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Guiding resuscitation in shock: base excess or lactate?
Critical Care ( IF 8.8 ) Pub Date : 2024-07-18 , DOI: 10.1186/s13054-024-05039-2
Micah Liam Arthur Heldeweg _{1,

2} , Thomas Langer _{3,

4} , František Duška ₂

Affiliation

Base excess (BE) is a widely used parameter derived from blood gas analysis. A recent international study showed that 40% of surveyed anesthesia and critical care clinicians use BE to guide (intraoperative) fluid management, and that 25% of respondents prefer BE over lactate [1]. This is surprising as lactate production is directly increased by hypovolemia-associated tissue hypoxia, whilst BE is a simple calculation of the metabolic component of acid-base derangement.

In the 1960s, measuring lactate was laborious and time-consuming: a typical colorimetric measurement of lactate took up to eight hours, clearly limiting its clinical point-of-care use [2]. At the same time, Astrup and Siggaard-Andersen introduced BE, a marker to quantify metabolic acid-base derangements independent of concomitant carbon dioxide variations, i.e. respiratory acid-base disorders. Modern BE is a simple mathematical expression that corrects changes in bicarbonate for carbon dioxide variation by using the slope of an experimentally determined carbon dioxide titration curve [3].

In contrast to lactate, BE was able to provide an instant and inexpensive quantification of a metabolic acidosis, occurring, for example, during circulatory shock. Unsurprisingly, in this context, many researchers considered BE a surrogate indicator of oxygen debt and hypovolemia. BE was ideal in the predominantly healthy traumatology population: a single surrogate marker for hemorrhagic shock severity that could be used as a therapeutic trigger for transfusion management. Investigations demonstrated that BE was more accurate at quantifying the magnitude of blood loss during hemorrhagic shock than clinicians’ visual estimates of blood loss, volume replacement counts, blood pressure, or heart rate [4].

Development of refined electrode-based lactate measurement methods enabled direct and rapid assessment, starting the era of routine lactate measurement in the 1980s [2]. Nonetheless, some authors deemed lactate as clinically less useful than BE because of potential confounding factors: inflammation, sympathetic stimulation, drugs such as metformin, hepatic failure, and exogenous lactate may all lead to a hyperlactatemia in the absence of oxygen debt [4]. Moreover, lactate normalization depends on its clearance and may be delayed despite effective resuscitative measures. Indeed, hyperlactatemia may reflect other pathophysiological mechanisms unrelated to hemorrhagic shock [5]. However, any increase in endogenous lactate, by definition, leads to a decrease in BE. Moreover, BE is a composite marker and may be influenced by more factors than only hyperlactatemia: changes in strong electrolytes, such as sodium and chloride, weak acids, such as albumin or phosphate, and other unmeasured acids, such as ketones and toxins. Notably, resuscitation with a 0.9% saline solution leads to a hyperchloraemic metabolic acidosis with a decreased BE [3].

Nonetheless, research in traumatology continued to employ BE. A landmark Critical Care cohort study heralded ‘the renaissance of BE’: investigators found that BE may be superior to traditional vital parameters (heart rate, systolic blood pressure, and Glasgow coma scale) for identification of transfusion requirements in traumatology patients [3]. BE was subsequently included in the guidelines and the ATLS classification of hypovolemic shock, an internationally-used teaching and management instrument for resuscitation. This established a paradigm in traumatology and resuscitation management that permeated into emergency medicine, anesthesia, and critical care [1]. Unfortunately, the original study did not perform a direct comparison of the performance of lactate versus BE to predict transfusion requirements [3].

Meanwhile, routine point-of-care testing spread across emergency and critical care settings worldwide, and mounting evidence supported the value of serial lactate measurements in the evaluation of critically ill patients and their response to (fluid) therapy. Clinicians widely embraced lactate as the best-available single high-sensitivity indicator of shock severity and a central therapeutic trigger in resuscitation protocols. In critical care, appraising lactate jointly with central mixed venous oxygen saturation may (partially) offset its limited specificity [5].

Currently lactate, an underlying metabolic substrate of tissue hypoxia, can be directly, reliably, and serially measured [2]. Considering BE its surrogate is, in our opinion, anachronistic. However, as these parameters provide different information, their joint evaluation remains informative. Indeed, if BE cannot be fully explained by hyperlactatemia, there may be a concurrent acid-base derangement, which should be identified and addressed. The presence of an ‘alactic’ BE may therefore be etiologically and prognostically valuable in traumatology, and perhaps, critically ill patients [1, 4]. There is a burning need for studies directly comparing the utility of metabolic parameters such as BE, lactate and alactic BE as tailored resuscitation trigger and prognostic markers in acute hypovolemia.

In conclusion, the current literature does not advocate for a single, optimal metabolic resuscitation trigger. Clinicians should integrate multiple metabolic variables with clinical parameters to decide the resuscitation strategy and evaluate its effect. Until direct comparisons are available, there is good rationale to suggest that, mechanistically, lactate is a more appropriate resuscitation trigger, whilst BE remains useful in identifying acid-base derangements superimposed on lactic acidosis.

No datasets were generated or analysed during the current study.

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Authors and Affiliations

Department of Intensive Care Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands
Micah Liam Arthur Heldeweg
Department of Anaesthesia and Intensive Care Medicine, The Third Faculty of Medicine, Charles University, FNKV University Hospital, Prague, Czech Republic
Micah Liam Arthur Heldeweg & František Duška
Department of Medicine and Surgery, University of Milan-Bicocca, Monza, Italy
Thomas Langer
Department of Anesthesia and Intensive Care Medicine, Niguarda Ca’ Granda, Milan, Italy
Thomas Langer

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MLAH, TL, and FD were responsible for the conception of the work. MLAH was responsible for the first draft of the manuscript. Subsequently all authors provided critical revisions for until the final manuscript was completed. All authors read and approved the final manuscript and ensured that questions related to the accuracy or integrity of any part of the work were investigated and resolved.

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Correspondence to Micah Liam Arthur Heldeweg.

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The authors declare no competing interests.

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Heldeweg, M.L.A., Langer, T. & Duška, F. Guiding resuscitation in shock: base excess or lactate?. Crit Care 28, 249 (2024). https://doi.org/10.1186/s13054-024-05039-2

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Received: 29 June 2024
Accepted: 13 July 2024
Published: 18 July 2024
DOI: https://doi.org/10.1186/s13054-024-05039-2

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Keywords

Base excess
Base deficit
Lactate
Metabolic acidosis
Resuscitation
Fluid management

中文翻译：

指导休克复苏：碱过量还是乳酸？

碱过剩 (BE) 是源自血气分析的广泛使用的参数。最近的一项国际研究表明，40% 的接受调查的麻醉和重症监护临床医生使用 BE 来指导（术中）液体管理，25% 的受访者更喜欢 BE 而不是乳酸 [1]。这是令人惊讶的，因为与低血容量相关的组织缺氧直接增加了乳酸的产生，而BE是酸碱紊乱的代谢成分的简单计算。

在 20 世纪 60 年代，测量乳酸既费力又耗时：典型的乳酸比色测量需要长达 8 小时，这明显限制了其临床现场使用 [2]。与此同时，Astrup 和 Siggaard-Andersen 引入了 BE，一种用于量化代谢酸碱紊乱的标记物，与伴随的二氧化碳变化无关，即呼吸性酸碱紊乱。现代 BE 是一个简单的数学表达式，通过使用实验确定的二氧化碳滴定曲线的斜率来校正碳酸氢盐随二氧化碳变化的变化 [3]。

与乳酸相比，BE 能够对代谢性酸中毒（例如在循环性休克期间发生的情况）进行即时且廉价的定量。毫不奇怪，在这种情况下，许多研究人员认为 BE 是氧债和低血容量的替代指标。 BE 在主要健康的创伤学人群中是理想的选择：失血性休克严重程度的单一替代标志物，可用作输血管理的治疗触发因素。研究表明，与临床医生对失血量、容量替代计数、血压或心率的视觉估计相比，BE 在量化失血性休克期间失血量方面更准确 [4]。

基于电极的精细乳酸测量方法的开发实现了直接、快速的评估，开启了 20 世纪 80 年代常规乳酸测量的时代 [2]。尽管如此，一些作者认为乳酸在临床上不如BE有用，因为存在潜在的混杂因素：炎症、交感神经刺激、二甲双胍等药物、肝衰竭和外源性乳酸都可能在没有氧债的情况下导致高乳酸血症[4]。此外，乳酸的正常化取决于其清除率，尽管采取了有效的复苏措施，但乳酸的正常化可能会延迟。事实上，高乳酸血症可能反映了与失血性休克无关的其他病理生理机制[5]。然而，根据定义，内源性乳酸的任何增加都会导致 BE 降低。此外，BE 是一个复合标志物，可能受到更多因素的影响，而不仅仅是高乳酸血症：强电解质（例如钠和氯化物）、弱酸（例如白蛋白或磷酸盐）以及其他未测量的酸（例如酮和毒素）的变化。值得注意的是，用 0.9% 盐水溶液复苏会导致高氯血症性代谢性酸中毒，同时 BE 降低[3]。

尽管如此，创伤学研究仍在继续使用BE。一项具有里程碑意义的重症监护队列研究预示着“BE 的复兴”：研究人员发现，在确定创伤科患者的输血需求方面，BE 可能优于传统的生命参数（心率、收缩压和格拉斯哥昏迷量表）[3]。 BE 随后被纳入指南和 ATLS 低血容量休克分类中，这是一种国际上使用的复苏教学和管理工具。这建立了创伤学和复苏管理的范例，并渗透到急诊医学、麻醉和重症监护领域[1]。不幸的是，最初的研究没有直接比较乳酸与 BE 的性能来预测输血需求 [3]。

与此同时，常规床旁检测遍布全球的急诊和重症监护机构，越来越多的证据支持连续乳酸测量在评估危重患者及其对（液体）治疗的反应中的价值。临床医生广泛认为乳酸是休克严重程度的最佳单一高灵敏度指标，也是复苏方案中的核心治疗触发因素。在重症监护中，联合评估乳酸和中心混合静脉血氧饱和度可能（部分）抵消其有限的特异性[5]。

目前，乳酸是组织缺氧的潜在代谢底物，可以直接、可靠、连续地测量[2]。我们认为，考虑到 BE 的替代品是不合时宜的。然而，由于这些参数提供不同的信息，它们的联合评估仍然提供信息。事实上，如果 BE 不能完全用高乳酸血症来解释，则可能存在并发的酸碱紊乱，应予以识别和解决。因此，“无乳酸”BE 的存在可能在创伤学、甚至危重患者中具有病因学和预后价值 [1, 4]。迫切需要直接比较代谢参数（例如 BE、乳酸和无乳酸 BE）作为急性低血容量的定制复苏触发因素和预后标志物的效用的研究。

总之，目前的文献并不提倡单一的、最佳的代谢复苏触发因素。临床医生应将多个代谢变量与临床参数相结合来决定复苏策略并评估其效果。在进行直接比较之前，有充分的理由表明，从机制上讲，乳酸是更合适的复苏触发因素，而 BE 在识别乳酸酸中毒叠加的酸碱紊乱方面仍然有用。

当前研究期间没有生成或分析数据集。

Heldeweg MLA、Stohlmann JAH、Loer SA。碱过量和乳酸用于指导围手术期液体管理：对参加 2022 年米兰 ESAIC 的麻醉师、住院医生和重症监护医生进行的调查。欧洲麻醉学杂志。 2023；40(8)：610–2。

文章 PubMed 谷歌学术
Weil MH，Tang W。用于指导重症监护的统计血液和血浆乳酸测量四十五年的演变。临床化学。 2009；55(11)：2053–4。 https://doi.org/10.1373/clinchem.2009.133553。

文章 CAS PubMed 谷歌学术
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Rixen D，西格尔 JH。实验室到临床的审查：氧债及其代谢与失血性和创伤后休克严重程度的量化指标相关。危重护理。 2005；9(5)：441–53。 https://doi.org/10.1186/cc3526。

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重症监护医学部，阿姆斯特丹大学医学中心，阿姆斯特丹，荷兰

迈卡·利亚姆·阿瑟·赫尔德韦格
捷克共和国布拉格查尔斯大学第三医学院麻醉与重症监护医学系、FNKV 大学医院

迈卡·利亚姆·阿瑟·赫尔德韦格 & 弗兰蒂谢克·杜斯卡
医学和外科系，米兰比可卡大学，蒙扎意大利
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