From vasospasm to early brain injury: new frontiers in subarachnoid haemorrhage research.

INTRODUCTION: Delayed vasospasm has traditionally been considered the most important determinant of poor outcome after subarachnoid haemorrhage (SAH). Consequently, most of the research and therapies are directed towards reducing the incidence of vasospasm (VSP). To date, however, clinical trials based on this strategy have not delivered a definitive treatment for preventing or reducing brain injury after SAH. This fact has caused a paradigm shift in research, which now focuses on early brain injury (EBI) occurring in the first 72 hours after SAH. It has also changed the idea of VSP's role in brain damage, and suggests the need for re-evaluating the pathophysiological process of SAH. DEVELOPMENT: This review examines the current state of knowledge on the pathophysiological mechanisms associated with EBI and summarises the diagnostic options currently available. CONCLUSION: It seems that the research approach needs to be changed so that investigators will focus on prevention of EBI, reduction of secondary brain complications and ultimately, the optimisation neurological outcome.

[Systemic capillary leak syndrome: hypoalbuminemia, hemoconcentration and shock. Presentation of a case]. / Síndrome de fuga capilar sistémica: hipoalbuminemia, hemoconcentración y shock. A propósito de un caso.

Systemic capillary leak syndrome is a rare disorder of unknown etiology and often recurrent episodes characterized by increased capillary permeability that allows a leakage of fluid and proteins from the circulatory system to the interstitial space leading to shock and massive edema. The lack of recognition of this disease may be due to its unespecific signs and symptons of presentation, its rapid clinical progression and high mortality of the acute episodes. General physicians are usually the first to evaluate patients with this kind of disorder, either in the pre-hospital situation, hospital emergency units or even (in the milder cases) in the health centers. Its poor outcome and the improvement in the prognosis, if appropriate treatment is initiated, leads us to emphasize the importance of recognizing this pathology in order to start the appropriate intensive care and emergency treatment.

[Arreflexic coma and MELAS syndrome]. / Coma arrefléxico en el síndrome de MELAS.

MELAS is a progressive neurodegenerative and fatal disease characterized by mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes. It is the result of a mitochondrial DNA mutation. Although the incidence of MELAS is currently unknown, it is suspected that approximately 1 out of every 5,000 persons world-wide have some type of defect in mitochondrial DNA. Cardinal clinical features observed in more than 90% of the patients include severe headache that may be associated with stroke-like episodes, seizures and the onset of symptoms before the age of 40 years. Diagnosis is established through genetic test or by with muscle biopsies that reveal the presence of ragged-red fibers. Prognosis is poor, with death at an early age. In this article, we present the clinical case of a 31-year old women diagnosed of MELAS syndrome who was admitted to the Intensive Care Unit of our hospital with arreflexic coma.

Síndrome de fuga capilar sistémica: hipoalbuminemia, hemoconcentración y shock. A propósito de un caso / Systemic capillary leak syndromhypoalbuminemia, hemoconcentration and shock. Presentation of a case

El síndrome de fuga capilar es un trastorno insólito, de etiología desconocida y presentación recurrente caracterizado por un aumento de la permeabilidad capilar, lo que permite la fuga de fluidos y proteínas desde el sistema circulatorio al espacio intersticial dando lugar a shock y edema masivo. Lo inespecífico de sus síntomas y signos de presentación, su rápida progresión clínica y la elevada tasa de mortalidad de los episodios agudos pueden haber derivado en la falta de reconocimiento del mismo. Son los médicos de familia los que habitualmente evalúan en primera instancia a los pacientes que sufren este trastorno clínico, bien sea desde los dispositivos de urgencias y emergencias, las unidades de urgencia hospitalaria o incluso (en los casos más leves) en consulta ambulatoria. Es su condición de fatalidad y la mejora del pronóstico, si se inicia un tratamiento adecuado, la que nos lleva a subrayar la importancia de reconocer dicho cuadro con el fin de aplicar una terapia intensiva y juiciosa de emergencias (AU)

Systemic capillary leak syndrome is a rare disorder of unknown etiology and often recurrent episodes characterized by increased capillary permeability that allows a leakage of fluid and proteins from the circulatory system to the interstitial space leading to shock and massive edema. The lack of recognition of this disease may be due to its unespecific signs and symptons of presentation, its rapid clinical progression and high mortality of the acute episodes. General physicians are usually the first to evaluate patients with this kind of disorder, either in the pre-hospital situation, hospital emergency units or even (in the milder cases) in the health centers. Its poor outcome and the improvement in the prognosis, if appropriate treatment is initiated, leads us to emphasize the importance of recognizing this pathology in order to start the appropriate intensive care and emergency treatment (AU)

Del vasoespasmo a la lesión cerebral precoz: una nueva frontera en la investigación de la hemorragia subaracnoidea / From vasospasm to early brain injury: new frontiers in subarachnoid haemorrhage research

Introducción: El vasoespasmo (VSP) ha sido tradicionalmente considerado como el principal determinante de mal pronóstico tras sufrir una hemorragia subaracnoidea (HSA). Como consecuencia, la mayoría de las líneas de investigación y los tratamientos están dirigidos hacia la reducción de la incidencia de dicho VSP. Hasta la fecha, sin embargo, los resultados de los ensayos clínicos basados en esta estrategia no se han traducido en un tratamiento definitivo capaz de prevenir o mejorarla lesión cerebraltras unaHSA. Este hecho ha provocado un cambio de paradigma en el interés investigativo, focalizándolo hacia la lesión cerebral precoz (LCP), que se produce en las primeras 72 h tras la HSA. Así mismo, ha modificado la visión que se tenía de la responsabilidad del VSP sobre el dano˜ cerebral y sugiere la necesidad de una re-evaluación del proceso fisiopatológico de la HSA. Desarrollo: Esta revisión examina el estado actual del conocimiento de los mecanismos fisiopatológicos relacionados con la LCP y resume las opciones diagnósticas disponibles en la actualidad. Conclusión: Parece necesario cambiar la dirección en la investigación de esta enfermedad, centrándose en la prevención de la LCP, la reducción de las complicaciones cerebrales secundarias y en última instancia, la optitimización de los resultados neurológicos (AU)

Introduction: Delayed vasospasm has traditionally been considered the mostimportant determinant of poor outcome after subarachnoid haemorrhage (SAH). Consequently, most of the research and therapies are directed towards reducing the incidence of vasospasm (VSP). To date, however, clinical trials based on this strategy have not delivered a definitive treatment for preventing or reducing brain injury after SAH. This fact has caused a paradigm shift in research, which now focuses on early brain injury (EBI) occurring in the first 72hours after SAH. It has also changed the idea of VSP’s role in brain damage, and suggests the need for re-evaluating the pathophysiological process of SAH. Development: This review examines the current state of knowledge on the pathophysiological mechanisms associated with EBI and summarises the diagnostic options currently available. Conclusion: It seems that the research approach needs to be changed so that investigators will focus on prevention of EBI,reduction of secondary brain complications and ultimately,the optimisation neurological outcome (AU)

Coma arrefl éxico en el síndrome de MELAS / Arrefl exic coma and MELAS syndrome

El síndrome MELAS es un desorden neurodegenerativo progresivo caracterizado por miopatía mitocondrial (M), encefalopatía (E), acidosis láctica (LA) y episodios tipo stroke-like (S), originado por una mutación en el ADN mitocondrial. Aunque no existen datos reales sobre su incidencia, se cree que alrededor de una de cada 5.000 personas presenta algún tipo de alteración del ADN mitocondrial. Los síntomas más frecuentes en más del 90% de los casos son la cefalea intensa acompañada de crisis comiciales y un inicio de los síntomas antes de los 40 años de edad. El diagnóstico se establece mediante un test genético o biopsia muscular que revele la presencia de fibras rojo-rasgadas. Su pronóstico es muy malo, los pacientes fallecen a edad temprana. En el presente artículo presentamos el caso clínico de una mujer de 31 años diagnosticada de síndrome de MELAS que ingresó en la Unidad de Cuidados Intensivos de nuestro hospital en situación de coma arrefléxico (AU)

MELAS is a progressive neurodegenerative and fatal disease characterized by mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes. It is the result of a mitochondrial DNA mutation. Although the incidence of MELAS is currently unknown, it is suspected that approximately 1 out of every 5000 persons world-wide have some type of defect in mitochondrial DNA. Cardinal clinical features observed in more than 90% of the patients include severe headache that may be associated with stroke-like episodes, seizures and the onset of symptoms before the age of 40 years. Diagnosis is established through genetic test or by with muscle biopsies that reveal the presence of ragged-red fibers. Prognosis is poor, with death at an early age. In this article, we present the clinical case of a 31-year old women diagnosed of MELAS syndrome who was admitted to the Intensive Care Unit of our hospital with arreflexic coma (AU)