The association of near-infrared spectroscopy-derived tissue oxygenation measurements with sepsis syndromes, organ dysfunction and mortality in emergency department patients with sepsis
1 Department of Emergency Medicine and Center for Vascular Biology Research, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA
2 Department of Emergency Medicine, Cooper University Hospital and the University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School at Camden, One Cooper Plaza, Camden, NJ 08103, USA
3 Department of Emergency Medicine, Detroit Receiving Hospital and Wayne State University, 4201 St Antoine 6G, UHC, Detroit, MI 48201, USA
4 Department of Emergency Medicine, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39211 USA
5 Technomics Research, LLC, 1815 Medina Road, Minneapolis, MN 55356, USA
6 Department of Critical Care, Cooper University Hospital and University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School at Camden, One Cooper Plaza, Camden, NJ 08103, USA
Critical Care 2011, 15:R223 doi:10.1186/cc10463Published: 22 September 2011
Near-infrared spectroscopy (NIRS) noninvasively measures peripheral tissue oxygen saturation (StO2). NIRS may be utilized along with a vascular occlusion test, in which limb blood flow is temporarily occluded and released, to quantify a tissue bed's rate of oxygen exchange during ischemia and recovery. The objective of this study was to test the hypothesis that NIRS-derived StO2 measures (StO2 initial, StO2 occlusion and StO2 recovery) identify patients who are in shock and at increased risk of organ dysfunction (Sequential Organ Failure Assessment (SOFA) score ≥ 2 at 24 hours) and dying in the hospital.
This prospective, observational study comprised a convenience sample of three cohorts of adult patients (age > 17 years) at three urban university emergency departments: (1) a septic shock cohort (systolic blood pressure < 90 after fluid challenge; the "SHOCK" cohort, n = 58), (2) a sepsis without shock cohort (the "SEPSIS" cohort, n = 60) and emergency department patients without infection (n = 50). We measured the StO2 initial, StO2 occlusion and StO2 recovery slopes for all patients. Outcomes were sepsis syndrome severity, organ dysfunction (SOFA score at 24 hours) and in-hospital mortality.
Among the 168 patients enrolled, mean initial StO2 was lower in the SHOCK cohort than in the SEPSIS cohort (76% vs 81%), with an impaired occlusion slope (-10.2 and 5.2%/minute vs -13.1 and 4.4%/minute) and an impaired recovery slope (2.4 and 1.6%/second vs 3.9 and 1.7%/second) (P < 0.001 for all). The recovery slope was well-correlated with SOFA score at 24 hours (-0.35; P < 0.001), with a promising area under the curve (AUC) for mortality of 0.81. The occlusion slope correlation with SOFA score at 24 hours was 0.21 (P < 0.02), with a fair mortality AUC of 0.70. The initial StO2 was significantly but less strongly correlated with SOFA score at 24 hours (-0.18; P < 0.04), with a poor mortality AUC of 0.56.
NIRS measurements for the StO2 initial, StO2 occlusion and StO2 recovery slope were abnormal in patients with septic shock compared to sepsis patients. The recovery slope was most strongly associated with organ dysfunction and mortality. Further validation is warranted.