Background

Pancreatitis is a common condition in dogs, but often perplexes the veterinarian in both the diagnosis and management.¹ Acute pancreatitis is defined as the presence of neutrophilic inflammation within the body of the pancreas, and potentially extending to the peri-acinar fat.² There is an absence of fibrosis or acinar atrophy, findings that are consistent with chronic pancreatitis.³ Often acute pancreatitis is accompanied by necrosis of the pancreas or peri-pancreatic tissue. In people, the presence of necrosis or infected necrosis is most often associated with increased morbidity and mortality. However, in dogs this has not been shown.

When necrosis or inflammation of the pancreas develops, there are localised effects of pain and ileus secondary to peritonitis. Vomiting may also develop due to this pain, as well as circulating emetics. In some dogs the inflammation, despite being acute, is limited to these local effects and the clinical presentation may not be severe. However, if there is activation of systemic inflammatory cascades, there can be significant complications such as cardiac arrhythmias, disseminated intravascular coagulation (DIC) and respiratory abnormalities. Additionally, local complications can also worsen, with development of extra-hepatic bile duct obstruction, profound ileus, pancreatic fluid collections (previously known as pancreatic pseudocysts) and haematemesis or haematochezia. Diabetes ketoacidosis may also be present at the time of initial presentation.

Diagnosis

Presentation of a middle-aged, overweight dog with an acute onset of vomiting and abdominal pain is highly suggestive of acute pancreatitis. However, these clinical signs are not specific for pancreatitis and other conditions such as septic peritonitis, intestinal foreign body obstruction, acute gastroenteritis, dietary indiscretion or metabolic disease such as renal failure should always be considered. Thorough history for evaluation of potential toxins or ingestion of foreign bodies should be undertaken along with a thorough physical examination. Physical findings can establish a clinical severity index score, which may potentially guide treatment.⁴

Routine biochemistry and haematology, ideally along with urine specific gravity, is necessary to rule out metabolic disease such as renal failure and to establish baseline electrolyte and acid-base status. The presence of gross lipaemia in the collected blood sample is highly suggestive of pancreatitis. There are no specific abnormalities to be found on routine blood tests that are confirmative for pancreatitis, but increased total lipase and amylase may be present. Unfortunately these assays are neither sensitive nor specific for the diagnosis of pancreatitis.⁵

Development of an assay that detects lipase specific to the pancreas has become widely available both as a quantitative assay (Spec-cPL) and a cage-side qualitative test (SNAP-cPL). Spec-cPL (and its precursor canine pancreas specific lipase immunoreactivity), has been reported to have a sensitivity ranging from 63 to 80%.⁶ The assay is more likely to be increased if the clinical disease is severe. The correlation between the SNAP test and the qualitative assay appears to be good, and one study has shown that Spec-cPL is highly specific in dogs without clinical signs of pancreatitis.⁷ However, our (as yet unpublished) observations are that in dogs which present with acute abdominal disease, the clinical utility of this test used as a single modality is only moderate. This is likely to be due to the fact that a number of conditions such as septic peritonitis may cause secondary pancreatic inflammation, and reliance on this test alone may lead to a false sense of security. To this end, the author recommends that this test should only be used in conjunction with diagnostic imaging.

Other laboratory based tests that can be considered include measurement of canine serum-pancreatic elastase-1. This test has been shown to be fairly sensitive in the diagnosis of pancreatitis⁸, again more so with severe disease.

Abdominal ultrasound is the diagnostic imaging modality most likely to assist in the diagnosis of pancreatitis in dogs. Improved technology and training has no doubt improved the sensitivity of this modality from previously published rates of approximately 66%⁵, but the true sensitivity is unknown and is likely to be highly operator dependent. With severe cases, the presence of peri-pancreatic fat necrosis gives the characteristic hyperechoic area around the pancreas, and the pancreas itself is often seen to be enlarged in size with variable echogenicity. Assessment of free abdominal fluid is also an important part of the diagnostic work-up to rule in or out septic peritonitis as the primary differential. Advanced imaging such as endoscopic ultrasound, CT or MRI has less of a place in the diagnosis of canine acute pancreatitis. Abdominal radiographs, although not generally useful for the diagnosis of pancreatitis, are essential to rule out surgical conditions such as pyometra or intestinal foreign body obstruction and should not be neglected or overlooked in general practice.

Management

The cornerstone of management of acute pancreatitis in the dog is to ensure that any fluid, acid-base and electrolyte imbalances are corrected. Crystalloids are the first line fluids used, with colloids reserved for those dogs with proven low oncotic pressure.

Pain is often a significant factor that prolongs the recovery of dogs. Multi-modality methods of providing analgesia may be necessary with refractory pain, and can be a combination of opioids (avoiding morphine due to the emetic effect) with other agents such as lignocaine or ketamine if necessary. Intra-abdominal bupivacaine may be of some benefit if there is not a large-volume effusion. Anti-emetics are also helpful in cases where vomiting persists. The author prefers the use of maropitant or prochlorperazine, as metoclopramide may theoretically be deleterious if there is antagonism of dopamine.

The use of antibiotics is controversial, as the condition is invariably sterile. However, if there appears to be a high risk of bacterial translocation then general broad spectrum antibiotics targeting gut bacteria may be indicated. To date there is no supportive evidence for the use of gastric acid suppression or constant rate dopamine infusion, and the administration of plasma in severe cases is expensive and lacks evidence for a defined clinical benefit.

The biggest change in management in pancreatitis in both people and dogs over the past decade has been the gradual switch from fasting (nil by mouth until recovered) to early enteral feeding in severe pancreatitis. Providing nutrition directly to the gut is both safe and well tolerated in dogs, with no increase in vomiting or pain observed in one study.⁹ Interventional nutrition is currently recommended in dogs with no nutritional intake for three or more days, and potentially may be of use earlier than that in dogs with severe disease. Further large studies are necessary before these conclusions can be proven. There is also no documented ideal diet to feed these dogs, but the current recommendation is to feed a low-fat diet, with pro-kinetics of potential benefit to assist in tolerating feeding.

Systemic complications such as diabetic ketoacidosis or cardiac arrhythmias also need to be treated on an individual basis. Local complications such as acute fluid collections or extra-hepatic bile duct obstruction have traditionally been surgically corrected, but these result in high mortality rates. The author currently monitors dogs with these problems via clinical assessment and abdominal ultrasound. If intervention is needed due to refractory pain or imminent rupture of the gall bladder, ultrasound guided needle drainage is the initial treatment of choice, followed by surgery only if there is documented rupture or the needle drainage fails to resolve the condition.

Upon discharge after recovery, dogs should ideally be fed a low-fat diet and supplemented with exocrine pancreatic enzymes for 4 weeks. At that point, fasting serum triglycerides and cholesterol should be checked to ensure there is not an underlying hyperlipidaemia causing the pancreatitis. Gradual transition back to a normal diet may begin at that point in time if tolerated.

References

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2.  Newman SJ, Steiner JM, Woosley K, et al. J Vet Diagn Invest 2006;18:115–118.

3.  Watson PJ, Roulois AJ, Scase T, et al. J Small Anim Pract 2007;48:609–618.

4.  Mansfield CS, James FE, Robertson ID. J Am Vet Med Assoc 2008;233:936–944.

5.  Mansfield CS, Jones BR. Aust Vet J 2000;78:416–422.

6.  Steiner JM, Newman S, Xenoulis P, et al. Vet Ther 2008;9:263–273.

7.  Neilson-Carley SC, Robertson JE, Newman S, et al. Am J Vet Res 2011;72:302–307.

8.  Mansfield CS, Jones BR, Watson PJ. J Vet Diag Invest 2011;23:In press.

9.  Mansfield CS, James FE, Steiner J, et al. J Vet Intern Med 2011;25:419–425.