Pancreatitis is the most common exocrine pancreatic disease in both dogs and cats. It can be acute or chronic, depending on whether or not the disease has led to permanent changes of the pancreatic parenchyma, mainly atrophy and/or fibrosis. Both acute and chronic pancreatitis can be 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, dietary indiscretion is believed to be a common risk factor in dogs. Severe blunt trauma, such as can be sustained during a traffic accident or in cats with high-rise syndrome, can cause pancreatitis. Surgery has been considered another risk factor for pancreatitis; 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 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 likely.
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 colocalization of both zymogen granules and lysosomes, leading to activation of trypsinogen to trypsin. 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 WBC 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.
Anorexia (91%), vomiting (90%), weakness (79%), abdominal pain (58%), dehydration (46%), and diarrhea (33%) are the most common clinical signs reported 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. The low rate of abdominal pain reported is remarkable given that >90% of human patients with pancreatitis report abdominal pain.
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 CBC 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 elevations in liver enzymes and bilirubin are common, nonspecific findings in both dogs and cats. 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. 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), and/or a pancreatic mass effect are highly specific for pancreatitis. Care should be taken not to over-interpret findings, as 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. Serum lipase and amylase activities have limited clinical usefulness in dogs and no usefulness in cats. In dogs, a patient-side test for the semiquantitative evaluation of serum pancreatic lipase immunoreactivity (SNAP cPL®) is now available. A negative SNAP cPL test suggests that canine pancreatitis is very unlikely. A positive test result suggests pancreatitis, and a serum sample for measurement of serum canine pancreatic lipase immunoreactivity (cPLI, now measured by a commercial assay, Spec cPL®) concentration should be evaluated to confirm the diagnosis and to determine a baseline concentration. This allows use of serum cPLI concentration as a monitoring tool for the disease. In both dogs and cats, serum PLI concentration (measured in dogs by Spec cPL and in cats by Spec fPL®) is highly specific for exocrine pancreatic function and is also the most sensitive diagnostic test for pancreatitis currently available (sensitivity >80%).
Abdominal exploratory laparotomy can also be used to definitively diagnose pancreatitis. However, even if the presence of pancreatitis seems obvious (eg, pancreatic congestion can easily be misdiagnosed as pancreatitis on gross examination), a biopsy specimen should be collected, as the definitive diagnosis of pancreatitis requires the identification of an inflammatory infiltrate during histopathology. It is difficult to exclude pancreatitis during abdominal exploratory laparotomy or even by pancreatic biopsy. In many cases, pancreatitis is localized to one lobe of the pancreas and may be missed when a single biopsy is being collected. Also, patients with severe pancreatitis are often poor anesthetic risks, and exploratory laparotomy 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. In those few cases in which the etiology 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 only suggested if the patient vomits uncontrollably (see Vomiting). Abdominal pain should be assumed to be present and treated until contrary evidence is available. Intermittent meperidine or butorphanol may be used in patients with mild or moderate abdominal pain. Patients with severe pain are often treated with a continuous-rate infusion 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 until adverse effects are identified. Many other treatments have been investigated in dogs, cats, and humans, but unfortunately none has been shown to be useful.
Patients 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 or hepatitis, inflammatory bowel disease, or diabetes mellitus). In dogs, feeding an ultra-low fat diet is crucial for treatment success. In cats, a moderately low-fat diet is recommended. Antinausea drugs are helpful for animals that may not eat due to nausea.
If patients do not respond to therapy, a trial with prednisone or prednisolone may be attempted. However, indiscriminate use of glucocorticoids in these patients should be discouraged.
The prognosis in mild cases is good, but prognosis in severe cases of pancreatitis is guarded in both dogs and cats. It can be challenging to identify severe cases early during the disease process and prevent complications in those animals.
Last full review/revision March 2012 by Jörg M. Steiner, DrMedVet, PhD, DACVIM, DECVIM-CA