemia, anemia, thrombocytopenia, leukocytosis and (less commonly) leukopenia 3 11. Previously, elevated serum lipase and amylase were used as markers for pancreatitis, but they are no longer recommended due to their lack of sensitivity and specificity. This is because both amylase and lipase originate from several tissues in addition to the pancreas, and traditional assays are not able to differentiate tissue of origin 12.

The canine pancreatic lipase immunoreactivity (cPLI) assay is the most sensitive and specific serum marker currently available for canine pancreatitis. Studies have evaluated the assay for detection of both clinical and histopathological pancreatitis cases, and it is notable that not all patients in the histopathological studies showed clinical signs of pancreatitis. The sensitivity of cPLI has been shown to improve in patients with moderate to severe pancreatitis. Furthermore, the assay loses specificity when a lower cut-off value (200 μg/L) is used for a positive diagnosis 12 13 14. A cage-side commercial assay is also available and has been shown to be highly sensitive 14; pancreatitis in dogs with a negative result on this test is unlikely.

More recently, a new assay for lipase activity has been developed using the substrate 1,2-o-dilauryl-rac-glycero glutaric acid-(6’-methylresorufin) ester (DGGR) and validated in dogs 15. This assay has been shown to have high agreement with the cPLI assay 16.

Diagnostic imaging

Pancreatitis may be suspected but not definitively diagnosed, based on abdominal radiographs. Radiographic findings in affected dogs have been reported to include loss of detail or increased radio-opacity in the right cranial abdomen, displacement of the duodenum to the right or pyloric antrum to the left, and gas in the descending duodenum or transverse colon 11. However, in this study radiographic abnormalities suggestive of acute pancreatitis were present in only 24% of dogs with fatal acute pancreatitis. 

Changes seen ultrasonographically with acute pancreatitis include an enlarged, hypoechoic pancreas, often with hyperechoic peri-pancreatic mesentery.
Figure 3. Changes seen ultrasonographically with acute pancreatitis include an enlarged, hypoechoic pancreas, often with hyperechoic peri-pancreatic mesentery. © Andrew Holdsworth/SCVS

The most commonly used diagnostic imaging tool for examining the canine pancreas is abdominal ultrasound. Changes seen ultrasonographically with acute pancreatitis include an enlarged, hypoechoic pancreas, often with hyperechoic peri-pancreatic mesentery (Figure 3). Additional abnormalities such as pancreatic pseudocysts, abscesses or masses, and peritoneal effusion may also be present 6 11 17. Hyperechoic areas within the pancreas may be seen, which could represent fibrosis 12. However, when used alone, the sensitivity of abdominal ultrasound to diagnose acute pancreatitis in dogs is generally low, reported in one study to be 68% 11.

Computed tomography (CT) is the most valuable imaging modality for diagnosing pancreatitis in people, but has been evaluated less in dogs. CT angiography findings in dogs with acute pancreatitis in a recent pilot study included an enlarged, homogeneously to heterogeneously attenuating and contrast-enhancing pancreas, with illdefined borders in all dogs 18. Although this was a small study, the results were promising, as CT angiography allowed the entire pancreas and common bile duct to be imaged; this proved to be superior to ultrasound in some of the dogs, where superimposition of gastrointestinal gas and fluid limited the ultrasound examination.


Because there is no specific cure, treatment is limited to supportive measures 6. The main complications of moderate to severe acute pancreatitis to be managed are anorexia, vomiting, abdominal pain, dehydration, electrolyte imbalances, and sometimes systemic inflammatory response syndrome (SIRS) 19 20. The following is a brief review of medical management and a more in-depth guide to nutritional management.

Fluid therapy 

Most dogs with pancreatitis have a history of vomiting or inappetence.
Figure 4. Most dogs with pancreatitis have a history of vomiting or inappetence. © Shutterstock

Continuous intravenous fluids are necessary for all but the mildest cases 19. Most dogs have a history of inappetence or vomiting (Figure 4), and fluids are required to restore hydration and replace electrolytes, with Lactated Ringer’s (Hartmann’s) solution the initial fluid of choice. Potassium supplementation may also be required. Colloids such as hydroxyethyl starch or fresh frozen plasma may be useful if there is decreased oncotic pressure (e.g., with hypoalbuminemia) but animals should be monitored closely for adverse effects such as coagulopathy 19 21.


Vomiting causes significant morbidity and worsening of dehydration and acid-base/electrolyte imbalance. Newer drugs such as maropitant and serotonin receptor antagonists (ondansetron, dolasetron) are more effective than older drugs such as metoclopramide 19 in reducing the incidence of emesis.


Abdominal pain may be difficult to recognize in affected dogs, so analgesics should be provided for most cases. Opioids (mu agonists) are typically the most effective drugs at relieving abdominal pain. NMDA antagonists (e.g., ketamine) and local anesthetics (e.g., lidocaine) may be used as a continuous rate infusion, either alone or in combination 19.


While corticosteroids have historically been regarded as a risk factor for pancreatitis, more recent evidence suggests they are not a cause and may in fact be beneficial in treatment. Low physiologic doses of short-acting corticosteroids are occasionally used to help manage moderate to severe inflammation (SIRS) associated with pancreatitis 19.


Traditional recommendations for the management of acute pancreatitis in dogs included fasting to “rest the pancreas” 22. It was thought that recommending nil per os (NPO) for 48-72 hours (or up to 5 days of anorexia) would reduce pancreatic stimulation and excessive release of enzymes 19 22. However, the pathogenesis most likely involves intracellular activation of proteolytic enzymes rather than excessive pancreatic stimulation 6, and there are numerous adverse consequences with prolonged NPO therapy. Protein malnutrition can lead to a catabolic state and hypoproteinemia. The gastrointestinal barrier may be compromised due to a combination of decreased intestinal blood flow, villus atrophy and decreased local immunoglobulin production, which is a risk factor for bacterial translocation and SIRS. Additionally, a loss of intestinal motility or even ileus can lead to worsening of vomiting and diarrhea 6.

Several studies have demonstrated the safety and efficacy of providing assisted enteral nutrition to dogs with experimental or naturally occurring pancreatitis 23 24 25 26. Total parenteral nutrition (TPN) has also been recommended, especially in cases of severe or refractory vomiting, although it can be associated with a higher rate of complications 6. Assisted enteral feeding is less expensive, readily available in general practice, and most likely safer; support early in the disease process, rather than later, is now becoming more widely recommended 6 20 26.

Feeding tubes are available in various sizes and materials. For cases of acute pancreatitis, the most common types are nasogastric (NG) tubes and esophagostomy (E) tubes 6. NG-tubes are easy to insert without the need for sedation and can remain in place for up to 7 days, which is usually long enough to allow recovery and resumption of voluntary intake. Only liquid diets can be fed through NG-tubes, which limits the choice of products. E-tube placement requires general anesthesia and a surgical approach, and critical patients should be stabilized before being anesthetized. A variety of diets can be fed through E-tubes; most wet (canned) dog foods can be blended with water so that the consistency is thin enough to flow through the tube without clogging 27 28.

The ideal diet for supporting dogs with pancreatitis has not yet been determined. In most cases, a highly digestible fat-restricted diet is the most appropriate choice 6 19 27 as high-fat diets are a potential risk for both pancreatitis and hyperlipidemia. A commonly accepted recommendation is to select commercial canine diets that do not exceed 20 grams of fat per 1,000 kcal (approximately 7% fat on a dry matter basis) 29. Several veterinary therapeutic diets are available that are formulated for gastrointestinal disease and are also fat-restricted. However, diets that are intended for management of obesity or fiber-responsive conditions may not be appropriate, as they are not highly digestible and require larger volumes of food to meet energy requirements. Commercially available liquid diets may not be fat-restricted but can be used in NG-tubes as long as careful monitoring is done to assess for post-feeding nausea, vomiting, abdominal discomfort, or other unwanted signs 27. Low-fat liquid diets are available in some countries.

A starting point for assisted feeding (NG- or E-tube) is to calculate the resting energy requirement (Table 1), the daily amount in kilocalories appropriate for a dog recovering from illness 6 19 27 28. Dogs with mild pancreatitis often start eating voluntarily within three days of the onset of anorexia, and in such cases feeding tubes are not necessary, but a gradual return to full feeding can be achieved using these guidelines. In dogs with moderate to severe pancreatitis, enteral nutrition (placement of a feeding tube) is recommended if anorexia has persisted for three days or longer and voluntary intake is not occurring 27 28

The resting energy requirement (RER) of a dog =
70 x BW(kg)0.75
A typical protocol is to give 1/3 of the calculated RER on day 1 of feeding, 2/3 of the RER on day 2, and the full RER on the third and subsequent days. For example, the RER for a 7kg dog is 301 kcal (70 x 7 0.75), so the amount fed would be 100 kcal on day 1, 200 kcal on day 2, and 300 kcal on day 3. Note that the daily amount should be divided into several small feeds, usually 4-6 times a day.

Table 1. Calculating the RER.

After recovery and discharge from the hospital, home care of patients with acute or chronic pancreatitis often includes medication and ongoing feeding of therapeutic diets 1 20 27. If the dog has hyperlipidemia or is at high risk of relapse, then food should be limited to highly digestible fat-restricted diets as noted previously 27 29. Other dogs may be able to tolerate diets that are moderate in fat (up to 40 grams/1,000 kcal or 15% on a dry matter basis) but, for most cases, higher-fat diets should be avoided long term, as well as table scraps and treats that contain excessive dietary fat.


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Melinda A. Wood

Melinda A. Wood

Dr Wood received her DVM from The Ohio State University College of Veterinary Medicine in 2003. Read more

Craig Datz

Craig Datz

Dr. Datz is a 1987 graduate of the Virginia-Maryland Regional College of Veterinary Medicine. Read more

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