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.

Metabolismo y terapia nutricional en el paciente quemado crítico: una revisión actualizada / Update on metabolism and nutrition therapy in critically ill burn patients

La quemadura grave induce estrés oxidativo severo, respuesta inflamatoria sistémica, hipermetabolismo e hipercatabolismo severo y persistente con sarcopenia secundaria, disfunción orgánica, sepsis y mayor mortalidad. El déficit energético, el balance negativo de proteínas y la deficiencia de micronutrientes antioxidantes durante la agresión térmica están asociados a malos resultados clínicos. En este contexto, una terapia nutricional personalizada, priorizando la nutrición enteral precoz, está indicada desde el inicio de la fase de resucitación. En las últimas 4 décadas se han estudiado diferentes intervenciones nutricionales y farmacológicas moduladoras de la respuesta inmune y metabólica. Dichas estrategias han demostrado ser capaces de minimizar la malnutrición aguda, modular la respuesta inmunoinflamatoria y mejorar los resultados clínicos. El propósito del presente estudio de revisión es analizar la evidencia más reciente sobre la respuesta metabólica y la terapia nutricional en el paciente quemado crítico

Major burn injury triggers severe oxidative stress, a systemic inflammatory response, and a persistent hypermetabolic and hypercatabolic state with secondary sarcopenia, multiorgan dysfunction, sepsis and an increased mortality risk. Calorie deficit, negative protein balance and antioxidant micronutrient deficiency after thermal injury have been associated to poor clinical outcomes. In this context, personalized nutrition therapy with early enteral feeding from the start of resuscitation are indicated. Over the last four decades, different nutritional and pharmacological interventions aimed at modulating the immune and metabolic responses have been evaluated. These strategies have been shown to be able to minimize acute malnutrition, as well as modulate the immunoinflammatory response, and improve relevant clinical outcomes in this patient population. The purpose of this updating review is to summarize the most current evidence on metabolic response and nutrition therapy in critically ill burn patients

Update on metabolism and nutrition therapy in critically ill burn patients. / Metabolismo y terapia nutricional en el paciente quemado crítico: una revisión actualizada.

Major burn injury triggers severe oxidative stress, a systemic inflammatory response, and a persistent hypermetabolic and hypercatabolic state with secondary sarcopenia, multiorgan dysfunction, sepsis and an increased mortality risk. Calorie deficit, negative protein balance and antioxidant micronutrient deficiency after thermal injury have been associated to poor clinical outcomes. In this context, personalized nutrition therapy with early enteral feeding from the start of resuscitation are indicated. Over the last four decades, different nutritional and pharmacological interventions aimed at modulating the immune and metabolic responses have been evaluated. These strategies have been shown to be able to minimize acute malnutrition, as well as modulate the immunoinflammatory response, and improve relevant clinical outcomes in this patient population. The purpose of this updating review is to summarize the most current evidence on metabolic response and nutrition therapy in critically ill burn patients.

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

Emulsiones lipídicas con aceite de pescado en el paciente crítico: análisis crítico y perspectivas futuras / Fish oil containing lipid emulsions in critically ill patients: Critical analysis and future perspectives

Las emulsiones lipídicas (EL) de tercera generación son una estrategia para disminuir el aporte de ácidos grasos de la serie omega-6 que presentan un efecto antiinflamatorio e inmunomodulador. En la actualidad la evidencia que sustenta el uso de las EL ricas en aceite de pescado (AP) en pacientes críticos que requieren nutrición parenteral o que reciben nutrición enteral (estrategia farmacológica) deriva mayormente de pequeños ensayos clínicos fase II. En los últimos 3 años han sido publicados diferentes revisiones sistemáticas y metaanálisis explorando los efectos clínicos de estas emulsiones. Recientemente, ha sido demostrado que estas EL podrían ser capaces de disminuir significativamente la incidencia de complicaciones infecciosas, así como los tiempos de ventilación mecánica y estancia hospitalaria. Sin embargo, se requiere de evidencia más robusta antes de una recomendación definitiva. Creemos que un estudio dosis respuesta es necesario antes de la realización de nuevos ensayos clínicos fase III comparando el uso de estas emulsiones ricas en AP contra EL ricas en soja en pacientes críticos (AU)

Third-generation lipid emulsions (LE) are soybean oil sparing strategies with immunomodulatory and antiinflammatory effects. Current evidence supporting the use of intravenous (i.v) fish oil (FO) LE in critically ill patients requiring parenteral nutrition or receiving enteral nutrition (pharmaconutrient strategy) mainly derives from small phase II clinical trials in heterogenous intensive care unit patient's population. Over the last three years, there have been published different systematic reviews and meta-analyses evaluating the effects of FO containing LE in the critically ill. Recently, it has been demonstrated that i.v FO based LE may be able to significantly reduce the incidence of infections as well as mechanical ventilation days and hospital length of stay. Nonetheless, more robust evidence is required before giving a definitive recommendation. Finally, we strongly believe that a dosing study is required before new phase III clinical trials comparing i.v FO containing emulsions versus other soybean oil strategies can be conducted (AU)

[Fish oil containing lipid emulsions in critically ill patients: Critical analysis and future perspectives]. / Emulsiones lipídicas con aceite de pescado en el paciente crítico: análisis crítico y perspectivas futuras.

Third-generation lipid emulsions (LE) are soybean oil sparing strategies with immunomodulatory and antiinflammatory effects. Current evidence supporting the use of intravenous (i.v) fish oil (FO) LE in critically ill patients requiring parenteral nutrition or receiving enteral nutrition (pharmaconutrient strategy) mainly derives from small phase ii clinical trials in heterogenous intensive care unit patient's population. Over the last three years, there have been published different systematic reviews and meta-analyses evaluating the effects of FO containing LE in the critically ill. Recently, it has been demonstrated that i.v FO based LE may be able to significantly reduce the incidence of infections as well as mechanical ventilation days and hospital length of stay. Nonetheless, more robust evidence is required before giving a definitive recommendation. Finally, we strongly believe that a dosing study is required before new phase iii clinical trials comparing i.v FO containing emulsions versus other soybean oil strategies can be conducted.

[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.

Farmaconutrición parenteral con selenio en la sepsis / Pharmaconutrition with parenteral selenium in sepsis

La enfermedad crítica se caracteriza por estrés oxidativo, el cual conduce a una disfunción orgánica múltiple, siendo dicha disfunción secundaria a sepsis la causa más frecuente de mortalidad en la unidad de cuidados intensivos. Durante las últimas 2 décadas, se ha acumulado una evidencia creciente a favor del uso de los micronutrientes antioxidantes en los pacientes críticos. De acuerdo con la evidencia reciente, la terapéutica con selenio puede ser considerada como la piedra angular dentro de las estrategias antioxidantes en la sepsis. El selenio, administrado como selenito de sodio o ácido selenioso, se comporta como un fármaco o nutrofármaco con efecto citotóxico y prooxidante cuando una dosis de carga en forma de bolo intravenoso es administrada en la fase precoz de la sepsis grave y el shock séptico. Hasta el momento, diversos estudios fase ii sobre suplementación de selenio han demostrado que esta estrategia es capaz de disminuir la mortalidad, la severidad de la disfunción orgánica y las infecciones. En el futuro próximo, nuevos estudios fase iii deberán confirmar los efectos de la farmaconutrición parenteral con selenio en la sepsis. En la presente revisión se discute la evidencia actual sobre la farmaconutrición con selenio en la sepsis

Critical illness is characterized by oxidative stress which leads to multiple organ failure, and sepsis-related organ dysfunction remains the most common cause of death in the intensive care unit. Over the last 2 decades, different antioxidant therapies have been developed o improve outcomes in septic patients. According to recent evidence, selenium therapy should be considered the cornerstone of the antioxidant strategies. Selenium given as selenious acid or sodium selenite should be considered as a drug or pharmaconutrient with prooxidant and cytotoxic effects when a loading dose in intravenous bolus form is administered, particularly in the early stage of severe sepsis/septic shock. To date, several phaseiitrials have demonstrated that selenium therapy may be able to decrease mortality, improve organ dysfunction and reduceinfections in critically ill septic patients. The effect of selenium therapy in sepsis syndrome must be confirmed by large, well designed phaseiiiclinical trials. The purpose of this review is to discuss current evidence on selenium pharmaconutrition in sepsis síndrome

[Pharmaconutrition with parenteral selenium in sepsis]. / Farmaconutrición parenteral con selenio en la sepsis.

Critical illness is characterized by oxidative stress which leads to multiple organ failure, and sepsis-related organ dysfunction remains the most common cause of death in the intensive care unit. Over the last 2 decades, different antioxidant therapies have been developed to improve outcomes in septic patients. According to recent evidence, selenium therapy should be considered the cornerstone of the antioxidant strategies. Selenium given as selenious acid or sodium selenite should be considered as a drug or pharmaconutrient with prooxidant and cytotoxic effects when a loading dose in intravenous bolus form is administered, particularly in the early stage of severe sepsis/septic shock. To date, several phase ii trials have demonstrated that selenium therapy may be able to decrease mortality, improve organ dysfunction and reduce infections in critically ill septic patients. The effect of selenium therapy in sepsis syndrome must be confirmed by large, well designed phase iii clinical trials. The purpose of this review is to discuss current evidence on selenium pharmaconutrition in sepsis syndrome.

Síndrome de lisis tumoral en terapia intensiva: encare diagnóstico y terapéutico / Tumor lysis syndrome in intensive therapy: diagnostic and therapeutic encare

El síndrome de lisis tumoral (SLT) es una complicación potencialmente letal provocada por la liberación masiva de ácidos nucleicos, potasio y fosfato hacia la circulación sistémica. Este cuadro es el resultado de la lisis celular de neoplasias, con frecuencia hematológicas, las cuales se caracterizan por una rápida capacidad de proliferación y alta sensibilidad a fármacos. Por otra parte, el SLT se puede observar por muerte celular espontánea previo al inicio del tratamiento citoreductor, agravándose luego de iniciada la quimioterapia. El SLT presenta una alta mortalidad, por lo que su prevención continúa siendo la medida terapéutica más importante. En la unidad de cuidados intensivos los médicos deben conocer su cuadro clínico, el cual se caracteriza por la existencia de graves trastornos del metabolismo hidroelectrolítico, en particular hiperpotasemia, hiperfosfatemia e hipocalcemia y por la aparición de una lesión renal aguda. Una adecuada intervención terapéutica implica la rápida admisión a unidad de cuidados intensivos, hidratación intravenosa y aporte de la enzima urato-oxidasa como las medidas más importantes. El objetivo de la presente revisión es proporcionar herramientas diagnósticas y terapéuticas que le permiten al médico intensivista reconocer la población en riesgo de desarrollar este síndrome, así como establecer una adecuada estrategia terapéutica y profiláctica (AU)

The tumor lysis syndrome (TLS) is a life-threatening complication caused by the massiverelease of nucleic acids, potassium and phosphate into the blood. This complication is theresult of tumor cell lysis, which may occur due to treatment of drug sensitive and is characterizedby rapid capacity of proliferation, that is often hematological origin. Moreover, the TLScan be observed before starting the treatment due to spontaneous tumor cell death, and frequentlyworsens when chemotherapy is initiated. TLS has high mortality, so that its prevention continues to be the most important therapeutic measure. In the intensive care unit (ICU), physicians should be aware of the clinical characteristics of TLS, which results in severe electrolytemetabolism disorders, especially hyperkalemia, hyperphosphatemia and hypocalcemia,and acute kidney injury which is a major cause of ICU mortality. An adequate strategy for themanagement of the TLS, combining hydration, urate oxidase, and an early admission to ICU can control this complication in most patients. The aim of this review is to provide diagnostic toolsthat allow to the ICU physician to recognize the population at high risk for developing the TLS,and outline a proper strategy for treating and preventing this serious complication (AU)

[Tumor lysis syndrome in intensive therapy: diagnostic and therapeutic encare]. / Síndrome de lisis tumoral en terapia intensiva: encare diagnóstico y terapéutico.

The tumor lysis syndrome (TLS) is a life-threatening complication caused by the massive release of nucleic acids, potassium and phosphate into the blood. This complication is the result of tumor cell lysis, which may occur due to treatment of drug sensitive and is characterized by rapid capacity of proliferation, that is often hematological origin. Moreover, the TLS can be observed before starting the treatment due to spontaneous tumor cell death, and frequently worsens when chemotherapy is initiated. TLS has high mortality, so that its prevention continues to be the most important therapeutic measure. In the intensive care unit (ICU), physicians should be aware of the clinical characteristics of TLS, which results in severe electrolyte metabolism disorders, especially hyperkalemia, hyperphosphatemia and hypocalcemia, and acute kidney injury which is a major cause of ICU mortality. An adequate strategy for the management of the TLS, combining hydration, urate oxidase, and an early admission to ICU can control this complication in most patients. The aim of this review is to provide diagnostic tools that allow to the ICU physician to recognize the population at high risk for developing the TLS, and outline a proper strategy for treating and preventing this serious complication.

Encefalopatía hiponatrémica y muerte cerebral en la intoxicación por éxtasis (3, 4-metilendioximetanfetamina) / Hyponatremic encephalopathy and brain death in Ecstasy (3, 4-methylenedioxymethamphetamine) intoxication

No disponible

Hiperglucemia de estrés y su control con insulina en el paciente crítico: evidencia actual / Stress hyperglycemia and its control with insulin in critically ill patients. Current evidence

Objetivo: Analizar la evidencia actual sobre el control de la glucemia con insulina en el paciente crítico. La hiperglucemia de estrés incrementa la morbimortalidad en el paciente crítico y se ha reconocido a la variabilidad de la glucemia como un predictor independiente de mortalidad. Inicialmente, los estudios Leuven han demostrado que el control estricto de la glucemia es capaz de reducir la mortalidad en pacientes críticos médicos y quirúrgicos. Sin embargo, esta estrategia terapéutica incrementa de modo significativo la incidencia de hipoglucemia grave. Recientemente, se han publicado los estudios Efficacy of Volume Substitution and Insulin Therapy in Severe Sepsis, GluControl y Normoglycemia in Intensive Care Evaluation and Survival Using Glucose Algorithm Regulation, los que han demostrado que el control estricto de la glucemia incrementa la mortalidad y la incidencia de hipoglucemia grave. Asimismo, un reciente metaanálisis indica que el control estricto de la glucemia podría ser beneficioso en pacientes críticos quirúrgicos. Futuras investigaciones deberían ser capaces de responder algunos interrogantes importantes surgidos a partir de los diferentes estudios existentes (AU)

Objective: To analyze the current evidence on glycemic control with insulin therapy in the critically ill. Recent findings: Stress hyperglycemia in critically ill patients has been associated with increased morbidity and mortality. Furthermore, current evidence suggests that glucose variability has a predictive value for hospital mortality. Initially, the Leuven studies showed that intensive insulin therapy was capable of reducing the mortality among surgical and medical ICU patients. Nevertheless, this strategy significantly increases the incidence of severe hypoglycemia. Three important trials on glucose control have been published recently: the VISEP, the Glucontrol study and the NICE-SUGAR. They have shown that strict control of glycemia is associated with a higher incidence of mortality and severe hypoglycemia. Furthermore, according to a recent meta-analysis, intensive insulin therapy may be beneficial for patients admitted to a surgical ICU. Further studies should be able to address some queries about these results on glycemic control in the critically ill (AU)

[Stress hyperglycemia and its control with insulin in critically ill patients: current evidence]. / Hiperglucemia de estrés y su control con insulina en el paciente crítico: evidencia actual.

OBJECTIVE: To analyze the current evidence on glycemic control with insulin therapy in the critically ill. RECENT FINDINGS: Stress hyperglycemia in critically ill patients has been associated with increased morbidity and mortality. Furthermore, current evidence suggests that glucose variability has a predictive value for hospital mortality. Initially, the Leuven studies showed that intensive insulin therapy was capable of reducing the mortality among surgical and medical ICU patients. Nevertheless, this strategy significantly increases the incidence of severe hypoglycemia. Three important trials on glucose control have been published recently: the VISEP, the Glucontrol study and the NICE-SUGAR. They have shown that strict control of glycemia is associated with a higher incidence of mortality and severe hypoglycemia. Furthermore, according to a recent meta-analysis, intensive insulin therapy may be beneficial for patients admitted to a surgical ICU. Further studies should be able to address some queries about these results on glycemic control in the critically ill.

[Selenium supplementation in critically ill patients: pharmacological issues and current evidence]. / Suplementación con selenio en el paciente crítico: aspectos farmacológicos y evidencia actual.

High dose intravenous selenium may be associated with a significant reduction in mortality among critically ill patients with systemic inflammation. Currently, parenteral selenium as sodium selenite seems to be a cornerstone of the antioxidant defence in the critically ill. So far, several clinical trials have evaluated the effects of selenium in monotherapy or as part of a multi-micronutrient approach, on relevant clinical end points for critically ill patients. Nonetheless, the results from these studies have sometimes been contradictory. We now have a better understanding of the pharmacokinetics of the initial and transient pro-oxidant effect of an intravenous bolus followed by the antioxidant effect of continuous infusion, which seems efficacious and safe among critically ill patients. Clinical confirmation of the potentially advantageous synergism between selenium and glutamine may soon be forthcoming but the most appropriate and the optimum time of supplementation remains undetermined. Short-term intravenous selenite (bolus injection plus continuous infusion) has shown to be safe and capable of optimizing serum selenium and antioxidant selenoenzymes activities. However, additional dose-ranging trials are necessary to elucidate an optimal and safe posology with confirmed pharmacokinetic profiles before more definitive phase III trials can be conducted.

Suplementación con selenio en el paciente crítico: aspectos farmacológicos y evidencia actual / Selenium supplementation in critically ill patients: Pharmacological issues and current evidence

Los antioxidantes y en particular el selenio parenteral parecen vincularse con una reducción significativa de la mortalidad en los pacientes críticos con Síndrome de Respuesta Inflamatoria Sistémica (SRIS). Actualmente, el selenio parenteral es considerado la piedra angular dentro de la estrategia de tratamiento antioxidante en los pacientes críticos. En los últimos años, diferentes estudios clínicos han evaluado el impacto clínico del uso de selenio intravenoso (selenito) aportado como monoterapia o asociado a otros micronutrientes antioxidantes ("cócteles antioxidantes"). Sin embargo, los resultados de estos estudios no han sido concluyentes. En la actualidad existe una mejor comprensión sobre la farmacocinética y farmacodinamia del selenio intravenoso, siendo reconocido el efecto pro-oxidante del bolo intravenoso inicial así como el efecto antioxidante de la infusión continua. Sin embargo, la dosis óptima y el tiempo de suplementación de selenio no han sido aun definidos planteándose la existencia de una posible sinergia entre selenio y glutamina parenteral. Esta revisión analiza la evidencia actual sobre la suplementación de selenio en pacientes críticos con SRIS. El uso de altas dosis de selenio por vía parenteral (bolo inicial e infusión continua) parece ser una estrategia segura y efectiva en optimizar los niveles séricos de selenio y la actividad de ciertas selenoenzimas antioxidantes tales como la Glutatión Peroxidasa y la Selenoproteína P. Sin embargo, son necesarios nuevos estudios sobre la posología y farmacocinética del selenio en pacientes críticos. Estas pesquisas deberían demostrar un beneficio definitivo del uso de selenio sobre end point clínicos de relevancia (AU)

High dose intravenous selenium may be associated with a significant reduction in mortality among critically ill patients with systemic inflammation. Currently, parenteral selenium as sodium selenite seems to be a cornerstone of the antioxidant defence in the critically ill. So far, several clinical trials have evaluated the effects of selenium in monotherapy or as part of a multi-micronutrient approach, on relevant clinical end points for critically ill patients. Nonetheless, the results from these studies have sometimes been contradictory. We now have a better understanding of the pharmacokinetics of the initial and transient pro-oxidant effect of an intravenous bolus followed by the antioxidant effect of continuous infusion, which seems efficacious and safe among critically ill patients. Clinical confirmation of the potentially advantageous synergism between selenium and glutamine may soon be forthcoming but the most appropriate and the optimum time of supplementation remains undetermined. Short-term intravenous selenite (bolus injection plus continuous infusion) has shown to be safe and capable of optimizing serum selenium and antioxidant selenoenzymes activities. However, additional dose-ranging trials are necessary to elucidate an optimal and safe posology with confirmed pharmacokinetic profiles before more definitive phase III trials can be conducted (AU)