Abstract
BackgroundSepsis is a leading cause of death despite appropriate management. There is increasing evidence that microcirculatory alterations might persist independently from macrohemodynamic improvement and are related to clinical evolution. Future efforts need to be directed towards microperfusion monitoring and treatment. This study explored the utility of thenar muscle oxygen saturation (StO2) and its changes during a transient vascular occlusion test (VOT) to measure the microcirculatory response to drotrecogin alfa (activated) (DrotAA) in septic patients.MethodsA prospective, observational study was performed in three general intensive care units at three university hospitals. We studied 58 patients with recent onset of severe sepsis or septic shock and at least two organ dysfunctions. Thirty-two patients were treated with DrotAA and 26 were not treated because of formal contraindication. StO2 was monitored using near-infrared spectroscopy (NIRS), and VOT was performed to obtain deoxygenation (DeOx) and reoxygenation (ReOx) slopes. Measurements were obtained before DrotAA was started and were repeated daily for a 96-hour period.ResultsPatients’ characteristics, outcome, severity, and baseline values of StO2, DeOx, and ReOx did not differ between groups. Treated patients significantly improved DeOx and ReOx values over time, whereas control patients did not. In treated patients, ReOx improvements were correlated to norepinephrine dose reductions. Early clinical response (SOFA improvement after 48 hours of treatment) was not associated to changes in VOT-derived slopes. In the treated group, the relative improvement of DeOx within 48 hours was able to predict mortality (AUC 0.91, p < 0.01).ConclusionsIn patients with severe sepsis or septic shock, DrotAA infusion was associated with improvement in regional tissue oxygenation. The degree of DeOx amelioration after 2 days in treated patients predicted mortality with high sensitivity and specificity. Thus, StO2 derived variables might be useful to evaluate the microcirculatory response to treatment of septic shock.
Highlights
Sepsis is a leading cause of death despite appropriate management
There is increasing evidence that persistent microcirculatory alterations are related to clinical evolution independently from macrohemodynamic improvement [4,5,6,7,8]
Patients Patients were recruited according to the following inclusion criteria: age >18 years old, with proven or suspected infection; infection was suspected when white blood cells were present in a normally sterile body fluid, or a viscera was perforated, or purulent sputum production was present associated with chest x-ray consistent with pneumonia, or a clinical syndrome of inflammation was associated with a high probability of infection, such as purpura fulminans or ascending cholangitis; presence of severe sepsis [25], with at least two sepsis-associated organ failures, newly developed, and not explained by an underlying disease or by the effects of concomitant therapy
Summary
Sepsis is a leading cause of death despite appropriate management. There is increasing evidence that microcirculatory alterations might persist independently from macrohemodynamic improvement and are related to clinical evolution. Sepsis is a leading cause of death in critically ill patients despite the use of modern antibiotics and resuscitation strategies [1]. Increased microvascular heterogeneity during sepsis mediated by the presence in varying degrees of stopped-flow capillaries, cell aggregation and thrombosis phenomena, vasoconstriction, and alteration of red cell flexibility among others [9] might be only partially reversed by macrohemodynamics resuscitation strategies. This strengthens the opinion that future research efforts need to be directed towards monitoring technologies and therapies targeting tissue microperfusion
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