Abstract:BackgroundAcute pancreatitis (AP) is common in dogs. Nevertheless, validated clinical severity index (CSI) scoring systems to assess severity and guide treatment in current, large-scale studies are unavailable.MethodsThis is a retrospective study including 109 dogs. Pancreatitis was diagnosed based on clinical signs, abdominal sonographic evidence, positive pancreatic lipase assays and experts’ assessment consensus.ResultsThe survival rate was 75 per cent (82 dogs). Azotaemia and presence of local complication… Show more
“…Indeed, several results that were borderline significant (ie, higher cPLI concentrations in nonsurvivors) might become significant in larger studies. Nevertheless, several present findings (eg, lack of association between cytokine concentrations and death, associations of ATA and CAPS score with death) are consistent with previous results, 25,32,33 strengthening our conclusions. Second, the dynamic nature of inflammation in naturally occurring AP largely depends on the duration of clinical signs, as evident in differences between early and late presentations.…”
Section: Discussionsupporting
confidence: 92%
“…4,5,11,31,32 The latter include SIRS and MODS, and their manifestations contribute to the CSI scores, which have been associated with the prognosis of AP in both humans and dogs. 4,5,11,[31][32][33] In our study, concentrations of pancreatic lipase (cPLI and DGGR lipase) and inflammatory cytokines did not differ between survivors and nonsurvivors of AP. The former finding is in disagreement with previous studies of AP in dogs, in which markedly increased cPLI concentrations 39 or serum lipase activities 40 were more frequent in nonsurvivors.…”
Section: Discussionmentioning
confidence: 39%
“…Local abdominal complications included peripancreatic or diffuse effusion, cholestasis, and intestinal ileus 31,33 . Systemic complications included: (1) acute kidney injury (AKI), diagnosed based on the International Renal Interest Society grading system 34 ; (2) disseminated intravascular coagulation (DIC), defined as presence of anomalies in each of the following categories: coagulation factor and platelet consumption (≥2 of the following: thrombocytopenia [platelet count, <143 × 10 9 /L], prolonged aPTT [aPTT, >20 s; RI, 17.4‐11.0 s] and PT [PT, >10 s; RI, 8.4‐6.0 s]), coagulation factor inhibitor consumption (hypoantithrombinemia [ATA <87%; RI, 87‐140%]) and increased fibrinolysis (D‐D concentration > 500 ng/mL; RI, <250 ng/mL) 35 ; (3) Hypercoagulability (suspected when PT, aPTT and platelet count were all within RI, while D‐D concentration was increased, or with presence of clinical or imaging evidence of thrombosis [ie, absent femoral pulse in absence of hypotension, Doppler‐ultrasonography evidence of a thrombus interrupting blood flow]) 36 ; and (4) SIRS diagnosed based on criteria used in the CAPS scoring system 32 (Appendix S1).…”
Section: Methodsmentioning
confidence: 99%
“…Clinical disease severity scores were assigned to each dog with AP using 3 previously published canine AP clinical scoring indexes (CSIs), 31,32 including a recently validated organ score CSI, 31,33 the canine acute pancreatitis severity (CAPS) and the simplified CAPS (sCAPS 32 ; Appendix S1).…”
Section: Clinical Scoring Indexes For Ap and Ap-associated Local Anmentioning
confidence: 99%
“…Local abdominal complications included peripancreatic or diffuse effusion, cholestasis, and intestinal ileus. 31,33 .…”
Section: Clinical Scoring Indexes For Ap and Ap-associated Local Anmentioning
Background: Acute pancreatitis (AP) presumably is associated with pancreatic protease activation, protease inhibitor (PI) depletion, and inflammatory mediator secretion. Objectives: Examine PIs and inflammatory mediator concentrations in dogs with AP and their association with death. Animals: Thirty-one dogs diagnosed with AP based on clinical signs, ultrasonographic findings, and increased canine pancreatic lipase immunoreactivity (cPLI) and 51 healthy control dogs. Methods: Antithrombin and α 2-antiplasmin activity (ATA and α 2 AP, respectively) and concentrations of α 1-proteinase inhibitor (α 1 PI), α 2-macroglobulin (α 2 MG), C-reactive protein (CRP), interleukins (ILs)-2,6,8 and tumor necrosis factor-α (TNF-α) were prospectively measured. Severity of AP was assessed by clinical severity scoring systems. Results: Mortality rate was 19%. Antithrombin activity was lower (P = .004) and maximal CRP, IL-6, and TNF-α concentrations higher (P < .04) in the AP group compared to the controls, whereas IL-2, IL-8, α 1 PI, and α 2 AP concentrations did not differ between groups. Serum α 2 MG concentration was not reliably detected. Serum cPLI, CRP, and IL-6 concentrations were significantly and positively correlated. The ATA was lower (P = .04), and canine acute pancreatitis severity (CAPS) scores higher
“…Indeed, several results that were borderline significant (ie, higher cPLI concentrations in nonsurvivors) might become significant in larger studies. Nevertheless, several present findings (eg, lack of association between cytokine concentrations and death, associations of ATA and CAPS score with death) are consistent with previous results, 25,32,33 strengthening our conclusions. Second, the dynamic nature of inflammation in naturally occurring AP largely depends on the duration of clinical signs, as evident in differences between early and late presentations.…”
Section: Discussionsupporting
confidence: 92%
“…4,5,11,31,32 The latter include SIRS and MODS, and their manifestations contribute to the CSI scores, which have been associated with the prognosis of AP in both humans and dogs. 4,5,11,[31][32][33] In our study, concentrations of pancreatic lipase (cPLI and DGGR lipase) and inflammatory cytokines did not differ between survivors and nonsurvivors of AP. The former finding is in disagreement with previous studies of AP in dogs, in which markedly increased cPLI concentrations 39 or serum lipase activities 40 were more frequent in nonsurvivors.…”
Section: Discussionmentioning
confidence: 39%
“…Local abdominal complications included peripancreatic or diffuse effusion, cholestasis, and intestinal ileus 31,33 . Systemic complications included: (1) acute kidney injury (AKI), diagnosed based on the International Renal Interest Society grading system 34 ; (2) disseminated intravascular coagulation (DIC), defined as presence of anomalies in each of the following categories: coagulation factor and platelet consumption (≥2 of the following: thrombocytopenia [platelet count, <143 × 10 9 /L], prolonged aPTT [aPTT, >20 s; RI, 17.4‐11.0 s] and PT [PT, >10 s; RI, 8.4‐6.0 s]), coagulation factor inhibitor consumption (hypoantithrombinemia [ATA <87%; RI, 87‐140%]) and increased fibrinolysis (D‐D concentration > 500 ng/mL; RI, <250 ng/mL) 35 ; (3) Hypercoagulability (suspected when PT, aPTT and platelet count were all within RI, while D‐D concentration was increased, or with presence of clinical or imaging evidence of thrombosis [ie, absent femoral pulse in absence of hypotension, Doppler‐ultrasonography evidence of a thrombus interrupting blood flow]) 36 ; and (4) SIRS diagnosed based on criteria used in the CAPS scoring system 32 (Appendix S1).…”
Section: Methodsmentioning
confidence: 99%
“…Clinical disease severity scores were assigned to each dog with AP using 3 previously published canine AP clinical scoring indexes (CSIs), 31,32 including a recently validated organ score CSI, 31,33 the canine acute pancreatitis severity (CAPS) and the simplified CAPS (sCAPS 32 ; Appendix S1).…”
Section: Clinical Scoring Indexes For Ap and Ap-associated Local Anmentioning
confidence: 99%
“…Local abdominal complications included peripancreatic or diffuse effusion, cholestasis, and intestinal ileus. 31,33 .…”
Section: Clinical Scoring Indexes For Ap and Ap-associated Local Anmentioning
Background: Acute pancreatitis (AP) presumably is associated with pancreatic protease activation, protease inhibitor (PI) depletion, and inflammatory mediator secretion. Objectives: Examine PIs and inflammatory mediator concentrations in dogs with AP and their association with death. Animals: Thirty-one dogs diagnosed with AP based on clinical signs, ultrasonographic findings, and increased canine pancreatic lipase immunoreactivity (cPLI) and 51 healthy control dogs. Methods: Antithrombin and α 2-antiplasmin activity (ATA and α 2 AP, respectively) and concentrations of α 1-proteinase inhibitor (α 1 PI), α 2-macroglobulin (α 2 MG), C-reactive protein (CRP), interleukins (ILs)-2,6,8 and tumor necrosis factor-α (TNF-α) were prospectively measured. Severity of AP was assessed by clinical severity scoring systems. Results: Mortality rate was 19%. Antithrombin activity was lower (P = .004) and maximal CRP, IL-6, and TNF-α concentrations higher (P < .04) in the AP group compared to the controls, whereas IL-2, IL-8, α 1 PI, and α 2 AP concentrations did not differ between groups. Serum α 2 MG concentration was not reliably detected. Serum cPLI, CRP, and IL-6 concentrations were significantly and positively correlated. The ATA was lower (P = .04), and canine acute pancreatitis severity (CAPS) scores higher
Background
Ultrasonographic gastrointestinal wall changes in dogs with acute pancreatitis (AP) are not well characterized in the literature. No detailed studies have described their prevalence, characteristics, distribution, or clinical relevance.
Hypothesis/Objectives
Describe the prevalence of ultrasonographic gastrointestinal wall changes in a population of dogs with AP and evaluate for associations between the presence of gastrointestinal wall changes and clinical or clinicopathological variables.
Animals
Referral population of 66 client‐owned dogs with AP.
Methods
Retrospective search of clinical records to identify dogs with AP. Clinical variables, clinicopathological variables and ultrasonographic findings were reported using descriptive statistics. A binary logistic regression model was used to evaluate for associations between the presence of gastrointestinal wall changes and clinical or clinicopathological variables.
Results
Sixty‐six dogs were included. Forty‐seven percent of dogs (95% confidence interval [CI], 35.0%‐59.0%; n = 31) with AP had ultrasonographic gastrointestinal wall changes. Gastrointestinal wall changes were most common in the duodenum and identified in 71% (n = 22) of affected dogs. Of dogs with gastrointestinal wall changes, 74.2% (n = 23) had wall thickening, 61.3% (n = 19) had abnormal wall layering, and 35.5% (n = 11) had wall corrugation. In the multivariable model, only heart rate remained an independent predictor of ultrasonographic gastrointestinal wall changes (P = .02).
Conclusions and Clinical Importance
Ultrasonographic gastrointestinal wall changes in this population of dogs with AP were common. Increased heart rate was the only independent predictor of gastrointestinal wall changes, which might imply more severe disease. Additional studies are required to elucidate whether ultrasonographic gastrointestinal wall changes reflect disease severity in AP.
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