Nozawa Hisataka, Tsuboi Norihiko, Oi Tadashi, Takezawa Yoshiki, Osawa Ichiro, Nishimura Nao, Nakagawa Satoshi
Department of Critical Care and Anesthesia, Critical Care Medicine, National Center for Child Health and Development, Tokyo, Japan.
J Pediatr Intensive Care. 2021 Aug 17;12(4):296-302. doi: 10.1055/s-0041-1733942. eCollection 2023 Dec.
From the perspective of the Stewart approach, it is known that expansion of the sodium chloride ion difference (SCD) induces alkalosis. We investigated the role of SCD expansion by furosemide-induced chloride reduction in pediatric patients with acute respiratory failure. We included patients admitted to our pediatric intensive care unit intubated for acute respiratory failure without underlying diseases, and excluded patients receiving extracorporeal circulation therapy (extracorporeal membrane oxygenation and/or renal replacement therapy). We classified eligible patients into the following two groups: case-those intubated who received furosemide within 24 hours, and control-those intubated who did not receive furosemide within 48 hours. Primary outcomes included SCD, partial pressure of carbon dioxide (PaCO ), and pH results from arterial blood gas samples obtained over 48 hours following intubation. Multiple regression analysis was also performed to evaluate the effects of SCD and PaCO changes on pH. Twenty-six patients were included of which 13 patients were assigned to each of the two groups. A total of 215 gas samples were analyzed. SCD (median [mEq/L] [interquartile range]) 48 hours after intubation significantly increased in the case group compared with the control group (37 [33-38] vs. 31 [30-34]; = 0.005). Although hypercapnia persisted in the case group, the pH (median [interquartile range]) remained unchanged in both groups (7.454 [7.420-7.467] vs. 7.425 [7.421-7.436]; = 0.089). SCD and PaCO were independently associated with pH ( < 0.001 for each regression coefficient). As a result, we provide evidence that SCD expansion with furosemide may be useful in maintaining pH within the normal range in pediatric patients with acute respiratory failure complicated by concurrent metabolic acidosis.
从斯图尔特方法的角度来看，已知氯化钠离子差（SCD）的扩大可诱发碱中毒。我们研究了速尿诱导的氯化物减少导致的SCD扩大在小儿急性呼吸衰竭患者中的作用。我们纳入了因急性呼吸衰竭而插管入住我们儿科重症监护病房且无基础疾病的患者，并排除了接受体外循环治疗（体外膜肺氧合和/或肾脏替代治疗）的患者。我们将符合条件的患者分为以下两组：病例组——在24小时内接受速尿治疗的插管患者，对照组——在48小时内未接受速尿治疗的插管患者。主要结局包括SCD、二氧化碳分压（PaCO₂）以及插管后48小时内采集的动脉血气样本的pH值结果。还进行了多元回归分析以评估SCD和PaCO₂变化对pH值的影响。共纳入26例患者，两组各13例。总共分析了215份气体样本。与对照组相比，病例组插管后48小时的SCD（中位数[mEq/L][四分位间距]）显著升高（37[33 - 38]对31[30 - 34]；P = 0.005）。尽管病例组持续存在高碳酸血症，但两组的pH值（中位数[四分位间距]）均保持不变（7.454[7.420 - 7.467]对7.425[7.421 - 7.436]；P = 0.089）。SCD和PaCO₂与pH值独立相关（每个回归系数的P均<0.001）。因此，我们提供的证据表明，速尿导致的SCD扩大可能有助于将并发代谢性酸中毒的小儿急性呼吸衰竭患者的pH值维持在正常范围内。
