Treating cerebral edema in diabetic ketoacidosis: caveats in extrapolating from traumatic brain injury*.
Treating cerebral edema in diabetic ketoacidosis: caveats in extrapolating from traumatic brain injury*.
复制标题
治疗糖尿病酮症酸中毒的脑水肿：从创伤性脑损伤推断的注意事项*。
DOI：
10.1097/pcc.0b013e31829f6c77
复制
发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Vavilala,MonicaS
中科院分区：
文献类型：
--
作者：
Vavilala,MonicaS
编辑724 www.PCcmJournal。组织，2013年9月，第14卷·第7号二级证据(19)。事实上，高渗剂与预后之间的关系可能取决于潜在的神经状况。例如，在一项针对各种情况下接受开颅手术的成人外科患者的研究中，他们被随机分为5毫升/公斤的20%甘露醇或3%高渗盐水，在保持正常碳酸血症和正常血容量的情况下，Rozet等人(20)报告了在脑放松或动静脉乳酸或脑脊液(CSF)乳酸增加方面没有差异，而3%高渗盐水随着时间的推移与更高的脑脊液钠浓度相关(20)。此外，甘露醇和高渗盐水的脑血管轮廓不同，这可能会对DKA的变化产生不同于其他神经疾病的影响。在本期《儿科重症护理医学》中，DeCourcey等人的研究报告称，在11年的研究期间，3%高渗盐水的使用量增加了四倍，这突显了经验性地将治疗从一种疾病状态推算到另一种疾病状态的问题。与他们的假设相反，他们认为DKA的死亡率下降可能是由于远离甘露醇，他们报告说，即使在对接受这种药物的倾向进行调整后，接受3%高渗盐水的患者的死亡率也更高。尽管这项研究不能明确回答高渗治疗与DKA相关性脑水肿和/或死亡率之间的关系这一问题，但DeCourcey等人(6)在与DKA相关性脑水肿的治疗相关的一些领域提供了思考的食粮。首先，这项研究表明，尽管缺乏佐证或指南，但美国各地的临床实践都倾向于使用高渗盐水。如果高渗盐水使DKA患者受益，这种变化可能不会有问题。然而，情况并非如此，数据是显著的，特别是考虑到与DKA相关的死亡率总体下降，这可能是由于其他治疗或评估做法的变化，如静脉输液或使用标准化的临床护理路径。DeCourcey等人的这项研究(6)强调了在DKA中使用3%高渗盐水的危害，这项研究的重要性质疑了我们经验性治疗外推的临床实践，并解决了对DKA患者而不是其他神经系统疾病患者的治疗进行批判性评估的必要性。DeCourcey等人(6)正确地指出，在DKA中使用这两种高渗剂的有效性仍然存在科学上的平衡。在进一步的澄清和研究之前，在经验性地采用从一种疾病状态(TBI)到另一种疾病状态(DKA)的治疗之前，应该考虑神经状况之间的潜在差异。
Editorials724 www. pccmjournal. org September 2013• Volume 14• Number 7 class II evidence (19). In fact, the relationship between hyperosmolar agent and outcome may depend on the underlying neurological condition. For example, in one study of adult surgical patients undergoing craniotomy for a variety of conditions who were randomized to receive either 5 mL/kg of 20% mannitol or 3% hypertonic saline, where normocapnia and euvolemia were maintained, Rozet et al (20) reported no difference in brain relaxation or arteriovenous lactate or increases in cerebrospinal fluid (CSF) lactate, whereas 3% hypertonic saline was associated with higher CSF Na concentrations over time (20). Furthermore, mannitol and hypertonic saline differ in their cerebrovascular profiles which may impact changes in DKA differently than in other neurological conditions. In this issue of Pediatric Critical Care Medicine, the study by DeCourcey et al (6) reporting a four-fold higher use of 3% hypertonic saline over the 11-year study period highlights the problem with empiric extrapolation of treatment from one disease state to another. Contrary to their hypothesis that declining mortality in DKA may be due to the shift away from mannitol, they report higher mortality among patients who received 3% hypertonic saline even after adjustment for the propensity to receive this medication. Although this study is not definitive in terms of answering the question relating hyperosmolar therapy with DKA-related cerebral edema and/or mortality, DeCourcey et al (6) offer food for thought in a number of areas pertaining to the treatment of DKA-related cerebral edema. First, the study demonstrates a change in clinical practice in favor of hypertonic saline across the United States, despite the absence of supporting evidence or guidelines. This change might not be problematic if hypertonic saline benefits patients with DKA. However, this is not the case and the data are significant, especially given the overall decline in DKA-related mortality, which may be due to change in other treatment or evaluation practices such as IV fluid administration or the use of standardized clinical care pathways. The importance of the study by DeCourcey et al (6) highlighting harm with the use of 3% hypertonic saline in DKA questions our clinical practice of empiric therapeutic extrapolation and addresses the need for critical evaluation of treatments in DKA from patients with DKA and not patients with other neurological conditions. DeCourcey et al (6) correctly point out that there continues to be scientific equipoise for efficacy in the use of the two hyperosmolar agents in DKA. Pending further clarification and studies, underlying differences between neurological conditions should be considered before empirically adopting treatments from one disease state (TBI) to another (DKA).