Abstract

ObjectiveTo estimate the incidence of raised cTnI after general anaesthesia in dogs and to explore major risk factors influencing this. Study designProspective clinical study. AnimalsA total of 107 (ASA physical status 1−2) dogs, 63% male and 37% female, median age 5 years (range 0.3–13.4), median weight 24.4 kg (range 4.2–66.5 kg) undergoing anaesthesia for clinical purposes. MethodsVenous blood samples were taken within 24 hours prior to induction and 24 hours after the termination of anaesthesia. Serum concentrations of cardiac troponin I were measured using a chemiluminescent enzyme immunometric assay with a lower level of detection of 0.20 ng mL−1 (below this level <0.20 ng mL−1). Continuous data were assessed graphically for normality and paired and unpaired data compared with the Wilcoxon signed ranks and Mann–Whitney U‐tests respectively. Categorical data were compared with the Chi squared or Fisher’s exact test as appropriate (p < 0.05). ResultsOf the 107 dogs recruited, 100 had pre‐ and post‐anaesthetic cTnI measured. The median pre‐anaesthesia cTnI was ‘<0.20’ ng mL−1 (range ‘<0.20’–0.43 ng mL−1) and the median increase from pre‐anaesthesia level was 0.00 ng mL−1 (range −0.12 to 0.61 ng mL−1). Fourteen dogs had increased cTnI after anaesthesia relative to pre‐anaesthesia (14%, 95% CI 7.2–20.8%, range of increase 0.03–0.61 ng mL−1). Six animals had cTnI levels that decreased (range 0.02–0.12 ng mL−1). Older dogs were more likely to have increased cTnI prior to anaesthesia (OR = 5.32, 95% CI 1.35–21.0, p = 0.007) and dogs 8 years and over were 3.6 times as likely to have an increased cTnI after anaesthesia (95% CI 1.1–12.4, p = 0.028). Conclusion and clinical relevanceIncreased cTnI after anaesthesia relative to pre‐anaesthesia levels was observed in a number of apparently healthy dogs undergoing routine anaesthesia.

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