{"id":19809,"date":"2019-12-19T15:01:30","date_gmt":"2019-12-19T15:01:30","guid":{"rendered":"https:\/\/todaysveterinarypractice.com\/?p=19809"},"modified":"2023-03-10T18:38:19","modified_gmt":"2023-03-10T18:38:19","slug":"diagnosing-acute-pancreatitis-in-dogs","status":"publish","type":"post","link":"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/hepatology\/diagnosing-acute-pancreatitis-in-dogs\/","title":{"rendered":"Diagnosing Acute Pancreatitis in Dogs"},"content":{"rendered":"

Pancreatitis in dogs is a significant illness and is considered to be the most common disease of the exocrine pancreas, although the exact prevalence is unknown.1-11<\/sup> A recent study evaluating dogs that had been necropsied found that 8% showed macroscopic evidence of pancreatitis and approximately 37% had microscopic lesions suggestive of either acute or chronic pancreatitis.12<\/sup><\/span><\/p>\n

The pancreas, a tubuloalveolar gland situated in the right cranial quadrant caudal to the stomach, is composed of two separate tissues, referred to as the exocrine and endocrine pancreata.1<\/sup> The exocrine pancreas, which comprises about 98% of the pancreatic mass, secretes zymogens (inactive pancreatic enzymes) and active enzymes that enable the digestion of carbohydrates, proteins, and triglycerides.<\/span><\/p>\n

Despite raised awareness of, increased knowledge about, and new diagnostic tests for pancreatitis, the mortality rate in dogs is high, ranging from 27% to 58%.2,5,8,10,13,14<\/sup> These rates are possibly overestimated, as they are based on study populations from referral institutions. Referred animals often have systemic effects associated with severe, complicated pancreatitis that requires intensive treatment and hospitalization rather than mild, self-limiting disease.4,13<\/sup><\/span><\/p>\n

The diagnosis of acute pancreatitis can be difficult because clinical signs and results of diagnostic testing are often nonspecific. This article addresses the diagnostic approach to patients with signs suggestive of pancreatitis; treatment of pancreatitis is addressed here<\/a>. <\/span><\/p>\n

Pathophysiology of Pancreatitis in Dogs<\/h2>\n

The underlying pathophysiology of acute pancreatitis is incompletely understood, with current understanding extrapolated from human and experimental models.1-3,15<\/sup> The pathogenesis is complex, involving multiple inflammatory pathways.15<\/sup> Regardless of the inciting cause, it is accepted that acute pancreatitis is initiated through dysregulated, uncontrolled activation of pancreatic proteolytic enzymes within acinar cells and the overwhelming of safeguards within the acinar cells and the systemic circulation.1,3,4,15-18<\/sup> Initially, this results in excessive activation of trypsin, which then results in further activation of all zymogens within pancreatic tissue.3,15,18,19<\/sup><\/span><\/p>\n

If more than 10% of acinar trypsin is activated and plasma protease inhibitors are depleted, pancreatic safeguards (i.e., pancreatic secretory trypsin inhibitor) are overwhelmed.3,15,18,19<\/sup> Release of the pancreatic <\/span>enzymes into the pancreatic tissue results in neutrophilic inflammation of the pancreatic and peripancreatic fat. <\/span>A complex and interdependent \u201ccytokine storm\u201d ensues, leading to production of reactive oxygen species, nitric oxide, and cytokines, as well as activation of other pathways (complement, kinin-kallikrein, and renin-angiotensin systems), which further perpetuates the local inflammatory reaction.3<\/sup> The end result is digestive enzyme damage not only to the acinar cell, but to the vascular endothelium, producing microcirculatory changes, vasoconstriction, capillary stasis, progressive ischemia, and edema of the pancreas.3,18<\/sup> Generated inflammatory free radicals and inflammatory cytokines may be released into the circulation, which may lead to organ failure (e.g., acute respiratory distress syndrome and acute kidney injury).20,21<\/sup><\/span><\/p>\n

Clinical Signs of Pancreatitis in Dogs<\/h2>\n

Acute pancreatitis is reversible unless the initial trigger persists or there is chronic recurrent inflammation.3,5,16,19<\/sup> In veterinary medicine, the pathologic description depends on histologic descriptions, with different forms of pancreatitis (e.g., acute necrotizing, acute, chronic) overlapping in clinical presentation.3,16<\/sup> <\/span><\/p>\n

No single clinical sign or combination of clinical signs is pathognomonic for pancreatitis.2,10,16<\/sup> Clinical signs are nonspecific and rely on the degree and severity of local pancreatic inflammation as well as the existence of concurrent systemic complications (<\/span>BOX 1<\/b><\/span>).2,3,19<\/sup><\/span><\/p>\n

BOX 1 Common Clinical Findings in Dogs With Acute Pancreatitis6,9,22\u201325<\/sup><\/div>
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