Managing the spectrum of canine pancreatitis
Managing the spectrum of canine pancreatitis
Caroline Mansfield BSc BVMS PhD DECVIM-CA
The University of Melbourne, 250 Princes Highway, Werribee, Victoria, Australia 3030. email@example.com
The definitions of pancreatitis can sometimes be challenging, as usually the terms used in textbooks refer to the histological classification, which does not always relate to the clinical presentation. Technically, acute pancreatitis is defined as a neutrophilic inflammation, without fibrosis or exocrine atrophy; and is usually present within the body of the pancreas and/or peri-pancreatic fat. Chronic pancreatitis (CP) is defined as a mononuclear (often lymphocytic) inflammation, with disruption of the pancreatic architecture due to concurrent fibrosis. The presence of nodular hyperplasia in the pancreas of dogs is now considered an incidental finding, with an increased presence in older animals.
Increasingly it is being recognised that mild, multi-focal inflammation within the pancreas occurs frequently, and as such some low-grade inflammation may be on the spectrum of normal for many animals, and not associated with any specific clinical signs. Likewise, due to the anatomical location of the pancreas, other abdominal or intestinal disease can cause ‘by-stander’ inflammation in the pancreas. This makes it very important to ensure that clinically we rule out other causes of acute abdominal disease in dogs before reaching a diagnosis of acute pancreatitis.
Obese and overweight dogs are at greater risk of pancreatitis, and this may be associated with abnormal dietary intake or indicate a general predisposition to inflammation associated with production of adipokines. In one retrospective survey, dogs with recent ingestion of unusual food items and garbage ingestion all showed an increased risk of developing pancreatitis, rather than dogs that appeared to have a higher intake of treats and snacks. It has also been observed that feeding a low-protein, high fat diet to dogs for prevention of struvite urolithiasis is linked with an increased incidence of pancreatitis.
None of the changes seen on routine clinical pathology are specific for pancreatitis but are useful in aiding in the diagnostic pathway. Some dogs may have overt lipaemia, which does increase the index of suspicion for pancreatitis. Serum lipase and amylase concentrations have been shown to increase in experimental and naturally occurring canine pancreatitis. However, neither enzyme is specific to the pancreas as they also originate from gastrointestinal mucosa and are excreted by the kidneys. Conversely, serum lipase and amylase concentrations can also be normal in dogs that do have pancreatitis.
Canine pancreatic lipase measures lipase that originates solely in the pancreas. The canine pancreatic-lipase immunoreactivity (cPLI) assay was developed into a commercially available specific canine pancreatic lipase (spec-CPL) sandwich ELISA, with results < 200 µg/L expected in healthy dogs, and results > 400 µg/L considered consistent with a diagnosis of pancreatitis. An in-clinic rapid semiquantitative assay (SNAP-cPL; Idexx Laboratories) is also available. In brief, a negative result for SNAP-cPL or cPLI means it is likely that the dog has disease other than acute pancreatitis. A positive result still requires confirmation and elimination of other disease by some other modality. This is especially true as approximately 25% of dogs with a positive SNAP cPL test presenting to a veterinary emergence centre had non-pancreatic disease as their primary presentation in one study. Conversely, there are a high number of false negative cPLI results in dogs with CP.
Diagnostic imaging is a vital component of the diagnostic work-up for dogs with possible pancreatitis. Radiography is not generally that helpful for diagnosis of pancreatitis but is essential to rule out intestinal obstruction or other clinical signs. Abdominal ultrasound is increasingly being considered the mainstay of diagnosis. Acute pancreatitis is usually diagnosed by ultrasound in both dogs and cats, seen as an enlarged, hypoechoic pancreas and peri-pancreatic necrosis (manifested as hyperechogenicity surrounding the pancreas). It is extremely difficult to elucidate sensitivity or specificity of ultrasound as it is both operator and equipment dependent. Likewise, we need to be sure to evaluate the entire abdomen to rule out other causes of disease.
Ultrasonographic changes for CP are poorly described, and not often present. It has also been shown that pancreatic duct dilatation, once considered a hallmark of CP in cats, may be an age-related change and not reflect inflammation. Modalities that are used commonly in people such as MRI, contrast-enhanced CT and endoscopic retrograde cholangiopancreatography (ERCP) are poorly described in animals. It is likely that they will be of minimal clinical benefit, due to the equipment and prolonged anaesthesia that is required.
There are no specific treatment modalities that are effective against pancreatitis. In acute pancreatitis, the aim is to treat the clinical consequences of the disease (dehydration, pain, nausea) and prevent further inflammation (interventional enteral nutrition). Therefore, the treatment of acute pancreatitis consists of:
IV fluid replacement
Analgesia aimed at preventing wind-up- so starting maximally and then titrating down but avoiding use of drugs that affect gastrointestinal motility if possible.
Interventional nutrition: tin dogs with moderate to severe disease, this should start within 3-5 days of when there has been no oral intake. An oeosphageal feeding tube ideally should be used, inserted when the animal is suitable for a general anaesthetic. Gradually increasing feeding volumes to resting energy requirements over 3 days is recommended, and normal convalescent diets appear to be adequate unless there is known pre-existing hyperlipidaemia.
Controlling vomiting is also necessary when there are ongoing fluid losses, and when it is suspected that nausea is contributing to hyporexia/anorexia. There is no single agent that has been shown to be most effective in acute pancreatitis. There is a theoretical advantage in using maropitant, as NK1-receptor antagonist, as substance P may be involved in visceral pain. If single-drug antiemetic therapy is not effective, then addition of ondansetron or metoclopramide may be necessary. Although there is a theoretical disadvantage with metoclopramide (as it is a dopamine receptor antagonist), if poor intestinal motility is thought to be contributing to nausea or anorexia, then its use may be indicated.
Antibiotics are not indicated in most dogs with AP, unless there is documented concurrent infection. Other treatments are generally aimed at treating complications as they occur and draining acute fluid collections that appear to be causing pain. In all animals, if a drug reaction is suspected, then of course the drug should be withdrawn. Follow-up assessment should consist of rechecking serum triglycerides and cholesterol 1-2 weeks after discharge. Long-term dietary management is then dictated by whether hyperlipidaemia is present or not. If it isn’t, the avoidance of trigger foods alone should be enough to minimise risk of recurrence.
Unfortunately, treatment options for CP are poorly explored. In animals with co-existing diseases such as inflammatory bowel disease or cholecystitis, treatment of the concurrent conditions takes priority, and often leads to resolution of clinical signs associated with CP. Therefore, the main priority in treating animals with CP is to look for and manage concurrent conditions.
The second priority is to look for underlying triggers for CP that can be corrected such as hyperlipidaemia. If cholesterol is high, and triglycerides are normal, then an underlying endocrinopathy should be investigated for, even though this may be problematic due to the influence of other disease on hormonal axis testing. If both triglycerides and cholesterol are increased, then an inherent defect in lipid metabolism is more likely. In the absence of an endocrinopathy, treatment should initially consist of feeding a low-fat, with < 15% DM as fat. This is achieved by feeding many of the prescription low fat, high fibre diets. Other treatments such as omega-3 supplementation (20-30 mg/kg/day) can also be used. If triglycerides (TG) alone are high and don’t decrease with dietary management then gemfibrosil (7.5-10 mg/kg PO q 12 hours) may be used. Usually treatment is not required to reduce cholesterol.
If no underlying cause is identified and it is thought CP is causing clinical signs, then the dilemma is whether to manage pain or try to reduce inflammation. Ideally, immune suppression should be used only when there is histological confirmation of inflammation within the pancreas. If the animal is not diabetic, prednisolone is the drug of choice for both immune suppression and to treat inflammation/fibrosis, albeit at different dosages for the different effects.
Cyclosporine is also a viable anti-inflammatory treatment option in diabetic dogs, but it is more expensive in medium to larger breeds. Azathioprine has been associated with causing pancreatitis in dogs, but this is a weak association. More importantly, it has not been shown that dogs with pre-existing idiopathic or dietary-induced pancreatitis are more likely to develop reactions to azathioprine. I have personally used azathioprine in dogs that have had previous bouts of pancreatitis with no adverse consequences, but always have warned the owner and monitored closely for side effects. When this drug works, it is much cheaper than cyclosporine and generally well tolerated. Other side effects include myelosuppression that needs to be monitored and the small risk of hepatotoxicity.
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McCord K, Morley PS, Armstrong J et al. A Multi‐Institutional Study Evaluating the Diagnostic Utility of the Spec cPL™ and SNAP® cPL™ in Clinical Acute Pancreatitis in 84 Dogs. Journal of Veterinary Internal Medicine. 2012; 26: 888-896