Background: In noncardiac critical disease in humans, myocardial injury as detected by cardiac troponin I and T (cTnI and cTnT) has been linked to high intensive care unit (ICU) death independent of prognostic composite scoring.Hypothesis: Presence of myocardial injury predicts short-term death in critically ill dogs with systemic inflammation and provides additional prognostic information when combined with established canine prognostic composite scores.Animals: Forty-two dogs admitted to the ICU with evidence of systemic inflammation and no primary cardiac disease. Methods: Prospective cohort study. Blood samples were obtained at ICU admission for the measurement of cTnI and cTnT, C-reactive protein, and several cytokines. The acute patient physiologic and laboratory evaluation (APPLE) score and the survival prediction index were calculated within the first 24 hours of admission. Receiver operating characteristic (ROC) curves were used to examine the prognostic capacity of each biomarker and severity score. Multiple logistic regression analysis was performed to evaluate whether cardiac markers significantly contributed to severity scores.Results: Twenty-eight day case fatality rate was 26% (11/ Conclusions and Clinical Importance: Markers of myocardial injury predict short-term death in dogs with systemic inflammation and cTnI significantly contributes to the APPLE score.

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Results indicated that dexmedetomidine can be used successfully to induce emesis in cats.

BackgroundMyocardial injury, detected by cardiac troponin I and T (cTnI and cTnT), has been associated with long‐term death in the noncardiac human intensive care unit (ICU).HypothesisPresence of myocardial injury predicts 1‐year case fatality in critically ill dogs with systemic inflammation.AnimalsThirty‐eight dogs with evidence of systemic inflammation and no primary cardiac disease.MethodsProspective cohort study. In dogs admitted to the ICU with evidence of systemic inflammation, blood samples were obtained at ICU admission for measurement of cTnI and cTnT, and cTnI was measured once daily during ICU hospitalization. Receiver operating characteristic (ROC) curves were used to examine prognostic capacity of admission cTnI, admission cTnT, and peak cTnI concentrations.ResultsOne‐year case fatality rate was 47% (18/38 dogs). Admission cTnI concentrations were (median [range]) 0.48 [0.004–141.50] ng/mL, and peak cTnI concentrations were 1.21 [0.021–141.50] ng/mL. Admission cTnT concentrations were 15 [<13–3744] ng/L. For each marker, non‐survivors had significantly higher concentrations than survivors (P = .0082–.038). ROC analyses revealed areas under curves [95% CI] of 0.707 [0.537–0.843] for peak cTnI and 0.739 [0.571–0.867] for admission cTnT, respectively. At the optimal cut‐off, concentrations were 1.17 ng/mL (peak cTnI) and 23 ng/L (admission cTnT), sensitivities were 72% and 72%, and specificities were 70% and 80%, respectively.Conclusions and Clinical ImportanceWhile peak cTnI and admission cTnT are significantly related to 1‐year case fatality in critically ill dogs with systemic inflammation, low sensitivities and specificities prevent their prediction of long‐term outcome in individual patients. Troponins might play a role in identification of dogs at long‐term risk of death.