Critical care (London, England) (CRIT CARE )

Publisher: Critical Care Forum

Description

Critical Care is a high quality, peer-reviewed, international clinical medical journal. Critical Care aims to improve the care of critically ill patients by acquiring, discussing, distributing, and promoting evidence-based information relevant to intensivists. The journal publishes commentaries, reviews, and research in all areas of intensive care and emergency medicine. Critical Care aims to provide a comprehensive overview of the intensive care field.

  • Impact factor
    4.72
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    Impact factor
  • 5-year impact
    5.25
  • Cited half-life
    4.40
  • Immediacy index
    0.98
  • Eigenfactor
    0.04
  • Article influence
    1.71
  • Website
    Critical Care website
  • Other titles
    Critical care (London, England: Online), Critical care, CC
  • ISSN
    1466-609X
  • OCLC
    44637976
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publications in this journal

  • Ciro Coletta, Katalin Módis, Gábor Oláh, Attila Brunyánszki, Daniela S Herzig, Edward R Sherwood, Zoltán Ungvári, Csaba Szabo
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    ABSTRACT: IntroductionThe goal of the current study was to investigate the effect of aging on the development of endothelial dysfunction in a murine model of sepsis, and to compare it with the effect of genetic deficiency of the endothelial isoform of nitric oxide synthase (eNOS).Methods Cecal ligation and puncture (CLP) was used to induce sepsis in mice. Survival rates were monitored and plasma indices of organ function were measured. Ex vivo studies included the measurement of vascular function in thoracic aortic rings, assessment of oxidative stress/cellular injury in various organs and the measurement of mitochondrial function in isolated liver mitochondria.ResultseNOS deficiency and aging both exacerbated the mortality of sepsis. Both eNOS deficient and aged mice exhibited a higher degree of sepsis-associated multiple organ dysfunction syndrome (MODS), infiltration of tissues with mononuclear cells and oxidative stress. A high degree of sepsis-induced vascular oxidative damage and endothelial dysfunction (evidenced by functional assays and multiple plasma markers of endothelial dysfunction) was detected in aortae isolated from both eNOS¿/¿ and aged mice. There was a significant worsening of sepsis-induced mitochondrial dysfunction, both in eNOS-deficient mice and in aged mice. Comparison of the surviving and non-surviving groups of animals indicated that the severity of endothelial dysfunction may be a predictor of mortality of mice subjected to CLP-induced sepsis.Conclusions Based on the studies in eNOS mice, we conclude that the lack of endothelial nitric oxide production, on its own, may be sufficient to markedly exacerbate the severity of septic shock. Aging markedly worsens the degree of endothelial dysfunction in sepsis, yielding a significant worsening of the overall outcome. Thus, endothelial dysfunction may constitute an early predictor and independent contributor to sepsis-associated MODS and mortality in aged mice.
    Critical care (London, England) 09/2014; 18(5):511.
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    ABSTRACT: IntroductionSodium bicarbonate (SBIC) was reported to be a promising approach to prevent cardiac surgery-associated acute kidney injury (CSA-AKI). However, the results remain controversial. We conducted a systematic review and meta-analysis to evaluate the efficacy and safety of SBIC on the prevention of CSA-AKI in adult patients undergoing cardiac surgery.Methods PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases were systematically searched. Randomized controlled trials (RCTs) assessing the effect of SBIC versus placebo on the prevention of CSA-AKI in adult patients undergoing cardiac surgery were included. Two investigators independently searched articles, extracted data, and assessed the quality of included studies. The primary outcome was the incidence of CSA-AKI. Meta-analysis was performed using random-effects models.ResultsFive RCTs involving 1079 patients were included in the meta-analysis. Overall, compared with placebo, SBIC was not associated with a reduced risk of CSA-AKI (relative risk [RR] 0.99; 95% confidence interval [CI] 0.78 to 1.24; P¿=¿0.911). SBIC failed to alter the clinical outcomes of hospital length of stay (weighted mean difference [WMD] 0.23 days; 95%CI ¿0.88 to 1.33 days; P¿=¿0.688), renal replacement therapy (RR 0.94; 95%CI 0.49 to 1.82; P¿=¿0.861), hospital mortality (RR 1.37; 95%CI 0.46 to 4.13; P¿=¿0.572), postoperative atrial fibrillation (RR 1.02; 95%CI 0.65 to 1.61; P¿=¿0.915). However, SBIC was associated with significant increased risks in longer duration of ventilation (WMD 0.64 hours; 95%CI 0.16 to 1.11 hours; P¿=¿0.008), longer ICU length of stay (WMD 2.06 days; 95%CI 0.54 to 3.58 days; P¿=¿0.008), and increased incidence of alkalemia (RR 2.21; 95%CI 1.42 to 3.42; P <0.001).ConclusionsSBIC could not reduce the incidence of CSA-AKI. Contrarily, SBIC prolongs the duration of ventilation and ICU length of stay, and increases the risk of alkalemia. Thus, SBIC should not be recommended for the prevention of CSA-AKI and perioperative SBIC infusion should be administrated with caution.
    Critical care (London, England) 09/2014; 18(5):517.
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    ABSTRACT: IntroductionImmobilization of hindlimb muscles in a shortened position results in an accelerated rate of inactivity-induced muscle atrophy and contractile dysfunction. Similarly, prolonged controlled mechanical ventilation (CMV) results in diaphragm inactivity and induces diaphragm muscle atrophy and contractile dysfunction. Further, the application of positive end-expiratory airway pressure (PEEP) during mechanical ventilation would result in shortened diaphragm muscle fibers throughout the respiratory cycle. Therefore, we tested the hypothesis that compared to CMV without PEEP; the combination of PEEP and CMV would accelerate CMV-induced diaphragm muscle atrophy and contractile dysfunction. To test this hypothesis, we combined PEEP with CMV or with assist-control mechanical ventilation (AMV) and determined the effects on diaphragm muscle atrophy and contractile properties.Methods The PEEP level (8 cm H2O) that did not induce lung over-distension or compromise circulation was determined. In vivo segmental length changes of diaphragm muscle fiber were then measured using sonomicrometry. Sedated rabbits were randomized into groups: surgical control, and those receiving CMV, AMV, continuous positive airway pressure (CPAP) with, or without PEEP for 2 days. In vitro diaphragmatic force, diaphragm muscle morphometry, myosin heavy-chain (MyHC) protein isoforms, caspase-3, insulin-like growth factor-1 (IGF-1), muscle atrophy F-box (MAFbx) and muscle ring finger-1 (MuRF1) mRNA were measured.ResultsPEEP shortened end-expiratory diaphragm muscle length by 15%, 14% and 12% with CMV, AMV and CPAP, respectively. Combined PEEP and CMV reduced tidal excursion of segmental diaphragm muscle length, consequently tidal volume (VT) decreased. VT was maintained with combined PEEP and AMV. CMV alone decreased maximal tetanic force (Po) production by 35% versus control (P <0.01). Combined PEEP and CMV did not decrease Po further. Po was preserved with AMV with or without PEEP. Diaphragm muscle atrophy did not occur in any fiber types. Diaphragm MyHC shifted to fast isoform in the combined PEEP and CMV group. In both CMV, and combined PEEP and CMV, IGF-1 mRNAs were suppressed, while Caspase-3, MAFbx and MuRF1 mRNA expression was elevated compared to control.Conclusions Two days of diaphragm muscle fiber shortening with PEEP did not exacerbate CMV-induced diaphragm muscle dysfunction.
    Critical care (London, England) 09/2014; 18(5):494.
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    ABSTRACT: IntroductionWe sought to investigate whether treatment of subnormal (<70%) central venous oxygen saturation (ScvO2) with inotropes or red blood cell (RBC) transfusion during early goal-directed therapy (EGDT) for septic shock is independently associated with in-hospital mortality.Methods Retrospective analysis of a prospective EGDT patient database drawn from 21 emergency departments with a single standardized EGDT protocol. Patients were included if, during EGDT, patients concomitantly achieved a central venous pressure (CVP) of ¿8 mm Hg and a mean arterial pressure (MAP) of ¿65 mm Hg while registering a ScvO2¿<¿70%. Treatment propensity scores for either RBC transfusion or inotrope administration were separately determined from independent patient sub-cohorts. Propensity-adjusted logistic regression analyses were conducted to test for associations between treatments and in-hospital mortality.ResultsOf 2595 EGDT patients, 572 (22.0%) met study inclusion criteria. The overall in-hospital mortality rate was 20.5%. Inotropes or RBC transfusions were administered for an ScvO2¿<¿70% to 51.9% patients. Patients were not statistically more likely to achieve an ScvO2 of ¿70% if they were treated with RBC transfusion alone (29/59, 49.2%, P¿=¿0.19), inotropic therapy alone (104/226, 46.0%, P¿=¿0.15) or both RBC and inotropic therapy (7/12, 58.3%, P¿=¿0.23) as compared to no therapy (108/275, 39.3%). Following adjustment for treatment propensity score, RBC transfusion was associated with a decreased adjusted odds ratio (aOR) of in-hospital mortality among patients with hemoglobin values less than 10 g/dL (aOR 0.42, 95% CI 0.18-0.97, P¿=¿0.04) while inotropic therapy was not associated with in-hospital mortality among patients with hemoglobin values of 10 g/dL or greater (aOR 1.16, 95% CI 0.69 to 1.96, P¿=¿0.57).Conclusions Among patients with septic shock treated with EGDT in the setting of subnormal ScvO2 values despite meeting CVP and MAP target goals, treatment with RBC transfusion may be independently associated with decreased in-hospital mortality.
    Critical care (London, England) 09/2014; 18(5):496.
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    ABSTRACT: IntroductionAssist in unison to the patient¿s inspiratory neural effort and feedback- controlled limitation of lung distension with neurally adjusted ventilatory assist (NAVA) may reduce the negative effects of mechanical ventilation on right ventricular function.Methods Heart-lung interaction was evaluated in 10 intubated patients with impaired cardiac function using esophageal balloons, pulmonary artery catheters and echocardiography. Adequate NAVA level identified by a titration procedure to breathing pattern (NAVAal), 50% NAVAal, and 200% NAVAal and adequate pressure support (PSVal, defined clinically), 50% PSVal, and 150% PSVal were implemented at constant positive end-expiratory pressure for 20 minutes each.ResultsNAVAal was 3.1¿±¿1.1cmH2O/¿V and PSVal was 17¿±¿2 cmH20. For all NAVA levels negative esophageal pressure deflections were observed during inspiration whereas this pattern was reversed during PSVal and PSVhigh. As compared to expiration, inspiratory right ventricular outflow tract velocity time integral (surrogating stroke volume) was 103¿±¿4%, 109¿±¿5%, and 100¿±¿4% for NAVAlow, NAVAal, and NAVAhigh and 101¿±¿3%, 89¿±¿6%, and 83¿±¿9% for PSVlow, PSVal, and PSVhigh, respectively (p¿<¿0.001 level-mode interaction, ANOVA). Right ventricular systolic isovolumetric pressure increased from 11.0¿±¿4.6 mmHg at PSVlow to 14.0¿±¿4.6 mmHg at PSVhigh but remained unchanged (11.5¿±¿4.7 mmHg (NAVAlow) and 10.8¿±¿4.2 mmHg (NAVAhigh), level-mode interaction p¿=¿0.005). Both indicate progressive right ventricular outflow impedance with increasing pressure support ventilation (PSV), but no change with increasing NAVA level.Conclusions Right ventricular performance is less impaired during NAVA compared to PSV as used in this study. Proposed mechanisms are preservation of cyclic intrathoracic pressure changes characteristic of spontaneous breathing and limitation of right-ventricular outflow impedance during inspiration, regardless of the NAVA level.Trial registrationClinicaltrials.gov Identifier: NCT00647361, registered March 19, 2008.
    Critical care (London, England) 09/2014; 18(5):499.
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    ABSTRACT: IntroductionEndotoxemia and the systemic inflammatory response syndrome have a significant impact on post-surgery outcome, particularly in the elderly. The cytokine response to endotoxin is altered by aging. We tested the hypothesis that vulnerability to endotoxemic cardiac depression increases with aging due to age-related augmentation of myocardial inflammatory responses.Methods Adult (4 to 6 months) and old (20 to 22 months) C57/BL6 mice were treated with endotoxin (0.5 mg/kg, iv). Left ventricle (LV) function was assessed using a microcatheter system. Chemokines and cytokines in plasma and myocardium were analyzed by enzyme-linked immunosorbent assay (ELISA). Mononuclear cells in the myocardium were examined using immunofluorescence staining.ResultsOld mice displayed worse LV function (cardiac output: 3.0¿±¿0.2 mL/min versus 4.4¿±¿0.3 mL/min in adult mice) following endotoxin treatment. The exaggerated cardiac depression in old mice was associated with higher levels of monocyte chemoattractant protein-1 (MCP-1) and keratinocyte chemoattractant (KC) in plasma and myocardium, greater myocardial accumulation of mononuclear cells, and greater levels of tumor necrosis factor-¿ (TNF-¿), interleukin 1ß (IL-1ß) and interleukin 6 (IL-6) in plasma and myocardium. Neutralization of MCP-1 resulted in greater reductions in myocardial mononuclear cell accumulation and cytokine production, and greater improvement in LV function in old mice while neutralization of KC had a minimal effect on LV function.Conclusion Old mice have enhanced inflammatory responses to endotoxemia that lead to exaggerated cardiac functional depression. MCP-1 promotes myocardial mononuclear cell accumulation and cardiodepressant cytokines production, and plays an important role in the endotoxemic cardiomyopathy in old mice. The findings suggest that special attention is needed to protect the heart in the elderly with endotoxemia.
    Critical care (London, England) 09/2014; 18(5):527.
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    ABSTRACT: IntroductionWhen alveoli collapse the traction forces exerted on their walls by adjacent expanded units may increase and concentrate. These forces may promote its re-expansion at the expense of potentially injurious stresses at the interface between the collapsed and the expanded units. We developed an experimental model to test the hypothesis that a local non-lobar atelectasis can act as a stress concentrator, contributing to inflammation and structural alveolar injury in the surrounding healthy lung tissue during mechanical ventilation.MethodsA total of 35 rats were anesthetized, paralyzed and mechanically ventilated. Atelectasis was induced by bronchial blocking: after five minutes of stabilization and pre-oxygenation with 100& oxygen, a silicon cylinder blocker was wedged in the terminal bronchial tree. Afterwards, the animals were randomized between two groups: 1) Tidal volume (VT)¿=¿10 ml/kg and positive end-expiratory pressure (PEEP)¿=¿3 cmH2O (VT10/PEEP3); and 2) VT¿=¿20 ml/kg and PEEP¿=¿0 cmH2O (VT20/zero end-expiratory pressure (ZEEP)). The animals were then ventilated during 180 minutes. Three series of experiments were performed: histological (n¿=¿12); tissue cytokines (n¿=¿12); and micro-computed tomography (microCT; n¿=¿2). An additional six, non-ventilated, healthy animals were used as controls.ResultsAtelectasis was successfully induced in the basal region of the lung of 26 out of 29 animals. The microCT of two animals revealed that the volume of the atelectasis was 0.12 and 0.21 cm3. There were more alveolar disruption and neutrophilic infiltration in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. Edema was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in the VT20/ZEEP than VT10/PEEP3 group. The volume-to-surface ratio was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. We did not find statistical difference in tissue interleukin-1ß and cytokine-induced neutrophil chemoattractant-1 between regions.Conclusions The present findings suggest that a local non-lobar atelectasis acts as a stress concentrator, generating structural alveolar injury and inflammation in the surrounding lung tissue.
    Critical care (London, England) 09/2014; 18(5):505.
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    ABSTRACT: IntroductionThe aim of this study was to evaluate the diagnostic and prognostic value of presepsin in patients with severe sepsis and septic shock during the first week of ICU treatment.Methods In total, 116 patients with suspected severe sepsis or septic shock were included during the first 24 hours of ICU treatment. Blood samples for biomarker measurements of presepsin, procalcitonin (PCT), interleukin 6 (IL-6), C reactive protein (CRP) and white blood cells (WBC) were drawn at days 1, 3 and 8. All patients were followed up for six months. Biomarkers were tested for diagnosis of severe sepsis, septic shock and sepsis at days 1, 3 and 8, and for all-cause mortality prognosis at 30 days and 6 months. Diagnostic and prognostic capacities were tested by determining diagnostic cutoff levels, goodness criteria, C-statistics and multivariable Cox regression models.ResultsPresepsin increased significantly from the lowest to most severe sepsis groups at days 1, 3 and 8 (test for linear trend P <0.03). Presepsin levels revealed valuable diagnostic capacity to diagnose severe sepsis and septic shock at days 1, 3 and 8 (range of diagnostic area under the curves (AUC) 0.72 to 0.84, P = 0.0001) compared to IL-6, PCT, CRP and WBC. Goodness criteria for diagnosis of sepsis severity were analyzed (¿sepsis, cutoff = 530 pg/ml; ¿severe sepsis, cutoff = 600 pg/ml; ¿septic shock, cutoff = 700 pg/ml; P <0.03). Presepsin levels revealed significant prognostic value for 30 days and 6 months all-cause mortality (presepsin: range of AUC 0.64 to 0.71, P <0.02). Patients with presepsin levels of the 4th quartile were 5 to 7 times more likely to die after six months than patients with lower levels. The prognostic value for all-cause mortality of presepsin was comparable to that of IL-6 and better than that of PCT, CRP or WBC.Conclusions Presepsin reveals valuable diagnostic capacity to differentiate sepsis severity compared to PCT, IL-6, CRP, WBC. Additionally, presepsin and IL-6 reveal prognostic value with respect to 30 days and 6 months all-cause mortality in patients with severe sepsis and septic shock throughout the first week of ICU treatment.Trial registrationClinicalTrials.gov NCT01535534. Registered 14 February 2012.
    Critical care (London, England) 09/2014; 18(5):507.
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    ABSTRACT: IntroductionPatients with severe acute exacerbations of asthma often receive inappropriate antibiotic treatment. We aimed to determine whether serum procalcitonin (PCT) levels can effectively and safely reduce antibiotic exposure in patients experiencing exacerbations of asthma.Methods In this randomized controlled trial, a total of 216 patients requiring hospitalization for severe acute exacerbations of asthma were screened for eligibility to participate in this study and 169 completed 12-month follow-up visit. Patients were randomized to either PCT-guided (PCT group) or standard antimicrobial therapy (control group). In the control group, patients received antibiotics according to the attending physician; in the PCT group, patients received antibiotics according to an algorithm based on serum PCT levels. The primary endpoint was antibiotic exposure; secondary endpoints were clinical recovery, length of hospital stay, clinical and laboratory parameters, spirometry, numbers of asthma exacerbations, emergency room visits, hospitalizations and need for corticosteroid use due to asthma.ResultsPCT guidance reduced antibiotic prescription (48.9% versus 87.8%, respectively; P <0.001) and antibiotic exposure (relative risk, 0.56; 95% confidence interval, 0.44 to 0.70; P <0.001) compared to standard therapy. There were no significant differences in clinical recovery, length of hospital stay, clinical, laboratory, spirometry outcomes in both groups. Numbers of asthma exacerbations, emergency room visits, hospitalizations and need for corticosteroid use due to asthma were similar during 12-month follow-up period.ConclusionA PCT-guided strategy allows antibiotic exposure to be reduced in patients with severe acute exacerbation of asthma without apparent harm.Trial registrationChinese Clinical Trial Register ChiCTR-TRC-12002534. Registered 26 September 2012.
    Critical care (London, England) 09/2014; 18(5):471.
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    ABSTRACT: IntroductionUnfractionated heparin (UFH) is the anticoagulant of choice for extracorporeal membrane oxygenation (ECMO), but bivalirudin can be used as an alternative. The purpose of the present study is to investigate the existence of a heparin-like effect (HLE) during heparin-free ECMO.Methods This is a retrospective study on patients treated with ECMO and receiving bivalirudin as the sole anticoagulant. Thromboelastography (TEG) tests with and without heparinase were recorded during the ECMO duration. A total of 41 patients (22 pediatrics and 19 adults) treated with ECMO after cardiac surgery procedures and receiving only bivalirudin-based anticoagulation were studied. Based on the presence of a different reaction time (R-time) between the TEG test with heparinase or without heparinase we defined the presence of a HLE. Survival to hospital discharge, liver failure, sepsis, bleeding and transfusion rate were analyzed for association with HLE with univariate tests.ResultsHLE was detected in 56.1% of the patients. R-times were significantly shorter in tests done with heparinase versus without heparinase during the first seven days on ECMO. Patients with HLE had a significantly (P¿=¿0.046) higher rate of sepsis (30%) than patients without HLE (5.6%) at a Pearson¿s chi-square test.ConclusionsA heparin-like effect is common during ECMO, and most likely due to a release of heparinoids from the glycocalyx and the mast cells, as a consequence of sepsis or of the systemic inflammatory reaction triggered by the contact of blood with foreign surfaces.
    Critical care (London, England) 09/2014; 18(5):504.
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    ABSTRACT: IntroductionEchocardiographic indices based on respiratory variations of superior and inferior vena cava diameters (¿SVC and ¿IVC, respectively) have been proposed as predictors of fluid responsiveness in mechanically ventilated patients but they have never been compared simultaneously in the same patient sample. The aim of this study was to compare the predictive value of these echocardiographic indices when concomitantly recorded in mechanically ventilated, septic patients.Methods Septic shock patients requiring hemodynamic monitoring were prospectively enrolled over a 1-year period in a mixed medical surgical ICU of a University Teaching Hospital (Toulouse, France). All patients were mechanically ventilated. Predictive indices were obtained by transesophageal and transthoracic echocardiography and were calculated as follows: (Dmax-Dmin) / Dmax for ¿SVC and (Dmax-Dmin) / Dmin for ¿IVC where Dmax and Dmin are the maximal or minimal diameter of SVC and IVC. Measurements were performed at baseline and after a 7 ml/kg volume expansion using a plasma expander. Patients were separated into responders (increase in cardiac index¿¿¿15%) and non-responders (increase in cardiac index¿<¿15%).ResultsAmong 44 included patients, 26 (59%) patients were responders (R). ¿SVC was significantly more accurate than ¿IVC to predict fluid responsiveness (the area under the ROC curve for ¿SVC and ¿IVC regarding assessment of fluid responsiveness were significantly different (0.74 (95% confidence interval (CI): 0.59 to 0.88) and 0.43 (95% CI: 0.25 to 0.61) respectively with P¿=¿0.012)). No significant correlation between ¿SVC and ¿IVC was found (r¿=¿0.005, P¿=¿0.98). The best threshold value to discriminate R from NR was 29% for ¿SVC with a 54% sensitivity and 89% specificity, and 21% for ¿IVC with a 38% sensitivity and 61% specificity.Conclusions¿SVC was better in predicting fluid responsiveness than ¿IVC in our cohort. It is worth noting that the sensitivity and specificity of ¿SVC and ¿IVC to predict fluid responsiveness were lower than those reported in the literature, highlighting the limits of using these indices in a heterogeneous sample of medical and surgical septic patients.
    Critical care (London, England) 09/2014; 18(5):473.
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    ABSTRACT: IntroductionDelirium is a frequent complication after cardiac surgery. Although various risk factors for postoperative delirium have been identified, the relationship between nocturnal breathing disorders and delirium has not yet been elucidated. This study evaluated the relationship between sleep-disordered breathing (SDB) and postoperative delirium in cardiac surgery patients without a previous diagnosis of obstructive sleep apnea.Methods In this prospective cohort study, 92 patients undergoing elective cardiac surgery with extracorporeal circulation were evaluated for both SDB and postoperative delirium. Polygraphic recordings were used to calculate the apnea-hypopnea index (AHI; mean number of apneas and hypopneas per hour recorded) of all patients preoperatively. Delirium was assessed during the first four postoperative days using the Confusion Assessment Method. Clinical differences between individuals with and without postoperative delirium were determined with univariate analysis. The relationship between postoperative delirium and those covariates that were associated with delirium in univiariate analysis was determined by multivariate logistic regression model.ResultsThe median overall preoperative AHI was 18.3 (interquartile range, 8.7 to 32.8). Delirium was diagnosed in 44 patients. The median AHI differed significantly between patients with and without postoperative delirium (28 versus 13; P¿=¿0.001). A preoperative AHI of 19 or higher was associated with an almost six-fold increased risk of postoperative delirium (odds ratio, 6.4; 95% confidence interval, 2.6 to 15.4; P <0.001). Multivariate logistic regression analysis showed that preoperative AHI, age, smoking, and blood transfusion were independently associated with postoperative delirium.Conclusion Preoperative SDB (for example, undiagnosed obstructive sleep apnea) were strongly associated with postoperative delirium, and may be a risk factor for postoperative delirium.
    Critical care (London, England) 09/2014; 18(5):477.
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    ABSTRACT: IntroductionHyperglycemia is a marker of poor prognosis in severe brain injuries. There is currently little data regarding the effects of intensive insulin therapy (IIT) on neurological recovery.MethodsA sub-group analysis of the randomized-controlled CGAO-REA study (NCT01002482) in surgical intensive care units (ICU) of two university hospitals. Patients with severe brain injury, with an expected ICU length of stay ¿48 hours were included. Patients were randomized between a conventional glucose management group (blood glucose target between 5.5 and 9 mmol.L¿1) and an IIT group (blood glucose target between 4.4 and 6 mmol.L¿1). The primary outcome was the day-90 neurological outcome evaluated with the Glasgow outcome scale.ResultsA total of 188 patients were included in this analysis. In total 98 (52%) patients were randomized in the control group and 90 (48%) in the IIT group. The mean Glasgow coma score at baseline was 7 (±4). Patients in the IIT group received more insulin (130 (68 to 251) UI versus 74 (13 to 165) UI in the control group, P¿=¿0.01), had a significantly lower morning blood glucose level (5.9 (5.1 to 6.7) mmol.L¿1 versus 6.5 (5.6 to 7.2) mmol.L¿1, P <0.001) in the first 5 days after ICU admission. The IIT group experienced more episodes of hypoglycemia (P <0.0001). In the IIT group 24 (26.6%) patients had a favorable neurological outcome (good recovery or moderate disability) compared to 31 (31.6%) in the control group (P¿=¿0.4). There were no differences in day-28 mortality. The occurrence of hypoglycemia did not influence the outcome.Conclusions In this sub-group analysis of a large multicenter randomized trial, IIT did not appear to alter the day-90 neurological outcome or ICU morbidity in severe brain injured patients or ICU morbidity.
    Critical care (London, England) 09/2014; 18(5):498.
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    ABSTRACT: IntroductionDengue Shock Syndrome (DSS) fluid resuscitation following the World Health Organization (WHO) guideline usually required large volumes of Ringer Lactate (RL) that may induce secondary fluid-overload. Our objective was to compare the effectiveness of the recommended volume of RL versus a smaller volume of a Hypertonic Sodium Lactate solution (HSL) in children suffering DSS. The primary endpoint was to evaluate the effect of HSL on endothelial cell inflammation, assessed by Soluble Vascular Cell Adhesion Molecule-1 (sVCAM-1) measurements. Secondarily, we considered the effectiveness of HSL in restoring hemodynamic fluid balance, acid¿base status, sodium and chloride balances as well as in-hospital survival.MethodsA prospective randomized single blind clinical trial including 50 DSS children conducted in the Pediatrics Department of Hasan Sadikin Hospital, Bandung, Indonesia. Only pediatric patients (2 to 14 year old) fulfilling the WHO criteria for DSS and new to resuscitation treatments were eligible. Patients were resuscitated with either HSL (5 ml.Kg BW¿1 in 15 minutes followed by 1 ml.Kg BW¿1.h¿1 for 12 hours), or RL (20 ml.Kg BW¿1 in 15 minutes followed by decreasing doses of 10, 7, 5, 3 ml.Kg BW¿1.h¿1 for 12 hours).ResultsIn total, 50 patients were randomized and included in outcome and adverse event analysis; 46 patients (8.2¿±¿0.5 years; 24.9¿±¿1.9 Kg; mean¿±¿sem) completed the protocol and were fully analyzed (24 and 22 subjects in the HSL and RL group respectively). Baseline (pre-bolus) data were similar in both groups. Hemodynamic recovery, plasma expansion, clinical outcome and survival rate were not significantly different in the two groups, whereas fluid accumulation was one third lower in the HSL than in the RL group. Moreover, HSL was responsible for a partial recovery from endothelial dysfunction, as indicated by the significant decrease in sVCAM-1.Conclusion Similar hemodynamic shock recovery and plasma expansion were achieved in both groups despite much lower fluid intake and fluid accumulation in the HSL group.Trial RegistrationClinicalTrials.gov NCT00966628. Registered 26 August 2009.
    Critical care (London, England) 09/2014; 18(5):466.
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    ABSTRACT: IntroductionSepsis and other infections are associated with late cardiovascular events. Although persistent inflammation is implicated, a causal relationship has not been established. We tested whether sepsis causes vascular inflammation and accelerates atherosclerosis.Methods Prospective randomized animal studies at a university research laboratory involving adult male apoE-deficient (apoE-/-) and young C57B/L6 wild-type (WT) mice are performed. In the primary study to determine whether sepsis accelerates atherosclerosis, we fed apoE-/- mice (n¿=¿46) an atherogenic diet for 4 months and then performed cecal ligation and puncture (CLP) followed by antibiotic therapy and fluid resuscitation or sham. We followed mice for up to five more months and assessed atheroma in the descending and root of the aorta. We also exposed 32 young WT mice to CLP or sham and followed for 5 days to determine the effects of sepsis on vascular inflammation.ResultsApoE-/- mice undergoing CLP had reduced activity over the first 14d (38% reduction compared to sham, P <0.001) and sustained weight loss versus sham (-6% versus +9% change in weight from CLP or sham to 5 m, P <0.001). Despite the weight loss, CLP mice had increased atheroma (46% by 3 months and 41% by 5 months increase in aortic surface area, P¿=¿0.03 and P¿=¿0.004, respectively) with increased macrophage infiltration into atheroma as assessed by immunofluorescence microscopy (0.52 versus 0.97 rfu, P¿=¿0.04). At 5 m, peritoneal cultures were negative but CLP mice had elevated serum levels of IL-6 and IL-10 (each P <0.05). WT mice undergoing CLP had increased expression of ICAM-1 in the aortic lumen versus sham at 24 hours (P¿=¿0.01) that persisted at 120 hours (P¿=¿0.006). Inflammatory and adhesion genes (TNF-¿, CCL2, and VCAM-1) and the adhesion assay, a functional measure of endothelial activation, were elevated at 72 hours and 120 hours in CLP versus sham (all P <0.05).Conclusions Using a combination of existing murine models for atherosclerosis and sepsis, we found that CLP, a model of intraabdominal sepsis, accelerates atheroma development. Accelerated atheroma burden was associated with prolonged systemic, endothelial, and intimal inflammation, and was not explained by ongoing infection. These findings support observations in humans and demonstrate the feasibility of a long-term follow-up murine model of sepsis.
    Critical care (London, England) 09/2014; 18(5):469.
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    ABSTRACT: IntroductionAcute kidney injury (AKI) is a common and feared complication of sepsis. The pathogenesis of sepsis-induced AKI is largely unknown and therapeutic interventions are mainly supportive. In the present study we tested the hypothesis that pharmacological inhibition of toll like receptor 4 (TLR4) would improve renal function and reduce renal damage in experimental sepsis, even after AKI had already developed.Methods Sheep were surgically instrumented and subjected to a 36 hour intravenous infusion of live Escherichia coli (E. coli). After 12 hours they were randomized to treatment with a selective TLR4 inhibitor (TAK-242) or vehicle.ResultsThe E.coli caused normotensive sepsis characterized by fever, increased cardiac index, hyperlactemia, oliguria and decreased creatinine clearance. TAK-242 significantly improved creatinine clearance and urine output. The increase in N-acetyl-beta-D-glucosaminidas, a marker of tubular damage, was attenuated. Furthermore, TAK-242 reduced the renal neutrophil accumulation and glomerular endothelial swelling caused by sepsis. These effects were independent of changes in renal artery blood flow and renal microvascular perfusion in both cortex and medulla. TAK-242 had no effect per se on the measured parameters.Conclusion These results show that treatment with a TLR4-inhibitor is able to reverse a manifest impairment in renal function caused by sepsis. In addition, the results provide evidence that the mechanism underlying the effect of TAK-242 on renal function does not involve improved macro-circulation or micro-circulation, enhanced renal oxygen delivery or attenuation of tubular necrosis. TLR4-mediated inflammation resulting in glomerular endothelial swelling may be an important part of the pathogenesis underlying gram-negative septic acute kidney injury.
    Critical care (London, England) 09/2014; 18(5):488.
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    ABSTRACT: IntroductionWhether red blood cell (RBC) transfusion is beneficial remains controversial. In both retrospective and prospective evaluations, transfusion has been associated with adverse, neutral, or protective effects. These varying results likely stem from a complex interplay between transfusion, patient characteristics, and clinical context. The objective was to test whether age, comorbidities, and clinical context modulate the effect of transfusion on survival.Methods Using the multiparameter intelligent monitoring in intensive care II database (v.2.6), a retrospective analysis of 9,809 critically ill patients evaluated the effect of RBC transfusion on 30-day and 1-year mortality. Propensity score modeling and logistic regression adjusted for known confounding and assessed the independent effect of transfusion on 30-day and 1-year mortality. Sensitivity analysis was performed using 3,164 transfused and non-transfused pairs matched according the previously validated propensity model for RBC transfusion.ResultsRBC transfusion did not affect 30-day or 1-year mortality in the overall cohort. Patients <55 years had increased odds of mortality (OR 1.71, P¿<¿0.01) with transfusion. Patients >75 years had lower odds of 30-day and 1-year mortality (OR 0.70, P¿<¿0.01) with transfusion. Transfusion was associated with worse outcome among patients undergoing cardiac surgery (OR 2.1, P¿<¿0.01). The propensity-matched population, corroborated findings identified by regression adjustment.Conclusion There is a complex relationship between RBC transfusion and clinical outcome. Our results show that transfusion is associated with improved outcomes in some cohorts and worse outcome in others depending on comorbidities and patient characteristics. As such, future investigations and clinical decisions evaluating the value of transfusion should account for variations in baseline characteristics and clinical context.
    Critical care (London, England) 08/2014; 18(4):487.
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    ABSTRACT: Intravenous fluids (IVFs) represent a basic therapeutic intervention utilized in septic shock. Unfortunately, the optimal method for administering IVFs to maximize patient outcomes is unknown. A meta-analysis of four randomized trials of goal-directed therapy did not demonstrate a significant reduction in mortality (odds ratio 0.609; 95% confidence interval 0.363 to 1.020; P = 0.059), whereas 18 trials with historical controls showed a significant increase in survival (odds ratio 0.580; 95% confidence interval 0.501 to 0.672; P < 0.0001). Based on these data, clinicians should be aware of the potential for harm due to the excessive administration of IVFs to patients with septic shock.
    Critical care (London, England) 08/2014; 18(4):481.
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    ABSTRACT: In the previous issue of Critical Care, Gu and colleagues reported the results of a systematic review and meta-analysis of randomized trials comparing high-frequency oscillatory ventilation (HFOV) with conventional ventilation in adults with acute respiratory distress syndrome (ARDS). In contrast to findings of prior meta-analyses, their main finding was that, despite reducing risks of oxygenation failure, HFOV does not improve survival in adults with ARDS.
    Critical care (London, England) 08/2014; 18(4):464.

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