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Background: Stress hyperglycaemia is common in the intensive care unit (ICU) setting and has been related to a worst outcome. Objective: The objective was to characterize the association of glucoregulatory hormones, mainly incretins, with the levels of glycaemia, and its relationship with outcome in ICU patients. Methods: We prospectively studied 60 patients. Stress hyperglycaemia was diagnosed when glycaemia was < 115 mg/dL. At ICU admission we determined glycaemia, insulin, glucagon, cortisol, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) plasma levels. Groups were compared using Kruskal-Wallis test. The association between glycaemia levels and glucoregulatory hormones was evaluated using linear regression. Results: Forty-five patients (75%) had hyperglycaemia. We observed no differences in glucoregulatory hormones levels between normo- and hyper- glycaemia groups. Glycaemia levels were not significantly correlated with insulin, glucagon, cortisol or GIP levels, but were correlated with GLP-1 (p = 0.04). GLP-1 was also correlated with cortisol (p = 0.01), but failed to show a significant correlation with insulin, glucagon or GIP levels. Lower levels of plasma GLP-1 were found in patients with stress hyperglycaemia requiring vasoactive support (p = 0.02). Conclusions: Glycaemia levels were correlated with GLP-1 levels in ICU patients. GLP-1 levels were also associated with cortisol. Patients with stress hyperglycaemia who required vasoactive support had lower incretin levels compared with those patients with stress hyperglycaemia who were hemodynamically stables. (ClinicalTrials.gov Identifier: NCT01087372).Antecedentes: La hiperglucemia de estrés es habitual en el contexto de la Unidad de cuidados intensivos (UCI) y se ha relacionado con un peor pronóstico. Objetivo: el objetivo fue caracterizar la asociación de hormonas glucorreguladoras, principalmente las incretinas, con las glucemias y su relación con el pronóstico de los pacientes de UCI. Métodos: Estudiamos de forma prospectiva a 60 pacientes. La hiperglucemia de estrés se diagnosticaba cuando la glucemia era < 115 mg/dl. En el ingreso en la UCI, determinamos la glucemia y las concentraciones plasmáticas de insulina, glucagón, cortisol, polipéptido insulinotropo dependiente de glucosa (GIP) y péptido-1 de tipo glucagón (GLP-1). Se compararon los grupos mediante la prueba de Kruskal-Wallis. La asociación entre las glucemias y las hormonas contrarreguladoras se evaluó mediante regresión linear. Resultados: 45 pacientes (75%) tenían hiperglucemia. No observamos diferencias en las concentraciones de hormonas glucorreguladoras entre los grupos de normo e hiperglucemia. Las glucemias no se correlacionaron de forma significativa con las concentraciones de insulina, glucagón, cortisol o GIP, pero sí con el GLP-1 (p = 0,04). El GLP-1 también se correlacionó con el cortisol (p = 0,01), pero no consiguió mostrar una correlación significativa con las concentraciones de insulina, glucagón o GIP. Se encontraron menores concentraciones plasmáticas de GLP-1 en los pacientes con hiperglucemia de estrés que requerían soporte vasoactivo (p = 0,02). Conclusiones: las glucemias se correlacionaron con las concentraciones de GLP-1 en los pacientes en UCI . Las concentraciones de GLP-1 también se asociaron con el cortisol. Los pacientes con hiperglucemia de estrés que necesitaron soporte vasoactivo tenían menores concentraciones de incretina en comparación con aquellos con hiperglucemia de estrés con estabilidad hemodinámica (ClinicalTrials.gov Identifier: NCT01087372).

Hipótesis: La suplementación endovenosa con el dipéptido N(2)-L-alanil-L-glutamina, en pacientes traumáticos ingresado en la UCI puede ejercer un efecto beneficioso en cuanto a reducción de la incidencia de infecciones, de la estancia en UCI y de la mortalidad, independientemente del tipo de nutrición (enteral o parenteral) administrada. Objetivos: El objetivo principal es medir la eficacia de la suplementación con el dipéptido, administrado de forma endovenosa, en reducir la incidencia de las complicaciones infecciosas, la mortalidad y la estancia en UCI de los pacientes traumáticos ingresados en la UCI. Otros objetivos secundarios son: 1) Evaluar la eficacia de L-alanil-L-glutamina en diferentes grupos de gravedad y en relación con los niveles plasmáticos de glutamina. 2) Recoger los posibles efectos adversos del dipéptido administrado de forma endovenosa. Metodología: Ensayo clínico prospectivo, multicéntrico, aleatorizado y doble ciego, con dos grupos paralelos de tratamiento, para evaluar eficacia frente a placebo. Los pacientes traumáticos ingresados en la UCI que cumplan los criterios de inclusión/no exclusión, serán aleatorizados para recibir L-alanil-L-glutamina o placebo, independientemente del tipo de nutrición que reciba el paciente (enteral o parenteral) El dipéptido será administrado como un farmaconutriente en forma de perfusión continua durante 24 horas y durante 5 días a 0,5 g/kg/día.Hypothesis: the endovenous administration of glutamine, independently of the type of nurtrition received, can reduce the ICU length of stay, the incidence of infections and the mortality in the traumatic patients admitted to the ICU. Objectives: The main objective is to assess the efficacy of glutamine suplementation, given intravenously, to reduce the incidence of infectious complications, mortality and ICU length of stay in the traumatic patients admitted to the ICU. Other objectives are: 1) to assess the efficacy of glutamine in different groups of patients according to the severity and the plasma levels of glutamine. 2) Record all the adverse events due to the intravenous administration of glutamine. Methods: prospective, randomized, doble-blind and multicenter study with two parallel groups: placebo and treatment group. The patients who fulfill the inclusion criteria will receive either glutamine or placebo, independently of the type on nutrition. Glutamine will be administered as a pharmaconutrient at 0.5 g/kg/day during 5 days as a continous perfusion.

Introducción y objetivos: El soporte nutricional en el enfermo crítico debe ser lo más ajustado a sus necesidades. La medición del GER por calorimetría indirecta (CI) es el "patrón oro", aunque las dificultades de la propia técnica condicionan su uso. El objetivo ha sido a partir de la medición del GER por CI en pacientes críticos con ventilación mecánica, desarrollar una fórmula simple para el cálculo del GER, basada en parámetros antropométricos, validarla y compararla con otras fórmulas predictivas (FP). Material y métodos: En 337 pacientes críticos se determinó el GER por CI en las primeras 48 horas de ingreso. Tras excluir pacientes febriles/hipotérmicos y con IMC < 18,5 kg/m² y > 40 kg/m², se consideraron 268 enfermos, adjudicados de manera aleatoria a dos grupos de 134 pacientes de características antropométricas similares. Un grupo (grupo A) se usó para la elaboración de la fórmula y otro (grupo B) para la validación y comparación con otras FP. Se consideraron como niveles de acierto, diferencias iguales o inferiores al 15 y 20% entre el GER medido y el calculado por distintas FP. Resultados: El grupo A tenía una edad media de 48 ± 20 años, un IMC de 26 ± 5 kg/m² y un GER de 1.870 ± 355 kcal/día. La fórmula resultante fue: GER/kg = 30 - (3 x Edad) - (3 x BMI) Edad: ≤ 50 años = 0 y > 50 años = 1. BMI: 18,5-24,9 = 0, 25-29,9 = 1 y 30-39,9 = 2. El grupo B tenía una edad media de 51 ± 19 años, un ICM de 25 ± 4 kcal/m² y el GER de 1.835 ± 332 kcal/día. En este grupo de validación, los porcentajes de acierto de la nueva fórmula descrita y de otras FP se presentan en la Tabla. Conclusiones: Se valida una fórmula fácil, que contempla factores de edad y sobrepeso/obesidad (ICM), para el cálculo del gasto energético de pacientes críticos en ventilación mecánica. [ABSTRACT FROM AUTHOR]

Introducción y objetivos: La glutamina (Gl) es un aminoácido esencial en situaciones de estrés metabólico. Se sugiere que al suplementarlo desciende la incidencia de complicaciones infecciosas. Los mecanismos por los que la Gl mejora la función inmunológica no están definidos. Estudios in vitro han demostrado que la Gl estimula la producción de radicales libres por monocitos lo que incrementaría su habilidad para eliminar microorganismos mediante fagocitosis. El objetivo de este estudio es comprobar si el tratamiento con nutrición parenteral (NPT) suplementada con Gl, usada en pacientes críticos, puede mejorar la función inmunológica por un aumento de la capacidad fagocítica de los monocitos. Material y métodos: Estudio prospectivo, aleatorizado y comparativo entre 2 grupos de pacientes críticos con NPT + Gl y con NPT sin Gl. El grupo control recibe NPT isocalórica e isonitrogenada. Estudio aprobado por el CEIC de las Illes Balears; en todos los casos se solicitó consentimiento informado. Las muestras de sangre periférica para estudiar TLR se extraerán antes de empezar el tratamiento, al final (50 día) y a los 14 días de haberse iniciado. Para estudiar la fagocitosis se ha utilizado E Coli marcado con GFP. Se han utilizado monocitos purificados mediante selección negativa a partir de sangre periférica y posteriormente infectados con E Coli con una multiplicidad de infección de 10 bacterias por monocito. Se ha empleado técnica de citometría de flujo para analizar la fagocitosis. Resultados preliminares de los primeros 11 pacientes (7 varones, 4 mujeres, edad media 45 años), 5 recibieron NPT suplementada con glutamina y 6 eran grupo control. Aunque con características basales similares, el grupo de glutamina tenía mayor gravedad medida por APACHE II, III y SOFA. Sin diferencias significativas entre ambos grupos respecto a fagocitosis (fig.) y aparición de complicaciones infecciosas. Conclusión: No hemos detectado hasta el momento un aumento de fagocitosis al suplementar la NPT con glutamina, respecto a un grupo control. Dado lo reducido del grupo de estudio y las diferencias en los índices de gravedad creemos necesario seguir el estudio intentando una muestra más homogénea. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) is a leading cause of disability and mortality globally, stemming from both primary mechanical injuries and subsequent secondary responses. Effective early management of moderate-to-severe TBI is essential to prevent secondary damage and improve patient outcomes. This review provides a comprehensive guide for the resuscitation and stabilization of TBI patients, combining clinical experience with current evidence-based guidelines. Key areas addressed in this study include the identification and classification of severe TBI, intubation strategies, and optimized resuscitation targets to maintain cerebral perfusion. The management of coagulopathy and special considerations for patients with concomitant hemorrhagic shock are discussed in depth, along with recommendations for neurosurgical interventions. This article further explores the role of multimodal neuromonitoring and targeted temperature management to mitigate secondary brain injury. Finally, it discusses end-of-life care in cases of devastating brain injury (DBI). This practical review integrates foundational and recent advances in TBI management to aid in reducing secondary injuries and enhancing long-term recovery, presenting a multidisciplinary approach to support acute care decisions in TBI patients.

Critical care management of aneurysmal subarachnoid hemorrhage (aSAH) remains a major challenge. Despite the recent publication of guidelines from the American Heart Association/American Stroke Association and the Neurocritical Care Society, there are many controversial questions in the intensive care unit (ICU) management of this population. The authors provide an analysis of common issues in the ICU and provide guidance on the daily management of this specific population of neurocritical care patients., (Copyright © 2023. Published by Elsevier España, S.L.U.)

Background: Individual extracerebral organ dysfunction is common after severe traumatic brain injury (TBI) and impacts outcomes. However, multiorgan failure (MOF) has received less attention in patients with isolated TBI. Our objective was to analyze the risk factors associated with the development of MOF and its impact in clinical outcomes in patients with TBI., Methods: This was an observational, prospective, multicenter study using data from a nationwide registry that currently includes 52 intensive care units (ICUs) in Spain (RETRAUCI). Isolated significant TBI was defined as Abbreviated Injury Scale (AIS) ≥ 3 in the head area with no AIS ≥ 3 in any other anatomical area. Multiorgan failure was defined using the Sequential-related Organ Failure Assessment as the alteration of two or more organs with a score of ≥ 3. We analyzed the contribution of MOF to crude and adjusted mortality (age and AIS head) by using logistic regression analysis. A multiple logistic regression analysis was performed to analyze the risk factors associated with the development of MOF in patients with isolated TBI., Results: A total of 9790 patients with trauma were admitted to the participating ICUs. Of them, 2964 (30.2%) had AIS head ≥ 3 and no AIS ≥ 3 in any other anatomical area, and these patients constituted the study cohort. Mean age was 54.7 (19.5) years, 76% of patients were men, and ground-level falls were the main mechanism of injury (49.1%). In-hospital mortality was 22.2%. Up to 185 patients with TBI (6.2%) developed MOF during their ICU stay. Crude and adjusted (age and AIS head) mortality was higher in patients who developed MOF (odds ratio 6.28 [95% confidence interval 4.58-8.60] and odds ratio 5.20 [95% confidence interval 3.53-7.45]), respectively. The logistic regression analysis showed that age, hemodynamic instability, the need of packed red blood cells concentrates in the initial 24 h, the severity of brain injury, and the need for invasive neuromonitoring were significantly associated with MOF development., Conclusions: MOF occurred in 6.2% of patients with TBI admitted to the ICU and was associated with increased mortality. MOF was associated with age, hemodynamic instability, the need of packed red blood cells concentrates in the initial 24 h, the severity of brain injury, and the need for invasive neuromonitoring., (© 2023. Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society.)

Traumatic brain injury (TBI) affects not only the brain but also peripheral organs like the heart and the lungs, which influences long-term outcomes. A heightened systemic inflammatory response is often induced after TBI, but the underlying pathomechanisms that contribute to co-morbidities remain poorly understood. Here, we investigated whether extracellular vehicles (EVs) containing inflammasome proteins are released after severe controlled cortical impact (CCI) in C57BL/6 mice and cause activation of inflammasomes in the heart that result in tissue damage. The atrium of injured mice at 3 days after TBI showed a significant increase in the levels of the inflammasome proteins AIM2, ASC, caspases-1, -8 and -11, whereas IL-1β was increased in the ventricles. Additionally, the injured cortex showed a significant increase in IL-1β, ASC, caspases-1, -8 and -11 and pyrin at 3 days after injury when compared to the sham. Serum-derived extracellular vesicles (EVs) from injured patients were characterized with nanoparticle tracking analysis and Ella Simple Plex and showed elevated levels of the inflammasome proteins caspase-1, ASC and IL-18. Mass spectrometry of serum-derived EVs from mice after TBI revealed a variety of complement- and cardiovascular-related signaling proteins. Moreover, adoptive transfer of serum-derived EVs from TBI patients resulted in inflammasome activation in cardiac cells in culture. Thus, TBI elicits inflammasome activation, primarily in the atrium, that is mediated, in part, by EVs that contain inflammasome- and complement-related signaling proteins that are released into serum and contribute to peripheral organ systemic inflammation, which increases inflammasome activation in the heart.

Objectives: To compare the ability of the Glasgow Coma Scale (GCS) score, the GCS Pupils (GCS-P) score, and the Pupil Reactivity Score (PRS) to predict mortality in patients with severe head injury., Material and Methods: Retrospective analysis of all patients with severe head injury and initial GCS scores of 8 or lower on initial evaluation for whom records included pupil dilation information and clinical course after admission to intensive care units of participating hospitals. We assessed the ability of each of the 3 scores (GCS, GCS-P, and PRS) to predict mortality using discrimination analysis. Discrimination was estimated by calculating the areas under the receiver operating characteristic curves (AUC) and 95% CIs., Results: A total of 1551 patients with severe head injury and pupil dilation records were studied. The mean age was 50 years, 1190 (76.7%) were males, and 592 (38.2%) died. No pupil dilation was observed in 905 patients (58.3%), 362 (23.3%) had unilateral mydriasis, and 284 (18.3%) had bilateral mydriasis. The GCS-P score was significantly better at predicting mortality, with an AUC of 0.77 (95% CI, 0.74-0.79), versus 0.69 (95% CI, 0.67-0.72) for the GCS, and 0.75 (95% CI, 0.72-0.77) for the PRS. As the GCS-P score decreased, mortality increased., Conclusion: The GCS-P was more useful than the GCS for predicting death after severe head injury.

Mechanisms involved in thyroid dysfunction in critically ill coronavirus disease 2019 (COVID-19) patients are not clear. Our objective was to correlate the thyroid response with the pro- and anti-inflammatory cytokines profile in critically ill COVID-19 patients. This was a prospective single-center study. We studied the relationship between continuous variables by using Pearson correlation and simple linear regression. Multiple logistic regression analysis was performed to analyze the factors independently associated with mortality. Seventy-eight patients were included in the study at intensive care unit (ICU) admission and 72 had a measurement of the thyroid and inflammatory profile at day 5. No significant correlations were found between thyroid stimulating hormone (TSH), free triiodothyronine (fT3) and free thyroxine (fT4) and inflammatory cytokines at ICU admission. At day 5, fT4, was inversely correlated with IL-10 (p = 0.035). IL-10 was associated with maximum lactate (p < 0.001) and SOFA score values (p = 0.012). The multiple logistic regression analysis showed that there was a significant relationship between IL-10 (day 5) and in-hospital mortality after adjusting by age and severity of illness. In conclusion, we found that the thyroid hormone profile and inflammatory cytokines had a weak correlation at ICU admission. Associations of interest between fT4 and IL-10 were found at day 5. IL-10 at day 5 was found to be correlated with low fT4 and markers of organ failure and death.

Our objective was to analyze the contribution of acute kidney injury (AKI) to the mortality of isolated TBI patients and its associated risk factors. Observational, prospective and multicenter registry (RETRAUCI) methods were used, from March 2015 to December 2019. Isolated TBI was defined as abbreviated injury scale (AIS) ≥ 3 head with no additional score ≥ 3. A comparison of groups was conducted using the Wilcoxon test, chi-square test or Fisher's exact test, as appropriate. A multiple logistic regression analysis was conducted to analyze associated risk factors in the development of AKI. For the result, overall, 2964 (30.2%) had AIS head ≥ 3 with no other area with AIS ≥ 3. The mean age was 54.7 (SD 19.5) years, 76% were men, and the ground-level falls was 49.1%. The mean ISS was 18.4 (SD 8). The in-hospital mortality was 22.2%. Up to 310 patients (10.6%) developed AKI, which was associated with increased mortality (39% vs. 17%, adjusted OR 2.2). Associated risk factors (odds ratio (OR) (95% confidence interval)) were age (OR 1.02 (1.01-1.02)), hemodynamic instability (OR 2.87 to OR 5.83 (1.79-13.1)), rhabdomyolysis (OR 2.94 (1.69-5.11)), trauma-associated coagulopathy (OR 1.67 (1.05-2.66)) and transfusion of packed red-blood-cell concentrates (OR 1.76 (1.12-2.76)). In conclusion, AKI occurred in 10.6% of isolated TBI patients and was associated with increased mortality.

Traumatic brain injury (TBI) has a complex pathology in which the initial injury releases damage associated proteins that exacerbate the neuroinflammatory response during the chronic secondary injury period. One of the major pathological players in the inflammatory response after TBI is the inflammasome. Increased levels of inflammasome proteins during the acute phase after TBI are associated with worse functional outcomes. Previous studies reveal that the level of inflammasome proteins in biological fluids may be used as promising new biomarkers for the determination of TBI functional outcomes. In this study, we provide further evidence that inflammatory cytokines and inflammasome proteins in serum may be used to determine injury severity and predict pathological outcomes. In this study, we analyzed blood serum from TBI patients and respective controls utilizing Simple Plex inflammasome and V-PLEX inflammatory cytokine assays. We performed statistical analyses to determine which proteins were significantly elevated in TBI individuals. The receiver operating characteristics (ROC) were determined to obtain the area under the curve (AUC) to establish the potential fit as a biomarker. Potential biomarkers were then compared to documented patient Glasgow coma scale scores via a correlation matrix and a multivariate linear regression to determine how respective biomarkers are related to the injury severity and pathological outcome. Inflammasome proteins and inflammatory cytokines were elevated after TBI, and the apoptosis-associated speck like protein containing a caspase recruitment domain (ASC), interleukin (IL)-18, tumor necrosis factor (TNF)-α, IL-4 and IL-6 were the most reliable biomarkers. Additionally, levels of these proteins were correlated with known clinical indicators of pathological outcome, such as the Glasgow coma scale (GCS). Our results show that inflammatory cytokines and inflammasome proteins are promising biomarkers for determining pathological outcomes after TBI. Additionally, levels of biomarkers could potentially be utilized to determine a patient's injury severity and subsequent pathological outcome. These findings show that inflammation-associated proteins in the blood are reliable biomarkers of injury severity that can also be used to assess the functional outcomes of TBI patients.

Background: The objectives of this study were to assess the association between serum caspase 1 levels and known clinical and radiological prognostic factors and determine whether caspase 1was a more powerful predictor of outcome after traumatic brain injury (TBI) than clinical indices alone, to determine the association between the serum levels of caspase 1 and the 6-month outcome, and to evaluate if there is any association between caspase 1 with clinical and radiological variables., Methods: This prospective and observational study was conducted in a university hospital and included patients with TBI who required hospital admission. Serum samples were collected at hospital admission and 24 h after TBI. Caspase 1 levels were determined by enzyme-linked immunosorbent assay. Receiver operating characteristic curves were obtained to test the potential of caspase 1 to predict mortality (Glasgow Outcome Scale Extended score of 1) and unfavorable outcome (Glasgow Outcome Scale Extended scores of 1-4). Multivariate logistic regression was used to assess the effect of serum caspase 1 levels, adjusted by known clinical and radiological prognostic indices, on the outcome., Results: One hundred thirty-two patients and 33 healthy controls were included. We obtained 6-month outcome in 118 patients. On admission, the mean serum levels of caspase 1 were higher in patients with TBI compared with controls (157.9 vs. 108.5 pg/mL; p < 0.05) but not at 24 h after TBI. Serum caspase 1 levels on admission were higher in patients with unfavorable outcomes (189.5 vs. 144.1 pg/mL; p = 0.009). Similarly, serum caspase 1 levels on admission were higher in patients who died vs. patients who survived (213.6 vs. 146.8 pg/mL; p = 0.03). A logistic regression model showed that the serum caspase 1 level on admission was an independent predictor of 6-month unfavorable outcomes (odds ratio 1.05; 95% confidence interval 1-1.11; p = 0.05). Caspase 1 levels were higher in patients with severe TBI compared with those with moderate TBI, those with mild TBI, and healthy controls (p < 0.001). We did not find any correlation between caspase 1 and the radiological variables studied., Conclusions: In this cohort of patients with TBI, we show that serum caspase 1 protein levels on admission are an independent prognostic factor after TBI. Serum caspase 1 levels on admission are higher in patients who will present unfavorable outcomes 6 months after TBI. Caspase 1 levels on admission are associated with the injury severity determined by the Glasgow Coma Scale., (© 2021. Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society.)

Our objective was to determine outcomes of severe chest trauma admitted to the ICU and the risk factors associated with mortality. An observational, prospective, and multicenter registry of trauma patients admitted to the participating ICUs (March 2015-December 2019) was utilized to collect the patient data that were analyzed. Severe chest trauma was defined as an Abbreviated Injury Scale (AIS) value of ≥3 in the thoracic area. Logistic regression analysis was used to evaluate the contribution of severe chest trauma to crude and adjusted ORs for mortality and to analyze the risk factors associated with mortality. Overall, 3821 patients (39%) presented severe chest trauma. The sample's characteristics were as follows: a mean age of 49.88 (19.21) years, male (77.6%), blunt trauma (93.9%), a mean ISS of 19.9 (11.6). Crude and adjusted (for age and ISS) ORs for mortality in severe chest trauma were 0.78 (0.68-0.89) and 0.43 (0.37-0.50) ( p < 0.001), respectively. In-hospital mortality in the severe chest trauma patients without significant traumatic brain injury (TBI) was 5.63% and was 25.71% with associated significant TBI ( p < 0.001). Age, the severity of injury (NISS and AIS-head), hemodynamic instability, prehospital intubation, acute kidney injury, and multiorgan failure were risk factors associated with mortality. The contribution of severe chest injury to the mortality of trauma patients admitted to the ICU was very low. Risk factors associated with mortality were identified.

The incidence of thyroid disfunction has not been analyzed in critically ill COVID-19 patients. Our objective was to analyze the relationship of the thyroid profile and in-hospital mortality in critically ill COVID-19 patients. This was a prospective single-center study involving critically ill COVID-19 patients admitted to the ICU of a tertiary University Hospital. Thyroid hormones were measured through drawing blood samples from a central venous catheter at ICU admission and on the fifth day. A multiple logistic regression analysis was performed to analyze the variables associated with mortality. The ability of the different thyroid hormones to predict in-hospital mortality was evaluated by calculating the receiver operating characteristics (ROCs) and the area under the curve (AUC). A total of 78 patients were included in the study at ICU admission; 72 had their thyroid profile measured at day 5. In-hospital mortality reached 29.5%. Multiple logistic regression analysis showed that variables associated with mortality were age and prior beta-blocker therapy at ICU admission and age fT4 at day 5. The AUC for in-hospital mortality predictions of fT4 at day 5 was 0.69. Thyroid responses are commonly observed in critically ill COVID-19 patients. fT4 at day 5 after ICU admission was associated with mortality.

Lung IL-6 is a promising biomarker for predicting respiratory failure during pulmonary infections. This biomarker is found in respiratory samples which need to be liquefied prior to analysis. Traditional liquefying methods use reducing agents such as dithiothreitol (DTT). However, DTT impairs immunodetection and does not liquefy highly viscous samples. We propose an enzymatic method that liquefies samples by means of generating O 2 bubbles with endogenous catalase. Low respiratory tract specimens from 48 mechanically ventilated patients (38 with SARS-CoV-2 infection) were treated with DTT or with the enzymatic method. We used turbidimetry to compare the liquefaction degree and IL-6 was quantified with ELISA. Finally, we used AUC-ROC, time-to-event and principal component analysis to evaluate the association between respiratory compromise or local inflammation and IL-6 determined with both methods. Enzymatically treated samples were better liquefied than those reduced by DTT, which resulted in higher ELISA signals. Lung IL-6 levels obtained with the enzymatic procedure were negatively correlated with the oxygenation index (PaO 2 /FiO 2 ) and the time of mechanical ventilation. The proposed enzymatic liquefaction method improves the sensitivity for lung IL-6 detection in respiratory samples, which increases its predictive power as a biomarker for evaluating respiratory compliance.

Background and Objective: Cerebral edema is a frequent and serious complication of traumatic brain injury (TBI). Diffusion tensor imaging (DTI) is considered a useful technique to assess white matter integrity after TBI. The objective of this prospective, observational study was to assess the characteristics of the vasogenic edema in the traumatic pericontusional tissue and compare it to the vasogenic edema found in brain tumors. We also included a control group., Methods: Using DTI, the Apparent diffusion coefficient (ADC) and Fractional anisotropy (FA) were measured in the area of vasogenic edema in both TBI and tumor patients. The measurements in the control group were done in the gray and white matter. We included 15 TBI patients, 18 tumor patients and 15 controls., Results: ADC and FA showed no differences between TBI and tumor patients (p=0.27 for AF; p=0.79 for ADC). Compared to healthy controls, TBI and tumor patients presented higher ADC values and lower FA values. The differences between TBI and controls were statistically significant (p<0.05)., Conclusions: In this prospective observational study using DTI-MRI in a selected group of mild and moderate TBI patients with vasogenic pericontusional edema we have shown that there were no significant differences of the ADC and FA values compared to brain tumor patients. Furthermore, healthy controls showed significant lower ADC values and higher FA values compared to TBI and tumor patients. Future studies, using DTI-MRI, should address whether any therapy has a favorable impact on the vasogenic edema of TBI patients with brain contusions., (Copyright © 2020 Sociedad Española de Neurocirugía. Published by Elsevier España, S.L.U. All rights reserved.)

Objective: To analyze factors associated with the development of early and late multiorgan failure (MOF) in trauma patients admitted to the intensive care unit (ICU)., Methods: Spanish Trauma ICU Registry (RETRAUCI). Data collected from 52 trauma ICU between March 2015 and December 2019. We analyzed the incidence, outcomes, and the risk factors associated with early (< 72 h) or late (beyond 72 h) MOF in trauma ICU patients. Multiple logistic regression analysis was performed to analyze associated factors., Results: After excluding patients with incomplete data, 9,598 trauma ICU patients constituted the study population. Up to 965 patients (10.1%) presented with MOF, distributed by early MOF in 780 patients (8.1%) and late MOF in 185 patients (1.9%). The multivariate analysis showed that early MOF was associated with: ISS ≥ 16 (OR 2.80), hemodynamic instability (OR from 2.03 to 43.05), trauma-associated coagulopathy (OR 2.32), and acute kidney injury (OR 4.10). Late MOF was associated with: age > 65 years (OR 1.52), hemodynamic instability (OR from 1.92 to 9.94), acute kidney injury (OR 4.22), and nosocomial infection (OR 17.23). MOF was closely related to mortality (crude OR (95% CI) 4.77 (4.22-5.40))., Conclusions: Multiorgan failure was recorded in 10% of trauma ICU patients, with early MOF being the predominant form. Early and late MOF forms were associated with different risk factors, suggesting different pathophysiological pathways. Early MOF was associated with higher severity of injury and severe bleeding-related complications and late MOF with advanced age and nosocomial infection., Competing Interests: The authors report no conflicts of interest., (Copyright © 2020 by the Shock Society.)