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Comparative Study
. 2009;13 Suppl 5(Suppl 5):S13.
doi: 10.1186/cc8011. Epub 2009 Nov 30.

Low tissue oxygen saturation at the end of early goal-directed therapy is associated with worse outcome in critically ill patients

Affiliations
Comparative Study

Low tissue oxygen saturation at the end of early goal-directed therapy is associated with worse outcome in critically ill patients

Alexandre Lima et al. Crit Care. 2009.

Abstract

Introduction: The prognostic value of continuous monitoring of tissue oxygen saturation (StO2) during early goal-directed therapy of critically ill patients has not been investigated. We conducted this prospective study to test the hypothesis that the persistence of low StO2 levels following intensive care admission is related to adverse outcome.

Methods: We followed 22 critically ill patients admitted with increased lactate levels (>3 mmol/l). Near-infrared spectroscopy (NIRS) was used to measure the thenar eminence StO2 and the rate of StO2 increase (RincStO2) after a vascular occlusion test. NIRS dynamic measurements were recorded at intensive care admission and each 2-hour interval during 8 hours of resuscitation. All repeated StO2 measurements were further compared with Sequential Organ Failure Assessment (SOFA), Acute Physiology and Chronic Health Evaluation (APACHE) II and hemodynamic physiological variables: heart rate (HR), mean arterial pressure (MAP), central venous oxygen saturation (ScvO2) and parameters of peripheral circulation (physical examination and peripheral flow index (PFI)).

Results: Twelve patients were admitted with low StO2 levels (StO2 <70%). The mean scores for SOFA and APACHE II scores were significantly higher in patients who persisted with low StO2 levels (n = 10) than in those who exhibited normal StO2 levels (n = 12) at 8 hours after the resuscitation period (P < 0.05; median (interquartile range): SOFA, 8 (7 to 11) vs. 5 (3 to 8); APACHE II, 32(24 to 33) vs. 19 (15 to 25)). There was no significant relationship between StO2 and mean global hemodynamic variables (HR, P = 0.26; MAP, P = 0.51; ScvO2, P = 0.11). However, there was a strong association between StO2 with clinical abnormalities of peripheral perfusion (P = 0.004), PFI (P = 0.005) and RincStO2 (P = 0.002). The persistence of low StO2 values was associated with a low percentage of lactate decrease (P < 0.05; median (interquartile range): 33% (12 to 43%) vs. 43% (30 to 54%)).

Conclusions: We found that patients who consistently exhibited low StO2 levels following an initial resuscitation had significantly worse organ failure than did patients with normal StO2 values, and found that StO2 changes had no relationship with global hemodynamic variables.

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Figures

Figure 1
Figure 1
Evolution of StO2 levels in our patient population stratified by low (StO2 <70%) and normal (StO2 ≥70%) values upon admission (T0) and 8 h after resuscitation (T8). ICU, intensive care unit; StO2, tissue oxygen saturation.
Figure 2
Figure 2
Box plotting demonstrating the outcome score values stratified by the StO2 levels 8 h after resuscitation: StO2 <70% (n = 10); StO2 ≥70% (n = 12). APACHE, Acute Physiology and Chronic Health Evaluation; SOFA, Sequential Organ Failure Assessment; StO2, tissue oxygen saturation. *Significant, Wilcoxon rank test.

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