Journal of Critical Care 42 (2017) 42–46

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Journal of Critical Care

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Stroke volume guided resuscitation in severe sepsis and septic shock

improves outcomes
Heath E. Latham a,⁎, Charles D. Bengtson a, Lewis Satterwhite a, Mindy Stites b, Dipti P. Subramaniam c,
G. John Chen c, Steven Q. Simpson a
a
Division of Pulmonary and Critical Care Medicine, The University of Kansas Medical Center, 3901 Rainbow Blvd, MS 3007, Kansas City, KS 66160, United States
b
Department of Nursing, The University of Kansas Medical Center, 3901 Rainbow Blvd, MS 2018, Kansas City, KS 66160, United States
c
Department of Internal Medicine, Division of Health Services Research, The University of Kansas Medical Center, 3901 Rainbow Blvd, MS 1037, Kansas City, KS 66160, United States

a r t i c l e i n f o a b s t r a c t

Keywords: To determine whether stroke volume (SV) guided fluid resuscitation in patients with severe sepsis and septic
Severe sepsis shock alters Intensive Care Unit (ICU) fluid balance and secondary outcomes, this retrospective cohort study eval-
Septic shock uated consecutive patients admitted to an ICU with the primary diagnosis of severe sepsis or septic shock. Co-
Sepsis horts were based on fluid resuscitation guided by changes in SV or by usual care (UC). The SV group
Bioreactance
comprised 100 patients, with 91 patients in the UC group. Net fluid balance for the ICU stay was lower in the
Stroke volume
SV group (1.77 L) than in the UC group (5.36 L) (p = 0.022). ICU length of stay was 2.89 days shorter (p =
Resuscitation
0.03) and duration of vasopressors was 32.8 h less (p = 0.001) in the SV group. SV group required less mechan-
ical ventilation (RR, 0.51; p = 0.0001). The SV group was less likely to require acute hemodialysis (6.25%) com-
pared with the UC group (19.5%) (RR, 0.32; p = 0.01). In multivariable analysis, SV was an independent predictor
of lower fluid balance, LOS, time on vasopressors, and not needing mechanical ventilation. This study demon-
strated that SV guided fluid resuscitation in patients with severe sepsis and septic shock was associated with re-
duced fluid balance and improved secondary outcomes.
© 2017 Elsevier Inc. All rights reserved.

1. Introduction
Severe sepsis and septic shock are characterized by peripheral vaso-
dilation associated with excessive release of inflammatory mediators
resulting in a decrease in systemic vascular resistance, decreased effec-
tive intravascular volume, and resultant tissue hypoperfusion [1]. Early
recognition, antibiotic initiation, and fluid resuscitation are integral
components of care for patients with severe sepsis and septic shock;
current Surviving Sepsis Guidelines recommend a fluid challenge of at
least 30 mL/kg of crystalloid as part of initial resuscitative efforts and
state that further fluid could be administered based upon improvement
in dynamic or static values [2-5].
Abbreviations: CO, cardiac output; CVP, central venous pressure; NICOM, non-invasive
cardiac output monitor; SAPS, Simplified Acute Physiology Score; ScvO2, central venous
oxygen saturation; SV, stroke volume; SVI, Stroke Volume Index.
⁎ Corresponding author.
E-mail addresses: hlatham@kumc.edu (H.E. Latham), cbengtson@kumc.edu
(C.D. Bengtson), lsatterwhite@kumc.edu (L. Satterwhite), mstites@kumc.edu (M. Stites),
dsubramaniam2@kumc.edu (D.P. Subramaniam), gchen2@kumc.edu (G.J. Chen),
ssimpson3@kumc.edu (S.Q. Simpson).
Multiple systematic reviews have shown that nearly half of patients
who were administered a fluid bolus in an ICU setting did not have a
corresponding increase in stroke volume (SV) or cardiac output (CO)
calling into question the utility of non-targeted fluid resuscitation in se-
vere sepsis and septic shock [6,7]. In addition, a retrospective analysis of
the Vasopressin in Septic Shock Trial and other studies of severe sepsis
and septic shock patients demonstrated that an increased positive
fluid balance is associated with increased morbidity and with mortality
[8-10]. In recent years, a number of hemodynamic monitoring devices
and techniques were validated to predict fluid responsiveness, includ-
ing pulse pressure variability, pulse contour analysis, and Doppler de-
rived techniques, each with its own benefits and flaws [11].
Bioreactance is a method that non-invasively measures hemody-
namic values, including SV and CO; it achieves these measurements by
detecting phase shifts in a small electrical current passed between elec-
trodes attached to the thorax [12]. It is comparable to other hemody-
namic measurement tools in assessing SV and CO, but it does not
require invasive monitoring [13,14]. Additionally, it is not affected by ar-
rhythmias or type of ventilation (positive or negative pressure). We
performed this retrospective analysis to evaluate the hypothesis that a
targeted volume resuscitation strategy that aimed to optimize stroke

http://dx.doi.org/10.1016/j.jcrc.2017.06.028
0883-9441/© 2017 Elsevier Inc. All rights reserved.
 H.E. Latham et al. / Journal of Critical Care 42 (2017) 42–46 43

volume via non-invasive bioreactance monitoring would result in a de- and duration of mechanical ventilation were compared using an un-
creased fluid balance and improved secondary outcomes in ICU patients paired t-test. Categorical variables including in-hospital mortality, re-
with severe sepsis and septic shock. quirement for mechanical ventilation, and requirement for dialysis
were compared using Fisher's exact test.
2. Materials and methods Multivariate analyses with linear and logistic regression were used
to determine predictive factors for the following eleven patient out-
After obtaining approval from the University of Kansas Institutional comes (dependent variables): fluid balance (4 h, 24 h, 48 h, and ICU
Review Board (00001653), we conducted a retrospective chart review LOS), hospital mortality, ICU LOS, need for mechanical ventilation and
and cohort analysis of patients with a diagnosis of severe sepsis or septic duration, need for vasopressor and duration, and need for acute hemo-
shock treated in the medical or transplant ICUs at the University of Kan- dialysis. The independent variables analyzed in each model were: use of
sas Hospital (Kansas City, KS) from April 1, 2014 to September 1, 2014. stroke volume guided resuscitation, age, gender, race, SAPS II score, ini-
Consecutive patients admitted to the medical or transplant ICUs were tial MAP, and presence of individual co-morbidities (pulmonary, cardio-
selected based on primary admission diagnosis codes for severe sepsis vascular, neurological, gastrointestinal, renal, and diabetes). The
and septic shock. The time interval for data collection was selected for multivariable analyses were computed using IBM SPSS Statistics for
evaluation because the non-invasive cardiac output monitoring Windows, Version 23.0 (Microsoft Corp. Redmond, WA). A two-tailed
(NICOM) device was available for use in our ICUs starting in April of p-value b 0.05 denoted statistical significance for all univariate compar-
2014. The stroke volume guided group of the study comprised patients isons and for predictor variables in the multivariate models.
with the primary admitting diagnosis of severe sepsis or septic shock, as
defined by the Surviving Sepsis Campaign International Guidelines
2012, who underwent stroke volume targeted fluid resuscitation guided
by NICOM (Cheetah-Medical, Newton Center, MA), during the initial 4 h
of their ICU course [2]. For comparison, we chose a similar group of
matched consecutive patients with the primary admitting diagnosis of Table 1
Comparison between SV and usual care groups.
severe sepsis or septic shock, as defined by the Surviving Sepsis Cam-
paign International Guidelines 2012, treated in the same ICU during SV-guided (%) Usual care p-Value
the same time period, but who had fluid resuscitation guided by usual Demographics
care at the discretion of the provider. No cases of severe sepsis or septic Patient no. 100 91
shock were excluded from analysis during the period of study, and vaso- Age, y 60 59 0.61
pressor use was not required to be included in the study. At the time of Gender (M/F) 49/51 45/45 1.00
SAPS II score 49.64 ± 1.60 49.25 ± 1.69 0.87
the study period and prior to implementing NICOM in our ICU, fluid re- Admit SVI pre-challenge 39
suscitation in the usual care group was primarily guided by serial lac- (on vasopressors)
tates, and bedside clinical assessment [15]. During the study period, Admit SVI post-challenge 45
fourteen separate Pulmonary and Critical Care faculty rotated, on aver- (on vasopressors)
Admit SVI pre-challenge 37
age, one week per month in the involved ICUs. Fluid management strat-
(no vasopressors)
egy was selected by individual attending or house staff physicians. Admit SVI post-challenge 44
All data were abstracted through the Epic (Verona, WI) electronic (no vasopressors)
medical record (EMR) and were collected and managed using REDCap ≥10% SVI increase 53/100 (53)
electronic data capture tools hosted at the University of Kansas Medical (all patients)
Lactate pre-challenge 3.01
Center [16]. Demographics and associated conditions were based on Lactate post-challenge 2.81
data prior to ICU admission. Patient acuity was calculated using Simpli- Admit pulse 96 102 0.12
fied Acute Physiology Score (SAPS) II and was based upon the worst Admit BP 96/53 112/65 0.0001
physiologic values in the 24 h surrounding their ICU admission. Net Admit MAP 65 78 0.0001
Admit creatininea 1.6 2.1 0.057
fluid balance was calculated using nurse documented hourly intake
Admit lactate 2.82 3.25 0.27
and output flowsheets; insensible losses were not calculated. The docu-
mentation of intake and output previous to admission to the ICU was in- Ethnicity
White 74 (74) 63 (68)
consistent throughout the data set; and therefore, the decision was
Black 14 (14) 19 (22)
made to only collect fluid balance data during the ICU admission, as Hispanic 6 (6) 5 (6)
this documentation was very consistent throughout the data set. Asian 3 (3) 1 (1)
At the time of NICOM implementation, our institution established a Other 3 (3) 3 (3)
standardized procedure for patients receiving SV-targeted fluid resusci- Co-morbidities
tation, involving either a passive leg raise or a 500 mL crystalloid bolus. Pulmonary 18 24 0.22
The procedure, once instituted, calls for patients with evidence of an SVI Cardiovascular 27 28 0.63
increase of ≥10% to receive repeated fluid boluses, until there is no fur- Neurological 15 21 0.20
GI 28 33 0.28
ther increase in SVI. For those patients undergoing SV-targeted fluid re- Renal 7 9 0.60
suscitation, the NICOM device was used within 4 h of admission to the Diabetes 24 25 0.62
ICU, and the above procedure was followed. Baseline lactate, ScvO2
Source of sepsis
and CVP measurements were obtained, when available, and in the SV
Pulmonary 39 46 0.11
group, post-volume challenge measurements were also recorded. Dura- Abdominal 27 23 0.87
tion of vasopressor use was calculated to the nearest hour, and number Urological 27 21 0.62
of vasopressors used was determined, regardless of duration of use. Me- Skin & soft tissue 8 13 0.17
Bacteremia 11 5 0.20
chanical ventilation and dialysis utilization was determined by any use
CNS 2 1 0.99
of those devices in a calendar day. Endocarditis 0 3 0.12
The univariate analyses were compared using Graphpad® PRISM 6 N1 source identified 11 20 0.05
software (La Jolla, CA). Demographics were compared using descriptive SAPS II = Simplified Acute Physiology Score II, SVI = Stroke Volume Index, MAP = Mean
statistics. The continuous variables of SAPS II, fluid balance (4 h, 24 h, Arterial Pressure, GI = Gastrointestinal.
48 h, and ICU Length of Stay (LOS)), ICU LOS, time on vasopressors, a
Creatinine of patients not receiving chronic hemodialysis at time of admission to ICU.
44 H.E. Latham et al. / Journal of Critical Care 42 (2017) 42–46

3. Results Table 2
Comparison of SV vs UC for patient outcomes in univariate analyses.

In the stroke volume group there were 100 patients identified, com- Patient outcomes SV UC p-Value
pared with 91 patients in the usual care group. The initial blood pressure Net-fluid balance – 4 h 808 ± 118 mL 926 ± 153 mL 0.54
and mean arterial pressure were higher in the usual care group. Other- Net-fluid balance – 24 h 1.68 ± 0.27 L 3.00 ± 0.36 L 0.004
wise, there were no significant differences between groups (Table 1). Net-fluid balance – 48 h 2.14 ± 0.39 L 4.16 ± 0.50 L 0.002
Use of stroke volume targeted resuscitation to guide fluid resuscitation Net-fluid balance – ICU LOS 1.77 ± 0.60 L 5.36 ± 1.01 L 0.002
In-hospital mortality 21/100 (21) 18/91 (20) 0.86
increased over the course of the study period, and fewer patients re-
ICU LOS – all patients (days) 6.22 ± 0.58 8.91 ± 0.96 0.015
ceived non-SV targeted resuscitation towards the end of the six ICU LOS – survivors (days) 5.98 ± 0.68 8.87 ± 1.18 0.03
month study period. Fifty-three percent of patients who received Mechanically ventilated 29/100 (29) 52/91 (57) 0.0001
NICOM measurement were found to be fluid responsive with a change Ventilator days 6.28 ± 1.40 6.71 ± 0.67 0.76
in the SVI by ≥ 10%. The mean SAPS II score was similar between the Vasopressor initiated 48/100 (48) 52/91 (57) 0.25
Vasopressor duration (hours) 32.08 ± 5.22 64.86 ± 8.39 0.001
SV (49.64 ± 1.60) and usual care (49.25 ± 1.69) groups (p = 0.87). Acute dialysis initiateda 6/96 (6.25) 16/82 (19.5) 0.01
We first performed univariate analyses comparing stroke volume
ICU = Intensive Care Unit, LOS = Length of Stay.
guided resuscitation versus usual care. Net fluid balance for the entire a
Excludes patients that required chronic hemodialysis prior to admission.
ICU length of stay was 1.77 ± 0.60 L in the SV group and 5.36 ±
1.01 L in the usual care group (p = 0.002). When further stratified by
time from admission in the ICU, there was no significant difference in
fluid balance at 4 h (SV 808 ± 118 mL vs usual care 926 ± 153 mL; p After the univariate analyses, we adjusted for independent variables
= 0.54). However, at 24 h and 48 h there were significant differences in multiple linear and logistic regression models. The results of these
in favor of decreased fluid balance in the SV group (SV 1.68 ± 0.27 L analyses follow. Tables detailing the results of each of the multivariate
vs usual care 3.00 ± 0.36 L; p = 0.004, and SV 2.14 ± 0.39 L vs usual regression models are available in the online supplement. Stroke vol-
care 4.16 ± 0.50 L; p = 0.002, respectively) (Fig. 1). At hospital dis- ume guided resuscitation was an independent predictor of a lower
charge, 21 patients in the SV group (21%) and 18 patients in the usual fluid balance at 24 h, 48 h, and at the ICU LOS (online supplement, Ta-
care group (19.8%) had died. The in-hospital mortality between the bles 2–4). There were no predictors of fluid balance at 4 h, but stroke
two groups did not differ significantly (relative risk, 0.98; 95% confi- volume guided resuscitation approached statistical significance at 4 h
dence interval (CI), 0.85 to 1.14; p = 0.86). When corrected for non-sur- into the ICU admission (online supplement, Table 1). The SAPS II score
vivors, there was a significantly lower ICU length of stay in the SV group was an independent predictor of a higher fluid balance with increasing
(SV 5.98 ± 0.68 days and usual care 8.87 ± 1.18 days; p = 0.03). Addi- severity of illness at 24 h, 48 h, and at the ICU LOS. Initial MAP and renal
tionally, patients in the SV group were less likely to require mechanical comorbidity were predictors of a lower fluid balance at 24 h. Age and
ventilation (relative risk, 0.51; CI 0.36 to 0.72; p = 0.0001). However, race were also predictors of fluid balance at 48 h. In addition to stroke
there was no significant difference in ventilator days for patients requir- volume guided resuscitation, age was a predictor of lower net fluid bal-
ing mechanical ventilation (SV 6.28 ± 1.40 days versus usual care 6.71 ance at the end of the ICU stay, but neurologic and GI co-morbidities
± 0.67 days; p = 0.76). There was no between group difference in the were predictors of a higher net fluid balance.
need for vasopressors or number of vasopressors required (relative The SAPS II score (odds ratio, 0.94; 95% CI, 0.916–0.917; p b 0.0001)
risk, 0.84; CI 0.64 to 1.10; p = 0.25; SV 1.60 ± 0.14 vasopressors needed and gastrointestinal co-morbidity, primarily end-stage liver disease,
versus usual care 1.86 ± 0.14 vasopressors needed, p = 0.19). However, (odds ratio, 0.19; 95% CI, 0.08–0.45; p b 0.0001) were the only indepen-
patients requiring vasopressors in the SV group received this therapy on dent predictors of in-hospital mortality (online supplement, Table 5).
average 32.08 ± 5.22 h which was significantly less than the 64.86 ± However, stroke volume guided resuscitation was an independent pre-
8.39 h in the usual care group (p = 0.001). When excluding patients ad- dictor of a shorter ICU length of stay while the SAPS II score was a pre-
mitted on chronic hemodialysis, patients in the SV group were less like- dictor of increasing length of stay with increased severity of illness
ly to require acute hemodialysis (6.25%) compared with the usual care (online supplement, Table 6). No other variables were predictors of
group (19.5%) (relative risk, 0.32; CI 0.13 to 0.78; p = 0.01). Table 2 ICU length of stay.
summarizes the comparison between stroke volume guided resuscita- Stroke volume guided resuscitation was an independent negative
tion and usual care in the univariate analyses. predictor of needing mechanical ventilation (odds ratio, 0.34; 95% CI,
0.15–0.80; p b 0.014) along with age and having a renal co-morbidity
on admission (online supplement, Table 7). SAPS II score, initial MAP,
and having diabetes as a co-morbidity were positive predictors of re-
quiring mechanical ventilation. The presence of a cardiac or a pulmo-
nary co-morbidity was not an independent predictor of the need for
mechanical ventilation. There were no independent predictors of dura-
tion of mechanical ventilation for those patients requiring it during the
ICU admission (online supplement, Table 8).
In the logistic regression model for initiating vasopressors, age and
race were negative predictors of requiring vasopressors while the
SAPS II score and gastrointestinal co-morbidity were independent pre-
dictors of needing vasopressors (online supplement, Table 9). However,
SV guided resuscitation was not an independent predictor of requiring
vasopressors. Stroke volume guided resuscitation was an independent
predictor of shorter duration of vasopressor use for those requiring va-
sopressor initiation (online supplement, Table 10). Neurologic and renal
co-morbidities on admit were predictors of longer duration of vasopres-
sor use.
Fig. 1. The fluid balance between the two groups was significantly less in the stroke
Finally, the multivariate analysis did not reveal any independent
volume (SV) group at 24 h, 48 h, and at the end of the ICU stay compared with the usual
care (UC) group. Dashed lines represent the difference in length of stay (LOS) between predictors for the need of acute hemodialysis (online supplement,
the two groups. Table 11). Table 3 summarizes the results of stroke volume guided
 H.E. Latham et al. / Journal of Critical Care 42 (2017) 42–46
Table 3
SV resuscitation results as an independent variable for patient outcomes in multivariate
analyses.
Outcome Results Confidence intervals
Net-fluid balance – 4 h −360.91 mL −727.16 to −5.340
Net-fluid balance – 24 h −1391.95 mL −2150.96 to −632.95
Net-fluid balance – 48 h −1485.26 mL −2496.60 to −473.92
Net-fluid balance – ICU LOS −2779.17 mL −4686.48 to −871.86
In-hospital mortality OR 0.58 0.23–1.47
ICU LOS – survivors −2.55 days −4.98 to −0.12
Mechanically ventilated OR 0.34 0.15–0.80
Ventilator days −2.15 days −5.24–0.97
Vasopressor initiated OR 0.57 0.26–1.24
Vasopressor duration −27.94 h −51.16 to −4.74
Acute dialysis initiateda OR 1.11 0.08–15.74
ICU = Intensive Care Unit, LOS = Length of Stay.
a SV-targeted group. Assuming there was no increased risk of renal failure
Excludes patients that required chronic hemodialysis prior to admission.
resuscitation as an independent variable for each of the multivariate
analyses of the eleven patient outcomes.
4. Discussion
Our study represents the first significant outcomes evaluation of
bioreactance guided stroke volume targeted fluid resuscitation in pa-
tients with severe sepsis and septic shock in the intensive care unit.
The results of this retrospective cohort study support our hypothesis
that net fluid balance is less positive when a volume resuscitation strat-
egy aimed at optimizing stroke volume is used in patients with severe
sepsis and septic shock. This was supported in both the univariate and
multivariate analyses. The difference in fluid balance for the ICU length
of stay could be confounded by a reduced ICU length of stay in the SV
group. However, the difference in fluid balance was evident at 24 and
48 h and persisted throughout the remainder of the ICU stay. The short-
ened length of stay in the SV group would not affect fluid balance at
these early time intervals. We believe fluid balances at 24 h and 48 h
are important markers to assess for volume overload, because multiple
studies identified these time intervals as important points of care to pre-
dict morbidity and mortality from a volume standpoint in the critically
ill [8,9,17]. The fluid balance at 4 was similar between the two groups.
We hypothesize this reflects the tendency of physicians to give volume
for hypotension or an elevated lactate when the patient is first admitted.
In the SV group, the absence of continued improvement in stroke vol-
ume likely served as an objective measure of adequate volume resusci-
tation to limit further fluid administration. However, the usual care
group likely received additional volume, whether it from boluses or
maintenance fluid, for refractory shock or elevated lactate. Hence, the
fluid balance progressively separated throughout the remainder of the
ICU admission.
The lower fluid balance in the SV group likely contributed to other ben-
eficial effects measured in the secondary outcomes, including shortened
ICU length of stay, reduced time on vasopressors, reduced requirement
for mechanical ventilation, and reduced requirement for hemodialysis.
With less administered volume in the SV group, it is logical that these pa-
tients had less pulmonary and peripheral edema and therefore would be
less likely to progress to respiratory failure requiring mechanical ventila-
tion. Another potential confounding factor for the increased rate of me-
chanical ventilation in the usual care group was the increase in
pulmonary and cardiac co-morbidities in the usual care group compared
to the SV group, albeit not statistically significant. However, these co-mor-
bidities were not independent predictors for requiring mechanical ventila-
tion in the multivariate analysis for this patient outcome.
It is less intuitive that patients with a lower fluid balance would re-
quire vasopressors for a significantly shorter length of time. To our
knowledge, this observation has not been reported in the literature.
There are a number of possible explanations including the vasodilatory
and inflammatory effects of hyperchloremia from saline infusion
45
previously demonstrated in animal sepsis models [18,19]. In addition,
it is possible that volume overload in the usual care group contributed
to endothelial cell activation leading to continued cytokine release and
p-Value prolonged systemic inflammatory response with vasodilatory effects
0.053 [20]. Regardless of the etiology, the reduced time on vasopressors was
b0.0001 likely a major contributing factor to the reduced ICU length of stay in
0.004 the SV group.
0.005
Another interesting finding was the increased requirement for he-
0.25
0.040 modialysis in the usual care group. There was no significant difference
0.01 in the admission creatinine between the two groups, although there
0.17 was a trend towards a higher creatinine in the usual care group. Recent
0.15 trials of severe sepsis and septic shock demonstrated dialysis rates be-
0.02
0.94
tween 13.4 and 18% [3,4,21]. Our usual care group had a corrected dial-
ysis rate of 19.5% compared to the corrected dialysis rate of 6.25% in the
in the usual care group, excess fluid balance could contribute to this out-
come as well. Our findings are consistent with a number of studies that
demonstrated a positive fluid balance was associated with an increased
risk for acute renal injury and trends towards increased need for hemo-
dialysis [22-24]. At the time of this study, fluid resuscitation in our insti-
tution was principally achieved via normal saline. Several studies
demonstrate the deleterious effects of chloride-rich fluids on renal func-
tion and increased risk of hemodialysis in the critically ill [25-27]. We
did not trend the chloride levels in our analysis, but further evaluation
of the patients requiring hemodialysis may be of interest.
We did not find a mortality difference between the two groups.
However, the mortality rate was approximately 20% for both groups,
which is consistent with the mortality of this patient population in re-
cent large clinical trials [3-5]. Given the small sample size, we expected
the study to be underpowered to detect a difference in mortality. In the
multivariate analysis for this patient outcome, the SAPS II score was an
independent predictor of mortality as any severity of illness score
should be.
Our study has limitations, the most important being its retrospective
nature. Thus, the results only serve to generate hypotheses for addition-
al prospective study and do not support definitive conclusions regard-
ing stroke volume targeted resuscitation practices. Furthermore, there
is potential for selection bias, as physicians independently determined
in which patients to use NICOM to guide volume resuscitation. Howev-
er, fourteen attending physicians and twelve pulmonary and critical
care fellows were involved in the care of these patients over the course
of the six month study period, which lessens the chances that systemat-
ic bias in patient selection for SV-targeted resuscitation was responsible
for the outcome differences observed between the two groups. This is
further supported by the nearly identical baseline SAPS-II scores of the
groups. Also, there were very few patients with documented CVP or
central venous O2 saturations, reflecting the then prevalent practice of
our physician group to use alternative markers, namely lactate levels,
to guide resuscitation in this patient population. Therefore, we could
not assess for any correlation of fluid balance with these markers be-
tween the two groups. In addition, documentation of fluid balance pre-
vious to admission to the ICU was inconsistent; and therefore, not
collected for the purpose of this study. Thus, the fluid balance in the
first 4 h of admission appears inadequate compared to the Surviving
Sepsis Campaign's recommended 30 mL/kg. However, documentation
of fluid balance on an hourly basis was consistent throughout the ICU
stay, and we believe this ensures an accurate comparison between the
two groups from time zero of the ICU stay, which we see as a strength.
Another strength to the study is that 53% of patients in the SV group
were fluid responsive, consistent with other publications indicating
that only half of critically ill patients are fluid responsive [6,7].
5. Conclusion
In conclusion, our retrospective cohort study demonstrated that op-
timization of stroke volume guided by bioreactance in patients with
46 H.E. Latham et al. / Journal of Critical Care 42 (2017) 42–46
severe sepsis and septic shock was associated with reduced fluid bal-
ance, duration of ICU stay, duration of vasopressors, and requirement
of mechanical ventilation and hemodialysis compared with usual care.
A randomized trial using a protocolized approach of stroke volume
targeted resuscitation in patients with severe sepsis and septic shock
is needed to further evaluate these findings.
Funding
This research did not receive any specific grant from funding agen-
cies in the public, commercial, or not-for-profit sectors.
Conflict of interest disclosures related to this manuscript
Dr Latham received consulting fees from Cheetah Medical in 2016.
None of the other authors of this manuscript have any financial or per-
sonal relationships that might inappropriately influence their actions
and create a conflict of interest relative to the content of this
manuscript.
Author contributions
Author contributions: Dr Latham is the corresponding author and
guarantor of the content of this manuscript, including all the data and
analysis. Dr Latham, Dr Bengtson, and Dr Simpson contributed substan-
tially to the study design, data collection, analysis, interpretation, and
the writing of this manuscript. Dr Satterwhite and Ms Stites contributed
substantially to the study design, data interpretation, and the writing of
this manuscript. Dr Subramaniam and Dr Chen contributed substantial-
ly to data analysis, data interpretation and writing of this manuscript.
Appendix A. Supplementary data
Supplementary data to this article can be found online at http://dx.
doi.org/10.1016/j.jcrc.2017.06.028.
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