Definitions

Pancreatitis in dogs shows a spectrum of disease from mild, subclinical to acute, necrotising and fatal. Pancreatitis is classified based on histopathological appearance. There is no ‘gold standard’ for histological description of pancreatitis in animals (unlike the liver). The author favours the definitions in human medicine, which define pancreatitis as ‘acute’ or ‘chronic’ based on its histological appearance and not how it appears clinically. These definitions are summarized in Table 1 below. Chronic pancreatitis (CP) is defined as ‘a continuing inflammatory disease characterized by the destruction of pancreatic parenchyma leading to progressive or permanent impairment of exocrine or endocrine function or both. The gold standard for diagnosis is histology, but this is rarely indicated or performed in dogs (or humans). Noninvasive diagnosis is difficult with the currently available diagnostic imaging, and blood tests have a lower sensitivity than for acute disease, which may explain why its prevalence is often underestimated.

Table 1. Proposed histopathological and functional definitions of acute and chronic pancreatitis in dogs based on human definitions

Histopathological descriptions are useful to understand the pathology and progression of the disease but are not very useful clinically, as most cases do not have a pancreatic biopsy performed and either chronic or acute pancreatitis episodes may be mild or severe, and either may be recurrent. However, recognizing the potential for underlying chronic disease in an animal that presents acutely is very important for long-term management, because it allows the clinician to realize that the dog may develop EPI or DM in the future, and to recognize and treat these appropriately.

Causes of Chronic Pancreatitis

The cause of CP in dogs is usually unknown. Any age or breed of dog can be affected, but the most typical signalment is a middle-aged to old dog, particularly a Cavalier King Charles Spaniel (CKCS), Cocker Spaniel, Collie, or Boxers in the UK. An independent large study of EPI in the UK found an increased prevalence in older CKCS, supporting this breed association. Some cases may represent chronic relapsing cases of acute disease, but many cases are truly ‘chronic’ from the outset, with an initial mononuclear infiltrate.

Autoimmune Chronic Pancreatitis in the English Cocker Spaniel

The particular form of chronic pancreatitis recognized in English Cocker Spaniels in the UK is thought to be an autoimmune. As in human autoimmune pancreatitis, it typically affects middle-aged to older dogs, with a higher prevalence in males, and at least 50% of affected dogs subsequently develop DM, EPI or both. Dogs also often have other concurrent autoimmune disease, particularly keratoconjunctivitis sicca and glomerulonephritis. There is often a mass-like lesion on ultrasound, and biopsies show a typical perilobular, diffuse fibrotic and lymphocytic disease centered on perilobular ducts and vessels, with loss of large ducts and hyperplasia of smaller ducts. Immunohistochemistry shows a preponderance of duct and vein-centered CD3+ lymphocytes (i.e., T-cells).

Recent work in humans has identified a strong association with plasma cells that secrete one subgroup of immunoglobulin G, IgG4. The disease in humans has been redefined as multisystemic because of the frequent involvement of other organs. It is now defined as IgG4-positive sclerosing disease, and concurrent keratoconjunctivitis sicca, sialoadenitis, biliary tract disease, and glomerulonephritis are common. Early work in English Cocker Spaniels also shows IgG4-positive plasma cells in the pancreas and kidney (Watson et al. 2012) and also demonstrated an association with a particular DLA (dog leukocyte antigen) in ECS, supporting the theory of autoimmunity (Bazelle et al. 2013). The disease in humans responds well to steroid therapy, including a reduction in insulin requirements in some diabetics. There are not yet any controlled trials evaluating the use of immunosuppressive drugs in English Cocker Spaniels with chronic pancreatitis, but there is now enough circumstantial evidence to justify their use in this particular breed. However, the clinician should note that this is very breed-specific; terriers in Britain, for example, have a different histopathologic and clinical picture of disease that does not appear to be autoimmune. The use of steroids in terriers with chronic pancreatitis is not recommended.

Clinical Signs

The clinical signs of pancreatitis obviously vary with the severity of the disease. It is only the severe, acute cases in dogs which show the classical signs of acute vomiting, cranial abdominal pain +/- “praying” stance. Concurrent colitis with the passage of small amounts of faeces with fresh blood is common due to local peritonitis affecting the transverse colon as it courses close to the left limb of the pancreas. Severe cases may present collapsed and dehydrated with signs of shock, and, in very severe cases, there may be renal shutdown, respiratory distress and DIC.

At the other end of the spectrum, low-grade acute or chronic cases may show few clinical signs: most commonly, anorexia with or without mild bouts of colitis and occasional vomiting, increased borborygmi and no or mild abdominal pain. Dogs with CP, regardless of the cause, most commonly present with mild intermittent gastrointestinal signs. Typically they have bouts of anorexia, occasional vomiting, mild hematochezia, and obvious postprandial pain, which often goes on for months to years without presentation to a veterinarian. The trigger for finally seeking veterinary attention is often an acute-on-chronic bout or the development of DM or EPI. Dogs may become more playful and less picky with their food when they are switched to a low-fat diet, suggesting they previously had postprandial pain. Chronic epigastric pain is a hallmark of the human disease and is sometimes severe enough to lead to opiate addiction or surgery, so it should not be overlooked or underestimated in small animal patients. In more severe, acute-on-chronic cases, the dogs are clinically indistinguishable from those with classical acute pancreatitis (see above) with severe vomiting, dehydration, shock, and potential multi-organ failure. There is a tendency for the first clinically severe bout to come at the end of a long (often years) subclinical phase of quietly progressive and extensive pancreatic destruction in dogs. It is very important for clinicians to be aware of this, as these dogs are at much higher risk of developing exocrine and/or endocrine dysfunction than those with truly acute pancreatitis; in addition, they usually already have protein-calorie malnutrition at presentation, which makes their management even more challenging. In some dogs, there are no obvious clinical signs until the development of EPI, DM or both. The development of EPI in a middle-aged to older dog of a breed not typical for pancreatic acinar atrophy has to increase the index of suspicion for underlying CP. The development of EPI or DM in a dog or cat with CP requires the loss of approximately 90% of exocrine or endocrine tissue function, respectively, implying considerable tissue destruction and ‘end-stage’ disease.