Sacha Gretchen L, Lam Simon W, Wang Lu, Duggal Abhijit, Reddy Anita J, Bauer Seth R
Department of Pharmacy, Cleveland Clinic, Cleveland, OH.
Department of Quantitative Health Sciences, Cleveland Clinic, Cleveland, OH.
Crit Care Med. 2022 Apr 1;50(4):614-623. doi: 10.1097/CCM.0000000000005317.
To determine the association of catecholamine dose, lactate concentration, and timing from shock onset at vasopressin initiation with in-hospital mortality.
Retrospective, observational study using segmented and multivariable logistic regression to evaluate the associations of catecholamine dose, lactate concentration, and timing from shock onset at vasopressin initiation with in-hospital mortality.
Multiple hospitals within the Cleveland Clinic Health System.
Adult patients who met criteria for septic shock based on the U.S. Centers for Disease Control and Prevention Adult Sepsis Event definition.
All patients received continuous infusion vasopressin as an adjunct to catecholamine vasopressors.
In total, 1,610 patients were included with a mean Acute Physiology and Chronic Health Evaluation III 109.0 ± 35.1 and Sequential Organ Failure Assessment 14.0 ± 3.5; 41% of patients survived the hospital admission. At the time of vasopressin initiation, patients had median (interquartile range) lactate concentration 3.9 mmol/L (2.3-7.2 mmol/L), norepinephrine-equivalent dose 25 µg/min (18-40 µg/min), and 5.3 hours (2.1-12.2 hr) elapsed since shock onset. The odds of in-hospital mortality increased 20.7% for every 10 µg/min increase in norepinephrine-equivalent dose up to 60 µg/min at the time of vasopressin initiation (adjusted odds ratio, 1.21 [95% CI, 1.09-1.34]), but no association was detected when the norepinephrine-equivalent dose exceeded 60 µg/min (adjusted odds ratio, 0.96 [95% CI, 0.84-1.10]). There was a significant interaction between timing of vasopressin initiation and lactate concentration (p = 0.02) for the association with in-hospital mortality. A linear association between increasing in-hospital mortality was detected for increasing lactate concentration at the time of vasopressin initiation, but no association was detected for time elapsed from shock onset.
Higher norepinephrine-equivalent dose at vasopressin initiation and higher lactate concentration at vasopressin initiation were each associated higher in-hospital mortality in patients with septic shock who received vasopressin.
确定去甲肾上腺素剂量、乳酸浓度以及血管加压素开始使用时距休克发作的时间与住院死亡率之间的关联。
采用分段和多变量逻辑回归的回顾性观察性研究,以评估去甲肾上腺素剂量、乳酸浓度以及血管加压素开始使用时距休克发作的时间与住院死亡率之间的关联。
克利夫兰诊所医疗系统内的多家医院。
根据美国疾病控制与预防中心成人脓毒症事件定义符合脓毒性休克标准的成年患者。
所有患者均接受持续输注血管加压素作为去甲肾上腺素类血管升压药的辅助治疗。
共纳入1610例患者,急性生理与慢性健康状况评分III平均为109.0±35.1,序贯器官衰竭评估评分为14.0±3.5;41%的患者存活至出院。在开始使用血管加压素时,患者的乳酸浓度中位数(四分位间距)为3.9 mmol/L(2.3 - 7.2 mmol/L),去甲肾上腺素等效剂量为25 μg/min(18 - 40 μg/min),自休克发作起已过去5.3小时(2.1 - 12.2小时)。在开始使用血管加压素时,去甲肾上腺素等效剂量每增加10 μg/min直至60 μg/min,住院死亡率的比值增加20.7%(校正比值比,1.21 [95% CI,1.09 - 1.34]),但当去甲肾上腺素等效剂量超过60 μg/min时未检测到关联(校正比值比,0.96 [95% CI,0.84 - 1.10])。血管加压素开始使用的时间与乳酸浓度之间存在显著交互作用(p = 0.02),与住院死亡率相关。在开始使用血管加压素时,随着乳酸浓度升高,住院死亡率呈线性增加,但未检测到与休克发作后经过时间的关联。
在接受血管加压素治疗的脓毒性休克患者中,开始使用血管加压素时较高的去甲肾上腺素等效剂量和较高的乳酸浓度均与较高的住院死亡率相关。