Ten physiological commandments for severe head injury.

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

Diez mandamientos fisiológicos a lograr durante el traumatismo craneoencefálico grave / Ten physiological commandments for severe head injury

Los avances en la monitorización cerebral multiparamétrica han permitido ahondar en el conocimiento de la fisiopatología del traumatismo craneoencefálico, y en cómo la terapéutica disponible puede modularla. Para ello, se antoja imprescindible conocer e interpretar una serie de principios fisiológicos y fisiopatológicos básicos que propician, por un lado, un entorno metabólico cerebral adecuado para prevenir un incremento de la lesión cerebral primaria y favorecer su recuperación, y por otro lado, permiten adaptar de forma individualizada los recursos terapéuticos a la situación concreta del paciente. En el presente artículo se exponen, en forma de decálogo, sustentados en dichas nociones, los objetivos fisiológicos a conseguir, junto con una serie de recomendaciones diagnósticas y terapéuticas que posibiliten su logro. Se hace énfasis en la consideración y análisis de las variables fisiológicas implicadas en el transporte de oxígeno al cerebro, como el gasto cardiaco y el contenido arterial de oxígeno, junto con sus condicionantes y las posibles alteraciones de cada uno de ellos. Cobran especial atención los elementos básicos que constituyen la neuroprotección fisiológica. Asimismo, se razonan las múltiples causas que provocan hipoxia cerebral y el modo de abordarlas y corregirlas. El aumento de la presión intracraneal, como elemento fisiopatológico, se examina, subrayándose para interpretarla la interconexión e influencia de la presión torácica y abdominal sobre la intracraneal. El tratamiento de la presión intracraneal debe efectuarse sobre un modelo de acciones escalonadas, cuyo inicio debería cimentarse más que en valores numéricos rígidos, en una reflexión fisiopatológica unida a la información de las lesiones tomográficas.(AU)

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

Ten physiological commandments for severe head injury. / Diez mandamientos fisiológicos a lograr durante el traumatismo craneoencefálico grave.

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

Hiperactividad simpática paroxística: una entidad que no debería pasar desapercibida / Paroxysmal sympathetic hyperactivity: An entity to keep in mind

La hiperactividad simpática paroxística es una urgencia neurológica potencialmente letal secundaria a múltiples lesiones cerebrales agudas adquiridas. Se caracteriza por rasgos clínicos de aparición cíclica y simultánea, consecuencia de una descarga simpática exacerbada. El diagnóstico es clínico, requiriendo elevados índices de alerta. Actualmente no existen criterios diagnósticos homogéneos que estén ampliamente difundidos y validados. El consenso reciente intenta arrojar luz sobre este oscuro panorama. Su fisiopatología es compleja y aún no ha sido elucidada con certeza; sin embargo, la teoría basada en el modelo excitación-inhibición es la que mejor explica los distintos aspectos de esta entidad, incluyendo la respuesta a la terapia con los fármacos disponibles. Los pilares terapéuticos se asientan sobre el reconocimiento precoz, evitar insultos secundarios y el desencadenamiento de los paroxismos. De ocurrir crisis simpáticas, es que estas se aborten de forma perentoria y que se prevengan. Cuanto más tarde en reconocerse el síndrome, peores serán los resultados

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

Paroxysmal sympathetic hyperactivity: An entity to keep in mind. / Hiperactividad simpática paroxística: una entidad que no debería pasar desapercibida.

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

Serum gelsolin levels in aneurismal subarachnoid hemorrhage: Preliminary results / Niveles séricos de gelsolina en pacientes con hemorragia subaracnoidea de origen aneurismático: resultados preliminaries

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Urotensinergic system genes in experimental subarachnoid hemorrhage / El sistema urotensinérgico en un modelo experimental de hemorragia subaracnoidea

Objective: Cerebral vasospasm, one of the main complications of subarachnoid hemorrhage (SAH), is characterized by arterial constriction and mainly occurs from day 4 until the second week after the event. Urotensin-II (U-II) has been described as the most potent vasoconstrictor peptide in mammals. An analysis is made of the serum U-II concentrations and mRNA expression levels of U-II, urotensin related peptide (URP) and urotensin receptor (UT) genes in an experimental murine model of SAH. Design: An experimental study was carried out. Setting: Experimental operating room of the Biomedicine Institute of Seville (IBiS), Virgen del Rocío University Hospital (Seville, Spain). Participants: 96 Wistar rats: 74 SAH and 22 sham intervention animals. Interventions: Day 1: blood sampling, followed by the percutaneous injection of 100μl saline (sham) or blood (SAH) into the subarachnoid space. Day 5: blood sampling, followed by sacrifice of the animals. Main variables of interest: Weight, early mortality, serum U-II levels, mRNA values for U-II, URP and UT. Results: Serum U-II levels increased in the SAH group from day 1 (0.62pg/mL [IQR 0.36-1.08]) today 5 (0.74pg/mL [IQR 0.39-1.43]) (p<0.05), though not in the sham group (0.56pg/mL [IQR 0.06-0.83] day 1; 0.37pg/mL [IQR 0.23-0.62] day 5; p=0.959). Between-group differences were found on day 5 (p<0.05). The ROC analysis showed that the day 5 serum U-II levels (AUC=0.691), URP mRNA (AUC=0.706) and UT mRNA (AUC=0.713) could discriminate between sham and SAH rats. The normal serum U-II concentration range in rats was 0.56pg/mL (IQR 0.06-0.83). Conclusion: The urotensinergic system is upregulated on day 5 in an experimental model of SAH (AU)

Objetivo: El vasoespasmo cerebral, una de las principales complicaciones secundarias a hemorragia subaracnoidea (HSA), se caracteriza por una constricción arterial que tiene lugar principalmente entre el día 4 y la segunda semana. La urotensina-II (U-II) ha sido definida como el péptido con mayor capacidad vasoconstrictora en mamíferos. Quisimos analizar los niveles séricos de U-II, así como los niveles de expresión de los genes de U-II, péptido relacionado con urotensina y receptor de urotensina, en un modelo murino experimental de HSA. Diseño: Estudio experimental. Ámbito: Quirófano experimental del Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocío. Participantes: Noventa y seis ratas Wistar: 74 con inyección percutánea de sangre (HSA), 22 con inyección percutánea de 100μL de salino (Sham). Intervenciones: Día 1: extracción de muestras de sangre. Posteriormente, inyección percutánea de 100μL de salino (Sham) o de sangre (HSA) en el espacio subaracnoideo. Día 5: extracción de muestras de sangre y sacrificio del animal. Principales variables de interés: Peso, mortalidad precoz, niveles séricos de U-II, valores de ARNm de U-II, péptido relacionado con urotensina y receptor de urotensina. Resultados: Observamos un incremento en los niveles de U-II sérica en el grupo HSA desde el día 1 (0,62pg/mL [RI 0,36-1,08]) al día 5 (0,74pg/mL [RI 0,39-1,43]) (p<0,05); pero no observamos tal diferencia en el grupo Sham (0,56pg/mL [RI 0,06-0,83] día 1; 0,37pg/mL [RI 0,23-0,62] día 5) (p=0,959). Se encontraron diferencias en los niveles de U-II entre ambos grupos al quinto día (p<0,05). El análisis de curvas ROC demostró que la U-II sérica al quinto día (AUC=0,691), ARNm de péptido relacionado con urotensina (AUC=0,706) y ARNm de receptor de urotensina (AUC=0,713) podían discriminar entre ratas Sham y HSA. Además, definimos un rango de normalidad para los niveles de U-II séricos en ratas: 0,56pg/mL (RI 0,06-0,83). Conclusión: Este estudio demuestra por primera vez que el sistema urotensinérgico ve incrementada su expresión en el quinto día en un modelo de HSA (AU)

Craniectomía descompresiva secundaria para el manejo de la hipertensión endocraneanal refractaria en el traumatismo craneoencefálico grave. Luces y sombras de los estudios recientes / Secondary decompressive craniectomy for the management of refractory endocraneal hypertension in severe traumatic brain injury. Lights and shadows from recent studies

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Sedación cooperativa: opción para el manejo de la agitación en el traumatismo craneoencefálico moderado / Cooperative sedation: An option for the management of agitation in moderate traumatic brain injury

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Urotensinergic system genes in experimental subarachnoid hemorrhage.

OBJECTIVE: Cerebral vasospasm, one of the main complications of subarachnoid hemorrhage (SAH), is characterized by arterial constriction and mainly occurs from day 4 until the second week after the event. Urotensin-II (U-II) has been described as the most potent vasoconstrictor peptide in mammals. An analysis is made of the serum U-II concentrations and mRNA expression levels of U-II, urotensin related peptide (URP) and urotensin receptor (UT) genes in an experimental murine model of SAH. DESIGN: An experimental study was carried out. SETTING: Experimental operating room of the Biomedicine Institute of Seville (IBiS), Virgen del Rocío University Hospital (Seville, Spain). PARTICIPANTS: 96 Wistar rats: 74 SAH and 22 sham intervention animals. INTERVENTIONS: Day 1: blood sampling, followed by the percutaneous injection of 100µl saline (sham) or blood (SAH) into the subarachnoid space. Day 5: blood sampling, followed by sacrifice of the animals. MAIN VARIABLES OF INTEREST: Weight, early mortality, serum U-II levels, mRNA values for U-II, URP and UT. RESULTS: Serum U-II levels increased in the SAH group from day 1 (0.62pg/mL [IQR 0.36-1.08]) to day 5 (0.74pg/mL [IQR 0.39-1.43]) (p<0.05), though not in the sham group (0.56pg/mL [IQR 0.06-0.83] day 1; 0.37pg/mL [IQR 0.23-0.62] day 5; p=0.959). Between-group differences were found on day 5 (p<0.05). The ROC analysis showed that the day 5 serum U-II levels (AUC=0.691), URP mRNA (AUC=0.706) and UT mRNA (AUC=0.713) could discriminate between sham and SAH rats. The normal serum U-II concentration range in rats was 0.56pg/mL (IQR 0.06-0.83). CONCLUSION: The urotensinergic system is upregulated on day 5 in an experimental model of SAH.