Feline pancreatitis (Proceedings)

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Feline pancreatitis (Proceedings)

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Aug 01, 2010

Disorders of the feline exocrine pancreas are common. Feline pancreatitis is classified as acute necrotizing, acute suppurative and chronic non-suppurative1. Acute pancreatitis is characterized by inflammation of the pancreas that is completely reversible upon removal of the underlying cause, while chronic pancreatitis is characterised by irreversible histological lesions such as fibrosis and atrophy2. Necrosis of pancreatic acinar cells and peripancretic fat with or without inflammation, hemorrhage, mineralization and fibrosis, describes acute necrotizing pancreatitis (ANP) 1. Acute suppurative pancreatitis differs in that neutrophilic inflammation is the predominant histologic lesion1. Chronic pancreatitis (CP) is characterized by lymphocytic inflammation, fibrosis and pancreatic acinar actrophy1. ANP and CP are most common, are clinically indistinguishable in the absence of a pancreatic biopsy1 and will be the focus of this discussion.

Pathogenesis and Etiology

Digestive enzymes are stored within pancreatic acinar cells as inactive enzyme precursors or zymogens (e.g. trypsinogen). After release into the intestinal lumen, trypsinogen is cleaved by enterokinase (secreted by duodenal mucosal cells) to its active form trypsin. In turn, trypsin activates other zymogens. Pancreatitis is characterized by inappropriate activation of zymogens within the pancreatic parenchyma2,3. In most patients this is due to fusion of lysosomal and zymogen granules within the pancreas, conversion of trypsinogen to trypsin and subsequent intra-pancreatic activation of other zymogens2,3. Unlike dogs, the feline pancreatic duct and common bile duct merge before emptying into the duodenum at the common bile duct, predisposing cats to pancreatic inflammation secondary to reflux of intestinal or biliary contents. Following zymogen activation, free radical–associated damage and pancreatic edema due to increased capillary permeability occur. Pancreatic inflammation extends locally to the stomach, duodenum, colon and potentially the adjacent hepatic parenchyma. Enzyme leakage into the bloodstream can overwhelm circulating antiproteases and potentially lead to hypotension, shock, disseminated intravascular coagulopathy (DIC), multiple organ failure and death2,3. It has been speculated that ANP and CP may have similar etiologies and pathogenesis and could represent a continuum of disease1. Accepted etiologies of feline ANP include biliary tract disease (most notably suppurative cholangitis), inflammatory bowel disease, pancreatic ischemia (e.g. hypotension, consequence of severe inflammation and edema, etc.), pancreatic duct obstruction (e.g. neoplasia, pancreatic fluke, duodenal foreign body, etc.), blunt abdominal trauma, infection (e.g. Toxoplasma gondii), organophosphate toxicosis and lipodystrophy1. There is currently insufficient evidence to consider hypercalcemia, drug reactions, high fat diet or obesity as risk factors for development of feline pancreatitis1. In many cases, no specific pre-disposing factor or inciting cause is identified. However, concurrent hepatobiliary or intestinal tract disease is common.