Comparison of stroke volume measurement between non-invasive bioreactance and esophageal Doppler in patients undergoing major abdominal-pelvic surgery

PURPOSE: Bioreactance is a non-invasive technology for measuring stroke volume (SV) in the operating room and critical care setting. We evaluated how the NICOM® bioreactance device performed against the CardioQ® esophageal Doppler monitor in patients undergoing major abdominal–pelvic surgery, focusing on the effect of different hemodynamic interventions. METHODS: SVNICOM and SVODM were simultaneously measured intraoperatively, including before and after interventions including fluid challenge, vasopressor boluses, peritoneal gas insufflation/removal, and Trendelenburg/reverse Trendelenburg patient positioning. RESULTS: A total of 768 values were collected from 21 patients. Pre- and post-intervention measures were recorded on 155 occasions. Bland–Altman analysis revealed a bias of 8.6 ml and poor precision with wide limits of agreement (54 and −37 ml) and a percentage error of 50.6%. No improvement in precision was detected after taking into account repeated measurements for each patient (bias: 8 ml; limits of agreement: 74 and −59 ml). Concordance between changes in SVNICOM and SVODM before and after interventions was also poor: 78.7% (all measures), 82.4% (after vasopressor administration), and 74.3% (after fluid challenge). Using Doppler SV as the reference technique, the area under the receiver operating characteristic curve assessing the ability of the NICOM device to predict fluid responsiveness was 0.81 (0.7–0.9). CONCLUSIONS: In patients undergoing major abdomino-pelvic surgery, SV values obtained by NICOM showed neither clinically or statistically acceptable agreement with those obtained by esophageal Doppler. Although, in the setting of this study, bioreactance technology cannot reliably replace esophageal Doppler monitoring, its accuracy for predicting fluid responsiveness was higher, up to approximately 80%

Optimising organ perfusion in the high-risk surgical and critical care patient: a narrative review

Maintenance or prompt restoration of an oxygen supply sufficient to facilitate adequate cellular metabolism is fundamental in maintaining organ function. This is particularly relevant when metabolic needs change markedly, for example in response to major surgery or critical illness. The consequences of inadequate tissue oxygenation include wound and anastomotic breakdown, organ dysfunction, and death. However, our ability to identify those at risk and to promptly recognise and correct tissue hypoperfusion is limited. Reliance is placed upon surrogate markers of tissue oxygenation such as arterial blood pressure and serum lactate that are insensitive to early organ compromise. Advances in oxygen sensing technology will facilitate monitoring in various organ beds and allow more precise titration of therapies to physiologically relevant endpoints. Clinical trials will be needed to evaluate any impact on outcomes, however accurate on-line monitoring of the adequacy of tissue oxygenation offers the promise of a paradigm shift in resuscitation and perioperative practice. This narrative review examines current evidence for goal-directed therapy in the optimisation of organ perfusion in high-risk surgical and critically ill patients, and offers arguments to support the potential utility of tissue oxygen monitoring

Levosimendan for the prevention of acute organ dysfunction in sepsis

BACKGROUND Levosimendan is a calcium-sensitizing drug with inotropic and other properties that may improve outcomes in patients with sepsis. METHODS We conducted a double-blind, randomized clinical trial to investigate whether levosimendan reduces the severity of organ dysfunction in adults with sepsis. Patients were randomly assigned to receive a blinded infusion of levosimendan (at a dose of 0.05 to 0.2 μg per kilogram of body weight per minute) for 24 hours or placebo in addition to standard care. The primary outcome was the mean daily Sequential Organ Failure Assessment (SOFA) score in the intensive care unit up to day 28 (scores for each of five systems range from 0 to 4, with higher scores indicating more severe dysfunction; maximum score, 20). Secondary outcomes included 28-day mortality, time to weaning from mechanical ventilation, and adverse events. RESULTS The trial recruited 516 patients; 259 were assigned to receive levosimendan and 257 to receive placebo. There was no significant difference in the mean (±SD) SOFA score between the levosimendan group and the placebo group (6.68±3.96 vs. 6.06±3.89; mean difference, 0.61; 95% confidence interval [CI], −0.07 to 1.29; P=0.053). Mortality at 28 days was 34.5% in the levosimendan group and 30.9% in the placebo group (absolute difference, 3.6 percentage points; 95% CI, −4.5 to 11.7; P=0.43). Among patients requiring ventilation at baseline, those in the levosimendan group were less likely than those in the placebo group to be successfully weaned from mechanical ventilation over the period of 28 days (hazard ratio, 0.77; 95% CI, 0.60 to 0.97; P=0.03). More patients in the levosimendan group than in the placebo group had supraventricular tachyarrhythmia (3.1% vs. 0.4%; absolute difference, 2.7 percentage points; 95% CI, 0.1 to 5.3; P=0.04). CONCLUSIONS The addition of levosimendan to standard treatment in adults with sepsis was not associated with less severe organ dysfunction or lower mortality. Levosimendan was associated with a lower likelihood of successful weaning from mechanical ventilation and a higher risk of supraventricular tachyarrhythmia. (Funded by the NIHR Efficacy and Mechanism Evaluation Programme and others; LeoPARDS Current Controlled Trials number, ISRCTN12776039.

Evidence for chemokine synergy during neutrophil migration in ARDS.

BACKGROUND: Acute respiratory distress syndrome (ARDS) is a life-threatening condition characterised by pulmonary oedema, respiratory failure and severe inflammation. ARDS is further characterised by the recruitment of neutrophils into the lung interstitium and alveolar space. OBJECTIVES: The factors that regulate neutrophil infiltration into the inflamed lung and our understanding of the pathomechanisms in ARDS remain incomplete. This study aimed at determining the role of the chemokine (C-C motif) ligand (CCL)2 and CCL7 in ARDS. METHODS: CCL2 and CCL7 protein levels were measured in bronchoalveolar lavage (BAL) fluid obtained from lipopolysaccharide(LPS)-challenged human volunteers and two separate cohorts of patients with ARDS. Neutrophil chemotaxis to ARDS BAL fluid was evaluated and the contribution of each was assessed and compared with chemokine (C-X-C motif) ligand 8 (CXCL8). Chemokine receptor expression on neutrophils from blood or BAL fluid of patients with ARDS was analysed by flow cytometry. RESULTS: CCL2 and CCL7 were significantly elevated in BAL fluid recovered from LPS-challenged volunteers and patients with ARDS. BAL fluid from patients with ARDS was highly chemotactic for human neutrophils and neutralising either CCL2 or CCL7 attenuated the neutrophil chemotactic response. Moreover, CCL2 and CCL7 synergised with CXCL8 to promote neutrophil migration. Furthermore, neutrophils isolated from the blood or BAL fluid differentially regulated the cell surface expression of chemokine (C-X-C motif) receptor 1 and C-C chemokine receptor type 2 during ARDS. CONCLUSION: This study highlights important inflammatory chemokines involved in regulating neutrophil migration, which may have potential value as therapeutic targets for the treatment of ARDS