Search

Resumen Los avances en la monitorizacion cerebral multiparametrica han permitido ahondar en el conocimiento de la fisiopatologia del traumatismo craneoencefalico, y en como la terapeutica disponible puede modularla. Para ello, se antoja imprescindible conocer e interpretar una serie de principios fisiologicos y fisiopatologicos basicos que propician, por un lado, un entorno metabolico cerebral adecuado para prevenir un incremento de la lesion cerebral primaria y favorecer su recuperacion, y por otro lado, permiten adaptar de forma individualizada los recursos terapeuticos a la situacion concreta del paciente. En el presente articulo se exponen, en forma de decalogo, sustentados en dichas nociones, los objetivos fisiologicos a conseguir, junto con una serie de recomendaciones diagnosticas y terapeuticas que posibiliten su logro. Se hace enfasis en la consideracion y analisis de las variables fisiologicas implicadas en el transporte de oxigeno al cerebro, como el gasto cardiaco y el contenido arterial de oxigeno, junto con sus condicionantes y las posibles alteraciones de cada uno de ellos. Cobran especial atencion los elementos basicos que constituyen la neuroproteccion fisiologica. Asimismo, se razonan las multiples causas que provocan hipoxia cerebral y el modo de abordarlas y corregirlas. El aumento de la presion intracraneal, como elemento fisiopatologico, se examina, subrayandose para interpretarla la interconexion e influencia de la presion toracica y abdominal sobre la intracraneal. El tratamiento de la presion intracraneal debe efectuarse sobre un modelo de acciones escalonadas, cuyo inicio deberia cimentarse mas que en valores numericos rigidos, en una reflexion fisiopatologica unida a la informacion de las lesiones tomograficas.

Advances in multiparametric brain monitoring have allowed us to deepen our knowledge of the physiopathology of head injury and how it can be treated using the therapies available today. It is essential to understand and interpret a series of basic physiological and physiopathological principles that, on the one hand, provide an adequate metabolic environment to prevent worsening of the primary brain injury and favour its recovery, and on the other hand, allow therapeutic resources to be individually adapted to the specific needs of the patient. Based on these notions, this article presents a decalogue of the physiological objectives to be achieved in brain injury, together with a series of diagnostic and therapeutic recommendations for achieving these goals. We emphasise the importance of considering and analysing the physiological variables involved in the transport of oxygen to the brain, such as cardiac output and arterial oxygen content, together with their conditioning factors and possible alterations. Special attention is paid to the basic elements of physiological neuroprotection, and we describe the multiple causes of cerebral hypoxia, how to approach them, and how to correct them. We also examine the increase in intracranial pressure as a physiopathological element, focussing on the significance of thoracic and abdominal pressure in the interpretation of intracranial pressure. Treatment of intracranial pressure should be based on a step-wise model, the first stage of which should be based on a physiopathological reflection combined with information on the tomographic lesions rather than on rigid numerical values.

Continuous monitoring of cerebral oxygenation and its application to the management of the severe neurological patient is a challenge for the management of patients with acute critical brain damage. Although several techniques have been described for monitoring brain, brain tissue oxygen monitoring provides relevant information about oxygen levels of brain tissue. However, the development of this technique has been associated with the need to answer not only some technical aspects of it as well as the meaning of the changes of the cerebral oxygenation in the neurocritical patient. The consensus document responds to various questions related to the monitoring of cerebral oxygenation by means of a cerebral oxygen tissue pressure sensor. For this purpose, a list of questions was prepared and a reviewed of the medical literature was made. The quality of the evidence and the degree of recommendation was evaluated using the GRADE methodology.

En las últimas décadas el sistema sanitario ha afrontado graves crisis de salud como el síndrome tóxico, la epidemia del virus H1N1, hasta la actual pandemia del COVID-19. Todas estas crisis comparten características comunes como la incertidumbre y sensación de pánico; el número ingente de afectados, leves en su mayoría, que pone a prueba la eficacia y organización del sistema sanitario; y, a destacar, que un alto porcentaje de pacientes precisa hospitalización debido a fallo respiratorio hipoxémico agudo, de los cuales, hasta un 10% pueden requerir ingreso en cuidados intensivos (UCI). Esto implica necesidad de incremento de camas críticas, de recursos electromédicos y de personal cualificado. La compra de respiradores implica esfuerzo económico, pero elementos fundamentales como el aumento de camas críticas o de personal es difícil de improvisar. Por otra parte, estudios como CESAR1 mostraron menor mortalidad cuando el paciente es tratado en UCI especializada con alto volumen de ingresos. Ante esta situación, la moderna tecnología basada en la trasformación digital podría ser de gran ayuda. ¿Qué beneficios podemos esperar en la UCI de los sistemas de información?

Paroxysmal sympathetic hyperactivity (PSH) is a potentially life-threatening neurological emergency secondary to multiple acute acquired brain injuries. It is clinically characterized by the cyclic and simultaneous appearance of signs and symptoms secondary to exacerbated sympathetic discharge. The diagnosis is based on the clinical findings, and high alert rates are required. No widely available and validated homogeneous diagnostic criteria have been established to date. There have been recent consensus attempts to shed light on this obscure phenomenon. Its physiopathology is complex and has not been fully clarified. However, the excitation-inhibition model is the theory that best explains the different aspects of this condition, including the response to treatment with the available drugs. The key therapeutic references are the early recognition of the disorder, avoiding secondary injuries and the triggering of paroxysms. Once sympathetic crises occur, they must peremptorily aborted and prevented. of the later the syndrome is recognized, the poorer the patient outcome.

Resumen La hiperactividad simpatica paroxistica es una urgencia neurologica potencialmente letal secundaria a multiples lesiones cerebrales agudas adquiridas. Se caracteriza por rasgos clinicos de aparicion ciclica y simultanea, consecuencia de una descarga simpatica exacerbada. El diagnostico es clinico, requiriendo elevados indices de alerta. Actualmente no existen criterios diagnosticos homogeneos que esten ampliamente difundidos y validados. El consenso reciente intenta arrojar luz sobre este oscuro panorama. Su fisiopatologia es compleja y aun no ha sido elucidada con certeza; sin embargo, la teoria basada en el modelo excitacion-inhibicion es la que mejor explica los distintos aspectos de esta entidad, incluyendo la respuesta a la terapia con los farmacos disponibles. Los pilares terapeuticos se asientan sobre el reconocimiento precoz, evitar insultos secundarios y el desencadenamiento de los paroxismos. De ocurrir crisis simpaticas, es que estas se aborten de forma perentoria y que se prevengan. Cuanto mas tarde en reconocerse el sindrome, peores seran los resultados.

Over the last few decades, the healthcare system has faced serious health crisis like the toxic syndrome or the H1N1 virus epidemic until the current COVID-19 pandemic. All of these crises share common features like uncertainty and a sensation of panic; also, the huge number of people affected by them—most of them mildly affected—puts the efficacy and organization of the entire healthcare system to the test. Also, a high percentage of these patients requires hospitalization due to acute hypoxemic respiratory failure. Up to 10% of these patients can end up requiring intensive care unit (ICU) admission. This requires more critical beds, electromedical resources, and skilled personnel available to cover these needs. Buying ventilators is a huge economic effort. However, increasing the number of critical beds or having more personnel is not easy to improvise. On the other hand, studies like the CESAR trial1 confirmed that mortality rate is lower when the patient is treated in a specialized ICU with a high volume of admissions. In the light of the current situation, modern technology based on digital transformation can help. What are the benefits we could expect from information systems at the ICU setting?

Cerebral damage secondary to the vasospasm due to subarachnoid hemorrhage (SAH) is an important cause of morbid-mortality. We propose the use of the PET tracer [18F]Fluoromisonidazole to visualize the hypoxia due to the vasospasm. On the other hand [18F]Fluoromisonidazole synthesis process was optimized, avoiding HPLC purification using SPE cartridges instead, and reducing some synthesis steps. [18F]Fluoromisonidazole in vitro stability was tested for ten hours, and in vivo PET/CT images showed higher cerebral uptake in hemorrhagic animals than in control rats., This research was in part supported by Spanish Regional Government of Andalusia with the research Grant PI-0136-2012 CSBS 2012 entitled “New therapeutic targets in spontaneous subarachnoid hemorrhage.” Andalusian Health System and also by the research Grant CTS 2482 entitled “Integration of the image PET/CT in a precision and Adaptive radiotherapy planning”. Spanish Regional Government of Andalusia.

Cerebral vasospasm, one of the main complications of subarachnoid hemorrhage (SAH), is characterized by arterial constriction and mainly occurs from day 4 until the second week after the event. Urotensin-II (U-II) has been described as the most potent vasoconstrictor peptide in mammals. An analysis is made of the serum U-II concentrations and mRNA expression levels of U-II, urotensin related peptide (URP) and urotensin receptor (UT) genes in an experimental murine model of SAH.An experimental study was carried out.Experimental operating room of the Biomedicine Institute of Seville (IBiS), Virgen del Rocío University Hospital (Seville, Spain).96 Wistar rats: 74 SAH and 22 sham intervention animals.Day 1: blood sampling, followed by the percutaneous injection of 100μl saline (sham) or blood (SAH) into the subarachnoid space. Day 5: blood sampling, followed by sacrifice of the animals.Weight, early mortality, serum U-II levels, mRNA values for U-II, URP and UT.Serum U-II levels increased in the SAH group from day 1 (0.62pg/mL [IQR 0.36-1.08]) to day 5 (0.74pg/mL [IQR 0.39-1.43]) (p0.05), though not in the sham group (0.56pg/mL [IQR 0.06-0.83] day 1; 0.37pg/mL [IQR 0.23-0.62] day 5; p=0.959). Between-group differences were found on day 5 (p0.05). The ROC analysis showed that the day 5 serum U-II levels (AUC=0.691), URP mRNA (AUC=0.706) and UT mRNA (AUC=0.713) could discriminate between sham and SAH rats. The normal serum U-II concentration range in rats was 0.56pg/mL (IQR 0.06-0.83).The urotensinergic system is upregulated on day 5 in an experimental model of SAH.

Digital transformation in healthcare is affecting all levels of care. Conceptually speaking, it involves technology but also cultural changes and acceptance. Adapting technology is beneficial in healthcare. Patient safety and the delivery of care have certainly improved with the advent of technological advances. Also, our ability to manage extended databases and have readily available resources for its use at all levels has also impacted healthcare. However, technology has also created obstacles and limitations such us alarm fatigue and lack of interoperability among systems, making it difficult to navigate information pathways. Smart ICU design contemplates the ability of the systems to communicate, facilitate, and re-create all elements of the delivery of medical care in the ICU. Concepts as action-reaction, real-time data collection, and integration of information as well as predictive algorithms are subject to growing research and discussion. A change on the culture of medical care from our actual system of delivery to the patient-centered one also benefits from technological innovation. The future of medical care, including ICU care, is personalized, centered in the singularity of the human being.

[Background] S100B and neuron-specific enolase (NSE) have been widely studied in diverse neurocritical pathologies, being recognized as the most promising biomarkers for brain injury assessment. However, their role in intracerebral hemorrhage (ICH) has not been widely analyzed., [Methods] This was an observational prospective cohort study of patients with ICH admitted to a neurocritical care unit. Blood samples were collected on admission and at 24 hours, 48 hours, and 72 hours. Patient outcomes were assessed at 6 months after the event., [Results] Thirty-six patients with ICH were included in the study. The mortality rate was 36%. Nonsurvivors had higher S100B values than survivors at admission, 24 hours, and 48 hours (P < 0.05). Likewise, S100B levels were higher in patients with poor outcomes (modified Rankin Scale [mRS] score >4) compared with those with good outcome (mRS score ≤3) in the 24-hour, 48-hour, and 72-hour samples. Receiver operating characteristic (ROC) curve analysis showed that S100B at admission, 24 hours, and 48 hours can discriminate between patients who survive and those who die as a consequence of ICH. The 48-hour sample (area under the ROC curve, 0.817; P = 0.003) reached the best values for sensitivity (75%) and specificity (80%); cutoff, 0.250 μg/L. For 6-month functional outcome, S100B protein could differentiate between groups at 24, 48, and 72 hours. The S100B 24-hour sample had the best values for sensitivity (82.6%) and specificity (72.7%), with a cutoff of 0.202 μg/L. We found no clear relationship between NSE values and clinical characteristics., [Conclusions] S100B protein acts as early predictor of mortality and functional outcome in patients with ICH. This biomarker measurement can provide additional information beyond clinical and radiologic findings to guide physicians in the management of these patients.

Continuous monitoring of cerebral oxygenation and its application to the management of the severe neurological patient is a challenge for the management of patients with acute critical brain damage. Although several techniques have been described for monitoring brain, brain tissue oxygen monitoring provides relevant information about oxygen levels of brain tissue. However, the development of this technique has been associated with the need to answer not only some technical aspects of it as well as the meaning of the changes of the cerebral oxygenation in the neurocritical patient. The consensus document responds to various questions related to the monitoring of cerebral oxygenation by means of a cerebral oxygen tissue pressure sensor. For this purpose, a list of questions was prepared and a reviewed of the medical literature was made. The quality of the evidence and the degree of recommendation was evaluated using the GRADE methodology.

Severe head injuries have a great socioeconomic and public health impact. Despite progress in diagnosis and treatment, no sufficiently reliable predictive models have been established for developing clinical trials and promoting effective therapeutic strategies capable of improving the prognosis. In the last decades, several brain damage biomarkers have been studied as potential diagnostic and prognostic tools in traumatic brain injury. However, all of them have limitations that preclude their universalized application. The properties of the known biomarkers –both those traditionally shown to correlate with severity and prognosis, and those recently announced as promising options– should be analyzed. New studies are needed to define their properties, both isolatedly and in combined use.

Severe head injuries have a great socioeconomic and public health impact. Despite progress in diagnosis and treatment, no sufficiently reliable predictive models have been established for developing clinical trials and promoting effective therapeutic strategies capable of improving the prognosis. In the last decades, several brain damage biomarkers have been studied as potential diagnostic and prognostic tools in traumatic brain injury. However, all of them have limitations that preclude their universalized application. The properties of the known biomarkers -both those traditionally shown to correlate with severity and prognosis, and those recently announced as promising options- should be analyzed. New studies are needed to define their properties, both isolatedly and in combined use.

To determine temporal profile and prognostic ability of S100B protein and neuron-specific enolase (NSE) for prediction of short/long-term mortality in patients suffering from severe traumatic brain injury (sTBI).Ninety-nine patients with sTBI were included in the study. Blood samples were drawn on admission and on subsequent 24, 48, 72, and 96 h.15.2% of patients died in NeuroCritical Care Unit, and 19.2% died within 6 months of the accident. S100B concentrations were significantly higher in patients who died compared to survivors. NSE levels were different between groups just at 48 h. In the survival group, S100B levels decreased from 1st to 5th sample (p 0.001); NSE just from 1st to 3rd (p 0.001) and then stabilized. Values of S100B and NSE in non-survival patients did not significantly vary over the four days post sTBI. ROC-analysis showed that all S100B samples were useful tools for predicting mortality, the best the 72 h sample (AUC 0.848 for discharge mortality, 0.855 for six-month mortality). NSE ROC-analysis indicated that just the 48-h sample predicted mortality (AUC 0.733 for discharge mortality, 0.720 for six-month mortality).S100B protein showed higher prognostic capacity than NSE to predict short/long-term mortality in sTBI patients.

Background and Purpose— Rho-kinase, an effector of RhoA, is associated with various cardiovascular diseases in circulating blood cells. However, the role of RhoA/Rho-kinase in peripheral blood mononuclear cells from patients with spontaneous aneurysmal subarachnoid hemorrhage (aSAH) has not yet been studied in relation to the severity of this disease. Therefore, we analyzed the expression and activity of RhoA as a possible biomarker in aSAH. Methods— Twenty-four patients with aSAH and 15 healthy subjects were examined. Peripheral blood mononuclear cells were collected, and RhoA activity and expression were determined by RhoA activation assay kit (G-LISA) and enzyme-linked immunosorbent assay tests, respectively. The severity of aSAH was determined from the World Federation of Neurological Surgeon scale, and vasospasm was evaluated using clinical symptoms, arteriography, and sonography. Results— RhoA expression was significantly increased in peripheral blood mononuclear cells from patients on days 0, 2, and 4 after aSAH versus healthy subjects ( P =0.036, 0.010, and 0.018, respectively, by U Mann–Whitney analysis). There was a significant correlation between RhoA expression and injury severity on days 2 and 4 (Spearman test, day 2: r =0.682, n=14, P =0.007; day 4: r =0.721, n=14, P =0.004). No significant correlation was observed on day 0 (day 0: r =0.131, n=6, P =0.805). Active RhoA was not significantly different in patients and healthy subjects on days 0, 2, and 4 ( P =0.243, 0.222, and 0.600, respectively) nor did it increase significantly on days 0 and 2 in patients with vasospasm versus patients without vasospasm ( P =0.064 and 0.519, respectively). In contrast, active RhoA was significantly higher on day 4 in patients who developed vasospasm versus patients without vasospasm ( P =0.028). Conclusions— Our preliminary results indicate that RhoA expression and activity in peripheral blood mononuclear cells might be related with aSAH severity and cerebral vasospasm. RhoA is a potential biomarker of the risks associated with aSAH.

{#article-title-2} We enjoyed reading the Burns et al.1 article about the evaluation of polyneuropathies but missed the discussion of critical illness polyneuropathy. It is the primary axonal degeneration of motor and sensory fibers that can lead to degeneration of muscle fibers. This occurs in critically ill patients, including those with systemic inflammatory response syndrome, sepsis with multiple organ dysfunction syndrome, hyperglycemia, or … Correspondence to: tmb8r{at}virginia.edu

To assess the utility of C-reactive protein (CRP) and procalcitonin (PCT) as biomarkers of infection in patients with severe burn injury.The present study included severe burn injury patients consecutively admitted to the Virgen del Rocío University Hospital (Andalucia, Spain) intensive care unit during a 12-month period. The variables of interest were: age, sex, mechanism of injury, percentage of burned body surface area, the Abbreviated Burn Severity Index (ABSI) and the absence/presence of sepsis. The authors analyzed serum levels of CRP and PCT at admission and every 48 h thereafter until intensive care unit discharge or death. Each determination was considered to be a sample or unit of analysis.A total of 157 determinations were analyzed from 17 severe burn injury patients. Fifty-four samples were considered to be septic, 25 of which corresponded to the first day of a new onset of sepsis. The mean duration of these symptoms was four days (interquartile range two to five days). Significant differences were found in the distributions of CRP and PCT values between sepsis and no-sepsis samples. Analysis of the changes in these biomarkers over time showed that PCT increase (ΔPCT) differentiated these diagnoses, whereas CRP increase (ΔCRP) did not. ROC curve analysis revealed that ΔPCT could predict positive sepsis samples (area under the curve 0.75 [95% CI 0.58 to 0.90]; P=0.003).These preliminary results showed that PCT had a better discriminatory capacity than CRP for identifying infectious processes in patients with severe burn injury. A larger sample size would be needed to confirm these results.Évaluer l’utilité de la protéine C réactive (PCR) et de la procalcitonine (PCT) comme biomarqueurs de l’infection chez des grands brûlés.La présente étude portait sur des grands brûlés admis consécutivement à l’unité de soins intensifs de l’hôpital universitaireAu total, les auteurs ont analysé 157 déterminants chez 17 grands brûlés. Cinquante-quatre échantillons étaient considérés comme septiques, dont 25 correspondaient au premier jour d’apparition du sepsis. Les symptômes duraient en moyenne quatre jours (plage interquartile de deux à cinq jours). Les auteurs ont constaté des différences importantes dans la répartition des valeurs de PCR et de PCT entre les échantillons de sepsis et sans sepsis. L’analyse des changements de ces biomarqueurs au fil du temps a révélé que l’augmentation de la PCT (ΔPCT) distinguait ces diagnostics, contrairement à l’augmentation de la PCR (ΔPCR). L’analyse de la courbe ROC a révélé que la ΔPCT pouvait prédire des échantillons de sepsis positifs (aire sous la courbe de 0,75 [95% IC 0,58 à 0,90]; P=0,003).Les résultats préliminaires démontrent que la PCT avait une meilleure capacité discriminatoire que la PCR pour dépister les processus infectieux chez des grands brûlés. Il faudrait un plus gros échantillon pour confirmer ces résultats.

Objective To analyze mortality and functional outcome in patients with severe spontaneous intracerebral hemorrhage (ICH), and identify the clinical characteristics, radiological findings and therapeutic procedures predictive of mortality in the Intensive Care Unit (ICU) and during hospitalization, as well as of poor functional results at 6 months. Design A prospective, observational study was carried out. Setting Neurocritical Care Unit of a university hospital. Patients Patients diagnosed with ICH were included over a period of 23 months. Variables of interest Demographic characteristics, cardiovascular risk factors, regular medication, laboratory test parameters, cranial CT findings, therapeutic procedures and outcome data. Intervention None. Results A total of 186 patients with ICH met the inclusion criteria. Surgery to evacuate ICH was performed in 25.8% of the patients. The mortality rate was 46.7%. The modified Rankin score at 6 months was 5 (RI: 4.6). Multivariate Cox regression analysis showed the presence of diabetes, prior anticoagulation, as well as APACHE II severity and the type of bleeding on the cranial CT scan to be predictors of mortality and poor functional outcomes. On the other hand, neurosurgical procedures and intracranial pressure (ICP) monitoring were associated with better outcomes. Conclusion The presence of comorbidities such as diabetes, or previous anticoagulation, as well as the CT findings were associated to poorer outcomes. In contrast, ICP monitoring and early neurosurgery were predictive of longer survival and better functional outcomes.

Resumen Objetivo Evaluar la mortalidad y el resultado funcional final de los pacientes con hemorragia intraparenquimatosa espontanea grave (HIP). Determinar las caracteristicas clinicas, radiologicas y terapeuticas con mayor poder predictivo sobre la mortalidad en la Unidad de Cuidados Intensivos (UCI) y durante el ingreso hospitalario, asi como sobre los malos resultados funcionales a los 6 meses. Diseno Estudio prospectivo, observacional. Ambito UCI de un hospital universitario. Pacientes Durante 23 meses se incluyo a aquellos pacientes con diagnostico de HIP. Variables de interes Datos demograficos, factores de riesgo cardiovascular, medicacion habitual, datos de laboratorio, tomografia craneal (TC), neuromonitorizacion, manejo terapeutico y evaluacion pronostica. Intervencion Ninguna. Resultados Se incluyo a un total de 186 pacientes. En el 25,8% se realizo evacuacion quirurgica de la HIP. La mortalidad fue del 46,7%. La mediana del Rankin modificado a los 6 meses fue de 5 (RI: 4;6). El analisis multivariante de regresion de Cox mostro que la presencia de diabetes, tratamiento previo con anticoagulantes, la gravedad segun APACHE II y el tipo de hemorragia en la TC de craneo se comportaron como variables predictoras de mortalidad y malos resultados funcionales, mientras que la realizacion de procedimientos neuroquirurgicos y la monitorizacion de la presion intracraneal (PIC) asociaron una mayor supervivencia y mejores resultados. Conclusion La presencia de comorbilidades, como la diabetes o el tratamiento previo con anticoagulantes, asi como los hallazgos de la TC se asociaron a peores resultados. Por contra, el marcador de mayor supervivencia y mejor resultado funcional era la monitorizacion de la PIC, asi como la cirugia precoz.

The aim of this study was to validate the S100B protein as a diagnostic tool for ruling out the presence of intracranial lesion (IL) after mild traumatic brain injury (mTBI). Subjects with a Glasgow Coma Scale (GCS) score of 15 and at least one neurological symptom post-trauma were selected from a large Spanish cohort.A number of 260 patients with mTBI were enrolled. Blood samples were extracted within 6 h and CT scan performed within 24 h post-injury. Blood samples were also drawn from 18 healthy subjects.CT scan revealed the presence of IL in 22 patients (8.5%). Patients with mTBI had higher S100B serum levels (p = 0.008) than the healthy subjects (p 0.001). The ROC analysis of S100B discriminated between patients with and without IL (AUC: 0.671; 95%CI: 0.574-0.769; p = 0.008). The multivariate analysis identified male gender (OR: 5.39; 95%CI: 1.45-20.10; p = 0.012), age 65 (OR: 2.97; 95%CI: 1.04-8.44; p = 0.041) and S100B level0.10 µg/L (OR: 7.93; 95%CI: 1.03-60.76; p = 0.046) as independent risk factors for IL in patients with mTBI.Measurement of S100B within 6 h of mTBI accurately predicts risk of IL in patients with a GCS score of 15 and at least one neurological symptom.

In neurocritically ill patients (NCPs), the use of hemoglobin level as the sole indicator for red blood cell transfusion (RBCT) can result in under- or over-transfusion. This randomized controlled trial was conducted to ascertain whether a transcranial oxygen saturation (rSO2) threshold, as measured by near-infrared spectroscopy, reduces RBCT requirements in anemic NCPs (closed traumatic brain injury, subarachnoid, or intracerebral hemorrhage), compared with a hemoglobin threshold alone. Patients with hemoglobin 70–100 g/L received RBCTs to attain an rSO2 > 60% (rSO2 arm) or to maintain hemoglobin between 85 and 100 g/L (hemoglobin arm). A total of 102 NCPs (51 in each group) were included in the intention-to-treat analysis, and 97 were included in the per-protocol analysis (51 and 46, respectively). Compared with those from the hemoglobin arm, patients in rSO2 arm received fewer RBC units (1.0 ± 0.1 vs. 1.5 ± 1.4 units/patient; p

BACKGROUND The aim of this work was to validate the IMPACT (International Mission for Prognosis and Analysis of Clinical Trials in TBI) model in a Spanish cohort of patients with moderate-severe TBI (traumatic brain injury). SETTING Two level I neurotrauma centers. PARTICIPANTS Patients admitted to these hospitals between 2011 and 2014 with a diagnosis of TBI and a Glasgow Coma Scale score of 12 or less. DESIGN Prospective observational study. MAIN MEASURES We collected prospectively the clinical variables included in the IMPACT models. Outcome evaluation was prospectively done at 6-month follow-up according to the Glasgow Outcome Scale. RESULTS A total of 290 patients were included in the study. Forty-seven patients (16.2%) died within 6 months post-TBI, and 74 patients (25.5%) had an unfavorable outcome. The Hosmer-Lemeshow test revealed that there was no difference between observed and predicted outcomes; hence, the 3 models displayed adequate calibration for predicting 6-month mortality or unfavorable outcome. The receiver operating characteristic curve indicated that the 3 models (Core, Extended, and Lab) could accurately discriminate between favorable and unfavorable outcomes, as well as between survival and mortality (P < .001). CONCLUSION The IMPACT model validates prediction of 6-month outcomes in a Spanish population of moderate-severe TBI. IMPACT Lab model is the one that presents a higher discriminative capacity. These results encourage the implementation of the IMPACT model as a prognostic tool in the management of patients with TBI.

Resumen Objetivo Evaluar si un modelo experimental de lesiones tipo masa (LM) transitoria en rata produce la liberacion precoz a sangre periferica de enolasa neuroespecifica (NSE) y proteina S100B como expresion del dano cerebral inducido. Diseno Estudio experimental con grupo control. Ambito Quirofano experimental del Instituto de Biomedicina (IBiS) del Hospital Universitario Virgen del Rocio. Participantes Catorce ratas adultas Wistar. Intervenciones Se extrajo muestra sanguinea basal y posteriormente se realizo: grupo LM, a traves de un trepano, se inflo el globo de una sonda con 500 μL/20 s; posteriormente, se realizaron 4 extracciones sanguineas cada 20 min. Grupo control, se repitieron de forma sistematica todos los pasos salvo que no se realizo trepano. Variables de interes principal Peso, mortalidad precoz, concentracion en suero de NSE y S100B. Resultados Encontramos diferencias entre las concentraciones de NSE y S100B a lo largo del tiempo dentro del propio grupo LM (p Conclusiones Las concentraciones en suero de NSE y S100B reflejan de forma precoz el dano cerebral que acontece sobre la sustancia gris y blanca en un modelo experimental de LM en rata.

The effects of human urotensin II (hUII) on the vascular tone of different animal species has been studied extensively. However, little has been reported on the vasoactive effects of rat urotensin (rUII) in murine models. The aim of the present study was to investigate the effects of rUII on vasoreactivity in rat basilar arteries. Basilar arteries from adult male Wistar rats (300-350 g) were isolated, cut in rings, and mounted on a small vessel myograph to measure isometric tension. rUII concentrations were studied in both resting and depolarized state. To remove endothelial nitric oxide effects from the rUII response, we treated selected arterial rings with Nω-nitro-L-arginine methyl ester (L-NAME). 10 μM rUII produced a potent vasoconstrictor response in rat basilar arteries with intact endothelium, while isometric forces remained unaffected in arterial rings treated with lower rUII concentrations. Although L-NAME did not have a significant effect on 10 μM rUII-evoked contraction, it slightly increased arterial ring contraction elicited by 1 μM rUII. In depolarized arteries, dose-dependent rUII increased depolarization-induced contractions. This effect was suppressed by L-NAME. Our results show that the rat basilar artery has a vasoconstrictor response to rUII. The most potent vasoconstrictor effect was produced by lower doses of rUII (0.1 and 1 μM) in depolarized arteries with intact endothelium. This effect could facilitate arterial vasospasm in vascular pathophysiological processes such as subarachnoid hemorrhage and hypertension, when sustained depolarization and L-type Ca(2+) channel activation are present.

Changes in Urotensin-II (U-II) concentration, a potent vasoconstrictor peptide, have been detected in various pathologies, but it has been impossible to define a normality range. We aimed to analyze the concordance and interchangeability between two enzyme immunoassay methods developed by Phoenix Pharmaceuticals, Inc. to measure U-II plasma concentration in rats: ELISA and fluorescent EIA. Assays resulted positively correlated (r = 0.850; p < 0.01). There was a significant difference between assays values (p < 0.001). The analysis of agreement (Bland and Altman plot) stated that the mean of the differences was 2.055 (SD ± 0.588). Hence, we concluded that the two U-II assays were correlated but not interchangeable.

Objetivo: Establecer el valor predictivo, para desarrollar deterioro neurológico tardío de origen isquémico (DNI), de un estudio doppler transcraneal (DTC) en pacientes con hemorragia subaracnoidea espontánea (HSA) en buena situación neurológica. Diseño: Estudio descriptivo-observacional desarrollado durante 3 años. Ámbito: Cuidados Críticos y Urgencias. Pacientes: Se incluyeron de forma consecutiva aquellos pacientes con HSA en buena situación neurológica (Hunt-Hess I-III). Variables de Interés: DNI (disminución en 2 puntos del GCS o déficit focal), velocidad media (VM) en arterias cerebrales medias, índice de Lindegaard (IL). Se consideró patrón sonográfico de vasoespasmo (PSV) cuando la VM fue>120cm/s y existía un IL>3. Resultados: La media de edad de los 122 pacientes fue de 54,1±13,7 años. El 57,3% eran mujeres. Se detectaron 24 pacientes con PSV (19,7%) encontrándose VM elevadas en 38 pacientes (31,1%). 21 pacientes desarrollaron DNI (VM 183+/-49cm/s), todos presentaron PSV. En los pacientes con DNI se detectó un aumento de VM de 22+/-5cm/s/24h durante los 3 primeros días. Al comparar aquellos pacientes que no presentaron VM elevadas (85 pacientes/VM 67+/-16,6cm/s) con respecto a los que desarrollaron DNI encontramos diferencias en las VM (p

S100B is a calcium-binding protein released into the blood from astroglial cells due to brain injury. Some authors have described a correlation between S100B serum concentration and severity of brain damage. There is not much information about the accuracy of urinary S100B for predicting outcome after severe traumatic brain injury (TBI). 55 patients with severe TBI were included in the study. Blood and urine samples were drawn to determine S100B levels on admission and on the subsequent 24, 48, 72 and 96 h. S100B concentrations (serum and urine) were significantly higher in patients who were dead a month after the accident compared to survivors. ROC-analysis showed that S100B at 24h post-severe TBI is a useful tool for predicting mortality (serum: AUC 0.958, urine: AUC 0.778). The best cut-offs for S100B were 0.461 μg/L and 0.025 μg/L (serum and urine respectively), with a sensitivity of 90% for both measurements and a specificity of 88.4% (serum) and 62.8% (urine). We can state that the determination of S100B levels both in urine and serum acts as a sensitive and an effective biomarker for the early prediction of mortality after severe TBI.

Cerebral microdialysis, introduced in experimental studies 40 years ago, has been used clinically since 1992 for the neurochemical monitoring of patients in intensive care. The principles underlying this technique are closely related to brain metabolism. The study of the metabolites detected at brain interstitial tissue level, through the semipermeable membrane of the device, allows us to assess different physiological pathways in the brain, analyzing the changes that occur when they become less efficient in terms of energy, and also detecting waste products secondary to tissue damage. Despite its current limitations, this technique provides relevant information for research and the clinical management of critical neurological patients.

La microdiálisis cerebral, introducida en estudios experimentales hace unos 40 años, ha sido empleada en la clínica desde 1992 para la monitorización neuroquímica de pacientes en unidades de cuidados intensivos. Los principios en los que se basa esta técnica se encuentran íntimamente ligados al metabolismo cerebral. El estudio de los metabolitos detectados en el intersticio tisular cerebral, a través de la membrana semipermeable de la que dispone el dispositivo, permite estimar la situación de las distintas rutas metabólicas fisiológicas cerebrales, analizando las modificaciones que se producen cuando estas tornan hacia rutas menos eficientes desde el punto de vista energético y detectando productos de desecho secundarios a la lesión tisular. A pesar de sus limitaciones actuales, esta técnica aporta información relevante para la investigación y el abordaje clínico de los pacientes neurocríticos. Cerebral microdialysis, introduced in experimental studies 40 years ago, has been used clinically since 1992 for the neurochemical monitoring of patients in intensive care. The principles underlying this technique are closely related to brain metabolism. The study of the metabolites detected at brain interstitial tissue level, through the semipermeable membrane of the device, allows us to assess different physiological pathways in the brain, analyzing the changes that occur when they become less efficient in terms of energy, and also detecting waste products secondary to tissue damage. Despite its current limitations, this technique provides relevant information for research and the clinical management of critical neurological patients.

This study tested the hypothesis that S100β is a useful screening tool for detecting intracranial lesion (IL) in patients with a normal level of consciousness after traumatic brain injury (TBI).One hundred and forty-three post-TBI patients without a decrease in consciousness (GCS = 15) and with at least one neurological symptom (e.g. transitory loss of consciousness, amnesia, headache, dizziness or vomiting) were prospectively included. A blood sample was drawn at 6-hours post-TBI. A routine CT scan was obtained within 24 hours post-injury. Diagnostic properties of S100β for IL prediction in CT scan findings were tested using ROC-analysis.A total of 15 patients (10.5%) had IL. Serum levels were significantly higher in these patients. Significant differences were found between S100β levels and CT scan findings (p = 0.007). ROC-analysis showed that S100β is a useful tool for detecting the presence of IL in CT scans (p = 0.007). In this series, the best cut-off for S100β is 0.130 µg L(-1), with 100% sensitivity and 32.81% specificity.Within the first 6 hours post-TBI, serum S100β seems to be an effective biochemical indicator of IL in patients without a decrease in consciousness. These results indicate that higher S100β cut-off values substantially improve the clinical relevance of this protein.

The present study outlines a series of questions and reflections upon the recent publication of Chesnut et al., who compared 2 approaches to the treatment of intracranial hypertension (ICH) in severe head injuries: one with and the other without intracranial pressure monitoring (ICP). The authors concluded that no improved outcome was observed in the treatment group guided by ICP monitoring. The main concerns relate to the degree of training of the physicians involved in the monitoring and management of ICH in the ICP group, as well as to the possible inter-observer variability in interpreting the CT scans, the capacity of clinical signs to guide the treatment of ICH, and the suitability of randomization. The analysis of this trial should not be taken to suggest the futility of ICP monitoring but rather the need to correctly use the information afforded by ICP monitoring, with emphasis on the importance of the definition of alternative methods for non-invasive monitoring.

To study the predictive capacity of early S100beta samples for long-term outcome prediction after severe TBI.Eighty-seven patients with severe TBI were studied. Clinical and CT scan were taken at admission. S100beta concentration was quantified at admission and 24, 48 and 72 hours post-TBI (days 0, 1, 2 and 3). Outcome was assessed 12 months after discharge using Glasgow Outcome Score (GOS).Significant negative correlations were found between 1-year GOS and S100beta concentrations on days 1-3, but not on day 0. Deceased patients showed higher S100beta concentration than survivors on days 1-3. Good (GOS = 4-5) vs poor outcome (GOS = 1-3) differed significantly on day 3. Death outcome was independently predicted by day 2 (2.37 microg l(-1)), day 3 (1.41 microg l(-1)) samples and absence of pupillary reaction. Poor outcome was predicted independently only by pupillary reaction and the 72-hour sample (1.1 microg l(-1)), but this predictive model was less satisfactory than the predictive model for death.A temporal profile of S100beta release from admission to 72 hours post-TBI is strongly recommended for use in identifying patients at risk of developing a worse outcome. The S100beta protein might be an early biomarker for predicting long-term outcome in patients with acute severe TBI.