Canine pancreatitis

Pancreatitis in dogs is a common and debilitating disease that may be acute or chronic in nature; Craig Datz and Melinda Wood review various aspects of the condition, including the etiology, the preferred diagnostic tests, and the options for treatment.

Craig Datz
DVM, MS, Dipl. ABVP, Dipl. ACVN

Melinda A. Wood
DVM, MS, Dipl. ACVIM

Introduction

Canine pancreatitis is an inflammatory disease of the pancreas that may be acute or chronic in nature. In acute cases, there are no permanent changes to the pancreas, whereas fibrosis and atrophy of the pancreas develop in the chronic scenario (1). Despite recent advances in available analytical tests, establishing a diagnosis can be challenging.

The cause for pancreatitis in an individual dog is typically idiopathic, but several risk factors have been suggested, including dietary indiscretion, obesity, and endocrine diseases such as diabetes mellitus, hyperadrenocorticism, and hypothyroidism and hypertriglyceridemia (2-5). Numerous drugs have been implicated as possible causes of pancreatitis, including potassium bromide, phenobarbital, thiazide diuretics and furosemide, L-asparaginase, azathioprine and organophosphates (3,6,7), and babesiosis has also been reported to be a causative agent (7).

Several studies have shown Miniature Schnauzers and Yorkshire Terriers to be at increased risk for developing acute pancreatitis (2-4). A study of chronic pancreatitis in US dogs demonstrated an increased prevalence in toy and non-sporting breeds (8), but a UK study on the same condition reported an increased risk in Cavalier King Charles Spaniels, English Cocker Spaniels, Boxers and Collies (9). 

Pathophysiology

Under normal conditions, several mechanisms protect the pancreas from autodigestion by digestive enzymes. Proteolytic enzymes synthesized within the pancreas are stored as inactive zymogens and are activated only once they have entered the duodenum. Pancreatic acinar cells synthesize and secrete pancreatic secretory trypsin inhibitor, and plasma contains several anti-proteases which both limit intra-pancreatic proenzyme activation and inactivate proteolytic enzymes if they have been released into the circulation (7) (10).

Pancreatitis develops because of premature activation of trypsinogen to trypsin within the acinar cells of the pancreas, leading to pancreatic cell destruction. Trypsin activation triggers activation of all other pancreatic zymogens, causing pancreatic autodigestion, inflammation and necrosis, as well as a systemic inflammatory reaction. In some cases, the effects can be severe and lead to multiorgan failure (7) (10). [...]