Near-infrared spectroscopy StO2 monitoring to assess the therapeutic effect of drotrecogin alfa (activated) on microcirculation in patients with severe sepsis or septic shock

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Abstract

Background

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. Future efforts need to be directed towards microperfusion monitoring and treatment. This study explored the utility of thenar muscle oxygen saturation (StO ₂) and its changes during a transient vascular occlusion test (VOT) to measure the microcirculatory response to drotrecogin alfa (activated) (DrotAA) in septic patients.

Methods

A 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. StO ₂ 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.

Results

Patients’ characteristics, outcome, severity, and baseline values of StO ₂, 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).

Conclusions

In 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, StO ₂ derived variables might be useful to evaluate the microcirculatory response to treatment of septic shock.

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Most cited references 24

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Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008

R Phillip Dellinger, Mitchell Levy, Jean M. Carlet … (2007)

Objective To provide an update to the original Surviving Sepsis Campaign clinical management guidelines, “Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock,” published in 2004. Design Modified Delphi method with a consensus conference of 55 international experts, several subsequent meetings of subgroups and key individuals, teleconferences, and electronic-based discussion among subgroups and among the entire committee. This process was conducted independently of any industry funding. Methods We used the GRADE system to guide assessment of quality of evidence from high (A) to very low (D) and to determine the strength of recommendations. A strong recommendation [1] indicates that an intervention's desirable effects clearly outweigh its undesirable effects (risk, burden, cost), or clearly do not. Weak recommendations [2] indicate that the tradeoff between desirable and undesirable effects is less clear. The grade of strong or weak is considered of greater clinical importance than a difference in letter level of quality of evidence. In areas without complete agreement, a formal process of resolution was developed and applied. Recommendations are grouped into those directly targeting severe sepsis, recommendations targeting general care of the critically ill patient that are considered high priority in severe sepsis, and pediatric considerations. Results Key recommendations, listed by category, include: early goal-directed resuscitation of the septic patient during the first 6 hrs after recognition (1C); blood cultures prior to antibiotic therapy (1C); imaging studies performed promptly to confirm potential source of infection (1C); administration of broad-spectrum antibiotic therapy within 1 hr of diagnosis of septic shock (1B) and severe sepsis without septic shock (1D); reassessment of antibiotic therapy with microbiology and clinical data to narrow coverage, when appropriate (1C); a usual 7–10 days of antibiotic therapy guided by clinical response (1D); source control with attention to the balance of risks and benefits of the chosen method (1C); administration of either crystalloid or colloid fluid resuscitation (1B); fluid challenge to restore mean circulating filling pressure (1C); reduction in rate of fluid administration with rising filing pressures and no improvement in tissue perfusion (1D); vasopressor preference for norepinephrine or dopamine to maintain an initial target of mean arterial pressure ≥ 65 mm Hg (1C); dobutamine inotropic therapy when cardiac output remains low despite fluid resuscitation and combined inotropic/vasopressor therapy (1C); stress-dose steroid therapy given only in septic shock after blood pressure is identified to be poorly responsive to fluid and vasopressor therapy (2C); recombinant activated protein C in patients with severe sepsis and clinical assessment of high risk for death (2B except 2C for post-operative patients). In the absence of tissue hypoperfusion, coronary artery disease, or acute hemorrhage, target a hemoglobin of 7–9 g/dL (1B); a low tidal volume (1B) and limitation of inspiratory plateau pressure strategy (1C) for acute lung injury (ALI)/acute respiratory distress syndrome (ARDS); application of at least a minimal amount of positive end-expiratory pressure in acute lung injury (1C); head of bed elevation in mechanically ventilated patients unless contraindicated (1B); avoiding routine use of pulmonary artery catheters in ALI/ARDS (1A); to decrease days of mechanical ventilation and ICU length of stay, a conservative fluid strategy for patients with established ALI/ARDS who are not in shock (1C); protocols for weaning and sedation/analgesia (1B); using either intermittent bolus sedation or continuous infusion sedation with daily interruptions or lightening (1B); avoidance of neuromuscular blockers, if at all possible (1B); institution of glycemic control (1B) targeting a blood glucose < 150 mg/dL after initial stabilization ( 2C ); equivalency of continuous veno-veno hemofiltration or intermittent hemodialysis (2B); prophylaxis for deep vein thrombosis (1A); use of stress ulcer prophylaxis to prevent upper GI bleeding using H2 blockers (1A) or proton pump inhibitors (1B); and consideration of limitation of support where appropriate (1D). Recommendations specific to pediatric severe sepsis include: greater use of physical examination therapeutic end points (2C); dopamine as the first drug of choice for hypotension (2C); steroids only in children with suspected or proven adrenal insufficiency (2C); a recommendation against the use of recombinant activated protein C in children (1B). Conclusion There was strong agreement among a large cohort of international experts regarding many level 1 recommendations for the best current care of patients with severe sepsis. Evidenced-based recommendations regarding the acute management of sepsis and septic shock are the first step toward improved outcomes for this important group of critically ill patients.

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The prognostic value of muscle StO2 in septic patients.

Jacques Creteur, Tiziana Carollo, Giulia Soldati … (2007)

To quantify sepsis-induced alterations in changes in muscle tissue oxygenation (StO(2)) after an ischemic challenge using near-infrared spectroscopy (NIRS), and to test the hypothesis that these alterations are related to outcome. Prospective study. Thirty-one-bed, university hospital Department of Intensive Care. Seventy-two patients with severe sepsis or septic shock, 18 hemodynamically stable, acutely ill patients without infection, and 18 healthy volunteers. Three-minute occlusion of the brachial artery using a cuff inflated 50[Symbol: see text]mmHg above systolic arterial pressure. Thenar eminence StO(2) was measured continuously by NIRS before (StO(2)baseline), during, and after the 3-min occlusion. Changes in StO(2) were assessed by the slope of increase in StO(2) during the first 14 s following the ischemic period and by the difference between the maximum StO(2) and StO(2)baseline (Delta). The slope was lower in septic patients than in controls and volunteers [2.3 (1.3-3.6), 4.8 (3.5-6.0), and 4.7 (3.2-6.3) %/s, p < 0.001]. Delta was also significantly lower in septic patients than in the other groups. Slopes were lower in septic patients with than without shock [2.0 (1.2-2.9) vs 3.2 (1.8-4.5) %/s, p < 0.05]. In 52 septic patients, in whom the slope was obtained every 24 h for 48 h, slopes were higher in survivors than in non-survivors and tended to increase in survivors but not in non-survivors. Altered recovery in StO(2) after an ischemic challenge is frequent in septic patients and more pronounced in the presence of shock. The presence and persistence of these alterations in the first 24[Symbol: see text]h of sepsis are associated with worse outcome.

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Use of non-invasive NIRS during a vascular occlusion test to assess dynamic tissue O(2) saturation response.

Patricio Polanco, M Pinsky, Hyung Suk Kim … (2008)

We assessed tissue O(2) saturation (StO(2)) and total hemoglobin (HbT) changes during a vascular occlusion test (VOT) as markers of O(2) consumption and cardiovascular reserve. Using the non-invasive InSpectra near infrared spectrometer, we studied the effect of VOT to StO(2) < 40% then release on thenar eminence StO(2) and HbT in 15 normal volunteers (controls) and 10 trauma patients. We repeated the VOT four times in controls and twice in patients, with controls exercising during the last VOT, and correlated StO(2) with HbT changes by linear regression analysis. StO(2) started to decrease 3-28 s post-occlusion (latency) in controls and then decreased in a linear fashion (-0.18 +/- 0.04% O(2)/s, mean +/- SD), while post-occlusion StO(2) recovery was rapid (5.20 +/- 1.19% O(2)/s). Exercise decreased latency (0-5 s) and increased desaturation rate (-0.18 and -0.69% O(2)/s, P < 0.005) without altering recovery. Trauma patients showed similar StO(2) desaturation rates, but slower recovery (5.20 +/- 1.19 vs. 2.88 +/- 1.71%/s, P < 0.0001). Repeated VOT gave similar recovery results within study groups. The hyperemic response was variable in both groups and, if present, was associated with an increased HbT. HbT pre- and post-VOT were significantly different within each subject. Although HbT slope of recovery correlated significantly with StO(2) recovery in trauma patients (rho 0.76), it was not in controls. One VOT defines StO(2) deoxygenation and recovery. That StO(2) and HbT recovery co-vary only in trauma patients suggests that pre-existing vasoconstriction was unmasked by the ischemic challenge consistent with increased sympathetic tone.

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Author and article information

Contributors

Jordi Masip

Jaume Mesquida

Cecilia Luengo

Gisela Gili

Gemma Gomà

Ricard Ferrer

Jean Louis Teboul

Didier Payen

Antonio Artigas

Journal

Journal ID (nlm-ta): Ann Intensive Care

Journal ID (iso-abbrev): Ann Intensive Care

Title: Annals of Intensive Care

Publisher: Springer

ISSN (Electronic): 2110-5820

Publication date Collection: 2013

Publication date (Electronic): 4 September 2013

Volume: 3

Page: 30

Affiliations

[1 ]Critical Care Department, Hospital de Sabadell, CIBER Enfermedades Respiratorias, Consorci Sanitari Universitari Parc Tauli, Universitat Autònoma de Barcelona, Parc Taulí s/n, Sabadell (Barcelona) CP 08208, Spain

[2 ]Department of Medicine, Intensive Care Unit, Critical Care Patient Unit, Hospital Clínico Universidad de Chile, Avenida Santos Dumontt 999, Independencia, Santiago, Chile

[3 ]Department of Anesthesiology & Critical Care Medicine, SAMU and Laboratory of Anesthesiology, Hospital Lariboisière, Paris, 2, rue Ambroise – Paré, 75010 Paris, 10ème, France

[4 ]Intensive Care Department, Mutua Terrassa University Hospital, University of Barcelona. CIBER Enfermedades Respiratorias, Plaça Doctor Robert, Terrassa (Barcelona) CP: 08221, Spain

[5 ]Service de Réanimation Médicale, Centre Hospitalo-Universitaire de Bicêtre, 78 rue du Général-Leclerc, Le Kremlin-Bicêtre 94 270, France

Article

Publisher ID: 2110-5820-3-30

DOI: 10.1186/2110-5820-3-30

PMC ID: 3847092

PubMed ID: 24007807

SO-VID: 9f1fb4bb-d934-4c7e-8655-0407e8749cd7

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.