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Fluid overload occurring as a consequence of overly aggressive fluid resuscitation may adversely affect outcome in hemodynamically unstable critically ill patients. Therefore, following the initial fluid resuscitation, it is important to identify which patients will benefit from further fluid administration.
To identify predictors of fluid responsiveness in hemodynamically unstable patients with signs of inadequate organ perfusion.
Data Sources and Study Selection
Search of MEDLINE and EMBASE (1966 to June 2016) and reference lists from retrieved articles, previous reviews, and physical examination textbooks for studies that evaluated the diagnostic accuracy of tests to predict fluid responsiveness in hemodynamically unstable adult patients who were defined as having refractory hypotension, signs of organ hypoperfusion, or both. Fluid responsiveness was defined as an increase in cardiac output following intravenous fluid administration.
Two authors independently abstracted data (sensitivity, specificity, and likelihood ratios [LRs]) and assessed methodological quality. A bivariate mixed-effects binary regression model was used to pool the sensitivities, specificities, and LRs across studies.
A total of 50 studies (N = 2260 patients) were analyzed. In all studies, indices were measured before assessment of fluid responsiveness. The mean prevalence of fluid responsiveness was 50% (95% CI, 42%-56%). Findings on physical examination were not predictive of fluid responsiveness with LRs and 95% CIs for each finding crossing 1.0. A low central venous pressure (CVP) (mean threshold <8 mm Hg) was associated with fluid responsiveness (positive LR, 2.6 [95% CI, 1.4-4.6]; pooled specificity, 76%), but a CVP greater than the threshold made fluid responsiveness less likely (negative LR, 0.50 [95% CI, 0.39-0.65]; pooled sensitivity, 62%). Respiratory variation in vena cava diameter measured by ultrasound (distensibility index >15%) predicted fluid responsiveness in a subgroup of patients without spontaneous respiratory efforts (positive LR, 5.3 [95% CI, 1.1-27]; pooled specificity, 85%). Patients with less vena cava distensibility were not as likely to be fluid responsive (negative LR, 0.27 [95% CI, 0.08-0.87]; pooled sensitivity, 77%). Augmentation of cardiac output or related parameters following passive leg raising predicted fluid responsiveness (positive LR, 11 [95% CI, 7.6-17]; pooled specificity, 92%). Conversely, the lack of an increase in cardiac output with passive leg raising identified patients unlikely to be fluid responsive (negative LR, 0.13 [95% CI, 0.07-0.22]; pooled sensitivity, 88%).
Conclusions and Relevance
Passive leg raising followed by measurement of cardiac output or related parameters may be the most useful test for predicting fluid responsiveness in hemodynamically unstable adults. The usefulness of respiratory variation in the vena cava requires confirmatory studies.
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Corresponding Author: Najib T. Ayas, MD, MPH, Division of Critical Care Medicine, St. Paul’s Hospital, 1081 Burrard St, Vancouver, BC, Canada V6Z 1Y6 (email@example.com).
Author Contributions: Drs Ayas and Bentzer had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of all the data analysis.
Study concept and design: Bentzer, Boyd, Sirounis, Ayas.
Acquisition, analysis, or interpretation of data: Bentzer, Griesdale, MacLean, Sirounis, Ayas.
Drafting of the manuscript: Bentzer, Boyd, Sirounis, Ayas.
Critical revision of the manuscript for important intellectual content: Bentzer, Griesdale, MacLean, Ayas.
Statistical analysis: Bentzer, Griesdale, Sirounis, Ayas.
Obtained funding: Bentzer.
Administrative, technical, or material support: Sirounis, Ayas.
Supervision: Boyd, Ayas.
Other (analyzing the original articles: MacLean.
Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Unrelated to the present article, Dr Ayas reports receipt of fees from RHS Medical for a presentation to family physicians. No other disclosures were reported.
Funding/Support: Dr Bentzer reports receipt of funding from ALF (Swedish [government funding to university hospitals for physician research and education]) (18401) and The Anna and Edwin Berger Foundation. Dr Griesdale reports receipt of funding from Vancouver General Hospital and the University of British Columbia Hospital Foundation Best of Health Fund. Dr Ayas reports receipt of funding from an established clinician scientist award from the Vancouver Coastal Health Research Institute.
Role of the Funder/Sponsor: The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript, and decision to submit the manuscript for publication.
Additional Contributions: We would like to acknowledge the following individuals who provided helpful advice on earlier versions of the manuscript: Charles Brudney, MB, CHB, and Martha Sue Carraway, MD, Durham VA Medical Center and Duke University, Durham, North Carolina; Alexander Fanaroff, MD, L. Kristin Newby, MD, and Cara O’Brien, MD, Duke University Medical Center, Durham, North Carolina. None of these individuals received compensation for their roles in the study.
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