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Diagnosis of Canine Pancreatitis
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Despite the fact that pancreatitis is a disease commonly encountered in first opinion practice, diagnosis can be far from straightforward, as Iwan Burgener describes in a paper that focuses on the pros and cons of the diagnostic options available.
Iwan A. Burgener
Prof. DVM, PhD, Dr. habil, Dip. ACVIM, Dip. ECVIM-CA.
Professor Burgener received his veterinary degree from the University of Bern, Switzerland in 1996. His career since then included various academic posts at the universities of Baton Rouge (USA), Bern, Leipzig and Utrecht before he moved to his current position as Professor and Chair of Small Animal Internal Medicine at Vienna, where he is also Head of the Small Animal Clinic. His research interests center around gastroenterology topics, and he has published over 60 articles in peer-reviewed publications, as well as being an ad hoc reviewer for more than 30 different scientific journals.
Key Points:
- Canine pancreatitis is a commonly encountered disease, but the pathophysiology is poorly understood, and the etiology remains unknown in most cases.
- Diagnosing pancreatitis remains a challenge for the clinician, due to a variety of factors; histology is still considered the gold standard for definitive diagnosis, but is rarely used.
Introduction
The synthesis and storage of digestive enzymes in the pancreas carries the risk of self-digestion and subsequent inflammation, i.e., pancreatitis. Strictly speaking, the term pancreatitis refers to inflammation (i.e., infiltration with inflammatory cells) of the exocrine pancreas, but it is also commonly expanded to include diseases of the exocrine pancreas characterized mainly by necrosis (necrotizing pancreatitis) or irreversible structural changes such as fibrosis (chronic pancreatitis), sometimes with only a minimal inflammatory component ( 1 ).
The exocrine pancreas has several mechanisms to prevent self-digestion (e.g., enzyme precursors, storage of enzymes in granules separated from lysosomes, localized high pH levels, good blood supply, etc.). Only if all these protective mechanisms are breached at the same time will pancreatitis develop. The disease itself proceeds in two stages. In the first stage, trypsin (activated from trypsinogen) is released, which in turn activates other digestive enzymes, leading to local changes such as edema, hemorrhage, infiltration with inflammatory cells, and necrosis of acinar cells and peripancreatic fat. In the second stage, the actual inflammatory process advances with recruitment of inflammatory cells and release of cytokines, which can lead to systemic organ disorders and ultimately death.
Pancreatitis is classified into acute (AP) and chronic forms (CP), depending on whether permanent histopathologic changes are absent (AP) or present (CP). Histologically, AP consists of neutrophilic inflammation associated with interstitial edema and necrosis of mesenteric fat (Figure 1). In CP, fibrosis is more prominent than inflammatory changes, with cystic degeneration of the tissue gradually increasing as the fibrosis increases. [...]
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