Diagnosis
Recent clinical studies in both dogs (Bostrom et al. 2013; Watson et al. 2007) and cats have confirmed CP as a clinically relevant disease, causing intermittent and/or on-going recurrent gastrointestinal signs and epigastric pain in a large number of affected animals.
The gastrointestinal signs of CP are typically low grade, waxing and waning anorexia and vomiting. Diarrhea is not a prominent feature until the development of exocrine pancreatic insufficiency (EPI) in the end stage of disease. However, animals with CP will often have large-bowel type diarrhea with some fresh blood a day or two after an episode, presumably due to irritation of the transverse colon as it passes close to the left limb of the pancreas.Some dogs with CP will present for the first time with an acute-on-chronic bout of pancreatitis, which looks clinically identical to classic acute pancreatitis, with sudden onset acute vomiting and severe abdominal pain. Some animals have recurrent acute flare-ups, often with no apparent trigger; others are presented during an acute exacerbation of disease with acute onset icterus due to extrahepatic biliary obstruction. Affected cats can also be icteric, although in cats this is more often due to concurrent cholangitis than to extrahepatic biliary obstruction.
Pain is a consistent and clinically important feature of CP. Chronic pancreatic pain is notoriously difficult to recognize and treat. Owners may be more aware of this pain than their veterinary surgeon, particularly in cats, which are very good at hiding pain in the consulting room. It is therefore very important for clinicians to be alert for signs of postprandial pain in the history and to work in partnership with owners for effective identification and treatment. The pain is not to be under-estimated: in humans, the pain of CP is often so severe that it leads to chronic opiate addiction or even total pancreatectomy.
Clinical signs suggestive of pain in dogs or cats with CP can include stretching or pacing around after eating; listlessness; discomfort when picked up, particularly around the abdomen; snappiness with owner and other animals when approached; and/or acquired food aversions particularly to high fat foods.Pain is particularly difficult to assess in cats but tends to present as similar behavior changes and a reduction in previous activity level. The pain of CP in humans can sometimes be referred to the lumbar spine, which has been described in dogs. However, some breeds affected with CP, such as the ECS, are also at increased risk of intervertebral disc disease so it is important to differentiate this from CP.
On clinical examination in dogs, the low- grade pain of CP is more difficult to recognize than the pain of acute disease. In the latter, palpation of any part of the abdomen usually elicits pain whereas with CP, the pain is only elicited over the pancreas. Dogs will usually show a pain response whereas cats rarely show pain on clinical examination even in the face of severe acute exacerbations of chronic disease.
Dogs and cats with CP may also show clinical signs consistent with chronic small intestinal maldigestion, with polyphagia, weight loss and dry coat. Some animals also have chronic steatorrhea with foul-smelling, voluminous feces although this does not appear to be a prominent feature in many animals developing EPI as an end stage of CP.
Confirmation of diagnosis of CP is challenging. Pancreatic histopathology is the most sensitive and specific test but pancreatic biopsies are not usually indicated because they are invasive and do not change the treatment. Diagnosis therefore has to rely on a combination of clinical signs, transcutaneous ultrasonography and pancreas specific blood tests such as lipase and canine- and felinespecific pancreatic lipase immunoreactivity. CP is therefore likely to be under-recognized because of the difficulty in obtaining a non- invasive diagnosis.
Affected animals also usually show clinicopathological evidence of a systemic inflammatory response often with neutrophilia and pre-renal azotemia. Some animals will show evidence of diabetes mel- litus. It is also important to measure serum trypsin-like immunoreactivity (TLI) and cobalamin in affected animals to assess for development of EPI. Cobalamin deficiency is common in dogs and cats with EPI because the pancreas is the only significant source of intrinsic factor, which is required for the absorption of cobalamin in the ileum. Dogs produce some intrinsic factor in their stomach, but the pancreas is the only source in cats. The sensitivity of a reduced TLI to diagnosis EPI in dogs and cats with CP is less than in dogs with pancreatic acinar atrophy. This is because ongoing pancreatic inflammation can increase the TLI back in to the normal range even in cases with clinically significant exocrine insufficiency.It is very important to undertake some form of diagnostic imaging in affected animals to rule out serious concurrent diseases such as gastrointestinal or biliary tract obstructions. It is not uncommon for pancreasspecific blood tests to be positive in animals with a concurrent more clinically significant disease such as gastrointestinal neoplasia or obstruction (Haworth et al. 2014).