Acute pancreatitis

What it is

In acute pancreatitis, trypsinogen is activated inside the acinar cells instead of in the intestinal lumen, and the activated enzymes digest the pancreas and the surrounding fat (autodigestion). Local inflammation, oedema and necrosis can spread to the peritoneum and trigger a systemic inflammatory response, with disseminated intravascular coagulation, acute kidney injury or respiratory complications in severe cases. Acute pancreatitis is potentially reversible, unlike chronic pancreatitis, which causes permanent fibrosis and loss of tissue. In most dogs no cause is found; risk factors include eating a fatty meal or dietary indiscretion, obesity, hypertriglyceridaemia, endocrine diseases and certain drugs.

Who it affects

Mainly middle-aged and older dogs. Breeds with a reported higher risk include the miniature schnauzer (associated with hypertriglyceridaemia), Yorkshire terrier and other terriers, and cocker spaniel. Dogs with diabetes mellitus, hyperadrenocorticism or hypothyroidism are at increased risk.

Anatomy involved

• Pancreas: the canine pancreas is V-shaped, with a right lobe in the mesoduodenum along the descending duodenum and a left lobe in the deep leaf of the greater omentum along the greater curvature of the stomach; the body lies at the pylorus. The right lobe is often the most affected.
• Duodenum: the pancreatic duct opens at the major duodenal papilla together with the bile duct, and the accessory pancreatic duct at the minor papilla; duodenal wall thickening and ileus are common.
• Liver and extrahepatic bile ducts: inflammation or fibrosis around the common bile duct can cause extrahepatic biliary obstruction and jaundice.

Clinical signs

Anorexia, vomiting, lethargy and cranial abdominal pain, sometimes shown as the "praying position" (forelimbs down, hindquarters up). Diarrhoea, fever or hypothermia and dehydration. Severe cases show shock, jaundice, bleeding tendencies and dyspnoea. Mild cases may have only nonspecific inappetence.

Diagnosis

• Pancreas-specific lipase (canine pancreatic lipase immunoreactivity, cPLI, or validated lipase assays): the most sensitive and specific blood test; a normal result makes pancreatitis unlikely.
• Abdominal ultrasound: enlarged, hypoechoic pancreas surrounded by hyperechoic peripancreatic fat, local fluid and duodenal changes; it also excludes other causes of acute abdomen.
• Blood work: inflammatory leucogram, raised liver enzymes and bilirubin, azotaemia, electrolyte disorders, hypertriglyceridaemia; coagulation profile in severe cases.
• The diagnosis combines clinical signs, lipase results and imaging; histopathology is rarely performed.

Treatment

Treatment is supportive: intravenous fluids, analgesia (often opioids), antiemetics (maropitant) and early enteral nutrition, which is preferred over prolonged fasting; a feeding tube is used if the dog does not eat. Severe cases may need plasma, management of coagulation and complications, and intensive care. Long-term, a low-fat diet is advised for dogs with recurrent pancreatitis or hypertriglyceridaemia. The prognosis is good in mild cases and guarded in severe necrotising forms.

In the cat

Pancreatitis is common in cats but often goes unnoticed because the signs are vague. Chronic pancreatitis, with lymphocytic infiltrates and fibrosis, predominates, and acute necrotising disease is less common than in the dog; both can coexist and flare up. No clear link with fatty meals or obesity has been shown.

• Anatomy: in most cats the pancreatic duct joins the common bile duct before opening at the major duodenal papilla, and only a minority have an accessory duct. This shared opening helps explain the frequent association of pancreatitis, cholangitis and inflammatory bowel disease (so-called triaditis).
• Signs: mainly lethargy and anorexia, with weight loss and dehydration; vomiting, abdominal pain and diarrhoea are less frequent than in the dog. Jaundice, hypothermia and, in severe cases, shock may occur. It is associated with diabetes mellitus and hepatic lipidosis.
• Diagnosis: feline pancreas-specific lipase (fPLI or lipase assays validated for the cat) together with ultrasound; neither is perfect on its own, and both are interpreted alongside the clinical signs.
• Treatment: fluids, analgesia (buprenorphine or other opioids), antiemetics such as maropitant and, above all, early nutritional support with appetite stimulants (mirtazapine, capromorelin) or a feeding tube, to prevent hepatic lipidosis. Cats have not been shown to need a low-fat diet. In chronic pancreatitis with triaditis the cholangitis and enteropathy are treated as well, and corticosteroids are used in some cases.

Key studies in the cat

• ACVIM consensus (Forman et al., 2021): the reference guide for pancreatitis in cats. Acute pancreatitis is far easier to diagnose than chronic pancreatitis, the diagnosis integrates all clinical and test information, and there is little evidence on management, especially of the chronic form.
• De Cock et al. (2007), histology of the whole pancreas of 115 cats at necropsy, whatever the cause of death. Lesions of pancreatitis were present in 67% of cats, and in 45% of those that had been clinically normal. Chronic pancreatitis (60%) was far more common than acute pancreatitis (15.7%) and increased with age.
• Fragkou et al. (2016), prospective study with biopsies of the intestine, liver and pancreas in 55 cats (27 with signs, 20 without and 8 normal). Of the 47 with inflammatory lesions, 57% had more than one organ affected; triaditis was found in 8 cats, all of them symptomatic (8 of 27), and pancreatitis alone in only 1.
• Lee et al. (2020), retrospective study of 274 sick cats in which Spec fPL was measured. Only 10% of cats unlikely to have pancreatitis tested positive, but 24% of cats with definite or probable pancreatitis tested negative: a positive result supports the diagnosis, a negative one does not rule it out. Only 9 cats had histological or cytological confirmation.
• Nivy et al. (2018), retrospective study of 157 cats hospitalised with pancreatitis. 77.7% survived to discharge and 86.6% of cases were idiopathic. Lethargy, pleural effusion, hypoglycaemia, ionised hypocalcaemia, azotaemia and persistent anorexia were more frequent in non-survivors, but none remained significant after correction for multiple comparisons.
• Wu et al. (2025), 3-week trial in 48 cats with presumed chronic pancreatitis. Owners chose symptomatic treatment alone or immunomodulation, and cats in the second group were randomised to prednisolone or cyclosporine. Cyclosporine lowered serum fPLI the most, but clinical improvement was greater with prednisolone. The trial was open-label and short, with a non-randomised control group.