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Pancreatitis in Small Animals

By Jörg M. Steiner, DrMedVet, PhD, DACVIM, DECVIM-CA, AGAF, Gastrointestinal Laboratory, Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A & M University

Pancreatitis is the most common exocrine pancreatic disease in both dogs and cats. It can be acute or chronic, depending on whether the disease has led to permanent changes of the pancreatic parenchyma, mainly atrophy and/or fibrosis. Both acute and chronic pancreatitis can be subclinical, mild and associated with vague clinical signs, or severe and associated with pancreatic necrosis and systemic complications. Thus a distinction between the two is clinically of little significance.

Etiology and Pathogenesis:

Most cases of pancreatitis in dogs and cats are idiopathic. However, several risk factors have been described. Miniature Schnauzers have been identified to be dramatically overrepresented in some studies, and it has been speculated that they may have a genetic predisposition similar to that in families of human patients with hereditary pancreatitis. Other studies have reported an increased prevalence in Yorkshire Terriers, Cocker Spaniels, Dachshunds, Poodles, sled dogs, or other breeds. Dietary indiscretion is believed to be a common risk factor in dogs. Also, hypertriglyceridemia in dogs, if severe (ie, generally serum concentrations ≥500 mg/dL), is considered a risk factor for pancreatitis. Hyperadrenocortiscism has been cited in some studies as a risk factor for pancreatitis in dogs. Severe blunt trauma, such as can be sustained during a traffic accident or in cats with high-rise syndrome, can also cause pancreatitis. Surgery has been considered another risk factor; however, most postsurgical cases of pancreatitis are now believed to be due to pancreatic hypoperfusion during anesthesia. Infectious diseases have been implicated, but the evidence for a cause and effect relationship is weak in most cases. In dogs, pancreatitis has been reported with Babesia canis or Leishmania infection. In cats, Toxoplasma gondii, Amphimerus pseudofelineus, and feline infectious peritonitis are considered most important.

Many drugs have been implicated in causing pancreatitis in people, but very few have been confirmed in dogs and cats. In general, most drugs should be viewed as potential causes of pancreatitis; cholinesterase inhibitors, calcium, potassium bromide, phenobarbital, l-asparaginase, estrogen, salicylates, azathioprine, thiazide diuretics, and vinca alkaloids are probably the most important.

Many different insults may ultimately lead to pancreatitis through a common pathway. Secretion of pancreatic juice decreases during the initial stages of pancreatitis. This is followed by co-localization of zymogen granules and lysosomes, leading to activation of trypsinogen to trypsin within the co-localized organelles. Trypsin, in turn, activates more trypsinogen and also other zymogens. Prematurely activated digestive enzymes lead to local damage of the exocrine pancreas with pancreatic edema, bleeding, inflammation, necrosis, and peripancreatic fat necrosis. The ensuing inflammatory process leads to recruitment of WBCs and cytokine production. The activated enzymes, and more importantly, the cytokines circulate in the bloodstream and lead to distant complications such as generalized inflammation, disseminated intravascular coagulation, disseminated lipodystrophy, pancreatic encephalopathy, hypotension, renal failure, pulmonary failure, myocarditis, or even multiorgan failure.

Clinical Findings:

Anorexia (91%), vomiting (90%), weakness (79%), abdominal pain (58%), dehydration (46%), and diarrhea (33%) have been reported as the most common clinical signs in dogs with severe pancreatitis. Clinical signs in cats with severe pancreatitis are even less specific, with anorexia (87%), lethargy (81%), dehydration (54%), weight loss (47%), hypothermia (46%), vomiting (46%), icterus (37%), fever (19%), and abdominal pain (19%) most commonly reported. Dogs and cats with milder forms of pancreatitis may be subclinical or may have only vague clinical signs, such as anorexia, lethargy, or diarrhea. The low rate of abdominal pain reported is remarkable given that >90% of human patients with pancreatitis report abdominal pain, so it is most likely due to lack of recognition in veterinary patients.


A history of dietary indiscretion combined with vomiting and abdominal pain may suggest pancreatitis in dogs, but most cats present with nonspecific histories and clinical signs. Findings on CBCs and serum biochemistry profiles may suggest an inflammatory disease process but are nonspecific. In dogs, thrombocytopenia and neutrophilia with a left shift are common. Azotemia and increases in liver enzymes and bilirubin are common, nonspecific findings in both dogs and cats. Thus, while basic blood work is not useful for the diagnosis of pancreatitis, it is crucial to systematically evaluate the animal and diagnose systemic complications. Abdominal radiographs may show decreased detail in the proximal abdominal cavity and displacement of abdominal organs, but these findings are also nonspecific and a diagnosis based on radiographic findings alone is not reliable. However, abdominal radiographs are valuable in animals suspected of having pancreatitis to exclude other differential diagnoses. Abdominal ultrasonography, if stringent criteria are applied, is highly specific for pancreatitis, but pancreatic enlargement and fluid accumulation around the pancreas alone are not sufficient for diagnosis. A combination of pancreatic enlargement, fluid accumulation around the pancreas, changes in echogenicity (ie, decreased echogenicity suggesting pancreatic necrosis, increased echogenicity around the pancreas suggesting peripancreatic fat necrosis, increased echogenicity suggesting pancreatic fibrosis), and/or a pancreatic mass effect are suggestive of pancreatitis. Care should be taken not to overinterpret findings, because modern ultrasonographic equipment has a very high resolution, and pancreatic nodular hyperplasia may lead to changes in echogenicity, falsely suggesting the presence of pancreatitis. Also, the sensitivity of abdominal ultrasonography is highly operator-dependent, with sensitivities as high as 35% in cats and 68% in dogs in the most experienced hands.

Several diagnostic markers for pancreatitis have been evaluated in dogs and cats. In general, the clinical usefulness of serum lipase and amylase activity is limited in dogs and even more so in cats. In-clinic tests for the semiquantitative evaluation of serum pancreatic lipase immunoreactivity are available. A negative semiquantitative test suggests that pancreatitis is very unlikely, whereas a positive test suggests pancreatitis. In the latter case, pancreatic lipase immunoreactivity (PLI) concentration should be measured in a serum sample and evaluated to confirm the diagnosis and to determine a baseline concentration. This allows use of serum PLI concentration as a monitoring tool for the disease. In both dogs and cats, serum PLI concentration is highly specific for exocrine pancreatic function and is also the most sensitive diagnostic test for pancreatitis currently available (sensitivity >80%). However, as for any disease, no test should be used in isolation for diagnosis, and all clinical findings should be used in conjunction to arrive at the most appropriate diagnosis.

Pancreatic cytology or histopathology can also be used to definitively diagnose pancreatitis. Fine-needle aspiration of the pancreas is safe and can show acinar cells and inflammatory cells, allowing a definitive diagnosis of pancreatitis. However, lack of inflammatory cells does not exclude pancreatitis, because the inflammatory infiltrate can be highly localized. Pancreatic biopsy for histopathologic evaluation may be associated with a higher risk of pancreatitis than fine-needle aspiration (due to more aggressive pancreatic handling and longer anesthesia). Also, even if the presence of pancreatitis seems obvious on macroscopic examination of the pancreas, a biopsy specimen should be collected because the definitive diagnosis of pancreatitis requires the identification of an inflammatory infiltrate during histopathology. Finally, animals with severe pancreatitis are often poor anesthetic risks, and exploratory laparotomy or even fine-needle aspiration may not be justified.


The mainstay of therapy of severe pancreatitis is supportive care with fluid therapy, vigorous monitoring, and early intervention to prevent systemic complications. Fluid therapy should be based on calculation of degree of dehydration (to be replaced over 4–8 hr if there is no contraindication), maintenance, and ongoing losses (eg, due to vomiting or diarrhea). In those few cases in which the cause is known, specific therapy against the inciting cause may be initiated. Antibiotics are of questionable value and should not be used routinely. Resting the pancreas is suggested only if the animal vomits uncontrollably (ie, the animal vomits frequently and violently despite appropriate antiemetic therapy) (see Vomiting). In fact, early nutritional support is considered a key component of successful treatment of human patients with severe pancreatitis. Also, enteral nutritional support is considered superior to parenteral nutrition. Animals that vomit should be treated with an entiemetic, such as maropitant (NK1 antagonist), ondansetron or dolasetron (HT3 antagonists), or in most animals a combination of both. Even animals that do not actively vomit may benefit from such antiemetic support, because they may be nauseated, leading to hyporexia or even anorexia. Metoclopramide is not considered effective as an antiemetic agent and should not be used in these animals. Abdominal pain should be assumed to be present and treated until contrary evidence is available. Intermittent meperidine, butorphanol, or buprenorphine may be used in animals with mild or moderate abdominal pain. Animals with severe pain are often treated with a constant-rate infusion of an opioid, such as morphine, fentanyl, or methadone, or with a combination therapy of fentanyl, ketamine, and lidocaine. Plasma appears to be helpful in severe cases of canine pancreatitis. It should be given daily until improvement is significant or adverse effects are identified. Many other treatments have been investigated in dogs, cats, and people, but unfortunately none has been shown to be useful.

Animals with mild forms of pancreatitis should be carefully assessed for the presence of risk factors (eg, hypertriglyceridemia, hypercalcemia, history of medications that can cause pancreatitis) and concurrent diseases (eg, cholangitis, hepatitis, inflammatory bowel disease, diabetes mellitus). In dogs, feeding an ultra-low-fat diet is crucial for treatment success. In cats, a moderately fat-restricted diet is recommended. Antiemetic drugs are helpful for animals that may not eat due to nausea.

If animals do not respond to therapy, a trial with prednisone (dogs), prednisolone (dogs and cats), or cyclosporine (dogs or cats) may be attempted. Cyclosporine is advantageous in animals with concurrent diabetes mellitus, because it has a smaller impact on insulin resistance than glucocorticoids. However, data are limited to date, and indiscriminate use of glucocorticoids or cyclosporine in dogs and cats with chronic pancreatitis should be discouraged.

The prognosis in mild cases is good, but prognosis in severe cases of pancreatitis is guarded in both dogs and cats. Systemic complications such as hypothermia, acidosis, hypocalcemia, and single- or multiple-organ failure are considered risk factors for a poor outcome. It can be challenging to identify severe cases early during the disease process and prevent complications in those animals.