氯离子浓度与住院犬患者发病率和死亡率关系的初步调查。

IF 1.7 Q2 VETERINARY SCIENCES
Veterinary medicine (Auckland, N.Z.) Pub Date : 2020-07-15 eCollection Date: 2020-01-01 DOI:10.2147/VMRR.S253759
Madeline B Libin, Joel G Weltman, Jennifer Prittie
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引用次数: 1

摘要

目的:探讨犬住院患者全血氯离子浓度与医院获得性AKI的关系。次要结局指标包括容量调整氯负荷、住院死亡率和ICU住院时间。患者和方法:这是一项前瞻性观察性研究。2018年2月至2019年7月,60只犬入住ICU并接受静脉输液治疗>24小时。校正后的氯化物和肌酐浓度每天两次。记录静脉输液总量和总氯离子负荷。容积调节氯负荷(VACL)是通过给氯除以给液量来计算的。医院获得性AKI定义为肌酐从基线到最大值≥26.5 μmol/L (0.3 mg/dL)或150%。同时记录存活至出院或未存活及ICU住院时间。结果:60例患者中有15例发生了医院获得性AKI。AKI组(中位数122.3 mmol/L)与非AKI组(中位数118.1 mmol/L;p = 0.0002)。60名患者中有6人出现了高氯血症。高绿血症患者更容易发生院内AKI (p=0.03)。住院≥2天的患者[Cl-]max明显高于住院时间较短的患者(121.8±5.9 mmol/L vs 117.5±4.3 mmol/L);p = 0.002)。60名患者中有8名非幸存者。最大校正氯化物和肌酐浓度在幸存者和非幸存者之间没有显著差异。AKI组和死亡率组间VACL无显著差异。结论:医院获得性AKI犬的最大校正氯离子浓度显著较高,即使在没有高氯血症的犬中也是如此。此外,在ICU住院时间较长的狗的最大校正氯浓度明显高于住院时间少于两天的狗。各结果组间VACL无显著差异。这项研究的结果表明,在急性肾损伤的发展过程中可能会观察到氯离子的变化。未来对危重犬的研究是有必要的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

A Preliminary Investigation into the Association of Chloride Concentration on Morbidity and Mortality in Hospitalized Canine Patients.

A Preliminary Investigation into the Association of Chloride Concentration on Morbidity and Mortality in Hospitalized Canine Patients.

A Preliminary Investigation into the Association of Chloride Concentration on Morbidity and Mortality in Hospitalized Canine Patients.

A Preliminary Investigation into the Association of Chloride Concentration on Morbidity and Mortality in Hospitalized Canine Patients.

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.

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