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Acute pancreatitis in canine patients

02 May 2020
11 mins read
Volume 11 · Issue 4
Figure 1. A patient undergoing a physical examination prior to ultrasound imaging.

Abstract

Canine acute pancreatitis (AP) is now commonly seen in veterinary practice. AP can be challenging to manage and patients may require intensive nursing care. This article aims to explain the pathophysiology of the disease, some of the common clinical findings, diagnostic testing available and treatment required by these patients. It will focus on the specific nursing care: analgesia and nutrition. The use of early enteral nutrition (EN) is now a well-established treatment method in human medicine for patients with pancreatitis, and should be considered in veterinary patients also. The benefits of EN over parenteral nutrition (PN) and suggested routes of administration will be discussed.

The pancreas is a lobulated organ that sits within the cranial abdomen, consisting of left and right lobes connected by a central body of tissue (Spielman, 2015). The pancreas is responsible for both endocrine (where substances are secreted directly into the bloodstream) and exocrine (where substances are secreted into a duct) functions. Endocrine functions of the pancreas involve islets of Langerhans cells which synthesise and release the hormones insulin and glucagon, involved in the regulation of blood sugar (Steiner, 2020). Surrounding these islet cells, and responsible for the exocrine function of the pancreas, are the acinar cells, which synthesise and secrete enzymes and zymogens involved in the digestion of food. Epithelial cells of the pancreatic ductules produce bicarbonate which acts as a buffer to the gastric acid in the duodenum (Gordon, 2011).

Pancreatitis is described as the most common exocrine disease affecting both canines and felines (Steiner, 2020). Premature activation of digestive enzymes results in pancreatic autodigestion, leading to pancreatitis. During episodes of pancreatitis, an apical block (secretory block) occurs, allowing zymogen and lysosomal granules to become co-localised within the acinar cell. The lysosomal protease cathepsin B activates trypsinogen, released from the zymogen granules, to trypsin. Production of trypsin continues until eventually the pancreatic secretory trypsin inhibitor (PSTI) is overwhelmed, at which point pancreatitis develops as the pancreatic digestive enzymes become activated within the acinar cell. In a normally functioning pancreas, both trypsinogen and cathepsin B would be released directly into the pancreatic duct (Mansfield, 2012).

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