[Haemostatic activation in head injury]. / Activación hemostática en el traumatismo creoencefálico.

A relationship between Central Nervous System and coagulation has been known since the work by Goodnight et al5. When an encephalic injury occurs tissue damage causes the release of thromboplastin-related products, mainly the Tissular Factor. This release produces an activation of the coagulation system specially through its extrinsic path. With this physiopathologic basis we attempt to improve the knowledge of this relation by performing a prospective study at the Intensive Care Unit of our Hospital. The study included 67 patients with cranioencephalic trauma alone, with an average Glasgow coma scale score of 10 and a control group consisting of 40 healthy subjects. Two peripheral vein blood extractions were performed, at admission and 24 hours later. Global coagulation parameters (prothrombin time, activated partial thromboplastin time, platelet count and fibrinogen), hypercoagulability markers (prothrombin fragments F1+2 and thrombin-antithrombin complex (TAT)) and thrombolisis markers (D-dimer) were determined. Our results show that early after head trauma an increase in fragments F1+2, TAT and Ddimer occur. After the first 24 hours a significant decrease in hypercoagulability markers levels is detected. Modification of the global coagulation parameters was also detected. In conclusion, early after a cranioencephalic trauma a simultaneous state of hypercoagulability and thrombolysis occur which may have the purpose of improving the hemostatic balance.

Activación hemostática en el traumatismo craneoencefálico / Haemostatic activation in head injury

Desde los estudios de Goodnight et al'., se conoce la relación entre el sistema nervioso central y el sistema de la coagulación sanguínea. Cuando se produce una lesión a nivel del encéfalo, la destrucción tisular produce la liberación de sustancias tromboplastínicas, principalmente Factor Tisular. Esta liberación produce una activación de la coagulación principalmente por la vía extrínseca. Ante esta base fisiopatológica nos planteamos avanzar en el estudio de esta relación, para lo cual realizamos un estudio prospectivo en el Servicio de Medicina Intensiva del Hospital Clínico Universitario "Lozano Blesa" de Zaragoza. El estudio esta formado por 67 pacientes con traumatismo craneoencefálico aislado, con un Glasgow medio de 10 puntos y un grupo control formado por 40 personas sanas. Realizamos dos extracciones de vena periférica, al ingreso y a las 24 horas de evolución. Determinamos parámetros globales de la coagulación (tiempo de protrombina, tiempo de tromboplastina parcial activado, recuento de plaquetas y fibrinógeno), marcadores de hipercoagulabilidad (fragmentos de la protrombina F1+2 y complejo trombina antitrombina) y marcadores de fibrinolisis (D-dímeros).Nuestros resultados muestran que de forma precoz se produce un aumento en los niveles de fragmentos F1+2, TAT y D-dímeros tras producirse un traumatismo craneoencefálico. Una vez transcurridas las primeras 24 horas de evolución hay un descenso significativo de los marcadores de hipercoagulabilidad. También hemos detectado una alteración en los parámetros globales de la coagulación. Así de forma precoz tras un traumatismo craneoencefálico se produce un estado simultáneo de hipercoagulabilidad y fibrinolisis, que quizá intente conseguir un equilibrio hemostático (AU)

Caloric supply in parenteral nutrition in the stress phase.

Due to the metabolic alterations following surgery, glucose is not completely oxidized but is converted into glycogen and lipids. Therefore we analysed 2 groups of 15 patients following surgery. They received parenteral nutrition with identical nitrogen (N = 0.28 g/kg/d) and lipid (1.5 g/kg/d) intake, whereby only the composition of carbohydrates was varied. Group I received exclusively glucose = 0.22 g/kg/h, and group II the combination fructose-glucose-xylitol in a proportion of 2:1:1 at the same infusion rate. The study lasted approximately 10 days. We found decreased exogenous insulin requirements and an increase in the NEFA levels with a maximum on the 3rd and 4th day in group II. There were no significant differences in the levels of either albumin, prealbumin or retinol-binding protein, nor were any hepatic or renal alterations related to the xylitol infusion observed. Xylituria was 6.13 +/- 3% of the amount infused. In our opinion, the partial substitution of glucose in group II led to a better utilisation of the infused energy supply, and to less insulin stimulation, which facilitated the mobilization of endogenous energy sources such as fatty acids, although we did not succeed in increasing the protein synthesis.