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PURPOSE: To evaluate whole blood chloride concentration and hospital-acquired AKI in hospitalized canine patients. Secondary outcome measures included the volume-adjusted chloride load, in-hospital mortality and length of ICU stay. PATIENTS AND METHODS: This is a prospective, observational study. Sixty dogs admitted to the ICU and receiving IV fluid therapy for >24 hours from February 2018 to July 2019. Corrected chloride and creatinine concentrations were obtained twice daily. Total volume of IV fluid and total chloride load were recorded. Volume-adjusted chloride load (VACL) was calculated by dividing the chloride administered by the volume of fluid administered. Hospital-acquired AKI was defined as an increase in creatinine of ≥26.5 µmol/L (0.3 mg/dL) or 150% from baseline to maximum. Survival to hospital discharge or non-survival and ICU length of stay were also recorded. RESULTS: Fifteen out of 60 patients developed hospital-acquired AKI. Maximum corrected chloride was significantly different in AKI group (median 122.3 mmol/L) vs non-AKI group (median 118.1 mmol/L; p=0.0002). Six out of 60 patients developed hyperchloremia. Hyperchloremic patients were significantly more likely to develop in-hospital AKI (p=0.03). Patients hospitalized ≥2 days had a significantly higher [Cl-]max compared to those with shorter ICU stay (121.8 ± 5.9 mmol/L vs 117.5 ± 4.3 mmol/L; p=0.002). Eight out of 60 patients were non-survivors. Maximum corrected chloride and creatinine concentrations were not significantly different between survivors and non-survivors. VACL was not significantly different between AKI or mortality groups. CONCLUSION: Maximum corrected chloride concentration was significantly higher in dogs with hospital-acquired AKI, even amongst dogs without hyperchloremia. Additionally, maximum corrected chloride concentrations were significantly higher in dogs hospitalized in the ICU longer compared to those hospitalized for fewer than two days. There was no significant difference in VACL in any of the outcome groups. Results from this study suggest alterations in chloride may be observed alongside the development of acute kidney injuries. Future studies in critically ill dogs are warranted.
RESUMO
OBJECTIVE: To evaluate the effect of two levels of partial neuromuscular block (NMB) on arytenoid abduction, tidal volume (VT) and peak inspiratory flow (PIF) in response to a hypercarbic challenge in anesthetized dogs. STUDY DESIGN: Prospective laboratory study. ANIMALS: Eleven healthy male Beagle dogs aged 3-5 years. METHODS: Dogs were anesthetized with propofol and dexmedetomidine infusions. The rima glottidis was observed via an endoscope placed through a laryngeal mask airway. Atracurium infusion was titrated to obtain two levels of partial NMB. The normalized glottal gap area (NGGA; glottal gap area normalized to height squared of rima glottidis) at peak inspiration during a hypercarbic challenge (10% CO2 inspired for 1 minute) was measured at baseline, during mild [train-of-four (TOF) ratio 0.4-0.6] and shallow (TOF ratio 0.7-0.9) NMB, and 30 minutes after spontaneous recovery from NMB. The VT and PIF were measured at the same time points and compared using anova for repeated measures and Tukey's post hoc tests. RESULTS: The NGGA and VT were significantly lower than baseline during both levels of partial NMB with no difference between mild and shallow NMB (p < 0.05). They returned to baseline values after spontaneous recovery from NMB. PIF was not altered significantly during partial NMB. CONCLUSIONS AND CLINICAL RELEVANCE: The NGGA and VT at peak inspiration in response to a hypercarbic challenge were reduced during partial NMB block, with decreased abduction of the arytenoid cartilages. This dysfunction was present even at shallow levels of NMB.
