OBJECTIVES:First, we aimed at assessing whether fluid responsiveness is predicted by the effects of an end-expiratory occlusion on the velocity-time integral of the left ventricular outflow tract. ...Second, we investigated whether adding the effects of an end-inspiratory occlusion and of an end-expiratory occlusion on velocity-time integral can predict fluid responsiveness with similar reliability than end-expiratory occlusion alone but with a higher threshold, which might be more compatible with the precision of echocardiography.
DESIGN:Diagnostic study.
SETTING:Medical ICU.
PATIENTS:Thirty mechanically ventilated patients in whom fluid administration was planned.
INTERVENTIONS:A 15-second end-expiratory occlusion and end-inspiratory occlusion, separated by 1 minute, followed by a 500-mL saline administration.
MEASUREMENTS AND MAIN RESULTS:Pulse contour analysis–derived cardiac index and velocity-time integral were measured during the last 5 seconds of 15-second end-inspiratory occlusion and end-expiratory occlusion and after fluid administration. End-expiratory occlusion increased velocity-time integral more in responders than in nonresponders to fluid administration (11% ± 5% vs 3% ± 1%, respectively; p < 0.0001), and end-inspiratory occlusion decreased velocity-time integral more in responders than in nonresponders (12% ± 5% vs 5% ± 2%, respectively; p = 0.0002). When adding the absolute values of changes in velocity-time integral observed during both occlusions, velocity-time integral changed by 23% ± 9% in responders and by 8% ± 3% in nonresponders. Fluid responsiveness was predicted by the end-expiratory occlusion–induced change in velocity-time integral with an area under the receiver operating characteristic curve of 0.938 (0.785–0.989) and a threshold value of 5%. Fluid responsiveness was predicted by the sum of absolute values of changes in velocity-time integral during both occlusions with a similar reliability (area under the receiver operating characteristic curve = 0.973 0.838–1.000) but with a threshold of 13%. Both sensitivity and specificity were 93% (68–100%).
CONCLUSIONS:If consecutive end-inspiratory occlusion and end-expiratory occlusion change velocity-time integral is greater than or equal to 13% in total, fluid responsiveness is accurately predicted. This threshold is more compatible with the precision of echocardiography than that obtained by end-expiratory occlusion alone.
OBJECTIVES:First, to validate bedside estimates of effective arterial elastance = end-systolic pressure/stroke volume in critically ill patients. Second, to document the added value of effective ...arterial elastance, which is increasingly used as an index of left ventricular afterload.
DESIGN:Prospective study.
SETTING:Medical ICU.
PATIENTS:Fifty hemodynamically stable and spontaneously breathing patients equipped with a femoral (n = 21) or radial (n = 29) catheter were entered in a “comparison” study. Thirty ventilated patients with invasive hemodynamic monitoring (PiCCO-2; Pulsion Medical Systems, Feldkirchen, Germany), in whom fluid administration was planned were entered in a “ dynamic” study.
INTERVENTIONS:In the “dynamic” study, data were obtained before/after a 500 mL saline administration.
MEASUREMENTS AND MAIN RESULTS:According to the “cardiocentric” view, end-systolic pressure was considered the classic index of left ventricular afterload. End-systolic pressure was calculated as 0.9 × systolic arterial pressure at the carotid, femoral, and radial artery level. In the “comparison” study, carotid tonometry allowed the calculation of the reference effective arterial elastance value (1.73 ± 0.62 mm Hg/mL). The femoral estimate of effective arterial elastance was more accurate and precise than the radial estimate. In the “dynamic” study, fluid administration increased stroke volume and end-systolic pressure, whereas effective arterial elastance (femoral estimate) and systemic vascular resistance did not change. Effective arterial elastance was related to systemic vascular resistance at baseline (r = 0.89) and fluid-induced changes in effective arterial elastance and systemic vascular resistance were correlated (r = 0.88). In the 15 fluid responders (cardiac index increases ≥ 15%), fluid administration increased end-systolic pressure and decreased effective arterial elastance and systemic vascular resistance (each p < 0.05). In the 15 fluid nonresponders, end-systolic pressure increased (p < 0.05), whereas effective arterial elastance and systemic vascular resistance remained unchanged.
CONCLUSIONS:In critically ill patients, effective arterial elastance may be reliably estimated at bedside (0.9 × systolic femoral pressure/stroke volume). We support the use of this validated estimate of effective arterial elastance when coupled with an index of left ventricular contractility for studying the ventricular-arterial coupling. Conversely, effective arterial elastance should not be used in isolation as an index of left ventricular afterload.
Summary
We present our findings on interpatient transmission, epidemic control measures, and the outcomes of a series of ten critically ill burn patients who were either colonized or infected with ...carbapenem-resistant
Acinetobacter baumannii
(CRAB). None of the five infected patients achieved clinical cure, and all experienced relapses. Microbiological failure was observed in 40% of the infected patients. The isolated CRAB strains were found to carry bla
OXA−23
and armA resistance genes. Despite the lack of clinical cure, all five infected patients survived and were discharged from the Burn Intensive Care Unit.
BackgroundAcute kidney injury (AKI) is a common condition in severely ill patients associated with poor outcomes. We assessed the associations between urinary neutrophil gelatinase-associated ...lipocalin (uNGAL), urinary liver-type fatty acid-binding protein (uLFABP), and urinary cystatin C (uCysC) concentrations and patient outcomes.MethodsWe assessed the predictive performances of uNGAL, uLFABP, and uCysC measured in the early phase of intensive care unit (ICU) management and at discharge from the ICU in severely ill patients for short- and long-term outcomes. The primary outcome was the occurrence of AKI during ICU stay; secondary outcomes were 28-day and 1-yr allcause mortality.ResultsIn total, 1,759 patients were admitted to the ICU, and 728 (41.4%) developed AKI. Median (interquartile range, IQR) uNGAL, uLFABP, and uCysC concentrations on admission were 147.6 (39.9-827.7) ng/mL, 32.4 (10.5-96.0) ng/mL, and 0.33 (0.12-2.05) mg/L, respectively. Biomarker concentrations on admission were higher in patients who developed AKI and associated with AKI severity. Three hundred fifty-six (20.3%) and 647 (37.9%) patients had died by 28 days and 1-yr, respectively. Urinary biomarker concentrations at ICU discharge were higher in non-survivors than in survivors. The areas under the ROC curve (95% confidence interval) of uLFABP for the prediction of AKI, 28-day mortality, and 1-yr mortality (0.70 0.67-0.72, 0.63 0.59-0.66, and 0.57 0.51-0.63, respectively) were inferior to those of the other biomarkers.ConclusionsuNGAL, uLFABP, and uCysC concentrations on admission were associated with poor outcomes. However, their predictive performance, individually and in combination, was limited. Further studies are required to confirm our results.
OBJECTIVES:The association between outcome and kidney injury detected at discharge from the ICU using different biomarkers remains unknown. The objective was to evaluate the association between ...1-year survival and kidney injury at ICU discharge.
DESIGN:Ancillary investigation of a prospective observational study.
SETTING:Twenty-one ICUs with 1-year follow-up.
PATIENTS:Critically ill patients receiving mechanical ventilation and/or hemodynamic support for at least 24 hours were included.
INTERVENTIONS:Serum creatinine, plasma Cystatin C, plasma neutrophil gelatinase-associated lipocalin, urinary neutrophil gelatinase-associated lipocalin, plasma Proenkephalin A 119-159, and estimated glomerular filtration rate (on serum creatinine and plasma Cystatin C) were measured at ICU discharge among ICU survivors.
MEASUREMENTS AND MAIN RESULTS:The association between kidney biomarkers at discharge and mortality was estimated using logistic model with and without adjustment for prognostic factors previously identified in this cohort. Subgroup analyses were performed in patients with discharge serum creatinine less than 1.5-fold baseline at ICU discharge. Among 1,207 ICU survivors included, 231 died during the year following ICU discharge (19.2%). Estimated glomerular filtration rate was significantly lower and kidney injury biomarkers higher at discharge in nonsurvivors. The association between biomarker levels or estimated glomerular filtration rate and mortality remained after adjustment to potential cofounding factors influencing outcome. In patients with low serum creatinine at ICU discharge, 25–47% of patients were classified as subclinical kidney injury depending on the biomarker. The association between kidney biomarkers and mortality remained and mortality was higher than patients without subclinical kidney injury. The majority of patients who developed acute kidney injury during ICU stay had elevated biomarkers of kidney injury at discharge even with apparent recovery based on serum creatinine (i.e., subclinical acute kidney disease).
CONCLUSIONS:Elevated kidney biomarkers measured at ICU discharge are associated with poor 1-year outcome, including in patients with low serum creatinine at ICU discharge.
Ketamine-associated cholestatic liver injury is reported in patients with severe burn injury, but its association with patient outcome is unclear. We investigated the relationship between ketamine ...exposure, cholestatic liver injury, and outcome of critically ill patients with burn injury.
In a retrospective study, patients with severe burn injury were analysed across two periods: unrestricted ketamine prescription (ketamine-liberal) and capped ketamine dosage (ketamine-restricted). The primary endpoint was cholestatic liver injury, and the secondary endpoint was 3-month mortality. Binary logistic regression models and the revised electronic causality assessment method were used to measure the strength of associations and causality assessment, respectively.
Of 279 patients (median age 51 IQR 31–67 years; 63.1% men; burned surface area 28.5%, IQR 20–45%), 155 (56%) were in the ketamine-liberal group, and 124 (44%) were in the ketamine-restricted group, with comparable clinical characteristics, except for ketamine exposure (median doses 265.0 IQR 0–8,021 mg and 20 IQR 0–105 mg, respectively; p <0.001). A dose- and time-dependent relationship was observed between ketamine exposure and cholestatic liver injury. Ketamine restriction was associated with a reduced risk of cholestatic liver injury (adjusted odds ratio 0.16, 95% CI 0.04–0.50; p = 0.003) and with a higher probability of 3-month survival (p = 0.035). The revised electronic causality assessment method indicated that ketamine was probably and possibly the cause of cholestatic liver injury for 14 and 10 patients, respectively. Cholangitis was not observed in the ketamine-restricted group. In propensity-matched patients, the risk of 3-month mortality was higher (adjusted odds ratio 9.92, 95% CI 2.76–39.05; p = 0.001) in patients with cholestatic liver injury and ketamine exposure ≥10,000 mg. Other sedative drugs were not associated with liver and patient outcome.
In this cohort, ketamine restriction was associated with less cholestatic liver injury and reduced 3-month mortality.
In a cohort of 279 critically ill patients with burn injury, ketamine was associated with a risk of liver bile duct toxicity. The risk was found to be dependent on both the dosage and duration of ketamine use. A restriction policy of ketamine prescription was associated with a risk reduction of liver injury and 3-month mortality. These findings have implications for the analgesia and sedation of critically ill patients with ketamine, with higher doses raising safety concerns.
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•In a burn ICU, implementing a ketamine restriction policy was associated with a reduced incidence of cholestatic liver injuries.•Ketamine-induced cholestatic liver injury was contingent on both time and dose, becoming apparent at cumulative doses >1,000 mg.•Association between cholestatic liver injury and mortality in patients with severe burn injury was solely observed in the presence of ketamine.•The introduction of ketamine restriction correlated with decreased cholestatic liver injury and mortality rates.
The aim of this study was to describe the prevalence, characteristics and outcome of critically burn patients with pulmonary HSV reactivation.
Retrospective, single-center cohort study in a burn ...critical care unit in a tertiary center, including all consecutive severely burn patients with bronchoalveolar lavage performed for pneumoniae suspicion and screened for HSV from January 2013 and April 2017. We used logistic regression to identify factors associated with HSV reactivation and outcomes.
94 patients were included, mean age was 51 (39-64) years; median total body surface area burned was 36 (25-54)% and ICU mortality 38%. Fifty-five patients (59%) had pulmonary HSV reactivation and 30 (55%) were treated with acyclovir. Patients with HSV reactivation were more severely ill with higher SOFA score at admission compared to patient without HSV reactivation (6 3-8 vs. 2 1-4, p < 0.0001 respectively). In multivariate analysis, sex, SOFA score at admission and smoke inhalation were significantly associated with HSV reactivation. Only septic shock was associated with 90-day mortality when HSV reactivation was not.
Pulmonary HSV reactivation is frequent among severely ill burn patients. Initial severity and smoke inhalation are risk factors. Antiviral treatment was not associated with outcome.
The delayed diagnosis of acute kidney injury (AKI) episodes and the lack of specificity of current single AKI biomarkers hamper its management. Urinary peptidome analysis may help to identify early ...molecular changes in AKI and grasp its complexity to identify potential targetable molecular pathways.
In derivation and validation cohorts totalizing 1170 major cardiac bypass surgery patients and in an external cohort of 1569 intensive care unit (ICU) patients, a peptide-based score predictive of AKI (7-day KDIGO classification) was developed, validated, and compared to the reference biomarker urinary NGAL and NephroCheck and clinical scores.
A set of 204 urinary peptides derived from 48 proteins related to hemolysis, inflammation, immune cells trafficking, innate immunity, and cell growth and survival was identified and validated for the early discrimination (< 4 h) of patients according to their risk to develop AKI (OR 6.13 3.96-9.59, p < 0.001) outperforming reference biomarkers (urinary NGAL and IGFBP7.TIMP2 product) and clinical scores. In an external cohort of 1569 ICU patients, performances of the signature were similar (OR 5.92 4.73-7.45, p < 0.001), and it was also associated with the in-hospital mortality (OR 2.62 2.05-3.38, p < 0.001).
An overarching AKI physiopathology-driven urinary peptide signature shows significant promise for identifying, at an early stage, patients who will progress to AKI and thus to develop tailored treatments for this frequent and life-threatening condition. Performance of the urine peptide signature is as high as or higher than that of single biomarkers but adds mechanistic information that may help to discriminate sub-phenotypes of AKI offering new therapeutic avenues.
Intravascular haemolysis has been associated with acute kidney injury (AKI) in different clinical settings (cardiac surgery, sickle cell disease). Haemolysis occurs frequently in critically ill burn ...patients. The aim of this study was to assess the predictive value of haptoglobin at admission to predict major adverse kidney events (MAKE) and AKI in critically ill burn patients.
We conducted a retrospective, single-centre cohort study in a burn critical care unit in a tertiary centre, including all consecutive severely burned patients (total burned body surface > 20% and/or shock and/or mechanical ventilation at admission) from January 2012 to April 2017 with a plasmatic haptoglobin dosage at admission.
A total of 130 patients were included in the analysis. Their mean age was 49 (34-62) years, their median total body surface area burned was 29% (15-51%) and the intensive care unit (ICU) mortality was 25%. Early haemolysis was defined as an undetectable plasmatic haptoglobin at admission. We used logistic regression to identify MAKE and AKI risk factors. In multivariate analysis, undetectable haptoglobin was associated with MAKE and AKI (respectively, OR 6.33, 95% CI 2.34-16.45, p < 0.001; OR 8.32, 95% CI 2.86-26.40, p < 0.001).
Undetectable plasmatic haptoglobin at ICU admission is an independent risk factor for MAKE and AKI in critically ill burn patients. This study provides a rationale for biomarker-guided therapy using haptoglobin in critically ill burn patients.
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