Explore diagnostic approaches, dietary strategies, and management considerations to help you improve outcomes for patients with pancreatic insufficiency in dogs and cats.
Pancreatic insufficiency in dogs and cats and other animal patients presents complex challenges, as both digestive enzyme deficits and hormonal imbalances can impact patient health. Effective management requires accurate diagnosis, an understanding of the underlying pathophysiology, and carefully tailored nutritional strategies. This article reviews current approaches to support you in optimizing care for affected patients.
Understanding EPI in pets
As part of the exocrine digestive and endocrine hormonal systems, the pancreas is necessary not only for digestion (and producing the enzymes that digest proteins, triglycerides, and complex carbohydrates), but also for the hormones insulin and glucagon. It secretes large amounts of bicarbonate to buffer the stomach acids, [copy missing here?] intrinsic factor for cobalamin absorption, and colipase, the co-factor used by pancreatic lipase for the efficient digestion of dietary fats.
Exocrine pancreatic acinar cells and their duct system open into the proximal duodenum (Figure 1). These cells synthesize and secrete digestive enzymes such as amylase and lipase, as well as their inactive proenzyme zymogens, including trypsinogen, chymotrypsinogen, proelastase and prophospholipase.
The pancreatic islets of Langerhans make up just 2% of the gland’s cells but contain all the important cell types that produce the hormones insulin, glucagon, and somatostatin (i.e. the alpha, beta, delta, and epsilon cells). These pancreatic cells all arise from progenitor multipotent stem cells, and function as discrete micro-endocrine organs.
The beta cells of the pancreas produce insulin and are more abundant than the alpha, delta, and epsilon cells; they account for about 50% of the islet cells in dogs. The alpha cells secrete glucagon; delta cells secrete somatostatin; and epsilon cells secrete ghrelin, which inhibits the beta-cell response to glucose and decreases insulin release.
When the production of these enzymes (exocrine) and hormones (endocrine) is insufficient, or the pancreas is damaged, it leads to pancreatic insufficiency in dogs and cats, exocrine pancreatic insufficiency in dogs and cats (EPI), and endocrine pancreatic insufficiency in dogs and cats (e.g. diabetes mellitus), which can be related and even co-exist. Additionally, pancreatic inflammation disrupts the flow of digestive enzymes into the digestive tract and allows them to leak into the abdomen (Figure 2). Because the kidneys and liver are located close to the pancreas, they are often affected, and the abdomen can become inflamed. Rapid enzymatic digestion of the exposed tissues occurs, along with serious clinical consequences. If bleeding occurs within the pancreas, shock and death can result.
Pancreatic hormones
Insulin
Insulin is initially formed as a single proinsulin polypeptide chain of 81 to 86 amino acid residues. It contains the A and B chains of the insulin molecule, as well as a connecting peptide. Enzymatic conversion follows and the insulin so formed is stored in membrane-limited secretory granules.
The liver, adipose cells, and muscle are three principal target sites for insulin. It increases the transfer of glucose and other substances into body cells and decreases the metabolic breakdown of fat, protein, and carbohydrates. The pancreatic islets of Langerhans are surrounded by the much more abundant acinar exocrine cells that secrete digestive enzymes into the ductal cells. The actions of insulin are opposed by glucagon, which is secreted by alpha cells.
Insulin allows blood glucose molecules to be used by the body’s cells to create energy. When glucose levels are low, the hormone glucagon causes the body to release its glycogen stores as energy. Glucagon’s primary role is to stimulate the liver to release stored glycogen as glucose and promote the production of more glucose from other sources (a process termed gluconeogenesis) to maintain a stable glucose level.
Extracellular calcium is required for insulin secretion, which can also be stimulated by other sugars (fructose, mannose, ribose), amino acids (leucine, arginine), hormones (glucagon, secretin), drugs (sulfonylurea, theophylline), short-chain fatty acids, and ketone bodies.
Glucagon
Glucagon is secreted by the alpha cells when blood glucose concentration becomes low and promotes the mobilization of energy-yielding nutrients by increasing glycogenolysis, gluconeogenesis, and lipolysis. It increases blood glucose by inducing hepatic glycogenolysis and gluconeogenesis. Glucagon is inhibited by hypercalcemia, insulin, GLP-1 (glucagon-like peptide-1) and somatostatin. Controlling glucagon in dogs is achieved with diet (more protein and fiber), exercise, and medication, if needed.
Insulin and glucagon act in tandem to maintain the glucose concentration in extracellular fluids. The relative amounts of insulin and glucagon are controlled by a glucose sensor in the pancreatic islets. Glucagon controls glucose release from the liver into the extracellular space, and insulin controls glucose transport from the extracellular space into insulin-sensitive tissues such as fat, muscle, and liver.
Somatostatin
Somatostatin was originally designated as a growth hormone–inhibiting hormone in the body, as it affects the secretion of other hormones within the hypothalamus, pancreas and gastrointestinal tract (GI), namely:
- Neurons in the hypothalamus inhibit the secretion of hormones coming from the pituitary gland, including growth hormone and thyroid-stimulating hormone.
- Delta cells in the pancreas inhibit the secretion of pancreatic hormones, including glucagon and insulin.
- Delta D-cells in the GI tract are found throughout the stomach and small intestine, with a high concentration in the pylorus. They decrease gastric secretion and the emission of GI hormones, such as secretin and gastrin.
Symptoms of pancreatitis
A variety of symptoms can be observed in the dog, including:
- Fever
- Increased appetite or loss of appetite (anorexia); appetite can also remain normal
- Weight loss from poor digestion (more common in cats)
- Dehydration
- Fatigue and sluggishness
- Mild to severe abdominal pain (may become more severe after eating)
- Depression
- Increased heart rate
- Difficulty breathing
Affected dogs often excrete large volumes of pale, fatty feces, termed steatorrhea. Young affected dogs have chronic diarrhea or very soft, bulky, fatty-looking feces, excessive appetites, occasional vomiting, and gradual weight loss over a period of months. The high level of fats in the stool may cause the hair coat around the anus and tail to appear and feel oily.
Causes of pancreatitis
EPI can be congenital (present from birth), inherited (genetic), or acquired from the effects of pancreatic infection, inflammation, or injury. Possible causes include genetic predisposition, nutritional factors (such as high blood levels of fat [lipemia] and calcium [hypercalcemia]), trauma to the pancreas, and certain drugs or toxins. Obesity linked to a high-fat and low-carbohydrate diet is also a risk factor.
- The most common cause of EPI in dogs is pancreatic acinar atrophy (PAA), especially when it appears in a dog under four years old. PAA appears to be an autoimmune disease, where the immune system attacks and destroys the pancreatic cells responsible for producing digestive enzymes.
- Pancreatic inflammation can occur after eating a large quantity of fatty foods. This typically happens around holiday periods, when pets are given table scraps they are unaccustomed to eating. Pancreatitis can be acute and occur rapidly. It affects both dogs and cats, although it is more common in cats. If treated promptly, permanent organ damage can usually be averted. However, if pancreatitis goes on chronically without treatment, severe organ damage can occur.
- Another predisposing cause of pancreatitis in both people and pets is the “leaky gut syndrome” of inflammatory bowel disease (IBD). Triggers that cause intestinal inflammation and damage to the gut lining include dietary proteins and allergens (glutens); low hydrochloric acid and gut enzymes; antibiotics and other drugs; microbial infections (bacteria, viruses, fungi, parasites) and pathogens; changes in blood sugars; presence of antibodies; organ failure; sex hormonal cycle changes including pregnancy and menopause; toxins like Clostridium, Salmonella and E.coli; and physical, physiological and emotional stress. Although unusual, the sting of a scorpion releases venom that can cause pancreatitis.
Diagnosing pancreatitis
Upon presentation to a veterinarian, a complete physical examination and series of lab tests should be performed to check for pancreatitis, diabetes, acid reflux, and even gallstones. X-rays and/or abdominal ultrasound imaging are used to look for evidence of any injury to the pancreas. Inflammation can damage the pancreatic insulin-producing cells, which could lead to diabetes.
Although pancreatitis is commonly seen in human beings, an estimated 90% of clinical or subclinical cases remain undiagnosed. Similarly, in dogs and cats, pancreatitis can be assumed to remain undiagnosed in the majority of cases. This is partly due to the nonspecific clinical presentation of these patients, but also because highly sensitive and specific clinical diagnostic tests for this disease were not available until the early 2000s.
Specific laboratory tests for pancreatitis
- Pancreatic trypsin-Like immunoreactivity (cTLI): This is the preferred diagnostic test for EPI in dogs and cats, especially when used in combination with measurements of cobalamin and folate. However, the sensitivities and specificities of different diagnostic tests for canine pancreatitis were recently compared: serum amylase activity showed a specificity of 57% and sensitivity of 62%, while serum lipase activity showed specificity of only 55% and a sensitivity of 73%. While these results could be marginally acceptable, almost 50% of dogs with an elevated serum amylase or lipase activity did not have pancreatitis.
The situation is even worse in cats, where serum amylase and lipase activities have been shown to have no clinical usefulness for diagnosing feline pancreatitis. Serum feline trypsin-like immunoreactivity (fTLI) concentration, while highly specific for feline pancreatitis, has a sensitivity of only 30% to 60%. However, the serum cTLI is still the most sensitive diagnostic tool currently available for pancreatitis in cats.
- Serum pancreatic lipase immunoreactivity (PLI): More recently, new assays for measuring serum pancreatic lipase immunoreactivity (PLI) have been developed and validated for both dogs and cats. Serum canine PLI (cPLI) has been shown to be highly specific for exocrine pancreatic function, and is highly sensitive for canine pancreatitis at the cutoff value of 200 µg/L. When compared to this test, sensitivity of serum cTLI concentration and serum lipase activity were much lower. Dogs with renal failure had normal cPLI, so this test can still be used to diagnose pancreatitis in these patients. The cPLI test is highly sensitive for canine pancreatitis. To date, clinical experience with the cPLI test has been excellent.
Serum fPLI has been evaluated in cats with experimental pancreatitis. In these cats, serum fPLI returned to normal concentrations many days after the fTLI, indicating that this test is likely to be more sensitive than serum TLI concentration. Initial results in feline clinical cases indicate that a serum fPLI concentration above 10 µg/L is highly suggestive of feline pancreatitis. However, chronic small intestinal disease compounded with chronic pancreatitis is more common than primary pancreatitis in cats. Feline cases with chronic GI disease should also be assessed and monitored periodically with measurements of serum cobalamin (vitamin B12) and folate concentrations.
In summary, serum PLI measurements have been validated for dogs and cats, and assays have been commercially available for about 15 years. Serum cPLI concentration has been shown to be both highly specific for EPI and highly sensitive for canine pancreatitis. Serum fPLI concentration can be elevated in the experimental and spontaneous pancreatitis of cats.
Adapted from Dr. David Williams, Head, Veterinary Clinical Medicine, University of IL, and consultant to GI Lab at Texas A & M University.
Treating pancreatitis
If mild or moderate, pancreatic inflammation can often be treated in a veterinarian’s office and will likely include fluid therapy with a colloid solution, electrolyte and potassium supplements, along with pancreatic enzyme replacement (e.g. Viokase®, Pancreazyme®). Any implicated medications should be stopped.
It is important to restrict the pet’s activity levels following treatment to allow for organ and tissue healing. Food and fluids will usually be stopped for a few days to give the pancreas time to rest, and to slow the production of digestive enzymes. Fluid therapy may be needed during this time to prevent dehydration.
Importantly, nutritional management is foremost in controlling and preventing further episodes of GI tract upset and pancreatitis. Treatment is usually required for the rest of the pet’s life. Note that if elevated folate levels are present, indicating small intestinal bacterial overgrowth (SIBO), tylosin antibiotic (e.g. Tylan®) is often used.
Drugs are used if vomiting occurs and persists. Severe cases of pancreatitis can often be saved with intraperitoneal lavage of canine or feline fresh-frozen plasma, as this blood product contains the alpha-1-antitrypsin protein that neutralizes the trypsin enzyme leaking out from the inflamed or damaged pancreas. Pain relief may be needed as well. Antibiotics are used to help prevent infection, and surgery may be necessary to relieve any blockages and remove severely damaged tissues.
More on nutritional management
EPI in pets can be controlled and treated by supporting digestion and overall health. Nutritional guidelines for managing pancreatitis and formulating therapeutic diets have largely depended upon experimental and retrospective studies, along with anecdotes, due to the limited availability of prospective studies. While fat has generally been considered the key nutrient for causing pancreatitis, other nutrients and dietary factors are involved and include energy density, digestibility, protein, carbohydrates, and fiber. Some experts assert that protein particle size may be of greater significance than dietary fat in the management of pancreatitis in cats.
For dogs with EPI, low-fat gastrointestinal diets are frequently recommended at first; whereas in cats, hydrolyzed diets are often initially considered. The presence or absence of comorbidity conditions is also important in formulating and managing appropriate diets, especially when considering the pet’s quality of life.
The terms “resting the gut” followed by the recent and novel “feed the gut” have been adopted for many of these cases. Allowing the gut to “rest” is intended to prevent stimulation of pancreatic secretions and minimize autodigestion and inflammation. However, fasting may have detrimental effects, including intestinal mucosal atrophy, enterocyte apoptosis, gut barrier dysfunction, and bacterial translocation. Providing the preferred enteral nutrition (EN) can help by reducing abdominal pain and the requirement for opioids, as well as lowering the likelihood of developing food sensitivities and intolerances.
Specific nutrient classes
Energy. It is necessary to maintain the pet’s daily energy requirements to avoid negative energy balance, as this increases protein turnover and can adversely affect the pancreas.
Fat. Some animal nutrition experts believe the management of naturally-occurring pancreatitis has overemphasized the role of fats. Less data is available for cats so their fat content should be evaluated on a case-by-case basis.
Protein. Excess dietary protein should be avoided as protein digestion stimulates pancreatic secretions in dogs.
Carbohydrates. When compared to fat and protein, carbohydrates are less stimulating to the pancreas.
Fiber. While prebiotic fibers can be beneficial, a diet high in viscous fiber should be avoided, particularly if pets are vomiting or regurgitating, because it slows gastric emptying.
Hypertriglyceridemia. Free fatty acids are hydrolyzed by pancreatic lipases, but when produced in excess amounts they can be toxic to pancreatic acinar cells. Moderate to high serum triglyceride concentrations often result in pancreatitis in dogs, and pets with diabetes mellitus are clearly at higher risk. Serum triglyceride concentrations >600 mg/dL require therapeutic management.
Using Omega-3 fatty acids provides clinical benefits. The recommended dose for treating dogs with hyperlipidemia is 120 mg of eicosapentaenoic acid and docosahexaenoic acid per kilogram of body weight.
Obesity. The inflammatory effects of adipose tissue likely causes the obesity seen with canine pancreatitis.
Chronic enteropathy (CE). In dogs and cats, CE is classified based on treatment response, with food-responsive enteropathy comprising approximately two-thirds of cases. When large intestinal bowel signs occur, fiber-enriched diets are recommended, which appear to also apply to cases of small intestinal disease.
Chronic kidney disease. As many renal diets are high in fat, this poses a potential risk of pancreatitis. Managing chronic kidney disease (CKD) optimally can slow disease progression and improve patient survival times.
Diabetes mellitus (DM). Some dogs with chronic pancreatitis develop DM. The pet’s body condition score (BCS) can assist with selecting a diet with appropriate caloric density.
Oral food intake. Recognizing and treating nausea is important when promoting oral food intake. To help increase intake, consider: use of preferred ingredients, textures, and flavors of food; warming the food to increase acceptance; handfeeding; moistening food; and providing a stress-free environment.
Assisted EN. Once the pet has been discharged from the vet hospital, owners should be counseled to avoid the risks associated with pancreatitis or its recurrence. These include: avoiding abrupt food change, ingestion of unusual food items, trash, and table scraps, and addressing obesity.
When oral or injectable cobalamin was given to dogs with EPI, serum cobalamin concentrations increased significantly. Additionally, in contrast to dogs with chronic enteritis, oral (not injectable) methylmalonic acid (MMA) supplementation was decreased after cobalamin supplementation. Note that MMA is a dicarboxylic acid involved in the metabolic breakdown of certain amino acids and odd-chain fatty acids. It also serves as a key indicator of vitamin B12 deficiency.
For dogs with EPI, pancreatic enzyme replacement therapy, oral cobalamin, and a highly digestible, low-fat diet are essential. In cases of diabetes mellitus due to endocrine pancreatic insufficiency, dietary management is aimed at stabilizing blood glucose levels through consistent defined feeding times and a carefully balanced diet.
When food can safely be resumed, a bland, low-fat, high-carbohydrate, easily digestible diet is recommended. If the pancreatitis was severe, or is chronic (recurring), a special bland low-fat diet may be needed permanently. When chronic pancreatitis is resolved and the patient is healed, EPI may no longer be a problem.
High-fat diets should be limited even for the long term, and protein levels should be kept at moderate levels of highly digestible and easily assimilated ingredients. The recovering pet should drink plenty of fresh water, and periodic checkups should be made with a veterinarian.
Managing pancreatic insufficiency in dogs and cats requires a balance of accurate diagnosis, tailored nutritional support, and ongoing monitoring to reduce relapse risk. By integrating dietary strategies with medical management, you can improve quality of life and long-term outcomes for your patients.
Genetic predisposition to pancreatitis
While pancreatitis can occur in any dog or cat breed, it occurs more frequently in cats, especially Siamese. In dogs, the most commonly affected breeds are the Miniature Schnauzer, Miniature Poodle, and American Cocker Spaniel. It also occurs in German Shepherd Dogs, Rough-coated Collies, Cairn Terriers, Akitas, West Highland White Terriers, Cardigan Welsh Corgis, Border Collies, Australian Heelers, Shetland Sheepdogs, and Australian Shepherds. In German Shepherds, PAA is considered an inherited condition.
Inflammation of the pancreas is also more common in females than in males, and in elderly pets. For Miniature Schnauzers, feeding a therapeutic low-fat diet or selecting a diet with 50% reduction in dietary fat is a reasonable first step. Fenofibrate may be added to the treatment protocol.
Preventing EPI re-occurrence
The following preventative measures can help prevent EPI from re-occurring:
- Implement steps for weight loss if the animal is overweight, and maintain an ideal weight
- Avoid high-fat diets
- Avoid drugs known to increase inflammation
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AUTHOR PROFILE
Dr. Jean Dodds received her veterinary degree in 1964 from the Ontario Veterinary College. In 1986, she established Hemopet, the first non-profit national blood bank program for animals. Today, Hemopet also runs Hemolife, an international veterinary specialty diagnostics service. Dr. Dodds has been a member of many committees on hematology, animal models of human disease and veterinary medicine. She received the Holistic Veterinarian of the Year Award from the AHVMA in 1994, has served two terms on the AHVMA’s Board of Directors, chairs their Communications Committee, and currently serves on the Board of the AHVMF, as well as its Research Grant and Editorial Committees.
