Subtle, nonspecific clinical signs coupled with no identifiable trigger make pancreatic disease an elusive diagnosis.
The pancreas is basically a bag of enzymes and hormones. The potent compounds it releases function as key activators needed for life. Sickness results when the pancreas becomes overzealous or, alternatively, slacks off.
The pancreas has two functional compartments: The endocrine pancreas releases compounds into the bloodstream, and the exocrine pancreas delivers its products to target organs via ducts. The endocrine portion consists of alpha, beta and delta cells that produce glucagon, insulin and somatostatin, respectively. In cats, the main disease of the endocrine pancreas is diabetes mellitus, sometimes resulting from insufficient insulin production.
The larger component—the exocrine pancreas—consists of acinar cells that make and secrete enzyme precursors, or zymogens. When mixed with pancreatic proteases situated in the intestinal lumen, these zymogens transform into digestive enzymes like amylase and lipase. The pancreas also secretes bicarbonate, which neutralizes stomach acid, antibacterial proteins, and intrinsic factor, which aids absorption of the vitamin cobalamin. Pancreatitis is the most frequently diagnosed condition involving the exocrine pancreas.
The endocrine and exocrine portions of the feline pancreas may conspire to produce disease, explained Scott Owens, DVM, MS, DACVIM, an internist at MedVet Indianapolis, at the Fetch dvm360 conference in San Diego. For instance, diabetes mellitus—more an issue of insulin resistance than deficiency in cats—can be triggered by pancreatitis. Though this association is unconfirmed in cats, one study links about 40% of diabetes cases with pancreatitis.1-4
Pancreatitis is the culmination of inappropriate activation of zymogens within the pancreas that cause autodigestion.5 Here, pancreatic endothelial membranes become damaged, microvascular circulation gets disrupted, free radicals are dispersed, and local ischemia, abscesses, edema and fat saponification result.
In dogs, this toxic cascade can often be traced back to a fatty meal or a trashcan raid. Most affected dogs vomit, demonstrate overt abdominal pain and stop eating altogether. But in cats, the disease usually has no obvious cause and is often silent.
“The signs are a lot less clear [in cats] than what we often associate with dogs,” Dr. Owens said. Often, the only clues are mild lethargy, reclusiveness, decreased appetite and possible weight loss. Fewer than half of these patients vomit, and only one in 10 has diarrhea.
Highly underdiagnosed in cats, pancreatitis is often acute-on-chronic once found. Necropsy studies have shown evidence of pancreatic inflammation in some 67% of cats, yet half of these had no history of associated clinical signs.
Dr. Owens shared the case of Gracie, a cat with a two-day history of lethargy and diarrhea. On presentation, Gracie was quiet, drooling and febrile (105.5ºF). Blood work showed severe neutropenia (with left shift), thrombocytopenia, borderline-high bilirubin, and normal amylase and lipase.
Dr. Owens’ differential diagnosis for Gracie was severe gastroenteritis, obstruction/intestinal perforation, pyelonephritis, feline panleukopenia and pancreatitis. The cat tested negative for parvovirus, but the Spec fPL (Idexx) was elevated at 19.1 µg/L (normal, 0–3.5 µg/L). Ultrasound revealed an enlarged pancreas with a thickness of 2 cm and a slightly dilated pancreatic duct. The diagnosis: severe pancreatitis.
Gracie was treated with fluids and broad-spectrum antibiotics (due to severe neutropenia), buprenorphine and an appetite stimulant. Within a few days, she was afebrile and her neutropenia was resolved. She went home on Hill’s Prescription Diet i/d because of a food hypersensitivity she’d developed while hospitalized.
Gracie is just one face of pancreatitis, Dr. Owens said. While most cats with pancreatitis are dehydrated on presentation, only 7% are hyperthermic; 68% are hypothermic as a result of poor perfusion. Fewer than two in 10 manifest abdominal pain, but 38% are icteric due to either associated hepatic lipidosis or inflammation around the bile duct leading to post-hepatic obstruction.
Blood work may show azotemia, neutrophilia/neutropenia and mild anemia, Dr. Owens said. The Spec fPL is typically elevated, despite normal serum amylase/lipase; the SNAP fPL and the serum trypsin-like immunoreactivity (TLI) tests are less useful due to low specificity and low sensitivity, respectively. Pyelonephritis should be ruled out by urinalysis.
Ultrasound, despite its poor sensitivity for pancreatitis in cats, might show an enlarged, hyperechoic pancreas, dilated pancreatic duct surrounded by edema, and saponified fat indicated by bright mesentery.
Crystalloids should replace fluid deficits over 24 hours, and be continued thereafter to maintain blood pressure and diuresis, said Dr. Owens. “You need to replenish before you can flush out the toxins.”
Colloids (VetStarch [Zoetis] or plasma) can be added if hypoalbuminemia and vasculitis/edema are present.
Once hydrated, dopamine, dobutamine or norepinephrine may be used to support blood pressure. For pain, which is often present but inapparent in cats, buprenorphine and fentanyl are effective. Antiemetics and appetite stimulants are important. Eating enables reperfusion of the damaged pancreas and resolution of any associated hepatic lipidosis.
In the case of triaditis—inflammatory bowel disease, cholangiohepatitis and pancreatitis—corticosteroids are a potent adjunctive treatment. Dietary changes, if indicated, are aimed at reducing allergens (for inflammatory bowel disease) rather than fat.
Exocrine pancreatic insufficiency (EPI) is often the antipodal end stage of chronic pancreatitis: The pancreas simply burns out.6 In one study, 10 of 16 affected cats had a known history of pancreatitis. Uncommon in cats, EPI results from the loss of acinar cells and the enzymes they manufacture; it is not clinically apparent until about 95% of pancreatic function is absent.
Unlike dogs with EPI, which typically present with a ravenous appetite and voluminous stools, feline patients often manifest weight loss only, although polyphagia, diarrhea and vomiting can occur. Diagnosis is confirmed by low serum trypsin-like immunoreactivity. Most cats respond quickly to supplemental pancreatic enzymes that can be sprinkled onto moistened food. Because EPI can hinder cobalamin absorption, serum cobalamin should be measured and, if low, treated with injectable vitamin B12.
Pancreatic adenocarcinoma is uncommon in cats and typically diagnosed by ultrasound. Signs include anorexia, weight loss, and alopecia and shiny skin on the ventrum. It carries a guarded prognosis, especially if metastasized at the time of diagnosis. In one study, 11 of 34 cats diagnosed with pancreatic adenocarcinoma had metastatic disease on presentation.7 The median survival for all subjects was three months, but it was slightly longer for those who underwent surgery and/or chemotherapy; 10% of cats lived for over one year.
Some less common feline pancreatic conditions include pancreatic cysts and abscesses (which are often secondary to severe pancreatitis) and parasitic infestation.
Zini E, Ferro S, Lunardi F, et al. Exocrine pancreas in cats with diabetes mellitus. Vet Pathol 2016;53(1):145-152.
Davison LJ. Diabetes mellitus and pancreatitis—cause or effect? J Small Anim Pract 2015;56(1):50-59.
Zini E, Hafner M, Osto M, et al. Predictors of clinical remission in cats with diabetes mellitus. J Vet Intern Med 2010;24(6):1314-1321.
Tschuor F et al. Remission of diabetes mellitus cannot be predicted by the arginine stimulation test. J Vet Intern Med 2011; 25:83-89.
Forman MA. Feline exocrine pancreatic disorders. In Bonagura JD, Twedt DC, eds: Kirk’s current veterinary therapy XV. St. Louis, MO: Elsevier Saunders; 2015:565-568.
Steiner JM. Exocrine pancreatic insufficiency in the cat. Top Companion Anim Med 2012;27(3):113-116.
Linderman MJ, Brodsky EM, deLorimier L-P, et al. Feline exocrine pancreatic carcinoma: a retrospective study of 34 cases. Vet Comp Oncol 2013;11(3):208-218.