Early goal-directed resuscitation of patients with septic shock: current evidence and future directions

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Abstract

Severe sepsis and septic shock are among the leading causes of mortality in the intensive care unit. Over a decade ago, early goal-directed therapy (EGDT) emerged as a novel approach for reducing sepsis mortality and was incorporated into guidelines published by the international Surviving Sepsis Campaign. In addition to requiring early detection of sepsis and prompt initiation of antibiotics, the EGDT protocol requires invasive patient monitoring to guide resuscitation with intravenous fluids, vasopressors, red cell transfusions, and inotropes. The effect of these measures on patient outcomes, however, remains controversial. Recently, three large randomized trials were undertaken to re-examine the effect of EGDT on morbidity and mortality: the ProCESS trial in the United States, the ARISE trial in Australia and New Zealand, and the ProMISe trial in England. These trials showed that EGDT did not significantly decrease mortality in patients with septic shock compared with usual care. In particular, whereas early administration of antibiotics appeared to increase survival, tailoring resuscitation to static measurements of central venous pressure and central venous oxygen saturation did not confer survival benefit to most patients. In the following review, we examine these findings as well as other evidence from recent randomized trials of goal-directed resuscitation. We also discuss future areas of research and emerging paradigms in sepsis trials.

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Most cited references 61

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Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares.

Paul E Marik, Michael Baram, Bobbak Vahid (2008)

Central venous pressure (CVP) is used almost universally to guide fluid therapy in hospitalized patients. Both historical and recent data suggest that this approach may be flawed. A systematic review of the literature to determine the following: (1) the relationship between CVP and blood volume, (2) the ability of CVP to predict fluid responsiveness, and (3) the ability of the change in CVP (DeltaCVP) to predict fluid responsiveness. MEDLINE, Embase, Cochrane Register of Controlled Trials, and citation review of relevant primary and review articles. Reported clinical trials that evaluated either the relationship between CVP and blood volume or reported the associated between CVP/DeltaCVP and the change in stroke volume/cardiac index following a fluid challenge. From 213 articles screened, 24 studies met our inclusion criteria and were included for data extraction. The studies included human adult subjects, healthy control subjects, and ICU and operating room patients. Data were abstracted on study design, study size, study setting, patient population, correlation coefficient between CVP and blood volume, correlation coefficient (or receive operator characteristic [ROC]) between CVP/DeltaCVP and change in stroke index/cardiac index, percentage of patients who responded to a fluid challenge, and baseline CVP of the fluid responders and nonresponders. Metaanalytic techniques were used to pool data. The 24 studies included 803 patients; 5 studies compared CVP with measured circulating blood volume, while 19 studies determined the relationship between CVP/DeltaCVP and change in cardiac performance following a fluid challenge. The pooled correlation coefficient between CVP and measured blood volume was 0.16 (95% confidence interval [CI], 0.03 to 0.28). Overall, 56+/-16% of the patients included in this review responded to a fluid challenge. The pooled correlation coefficient between baseline CVP and change in stroke index/cardiac index was 0.18 (95% CI, 0.08 to 0.28). The pooled area under the ROC curve was 0.56 (95% CI, 0.51 to 0.61). The pooled correlation between DeltaCVP and change in stroke index/cardiac index was 0.11 (95% CI, 0.015 to 0.21). Baseline CVP was 8.7+/-2.32 mm Hg [mean+/-SD] in the responders as compared to 9.7+/-2.2 mm Hg in nonresponders (not significant). This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVP/DeltaCVP to predict the hemodynamic response to a fluid challenge. CVP should not be used to make clinical decisions regarding fluid management.

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Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature.

Paul E Marik, Rodrigo Cavallazzi, Tajender Vasu … (2009)

: A systematic review of the literature to determine the ability of dynamic changes in arterial waveform-derived variables to predict fluid responsiveness and compare these with static indices of fluid responsiveness. The assessment of a patient's intravascular volume is one of the most difficult tasks in critical care medicine. Conventional static hemodynamic variables have proven unreliable as predictors of volume responsiveness. Dynamic changes in systolic pressure, pulse pressure, and stroke volume in patients undergoing mechanical ventilation have emerged as useful techniques to assess volume responsiveness. : MEDLINE, EMBASE, Cochrane Register of Controlled Trials and citation review of relevant primary and review articles. : Clinical studies that evaluated the association between stroke volume variation, pulse pressure variation, and/or stroke volume variation and the change in stroke volume/cardiac index after a fluid or positive end-expiratory pressure challenge. : Data were abstracted on study design, study size, study setting, patient population, and the correlation coefficient and/or receiver operating characteristic between the baseline systolic pressure variation, stroke volume variation, and/or pulse pressure variation and the change in stroke index/cardiac index after a fluid challenge. When reported, the receiver operating characteristic of the central venous pressure, global end-diastolic volume index, and left ventricular end-diastolic area index were also recorded. Meta-analytic techniques were used to summarize the data. Twenty-nine studies (which enrolled 685 patients) met our inclusion criteria. Overall, 56% of patients responded to a fluid challenge. The pooled correlation coefficients between the baseline pulse pressure variation, stroke volume variation, systolic pressure variation, and the change in stroke/cardiac index were 0.78, 0.72, and 0.72, respectively. The area under the receiver operating characteristic curves were 0.94, 0.84, and 0.86, respectively, compared with 0.55 for the central venous pressure, 0.56 for the global end-diastolic volume index, and 0.64 for the left ventricular end-diastolic area index. The mean threshold values were 12.5 +/- 1.6% for the pulse pressure variation and 11.6 +/- 1.9% for the stroke volume variation. The sensitivity, specificity, and diagnostic odds ratio were 0.89, 0.88, and 59.86 for the pulse pressure variation and 0.82, 0.86, and 27.34 for the stroke volume variation, respectively. : Dynamic changes of arterial waveform-derived variables during mechanical ventilation are highly accurate in predicting volume responsiveness in critically ill patients with an accuracy greater than that of traditional static indices of volume responsiveness. This technique, however, is limited to patients who receive controlled ventilation and who are not breathing spontaneously.

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Author and article information

Contributors

Ravi G. Gupta: guptar4@vcu.edu

Journal

Journal ID (nlm-ta): Crit Care

Title: Critical Care

Publisher: BioMed Central (London )

ISSN (Print): 1364-8535

ISSN (Electronic): 1466-609X

Publication date (Electronic): 28 August 2015

Publication date PMC-release: 28 August 2015

Publication date (Print): 2015

Volume: 19

Issue: 1

Electronic Location Identifier: 286

Affiliations

[ ]Division of Pulmonary Disease and Critical Care Medicine, Department of Internal Medicine, Virginia Commonwealth University School of Medicine, P.O. Box 980050, Richmond, VA 23298 USA

[ ]Division of General Internal Medicine, Department of Internal Medicine, Virginia Commonwealth University School of Medicine, P.O. Box 980070, Richmond, VA 23298 USA

[ ]Division of Infectious Diseases, Department of Internal Medicine, Virginia Commonwealth University School of Medicine, P.O. Box 980019, Richmond, VA 23298 USA

Article

Publisher ID: 1011

DOI: 10.1186/s13054-015-1011-9

PMC ID: 4552276

PubMed ID: 26316210

SO-VID: c0bb0d84-8362-48f1-bffd-c74ec2636e7e

License:

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.