Moffett Brady S, Tsang Rocky, Kennedy Curt, Bronicki Ron A, Akcan-Arikan Ayse, Checchia Paul A
1Department of Pharmacy,Texas Children's Hospital,Houston,Texas,United States of America.
2Department of Pediatrics,Baylor College of Medicine,Houston,Texas,United States of America.
Cardiol Young. 2017 Aug;27(6):1104-1109. doi: 10.1017/S1047951116002122. Epub 2016 Nov 11.
Sequential nephron blockade using intravenous chlorothiazide is often used to enhance urine output in patients with inadequate response to loop diuretics. A few data exist to support this practice in critically ill infants.
We included 100 consecutive patients <1 year of age who were administered intravenous chlorothiazide while receiving furosemide therapy in the cardiac ICU in our study. The primary end point was change in urine output 24 hours after chlorothiazide administration, and patients were considered to be responders if an increase in urine output of 0.5 ml/kg/hour was documented. Data on demographic, clinical, fluid intake/output, and furosemide and chlorothiazide dosing were collected. Multivariable regression analyses were performed to determine variables significant for increase in urine output after chlorothiazide administration.
The study population was 48% male, with a mean weight of 4.9±1.8 kg, and 69% had undergone previous cardiovascular surgery. Intravenous chlorothiazide was initiated at 89 days (interquartile range 20-127 days) of life at a dose of 4.6±2.7 mg/kg/day (maximum 12 mg/kg/day). Baseline estimated creatinine clearance was 83±42 ml/minute/1.73 m2. Furosemide dose before chlorothiazide administration was 2.8±1.4 mg/kg/day and 3.3±1.5 mg/kg/day after administration. A total of 43% of patients were categorised as responders, and increase in furosemide dose was the only variable significant for increase in urine output on multivariable analysis (p<0.05). No graphical trends were noted for change in urine output and dose of chlorothiazide.
Sequential nephron blockade with intravenous chlorothiazide was not consistently associated with improved urine output in critically ill infants.
对于对袢利尿剂反应不足的患者,静脉注射氯噻嗪进行序贯肾单位阻滞常用于增加尿量。但支持在危重症婴儿中采用这种做法的数据较少。
我们纳入了100例年龄小于1岁的连续患者,这些患者在我们研究的心脏重症监护病房接受呋塞米治疗时接受了静脉注射氯噻嗪。主要终点是氯噻嗪给药后24小时尿量的变化,如果记录到尿量增加0.5 ml/kg/小时,则患者被视为有反应者。收集了人口统计学、临床、液体出入量以及呋塞米和氯噻嗪给药剂量的数据。进行多变量回归分析以确定氯噻嗪给药后尿量增加的显著变量。
研究人群中男性占48%,平均体重为4.9±1.8 kg,69%曾接受过心血管手术。静脉注射氯噻嗪在出生后89天(四分位间距20 - 127天)开始,剂量为4.6±2.7 mg/kg/天(最大12 mg/kg/天)。基线估计肌酐清除率为83±42 ml/分钟/1.73 m²。氯噻嗪给药前呋塞米剂量为2.8±1.4 mg/kg/天,给药后为3.3±1.5 mg/kg/天。共有43%的患者被归类为有反应者,多变量分析显示呋塞米剂量增加是尿量增加的唯一显著变量(p<0.05)。未观察到尿量变化与氯噻嗪剂量之间的图形趋势。
在危重症婴儿中,静脉注射氯噻嗪进行序贯肾单位阻滞与尿量改善之间并无一致关联。