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.

Meningitis bacteriémica por Streptococcus pyogenes, complicada con endoftalmitis bilateral / Bacteremic meningitis due to Streptococcus pyogenescomplicated by bilateral endophthalmitis

No disponible

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.

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.