Feeding Dogs with Pancreatitis
World Small Animal Veterinary Association Congress Proceedings, 2016
Lisa Weeth1, DVM, DACVN, MRCVS; Frederic Gaschen2, Dr. med. vet., Dr. habil., DACVIM (SAIM), DECVIM-CA
1Clinical Nutrition, Weeth Nutrition Services, Edinburgh, UK; 2Veterinary Clinical Sciences,
School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, USA

Inflammation of the pancreas is the most common exocrine pancreatic disorder affecting dogs. True prevalence of acute and chronic pancreatitis in the dog population is not known, but histological evidence of chronic inflammatory changes to the pancreas have been seen on post-mortem examination of up to one-third of dogs presenting to first opinion practices. Pancreatitis is a painful and potentially life-threatening condition and given the pancreas' role in normal digestion, feeding of animals with active pancreatic inflammation can greatly influence clinical signs and outcomes.


The pancreas has two main roles in digestion: 1) the production of insulin (i.e., an endocrine function) and 2) the production of digestive enzymes such as amylase, lipase, and trypsin, which are secreted into the lumen of the duodenum where they facilitate break down of ingested starches, fats, and proteins (i.e., an exocrine function). These exocrine enzymes are produced in their pro-enzyme, or inactive forms, and packaged into zymogens granules. Under normal circumstances the presence of fat and protein in the duodenum stimulate secretion of cholecystokinin (CCK) from the enterocytes, which in turn stimulates pancreatic contraction to releases zymogens and pancreatic-derived bicarbonate into the pancreatic duct. Within the pancreas, bicarbonate and zymogens granules are kept isolated from one another during production and storage to prevent premature activation, but once in the duodenal lumen bicarbonate causes a rise in luminal pH resulting in activation of the digestive enzymes. Premature activation of exocrine enzymes within the pancreas itself and subsequent auto-digestion is responsible for the clinical signs in affected dogs and can be fatal if left untreated. Acute pancreatitis (AP) typically has a sudden onset with more pronounced and severe clinical signs (i.e., vomiting, anorexia, and abdominal pain) while clinical signs of chronic pancreatitis (CP) are often vague (i.e., lethargy, decreased food intake, and weight loss).

Risk Factors

Acute versus chronic pancreatitis is largely a histological distinction but clinical signs and inciting causes between the two types can also vary. There are a number of known causes for AP in dogs, but the most common triggers are consumption of a non-food item, feeding of table scraps, and eating garbage or other household food waste. The exact mechanism for this disease is not yet known, but the rapid increase in circulating fatty acids may play a role in activation of pancreatic enzymes within the pancreatic acini. Additional factors associate with an increased risk of pancreatitis include breeds predispositions to hypertriglyceridemia, such as seen in miniature Schnauzers and Yorkshire terriers; medications, such as potassium bromide and phenobarbital; and obesity. Dogs with mild pancreatitis may vomit, refuse food, or seem lethargic at home; those with chronic, low-grade pancreatitis may have vague signs such as an intermittently poor appetite and weight loss over a period of weeks to months; severe pancreatitis can cause not only vomiting, food refusal, and lethargy, but diarrhea, fever, and marked abdominal pain. Severe pancreatitis, if left untreated, can also result in circulatory collapse, systemic inflammatory response syndrome or sepsis, disseminated intravascular coagulation, and death.


Currently, the clinical diagnosis of canine AP relies on a combination of four factors: the presence of typical clinical signs, elimination of other possible differential diagnoses (after evaluation of a minimal database consisting of CBC, biochemistry profile, and urinalysis), increased pancreatic lipase immunoreactivity (PLI) or DGGR lipase, and presence of typical ultrasonographic lesions of the pancreas and surrounding tissue. The diagnosis of CP is more challenging: the clinical signs are often vague, or identical to AP in some cases, and laboratory tests used for AP diagnosis as well as abdominal ultrasound are less sensitive for CP. Therefore, it is extremely important for clinicians to keep the disease "on their radar" when they see dogs with vague GI-related signs.

Medical and Dietary Management

The treatment of AP in dogs is supportive and consists of 4 essential parts: 1) rapid restoration of water and electrolyte balance, 2) control of vomiting with antiemetics, 3) pain control, and 4) early enteral nutrition. In addition, one of the authors (FG) commonly uses prokinetics early in the course of the disease for moderate to severe cases, as it is likely that GI hypomotility will contribute to delayed recovery (and perpetuate nausea, vomiting, and hyporexia). Commonly used prokinetics include metoclopramide, preferably given as a constant rate infusion (CRI) (1–2 mg/kg/24 h), and erythromycin lactobionate (reconstitute based on manufacturer's recommendations, 0.5–1 mg/kg IV q 8 h, or as 1.5–3 mg/kg/24 h as a CRI). Based on a recent review from the UK, the treatment of CP includes: assessing pain and providing analgesia as needed, providing adequate nutrition, and assessing and addressing functional loss.

While fasting is necessary in animals that are nauseous and vomit frequently, it is not recommended to fast a dog for more than 48 to 72 hours from the time it stopped eating in the home environment. Prolonged food deprivation can lead to immune suppression, delayed healing and increased risk of bacterial translocation across the intestinal mucosa (with risk of sepsis). The goals of nutritional therapy are to provide sufficient calories and nutrients to allow for patient recovery while minimizing pancreatic stimulation. Given that pancreatic inflammation causes disruption of normal digestive processes, nutritional therapy must involve gradual introduction of a highly digestible, low to moderate fat containing food. Over-the-counter commercial diets are less digestible and often higher in fat than veterinary-prescribed therapeutic diets and as a general rule over-the-counter diets should be avoided during the recovery period.

One study of early nutritional support in dogs with AP found good tolerance to assisted nutritional support through an esophagostomy tube with significantly fewer incidences of regurgitation and vomiting compared to dogs given parenteral nutrition. These finding suggest that dogs with an expected prolonged anorexia due to AP may benefit from placement of an assisted feeding device such as a nasoesophageal or esophagostomy tube.

The degree of dietary fat restriction required for a dog with pancreatitis will vary with the underlying cause and chronicity of the condition. A dog that developed AP after ingestion of a single high fat meal may tolerate a moderate fat (i.e., 25–35% fat on a metabolizable energy - ME - basis) diet during recovery and for long-term treatment, while one with CP and already eating a moderate fat diet at the time of diagnosis would benefit from a more restricted fat intake (i.e., less than 20% fat on a ME basis). The optimal long-term diet choice for a dog with pancreatitis will depend on the inciting cause (genetics, medication, hypertriglyceridemia, or high fat intake). Irrespective of underlying cause, dogs with a history of pancreatitis should not be fed diets with >45% fat on a ME basis due to the risk of recurrence.


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Speaker Information
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Frederic Gaschen, Dr. med. vet., Dr. habil., DACVIM, DECVIM-CA
Veterinary Clinical Sciences
School of Veterinary Medicine
Louisiana State University
Baton Rouge, LA, USA

Clinical Nutrition
Weeth Nutrition Services
Edinburgh, UK

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