Pancreatitis: first steps and dietary essentials... - Veterinary Practice
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Pancreatitis: first steps and dietary essentials…

of Royal Canin
examines the
factors involved
in treating
from a
nutritional standpoint

PANCREATIC DISORDERS ARE COMMONLY SEEN in clinical practice, with pancreatitis the most common disease of the exocrine pancreas in the dog. The clinical picture is characterised by non-specific gastrointestinal signs and a range of disease from very mild to severe is presented. Pancreatitis can be divided into acute or chronic forms depending on whether the disease has led to permanent histopathological changes in the pancreatic parenchyma such as fibrosis and/or atrophy.1 Pancreatitis describes inflammation of the exocrine pancreas, which occurs when there is premature activation of digestive enzymes. More specifically, the common pathway is suggested to be the inappropriate early activation of the zymogen trypsinogen to trypsin within the pancreatic acini, resulting in pancreatic inflammation, tissue necrosis, systemic inflammation and potentially the development of systemic inflammatory response syndrome (SIRS) and disseminated intravascular coagulopathy (DIC). Most cases of pancreatitis in dogs are idiopathic. Several breed predispositions have been identified with acute pancreatitis most commonly reported in small breed dogs with miniature schnauzers and terriers overrepresented. 2 Chronic pancreatitis is more commonly seen in Cavalier King Charles spaniels, cocker spaniels, collies and boxers.3 Dogs of any age can develop the disease; however, it is more commonly seen in animals middle-aged to old (>5 years of age). Certain risk factors have been described including endocrine disease, hypercalcaemia, obesity, trauma and various drugs and toxins.1,4,5 The nutritional factors that have been reported anecdotally include dietary indiscretion and consumption of more dietary fat than normal for a particular dog.6 The possibility that a dog may be suffering from pancreatitis is suspected on interpretation of an animal’s history, results of physical examination and presence of predisposing factors. While no clinical signs (or combination) are considered pathognomic for either acute or chronic ancreatitis, cranial abdominal pain, often in combination with a hunched stance and vomiting are the most common presenting signs in cases of acute pancreatitis.7 Dogs with chronic pancreatitis may display vague signs of anorexia, hyporexia, lethargy, or behavioural changes, and an acute trigger may not be immediately identified in these patients.8 Because many other diseases can cause these symptoms, further investigations are required to rule out other conditions and to reach a diagnosis of pancreatitis. The “gold standard” for diagnosis is pancreatic histopathology, which is rarely indicated or performed, with no other diagnostic test offering 100% sensitivity or specificity. Routine haematology and biochemistry can lead to a suspicion of pancreatitis; the results are often non-specific and instead are best used to provide information on the general condition of the patient and rule out the other disease processes. The canine pancreatic lipase immunoreactivity (cPLI) is an enzymelinked assay developed to measure pancreatic lipase activity. It is currently considered to be the most specific and sensitive serum test for the diagnosis of pancreatitis in the dog.1 Abdominal ultrasonography is the most widely used imaging modality for diagnosing pancreatitis. A combination of pancreatic enlargement, fluid accumulation around the pancreas, and changes in echogenicity are all suggestive of pancreatitis. However, the sensitivity of ultrasonography when used alone to diagnose pancreatitis is highly operator-dependent and often very low. Therefore, the best combination for specific diagnosis of pancreatitis in the dog is elevated cPLI and ultrasound findings comparable with pancreatitis.9 Despite recent advances in diagnostics, it is increasingly recognised that accurate clinical diagnosis of pancreatitis can be challenging. While it is impossible to differentiate between acute and chronic forms of the disease on clinical signs alone, this is not important for short-term emergency management. Therapies for pancreatitis are largely supportive with the mainstays including resolution of any predisposing factors, analgesia, control of vomiting, treatment of bacterial complications, correction of acid-base and electrolyte balances and maintenance of adequate tissue perfusion and oxygen delivery. Nutritional support plays a central role in the management of pancreatitis in people.10,11 However, in veterinary medicine the traditional approach has been to withhold food with the view that this limits autodigestion by decreasing pancreatic stimulation and enzyme release. More recently it is felt this approach is unwarranted and could lead to malnutrition and impaired gastrointestinal barrier function as lack of enteral nutrition induces a reduction in the thickness of the intestinal mucosa and the height of the villi, leading to increased intestinal permeability – ultimately exposing the animal to septic complications via bacterial translocation.12 When implementing enteral feeding, a highly-digestible diet that is appropriate in terms of protein and fat content is recommended. Specialists generally advise that a low-fat diet be given4,13 and while the definition of “low fat” is not well-established, the general consensus is less than 30g per 1,000kcal.14 There are several clinical diets available that meet these requirements such as Royal Canin Gastrointestinal low-fat diet, which is available in both a dry and wet formulation as well as a liquid formulation to facilitate tube feeding. Foods should be re-introduced very gradually to avoid pancreatic secretion and this is dependent on the duration of patient anorexia. If a patient has been anorexic for more than three to five days, it is recommended to feed only one-third of the resting energy requirement (RER) on day one and then gradually increasing calories if tolerated to reach full RER usually by day three.15 Ideally food should be re-introduced at the same time as the instigation of other treatment; however, this is often delayed due to the presence of vomiting and gastroduodenal ileus; both common presentations in acute pancreatitis. Non-vomiting dogs with mild clinical signs should have food re-introduced as soon as possible12 with small amounts of warmed food offered intermittently in a low-stress environment. If the animal is vomiting and requires pharmacological control, food can be re-introduced after 12 to 24 hours. In anorexic animals, enteral nutrition is preferable to total parental nutrition and a feeding tube should be placed (e.g. naso-oesophageal, oesophageal, etc.), taking into account both the severity of clinical signs and the type of disease present. Dogs with acute pancreatitis may go on to make a full recovery without displaying either clinical or histopathological features of chronic disease. Following discharge, providing the patient is eating well and clinically stable, the goal is to slowly transition the patient from a low-fat diet received during hospitalisation to a diet otherwise optimal for the pet’s age and health. Continued avoidance of risk factors such as ingestion of table scraps or dietary indiscretion is advised. Dietary modification is probably the most important component of long-term management of dogs with chronic pancreatitis with lifelong fat restriction recommended.6 Pancreatitis is a common condition seen in clinical practice in dogs; however, establishing a diagnosis can be difficult with no diagnostic test 100% sensitive or specific. Alongside other therapies, nutrition plays an integral role in the successful management of both acute and chronic cases with early intervention recommended. Acute cases in particular may benefit from assistive feeding; however, ultimately the timing and route of administration are dependent upon the severity of clinical signs and the type of disease present. A highly-digestible diet appropriate in terms of protein and low in fat (less than 30g per 1,000kcal) is advised initially for acute cases with chronic cases requiring lifelong fat restriction.

  • To watch a Royal Canin-hosted webinar on pancreatitis, visit the vet portal https://vetportal.royalcanin.


  1. Xenoulis, P. G. (2016). Diagnosis of pancreatitis in dogs and cats. J Small Anim Pract 56: 13-26.
  2. Watson, P. J., Roulois, A., Scase, T. et al. (2007) Prevalence and breed distribution of chronic pancreatitis at post-mortem examination in first-opinion dogs. J Small Anim Pract 48: 609-618.
  3. Bishop, M. A., Xenoulis, P. G., Levinski, M. D. et al. (2010) dentification of variants of the SPINK1gene and their association with pancreatitis in Miniature Schnauzers. American Journal of Veterinary Research 71: 527-533.
  4. Watson, P. (2015). Pancreatitis in dogs and cats: Definitions and pathophysiology. J Small Anim Pract 56: 3-12.
  5. Xenoulis, P. G., Suchodolski, J. S. and Steiner, J. M. (2008). Chronic pancreatitis in dogs and cats. Compend Cont Ed Pract Vet 30 (3): 166-180.
  6. Lem, K. Y., Fosgate, G. T., Norby, B. et al. (2008). Associations between dietary factors and pancreatitis in dogs. JAVMA 233: 1,425-1,431.
  7. Hess, R. S., Saunders, H. M., Van Winkle, T. J. et al. (1998) Clinicopathologic radiographic and ultrasonographic abnormalities in dogs with fatal acute pancreatitis: 70 cases. JAVMA 213: 665-670.
  8. Andreson, N. V., Low, D. G. (1965) Diseases of the Canine Pancrease: A comparative summary of 103 cases. Anim Hosp 1: 263-373.
  9. Steiner, J. M., Newman, S., Xenoulis, P. G. et al. (2008) Sensitivity of serum markers for pancreatitis in dogs with acroscopic evidence of pancreatitis. Vet Ther 9 (4): 263-273.
  10. Nathens, A. B., Curtis, J. R., Beale, R. J. et al. (2004). Management of the critically ill patient with severe acute ancreatitis. Crit Care Med 32 (12): 2,524-2,536.
  11. Ioannidis, O., Lavrentieva, A. and Botsois, D. (2008) Nutritional support in acute pancreatitis. JOP 9 (4): 275-390.
  12. Qin, H. L., Su, Z. D., Hu, H. L. et al. (2007). Effect of parenteral and early intrajejunal nutrition on pancreatic digestive enzyme synthesis, storage and discharge in dog models of acute pancreatitis. World J Gastroenterol 13 (7): 1,123-1,128.
  13. Williams, D. A., Steiner, J. M. (2005) Canine exocrine pancreatic disease. In Ettinger, S. J., Feldman, E. C. (eds): Textbook of Veterinary Internal Medicine. 6th ed. St Louis: Elsevie; pp1,482-1,488.
  14. Shmalberg, J. (2016) To Feed or Not to Feed? Controversies in the nutritional management of pancreatitis. Today’s Veterinary Practice 6 (6): 45-51.
  15. Freeman, L., Labato, M., Rush, J. et al. (1995) Nutritional Support in pancreatitis; a retrospective study. J Vet Energ Crit Care 5 (1): 32-41.

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