ACVIM consensus statement on pancreatitis in cats

Abstract

Background: Pancreatitis in cats, although commonly diagnosed, still presents many diagnostic and management challenges.

Objective: To summarize the current literature as it relates to etiology, pathogenesis, diagnosis, and management of pancreatitis in cats and to arrive at clinically relevant suggestions for veterinary clinicians that are based on evidence, and where such evidence is lacking, based on consensus of experts in the field.

Animals: None.

Methods: A panel of 8 experts in the field (5 internists, 1 radiologist, 1 clinical pathologist, and 1 anatomic pathologist), with support from a librarian, was formed to assess and summarize evidence in the peer reviewed literature and complement it with consensus clinical recommendations.

Results: There was little literature on the etiology and pathogenesis of spontaneous pancreatitis in cats, but there was much in the literature about the disease in humans, along with some experimental evidence in cats and nonfeline species. Most evidence was in the area of diagnosis of pancreatitis in cats, which was summarized carefully. In contrast, there was little evidence on the management of pancreatitis in cats.

Conclusions and clinical importance: Pancreatitis is amenable to antemortem diagnosis by integrating all clinical and diagnostic information available, and recognizing that acute pancreatitis is far easier to diagnose than chronic pancreatitis. Although both forms of pancreatitis can be managed successfully in many cats, management measures are far less clearly defined for chronic pancreatitis.

Keywords: cat; diagnosis; etiology; gastroenterology; management; pancreas; pancreatitis; pathophysiology.

FIGURE 1

Mechanisms that protect the pancreas from premature activation of zymogens (panel A). Events that can lead to acute pancreatitis due to premature activation of trypsinogen (panel B)

FIGURE 2

Local and systemic inflammation ensues in acute pancreatitis, which is independent of trypsin activation, but dependent on ongoing stimulation of the NFκB pathway

FIGURE 3

The pathophysiological mechanisms relevant for chronic pancreatitis that occur independently of trypsin activation and acute pancreatitis

FIGURE 4

Sagittal plane abdominal ultrasound image of the left pancreatic limb in a cat with acute pancreatitis performed with an 8.5 MHz curved array transducer. The left limb of the pancreas is enlarged (1.65 cm), diffusely hypoechoic, and surrounded by a halo of hyperechoic mesentery

FIGURE 5

Sagittal plane abdominal ultrasound image using an 8.5 MHz curved array transducer of the left pancreatic limb of a cat with chronic pancreatitis. The pancreas is mildly enlarged at 1.5 cm (X‐X). The pancreatic parenchyma is diffusely heterogenous and has a mottled echotexture. The surrounding mesentery is unremarkable

FIGURE 6

Pancreatic aspirate from a cat. Modified Wright's stain. 50× magnification. There is a cluster of acinar cells (arrow) surrounded by erythrocytes and many nondegenerate neutrophils (arrowheads), consistent with suppurative pancreatic inflammation

FIGURE 7

Histopathologic image of acute pancreatitis in a cat showing fat necrosis (star) and focal suppurative infiltration (arrow) with early focal acinar‐to‐ductal metaplasia (arrowhead). Scale bar = 100 μm

FIGURE 8

Histopathologic image of chronic pancreatitis in a cat, showing moderate lymphocytic infiltration (star), interlobular and intralobular fibrosis (arrows), and acinar‐to‐ductal metaplasia (arrowheads). Scale bar = 100 μm

FIGURE 9

Nasoesophageal (A) and esophagostomy (B) tubes are the most practical tubes for alimentary support of cats with acute pancreatitis