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Today's Ve T erinary Prac T ice | s eptember/ o ctober 2016 | tvpjournal.com a c ase of c anine a cu T e Pancrea T i T is Peer r eviewed 56 coagulation factors on days 1, 5, and 6. Clopidogrel (18.75 mg PO Q 24 H) was administered to inhibit platelet activity. Additional Supportive Care On day 7 of hospitalization, all IV fluids and medications were discontinued and Sidney was discharged on oral medications, including tramadol (25 mg PO Q 8 H), clopidogrel (18.75 mg PO Q 48 H), and maropitant (24 mg PO Q 24 H). In an attempt to prevent a recurrent episode of acute pancreatitis, an ultra low fat diet was recommended and any treats with high fat content were discouraged. FOLLOW-UP Sidney was discharged after 7 days of hospitalization and was presented for a recheck 3 days after discharge. Sidney's owners reported that she had a good appetite, and there were no signs of abdominal pain. No vomiting or diarrhea was identified. PROGNOSIS The prognosis for dogs with acute pancreatitis varies and largely depends on disease severity. There is no universally accepted severity score for pancreatitis that allows prediction of prognosis available in veterinary medicine. In general, systemic complications can indicate severe pancreatitis and a poor prognosis. 1 A recent study 2 suggested that serum paraoxonase 1 activity, combined with triglyceride and C-reactive protein concentrations, can help evaluate disease severity, but further studies are warranted. In Sidney's case, prognosis was poor to guarded when she was hospitalized, but upgraded to fair to good upon discharge. However, long-term follow-up was not achieved. ACUTE PANCREATITIS: DIAGNOSTICS Even with the advanced diagnostic modalities currently available, accurate diagnosis of acute pancreatitis is still challenging. Practically, acute pancreatitis in dogs is usually diagnosed with a combination of history, clinical signs, abnormally high serum cPLI concentration (as measured by Spec cPL), and abdominal ultrasonographic images consistent with pancreatitis. Concurrently, other intra-abdominal diseases that could cause similar clinical signs are excluded by assessment of laboratory test results, survey abdominal radiographs, and abdominal ultrasonography. Pancreatic Lipase Immunoreactivity Measurement of serum cPLI concentration is considered highly sensitive and specific for pancreatitis. The SNAP test provides semiquantitative estimation of cPLI concentration. A negative result rules out pancreatitis with high likelihood, whereas a positive result is consistent with pancreatitis and may require follow-up with the Spec cPL test. 6,7 Update on Pathophysiology of Pancreatitis The exact mechanism of development of naturally occurring acute pancreatitis in dogs is still poorly understood. It has been postulated that pancreatitis develops as a result of autodigestion and severe inflammation caused by inappropriate premature activation and secretion of proteases (especially trypsinogen to trypsin) within pancreatic acinar cells. Pancreatitis and subsequent peripancreatic fat necrosis can cause focal or generalized peritonitis, and most pancreatitis cases in dogs are sterile. Several protective mechanisms exist to prevent pancreatic autodigestion, including: ` Concurrent secretion of pancreatic secretory trypsin inhibitor (PSTI, also known as SPINK 1) with trypsinogen secretion ` Unidirectional flow of pancreatic juice in the pancreatic duct ` Plasma protease inhibitors (alpha1-proteinase inhibitor and alpha2-macroglobulin). Studies in human medicine 3,4 suggest that a compensatory anti-inflammatory response plays an important role in limiting progression of inflammation locally by upregulating anti- inflammatory cytokines, such as IL-10 or IL-11, but no study has been performed to confirm this in dogs. When these protective mechanisms fail to prevent damage to pancreatic acinar cells, severe inflammation is caused by secreted proinflammatory cytokines from neutrophils and macrophages. A sterile inflammatory peritoneal effusion can occur due to localized peritonitis and the coagulation cascade can be activated, resulting in DIC. Lungs, kidneys, and livers are especially vulnerable to damage, causing multiple organ failure due to extensive distribution of capillary vessels. In human medicine, multi-organ failure is recognized as having more important relation to mortality in acute pancreatitis than severity of the disease itself 3,5 even though no data is available for dogs.