Efecto de la infusión de lactato de sodio 0.5 molar sobre el medio interno de pacientes críticos / Effect of half-molar sodium lactate infusion on biochemical parameters in critically ill patients

Objetivo Evaluar el impacto de la infusión de lactato de sodio 0,5M sobre variables del medio interno y sobre la presión intracraneana en pacientes críticos. Diseño Estudio prospectivo experimental de cohorte única. Ámbito Unidad de cuidados intensivos de un hospital universitario. Pacientes Pacientes con shock y neurocríticos con hipertensión intracraneana. Intervenciones Se infundió una carga de 500 cc de infusión de lactato de sodio 0,5M en 15 min y se midió el nivel plasmático de sodio, potasio, magnesio, calcio, cloro, lactato, bicarbonato, PaCO2 arterial, pH, fosfato y albúmina en 3 tiempos: T0 preinfusión; T1 a los 30 min y T2 a los 60 min postinfusión. Se midieron la presión arterial media y presión intracraneana en T0 y T2. Resultados Recibieron el fluido N=41: n=19 como osmoagente y 22 como expansor. Se constató alcalosis metabólica: T0 vs. T1 (p=0,007); T1 vs. T2 (p=0,003). La natremia aumentó en los 3 tiempos (T0 vs. T1; p<0,0001; T1 vs. T2; p=0,0001). Se demostró un descenso de la presión intracraneana (T0: 24,83±5,4 vs. T2: 15,06±5,8; p <0,001). El lactato aumentó inicialmente (T1) con un rápido descenso (T2) (p <0,0001), incluso en aquellos pacientes con hiperlactatemia basal (p=0,002). Conclusiones La infusión de lactato de sodio 0,5M genera alcalosis metabólica, hipernatremia, disminución de la cloremia y un cambio bifásico del lactato, y muestra eficacia en el descenso de la presión intracraneana en pacientes con daño encefálico agudo. (AU)

Objective To evaluate the impact of the infusion of sodium lactate 500ml upon different biochemical variables and intracranial pressure in patients admitted to the intensive care unit. Design A prospective experimental single cohort study was carried out. Scope Polyvalent intensive care unit of a university hospital. Patients Critical patients with shock and intracranial hypertension. Procedure A 500ml sodium lactate bolus was infused in 15min. Plasma levels of sodium, potassium, magnesium, calcium, chloride, lactate, bicarbonate, PaCO2, pH, phosphate and albumin were recorded at 3timepoints: T0 pre-infusion; T1 at 30minutes, and T2 at 60minutes post-infusion. Mean arterial pressure and intracranial pressure were measured at T0 and T2. Results Forty-one patients received sodium lactate: 19 as an osmotically active agent and 22 as a volume expander. Metabolic alkalosis was observed: T0 vs. T1 (P=0.007); T1 vs. T2 (P=0.003). Sodium increased at the 3time points (T0 vs. T1, P<0.0001; T1 vs. T2, P=0.0001). In addition, sodium lactate decreased intracranial pressure (T0: 24.83±5.4 vs. T2: 15.06±5.8; P<0.001). Likewise, plasma lactate showed a biphasic effect, with a rapid decrease at T2 (P<0.0001), including in those with previous hyperlactatemia (P=0.002). Conclusions The infusion of sodium lactate is associated to metabolic alkalosis, hypernatremia, reduced chloremia, and a biphasic change in plasma lactate levels. Moreover, a decrease in intracranial pressure was observed in patients with acute brain injury. (AU)

Effect of half-molar sodium lactate infusion on biochemical parameters in critically ill patients.

OBJECTIVE: To evaluate the impact of the infusion of sodium lactate 500ml upon different biochemical variables and intracranial pressure in patients admitted to the intensive care unit. DESIGN: A prospective experimental single cohort study was carried out. SCOPE: Polyvalent intensive care unit of a university hospital. PATIENTS: Critical patients with shock and intracranial hypertension. PROCEDURE: A 500ml sodium lactate bolus was infused in 15min. Plasma levels of sodium, potassium, magnesium, calcium, chloride, lactate, bicarbonate, PaCO2, pH, phosphate and albumin were recorded at 3 timepoints: T0 pre-infusion; T1 at 30min, and T2 at 60min post-infusion. Mean arterial pressure and intracranial pressure were measured at T0 and T2. RESULTS: Forty-one patients received sodium lactate: 19 as an osmotically active agent and 22 as a volume expander. Metabolic alkalosis was observed: T0 vs. T1 (p=0.007); T1 vs. T2 (p=0.003). Sodium increased at the 3 timepoints (T0 vs. T1, p<0.0001; T1 vs. T2, p=0.0001). In addition, sodium lactate decreased intracranial pressure (T0: 24.83±5.4 vs. T2: 15.06±5.8; p<0.001). Likewise, plasma lactate showed a biphasic effect, with a rapid decrease at T2 (p<0.0001), including in those with previous hyperlactatemia (p=0.002). CONCLUSIONS: The infusion of sodium lactate is associated to metabolic alkalosis, hypernatremia, reduced chloremia, and a biphasic change in plasma lactate levels. Moreover, a decrease in intracranial pressure was observed in patients with acute brain injury.

Hipoxemia real y espuria en un paciente con hiperleucocitosis extrema / Real and spurious hypoxemia in a patient with extreme hyperleukocytosis

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Cerebral Critical Closing Pressure: Is the Multiparameter Model Better Suited to Estimate Physiology of Cerebral Hemodynamics?

BACKGROUND: Cerebral critical closing pressure (CrCP) is the level of arterial blood pressure (ABP) at which small brain vessels close and blood flow stops. This value is always greater than intracranial pressure (ICP). The difference between CrCP and ICP is explained by the tone of the small cerebral vessels (wall tension). CrCP value is used in several dynamic cerebral autoregulation models. However, the different methods for calculation of CrCP show frequent negative values. These findings are viewed as a methodological limitation. We intended to evaluate CrCP in patients with severe traumatic brain injury (TBI) with a new multiparameter impedance-based model and compare it with results found earlier using a transcranial Doppler (TCD)-ABP pulse waveform-based method. METHODS: Twelve severe TBI patients hospitalized during September 2005-May 2007. Ten men, mean age 32 years (16-61). Four had decompressive craniectomies (DC); three presented anisocoria. Patients were monitored with TCD cerebral blood flow velocity (FV), invasive ABP, and ICP. Data were acquired at 50 Hz with an in-house developed data acquisition system. We compared the earlier studied "first harmonic" method (M1) results with results from a new recently developed (M2) "multiparameter method." RESULTS: M1: In seven patients CrCP values were negative, reaching -150 mmHg. M2: All positive values; only one lower than ICP (ICP 60 mmHg/ CrCP 57 mmHg). There was a significant difference between M1 and M2 values (M1 < M2) and between ICP and M2 (M2 > ICP). CONCLUSION: M2 results in positive values of CrCP, higher than ICP, and are physiologically interpretable.

Lactato de sodio 0, 5 molar: ¿el agente osmótico que buscamos? / Half-molar sodium-lactate: The osmotic agent we are looking for?

La hipertensión intracraneana (HIC) es el factor modificable con mayor impacto pronóstico predictivo negativo en el paciente neurocrítico. La terapia osmótica constituye la medida específica de primer nivel más importante para controlar la HIC. El manitol al 20% y el cloruro de sodio hipertónico al 3, 7,5, 10 y 23% son los agentes osmóticos más comúnmente utilizados en la práctica clínica. En los últimos años ha sido incorporado el lactato de sodio 0,5M como agente osmótico. El lactato como anión acompañante del sodio evita la hipercloremia y sus efectos adversos (acidosis hiperclorémica, inflamación sistémica, insuficiencia renal aguda); asimismo, el lactato puede ser utilizado por la neuroglia como sustrato energético para el cerebro dañado. El lactato de sodio 0,5M tendría además un efecto más potente y prolongado mediante un descenso de la osmolaridad intracelular e inhibición de los mecanismos de control del volumen neuronal. Trabajos pioneros en pacientes con traumatismo craneoencefálico grave han mostrado un efecto más pronunciado que el manitol en el control de la HIC. Asimismo, en este grupo de pacientes parece ser beneficioso en la prevención de HIC. Sin embargo, estos resultados prometedores necesitan ser corroborados en futuras investigaciones

Intracranial hypertension (ICH) is the most important modifiable factor with predictive negative value in brain injury patients. Osmotherapy is the most important first level specific measure in the treatment of ICH. Mannitol 20%, and 3, 7.5, 10, and 23% hypertonic sodium chloride are the most commonly used osmotic agents in the neurocritical care setting. Currently, controversy about the best osmotic agent remains elusive. Therefore, over the past few years, half-molar sodium lactate has been introduced as a new osmotic agent to be administered in the critically ill. Lactate is able to prevent hyperchloremia, as well as its adverse effects such as hyperchloremic acidosis, systemic inflammation, and acute kidney injury. Furthermore, lactate may also be used by glia as energy substrate in brain injury patients. Half-molar sodium lactate would also have a more potent and long-lasting effect decreasing intracellular osmolarity and by inhibiting neuronal volume control mechanisms. Pioneering researches in patients with traumatic brain injury have shown a more significant effect than mannitol on the control of ICH. In addition, in this group of patients this solution appears to be beneficial in preventing episodes of ICH. However, future research is necessary to corroborate or not these promising results

[Half-molar sodium-lactate: The osmotic agent we are looking for?]. / Lactato de sodio 0,5 molar: ¿el agente osmótico que buscamos?

Intracranial hypertension (ICH) is the most important modifiable factor with predictive negative value in brain injury patients. Osmotherapy is the most important first level specific measure in the treatment of ICH. Mannitol 20%, and 3, 7.5, 10, and 23% hypertonic sodium chloride are the most commonly used osmotic agents in the neurocritical care setting. Currently, controversy about the best osmotic agent remains elusive. Therefore, over the past few years, half-molar sodium lactate has been introduced as a new osmotic agent to be administered in the critically ill. Lactate is able to prevent hyperchloremia, as well as its adverse effects such as hyperchloremic acidosis, systemic inflammation, and acute kidney injury. Furthermore, lactate may also be used by glia as energy substrate in brain injury patients. Half-molar sodium lactate would also have a more potent and long-lasting effect decreasing intracellular osmolarity and by inhibiting neuronal volume control mechanisms. Pioneering researches in patients with traumatic brain injury have shown a more significant effect than mannitol on the control of ICH. In addition, in this group of patients this solution appears to be beneficial in preventing episodes of ICH. However, future research is necessary to corroborate or not these promising results.

Hiponatremias en el paciente neurocrítico: enfoque terapéutico basado en la evidencia actual / Hyponatremia in the neurocritical care patient: An approach based on current evidence

En el paciente neurocrítico la hiponatremia es la distonía más frecuente, comportándose como un predictor pronóstico. Clásicamente, el cerebro perdedor de sal y la secreción inadecuada de hormona antidiurética han sido las 2 entidades responsables de explicar la mayor parte de los casos de hiponatremia en estos pacientes. Sin embargo, en virtud de la dificultad en establecer el estado de la volemia en el paciente crítico, el diagnóstico diferencial es con frecuencia difícil de establecer. Por otra parte, en el paciente neurocrítico el diagnóstico diferencial entre ambos síndromes no ha demostrado ser de utilidad debido a que el cloruro de sodio hipertónico es la piedra angular en el tratamiento de ambos cuadros, y la restricción hídrica con frecuencia está contraindicada. Es por ello que ha surgido el concepto de «cerebro falto de sal», lo cual traduce la necesidad del aporte de sodio como estrategia terapéutica en todos los casos

In the neurocritical care setting, hyponatremia is the commonest electrolyte disorder, which is associated with significant morbimortality. Cerebral salt wasting and syndrome of inappropriate antidiuretic hormone have been classically described as the 2 most frequent entities responsible of hyponatremia in neurocritical care patients. Nevertheless, to distinguish between both syndromes is usually difficult and useless as volume status is difficult to be determined, underlying pathophysiological mechanisms are still not fully understood, fluid restriction is usually contraindicated in these patients, and the first option in the therapeutic strategy is always the same: 3% hypertonic saline solution. Therefore, we definitively agree with the current concept of “cerebral salt wasting”, which means that whatever is the etiology of hyponatremia, initially in neurocritical care patients the treatment will be the same: hypertonic saline solution

Hyponatremia in the neurocritical care patient: An approach based on current evidence.

In the neurocritical care setting, hyponatremia is the commonest electrolyte disorder, which is associated with significant morbimortality. Cerebral salt wasting and syndrome of inappropriate antidiuretic hormone have been classically described as the 2 most frequent entities responsible of hyponatremia in neurocritical care patients. Nevertheless, to distinguish between both syndromes is usually difficult and useless as volume status is difficult to be determined, underlying pathophysiological mechanisms are still not fully understood, fluid restriction is usually contraindicated in these patients, and the first option in the therapeutic strategy is always the same: 3% hypertonic saline solution. Therefore, we definitively agree with the current concept of "cerebral salt wasting", which means that whatever is the etiology of hyponatremia, initially in neurocritical care patients the treatment will be the same: hypertonic saline solution.

Bedside study of cerebral critical closing pressure in patients with severe traumatic brain injury: a transcranial Doppler study.

OBJECTIVE: Cerebral critical closing pressure (CrCP) is the arterial pressure (AP) below which small arterial cerebral vessels collapse. Our objective was to estimate cerebral CrCP in 12 severe TBI patients, relating transcranial Doppler flow velocity (FV) and AP data. METHODS: FV, intracranial pressure (ICP) and invasive AP were prospectively acquired at 50 Hz. CrCP was estimated using three methods (M): M(1): amplitude ratio of FV/AP first harmonics; M(2): AP axis intersection of the regression line between systolic and diastolic values of FV and AP; M(3): AP axis intersection of the regression line between decreasing AP and FV simultaneous values. RESULTS: There were 12 patients. Frequent negative CrCP values were found. Average M(1):-12 mmHg; M(2):-33 mmHg; M(3):-43 mmHg. Correlation between the three methods was significant (P < 0.01). M(1) showed the lowest range and more positive values. The better limits of agreement (Bland and Altman test) were between M(2) and M(3). CONCLUSIONS: The frequently found negative values do not allow us for the moment, to use any of these three methods for clinical guidance.

Development of a multimodal monitoring platform for medical research.

A low cost multimodal monitoring and signal processing platform is presented. A modular and flexible system was developed, aimed to continuous acquisition of several biological variables at patient bed-head and further processing with application specific algorithms. System hardware is made of a six-channel isolation and signal conditioning front-end along with a high resolution analog-to-digital converter board connected to a standard laptop. Whole system hardware is compact and light weight, which ensures portability and ease of use at intensive care units. System software is divided in three modules: Acquisition, Signal Processing and Patients Data Management. The first one allows configuring each acquisition channel parameters, depending on the biological variable connected to it, and to store up to several hours of continuous data. Signal processing module implements novel algorithms for research purposes like dynamic cerebral autoregulation, optimal perfusion pressure, critical closing pressure or pulsatility index. It is flexible enough to easily add new processing algorithms, export data to different formats and create graphical reports. Patients data management module organizes acquired records, which allows selecting cases for new studies based on different criteria like monitored variables or pathological information. In this work, whole system architecture is described and algorithms included into the cerebral hemodynamics toolbox are presented along with experimental results.

Cerebral CO2 reactivity in severe head injury. A transcranial Doppler study.

BACKGROUND: Cerebral circulation is profoundly affected by changes in PaCO2. CO2 manipulation plays a basic role in the management of intracranial hypertension; CO2 reactivity (CO2R) defines the changes in CBF in response to changes in PaCO2. Transcranial Doppler has allowed exploring its effects "on line". MATERIALS AND METHODS: We conducted a prospective clinical trial, with the objective of studying CO2R in severe head injury patients. Sixteen severe traumatic brain injury patients, mechanically ventilated, were included. Monitoring of MAP, ICP, CPP, SjO2, ETCO2, and cerebral blood flow velocity (CBFV) was performed. Taking into account basal cerebral hemodynamic pattern, minute ventilation was modified to attain a negative ("A") or positive ("B") deltaPCO2. CO2R was calculated as: CO2R = % deltaCBFV/deltaETCO2 in mmHg (normal value 3.7 +/- 1%/mmHg). CO2R was compared with deltaICP/ deltaPCO2 in each patient. FINDINGS: Three patients were excluded because the change in ETCO2 was too low (deltaETCO2 < 3 mmHg). The median value of CO2R in the total group of 13 patients was 3.38. In "A" the values tended to be lower than in "B". There were four low CO2R values in "A" and none in "B". There was no significant correlation between CO2R and deltaICP/deltaPCO2. CONCLUSIONS: The different "A" and "B" behavior might be due to dissimilar mechanisms involved in the basis of vasodilatation and vasoconstriction. Changes in ventilation must be performed with caution, avoiding sudden increases in CO2 that may increase ICP. The absence of correlation between CO2R and deltaICP/deltaPCO2 is explained, at least partially, by different cranio-cerebral compliance in each patient. Therefore, induced blood volume changes are not directly transmitted to ICP, but their effects depend on the shape of the pressure-volume curve and the position on the curve in which each situation is working.

Indomethacin and cerebral autoregulation in severe head injured patients: a transcranial Doppler study.

OBJECTIVE: To assess the effect of indomethacin on cerebral autoregulation, systemic and cerebral haemodynamics, in severe head trauma patients. DESIGN: Prospective, controlled clinical trial, with repeated measurements. SETTINGS: A 12-bed adult general intensive care unit in a third level referral university hospital. PATIENTS: 16 severely head injured patients, 14 males, age range 17-60. INTERVENTIONS: Indomethacin was administrated as a load plus continuous infusion. Indomethacin reactivity was assessed as the estimated cerebral blood flow change elicited by the load. Dynamic and static cerebral autoregulation tests were performed before indomethacin administration, and during its infusion. MEASUREMENTS AND MAIN RESULTS: Systemic and cerebral haemodynamic changes were assessed through continuous monitoring of mean arterial pressure, transcranial Doppler cerebral blood flow velocity, intracranial pressure, cerebral perfusion pressure, and jugular venous oxygen saturation. Indomethacin loading dose was immediately followed by a cerebral blood flow median decrease of 36 or 29% (p = ns) evaluated by two different methods, by an ICP decrease and by an AVDO(2) increase from 3.52 to 6.15 mL/dL (p = 0.002). Dynamic autoregulation increased from a median of 28 to 57% (p<0.05) during indomethacin infusion; static autoregulation also increased, from a median of 72 to 89% (p = ns). CONCLUSIONS: Indomethacin decreased intracranial pressure and cerebral blood flow, and increased cerebral perfusion pressure, while maintaining tissue properties of further extracting O(2). The increase in both autoregulatory values reveals an enhancement of cerebral microvasculature reactivity under indomethacin, during hypertensive and--especially--during hypotensive situations.

[Effects of dexmedetomidine on intracranial hemodynamics in severe head injured patients]. / Efectos de la dexmedetomidina sobre la hemodinámica intracraneal en pacientes con lesión encefálica traumatica grave.

Dexmedetomidine, an alpha 2 adrenergic agonist, with distinctive characteristics when compared to traditional plans, namely: conscious sedation, sympatholysis and lack of respiratory depression, represents an attempt to improve the sedoanalgesia of critically ill patients. OBJECTIVE. To study dexmedetomidine's effect on intracranial hemodynamic and hemometabolic parameters in severe head injured patients. MATERIAL AND METHODS. Prospective study on the effect of Dexmedetomidine on twelve severe head injured patients (Glasgow Coma Scale score

Efectos de la dexmedetomidina sobre la hemodinámica intracraneal en pacientes con lesión encefálica traumatica grave / Effects of dexmedetomidine on intracranial hemodynamics in severe head injured patients

La dexmedetomidina, un agonista adrenérgico selectivoalfa2, constituye un intento de mejorar la sedoanalgesia de los pacientes críticos, por sus efectos distintivos en comparación a los planes tradicionales como son: sedación consciente, simpaticolisis y ausencia de depresión respiratoria. Objetivo. Estudiar el efecto de la dexmedetomidina, un nuevo agonista alfa28, sobre la hemodinámica intracraneal y sobre los parámetros hemometabólicos cerebrales en un grupo de pacientes con trauma craneoencefálico grave. Material y métodos. Estudio prospectivo de los pacientes con lesión encefálica traumática grave (Glasgow Coma Scale <= 8) ingresados en un Centro de Tratamiento Intensivo (CTI) que recibieron monitorización de la presión intracraneal (PIC) y monitorización de saturación de O2 del bulbo yugular (SjO2). Se realizó una perfusión intravenosa de la droga durante 3 horas, en dosis progresivas (0.2, 0.4 y 0.7 ug/kg/h), previa suspensión de otros sedantes y analgésicos. Resultados. Se estudiaron 12 pacientes sin hipertensión intracraneal. No se encontraron diferencias significativas entre los valores de PIC y presión arterial media (PAM) tras la infusión de la droga en relación con los valores basales. La presión de perfusión cerebral (PPC) mostró una tendencia a disminuir durante el estudio (efecto marginal, p=0.058). Se encontró un descenso significativo de la frecuencia cardíaca (FC) (p<0.0001) en relación a los valores basales. No se hallaron diferencias significativas en los parámetros hemometabólicos cerebrales (SjO2 y CEO2).Conclusión. A las dosis utilizadas, la dexmede-tomidina fue segura, no asociándose a alteraciones significativas de la hemodinámica intracraneal ni del metabolismo sanguíneo cerebral en pacientes en la etapa aguda del trauma craneoencefálico grave (TECG)

Dexmedetomidine, an alpha2 adrenergic agonist, with distinctive characteristics when compared to traditional plans, namely: conscious sedation, sympatholysis and lack of respiratory depression, represents an attempt to improve the sedoanalgesia of critically ill patients.Objective. To study dexmedetomidine´s effect on intracranial hemodynamic and hemometabolic parameters in severe head injured patients. Material and methods. Prospective study on the effect of Dexmedetomidine on twelve severe head injured patients (Glasgow Coma Scale score <= 8) admitted to an intensive care unit, with intracranial pressure < 20 mmHg and O2 saturation monitoring of blood from jugular bulb. The drug was perfused intravenously during 3 hours, in progressive doses (0.2, 0.4 y 0.7 ug/kg/h). All other sedo-analgesia medication had been previously withdrawn. Results. No significant differences were found in intracranial pressure, mean arterial pressure and cerebral hemometabolic parameters after infusion of dexmedetomidine in relation to basal values. Cerebral perfusion pressure showed a trend to decrease during the drug infusion (marginal effect, p =.058). Cardiac frequency decreased significantly after the drug administration. Conclusions. At the doses utilized, dexmedetomidine was safe, and it was not associated with significant changes in intracranial hemodynamics, nor in cerebral hemometabolic parameters, in a group of severe head injured patients

Comparison between two static autoregulation evaluation methods.

Cerebral static autoregulation (AR) was evaluated at bedside in 14 severely head injured patients. 16 investigations were performed. Cerebral perfusion pressure (CPP) was increased by infusing vasopressors during one hour, and registered every 2-5 minutes. CBF was simultaneously estimated by: 1) middle cerebral artery mean flow velocity (FV) monitoring with Transcranial Doppler (TDC), and 2) the reciprocal of arteriovenous oxygen content difference, calculated from basal and hypertensive arterial and jugular bulb blood samples. AR assessment: For TCD results, linear regression method was used, studying two pairs of variables: a) %FV-CPP (the regression slope was the main AR value adopted) and b) % cerebrovascular resistance (CVR)-%CPP. For the AVDO2 method, autoregulation was considered preserved if estimated % delta CBF/delta PPE < 1%/mm Hg. TCD method clearly defined three groups. Group 1 and 2 (8 and 5 investigations) were considered as two grades of preserved AR, and the third one (3 cases) as impaired AR. AVDO2 method: 12 studies were evaluated. 10 showed preserved AR, and 2 impaired AR. There was coincidence of results from both methods in 10 out of 12 studies. (0.83).

[First tier measures in the treatment of intracranial hypertension in the patient with severe craniocerebral trauma. Proposal and justification of a protocol]. / Medidas de primer nivel en el tratamiento de la hipertensión intracraneal en el paciente con un traumatismo craneoencefálico grave. Propuesta y justificación de un protocolo.

The management of severe head injuries in general and that of high intracranial pressure (ICP) in particular are among the most challenging tasks in neurocritical care. One of the difficulties still faced by clinicians is that of reducing variability among centers when implementing management protocols. The purpose of this paper is to propose a standardized protocol for the management of high ICP after severe head injury, consistent with recently published clinical practice guidelines and other clinical evidence such as that provided by the systematic reviews of the Cochrane Collaboration. Despite significant advances in neuromonitoring, deeper insight into the physiopathology of severe brain trauma and the many therapeutic options available, standardized protocols are still lacking. Recently published guidelines provide sketchy recommendations without details on how and when to apply different therapies. Consequently, great variability exists in daily clinical practice even though different centers apply the same evidence-based recommendations. In this paper we suggest a structured protocol in which each step is justified and integrated into an overall strategy for the management of severe head injuries. The most recent data from both the preliminary and definitive results of randomized clinical trials as well as from other sources are discussed. The main goal of this article is to provide neurotraumatology intensive care units with a unified protocol that can be easily modified as new evidence becomes available. This will reduce variation among centers when applying the same therapeutic measures. This goal will facilitate comparisons in outcomes among different centers and will also enable the implementation of more consistent clinical practice in centers involved in multicenter clinical trials.

Medidas de primer nivel en el tratamiento de la hipertensión intracraneal en el paciente con un traumatismo craneoencefálico grave. Propuesta y justificación de un protocolo / First tier therapeutic measures in the management of high intracranial pressure after severe head injury. Rationale and proposal for a protocol

El manejo de los traumatismos craneoencefálicos graves en general y de aquéllos que presentan una hipertensión intracraneal en particular, es uno de los desafíos más importantes en el manejo del paciente neurocrítico. Una de las principales dificultades con las que aún se enfrentan los clínicos es la de intentar reducir la variabilidad que todavía existe entre centros en la implementación de protocolos de tratamiento en estos pacientes. El objeto de este artículo es proponer un protocolo estandarizado para el manejo de la hipertensión intracraneal en los traumatismos craneoencefálicos graves (TCEG), que siga las directrices propuestas por las guías de práctica clínica recientemente publicadas y también otra evidencia clínica, como la aportada por las revisiones sistemáticas de la Colaboración Cochrane. A pesar de los avances significativos en la neuromonitorización que han permitido profundizar en la fisiopatología de los TCEG, y de las diversas opciones terapéuticas disponibles, aún no existen protocolos estandarizados para el tratamiento de estos pacientes. Aunque las guías de práctica clínica, recientemente publicadas, ofrecen recomendaciones generales, no aportan detalles explícitos sobre cómo y cuando aplicar estas recomendaciones terapéuticas. Como consecuencia, existe todavía una gran variabilidad en la práctica clínica diaria incluso entre aquellos centros que aplican las mismas medidas terapéuticas. En este artículo se propone un protocolo estructurado, en el que cada paso se justifica e integra dentro de una estrategia global para el manejo de los traumatismos craneoencefálicos graves. Se discuten los datos disponibles más recientes, procedentes de ensayos clínicos controlados tanto preliminares como definitivos, así como de otras fuentes. El principal objetivo de este artículo es dotar a las unidades de neurocríticos de un protocolo unificado que pueda ser fácilmente modificado a medida que se disponga de nueva información basada en evi dencia clase I o II. Esto permite reducir la variabilidad que existe entre centros que aplican las mismas medidas terapéuticas. Por otra parte, este protocolo puede facilitar la comparación de los resultados neurológicos entre diferentes hospitales haciendo más fácil a su vez la implantación de una práctica clínica más uniforme en aquellos centros implicados en estudios clínicos multicéntricos. (AU)

[The use of moderate hypothermia in the treatment of patients with severe craniocerebral trauma]. / Reflexiones sobre el uso de la hipotermia moderada en el tratamiento del paciente con un traumatismo craneoencefálico grave.

Traumatic brain injury initiates several metabolic processes that can increase the primary injury. It is well established that in severe head injuries, posttraumatic secondary insults, such as brain hypoxia, hypotension or anemia, exacerbate neuronal injury and lead to a poorer outcome. Experimental and clinical evidence suggests that moderate hypothermia (32-34 degrees C), may limit some of these deleterious secondary metabolic responses. Recent laboratory studies and prospective controlled clinical trials of induced moderate hypothermia for relatively short periods (24-48 h) in patients with severe head injury, have demonstrated good intracranial pressure control and better outcome when compared with patients maintained in normothermia and given conventional treatment. Despite its proven clinical role in neuroprotection, hypothermia research has been inconstantly followed for various reasons. In this paper we review the mechanisms of neuroprotection in hypothermia, the different preclinical and clinical studies that favor its use as a neuroprotector in severe head injury or in patients in whom high intracranial pressure is refractory to first tier measures. The evidence that favors hypothermia is discussed. We also discuss the negative results of the still unpublished multicentre trial on prophylactic moderate hypothermia developed in the USA. The main problem with moderate hypothermia is the lack of a systematic methodology to induce and maintain it. Also, optimal duration of its use and the methodology and timing for rewarming have not been determined. Consequently, the results of different trials are difficult to analyze and compare. However, most evidence suggests that hypothermia provides remarkable protection against the adverse effects of neuronal damage that is exacerbated by secondary injury. Further prospective controlled trials with clearly defined methodology are needed before this method is implemented in daily clinical practice. The most important task for the years to come may be to focus on refining this procedure, defining the optimal time of cooling and rewarming and to optimize the methods of rapidly inducing and maintaining low temperature. It is also essential to define the most appropriate method and velocity of the rewarming phase, in which many successfully controlled patients deteriorate and die.